Once calm, effective communication is established, the health care provider
should first determine whether the patient is conscious and breathing and has a pulse.
If life-threatening symptoms have occurred, the caller should call 9-1-1 for
emergency services. If the health care provider does not have the knowledge or
resources to provide poison information, he or she should refer the caller to the
closest poison control center. Information on the location and phone number of the
nearest poison control center can be found at http://www.aapcc.org or by calling 1-
800-222-1222 in the United States.
Management of poisoned or overdosed patients is primarily based on symptomatic
and supportive care. Specific antidotes exist only for a small percentage of the
thousands of potential drugs and chemicals that can cause a poisoning.
The first aspect of patient management should always be basic support of airway,
breathing, and circulation (the “ABCs”). The assessment and treatment of the
potentially poisoned patient can be separated into seven primary functions: (a)
gathering history of exposure, (b) evaluating clinical presentation (i.e.,
“toxidromes”), (c) evaluating clinical laboratory patient data, (d) removing the toxic
source (e.g., irrigating eyes, decontaminating exposed skin), (e) considering antidotes
and specific treatment, (f) enhancing systemic clearance, and (g) monitoring
Comprehensive historical information about the toxic exposure should be gathered
from as many different sources as possible (e.g., patient, family, friends, prehospital
health care providers). This information should be compared for consistency and
evaluated relative to clinical findings and laboratory results. The patient’s history of
the exposure is often inaccurate and should be confirmed with objective
22,23,25 For example, a patient who presents to an ED with a supposed
hydrocodone and carisoprodol overdose is expected to be lethargic or comatose. If
the patient arrives wide awake with tachycardia and agitation, the clinician should
suspect exposure to other substances.
Specific information should be sought concerning the patient’s state of
consciousness, symptoms, probable intoxicant(s), and maximal amount and dosage
form(s) of substance ingested, as well as when the exposure occurred. Medications,
allergies, and prior medical problems also should be ascertained to facilitate
development of treatment plans (e.g., a history of renal failure may indicate the need
for hemodialysis to compensate for decreased renal drug clearance).
EVALUATING CLINICAL PRESENTATION AND TOXIDROMES
A thorough physical examination is needed to characterize the signs and symptoms of
overdose, and it should be conducted serially to determine the evolution or resolution
of the patient’s intoxication. An evaluation of the presenting signs and symptoms can
provide clues to the drug class causing the toxicity, confirm the historical data
surrounding the toxic exposure, and suggest initial treatment.
asymptomatic on presentation, even though a potentially severe exposure has
occurred, if absorption of the drug or toxic substance is incomplete or if the
substance has not yet been metabolized to a toxic substance.
Characteristic toxidromes (i.e., a constellation of signs and symptoms consistent
with a syndrome) can be associated with some specific classes of drugs.
most common toxidromes are those associated with anticholinergic activity,
increased sympathetic activity, and central nervous system (CNS) stimulation or
depression. Anticholinergic drugs can increase heart rate and body temperature,
decrease gastrointestinal (GI) motility, dilate pupils, and produce drowsiness or
delirium. Sympathomimetic drugs can increase CNS activity, heart rate, body
temperature, and blood pressure (BP). Opioids, sedatives, hypnotics, and
antidepressants can depress the CNS, but the specific class of CNS depressant often
Classic findings may not be present for all drugs within a therapeutic class. For
example, opioids generally induce miosis, but
meperidine can produce mydriasis. Furthermore, the association of symptoms with
a particular class of toxic substances is difficult when more than one substance has
been ingested. Practitioners should not focus only on the specific clinical findings
associated with a toxidrome. Rather, they should consider all subjective and
objective data gathered from the history of exposure, the patient’s medical history,
physical examination, and laboratory findings.
INTERPRETATION OF LABORATORY DATA
A urine drug screen can be useful in identifying the presence of drugs and their
metabolites in selected patients but is not indicated in all cases of drug overdose.
Urine drug screens can be useful in a patient with coma of unknown etiology, when
the presented history is inconsistent with clinical findings, or when more than one
drug might have been ingested.
Pharmacokinetic Considerations
The absorption, distribution, metabolism, and elimination of drugs in the overdosed
patient can be quite different than when the drug is taken in usual therapeutic
29–31 The expected pharmacodynamic and pharmacokinetic features of drugs can
be substantially altered by large drug overdoses, especially with drugs that exhibit
dose-dependent pharmacokinetics. The rate of drug absorption is generally slowed
by large overdoses, and the time to reach peak serum drug concentrations can be
32,34 For example, peak serum concentrations of phenytoin can be delayed for
2 to 7 days after an orally ingested overdose.
35,36 The volume of distribution of an
overdosed drug can be increased, and when usual metabolic pathways become
saturated, secondary clearance pathways can be important. For example, large
overdoses of acetaminophen saturate glutathione mechanisms of metabolism,
When the pharmacokinetic parameters of an overdosed drug are altered, serial
plasma concentration measurements can better define the absorption, distribution, and
clearance phases of the ingested substance. Pharmacokinetic parameters that have
been derived from therapeutic doses should not be used to predict whether
absorption is complete or to predict the expected duration of intoxication caused by
After the airway and the cardiopulmonary system are supported, efforts should be
directed toward removing the toxic substance from the patient (i.e.,
22,40 Decontamination presumes that both the dose and the duration
of toxin exposure are important in determining the extent of toxicity and that
prevention of continued exposure will decrease toxicity.
29–31,40 This intuitive concept
is clearly relevant to ocular, dermal, and respiratory exposures, when local tissue
damage is the primary problem. Respiratory decontamination involves removing the
patient from the toxic environment and providing fresh air or oxygen to the patient.
Decontamination of skin and eyes involves flushing the affected area with large
volumes of water or saline to physically remove the toxic substance from the
Gastrointestinal Decontamination
Because most poisonings and overdoses result from oral ingestions, measures to
decrease or prevent continued GI absorption have commonly been used to limit the
22,23,37 GI decontamination should be considered if the ingestion is
large enough to produce potentially significant toxicity, or if the potential severity of
the ingestion is unknown and the time since ingestion is less than 1 hour. The
following methods have historically been used: (a) evacuation of gastric contents by
emesis or gastric lavage, (b) administration of activated charcoal as an adsorbent to
bind the toxic substance remaining in the GI tract, (c) use of cathartics or whole
bowel irrigation (WBI) to increase the rectal elimination of unabsorbed drug, or (d)
a combination of any of these methods.
The efficacy of GI decontamination varies, depending on when the process is
initiated relative to the time of ingestion, dose ingested, and other factors.
Furthermore, ipecac-induced emesis, gastric lavage, cathartics, and activated
charcoal are not directly associated with improved patient outcomes.
The most appropriate method for GI tract decontamination remains unclear
because sound comparative data for different methods of GI decontamination are not
available. Clinical research in healthy subjects, by necessity, must use nontoxic
doses of drugs. Studies using nontoxic doses are not applicable to the overdose
situation because alterations in GI absorption can occur with large doses. In addition,
low-dose studies generally rely on pharmacokinetic end points such as peak plasma
concentrations, area under the plasma concentration–time curve, or quantity of drug
In contrast, clinical studies of GI decontamination
methods in patients who have ingested toxic doses of a substance use clinical
outcomes or a directional change in serum drug concentrations.
trials are not standardized with respect to the dose ingested or to the time interval
between drug ingestion and GI decontamination.
Ipecac-Induced Emesis and Gastric Lavage
Ipecac-induced emesis and gastric lavage primarily remove substances from the
stomach. Their efficacy is affected significantly by the time the ingested substance
remains in the stomach. Gastric lavage and ipecac-induced emesis are most effective
when implemented before the substance moves past the stomach into the intestine
The commonly used adult gastric lavage tube (36F) has an internal diameter too
small to allow recovery of large tablet or capsule fragments. An even smaller
diameter lavage tube is used for children.
42 Gastric lavage may be useful only if large
amounts of a liquid substance were ingested and the patient arrived within 1 hour of
45 However, patients usually arrive in the ED more than an hour after
ingestion, when absorption of the toxin has most likely already occurred. As a result,
the efficacy of these procedures in overdose situations is minimal, and no studies
have confirmed that use of gastric lavage or ipecac-induced emesis improves the
41,42,47 For these reasons, ipecac is no longer used, and gastric
lavage is used only in rare, specific situations.
In 1963, a review article concluded that activated charcoal was the most valuable
agent available for the treatment of poisoning.
48 This conclusion was based only on
studies in fasting patients who had nontoxic exposures. Nevertheless, data from those
studies were extrapolated to poisoned patients. Since then, activated charcoal has
become the preferred method of GI decontamination for the treatment of toxic
The goal of the therapy is to decrease the absorption of the substance and reduce
43 Unfortunately, there are no satisfactorily designed
clinical studies assessing benefit from the use of activated charcoal to guide the use
of this therapy. There is also no evidence that the administration of activated
charcoal improves clinical outcomes.
The use of activated charcoal at a dose of 1 g/kg should be considered when the
patient has ingested a toxic substance that is known to be absorbed by activated
charcoal within 1 hour of the ingestion. The potential for benefit is unknown if the
activated charcoal is given more than 1 hour after ingestion.
iron and lithium are not absorbed by activated charcoal. Other forms of GI
decontamination must be used to remove those substances from the GI tract.
Generally the use of activated charcoal is safe. Although there are relatively few
reports of adverse effects from the use of activated charcoal, there are numerous
reports of complications, usually involving aspiration. It is essential that the patient
has an intact or protected airway (intubation) before activated charcoal is
administered, especially in drowsy patients or patients who may rapidly become
Vomiting with aspiration of activated charcoal occurs in about 5% of patients who
43,49–51 The resulting pulmonary problems can be caused by
aspiration of acidic stomach contents or the charcoal. Decreased oxygenation can
occur immediately, or pulmonary effects can occur later.
distress syndrome has resulted after the unintentional instillation of charcoal into the
51 Aspiration of charcoal can result in chronic lung disease or fatalities, whereas
the toxic exposure, for which the charcoal was administered, is often not lethal or
Historically, sorbitol (a cathartic) was often administered with activated charcoal to
enhance passage of the charcoal–substance complex through the GI tract. However,
decreased transit time through the bowel has not been proven to decrease absorption
because drug absorption does not take place in the large bowel.
associated with vomiting and aspiration.
44 Hypernatremia can also develop
subsequent to the administration of repeat doses of activated charcoal with
57,58 Currently, most EDs use aqueous activated charcoal mixtures rather than
charcoal–sorbitol combinations. Because cathartics are not effective in reducing drug
absorption or increasing patient outcome, their use is no longer advised.
WBI with a polyethylene glycol–balanced electrolyte solution (e.g., Colyte,
GoLYTELY) can successfully remove substances from the entire GI tract in a period
of several hours. WBI is effective with ingestions of sustained-release dosage forms,
as well as substances that form bezoars (concretions of tablets or capsules), such as
23,45,59 WBI is also indicated when the toxic agent is not
adsorbed by activated charcoal (e.g., body-packer packets, lithium, iron,
22,23,45,59 This method of GI decontamination takes much longer to complete
and is associated with poor patient compliance because large volumes of fluid (2
L/hour for adults until the effluent is clear) need to be ingested to be effective.
nasogastric (NG) tube can be inserted, and the WBI fluid can be administered via NG
tube so that lack of patient compliance is no longer a factor.
ANTIDOTES AND SPECIFIC TREATMENTS
An antidote is a drug that neutralizes or reverses the toxicity of another substance.
Some antidotes can displace a drug from receptor sites (e.g., naloxone for opioids,
flumazenil for benzodiazepines), and some can inhibit the formation of toxic
metabolites (e.g., N-acetylcysteine [NAC] for acetaminophen, fomepizole for
23,60,61 Some treatments are highly effective for the management of
individual drug overdoses but do not meet the definition of an antidote. For example,
sodium bicarbonate is used to treat the cardiotoxicity arising from tricyclic
antidepressant (TCA) overdoses, and benzodiazepines are used to treat CNS toxicity
associated with cocaine and amphetamine overdoses.
62–64 However, it is important to
note that for antidotes to be effective, they must be readily available at the health care
facility in adequate doses to treat the patient in a timely manner.
Hemodialysis and manipulation of urine pH can enhance the clearance of substances.
Hemodialysis can successfully treat some specific intoxications (e.g., methanol,
ethylene glycol, aspirin, theophylline, lithium). Hemodialysis can also be used in
patients with severe acid–base disturbances or renal dysfunction.
the urine can enhance the elimination of drugs such as aspirin and phenobarbital.
Selecting the appropriate parameters and length of time to monitor a patient who has
been exposed to a toxic agent requires knowledge of toxic effects and the time course
33,34 Most patients who are at risk for moderate or severe toxicity
should be monitored in an intensive care unit (ICU) with careful assessments of
cardiac, pulmonary, and CNS function.
ASSESSMENT OF SALICYLATE INGESTION
tablets. What additional information should be obtained from or given to A.J. at this time?
Obtaining an initial assessment of the patient’s status is essential. The caller’s
telephone number should be obtained in the event that the call is disconnected, initial
recommendations need to be modified, or subsequent follow-up is needed. The health
care provider should ask for patient-specific information with questions that are
nonthreatening and nonjudgmental. The caller should be reassured that calling for
help was the right thing to do.
Evaluating Clinical Presentation
CASE 5-1, QUESTION 2: On further questioning, A.J. states that R.J. is crying and complaining of a
assess the potential for toxicity in R.J.?
To determine the potential toxicity for an unintentional ingestion, it is important to
assess the presence of symptoms and to identify the substance ingested. Inquiries
should begin with open-ended questions to determine the facts that the caller is
certain of versus what may have been assumed. The answers usually point to more
specific information that is needed to accurately assess the exposure.
R.J’s symptoms presently are not life-threatening. His behavior is consistent with
being scared in response to the mother’s anxiety. Once it has been established that the
child does not need immediate life-saving treatment, the caller is generally more
willing and able to answer additional questions.
A.J. already has provided information about the child’s symptoms. More
information is needed to determine the identity of the ingested substance, the time of
units in a full container, and the number of remaining dosage units in the container.
The parent should be advised to look for tablets under beds, rugs, or other locations
out of sight (e.g., wastepaper baskets, toilets, pet food dishes, pockets). The dosage
forms in the container should be identical in appearance, and the contents should be
what are stated on the label. Information concerning the child’s weight and health
status, as well as whether the child is taking other medications, is also important. The
child’s weight is useful in determining the maximum milligram per kilogram dose of
When more than one child is present during an ingestion, the caller should be
questioned as to whether other children also could have participated in the ingestion.
In this situation, the children could have shared equally in the missing medication, all
of the drug could have been fed to one child, or all of the drug could have been
ingested by the oldest or most aggressive child. When it is unclear how much is
missing among a group of children, each child should be evaluated and managed as if
he or she may have ingested the total missing quantity.
treatment is needed for this child?
The maximal dose of aspirin ingested by this child is likely to be much less than
the minimal dose required to cause significant symptoms based on his weight for his
age (i.e., 42 pounds or approximately 19 kg). A dose of 150 mg/kg of aspirin is the
smallest dose at which treatment or assessment at a health care facility is
68,71 A.J. is likely to have ingested a maximum of 567 mg of aspirin (i.e.,
seven 81-mg tablets), which is about 29.8 mg/kg (567 mg divided by 19 kg). If this
child is healthy, takes no medications, and is not allergic to aspirin, the child does
not require any treatment. With this history of ingestion, the only adverse effect that
might occur is some mild nausea. Providing information to the mother that her child
had not ingested a toxic or dangerous amount will be reassuring.
For many years, aspirin was the most common cause of unintentional poisoning
and poisoning deaths among children.
71–73 However, safety closure packaging and
reduction of the total aspirin content in a full bottle of children’s aspirin to
approximately 3 g has steadily reduced the frequency of pediatric aspirin poisoning
72–74 Although acute aspirin poisoning remains a problem, the largest
percentage of life-threatening intoxications now results from therapeutic overdose.
Therapeutic overdoses occur when a dose is given too frequently, when both parents
unknowingly dose the child with the drug, or when too large a dose is given.
Therapeutic overdoses are especially problematic when excessive doses are given
for a prolonged period and the drug is able to accumulate.
Follow-up telephone consultation on toxic ingestions is important to identify children
who unexpectedly develop symptoms that might need to be treated. A telephone call
to A.J. 6 to 24 hours after her initial call would be appropriate to follow up on the
child. On a call back to A.J., the parent stated that she gave R.J. lunch at the
appropriate time. R.J. then watched cartoons, took his usual nap, and remained
QUESTION 1: A.S., a 71-year-old, 59-kg woman with a history of chronic headaches, has taken 10 to 12
Blood urea nitrogen (BUN), 38 mg/dL
Arterial blood gas (ABG) values (room air) were as follows: pH, 7.14; PCO2
Is A.S. at high risk because of her ingestion?
The symptoms and severity of salicylate intoxication depend on the dose
consumed; the patient’s age; and whether the ingestion was acute, chronic, or a
73,75,76 This case illustrates an acute ingestion in someone who
has also chronically ingested aspirin. Acute ingestion of 150 to 300 mg/kg of aspirin
is likely to produce mild-to-moderate intoxication, greater than 300 mg/kg indicates
severe poisoning, and greater than 500 mg/kg is potentially lethal.
ingested approximately 523 mg/kg, has taken a potentially lethal dose. Chronic
salicylate intoxication is usually associated with ingestion of greater than 100
mg/kg/day for more than 2 days.
68,71 A.S. has been taking 66 mg/kg/day for her
headaches in addition to her acute ingestion. A.S. demonstrates many of the findings
typical of severe acute salicylism (see Pathophysiology of Salicylate Intoxication and
Assessment of Toxicity sections). A.S.’s prognosis is potentially poor because she is
elderly and has taken a potentially lethal overdose of aspirin.
Pathophysiology of Salicylate Intoxication
Toxicity from salicylate exposure results in direct irritation of the GI tract, direct
stimulation of the CNS respiratory center, stimulation of the metabolic rate, lipid and
carbohydrate metabolism disturbances, and interference with hemostasis.
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