Approach to the poisoned patient

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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.

Approach

• Stabilize the patient using a modified ABCDE approach that includes toxicology-specific considerations, for example:
  • Airway: Anticipate airway loss due to impending obstruction or depressed mental status and consider prophylactic airway protection.
  • Breathing: Consider the effect of the toxin on the respiratory drive.
  • Circulation: Check ECG to identify and treat cardiotoxic substance exposure.
  • Disability: Treat alterations in glucose metabolism and/or toxic seizures.
  • Exposure: Look for clues for the underlying toxin and perform surface decontamination.
• Evaluate for classic toxidromes as well as for signs and symptoms of specific poisonings.
• Determine if GI decontamination, enhanced elimination techniques, and/or specific antidotes are required during or after stabilization.
• Once the patient has been stabilized, continue the toxicological risk assessment.

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

The combination of hypotension and bradycardia suggests the ingestion of beta blockers, calcium channel blockers, digoxin, guanfacine, or clonidine. ^[2]

Airway ^[2][3][4][5]

Assessment

• Airway obstruction or injury
  • Caustic agents
  • Toxic inhalation injuries
  • Toxic seizures
• ↑ Risk of aspiration or bronchial obstruction
  • Loss of airway protective reflexes
  • Excessive vomiting or hematemesis

Management

• Airway obstruction
  • Caustic or inhalation injury: high risk of difficult airway
    • Call for help: e.g., anesthesia.
    • Perform intubation as soon as possible. ^[6][7]
  • Uncontrollable seizures: Abort convulsive activity and perform RSI.
• Loss of airway protection
  • Begin basic airway maneuvers.
  • Consider early intubation for patients expected to deteriorate with:
    • Severely depressed mental status or coma ^[8]
    • ↑ Risk of aspiration: e.g., excessive vomiting
    • ↑ Risk of status epilepticus
• Transient airway compromise (e.g., isolated GHB toxicity, post-ictal period): Consider basic airway maneuvers alone with close airway monitoring. ^[9]

Breathing ^[2][3][4][5]

Assessment

• ↓ RR
  • Opioids
  • Sedative-hypnotics
• ↑ RR or Kussmaul respirations
  • Stimulants (e.g., amphetamines, cocaine)
  • Acute salicylate ingestion
  • Compensation for toxin-induced metabolic acidosis (e.g., toxic alcohols)
  • Aspiration pneumonia

Management

• All patients
  • Start SpO₂ monitoring and provide oxygen therapy as needed.
  • Begin BMV if signs of respiratory failure.
  • Consider ABG/VBG to screen for acid-base disorders.
• CO toxicity
  • Administer high-flow 100% O₂.
  • Interpret pulse oximetry with caution in patients with CO toxicity. ^[2]
• Opioid-induced respiratory depression or respiratory arrest: Administer naloxone for opioid overdose.
• Consider intubation and mechanical ventilation for:
  • Respiratory failure unresponsive to antidotes (e.g., naloxone)
  • Significant acidemia and evidence of respiratory muscle fatigue (see “High-risk indications for invasive mechanical ventilation”)

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

Circulation ^[2][3][4][5]

Assessment

• Hypotension: opioids, digoxin, antihypertensives
• Hypertension
  • Central neurological complication (e.g., cocaine-associated stroke)
  • Sympathomimetics
• Toxin-induced rhythm and conduction abnormalities
  • Bradycardia: beta blockers, CCBs
  • Narrow complex tachycardia: vasodilators, sympathomimetics
  • QRS widening and wide complex tachycardia: sodium channel blockers (e.g., TCAs, antiarrhythmics) ^[10]

Management

• All patients
  • Start continuous cardiac monitoring and consider hemodynamic monitoring for patients with shock.
  • Establish adequate IV access.
  • Provide immediate hemodynamic support as needed (e.g., IV fluid resuscitation)
• Toxin-induced bradycardia
  • Administer atropine and follow the “Adult unstable bradycardia algorithm.”
  • If there are muscarinic cholinergic symptoms, give high-dose atropine. ^[11]
  • See “Cardiovascular drug poisoning” for further details.
• Toxin-induced tachyarrhythmias
  • Consider benzodiazepines (e.g., lorazepam ) if stimulants are suspected.
  • Administer 8.4% sodium bicarbonate for severe sodium channel blocker toxicity (e.g., TCA toxicity). ^{[3][12][13][14]}
• Toxin-induced hypotension: typically requires treatment with adrenergic vasopressors ^[13]
  • Negative inotropes: Epinephrine is preferred. ^[4][15]
  • Peripheral vasodilators: Norepinephrine is preferred. ^[15]
  • See “Vasopressors” for information on dosages.
• Cardiovascular drug poisoning: e.g., beta-blocker poisoning, CCB poisoning, digoxin poisoning
  • Consider toxin-specific antidotes in addition to immediate hemodynamic support, such as:
    • High-dose euglycemic insulin therapy
    • Calcium for drug poisoning
    • High-dose glucagon
    • Digoxin immune fab
    • Intravenous lipid emulsion therapy
    • Methylene blue for drug poisoning
  • Consider ECMO for refractory life-threatening cases.
  • See “Cardiovascular drug poisoning” for further details.

Disability ^[2][3][4][5]

Assessment

• Pupillary changes: examine closely for mydriasis and miosis (see “Classic toxidromes”).
• Hypoglycemia: insulin and oral hypoglycemics
• Toxic seizures ^[2]
  • Insulin and oral hypoglycemics
  • Antidepressants
  • Sympathomimetics
  • Lead
  • Lithium
  • Isoniazid
• Withdrawal seizures: e.g., from alcohol, benzodiazepines

Management

• Altered mental status
  • Do not administer a “coma cocktail” empirically. Consider each antidote on an individual basis. ^{[2] [2][16]}
  • Consider naloxone for opioid-induced coma. ^[17]
  • Give D₅₀W for hypoglycemia.
  • Give thiamine if there are risk factors for Wernicke encephalopathy (e.g., malnourishment, alcohol use disorder). ^[13]
  • Reevaluate mental status frequently.
• Toxic seizures ^[2][18]
  • First-line: benzodiazepines (e.g., lorazepam )
  • Second-line: barbiturates (e.g., phenobarbital )
  • Treat underlying poisoning.
    • Drugs: See “TCA poisoning,” “Salicylate poisoning,” “Local anesthetic systemic toxicity,” “Bupropion poisoning,” “Antipsychotic poisoning,” “Lithium poisoning,” and “Stimulant intoxication.”
    • Environmental: See “Organophosphates,” “Cyanide poisoning,” “Carbon monoxide poisoning,” “Snake envenomation,” “Metal toxicity,” and “Mushroom poisoning.”
  • Identify and treat toxin-induced hypoglycemia or hyponatremia.
  • Consult neurology and toxicology for refractory seizures.
• Cyanide toxicity: Administer hydroxocobalamin OR sodium nitrite followed immediately by sodium thiosulfate .

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. ^[14][19]

Exposure ^[2][3][4][5]

Assessment

• Skin abnormalities
  • Evidence of chemical exposure
  • Transdermal medication patches
  • Track marks
  • See “Focused physical examination” for other skin findings.
• Hyperthermia: See “Differential diagnosis of drug-induced hyperthermia.”

Management

• Chemical or radiological exposures
  • Remove all of the patient's clothing.
  • Immediately irrigate the body.
  • Avoid irrigation with water if the patient was exposed to an alkali metal.
  • See also “Surface decontamination.”
• Hyperthermia
  • Discontinue causative agent (see “Serotonin syndrome” and “Neuroleptic malignant syndrome”).
  • Begin active cooling, e.g., mist and fan.

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 what is described here.

In patients taking serotonergic medications, clonus and hyperreflexia should raise suspicion for serotonin syndrome. ^[20]

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 ^[2][14]

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 ^[2][11][14]

• 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 ^[2][14]
  • 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
  • Examination of the skin, eyes, abdomen, and neurological system
  • Identification of classic toxidromes
  • Identification of cardinal signs of specific toxins

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

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

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. ^[21]

Diagnostics ^{[2][4][13][14]}

• 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][4]
  • 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. ^[2]

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

• BMP
  • Electrolyte abnormalities
    • Hyponatremia (e.g., due to MDMA)
    • Hyperkalemia (e.g., due to digoxin)
    • Hypokalemia (e.g., due to albuterol or theophylline)
  • Hypoglycemia (e.g., due to insulin and/or oral hypoglycemics)
  • Acute kidney injury (e.g., due to ethylene glycol or rhabdomyolysis) ^[2]
  • Anion gap and osmolar gap : ↑ with multiple toxins
• Liver chemistries: may be deranged in acetaminophen overdose or alcohol intoxication
• Acetaminophen level: the only specific toxin routinely screened ^[4]
• ECG ^[14][20]
  • Bradycardia and atrioventricular block (e.g., due to digoxin, beta blockers, or calcium channel blockers)
  • QRS prolongation and right axis deviation (e.g., due to tricyclic antidepressants)
  • QT prolongation (e.g., due to citalopram, antipsychotics)

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) ^[2]

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. ^[13]

Additional testing

• ABG: to help identify acid-base disorders
• Lactate and/or ketones: to further evaluate metabolic acidosis
• CPK: for suspected rhabdomyolysis
• Quantitative drug levels can be helpful to guide management for the following toxins: ^[2]
  • Digoxin
  • Ethanol
  • Lithium
  • Salicylates
  • Iron
  • Methotrexate
  • Theophylline
  • Phenobarbital
  • Valproic acid
  • Phenytoin
  • Carbamazepine

Imaging ^[2][20]

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

• X-ray chest: Consider if there is concern for pulmonary complications (e.g., aspiration, ARDS). ^[20]
• CT head: Perform routinely for patients with altered mental status that is not clearly attributable to a specific toxic exposure. ^[2]
• CT or MRI esophagus: Consider if there is suspicion for esophageal caustic injury.
• X-ray or CT abdomen: Consider if there is concern for ingestion of select radiopaque substances, e.g.: ^[22]
  • Heavy metals (e.g., iron, lead, arsenic, mercury) ^[20]
  • Packets containing substances such as opiates or cocaine ^[2]
  • Chloral hydrate
  • Phenothiazines
  • Numerous sustained-release or enteric-coated substances
  • Numerous industrial solvents (e.g., carbon tetrachloride)

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. ^[22]

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. ^[2][13]

Body 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 body surface decontamination and specialized PPE.
• Exposures to such toxins may be the result of:
  • Deliberate release
  • Household, industrial, or agricultural exposure

Clinical applications

Body 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: ^[23]
  • History of intentional overdose with a chemical substance
  • Strong or unusual odor (see “Odors” in “Focused physical examination”)
  • Unidentified substances contaminating skin or clothing
  • Signs and symptoms of a cholinergic toxidrome
  • Chemical burns or inflamed mucous membranes
• Substances typically requiring body surface decontamination ^[24]
  • 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 body 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”). ^[25][26]
  • 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 ^[23][27]
  • 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. ^[28][29]

Gastrointestinal decontamination ^{[2][4][13][14]}

• 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. ^[30][31][32]
• Balance the risk and benefits for each individual patient in consultation with a specialist.

The use of ipecac to induce vomiting is no longer recommended by the American Academy of Clinical Toxicology. ^[33]

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. ^[12][34]

• 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. ^[13][14]

General considerations ^[12][37][38]

• 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 ^[14]
    • Are associated with ↑ risk of dosing errors
  • The risks of administration:
    • Depend on patient-specific risk factors ^[12][37]
    • Can be outweighed by possible benefits if the patient is extremely sick.
    • Typically increase when co-ingestions have occurred ^[12]
• 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: ^[38]
    • Clinical signs and symptoms (e.g., blood pressure, if administering calcium to treat a calcium channel blocker overdose)
    • Time to clinical response (delayed response may suggest the need for redosing or reconsideration of the diagnosis)
    • Laboratory values (e.g., prothrombin time, if administering vitamin K to treat a warfarin overdose)

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

Specific antidotes

If further expert help is required: call Poison Control, available 24/7 at 1-800-222-1222 in the US.

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

• Cardiorespiratory ^[5][13]
  • Manage persistent hypotension: Ensure adequate fluid resuscitation and consider vasopressors (see “Shock”).
  • Prevent arrhythmias, e.g., due to QTc prologation, wide QRS complex, or AV block. ^[12]
  • Provide oxygen therapy; consider mechanical ventilation as needed to optimize gas exchange.
• Metabolic ^[5][13][39]
  • Correct electrolyte derangements (e.g., hypokalemia, hypomagnesemia, hyponatremia).
  • Manage severe metabolic acidosis.
    • Adjust tidal volume and respiratory rate as needed (see “Ventilation strategy for severe acidosis”).
    • Consider administration of IV 8.4% sodium bicarbonate.
  • Manage hypoglycemia.
    • Encourage oral carbohydrate intake and ensure resolution of hypoglycemia.
    • If the patient is unconscious: IV 50% dextrose in water
    • If insulin or sulfonlyurea-related: Consider a continuous dextrose infusion (e.g., 10% dextrose in 0.9% NaCl).
    • Monitor glucose and potassium levels.
    • Consider prophylactic dextrose in patients with salicylate toxicity to avoid cerebral hypoglycemia.
    • See “Treatment of hypoglycemia” for more information.
• Temperature (hyperthermia) ^[5][13]
  • If core temperature is > 39°C: Use active cooling techniques.
  • If due to sympathetic stimulation: Use benzodiazepines (e.g., lorazepam ).
  • If resistant to cooling measures: Consult toxicologist for advanced treatment strategies.

Many cases of poisoning can be effectively managed with supportive care alone. ^[2]

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

Monitoring

• Duration of observation ^[2]
  • 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 . ^[38]
    • Patient-related: Symptoms do not resolve with supportive treatment or complications occur.
• Cardiotoxicity ^[2]
  • Consider serial ECGs and continuous cardiac monitoring if:
    • The ingested substance was cardiotoxic (e.g., calcium channel blockers, digoxin)
    • Multiple substances were ingested
    • The ingested substance is unknown
  • For patients with rhythm disturbances, monitor the following: ^[12]
    • 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) ^[2]
• Monitor for complications, including: ^[5]
  • Rhabdomyolysis (due to direct toxic effects, resulting seizures, or prolonged hyperthermia)
  • Urinary retention (due to anticholinergic effects)

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.

Disposition

Discuss disposition with a toxicologist or poison control center based on individual toxicological risk assessment.

• Most patients require admission for stabilization, treatment, observation, and/or involuntary commitment.
• Select patients may be discharged with instructions, e.g.:
  • Clinically stable after unintentional, nontoxic exposures
  • PLUS reliable history, support network, and follow-up
• Consult critical care early for all unstable patients or high-risk toxicological risk assessment.
• Intentional poisoning: Consult psychiatry.
• Substance abuse: Refer for counseling or rehabilitation if patient agrees.

All patients

• Don appropriate PPE.
• Perform an ABCDE approach with toxicology-specific considerations.
  • Consider intubation for airway protection.
  • Provide oxygen therapy and mechanical ventilation as needed.
  • Provide immediate hemodynamic support as needed.
• Identify classic toxidromes or signs of specific poisoning.
• Consider the need for body surface decontamination or time-sensitive GI decontamination.
• Administer antidotes for immediate threats to life e.g., naloxone, atropine, dextrose.
• Identify and treat life-threatening complications: e.g., cardiac arrhythmias, seizures.
• Consult critical care as needed.
• Provide aggressive supportive care:
  • IV fluid therapy
  • Correction of electrolyte and metabolic derangements.
  • Maintenance of normothermia
• Perform toxicological risk assessment.
• Obtain focused toxicological history and physical examination.
  • Obtain collateral history as needed (e.g., EMS, family, medical records)
  • Quantify amount, time, and route of toxic exposure(s).
  • Determine suicidal risk of patients with intentional exposure.
• Obtain routine studies (BMP, liver chemistry, acetaminophen level, ECG).
• Consult a toxicologist or poison center for input as needed.

Management to consider based on toxicological risk assessment

• GI decontamination: e.g., activated charcoal
• Enhanced elimination techniques: e.g., hemodialysis
• Antidotes: e.g., N-Acetylcysteine
• Additional laboratory studies and imaging
• Consults: e.g., psychiatry, nephrology, neurology.
• Serial ECGs and continuous cardiac monitoring: e.g., for patients with rhythm disturbances, cardiotoxic substances, multiple substances, unknown substances
• Monitor serial drug levels if relevant to the substance ingested.
• Determine the duration of observation according to patient risk.
• Consider admission for:
  • Symptomatic patients.
  • Asymptomatic patients expected to experience delayed toxicity
• Consider ICU admission for patients with:
  • Need for advanced airway management OR high risk of airway compromise
  • Need for mechanical ventilation OR high risk of respiratory failure
  • Need for vasoactive medications OR high risk of hemodynamic instability
  • High risk of life-threatening complications: e.g., cardiac arrhythmias, seizures, cerebral edema, multiorgan failure
  • Need for hemodialysis
• Consider reassurance and discharge with instructions for patients with unintentional nontoxic exposures

Definitions ^[40][41][42]

• Body packing: intentional or coerced ingestion of large quantities of a controlled substance (e.g., narcotics, cocaine, amphetamines) in packaging that prevents absorption, typically for smuggling purposes
• Body stuffing: ingestion or intracavitary concealment of small amounts of drugs to avoid arrest

A patient's concealment of drugs, involvement with drug trafficking, or lack of cooperation with health providers may be involuntary. Beware of implicit biases during the clinical encounter.

Clinical features ^[40][41][42]

Clinical manifestations, e.g., opioid toxidrome, sympathomimetic toxidrome, depend on the substance and amount absorbed.

• Body stuffing: often symptomatic
• Body packing
  • Unruptured packet: typically asymptomatic; clinical features of bowel obstruction may occur.
  • Ruptured packet
    • Subtle features initially
    • Fulminant, life-threatening poisoning (e.g., respiratory failure, shock, coma, cardiac arrest) can rapidly develop.

Diagnostics ^[40][41][42]

Body stuffing is a clinical diagnosis. Obtain confirmatory imaging if body packing is suspected.

• Abdominal x-ray
  • Indicated as a screening tool or for rapid confirmation
  • Reported sensitivity ranges from 40 to 90% ^[43]
• CT abdomen: indicated if x-ray findings are equivocal

Management ^[40][41][42]

• All symptomatic patients: Manage associated poisoning.
  • See “Management of opioid overdose.”
  • See “Management of stimulant intoxication.”
• Body packing
  • Consider GI decontamination with whole bowel irrigation.
  • Admit patients for observation until all packets have passed (ICU monitoring may be required).
  • If symptoms of a ruptured packet occur:
    • Begin acute stabilization.
    • Administer high doses of indicated antidotes, e.g., naloxone for opioid overdose.
    • Consult surgery for urgent operative GI decontamination, e.g., for stimulant packets.
  • Identify and treat GI perforation and bowel obstruction.
• Patients with red flags for human trafficking: See “Management of human trafficking.”

A ruptured packet in a patient with body packing is an acute life-threatening emergency. It often requires respiratory support, hemodynamic stabilization, large quantities of antidotes, and/or surgical intervention.