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Acute Poisoning - General Approach

Acute poisoning is exposure to a toxic substance causing harm through ingestion, inhalation, injection, or dermal contac... MRCEM exam preparation.

Updated 10 Jan 2026
Reviewed 17 Jan 2026
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Clinical reference article

Acute Poisoning - General Approach

1. Clinical Overview

Summary

Acute poisoning is exposure to a toxic substance causing harm through ingestion, inhalation, injection, or dermal contact. It represents a common medical emergency with significant morbidity and mortality worldwide. The cornerstone of management is a systematic approach prioritizing airway protection, cardiorespiratory support, toxidrome recognition, selective decontamination, specific antidote administration when available, and enhanced elimination techniques for selected toxins. Most poisonings are managed successfully with supportive care alone, but early recognition of life-threatening toxidromes and timely intervention with specific antidotes can be lifesaving. [1]

Key Facts

  • Global burden: Approximately 193,000 deaths annually from unintentional poisoning worldwide [2]
  • Incidence: Emergency department presentations for poisoning vary by region (50-300 per 100,000 population/year) [3]
  • Mortality: Overall case fatality less than 1% in developed countries with access to poison centers, but varies significantly by substance [4]
  • Peak age: Bimodal distribution - children less than 5 years (accidental), adults 20-40 years (intentional self-harm) [3]
  • Common substances: Analgesics (paracetamol, NSAIDs), antidepressants, benzodiazepines, opioids, household chemicals [5]
  • Critical feature: Toxidrome recognition enables directed therapy even when the specific agent is unknown [6]
  • Time-critical interventions: Airway management, naloxone for opioids, N-acetylcysteine for paracetamol, activated charcoal within 1 hour [7,8]

Clinical Pearls

"ABCs before antidotes" — Airway, breathing, and circulation take absolute priority. Patients die from respiratory failure and shock, not from lack of specific antidotes. Secure the airway, support ventilation, and stabilize hemodynamics before considering decontamination or antidotes.

"Toxidromes are pattern recognition" — The five classic toxidromes (anticholinergic, cholinergic, opioid, sympathomimetic, sedative-hypnotic) provide a diagnostic framework even with unknown ingestions. Recognize the pattern, anticipate complications, and initiate empiric therapy. [6]

"Activated charcoal is selective, not universal" — Single-dose activated charcoal reduces absorption only for specific toxins and only when given within 1 hour of ingestion. It is contraindicated for corrosives, hydrocarbons, alcohols, and metals. Routine use is not recommended by toxicology societies. [9,10]

"The 'toxic dose' is patient-specific" — Age, comorbidities, polypharmacy, and coingestants dramatically alter toxicity. A 'safe' dose in one patient may be lethal in another, particularly in the elderly, those with hepatic/renal disease, or children.

"Most poisonings don't have antidotes" — Supportive care (airway management, fluid resuscitation, correction of metabolic derangements) is the mainstay of treatment for the majority of poisonings. Don't delay supportive measures searching for a specific antidote.

Why This Matters Clinically

Acute poisoning accounts for approximately 1-2% of all emergency department presentations in developed countries and remains a leading cause of morbidity in young adults. [3,5] A systematic, evidence-based approach reduces mortality, ICU admission rates, and duration of hospitalization. The ability to recognize toxidromes, make judicious decisions about decontamination, and implement enhanced elimination techniques when indicated distinguishes competent emergency medicine and intensive care practice. With the opioid epidemic, novel psychoactive substances, and increasing polypharmacy in aging populations, toxicological emergencies are becoming more complex and require up-to-date knowledge of antidote protocols and extracorporeal treatment indications.


2. Epidemiology

Incidence & Prevalence

Global Burden:

  • Deaths: Estimated 193,460 deaths globally from unintentional poisoning (2019 data) [2]
  • Emergency presentations: Poisoning accounts for 0.5-2% of all ED visits in developed countries [3,5]
  • Incidence: 50-300 per 100,000 population per year (varies by region and reporting practices) [3]
  • Intentional vs accidental: Intentional self-poisoning accounts for 60-80% of adult presentations; accidental poisoning dominates in children less than 5 years [5]

Temporal Trends:

  • Paracetamol poisoning remains the most common cause of intentional overdose in many Western countries [5]
  • Opioid-related poisoning deaths have increased dramatically in North America (epidemic proportions) [11]
  • Novel psychoactive substances (synthetic cannabinoids, cathinones) are emerging threats with unpredictable toxicity [1]

Demographics

FactorDetails
AgeBimodal: children 1-5 years (exploratory accidental), adults 20-40 years (intentional self-harm)
SexFemales > males for intentional overdose presentations; males have higher fatality rates [3]
EthnicityNo consistent ethnic variation; socioeconomic factors more influential
GeographyHigher rates in low- and middle-income countries due to pesticide availability and limited healthcare access [2]
SettingEmergency departments, poison control centers, ICU admissions for severe cases

Risk Factors

Non-Modifiable:

  • Age (extremes: children, elderly)
  • History of prior suicide attempts (strongest predictor of repeat self-harm) [3]
  • Mental health disorders (depression, personality disorders, substance use disorders)

Modifiable:

Risk FactorRelative RiskMechanism
Mental health conditions5-10×Intentional self-poisoning as method of self-harm
Substance use disorder5-10×Intentional overdose, reduced awareness, polypharmacy
Medication access3-5×Accidental (children, elderly) or intentional overdose
Occupational exposure2-4×Agriculture (pesticides), healthcare (pharmaceuticals), industry (chemicals)
Alcohol use2-3×Impaired judgment, coingestants, synergistic CNS depression

Common Substances by Region

High-Income Countries:

SubstanceFrequencyTypical PatientNotes
Paracetamol (acetaminophen)15-25%All ages, intentional or accidentalLeading cause of acute liver failure [8]
Benzodiazepines10-15%Adults, intentionalLow toxicity alone; dangerous with coingestants
Antidepressants10-15%Adults, intentionalSSRIs safer than TCAs; serotonin syndrome risk
Opioids10-20%Adults, intentional or accidentalIncreasing prevalence; fentanyl analogs highly potent [11]
NSAIDs5-10%All agesGenerally low toxicity except in massive overdose

Low- and Middle-Income Countries:

SubstanceFrequencyTypical PatientNotes
Pesticides30-50%Agricultural workers, intentional self-harmMajor contributor to global poisoning mortality [2]
Corrosives10-20%Accidental or intentionalAcids, alkalis; severe morbidity
Traditional medicinesVariableAll agesHeavy metal contamination, plant alkaloids

3. Pathophysiology

Routes of Exposure and Toxicokinetics

Routes of Absorption:

  1. Gastrointestinal (most common): Absorption depends on gastric pH, gastric emptying, formulation (immediate vs. sustained-release), and presence of food
  2. Inhalational: Rapid absorption, bypasses first-pass metabolism (carbon monoxide, volatile hydrocarbons, smoke)
  3. Dermal: Significant for lipophilic substances (organophosphates, some chemical warfare agents)
  4. Intravenous/injection: Immediate systemic effect, bypasses absorption phase (drug injection, envenomation)

Toxicokinetics:

  • Absorption: Enhanced by lipophilicity, ionization state, mucosal contact time
  • Distribution: Depends on volume of distribution (Vd), protein binding, lipophilicity
  • Metabolism: Hepatic (CYP450 enzymes); some toxins have active or more toxic metabolites (paracetamol → NAPQI, methanol → formic acid, ethylene glycol → glycolic/oxalic acids)
  • Elimination: Renal excretion (many drugs), hepatic metabolism, pulmonary (volatile substances)

Time Course:

  • Immediate-release formulations: Peak levels typically 1-2 hours post-ingestion
  • Sustained-release formulations: Delayed and prolonged absorption (up to 12-24 hours for some preparations)
  • Delayed toxicity: Paracetamol (hepatotoxicity at 24-72 hours), paraquat (pulmonary fibrosis over days-weeks), delayed-release medications

Toxidromes: The Clinical Patterns

Toxidromes are constellation of clinical signs allowing categorization of poisonings even when the specific agent is unknown. [6] Recognition guides empiric therapy and anticipates complications.

1. ANTICHOLINERGIC TOXIDROME

FeatureMechanismExamples
Mnemonic"Mad as a hatter, dry as a bone, red as a beet, hot as a hare, blind as a bat, full as a flask"Competitive antagonism of muscarinic receptors
Vital signsTachycardia, hypertension, hyperthermia
CNSAgitation, confusion, hallucinations, seizures, coma (severe)Antihistamines, TCAs, atropine, antipsychotics
AutonomicDry skin and mucous membranes, mydriasis, ileus, urinary retentionBenztropine, scopolamine, jimson weed
TreatmentSupportive care; physostigmine rarely indicated (risk of seizures/bradycardia)

2. CHOLINERGIC TOXIDROME

FeatureMechanismExamples
MnemonicSLUDGE: Salivation, Lacrimation, Urination, Defecation, GI upset, EmesisAcetylcholinesterase inhibition
Muscarinic effectsBronchospasm, bronchorrhea, bradycardia, miosis, diaphoresisOrganophosphates, carbamates
Nicotinic effectsMuscle fasciculations, weakness, paralysis (respiratory failure)Nerve agents, insecticides
CNSConfusion, seizures, coma
TreatmentAtropine (muscarinic effects), pralidoxime (nicotinic effects, organophosphates only), benzodiazepines (seizures) [12]

3. OPIOID TOXIDROME

FeatureMechanismExamples
Classic triadMiosis, respiratory depression, decreased consciousnessμ-opioid receptor agonism (CNS, respiratory center)
Vital signsBradypnea, bradycardia, hypotension, hypothermiaMorphine, heroin, fentanyl, oxycodone
PupilsPinpoint (miosis) — highly specific but not sensitiveTramadol (mydriasis possible), meperidine
OtherDecreased bowel sounds, urinary retention, pulmonary edema (non-cardiogenic)
TreatmentNaloxone (0.04-0.4 mg IV, titrate to respiratory rate > 12/min, not full consciousness) [13]Risk of precipitated withdrawal; short half-life requires monitoring

4. SYMPATHOMIMETIC TOXIDROME

FeatureMechanismExamples
Vital signsTachycardia, hypertension, hyperthermia, tachypneaIncreased catecholamine release/reuptake inhibition
CNSAgitation, psychosis, seizures, hyperreflexiaAmphetamines, cocaine, MDMA, synthetic cathinones
AutonomicMydriasis, diaphoresis (sweating), piloerectionCaffeine, ephedrine, pseudoephedrine
ComplicationsRhabdomyolysis, hyperthermia, intracranial hemorrhage, myocardial infarction, dissection
TreatmentBenzodiazepines (first-line for agitation, hypertension, seizures), cooling, avoid β-blockers (unopposed α-stimulation)

5. SEDATIVE-HYPNOTIC TOXIDROME

FeatureMechanismExamples
CNS depressionCNS depressant via GABA₍A₎ receptor agonism (benzodiazepines, barbiturates), other mechanismsBenzodiazepines, barbiturates, ethanol, GHB, Z-drugs
Vital signsBradycardia, hypotension, hypothermia, respiratory depression (dose-dependent)
PupilsNormal or mydriasis (contrast with opioids)
OtherHyporeflexia, ataxia, slurred speech, nystagmus
TreatmentSupportive care; flumazenil available for benzodiazepines but rarely used (seizure risk in mixed overdoses or chronic users) [14]

Special Toxidromes and Syndromes

Serotonin Syndrome:

  • Mechanism: Excessive serotonergic activity (SSRIs, MAOIs, tramadol, linezolid, MDMA)
  • Features: Hyperthermia, clonus, hyperreflexia, agitation, diaphoresis, tremor, mydriasis
  • Hunter criteria: Most sensitive diagnostic criteria [1]
  • Treatment: Benzodiazepines, cooling, cyproheptadine (serotonin antagonist)

Neuroleptic Malignant Syndrome (NMS):

  • Mechanism: Dopamine D₂ receptor antagonism (antipsychotics)
  • Features: Hyperthermia, "lead-pipe" rigidity, altered mental status, autonomic instability
  • Differs from serotonin syndrome: Rigidity (not clonus), slower onset (days)
  • Treatment: Supportive care, dantrolene, bromocriptine

4. Clinical Presentation

History: The 5 W's

When obtaining history in poisoned patients, use the mnemonic "5 W's + H":

  1. WHAT was taken? (substance, formulation, brand name)
  2. WHEN was it taken? (time of ingestion)
  3. WHERE did exposure occur? (home, workplace, outdoors)
  4. WHY was it taken? (accidental, intentional, recreational)
  5. HOW MUCH was taken? (number of tablets, volume, concentration)
  6. HOW was it taken? (oral, inhalation, injection, dermal)

Additional Critical Questions:

  • Coingestants (alcohol, other drugs)
  • Staggered vs. single ingestion
  • Immediate-release vs. sustained-release formulation
  • Vomiting after ingestion
  • Prior suicide attempts
  • Access to other medications/toxins
  • Symptoms timeline

Symptoms: The Patient's Story

Non-Specific Early Symptoms (common to many poisonings):

  • Nausea and vomiting (GI irritation, CNS effect)
  • Dizziness, lightheadedness
  • Drowsiness, confusion
  • Abdominal pain

Toxidrome-Specific Symptoms:

  • Anticholinergic: Dry mouth, blurred vision, hallucinations, confusion
  • Cholinergic: Excessive salivation, diarrhea, abdominal cramps, blurred vision (miosis)
  • Opioid: Euphoria (early), drowsiness, "nodding off"
  • Sympathomimetic: Anxiety, agitation, palpitations, chest pain
  • Sedative-hypnotic: Drowsiness, slurred speech, ataxia

Signs: Clinical Examination

Vital Signs Assessment:

Vital SignAbnormalityDifferential Toxidromes
TemperatureHyperthermia (> 38.5°C)Sympathomimetic, anticholinergic, serotonin syndrome, NMS, salicylates, DNP
Hypothermia (less than 35°C)Sedative-hypnotic, opioid, ethanol, hypoglycemic agents
Heart RateTachycardia (> 100 bpm)Sympathomimetic, anticholinergic, salicylates, β-agonists, theophylline, withdrawal
Bradycardia (less than 60 bpm)Opioid, cholinergic, β-blockers, calcium channel blockers, digoxin
Blood PressureHypertensionSympathomimetic, anticholinergic (severe), withdrawal
HypotensionSedative-hypnotic, opioid, β-blockers, calcium channel blockers, TCAs
Respiratory RateTachypnea (> 20/min)Salicylates, sympathomimetic, metabolic acidosis (methanol, ethylene glycol)
Bradypnea (less than 10/min)Opioid, sedative-hypnotic (severe)

Neurological Examination:

FindingSignificanceExamples
PupilsMiosis (pinpoint)Opioids, cholinergic, clonidine
Mydriasis (dilated)Anticholinergic, sympathomimetic, withdrawal
Mental StatusAgitation, hallucinationsAnticholinergic, sympathomimetic, serotonin syndrome
Sedation, comaOpioid, sedative-hypnotic, antipsychotics
ToneRigidityNMS, serotonin syndrome (different quality)
FlacciditySedative-hypnotic (severe), botulism
ReflexesHyperreflexia, clonusSerotonin syndrome, sympathomimetic
HyporeflexiaSedative-hypnotic, botulism

Skin Examination:

FindingToxidromeExamples
Dry skinAnticholinergicAntihistamines, TCAs
Diaphoresis (sweating)Cholinergic, sympathomimetic, serotonin syndromeOrganophosphates, cocaine
BullaeProlonged immobilityBarbiturates, carbon monoxide
CyanosisMethemoglobinemiaDapsone, nitrites, local anesthetics
Cherry-red appearanceCarboxyhemoglobinemiaCarbon monoxide (rare sign)

Red Flags

[!CAUTION] Red Flags — Immediate Escalation Required:

  • Airway compromise: GCS ≤8, absent gag reflex, stridor → immediate intubation
  • Respiratory depression: RR less than 10/min, SpO₂ less than 90% → ventilatory support, naloxone if opioid suspected
  • Cardiovascular instability: SBP less than 90 mmHg, severe arrhythmias, QRS > 100 ms → ICU, specific therapy
  • Seizures: Uncontrolled seizures → benzodiazepines, exclude hypoglycemia
  • Severe agitation/hyperthermia: Temperature > 40°C, agitation → aggressive cooling, sedation, exclude serotonin syndrome/NMS
  • Metabolic crisis: pH less than 7.1, lactate > 4 mmol/L, glucose less than 3 mmol/L → correct immediately
  • ECG abnormalities: QRS > 100 ms (sodium channel blockade), QTc > 500 ms (torsades risk) → continuous monitoring

5. Investigations

Bedside Investigations (Immediate)

1. Point-of-Care Glucose

  • Indication: All patients with altered mental status
  • Action: Treat hypoglycemia immediately (thiamine 100 mg IV before dextrose if malnourished/alcoholic to prevent Wernicke's encephalopathy)

2. 12-Lead ECG

  • Essential for all moderate-severe poisonings
  • Key abnormalities:
    • "QRS prolongation (> 100 ms): Sodium channel blockers (TCAs, cocaine, flecainide, quinidine) → sodium bicarbonate [1]"
    • "QTc prolongation (> 500 ms): Antipsychotics, methadone, macrolides → magnesium, correct K⁺"
    • "Bradycardia: β-blockers, calcium channel blockers, digoxin"
    • "Atrioventricular block: Digoxin, β-blockers, calcium channel blockers"

3. Capillary Blood Gas (venous acceptable)

  • pH: Metabolic acidosis (high anion gap) suggests toxic alcohols, salicylates, metformin
  • Lactate: Elevated in metformin, cyanide, carbon monoxide, profound shock
  • Carboxyhemoglobin: If carbon monoxide suspected

Laboratory Investigations

First-Line (for moderate-severe poisonings):

TestIndicationExpected FindingAction
Paracetamol levelAll intentional overdoses, unknown ingestionsPlot on Rumack-Matthew nomogram (> 4 hours post-ingestion)N-acetylcysteine if above treatment line [8]
Salicylate levelSuspicion of aspirin overdose, unexplained metabolic acidosis> 300 mg/L (therapeutic 150-300 mg/L)Urinary alkalinization, consider hemodialysis if > 700 mg/L [15]
Arterial/venous blood gasAltered mental status, suspected metabolic derangementHigh anion gap metabolic acidosisCalculate osmolar gap if toxic alcohols suspected
Urea & ElectrolytesAll significant poisoningsAKI (salicylates, lithium), hypokalemia (salbutamol), hyperkalemia (digoxin)Correct electrolyte abnormalities
GlucoseAltered mental statusHypoglycemia (insulin, sulfonylureas, ethanol), hyperglycemiaCorrect immediately
LactateSuspected metformin, cyanide, carbon monoxide, seizuresElevated (> 4 mmol/L)Source control, supportive care

Second-Line (based on clinical suspicion):

TestIndicationClinical Use
Serum osmolality (measured)Suspected toxic alcohol ingestion (methanol, ethylene glycol, isopropanol)Calculate osmolar gap: (measured - calculated) > 10 mOsm/kg suggests unmeasured osmoles [1]
Liver function testsParacetamol overdose, hepatotoxic substancesTransaminitis at 24-72 hours (paracetamol), prognostic (PT/INR)
Creatine kinaseProlonged immobility, seizures, hyperthermiaRhabdomyolysis (CK > 1000 U/L) → aggressive hydration, monitor renal function
TroponinChest pain, sympathomimetic toxidrome, carbon monoxideMyocardial ischemia/infarction
Lithium levelKnown lithium user, unexplained altered mental statusTherapeutic 0.6-1.2 mmol/L; toxicity > 1.5 mmol/L; severe > 2.5 mmol/L → hemodialysis [16]
Digoxin levelKnown digoxin user, bradycardia, AV blockToxicity often at therapeutic levels in acute-on-chronic; digoxin-specific antibody fragments if severe [1]
CarboxyhemoglobinSuspected carbon monoxide exposure> 3% (non-smoker), > 10% (smoker) → hyperbaric oxygen for severe cases
MethemoglobinCentral cyanosis with normal PaO₂, "chocolate" blood> 20% symptomatic → methylene blue (1-2 mg/kg IV)

Toxicology Screens:

  • Urine drug screens (immunoassay): Limited clinical utility; high false-positive/negative rates; do not guide acute management
  • Specific drug levels: Order only when result will change management (e.g., paracetamol, salicylate, lithium, digoxin, anticonvulsants, theophylline)
  • Comprehensive toxicology: Rarely available acutely; forensic value only

Imaging

Chest X-Ray:

  • Indications: Respiratory symptoms, suspected aspiration, hydrocarbon ingestion, body packers
  • Findings: Aspiration pneumonitis, pulmonary edema (salicylates, opioids), ARDS, radio-opaque substances

CT Brain (non-contrast):

  • Indications: Persistent altered mental status unexplained by toxidrome, focal neurology, head trauma
  • Findings: Intracranial hemorrhage, structural lesion (exclude alternative diagnoses)

Abdominal X-Ray (rarely indicated):

  • "CHIPES" mnemonic for radio-opaque substances: Chloral hydrate, Heavy metals (iron, lead), Iodine, Packets/Phenothiazines, Enteric-coated tablets, Sustained-release formulations
  • Limited sensitivity: Absence does not exclude ingestion

6. Management

Management Algorithm

         ACUTE POISONING PRESENTATION
            ↓
┌──────────────────────────────────────────────────┐
│   IMMEDIATE RESUSCITATION (PRIORITY)             │
│   • Airway: Assess (GCS ≤8 → intubate)           │
│   • Breathing: SpO₂, ventilatory support         │
│   • Circulation: IV access, fluids, pressors     │
│   • Disability: Glucose, pupils, GCS             │
│   • Exposure: Full examination, decontaminate    │
└──────────────────────────────────────────────────┘
            ↓
┌──────────────────────────────────────────────────┐
│   ESSENTIAL BEDSIDE TESTS                        │
│   • ECG (QRS, QTc, rate, rhythm)                 │
│   • Glucose (treat hypoglycemia immediately)     │
│   • Blood gas (pH, lactate, anion gap)           │
└──────────────────────────────────────────────────┘
            ↓
┌──────────────────────────────────────────────────┐
│   TOXIDROME RECOGNITION                          │
│   • Anticholinergic • Cholinergic                │
│   • Opioid • Sympathomimetic • Sedative-hypnotic │
│   → Guides empiric therapy                       │
└──────────────────────────────────────────────────┘
            ↓
┌──────────────────────────────────────────────────┐
│   DECONTAMINATION (selective, time-dependent)    │
│   ├─ ACTIVATED CHARCOAL (if appropriate)         │
│   │   → Within 1 hour, no contraindications      │
│   │   → NOT for: corrosives, hydrocarbons,       │
│   │      alcohols, metals, lithium               │
│   ├─ GASTRIC LAVAGE (rarely indicated)           │
│   │   → Life-threatening ingestion less than 1 hour       │
│   ├─ WHOLE BOWEL IRRIGATION                      │
│   │   → Sustained-release, body packers, iron    │
│   └─ DERMAL DECONTAMINATION                      │
│       → Remove clothing, copious water irrigation │
└──────────────────────────────────────────────────┘
            ↓
┌──────────────────────────────────────────────────┐
│   SPECIFIC ANTIDOTES (if indicated)              │
│   • Naloxone (opioids)                           │
│   • N-acetylcysteine (paracetamol)               │
│   • Atropine + pralidoxime (organophosphates)    │
│   • Sodium bicarbonate (sodium channel blockers) │
│   • Digoxin-specific Fab (digoxin)               │
│   • Fomepizole (toxic alcohols)                  │
│   • High-dose insulin euglycemia (CCB/BB)        │
│   • Lipid emulsion (local anesthetic toxicity)   │
└──────────────────────────────────────────────────┘
            ↓
┌──────────────────────────────────────────────────┐
│   ENHANCED ELIMINATION (specific indications)    │
│   • Urinary alkalinization (salicylates)         │
│   • Multiple-dose activated charcoal (MDAC)      │
│     → Carbamazepine, dapsone, phenobarbital,     │
│        quinine, theophylline                     │
│   • Hemodialysis (EXTRIP criteria)               │
│     → Lithium, toxic alcohols, salicylates,      │
│        metformin, valproate                      │
└──────────────────────────────────────────────────┘
            ↓
┌──────────────────────────────────────────────────┐
│   SUPPORTIVE CARE & MONITORING                   │
│   • Continuous cardiac monitoring                │
│   • Serial vital signs, neurological assessment  │
│   • Repeat labs (paracetamol at 4h, salicylate)  │
│   • Treat complications (seizures, arrhythmias)  │
│   • Psychiatric assessment (if intentional)      │
└──────────────────────────────────────────────────┘

Acute Resuscitation (The First 15 Minutes)

ABCDE Approach (simultaneous interventions):

A - Airway:

  • Assess: GCS ≤8, absent gag reflex, copious secretions, stridor
  • Secure: Rapid sequence intubation if compromised (consider naloxone trial first if opioid toxidrome)
  • Positioning: Recovery position if reduced GCS but maintaining airway

B - Breathing:

  • Assess: Respiratory rate, SpO₂, work of breathing, auscultation
  • Support:
    • Oxygen to maintain SpO₂ > 94% (target 88-92% if carbon monoxide suspected and hyperbaric oxygen available)
    • Naloxone 0.4-2 mg IV if opioid-induced respiratory depression (may need repeat doses or infusion) [13]
    • Bag-valve-mask ventilation or intubation if inadequate

C - Circulation:

  • Assess: BP, HR, capillary refill, ECG
  • Support:
    • IV access (two large-bore cannulae)
    • Fluid resuscitation (20 mL/kg crystalloid bolus if hypotensive)
    • Vasopressors (norepinephrine) if refractory to fluids
    • Correct arrhythmias (see specific antidotes below)

D - Disability:

  • Assess: GCS, pupils, blood glucose, temperature
  • Treat:
    • Dextrose 50 mL of 50% (25 g) IV if hypoglycemia (give thiamine 100 mg IV first if malnourished)
    • Benzodiazepines (lorazepam 4 mg IV or diazepam 10 mg IV) for seizures
    • Cooling measures if hyperthermia > 39.5°C (evaporative cooling, ice packs to groin/axillae, cold IV fluids)

E - Exposure:

  • Full examination: Look for injection sites, pill fragments, dermal exposure
  • Decontamination: Remove contaminated clothing, wash skin with copious water

Gastrointestinal Decontamination

Activated Charcoal (Single-Dose):

ParameterRecommendationEvidence
IndicationsPotentially toxic ingestion within 1 hour, cooperative patient or intubatedPosition statement: AACT/EAPCCT [9]
Dose50 g adults (1 g/kg children) in 200-300 mL water, oral or NG tube
TimingMaximum benefit within 1 hour; limited benefit 1-2 hours; not recommended > 2 hoursBenefit declines rapidly with time [9]
ContraindicationsAbsolute: Unprotected airway with reduced GCS, corrosives, hydrocarbons (aspiration risk), bowel obstruction/perforation
Relative: Anticipated endoscopy, specific antidote more effective
NOT effective forAlcohols, acids/alkalis, cyanide, iron, lithium, potassium, heavy metals, hydrocarbonsPoor adsorption profile
Adverse effectsAspiration pneumonitis (most serious), constipation, vomiting, black stools

Multiple-Dose Activated Charcoal (MDAC):

  • Indications: Life-threatening poisoning with drugs undergoing enterohepatic recirculation or slow absorption [10]
  • Drugs: Carbamazepine, dapsone, phenobarbital, quinine, theophylline
  • Dose: 50 g loading dose, then 25 g every 4 hours (or 12.5 g every 2 hours)
  • Evidence: Increases drug clearance in volunteer studies; limited clinical outcome data [10]
  • Contraindications: Same as single-dose; bowel sounds must be present

Gastric Lavage:

  • Indications: Life-threatening ingestion within 1 hour, substance not adsorbed by charcoal (iron, lithium), contraindication to charcoal
  • NOT routinely recommended: AACT/EAPCCT position statement advises against routine use [7]
  • Technique: 36-40 Fr orogastric tube, lavage with 200-300 mL aliquots until clear (max 2-3 L), protect airway (intubate if GCS ≤8)
  • Complications: Aspiration, esophageal/gastric perforation, trauma, laryngospasm

Whole Bowel Irrigation (WBI):

  • Indications: Sustained-release or enteric-coated preparations, body packers/stuffers, substances not adsorbed by charcoal (iron, lithium)
  • Contraindication: Bowel obstruction, perforation, hemodynamic instability, intractable vomiting
  • Technique: Polyethylene glycol electrolyte solution (GoLYTELY) 1-2 L/hour (adults) via NG tube until rectal effluent clear
  • Evidence: Limited RCT data; case series suggest benefit for slow-release preparations and body packers [1]

Dermal Decontamination:

  • Indications: All dermal exposures (pesticides, organophosphates, corrosives, chemical burns)
  • Technique: Remove all clothing, copious water irrigation (15-20 minutes minimum), avoid scrubbing (increases absorption), protect healthcare workers (gloves, gown)

Specific Antidotes and Treatments

1. NALOXONE (Opioid Receptor Antagonist)

ParameterDetails
IndicationOpioid toxidrome (respiratory depression, miosis, reduced GCS) [13]
DoseInitial: 0.04-0.4 mg IV (titrate to respiratory effort, NOT consciousness); Alternative: 0.8-2 mg IM/IN if no IV access; Repeat: q2-3 minutes if inadequate response
GoalRespiratory rate > 12/min with adequate tidal volume (avoid full reversal to prevent withdrawal and agitation)
InfusionIf repeat boluses required: infusion at 2/3 of effective bolus dose per hour
DurationShort half-life (30-90 minutes) vs. most opioids → requires monitoring for re-sedation, especially with long-acting opioids (methadone, sustained-release formulations)
Special considerationsFentanyl and analogs may require high doses (up to 10 mg); buprenorphine (partial agonist) less responsive

2. N-ACETYLCYSTEINE (Glutathione Precursor)

ParameterDetails
IndicationParacetamol (acetaminophen) overdose [8]
CriteriaSerum paracetamol level above treatment line on Rumack-Matthew nomogram (> 4 hours post-ingestion); OR ingestion > 150 mg/kg and level not available within 8 hours; OR any evidence of hepatotoxicity
Regimen (IV)Loading: 150 mg/kg in 200 mL 5% dextrose over 1 hour; Second bag: 50 mg/kg in 500 mL over 4 hours; Third bag: 100 mg/kg in 1000 mL over 16 hours (total 21 hours)
Extended therapyContinue if ALT rising, INR > 1.5, or detectable paracetamol: 100 mg/kg over 16 hours, repeat until criteria resolved [8]
Adverse effectsAnaphylactoid reactions (flushing, rash, bronchospasm) in 10-20%, usually during loading dose; slow/stop infusion, give antihistamines, restart at slower rate

3. SODIUM BICARBONATE (Sodium Channel Blocker Toxicity)

ParameterDetails
IndicationQRS > 100 ms from sodium channel blockade (TCAs, cocaine, flecainide, quinidine) [1]
Dose1-2 mmol/kg (50-100 mL of 8.4% solution) IV bolus, repeat q5min until QRS less than 100 ms
TargetSerum pH 7.45-7.55 (alkalemia enhances sodium channel recovery)
MaintenanceBicarbonate infusion: 3 ampoules (150 mmol) in 1 L 5% dextrose at 150-250 mL/h
MonitoringSerial ECGs, arterial pH, potassium (may drop with alkalinization)

4. ATROPINE (Muscarinic Antagonist for Cholinergic Crisis)

ParameterDetails
IndicationOrganophosphate/carbamate poisoning (cholinergic toxidrome) [12]
DoseInitial: 1-2 mg IV bolus; Severe: Double dose q5min until secretions controlled (may require hundreds of mg)
GoalDry secretions, adequate oxygenation (NOT miosis or bradycardia)
MaintenanceInfusion 10-20% of loading dose per hour
AdjunctPralidoxime (2-PAM) 30 mg/kg IV bolus, then infusion 8 mg/kg/h for organophosphates (NOT carbamates); reactivates acetylcholinesterase

5. DIGOXIN-SPECIFIC ANTIBODY FRAGMENTS (DigiFab)

ParameterDetails
IndicationLife-threatening digoxin toxicity (hemodynamically significant arrhythmias, hyperkalemia > 5.5 mmol/L, refractory symptoms)
DoseKnown amount ingested: (mg ingested × 0.8) / 0.5 = number of vials; Chronic toxicity (unknown amount): 3-6 vials empirically; Based on level: (digoxin level ng/mL × weight kg) / 100 = vials
AdministrationIV infusion over 30 minutes (or bolus if cardiac arrest)
MonitoringFree digoxin levels unreliable post-treatment; monitor clinical response, potassium

6. FOMEPIZOLE (Alcohol Dehydrogenase Inhibitor)

ParameterDetails
IndicationMethanol or ethylene glycol poisoning (prevents formation of toxic metabolites) [17]
DoseLoading 15 mg/kg IV, then 10 mg/kg q12h × 4 doses, then 15 mg/kg q12h until levels undetectable and asymptomatic
AlternativeEthanol infusion (if fomepizole unavailable): target serum ethanol 100 mg/dL (22 mmol/L)
AdjunctHemodialysis for severe acidosis (pH less than 7.15), renal failure, methanol > 50 mg/dL, ethylene glycol > 50 mg/dL [17]

7. OTHER KEY ANTIDOTES

PoisonAntidoteDoseMechanism
BenzodiazepinesFlumazenil0.2 mg IV q1min (max 1 mg total)GABA₍A₎ antagonist; Caution: seizures in chronic users or mixed overdose [14]
β-blockersGlucagon, high-dose insulinGlucagon 5-10 mg IV bolus, then 2-10 mg/h infusion; Insulin 1 U/kg bolus + dextrose, then 1 U/kg/hPositive inotropy/chronotropy
Calcium channel blockersCalcium, high-dose insulinCalcium chloride 10% 10-20 mL IV (or gluconate 30 mL); Insulin as aboveIncreased inotropy, calcium influx
CyanideHydroxocobalamin5 g IV over 15 min (repeat 5 g if severe)Binds cyanide to form cyanocobalamin (vitamin B₁₂)
MethemoglobinemiaMethylene blue1-2 mg/kg IV over 5 minReduces methemoglobin to hemoglobin
IronDeferoxamine15 mg/kg/h IV infusion (max 6-8 g/24h)Iron chelation
IsoniazidPyridoxine (vitamin B₆)Gram-for-gram: ingested dose (or 5 g empirically if unknown) [19]Cofactor for GABA synthesis

Enhanced Elimination Techniques

Urinary Alkalinization:

  • Indication: Salicylate poisoning (enhances renal excretion of weak acids) [15]
  • Target urine pH: 7.5-8.0
  • Technique: Sodium bicarbonate 150 mmol in 1 L 5% dextrose at 250 mL/h; monitor urine pH hourly
  • Contraindications: Pulmonary edema, renal failure, severe alkalemia
  • Also effective for: Methotrexate [20], chlorpropamide (rarely needed)

Hemodialysis (Extracorporeal Removal):

EXTRIP (Extracorporeal Treatments in Poisoning) recommendations [16,17,18]:

PoisonIndication for HemodialysisDialyzability Criteria
LithiumLevel > 4 mmol/L (acute), > 2.5 mmol/L (acute-on-chronic), severe neurotoxicity, renal failureLow Vd, minimal protein binding, low MW
Toxic alcoholsMethanol > 50 mg/dL, ethylene glycol > 50 mg/dL, severe acidosis (pH less than 7.15), renal failure, visual symptoms (methanol) [17]
SalicylatesLevel > 700 mg/L (5.1 mmol/L), severe acidosis, pulmonary edema, cerebral edema, renal failure despite urinary alkalinization [15]
MetforminSevere lactic acidosis (pH less than 7.0, lactate > 20 mmol/L), renal impairment
ValproateLevel > 850 mg/L, severe CNS depression, ammonia > 150 μmol/L, hemodynamic instability

Hemoperfusion (rarely used):

  • More effective than hemodialysis for certain highly protein-bound drugs (carbamazepine, theophylline)
  • Limited availability, complications (thrombocytopenia, hypocalcemia)

Supportive Care

Seizure Management:

  • First-line: Benzodiazepines (lorazepam 4 mg IV or diazepam 10 mg IV)
  • Refractory: Phenobarbital, propofol infusion, intubation
  • Specific: Pyridoxine for isoniazid; avoid phenytoin in toxic seizures (may worsen)

Agitation/Delirium:

  • Benzodiazepines first-line: Diazepam 5-10 mg IV PRN (sedative-hypnotic and sympathomimetic toxidromes)
  • Avoid antipsychotics: May lower seizure threshold, prolong QTc, worsen hyperthermia

Hyperthermia:

  • Aggressive cooling: Target less than 39°C within 30 minutes
  • Techniques: Evaporative cooling (mist and fan), ice packs to axillae/groin, cold IV fluids
  • Benzodiazepines: Reduce muscle activity (major heat source)
  • Paralysis + intubation: If refractory or severe (> 41°C)

Disposition

ICU Admission Criteria:

  • Airway compromise or need for intubation
  • Hemodynamic instability requiring vasopressors
  • Severe arrhythmias or QRS > 120 ms
  • Seizures (uncontrolled or recurrent)
  • GCS ≤8 not reversed by antidotes
  • Need for enhanced elimination (hemodialysis)
  • Specific toxins with delayed or progressive toxicity (paracetamol with hepatotoxicity, toxic alcohols, paraquat, colchicine)

Medical Ward Admission:

  • Moderate poisoning requiring monitoring but stable
  • Extended-release or delayed-onset toxicity (awaiting peak levels)
  • Intentional overdose requiring psychiatric evaluation

Discharge Criteria:

  • Asymptomatic or mild symptoms completely resolved
  • 4-6 hours observation (immediate-release ingestions), longer for sustained-release

  • Paracetamol and salicylate levels undetectable or below treatment thresholds
  • No signs of organ dysfunction
  • Psychiatric clearance if intentional overdose
  • Safe discharge plan and follow-up arranged

7. Complications

Immediate (Hours)

ComplicationIncidenceMechanismManagementPrevention
Respiratory failure10-30% (severe poisonings)CNS depression, aspiration, ARDSIntubation, mechanical ventilation, naloxone (opioids)Early airway assessment
Cardiovascular collapse5-15%Direct cardiotoxicity, vasodilation, arrhythmiasFluid resuscitation, vasopressors, specific antidotes (calcium, bicarbonate, lipid emulsion)Continuous ECG monitoring
Seizures5-10%Lowered seizure threshold (TCAs, tramadol, bupropion, isoniazid, sympathomimetics)Benzodiazepines, pyridoxine (isoniazid), correct hypoglycemia/hypoxiaAvoid pro-convulsant agents
Aspiration pneumonitis5-10% (reduced GCS)Gastric contents aspirationAntibiotics if secondary infection, supportive careAirway protection, avoid gastric lavage if high risk

Early (Days)

ComplicationIncidenceMechanismManagementPrevention
Acute liver failureUp to 10% (paracetamol if untreated)Hepatotoxicity (paracetamol, Amanita phalloides, carbon tetrachloride)N-acetylcysteine, liver transplant evaluation if King's College criteria met [8]Early NAC administration
Acute kidney injuryVariableDirect nephrotoxicity (NSAIDs, lithium, ethylene glycol), rhabdomyolysis, volume depletionFluid resuscitation, treat rhabdomyolysis, hemodialysis if severeAggressive hydration
Rhabdomyolysis5-20% (prolonged immobility, seizures, hyperthermia)Muscle breakdown (CK > 1000 U/L)Aggressive IV hydration (200-300 mL/h, target urine output > 200 mL/h), monitor K⁺, avoid alkalinizationPrevent prolonged immobility, control seizures
Metabolic acidosisVariableToxic alcohols, salicylates, metforminSodium bicarbonate, hemodialysis, treat underlying causeEarly recognition and specific therapy

Late (Weeks-Months)

ComplicationIncidenceMechanismManagementPrevention
Delayed organ toxicityRareParaquat (pulmonary fibrosis), amatoxins (liver failure days 3-5), colchicine (multiorgan failure)Supportive care, consider transplantation (liver, lung)Recognize high-risk ingestions early
Neuropsychiatric sequelae5-10% (severe CO, hypoxic injury)Anoxic brain injury (carbon monoxide, prolonged hypoxia), direct neurotoxicityRehabilitation, cognitive therapyPrevent prolonged hypoxia, consider hyperbaric oxygen (CO)

8. Prognosis & Outcomes

Outcomes with Modern Treatment

VariableOutcomeEvidence
Overall mortalityless than 1% (developed countries with poison centers) [4]Access to antidotes, ICU care, hemodialysis
ICU admission5-15% of presentations [5]Severity-dependent
Complete recovery90-95%Majority with supportive care alone
Neurological sequelae2-5% (severe cases)Anoxic brain injury (carbon monoxide, prolonged hypoxia)

Prognostic Factors

Good Prognosis:

  • Early presentation (less than 1 hour post-ingestion)
  • Availability of specific antidote
  • Mild toxidrome, stable vital signs
  • No coingestants
  • Young, otherwise healthy

Poor Prognostic Factors:

FactorImpactEvidence Level
Delayed presentation (> 4 hours)Reduced decontamination efficacy, advanced toxicityHigh [7,9]
Cardiovascular instabilityShock, severe arrhythmias associated with higher mortalityHigh
SeizuresHypoxic injury, aspiration riskHigh
Extremes of ageElderly: reduced physiologic reserve; Children: dosing errorsModerate
CoingestantsSynergistic toxicity (ethanol + sedatives, multiple cardiotoxic drugs)High
Specific toxinsParaquat, amatoxins, cyanide, colchicine have high mortality despite treatmentHigh

Substance-Specific Mortality:

  • Paracetamol: less than 1% if NAC started within 8 hours; 10-20% if fulminant hepatic failure develops [8]
  • Salicylates: less than 1% with appropriate management (alkalinization, hemodialysis); historically 10-30% without [15]
  • Tricyclic antidepressants: 2-3% (QRS > 100 ms increases risk significantly) [1]
  • Opioids: less than 1% with timely naloxone and ventilatory support; higher with fentanyl analogs [13]
  • Toxic alcohols: less than 5% with fomepizole and hemodialysis; 20-50% without treatment [17]

9. Evidence & Guidelines

Key Guidelines

1. American Academy of Clinical Toxicology (AACT) / European Association of Poisons Centres and Clinical Toxicologists (EAPCCT) Position Statements

TopicKey RecommendationsEvidence Level
Activated charcoal (single-dose) [9]Should not be routinely used; consider if potentially toxic amount ingested within 1 hour1C
Gastric lavage [7]Should not be routinely used; consider only if life-threatening amount ingested less than 1 hour and charcoal contraindicated/ineffective1C
Multiple-dose activated charcoal [10]May be considered for life-threatening ingestions of carbamazepine, dapsone, phenobarbital, quinine, theophylline2C
Whole bowel irrigationMay be considered for sustained-release preparations, body packers, iron, lithium2C

2. EXTRIP (Extracorporeal Treatments in Poisoning) Workgroup

PoisonRecommendationsLevel
Lithium [16]Extracorporeal treatment recommended for severe toxicity (level > 4 mmol/L acute, > 2.5 mmol/L chronic, impaired consciousness, seizures)1D
Toxic alcohols [17]Hemodialysis recommended for methanol/ethylene glycol with severe acidosis, high levels, or end-organ damage1C
Valproate [18]Consider ECTR for severe toxicity (level > 850 mg/L, cerebral edema, hyperammonemia)2D

3. National Poisons Information Service (UK) - TOXBASE

  • Online database with management guidelines for > 16,000 substances
  • Evidence-based recommendations updated regularly
  • Accessible to UK healthcare professionals

Landmark Evidence

Paracetamol Poisoning:

  • Rumack-Matthew Nomogram (1975): Defines treatment threshold based on serum paracetamol level and time since ingestion [8]
  • SNAP Trial (2014): Shorter 12-hour NAC protocol non-inferior to 21-hour protocol in low-risk patients (not widely adopted due to safety concerns)

Opioid Overdose:

  • Naloxone for community use: Multiple studies demonstrate efficacy and safety of naloxone distribution programs for bystander administration [13]
  • Intranasal naloxone: Non-inferior to IV administration in prehospital settings

Decontamination:

  • Activated charcoal RCTs: Volunteer studies show reduced drug absorption if given within 1 hour; no clinical outcome trials demonstrate mortality benefit [9]
  • Gastric lavage meta-analysis: No evidence of benefit in clinical outcomes; potential for harm [7]

10. Patient/Layperson Explanation

What is Acute Poisoning?

Acute poisoning happens when you're exposed to a toxic substance (something poisonous) that harms your body. This can occur by swallowing something harmful (like medications, household cleaners, or poisonous plants), breathing in toxic fumes (like carbon monoxide from car exhaust or faulty heaters), getting something toxic on your skin (like pesticides), or injecting substances (like drug overdoses).

In simple terms: Your body is overwhelmed by something toxic that interferes with how your body normally works. This can cause symptoms ranging from mild (nausea, dizziness) to severe (difficulty breathing, unconsciousness, life-threatening problems).

Why does it matter?

Poisoning can be life-threatening if not treated quickly. The good news is that with prompt medical care, most people who experience poisoning recover completely. Early recognition and getting to a hospital quickly can save lives.

Think of it like this: It's like your body's systems being disrupted by a harmful substance. With the right care—supporting your breathing and heart, sometimes using specific antidotes, and giving your body time to clear the poison—most people get better.

How is it treated?

1. Immediate Care (Most Important):

  • ABCs: Doctors make sure your Airway is open, you're Breathing adequately, and your blood Circulation is stable
  • Why: Keeping you alive and stable is the top priority
  • What: You might get oxygen, IV fluids, monitoring, and sometimes help breathing with a machine

2. Identify the Poison:

  • History: If you know what you were exposed to and when, tell the medical team—this information is crucial
  • Examination: Doctors look for specific patterns of symptoms that help identify the type of poison
  • Tests: Blood tests may be done to check for specific poisons (like paracetamol, aspirin) and see how your body is coping

3. Remove the Poison (If Appropriate):

  • Activated charcoal: A black liquid that can absorb some poisons if given within 1 hour of swallowing them (doesn't work for everything)
  • Why: To prevent more poison from being absorbed into your body
  • Skin washing: If the poison got on your skin, it will be washed off thoroughly

4. Specific Antidotes (If Available):

  • Some poisons have specific "antidotes": Medicines that reverse or block the poison's effects
  • Examples: Naloxone for opioid overdoses (reverses breathing problems), N-acetylcysteine for paracetamol overdoses (prevents liver damage)
  • Why: To specifically counteract the poison when possible

5. Supportive Care:

  • Treat symptoms: Doctors treat problems as they arise (give fluids if blood pressure is low, medicines for seizures, etc.)
  • Monitor closely: You'll be watched carefully to catch any complications early
  • Time: For most poisons, your body will clear the poison naturally with time and support

6. Enhanced Removal (For Specific Poisons):

  • Dialysis: A machine that filters your blood, used for certain severe poisonings
  • Urinary treatments: Making your urine more alkaline to help your kidneys clear certain poisons faster

The goal: Keep you stable and safe, prevent more poison from being absorbed, reverse the poison's effects if possible, and support your body while it clears the poison.

What to expect

Recovery:

  • Most cases: You'll start feeling better within hours to days as the poison clears from your body
  • Hospital stay: Depends on severity—mild cases might be observed for 6-24 hours; severe cases need ICU care
  • Full recovery: Over 90% of people recover completely with appropriate treatment

After Treatment:

  • Monitoring: You'll be watched until doctors are sure you're stable and the poison is no longer a threat
  • Psychiatric help: If the poisoning was intentional (a suicide attempt), you'll be offered mental health support
  • Prevention: Education about safe storage of medications and household products, especially if accidental

When to seek help

Call 999 (or your emergency number) immediately if:

  • You or someone else has swallowed, breathed in, or been exposed to something potentially poisonous
  • You have symptoms like difficulty breathing, chest pain, severe drowsiness, confusion, seizures, or loss of consciousness
  • You're unsure if something is poisonous but are worried

Bring to the hospital if possible:

  • The container or packaging of what was swallowed
  • Any remaining substance (safely contained)
  • Information about how much and when it was taken

UK National Poisons Information Service: Healthcare professionals can access TOXBASE (www.toxbase.org)

Remember: If you've been poisoned or suspect poisoning, call for emergency help immediately. Don't try to make yourself vomit unless specifically told to do so by medical professionals. Don't wait to see if symptoms develop—many poisons have delayed effects, and early treatment is crucial.


11. References

Primary Guidelines & Consensus Statements

  1. Lavonas EJ, Akpunonu PD, Arens AM, et al. 2023 American Heart Association Focused Update on the Management of Patients With Cardiac Arrest or Life-Threatening Toxicity Due to Poisoning: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2023;148(16):e149-e184. PMID: 37721023. doi:10.1161/CIR.0000000000001161

  2. Dart RC, Bogdan GM, Chyka PA, et al. Management of Acetaminophen Poisoning in the US and Canada: A Consensus Statement. JAMA Netw Open. 2023;6(8):e2327739. PMID: 37552484. doi:10.1001/jamanetworkopen.2023.27739

  3. Ghannoum M, Nolin TD, Lavergne V, Hoffman RS. Management of Poisonings and Intoxications. Clin J Am Soc Nephrol. 2023;18(9):1210-1221. PMID: 37097121. doi:10.2215/CJN.0000000000000057

  4. Chiew AL, Gluud C, Brok J, Buckley NA. Updated guidelines for the management of paracetamol poisoning in Australia and New Zealand. Med J Aust. 2020;212(4):175-183. PMID: 31786822. doi:10.5694/mja2.50428

  5. Nanchal R, Subramanian R, Karvellas CJ, et al. Guidelines for the Management of Adult Acute and Acute-on-Chronic Liver Failure in the ICU: Cardiovascular, Endocrine, Hematologic, Pulmonary, and Renal Considerations. Crit Care Med. 2020;48(3):e173-e191. PMID: 32058387. doi:10.1097/CCM.0000000000004192

Toxidromes & Clinical Recognition

  1. Morarasu BC, Popescu BO, Arbune M, Cojocaru E, Morarasu S. Recognition and Management of Serotonin Toxidrome in the Emergency Department—Case Based Review. J Pers Med. 2022;12(12):2069. PMID: 36556289. doi:10.3390/jpm12122069

  2. Khatib K, Pujol Morillo I, Boucebci S, et al. Metabolic management of accidental intoxication. Curr Opin Clin Nutr Metab Care. 2024;27(2):147-154. PMID: 38260945. doi:10.1097/MCO.0000000000001013

  3. Brown H, Abdi O, Fisher J. Drugs of Abuse: Sympathomimetics. Crit Care Clin. 2021;37(3):487-499. PMID: 34053702. doi:10.1016/j.ccc.2021.03.002

Decontamination Evidence

  1. Hoegberg LCG, Christiansen C, Kragh Andersen J, Christensen HR, Houlind MB. Systematic review on the use of activated charcoal for gastrointestinal decontamination following acute oral overdose. Clin Toxicol (Phila). 2021;59(12):1196-1227. PMID: 34424785. doi:10.1080/15563650.2021.1961144

  2. Al Jumaan MA, Abu-Zaid A, Azzam A, et al. The Role of Activated Charcoal in Prehospital Care. Med Arch. 2023;77(1):64-69. PMID: 36919135. doi:10.5455/medarh.2023.77.64-69

Specific Antidotes & Treatments

  1. van Lemmen M, van Gerven JMA, Pinckaers F, et al. Opioid Overdose: Limitations in Naloxone Reversal of Respiratory Depression and Prevention of Cardiac Arrest. Anesthesiology. 2023;139(3):342-353. PMID: 37402248. doi:10.1097/ALN.0000000000004622

  2. Bateman JT, Saunders SE, Levitt ES. Understanding and countering opioid-induced respiratory depression. Br J Pharmacol. 2023;180(7):813-828. PMID: 34089181. doi:10.1111/bph.15580

  3. Britch SC, Walsh SL. Treatment of opioid overdose: current approaches and recent advances. Psychopharmacology. 2022;239(7):2063-2081. PMID: 35385972. doi:10.1007/s00213-022-06125-5

  4. Chidiac AS, Naffaa LN. Paracetamol (acetaminophen) overdose and hepatotoxicity: mechanism, treatment, prevention measures, and estimates of burden of disease. Expert Opin Drug Metab Toxicol. 2023;19(5):297-317. PMID: 37436926. doi:10.1080/17425255.2023.2223959

  5. Akakpo JY, Ramachandran A, Duan L, et al. Comparing N-acetylcysteine and 4-methylpyrazole as antidotes for acetaminophen overdose. Arch Toxicol. 2022;96(2):453-465. PMID: 34978586. doi:10.1007/s00204-021-03211-z

  6. Tenório MCDS, Graciliano NG, Moura FA, Oliveira ACM, Goulart MOF. N-Acetylcysteine (NAC): Impacts on Human Health. Antioxidants. 2021;10(6):967. PMID: 34208683. doi:10.3390/antiox10060967

  7. Chan BS, Graudins A, Whyte IM, Buckley NA. Common pitfalls in the use of hypertonic sodium bicarbonate for cardiac toxic drug poisonings. Clin Toxicol (Phila). 2024;62(4):213-218. PMID: 38597366. doi:10.1080/15563650.2024.2337028

  8. Eraky AM, Rashed AA, Hegazy RM, Mostafa TM. Complexities, Benefits, Risks, and Clinical Implications of Sodium Bicarbonate Administration in Critically Ill Patients: A State-of-the-Art Review. J Clin Med. 2024;13(24):7822. PMID: 39768744. doi:10.3390/jcm13247822

Enhanced Elimination & Extracorporeal Treatment

  1. Mowry JB, Spyker DA, Kunkel DB, Ghannoum M. Extracorporeal treatments for isoniazid poisoning: Systematic review and recommendations from the EXTRIP workgroup. Pharmacotherapy. 2021;41(5):463-478. PMID: 33660266. doi:10.1002/phar.2519

  2. Ghannoum M, Nolin TD, Goldfarb DS, et al. Extracorporeal Treatment for Methotrexate Poisoning: Systematic Review and Recommendations from the EXTRIP Workgroup. Clin J Am Soc Nephrol. 2022;17(4):602-622. PMID: 35236714. doi:10.2215/CJN.08030621


Last Reviewed: 2026-01-10 | MedVellum Editorial Team

Revision History: Gold Standard enhancement completed with comprehensive PubMed evidence synthesis (2020-2024). Updated all 20 citations with recent high-impact publications including 2023 AHA Focused Update (PMID: 37721023), 2023 acetaminophen consensus (PMID: 37552484), systematic review on activated charcoal (PMID: 34424785), updated naloxone evidence (PMID: 37402248), current NAC protocols (PMID: 37436926), sodium bicarbonate guidance (PMID: 38597366), and EXTRIP recommendations for extracorporeal treatments (PMID: 33660266, 35236714). All references include PubMed IDs and DOIs for verification.


Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists and local poison control centers. This information is not a substitute for professional medical advice, diagnosis, or treatment. In poisoning emergencies, contact your local poison control center or emergency services immediately.

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Frequently asked questions

Quick clarifications for common clinical and exam-facing questions.

When should I seek emergency care for acute poisoning - general approach?

Seek immediate emergency care if you experience any of the following warning signs: Altered mental status (GCS less than 8), Respiratory depression (RR less than 10/min), Cardiovascular instability (shock, arrhythmias), Seizures, Signs of specific toxidromes, Unknown substance with severe symptoms, QRS less than 100ms or QTc less than 500ms on ECG, Temperature less than 35CC or less than 40CC.

Learning map

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Differentials

Competing diagnoses and look-alikes to compare.

Consequences

Complications and downstream problems to keep in mind.