Poisoning is a systemic disease caused by the entry of chemical substances into the human body at toxic levels, leading to damage to tissues and organs. The chemical substances responsible for poisoning are referred to as toxins. Based on the source and usage of these toxins, they can be categorized as follows:

Industrial toxins
Medications
Pesticides
Toxic plants and animals

The study of poisoning aims to understand the pathways through which toxins enter the body and the mechanisms by which they cause harm. Acquiring and applying this knowledge helps in guiding the prevention, diagnosis, and treatment of poisoning-related diseases.

Based on the toxicity, dosage, and duration of exposure, poisoning can generally be classified into two types: acute poisoning and chronic poisoning. Acute poisoning refers to large-dose exposure at one time or multiple exposures within 24 hours to one or more toxic substances, resulting in acute pathological changes. It typically presents with rapid onset, severe symptoms, and swift progression, potentially life-threatening if not treated promptly. Chronic poisoning refers to prolonged exposure where toxins accumulate in the body, leading to poisoning. This type develops slowly and has a long course, often lacking specific diagnostic markers, making misdiagnosis and missed diagnosis more likely.

Therefore, for suspected cases of chronic poisoning, it is essential to perform detailed medical history assessments, physical examinations, and relevant laboratory analyses of toxins. Chronic poisoning is often occupational in origin.

Causes and Mechanisms of Poisoning

Causes

Occupational Poisoning

Poisoning may occur during production processes due to exposure to toxic raw materials, intermediates, or finished products, especially when proper protective measures are not followed. Inadequate adherence to safety and protective protocols during storage, use, and transportation can also result in poisoning.

Non-occupational Poisoning

Non-occupational poisoning can occur due to accidental ingestion, unintended exposure to toxic substances, medication overdoses, intentional self-harm, or acts of poisoning aimed to harm others. A large amount of toxin entering the body under these circumstances can lead to poisoning.

Mechanisms of Poisoning

Toxin Absorption Pathways

Pathways for Toxin Entry

Toxins commonly enter the body through the gastrointestinal tract, respiratory tract, or skin and mucous membranes. The speed, intensity, and manifestations of the toxic effects depend on the route of entry and the absorption rate of the toxin.

Gastrointestinal Tract

This is a common route in non-occupational poisoning, such as that caused by toxic foods, organophosphorus insecticides (OPIs), and sedative-hypnotic drugs which are often ingested orally. Toxins are seldom absorbed through the mucous membranes of the mouth or esophagus. Compounds like OPIs and cyanides are minimally absorbed in the stomach but are primarily absorbed in the small intestine after being altered by intestinal fluids and enzymes. The toxins then enter the bloodstream, undergo detoxification in the liver, and are distributed to tissues and organs throughout the body.

Respiratory Tract

Due to the large surface area of the alveoli and the rich blood supply in pulmonary capillaries, toxins inhaled through the respiratory tract are absorbed into the bloodstream 20 times faster than those absorbed through the gastrointestinal tract. This results in rapid onset of poisoning symptoms and rapid disease progression. For example, cases of carbon monoxide poisoning are common in non-occupational settings, while occupational poisoning often involves toxins inhaled as dust, fumes, vapors, or gases.

Skin and Mucous Membranes

The surface of healthy skin has a lipid layer that can prevent the penetration of water-soluble toxins. However, certain fat-soluble toxins (e.g., benzene, aniline, nitrobenzene, ether, chloroform, or organophosphorus compounds) can be absorbed through the sebaceous glands and cause poisoning after skin contact. Toxins that damage the skin (e.g., arsenic compounds or mustard gas) can also be absorbed through the skin, resulting in poisoning. Factors such as sweating or skin injuries can accelerate toxin absorption. Some toxins may also be absorbed through the conjunctiva. In cases of snakebites, venom can enter the bloodstream through the wound, causing poisoning.

Toxin Metabolism

After entering the bloodstream, toxins bind to certain components in red blood cells or plasma and are distributed throughout body tissues and cells. Lipid-soluble, non-electrolyte toxins accumulate in fatty tissues and certain nervous tissues, while non-lipid-soluble, non-electrolyte toxins have limited ability to penetrate cell membranes. Electrolyte toxins (e.g., lead, mercury, manganese, arsenic, and fluoride) may exhibit uneven distribution within the body.

Most toxins undergo metabolism in the liver through oxidation, reduction, hydrolysis, or conjugation before interacting with chemicals in tissues and cells, resulting in decomposition or the synthesis of new compounds. For instance, ethanol is oxidized to carbon dioxide and water, ethylene glycol is oxidized to oxalic acid, and benzene is oxidized to phenol. In most cases, the toxicity of a substance is reduced after metabolism, constituting a detoxification process. However, in some cases, toxin metabolism can result in increased toxicity, such as the conversion of parathion into the more toxic paraoxon.

Toxin Excretion

Most toxins that enter the human body are excreted after undergoing metabolism. The excretion rate depends on the solubility of the toxin in tissues, its volatility, and the functional state of excretory and circulatory organs. The kidney is the main organ for detoxification, and water-soluble toxins are excreted more rapidly, with diuretics able to accelerate their elimination. Heavy metals and alkaloids are primarily excreted through the gastrointestinal tract. Toxins such as lead, mercury, and arsenic can also be excreted through breast milk, which may cause poisoning in breastfeeding infants. Volatile toxins (e.g., chloroform, ether, alcohol, and hydrogen sulfide) are expelled in their original form via the respiratory tract, with greater tidal volume enhancing the excretion process. Some fat-soluble toxins can be excreted through sebaceous and mammary glands, while a few toxins excreted via sweat can lead to dermatitis. Certain toxins accumulate in specific organs or tissues within the body and are excreted more slowly, with release potentially causing poisoning once again.

Mechanisms of Toxicity

Toxins vary widely in type, and the mechanisms through which they cause poisoning differ. These mechanisms primarily include the following:

Corrosive Effects

Strong acids or bases absorb water from tissues and combine with proteins or fats, leading to denaturation and necrosis of tissue cells at the contact site.

Hypoxia in Tissues and Organs

Toxins such as carbon monoxide, hydrogen sulfide, or cyanides interfere with oxygen absorption, transport, or utilization. The brain and myocardium, which are sensitive to hypoxia, are particularly prone to toxic damage.

Anesthetic Effects

Lipophilic toxins (e.g., organic solvents and inhaled anesthetics) readily cross the blood-brain barrier to enter brain tissue, suppressing its function.

Enzyme Inhibition

Certain toxins and their metabolites exert toxic effects by inhibiting enzyme activity. For example, organophosphorus insecticides (OPIs) inhibit cholinesterase (ChE), cyanides inhibit cytochrome oxidase, and toxins containing metal ions inhibit enzymes with thiol groups.

Disruption of Cellular or Organelle Function

In the body, carbon tetrachloride is metabolized by enzymes to form chloroform free radicals. These free radicals react with unsaturated fatty acids in hepatocyte membranes, triggering lipid peroxidation, compromising membrane integrity, causing lysosomal rupture, leading to mitochondrial and endoplasmic reticulum degeneration, and resulting in hepatocyte necrosis. Phenolic compounds such as dinitrophenol, pentachlorophenol, and gossypol can decouple oxidative phosphorylation in mitochondria, hindering the formation and storage of adenosine triphosphate (ATP).

Competition with Relevant Receptors

For example, excessive atropine can cause toxic effects by competitively blocking muscarinic receptors.

Factors Affecting Toxin Action

Properties of Toxins

The toxicity of a toxin is closely related to its chemical structure and physical-chemical properties. For instance, the smaller the aerosol particles of a toxic substance in the air, the more easily they are inhaled into the lungs, thereby increasing toxicity. Moreover, the route of toxin entry, dosage, and duration of exposure directly impact the effects of the toxin on the body.

State of the Body

Several factors, such as gender, age, nutritional and health status, living habits, and response to toxin toxicity, influence outcomes following poisoning. Even with the same toxin, prognosis may vary. For example, the nervous systems of infants and young children are more tolerant to hypoxia and thus exhibit some resistance to carbon monoxide poisoning, whereas elderly individuals exhibit the opposite. Malnutrition, extreme fatigue, and diseases involving vital organs (e.g., heart, lungs, liver, or kidneys) can reduce the body's ability to detoxify or eliminate toxins. Individuals with liver cirrhosis, for example, experience impaired liver function and lower glycogen levels, reducing their capacity to resist and detoxify toxins. Intake of toxins at levels below lethal doses can still prove fatal in such cases.

Interactions Between Toxins

The simultaneous ingestion of two or more toxins can result in additive or counteractive toxic effects. For example, carbon monoxide can enhance the toxicity of hydrogen sulfide, and alcohol can increase the toxicity of carbon tetrachloride or aniline. Conversely, certain substances, such as datura, may counteract the toxic effects of OPIs.

Clinical Manifestations

Acute Poisoning

The presentation of acute poisoning varies depending on the chemical substance involved. Severe poisoning often results in common signs such as cyanosis, coma, convulsions, respiratory distress, shock, and oliguria.

Manifestations in Skin and Mucous Membranes

Burns to Skin and Oral Mucosa

These are observed with corrosive toxins such as strong acids, strong bases, formaldehyde, phenol, cresol soap solutions, and paraquat. For example, nitric acid burns result in yellow scabs, hydrochloric acid burns produce brown scabs, and sulfuric acid burns cause black scabs on affected tissues.

Skin Color Changes

Cyanosis may occur due to poisoning by substances that reduce oxygenated hemoglobin levels in the blood. Poisoning caused by nitrites, aniline, or nitrobenzene results in increased levels of methemoglobin and cyanosis.

Skin redness is seen in carbon monoxide poisoning, where the skin and mucous membranes appear cherry red.

Jaundice can occur due to toxins like poisonous mushrooms, fish bile, or carbon tetrachloride that damage the liver.

Eye Manifestations

Pupil dilation can occur in poisoning by atropine or scopolamine.

Pupil constriction is noted in poisoning by OPIs or carbamate insecticides.

Optic neuritis can result from methanol poisoning.

Neurological Manifestations

Coma

This is associated with poisoning from hypnotics, sedatives, or anesthetics; organic solvents; asphyxiating toxins (such as carbon monoxide, hydrogen sulfide, and cyanides); methemoglobin-inducing toxins; and pesticides (such as organophosphorus insecticides (OPIs), pyrethroid insecticides, or methyl bromide).

Delirium

This is observed in cases of poisoning caused by atropine, ethanol, or antihistamines.

Muscle Tremors

These are identified in poisoning from OPIs, carbamate pesticides, acute isoniazid poisoning, acrylamide, or lead.

Convulsions

These occur in cases of poisoning by asphyxiating toxins, organochlorine or pyrethroid insecticides, tetramine (tetramethyl disulfotetramine, commonly known as "rat poison"), plants (such as poisonous mushrooms, datura, and bitter almonds), medications (such as isoniazid, theophyllines, and atropine), and heavy metals (such as lead and thallium).

Paralysis

This is detected in poisoning caused by snake venom, arsenic trioxide, soluble barium salts, or tri-ortho-cresyl phosphate.

Mental Disorders

These are linked to poisoning by carbon monoxide, carbon disulfide, alcohol, atropine, organic solvents, antihistamines, or withdrawal syndrome associated with drug dependence.

Respiratory System Manifestations

Characteristic Odors in Exhaled Breath

Ethanol poisoning produces an alcoholic smell; cyanide poisoning presents the smell of bitter almonds; poisoning by OPI, yellow phosphorus, dimethyl sulfoxide, thallium, or arsenic produces a garlic-like smell. Phenol or cresol soap solution poisoning results in a phenolic odor, nitrobenzene poisoning produces a smell resembling shoe polish, zinc or aluminum phosphide poisoning creates a fishy smell, and toluene or other solvents often produce a glue-like odor.

Increased Respiratory Rate

Respiratory stimulation occurs in cases of poisoning by salicylates or methanol, and exposure to irritant gases (such as nitrogen dioxide, hydrogen fluoride, hydrogen sulfide, hydrogen chloride, hydrogen bromide, phosphine, or sulfur dioxide) may lead to rapid breathing.

Decreased Respiratory Rate

Respiratory depression occurs due to central respiratory inhibition in cases of poisoning by hypnotics or morphine, resulting in slower breathing.

Pulmonary Edema

Poisoning induced by inhalation of irritant gases (such as phosgene, nitrogen dioxide, chlorine gas, ammonia, alkyl bromides, or acrolein), high concentrations of cadmium fumes or cadmium compound dust, or poisons like OPI and paraquat often causes pulmonary edema.

Cardiovascular System Manifestations

Cardiac Arrhythmias

Poisoning from substances like digitalis, oleander, or bufotoxin results in excitation of the vagus nerve. Poisoning by sympathomimetic drugs or tricyclic antidepressants leads to sympathetic nerve stimulation. The mechanisms of arrhythmias caused by theophylline poisoning are varied.

Cardiac Arrest

This is caused by:

Myocardial Toxicity: Associated with poisoning by substances such as digitalis, quinidine, antimonials, or emetine.
Hypoxia: Observed in poisoning caused by asphyxiating gases, including carbon monoxide, hydrogen sulfide, cyanides, or aniline.
Severe Hypokalemia: Resulting from poisoning by soluble barium salts, gossypol, or potassium-depleting diuretics.

Shock

Severe burns caused by strong acids or bases lead to plasma leakage; vomiting and diarrhea due to arsenic trioxide poisoning result in significant fluid loss; and inhibitory effects on vascular centers from anesthetic overdose or severe barbiturate poisoning cause peripheral vasodilation. These mechanisms may result in absolute or relative reductions in circulating blood volume and lead to shock.

Urinary System Manifestations

Acute kidney injury may occur following nephrotoxic poisoning. Tubular obstruction can result from hemolytic products caused by acute arsenic hydride poisoning. Renal ischemia or tubular necrosis may occur in cases of poisoning involving cephalosporins, aminoglycoside antibiotics, toxic mushrooms, or snake venom, leading to acute renal failure with reduced or absent urine output.

Hematological System Manifestations

Hemolytic anemia and jaundice may occur following poisoning by substances such as arsenic hydride, aniline, or nitrobenzene. Overdoses of salicylates, heparin, dicoumarol, warfarin, bromadiolone, or poisoning by substances like sodium fluoroacetate and snake venom may result in coagulation disorders and bleeding. Leukopenia may develop due to chloramphenicol, antineoplastic drugs, or benzene poisoning.

Fever

Fever has been observed in cases of poisoning by substances such as atropine, dinitrophenol, or gossypol.

Chronic Poisoning

Neurological Manifestations

Dementia is associated with chronic poisoning by substances such as tetraethyl lead or carbon monoxide; parkinsonism syndrome is linked to carbon monoxide, phenothiazines, or manganese poisoning; and peripheral neuropathy results from chronic poisoning by lead, arsenic, or OPIs.

Gastrointestinal System Manifestations

Toxic liver disease may develop following poisoning by arsenic, carbon tetrachloride, trinitrotoluene, or vinyl chloride.

Urinary System Manifestations

Toxic kidney damage may result from chronic poisoning by cadmium, mercury, or lead.

Hematological System Manifestations

Benzene or trinitrotoluene poisoning can cause leukopenia or aplastic anemia.

Skeletal System Manifestations

Fluorosis may occur due to chronic fluoride poisoning, while mandibular necrosis can result from yellow phosphorus poisoning.

Diagnosis

Poisoning diagnosis typically involves assessment based on exposure history, clinical manifestations, laboratory analysis of toxic substances, and investigation of the surrounding environment for the presence of toxins. The diagnosis is made after excluding other diseases with similar symptoms. In cases of acute poisoning, information is usually gathered from the patient’s colleagues, family members, caregivers, friends, or eyewitnesses. In cases of deliberate poisoning, the patient may be unable or unwilling to provide an accurate medical history. For chronic poisoning cases, neglecting the patient's history and investigating potential causes may easily lead to misdiagnosis or missed diagnosis. The diagnosis of occupational poisoning requires careful consideration.

Medical History

The medical history generally includes details about the timing of toxic exposure, the environment and route of poisoning, the name and dose of the toxic substance, initial treatment, and the individual’s past lifestyle and health status.

History of Toxic Exposure

For poisoning in daily life, such as suspected ingestion of toxic substances, details about the patient’s living conditions prior to the onset of symptoms, mental state, long-term medication use, any leftover drug containers or packages, and whether any household medications are missing are relevant to determining the timing and dosage of ingestion. For carbon monoxide poisoning, situations involving indoor stoves, chimneys, gas supplies, and other individuals in the same space may need to be assessed. Food poisoning often occurs in groups, but in sporadic cases, investigating whether individuals who consumed the same meal have similar symptoms is necessary. Regional outbreaks of poisoning may result from water or food contamination, calling for epidemiological investigations where required. For occupational poisoning, a detailed occupational history is essential, including job type, years of experience, type and duration of exposure to toxins, working conditions, protective measures, and whether similar incidents have occurred. In general, the circumstances at the site of poisoning and any evidence of toxic substance exposure should be clarified for any suspected case of poisoning.

Past Medical History

The patient’s health condition before onset, lifestyle habits, personal interests, emotional and behavioral changes, medication use, and financial situation are factors that should be reviewed. These aspects contribute to analyzing and identifying the possibility of poisoning.

Clinical Manifestations

Poisoning should be suspected in patients with sudden, unexplained symptoms such as coma, vomiting, convulsions, respiratory distress, or shock. Additionally, unexplained cyanosis, peripheral neuropathy, bleeding, anemia, leukopenia, thrombocytopenia, or liver damage may indicate poisoning.

Treatment

Principles of Treatment

These include:

Immediate termination of exposure to the toxic substance.
Emergency resuscitation and symptomatic supportive treatment.
Elimination of unabsorbed toxins from the body.
Administration of specific antidotes.
Prevention of complications.

Acute Poisoning Treatment

Termination of Ongoing Exposure to the Toxic Substance

Patients should be promptly removed from the site of poisoning and transferred to areas with fresh air. Contaminated clothing should be removed. Skin and hair should be washed with warm water or soap to remove toxins, while the affected eyes should be thoroughly rinsed with water to eliminate any toxins. Clearing of toxins from wounds should also be performed. Specific requirements for cleaning and removal based on particular toxic substances are outlined in Table 1.

Table 1 Specific cleaning requirements for toxic substances

Emergency Resuscitation and Symptomatic Supportive Treatment

The purpose of resuscitation and supportive treatment is to protect and restore the function of vital organs, enabling critically ill patients to navigate through life-threatening stages. For patients with acute poisoning and coma, measures should focus on maintaining airway patency and preserving respiratory and circulatory function, while monitoring consciousness, body temperature, pulse, respiration, and blood pressure. Patients with severe poisoning may develop conditions such as cardiac arrest, shock, circulatory failure, respiratory failure, renal failure, and disturbances in fluid-electrolyte or acid-base balance, where immediate and effective emergency resuscitation measures are necessary to stabilize vital signs. For cases with convulsions, anticonvulsant drugs such as phenobarbital, pentobarbital, or diazepam may be used. In cases of cerebral edema, mannitol or sorbitol combined with dexamethasone may be administered. Nutritional support through nasal feeding or parenteral methods may also be provided.

Removal of Unabsorbed Toxins from the Body

Early removal of toxins from the gastrointestinal tract in orally ingested poisoning cases can significantly improve the patient’s condition, with earlier and more thorough clearance being more effective.

Induction of Vomiting

Applicable in cases of accidental poisoning when gastric lavage cannot be performed. Vomiting induction may be considered for conscious and cooperative patients with oral poisoning. However, due to the risk of aspiration, delayed administration of activated charcoal, and complications such as esophageal tearing, gastric perforation, or bleeding, this method has become less commonly applied in clinical practice. It is contraindicated in patients who have ingested corrosive substances, who exhibit coma, convulsions, or shock, lack a gag reflex, have had recent gastrointestinal bleeding or esophagogastric varices, or in pregnant women.

Physical Methods of Stimulation

Vomiting can be triggered by stimulating the posterior pharyngeal wall or the base of the tongue using fingers, tongue depressors, or chopsticks. If the initial attempt is ineffective, warm water (200–300 ml) can be consumed, followed by repeated stimulation to induce vomiting. This process continues until clear gastric contents are expelled.

Drug-Induced Vomiting

This method is rarely used in clinical practice.

Derived from morphine, apomorphine is a semi-synthetic central emetic that has a strong dopaminergic receptor agonist effect. It acts directly on the medullary chemoreceptor zone, stimulating the vomiting center and inducing intense emesis. A dose of 2–5 mg is administered via subcutaneous injection, and vomiting typically occurs within 5–10 minutes. Drinking 200–300 ml of water prior to administration enhances the emetic effect. Apomorphine is contraindicated in cases of narcotic poisoning, severe cardiovascular diseases, or gastric and duodenal ulcers.

Ipecac syrup directly stimulates gastrointestinal mucosal receptors and has a reflexive effect on the vomiting center, resulting in emesis. A 30 ml dose is orally administered, followed by intake of 200 ml of water. Vomiting occurs within 20 minutes and persists for 30–120 minutes.

Gastric Lavage

Indications

Gastric lavage is suitable for poisoning cases within 1 hour of oral toxin ingestion. It can also be extended to 4–6 hours in cases of toxins that are slowly absorbed or when gastric motility is diminished. In cases of acute severe poisoning where no specific antidote is available, gastric lavage may still be considered even if more than 6 hours have passed since ingestion.

Contraindications

Gastric lavage is contraindicated in cases where corrosive toxins have been ingested, in patients with esophageal varices, or in those experiencing convulsions or coma.

Method of Gastric Lavage

During lavage, the patient's head is positioned slightly lower and turned to one side. A large-diameter gastric tube, lubricated with liquid paraffin, is inserted orally to a depth of approximately 50 cm. Successful placement in the stomach is confirmed by the extraction of gastric contents. If uncertain, air can be injected into the tube, and the presence of a "gurgling" sound in the gastric region confirms placement. Initial gastric contents are suctioned and preserved for toxicological analysis. Warm water at approximately 35°C is then repeatedly introduced into the stomach in 200–300 ml increments, ensuring fluid input-output balance, as excessive volumes may propel toxins into the intestines. Lavage is continued until clear fluid is retrieved. When removing the gastric tube, its distal end should be clamped to prevent reflux of liquids into the trachea.

Selection of Lavage Fluids

Warm water is most commonly used for gastric lavage. Specific lavage fluids may be employed based on the type of ingested toxin, as outlined below:

Solvents: For fat-soluble toxins (e.g., gasoline or kerosene), liquid paraffin (150–200 ml) can be used initially to dissolve and prevent absorption of the toxin before lavage.
Antidotes: Antidotes can neutralize, oxidize, or precipitate toxins, rendering them non-toxic.
Neutralizing Agents: Weak acids (e.g., vinegar or fruit juices) neutralize strong alkalis, while weak bases (e.g., milk of magnesia or aluminum hydroxide gel) neutralize strong acids. Sodium bicarbonate is avoided as it produces carbon dioxide gas in acidic environments, increasing the risk of perforation.
Precipitating Agents: Certain chemicals react with toxins to form substances with low solubility and reduced toxicity. Examples include calcium lactate or calcium gluconate reacting with fluorides or oxalates to produce insoluble calcium fluoride or calcium oxalate. Sodium sulfate (2–5%) reacts with soluble barium salts to form insoluble barium sulfate. Silver nitrate reacts with saline to produce insoluble silver chloride.
Oxidizing Agents: Potassium permanganate (1:5,000 solution) oxidizes alkaloids and toxins from mushrooms to detoxify them.
Gastric Mucosal Protectants: When corrosive toxins are ingested, gastric lavage is contraindicated, but mucosal protectants such as milk, egg whites, rice water, or vegetable oil can be used to protect the gastric lining.

Complications of Gastric Lavage

Potential complications include gastric perforation or bleeding, aspiration pneumonia, or asphyxia.

Activated Charcoal Adsorption

Activated charcoal is a powerful adsorbent capable of binding a wide range of toxins. However, certain substances, such as ethanol, strong acids, strong alkalis, potassium, iron, lithium, iodine, and cyanides, are poorly adsorbed by activated charcoal. Its effectiveness depends on timely administration, ideally within 1 hour of toxin ingestion. The adsorption process is saturation-dependent, requiring sufficient quantities of charcoal relative to the toxin. An initial dose of 1–2 g/kg is mixed with 200 ml of water and administered via a gastric tube. Repeat doses of 0.5–1.0 g/kg can be given every 2–4 hours until symptoms improve. For para-aminosalicylic acid poisoning, the ideal charcoal-to-toxin ratio is 10:1, with a recommended dose of 25–100 g. Common complications include vomiting, intestinal obstruction, and aspiration pneumonia.

Catharsis

Stand-alone use of cathartics to eliminate intestinal toxins in acute poisoning cases is not recommended. Lipid-based laxatives are avoided due to their potential to enhance absorption of fat-soluble toxins. Following gastric lavage or activated charcoal administration, cathartics may be introduced. Commonly used agents include mannitol, sorbitol, magnesium sulfate, sodium sulfate, and compound polyethylene glycol electrolyte powder. Magnesium sulfate is typically administered in a dose of 15 g, dissolved in water and delivered orally or via gastric tube. Excess magnesium absorption may suppress the central nervous system. Cathartics are contraindicated in patients with renal or respiratory failure, coma, or late-stage poisoning from substances like zinc phosphide or organophosphorus insecticides.

Enemas

Excluding cases involving corrosive toxins, enemas are applied for cases of oral poisoning that occurred more than 6 hours earlier, when cathartics are ineffective, and for toxins that inhibit intestinal peristalsis, such as barbiturates, atropine alkaloids, or opioids. A 1% warm soap solution is repeatedly used for enemas.

Whole Bowel Irrigation

Whole bowel irrigation reduces toxin absorption in the body by accelerating intestinal excretion. This method is utilized for poisoning involving heavy metals, sustained-release medications, enteric-coated drugs, or cases involving ingestion of concealed drugs within the gastrointestinal tract. Polyethylene glycol solutions, which are not absorbed by the body and do not disrupt fluid and electrolyte balance, are used for whole bowel irrigation.

Promotion of Elimination of Absorbed Toxins

Enhanced Diuresis and Modification of Urinary pH

Enhanced Diuresis

Enhancing urine output facilitates the excretion of toxins, particularly for toxins excreted directly by the kidney in their unchanged form. The method includes:

Rapid and high-volume intravenous infusion of 5%–10% glucose solution or 5% glucose-saline solution at a rate of 500–1,000 ml per hour.
Concurrent intravenous administration of furosemide (20–80 mg). This treatment is not recommended for individuals with cardiac, pulmonary, or renal dysfunction.

Modification of Urinary pH

Depending on the acid-base characteristics of the toxin, pH-modifying solutions are selected to promote excretion.

Alkalization of Urine: For poisoning by weak acidic toxins (e.g., barbiturates or salicylates), intravenous administration of sodium bicarbonate raises urine pH (≥8.0), enhancing toxin excretion.
Acidification of Urine: For poisoning by alkaline toxins (e.g., amphetamines, strychnine, or phencyclidine), intravenous administration of vitamin C (4–8 g/day) or ammonium chloride (2.75 mmol/kg, every 6 hours) lowers urine pH (<5.0), promoting toxin elimination.

Oxygen Therapy**

In cases of carbon monoxide poisoning, oxygen administration increases the dissociation of carboxyhemoglobin, thereby accelerating carbon monoxide elimination. Hyperbaric oxygen therapy is considered a specific treatment for carbon monoxide poisoning.

Blood Purification

Blood purification techniques are applied in cases of significantly elevated blood toxin levels, severe poisoning, prolonged unconsciousness, complications, or cases where the condition continues to deteriorate despite intensive supportive treatments.

Hemodialysis

This method removes toxins with low molecular weight and poor lipid solubility (e.g., barbiturates, salicylates, methanol, theophylline, ethylene glycol, and lithium) from the bloodstream. Short-acting barbiturates, glutethimide, and organophosphorus insecticides are typically not suitable for hemodialysis due to their lipid solubility. Poisoning from chlorates or dichromates, causing acute renal failure, often necessitates hemodialysis as the preferred method. Hemodialysis performed within 12 hours of poisoning yields optimal results, whereas delayed treatment may render toxins bound to plasma proteins less amenable to dialysis.

Hemoperfusion

Hemoperfusion involves passing blood through a column containing activated charcoal or resin to adsorb toxins before returning the blood to the patient. This method is effective for lipid-soluble toxins or those bound to proteins, allowing for the removal of barbiturates and paraquat, among others. Hemoperfusion is one of the most commonly used interventions for managing poisoning. However, this process can adsorb normal blood components such as platelets, white blood cells, clotting factors, glucose, and divalent cations. Post-treatment monitoring of blood composition is therefore required.

Plasmapheresis

This method removes free toxins or toxins bound to proteins, especially biological toxins (e.g., snake venom, mushroom toxins) and hemolytic toxins such as arsine. Typically, 3–5 liters of plasma are exchanged over several hours.

Antidotes

Antidotes for Metal Poisoning

Most antidotes for metal poisoning are chelating agents. Commonly used chelating agents include amino carboxylates and sulfhydryl-based compounds.

Disodium Calcium Ethylenediaminetetraacetate (EDTA Ca-Na₂)

This amino carboxyl chelating agent is the most widely used and forms stable, soluble complexes with various metals for excretion, primarily used in treating lead poisoning. The typical dose is 1 g diluted in 250 ml of 5% glucose solution and administered via intravenous infusion once daily for 3 consecutive days, forming a single treatment cycle that can be repeated after a 3–4 day interval.

Dimercaprol (BAL)

Containing reactive sulfhydryl (–SH) groups, this antidote forms non-toxic, poorly dissociated but soluble chelates with certain metals, allowing their excretion via urine. It also recovers enzymatic activity by displacing metals bound to enzymes. Dimercaprol is used in treating arsenic and mercury poisoning. For acute arsenic poisoning, a dose of 2–3 mg/kg is administered intramuscularly every 4–6 hours over the first 1–2 days, followed by twice-daily injections from day 3 to day 10. Common side effects include nausea, vomiting, abdominal pain, headache, and palpitations.

Sodium Dimercaptopropane Sulfonate (DMPS)

This chelating agent has a similar mechanism to dimercaprol but demonstrates better efficacy with fewer side effects. It is primarily used for mercury, arsenic, copper, or antimony poisoning. For mercury poisoning, a 5% DMPS solution (5 ml) is administered intramuscularly once daily over 3 consecutive days, with a 4-day interval before repeating the treatment cycle.

Sodium Dimercaptosuccinate (DMS)

This antidote is reserved for poisoning involving antimony, lead, mercury, arsenic, or copper. For acute antimony poisoning presenting with arrhythmias, an initial dose of 2.0 g is diluted in 10–20 ml of water for injection and administered via slow intravenous infusion. Subsequent doses of 1.0 g are given hourly for 4–5 times.

Antidote for Methemoglobinemia

Low doses of methylene blue are effective in reducing methemoglobin to normal hemoglobin and are used to treat methemoglobinemia caused by nitrites, aniline, or nitrobenzene poisoning. The dosage involves intravenous administration of 5–10 ml of a 1% methylene blue solution (1–2 mg/kg) after dilution, and repeated use may be considered based on the clinical situation. Leakage of the injection solution can cause tissue necrosis.

Antidote for Cyanide Poisoning

For cyanide poisoning, immediate inhalation of amyl nitrite is required, followed by slow intravenous administration of 10 ml of a 3% sodium nitrite solution. This is then followed by slow intravenous administration of 50 ml of a 50% sodium thiosulfate solution. A suitable dose of nitrite oxidizes hemoglobin to form a specific amount of methemoglobin, which then binds with cyanide in the blood to form cyanomethemoglobin. Methemoglobin can also sequester cyanide ions from oxidized cytochrome oxidase. Cyanide ions subsequently react with sodium thiosulfate to form low-toxicity thiocyanate, which is excreted from the body.

Fomepizole

Fomepizole and ethanol are effective antidotes for poisoning caused by ethylene glycol and methanol. Both substances are inhibitors of alcohol dehydrogenase (ADH), with fomepizole having a stronger inhibitory effect. Ethylene glycol can lead to kidney failure, while methanol can cause visual impairment or blindness. Administration of fomepizole before the onset of poisoning symptoms, following exposure to methanol or ethylene glycol, prevents toxicity. Administration after symptoms develop prevents further progression of the condition. Use of fomepizole can avoid the need for hemodialysis in cases where kidney damage from ethylene glycol is not severe. A loading dose of 15 mg/kg is diluted in 100 ml or more of normal saline or 5% glucose solution and infused over a period of at least 30 minutes. Maintenance doses of 10 mg/kg are administered every 12 hours for four consecutive doses.

Octreotide

Octreotide inhibits pancreatic β-cell activity and is used to treat hypoglycemia caused by overdose of sulfonylurea drugs. Its insulin-inhibiting effect is twice that of somatostatin. The recommended adult dose is 50–100 μg, administered subcutaneously or via intravenous infusion every 8–12 hours.

Glucagon

Glucagon induces the release of catecholamines and serves as an antidote for poisoning caused by β-receptor antagonists and calcium channel blockers. It is also applicable for overdoses of procaine, quinidine, and tricyclic antidepressants. Bradycardia and hypotension are the main indications for its use. The initial dose ranges from 5–10 mg via intravenous injection, and repeated doses are permissible. Maintenance doses are administered at an infusion rate of 1–10 mg/h. Common side effects include nausea and vomiting.

Antidotes for Central Nervous System Depressants

Naloxone

Naloxone is an opioid receptor antagonist and serves as an antidote for opioid poisoning. It has a specific antagonistic effect on respiratory depression induced by opioid analgesics. Naloxone is also effective in arousing patients from acute alcohol poisoning and has some efficacy in poisoning caused by sedative-hypnotic drugs such as diazepam. Under stress, the release of β-endorphins from the anterior pituitary can cause cardio-pulmonary dysfunction, which naloxone may counteract. A dose of 0.4–0.8 mg is administered via intravenous injection, with a second dose administered after one hour in severe cases.

Flumazenil

Flumazenil is the antidote for poisoning caused by benzodiazepines.

Antidotes for Organophosphorus Insecticide (OPI) Poisoning

Treatment involves the use of atropine, penehyclidine hydrochloride, and pralidoxime iodide (PAM-I).

Prevention of Complications

During seizures, measures should be taken to protect individuals from injury. For patients requiring prolonged bed rest, measures such as regular repositioning are essential to prevent complications like aspiration pneumonia, pressure sores, or thromboembolic disorders.

Treatment of Chronic Poisoning

Antidotal Therapy

Antidotal therapy for chronic poisoning caused by lead, mercury, arsenic, manganese, and other metals can be administered using metal chelating agents, as detailed in the section on "Treatment of Acute Poisoning."

Symptomatic Treatment

For poisoning cases involving peripheral neuropathy, tremor-paralysis syndrome, toxic liver disease, toxic kidney disease, leukopenia, thrombocytopenia, or aplastic anemia, treatments are referenced in the respective clinical sections.

Prevention

Enhancing Public Awareness of Poison Prevention

Public awareness of poison prevention is promoted based on actual circumstances and local conditions in factories, rural areas, and urban communities. Educational campaigns introduce knowledge about the prevention and first aid of poisoning. In early winter, common practices for preventing carbon monoxide poisoning are highlighted. During pesticide spraying periods or seasons for rodent, mosquito, and fly control, information on preventing pesticide poisoning is shared with the public.

Strengthening the Management of Toxic Substances

Strict adherence to regulations regarding the management, protection, and use of toxic substances is emphasized. Storage of toxic substances is closely monitored to prevent leaks, spills, or drips of chemicals. Work areas handling toxic materials in factories and mining sites are managed with measures such as localized and centralized ventilation to expel toxins. Compliance with the maximum allowable concentration of toxic substances in workplace air is enforced, and protective measures against toxins are strengthened. Wastewater, exhaust gases, and solid waste are carefully managed to avoid contamination.

Preventing Chemical Food Poisoning

The potential toxicity of special foods is considered before consumption. Toxic or spoiled animal and plant-based foods are avoided. Edible fungi with uncertain toxicity are not consumed. Items such as pufferfish, cassava, and aconite are processed adequately to eliminate toxicity before consumption, and any uncertainty about their safety precludes their use as food. Acidic foods like soft drinks or fruit juices are not stored in galvanized containers.

Preventing Accidental Ingestion of Toxic Substances or Overdose

Containers holding medications or chemical substances are clearly labeled. Hospitals, households, and childcare institutions manage disinfectants and pesticides carefully. Hospitals implement strict verification protocols for dispensing and administering medications to avoid accidental consumption or overdose. Household medications are locked away and kept out of the reach of children, with designated individuals responsible for dispensing medications for psychiatric patients.

Preventing Endemic Poisoning Diseases

Excessive fluoride levels in drinking water can lead to endemic fluorosis, which can be mitigated by methods such as drilling deep wells or changing water sources. High barium levels in local well water can cause endemic paralysis, and efforts to reduce barium concentrations in drinking water are employed. Gossypol in cottonseed oil can result in poisoning after consumption. Treating cottonseed oil with alkali to convert gossypol into gossypol sodium eliminates its toxicity.