Version May 2024
INTRODUCTION — Accidental and intentional poisonings or drug overdoses constitute a significant source of aggregate morbidity, mortality, and health care expenditure worldwide. In 2021, over two million cases of known or suspected human toxic exposures were managed by United States poison control centers [1].
The general approach and initial management of patients with suspected or confirmed poisoning will be reviewed here. Specific issues relating to the management of common drug overdoses are discussed separately (see appropriate topic reviews). Topics devoted to the management of the critically ill adult and the child with an unknown overdose are found separately.
●(See "Initial management of the critically ill adult with an unknown overdose".)
●(See "Approach to the child with occult toxic exposure".)
EPIDEMIOLOGY — Accidental and intentional poisoning from both licit and illicit substances remains a major cause of morbidity and mortality worldwide [1,2]. In the United States, the America’s Poison Centers (APC) reported over two million human cases in 2021 [1]. While the overall mortality rate reported by the APC was just under 0.08 percent, 30 percent of cases required management at a health care facility, and 7.9 percent of cases required hospital admission. Fatal ingestions are very uncommon in patients under 12 years of age.
In the United States between 2016 and 2019, there were an estimated 270,000 emergency department visits related to medications used for self-harming behaviors and an additional 1.4 million visits related to therapeutic use of medications [3]. Rates of poisoning cases among emergency department patients appear similar in other industrialized nations [4]. Most cases involving children under age six involved nonintentional ingestion, whereas most fatalities in adults (age 20 and older) were suicidal [1]. While females account for slightly more than one-half of all human exposures reported to United States poison control centers, males account for approximately one-half of all fatal ingestions [1,5].
As of 2008, poisoning had become the leading cause of injury-related death in the United States, surpassing motor vehicle collisions. In 2021, more than 102,000 Americans died of poisoning [6]. The majority of these cases involve an opioid. The number of Americans dying from opioid overdose remain high.
The contribution of poisoning to suicide cases varies by region: suicidal poisoning is especially prevalent in Scandinavian countries and the United Kingdom, while the burden of suicidal poisonings is relatively less in most of Eastern Europe and Central and South America [7].
Among ingestions warranting consultation with a medical toxicologist, the most common drug classes involved were opioids (15.9 percent), ethanol (14.9 percent), non-opioid analgesics (12.8 percent), and antidepressants (9.0 percent) [5]. Reviews of self-poisoning cases in the United Kingdom found that analgesics and antidepressants were the most commonly encountered drugs in poisoning cases, but opioids are now the most common cause of fatal overdose [4,8,9]. However, trends vary in other regions. A study of Norwegian patients reported the most prevalent drugs (aside from ethanol) to be acetaminophen, opioids, and gamma hydroxybutyrate (GHB) [10]. A German study of intensive care unit (ICU) admissions for poisoning found benzodiazepines, antidepressants, and antihistamines to be the most commonly encountered drugs, again excluding ethanol [11]. A report of Israeli poison center data found that analgesics, cleaning products, and antimicrobials were the xenobiotics most frequently reported in poisonings [12], while a review of Turkish ICU admissions for acute poisoning found antidepressants and analgesics to be most common among single-agent ingestions [13]. In Africa and East Asia, pesticides account for more poisoning cases than medications [14,15].
OVERVIEW OF APPROACH — Clinicians who treat poisoned patients should have a systematic and consistent approach to evaluation and management. It is important to note that drug poisoning can produce a wide range of symptoms and clinical findings and may occur in isolation or with other pathology (eg, trauma, infection). Presentation depends upon the agent ingested, whether the ingestion is acute or chronic, baseline prescription medications a patient may be taking, baseline health status of the patient (eg, liver or kidney disease), and whether the ingestion involves a single drug or co-ingestants. Initial management is focused on pattern recognition and acute stabilization. A focused history and physical examination are of great importance in recognizing that poisoning has occurred and determining the type of poisoning. Management is directed to the provision of supportive care, prevention of poison absorption, and, when applicable, the use of antidotes and enhanced elimination techniques. Meticulous supportive care is paramount.
INITIAL EVALUATION AND TREATMENT — A brief initial screening examination should be performed on all patients to identify immediate measures required to stabilize and prevent deterioration of the patient. Assess the airway, vital signs, mental status, pupil size, and skin temperature and moisture. Immediate diagnostic studies to be performed include pulse oximetry, continuous cardiac monitoring, an electrocardiogram (ECG), and a capillary glucose measurement (in altered patients). Intravenous (IV) access should be obtained in all cases of serious ingestion.
In patients with suspected trauma, maintain in-line cervical immobilization. Assess the airway and perform tracheal intubation if there is significant doubt about the patient's ability to protect their airway and avoid aspiration and there is no apparent reversible cause (eg, opioid overdose with naloxone). Provide advanced cardiac life support measures as required. (See "Initial management of the critically ill adult with an unknown overdose" and "Initial management of trauma in adults" and "The decision to intubate" and "Rapid sequence intubation in adults for emergency medicine and critical care" and "Advanced cardiac life support (ACLS) in adults".)
In patients with altered consciousness, a capillary glucose should be performed. Patients who are hypoglycemic should immediately be given dextrose (25g in adults, 0.5g/kg in children). Administer IV naloxone to patients with respiratory depression and signs, symptoms, or a history suggestive of opioid intoxication [16]. (See "Wernicke encephalopathy", section on 'Treatment' and "Acute opioid intoxication in adults", section on 'Basic measures and antidotal therapy'.)
The notion that thiamine must be given prior to dextrose to avoid precipitating Wernicke encephalopathy is unsupported [17]. Uptake of thiamine into cells is slower than that of dextrose [18], and withholding dextrose until the administration of thiamine is complete may prove detrimental to those with actual hypoglycemia.
Rapid bedside glucometers are the most expedient method to determine the presence of hypoglycemia. Empiric administration of dextrose is recommended for the patient with altered consciousness when bedside glucose measurements are low, borderline low, or not immediately available; or the accuracy of the results is questionable. Follow-up finger-stick or serum glucose measurements should be obtained in patients with a persistent altered mental status, as hypoglycemia may develop during the later stages of some poisonings.
Be certain to expose the patient completely and look for signs of trauma, drug use (eg, needle tracks), infection, or extremity swelling. Measure the core body temperature in comatose or encephalopathic patients. Patient decontamination should then be initiated if indicated. Obtain an ECG to assess for drug-related cardiotoxicity. (See 'Electrocardiography' below.)
Search clothing, wallets, and pocketbooks for pills, pill bottles, or drug-related equipment, but take care when doing so to avoid a needle stick. A medical alert bracelet or necklace may provide important history. A more detailed diagnostic evaluation can then ensue. (See "Gastrointestinal decontamination of the poisoned patient".)
DIAGNOSIS OF POISONING — The history, physical examination, and routine and toxicologic laboratory evaluations are used to establish and confirm the diagnosis of poisoning.
History — The history, although intuitively the source of the most helpful information for identifying the etiology of poisoning, is often unreliable when provided by a patient following intentional ingestion [19-21]. In one prospective survey, the initial clinical history fully correlated with confirmatory testing in only 31 percent of cases [22]. The patient's ability to provide a reliable history is often impaired by direct drug effects or psychiatric illness [23]. Therefore, the patient's history should be confirmed whenever possible and correlated with the signs, symptoms, and laboratory data expected from poisoning with the agent(s) implicated by history. When the patient is unable or unwilling to give a reliable history regarding poison exposure, information should be sought from paramedics, police, coworkers, family, friends, and primary care clinician, as well as from medical records and pharmacists. A review of electronic prescription drug monitoring programs may be helpful.
A thorough search of the exposure environment should be conducted for pill bottles or a suicide note, which may provide clues to etiologic agent(s). Knowledge of drugs prescribed for the patient or the patient's family or friends and to which he or she could have had access may prove important.
Unknown pills or chemicals may be identified by consultation with a regional poison control center, computerized drug or poison identification system, or product manufacturer (eg, material data safety sheet). An excellent pill identification tool is available through Lexicomp (Lexicomp Drug I.D. program). An additional Lexicomp subscription may be required; for those without access to Lexicomp, another useful pill identifier can be found in the following reference [24]. United States poison control centers can be reached through a toll-free line (1-800-222-1222). Contact information for poison centers around the world is provided separately. (See 'Additional resources' below.)
It is critical to inquire specifically about the use of over-the-counter medications, traditional or herbal remedies, and dietary supplements as these are often not considered to be medications by the patient and may not be volunteered during routine questioning about "drugs." In addition, patients or secondary sources providing history may misidentify drugs. Over-the-counter products may be confused (eg, acetaminophen versus aspirin) or prescription medications may be mistaken for each other (eg, clonazepam versus clonidine). Lastly, drugs of abuse may only be identified by colloquial or slang terms (eg, "ecstasy" for 3,4-methylenedioxymethamphetamine [MDMA], or "bath salts" for synthetic cathinones) [23]. Beware of co-ingestants.
Physical examination — The physical examination of symptomatic poisoned patients may provide invaluable clues to the agent involved. The mental status, vital signs, and pupillary examination are the most useful elements and allow classification of the patient into either a state of physiologic excitation or depression [25].
●Physiologic excitation (manifested by central nervous system stimulation and increased pulse, blood pressure, respiratory rate and depth, and temperature) is most commonly caused by anticholinergic, sympathomimetic, or central hallucinogenic agents; or by drug withdrawal states. (See "Anticholinergic poisoning" and "Cocaine: Acute intoxication" and "Methamphetamine: Acute intoxication" and "Acute amphetamine and synthetic cathinone ("bath salt") intoxication" and "Phencyclidine (PCP) intoxication in adults" and "Intoxication from LSD and other common hallucinogens" and "Management of moderate and severe alcohol withdrawal syndromes" and "Gabapentinoid poisoning and withdrawal", section on 'Withdrawal syndromes' and "GABA-B agonist (baclofen, phenibut) poisoning and withdrawal", section on 'Withdrawal syndromes'.)
●Physiologic depression (manifested by a depressed mental status, blood pressure, pulse, respiratory rate and depth, and temperature) is most commonly precipitated by sedative-hypnotic agents, opioids, cholinergic (parasympathomimetic) agents, sympatholytics, or alcohols (ethanol, isopropanol, methanol, or ethylene glycol). (See "Organophosphate and carbamate poisoning" and "Acute opioid intoxication in adults" and "Benzodiazepine poisoning" and "Ethanol intoxication in adults" and "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis" and "Gabapentinoid poisoning and withdrawal" and "GABA-B agonist (baclofen, phenibut) poisoning and withdrawal" and "Barbiturate (phenobarbital) poisoning".)
●Mixed physiologic effects may occur in polydrug overdoses or following exposure to certain metabolic poisons (eg, hypoglycemic agents, salicylates, cyanide), membrane-active agents (eg, volatile inhalants, antiarrhythmic drugs, local anesthetic agents), heavy metals (eg, iron, arsenic, mercury, lead), or agents with multiple mechanisms of action (eg, tricyclic antidepressants, many antipsychotics). (See "Metformin poisoning" and "Sulfonylurea agent poisoning" and "Salicylate (aspirin) poisoning: Clinical manifestations and evaluation" and "Cyanide poisoning" and "Acute iron poisoning" and "Tricyclic antidepressant poisoning" and "First-generation (typical) antipsychotic medication poisoning" and "Second-generation (atypical) antipsychotic medication poisoning".)
Following the initial diagnostic evaluation and stabilization, other physical findings should be sought to further define a particular toxic syndrome (toxidrome) and to narrow the potential etiologies of poisoning. The following table describes the major characteristics of the common toxidromes and was created to make comparisons easier and assist with diagnosis (table 1). Of note, a particular patient may not manifest all the symptoms or findings typically associated with a given toxidrome. As one example, despite being anticholinergic, tricyclic antidepressants may cause miosis due to competing effects from activation of muscarinic and alpha receptors. If a patient has a mixed overdose (eg, heroin and methamphetamine), pupils will likely be midrange rather than pinpoint or dilated. Even in the case of a pure overdose, anoxic injury may obscure findings once the drug has been metabolized.
Diagnosis of a poisoning may be assisted by the following physical findings [23,26]:
●Characteristic odors (table 2)
●Pupillary findings (table 3)
●Neuromuscular abnormalities (table 4)
●Mental status alterations (table 5)
●Skin findings (table 6)
●Temperature alterations (table 7)
●Blood pressure and heart rate alterations (table 8)
●Respiratory disturbances (table 9)
Discrepancies between the physical examination and the history may reflect an inaccurate ingestion history, a brief or prolonged time interval between exposure and physical examination, or the effects of the patient's regular cardiovascular medications in masking the expected physiologic response. The physical examination, particularly the evaluation of mental status and vital signs, should be repeated frequently (approximately every hour, depending upon the patient's condition) to determine the course of poisoning and the need for further intervention.
Electrocardiography — Electrocardiographic (ECG) abnormalities may provide diagnostic and prognostic information, and an ECG should be performed on all patients who are symptomatic or who have been exposed to potentially cardiotoxic agents or unknown substances (table 10) [27]. Particular attention should be paid to the duration of the QRS and QTc intervals. Many drugs cause sodium channel blockade (eg, cocaine, tricyclic antidepressants, carbamazepine), which causes prolongation of the QRS interval. Many other drugs block potassium efflux (eg, most antipsychotics, sotalol), which causes prolongation of the QT interval. Toxin-induced QRS interval prolongation, of the type seen with tricyclic antidepressant poisoning, warrants immediate intervention most often with sodium bicarbonate. (See "Tricyclic antidepressant poisoning", section on 'Electrocardiogram'.)
Radiographic studies — Imaging studies are not required in every patient but may be useful in several situations [28,29]:
●Certain radiopaque toxins (summarized by the mnemonic "CHIPES") may be visualized by plain film radiographs (table 11 and image 1).
●Ingested drug packets of "body packers" or "body stuffers" may be seen on imaging, such as plain films (image 2), computed tomography (image 3), ultrasound, and magnetic resonance imaging. However, diagnostic imaging is not always required, especially in body stuffers, which is discussed separately. (See "Internal concealment of drugs of abuse (body packing)", section on 'Diagnostic imaging' and "Acute ingestion of illicit drugs (body stuffing)", section on 'Imaging'.)
●Noncardiogenic pulmonary edema and/or the acute respiratory distress syndrome due to exposure to certain toxic agents may be suggested by the appearance of the chest radiograph (table 12 and image 4). Any poisoning that causes significant central nervous system depression creates a risk for aspiration. Signs of aspiration may be evident on the chest radiograph.
Abdominal ultrasound does not appear to be a reliable method of detecting ingested medications [30,31].
Toxicology screens (drug testing) — Toxicology screening is rarely necessary when patients with an unintentional ingestion are asymptomatic or have clinical findings that are consistent with the medical history. However, screening for acetaminophen and salicylates is strongly recommended for patients with an uncertain history or intentional poisoning; few early signs may be present following lethal doses of these agents, and specific treatments are available and highly effective if implemented early. One retrospective study found detectable serum acetaminophen concentrations in 9.6 percent of all overdose patients; almost one-third of this subset denied ingestion of acetaminophen [32]. Other less common xenobiotics with potential for delayed toxicity ("toxic time bombs") that demand a high index of suspicion for diagnosis are listed in the table (table 13). (See "Acetaminophen (paracetamol) poisoning in adults: Pathophysiology, presentation, and evaluation" and "Clinical manifestations and diagnosis of acetaminophen (paracetamol) poisoning in children and adolescents" and "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis" and "Clinical manifestations and evaluation of mushroom poisoning" and "Sulfonylurea agent poisoning".)
"Drugs of abuse" immunoassay urine screens can be used to detect opiates, benzodiazepines, cocaine metabolites, barbiturates, tricyclic antidepressants, tetrahydrocannabinol, and phencyclidine. Some assays include screens for methadone, oxycodone, fentanyl, and buprenorphine. These assays are inexpensive and provide rapid results, usually within one hour. However, due to high rates of false positives and false negatives, these tests should not be relied upon to establish a diagnosis. Testing for drugs of abuse is reviewed in detail separately; a table summarizing common urine drug testing assays is provided (table 14). (See "Testing for drugs of abuse (DOAs)" and "Substance use disorders: Clinical assessment".)
Of note, positive and negative screen tests do not provide absolute confirmation or refutation of a poisoning, and further evaluation may be required. In some cases, a negative screen may reflect a drug concentration below the threshold for detection when the specimen is obtained. Some drugs may simply be missed by the assay even when signs of toxicity are present. As an example, a patient may be comatose and apneic from fentanyl despite a urine drug screen negative for opiates. Conversely, high concentrations of certain drugs may be due to a false-positive result. As an example, diphenhydramine can cause a false-positive result for tricyclic antidepressants [33]. In some cases, a test may be positive due to small quantities of a drug that is present, but that drug is not responsible for the acute toxicity experienced by the patient. As an example, a patient may have used cocaine three days prior but presents comatose and apneic following an acute fentanyl ingestion. In this case, the cocaine screen would likely be positive, but the opioid screen negative. Any rapid immunoassay test requires confirmatory testing prior to legal action (eg, removal of a child from parental custody). (See "The substance-exposed child: Clinical features and diagnosis", section on 'Toxicology testing'.)
Comprehensive qualitative toxic screening of urine, blood, or meconium (commonly by liquid or gas chromatography and mass spectrometry) is of limited clinical utility. Such screening is expensive, commonly requires hours or days for results, often does not predict or define the severity of poisoning, detects unsuspected drugs in only a minority of patients, rarely leads to changes in patient management and disposition, and is unlikely to affect patient outcome [34-37]. Thus, comprehensive toxicology screening should be reserved for patients with severe or unexplained toxicity or for cases with legal implications. Urine is the optimal matrix for analysis (as opposed to serum or whole blood) due to the longer window for detection and higher concentrations of drugs or their metabolites.
Select quantitative assays have circumscribed roles in the management of poisoned patients. They are useful in guiding the management of certain intoxications when interpreted in conjunction with clinical status and the timing of poisoning (table 15).
Other laboratory studies — Certain laboratory abnormalities are characteristic of specific agents (table 16 and table 17). Symptomatic patients and those with an unreliable or unknown history should, at a minimum, undergo urinalysis and measurement of serum electrolytes, blood urea nitrogen (BUN), creatinine, and glucose. Measurements of serum ketones, creatine kinase, liver function tests, lipase, ionized calcium, and magnesium should also be performed in most significantly ill patients. Additional testing may be useful in specific circumstances, such as serum osmolality in suspected toxic alcohol ingestion. Routine urine pregnancy testing is strongly recommended in all women of childbearing age. Acetaminophen and salicylate concentrations should be obtained in most intentional ingestions.
The ordering of other laboratory studies should be individualized and is somewhat dependent upon the results of initial laboratory studies:
●Blood gas, co-oximetry, and serum lactate measurements may be necessary in patients with acid-base, cardiovascular, neurologic, or respiratory disturbances. Co-oximetry can aid in the rapid diagnosis of carbon monoxide poisoning and methemoglobinemia. (See "Carbon monoxide poisoning" and "Methemoglobinemia".)
In general, co-oximetry results are the same whether venous or arterial blood is used. Thus, arterial blood is not required when evaluating a patient for carbon monoxide toxicity. However, it may be useful to compare the partial pressure of oxygen (PO2) from venous and arterial blood samples when evaluating the effects of a toxin that blocks the electron transport chain (eg, cyanide). (See "Cyanide poisoning".)
●Any patient with an acid-base disturbance, increased serum osmolal gap, or oxygen saturation gap (>5 percent difference between measured and calculated value) should have a toxic etiology ruled out (table 18 and table 19). Detection of a serum osmolal gap with any alcohol intoxication occurs only when the serum osmolality is measured by freezing point depression; the osmotic contribution of volatile alcohols is not included when using a vapor pressure osmometer, which assumes that only water is in the vapor phase. (See "Serum osmolal gap" and "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)
●The presence of an anion gap metabolic acidosis may be the first clue to a toxic ingestion and should prompt consideration of such causes as salicylates, ethylene glycol, and methanol. Serum creatinine, glucose, ketones, and lactate also should be measured to detect other potential causes of an anion gap acidosis. (See "Approach to the adult with metabolic acidosis" and "Salicylate (aspirin) poisoning: Clinical manifestations and evaluation" and "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)
●The presence of an abnormally elevated serum creatinine with a normal BUN may be seen with alcoholic ketoacidosis, diabetic ketoacidosis, or isopropyl alcohol poisoning. High serum concentrations of acetone, a metabolite of isopropyl alcohol, interfere with colorimetric creatinine assays, causing falsely elevated values [38]. Another clue to such a false elevation is a high creatinine on a chemistry panel but a normal creatinine on a blood gas or point-of-care assay, which rely on enzymatic detection methods. (See "Fasting ketosis and alcoholic ketoacidosis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis" and "Isopropyl alcohol poisoning".)
●Blood concentrations of isopropyl alcohol and beta-hydroxybutyrate should be measured in patients with an elevated osmolal gap without metabolic acidosis. (See "Isopropyl alcohol poisoning", section on 'Serum isopropyl alcohol and acetone levels' and "Fasting ketosis and alcoholic ketoacidosis", section on 'Direct measurement of serum beta-hydroxybutyrate'.)
POISONING MANAGEMENT — Optimal management of the poisoned patient depends upon the specific poison(s) involved, the presenting and predicted severity of illness, and elapsed time between exposure and presentation. Treatment variably includes supportive care, decontamination, antidotal therapy, and enhanced elimination techniques. Assistance can be obtained from a medical toxicologist or consultation with a regional poison control center. In the United States, poison control centers can be reached through a toll-free line (1-800-222-1222). If available, direct consultation with a medical toxicologist is often helpful. Contact information for poison centers around the world is provided separately (see 'Additional resources' below).
Decontamination — Following initial patient stabilization, patient decontamination may be performed if indicated. The sooner decontamination is performed, the more effective it is at preventing poison absorption. Copious water or saline irrigation for non-metallic topical exposures (table 20) and administration of activated charcoal for ingestions are the preferred methods of decontamination in most cases. In general, decontamination of a topical chemical exposure should be performed before the patient is brought into the emergency department. Activated charcoal should only be administered to a patient with a patent airway who is not expected to lose airway patency. In certain circumstances, other methods of gastrointestinal decontamination may be warranted, such as whole-bowel irrigation, endoscopy, surgery, dilution, and cathartics. (See "Topical chemical burns: Initial evaluation and management" and "Gastrointestinal decontamination of the poisoned patient".)
The role of decontamination in the management of specific toxins is reviewed in topics devoted to the poisoning in question; general discussions of methods for decontamination, including the evidence for their effectiveness, are found separately. (See "Gastrointestinal decontamination of the poisoned patient" and "Enhanced elimination of poisons".)
Antidotes — Supportive care is the cornerstone of the treatment of the poisoned patient, and the adage "treat the patient, not the poison" is the guiding principle of medical toxicology. However, there are instances in which prompt administration of a specific antidote is potentially lifesaving.
Antidote administration is appropriate when there is a poisoning for which an antidote exists, the actual or predicted severity of poisoning warrants its use, and the expected benefits of therapy outweigh its associated risks. Antidotes dramatically reduce morbidity and mortality in certain intoxications, but they are unavailable for most toxic agents and therefore are used in only a small fraction of cases [39].
Antidotes reduce or reverse poison effects by a variety of means. They may prevent absorption, bind and neutralize poisons directly, antagonize end-organ effects, or inhibit conversion to more toxic metabolites.
The pharmacokinetics of both the toxin and the antidote must be considered. Toxicity may recur if the antidote is eliminated more rapidly than the ingested substance, particularly if the antidote acts by antagonizing end-organ effects or inhibiting conversion to toxic metabolites. As an example, naloxone reverses opioid-induced somnolence and respiratory depression, but symptoms recur in approximately one-third of cases because the elimination half-life of naloxone is only 30 to 90 minutes [40,41]. Thus, in certain situations antidotes may require repeated administration. (See "Acute opioid intoxication in adults", section on 'Basic measures and antidotal therapy'.)
Although a response to empirically administered antidotes can be used to suggest a suspected diagnosis, their indiscriminate use can potentially increase patient morbidity. As an example, routine administration of flumazenil to comatose patients suspected of benzodiazepine overdose may precipitate seizures, particularly if a proconvulsant drug has also been ingested, which is discussed in detail separately. (See "Benzodiazepine poisoning", section on 'Role of antidote (flumazenil)'.)
Enhanced elimination techniques — Procedures to enhance elimination of poisons include forced diuresis, urine ion trapping, hemodialysis, hemoperfusion, hemofiltration, and exchange transfusion. Various measures may be useful in selected circumstances. (See "Enhanced elimination of poisons".)
Supportive care — Supportive care is the most important aspect of treatment and frequently is sufficient to effect complete patient recovery. Supportive care for the poisoned patient is generally similar to that utilized for other critically ill patients, but certain issues are managed slightly differently:
●Airway protection – Airway protection with tracheal intubation should be performed early in the poisoned patient with depressed mental status, unless the cause is easily reversible (eg, opioid intoxication or hypoglycemia) because of the high risk for aspiration and its associated complications. Tracheal intubation is not routinely indicated exclusively for the purpose of gastric decontamination. Tracheal intubation with mechanical ventilation is also indicated in the presence of severe acid-base disturbances or acute respiratory failure. Particularly when intubating a severely acidemic patient (eg, severe salicylate toxicity), it is important to prevent the development of a respiratory acidosis through inadequate minute ventilation. (See "Initial management of the critically ill adult with an unknown overdose", section on '"A": Airway stabilization' and "Rapid sequence intubation in adults for emergency medicine and critical care" and "Approach to the difficult airway in adults for emergency medicine and critical care", section on 'High-risk physiology present' and "Mechanical ventilation of adults in the emergency department".)
Occasionally, the management of high-grade physiologic stimulation may require sedation and/or paralysis with mechanical ventilation to limit the extent of complications such as hyperthermia, acidosis, and rhabdomyolysis. One rare exception to this important principle of aggressive airway management is salicylate poisoning, in which mechanical ventilation should be avoided unless absolutely necessary. (See "Salicylate (aspirin) poisoning: Management", section on 'ABCs and supportive care'.)
●Hypotension – Hypotension should be managed initially with boluses of isotonic intravenous (IV) fluids. Vasopressors are required when hypotension does not resolve with volume expansion. In general, direct-acting vasopressors, such as norepinephrine or epinephrine, are favored over indirect-acting agents, such as dopamine. The superiority of direct-acting agents has been demonstrated in the setting of tricyclic antidepressant poisoning [42,43]. (See "Initial management of the critically ill adult with an unknown overdose", section on 'Hypotension' and "Use of vasopressors and inotropes" and "Tricyclic antidepressant poisoning".)
●Hypertension – Hypertension in agitated patients is best treated initially with nonspecific sedatives such as benzodiazepines [44]. When hypertension necessitates specific therapy because of associated end-organ dysfunction, preferred treatments include calcium-channel blocking agents, phentolamine, labetalol, or nitroprusside. The use of beta-blockers alone for patients with sympathetic hyperactivity (eg, cocaine intoxication) is generally not recommended because it may result in unopposed alpha-adrenergic stimulation and intensified vasoconstriction [44,45]. The use of a beta-blocker after vasodilation has been achieved through alpha blockade (eg, phentolamine) or another vasodilator (eg, nitroprusside) is acceptable in these circumstances. In addition, a positive drug screen result for cocaine or amphetamines in an otherwise asymptomatic, non-tachycardic patient should not be considered a contraindication for beta-blockers. (See "Cocaine: Acute intoxication" and "Acute amphetamine and synthetic cathinone ("bath salt") intoxication" and "Methamphetamine: Acute intoxication".)
●Ventricular tachycardia – Sodium bicarbonate is first-line therapy for ventricular tachycardias when they occur in the context of intoxication from a drug with sodium channel-blocking properties (eg, tricyclic antidepressants, carbamazepine, cocaine). Types IA (eg, procainamide), IC, and III antiarrhythmic agents are not recommended and are potentially dangerous since they may further impair cardiac conduction. Hypertonic saline may be preferable to sodium bicarbonate for treatment of intraventricular conduction delay due to flecainide toxicity. (See "Initial management of the critically ill adult with an unknown overdose", section on 'Monomorphic, wide-complex tachycardia' and "Tricyclic antidepressant poisoning", section on 'Sodium bicarbonate for cardiac toxicity' and "Major side effects of class I antiarrhythmic drugs", section on 'Flecainide'.)
Overdrive pacing with isoproterenol or a temporary pacemaker may be effective in patients with drug-induced torsades de pointes and prolonged QT intervals on electrocardiogram (ECG). IV magnesium sulfate can also be administered. Digoxin-poisoned patients with life-threatening tachyarrhythmias or bradyarrhythmias should be treated with specific antigen-binding (Fab) fragments (Digibind). (See "Digitalis (cardiac glycoside) poisoning" and "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management".)
●Bradyarrhythmia – Bradyarrhythmias associated with hypotension should be treated in the standard fashion with atropine and/or temporary pacing. However, in patients with calcium channel blocker or beta blocker intoxication, the administration of calcium, glucagon, vasopressors, isoproterenol, high-dose insulin, or other therapies may obviate the need for a temporary pacemaker. Patients who have ingested clonidine are an exception to the general rule that direct-acting vasopressors are preferred over indirect-acting agents. Such patients have decreased sympathomimetic tone due to decreased release of sympathomimetic neurotransmitters, which is overcome by dopamine. (See "Initial management of the critically ill adult with an unknown overdose", section on 'Bradycardia with hypotension' and "Calcium channel blocker poisoning" and "Beta blocker poisoning" and "Clonidine, xylazine, and related imidazoline poisoning".)
●Seizure – Seizures generally are best treated with benzodiazepines, followed by barbiturates if necessary. Phenytoin is typically not recommended to control seizures in poisoned patients [46]. One possible exception is seizures caused by dalfampridine (4-aminopyridine), which may respond to phenytoin in addition to benzodiazepines. By extension, other anticonvulsants, such as levetiracetam, are unlikely to be successful in controlling toxin-induced seizures. Seizures caused by certain agents may require specific antidotes for their successful termination (eg, pyridoxine for isoniazid toxicity, glucose for hypoglycemic agents). (See "Initial management of the critically ill adult with an unknown overdose", section on '"D": Disability and neurological stabilization' and "Beta blocker poisoning" and "Theophylline poisoning" and "Isoniazid (INH) poisoning" and "Metformin poisoning" and "Sulfonylurea agent poisoning".)
●Agitation – Drug-associated agitation is generally best treated with benzodiazepines. Severe agitation refractory to benzodiazepines may respond to phenobarbital or propofol, although tracheal intubation is typically required. (See "Sedative-analgesia in ventilated adults: Management strategies, agent selection, monitoring, and withdrawal".).
Agitation associated with certain toxidromes may be best treated with specific agents (eg, physostigmine for the anticholinergic syndrome) [47]. (See "Anticholinergic poisoning", section on 'Antidotal therapy with physostigmine for severe toxicity'.)
●Hyperthermia – Severe hyperthermia secondary to drug toxicity (eg, sympathomimetic overdose, serotonin syndrome, or neuroleptic malignant syndrome) may require aggressive treatment, possibly including ice water immersion [48]. Descriptions of such cooling techniques, including ice water immersion, are provided separately. (See "Initial management of the critically ill adult with an unknown overdose", section on '"E": Exposure and elimination' and "Severe nonexertional hyperthermia (classic heat stroke) in adults", section on 'Cooling measures and temperature monitoring' and "Exertional heat illness in adolescents and adults: Management and prevention", section on 'Rapid cooling'.)
Antipyretics, such as acetaminophen or ibuprofen, are unlikely to alleviate drug-induced hyperthermia but may be useful for treatment of fever due to complications (eg, aspiration).
DISPOSITION — Following initial evaluation, treatment, and a short period of observation, disposition of the patient is based upon the observed and predicted severity of toxicity. Patients who develop only mild toxicity and who have only a low predicted severity can be observed in the emergency department until they are asymptomatic. An observation period of four to six hours is usually adequate for this purpose. Patients with moderate observed toxicity or those who are at risk for such on the basis of history or initial laboratory data should be admitted to an intermediate-care floor or an appropriate observation unit for continued monitoring and treatment. Patients with significant toxicity should be admitted to an intensive care unit (ICU) (table 21). All patients with intentional overdose require psychiatric assessment prior to discharge.
One retrospective study of 209 patients with drug overdoses suggested that clinical assessment in the emergency department could reliably identify patients who are at high risk for complications and require ICU care [49]. The presence of any of eight clinical criteria predicted a complicated hospital course that could be best managed in an ICU:
●Partial pressure of carbon dioxide (PaCO2) >45 mmHg
●Need for emergency intubation
●Post-ingestion seizures
●Unresponsiveness to verbal stimuli
●Non-sinus cardiac rhythm
●Second- or third-degree atrioventricular block
●Systolic blood pressure <80 mmHg
●QRS duration ≥0.12 seconds
None of the 151 patients who lacked these risk factors developed a high-risk condition after admission, and none required transfer to the ICU. The authors estimated that use of these predictors in similar patient populations could eliminate over one-half of intensive care days for poisoning without compromising the quality of care. A subsequent prospective study confirmed the importance of several of the criteria listed above (respiratory depression, hypotension, arrhythmia) and also noted that older age (over 61 years), abnormal body temperature, and suicidal intent were associated with an increased risk of death following poisoning [50].
ADDITIONAL RESOURCES
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" and "Society guideline links: Poisoning prevention".)
SUMMARY AND RECOMMENDATIONS
●Toxicology consultation – Assistance can be obtained from regional poison control centers or a bedside consultation with a medical toxicologist. United States poison control centers can be reached through a toll-free line (1-800-222-1222). Contact information for poison centers around the world is provided separately. (See 'Additional resources' above and "Society guideline links: Regional poison control centers".)
●Avoid unnecessary interventions – While poisonings can be fatal, the large majority of patients presenting with a toxic exposure suffer minimal morbidity and recover fully. Thus, it is important to weigh the risks of interventions against the potential benefits, which, for many patients, are relatively small. (See 'Epidemiology' above.)
●Initial stabilization – Stabilization procedures are paramount in patients with a compromised airway, inadequate gas exchange, or marginal hemodynamics. (See 'Initial evaluation and treatment' above and "Initial management of the critically ill adult with an unknown overdose", section on 'Systematic evaluation: The "ABCDE" approach'.)
●History – Obtain a thorough history of actual and potential exposures. Use information from friends, family, and prehospital personnel when available. Always inquire specifically about the use of over-the-counter drugs and traditional or herbal remedies in cases of intentional overdose. (See 'History' above.)
●Physical examination – Perform a thorough physical examination to ascertain signs of a potential toxidrome as well as complications of the toxic exposure, such as trauma. The following table describes the major characteristics of the common toxidromes (table 1). Diagnosis of a potential toxin may be assisted with the following particular physical findings (see 'Physical examination' above):
•Characteristic odors (table 2)
•Pupillary findings (table 3)
•Neuromuscular abnormalities (table 4)
•Mental status alterations (table 5)
•Skin findings (table 6)
•Temperature alterations (table 7)
•Blood pressure and heart rate alterations (table 8)
•Respiratory disturbances (table 9)
●Diagnostic testing and imaging – Perform a focused laboratory and radiographic evaluation that is guided by the severity of the patient's clinical status and the suspected toxins. Symptomatic patients and those with an unknown or unreliable history should, at a minimum, have measurements of serum electrolytes, renal function, and blood glucose. A urinalysis should also be performed. Calculation of the osmolal and anion gaps may help guide further evaluation of the toxic agent. An electrocardiogram (ECG) should be performed on all patients who are symptomatic or who have been exposed to potentially cardiotoxic agents. Obtain a pregnancy test in females of childbearing age. (See 'Radiographic studies' above and 'Other laboratory studies' above and 'Electrocardiography' above.)
●Drug testing – Toxicology screening is rarely necessary when patients with an unintentional ingestion are asymptomatic or have clinical findings that are consistent with the medical history. Screening for acetaminophen and salicylates is strongly recommended for patients with an uncertain history, intentional poisoning, or unexplained toxicity. Obtain quantitative drug concentrations if the results will help guide management (table 15). "Drugs of abuse" immunoassay urine screens (table 14) provide less expensive and more timely results than comprehensive qualitative assays using gas chromatography or mass spectrometry, but neither are likely to change management, and routine urine drug screens are not recommended. (See 'Toxicology screens (drug testing)' above and "Testing for drugs of abuse (DOAs)".)
●Supportive care and intensive care unit (ICU) criteria – Supportive care in conjunction with decontamination procedures is sufficient for the vast majority of patients with toxic exposures. The decision to admit a patient with a toxic exposure to an intensive care setting is based upon clinical criteria that relate to the stability of the airway, respiratory system, and cardiovascular system; and the patient's level of consciousness (table 21). (See 'Poisoning management' above and 'Disposition' above.)
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