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Initial management of the critically ill adult with an unknown overdose

Initial management of the critically ill adult with an unknown overdose
Literature review current through: Jan 2024.
This topic last updated: Dec 21, 2023.

INTRODUCTION — Poisoning is a leading cause of death especially in the young, in whom it is the leading cause of non-traumatic cardiac arrest under the age of 35 years. Overdose, both intentional and unintentional, has also become the leading cause of injury-related death in the United States, exceeding the number of deaths due to firearms, falls, or motorized vehicle collisions [1,2].

Severely poisoned patients may present in extremis. Such patients require an organized, targeted resuscitation despite incomplete, uncertain, or even erroneous information. A "generic" approach based upon the advanced cardiac life support (ACLS) protocols intended for cardiac patients is suboptimal [3,4]. It can lead to missed opportunities for specific life-saving interventions and may at times be harmful.

This topic will describe an approach to the resuscitation of the critically ill poisoned adult patient when the identity of the causative agent(s) is initially unknown. The general approach to the poisoned patient and the management of specific poisonings are described separately. (See "General approach to drug poisoning in adults".)

INITIAL DATA ACQUISITION — Any readily available information about the patient and the poisoning should be obtained from pre-hospital care providers, other first responders (including witnesses, firemen, police, friends, and family), and from medical records. Medication or chemical product containers, material safety data sheets, pharmacy records, and institutional or patient lists of prescribed medication can be helpful. In addition, the setting and circumstances may help to identify the toxin(s) involved and select interventions. As examples, recreational ingestion of illicit alcohol (eg, containing methanol), inhalation of toxic gases in an enclosed space, or accidental industrial releases/fires suggest the need to prepare for multiple victims. A person who rapidly decompensates after being taken into police custody may have "stuffed" or "packed" large amounts of illicit drugs requiring the immediate removal of the leaking package from a body cavity [5]. (See "General approach to drug poisoning in adults", section on 'History' and "Acute ingestion of illicit drugs (body stuffing)" and "Internal concealment of drugs of abuse (body packing)".)

FIRST PRIORITIES — In addition to securing the airway, breathing, and circulation (ABC's) as with any critically ill or injured patient, the resuscitation leader must consider two additional imperatives that may arise with severely poisoned patients: preserving the operational capacity of the emergency health care system and ensuring the safety of health care workers. These priorities are addressed concurrently as part of the primary assessment.

Multiple casualty and mass casualty incidents may involve toxic exposures and challenge health care systems of any size. Even a single patient contaminated or potentially contaminated with a highly potent toxin (eg, a radioactive isotope or nerve agent such as sarin) can disable an entire emergency department (ED).

Highly potent toxins can directly threaten the health of clinicians and rescue personnel when proper protection is not used. However, such agents are extremely rare outside of a large-scale industrial accident, major transportation accident, or terrorist attack. Opioid toxicity is extremely unlikely following incidental dermal contact with fentanyl or fentanyl analogs despite concerns by first responders while rendering first aid and resuscitation to a patient with opioid intoxication [6,7]. Routine measures are sufficient for nearly all single-patient encounters involving consumer products and common chemicals. If readily available, nitrile gloves, safety goggles, and a water-resistant gown can be worn for additional security when dealing with extensive solid particle contamination, liquid spills, or emesis following an unknown exposure. However, locating such protective equipment should not delay the delivery of lifesaving care without clear reason to suspect a highly toxic agent [8].

Ideally, surface decontamination should be performed at or near the scene (ie, prior to transport) or before the patient is brought into the clean area of the ED (if not performed in the pre-hospital setting). Clothing soiled with chemicals or bodily fluids should be placed in appropriate closed containers and disposed of properly. Decontamination procedures and the chemical and biologic agents likely to be involved in an exposure are discussed separately. (See "Topical chemical burns: Initial evaluation and management" and "Chemical terrorism: Rapid recognition and initial medical management" and "Identifying and managing casualties of biological terrorism".)

RAPID FIRST LOOK: EXAMINATION, MONITORING, AND TESTING — A rapid systematic examination should be performed while resuscitative measures are initiated. The class of toxin involved may be suggested by characteristic combinations of symptoms and signs (so-called "toxidromes"). The "toxidrome-oriented" physical examination consists of: vital signs; level of alertness; pupil size and position; mucous membrane moisture and secretions; skin temperature and moisture; presence or absence of bowel sounds; and motor tone. Alertness can be categorized simply as alert, responsive to voice, responsive to pain, or unresponsive, which is preferred over the Glasgow Coma Scale (GCS) to characterize the mental status of a poisoned patient. The findings of this rapid initial examination may provide valuable insight into the class of toxin involved. The major toxidromes and their associated findings are summarized in the accompanying table (table 1). Disturbances in temperature (table 2), heart rate and blood pressure (table 3), and respiration (table 4) can also suggest a toxin class.

In addition to the findings above, the clinician should look for signs of trauma (self-inflicted or accidental), recent intravenous drug use, transdermal patches, and seizures (eg, incontinence, lateral tongue laceration). Cervical spine precautions may be needed if major trauma is suspected.

The clinical team should immediately obtain intravenous access, apply a cardiac monitor and pulse oximeter, and provide high flow oxygen by non-rebreather face mask, as needed. The following laboratory tests should usually be obtained:

Point-of-care capillary blood glucose

Complete blood count

Basic serum electrolytes, BUN, and creatinine

Serum lactate

Venous or arterial blood gas, including carboxyhemoglobin and methemoglobin level in appropriate circumstances (eg, smoke inhalation or cyanosis not improving with supplemental oxygen, respectively)

Serum acetaminophen and salicylate concentrations following self-harm attempt


Other specific drug concentrations as indicated (eg, ethanol, theophylline, digoxin, anti-epileptics)

An initial urine sample can be retained for comprehensive drug testing in a critically-ill patient with an unclear etiology, a prolonged clinical course, or an unusual clinical course (eg, multiple substances creating mixed toxicity). Unlike the commonly available urine "drug of abuse screen," which is an immunoassay that rarely alters the initial management of most patients, comprehensive drug testing requires specialized expertise and equipment, which are generally not available in most hospital laboratories and thus have long turnaround times. The first available urine sample is generally preferred, ideally obtained from the initial catheterization without intraurethral lidocaine, which may mask the presence of other substances. (See "Testing for drugs of abuse (DOAs)".)

More detailed information about these initial tests is provided separately. (See "General approach to drug poisoning in adults".)

SYSTEMATIC EVALUATION: THE "ABCDE" APPROACH — We have adapted the basic "ABC" (airway, breathing, circulation) approach used in cardiac and trauma resuscitation for the initial management of the critically ill adult with an unknown overdose. The steps are organized according to the issues that pose the most immediate life threats; problems are managed immediately in the order encountered. Important modifications for the poisoned patient are described in each section below.

"A": Airway stabilization — Patients who cannot protect their airway should be tracheally intubated immediately. The evaluation of the patency or protection of the airway is discussed separately. (See "The decision to intubate", section on 'Is patency or protection of the airway at risk?'.)

Exceptions include suspected opioid overdose and severe hypoglycemia. If opioid toxicity is suspected (table 1), administer naloxone while assuring adequate oxygenation and ventilation [9]. Use small doses initially (eg, 0.04 or 0.05 mg intravenously or 0.1 mg intramuscularly) when opioid dependence is possible and ventilation can be maintained, doubling the dose until reversal of respiratory depression is achieved. Severe hypoglycemia should also be ruled out (with a point-of-care capillary blood glucose) as a cause of depressed mental status prior to intubation. (See "Acute opioid intoxication in adults", section on 'Basic measures and antidotal therapy'.)

Do not routinely administer flumazenil for possible benzodiazepine overdose, as the risk benefit ratio of this agent is poor, and withdrawal seizures can develop [9]. The use of flumazenil (and scenarios where it may be appropriate) is discussed separately. (See "Benzodiazepine poisoning", section on 'Role of antidote (flumazenil)'.)

Placing a nasopharyngeal airway (ie, nasal trumpet) may be sufficient to overcome upper airway obstruction from central nervous system depression (CNS) and preclude the need for tracheal intubation in a patient who has ingested a short-acting sedative (eg, ethanol, gamma-hydroxybutyrate) and whose clinical course is likely to improve. (See "Basic airway management in adults", section on 'Nasopharyngeal airway'.)

We do not solely use a Glasgow Coma Scale (GCS) (table 5) ≤8 to identify the need for tracheal intubation in an unresponsive poisoned patient who is protecting their airway, maintaining adequate oxygen saturation, hemodynamically stable, and expected to not deteriorate based on the suspected ingestion (eg, short-acting sedative such as ethanol). The GCS was developed to classify injury severity and prognosticate in patients with traumatic brain injury (TBI); a GCS ≤8 represents severe TBI and is generally used as an indication for tracheal intubation. However, unlike comatose patients with TBI, poisoned patients generally have a much better prognosis despite having a low GCS. The prognosis is particularly favorable in patients intoxicated with short-acting sedatives (eg, ethanol) since they typically present for care at or near the time of maximal CNS depression and improve rapidly if they have a patent airway and spontaneous respiration. For these patients, the risks of tracheal intubation (eg, hemodynamic instability, hypoxia, dental injury, barotrauma, ventilator-associated pneumonia) are unlikely to outweigh the expected benefit (ie, aspiration prevention). Evidence includes a multicenter trial of 225 adult patients with acute poisoning and a GCS ≤8 randomized to have selective tracheal intubation based on respiratory distress (ie, pulse oximetry <90 percent despite nasal canula oxygen), seizure, vomiting, or shock (ie, systolic blood pressure <90 mmHg after 1 liter of crystalloid fluid) versus routine care with permissive intubation at the discretion of the treating physician. Patients in the selective arm were less likely to undergo mechanical ventilation (18.1 versus 59.6 percent, absolute difference -42.5, 95% CI -30.9 to -54.1), less likely to be admitted to the intensive care unit (39.7 versus 66.1 percent, absolute difference -29.2, 95% CI -17.4 to -41), experienced fewer adverse events from intubation (6 versus 14.7 percent, absolute difference -8.6, 95% CI -0.7 to -16.6), less likely to develop pneumonia (5.4 versus 15 percent, absolute difference -9.6, 95% CI -17.5 to -1.7), and had a shorter hospital length of stay (median 21.5 versus 37 hours, relative risk 0.74, 95% CI 0.53-1.03); the latter finding did not achieve statistical significance [10]. Importantly, the trial excluded patients who required immediate tracheal intubation (signs of respiratory distress, clinical suspicion of any brain injury, seizure, shock) or had cardiotoxic drug overdoses. Also, patients were young (mean age 33 years), there were no deaths, most patients ingested sedatives (ethanol was 67 percent), and almost all exposures involved substances that would be expected to have a benign course.

Unless the patient is moribund, rapid sequence intubation with pre-oxygenation and neuromuscular blockade is typically the best approach to securing the airway [11]. Rocuronium is preferred over succinylcholine in cases of suspected organophosphate poisoning and acute digoxin toxicity. In organophosphate poisoning, succinylcholine may have a markedly prolonged duration of action, as the cholinesterases which degrade it are inactivated by the toxin. Digoxin poisoning may produce hyperkalemia, a contraindication to succinylcholine use. (See "Rapid sequence intubation in adults for emergency medicine and critical care" and "Organophosphate and carbamate poisoning", section on 'Initial resuscitation' and "Digitalis (cardiac glycoside) poisoning", section on 'Management'.)

Patients with a caustic ingestion who manifest stridor and drooling are ideally tracheally intubated early by the most experienced clinician available using an awake approach. An alternate strategy for securing the airway, and the means to establish a surgical airway if necessary, must be immediately available. (See "Approach to the difficult airway in adults for emergency medicine and critical care", section on 'Awake techniques'.)

"B": Breathing — Administer supplemental oxygen as needed to all critically ill patients with a suspected overdose. End tidal carbon dioxide monitoring (ie, capnography) can provide information regarding adequacy of ventilation in obtunded or unconscious patients, especially since the administration of supplemental oxygen renders pulse oximetry less effective as an early warning device for hypoventilation. (See "Carbon dioxide monitoring (capnography)".)

Several toxins interfere with oxygenation and ventilation. Carbon monoxide poisoning can cause severe hypoxia despite falsely normal pulse oximetry readings. In cases of methemoglobinemia, the pulse oximeter may read around 85 percent despite visible cyanosis. Other toxicologic causes of cellular hypoxia despite normal oxygen saturation include cyanide, hydrogen sulfide, and sodium azide. Patients with profound tissue hypoxia from these toxins require endotracheal intubation and mechanical ventilation using 100 percent oxygen. (See "Carbon monoxide poisoning" and "Methemoglobinemia" and "Cyanide poisoning".)

Patients with aspirin poisoning are initially tachypneic and hyperpneic due to the stimulatory effects of aspirin upon the respiratory center of the medulla. This hyperventilation is beneficial, and intubation should be avoided if possible because it is difficult to replicate such high minute ventilation with mechanical ventilation. Nevertheless, patients unable to protect their airway must be intubated and hyperventilated. Severe aspirin poisoning can cause precipitous decompensation and death shortly after intubation, and such patients require specific and aggressive resuscitation, including treatment with sodium bicarbonate, high minute ventilation, and immediate hemodialysis. (See "Salicylate (aspirin) poisoning: Management", section on 'ABCs and supportive care'.)

Patients with profound metabolic acidosis due to other toxins (eg, methanol, ethylene glycol) can also develop extremely high compensatory minute ventilation. These patients may be acidemic despite a PaCO2 near 10 mmHg. When this high minute ventilation rate slows (eg, due to seizures, fatigue, or iatrogenic sedation or paralysis), the arterial pH falls abruptly, sometimes well below 7. As such, patients with severe metabolic acidosis due to poisoning are at risk of decompensating rapidly from respiratory failure. Such patients should be intubated for any sign of impending respiratory failure, either clinically or on blood gas testing. A seemingly normal PaCO2 of 30 to 40 mmHg in the face of a severe metabolic acidosis is evidence of respiratory failure. (See "Methanol and ethylene glycol poisoning: Management", section on 'Overview of management'.)

When intubating hyperpneic patients with severe metabolic acidosis, we suggest the following approach:

Administer one to three 50 mL amps of 7.5 to 8.4 percent sodium bicarbonate via intravenous bolus before and after intubation.

Avoid sedation until just prior to tracheal intubation.

Optimize the likelihood of first-pass success by using neuromuscular blockade and sound technique; the most experienced intubator available should perform the procedure. (See "Rapid sequence intubation in adults for emergency medicine and critical care" and "Direct laryngoscopy and endotracheal intubation in adults".)

Maximize minute ventilation once intubated, while following peak airway pressures and arterial blood gases. Initial settings could be 12 mL/kg at 20 breaths per minute for an adult, with frequent reassessment of acidemia and signs of barotrauma. As the acidosis resolves, minute ventilation should be reduced. (See "Mechanical ventilation of adults in the emergency department".)

Organize immediate hemodialysis if a dialyzable toxin (eg, aspirin, methanol, ethylene glycol) is responsible.

"C": Circulation

Asystole and ventricular fibrillation — Asystole and ventricular fibrillation are managed according to standard ACLS protocols (algorithm 1). (See "Advanced cardiac life support (ACLS) in adults", section on 'Pulseless ventricular tachycardia and ventricular fibrillation' and "Advanced cardiac life support (ACLS) in adults", section on 'Asystole and pulseless electrical activity'.)

Hypotension — Hypotension is treated with a rapid intravenous (IV) infusion of up to 2 L of isotonic crystalloid, followed by a norepinephrine infusion or small boluses of phenylephrine, pending more specific information (eg, bedside echocardiography, point-of-care ultrasonography) to guide therapy. (See "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock".)

At times, the dose of vasopressor or inotrope needed to achieve a response may be much higher than doses used for non-poisoned patients [12]. Circulatory assist devices (eg, intraaortic balloon pump) and extracorporeal life support (eg, circulatory bypass pump or veno-arterial extracorporeal membrane oxygenation) may be needed in refractory shock [13,14]. Ingestions that have been successfully managed with extracorporeal life support are listed in the table (table 6). (See "Extracorporeal life support in adults in the intensive care unit: Overview".)

Selected antidotes can be administered empirically to hypotensive patients when circumstances suggest a specific etiology. A list of these antidotes with empiric dosing guidelines is provided (table 7).

Despite numerous case reports of its use for refractory shock, there is scant evidence of benefit for lipid emulsion therapy when used for drug toxicity other than local anesthetics, and its routine use is not recommended [15,16]. Methylene blue has also been proposed for empirical use to treat refractory shock in overdose based on a similarly limited evidence base [17]. (See "Calcium channel blocker poisoning", section on 'Lipid emulsion therapy' and "Local anesthetic systemic toxicity" and "Methemoglobinemia", section on 'Methylene blue (MB)'.)

Bradycardia with hypotension — Bradycardia with hypotension suggests an overdose with digoxin, calcium channel blockers, or beta blockers. Digoxin toxicity may be characterized by increased automaticity, depressed AV nodal conduction, characteristic repolarization changes, and gastrointestinal symptoms. Beta-blocker toxicity can be accompanied by hypoglycemia and, in the case of propranolol, sodium channel blockade with widening of the QRS complex and seizures. Overdose with calcium channel blockers usually causes hyperglycemia and a relatively well-preserved mental status despite hypotension. Specific therapy for each agent is available and discussed separately. (See "Digitalis (cardiac glycoside) poisoning" and "Dosing regimen for digoxin-specific antibody (Fab) fragments in patients with digoxin toxicity" and "Calcium channel blocker poisoning", section on 'Management' and "Beta blocker poisoning", section on 'Management'.)

Monomorphic, wide-complex tachycardia — Monomorphic, wide-complex tachycardia in the setting of poisoning is commonly supraventricular in origin with aberrancy due to sodium channel blockade. Many poisons can cause sodium channel blockade, including tricyclic antidepressants, antihistamines, Type IA antiarrhythmics, and cocaine. The treatment is sodium bicarbonate 50 to 100 mEq given as an intravenous (IV) bolus, and repeated as necessary, until the QRS interval is <100 msec in the limb leads, or until arterial pH approaches 7.55. Other Type I antiarrhythmics (eg, procainamide) should be avoided. (See "Tricyclic antidepressant poisoning", section on 'Sodium bicarbonate for cardiac toxicity' and "Anticholinergic poisoning" and "Cocaine: Acute intoxication".)

Polymorphic ventricular tachycardia — Polymorphic ventricular tachycardia (torsade de pointes) is occasionally seen following overdose with Types IA, IC, and III antiarrhythmics; pentamidine; antipsychotics; arsenicals; antifungals; and antihistamines. This arrhythmia is treated with 2 g magnesium sulfate IV given over two to five minutes. Up to two additional doses may be given as needed. Overdrive pacing with isoproterenol or overdrive electrical pacing may also be used, as bradycardia potentiates this arrhythmia [18]. (See "Advanced cardiac life support (ACLS) in adults", section on 'Irregular wide complex'.)

Narrow complex tachycardia — Narrow complex tachycardia and hypertension due to drug overdose or withdrawal are usually due to hyperadrenergic states, as seen with cocaine, amphetamine, and other sympathomimetics. Treatment consists primarily of benzodiazepines, and perhaps phentolamine for severe hypertension [19,20]. Refractory hypertension may also be treated with nitroglycerin (in the setting of cardiac ischemia), clevidipine, nicardipine, or nitroprusside. Beta-blockers and antipsychotics should be avoided [21,22]. Synchronized cardioversion is rarely effective. (See "Cocaine: Acute intoxication", section on 'Initial management' and "Methamphetamine: Acute intoxication", section on 'Management'.)

"D": Disability and neurological stabilization — Once the airway, breathing, and circulation are secured, attention is next directed towards neurologic stabilization. The so-called "coma cocktail" of dextrose, oxygen, naloxone, and thiamine given empirically is an outdated concept and has been replaced by selective use of each component as necessary [9,23]. Hypoglycemia can present as any alteration of mental status, including confusion, seizures, focal deficits, and coma. Treat these symptoms with intravenous dextrose when the glucometer reports a low or low-normal capillary blood glucose.

Naloxone is indicated for the reversal of respiratory depression in the setting of known or suspected opioid toxicity (see "Acute opioid intoxication in adults", section on 'Basic measures and antidotal therapy'). Flumazenil should not be used, even when benzodiazepine toxicity is suspected, because it can precipitate benzodiazepine withdrawal, causing seizures (see "Benzodiazepine poisoning", section on 'Role of antidote (flumazenil)'). Thiamine may be administered safely before glucose, but is unlikely to reverse coma [24]. Physostigmine is no longer used as a non-specific analeptic but does play a selected role in the management of anticholinergic (antimuscarinic) poisoning. (See "Anticholinergic poisoning", section on 'Antidotal therapy with physostigmine for severe toxicity'.)

Seizures due to poisoning or withdrawal are best treated with escalating doses of benzodiazepines (eg, diazepam 5 mg IV, repeated and doubled every 5 to 10 minutes as necessary for refractory seizures) (table 8). Phenytoin is usually ineffective and can cause toxicity due to the propylene glycol solvent. Propofol has superseded the barbiturates and inhalational anesthetics as second-line therapy for benzodiazepine-resistant seizures [25]. When seizures are likely due to sodium channel blockade, intravenous sodium bicarbonate should be administered in addition to benzodiazepines. Dosing is described above (see '"C": Circulation' above). High doses of pyridoxine (5 g IV) should be given to patients in status epilepticus believed to be caused by isoniazid overdose or monomethylhydrazine poisoning (eg, Gyromitra mushrooms). (See "Isoniazid (INH) poisoning".)

Causes other than overdose may be responsible for coma or depressed mental status in the poisoned patient. This is discussed separately. (See "Stupor and coma in adults".)

"E": Exposure and elimination — This phase of management aims to remove clothing, transdermal medication patches, and other external contaminants, to measure core temperature and treat hypothermia or hyperthermia as necessary, to identify self-inflicted or accidental trauma, and to search personal items for concealed drugs, weapons of self-harm, or clues regarding medical history and the nature of the overdose.

Severe hyperthermia (greater than 40°C) usually requires paralysis, sedation, and ice bath cooling (see "Severe nonexertional hyperthermia (classic heat stroke) in adults", section on 'Management'). Severe hypothermia (less than 30°C) is also treated aggressively with rapid rewarming (see "Accidental hypothermia in adults", section on 'Management'). Therapeutic hypothermia should be administered to unconscious patients with return of spontaneous circulation after circulatory arrest. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Temperature management'.)

Methods of enhancing the elimination of poisons, such as gastric lavage, activated charcoal, whole bowel irrigation, and hemodialysis, may be helpful for selected patients (see "Gastrointestinal decontamination of the poisoned patient"). Circumstances may suggest the presence of concealed drug packages in the GI tract or vagina. (See "Internal concealment of drugs of abuse (body packing)".)

CESSATION OF RESUSCITATIVE EFFORTS — Unlike most cardiac arrest patients, prolonged resuscitation efforts are not necessarily futile for poisoned patients [26-28]. Neurologically intact survival after more than 60 minutes of pulseless arrest and external chest compressions is possible [29-31]. Prolonged resuscitative efforts including extracorporeal circulatory assistance may be warranted for previously healthy patients with witnessed cardiac arrest following drug overdose [13,32]. Even if neurologic recovery is not possible, selected patients poisoned with neurotoxins such as methanol, carbon monoxide, and cyanide can serve as organ donors.


Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)

Society guideline links — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General measures for acute poisoning treatment" and "Society guideline links: Treatment of acute poisoning caused by specific agents other than drugs of abuse".)


Protection of clinicians and emergency department (ED) – While resuscitating a critically ill adult with an unknown poisoning, the clinician must preserve the operational capacity of the emergency health care system and ensure the safety of health care workers. In addition to multiple casualty scenarios, even a single patient contaminated or potentially contaminated with a highly potent toxin can disable an entire ED. (See 'First priorities' above and 'Initial data acquisition' above.)

Examination and identification of toxin – During the resuscitation, characteristic combinations of selected findings (so called "toxidromes") (table 1) should be rapidly sought, including: vital signs; level of alertness; pupil size and position; mucous membrane moisture and secretions; skin temperature and moisture; presence or absence of bowel sounds; and motor tone. Diagnostic tests to be obtained as part of the initial evaluation are described in the text. (See 'Rapid first look: Examination, monitoring, and testing' above.)

Management – A systematic approach is essential to the resuscitation of the critically ill adult with an unknown overdose and can be adapted from the basic "ABC" (airway, breathing, circulation) scheme used for cardiac arrest and trauma patients. An exception is that we do not solely use a Glasgow Coma Scale ≤8 to identify the need for tracheal intubation in an unresponsive poisoned patient who is protecting their airway, maintaining adequate oxygen saturation, hemodynamically stable, and expected to not deteriorate based on the suspected ingestion. The steps are organized according to the issues that pose the most immediate life threats: airway, breathing, circulation, disability (neurologic stabilization), and exposure & elimination. Problems are managed immediately and concurrently as identified. (See 'Systematic evaluation: The "ABCDE" approach' above.)

Prolonged resuscitation – Unlike most cardiac arrest patients, prolonged resuscitation efforts are not necessarily futile for poisoned patients. Neurologically intact survival after more than 60 minutes of pulseless arrest and external chest compressions is possible in some instances. (See 'Cessation of resuscitative efforts' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Stephen J Traub, MD, former section editor of the toxicology program, for 20 years of dedicated service.

  1. Tanz LJ, Dinwiddie AT, Mattson CL, et al. Drug Overdose Deaths Among Persons Aged 10-19 Years - United States, July 2019-December 2021. MMWR Morb Mortal Wkly Rep 2022; 71:1576.
  2. Spencer MR, Miniño AM, Warner M. Drug Overdose Deaths in the United States, 2001-2021. NCHS Data Brief 2022; :1.
  3. Albertson TE, Dawson A, de Latorre F, et al. TOX-ACLS: toxicologic-oriented advanced cardiac life support. Ann Emerg Med 2001; 37:S78.
  4. Panchal AR, Bartos JA, Cabañas JG, et al. Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2020; 142:S366.
  5. Traub SJ, Hoffman RS, Nelson LS. Body packing--the internal concealment of illicit drugs. N Engl J Med 2003; 349:2519.
  6. Del Pozo B, Sightes E, Kang S, et al. Can touch this: training to correct police officer beliefs about overdose from incidental contact with fentanyl. Health Justice 2021; 9:34.
  7. Moss MJ, Warrick BJ, Nelson LS, et al. ACMT and AACT Position Statement: Preventing Occupational Fentanyl and Fentanyl Analog Exposure to Emergency Responders. J Med Toxicol 2017; 13:347.
  8. De Groot R, Van Zoelen GA, Leenders MEC, et al. Is secondary chemical exposure of hospital personnel of clinical importance? Clin Toxicol (Phila) 2021; 59:269.
  9. Sivilotti ML. Flumazenil, naloxone and the 'coma cocktail'. Br J Clin Pharmacol 2016; 81:428.
  10. Freund Y, Viglino D, Cachanado M, et al. Effect of Noninvasive Airway Management of Comatose Patients With Acute Poisoning: A Randomized Clinical Trial. JAMA 2023; 330:2267.
  11. Adnet F, Borron SW, Finot MA, et al. Intubation difficulty in poisoned patients: association with initial Glasgow Coma Scale score. Acad Emerg Med 1998; 5:123.
  12. Skoog CA, Engebretsen KM. Are vasopressors useful in toxin-induced cardiogenic shock? Clin Toxicol (Phila) 2017; 55:285.
  13. de Lange DW, Sikma MA, Meulenbelt J. Extracorporeal membrane oxygenation in the treatment of poisoned patients. Clin Toxicol (Phila) 2013; 51:385.
  14. Upchurch C, Blumenberg A, Brodie D, et al. Extracorporeal membrane oxygenation use in poisoning: a narrative review with clinical recommendations. Clin Toxicol (Phila) 2021; 59:877.
  15. Gosselin S, Hoegberg LC, Hoffman RS, et al. Evidence-based recommendations on the use of intravenous lipid emulsion therapy in poisoning(). Clin Toxicol (Phila) 2016; 54:899.
  16. Levine M, Hoffman RS, Lavergne V, et al. Systematic review of the effect of intravenous lipid emulsion therapy for non-local anesthetics toxicity. Clin Toxicol (Phila) 2016; 54:194.
  17. Warrick BJ, Tataru AP, Smolinske S. A systematic analysis of methylene blue for drug-induced shock. Clin Toxicol (Phila) 2016; 54:547.
  18. Chan A, Isbister GK, Kirkpatrick CM, Dufful SB. Drug-induced QT prolongation and torsades de pointes: evaluation of a QT nomogram. QJM 2007; 100:609.
  19. Burns MJ, Dickson EW, Sivilotti ML, Cuenoud H. Phentolamine reduces myocardial injury and mortality in a rat model of phenylpropanolamine poisoning. J Toxicol Clin Toxicol 2001; 39:129.
  20. Wood DM, Dargan PI, Hoffman RS. Management of cocaine-induced cardiac arrhythmias due to cardiac ion channel dysfunction. Clin Toxicol (Phila) 2009; 47:14.
  21. Wu S, Pearl-Davis MS, Manini AF, Hoffman RS. Use of antipsychotics to treat cocaine toxicity? Acad Emerg Med 2008; 15:105; author reply 106.
  22. Hoffman RS. Cocaine and beta-blockers: should the controversy continue? Ann Emerg Med 2008; 51:127.
  23. Hoffman RS, Goldfrank LR. The poisoned patient with altered consciousness. Controversies in the use of a 'coma cocktail'. JAMA 1995; 274:562.
  24. Jackson R, Teece S. Best evidence topic report. Oral or intravenous thiamine in the emergency department. Emerg Med J 2004; 21:501.
  25. Fletcher ML, Sarangarm P, Nash J, et al. A systematic review of second line therapies in toxic seizures. Clin Toxicol (Phila) 2021; 59:451.
  26. Morrison LJ, Verbeek PR, Zhan C, et al. Validation of a universal prehospital termination of resuscitation clinical prediction rule for advanced and basic life support providers. Resuscitation 2009; 80:324.
  27. Kellermann AL, Hackman BB, Somes G. Predicting the outcome of unsuccessful prehospital advanced cardiac life support. JAMA 1993; 270:1433.
  28. Bonnin MJ, Pepe PE, Kimball KT, Clark PS Jr. Distinct criteria for termination of resuscitation in the out-of-hospital setting. JAMA 1993; 270:1457.
  29. Ramsay ID. Survival after imipramine poisoning. Lancet 1967; 2:1308.
  30. Southall DP, Kilpatrick SM. Imipramine poisoning: survival of a child after prolonged cardiac massage. Br Med J 1974; 4:508.
  31. Orr DA, Bramble MG. Tricyclic antidepressant poisoning and prolonged external cardiac massage during asystole. Br Med J (Clin Res Ed) 1981; 283:1107.
  32. International Liaison Committee on Resuscitation. 2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Part 4: Advanced life support. Resuscitation 2005; 67:213.
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