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Approach to the poisoned patient

Last updated: June 15, 2021

Summarytoggle arrow icon

This article provides a general approach to patients with known or suspected acute poisoning from exposure to a wide variety of potentially toxic substances, including medications, recreational drugs, and common household products. Although fewer than 1% of poisonings are fatal, acute poisoning can be a challenging medical emergency. Successful management of poisoned patients involves adapting the ABCDE approach to include toxicological considerations (including expedient recognition of various classic toxidromes), performing a toxicology-focused history and physical examination, and tailoring management based on an individualized risk assessment of each patient. The risk assessment depends on patient characteristics such as age and comorbidities, as well as characteristics of the exposure, including type, route, dosage, timing, and whether the exposure was intentional or unintentional, and typically involves consultation with a toxicologist or regional poison control center (in the United States, Poison Control is available 24/7 at 1-800-222-1222). Many patients can be managed with supportive care alone and careful monitoring. Frequent reevaluation of the patient is essential, since the pharmacokinetics of a substance are altered in situations of overdose, and the clinical presentation can be dynamic as the substance is metabolized. For most serious toxic exposures, specific treatment strategies are required that include decontamination methods to reduce absorption (e.g., activated charcoal), enhanced elimination therapies (e.g., hemodialysis), or specific antidotes (e.g., naloxone for opioid toxicity, or N-acetylcysteine for acetaminophen toxicity). The monitoring and disposition requirements and the risk of complications can be estimated through a careful toxicological risk assessment and reassessment.

General principles

Anticipate and prepare for changes in hemodynamic and mental status, as toxins are metabolized gradually.

Modifications to the ABCDE approach

ABCDE approach: toxicology-specific considerations [1][2][3][4]
Alterations and possible causes Management
Airway
Breathing [9]
Circulation
Disability
Exposure
  • Chemical or radiological exposures: providers trained in decontamination should:
    • Remove all of the patients clothing
    • Immediately irrigate the body
    • Avoid irrigation with water if the patient was exposed to an alkali metal
    • See also “Surface decontamination.”
  • Hyperthermia

The combination of hypotension and bradycardia suggests the ingestion of beta blockers, calcium channel blockers, digoxin, guanfacine, or clonidine. [3]

In mechanically ventilated patients with severe metabolic acidosis, optimize tidal volume and respiratory rate to match the patient's respiratory compensation.

Do not treat toxic seizures with phenytoin, which can worsen the cardiotoxic effects of certain drugs (tricyclic antidepressants, theophylline, and cocaine) and is ineffective in seizures caused by withdrawal or isoniazid. [16][23]

Classic toxidromes

Recognition of classic toxidromes is essential to the evaluation of patients poisoned with an unknown substance. Note that, in practice, toxidromes may manifest more subtly than described here.

Classic toxidromes [2][3][13]
Class of drug Vital signs Mental status Pupils Other examination findings
Sedative-hypnotics
  • Poor reactivity to light
Opioids
  • Decreased bowel sounds
Cholinergics (muscarinic)
  • ↓ HR
  • Variable RR
  • ↓ BP
  • SaO2
  • Can be altered or normal
  • Wheezing/bronchospasm
  • Signs and symptoms of ↑ secretions (bronchorrhea, salivation, lacrimation, urination, defecation, vomiting, sweating)
  • Gastrointestinal cramps
  • DUMBBELLSS
Cholinergics (nicotinic)
  • ↑ HR
  • ↑ BP
  • Normal
Anticholinergics
Serotonin
  • Hyperthermia
  • ↑ HR
  • ↑ RR
  • ↑/↓ BP (Variability in BP is a feature of autonomic instability.)
Sympathomimetics

In patients taking serotonergic medications, clonus and hyperreflexia should raise suspicion for serotonin syndrome. [24]

For patients with anticholinergic syndrome, remember: blind as a bat, mad as a hatter, red as a beet, hot as a hare, and dry as a bone!

Rationale

  • Goal of risk assessment
    • Categorize the risk presented by a toxic exposure along the following spectrum (from high to low):
      • Immediate threat to life and/or cognitive function
      • Potential for permanent organ damage
      • Potential for developing a complication (e.g., seizures, cardiac arrhythmias) that could increase the risk level
      • Uncertain risk (further monitoring is required)
      • Low risk (e.g., does not meet the threshold of toxic ingestion)
    • Guide interventions that help convert:
      • Potentially fatal toxic exposures to nonfatal toxic exposures
      • Potentially toxic exposures to nontoxic exposures
  • Decisions affected by risk assessment
    • Decontamination: indications, risk-benefit analysis, timing, method
    • Antidote use: indications, risk-benefit analysis, dosing
    • Supportive care requirements: hemodynamic and metabolic support, necessary consults
    • Monitoring requirements: airway, cardiac, neurological
    • Disposition: discharge from ED, ward admission, ICU admission, interfacility transfer

Approach [3][16]

Risk assessment in toxicology does not involve a specific scoring system but instead refers to a conceptual process based on the overall clinical evaluation.

  • All patients: Perform focused toxicological history and physical examination
  • Diagnostics
    • Obtain a limited set of routine studies for most patients.
    • Consider additional laboratory studies and imaging for specific scenarios, such as:
      • Refining the diagnosis
      • Identifying or evaluating complications or abnormal results of routine studies
      • Guiding further management, for example:
        • Determining the need for enhanced elimination or a particular antidote
        • Monitor the response to treatment .
  • Evaluate the clinical hypothesis
    • Consider whether the exam and diagnostic findings are consistent with the range of possible presentations suggested by the history.
    • History obtained initially can be unreliable for various reasons, for example:
      • Only secondhand information is available (i.e., the patient is unresponsive or altered).
      • Patients may feel the need to conceal information about the exposure.
  • Consult additional resources as needed, such as:
    • US Poison Control national hotline: 1-800-222-1222
    • Online drug databases or pill identifier tools (see “Tips & links”)
    • Safety data sheets (SDS) for occupational exposures

While some substances (e.g., those with a narrow therapeutic window) inherently have more toxic potential than others, the dose of the substance is a primary determinant of the clinical effects seen. In other words: “The dose makes the poison.”

Focused toxicological history and physical examination [3][13][16]

  • Sources of information
    • Obtain as much information directly from patients as possible, reassuring them about confidentiality. (e.g., regarding the use of illicit substances)
    • Seek collateral sources of information if the patient is unable or unwilling to answer questions, and/or there are inconsistencies between the history and physical examination.
      • EMS providers
      • Family/friends
      • Chart review or pharmacy
      • Witnesses or bystanders
  • Key historical elements
    • Drug-related: e.g., drug class, immediate vs. extended-release formulation, amount, time of ingestion [3][16]
    • Patient-related: e.g., age, comorbidities, clinical status
    • Attempt to quantify the toxic dose ingested per kg of weight.
    • Consider the possibility of multiple co-ingested substances.
  • Key physical examination elements

Clinical effects of a given substance at toxic (supratherapeutic) doses can vary dramatically from the expected side effects at therapeutic doses.

Focused toxicological history [3][13][16]
Questions Description
Who?
  • Patient characteristics: confer an increased risk
What?
  • Exposure characteristics: confer an increased risk
    • High dose
    • High toxicity (e.g., narrow therapeutic index)
    • Extended-release formulation
    • Any co-ingestions
  • Unknown toxin: attempt to identify by asking about:
    • All recently prescribed medications
    • Any nonprescribed medications, supplements, herbals, etc.
    • Occupation and hobbies
    • If bottles are found, do not rely solely on labels, since patients may use bottles to store other medications. Use a pill identifier tool; see “Tips & Links.” [3]
How?
  • Route of exposure: e.g., oral, intravenous, transdermal, rectal
When?
  • Important times to document
    • Exact time and duration of exposure [3]
    • Time elapsed since exposure
    • Time of symptom onset
Why?
  • Unintentional exposure
    • Iatrogenic: e.g., incorrect dose prescribed or given
    • Patient-related: e.g., misunderstanding regarding prescribed dose, inability to read or understand the bottle label, new or worsening cognitive disorder.
  • Intentional exposure

Reevaluate the clinical hypothesis if physical findings and diagnostic studies are inconsistent with toxic effects that are expected from the history of the exposure.

Focused toxicological physical examination [3][13][16]
Examination Description
Weight
Odors
Skin
Eyes and mucous membranes
Abdomen
Neurological exam

Reassess the patient frequently! Examination findings can be dynamic as the toxin metabolizes.

Intoxication with certain substances can cause the loss of some brainstem reflexes. Multiple society guidelines state that diagnosis of brain death can only be made in the absence of intoxication. [25]

Diagnostics [2][3][15][16]

  • Investigations should be guided by history and examination findings.
  • Clearly document the time blood was drawn, so that results can be accurately interpreted.
  • General serum or urine screening panels for multiple toxins are not routinely recommended, because: [2][3]
    • They do not include all toxins.
    • Results often do not return in time to affect acute management.
    • Both false-negative and false-positive results can occur.
    • Drugs or their metabolites may be detected in urine for days after any clinical symptoms have resolved; therefore, results may not explain the current presentation. [3]

Abnormalities (e.g., metabolic acidosis, other metabolic derangements, elevated liver enzymes) increase the risk of complications; treat appropriately and consider extended observation, admission, and involvement of critical care as necessary.

Routine tests

Classic causes of high anion gap metabolic acidosis: CAT MUDPILES (Cyanide/Carbon monoxide, Aspirin/Alcoholic ketoacidosis, Toluene, Methanol/Metformin, Uremia, Diabetic ketoacidosis, Paraldehyde/Propylene glycol, Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates) [3]

Classic causes of high osmolar gap: ME DIE (Methanol, Ethylene glycol, Diuretics (mannitol)/Diabetic ketoacidosis, Isopropyl alcohol, Ethanol)

Acetaminophen levels may not be detectable if the patient presents > 18 hours after overdose. [15]

Additional testing

Imaging [3][24]

There is no indication for routine imaging in poisoned patients, but the following studies may be of use in certain situations.

To remember foreign substances with a radiopaque appearance on abdominal radiography, think of CHIPES: Chloral hydrate, Heavy metals, Iodides, Phenothiazines, Enteric-coated or sustained-release substances, and Solvents. [26]

Decontamination is a time-sensitive intervention to prevent further toxicity of certain subtances. It should be considered urgently as the window of opportunity for life-saving benefits is often narrow. [3][15]

Surface decontamination

  • Involves the removal of any residual toxin from the patient's skin and mucus membranes to:
    • Prevent further transdermal and/or inhalational exposure
    • Protect healthcare providers from contamination
  • Decontamination of dermal or ocular exposures should be addressed during the exposure component of the ABCDE approach.
  • Healthcare providers should routinely use universal precautions as minimum protection.
  • Certain toxins require more aggressive surface decontamination and specialized PPE.
  • Exposures to such toxins may be the result of:
    • Deliberate release
    • Household, industrial, or agricultural exposure

Clinical applications

Surface decontamination should be considered in any case of known or suspected exposure to chemical, biological, radiologic, or nuclear (CBRN) hazards.

  • Suspect chemical contamination if any of the following are present: [27]
  • Substances typically requiring surface decontamination [28]
    • Solvents
    • Organophosphates
    • Paraquat
    • Hydrofluoric acid
    • Heavy metals (e.g., methylmercury)
    • Cyanide
    • Radioactive particles

Patients who have been exposed to radiation but have no radioactive materials on their person do not require surface decontamination.

Approach

  • Prior to decontamination
    • Use the appropriate level of PPE protection according to the Occupational Health and Safety Administration/Environmental Protection Agency categories (e.g., Level A, B, or C; see “Tips & links”). [29][30]
    • Activate necessary protocols (e.g., for hazardous exposures, mass casualties).
    • Notify external agencies according to hospital and state requirements (e.g., fire department, health department, CDC).
  • Procedure: Decontaminate the patient prior to entering patient care areas [27][31]
    • Carefully and completely remove all clothing.
    • Double-bag clothing in sealed and labeled biohazard bags.
    • Wash exposed areas with copious amounts of water (and soap, if possible) for 10–15 minutes, while sponging areas gently.
      • Wash any exposed open wounds and eyes (if exposed) first.
      • Continue to wash the rest of the body, working from head to toe.
      • Prevent water runoff from touching eyes, nose, mouth, or any unexposed areas.
      • After the initial wash of eyes and/or open wounds, use water or saline to irrigate them for another 5–10 minutes.
    • In situations of deliberate release, the “rinse-wipe-rinse” approach is recommended. [32][33]

Gastrointestinal decontamination [2][3][15][16]

  • This refers to the removal of a toxin from the body before it is absorbed by the GI tract
  • The American Academy of Clinical Toxicology (AACT) discourages routine use of these interventions, as risks often outweigh relatively limited benefits. [34][35][36]
  • Balance the risk and benefits for each individual patient in consultation with a specialist.
Approach to GI decontamination methods [2][3][15]
Strategy Description Cautions
Single-dose activated charcoal
  • Method: oral or nasogastric administration of activated charcoal [3][34]
  • Most effective for single toxic ingestions occurring ≤ 1 hour prior to presentation
  • Consider for single ingestions of slowly metabolized toxins occurring > 1 hour from presentation, such as: [15]
    • Substances that prolong GI transit (e.g., TCAs)
    • Extended-release formulations
Whole bowel irrigation
  • Method: oral or nasogastric administration of large volumes of an osmotically balanced solution (e.g., polyethylene glycol electrolyte solution) to flush the bowel [2][15][35]
  • Consider for significant ingestions of : [35]
    • Drug-containing packets (ingested for purposes of smuggling)
    • Enteric-coated tablets
    • Sustained-release formulations
    • Drugs poorly absorbed by activated charcoal (e.g., iron, lithium)
Gastric lavage
  • Method: administration of warm saline or water via a large-bore orogastric tube, followed by aspiration of the fluid, in order to remove pills and pill debris. [2][36]
  • No clear indications
  • Should only be performed in extremely rare situations and by experienced individuals [2]

The use of ipecac to induce vomiting is no longer recommended by the American Academy of Clinical Toxicology. [37]

Activated charcoal does not adsorb metals (e.g., iron, mercury, arsenic, lead, lithium), alcohols (e.g., ethanol, methanol, ethylene glycol), organic solvents (e.g., acetone), acids, bases, or cyanides. [14][38]

  • This refers to the removal of a toxin from the body after it has been absorbed by the GI tract.
  • These are only indicated for a small number of toxins with specific pharmacokinetics .
  • Consult a toxicologist or poison control unit before implementing one of these methods. [15][16]
Approach to enhanced elimination methods [2][3][14][15]
Strategy Description

Cautions

Multidose activated charcoal (MDAC)

Urine alkalinization

  • Risks include:
  • Normokalemia must be maintained in order for alkalinization to occur.
    • Correct hypokalemia before beginning the infusion.
    • Supplement potassium during the infusion. [15]
    • Monitor urinary pH and BMP (for acid-base balance and potassium level) every 1–2 hours.
Extracorporeal elimination techniques

General considerations [14][41][42]

  • Prior to administration
    • There is minimal high-quality evidence to support the use of most antidotes.
    • Antidotes are typically most useful for drugs that have delayed, potentially severe consequences.
    • Antidotes are used infrequently, and as a consequence:
      • May not be immediately available [16]
      • Are associated with ↑ risk of dosing errors
    • The risks of administration:
      • Depend on patient-specific risk factors [14][41]
      • Can be outweighed by possible benefits if the patient is extremely sick.
      • Typically increase when co-ingestions have occurred [14]
  • During administration
    • Many antidotes are titrated according to specific clinical effects rather than administered as a fixed dose.
    • Avoid excess dosing of antidotes.
    • Stop treatment at the desired therapeutic endpoint.
    • Relevant monitoring markers include: : [42]

Consult poison control before administering antidotes unless these are time-sensitive life-saving treatments (e.g., naloxone, atropine, 8.4% NaHCO3)

Specific antidotes

Toxins and their antidotes [2][14][41]
Poisoning type Additional information (antidote)
Sedative-hypnotic
Opioid
Cholinergic
Anticholinergic
Serotonin
Sympathomimetic
Other medications
Other substances

Intravenous lipid emulsion therapy [43]

Aggressive supportive care is essential to the successful management of poisoned patients, irrespective of the need for other interventions (e.g., decontamination, antidotes).

Toxins with no specific antidote
Poisoning type Additional information
Recreational substances
Other

Many cases of poisoning can be effectively managed with supportive care alone. [3]

Consider 3% hypertonic saline to treat severe MDMA-induced hyponatremia causing cerebral edema or seizures.

  • Duration of observation [3]
    • May be limited to 6 hours for intentional ingestion, if:
      • Peak toxicity is expected to be reached within that time
      • Overall level of toxicity is predicted to be low
      • Patient remains asymptomatic
      • Patient has received a psychiatric consult
    • May be longer (> 24 hours) in the following situations:
      • Substance-related: extended-release formulation, delayed peak effects , delayed toxicity , or active metabolites . [42]
      • Patient-related: Symptoms do not resolve with supportive treatment or complications occur.
  • Cardiotoxicity [3]
    • Consider serial ECGs and continuous cardiac monitoring if:
    • For patients with rhythm disturbances, monitor the following: [14]
      • QRS and QT intervals with serial ECGs (e.g., every 2–4 hours)
      • Serum electrolytes: Maintain K+ levels > 4 mEq/L.
      • Acid-base status: Correct metabolic acidosis.
  • Consider the need for serial drug levels: for drugs with unpredictable absorption kinetics (e.g., salicylates, valproic acid) [3]
  • Monitor for complications, including: [4]

In overdose, the pharmacokinetics of drugs are altered: The elimination half-life is not the same as when the drug is administered at therapeutic levels.

All patients

Management to consider based on toxicological risk assessment

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