General Approach To Drug Poisoning in Adults

20/7/2017 General approach to drug poisoning in adults - UpToDate
Official reprint from UpToDate

www.uptodate.com 2017 UpToDate
General approach to drug poisoning in adults
Author: Sean H Rhyee, MD, MPH

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: Jun 2017. | This topic last updated: Aug 10, 2016.
INTRODUCTION Accidental and intentional poisonings or drug overdoses constitute a significant source
of aggregate morbidity, mortality, and health care expenditure worldwide. Millions of poisonings and drug
overdoses occur annually in the United States alone [1,2].
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). A topic devoted to the management of the critically ill patient with
an unknown overdose is found separately. (See "Initial management of the critically ill adult with an unknown
overdose".)
EPIDEMIOLOGY Accidental and intentional poisoning from both licit and illicit substances remains a major
cause of morbidity and mortality worldwide [3-7]. In the United States, the American Association of Poison
Control Centers (AAPCC) reported over 2.1 million human exposure calls in 2014. While the overall mortality
rate reported by the AAPCC was 0.07 percent, 28.3 percent of cases required management at a health care
facility and 7.9 percent of cases required hospital admission [2]. Between 2008 and 2011 in the United
States, 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 presenting with drug poisoning
required hospital admission, compared with 12.7 percent for non-poisoning related presentations [8]. Rates of
poisoning cases among ED patients appear similar in other industrialized nations [9].
As of 2008, poisoning has become the leading cause of injury-related death in the United States, surpassing
motor vehicle collisions. The majority of poisoning fatalities were related to drugs, with 36,500 cases in 2008
[10]; most overdoses involved prescription drugs [11]. Patients aged 35 to 54 years accounted for the highest
number of poisonings, but patients between the ages of 18 and 20 had the highest rate. 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 [12].
Among adults, the AAPCC reported the most common exposures were due to analgesics (11.3 percent),
sedatives and antipsychotics (5.9 percent), and antidepressants (4.4 percent). A review of a toxicology case
registry noted similar findings, with sedatives, analgesics and antidepressants accounting for the most
frequently mentioned exposures [13]. Reviews of self-poisoning cases in the United Kingdom and Spain
found that analgesics, benzodiazepines, and antidepressants were the most commonly encountered drugs
[9,14]. However, trends vary in other geographic regions. In a study of Norwegian patients, the most
prevalent drugs (aside from ethanol) were acetaminophen, opioids, and gamma hydroxybutyrate (GHB) [15].
A German study of intensive care unit (ICU) admissions found benzodiazepines, antidepressants and
antihistamines were the most commonly encountered drugs, again excluding ethanol [16]. A report of Israeli
poison center data found that antimicrobials were the most frequently reported drugs, second only to
analgesics (including opioids) [17].
https://www-uptodate-com.bibliotecavirtual.udla.edu.ec/contents/general-approach-to-drug-poisoning-in-adults/print?source=search_result&sear 1/32
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. 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 several coingestants. Initial management is focused on acute stabilization.
The history and physical examination are of great importance in recognizing that poisoning has occurred.
Management is directed to the provision of supportive care, prevention of poison absorption, and, when
applicable, the use of antidotes and enhanced elimination techniques [18].
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
vital signs, mental status, and pupil size, skin temperature and moisture, and perform pulse oximetry,
continuous cardiac monitoring, and an electrocardiogram. Obtain intravenous access and a finger-stick
glucose measurement. In patients with suspected occult trauma, maintain in-line cervical immobilization.
Assess the airway and perform endotracheal intubation if there is significant doubt about the patient's ability
to protect their airway and avoid aspiration. 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".)
Patients with altered consciousness should prompt administration of intravenous thiamine to prevent
Wernicke's encephalopathy and 25 g of dextrose (50 mL of a 50 percent solution) to treat hypoglycemia,
unless these diagnoses can be rapidly excluded. Administer intravenous naloxone to patients with signs,
symptoms, or a history suggestive of opioid intoxication [18,19]. (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
largely unsupported [20]. Uptake of thiamine into cells is slower than that of dextrose [21], 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, infection, or extremity
swelling. Measure the core body temperature. Patient decontamination should then be initiated (if indicated).
Obtain an electrocardiogram to assess for drug-related cardiotoxicity (see section on electrocardiogram
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 more detailed diagnostic evaluation can then ensue. (See
"Gastrointestinal decontamination of the poisoned patient".)
DIAGNOSIS OF POISONING The history, physical examination, and routine and toxicological 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 [22,23]. In
one prospective survey, the initial clinical history fully correlated with confirmatory testing in only 27 percent of
cases [24]. The patient's ability to provide a reliable history is often impaired by direct drug effects or
psychiatric illness [18]. 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, primary
care clinician, and pharmacist.
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 to which he or she could have had access may also 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) [18].
Physical examination The physical examination of symptomatic poisoned patients may provide
invaluable clues to the agent involved. The mental status, vital signs, and pupillary examination are the most
useful elements and allow classification of the patient into either a state of physiologic excitation or
depression [25].
Physiologic excitation, manifested by central nervous system stimulation and increased pulse, blood
pressure, respiratory rate and depth, and temperature, is most commonly caused by anticholinergic,
sympathomimetic, or central hallucinogenic agents, or by drug withdrawal states. (See "Anticholinergic
poisoning" and "Cocaine: Acute intoxication" and "Methamphetamine: Acute intoxication" and "Acute
amphetamine and synthetic cathinone (bath salt) intoxication" and "Phencyclidine (PCP) intoxication in
adults" and "Intoxication from LSD and other common hallucinogens" and "Management of moderate
and severe alcohol withdrawal syndromes".)
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, opiates, 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".)
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). However, a particular patient may not manifest all the
symptoms or findings typically associated with a given toxidrome. The diagnosis may be assisted by [18,26]:
Characteristic odors (table 2)
Pupillary findings (table 3)
Neuromuscular abnormalities (table 4)
Mental status alterations (table 5)
Skin findings (table 6)
Temperature alterations (table 7)
Blood pressure and heart rate alterations (table 8)
Respiratory disturbances (table 9)
Discrepancies between the physical examination and the history may reflect an inaccurate ingestion history
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) [27]. Particular attention should be paid to the duration of
the QRS and QTc intervals. Toxin-induced QRS interval prolongation, of the type seen with tricyclic
antidepressant poisoning, may warrant immediate intervention. (See "Tricyclic antidepressant poisoning".)
Radiographic studies Imaging studies are not required in every patient but may be useful in several
situations [28,29]:
Certain radiopaque toxins (summarized by the mnemonic "CHIPES") may be visualized by plain film
radiographs (table 11 and image 1).
Ingested drug packets of "body packers" may be seen on plain films (image 2). (See "Internal
concealment of drugs of abuse (body packing)".)
Abdominal ultrasound does not appear to be a reliable method of detecting ingested medications [30,31].
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).
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 [32]. 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 diagnosis" 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). These assays are inexpensive and provide rapid results, usually within one hour. Positive and negative
screens for drugs do not absolutely confirm or refute poisoning diagnoses and require further evaluation. As
an example, a negative screen may reflect a drug concentration below the threshold limit of detection due to
timing of the specimen before or after peak concentration. Conversely, high concentrations of certain drugs
may be due to a false positive result. As an example, diphenhydramine can cause false positive results in
assays screening for tricyclic antidepressants [33]. In some instances, a positive test may reflect an earlier
ingestion that does not account for the patient's presentation. Testing for drugs of abuse is reviewed in detail
separately. (See "Testing for drugs of abuse (DOA)" and "Clinical assessment of substance use disorders".)
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 six hours 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 [24,34-36]. 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 15).
Other laboratory studies Certain laboratory abnormalities are characteristic of specific agents (table 16
and table 17). Symptomatic patients and those with an unreliable or unknown history should, at a minimum,
undergo urinalysis and measurement of serum electrolytes, 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.
The ordering of other laboratory studies should be individualized and is somewhat dependent upon the
results of initial laboratory studies:
Arterial 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 "Clinical features, diagnosis, and treatment of methemoglobinemia".)
Any patient with an acid-base disturbance, increased serum osmolal gap, or oxygen saturation gap (>5
percent difference between measured and calculated value) should have a toxic etiology ruled out (table
18 and table 19). Detection of a 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".)
The presence of an anion gap metabolic acidosis may be the first clue to a toxic ingestion and should
prompt consideration of etiologies such as salicylates, ethylene glycol, and methanol; serum creatinine,
glucose, ketones, and lactate also should be measured to detect other causes of the anion gap acidosis.
(See "Approach to the adult with metabolic acidosis" and "Salicylate (aspirin) poisoning in adults" and
"Methanol and ethylene glycol poisoning".)
The presence of an abnormally elevated serum creatinine with a normal BUN may be seen with
isopropyl alcohol poisoning (or with diabetic ketoacidosis). High serum levels of acetone, which are
formed as a metabolite of isopropyl alcohol, interfere with colorimetric creatinine assays, resulting in
falsely elevated values [37]. (See "Isopropyl alcohol poisoning".)
Measurement of isopropyl alcohol concentration in blood should be obtained 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 regional poison control centers. 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.
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. 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" 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, expected benefits of therapy outweigh its associated risk,
and there are no contraindications. 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 [38].
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 60 to 90 minutes [19,39] (see "Acute opioid
intoxication in adults", section on 'Basic measures and antidotal therapy'). Thus, in certain situations
antidotes may require repeated administration or continuous infusion.
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
are 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 by endotracheal 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,
particularly when gastric decontamination procedures need to be undertaken [40]. 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. 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, 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 [41,42]. (See "Tricyclic antidepressant poisoning".)
Hypertension Hypertension in agitated patients is best treated initially with nonspecific sedatives such
as benzodiazepines [43]. 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 [43,44]. 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 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 with tricyclic antidepressants or other membrane-active agents.
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 "Acquired long QT
syndrome" and "Digitalis (cardiac glycoside) poisoning".)
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, or high dose insulin may obviate the need
for further measures. 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 [45].
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 agitated behavior is generally best treated with benzodiazepine

administration, supplemented with high potency neuroleptics (eg, haloperidol) as needed [46] (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) [47]. (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 [48]. 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'.)
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 20).
All patients with intentional overdose require psychiatric assessment prior to discharge.
One retrospective study of 209 patients with drug overdoses suggested that clinical assessment in the
emergency department could reliably identify patients who are at high risk for complications and require ICU
care [49]. The presence of any of eight clinical criteria predicted a complicated hospital course that could be
best managed in an ICU:
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 [50].
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 clinical and/or 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.
SUMMARY AND RECOMMENDATIONS While poisonings can be fatal, the vast majority of patients
presenting with a toxic exposure suffer minimal morbidity and recover fully. As a result, it is important to
weigh the risks of interventions against the potential benefits which, for many patients, are relatively small.
Assistance can be obtained from regional poison control centers. 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.
The essential elements of care for the poisoned patient include the following:
Institute stabilization procedures in patients with a compromised airway, inadequate gas exchange, or
marginal hemodynamics. (See 'Initial evaluation and treatment' above.)
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.)
Perform a thorough physical examination to ascertain signs of a potential toxidrome as well as

complications of the toxic exposure. 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.)
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.)
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.)
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 should be based upon clinical criteria that relate to the stability of the airway, respiratory system,
cardiovascular system, and the patient's level of consciousness. (See 'Poisoning management' above
and 'Disposition' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
Topic 324 Version 18.0
GRAPHICS
Common poisoning syndromes (toxidromes)
Mental Other Examples of

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

agitation, tachycardia, tremors, amphetamines,
hallucinations, hypertension, hyperreflexia, cathinones, ephedrine,
paranoia widened pulse seizures pseudoephedrine,
pressure, phenylpropanolamine,
tachypnea, theophylline, caffeine
hyperpnea
Anticholinergic Hypervigilance, Mydriasis Hyperthermia, Dry flushed skin, Antihistamines, tricyclic

agitation, tachycardia, dry mucous antidepressants,
hallucinations, hypertension, membranes, cyclobenzaprine,
delirium with tachypnea decreased bowel orphenadrine,
mumbling sounds, urinary antiparkinson agents,
speech, coma retention, antispasmodics,
myoclonus, phenothiazines,
choreoathetosis, atropine, scopolamine,
picking behavior, belladonna alkaloids
seizures (rare) (eg, Jimson Weed)
Hallucinogenic Hallucinations, Mydriasis Hyperthermia, Nystagmus Phencyclidine, LSD,

perceptual (usually) tachycardia, mescaline, psilocybin,
distortions, hypertension, designer
depersonalization, tachypnea amphetamines (eg,
synesthesia, MDMA ["Ecstasy"],
agitation MDEA)
Opioid CNS depression, Miosis Bradypnea, Hyporeflexia, Opioids (eg, heroin,

coma apnea pulmonary edema, morphine, methadone,
characteristic; needle marks oxycodone,
May develop: hydromorphone),
hypothermia, diphenoxylate
bradycardia,
hypotension
Sedative-hypnotic CNS depression, Variable Often normal, Hyporeflexia Benzodiazepines,

confusion, stupor, but may barbiturates,
coma develop: carisoprodol,
hypothermia, meprobamate,
bradycardia, glutethimide, alcohols,
hypotension, zolpidem
apnea,
bradypnea
Cholinergic Confusion, coma Miosis Bradycardia, Salivation, urinary Organophosphate and

hypertension and fecal carbamate insecticides,
orhypotension, incontinence, nerve agents, nicotine,
tachypnea or diarrhea, emesis, pilocarpine,
bradypnea diaphoresis, physostigmine,
lacrimation, GI edrophonium,
cramps, bethanechol,
bronchoconstriction, urecholine
muscle
fasciculations and
weakness, seizures
Serotonin Confusion, Mydriasis Hyperthermia, Tremor, myoclonus, MAOIs alone or with:

syndrome agitation, coma tachycardia, hyperreflexia, SSRIs, meperidine,
hypertension, clonus, diaphoresis, dextromethorphan,
tachypnea flushing, trismus, TCAs, L-tryptophan
rigidity, diarrhea
https://www-uptodate-com.bibliotecavirtual.udla.edu.ec/contents/general-approach-to-drug-poisoning-in-adults/print?source=search_result&sea 10/32
LSD: lysergic acid diethylamide; CNS: central nervous system; GI: gastrointestinal; MAOI: monoamine oxidase inhibitor;
SSRI: serotonin reuptake inhibitor; TCA: tricyclic antidepressant.
Graphic 71268 Version 16.0
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 Hydromorphone
Phenytoin
Amphetamines Oxycodone
Methylphenidate Hydrocodone
Lithium
Cathinones Codeine Ethanol
Anticholinergics Propoxyphene Toxic alcohols

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

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

Propranolol Lithium Anticholinergics
Insecticides (eg, organophosphates, Antipsychotics TCAs

carbamates) Antihistamines
Sympathomimetics
Lidocaine and other local Antiepileptics
Cocaine
anesthetics Phenytoin
Theophylline
Sympathomimetics Amphetamines Carbamazepine
Cocaine Caffeine Weakness/paralysis

Amphetamines Albuterol
Barium (hypokalemia)
Theophylline Methylphenidate
Magnesium
Caffeine Cathinones
Nicotine Solvent abuse
Anticholinergics
Drug withdrawal states Toluene
Antihistamines
Gasoline
Antidepressants TCAs
Heavy metals
TCAs Drug withdrawal states
Bupropion Mercury
Heavy metals
Citalopram Thallium
Rigidity/parkinsonism Insecticides
Escitalopram
Fluvoxamine Antipsychotics (neuroleptics) Organophosphates
Venlafaxine Metoclopramide Carbamates
Amoxapine Nicotine
Amoxapine
Maprotiline
Carbon monoxide (delayed) Botulism
Antipsychotics
Methanol Neurotoxic snake envenomation
Phenothiazines
Ethylene glycol Tick paralysis
Clozapine
Phencyclidine Seafood poisoning
Salicylates
Paralytic shellfish
Camphor MAOIs
Pufferfish (fugu)
Isoniazid Serotonin syndrome
Chemical nerve agents (eg, soman, Black widow spider bite

VX) Lithium
Lithium Methaqualone
Hypoglycemic agents MPTP (designer meperidine)
Cyanide Manganese
Carbon monoxide Strychnine
Meperidine Carbon disulfide
Propoxyphene Cyanide
Orphenadrine Malignant hyperthermia
Antihistamines (rare) Neuroleptic malignant syndrome
Lindane Postanoxic injury from any agent
Gyromitra-containing mushrooms
Heavy metals
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
Clonidine
Ketamine
Sedative-hypnotics Designer amphetamines
Benzodiazepines Synthetic cannabinoids
Barbiturates
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 Cyanotic Desquamation

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

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
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 Cyanide
TCAs (early) Oxymetazoline
antagonists
Phenothiazines (some) Cholinergic agents Carbon monoxide (late)
Phenothiazines
Antiparkinson agents Organophosphates Opioids
TCAs
Muscle relaxants Carbamates
Hydralazine Sedative-hypnotics
Clozapine Steroid hormones
Heavy metals (acute) Barbiturates
Central hallucinogens Glucocorticoids
Iron Benzodiazepines
Designer amphetamines Mineralocorticoids
Arsenic Cholinergics
Lysergic acid diethylamide Estrogen
Colchicine Organophosphates
(LSD)
Progesterone
Carbamates
Phencyclidine (PCP)
Androgens
Nitrates
Synthetic cannabinoids Antiarrhythmics
Yohimbine Sodium nitroprusside
Envenomations
Heavy metals
Black widow spider bite
Lead
Scorpion stings
Disulfiram reaction (early)
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
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

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

Cocaine Amphetamines Antipsychotics
Cardiac glycosides
Theophylline Theophylline
Digoxin Antihistamines
Caffeine Antidepressants
Digitoxin Diphenhydramine
Methylphenidate TCAs
Red squill Astemizole
Ephedrine
Digitalis lanata Antipsychotics Terfenadine
Pseudoephedrine
Digitalis purpurea Phenothiazines Antiarrhythmics
Albuterol
Bufotenin Chlorinated hydrocarbons Quinidine
Dobutamine
Oleander Chloral hydrate Disopyramide
Epinephrine
Alpha-adrenergic agonists Solvents Procainamide
Dopamine
Phenylpropanolamine Fluoride Propafenone
Anticholinergics
Clonidine Flecainide, encainide
Antihistamines
Cardiac glycosides
Imidazolines Amiodarone
TCAs Potassium
Cholinergics Calcium channel blockers
Phenothiazines (rare)
Organophosphates
Clozapine Beta blockers (rare)
Carbamates
Atropine
Propoxyphene
Opioids Scopolamine
Organophosphate
Sedative-hypnotics Thyroid hormone insecticides
Magnesium Cellular asphyxiants Antimicrobials
Carbon monoxide Amantadine
Drug withdrawal states 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.
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,
moderate to heavy use hemp seed oil
Opiates 1 to 3 days Rifampin, fluoroquinolones, poppy seeds,

quinine in tonic water
Phencyclidine 7 to 14 days Ketamine, dextromethorphan
Adapted from: The Medical Letter 2002; 44:71.
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
Laboratory abnormalities associated with certain toxins or drugs
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, Sulfonamides Nitroprusside
seizures, 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 Increased oxygen saturation gap (>5

[SD] m0sm/L) percent 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 (Glasgow coma scale 6)
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
Extremes of temperature (eg, hyperthermia with T >104F)
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

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

General Approach To Drug Poisoning in Adults - UpToDate

Uploaded by

Copyright:

Available Formats

20/7/2017 General approach to drug poisoning in adults - UpToDate

Official reprint from UpToDate

Author: Sean H Rhyee, MD, MPH

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)

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

Agitation Drug-associated agitated behavior is generally best treated with benzodiazepine

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

PaCO2 >45 mmHg

Perform a thorough physical examination to ascertain signs of a potential toxidrome as well as

Use of UpToDate is subject to the Subscription and License Agreement.

Topic 324 Version 18.0

Common poisoning syndromes (toxidromes)

Mental Other Examples of

Sympathomimetic Hyperalert, Mydriasis Hyperthermia, Diaphoresis, Cocaine,

Anticholinergic Hypervigilance, Mydriasis Hyperthermia, Dry flushed skin, Antihistamines, tricyclic

Hallucinogenic Hallucinations, Mydriasis Hyperthermia, Nystagmus Phencyclidine, LSD,

Opioid CNS depression, Miosis Bradypnea, Hyporeflexia, Opioids (eg, heroin,

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

Cholinergic Confusion, coma Miosis Bradycardia, Salivation, urinary Organophosphate and

Serotonin Confusion, Mydriasis Hyperthermia, Tremor, myoclonus, MAOIs alone or with:

Graphic 71268 Version 16.0

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 Codeine Ethanol

Anticholinergics Propoxyphene Toxic alcohols

Muscle relaxants Cholinergics Serotonin syndrome

Graphic 61723 Version 7.0

Drug- and toxin-induced movement disorders

Seizures Tremors/myoclonus Choreoathetosis

Insecticides (eg, organophosphates, Antipsychotics TCAs

Cocaine Caffeine Weakness/paralysis

Chemical nerve agents (eg, soman, Black widow spider bite

Graphic 64472 Version 9.0

Drug- and toxin-induced mental status alterations

Central nervous system depression Agitation

Simple asphyxiants Antihistamines

Carbon dioxide Atropine

Inert gases Scopolamine

Graphic 80618 Version 8.0

Drug- and toxin-induced skin abnormalities

Red and flushed Pale and Cyanotic Desquamation

Coprinus Nerve agents

Graphic 74778 Version 6.0