Poisoning or overdose
Exam Tips
- In any altered consciousness with unclear cause, check glucose immediately and consider poisoning early.
- Do not be reassured by a well-looking patient after paracetamol overdose; early symptoms may be minimal before hepatotoxicity evolves.
- For single acute paracetamol ingestion, the 4-hour blood level (or later) drives antidote decisions; earlier levels are not interpretable.
- Memorise high-risk paediatric agents where very small amounts can be lethal (especially methadone, tricyclics, calcium-channel blockers, beta-blockers, oral hypoglycaemics).
- Mixed overdoses are common, so toxidromes can overlap; serial observations and repeat ECGs are high-yield in OSCE/viva answers.
- See Figure: Rumack-Matthew paracetamol nomogram and classic toxidrome comparison tables in emergency toxicology chapters.
Definition
Poisoning (including overdose) is a clinical state caused by exposure to a toxic amount of a medicine, chemical, biological toxin, or drug of misuse via ingestion, inhalation, injection, dermal, or ocular routes. In UK practice, overdose usually refers to taking more than the intended dose of a drug (prescribed, over-the-counter, or illicit), and may be accidental (for example dosing errors) or deliberate self-poisoning as part of self-harm.
Pathophysiology
Toxicity occurs when exposure dose, rate, and route exceed the body’s capacity for distribution, metabolism, and elimination, leading to target-organ dysfunction. Core mechanisms include direct cellular injury (for example paracetamol metabolite NAPQI causing hepatocyte necrosis when glutathione is depleted), receptor-mediated excess or blockade (opioid mu-agonism causing respiratory depression; anticholinergic or sympathomimetic syndromes), membrane/channel effects (for example tricyclic antidepressant sodium-channel blockade causing QRS widening and ventricular arrhythmia), and metabolic derangement (salicylate-induced respiratory alkalosis with later metabolic acidosis, mitochondrial uncoupling with hyperthermia). Mixed ingestions are common, so toxidromes may overlap and evolve over hours; delayed toxicity can occur even when early examination is relatively normal.
Risk Factors
- Age under 6 years (exploratory accidental ingestion), especially poor medicine storage at home
- Adolescence and young adulthood (approximately 15-35 years) with deliberate self-poisoning risk
- Psychiatric illness, previous self-harm, substance misuse, and social stressors
- Polypharmacy, poor eyesight, cognitive impairment, and dosing confusion (including duplicate paracetamol-containing products)
- Access to high-risk agents (opioids including methadone, tricyclic antidepressants, antipsychotics, beta-blockers, calcium-channel blockers, oral hypoglycaemics)
- Comorbidity and older age increasing morbidity/mortality after similar ingested doses
Clinical Features
Symptoms
- Often none initially (especially early paracetamol overdose)
- Nausea, vomiting, abdominal pain, dizziness, headache
- Drowsiness, confusion, agitation, behavioural change, reduced consciousness
- Tinnitus, hyperventilation, diaphoresis (suggestive of salicylate toxicity)
- Palpitations, chest pain, tremor, seizures
- Dyspnoea or slow breathing (opioid or sedative co-ingestion)
Signs
- Altered GCS, pinpoint or dilated pupils depending on toxidrome
- Abnormal respiratory rate (depression or hyperventilation), hypoxia
- Tachycardia or bradycardia, hypotension or hypertension
- ECG abnormalities (QRS prolongation, QT prolongation, arrhythmias)
- Sweating, flushing, dry mucosae, urinary retention, hyperthermia (toxidrome clues)
- Right upper quadrant tenderness and evolving jaundice in delayed hepatotoxicity
Investigations
Management
Lifestyle Modifications
- Call emergency services/urgent hospital referral for suspected significant ingestion, unknown amount, symptoms, or high-risk agent
- Remove ongoing exposure (fresh air for inhaled toxins, contaminated clothing removal, skin/eye irrigation)
- Bring medication packets/containers and timing details to hospital to improve risk stratification
- After medical stabilisation, complete psychosocial and self-harm assessment before discharge when intentional overdose is suspected
- Harm-reduction counselling: secure storage, avoid duplicate combination products (especially paracetamol), substance-use support
Pharmacological Treatment
GI decontamination
- Activated charcoal 50 g orally for adults (child: 1 g/kg up to 50 g), ideally within 1 hour of ingestion
Use when a potentially toxic dose is recent and airway is protected. Contraindicated in unprotected airway, significant aspiration risk, caustic ingestion, or hydrocarbons with high aspiration potential unless expert advice supports use.
Paracetamol antidote
- Acetylcysteine IV: 100 mg/kg over 2 hours then 200 mg/kg over 10 hours (total 300 mg/kg over 12 hours)
Start promptly when indicated by nomogram/timing uncertainty or delayed presentation. Monitor for anaphylactoid reactions (rash, wheeze, hypotension); manage reaction and restart at slower rate once stable. Continue/extend treatment if paracetamol remains detectable or LFT/INR worsen.
Opioid toxicity reversal
- Naloxone IV 400 micrograms, repeated every 2-3 minutes to restore ventilation (usual cumulative ceiling 10 mg before reconsidering diagnosis)
- Intramuscular naloxone 400 micrograms if IV access delayed
Titrate to adequate respiration rather than full wakefulness. Observe for renarcotisation because naloxone duration is shorter than many opioids; infusion may be required. In dependent patients, rapid reversal can precipitate acute withdrawal and agitation.
Tricyclic antidepressant cardiotoxicity
- Sodium bicarbonate 8.4%: 50 mmol IV bolus, repeated as needed for QRS widening/hypotension/ventricular arrhythmia
Aim for ECG narrowing and haemodynamic improvement with careful blood gas/alkalosis monitoring. Avoid class Ia and Ic antiarrhythmics. Early critical care input is advised.
Hypoglycaemia (including sulfonylurea overdose)
- Dextrose IV (for example 10% dextrose 150-200 mL bolus in adults, then infusion titrated to glucose)
- Octreotide 50-100 micrograms subcutaneously every 6-12 hours (adult) for recurrent sulfonylurea-induced hypoglycaemia
Frequent glucose monitoring is essential. Rebound hypoglycaemia is common with sulfonylureas; observation must continue after apparent recovery.
Benzodiazepine reversal (selected cases only)
- Flumazenil 200 micrograms IV over 15 seconds, then 100 micrograms at 60-second intervals up to 1 mg if needed
Avoid routine use in undifferentiated overdose. Contraindicated or high risk in mixed overdose (especially tricyclics/pro-convulsants), seizure disorders, and benzodiazepine dependence due to risk of refractory seizures/arrhythmias.
Surgical / Interventional
- No routine surgical treatment; consider extracorporeal removal (for example haemodialysis) in severe dialysable poisonings such as salicylate, lithium, methanol, or ethylene glycol after specialist toxicology advice
Complications
- Acute liver failure, encephalopathy, and coagulopathy (notably after severe paracetamol toxicity)
- Respiratory failure and aspiration pneumonia
- Seizures, coma, hypoxic brain injury
- Life-threatening arrhythmias and cardiovascular collapse
- Acute kidney injury, rhabdomyolysis, metabolic acidosis
- Death, with higher risk in opioid/poly-drug exposure and delayed presentation
Prognosis
Outcome is highly dependent on agent, dose, co-ingestants, and time to treatment. Most preschool accidental ingestions are low severity (clinically serious cases are uncommon), but a small set of high-risk drugs can be fatal even in one or two adult tablets/sachets for toddlers. In UK adults, poisoning remains a major cause of death, especially with opioids and poly-drug use; early risk assessment and antidote treatment markedly improve outcomes.
Sources & References
🏥BMJ Best Practice(1)
✅NICE Guidelines(1)
- Poisoning or overdose[overview]