General Approach To Drug Poisoning in Adults

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General approach to drug poisoning in adults

Author: Michael D Levine, MD
Section Editor: Stephen J Traub, MD
Deputy Editor: Jonathan Grayzel, MD, FAAEM
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2020. | This topic last updated: Jul 01, 2020.
INTRODUCTION
Accidental and intentional poisonings or drug overdoses constitute a significant source of aggregate morbidity,
mortality, and health care expenditure worldwide. In 2018, over two million calls were made to United States
poison control centers regarding known or suspected human toxicities [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" and "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 American Association of Poison Control Centers
(AAPCC) reported over two million human exposure calls in 2018 [1]. While the overall mortality rate reported
by the AAPCC was just under 0.07 percent, 31 percent of cases required management at a health care
facility, and 8.4 percent of cases required hospital admission.
In the United States between 2008 and 2011, there were an estimated 1.1 million annual emergency
department (ED) visits related to drug poisoning, or 35.4 visits per 10,000 persons; 24.5 percent of these
patients required hospital admission, compared with 12.7 percent for non-poisoning related presentations [3].
Rates of poisoning cases among ED 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 half of all human exposures
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reported to United States poison control centers, males account for just over 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 2017, more than 70,000 Americans died of a drug overdose, with 68 percent
involving an opioid [6]. 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 analgesics (15.2 percent), antidepressants (11.4 percent), and opioids (10.9 percent) [5].
Reviews of self-poisoning cases in the United Kingdom and Spain found that analgesics, benzodiazepines,
and antidepressants were the most commonly encountered drugs in poisoning cases [4,8]. 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) [9]. 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 [10]. A report of Israeli poison center data found that
analgesics, cleaning products, and antimicrobials were the xenobiotics most frequently reported in poisonings
[11], while a review of Turkish ICU admissions for acute poisoning found antidepressants and analgesics to
be most common among single agent ingestions [12]. In Africa and East Asia, pesticides account for more
poisoning cases than medications [13,14].
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, and whether the ingestion involves a single drug or coingestants. 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, and a capillary glucose measurement (in
altered patients). Intravenous access should be obtained in all cases of serious ingestion.
In patients with suspected occult 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. In cases of suspected opioid toxicity, a brief trial of naloxone may be performed prior to
performing tracheal intubation, provided ventilation can be assisted using noninvasive measures. 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 for adults outside the operating room" 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
intravenous naloxone to patients with signs, symptoms, or a history suggestive of opioid intoxication [15].
(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's encephalopathy is
unsupported [16]. Uptake of thiamine into cells is slower than that of dextrose [17], 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 or borderline-low, 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 electrocardiogram to assess for drug-
related cardiotoxicity. (See 'Electrocardiography' below.)
Search clothing, wallets, and pocket books 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 [18,19]. In
one prospective survey, the initial clinical history fully correlated with confirmatory testing in only 31 percent of
cases [20]. The patient's ability to provide a reliable history is often impaired by direct drug effects or
psychiatric illness [21]. 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, and the patient's employer, family, friends, and primary
care clinician, as well as from medical records and pharmacists.
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). United States poison control
centers can be reached through a toll-free line (1-800-222-1222). The World Health Organization (WHO)
provides a listing of international poison centers at its website.
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, keep in mind that 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
MDMA, or "bath salts" for synthetic cathinones) [21].
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 [22].
● 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".)
● Physiologic depression, manifested by a depressed mental status, blood pressure, pulse, respiratory rate
and depth, and temperature, is most commonly precipitated by ethanol, other sedative-hypnotic agents,
opioids, cholinergic (parasympathomimetic) agents, sympatholytics, or toxic alcohols (methanol or
ethylene glycol). (See "Organophosphate and carbamate poisoning" and "Acute opioid intoxication in
adults" and "Benzodiazepine poisoning and withdrawal" and "Ethanol intoxication in adults" and
"Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)
● 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). (See "Metformin poisoning" and
"Sulfonylurea agent poisoning" and "Salicylate (aspirin) poisoning in adults" and "Cyanide poisoning" and
"Acute iron poisoning" and "Tricyclic antidepressant 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 mid-range 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 [21,23]:
● 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 or
a brief or prolonged time interval between exposure and physical examination. 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 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 (table 10) [24]. 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. (See "Tricyclic antidepressant poisoning".)
Radiographic studies — Imaging studies are not required in every patient but may be useful in several
situations [25,26]:
● 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" may be seen on plain films (image 2). (See "Internal
concealment of drugs of abuse (body packing)" and "Acute ingestion of illicit drugs (body stuffing)".)
● Abdominal ultrasound does not appear to be a reliable method of detecting ingested medications [27,28].
● 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
3). Any poisoning that causes significant central nervous system depression creates a risk for aspiration.
Signs of aspiration may be evident on the chest radiograph.
Toxicology screens (drug testing) — Toxicology screening is rarely necessary when patients with a non-
intentional 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 [29]. Other less common "toxic time bombs" for
which diagnosis demands a high index of suspicion are listed in the table (table 13). (See "Acetaminophen
(paracetamol) poisoning in adults: Pathophysiology, presentation, and evaluation" and "Acetaminophen
(paracetamol) poisoning in adults: Treatment" and "Salicylate (aspirin) poisoning in adults".)
"Drugs of abuse" immunoassay screens can be used to detect opioids, benzodiazepines, cocaine
metabolites, barbiturates, tricyclic antidepressants, tetrahydrocannabinol, and phencyclidine in urine (table
14). Some assays include screens for methadone or methamphetamine. These assays are inexpensive and
provide rapid results, usually within one hour. Testing for drugs of abuse is reviewed in detail separately; a
table summarizing common urine drug testing assays is provided (table 15). (See "Testing for drugs of abuse
(DOA)" and "Clinical assessment of substance use disorders".)
Of note, positive and negative screen tests do not provide absolute confirmation or refutation of a poisoning,
and further evaluation may be required. As an example, 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 opioids. 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 [30]. 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.
In contrast to the rapid immunoassay screens, comprehensive qualitative toxic screening of urine, blood, or
other body fluids (commonly by liquid and gas chromatography and mass spectrometry) 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 [31-34]. Thus, comprehensive toxicology screening
should be reserved for patients with severe or unexplained toxicity. 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.
Quantitative assays have defined 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 16).
Other laboratory studies — Certain laboratory abnormalities are characteristic of specific agents (table 17
and table 18). Symptomatic patients and those with an unreliable or unknown history should, at a minimum,
undergo urinalysis and measurement of serum electrolytes, BUN, creatinine, and glucose. Measurements of
serum osmolality, ketones, creatine kinase, liver function tests, lipase, ionized calcium, and magnesium
should also be performed in most significantly ill patients. 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 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
19 and table 20). Detection of a plasma osmolal gap with any alcohol intoxication occurs only when the
plasma 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 in
adults" 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 [35]. 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.
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). The
World Health Organization (WHO) provides a listing of international poison centers at its website. If available,
direct consultation with a medical toxicologist is often helpful.
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 topical exposures and administration of activated charcoal for ingestions
are the preferred methods of decontamination in most cases. Decontamination of a topical chemical exposure
should be performed before the patient is brought into the emergency department. In certain circumstances,
other methods of gastrointestinal decontamination may be warranted, such as gastric lavage, whole bowel
irrigation, endoscopy, surgery, dilution, and cathartics. (See "Topical chemical burns: Initial assessment and
management" and "Gastrointestinal decontamination of the poisoned patient", section on 'Activated
charcoal'.)
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 life-saving.
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 [36].
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 [37,38]. 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 confirm 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, and is therefore NOT recommended. (See "Benzodiazepine
poisoning and withdrawal", section on '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, it is
important to prevent the development of a respiratory acidosis through inadequate minute ventilation.
(See "Rapid sequence intubation for adults outside the operating room" 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 in adults".)
● Hypotension – Hypotension should be managed initially with boluses of isotonic intravenous 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 [39,40]. (See "Use of vasopressors and inotropes" and "Tricyclic
antidepressant poisoning".)
● Hypertension – Hypertension in agitated patients is best treated initially with nonspecific sedatives such
as benzodiazepines [41]. 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 [41,42]. 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.
(See "Tricyclic antidepressant poisoning", section on 'Sodium bicarbonate for cardiac toxicity'.)
Overdrive pacing with isoproterenol or a temporary pacemaker may be effective in patients with drug-
induced torsades de pointes and prolonged QT intervals on ECG. Intravenous magnesium sulfate can
also be administered. Digoxin-poisoned patients with life-threatening tachyarrhythmias or
bradyarrhythmias should be treated with specific Fab fragments (Digibind). (See "Digitalis (cardiac
glycoside) poisoning" and "Acquired long QT syndrome: Clinical manifestations, diagnosis, and
management".)
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● 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 "Calcium channel blocker
poisoning" and "Beta blocker poisoning" and "Clonidine 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 [43]. One
possible exception is seizures caused by dalfampridine (f-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 "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-analgesic medications in critically ill adults: Selection, initiation,
maintenance, and withdrawal" and "Assessment and emergency management of the acutely agitated or
violent adult", section on 'Chemical sedation'.).
Agitation associated with certain toxidromes may be best treated with specific agents (eg, physostigmine
for the anticholinergic syndrome) [44]. (See "Anticholinergic poisoning", section on 'Antidotal therapy with
physostigmine'.)
● 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 [45]. Descriptions of such cooling techniques, including ice water
immersion, are provided separately. (See "Severe nonexertional hyperthermia (classic heat stroke) in
adults", section on 'Cooling measures' and "Exertional heat illness in adolescents and adults:
Management and prevention", section on 'Cooling measures'.)
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 [46]. The presence of any of eight clinical criteria predicted a complicated hospital course that could be
best managed in an ICU:
● 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 less than 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 [47].
ADDITIONAL RESOURCES
Regional poison control centers in the United States are available at all times for consultation on patients who
are 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 and/or inpatient care. Whenever
available, these are invaluable resources to help in the diagnosis and management of ingestions or
overdoses. The World Health Organization (WHO) provides a listing of international poison centers at its
website.
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".)
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). The World Health Organization (WHO) provides a listing of
international poison centers at its website.
● 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.
● Initial stabilization – Institute 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".)
● 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. The following table describes the major
characteristics of the common toxidromes (table 1). Look for signs of trauma. The topic contains multiple
tables that describe the association between particular physical findings and potential toxins. (See
'Physical examination' above.)
Diagnosis of a poisoning may be assisted by the following physical findings:
• 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
should be performed on all patients who are symptomatic or who have been exposed to potentially
cardiotoxic agents. Obtain a pregnancy test in women of child-bearing age. (See 'Radiographic studies'
above and 'Other laboratory studies' above and 'Electrocardiography' above.)
● Drug testing — Obtain a "toxic screen" of blood and/or urine in patients with severe or unexplained
toxicity. Limited immunoassay screens are adequate for most cases of intentional overdose and provide
less expensive and more timely results than comprehensive qualitative assays using gas
chromatography or mass spectrometry. 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. (See 'Toxicology screens
(drug testing)' above and "Testing for drugs of abuse (DOA)".)
● 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 are based upon clinical
criteria that relate to the stability of the airway, respiratory system, cardiovascular system, and the
patient's level of consciousness (table 21). (See 'Poisoning management' above and 'Disposition' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
Topic 324 Version 24.0
GRAPHICS
Common poisoning syndromes (toxidromes)
Mental Other Examples of toxic

Toxidrome Pupils Vital signs
status manifestations agents
Sympathomimetic Hyperalert, Mydriasis Hyperthermia, Diaphoresis, tremors, Cocaine, amphetamines,

agitation, tachycardia, hyperreflexia, seizures cathinones, ephedrine,
hallucinations, hypertension, pseudoephedrine,
paranoia widened pulse phenylpropanolamine,
pressure, theophylline, caffeine
tachypnea,
hyperpnea
Anticholinergic Hypervigilance, Mydriasis Hyperthermia, Dry flushed skin, dry Antihistamines, tricyclic
agitation, tachycardia, mucous membranes, antidepressants,
hallucinations, hypertension, decreased bowel sounds, cyclobenzaprine, orphenadrine,
delirium with tachypnea urinary retention, antiparkinson agents,
mumbling myoclonus, antispasmodics,
speech, coma choreoathetosis, picking phenothiazines, atropine,
behavior, seizures (rare) scopolamine, belladonna
alkaloids (eg, Jimson Weed)
Hallucinogenic Hallucinations, Mydriasis Hyperthermia, Nystagmus Phencyclidine, LSD, mescaline,

perceptual (usually) tachycardia, psilocybin, designer
distortions, hypertension, amphetamines (eg, MDMA
depersonalization, tachypnea ["Ecstasy"], MDEA)
synesthesia,
agitation
Opioid CNS depression, Miosis Bradypnea, Hyporeflexia, pulmonary Opioids (eg, heroin, morphine,
coma apnea edema, needle marks methadone, oxycodone,
characteristic; hydromorphone),
may develop: diphenoxylate
hypothermia,
bradycardia,
hypotension
Sedative-hypnotic CNS depression, Variable Often normal, Hyporeflexia Benzodiazepines, barbiturates,

confusion, stupor, but may carisoprodol, meprobamate,
coma develop: glutethimide, alcohols,
hypothermia, zolpidem
bradycardia,
hypotension,
apnea,
bradypnea
Cholinergic Confusion, coma Miosis Bradycardia, Salivation, urinary and Organophosphate and
hypertension fecal incontinence, carbamate insecticides, nerve
or diarrhea, emesis, agents, nicotine, pilocarpine,
hypotension, diaphoresis, lacrimation, physostigmine, edrophonium,
tachypnea or GI cramps, bethanechol, urecholine
bradypnea bronchoconstriction,
muscle fasciculations and
weakness, seizures
Serotonin Confusion, Mydriasis Hyperthermia, Tremor, myoclonus, MAOIs alone or with: SSRIs,
syndrome agitation, coma tachycardia, hyperreflexia, clonus, meperidine,
hypertension, diaphoresis, flushing, dextromethorphan, TCAs, L-
tachypnea trismus, rigidity, diarrhea tryptophan
LSD: lysergic acid diethylamide; MDMA: 3,4-methylenedioxymethamphetamine; MDEA: methylenedioxymethamphetamine; CNS: central
nervous system; GI: gastrointestinal; MAOI: monoamine oxidase inhibitor; SSRI: selective serotonin reuptake inhibitor; TCA: tricyclic
antidepressant.
Graphic 71268 Version 21.0
Drug- and toxin-associated odors
Odor Agent(s)
Acetone (fruity) Ethanol, isopropyl alcohol, chloroform, salicylates
Bitter almonds Cyanide
Garlic Arsenic, organophosphates, phosphorus, thallium, selenium
Mothballs Naphthalene, paradichlorobenzene
Kerosene (petroleum distillate) Organophosphates, parathion
Freshly mown hay Phosgene
Rotten eggs Hydrogen sulfide
Wintergreen Methyl salicylate
Drug- and toxin-induced ocular abnormalities
Mydriasis Miosis Nystagmus

Sympathomimetics Opioids Barbiturates
Cocaine Heroin Carbamazepine
Caffeine Morphine
Phencyclidine
Ephedrine Fentanyl
Phenytoin
Amphetamines Hydromorphone
Methylphenidate Oxycodone
Lithium
Cathinones Hydrocodone Ethanol
Anticholinergics Codeine Toxic alcohols

Atropine Propoxyphene
Organophosphates
Scopolamine Sedative-hypnotics
Scorpion stings
TCAs Barbiturates
Strychnine
Antihistamines Benzodiazepines
Antiparkinson agents Alcohols (with deep coma) MAOIs
Muscle relaxants Zolpidem and related medications Serotonin syndrome

Antispasmodics Cholinergics Ketamine
Phenothiazines (some) Nerve agents
Plants (with belladonna alkaloids) Organophosphate insecticides
Hallucinogens Carbamate insecticides
LSD Pilocarpine
Mescaline Edrophonium
Psilocybin Physostigmine
Designer amphetamines Sympatholytics
Miscellaneous Clonidine
Glutethimide Oxymetazoline
MAOIs Tetrahydrazoline
Nicotine Antipsychotics
Serotonin syndrome Miscellaneous
Drug withdrawal states Phencyclidine
Drug- and toxin-induced movement disorders
Seizures Tremors/myoclonus Choreoathetosis

Propranolol Lithium Cocaine
Insecticides (eg, organophosphates, Antipsychotics Anticholinergics

carbamates) TCAs
Sympathomimetics
Lidocaine and other local anesthetics Cocaine Antihistamines
Sympathomimetics Theophylline Antiepileptics
Cocaine Amphetamines Phenytoin
Amphetamines Caffeine Carbamazepine
Theophylline Albuterol
Weakness/paralysis
Caffeine Methylphenidate
Barium (hypokalemia)
Nicotine Cathinones
Magnesium
Withdrawal from GABA agonists or Anticholinergics
Carisoprodol Antihistamines Solvent abuse
Antidepressants TCAs Toluene
TCAs Drug withdrawal states Gasoline
Bupropion Heavy metals

Carisoprodol
Citalopram Mercury
Heavy metals
Escitalopram Thallium
Fluvoxamine Rigidity/parkinsonism Insecticides
Venlafaxine Antipsychotics (neuroleptics) Organophosphates
Amoxapine Carbamates
Metoclopramide
Maprotiline
Amoxapine Nicotine
Antipsychotics
Carbon monoxide (delayed) Botulism
Phenothiazines
Methanol Neurotoxic snake envenomation
Clozapine
Ethylene glycol Tick paralysis
Salicylates
Phencyclidine Seafood poisoning
Camphor
Paralytic shellfish
Isoniazid MAOIs
Pufferfish (fugu)
Chemical nerve agents (eg, soman, VX) Serotonin syndrome
Lithium Black widow spider bite
Hypoglycemic agents Lithium
Cyanide Methaqualone
Carbon monoxide MPTP (designer meperidine)
Meperidine Manganese
Propoxyphene Strychnine
Orphenadrine Carbon disulfide
Antihistamines (rare) Cyanide
Lindane Malignant hyperthermia
Gyromitra-containing mushrooms Neuroleptic malignant syndrome
Heavy metals Postanoxic injury from any agent
Antimicrobials
Imipenem
Penicillins
Drug- and toxin-induced mental status alterations
Central nervous system depression Agitation

Anticholinergics Amantadine
Antihistamines Sympathomimetics
Belladonna alkaloids Amphetamines
Phenothiazines Cocaine
Antidepressants Caffeine
Cyclic antidepressants Phenylpropanolamine
Selective serotonin reuptake inhibitors Theophylline
Monoamine oxidase inhibitors Cathinones
Antipsychotics Anticholinergics
Simple asphyxiants Antihistamines
Carbon dioxide Atropine
Inert gases Scopolamine

Antiparkinson agents
Cellular asphyxiants
Antispasmodics
Carbon monoxide
Muscle relaxants
Cyanide
Plants containing belladonna alkaloids
Hydrogen sulfide
Phenothiazines
Methemoglobinemia
Tricyclic antidepressants
Lithium
Salicylates
Cholinergics
Central hallucinogens
Organophosphates
Lysergic acid diethylamide (LSD)
Carbamates
Phencyclidine
Sympatholytics
Mescaline
Beta blockers
Psilocybin
Sedative-hypnotics Ketamine
Benzodiazepines Designer amphetamines
Barbiturates Synthetic cannabinoids
Alpha-2 adrenergic agonists (eg clonidine, dexmedetomidine) Drug withdrawal states
Muscle relaxants Lithium
Hypoglycemic agents Carbon monoxide
Heavy metals Hypoglycemic agents
Opiates Heavy metals
Antiepileptics
Mushrooms
Salicylates
Gamma-hydroxybutyrate
Volatile inhalants
Alcohols
Drug- and toxin-induced skin abnormalities
Red and flushed Pale and diaphoretic Cyanotic Desquamation

Anticholinergic agents Sympathomimetics Methemoglobinemia Stevens-Johnson syndrome
Antihistamines Cocaine Sulfhemoglobinemia Toxic epidermal necrolysis
TCAs Amphetamines
Hypoxemia Boric acid
Atropine Theophylline
Heavy metals
Scopolamine Caffeine
Arsenic
Belladonna alkaloids Ephedrine
Mercury
Phenothiazines Phenylpropanolamine
Thallium
Boric acid Cathinones
Disulfiram reaction Cholinergic agents
Disulfiram/ethanol Organophosphates
Cephalosporins/ethanol Carbamates
Solvents/ethanol Nerve agents
Coprinus mushrooms/ethanol Central hallucinogens
Monosodium glutamate Lysergic acid diethylamide

(LSD)
Scombroid fish poisoning
Phencyclidine
Rifampin Mescaline
Carbon monoxide (rare) Psilocybin
Designer amphetamines
Synthetic cannabinoids
Arsenic
Salicylates
Drug- and toxin-induced temperature abnormalities
Hyperthermia Hypothermia
Increased heat production Opioids
Muscular hyperactivity/rigidity Sedative-hypnotics
Sympathomimetics Benzodiazepines
Barbiturates
Cocaine
Alcohols
Amphetamines
Phenylpropanolamine Sympatholytics
Ephedrine Beta blockers
Cathinones Clonidine
Anticholinergics Alpha-adrenergic antagonists
Drug withdrawal states Hypoglycemic agents
Lithium Antipsychotics
Central hallucinogens General anesthetic agents
Phencyclidine Carbon monoxide
Lysergic acid diethylamide (LSD) Drugs which cause flaccid coma

Designer amphetamines (MDMA, MDEA)
Synthetic cannabinoids
Drugs causing recurrent seizures

Isoniazid
Theophylline
Phenethylamines
Strychnine
Neuroleptic malignant syndrome
Serotonin syndrome
MAO inhibitors
Malignant hyperthermia
Impaired heat dissipation
Impaired sweating
Anticholinergic agents
Antihistamines
Phenothiazines
Tricyclic antidepressants
Increased metabolic rate
Uncoupled oxidative phosphorylation

Salicylates
Dinitrophenol, pentachlorophenol
Thyroid hormone
Drug- and toxin-induced changes in blood pressure and pulse
Hypertension with Hypertension with Hypotension with Hypotension with

tachycardia bradycardia tachycardia bradycardia
Sympathomimetics Alpha-adrenergic agonists Beta-adrenergic agonists Beta-blockers
Amphetamines Phenylpropanolamine Theophylline Calcium-channel blockers
Cocaine Phenylephrine Albuterol
Cardiac glycosides
Ephedrine Phentermine Isoproterenol
Digoxin
Pseudoephedrine Ergot alkaloids Terbutaline
Digitalis purpurea
Theophylline Caffeine
Sumatriptan Oleander
Caffeine Disulfiram reaction (late)
Clonidine (early) Red squill
Methylphenidate
Toxic alcohols Bufotenin
Cathinones
Guanfacine
Isopropyl alcohol Clonidine
Anticholinergics Imidazolines
Carbon monoxide Alpha-methyldopa
Antihistamines Tetrahydrozoline
Alpha-adrenergic antagonists Cyanide
TCAs (early) Oxymetazoline
Phenothiazines
Phenothiazines (some) Cholinergic agents Carbon monoxide (late)
TCAs
Antiparkinson agents Organophosphates Opioids
Hydralazine
Muscle relaxants Carbamates
Sedative-hypnotics
Clozapine
Heavy metals (acute)
Steroid hormones
Barbiturates
Iron
Central hallucinogens Glucocorticoids Benzodiazepines
Arsenic
Designer amphetamines Mineralocorticoids
Cholinergics
Lysergic acid diethylamide
Colchicine
Estrogen
Organophosphates
(LSD) Nitrates
Progesterone
Carbamates
Phencyclidine (PCP)
Androgens Sodium nitroprusside
Synthetic cannabinoids Antiarrhythmics
Yohimbine
Envenomations
Heavy metals
Black widow spider bite
Lead
Scorpion stings
Disulfiram reaction (early)
Drug withdrawal states
MAOIs (foods with tyramine)
Nicotine
Cholinergic agents
(sometimes)
Organophosphates
Carbamates
Thyroid hormone
Drugs and toxins associated with respiratory dysfunction
Tachypnea/hyperventilation Bradypnea/hypoventilation
Sympathomimetics CNS depressants
Amphetamines Opioids
Cocaine Sedative-hypnotics
Caffeine Alcohols
Theophylline Antidepressants
Nicotine Antipsychotics
Cathinones Sympatholytics
Central hallucinogens Volatile inhalants (solvents)
Lysergic acid diethylamide (LSD) Cholinergics
Phencyclidine Muscle relaxants
Designer amphetamines Antiepileptics
Synthetic cannabinoids Respiratory muscle failure
Anticholinergics Botulism
Carbamates
Drug withdrawal states
Neurotoxic snake envenomation
Salicylates
Neuromuscular blocking agents
Dinitrophenol, pentacholorphenol Organophosphates
Drug-associated hepatic failure Paralytic shellfish poisoning (saxitoxin)
Acetaminophen Puffer fish poisoning (tetrodotoxin)
Amanita mushrooms Strychnine
Cellular asphyxiants Tetanus
Carbon monoxide
Cyanide
Hydrogen sulfide
Methemoglobinemia
Toxins that induce pulmonary edema

Opioids
Pulmonary irritants
Drugs that induce metabolic acidosis (respiratory

compensation)
Methanol
Ethylene glycol
Alcoholic ketoacidosis
Iron
Isoniazid
Drug- and toxin-induced electrocardiographic abnormalities
Bradycardia/AV Supraventricular Ventricular QRS and QT interval

blockade tachycardia tachycardia prolongation
Beta blockers Sympathomimetics Sympathomimetics Antidepressants
Calcium channel blockers Amphetamines Cocaine Citalopram

Cocaine Amphetamines Escitalopram
Cardiac glycosides
Theophylline Theophylline Venlafaxine
Digoxin
Caffeine Antidepressants Desvenlafaxine
Digitoxin
Methylphenidate TCAs Tricyclic antidepressants
Red squill
Ephedrine Antipsychotics
Digitalis lanata Antipsychotics
Pseudoephedrine
Digitalis purpurea Phenothiazines Antihistamines
Albuterol
Bufotenin Chlorinated hydrocarbons Diphenhydramine
Dobutamine
Oleander Chloral hydrate Astemizole
Epinephrine
Alpha-adrenergic agonists Solvents Terfenadine
Dopamine
Phenylpropanolamine Fluoride Antiarrhythmics
Anticholinergics
Clonidine Quinidine
Antihistamines
Cardiac glycosides
Imidazolines Disopyramide
TCAs Potassium
Cholinergics Procainamide
Phenothiazines
Organophosphates Propafenone
Clozapine
Carbamates Flecainide, encainide
Atropine
Amiodarone
Opioids Scopolamine
Calcium channel blockers
Sedative-hypnotics Thyroid hormone (rare)
Magnesium Cellular asphyxiants Beta blockers (rare)
Carbon monoxide Propoxyphene
Drug withdrawal states Organophosphate

insecticides
Antimicrobials
Amantadine
Azithromycin
Chloroquine
Erythromycin
Pentamidine
Quinine
Quinolones (eg, ciprofloxacin)
Arsenic
Thallium
Fluoride
Citrate
Lithium
Agents possibly radiopaque on plain x-ray
C Chlorinated hydrocarbons (eg, chloral hydrate, carbon tetrachloride)
Calcium salts (eg, calcium carbonate)
Crack vials
H Heavy metals (eg, iron, arsenic, mercury, thallium, lead)
I Iodinated compounds (eg, thyroxine)
P Psychotropics (eg, phenothiazines, lithium, cyclic antidepressants)
Packets of drugs (eg, cocaine and heroin "body packers")
Play-Doh
Potassium salts
E Enteric-coated tablets (eg, aspirin)
S Salicylates
Sodium salts
Sustained-release preparations
Abdominal radiograph in iron overdose
Abdominal radiograph showing radiopaque iron (ferrous sulfate) tablets

visualized in the stomach of an intentional overdose patient (arrow).
Courtesy of Michael J Burns, MD.
Drug packet ingestion
Abdominal radiograph showing radiopaque drug packets ingested by a "body

packer."
Courtesy of Michael J Burns, MD.
Agents associated with noncardiogenic pulmonary edema
Irritant gases Opiates

Ammonia Heroin
Chlorine Methadone
Hydrogen sulfide Sedative-hypnotics
Nitrogen oxides Ethchlorvynol
Phosgene
Smoke
Cyanide
Sulfur dioxide
Carbon monoxide
Metal oxides
Salicylates
Acid and alkaline gases
Aldehydes
Organophosphates
Isocyanates Phencyclidine
Polymers Paraquat
Volatile inhalants (hydrocarbons) Ethylene glycol
Gasoline
Heavy metals
Kerosene
Sympathomimetics
Butane
Beta blockers
Beryllium
Calcium-channel blockers
Any agent that causes prolonged hypoxia or hypotension may result in the acute respiratory distress syndrome.
Chest radiograph of acute respiratory distress syndrome (ARDS) following trauma
Chest radiograph demonstrates extensive diffuse bilateral pulmonary consolidation in a patient with ARDS following trauma. The
patient is intubated.
Toxic time bombs (delayed clinical toxicity)
Acetaminophen Drug packet ingestion (heroin, cocaine)
Pennyroyal oil Oral hypoglycemic agents
Carbon tetrachloride Diphenoxylate
Mushrooms Methylene chloride

Amanita (amatoxin) Paraquat/diquat
Lepiota (amatoxin)
Cyanogenic glycosides
Gyromitra (gyromitrin)
Flouride
Cortinarius (orellanine/orelline)
Warfarin/superwarfarin
Toxic alcohols
Brodifacoum
Ethylene glycol
Methanol
Neurotoxic snake envenomation
Sustained-release preparations Antimetabolites
Calcium-channel blockers Colchicine
Beta-blockers Methotrexate
Lithium Alkylating agents
Theophylline Fat-soluble organophosphate insecticides
Enteric-coated preparations Ergotamines

Aspirin Heavy metals
Monoamine oxidase inhibitors Lead
Thallium
Mercury
Urine testing for drugs of abuse (addictive drugs)
Drugs causing false-positive

Drug Duration of detectability in urine
preliminary urine screens
Amphetamines 2 to 3 days Ephedrine, pseudoephedrine, phenylephrine,

selegiline, chlorpromazine, trazodone, bupropion,
desipramine, amantadine, ranitidine
Cocaine 2 to 3 days Topical anesthetics containing cocaine
Marijuana 1 to 7 days (light use); 1 month with chronic Ibuprofen, naproxyn, dronabinol, efavirenz, hemp
moderate to heavy use seed oil
Opiates 1 to 3 days Rifampin, fluoroquinolones, poppy seeds, quinine

in tonic water
Phencyclidine 7 to 14 days Ketamine, dextromethorphan
Adapted from: Tests for drugs of abuse. The Medical Letter 2002; 44:71.
Summary of urine drug testing assays
Time frame
for positive urine
assay with acute False positives
Substance
Drug exposure* (false positivity Comments
detected
(time frame for varies by assay)
chronic exposure in
parentheses)
Amphetamine 1 to 2 days (2 to 4 days) Amphetamine Amphetamine assays have Many assays include MDMA
molecule poor specificity due to and methamphetamine, but
structural similarity of many this varies by manufacturer.
drugs, herbal supplements, Refer to manufacturer's
and medications. literature.
False positives result from Over 100 "designer"
structurally similar amphetamines exist, dozens
substances, drugs that are of which are widely available
metabolized to structurally for purchase on the internet.
similar molecules in vivo, These may not be detected
and structurally dissimilar by routine screening.
molecules. Atomoxetine and
Nasal decongestants, methylphenidate are not
including l- detected by routine
methamphetamine, screening.
phenylephrine,
pseudoephedrine; herbal
products, including
ephedrine, synephrine;
amphetamine analogues;
medications including
bupropion, selegiline,
propranolol, atenolol.
Benzodiazepines 1 to 5 days (most) Oxazepam Oxaprozin Due to poor sensitivity of

2 to 30 days for diazepam (most common) assays, not recommended
Various as a urine immunoassay in
Chronic use does not
benzodiazepine the emergency setting.
significantly alter window of
detection metabolites No single assay is known to
detect all benzodiazepines.
Depending on metabolites
detected, commonly used
benzodiazepines such as
alprazolam and lorazepam
might not be detected.
"Z" drugs (eszopiclone,
zaleplon, zolpidem,
zopiclone) are not detected
by benzodiazepine
screening.
Detection depends on half-
life of metabolites, which is
generally several days, but
for diazepam and
chlordiazepoxide may be >1
week.
Cocaine 2 days (7 days) Benzoylecgonine Coca tea, Coca leaves Cocaine assays have high
(cocaine specificity and overall
metabolite) accuracy.
GHB <24 hours GHB Endogenous Detection is difficult because

neurotransmitter naturally of brief half-life and
technical problems.
Chronic use does not present in minute GHB detection is possible
significantly alter detection quantities. but requires specific assay.
Congeners GBL and 1,4
butanediol are detected by
GHB screening.
Often included as part of
date rape screening panel.
Ketamine 1 to 3 days Ketamine, Not detected by routine

norketamine screening assays, must be
ordered as a standalone
test.
LSD 1 to 3 days 2-oxo-3- Not commonly used in

hydroxyLSD clinical settings.
(LSD
metabolite)
Marijuana 1 to 3 days (>1 month) 11-nor-9- Hemp-containing foods. False positive urine testing
carboxy-delta9- Early, rare reports of false due to secondhand smoke
THC (THC positives from NSAIDs exposure is considered
metabolite) associated with assays that impossible.
are no longer in use. Consumption of hemp-
containing foods is
extremely unlikely to cause
a positive test.
Differentiation between
positive tests from
marijuana use and hemp oil
is generally not possible.
No longer recommended as
a required urine
immunoassay due to the
extended time frame for a
positive test and lack of
evidence of relevant acute
adverse effects.
Synthetic cannabinoids that
are widely abused are not
detected by routine urine
assays.
Opioids 1 to 3 days Codeine or Poppy seeds In recognition that poppy

morphine seed consumption may
cause positive tests, the
threshold for detection in
urine was substantially
raised. Using the
recommended threshold,
poppy seed consumption is
unlikely to cause positive
results. However, not all
institutions use the
recommended threshold.
Routine opioid screening
does not detect synthetic
opioids, such as
buprenorphine, fentanyl,
methadone, meperidine,
pentazocine, propoxyphene,
tramadol, and loperamide.
Oxycodone is poorly
detected by many routine
opioid screening assays.
Specific assays are required.
Methadone 1 to 5 days Methadone Doxylamine Due to problems with
EDDP (methadone noncompliance and diversion,
metabolite) assays detect both methadone
and the methadone metabolite
EDDP.
Noncompliant patients who are
diverting their methadone to
other abusers commonly try to
add methadone to their urine
samples to demonstrate
compliance.
Propoxyphene 3 to 10 days Norpropoxyphene

(propoxyphene
metabolite)
PCP 4 to 7 days PCP Dextromethorphan, Dozens of congeners of PCP

diphenhydramine, with similar clinical effects
doxylamine, ketamine, exist, and these are variably
tramadol, and venlafaxine detected or not detected by
PCP screening.
Many causes of false-
positive screening exist, and
due to the low prevalence of
PCP use in most settings,
the likelihood of a true
positive test is low.
GHB: gamma-hydroxybutanoic acid; GBL: gamma-butyrolactone; LSD: lysergic acid diethylamide; THC: tetrahydrocannabinol; NSAIDs:
nonsteroidal antiinflammatory drugs; PCP: phencyclidine.
*Generally, screening tests for particular drugs become positive within minutes to hours once the drug becomes bioavailable.
Courtesy of Robert J Hoffman, MD.
Quantitative drug levels that may direct therapy
Acetaminophen
Carboxyhemoglobin
Methemoglobin
Digoxin
Lithium
Theophylline
Salicylate
Paraquat
Iron
Methanol
Ethylene glycol
Antiepileptic agents
Carbamazepine
Phenytoin
Valproic acid
Heavy metals
Lead
Mercury
Drug- and toxin-induced electrolyte abnormalities
Hyperkalemia Hyperglycemia
Cardiac glycosides Beta-adrenergic agonists
Fluoride Albuterol
Theophylline
Hypokalemia
Epinephrine
Beta-adrenergic agonists Caffeine
Albuterol Calcium channel blockers
Theophylline
Iron
Epinephrine
Vacor (rodenticide)
Methylphenidate
Caffeine Hypoglycemia
Diuretics Ackee fruit (unripe)
Toluene Beta blockers
Barium Insulin
Hypocalcemia Oral hypoglycemic agents
Ethylene glycol Ethanol
Oxalate Quinine
Fluoride Salicylate
Drugs and toxins capable of causing rhabdomyolysis, hepatotoxicity, or methemoglobinemi

a
Rhabdomyolysis Hepatotoxicity Methemoglobinemia

Sympathomimetics Acetaminophen Nitrates
Cocaine Ethanol Nitroglycerin
Amphetamines Well water
Amanita mushrooms
Cathinones Silver nitrate
Isoniazid
Anticholinergics Nitrites
Phenytoin
Central hallucinogens Amyl nitrite
Halogenated hydrocarbons (Iso)butyl nitrite
Phencyclidine
Carbon tetrachloride
LSD Trinitrotoluene
Designer amphetamine
Heavy metals
Aniline dyes
Synthetic cannabinoids Iron
Phenazopyridine
Neuroleptics (NMS) Gyromitra mushrooms
Chlorates
Malignant hyperthermia Paraquat
Dapsone
Serotonin syndrome Phenylbutazone
Hydrazines
Ethanol Phosphorus (yellow)
Local anesthetics
Toluene Methotrexate
Benzocaine
Isoniazid Rifampin Lidocaine
Strychnine Oral contraceptives Prilocaine
Antidepressants Vinyl chloride Phenacetin
Sedative-hypnotics Androgens Toluidine
Snake bite Alpha-methyldopa Toluenediamine
Tetanus Halothane Sulfonamides
Opioids Valproic acid Aromatic amines
Toxic alcohols Tetracycline Nitrobenzene
Cellular asphyxiants Erythromycin estolate Chloroquine
Corticosteroids Dimethylformamide Primaquine
Any agent that causes extreme Allopurinol Naphthalene

agitation, hyperthermia, seizures, Sulfonamides Nitroprusside
prolonged coma
Pennyroyal oil Chlorobenzene
Salicylates Nitrous gases (arc welders)
Chlorpromazine Metoclopramide
Troglitazone Phenols
Pyrrolizidine alkaloids (plants) Pyridine
Nitrofurantoin Arsine
Drug- and toxin-induced alterations in the anion gap
Increased anion gap with Increased anion gap with Decreased anion gap
metabolic acidosis metabolic acidosis (<6 meq/L)
(>13 meq/L)* (>13 meq/L) (cont) Hypermagnesemia
Methanol Salicylates Hypercalcemia
Ethylene glycol Dinitrophenol Bromide
Ethanol (alcoholic ketoacidosis) Inorganic acid Nitrates
Salicylates Metformin Lithium
Isoniazid Phenformin Iodide
Iron Paraldehyde Spironolactone
Glycol ethers Formaldehyde Ammonium chloride
NSAID Toluene Acetazolamide
Ketoprofen Sulfur (elemental)
Naproxen
Colchicine
Phenylbutazone
Fluroacetate
Sympathomimetics
Cocaine
Carbon monoxide
Theophylline
Cyanide
Caffeine
Hydrogen sulfide
Cathinones
Methemoglobinemia
Albuterol
Propylene glycol
Benzyl alcohol
Phenol
Strychnine
Vacor
* Any poison causing seizure, hypoxemia, shock (hypotension), cellular anoxia, or rhabdomyolysis will result in a high anion gap
metabolic acidosis from increased serum lactic acid concentrations.
Increased osmolal and oxygen saturation gaps
Increased osmolal gap (normal 5 ± 7 [SD] Increased oxygen saturation gap (>5 percent
m0sm/L) difference)
Acetone Carbon monoxide
Ethanol Cyanide
Ethylene glycol Sulfhemoglobinemia
Glycerol Hydrogen sulfide
Hypermagnesemia (>9.5 mEq/L) Methemoglobin
Isopropyl alcohol
Mannitol
Methanol
Propylene glycol
Benzyl alcohol
Sorbitol
Ethyl ethers
Glycol ethers
Criteria for ICU admission of poisoned patient
CNS depression, including significant lethargy, coma
Agitation requiring chemical or physical restraint
Respiratory depression (PCO2 >45 mmHg), hypoxia or respiratory failure (ARDS), and/or endotracheal intubation
Hypotension (SBP ≤80 mmHg)
Seizures that are prolonged or recurring
Second or third degree AV block on ECG
Nonsinus cardiac rhythm on ECG
Significant acid-base disturbances (eg, metabolic acidosis with pH ≤7.2)
Significant metabolic abnormalities requiring close monitoring or aggressive correction (eg, symptomatic hypoglycemia following
sulfonylurea or insulin overdose)
Extremes of temperature (eg, hyperthermia with T >104°F)
Poisoning with a "toxic time bomb"

Ingested drug packets, sustained-release preparations
Quantitative level of drug which predicts unfavorable outcome
Need for invasive hemodynamic monitoring (eg, pulmonary artery catheter or arterial line) or cardiac pacing
Need for whole bowel irrigation to enhance GI elimination of poison
Need for emergency hemodialysis, hemoperfusion, hemofiltration
Need for emergency antidote which requires close monitoring (eg, crotalid antivenin, Digibind, physostigmine, naloxone drip)
Ischemic chest pain from toxin (eg, cocaine, carbon monoxide)
TCA or other drug exposure with QRS >120 msec or QTc >500 msec

General Approach To Drug Poisoning in Adults - UpToDate

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7/8/2020 General approach to drug poisoning in adults - UpToDate

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INITIAL EVALUATION AND TREATMENT

Diagnosis of a poisoning may be assisted by the following physical findings [21,23]:

● Characteristic odors (table 2)

Electrocardiography — Electrocardiographic abnormalities may provide diagnostic and prognostic

Decontamination — Following initial patient stabilization, patient decontamination may be performed if

● Bradyarrhythmia – Bradyarrhythmias associated with hypotension should be treated in the standard

● Hyperthermia – Severe hyperthermia secondary to drug toxicity (eg, sympathomimetic overdose,

● PaCO2 >45 mmHg

SOCIETY GUIDELINE LINKS

SUMMARY AND RECOMMENDATIONS

● Physical examination – Perform a thorough physical examination to ascertain signs of a potential

Diagnosis of a poisoning may be assisted by the following physical findings:

• Characteristic odors (table 2)

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Topic 324 Version 24.0

Common poisoning syndromes (toxidromes)

Mental Other Examples of toxic

Sympathomimetic Hyperalert, Mydriasis Hyperthermia, Diaphoresis, tremors, Cocaine, amphetamines,

Hallucinogenic Hallucinations, Mydriasis Hyperthermia, Nystagmus Phencyclidine, LSD, mescaline,

Sedative-hypnotic CNS depression, Variable Often normal, Hyporeflexia Benzodiazepines, barbiturates,

Graphic 71268 Version 21.0

Drug- and toxin-associated odors

Acetone (fruity) Ethanol, isopropyl alcohol, chloroform, salicylates

Bitter almonds Cyanide

Garlic Arsenic, organophosphates, phosphorus, thallium, selenium

Mothballs Naphthalene, paradichlorobenzene

Kerosene (petroleum distillate) Organophosphates, parathion

Freshly mown hay Phosgene

Rotten eggs Hydrogen sulfide

Wintergreen Methyl salicylate

Graphic 76045 Version 3.0

Drug- and toxin-induced ocular abnormalities

Mydriasis Miosis Nystagmus

Cathinones Hydrocodone Ethanol

Anticholinergics Codeine Toxic alcohols

Muscle relaxants Zolpidem and related medications Serotonin syndrome

Graphic 61723 Version 8.0

Drug- and toxin-induced movement disorders

Seizures Tremors/myoclonus Choreoathetosis

Insecticides (eg, organophosphates, Antipsychotics Anticholinergics

Sympathomimetics Theophylline Antiepileptics

Cocaine Amphetamines Phenytoin

Amphetamines Caffeine Carbamazepine

Antidepressants TCAs Toluene

TCAs Drug withdrawal states Gasoline

Bupropion Heavy metals

Lithium Black widow spider bite

Hypoglycemic agents Lithium

Carbon monoxide MPTP (designer meperidine)

Orphenadrine Carbon disulfide

Antihistamines (rare) Cyanide

Lindane Malignant hyperthermia

Gyromitra-containing mushrooms Neuroleptic malignant syndrome

Heavy metals Postanoxic injury from any agent

Graphic 64472 Version 10.0

Drug- and toxin-induced mental status alterations

Central nervous system depression Agitation

Simple asphyxiants Antihistamines

Carbon dioxide Atropine

Inert gases Scopolamine