Antidotes and management of common poisonings

• Poisoning is common and usually survivable: most patients need good supportive care, observation and the right antidote rather than invasive decontamination.
• The first job is always the same: airway, breathing, circulation, disability and exposure (ABCDE), then remove the source of toxin and call the local poison centre.
• Activated charcoal helps only for certain toxins and works best when given early; for acids, alkalis, alcohols, iron and lithium it does not help.
• Antidotes exist for many, but not all, poisons. When an antidote is unavailable, the treatment is supportive care plus, where needed, enhancement of elimination such as alkalinisation or dialysis.
• Where guidance conflicts between sources or regions, the safer value is given and the difference is stated.

By the end of this page you should be able to:

1. Carry out the stepwise resuscitation and stabilisation of a poisoned patient, including a focused history and examination.
2. Recognise the common toxidromes and use them to identify the toxin when the history is unreliable.
3. Decide which patients need decontamination, which method to use, and when activated charcoal is and is not indicated.
4. State the antidote or specific treatment, with adult dosing, for the common poisonings listed here.
5. Manage an unknown overdose using an algorithm, including enhanced elimination and dialysis triggers.
6. Recognise acid and alkali ingestion and plan endoscopy, airway protection and surgical referral.

Poisoning covers any harmful exposure to a drug, chemical, plant, animal product or environmental agent. Most poisonings are self-limited and resolve with observation alone, but a small number progress quickly to seizures, arrhythmia, hypotension, renal failure or liver failure. The clinician's task is therefore triage: spot the dangerous exposures early, support the patient, give the right antidote at the right time, and avoid iatrogenic harm from unnecessary decontamination.

This page is written for adults. Children are more sensitive to many toxins per kilogram of body weight, take tiny lethal doses of iron or certain cardiac drugs, and need paediatric-specific dosing and safeguarding; the principles of assessment and triage are the same. Because the same poison often reaches the patient with a different name in different countries, generic drug names are used throughout (paracetamol is acetaminophen in North America). ^[1]

The first priorities are airway, breathing, circulation, disability and exposure (ABCDE), exactly as in any other critically ill patient. Remove the patient from the source of toxin and stop any ongoing exposure (for example, remove contaminated clothing and wash skin, or stop an infusion). Protect the airway early: many toxins depress consciousness or impair swallowing, and aspiration is the commonest iatrogenic complication of poisoning care.

Practical steps during stabilisation include these, given as typical practice and adjusted to the patient:

• Oxygen and ventilation. Give oxygen and ventilate if the respiratory drive is depressed. Do not rely on pulse oximetry alone in carbon monoxide or cyanide exposure; a normal reading can be misleading.
• Circulation. Start intravenous fluids for hypotension. Most overdoses produce a mixed picture, so use the clinical response and bedside ultrasound rather than a single formula.
• Glucose. Check a bedside glucose in every altered patient; give dextrose for hypoglycaemia. Give thiamine first in patients at risk of deficiency (chronic alcohol use, malnutrition).
• Naloxone. Give naloxone early when opioid overdose is suspected, because respiratory depression is the lethal event and naloxone is safe. See the opioid section below.
• Cardiac monitoring and ECG. Obtain a 12-lead ECG in every significant poisoning. Look in particular for QRS widening, QT prolongation and arrhythmias, which point to sodium-channel blockers, potassium-channel blockers or cardiotoxic drugs.
• Temperature. Hypothermia and hyperthermia both occur; active warming or cooling may be required.
• Seizures. Stop seizures with benzodiazepines first line. Do not give flumazenil to a poisoned patient who has seized.

Poison centres exist for exactly this purpose and should be consulted early. In the United Kingdom the National Poisons Information Service runs TOXBASE (www.toxbase.org) for professionals and the public reach it through NHS 111. In the United States the Poison Help Line is 1-800-222-1222 and is available to clinicians and the public 24 hours a day. ^[2] In many countries a national or regional centre does not exist; every clinician should know, before they need it, where their local toxicology advice comes from.

A clear history is usually available, even in an overdose, because the patient, relatives, ambulance staff or bystanders know what happened. Record:

• What was taken: name, strength, formulation (immediate-release, extended-release, enteric-coated), and whether other drugs were involved.
• How much, in tablets or millilitres and in milligrams or grams. Patients and relatives often under- or over-estimate; look at the empty containers.
• When, and whether the ingestion was acute or repeated over days (repeated supratherapeutic ingestion cannot be plotted on a single-dose nomogram).
• Route: swallowed, inhaled, injected, absorbed through skin, inserted.
• Co-ingestants, including alcohol, over-the-counter drugs and household products. Two poisons are common: paracetamol and salicylates are routinely present in significant ingestions and are dangerous, so they should be measured in every substantial overdose.
• Intent: accidental, recreational, self-harm. This changes observation, psychiatric assessment and disposition.
• Medical history, especially liver, kidney, heart and lung disease, pregnancy, and current medications.

The examination should be systematic: vital signs, mental status, pupils, skin, mucous membranes, bowel sounds, respiratory secretions and odour. Toxidromes (patterns of signs) often identify the drug class when the history is poor or the patient cannot speak. The absence of sweating is a useful clue to anticholinergic poisoning rather than sympathomimetic poisoning. ^[4]

Investigations should be targeted to the suspected toxin. A thorough history plus an ECG, glucose, paracetamol and salicylate levels, and an arterial blood gas covers most serious cases. ^[2] Sensible minimum tests for a significant unknown ingestion are:

• Paracetamol and salicylate levels in every significant ingestion (both are commonly present and dangerous).
• Urea, electrolytes and creatinine, liver function tests, coagulation screen, full blood count.
• Arterial or venous blood gas with lactate, glucose and anion gap; the osmolar gap early after a toxic alcohol. ^[2]
• ECG for sodium and potassium channel effects (QRS width, QTc).
• Pregnancy test in women of childbearing age.
• Drug screens and expanded toxicology only when they change management. Many screens are qualitative, slow to return and misleading, and they rarely change the initial treatment.

Substance-specific levels are taken when the result changes treatment: serum paracetamol at 4 hours for immediate-release products, serum iron at 4 to 6 hours, digoxin level with ECG, serum ethanol, methanol and ethylene glycol levels where available. ^[7]

Gastrointestinal decontamination used to be routine and is not anymore. The American Academy of Clinical Toxicology and the European Association of Poisons Centres and Clinical Toxicologists consensus statements and current reviews agree that most patients need supportive care only, with the decision based on the agent, the dose, the time since ingestion, the clinical state and the patient's airway, ideally with poison-centre advice. ^[3]

Key points from the consensus position papers:

• Activated charcoal is most useful when given early, within about 1 hour. It may still help for up to about 4 hours after large ingestions, delayed-release formulations or drugs that slow gut motility. Its usefulness later is uncertain and it has never been shown to improve mortality. ^[3]
• Activated charcoal does not adsorb acids, alkalis, alcohols, metals (including iron and lithium) or electrolytes. ^[3]
• Routine use of sorbitol or other cathartics in combination with activated charcoal is not advised; dilution with water or milk is no longer recommended. Give a single cathartic (such as sorbitol) with the first dose of charcoal only if it aids acceptability. ^[3]
• Airway protection comes first. A protected airway (endotracheal intubation) is required before giving charcoal to a drowsy patient. Pulmonary aspiration of charcoal is the major avoidable harm. ^[3]
• Multi-dose activated charcoal (MDAC) is valuable for life-threatening ingestions of carbamazepine, dapsone, phenobarbital, phenytoin, quinine, valproate, theophylline and cardiac glycosides (to reduce enterohepatic recirculation). ^[3]
• Ingested concentrations count as elemental amounts. For iron, a 325 mg ferrous sulphate tablet contains about 65 mg of elemental iron. ^[7]

When the toxin has already been absorbed, elimination can sometimes be speeded up:

• Urinary alkalinisation is a form of enhanced elimination for salicylates (and some other weak acids) using intravenous sodium bicarbonate, discussed in the salicylate section.
• Haemodialysis removes the toxin and corrects acid-base and electrolyte abnormalities. It is indicated for severe salicylate poisoning; for methanol and ethylene glycol with severe acidosis or organ dysfunction; for lithium; for theophylline; and for severe iron in some cases. It is ineffective for tricyclic antidepressants because of high protein binding and large volume of distribution. ^[10]
• Supportive extracorporeal life support such as extracorporeal membrane oxygenation (ECMO) is reserved for beta-blocker or calcium-channel-blocker poisoning that remains hypotensive despite maximal medical therapy. ^[5]

Most poisoned patients arrive without a clear history. The algorithm below is the usual approach: stabilise, identify the toxin and population, look for toxidromes, obtain targeted tests, treat specifically, and use charcoal or dialysis only when they help.

Many patients with an intentional ingestion also need a period of observation even when they look well at presentation, because several toxins (paracetamol, iron, salicylates, lithium, sustained-release preparations) have delayed or biphasic toxicity. Defer discharge until the toxin, the dose and the time window are understood.

The table is a rapid reference. Doses are typical adult doses; children, older adults, renal or hepatic impairment and pregnancy need adjustment. Always cross-check with the product label and local toxicology advice.

A note on the salicylate dose line: severity is "mild 40 to 80, moderate 80 to 100, severe above 100 mg per dL" by serum salicylate level. ^[10] Laboratories may report salicylate in different units, so check the units on the report before comparing with these thresholds. ^[10]

Paracetamol overdose is the leading cause of acute liver failure in many countries. Adults are generally at risk after more than 12 g over 24 hours, a single dose of 7.5 to 10 g, or more than 150 mg per kg; in healthy children aged 1 to 6 years the figure is a single dose of 150 to 200 mg per kg. ^[1] Toxicity tends to be silent at first: nausea and vomiting, then a quiet phase, then rising transaminases from 24 hours and peak values often above 10,000 international units per litre at 72 to 96 hours, with jaundice, encephalopathy and renal failure in severe cases. ^{[1] [5]}

Diagnosis rests on the serum paracetamol concentration, ideally taken 4 hours after ingestion for immediate-release products (immediately if later), and plotted on the Revised Rumack-Matthew nomogram. The treatment threshold is 150 micrograms per mL, or 990 micromol per L, at 4 hours, falling to 4.69 micrograms per mL, or 31.3 micromol per L, at 24 hours. ^[1] For extended-release formulations or co-ingestion with anticholinergics or opioids, repeat the level 4 to 6 hours later if the first level is above 10 micrograms per mL but below the treatment line; repeated supratherapeutic ingestions over more than 24 hours cannot be plotted on the nomogram, so decisions rely on the history, the level and the transaminases. ^[1] Activated charcoal may be given within the first 4 hours, and is most useful within the first hour or two, especially for large or extended-release ingestions. ^[1]

N-acetylcysteine (NAC) replenishes glutathione and binds the toxic metabolite N-acetyl-p-benzoquinoneimine (NAPQI). It is highly effective when started within 8 hours of an acute ingestion, with equal benefit whether given at 0 to 4 hours or 4 to 8 hours, and it may still help later or when liver injury is present. ^[1] Oral NAC is 140 mg per kg as a loading dose followed by 70 mg per kg every 4 hours for 17 further doses (72 hours in total); patients over 100 kg receive a maximum loading dose of 100 mg per kg. The intravenous 21-hour regimen gives 150 mg per kg over 1 hour, then 50 mg per kg over 4 hours, then 100 mg per kg over 16 hours; later protocols continue a single infusion of 12.5 to 15 mg per kg per hour until the stopping criteria are met. ^[1][2] NAC may be stopped when the paracetamol level is below 10 micrograms per mL, the INR is below 2.0, and the aminotransferases are normal for the patient or have fallen at least 25 to 50 percent from their peak, with the patient clinically well; high-risk ingestions (more than 30 g, or a 4-hour level above 300 micrograms per mL) may need intubation, fluids, vasopressors, a higher dose of NAC and haemodialysis. ^[1] When the timing is unknown or the level will be delayed beyond 8 hours, start NAC while waiting for the result. ^[1]

Many drug classes produce anticholinergic effects: antihistamines, antispasmodics, tricyclic antidepressants, antipsychotics and some plants. The picture is tachycardia, dry flushed skin, dilated pupils, ileus, urinary retention, agitation and hyperthermia without sweating. ^[4] Most patients do well with supportive care. Agitation is treated first with intravenous benzodiazepines, which may need large doses; cooling and fluids are given for hyperthermia; intravenous sodium bicarbonate is used for a wide QRS. ^[4]

Physostigmine, a centrally and peripherally active acetylcholinesterase inhibitor, is reserved for pure anticholinergic poisoning with both central and peripheral features that is refractory to benzodiazepines. Give 0.5 to 2 mg IV in adults and 0.02 mg per kg IV in children, to a maximum of 0.5 mg, with resuscitation equipment (including atropine) ready; it may be repeated after about 30 minutes if symptoms recur. ^[4] Its benefit is in selected pure cases and it is avoided in tricyclic antidepressant overdose, where it has been associated with asystole.

Organophosphate insecticides and nerve agents (sarin, soman, tabun, VX) phosphorylate acetylcholinesterase, producing a cholinergic crisis. The presentation is salivation, lacrimation, urination, defecation, diaphoresis, miosis, bronchorrhoea, bronchospasm, bradycardia and, later, muscle fasciculations, weakness, seizures and respiratory failure. ^[2] Initial decontamination of skin and eyes matters for both the patient and staff.

Treatment follows airway, breathing and circulation. Atropine competitively blocks acetylcholine at muscarinic receptors and is given in doses of 2 to 5 mg IV in adults and 0.05 mg per kg IV in children, doubling every 3 to 5 minutes until secretions and bronchospasm clear (titrating to drying of pulmonary secretions rather than to pupil size). ^[2] Pralidoxime (2-PAM) reactivates acetylcholinesterase and is given as at least 30 mg per kg IV in adults and 25 to 50 mg per kg in children; it is most effective before the agent ages on the enzyme. Oximes are controversial and of uncertain benefit in some organophosphates, particularly in the developing world. ^[2] Diazepam treats seizures, which are more common in children, and Suxamethonium should be avoided during intubation of an organophosphate-poisoned patient. ^[2]

Beta blockers produce bradycardia, hypotension and, with the lipophilic agents, altered mental status; co-ingestion with calcium channel blockers is particularly dangerous. Hypoglycaemia points towards beta blockers rather than calcium channel blockers. Symptoms usually appear within 1 to 2 hours, although sotalol may be delayed up to 20 hours. ^[5]

Treatment is glucagon first (3 to 5 mg IV, 50 micrograms per kg in children), repeated with 4 to 10 mg after 5 minutes if there is no improvement, with an antiemetic because glucagon causes vomiting; glucagon has no controlled trial evidence but is considered the treatment of choice, and it may cause hyperglycaemia and hypocalcaemia. Calcium, high-dose insulin and euglycaemia (1 unit per kg insulin bolus with 0.5 g per kg glucose, then 0.5 to 2 units per kg per hour, keeping glucose at 100 to 200 mg per dL) is used when glucagon and fluids fail. Sodium bicarbonate is given for QRS widening, magnesium for QTc prolongation, vasopressors for hypotension, and benzodiazepines for seizures. ^[2][5] Gastric lavage may be needed after massive early ingestions, activated charcoal helps for patients presenting after an hour, whole-bowel irrigation is considered for sustained-release preparations, and the water-soluble agents (atenolol, nadolol, sotalol) may respond to enhanced elimination such as multi-dose charcoal, haemoperfusion or dialysis. Extracorporeal membrane oxygenation is reserved for collapse. ^[5]

Calcium channel blockers cause myocardial depression, hypotension, bradycardia and atrioventricular block; verapamil and diltiazem produce more bradycardia, while dihydropyridines such as amlodipine tend to produce hypotension with reflex tachycardia. The treatments overlap with beta blockers: calcium as chloride or gluconate, glucagon, high-dose insulin, lipid emulsion for refractory hypotension and vasopressors. ^[2] Calcium dosing is 10 to 20 mL of 10 percent calcium chloride, or 30 to 60 mL of 10 percent calcium gluconate, intravenously, repeatable every 15 to 20 minutes up to four further doses, or given as a continuous infusion. ^[2] Hyperglycaemia is a helpful marker because calcium channel blockers suppress insulin release. ^[5]

Digoxin toxicity is usually chronic rather than acute, worsened by renal impairment, hypokalaemia, hypomagnesaemia, hypercalcaemia and interacting drugs. It causes gastrointestinal upset, visual disturbance (yellow or green halos), arrhythmias and, in acute overdose, severe hyperkalaemia. Activated charcoal may be given; gastric lavage is avoided because of vagal stimulation. ^[2] The antidote is digoxin-specific Fab, indicated for life-threatening arrhythmias, high-grade atrioventricular block, hypotension, symptomatic bradycardia, potassium above 5 mmol per L in acute overdose, acute ingestions above 10 mg in adults or 4 mg in children, and a digoxin concentration above 15 ng per mL at any time or above 10 ng per mL 6 hours after ingestion. ^[2] Fab is dosed in vials as the total milligrams ingested divided by 0.5, or as the digoxin level in ng per mL multiplied by weight in kg divided by 100; ten to twenty vials empirically for critical illness after acute overdose, three to six vials for chronic toxicity in adults, and one to two in children. ^[2] Take care not to reverse chronically digoxin-dependent patients completely, and monitor for relapse because Fab has a shorter half-life than digoxin. ^[2] Oleander, foxglove and other cardioactive steroid plants are treated the same way, although dosing is less certain.

Bleeding is the major complication of heparin. The specific reversal agent is protamine sulphate, which binds heparin to an inactive complex with an effect within about 5 minutes. Give 1 mg of protamine for about 100 units of unfractionated heparin remaining in the body, by slow intravenous push with a maximum of 50 mg over 10 minutes, because rapid or excessive doses cause hypotension, pulmonary hypertension and anaphylaxis. ^[13] Protamine only partly reverses low-molecular-weight heparin (anti-Xa activity is never fully reversed, to about 60 percent for enoxaparin and 60 to 75 percent for dalteparin), and should be calculated against the time since the last dose because of heparin's short half-life. ^[13]

Warfarin is a vitamin K antagonist. For raised INR without bleeding, stop the drug and use low-dose oral vitamin K; do not give prophylactic vitamin K for an intentional overdose, because the half-life of warfarin far exceeds that of vitamin K and the INR can bounce back. ^[2] For a patient with bleeding, give 10 mg of intravenous vitamin K over 20 to 60 minutes plus 4-factor prothrombin complex concentrate or fresh frozen plasma; vitamin K alone takes hours, so serious bleeding needs clotting factors. ^[2] Oral vitamin K works in 12 to 24 hours; subcutaneous vitamin K is unreliable and should be avoided. Superwarfarins (long-acting rodenticides) are far more potent than warfarin and may need prolonged high-dose vitamin K and serial INR checks for weeks. ^[2]

Iron has five clinical stages: early vomiting, abdominal pain and haematemesis within the first 6 hours; a misleading latent phase; shock, acidosis and hepatic injury at 6 to 72 hours; hepatic failure; and, weeks later, gastric outlet obstruction. ^[7] Severity is based on elemental iron: less than 20 mg per kg is generally nontoxic, 20 to 60 mg per kg moderate, and above 60 mg per kg severe and potentially fatal. ^[7] Serum iron peaks at 4 to 6 hours: below 350 micrograms per dL suggests mild poisoning, 350 to 500 micrograms per dL moderate, and above 500 micrograms per dL severe systemic toxicity. ^[7] Activated charcoal does not bind iron and must not be used; whole-bowel irrigation with polyethylene glycol helps move unabsorbed tablets. Intravenous deferoxamine is the chelator for moderate or severe poisoning, given as 15 mg per kg per hour (maximum 35 mg per kg per hour, maximum 6 g per day) for about 24 hours. ^[7] Iron containers and prenatal tablets should be stored locked and out of reach of children. ^[7]

Lead poisoning is usually chronic and asymptomatic at low levels, where even small rises reduce intelligence quotient in children; higher exposures cause irritability, abdominal pain, anaemia and basophilic stippling; above 70 to 100 micrograms per dL there may be encephalopathy. ^[8] Management begins with identifying and removing the source, removing retained lead fragments, and repleting iron, calcium and zinc. Chelation is indicated for children with a blood lead above 45 micrograms per dL, adults above 70 to 100 micrograms per dL, and anyone with encephalopathy: dimercaprol 75 mg per m2 intramuscularly every 4 hours for 5 days when severe, followed by edetate calcium disodium; succimer orally for milder or asymptomatic cases. ^[2][8] Chelators can mobilise lead from bone back into soft tissue, so source removal matters more than chelation. ^[8]

Both are metabolised by alcohol dehydrogenase to toxic acids: methanol to formic acid (metabolic acidosis and visual loss) and ethylene glycol to glycolic and oxalic acids (acidosis and renal injury from calcium oxalate). Ethylene glycol has a sweet taste and is found in antifreeze; methanol in windscreen wash, solvents and illicit spirits. ^[2] The parent alcohols are relatively nontoxic, so treatment is to block their metabolism.

Treat with fomepizole (ethanol if fomepizole is unavailable) when the methanol concentration is at or above 32 mg per dL or the ethylene glycol concentration at or above 62 mg per dL, after a recent ingestion with an osmolar gap above 25, or when a suspected ingestion is accompanied by two or more of arterial pH below 7.3, bicarbonate below 20 mmol per L, osmolar gap above 25, urinary oxalate crystals or visual disturbance. ^[2] The fomepizole regimen is 15 mg per kg intravenously as a loading dose, then 10 mg per kg every 12 hours for four doses, then 15 mg per kg every 12 hours. Ethanol can be given at 15 mL per kg loading of 5 percent intravenous solution (half that concentration for 10 percent) with maintenance infusions that vary with drinker status and dialysis. ^[2] Haemodialysis is added for renal dysfunction, severe metabolic acidosis or electrolyte disturbance; for methanol, fomepizole with dialysis is commonly used, whereas ethylene glycol often does not need dialysis if treated early. ^[2] Adjunctive thiamine, pyridoxine and magnesium support ethylene glycol metabolism. ^[2]

Opioids kill by respiratory depression. The triad is drowsiness, hypoventilation and miosis, although miosis may be absent, particularly with pethidine, mixed overdoses or in tolerant users. ^[9] Airway management and ventilation come first; naloxone is a pure opioid antagonist with onset in minutes and duration of about 1 hour. Give 0.4 to 1 mg intravenously in adults and 0.1 mg per kg in children; in suspected chronic users start 0.04 to 0.4 mg IV every 1 to 3 minutes to avoid precipitating severe withdrawal; repeat every 2 to 3 minutes and consider a continuous infusion for long-acting agents such as methadone. ^[9] For apnoea or impending arrest escalate the dose rapidly and intubate early rather than waiting for a response. ^[9] Higher doses are needed for diphenoxylate, methadone, pentazocine and other partial or mixed agonists. ^[9] Observe for 12 to 24 hours after reversal because naloxone is short-acting and recurrence of respiratory depression is common with long-acting opioids and with non-cardiogenic pulmonary oedema. ^[9]

Salicylate poisoning creates a mixed picture: direct stimulation of the respiratory centre produces respiratory alkalosis, while uncoupling of oxidative phosphorylation produces metabolic acidosis, hyperthermia, tinnitus, sweating and, at high levels, cerebral and pulmonary oedema. ^[10] Severity by serum salicylate level is mild at 40 to 80 mg per dL, moderate at 80 to 100 mg per dL and severe above 100 mg per dL, but symptoms lag and patients can deteriorate quickly, especially children. ^[10]

Patients are volume-depleted, so resuscitate with dextrose 5 percent with 3 ampoules of sodium bicarbonate (150 mEq in 1000 mL), aiming for a urine output of 2 to 3 mL per kg per hour and repleting potassium. ^[10] Urinary alkalinisation enhances elimination: the same bicarbonate regimen raises urine pH and converts salicylate to its ionised form, which the kidney excretes, while a bolus of 1 to 2 mEq per kg of sodium bicarbonate is useful at intubation because ventilation cannot compensate as well. ^[10] Keep the pH corrected and avoid worsening acidosis. ^[10] Haemodialysis is indicated for levels above 100 mg per dL after acute ingestion, severe acidosis or hypotension despite fluids, mechanical ventilation, renal failure or evidence of end-organ damage such as seizures, pulmonary or cerebral oedema. ^[10] Activated charcoal may help for recent ingestions, including extended-release aspirin, and early gastric lavage is considered for large acute ingestions of enteric-coated aspirin. ^[10] Whole-bowel irrigation has not been shown to help and may increase absorption. ^[10]

Tricyclic antidepressants have a narrow therapeutic index and block sodium and potassium channels, muscarinic, alpha-adrenergic and histamine receptors. Toxicity begins within 30 to 40 minutes. A 12-lead ECG is mandatory: QRS above 100 ms predicts seizures and above 160 ms predicts arrhythmias, and an R wave in aVR greater than 3 mm or an R/S ratio in aVR above 0.7 also predicts seizures and arrhythmias. ^[11] Ingestions of 10 to 20 mg per kg may be life-threatening. ^[11]

Supportive care comes first. Activated charcoal may be given when the airway is protected, up to 2 hours after ingestion, and it may work longer when bowel sounds are reduced. ^[11] Correct acidosis aggressively because acidosis worsens cardiac and cerebral toxicity. Sodium bicarbonate, 1 to 2 mEq per kg by bolus and repeated as needed, is indicated for haemodynamic instability, seizures, dysrhythmias and QRS above 100 ms, aiming to narrow the QRS and keep serum pH at 7.5 to 7.55. ^[2][11] Seizures respond to benzodiazepines; hypotension is treated with fluids then noradrenaline if needed; refractory arrhythmias may need lipid emulsion, and temporary pacing can be used for refractory bradycardia. ^[11] Physostigmine, class IA/IC/III antiarrhythmics and flumazenil must be avoided, and dialysis and haemoperfusion are ineffective because of high protein binding and large volume of distribution. ^[11]

Caustics cause severe morbidity and occur in all ages; about 80 percent of US cases are children, often accidental ingestions of household cleaners in small amounts, while intentional ingestions involve large volumes of concentrated agents. ^[12] The oesophagus is most vulnerable to alkalis, the stomach to acids. Acids (pH below 3) tend to cause coagulative necrosis with a protective eschar, whereas alkalis (pH above 11) cause liquefactive necrosis and deeper penetration; in practice strong acids and strong alkalis are equally capable of full-thickness injury. ^[12]

Management is airway first: drooling, stridor, respiratory distress and hypoxia mean early intubation, preferably fiberoptic, and tracheostomy for upper-airway oedema. Secure multi-site intravenous access and resuscitate. ^[12] Do not induce vomiting, do not neutralise the pH (exothermic injury with no human outcome benefit) and do not dilute with water or milk in current practice. ^[12] Activated charcoal is reserved for metal caustics such as zinc or mercuric chloride. ^[12] Blind nasogastric tube placement is dangerous; tubes, if needed, go in under direct endoscopic vision. ^[12]

Upper endoscopy is the gold standard and should be done within 24 hours for symptomatic patients (posterior pharyngeal burns, stridor, chest or abdominal pain, inability to tolerate liquids) and for any intentional ingestion; asymptomatic patients without mucosal burns may be observed and may not need endoscopy. Endoscopy up to 96 hours may be safe with gentle insufflation. Injuries are graded on the Zargar scale from 0 to 3b, and the risk of stricture rises with the grade of injury. Corticosteroids are controversial and are not used routinely, though high-dose methylprednisolone has been used for grade 2b injuries. Pneumomediastinum, peritonitis, shock or high-grade injury needs emergent surgical consultation. ^[12] Eye and skin exposures need immediate copious irrigation. ^[12]

Discharge is reasonable for trivial exposures with no symptoms and no delayed-toxicity risk, but most significant ingestions need observation because delayed toxicity is common (paracetamol, iron, salicylates, lithium, sustained-release preparations). Admit to a monitored bed for anything serious; admit to intensive care for respiratory or haemodynamic instability, arrhythmias, acidosis, altered consciousness or the need for dialysis. Patients after intentional overdose need mental-health and social assessment before discharge. ^[9]

• Most poisoned patients need supportive care, observation and the correct antidote, not routine gastric emptying. ^[3]
• Airway, breathing and circulation come first; protect the airway before giving charcoal. ^[3]
• Paracetamol has an 8-hour window for N-acetylcysteine; always obtain a level at 4 hours and plot it on the Rumack-Matthew nomogram. ^[1]
• Iron is staged and delayed: deferoxamine by infusion at 15 mg per kg per hour for serum iron above 500 micrograms per dL. ^[7]
• Opioid and benzodiazepine overdose kill by respiratory depression; naloxone reverses opioids but flumazenil is not routine for benzodiazepines. ^[6][9]
• Beta blocker and calcium channel blocker overdose are treated with calcium, glucagon and high-dose insulin, with ECMO as rescue. ^[2][5]
• Salicylate poisoning needs urinary alkalinisation and sometimes dialysis; levels are severity thresholds of 40 to 80, 80 to 100 and above 100 mg per dL. ^[10]
• Tricyclic toxicity is treated with sodium bicarbonate for QRS above 100 ms or haemodynamic instability. ^[2][11]
• Activated charcoal helps only for adsorbed toxins, mostly within the first hour, and never for acids, alkalis, alcohols, iron, lithium or hydrocarbons. ^[3]
• Methanol and ethylene glycol are treated with fomepizole; target concentrations are 32 mg per dL and 62 mg per dL. ^[2]
• Caustics are managed with airway protection, endoscopy within 24 hours and surgery for perforation or mediastinitis; no neutralisation and no blind tubes. ^[12]
• tPA bleeding has no specific reversal; stop the drug and consider antifibrinolytics and cryoprecipitate when fibrinogen is low. ^[14]

Poisoning and ingestions in children (paediatrics) covers childhood exposures, iron, button batteries and caustics in a younger population. Useful follow-ons include management of the comatose patient, acid-base disorders, and the emergency assessment of chest pain, palpitations and acute confusion, which can be linked via TopicLink once verified.