The Overdose Unknown: The General Approach to the Poisoned Patient

Dr Neeraj Manikath , claude.ai

Abstract

Acute poisoning represents a significant challenge in critical care, with over 2 million toxic exposures reported annually to poison control centers in the United States alone. The poisoned patient often presents with an unclear history, multiple substance exposures, and rapidly evolving clinical manifestations. This review provides a systematic, evidence-based approach to the management of the undifferentiated poisoned patient, emphasizing the primacy of supportive care, toxidrome recognition, and judicious use of antidotes. We integrate current guidelines with practical clinical pearls to guide the postgraduate trainee through the critical first hours of managing these complex patients.

Keywords: Toxicology, poisoning, toxidrome, antidotes, critical care, overdose

Introduction

The emergency department and intensive care unit serve as the front lines for managing acute poisonings, yet the majority of clinicians receive limited formal training in clinical toxicology. The undifferentiated poisoned patient presents a unique diagnostic challenge: the substance may be unknown, co-ingestions are common (occurring in 30-50% of intentional overdoses), and the clinical presentation may not manifest for hours after exposure.[1,2]

The fundamental principle guiding the management of any poisoned patient is deceptively simple: excellent supportive care saves more lives than any specific antidote. Most patients survive toxic exposures through meticulous attention to airway management, hemodynamic support, and prevention of secondary complications. This review focuses on the systematic approach to the patient with an unknown overdose, providing a framework applicable to virtually any poisoning scenario.

Pearl: The mnemonic "ABCDE" in toxicology stands for: Airway, Breathing, Circulation, Decontamination, and Enhanced Elimination—a framework that organizes priorities even when the toxin remains unknown.

The Primary Survey: Airway, Breathing, and the Glasgow Coma Scale

Airway Assessment and Management

The first priority in any poisoned patient is airway assessment. Altered mental status occurs in approximately 15-20% of serious poisonings and represents the most common indication for intensive care admission.[3] Unlike trauma scenarios where cervical spine protection dominates airway management, the poisoned patient's airway concerns center on three mechanisms:

Central nervous system depression leading to loss of protective reflexes
Hypersalivation or secretions (particularly with cholinergic or sedative toxins)
Seizures compromising airway patency

The decision to intubate a poisoned patient should be based on clinical assessment rather than an arbitrary Glasgow Coma Scale (GCS) cutoff. Traditional teaching suggests intubation for GCS ≤8, but this rule lacks validation in the toxicology literature. Instead, assess for:

Inability to protect the airway (absent gag reflex, pooling secretions)
Inadequate ventilation (respiratory acidosis, hypoxemia)
Anticipated clinical deterioration (large ingestion of delayed-release formulation, progressive symptoms)
Need for decontamination procedures (gastric lavage, though rarely indicated)

Hack: Before reaching for the laryngoscope, consider temporizing measures. Naloxone can rapidly reverse opioid-induced respiratory depression and may obviate intubation. Similarly, repositioning and basic airway maneuvers buy time for assessment while antidotes take effect.

Oyster: Avoid succinylcholine in poisoned patients when possible, particularly with organophosphate exposure. These patients have depleted pseudocholinesterase levels, leading to prolonged paralysis.[4] Rocuronium with sugammadex reversal offers a safer alternative with predictable offset.

Breathing and Ventilation

Once the airway is secured (or preserved), assess ventilation adequacy. Several toxins cause distinctive respiratory patterns:

Respiratory depression: Opioids, sedative-hypnotics, barbiturates
Tachypnea: Salicylates (respiratory alkalosis initially), toxic alcohols, sympathomimetics
Bradypnea: Clonidine, opioids, GHB

Arterial blood gas analysis provides critical information beyond oxygenation status. The anion gap metabolic acidosis serves as a red flag for specific toxins, remembered by the mnemonic GOLDMARK:

Glycols (ethylene glycol, propylene glycol)
Oxoproline (from chronic acetaminophen use)
L-lactate (from metformin, cyanide, carbon monoxide, seizures)
D-lactate (propylene glycol, short bowel syndrome)
Methanol
Aspirin (salicylates)
Renal failure (uremia)
Ketoacidosis (alcoholic, diabetic, starvation)

Pearl: Calculate the osmolar gap in any patient with unexplained altered mental status and anion gap metabolic acidosis. An osmolar gap >10 mOsm/kg suggests toxic alcohol ingestion (methanol, ethylene glycol, isopropanol). The formula: Osmolar gap = Measured osmolality - Calculated osmolality, where Calculated osmolality = 2(Na+) + (Glucose/18) + (BUN/2.8) + (Ethanol/4.6).[5]

Glasgow Coma Scale and Mental Status Assessment

The GCS, while imperfect, provides a standardized method for documenting and tracking mental status changes. However, in toxicology, the trajectory matters more than the absolute number. Document:

Pupil size and reactivity (critical for toxidrome identification)
Response to naloxone or flumazenil (if administered)
Temporal progression (improving, stable, or deteriorating)

Serial assessments every 15-30 minutes in the acute phase can guide management decisions and predict the need for escalation of care.

Hack: The "Talk Test" provides a rapid functional assessment: Can the patient state their name, location, and follow simple commands? If yes, the airway is likely patent, ventilation adequate, and perfusion sufficient to maintain consciousness—buying time for further evaluation.

The Toxidrome Recognition: Opioid, Sympathomimetic, Anticholinergic, Cholinergic, Sedative

Toxidrome recognition represents the cornerstone of clinical toxicology. A toxidrome is a constellation of signs and symptoms that suggest exposure to a particular class of substances, allowing for rational empiric therapy even when the specific agent remains unknown.[6] While many poisonings present with mixed or atypical features, recognizing classic patterns guides initial management.

The Opioid Toxidrome

Classic Triad: Miosis, respiratory depression, decreased level of consciousness

Mechanism: Mu-opioid receptor agonism in the CNS, causing decreased respiratory drive, altered consciousness, and miosis through Edinger-Westphal nucleus effects.

Clinical Features:

Pinpoint pupils (1-2mm) reactive to light
Respiratory rate <12/min with decreased tidal volume
GCS typically 3-10
Decreased bowel sounds
Hypothermia (from reduced thermogenesis)
Track marks or other stigmata of injection drug use

Expanded Differential:

Prescription opioids: morphine, oxycodone, hydrocodone, fentanyl
Illicit opioids: heroin, illicit fentanyl analogs, carfentanil
Atypical opioids: tramadol (also inhibits serotonin/norepinephrine reuptake), tapentadol
Opioid-like substances: clonidine, loperamide (in massive overdose)

Pearl: Not all CNS depressants cause miosis. If pupils are normal or dilated with respiratory depression, consider co-ingestion, hypoxic brain injury, or non-opioid sedatives. Meperidine can paradoxically cause mydriasis due to anticholinergic properties.

Oyster: Massive exposure to synthetic opioids (fentanyl, carfentanil) may require milligrams rather than micrograms of naloxone. Chest wall rigidity can occur with rapid IV fentanyl administration, preventing ventilation despite an open airway—this requires paralysis and intubation, not just naloxone.[7]

The Sympathomimetic Toxidrome

Classic Features: Hypertension, tachycardia, hyperthermia, mydriasis, diaphoresis, agitation

Mechanism: Excessive adrenergic stimulation through various mechanisms—increased catecholamine release (amphetamines, cocaine), decreased reuptake (cocaine), direct receptor agonism (synthetic cathinones), or MAO inhibition.

Clinical Features:

Vital signs: HR >100 bpm, BP often >160/100 mmHg, temperature >38.5°C
Dilated pupils (4-8mm) reactive to light
Diaphoretic skin (wet)
Hyperreflexia, tremor, myoclonus
Agitation, paranoia, hallucinations
Mydriasis with horizontal nystagmus suggests phencyclidine (PCP)

Agents:

Classical stimulants: cocaine, amphetamines, methamphetamine
Substituted amphetamines: MDMA (ecstasy), methylone
Synthetic cathinones: bath salts, mephedrone
Over-the-counter: pseudoephedrine, caffeine (massive doses)
Prescription: phentermine, methylphenidate, bupropion
Withdrawal states: alcohol, benzodiazepines

Pearl: The presence of diaphoresis distinguishes sympathomimetic from anticholinergic toxidromes—both cause tachycardia, hypertension, and mydriasis, but anticholinergic patients have dry, flushed skin.

Hack: Benzodiazepines are first-line for sympathomimetic toxicity. Titrate large doses (midazolam 0.1-0.2 mg/kg IV bolus, repeated as needed) to control agitation, which reduces oxygen consumption, heat generation, and cardiovascular stress. Avoid beta-blockers as monotherapy—unopposed alpha stimulation can worsen hypertension.[8]

The Anticholinergic Toxidrome

Classic Description: "Blind as a bat, red as a beet, hot as a hare, dry as a bone, mad as a hatter"

Mechanism: Muscarinic acetylcholine receptor antagonism, causing both central and peripheral effects.

Clinical Features:

Central: Agitation, confusion, delirium, hallucinations (often visual), mumbling speech, myoclonus, seizures
Peripheral:
- Mydriasis (dilated pupils 6-9mm, poorly reactive or non-reactive)
- Dry mucous membranes, decreased secretions
- Decreased or absent bowel sounds
- Urinary retention
- Flushed, dry skin
- Hyperthermia (from inability to sweat)
- Tachycardia (from vagal blockade)

Agents:

Antihistamines: diphenhydramine, hydroxyzine, doxylamine
Psychiatric medications: tricyclic antidepressants, olanzapine, clozapine
Antiparkinson drugs: benztropine, trihexyphenidyl
Antispasmodics: oxybutynin, dicyclomine
Plants: jimsonweed (Datura), deadly nightshade (Atropa belladonna)
Mushrooms: Amanita muscaria
Over-the-counter sleep aids: most contain diphenhydramine

Oyster: Tricyclic antidepressants deserve special mention—they cause anticholinergic effects PLUS sodium channel blockade (causing QRS widening and arrhythmias) and alpha-blockade (hypotension). A QRS >100 ms predicts seizures, and >160 ms predicts ventricular arrhythmias. Sodium bicarbonate (bolus 1-2 mEq/kg) is the specific treatment for TCA-induced cardiac toxicity.[9]

Pearl: Central anticholinergic syndrome can occur with therapeutic doses of medications in susceptible populations (elderly, polypharmacy). Consider this diagnosis in elderly patients with acute delirium—particularly if they recently started an antihistamine, bladder medication, or muscle relaxant.

The Cholinergic Toxidrome

Classic Features: SLUDGE syndrome (Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis) plus the "Killer Bs" (Bronchospasm, Bronchorrhea, Bradycardia)

Mechanism: Excess acetylcholine at muscarinic and nicotinic receptors, typically from acetylcholinesterase inhibition.

Clinical Features:

Muscarinic effects:

Increased secretions (salivation, lacrimation, bronchorrhea)
Miosis (pinpoint pupils)
Bronchospasm, bronchorrhea
Bradycardia
Urination, defecation
Emesis
Diaphoresis (although sweating is technically nicotinic)

Nicotinic effects:

Muscle fasciculations followed by weakness or paralysis
Tachycardia (early, from sympathetic ganglia stimulation)
Hypertension
Mydriasis (can occur early, confusing the picture)

Central effects:

Anxiety, confusion, coma
Seizures
Respiratory depression

Agents:

Organophosphate insecticides (malathion, parathion, chlorpyrifos)
Carbamate insecticides (aldicarb, carbaryl)
Nerve agents (sarin, VX, soman)
Medications: physostigmine, pyridostigmine, donepezil, rivastigmine
Certain mushrooms: Inocybe and Clitocybe species

Pearl: The "two PAMs and an atropine" approach for organophosphate poisoning: Pralidoxime (2-PAM) 1-2 g IV over 30 minutes, repeated as needed, reactivates acetylcholinesterase if given early (<24-48 hours). Atropine 2-5 mg IV bolus, doubled every 5 minutes until bronchial secretions dry (may require hundreds of milligrams). Think of atropine as "drying the patient" rather than treating by vital signs.[10]

Hack: In resource-limited settings or with delayed presentation beyond the pralidoxime window, high-dose atropine alone can be life-saving. The endpoint is dried bronchial secretions, not pupil size or heart rate.

The Sedative-Hypnotic Toxidrome

Classic Features: CNS depression, respiratory depression, normal pupils, normal or decreased temperature

Mechanism: Enhancement of GABA-A receptor function (benzodiazepines, barbiturates) or other CNS depressant mechanisms.

Clinical Features:

Decreased level of consciousness (GCS variable, 3-14)
Respiratory depression (rate and/or tidal volume)
Normal or slightly dilated pupils (3-5mm), reactive
Hypotension (with massive overdose or barbiturates)
Hypothermia
Decreased or normal reflexes
Normal bowel sounds

Agents:

Benzodiazepines: diazepam, alprazolam, clonazepam, lorazepam
Barbiturates: phenobarbital, butalbital
Non-benzodiazepine hypnotics: zolpidem, eszopiclone, zaleplon
Gamma-hydroxybutyrate (GHB) and precursors
Ethanol
Baclofen
Carisoprodol (metabolizes to meprobamate)

Distinguishing from Opioids:

Normal-sized pupils (not miotic)
Less profound respiratory depression per degree of sedation
Slower onset (most sedatives have longer time to peak effect than opioids)
Context clues (prescription bottles, known anxiety disorder history)

Pearl: GHB deserves special mention—it causes profound but brief CNS depression (often GCS 3-4), typically resolving spontaneously within 2-6 hours. Patients may require intubation but wake precipitously, becoming agitated and attempting self-extubation. Bradycardia is common. The key is supportive care; most patients can be managed with close observation rather than intubation if respiratory drive remains adequate.[11]

Oyster: Benzodiazepine tolerance means that patients on chronic benzodiazepines may ingest quantities that would be lethal to opioid-naive individuals yet present with minimal symptoms. Conversely, benzodiazepine-naive patients may experience profound CNS depression from therapeutic doses.

Mixed and Atypical Toxidromes

Clinical reality rarely matches textbook toxidromes perfectly. Consider:

Serotonin syndrome: Hyperthermia, clonus, hyperreflexia, autonomic instability—overlaps with sympathomimetic but has distinctive neuromuscular hyperactivity (particularly ocular clonus and lower extremity clonus)
Neuroleptic malignant syndrome: Rigidity (lead-pipe), hyperthermia, altered mental status—develops over days, not hours
Salicylate toxicity: Mixed acid-base disturbances (respiratory alkalosis plus anion gap metabolic acidosis), tinnitus, hyperpnea
Toxic alcohol ingestion: Osmolar gap early, anion gap later, visual symptoms (methanol), flank pain (ethylene glycol)

Hack: When the presentation doesn't fit a classic toxidrome, consider: (1) co-ingestion, (2) complications of the ingestion (hypoxic brain injury, aspiration, rhabdomyolysis), (3) non-toxicologic etiology, or (4) rare poison.

The Universal Antidotes: Naloxone, Flumazenil, Deferoxamine, N-Acetylcysteine

The term "universal antidotes" is a misnomer—no antidote applies to all poisonings—but certain antidotes have such broad applicability or critical importance that every intensivist must know them intimately.

Naloxone: The Opioid Reversal Agent

Mechanism: Competitive antagonist at mu, kappa, and delta opioid receptors

Indications:

Suspected opioid toxicity with respiratory depression (RR <10-12/min)
Altered mental status with miosis in appropriate context
Diagnostic trial in undifferentiated coma with respiratory depression

Dosing:

Initial: 0.04-0.4 mg IV (40-400 mcg), titrated to respiratory effort, NOT full consciousness
Goal: Adequate ventilation and airway protection, not complete reversal
Escalation: Double the dose every 2-3 minutes if no response (up to 10-15 mg total for suspected synthetic opioid overdose)
Infusion: If repeat boluses needed, start continuous infusion at two-thirds of the effective bolus dose per hour (e.g., if 2 mg total bolus was effective, infuse 1.3 mg/hr)

Routes of Administration:

IV: Preferred, onset 1-2 minutes
IM/SC: Onset 5-10 minutes, useful in prehospital setting
Intranasal: 2-4 mg (absorbed transmucosally), onset 5-10 minutes
Endotracheal: 2-2.5× IV dose (rarely necessary with IN availability)

Duration: 30-90 minutes (shorter than most opioids), necessitating observation for renarcotization

Pearl: Titrate to respiratory effort, not consciousness. The goal of naloxone is to restore adequate spontaneous ventilation, not to achieve full alertness. Over-reversal precipitates acute opioid withdrawal (agitation, tachycardia, hypertension, vomiting), increases the risk of aspiration, and may cause the patient to abscond before evaluation is complete.

Oyster: Naloxone does not reverse buprenorphine effectively at standard doses due to buprenorphine's high receptor affinity and slow dissociation. Massive doses (10-15 mg) may be required, or mechanical ventilation may be necessary until buprenorphine redistributes.[12]

Controversy: The proliferation of synthetic opioids (illicit fentanyl analogs) has changed prehospital and emergency naloxone use. Some patients require unprecedented doses, and case reports describe naloxone doses exceeding 20 mg. This has led to debate about appropriate initial dosing—should we start higher? Current consensus favors starting low (preserving the option for partial reversal) but being prepared to escalate rapidly and dramatically.[7]

Hack: If you suspect opioid overdose but naloxone is unavailable (or while preparing it), bag-valve-mask ventilation is the immediate life-saving intervention. Opioid-induced respiratory depression responds well to positive pressure ventilation, and adequate oxygenation prevents anoxic brain injury while definitive treatment is prepared.

Flumazenil: The Controversial Benzodiazepine Antagonist

Mechanism: Competitive antagonist at the GABA-A benzodiazepine receptor

Indications (controversial):

Accepted: Iatrogenic benzodiazepine oversedation (procedure-related)
Controversial: Suspected isolated benzodiazepine overdose

Dosing:

Initial: 0.2 mg IV over 30 seconds
Repeat: 0.3 mg at 1 minute if no response
Further: 0.5 mg every 1 minute up to cumulative 3 mg
Infusion: 0.1-0.5 mg/hr if repeat boluses required

Duration: 40-80 minutes (shorter than most benzodiazepines)

Contraindications (relative and absolute):

Seizure disorder or risk: Removes GABA-ergic anticonvulsant effect
Chronic benzodiazepine use: Precipitates withdrawal seizures
Co-ingestion with pro-convulsant (TCAs, cocaine, tramadol, bupropion): Unmasks seizure activity
Increased intracranial pressure: Benzodiazepine effect may be protective
QRS widening on ECG: Suggests TCA co-ingestion

Oyster: Flumazenil is rarely indicated in the poisoned patient. Unlike naloxone, which addresses life-threatening respiratory depression, isolated benzodiazepine overdose rarely causes death with supportive care. The risk of precipitating seizures (potentially refractory status epilepticus) in unrecognized polypharmacy overdose outweighs benefits in most scenarios.[13]

When to Consider: The narrow window for flumazenil use includes:

Known iatrogenic benzodiazepine administration (post-procedure)
Confirmed isolated benzodiazepine ingestion (witnessed, confirmatory testing)
No seizure history or pro-convulsant co-ingestion
Hemodynamic stability

Pearl: In cases of suspected hepatic encephalopathy with benzodiazepine contribution, flumazenil may clarify mental status and guide further management. However, this is best done in consultation with toxicology or hepatology specialists.

Hack: The best approach to benzodiazepine overdose is supportive care—airway protection if needed, monitoring for aspiration, and allowing time for metabolism and elimination. Most patients awaken within 12-24 hours without intervention.

Deferoxamine: The Iron Chelator

Mechanism: Binds free iron, forming ferrioxamine, which is renally excreted

Indications:

Confirmed: Serum iron >500 mcg/dL
Empiric: Suspected significant iron ingestion with clinical toxicity (persistent vomiting, hematemesis, shock, altered mental status, metabolic acidosis)
Consider: Serum iron 350-500 mcg/dL with symptoms

Dosing:

Continuous IV infusion: 15 mg/kg/hr (maximum 6-8 g/24hr traditionally, though higher doses used in severe toxicity)
Duration: Until clinical improvement and iron level <100 mcg/dL, typically 12-48 hours

Monitoring:

Serum iron levels every 4-6 hours
Urine color (classically "vin rosé" or rust-colored from ferrioxamine excretion, though absence doesn't exclude efficacy)
Metabolic acidosis resolution
Vital sign normalization

Pearl: The traditional "vin rosé" urine color from ferrioxamine is neither sensitive nor specific for the need to continue deferoxamine. Base decisions on clinical status (resolution of acidosis, hemodynamic stability) and decreasing iron levels rather than urine color alone.[14]

Oyster: Deferoxamine can cause acute respiratory distress syndrome (ARDS) with prolonged administration (>24-48 hours), particularly at higher doses. This mandates careful risk-benefit assessment and aggressive supportive lung care. Consider consultation with a medical toxicologist for severe cases requiring extended chelation.

Stages of Iron Toxicity:

Stage I (0.5-6 hours): GI symptoms (vomiting, diarrhea, abdominal pain, hematemesis)
Stage II (6-24 hours): Apparent recovery (latent phase)
Stage III (12-48 hours): Shock, metabolic acidosis, coagulopathy, hepatotoxicity
Stage IV (2-6 weeks): Gastric outlet obstruction from scarring

Hack: In the child with suspected iron ingestion, abdominal radiography can help. Iron tablets are radiopaque, and the presence of multiple tablets warrants aggressive decontamination (whole bowel irrigation) even before serum levels return.

N-Acetylcysteine (NAC): The Acetaminophen Antidote

Mechanism: Replenishes glutathione stores, provides alternative substrate for NAPQI (toxic metabolite), and has antioxidant and anti-inflammatory effects

Indications:

Confirmed: Acute acetaminophen ingestion with level above treatment line on Rumack-Matthew nomogram (4-hour level >150 mcg/mL)
Empiric: Suspected toxic ingestion (>7.5 g or >150 mg/kg in adults) with delayed presentation where levels cannot be interpreted
Extended-release or chronic: Cannot use nomogram; treat if any measurable level with suspicion of toxic ingestion
Uncertain timing: Treat if any detectable acetaminophen level and suspicion of overdose

Traditional 21-Hour IV Protocol (FDA-approved in US):

Loading dose: 150 mg/kg in 200 mL D5W over 1 hour
Second dose: 50 mg/kg in 500 mL D5W over 4 hours
Third dose: 100 mg/kg in 1000 mL D5W over 16 hours
Total: 300 mg/kg over 21 hours

Modified Protocols:

12-hour protocol: Used in some countries, equivalent efficacy for most patients
Extended therapy: Continue 100 mg/kg over 16 hours (repeat third dose) if:
- Acetaminophen level still detectable
- AST/ALT rising or peaked but not improving
- Massive ingestion
- Evidence of hepatotoxicity

Oral NAC Protocol (alternative when IV unavailable):

Loading dose: 140 mg/kg PO
Maintenance: 70 mg/kg PO every 4 hours for 17 additional doses (total 72 hours)
Limitations: Vomiting (may require antiemetics or NG tube), slower absorption

Pearl: When in doubt, treat. NAC has an exceptional safety profile (anaphylactoid reactions occur but are rarely serious), and hepatotoxicity from untreated acetaminophen overdose carries significant morbidity and mortality. The mnemonic "Better NAC than sorry" captures this principle.

Oyster: Anaphylactoid reactions to IV NAC occur in 10-20% of patients, typically during the loading dose (which has the highest infusion rate). Reactions include flushing, urticaria, angioedema, bronchospasm, and hypotension. Management:

Stop the infusion temporarily
Administer antihistamines (diphenhydramine 25-50 mg IV, ranitidine 50 mg IV)
For bronchospasm: Albuterol nebulizer
For hypotension: Fluid bolus
Resume NAC at slower rate once reaction resolves

True IgE-mediated anaphylaxis is exceedingly rare; these are rate-related histamine-release reactions, and NAC can almost always be continued at a slower rate.[15]

Hack: For patients presenting >24 hours after ingestion with established hepatotoxicity (transaminitis, coagulopathy, encephalopathy), extend NAC therapy beyond the standard 21 hours. Continue NAC infusion at 100 mg/kg over 16 hours (repeating the third dose) until clinical improvement occurs (normalizing transaminases, improving coagulopathy, improving mental status). Some patients require NAC for days to weeks until liver function recovers or transplantation occurs.[16]

Rumack-Matthew Nomogram Limitations:

Only valid for acute, single-time-point ingestions
Cannot be used if timing uncertain
Not applicable to chronic or repeated supratherapeutic ingestion
4-hour level must be drawn at least 4 hours post-ingestion (earlier levels cannot be interpreted)

Alternative Approach for Extended-Release Acetaminophen:

Obtain levels at 4 hours AND 8 hours post-ingestion
Treat if either level is above treatment line
The second level captures delayed absorption

Enhanced Elimination: The Role of Activated Charcoal and Urine Alkalinization

While preventing absorption and enhancing elimination sound appealing, these interventions have narrower indications than historically believed. The era of aggressive gastric emptying (ipecac, gastric lavage) has largely passed, replaced by selective use of activated charcoal and targeted manipulation of elimination kinetics.

Gastrointestinal Decontamination

Activated Charcoal

Mechanism: Adsorbs toxins in the GI tract through Van der Waals forces, preventing systemic absorption

Dose:

Adults: 50-100 g PO or via NG tube
Children: 1 g/kg (maximum 50 g)
Given as aqueous slurry (typically premixed formulations)

Indications:

Potentially toxic ingestion of adsorbable substance
Timing: Most effective within 1 hour of ingestion, but may offer benefit up to 2-4 hours for:
- Agents delaying gastric emptying (anticholinergics, opioids)
- Sustained-release formulations
- Large ingestions with delayed absorption
- Substances with enterohepatic recirculation

Substances NOT adsorbed by activated charcoal (mnemonic: PHAILS):

Petroleum distillates (gasoline, kerosene)
Heavy metals (iron, lead, lithium)
Acids and alkalis (caustics)
Ions (lithium, potassium)
Liquid hydrocarbons
Solvents (alcohols, glycols)

Contraindications:

Absolute:
- Unprotected airway with altered mental status (aspiration risk)
- GI perforation or obstruction
- Caustic ingestion
Relative:
- Recent GI surgery
- Ingestion of substance not adsorbed by charcoal
- Presentation >2 hours after ingestion of typical-release formulation

Pearl: The risk-benefit calculation for activated charcoal hinges on aspiration risk. A patient with GCS <10 who cannot protect their airway should either be intubated before charcoal administration or charcoal should be foregone. Charcoal aspiration causes severe pneumonitis with high mortality.[17]

Multiple-Dose Activated Charcoal (MDAC):

Used to enhance elimination of certain drugs through "gastrointestinal dialysis"—interrupting enterohepatic/enteroenteric recirculation.

Indications:

Carbamazepine
Dapsone
Phenobarbital
Quinine
Theophylline
Possibly: salicylates, valproic acid

Dosing:

25-50 g every 2-4 hours (adult)
0.5 g/kg every 2-4 hours (pediatric)
Continue until clinical improvement or drug levels decline

Monitoring: Bowel sounds and stool output (ensure charcoal passage, avoid obstruction)

Oyster: MDAC is underutilized in modern practice, partly due to limited evidence from randomized trials and partly due to concerns about patient tolerability. However, for specific life-threatening ingestions (carbamazepine causing refractory seizures, theophylline causing ventricular arrhythmias), MDAC can significantly reduce drug levels and improve outcomes when extracorporeal methods are unavailable or delayed.[18]

Hack: Pre-medicate with ondansetron (4-8 mg IV) before charcoal administration to reduce vomiting. Vomiting charcoal increases aspiration risk and reduces efficacy. If the patient vomits the first dose, repeat it—one successful dose is better than none.

Gastric Lavage: The Dying Art

Once a cornerstone of poisoning management, gastric lavage has fallen from favor due to:

Limited efficacy (retrieves <30% of gastric contents even when performed immediately)
Significant complications (esophageal perforation, aspiration, vagal stimulation)
No mortality benefit in clinical trials

Current Limited Indications:

Life-threatening ingestion within 1 hour
No safer alternative available
Substance not adsorbed by charcoal
Protected airway (intubated)

Technique (if performed):

Large-bore orogastric tube (36-40 French in adults)
Left lateral decubitus position, head down
Aspirate gastric contents
Lavage with 200-300 mL aliquots of normal saline until clear (typically 2-5 L total)
Administer activated charcoal through tube after lavage

Pearl: Gastric lavage is essentially obsolete for most poisonings. The phrase "treat the patient, not the poison" encapsulates modern toxicology—supportive care outperforms aggressive decontamination in virtually all scenarios.

Whole Bowel Irrigation (WBI)

Mechanism: Large-volume polyethylene glycol electrolyte solution flushes GI tract without fluid/electrolyte shifts

Indications:

Body packers/stuffers: Cocaine, heroin packets
Sustained-release formulations: Calcium channel blockers, iron
Substances not adsorbed by charcoal: Iron, lithium, lead
Massive ingestions where tablet burden exceeds charcoal capacity

Dosing:

Adults: 1.5-2 L/hour via NG tube until rectal effluent clear
Children: 25-40 mL/kg/hour
Continue until clear rectal effluent (typically 4-6 hours)

Contraindications:

Bowel obstruction or perforation
GI bleeding
Hemodynamic instability
Unprotected airway
Ileus

Oyster: WBI creates a logistical challenge—patients require frequent bedside nursing for bowel management, and the large fluid volumes raise aspiration concerns. Place patients on a commode or use rectal tubes for containment. Ensure adequate airway protection before initiating.

Hack: For iron ingestion where abdominal radiograph shows retained tablets after initial charcoal, WBI can mechanically remove iron tablets that charcoal cannot adsorb. This combination approach (charcoal for co-ingestants, WBI for iron) may be optimal for mixed overdoses.

Enhanced Elimination Techniques

Urine Alkalinization

Mechanism: Increases renal elimination of weak acids by ion trapping—alkaline urine (pH 7.5-8.5) ionizes weak acids, preventing tubular reabsorption

Indications:

Salicylate poisoning (primary indication)
Chlorpropamide overdose (rare)
Methotrexate toxicity (in oncology settings)
Phenobarbital poisoning (MDAC preferred if tolerated)

Technique:

Bolus: Sodium bicarbonate 1-2 mEq/kg (typically 50-100 mEq) IV over 30-60 minutes
Infusion: Add 150 mEq (3 amps) sodium bicarbonate to 1 L D5W, infuse at 200-250 mL/hr
Monitoring:
- Urine pH every 2 hours (goal 7.5-8.5)
- Serum pH, electrolytes, calcium every 2-4 hours
- Adjust infusion to maintain target urine pH
Titration: Increase or decrease infusion rate by 50 mL/hr based on urine pH

Goals:

Urine pH: 7.5-8.5
Serum pH: 7.45-7.55 (avoid severe alkalemia)
Urine output: 2-3 mL/kg/hr

Complications:

Hypokalemia: Alkalemia drives K+ intracellularly; aggressive repletion required (maintain K+ >4.0 mEq/L)
Volume overload: Large sodium load, monitor for pulmonary edema
Hypocalcemia: Alkalemia decreases ionized calcium
Metabolic alkalosis: Particularly if continued beyond indication

Pearl: Adequate urine alkalinization is impossible without correcting hypokalemia. The kidney will preferentially reabsorb K+ over excreting H+ when potassium-depleted, making alkalinization ineffective. Aggressively supplement potassium (20-40 mEq/L in maintenance fluids) from the start.

Salicylate Toxicity—Special Considerations:

Salicylate poisoning causes unique acid-base derangements:

Respiratory alkalosis: Direct stimulation of medullary respiratory center
Anion gap metabolic acidosis: Uncoupling oxidative phosphorylation, lactate production
Mixed: Both disturbances occur simultaneously

Why Alkalinization Matters:

Salicylate CNS toxicity correlates with brain salicylate concentration
Acidemia (systemic or CNS) drives salicylate into CNS (ion trapping in reverse)
CRITICAL: Intubation and mechanical ventilation can be fatal in salicylate toxicity if minute ventilation is not matched to the patient's compensatory hyperventilation—loss of respiratory alkalosis causes catastrophic acidemia and brain salicylate accumulation[19]

Hack: If a patient with salicylate toxicity requires intubation, match their spontaneous minute ventilation (typically 30-40 L/min). Use volume control mode with:

Tidal volume 8-10 mL/kg
Respiratory rate 30-40/min
Monitor end-tidal CO2 and blood gas closely
Consider hemodialysis as alternative to intubation when possible

Oyster: The salicylate level in chronic toxicity correlates poorly with clinical severity. Elderly patients on chronic salicylate therapy can develop life-threatening toxicity with "therapeutic" or mildly elevated levels (30-50 mg/dL). Treat based on clinical status (altered mental status, metabolic acidosis, pulmonary edema), not just the level.[20]

Hemodialysis and Extracorporeal Removal

While beyond the scope of "enhanced elimination" techniques applicable to all poisonings, recognize indications for dialysis:

Mnemonic for Dialyzable Poisons: SLIME

Salicylates
Lithium
Isopropanol (rarely necessary)
Methanol
Ethylene glycol

Additional Indications:

Valproic acid (severe toxicity)
Carbamazepine (refractory seizures)
Theophylline (level >100 mg/L)
Metformin (with severe lactic acidosis)

General Criteria for Dialysis:

Severe toxicity despite maximal supportive care
Drug is dialyzable (low molecular weight, low volume of distribution, minimal protein binding)
Clinical deterioration or life-threatening complications
Toxic metabolite production (methanol, ethylene glycol)

Pearl: Consult nephrology and toxicology early when considering dialysis. Many ICUs lack experience with poison-specific dialysis kinetics, and toxicology can guide duration and endpoints.

When to Consult the Poison Control Center (Hint: Always)

The Value of Toxicology Consultation

The poison control center represents an underutilized resource in critical care. In the United States, the Poison Help line (1-800-222-1222) connects to regional centers staffed 24/7 by specialists in poison information (nurses, pharmacists) with medical toxicologist backup. Services are free and confidential.

When to Call:

Always for unknown or poly-pharmacy overdoses
Any poisoning with atypical presentation
Unfamiliar antidote dosing or availability questions
Pediatric poisonings (different pharmacokinetics)
Occupational or environmental exposures
When considering unusual therapies (lipid emulsion, hemodialysis)
For prognostic information and disposition guidance

What They Provide:

Evidence-based treatment recommendations from current literature
Antidote availability and sourcing (many antidotes are not stocked in every hospital)
Follow-up calls to track clinical course and adjust recommendations
Documentation for medicolegal purposes
Transfer assistance to toxicology centers for complex cases
Access to medical toxicologists for complex consultations

Pearl: Document the poison control center case number in your medical record. This facilitates continuity if multiple providers are involved and provides medicolegal protection by demonstrating consultation with specialists.

Medical Toxicology Consultation

Beyond poison control center phone support, consider formal medical toxicology consultation for:

Absolute Indications:

Exotic or rare poisons (colchicine, cardiac glycosides, heavy metals)
Poisonings requiring specialized antidotes (digoxin immune Fab, antivenoms)
Extracorporeal removal considerations
Body packers/stuffers requiring surgical decisions
Prolonged toxicity requiring ICU-level toxicology expertise

Relative Indications:

Failure to improve with standard management
Diagnostic uncertainty despite workup
Multiple organ system involvement
Pregnancy with significant poisoning
Medicolegal complexity (assault, workplace exposure, self-harm in special populations)

Access Points:

Poison control center can facilitate toxicology consult
American College of Medical Toxicology (ACMT) maintains consultant directory
Many tertiary centers have toxicology services
Telemedicine toxicology increasingly available

Hack: Build a relationship with your regional poison control center and toxicology service before you need them urgently. Understand their capabilities, response times, and preferred communication methods. In a crisis, you'll have established channels rather than cold-calling for help.

What Information to Provide

When consulting poison control or toxicology:

Essential Information:

Patient demographics: Age, weight, sex
Substance(s): Name, formulation, dose, timing
Route: Ingestion, inhalation, dermal, injection
Intent: Intentional, unintentional, recreational
Clinical status: Vital signs, GCS, pupils, skin findings
Interventions: Decontamination, antidotes, supportive care given
Laboratory data: Specific levels, electrolytes, acid-base status
Co-morbidities: Liver/kidney disease, psychiatric history, medications

Optimize the Consultation:

Have pill bottles or substance containers available
Take photographs of substances, labels, or packaging
Be prepared to describe the clinical trajectory
Have someone available to take detailed notes
Ask specific questions (antidote dosing, lab monitoring, prognosis, disposition)

Oyster: Poison control centers track exposures for epidemiologic surveillance. Your call contributes to understanding emerging threats (novel psychoactive substances, contaminated drug supplies, product recalls). This public health function benefits future patients.

Putting It All Together: The Systematic Approach

The First 15 Minutes

When an undifferentiated poisoned patient arrives:

Immediate Actions (Simultaneous):

Primary survey: Airway, breathing, circulation
Continuous monitoring: Cardiac monitor, pulse oximetry, blood pressure
IV access: At least one large-bore IV
Point-of-care glucose: Hypoglycemia mimics intoxication
12-lead ECG: QRS width, QTc, conduction abnormalities
Supplemental oxygen: Maintain SpO2 >94%

History (AMPLE + toxicology-specific):

Allergies
Medications (patient's, household members')
Past medical history (psychiatric, substance use, chronic pain)
Last meal (affects absorption kinetics)
Events (what, when, why, how much, witnesses)
Additional: Suicide note, pill bottles, paraphernalia, collateral from EMS/family

Physical Examination:

Vital signs: Include temperature (core if altered)
Toxidrome assessment: Systematically evaluate pupils, skin, bowel sounds, reflexes, mental status
Focused exam: Needle tracks, burns (caustics), trauma (fall from sympathomimetic agitation)

Initial Laboratories:

Basic metabolic panel: Anion gap calculation
Hepatic function: AST, ALT, INR (if acetaminophen concern)
Arterial or venous blood gas: Acid-base status, lactate
Serum osmolality: Calculate osmolar gap
Acetaminophen level: Screen everyone with intentional overdose
Salicylate level: Low threshold for checking
Ethanol level: Common co-ingestant
Urine pregnancy test: All females of childbearing age
ECG: Already done, interpret carefully

Targeted Levels (based on history/presentation):

Specific drugs mentioned by patient
Toxins suggested by toxidrome
Institutional "toxic screen" panels vary in utility

Pearl: The "toxic screen" or "urine drug screen" rarely changes acute management. These tests identify classes of substances (opioids, benzodiazepines, amphetamines) but:

Don't detect many toxins (synthetic opioids, novel psychoactive substances)
Don't provide quantitative levels
Have false positives (cross-reactivity)
Have false negatives (synthetic substances)
Results delayed (hours)

Treat the patient, not the tox screen. Clinical toxidrome recognition guides management better than laboratory testing for most poisonings.[21]

The First Hour

Stabilization:

Airway secured if needed (clinical assessment, not GCS alone)
Antidote administered if indicated:
- Naloxone for opioid toxidrome with respiratory depression
- Sodium bicarbonate for wide QRS from suspected TCA/sodium channel blocker
- Consider empiric thiamine, dextrose if altered + hypoglycemia risk
Decontamination decision made:
- Activated charcoal if appropriate timing and protected airway
- Whole bowel irrigation if indicated (body packer, sustained-release, iron)
Enhanced elimination initiated if indicated:
- Urine alkalinization for salicylates
- MDAC for appropriate substances

Consultation:

Poison control center called (always)
Toxicology consultation if complex
Psychiatry notification if intentional self-harm (but defer formal evaluation until medically stable)
Nephrology if dialysis considered
Social work/child protective services if pediatric non-accidental poisoning suspected

Disposition Planning:

ICU admission criteria:
- Ongoing hemodynamic instability
- Respiratory support required
- Altered mental status requiring frequent reassessment
- Antidote infusions requiring close monitoring
- Anticipated deterioration (delayed-onset toxins)
- Body packer (observation for packet rupture)
Monitored bed criteria:
- Symptomatic but stable
- Substances with delayed effects (acetaminophen, ASA, iron)
- Need for serial examinations
- MDAC or other frequent interventions
Medical floor/observation:
- Asymptomatic with non-toxic screening levels
- Psychiatric hold after medical clearance
- Delayed presentations with normal labs
Discharge:
- Minimal exposure with completely asymptomatic course
- Reliable patient with psychiatric follow-up arranged
- Pediatric unintentional exposure with clear innocuous substance

Oyster: "Medical clearance" for psychiatric admission is often poorly defined. Ensure the patient is:

Hemodynamically stable with normal vital signs
Alert and oriented, back to baseline mental status
Cleared from medical complications (aspiration, rhabdomyolysis)
Acetaminophen and salicylate levels non-toxic (or appropriate NAC completed)
ECG normalized if previously abnormal
Physical exam normal

Document clearly what you're clearing and what residual risk remains (e.g., "Medically cleared from toxicology standpoint; psychiatric team to assess capacity and safety for discharge").

The First 24 Hours

Ongoing Management:

Serial assessments: Vital signs, mental status, toxidrome evolution every 1-4 hours based on severity
Repeat laboratories: Based on specific poison (e.g., acetaminophen at 4 hours and 24 hours, salicylate every 4 hours until declining)
Supportive care optimization:
- Fluids for rhabdomyolysis prophylaxis (sympathomimetics)
- Benzodiazepines for agitation, seizures
- Antiemetics for persistent vomiting
- DVT prophylaxis if prolonged immobility
- Aspiration precautions if altered
Antidote titration: Adjust naloxone infusion, continue/discontinue NAC, monitor for deferoxamine complications
Enhanced elimination assessment: Is MDAC being tolerated? Is urine alkalinization achieving target pH?
Complication surveillance:
- Aspiration pneumonitis
- Rhabdomyolysis
- Acute kidney injury
- Hepatotoxicity
- Cardiovascular complications
- Seizures

Communication:

Update poison control center with clinical course
Coordinate with psychiatry for intentional overdoses
Family meetings if prolonged course expected
Documentation of decision-making and consultations

Clinical Pearls and Oysters: High-Yield Teaching Points

Pearls for the Poisoned Patient

Supportive care trumps antidotes: The vast majority of poisoned patients survive with good airway management, hemodynamic support, and prevention of complications. Don't delay supportive care while searching for exotic antidotes.
The patient is the best "tox screen": Physical examination (pupils, skin, vital signs, mental status) provides more immediately useful information than laboratory testing for guiding initial management.
When you hear hoofbeats, think horses (but keep zebras in mind): Common things are common (acetaminophen, benzodiazepines, alcohol, opioids), but remain alert for rare but deadly toxins (colchicine, cardiac glycosides, toxic alcohols).
The antidote to most poisonings is time: With adequate supportive care, most xenobiotics are metabolized and eliminated without specific interventions. Patience is therapeutic.
Co-ingestion is the rule, not the exception: 30-50% of intentional overdoses involve multiple substances. Screen broadly, treat the clinical picture, and expect the unexpected.
Treat responsive patients as though they're telling the truth, unresponsive patients as though they're not: Believe the history when the patient is alert, but when obtunded, assume the worst (bigger ingestion, more substances, earlier timing).
The most dangerous time is 4-6 hours post-ingestion: Many delayed-onset toxins (acetaminophen, ASA, iron, sustained-release formulations) look benign initially. Early reassurance followed by unexpected deterioration is the pattern.
QRS duration is the most important ECG parameter in overdose: Wide QRS (>100 ms) suggests sodium channel blockade (TCAs, cocaine, diphenhydramine, propranolol, quinidine, local anesthetics) and mandates aggressive treatment with sodium bicarbonate and cardiac monitoring.
Agitation kills: Sympathomimetic toxicity causes death through hyperthermia, rhabdomyolysis, and cardiovascular collapse—all preventable with adequate sedation. Titrate benzodiazepines aggressively.
The pupils don't lie (usually): Pupil examination is remarkably reliable for toxidrome identification, but remember: miosis doesn't always mean opioids (clonidine, pontine stroke, organophosphates), and mydriasis doesn't always mean anticholinergic (sympathomimetics, serotonin syndrome).

Oysters (Dangerous Pitfalls)

The "stable" body packer is never stable: Cocaine or heroin packets in the GI tract represent ticking time bombs. Packet rupture causes massive, often lethal toxicity. Admit to ICU, consult surgery, consider WBI, have antidotes ready.
Intubating the salicylate patient without matching their minute ventilation is potentially fatal: Loss of compensatory hyperventilation causes precipitous acidemia and brain salicylate accumulation. Match their pre-intubation ventilation (often 30-40 L/min) or consider hemodialysis as an alternative to intubation.
Beta-blocker and calcium channel blocker toxicity can masquerade as septic shock: Profound vasodilatory shock with relative bradycardia—don't miss this diagnosis by assuming all shock is septic. History is critical; treatment differs dramatically (high-dose insulin, calcium, glucagon, lipid emulsion vs. antibiotics).
Hypoglycemia is not just for diabetics: Ethanol, beta-blockers, sulfonylureas, salicylates, and insulin can all cause profound hypoglycemia. Check glucose in every altered patient, even without diabetes history.
Serotonin syndrome can kill quickly: This is not a benign condition. Hyperthermia >41°C, rigidity, rhabdomyolysis, DIC, and multi-organ failure develop rapidly. Aggressive cooling, benzodiazepines, cyproheptadine, and sometimes paralysis/intubation are required. Stop all serotonergic agents.
Delayed acetaminophen hepatotoxicity occurs despite normal initial presentation: The patient who presents 2 hours post-ingestion with no symptoms still needs a 4-hour level and possible NAC. Hepatotoxicity peaks at 3-4 days, long after the patient feels fine.
Chronic salicylate toxicity in the elderly is more dangerous than acute overdose: Elderly patients develop toxicity at lower levels, present with non-specific symptoms (confusion, tachypnea), and have higher mortality. Always check ASA level in elderly patients with unexplained altered mental status or acid-base disturbances.
Propofol infusion syndrome looks like toxic ingestion: Profound lactic acidosis, rhabdomyolysis, cardiovascular collapse, and renal failure—but the "poison" is iatrogenic. Consider this in ICU patients on prolonged propofol infusions, especially children or patients receiving >4 mg/kg/hr for >48 hours.
Lipid emulsion therapy is not benign: While potentially life-saving for lipophilic drug overdose (local anesthetics, calcium channel blockers, beta-blockers, TCAs), lipid emulsion causes pancreatitis, fat embolism, and interference with laboratory testing. Consult toxicology before administration in most cases (except local anesthetic systemic toxicity, where it's first-line).[22]
The "hangover" that won't quit might be toxic alcohol ingestion: Persistent altered mental status, worsening acidosis, and osmolar gap hours after suspected ethanol ingestion suggest methanol or ethylene glycol. These require fomepizole and hemodialysis, not just supportive care.

Conclusion

The management of the poisoned patient remains one of the most challenging and intellectually stimulating aspects of critical care medicine. While specific antidotes and targeted therapies capture attention, the foundation of successful outcomes rests on meticulous supportive care, systematic clinical assessment, and early consultation with toxicology experts.

The approach outlined in this review—beginning with the primary survey, proceeding through toxidrome recognition, judiciously applying antidotes, considering enhanced elimination when appropriate, and always consulting poison control—provides a framework applicable to virtually any poisoning scenario. As the landscape of toxic exposures evolves with novel psychoactive substances, designer drugs, and emerging pharmaceuticals, this systematic approach remains constant.

Remember: treat the patient, not the poison. Excellent airway management, hemodynamic support, seizure control, and prevention of complications will save more lives than memorizing every antidote. When in doubt, call poison control—their expertise is available 24/7, free of charge, and can make the difference between good and excellent care.

The poisoned patient challenges us to be both systematic and creative, evidence-based yet pragmatic, and above all, to remember that behind every toxidrome is a person whose life may depend on our ability to synthesize disparate clues into coherent action.

References

Mowry JB, Spyker DA, Brooks DE, et al. 2015 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 33rd Annual Report. Clin Toxicol (Phila). 2016;54(10):924-1109.
Zimmerman JL. Poisonings and overdoses in the intensive care unit: general and specific management issues. Crit Care Med. 2003;31(12):2794-2801.
Mokhlesi B, Leikin JB, Murray P, Corbridge TC. Adult toxicology in critical care: Part I: general approach to the intoxicated patient. Chest. 2003;123(2):577-592.
Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide poisoning. Lancet. 2008;371(9612):597-607.
Kraut JA, Kurtz I. Toxic alcohol ingestions: clinical features, diagnosis, and management. Clin J Am Soc Nephrol. 2008;3(1):208-225.
Manini AF, Nelson LS, Skolnick AH, et al. Electrocardiographic predictors of adverse cardiovascular events in suspected poisoning. J Med Toxicol. 2010;6(1):106-115.
Somerville NJ, O'Donnell J, Gladden RM, et al. Characteristics of Fentanyl Overdose — Massachusetts, 2014–2016. MMWR Morb Mortal Wkly Rep. 2017;66(14):382-386.
Richards JR, Albertson TE, Derlet RW, et al. Treatment of toxicity from amphetamines, related derivatives, and analogues: A systematic clinical review. Drug Alcohol Depend. 2015;150:1-13.
Kerr GW, McGuffie AC, Wilkie S. Tricyclic antidepressant overdose: a review. Emerg Med J. 2001;18(4):236-241.
Peter JV, Sudarsan TI, Moran JL. Clinical features of organophosphate poisoning: A review of different classification systems and approaches. Indian J Crit Care Med. 2014;18(11):735-745.
Mason PE, Kerns WP 2nd. Gamma hydroxybutyric acid (GHB) intoxication. Acad Emerg Med. 2002;9(7):730-739.
Gowing L, Ali R, White JM. Buprenorphine for the management of opioid withdrawal. Cochrane Database Syst Rev. 2017;2(2):CD002025.
Weinbroum AA, Flaishon R, Sorkine P, Szold O, Rudick V. A risk-benefit assessment of flumazenil in the management of benzodiazepine overdose. Drug Saf. 1997;17(3):181-196.
Tenenbein M. Benefits of parenteral deferoxamine for acute iron poisoning. J Toxicol Clin Toxicol. 1996;34(5):485-489.
Bateman DN, Dear JW, Thanacoody HK, et al. Reduction of adverse effects from intravenous acetylcysteine treatment for paracetamol poisoning: a randomised controlled trial. Lancet. 2014;383(9918):697-704.
Bunchorntavakul C, Reddy KR. Acetaminophen (APAP or N-Acetyl-p-Aminophenol) and Acute Liver Failure. Clin Liver Dis. 2018;22(2):325-346.
Position paper: single-dose activated charcoal. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 1997;35(7):721-741.
Position statement and practice guidelines on the use of multi-dose activated charcoal in the treatment of acute poisoning. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 1999;37(6):731-751.
Stolbach AI, Hoffman RS, Nelson LS. Mechanical ventilation was associated with acidemia in a case series of salicylate-poisoned patients. Acad Emerg Med. 2008;15(9):866-869.
Juurlink DN, Gosselin S, Kielstein JT, et al. Extracorporeal Treatment for Salicylate Poisoning: Systematic Review and Recommendations from the EXTRIP Workgroup. Ann Emerg Med. 2015;66(2):165-181.
Mokhlesi B, Leiken JB, Murray P, Corbridge TC. Adult toxicology in critical care: Part II: specific poisonings. Chest. 2003;123(3):897-922.
American College of Medical Toxicology. ACMT Position Statement: Guidance for the Use of Intravenous Lipid Emulsion. J Med Toxicol. 2017;13(1):124-125.

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