Poisoning and overdose

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Poisoning is a clinical problem of exposure, timing and physiological effect. A substance may be harmless at one dose and lethal at another, while delayed absorption, active metabolites and organ impairment change the course. Product names from illicit markets are particularly unreliable. A working toxidrome can justify immediate treatment, but neither a familiar story nor a positive screening test excludes injury or another medical diagnosis.

Assessment also needs to establish why the exposure occurred and what support will make discharge safe. Accidental medication errors, dependence, self-harm, coercion and occupational exposure require different follow-up. Physical treatment and psychosocial assessment should be coordinated. Improvement after an antidote is only one part of the disposition decision: anticipated recurrence, capacity, biochemical injury and ongoing risk remain relevant.

Key points

Treat dangerous physiology before waiting to identify the exact poison or obtain a screening result.
Ask what was taken, the amount, formulation, time, route and co-ingestants; retain uncertainty rather than converting an estimate into a fact.
A normal initial examination does not exclude delayed toxicity from modified-release preparations or hepatotoxic overdose.
Use targeted concentrations such as paracetamol or salicylate when relevant; routine urine drug screens rarely guide acute treatment.
Naloxone aims to restore breathing and airway protection, not necessarily complete wakefulness.
A paracetamol nomogram is unsuitable when ingestion is staggered or timing is uncertain; seek the current NPIS pathway and start indicated treatment promptly.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Intentional and accidental ingestion

Overdose may follow self-harm, dosing error, recreational use or exposure to an incorrectly labelled product. Establish formulation and timing because delayed-release preparations change the expected onset and duration.

Non-oral exposure

Inhalation, injection, dermal contamination and ocular exposure can produce local or systemic toxicity. Staff protection and decontamination requirements depend on the route and specific agent.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Receptor-mediated toxicity
Opioids suppress respiratory drive through receptor effects; naloxone competitively reverses these actions. Different durations of action explain why respiratory depression can recur after a seemingly successful response.
2
Metabolic injury
Paracetamol overdose can overwhelm detoxification of a reactive metabolite and injure hepatocytes. Acetylcysteine supports protective pathways, with greatest benefit from prompt treatment before established severe injury.
3
Conduction and cellular effects
Some toxins impair sodium channels, repolarisation or cellular energy production. ECG abnormalities and acidaemia may therefore identify life-threatening mechanisms before the exact substance has been confirmed.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Opioid pattern

Depressed respiratory rate and depth with reduced awareness, often with small pupils, suggest opioid toxicity. Co-ingestants may alter the pupil findings, and potent or long-acting opioids can produce recurrent depression after initial reversal.

Excited or hyperthermic pattern

Agitation, tachycardia, sweating, clonus or rigidity can indicate stimulant or serotonergic toxicity, while dry skin and urinary retention suggest antimuscarinic effects. Severe hyperthermia and seizures need immediate treatment and specialist advice.

Cardiac conduction toxicity

Syncope, hypotension, broad QRS complexes or marked QT prolongation after overdose can precede arrest. Obtain serial ECGs and urgent toxicology support; ordinary arrhythmia treatment may be inappropriate for a specific poison.

Occult or delayed organ injury

Paracetamol overdose can initially cause few symptoms despite substantial hepatic risk. Modified-release ingestion, body packing and some metabolic poisons can also deteriorate after an apparently reassuring early assessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Glucose and repeated blood gasesFirst step
Why
Identify reversible metabolic threats and follow ventilation, acidaemia and lactate.
Interpretation and limitations
Interpret results alongside the toxidrome. A widening anion gap or persistent acidaemia may prompt targeted investigation for a metabolic poison; a single early normal gas does not exclude later toxicity.
02
Twelve-lead ECG with rhythm monitoring
Why
Detect conduction, repolarisation and rhythm disturbances that change urgent treatment.
Interpretation and limitations
Measure QRS duration and assess QT in context. Repeat the ECG when symptoms evolve or the agent can cause delayed cardiotoxicity, rather than relying on the first tracing alone.
03
Timed paracetamol concentration and hepatic assessment
Why
Determine treatment need in an appropriate single acute ingestion and assess organ injury.
Interpretation and limitations
For a reliably timed single ingestion, obtain the concentration at four hours or later and interpret against the UK treatment line. Uncertain or staggered ingestion requires a different pathway, with liver tests and INR informing subsequent care.
04
Selected drug levels and organ tests
Why
Clarify exposures where measured concentrations guide treatment or observation.
Interpretation and limitations
Request salicylate, lithium or other assays when the history and findings warrant, including repeat sampling for delayed peaks. Renal function, electrolytes and clotting help identify complications and treatment constraints.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Primary neurological disease

Intracranial haemorrhage, stroke, seizure and central nervous system infection can mimic intoxication. Focal findings, injury history or failure to improve should reopen the neurological assessment.

Metabolic illness

Hypoglycaemia, electrolyte abnormalities, hypercapnia and hepatic or uraemic encephalopathy can resemble sedative poisoning. Bedside glucose and targeted blood tests are necessary even when drug exposure is plausible.

Mixed exposure

Several agents may produce conflicting signs, such as stimulation with simultaneous respiratory depression. A partial antidote response supports one component but does not exclude additional toxicity or another illness.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Worked caseRecurrent respiratory depression after opioid reversalFirst stepAn adult with suspected illicit opioid use has a pulse, respiratory rate six/min and reduced consciousness. Airway support and bag-mask ventilation are started; IV access is available.

1Call experienced help and provide effective ventilation with oxygen while attaching ECG, oximetry and capnography where available. Check glucose and look for injury or co-ingestion in parallel.
2Titrate small IV naloxone doses to respiratory recovery in this non-arrest setting. After a total 400 micrograms, respiratory rate rises to twelve/min with adequate depth and airway protection, although the patient remains sleepy.
3Recognise this as an appropriate respiratory endpoint rather than an automatic indication to force complete arousal. Continue direct observation and reassess the reliability of spontaneous ventilation.
4Twenty minutes later breathing deteriorates again. Resume assistance and give further titrated naloxone; seek monitored admission and an infusion plan because recurrent depression suggests the opioid is outlasting the antagonist.
5Verify a sustained response under the chosen support and document each bolus and time. Before eventual discharge, meet the exposure-specific observation requirements and arrange drug-service support and overdose-prevention advice.

02Paracetamol branchAn uncertain ingestion historyAn adult reports taking repeated excessive paracetamol doses throughout the evening and cannot reliably identify when the first or last dose was taken.

1Obtain the available packet, estimated dose and co-ingestants, but do not plot an invented time on a nomogram. Send paracetamol concentration, liver tests, INR, renal function and other clinically indicated tests.
2Use current TOXBASE or NPIS advice and initiate acetylcysteine when indicated for the uncertain or staggered overdose, without waiting for a deceptively low concentration to provide reassurance.
3Monitor for infusion reactions and repeat the required blood tests before the planned treatment endpoint. Continuing liver injury or other treatment criteria may require further acetylcysteine and specialist liver-unit discussion.

03Decontamination branchConsidering activated charcoalA patient presents soon after a potentially toxic oral ingestion and the team is considering gastrointestinal decontamination.

1Establish whether the agent binds to charcoal, the likely dose and elapsed time, and whether the airway is protected. Consult the specific poison guidance when the exposure or benefit is uncertain.
2Consider single-dose charcoal for a relevant ingestion usually within one hour; do not give it to an obtunded patient with an unprotected airway or for an agent where aspiration risk outweighs benefit.
3Do not use routine gastric lavage. Continue monitoring and antidotal treatment where indicated; charcoal does not remove an already absorbed toxin or replace resuscitation.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Reverse opioid-mediated respiratory depression in the acute overdose context.

Naloxone for non-arrest opioid respiratory depression

With airway and ventilation support, give 100–200 micrograms IV every 60 seconds, titrating to adequate breathing and protective reflexes. Larger cumulative doses may be needed; recurrent toxicity requires repeated boluses and a senior infusion plan.

Respiratory arrest or peri-arrest needs the separate urgent RCEM escalation regimen alongside resuscitation. Excess reversal may precipitate withdrawal. The opioid may last longer than naloxone, and mixed poisoning can limit response.

Prevent or reduce hepatic injury when paracetamol exposure meets treatment criteria.

Acetylcysteine for paracetamol overdose

The authorised IV course is 150 mg/kg over 1 hour, then 50 mg/kg over 4 hours, then 100 mg/kg over 16 hours: 300 mg/kg over 21 hours. Use the prescribed product’s dilution chart and a ceiling weight of 110 kg.

Alternative local regimens require their own approved protocol. Review tests before stopping; further treatment may be needed. Adapt diluent volume for low weight or fluid restriction and manage reactions promptly with senior or NPIS advice.

Reduce absorption of a clinically important ingested substance that binds to charcoal, after the airway and expected benefit have been assessed.

Activated charcoal for selected recent oral poisonings

For an eligible adult, give 50 g orally as a single dose, preferably within 1 hour of ingestion. Use the product preparation instructions and obtain agent-specific NPIS advice; repeated dosing is a separate specialist decision.

Do not give with an unprotected airway or after caustic, foaming or hydrocarbon ingestion. It does not usefully adsorb alcohols, iron or lithium. Consider obstruction or ileus and aspiration risk; charcoal must never delay resuscitation or a needed antidote.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Aspiration and respiratory arrest

Reduced awareness and vomiting threaten the airway, while respiratory depressants reduce ventilation directly. Supportive airway care remains essential even when an effective antidote is available.

Delayed organ failure

Hepatic, renal or muscle injury can emerge after an initially mild presentation. Observation and repeat laboratory assessment should reflect the expected toxic course rather than current symptoms alone.

Recurrent poisoning or self-harm

Without coordinated follow-up, the circumstances leading to overdose may persist. Appropriate psychosocial assessment, medicine review, harm-reduction advice and service referral are needed before the episode is considered resolved.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Reassess respiratory rate, depth, airway reflexes and conscious level repeatedly after naloxone; record oxygen support because saturation alone can conceal persistent hypoventilation.
Repeat ECGs, electrolytes and acid-base tests according to the toxin and course, and escalate new QRS widening, arrhythmia, seizures or hyperthermia immediately.
Check appropriate liver, clotting and paracetamol results before completing acetylcysteine; do not stop solely because the final scheduled bag has ended.
For opioid overdose, RCEM generally requires at least four hours after the last naloxone and six hours after use, with longer observation for long-acting agents and an individualised admission or discharge decision.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Antidote availability is an operational issue

Some antidotes are held regionally. Early NPIS contact in severe poisoning can mobilise supplies while the team continues immediate supportive treatment and investigates the exposure.

An infusion needs an explicit calculation

For recurrent opioid depression, RCEM bases the initial hourly naloxone infusion on sixty percent of the effective bolus needed at the second reversal. Confirm concentration, pump rate and close observation with the senior team.

Capacity must be assessed specifically

A wish to leave does not establish or remove capacity. Assess understanding, retention, use or weighing of information and communication for the decision at that time, seeking senior support where intoxication complicates assessment.

Prevention is part of treatment

After a non-fatal overdose, offer appropriate drug-service referral and discuss access to take-home naloxone and training. Self-harm presentations also require psychosocial assessment and a coordinated safety plan.

11Common pitfallsFrequent interpretation and management errors.

01
Do not regard a negative urine drug screen as evidence that a dangerous poisoning is excluded.
02
Do not use flumazenil routinely in an unexplained mixed overdose, where withdrawal or proconvulsant co-ingestion may make reversal hazardous.
03
Do not administer activated charcoal to an unprotected airway or assume it treats alcohols, metals and other poorly adsorbed agents.
04
Do not discharge merely because the patient is awake: delayed toxicity, recurrent sedation, organ injury and ongoing psychosocial risk still require assessment.

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