Poisoning — Symptoms, Causes & Treatment | MyMedicPlus

Poisoning is defined as harmful physiological exposure to any quantity of a toxic substance sufficient to cause tissue injury, organ dysfunction, or death. Routes of exposure include ingestion (most common), inhalation, dermal absorption, injection, and envenomation. Poisoning may be: accidental (the most common scenario in children under 5, driven by unsupervised access to medications, household chemicals, and plants); intentional self-harm (the predominant aetiology of serious and fatal poisoning in adults in high-income countries — constituting a simultaneous toxicological and psychiatric emergency); occupational or environmental (industrial chemical exposures, agricultural pesticide use); iatrogenic (drug-drug interactions, dosing errors); and criminal poisoning (rare). In high-income countries, medication overdoses are the leading cause of poisoning deaths: paracetamol (acetaminophen — responsible for approximately 50% of acute liver failure in the UK), opioids (responsible for the opioid overdose epidemic with 80,000+ deaths per annum in the USA), benzodiazepines, tricyclic antidepressants, and SSRIs. In low- and middle-income countries, organophosphate and carbamate pesticide self-poisoning is the largest single cause of poisoning mortality — responsible for an estimated 200,000 deaths per year globally, predominantly among agricultural workers. Carbon monoxide is the most common cause of environmental poisoning death in the UK. Globally, poisoning claims approximately 100,000-120,000 lives per year from unintentional causes and many more from intentional overdose. Immediate access to a regional Poison Control Centre (UK: NHS 111; USA: 1-800-222-1222; India: 1800-116-117) is critical for initial management guidance.

Pharmaceutical agents: paracetamol (acetaminophen — toxicity occurs through saturation of normal glucuronidation/sulphation pathways, diverting metabolism towards the reactive NAPQI metabolite that depletes glutathione and causes direct hepatocellular necrosis; the Rumack-Matthew nomogram guides N-acetylcysteine treatment decisions); opioids (morphine, heroin, fentanyl, codeine, tramadol — cause respiratory depression through mu-opioid receptor agonism in brainstem respiratory centres; fentanyl is 50-100x more potent than morphine and is the primary driver of the US opioid epidemic); benzodiazepines (CNS and respiratory depression — rarely fatal alone but extremely dangerous in combination with opioids or alcohol); tricyclic antidepressants (amitriptyline, imipramine — cause fatal ventricular arrhythmias through fast sodium channel blockade causing QRS prolongation above 100ms, plus anticholinergic toxidrome; sodium bicarbonate is the specific antidote); SSRIs (citalopram, fluoxetine — cause serotonin syndrome in overdose or drug-drug interaction with MAOIs, tramadol, or linezolid). Carbon monoxide (CO): colourless, odourless gas from incomplete combustion — binds haemoglobin with 200x the affinity of oxygen, causing tissue hypoxia; standard SpO2 is falsely normal — CO-oximetry is required for diagnosis. Natural toxins: Amanita phalloides (death cap mushroom — amatoxin causes severe delayed hepatotoxicity 6-24 hours after ingestion, responsible for 90% of mushroom fatality deaths worldwide); snake envenomation (haemotoxic, neurotoxic, or cytotoxic — managed with species-specific antivenom); digitalis glycosides (foxglove, oleander — bradyarrhythmias and heart block). Household chemicals: caustic alkalis (sodium hydroxide drain cleaners) and acids cause oropharyngeal and oesophageal burns; button battery ingestion in children causes alkaline tissue liquefaction and oesophageal perforation within hours — a surgical emergency.

Recognition of toxidromes (toxin-specific symptom clusters) allows rapid identification of the agent class before laboratory results. Cholinergic toxidrome (organophosphate/carbamate pesticides, nerve agents — sarin, VX): SLUDGE/DUMBELS — Salivation, Lacrimation, Urination, Defecation, GI cramping, Emesis (muscarinic effects), plus Bradycardia, Bronchospasm, Bronchorrhoea, Miosis (bilateral pinpoint pupils), and Muscle fasciculations/weakness (nicotinic effects); the combination of bronchospasm, bradycardia, and miosis is nearly diagnostic. Opioid toxidrome: the classic triad — respiratory depression (rate below 10/min, shallow), miosis (pinpoint pupils, reactive to light), and reduced consciousness — any two features in an unconscious patient should prompt empirical naloxone 0.4mg IV/IM/intranasal immediately. Sympathomimetic toxidrome (cocaine, amphetamines, MDMA, pseudoephedrine): tachycardia, hypertension, mydriasis (dilated pupils), hyperthermia, and agitation — may progress to hypertensive crisis, stroke, coronary vasospasm, ventricular arrhythmia, and hyperthermia-related rhabdomyolysis. Anticholinergic toxidrome (TCAs, antihistamines, antipsychotics, atropine, Jimson weed): 'dry as a bone, red as a beet, blind as a bat, mad as a hatter, hot as a hare' — dry flushed skin, mydriasis, confusion/delirium, urinary retention, hyperthermia, tachycardia; diaphoresis and urinary retention distinguish from sympathomimetic. Serotonin syndrome (SSRIs plus MAOIs, tramadol, or linezolid): clonus (spontaneous, inducible, or ocular — highly specific), agitation, hyperreflexia, diaphoresis, and hyperthermia in severe cases; the Hunter criteria are most specific for diagnosis. Carbon monoxide poisoning: throbbing frontal headache (90% of cases), nausea, dizziness, weakness, and confusion; severe poisoning (COHb above 30-40%) causes syncope, seizures, pulmonary oedema, and coma; cherry-red skin is a post-mortem finding and unreliable in living patients.

Clinical history (time, agent, amount, route, intentionality) combined with toxidrome recognition is the primary diagnostic approach. Consult National Poison Control Center for guidance. Blood tests: paracetamol level at 4 hours post-ingestion (mandatory in all overdoses), salicylate level, BMP (glucose, electrolytes, renal function), LFTs, FBC, arterial blood gas (pH, lactate), prothrombin time (coagulopathy in warfarin, hepatotoxins). ECG: QTc prolongation (risk of torsades de pointes from many drugs), QRS widening (TCA toxicity). Urine drug screen (qualitative, limited utility in acute management). CO-oximetry for CO poisoning (SpO2 unreliable). A systematic diagnostic approach that carefully combines a thorough clinical history, detailed physical examination findings, and appropriately targeted laboratory and imaging investigations is essential to accurately distinguish this condition from closely mimicking disorders and to guide safe and effective treatment selection. Early specialist referral — particularly when the diagnosis is uncertain or when initial treatments fail — optimises diagnostic accuracy and reduces unnecessary delays to effective management.

Immediate priorities: secure airway (endotracheal intubation if GCS under 8 or respiratory failure), establish IV access, correct hypoglycemia (glucose), treat seizures (benzodiazepines). Decontamination: activated charcoal (50g orally) within 1 hour of ingestion of an absorbable toxin in a conscious patient reduces absorption. Specific antidotes: N-acetylcysteine (NAC) for paracetamol — the most important antidote, highly effective if started within 8 hours; naloxone for opioid overdose (IV/IM/IN, 0.4mg titrated); atropine plus pralidoxime for organophosphate poisoning; methylene blue for methemoglobinemia; flumazenil for benzodiazepines (use with caution — precipitates seizures in mixed overdose); hydroxocobalamin for CN poisoning; 100% oxygen for CO poisoning. Regular monitoring of treatment response, early detection of side effects, and ongoing assessment of disease progression are essential components of optimising patient outcomes over the long term. Treatment plans should be proactively reviewed and appropriately adjusted based on clinical response, patient-reported tolerability, changing patient circumstances, and continuously evolving evidence-based clinical guidelines. Meaningful shared decision-making between patients and their healthcare team, incorporating patient values and treatment preferences, consistently improves both treatment adherence and long-term outcomes.

Paracetamol overdose without timely NAC treatment causes acute liver failure with peak hepatotoxicity at 72-96 hours and may require liver transplantation (King's College criteria guide transplant referral). Opioid overdose causes fatal respiratory depression and hypoxic brain injury — major contributor to overdose death epidemic. TCA overdose causes refractory cardiac arrhythmias (sodium bicarbonate is the antidote for QRS prolongation). Aspiration pneumonia from loss of protective airway reflexes. Organophosphate toxicity causes prolonged cholinergic crisis requiring intensive ICU management for days to weeks.

Medication safety: store all medications in the original child-resistant container in a locked cabinet inaccessible to children; dispose of unused medications at pharmacy take-back programmes; never leave medications on kitchen worktops or in handbags accessible to children. Carbon monoxide prevention: install at least one CO detector per floor near sleeping areas; service all gas appliances (boiler, gas hob, wood burner) annually by a registered Gas Safe engineer; never use a BBQ, camping stove, or petrol generator indoors or in enclosed spaces; CO detectors should be replaced every 5-7 years. Paracetamol pack size restriction: UK legislation limiting paracetamol packs to 32 tablets in pharmacies and 16 in general retail (implemented 1998) reduced paracetamol overdose deaths by 43% and liver transplantation for paracetamol toxicity by 61% — the most effective single poisoning prevention intervention ever implemented. Opioid harm reduction: take-home naloxone kits for people who use opioids and their families (naloxone is increasingly available over the counter); prescribing naloxone alongside opioid prescriptions for chronic pain patients; opioid substitution therapy (methadone, buprenorphine); prescription drug monitoring programmes. Mushroom safety: never forage wild mushrooms without expert mycological identification — the death cap (Amanita phalloides) closely resembles edible species and causes 90% of mushroom fatality deaths worldwide; educate children about plant and mushroom toxicity. Psychiatric follow-up: every patient presenting after intentional self-poisoning must receive a psychiatric assessment and a documented safe discharge plan before leaving the emergency department — this is a NICE quality standard; restricting access to highly lethal means (pesticides) in suicidal individuals is one of the most effective suicide prevention strategies.

Call emergency services immediately (999/911) for any suspected poisoning or overdose — do not wait for symptoms to develop. Bring the container, label, or substance details to the emergency department. Do not induce vomiting unless specifically advised by Poison Control — this can cause additional harm with some substances. Call your regional Poison Control Centre for immediate guidance on ingestion of household chemicals, medications, plants, or animals. Do not wait for symptoms — some poisons (e.g., paracetamol overdose) cause delayed but severe liver damage with symptoms appearing hours to days later. Seek immediate care for: ingestion of any medication in a dose above therapeutic range, household chemical ingestion, suspected carbon monoxide exposure (headache, nausea, confusion in multiple people in same building), or any ingestion in a child. Remove from exposure immediately for chemical exposure.