Acute Poisoning - General Approach
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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
| Factor | Details |
|---|---|
| Age | Bimodal: children 1-5 years (exploratory accidental), adults 20-40 years (intentional self-harm) |
| Sex | Females > males for intentional overdose presentations; males have higher fatality rates [3] |
| Ethnicity | No consistent ethnic variation; socioeconomic factors more influential |
| Geography | Higher rates in low- and middle-income countries due to pesticide availability and limited healthcare access [2] |
| Setting | Emergency 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 Factor | Relative Risk | Mechanism |
|---|---|---|
| Mental health conditions | 5-10× | Intentional self-poisoning as method of self-harm |
| Substance use disorder | 5-10× | Intentional overdose, reduced awareness, polypharmacy |
| Medication access | 3-5× | Accidental (children, elderly) or intentional overdose |
| Occupational exposure | 2-4× | Agriculture (pesticides), healthcare (pharmaceuticals), industry (chemicals) |
| Alcohol use | 2-3× | Impaired judgment, coingestants, synergistic CNS depression |
Common Substances by Region
High-Income Countries:
| Substance | Frequency | Typical Patient | Notes |
|---|---|---|---|
| Paracetamol (acetaminophen) | 15-25% | All ages, intentional or accidental | Leading cause of acute liver failure [8] |
| Benzodiazepines | 10-15% | Adults, intentional | Low toxicity alone; dangerous with coingestants |
| Antidepressants | 10-15% | Adults, intentional | SSRIs safer than TCAs; serotonin syndrome risk |
| Opioids | 10-20% | Adults, intentional or accidental | Increasing prevalence; fentanyl analogs highly potent [11] |
| NSAIDs | 5-10% | All ages | Generally low toxicity except in massive overdose |
Low- and Middle-Income Countries:
| Substance | Frequency | Typical Patient | Notes |
|---|---|---|---|
| Pesticides | 30-50% | Agricultural workers, intentional self-harm | Major contributor to global poisoning mortality [2] |
| Corrosives | 10-20% | Accidental or intentional | Acids, alkalis; severe morbidity |
| Traditional medicines | Variable | All ages | Heavy metal contamination, plant alkaloids |
3. Pathophysiology
Routes of Exposure and Toxicokinetics
Routes of Absorption:
- Gastrointestinal (most common): Absorption depends on gastric pH, gastric emptying, formulation (immediate vs. sustained-release), and presence of food
- Inhalational: Rapid absorption, bypasses first-pass metabolism (carbon monoxide, volatile hydrocarbons, smoke)
- Dermal: Significant for lipophilic substances (organophosphates, some chemical warfare agents)
- 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
| Feature | Mechanism | Examples |
|---|---|---|
| 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 signs | Tachycardia, hypertension, hyperthermia | |
| CNS | Agitation, confusion, hallucinations, seizures, coma (severe) | Antihistamines, TCAs, atropine, antipsychotics |
| Autonomic | Dry skin and mucous membranes, mydriasis, ileus, urinary retention | Benztropine, scopolamine, jimson weed |
| Treatment | Supportive care; physostigmine rarely indicated (risk of seizures/bradycardia) |
2. CHOLINERGIC TOXIDROME
| Feature | Mechanism | Examples |
|---|---|---|
| Mnemonic | SLUDGE: Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis | Acetylcholinesterase inhibition |
| Muscarinic effects | Bronchospasm, bronchorrhea, bradycardia, miosis, diaphoresis | Organophosphates, carbamates |
| Nicotinic effects | Muscle fasciculations, weakness, paralysis (respiratory failure) | Nerve agents, insecticides |
| CNS | Confusion, seizures, coma | |
| Treatment | Atropine (muscarinic effects), pralidoxime (nicotinic effects, organophosphates only), benzodiazepines (seizures) [12] |
3. OPIOID TOXIDROME
| Feature | Mechanism | Examples |
|---|---|---|
| Classic triad | Miosis, respiratory depression, decreased consciousness | μ-opioid receptor agonism (CNS, respiratory center) |
| Vital signs | Bradypnea, bradycardia, hypotension, hypothermia | Morphine, heroin, fentanyl, oxycodone |
| Pupils | Pinpoint (miosis) — highly specific but not sensitive | Tramadol (mydriasis possible), meperidine |
| Other | Decreased bowel sounds, urinary retention, pulmonary edema (non-cardiogenic) | |
| Treatment | Naloxone (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
| Feature | Mechanism | Examples |
|---|---|---|
| Vital signs | Tachycardia, hypertension, hyperthermia, tachypnea | Increased catecholamine release/reuptake inhibition |
| CNS | Agitation, psychosis, seizures, hyperreflexia | Amphetamines, cocaine, MDMA, synthetic cathinones |
| Autonomic | Mydriasis, diaphoresis (sweating), piloerection | Caffeine, ephedrine, pseudoephedrine |
| Complications | Rhabdomyolysis, hyperthermia, intracranial hemorrhage, myocardial infarction, dissection | |
| Treatment | Benzodiazepines (first-line for agitation, hypertension, seizures), cooling, avoid β-blockers (unopposed α-stimulation) |
5. SEDATIVE-HYPNOTIC TOXIDROME
| Feature | Mechanism | Examples |
|---|---|---|
| CNS depression | CNS depressant via GABA₍A₎ receptor agonism (benzodiazepines, barbiturates), other mechanisms | Benzodiazepines, barbiturates, ethanol, GHB, Z-drugs |
| Vital signs | Bradycardia, hypotension, hypothermia, respiratory depression (dose-dependent) | |
| Pupils | Normal or mydriasis (contrast with opioids) | |
| Other | Hyporeflexia, ataxia, slurred speech, nystagmus | |
| Treatment | Supportive 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":
- WHAT was taken? (substance, formulation, brand name)
- WHEN was it taken? (time of ingestion)
- WHERE did exposure occur? (home, workplace, outdoors)
- WHY was it taken? (accidental, intentional, recreational)
- HOW MUCH was taken? (number of tablets, volume, concentration)
- 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 Sign | Abnormality | Differential Toxidromes |
|---|---|---|
| Temperature | Hyperthermia (> 38.5°C) | Sympathomimetic, anticholinergic, serotonin syndrome, NMS, salicylates, DNP |
| Hypothermia (less than 35°C) | Sedative-hypnotic, opioid, ethanol, hypoglycemic agents | |
| Heart Rate | Tachycardia (> 100 bpm) | Sympathomimetic, anticholinergic, salicylates, β-agonists, theophylline, withdrawal |
| Bradycardia (less than 60 bpm) | Opioid, cholinergic, β-blockers, calcium channel blockers, digoxin | |
| Blood Pressure | Hypertension | Sympathomimetic, anticholinergic (severe), withdrawal |
| Hypotension | Sedative-hypnotic, opioid, β-blockers, calcium channel blockers, TCAs | |
| Respiratory Rate | Tachypnea (> 20/min) | Salicylates, sympathomimetic, metabolic acidosis (methanol, ethylene glycol) |
| Bradypnea (less than 10/min) | Opioid, sedative-hypnotic (severe) |
Neurological Examination:
| Finding | Significance | Examples |
|---|---|---|
| Pupils | Miosis (pinpoint) | Opioids, cholinergic, clonidine |
| Mydriasis (dilated) | Anticholinergic, sympathomimetic, withdrawal | |
| Mental Status | Agitation, hallucinations | Anticholinergic, sympathomimetic, serotonin syndrome |
| Sedation, coma | Opioid, sedative-hypnotic, antipsychotics | |
| Tone | Rigidity | NMS, serotonin syndrome (different quality) |
| Flaccidity | Sedative-hypnotic (severe), botulism | |
| Reflexes | Hyperreflexia, clonus | Serotonin syndrome, sympathomimetic |
| Hyporeflexia | Sedative-hypnotic, botulism |
Skin Examination:
| Finding | Toxidrome | Examples |
|---|---|---|
| Dry skin | Anticholinergic | Antihistamines, TCAs |
| Diaphoresis (sweating) | Cholinergic, sympathomimetic, serotonin syndrome | Organophosphates, cocaine |
| Bullae | Prolonged immobility | Barbiturates, carbon monoxide |
| Cyanosis | Methemoglobinemia | Dapsone, nitrites, local anesthetics |
| Cherry-red appearance | Carboxyhemoglobinemia | Carbon 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):
| Test | Indication | Expected Finding | Action |
|---|---|---|---|
| Paracetamol level | All intentional overdoses, unknown ingestions | Plot on Rumack-Matthew nomogram (> 4 hours post-ingestion) | N-acetylcysteine if above treatment line [8] |
| Salicylate level | Suspicion 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 gas | Altered mental status, suspected metabolic derangement | High anion gap metabolic acidosis | Calculate osmolar gap if toxic alcohols suspected |
| Urea & Electrolytes | All significant poisonings | AKI (salicylates, lithium), hypokalemia (salbutamol), hyperkalemia (digoxin) | Correct electrolyte abnormalities |
| Glucose | Altered mental status | Hypoglycemia (insulin, sulfonylureas, ethanol), hyperglycemia | Correct immediately |
| Lactate | Suspected metformin, cyanide, carbon monoxide, seizures | Elevated (> 4 mmol/L) | Source control, supportive care |
Second-Line (based on clinical suspicion):
| Test | Indication | Clinical 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 tests | Paracetamol overdose, hepatotoxic substances | Transaminitis at 24-72 hours (paracetamol), prognostic (PT/INR) |
| Creatine kinase | Prolonged immobility, seizures, hyperthermia | Rhabdomyolysis (CK > 1000 U/L) → aggressive hydration, monitor renal function |
| Troponin | Chest pain, sympathomimetic toxidrome, carbon monoxide | Myocardial ischemia/infarction |
| Lithium level | Known lithium user, unexplained altered mental status | Therapeutic 0.6-1.2 mmol/L; toxicity > 1.5 mmol/L; severe > 2.5 mmol/L → hemodialysis [16] |
| Digoxin level | Known digoxin user, bradycardia, AV block | Toxicity often at therapeutic levels in acute-on-chronic; digoxin-specific antibody fragments if severe [1] |
| Carboxyhemoglobin | Suspected carbon monoxide exposure | > 3% (non-smoker), > 10% (smoker) → hyperbaric oxygen for severe cases |
| Methemoglobin | Central 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):
| Parameter | Recommendation | Evidence |
|---|---|---|
| Indications | Potentially toxic ingestion within 1 hour, cooperative patient or intubated | Position statement: AACT/EAPCCT [9] |
| Dose | 50 g adults (1 g/kg children) in 200-300 mL water, oral or NG tube | |
| Timing | Maximum benefit within 1 hour; limited benefit 1-2 hours; not recommended > 2 hours | Benefit declines rapidly with time [9] |
| Contraindications | Absolute: Unprotected airway with reduced GCS, corrosives, hydrocarbons (aspiration risk), bowel obstruction/perforation | |
| Relative: Anticipated endoscopy, specific antidote more effective | ||
| NOT effective for | Alcohols, acids/alkalis, cyanide, iron, lithium, potassium, heavy metals, hydrocarbons | Poor adsorption profile |
| Adverse effects | Aspiration 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)
| Parameter | Details |
|---|---|
| Indication | Opioid toxidrome (respiratory depression, miosis, reduced GCS) [13] |
| Dose | Initial: 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 |
| Goal | Respiratory rate > 12/min with adequate tidal volume (avoid full reversal to prevent withdrawal and agitation) |
| Infusion | If repeat boluses required: infusion at 2/3 of effective bolus dose per hour |
| Duration | Short half-life (30-90 minutes) vs. most opioids → requires monitoring for re-sedation, especially with long-acting opioids (methadone, sustained-release formulations) |
| Special considerations | Fentanyl and analogs may require high doses (up to 10 mg); buprenorphine (partial agonist) less responsive |
2. N-ACETYLCYSTEINE (Glutathione Precursor)
| Parameter | Details |
|---|---|
| Indication | Paracetamol (acetaminophen) overdose [8] |
| Criteria | Serum 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 therapy | Continue if ALT rising, INR > 1.5, or detectable paracetamol: 100 mg/kg over 16 hours, repeat until criteria resolved [8] |
| Adverse effects | Anaphylactoid 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)
| Parameter | Details |
|---|---|
| Indication | QRS > 100 ms from sodium channel blockade (TCAs, cocaine, flecainide, quinidine) [1] |
| Dose | 1-2 mmol/kg (50-100 mL of 8.4% solution) IV bolus, repeat q5min until QRS less than 100 ms |
| Target | Serum pH 7.45-7.55 (alkalemia enhances sodium channel recovery) |
| Maintenance | Bicarbonate infusion: 3 ampoules (150 mmol) in 1 L 5% dextrose at 150-250 mL/h |
| Monitoring | Serial ECGs, arterial pH, potassium (may drop with alkalinization) |
4. ATROPINE (Muscarinic Antagonist for Cholinergic Crisis)
| Parameter | Details |
|---|---|
| Indication | Organophosphate/carbamate poisoning (cholinergic toxidrome) [12] |
| Dose | Initial: 1-2 mg IV bolus; Severe: Double dose q5min until secretions controlled (may require hundreds of mg) |
| Goal | Dry secretions, adequate oxygenation (NOT miosis or bradycardia) |
| Maintenance | Infusion 10-20% of loading dose per hour |
| Adjunct | Pralidoxime (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)
| Parameter | Details |
|---|---|
| Indication | Life-threatening digoxin toxicity (hemodynamically significant arrhythmias, hyperkalemia > 5.5 mmol/L, refractory symptoms) |
| Dose | Known 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 |
| Administration | IV infusion over 30 minutes (or bolus if cardiac arrest) |
| Monitoring | Free digoxin levels unreliable post-treatment; monitor clinical response, potassium |
6. FOMEPIZOLE (Alcohol Dehydrogenase Inhibitor)
| Parameter | Details |
|---|---|
| Indication | Methanol or ethylene glycol poisoning (prevents formation of toxic metabolites) [17] |
| Dose | Loading 15 mg/kg IV, then 10 mg/kg q12h × 4 doses, then 15 mg/kg q12h until levels undetectable and asymptomatic |
| Alternative | Ethanol infusion (if fomepizole unavailable): target serum ethanol 100 mg/dL (22 mmol/L) |
| Adjunct | Hemodialysis for severe acidosis (pH less than 7.15), renal failure, methanol > 50 mg/dL, ethylene glycol > 50 mg/dL [17] |
7. OTHER KEY ANTIDOTES
| Poison | Antidote | Dose | Mechanism |
|---|---|---|---|
| Benzodiazepines | Flumazenil | 0.2 mg IV q1min (max 1 mg total) | GABA₍A₎ antagonist; Caution: seizures in chronic users or mixed overdose [14] |
| β-blockers | Glucagon, high-dose insulin | Glucagon 5-10 mg IV bolus, then 2-10 mg/h infusion; Insulin 1 U/kg bolus + dextrose, then 1 U/kg/h | Positive inotropy/chronotropy |
| Calcium channel blockers | Calcium, high-dose insulin | Calcium chloride 10% 10-20 mL IV (or gluconate 30 mL); Insulin as above | Increased inotropy, calcium influx |
| Cyanide | Hydroxocobalamin | 5 g IV over 15 min (repeat 5 g if severe) | Binds cyanide to form cyanocobalamin (vitamin B₁₂) |
| Methemoglobinemia | Methylene blue | 1-2 mg/kg IV over 5 min | Reduces methemoglobin to hemoglobin |
| Iron | Deferoxamine | 15 mg/kg/h IV infusion (max 6-8 g/24h) | Iron chelation |
| Isoniazid | Pyridoxine (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]:
| Poison | Indication for Hemodialysis | Dialyzability Criteria |
|---|---|---|
| Lithium | Level > 4 mmol/L (acute), > 2.5 mmol/L (acute-on-chronic), severe neurotoxicity, renal failure | Low Vd, minimal protein binding, low MW |
| Toxic alcohols | Methanol > 50 mg/dL, ethylene glycol > 50 mg/dL, severe acidosis (pH less than 7.15), renal failure, visual symptoms (methanol) [17] | |
| Salicylates | Level > 700 mg/L (5.1 mmol/L), severe acidosis, pulmonary edema, cerebral edema, renal failure despite urinary alkalinization [15] | |
| Metformin | Severe lactic acidosis (pH less than 7.0, lactate > 20 mmol/L), renal impairment | |
| Valproate | Level > 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)
| Complication | Incidence | Mechanism | Management | Prevention |
|---|---|---|---|---|
| Respiratory failure | 10-30% (severe poisonings) | CNS depression, aspiration, ARDS | Intubation, mechanical ventilation, naloxone (opioids) | Early airway assessment |
| Cardiovascular collapse | 5-15% | Direct cardiotoxicity, vasodilation, arrhythmias | Fluid resuscitation, vasopressors, specific antidotes (calcium, bicarbonate, lipid emulsion) | Continuous ECG monitoring |
| Seizures | 5-10% | Lowered seizure threshold (TCAs, tramadol, bupropion, isoniazid, sympathomimetics) | Benzodiazepines, pyridoxine (isoniazid), correct hypoglycemia/hypoxia | Avoid pro-convulsant agents |
| Aspiration pneumonitis | 5-10% (reduced GCS) | Gastric contents aspiration | Antibiotics if secondary infection, supportive care | Airway protection, avoid gastric lavage if high risk |
Early (Days)
| Complication | Incidence | Mechanism | Management | Prevention |
|---|---|---|---|---|
| Acute liver failure | Up 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 injury | Variable | Direct nephrotoxicity (NSAIDs, lithium, ethylene glycol), rhabdomyolysis, volume depletion | Fluid resuscitation, treat rhabdomyolysis, hemodialysis if severe | Aggressive hydration |
| Rhabdomyolysis | 5-20% (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 alkalinization | Prevent prolonged immobility, control seizures |
| Metabolic acidosis | Variable | Toxic alcohols, salicylates, metformin | Sodium bicarbonate, hemodialysis, treat underlying cause | Early recognition and specific therapy |
Late (Weeks-Months)
| Complication | Incidence | Mechanism | Management | Prevention |
|---|---|---|---|---|
| Delayed organ toxicity | Rare | Paraquat (pulmonary fibrosis), amatoxins (liver failure days 3-5), colchicine (multiorgan failure) | Supportive care, consider transplantation (liver, lung) | Recognize high-risk ingestions early |
| Neuropsychiatric sequelae | 5-10% (severe CO, hypoxic injury) | Anoxic brain injury (carbon monoxide, prolonged hypoxia), direct neurotoxicity | Rehabilitation, cognitive therapy | Prevent prolonged hypoxia, consider hyperbaric oxygen (CO) |
8. Prognosis & Outcomes
Outcomes with Modern Treatment
| Variable | Outcome | Evidence |
|---|---|---|
| Overall mortality | less than 1% (developed countries with poison centers) [4] | Access to antidotes, ICU care, hemodialysis |
| ICU admission | 5-15% of presentations [5] | Severity-dependent |
| Complete recovery | 90-95% | Majority with supportive care alone |
| Neurological sequelae | 2-5% (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:
| Factor | Impact | Evidence Level |
|---|---|---|
| Delayed presentation (> 4 hours) | Reduced decontamination efficacy, advanced toxicity | High [7,9] |
| Cardiovascular instability | Shock, severe arrhythmias associated with higher mortality | High |
| Seizures | Hypoxic injury, aspiration risk | High |
| Extremes of age | Elderly: reduced physiologic reserve; Children: dosing errors | Moderate |
| Coingestants | Synergistic toxicity (ethanol + sedatives, multiple cardiotoxic drugs) | High |
| Specific toxins | Paraquat, amatoxins, cyanide, colchicine have high mortality despite treatment | High |
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
| Topic | Key Recommendations | Evidence Level |
|---|---|---|
| Activated charcoal (single-dose) [9] | Should not be routinely used; consider if potentially toxic amount ingested within 1 hour | 1C |
| Gastric lavage [7] | Should not be routinely used; consider only if life-threatening amount ingested less than 1 hour and charcoal contraindicated/ineffective | 1C |
| Multiple-dose activated charcoal [10] | May be considered for life-threatening ingestions of carbamazepine, dapsone, phenobarbital, quinine, theophylline | 2C |
| Whole bowel irrigation | May be considered for sustained-release preparations, body packers, iron, lithium | 2C |
2. EXTRIP (Extracorporeal Treatments in Poisoning) Workgroup
| Poison | Recommendations | Level |
|---|---|---|
| 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 damage | 1C |
| 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
-
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
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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
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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
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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
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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
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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
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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
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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
-
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
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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
-
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
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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
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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
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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
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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
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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
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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
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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
-
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
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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
Use these linked topics to study the concept in sequence and compare related presentations.
Consequences
Complications and downstream problems to keep in mind.