Cannabis (Marijuana) : Acute Intoxication - UpToDate

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Cannabis (marijuana): Acute intoxication

Author: George Sam Wang, MD
Section Editors: Michele M Burns, MD, MPH, Stephen J Traub, MD
Deputy Editor: Michael Ganetsky, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2022. | This topic last updated: Apr 21, 2022.
INTRODUCTION
This topic discusses the epidemiology, toxicity, clinical manifestations, and management of
acute intoxication with cannabis.
The clinical manifestations and management of toxicity from synthetic cannabinoids, medical
uses of cannabinoids, and the manifestations and treatment of cannabis use disorder are
provided separately:
● (See "Synthetic cannabinoids: Acute intoxication".)
● (See "Cancer pain management: Role of adjuvant analgesics (coanalgesics)", section on

'Cannabis and cannabinoids'.)
● (See "Symptom management of multiple sclerosis in adults", section on 'Cannabinoids'.)
● (See "Assessment and management of nausea and vomiting in palliative care", section
on 'Cannabinoids and cannabis'.)
● (See "Overview of the management of epilepsy in adults", section on 'Alternative

therapies'.)
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● (See "Cannabis use: Epidemiology, pharmacology, comorbidities, and adverse effects"

and "Cannabis use disorder in adults".)
EPIDEMIOLOGY
According to the World Health Organization (WHO), 147 million people, or 2.5 percent of the
world population, use cannabis, making it the world's most widely cultivated, trafficked, and
abused illicit substance [1]. Use is high in the adolescent age group. As an example, among
surveyed adolescents in the United States, approximately 6 percent of 8th graders, 17 percent
of 10th graders, and 21 percent of 12th graders reported cannabis use in the past month [2].
Some countries have legalized cannabis, including Uruguay and Canada [3,4]. At the United
States federal level, cannabis products are classified as Schedule I (ie, no currently accepted
medical use and a high potential for abuse) [3,5,6]. However, over 30 states have
decriminalized medical cannabis or are reviewing legislation to allow low-dose delta-9
tetrahydrocannabinol (THC) products for specific medicinal indications. As of 2021, 18 states
have allowed the retail sale and possession of recreational cannabis [7].
The public health impact of decriminalization or legalization of recreational cannabis use

includes the following:
● Both decriminalization and legalized recreational use have been associated with
increased unintentional pediatric ingestions [8-16]. As an example, after legalization of
recreational cannabis use in Colorado, annual calls to the regional poison control center
for pediatric cannabis exposure increased 34 percent on average to 6 cases per 100,000
population, which was almost twice the rate for the rest of the United States [10].
Exposure to recreational cannabis accounted for about half of cases. Rates of hospital
visits at a large regional children's hospital system also increased significantly during
the period of the study, although the total number of presenting patients (81) was
small.
● The impact of cannabis legalization on prevalence of use among youth is mixed. In

regions with medical cannabis availability, diversion of drug from registered users may
encourage adolescent abuse [17]. The National Survey on Drug Use and Health cross-
sectional survey reported a small increase in cannabis use disorder in the adolescent
and young adult population in the regions of the United States that have legalized
recreational cannabis [18]. On the other hand, a separately administered high school
survey in Colorado has not demonstrated a significant increase in admitted cannabis
use in high school students. However, there was a significant increase in use of
alternative forms of cannabis, with dabbing increasing to 10.2 percent and vaporizing
to 6.8 percent in 2019 among cannabis users [19].
● Approximately 1 in 20 pregnant women report cannabis use some time during

pregnancy. The prevalence of use in this population has continued to increase in the
United States, most notable in states that have legalized medical and recreational
cannabis. Common reasons for use included self-treatment of stress, anxiety, nausea,
vomiting, and pain. (See "Substance use during pregnancy: Overview of selected
drugs", section on 'Cannabis (marijuana)'.)
● In other countries where cannabis can be used legally, rates of usage vary. In the
European Union, cannabis use in 2020 for those aged 15 to 34 was estimated at 15.4
percent, ranging from 3.4 percent in Hungary to 21.8 percent in France [20]. Thus, the
impact of decriminalization or legalization on the subsequent prevalence of cannabis
use is not easily predicted and varies depending upon the specifics of enacted
regulations [3].
PHARMACOLOGY AND TOXICITY
Site of action — The cannabinoid receptor is a G-protein-coupled receptor, which inhibits

adenylyl cyclase and stimulates potassium conductance. There are two known cannabinoid
receptors: CB1 and CB2 [21-23]:
● CB1 is found in the central nervous system including the basal ganglia, substantia
nigra, cerebellum, hippocampus, and cerebral cortex. It acts presynaptically and inhibits
release of several neurotransmitters including acetylcholine, L-glutamate, gamma
amino butyric acid (GABA), norepinephrine, dopamine, and 5-hydroxytryptamine.
● CB2 is found peripherally in the immune system tissues (eg, splenic macrophages and B
lymphocytes), peripheral nerve terminals, and vas deferens. It is postulated that it plays
a role in regulation of immune responses and inflammatory reactions. Anandamide and
palmitoylethanolamide are known endogenous cannabinoid receptor ligands.
Pharmacokinetics — Delta-9 tetrahydrocannabinol (THC) is the most psychoactive

cannabinoid. The pharmacokinetics and pharmacodynamics of THC vary by route of
exposure as follows [21,23-31]:
● Inhaled cannabis – After inhalation of cannabis smoke, onset of psychoactive effects

occurs rapidly, with peak effects felt at 15 to 30 minutes and lasting up to four hours.
These effects mirror plasma THC concentrations. Approximately 2 to 3 mg of inhaled
THC is sufficient to produce drug effects in a naïve user. Pulmonary bioavailability varies
from 10 to 35 percent of an inhaled dose and is determined by the depth of inhalation
along with the duration of puffing and breath holding.
● Ingested cannabis – When compared with inhalation, cannabis ingestion has a delayed
onset of psychoactive effects that ranges from 30 minutes to three hours. Clinical
effects may last up to 12 hours. Orally administered cannabis has low bioavailability (5
to 20 percent) because of chemical degradation in gastric acid and substantial first-pass
metabolism in the liver. In naïve users, psychotropic effects occur with 5 to 20 mg of
ingested THC.
THC is lipid soluble, highly protein bound (95 to 99 percent), and has a volume of distribution
of 2.5 to 3.5 L/kg [21,27].
THC metabolism occurs via hepatic cytochrome oxidases, CYP2C9 and 3A4. The primary
active metabolite is 11-hydroxy THC (11-OH THC), and the inactivated metabolite is THC-
carboxylic acid (THC-COOH) [21]. After metabolism, THC is mostly excreted as hydroxylated
and carboxylated metabolites via feces (65 percent) and urine (20 percent) [21]. Although
difficult to measure, the acute elimination half-life of THC is slow, ranging from 25 to 36
hours [21]. This lengthy half-life is likely due to slow release from lipid storage compartments
and enterohepatic circulation. Elimination half-life is longer in regular cannabis users.
THC crosses the placenta with fetal plasma concentrations 10 to 30 percent of maternal
concentrations. Limited data demonstrate that THC also accumulates in breast milk, peaking
at four hours after maternal smoking, and can be detectable in breast milk at least six days
after last maternal use. (See "Infants with prenatal substance use exposure" and "Substance
use during pregnancy: Overview of selected drugs", section on 'Cannabis (marijuana)'.)
Cannabis formulations — There are a variety of subspecies and strains of cannabis;

Cannabis sativa is one of the most commonly used for recreational purposes. Cannabis sativa
contains over 500 different clinical compounds and over 60 known cannabinoids; of these,
THC is the most psychoactive and is responsible for most symptoms of intoxication [21,25].
The dried flower of the cannabis plant has a large range of THC content, ranging from 1 to 20
percent of the total weight; however, much variability exists among cannabis samples [32]. In
general, cannabis potency has increased over the past 20 years [33]. Common slang terms
for cannabis include "pot," "grass," "dope," "MJ," "Mary Jane," "doobie," "hooch," "weed,"
"hash," "reefer," and "ganja."
Chemical analogues of THC called "synthetic cannabinoids" may have been available in
Europe as early as 2004 and were first reported in the United States in December 2008. The
clinical effects can be similar to natural cannabis intoxication but may also result in more
severe life-threatening symptoms. Acute intoxication from synthetic cannabinoids is
discussed separately. (See "Synthetic cannabinoids: Acute intoxication".)
Recreational use — Recreational cannabis use often consists of smoking the dried flower in
the form of rolled cigarettes (joints) and water bongs [34]. THC is also extracted using various
solvents (butane, ethanol, hexane, isopropanol) to create highly concentrated products (60 to
99 percent of THC by weight) including oils and tinctures called "wax," "dabs," "budder," and
"shatters" [35-37]. In addition to being smoked, these highly concentrated products are
vaporized (eg, using electronic cigarettes [38,39]) or mixed in food products (such as baked
goods, candies, and other food and beverages) and ingested ("edibles").
In regions where cannabis use is legal, concentrated forms are popular and may pose a risk
of unintentional ingestion by young children or excessive use by adolescents and adults [40-
42]. As an example, in Colorado, some companies have produced packaging for cannabis
products that mimic popular candy, although state law prohibits packaging and advertising
that targets children [43]. Furthermore, many of these products contain up to four times the
suggested adult serving size dose of 5 to 10 mg. Cannabis edible product ingestions have
significantly increased in young children, with a greater proportion of calls due to edible
product ingestion in states that have legalized cannabis [15].
Medicinal use — Medicinal cannabis is supplied as dried flowers of the Cannabis sativa
plant that are smoked as described for recreational cannabis use (see 'Recreational use'
above). Derivatives of cannabinoids are also available as pharmaceuticals in some countries
including oral preparations (dronabinol and nabilone) and a spray for buccal use
(nabiximols).
Cannabis and its components have been proposed for various medicinal purposes, such as
chronic severe pain (eg, due to cancer), refractory nausea and vomiting, anorexia and
cachexia, glaucoma, and seizures [22,44]. However, none have been proven to have greater
efficacy than other currently available medications.
Of these indications, medical cannabis is most frequently prescribed for severe or chronic
pain. An oromucosal spray containing THC and cannabidiol (CBD; Sativex, also called
nabiximols) has been shown to have some efficacy as a multipurpose analgesic in
combination with traditional therapy and is approved for use in Canada and elsewhere but
not in the United States. No controlled studies demonstrate the efficacy of inhaled cannabis
as an adjunct to traditional pain medications for patients with cancer-related pain (see
"Cancer pain management: Role of adjuvant analgesics (coanalgesics)", section on 'Cannabis
and cannabinoids'). Trials in patients with multiple sclerosis have failed to show consistent
pain reduction. (See "Symptom management of multiple sclerosis in adults", section on
'Cannabinoids'.)
Although inhaled, buccal, or ingested cannabis has shown some efficacy for refractory
nausea and vomiting or glaucoma [45,46], consensus expert guidelines do not support its
use. (See "Cancer pain management: Role of adjuvant analgesics (coanalgesics)", section on
'Cannabis and cannabinoids' and "Assessment and management of nausea and vomiting in
palliative care", section on 'Cannabinoids and cannabis'.)
In addition, cannabinoids, specifically CBD, have been studied for the treatment of refractory
epilepsy in children as discussed separately. (See "Dravet syndrome: Management and
prognosis", section on 'Cannabidiol' and "Epilepsy syndromes in children", section on

'Lennox-Gastaut syndrome'.)
Toxic effects — Recreational cannabis intake to achieve psychoactive effects can often result
in adverse effects because there is no clear demarcation between doses that achieve
symptoms desired by a cannabis user and noxious effects.
In adolescents and adults, inhaled doses of 2 to 3 mg of THC and ingested doses of 5 to 20

mg of THC impair attention, concentration, short-term memory, and executive functioning
[21,23-31,47-53]. More severe adverse effects may occur at doses >7.5 mg/m2 of THC,
including nausea, postural hypotension, delirium, panic attacks, anxiety, and myoclonic
jerking [48,49]. Acute psychosis has also been associated with use of higher
potency/concentrated cannabis products [54,55].
Toxicity in children is most often reported after ingestion of a highly concentrated food
product [8,9,15,56-61] or hashish resin [62]. Estimated oral doses from 5 to 300 mg in
pediatrics have caused a range of symptoms such as mild sleepiness, ataxia, behavior
changes, excessive and purposeless motor activity of the extremities (hyperkinesis), coma,
and respiratory depression with more severe intoxication correlated with higher estimated
doses. For example, in a small cohort of 38 children presenting to an emergency department
for acute cannabis intoxication after ingestion, degree of symptoms corresponded to an
estimated dose as follows: 3.2 mg/kg of THC led to observation and minimal medical
intervention, 7.2 mg/kg of THC led to admission to an inpatient floor and moderate medical
intervention, and 13 mg/kg of THC led to admission to an intensive care unit and major
medical interventions [63]. Patients without prior THC exposure more commonly had
lethargy or somnolence and had a longer duration of clinical symptoms. Similarly, as
concentrated hashish resin has become more available in France, a corresponding increase
in the number of annual admissions and severity of symptoms has occurred among infants
and young children [62,64].
CLINICAL MANIFESTATIONS
The clinical manifestations of acute cannabis intoxication vary according to age.
Neurologic abnormalities are more prominent in children and include ataxia, excessive and
purposeless motor activity of the extremities (hyperkinesis), seizures, lethargy, and
prolonged coma, which may be life threatening [8,9,56-62].
Acute cannabis intoxication is an unusual primary complaint in adolescents and adults.

Patients who come to medical attention are more likely to have hyperemesis or behavioral
problems (eg, dysphoria or agitation) caused by adverse cannabis effects or medical
emergencies (eg, bronchospasm or pneumothorax) associated with the method of
inhalation. Although rare, chest pain with myocardial infarction in young adults without any
prior history of coronary artery abnormalities has been described [65-69]. The issue of
causation is unclear, however, in light of the frequency of cannabis use in the general
population and the presence of unsuspected atherosclerosis or other cardiac conditions in
some of these patients.
Children — In children, acute cannabis intoxication typically occurs after exploratory

ingestion of cannabis intended for adult use [8-10,57-61,70,71]. Less commonly, intentional
exposure of children by caretakers, including encouragement of cannabis inhalation to
promote sleepiness and to decrease activity, has been reported [72]. Pediatric ingestions of
cannabis products happen more frequently in regions with decriminalization or legalization
of cannabis use [8-15,73]. (See 'Epidemiology' above.)
After limited exposures, children may display sleepiness, euphoria, irritability, and other
changes in behavior [8,9,57-61,70,72-74]. Vital signs may show sympathomimetic effects (eg,
tachycardia and hypertension) or, in patients with depressed mental status, bradycardia.
Nausea, vomiting, conjunctival injection, nystagmus, ataxia, and (in verbal children) slurred
speech may also be present. Dilated pupils have frequently been reported, although miosis
has also been described [74-77].
In large overdoses (eg, ingestion of edible products, concentrated oils, or hashish), coma
with apnea or depressed respirations can occur [8-10,57-62,71,74].
Although not typical of pediatric cannabis intoxication, seizures have also been reported
[58,70,71,76]. In one instance, cocaine was also found on urine screening [76]. In one
retrospective series of 29 children under age three admitted with documented cannabis
exposure, seizures occurred in four patients, all of whom had ingested hashish resin [70].
Adolescents and adults — The physiologic signs of cannabis intoxication in adolescents and
adults can include [21,23,24]:
● Tachycardia
● Increased blood pressure or, especially in older adults, orthostatic hypotension
● Increased respiratory rate
● Conjunctival injection (red eye)
● Dry mouth
● Increased appetite
● Nystagmus
● Ataxia
● Slurred speech
Complications associated with inhalation use include:
● Acute exacerbations and poor symptom control in patients with asthma [78]. (See
"Acute exacerbations of asthma in adults: Emergency department and inpatient
management".)
● Pneumomediastinum and pneumothorax suggested by tachypnea, chest pain, and

subcutaneous emphysemas caused by deep inhalation with breath-holding [79]. (See
"Spontaneous pneumomediastinum in children and adolescents" and "Pneumothorax:
Definitive management and prevention of recurrence".)
● Rarely, angina, myocardial infarction, and cardiac dysrhythmias [80-83]. (See "Initial
evaluation and management of suspected acute coronary syndrome (myocardial
infarction, unstable angina) in the emergency department".)
The risk for myocardial infarction among regular cannabis users has been found to be
significantly elevated over baseline risk in nonusers [69,80].
Cannabis intoxication in adolescents and adults also results in the following neuropsychiatric
effects:
● Mood, perception, thought content – Ingestion typically leads to feeling "high,"

marked by a euphoric, pleasurable feeling and a decrease in anxiety, alertness,
depression, and tension. However, first-time cannabis users, as well as anxious or
psychologically vulnerable individuals, may experience anxiety, dysphoria, and panic
[24]. Increased sociability usually occurs during intoxication, although dysphoric
reactions may be accompanied by social withdrawal. Inexperienced users who ingest
cannabis products may not be aware that effects may not be felt for up to three hours,
which may cause them to continue to consume high-potency products with an
increased likelihood of dysphoria. (See 'Pharmacokinetics' above.)
Perceptual changes include the sensation that colors are brighter and music is more
vivid [24]. Time perception is distorted in that perceived time is faster than clock time.
Spatial perception can also be distorted, and high doses of potent cannabis products
may cause hallucinations. Mystical thinking, increased self-consciousness, and
depersonalization may occur, as well as transient grandiosity, paranoia, and other signs
of psychosis [24,84]. Acute intoxication from THC can also lead to acute psychotic
symptoms, which are worsened with higher doses of THC [55,85].
● Cognition, psychomotor performance – Cannabis use slows reaction time and impairs
attention, concentration, short-term memory, and risk assessment. These effects are
additive when cannabis is used in conjunction with other central nervous system
depressants [24]. Acute cannabis use also impairs motor coordination and interferes
with the ability to complete complex tasks that require divided attention [86].
Impairment of cognition, coordination, and judgment lasts much longer than the
subjective mood change of feeling "high." Psychomotor impairment lasts for 12 to 24
hours due to accumulation of cannabis in adipose tissue, slow release of THC from fatty
tissue stores, and enterohepatic recirculation. However, a cannabis user may think that
they are no longer impaired until several hours after the acute mood-altering effects
have resolved. As an example, a placebo-controlled trial with licensed pilots found that
smoking cannabis impaired performance on a flight simulator for up to 24 hours,
although only one of the nine subjects recognized this impairment [87].
Acute psychomotor impairments interfere with the ability to operate other heavy
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machinery, such as automobiles, trains, and motorcycles. A meta-analysis of nine

studies found an association between cannabis intoxication and an increased risk of a
motor vehicle collision involving serious injury or death [24,52,88,89]. Drivers using
cannabis are two to seven times more likely to be responsible for accidents compared
with drivers not using any drugs or alcohol [90]. Furthermore, the probability of causing
an accident increases with plasma levels of THC [52].
DIAGNOSIS
Children — Diagnosis of cannabis intoxication in young children based solely on clinical

criteria can be difficult because a history of exposure is often lacking, and the symptoms of
cannabis exposure are nonspecific. Thus, ancillary studies are often needed to exclude other
causes of altered mental status (see 'Other ancillary studies' below). Urine drug screens help
confirm the diagnosis because any positive result in a symptomatic child likely represents an
acute exposure. (See 'Drug testing for cannabinoids' below.)
Adolescents and adults — Acute cannabis intoxication is a clinical diagnosis in adolescents

and adults. Urine drug screens are less helpful in adolescents and adults for the diagnosis of
acute intoxication. Although testing is usually positive several hours after acute exposure, it
can also be positive well after symptoms have resolved. As an example, positive results for
THC metabolites have been reported up to 10 days after weekly use and up to 25 days after
daily use [91]. Thus, cannabis testing does not provide any specific information on the
timeline of exposure or correlate with severity of intoxication.
Pure cannabidiol (CBD) should not result in a positive THC urine drug screen. However, CBD
products may contain THC, which will result in a positive urine drug screen [92]. Confirmatory
testing evaluating individual cannabinoids and respective metabolites can help determine
the specific exposure.
Selected adolescents and adults with chest pain may warrant an electrocardiogram (ECG),
cardiac biomarkers, or chest radiograph to identify associated myocardial ischemia or
pneumomediastinum. (See 'Other ancillary studies' below.)
Drug testing for cannabinoids — Hospital testing for cannabis typically consists of a urine
drug screen. (See 'Diagnosis' above.)
Standard urine drug screens that are available in most health care facilities consist of
immunoassays that detect THC metabolites, primarily the main metabolite THC-COOH. The
lower limits of detection range from 20 to 100 ng/mL, depending upon the specific assay
[93]. The Substance Abuse and Mental Health Services Administration (SAMHSA) standard is
50 ng/mL, with confirmatory testing using 15 ng/mL, as the lower limit of detection [94].
Immunoassays for THC do not detect synthetic cannabinoids, which are structurally distinct
from THC.
In situations where a positive screen for cannabis has legal implications or may impact
school attendance or sports participation, individuals may claim that the test results from
passive inhalation of cannabis smoked by others. In adolescents and adults, it is difficult to
achieve sufficient concentrations from secondhand smoke from typical cannabis cigarettes to
detect metabolite concentrations above most urine drug screen limits [95-99]. However,
studies using products with higher THC content (typical of what is more commonly used
since 2005) have not been performed. There has been a case report of an infant becoming
symptomatic after passive cannabis smoke exposure [100]. Metabolites of THC have been
detectable in a cohort of children hospitalized for bronchiolitis exposed to passive cannabis
smoke, although below the limits of detection of standard immunoassays [101].
False positives for cannabinoids are rare because the chemical structure is unique and
immunoassays are targeted toward metabolites of THC. Reported false positives for THC
include: dronabinol, efavirenz, proton pump inhibitors, hemp seed oil, nonsteroidal
antiinflammatory drugs (NSAIDs), and baby wash products in infants [102-107]. Most
package inserts for commercially available immunoassays will list possible false positives for
their cannabinoid assay. If required for clinical or social indications, confirmatory testing of
urine, blood, or serum can be sent to reference labs by gas chromatography and mass
spectrophotometry. However, results of confirmatory testing do not return quickly enough to
affect clinical care.
Other ancillary studies — Most adolescents and adults do not warrant any testing for the
diagnosis or treatment of uncomplicated acute cannabis intoxication. Patients with chest
pain suggestive of myocardial ischemia or infarction warrant a 12-lead ECG and possibly
cardiac biomarkers (eg, troponin T or I). (See "Troponin testing: Clinical use", section on
'Diagnosis of acute MI'.)
Chest radiograph may assist in the diagnosis of stable patients with chest pain indicative of a
spontaneous pneumothorax. However, patients with signs of a tension pneumothorax
should undergo decompression prior to chest radiography. Bedside ultrasound may assist
with rapid diagnosis of pneumothorax in these unstable patients. (See "Bedside pleural
ultrasonography: Equipment, technique, and the identification of pleural effusion and
pneumothorax".)
Children may warrant testing for other potential causes of altered mental status depending
upon whether the exposure is known and based upon specific physical findings including
rapid blood glucose, electrolytes, blood gas analysis, lumbar puncture, and neuroimaging
(eg, computed tomography [CT] of the head). Neuroimaging should be avoided in known
cannabis exposures unless focal neurologic findings are also present or concerns for other
etiologies such as head trauma exist. (See 'Differential diagnosis' below.)
DIFFERENTIAL DIAGNOSIS
Children — The differential diagnosis for cannabis exposure in children is broad because
toxicity most commonly presents as altered behavior, lethargy, or coma. When history of
exposure is lacking, a positive rapid urine drug screen for cannabinoids is helpful for
identifying cannabis as the likely culprit in children too young to be using cannabis
recreationally. (See 'Drug testing for cannabinoids' above.)
Some common medical causes of lethargy and coma are listed here with features that
distinguish them from cannabis intoxication (see "Evaluation of stupor and coma in children",
section on 'Etiologies'):
● Hypoglycemia – Low rapid blood sugar (see "Causes of hypoglycemia in infants and
children")
● Electrolyte imbalance (eg, hyponatremia or hypocalcemia) – Low serum sodium or

calcium (see "Hyponatremia in children: Etiology and clinical manifestations" and
"Etiology of hypocalcemia in infants and children")
● Central nervous system infection (eg, meningitis or encephalitis) – Fever and/or

meningismus
● Traumatic brain injury, especially abusive head trauma – Child abuse may present
with intracranial injury (eg, subdural hematoma) without an appropriate mechanism by
history, retinal hemorrhages, skin bruising, and/or fractures (see "Child abuse:
Evaluation and diagnosis of abusive head trauma in infants and children", section on
'Clinical features')
A positive urine drug screen for metabolites of cannabis also helps differentiate cannabis
intoxication from poisoning with other agents but is not immediately available in most
facilities. Toxicologic causes of lethargy and coma in children are extensive ( table 1). The
following agents and important clinical features that distinguish them from cannabis
intoxication include:
● Opioids – Lethargy and coma following cannabis ingestion does not respond to
naloxone, which differentiates it from toxicity caused by opioid analgesics. (See "Opioid
intoxication in children and adolescents", section on 'Clinical manifestations'.)
● Sedative/hypnotic agents – Cannabis toxicity typically causes more tachycardia or

seizure-like activity than sedatives/hypnotics. (See "Benzodiazepine poisoning and
withdrawal", section on 'Clinical features of overdose' and "Meprobamate poisoning",
section on 'Clinical features of overdose'.)
● Ethanol – A sickly sweet breath odor, hypoglycemia (when present), and an elevated
blood alcohol concentration are important findings of ethanol intoxication. (See
"Ethanol intoxication in children: Clinical features, evaluation, and management",
section on 'Clinical features'.)
● Oral hypoglycemic agents – Patients typically have a normal mental status and
examination unless hypoglycemia is present. Cannabis intoxication is not associated
with hypoglycemia. (See "Sulfonylurea agent poisoning", section on 'History and
physical examination'.)
● Clonidine – Some patients with coma from clonidine poisoning will respond to naloxone
administration. Patients will also show more signs of hemodynamic instability such as
bradycardia and hypotension. (See "Clonidine and related imidazoline poisoning",
section on 'Clinical features and diagnosis'.)
● Antihistamines – Significant toxicity is often associated with anticholinergic findings

(dilated pupils, flushing, dry skin and mouth, decreased breath sounds, and delirium
with seizures). (See "Anticholinergic poisoning" and "Anticholinergic poisoning", section
on 'Clinical features of overdose'.)
● Carbon monoxide – Other members of the household may have flu-like symptoms in
patients with carbon monoxide poisoning, and carboxyhemoglobin will be elevated.
(See "Carbon monoxide poisoning", section on 'Clinical presentation'.)
● Psychotropic agents (eg, antipsychotic or antidepressant agents) – These agents

often are associated with anticholinergic findings as described above and may be
associated with arrhythmias or electrocardiographic (ECG) abnormalities (eg, prolonged
QRS or QT intervals). (See "First-generation (typical) antipsychotic medication
poisoning", section on 'Clinical features of overdose' and "Second-generation (atypical)
antipsychotic medication poisoning", section on 'Clinical features of overdose'.)
Adolescents and adults — Several other commonly used recreational drugs have some
overlapping clinical features with cannabis intoxication in adolescents and adults, including:
● Cocaine (see "Cocaine: Acute intoxication", section on 'Clinical manifestations')
● Amphetamines and methcathinones (bath salts) (see "Acute amphetamine and

synthetic cathinone ("bath salt") intoxication", section on 'Clinical features of overdose'
and "Methamphetamine: Acute intoxication", section on 'Clinical features')
● Lysergic acid diethylamide (LSD) and other hallucinogens (eg, phencyclidine [PCP],
dextromethorphan, or psilocybin) (see "Intoxication from LSD and other common
hallucinogens", section on 'General clinical features of intoxication')
● MDMA (ecstasy) (see "MDMA (ecstasy) intoxication", section on 'Clinical features')
● Synthetic cannabinoids (see "Synthetic cannabinoids: Acute intoxication", section on

'Clinical manifestations')
Cannabis is frequently used recreationally with these drugs or may serve as a vehicle for use
(eg, lacing cannabis cigarettes with PCP). Thus, investigation for other intoxicants is indicated
if symptoms are prolonged beyond a few hours or if other marked physiologic abnormalities
exist such as hyperthermia, acidosis, significant rhabdomyolysis, or end-organ toxicity.
Synthetic cannabinoids (eg, Spice or K2) cause findings that are very similar to cannabis
intoxication but are more frequently associated with more pronounced sympathomimetic
effects, aggressive behavior and agitation, dystonia, and seizures. A urine drug screen for
cannabinoids will be negative after synthetic cannabinoid use. (See "Synthetic cannabinoids:
Acute intoxication", section on 'Clinical manifestations'.)
Cannabis use may exacerbate pre-existing mental illness (eg, psychosis, anxiety, or
depression). Thus, clinicians should ask about cannabis use in patients who display new
onset or worsening of known psychiatric disease.
MANAGEMENT
The management of cannabis intoxication consists of supportive care. Because of the

differences in toxic manifestations, the management differs significantly by age.
Children — Children with cannabis exposure are much more likely to demonstrate severe or
life-threatening toxicity consisting of excessive and purposeless motor activity (hyperkinesis),
seizures, or deep coma. Consultation with a regional poison control center and a medical
toxicologist is encouraged for all symptomatic exposures. (See 'Additional resources' below.)
Central nervous system depression — Severe central nervous system depression from
cannabis exposure is unique to the pediatric population and can present with profound
depression, lethargy, and coma.
Treatment is supportive and consists of the following measures:
● Maintain airway, breathing, and circulation. Patients with lethargy and coma should
receive supplemental oxygen, assessment and support of airway and breathing, and
vascular access. Patients with apnea or at risk for aspiration should undergo rapid
sequence endotracheal intubation and receive assisted ventilation ( table 2). (See
"Emergency endotracheal intubation in children", section on 'Indications' and "Rapid
sequence intubation (RSI) outside the operating room in children: Approach", section on
'Indications'.)
● Measure rapid blood glucose to exclude hypoglycemia ( table 3).
● Administer naloxone to patients presenting with features of opioid intoxication.

Naloxone will not reverse coma due to cannabis toxicity ( table 4).
The duration of coma is typically one to two days [59,60,75,76]. Full recovery is expected with
supportive care.
Seizures — Seizures have rarely been described after cannabis intoxication in children and
may be associated with co-ingestants (eg, cocaine) [58,60,62,76]. Initial treatment of toxin-
associated seizures consists of benzodiazepines (eg, lorazepam or midazolam). If seizures
persist despite multiple doses of benzodiazepines, then treatment for status epilepticus
caused by toxins, as described in the table and algorithm, is warranted ( table 5 and
algorithm 1). (See "Management of convulsive status epilepticus in children".)
Agitation — Dysphoria with agitation is not a common presentation in pediatric cannabis

exposure. However, if symptoms of marked anxiety or agitation develop, benzodiazepines
(eg, lorazepam) are frequently effective and have a low adverse effect profile.
Adolescents and adults
Mild intoxication — Mild intoxication with dysphoria is a common presentation in either

naïve or chronic cannabis users after ingestion or inhalation of a high-potency product such
as an edible or concentrate. Most patients can be managed with a dimly lit room,
reassurance, and decreased stimulation. Short-acting benzodiazepines (eg, lorazepam) can
be helpful in controlling symptoms of anxiety and have a low side effect profile.
Severe intoxication — Severe physiologic effects are rare after cannabis use, and their
presence should prompt the clinician to consider co-ingestion of other recreational drugs
(including cocaine, amphetamines, and phencyclidine) or coexisting mental illness. (See

'Adolescents and adults' above.)
Marked agitation or combativeness not responsive to reassurance and benzodiazepines may

necessitate the use of other medications, depending upon the cause, and is rarely
encountered with intoxication from cannabis alone. The approach to sedation of the acutely
agitated or violent adult is discussed in detail separately. (See "Assessment and emergency
management of the acutely agitated or violent adult", section on 'Chemical sedation'.)
Chest pain — Chest pain in association with cannabis use should be managed according to
etiology as follows:
● Acute coronary syndrome – Substernal squeezing chest pain suggestive of myocardial

ischemia or infarction may occur rarely in association with cannabis use
[65,66,68,69,81,82]. Patients complaining of chest pain suggestive of coronary
insufficiency should be evaluated for acute coronary syndrome and treated accordingly
( table 6). (See "Initial evaluation and management of suspected acute coronary
syndrome (myocardial infarction, unstable angina) in the emergency department",
section on 'Clinical presentation' and "Initial evaluation and management of suspected
acute coronary syndrome (myocardial infarction, unstable angina) in the emergency
department", section on 'Management'.)
● Pneumothorax or pneumomediastinum – Inhalation and breath-holding during

cannabis use may cause a pneumothorax or pneumomediastinum with sharp, pleuritic
chest pain and subcutaneous crepitus. Management of a pneumothorax depends upon
its size and includes oxygen administration and, if necessary, evacuation with needle
decompression or chest tube insertion. (See "Treatment of secondary spontaneous
pneumothorax in adults", section on 'Initial management of first event'.)
No specific treatment is necessary for uncomplicated pneumomediastinum. (See

"Spontaneous pneumomediastinum in children and adolescents", section on
'Management'.)
● Asthma exacerbation – Cannabis use may cause chest tightness with bronchospasm
and wheezing. Standard therapy for status asthmaticus should be provided ( table 7).
(See "Acute exacerbations of asthma in adults: Emergency department and inpatient

management".)
Gastrointestinal decontamination — Activated charcoal has little efficacy in patients with

symptomatic cannabis intoxication because they generally present well after the time of
ingestion (three hours or longer). In young children, clinical toxicity after ingestion may also
include rapid onset of altered mental status or vomiting, which may raise the risk of
aspiration if activated charcoal is administered. In addition, the clinical effects of cannabis
ingestion are often self-limited without gastrointestinal decontamination, and good
outcomes occur with supportive care alone.
There is no role for gastrointestinal decontamination after toxicity caused by inhaled

cannabis.
Cannabis hyperemesis syndrome — Cannabis hyperemesis syndrome (CHS) is typically

seen with chronic cannabis use in older adolescents and adults. It can also occur after acute
or acute-on-chronic use [108,109].
● Clinical manifestations – Patients may complain of cyclic abdominal pain, vomiting, or

nausea that is typically relieved by hot showers or baths. Acute treatment consists of
symptomatic care including intravenous (IV) fluid hydration, antiemetics, and
benzodiazepines [110,111]. Cessation of cannabis use is also recommended.
● Management – For cannabis users who present for the first time with mild abdominal
pain and vomiting likely due to CHS, our approach is as follows:
• Administer antiemetics (eg ondansetron [preferred] or metoclopramide). Give

benzodiazepines (eg, lorazepam) if vomiting persists.
• Provide fluid repletion (eg, 1 L of normal saline or buffered crystalloid solution such
as lactated Ringer over one hour).
• Perform evaluation to exclude other etiologies for the symptoms or potential

complications of excessive vomiting:
- Complete blood count with differential
- Serum electrolytes
- Blood urea nitrogen and serum creatinine
- Serum lipase
- Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST)
- Radiographic imaging if concern for esophageal or bowel perforation,
cholecystitis, or bowel obstruction; choice of imaging depends upon specific
concern and may include plain radiographs (eg, posteroanterior and lateral
chest, supine and upright abdomen) or abdominal ultrasound
• For patients who do not respond to supportive measures (conventional antiemetics

and fluid repletion) and for whom alternative causes of nausea, vomiting, and
abdominal pain have been excluded, we suggest a trial of topical capsaicin.
• For patients who are refractory to all prior interventions and persist with moderate
to severe abdominal pain and vomiting, we suggest droperidol (observational
studies have used 0.625 or 1.25 mg) or haloperidol (0.05 to 0.1 mg/kg, maximum
single dose 2.5 mg).
We advise all patients with CHS to forego further cannabis use and offer mental health
or substance use treatment referral (see "Cannabis use disorder in adults"). The patient
must understand that it may take several weeks of cannabis abstinence for symptoms
to resolve and that symptoms may worsen or return if cannabis is resumed. However, it
is difficult for many patients to abruptly abstain from cannabis use. For these patients,
the clinician can advise use of products with decreased potency and reduced frequency
of use with an ultimate goal of abstinence.
For patients with protracted symptoms who present repeatedly to the emergency
department with frequent vomiting and retching, it is reasonable to individualize
treatment, which may involve earlier or primary use of droperidol or haloperidol to
control symptoms. An evaluation to exclude other etiologies of symptoms or
complications of repeated vomiting are still appropriate in these patients, especially
those whose symptoms are poorly controlled.
Evidence for the use of capsaicin and dopamine antagonists for CHS include:
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• Capsaicin – Limited observational evidence (case reports and case series) suggests
that topical capsaicin cream (supplied in concentrations of 0.025 to 0.1%) applied
once in a thin film over the abdomen may improve acute severe abdominal pain and
emesis in patients not responsive to ondansetron or benzodiazepines [108,112-116].
It is hypothesized that capsaicin may provide relief by its potent agonism on the
transient receptor potential vanilloid 1 (TRPV1) receptor. In a small retrospective
cohort of 43 patients treated for CHS in the emergency department, use of capsaicin
cream decreased total medications administered and reduced opioid requirements;
two-thirds of patients required no further treatment prior to discharge [117]. In a
separate retrospective cohort study of 201 patients with CHS, capsaicin cream was
associated with greater efficacy for symptom relief than other treatments but was
not associated with lower rates of admission or return emergency department visits
within 24 hours [118]. Thus, capsaicin may be useful in the acute treatment of CHS.
However, our experience suggests that patients may not tolerate the discomfort of
capsaicin use at home.
• Dopamine antagonists – Case reports have documented the successful use of

dopamine antagonists such as haloperidol and droperidol to abort severe episodes
of hyperemesis. [108,119-121]. In a randomized, blinded trial of 33 adults with
cannabis use and active emesis, haloperidol was superior to ondansetron in
improvement of self-rated abdominal pain and nausea and decreased time to
discharge from the emergency department [122]. (See "Cyclic vomiting syndrome",
section on 'Chronic cannabis use'.)
DISPOSITION
Disposition is determined by several factors including patient age, social circumstances,

duration of toxicity, and type of symptoms as follows:
● Children – The duration of symptoms after acute cannabis exposure in children can
vary from 4 to 48 hours depending upon the dose ingested [8,9]. Patients with
persistent vomiting, altered mental status, seizures, or excessive, purposeless motor
activity (hyperkinesis) warrant hospital admission.
Patients who remain asymptomatic or become asymptomatic following exploratory

ingestion of legally acquired cannabis products may be discharged after a brief
observation period (eg, four to six hours after ingestion).
Regardless of whether cannabis is legal in a given jurisdiction, any concerns about the
nature of a cannabis exposure in a child warrant involvement of a child abuse or social
work team to determine additional social evaluation and potential need for reporting to
child protection services. (See "Child abuse: Social and medicolegal issues", section on
'Reporting suspected abuse'.)
● Adolescents and adults – Most symptoms after acute cannabis use in adults and
adolescents resolve within a few hours and will not require hospital admission.
Hospital admission may rarely be needed for prolonged delirium or agitation requiring
repeated doses of benzodiazepines or antipsychotics. These patients should also be
screened for substance use disorders and mood disorders, and, if needed, undergo
psychiatric consultation and appropriate referrals to substance-use treatment
programs. (See "Cannabis use disorder in adults".)
The disposition for patients with complications of cannabis use depends upon the
degree of illness and response to therapy. Patients with proven myocardial infarction or
pneumothorax requiring chest tube thoracostomy warrant hospital admission to an
appropriate level of care.
ADDITIONAL RESOURCES
Regional poison control centers — Regional poison control centers in the United States are
available at all times for consultation on patients with known or suspected poisoning, and
who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-
222-1222). In addition, some hospitals have medical toxicologists available for bedside
consultation. Whenever available, these are invaluable resources to help in the diagnosis and
management of ingestions or overdoses. Contact information for poison centers around the
world is provided separately. (See "Society guideline links: Regional poison control centers".)
The Partnership at Drugfree.org maintains a drug guide for 40 commonly abused drugs
including common slang terms.
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: Cannabis use disorder and withdrawal" and "Society guideline links: General
measures for acute poisoning treatment" and "Society guideline links: Poisoning prevention"
and "Society guideline links: Treatment of acute poisoning caused by recreational drug or
alcohol use".)
SUMMARY AND RECOMMENDATIONS
● Epidemiology – Serious cannabis intoxication is rare in adolescents and adults.

Exploratory ingestions of cannabis products have caused life-threatening toxicity in
young children. (See 'Epidemiology' above and 'Children' above.)
● Clinical manifestations
• Children – Ingestion of cannabis by young children may cause (see 'Children' above):
- Life-threatening coma with apnea or depressed respirations

- Seizures
- Effects of intoxication as described below for older patients (limited exposures)
Children may warrant testing for other potential causes of altered mental status
depending upon whether the exposure is known and based upon specific physical
findings. (See 'Other ancillary studies' above and 'Children' above.)
• Adolescents and adults – Cannabis intoxication in adolescents and adults causes

(see 'Adolescents and adults' above):
- Tachycardia
- Blood pressure changes (hypertension, or in older adults, orthostatic
hypotension)
- Conjunctival injection
- Dry mouth
- Increased appetite
- Nystagmus
- Signs of intoxication such as ataxia, slurred speech, euphoria, perceptual
changes, and psychomotor impairment
Chest pain may arise from pneumothorax, exacerbation of pulmonary disease such
as asthma, or (uncommonly) myocardial ischemia. (See 'Adolescents and adults'
above.)
Investigation for other intoxicants may be indicated if symptoms are prolonged, or if

other marked physiologic abnormalities exist such as hyperthermia, acidosis,
significant rhabdomyolysis, or end-organ toxicity. Otherwise, no specific testing is
necessary. (See 'Adolescents and adults' above.)
● Diagnosis – Regardless of age, acute cannabis intoxication is a clinical diagnosis. Urine

drug screens can be helpful in confirming the diagnosis in young children because any
positive result identifies acute exposure in the setting of major toxicity. Urine drug
screens are less helpful in adolescents and adults and are not routinely needed for
diagnosis or management. (See 'Diagnosis' above and 'Drug testing for cannabinoids'
above.)
● Management
• Supportive care – Expected toxicity and treatment differs by age:
- Children – Young children may require management of coma and respiratory

depression, which frequently requires endotracheal intubation along with
exclusion of hypoglycemia and other causes of altered mental status.
For children with marked anxiety or agitation, we suggest treatment with a

benzodiazepine (eg, lorazepam) (Grade 2C). (See 'Agitation' above.)
Lorazepam is also warranted for patients who develop seizures; convulsive

status epileptics requires further treatment as summarized in the algorithm (
algorithm 1) and discussed in detail separately. (See "Management of
convulsive status epilepticus in children".)
Any concerns about the nature of a cannabis exposure in a child requires

involvement of a child abuse or social work team to determine additional social
evaluation and potential need for reporting to child protection services. (See
'Disposition' above.)
- Adolescents and adults – Mild intoxication with dysphoria can be managed

with a dimly lit room, reassurance, and decreased stimulation. For patients with
ongoing anxiety despite these measures, we suggest benzodiazepines (eg, oral
lorazepam) (Grade 2C). (See 'Mild intoxication' above.)
Marked agitation or combativeness should prompt consideration of a possible

co-ingestion (eg, cocaine, amphetamines, phencyclidine [PCP]) or coexisting
mental illness. Management of the acutely agitated or violent adult is discussed
in detail separately. (See "Assessment and emergency management of the
acutely agitated or violent adult", section on 'Chemical sedation'.)
Chest pain in association with cannabis use requires identification and

treatment of the underlying etiology (eg, acute coronary syndrome,
pneumothorax, or asthma exacerbation). (See 'Chest pain' above.)
• Gastrointestinal decontamination – For patients who ingest cannabis or cannabis-

containing products or food, we suggest not administering activated charcoal
because of the potential for rapid onset of altered mental status with apnea or
seizures in young children and lack of efficacy in otherwise symptomatic patients
(Grade 2C). (See 'Gastrointestinal decontamination' above.)
• Cannabis hyperemesis syndrome (CHS) – CHS is a clinical syndrome of cyclic

abdominal pain, vomiting, or nausea in older adolescents and adults with chronic
cannabis use. Relief of symptoms with hot showers or baths is a common feature.
Management includes (see 'Cannabis hyperemesis syndrome' above):
- Antiemetic therapy – We suggest ondansetron as the first-line agent (Grade 2C);

metoclopramide is a reasonable alternative. If vomiting persists, we suggest a
benzodiazepine (eg, lorazepam) (Grade 2C).
- Fluid repletion.
- Laboratory evaluation to exclude other etiologies or to identify complications of

excessive vomiting.
- For patients unresponsive to supportive measures (conventional antiemetics

and fluid repletion) and for whom alternative causes of nausea, vomiting, and
abdominal pain have been excluded, we suggest a trial of topical capsaicin
(Grade 2C).
- For patients with persistent moderate to severe abdominal pain and vomiting
despite the above interventions, we suggest droperidol or haloperidol (Grade
2C).
- All patients should receive counseling regarding the need to decrease cannabis
use (both potency of products and frequency of use) and referral to support
abstinence.
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Topic 97099 Version 42.0
GRAPHICS
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
Cellular asphyxiants Antiparkinson agents
Carbon monoxide Antispasmodics
Cyanide Muscle relaxants
Hydrogen sulfide Plants containing belladonna alkaloids
Methemoglobinemia Phenothiazines
Lithium Tricyclic antidepressants
Cholinergics Salicylates
Organophosphates Central hallucinogens
Carbamates Lysergic acid diethylamide (LSD)
Sympatholytics Phencyclidine
Beta blockers Mescaline
Sedative-hypnotics Psilocybin
Benzodiazepines Ketamine
Barbiturates Designer amphetamines
Alpha-2 adrenergic agonists (eg clonidine, Synthetic cannabinoids

dexmedetomidine)
Drug withdrawal states
Muscle relaxants
Lithium
Hypoglycemic agents
Carbon monoxide
Heavy metals
Hypoglycemic agents
Opiates
Heavy metals
Antiseizure medications
Mushrooms
Salicylates
Gamma-hydroxybutyrate
Volatile inhalants
Alcohols
Graphic 80618 Version 10.0
Rapid overview of rapid sequence intubation in children
Preparation - Utilize an active checklist to:
Begin preoxygenation as described below.
Identify conditions that will affect choice of medications (eg, increased intracranial pressure,
septic shock, bronchospasm, status epilepticus, or, if succinylcholine use is planned, absolute
contraindications for its use as listed below).
Identify conditions that will predict difficult intubation or bag-mask ventilation (eg, small chin,
inability to fully open the mouth, upper airway trauma, or infection).
Assemble equipment and check for function.
Develop contingency plan for failed intubation (refer to UpToDate topics on devices for difficult
endotracheal intubation).
Preoxygenation
Begin preoxygenation as soon as rapid sequence intubation is potentially needed:
Spontaneously breathing: 100% FiO 2 (>7 L/min oxygen flow) by nonrebreather mask for 3
minutes
Apneic or inadequate breathing: Bag-mask ventilation with small tidal breaths using
100% FiO 2
During induction and paralysis, provide apneic oxygenation via nasal cannula at flow rate
of 1 L/kg/min (maximum flow 15 L/min)
Administer oxygen at the highest concentration available.
Pretreatment (optional)
Atropine: Although not routinely recommended, many experts suggest atropine as

pretreatment for:
Children ≤1 year
Children in shock
Children <5 years receiving succinylcholine
Older children receiving a second dose of succinylcholine
Dose: 0.02 mg/kg IV without a minimum dose (maximum single dose 1 mg; if no IV access, can
be given IM).
Induction (sedation)
Etomidate:
Safe with hemodynamic instability, neuroprotective, transient adrenal cortico-

suppression. Do not use routinely in patients with septic shock.
Dose: 0.3 mg/kg IV.
Ketamine:
Safe with hemodynamic instability if patient is not catecholamine depleted. Use in
patients with bronchospasm and septic shock. Use with caution in hypertensive patients
with increased intracranial pressure.
Dose: 1 to 2 mg/kg IV (if no IV access, can be given IM dose: 3 to 7 mg/kg).
Propofol:
Causes hypotension. May use in hemodynamically stable patients with status epilepticus.
Dose 1 to 1.5 mg/kg IV.
Midazolam:
May use in hemodynamically stable patients with status epilepticus. Time to clinical effect
is longer; inconsistently induces unconsciousness. May cause hemodynamic instability at
doses required for sedation.
Dose: 0.2 to 0.3 mg/kg IV (maximum dose 10 mg; onset of effect requires 2 to 3 minutes).
Fentanyl:
Optional for cardiogenic shock or catecholamine-depleted shock (eg, persistent
hypotension despite vasopressor therapy). Limited evidence in children.
Dose 1 to 5 mcg/kg titrated to effect. Start at lower end of range in hypotensive patients.
Give over 30 to 60 seconds to avoid respiratory depression or chest wall rigidity.
Paralytic
Rocuronium:
Use for children with contraindication for succinylcholine or as primary paralytic if
sugammadex is immediately available.
Dose: 1 mg/kg IV.*
Succinylcholine:
Do not use with extensive crush injury with rhabdomyolysis, chronic skeletal muscle
disease (eg, Becker muscular dystrophy) or denervating neuromuscular disease (eg,
cerebral palsy with paralysis); 48 to 72 hours after burn, multiple trauma, or denervating
injury; patients with history or malignant hyperthermia; or pre-existing hyperkalemia.
Dose: Infants and children ≤2 years: 2 mg/kg IV, older children and adolescents: 1 to 1.5
mg/kg IV (if IV access unobtainable, can be given IM, dose: 4 mg/kg) ¶ .
Protection and positioning
Maintain manual cervical spine immobilization during intubation in the trauma patient.
If cervical spine injury is not potentially present, put the patient in the "sniffing position" (ie,
head forward so that the external auditory canal is anterior to the shoulder and the nose and
mouth point to the ceiling).
Utilize external laryngeal manipulation or, in infants, gentle cricoid pressure to optimize the
view of the glottis during direct laryngoscopy if the initial view is suboptimal or inadequate
despite correct laryngoscope blade positioning. Δ
Positioning, with placement
Confirm tracheal tube placement with end-tidal CO 2 detection and auscultation.
Postintubation management
Obtain a chest radiograph to confirm the depth of tracheal tube insertion.
Provide ongoing sedation (eg, midazolam), analgesia (eg, fentanyl 1 mcg/kg), and, if indicated,
paralysis. ◊
If IV access is not rapidly obtained, intraosseous administration of drugs is an acceptable

alternative.
IM: intramuscularly; IV: intravenously; CO 2 : carbon dioxide; FiO 2 : fraction of inspired oxygen.
* Sugammadex in a dose of 16 mg/kg can provide immediate reversal of paralysis when given
approximately 3 minutes after a single dose of rocuronium or vecuronium. Vecuronium may be
used in children with contraindications to succinylcholine and when rocuronium is not available.
Suggested dose for rapid sequence intubation: vecuronium 0.15 to 0.2 mg/kg. Patients may
experience prolonged and unpredictable duration of paralysis at this dose.
¶ Defasciculating agents (eg, rocuronium or vecuronium at one-tenth of the paralyzing dose) are
not routinely recommended for children receiving succinylcholine. Onset of paralysis is slower by
the IM route; the clinician must ensure full pre-oxygenation prior to administration, whenever
possible, and be prepared to perform bag-mask ventilation if desaturation occurs before the
patient is fully paralyzed for endotracheal intubation.
Δ Bimanual laryngoscopy, also called external laryngeal manipulation (ELM), entails manipulating
the thyroid cartilage or hyoid bone with the right hand during laryngoscopy in order to improve
the view of the glottis. For a description of how to perform ELM, refer to topics on emergency
endotracheal intubation in children and rapid sequence intubation in children.
◊ If decompensation occurs after successful intubation, use the DOPE mnemonic to find the
cause:
D: Dislodgement of the tube (right mainstem or esophageal)
O: Obstruction of tube
P: Pneumothorax
E: Equipment failure (ventilator malfunction, oxygen disconnected or not on)
Rapid overview for diagnosis and treatment of hypoglycemia in

adolescents and children (other than neonates) in the Emergency
Department
Clinical features
Any patient with acute lethargy or coma should have an immediate measurement of blood
glucose to determine if hypoglycemia is a possible cause
Other findings of hypoglycemia are nonspecific* and vary by age:
Infants Older children and adolescents
Irritability Neurogenic (autonomic) Neuroglycopenic response

Lethargy response Irritability
Jitteriness Sweating Confusion
Feeding problems Tachycardia Uncharacteristic
Hypothermia Palpitations behavior
Hypotonia Tremor Weakness
Tachypnea Nervousness Lethargy
Cyanosis Hunger Loss of consciousness
Apnea Paresthesias Seizures
Seizures Pallor Coma
Occasionally, transient
focal neurologic deficits
Diagnosis
Obtain rapid bedside point-of-care glucose concentration (and beta-hydroxybutyrate, if

available as a point-of-care measurement)
Confirm the presence of hypoglycemia with a plasma glucose measurement (drawn close in
time to the point-of-care sample)
Treat, as outlined below, if the bedside value is low (<70 mg/dL [3.89 mmol/L]) in
symptomatic patients
For all infants and young children who are not being treated for diabetes mellitus or do not
have a known cause for hypoglycemia, obtain a blood sample for additional diagnostic
studies prior to glucose administration, if possible, and collect the first voided urine after the
hypoglycemic event. ¶
Treatment
Do not delay treatment if symptomatic hypoglycemia is suspected. However, every

reasonable effort should be made to obtain a rapid plasma glucose measurement
(fingerstick or point-of-care device) prior to administering glucose.
Give glucose based upon the patient's level of consciousness and ability to swallow
safely (ie, alert enough to do so and with intact gag reflex) as follows:
Conscious and able to drink and swallow safely:
Administer 0.3 g/kg (10 to 20 g) of a rapidly-absorbed carbohydrate. May repeat in

10 to 15 minutes.
Options include any one of the following:
Glucose tablets (5 g per tablet)

Glucose gel (15 g per tube)
Sweetened fruit juice: 12 g carbohydrate per 4 oz (120 mL)
Regular soda (not diet): 18 g carbohydrate per 6 oz (180 mL)
Honey: 17 g carbohydrate per 1 tablespoon (15 mL)
Table sugar (granulated sugar): 12.5 g sugar per 1 tablespoon
Altered mental status, unable to swallow, or does not respond to oral glucose
administration within 15 minutes:
Give an initial IV bolus of glucose of 0.25 to 0.5 g/kg of dextrose (maximum single
dose 25 g). Δ The volume and concentration of glucose bolus is infused slowly at 2
to 3 mL per minute and based upon age:
Infants and children up to 12 years: 2.5 to 5 mL/kg of 10% dextrose solution

(D10W), or 1 to 2 mL/kg of 25% dextrose (D25W). D10W is typically used in
infants and children <5 years of age. (10% dextrose is 100 mg/mL; 25% dextrose
is 250 mg/mL.)
Adolescents ≥12 years: 1 to 2 mL/kg of D25W
Unable to receive oral glucose and unable to obtain IV access:
Give glucagon 0.5 mg (for <25 kg body weight) or 1 mg (for ≥25 kg body weight)
IM or SQ (maximum dose 1 mg): ◊
Perform blood glucose monitoring every 10 to 15 minutes as the effects of

glucagon may be transient
Establish vascular access as soon as possible; if unable to achieve access and
hypoglycemia persists or is recurrent, ensure the airway is protected and, if not,
secure it with rapid sequence intubation. Then place a nasogastric tube and
administer 0.2 to 0.25 g/kg dextrose using volume and concentration guidance
for IV administration above.
After initial hypoglycemia is reversed, provide additional glucose and treatment based upon
suspected etiology:
For patients with type 1 diabetes mellitus: Give a normal diet; initiate IV dextrose-
containing fluids if intake is inadequate.
For patients with an underlying hypoglycemic disorder or with an unknown cause of
hypoglycemia: Administer an intravenous infusion of dextrose 10%:
For infants, start with initial glucose infusion rate (GIR) of 5 to 6 mg/kg/minute
For older children, start with GIR of 2 to 3 mg/kg/minute
Calculation to convert target GIR to infusion rate:
Rate of dextrose infusion (mL/hr) = GIR (mg/kg/minute) × 6 × weight (kg) ÷
dextrose percentage of fluid (eg, 5 for 5% dextrose [D5W] or 10 for D10W)
Titrate infusion to maintain plasma glucose in a safe and appropriate range (70 to
120 mg/dL [3.89 to 8.33 mmol/L]).
Patients who have ingested a long-acting hypoglycemia agent such as a sulfonylurea
may require prolonged treatment until the effect wears off. Selected patients may also
warrant treatment with octreotide. (Refer to UpToDate topic on sulfonylurea poisoning.)
Measure a rapid plasma glucose 15 to 30 minutes after the initial IV glucose bolus and then
monitor every 30 to 60 minutes until stable (minimum of four hours) to ensure that plasma
glucose concentration is maintained in the normal range (>70 to 100 mg/dL [>3.89 to 5.55
mmol/L])
Obtain pediatric endocrinology consultation for patients with persistent hypoglycemia and
for hypoglycemia of unknown cause
Obtain medical toxicology consultation for patients with ingestion of oral hypoglycemic
agents by calling a regional poison control center. §
Admit the following patients:
Cannot maintain normoglycemia with oral intake
Hypoglycemia of unknown cause
Ingestion of long-acting hypoglycemic agents
Recurrent hypoglycemia during the period of observation
IV: intravenous; IM: intramuscular; SQ: subcutaneous; D10W: 10% dextrose in water; D25W: 25%
dextrose in water; D50W: 50% dextrose in water; GIR: glucose infusion rate.
* These findings may also occur in infants with sepsis, congenital heart disease, respiratory
distress syndrome, intraventricular hemorrhage, other metabolic disorders, and in children and
adolescents with a variety of underlying conditions.
¶ Specific laboratory studies to obtain in children include blood samples for glucose, insulin, C-
peptide, beta-hydroxybutyrate, lactate (free flowing blood must be obtained without a
tourniquet), plasma acylcarnitines, free fatty acids, growth hormone, and cortisol.
Δ Higher doses of glucose (eg, 0.5 to 1 g/kg [5 to 10 mL/kg of 10% dextrose in water or 2 to 4
mL/kg of 25% dextrose in water]) is recommended by the Pediatric Advanced Life Support course
and may be needed to correct hypoglycemia caused by excess insulin administration or
sulfonylurea ingestion. (For more detail, refer to UpToDate topic on sulfonylurea agent
poisoning.)
◊ Glucagon will reverse hypoglycemia caused by excess endogenous or exogenous insulin and
will not be effective in patients with inadequate glycogen stores (prolonged fasting), ketotic
hypoglycemia, or are unable to mobilize glycogen (glycogen storage diseases). Of note, children
may exhaust their glycogen stores in as little as 12 hours. Other conditions in which glycogen
cannot be effectively mobilized include ethanol intoxication in children, adrenal insufficiency, and
certain inborn errors of metabolism (eg, a disorder of glycogen synthesis and glycogen storage
diseases).
§ To access a regional poison control center in the United States, call 1-800-222-1222. Contact
information for poison centers around the world is available at the following website:
https://www.liquidglassnanotech.com/poison-emergency-center-contact-numbers/.
Opioid intoxication in children and adolescents: Rapid overview
To obtain emergency consultation with a medical toxicologist, in the United States, call 1-800-222-
1222, or the nearest international regional poison center. Contact information for regional poison
centers around the world is available at the website referenced below. [1]
Clinical features*
Depressed mental status ranging from lethargy to coma
Miotic pupils (often pinpoint) Δ
Depressed respirations including apnea
Bradycardia and hypotension
Decreased to absent bowel sounds
Track marks (adolescents with IV drug abuse)
Ancillary studies ◊
Blood glucose and pulse oximetry in patients with coma and depressed respirations
Serum ethanol level, especially in adolescents with recreational or suicidal overdose
Serum acetaminophen if suicidal intent or ingestion of combination medications (eg,

acetaminophen with oxycodone)
Electrocardiogram in patients intoxicated with methadone (prolonged QTc) or propoxyphene

(prolonged QRS)
Chest radiograph in patients with persistent respiratory findings that suggest pulmonary
aspiration or noncardiogenic pulmonary edema
Urinalysis, serum electrolytes, blood urea nitrogen, creatinine, and creatine kinase in patients with
prolonged immobilization or muscular rigidity at risk for rhabdomyolysis
Rapid urine pregnancy test in postmenarchal girls
Rapid urine testing for opioids in young children and infants with coma from unknown cause or in
whom intentional poisoning by a caretaker is suspected
Treatment
Support airway and breathing using bag-mask ventilation with 100 percent inspired oxygen until
naloxone is administered
Give naloxone for deep coma and respiratory depression as follows § :
¥
- Children <20 kg: 0.1 mg/kg IV or IO (maximum 2 mg per dose) except neonates ¥
- Children over 20 kg: 2 mg IV or IO
- Adolescents suspected of opioid addiction: 0.04 to 0.4 mg per dose repeated every 3-5
minutes and titrated to patient response
- If no effect, repeat the naloxone dose every one to two minutes to a maximum total dose of 10
mg
- Patients with recurrent toxicity may receive additional bolus doses or a continuous naloxone
infusion. Begin the infusion rate at 2/3 of the total dose of naloxone needed to restore
breathing, delivered every hour.
If the patient develops respiratory depression despite the naloxone infusion (this may
happen 20 to 30 minutes after starting infusion) administer a naloxone bolus (using half the
original effective bolus dose) and repeat if necessary until adequate ventilation returns, then
increase the infusion rate
If the patient develops signs of opioid withdrawal, stop the infusion. If respiratory
depression returns, start the infusion at half the original rate.
Give activated charcoal (1 gram/kg orally or by nasogastric tube, maximum dose 50 grams) to alert
young children and adolescents who present within one hour of oral overdose ‡
In cases of suspected child abuse, consult an experienced children protection team (if available)
and report suspicion to the appropriate governmental agency
Consult psychiatry for patients with substance abuse or suicidal intent
IO: intraosseous; AC: activated charcoal; ET: endotracheal tube; IM: intramuscular.
* The diagnosis of opioid intoxication is based upon clinical features and response to antidotal
therapy.
Δ Small pupils are not always present in children and adolescents with opioid intoxication.
◊ Other ancillary studies may be indicated in selected patients in whom trauma, infection, or
other etiologies besides poisoning are suspected. Refer to UpToDate topics on stupor and coma
in children and pediatric occult toxic exposures.
§ Naloxone may also be given intramuscularly or intratracheally via endotracheal tube (ET) in
children or adolescents with poor IV access. If an endotracheal tube is present, ET administration
is preferred over intramuscular, if IV and IO routes not available. ET dose is approximately two to
three times IV dose.
¥ Naloxone administration is not recommended as part of initial resuscitation of neonates in the
delivery room. Refer to UpToDate topics on neonatal resuscitation.
‡ AC should be withheld in patients who are sedated and may not be able to protect their airway,
unless endotracheal intubation is performed first or naloxone therapy is effective in maintaining
an alert state. Endotracheal intubation should not be performed solely for the purpose of giving
AC.
Reference:
1. Poison emergency center contact numbers. Liquid Glass Nanotech. Available at:
https://www.liquidglassnanotech.com/poison-emergency-center-contact-numbers/ (Accessed on May 25, 2021).
Initial management of status epilepticus in children
Timeline* Assessment Supportive care Seizure therapy
0 to 5 Obtain initial vital signs, Open airway Benzodiazepine:

minutes including temperature
Suction secretions Lorazepam 0.1 mg/kg IV
or IO, maximum 4 mg
Administer 100% O 2
OR
Identify airway Place continuous
obstruction and cardiorespiratory Diazepam 0.2 mg/kg IV
hypoxemia monitors and pulse or IO, maximum 10 mg
oximetry IV or IO access not
Identify impaired Perform bag-valve-mask achieved within 3
oxygenation or ventilation, as needed minutes:
ventilation Buccal midazolam 0.3 to
Prepare for RSI*
0.5 mg/kg, maximum 10
Obtain rapid bedside Establish IV or IO access
mg
blood glucose and other
studies, as indicated ¶ OR
Evaluate for signs of Treat hypoglycemia (IV IM midazolam 0.1 to 0.2

sepsis/meningitis dextrose 0.25 to 0.5 g/kg) mg/kg, maximum 10 mg
OR
Evaluate for signs of head Treat fever
trauma (acetaminophen 15 Rectal diazepam (Diastat
mg/kg rectally) gel or injection solution
given rectally) 0.5 mg/kg,
maximum 20 mg
5 to 10 Reevaluate vital signs, Maintain monitoring, Benzodiazepine: second

minutes airway, breathing, and ventilatory support, and dose
circulation vascular access
Evaluate for signs of Give antibiotics if signs of

trauma, sepsis, sepsis or meningitis Δ
meningitis, or
encephalitis
10 to 15 Reevaluate vital signs, Maintain monitoring, Levetiracetam 60 mg/kg

minutes airway, breathing, and ventilatory support, and IV or IO, maximum single
circulation vascular access dose 4500 mg
Place second IV OR
RSI potentially indicated* Fosphenytoin 20 mg PE

per kg IV or IO, maximum
single dose 1500 mg ◊
OR
Valproate 20 to 40 mg/kg
IV or IO
OR
Phenobarbital 20 mg/kg
IV or IO, maximum 1 g
(expect a respiratory
depression with apnea) ¥
15 to 30 Reevaluate vital signs, Maintain monitoring, Fosphenytoin (if not

minutes airway, breathing, and ventilatory support, and already given) 20 mg PE
circulation vascular access per kg IV or IO ◊
Obtain continuous EEG OR

monitoring, if available Valproate (if not already
given) 20 to 40 mg/kg IV
or IO
OR
Phenobarbital (if not

already given) 20 mg/kg
IV or IO, maximum 1 g (10
mg/kg if phenobarbital
already given) ¥
OR
Levetiracetam (if not

already given) 60 mg/kg
IV or IO
AND
Pyridoxine 100 mg IV or
IO in infants <1 year of
age
Pyridoxine 70 mg/kg IV
or IO, maximum 5 g, if
INH poisoning suspected
Obtain pediatric
neurology consultation ‡
RSI: rapid sequence endotracheal intubation; IV: intravenous; IO: intraosseous; IM: intramuscular;
O 2 : oxygen; PE: phenytoin equivalents; EEG: electroencephalogram; INH: isoniazid.
* Rapid sequence intubation should be performed if airway, ventilation, or oxygenation cannot
be maintained and if the seizure becomes prolonged.
¶ For ancillary studies to obtain in children with status epilepticus, refer to UpToDate topics on
status epilepticus in children.
Δ Empiric antibiotic regimens vary depending on patient susceptibility and likely pathogen.
◊ Do not exceed 2 mg PE/kg per minute (maximum rate: 150 mg per minute). If fosphenytoin not
available, may use phenytoin 20 mg/kg IV, do not exceed 1 mg/kg per minute (maximum rate: 50
mg per minute). Both fosphenytoin and phenytoin infusion require cardiac monitoring. Phenytoin
and fosphenytoin may be less effective for the treatment of seizures due to toxins or drugs and
may intensify seizures caused by cocaine, other local anesthetics, theophylline, or lindane. In
such cases, levetiracetam, valproate, or phenobarbital should be used.
¥ When administering phenobarbital, the maximum infusion rate is 2 mg/kg per minute with a
ceiling of 50 mg/min. Anticipate respiratory depression.
‡ In patients with ongoing seizure activity despite two initial doses of benzodiazepine and a
second-therapy antiseizure medication, preparation for a continuous infusion of midazolam,
propofol, or pentobarbital should occur simultaneously with administration of a third-therapy
antiseizure medication.
Approach to treatment of convulsive status epilepticus in children and adolescen
This algorithm summarizes our suggested approach to antiseizure treatment for convulsive status epilepticus
unremitting seizure lasting >5 minutes or frequent clinical seizures without an interictal return to the baseline
with CSE require simultaneous, rapid initiation of monitoring, including frequent core temperature measurem
recognition and treatment of hypoglycemia and other potential underlying causes, such as complex febrile se
infection, sepsis, and traumatic brain injury. Refer to UpToDate topics on pediatric CSE for additional details.
EMS: emergency medical services; IV: intravenous; IO: intraosseous; ICP: intracranial pressure; IM: intramuscu
intensive care unit; RSI: rapid sequence endotracheal intubation; NCSE: nonconvulsive status epilepticus; RSE:
* Rapid sequence intubation should be performed if airway, ventilation, or oxygenation cannot be maintained
¶ For ancillary studies to obtain in children with status epilepticus, refer to UpToDate topics on status epileptic
Δ Common causes of pediatric CSE are listed here. If isoniazid poisoning is suspected, pyridoxine should be ad
discussion of causes of CSE in children, refer to UpToDate's topic on pediatric CSE.
◊ Additional evaluation may include neuroimaging if CSE is the first presentation of epilepsy or if there are ne
increased ICP, or prolonged duration of depressed consciousness (ie, for >1 to 2 hours after the episode). For
with CSE, refer to UpToDate topics on pediatric CSE.
§ Refer to text for dosing intranasal midazolam.
¥ Phenytoin and fosphenytoin may be less effective for the treatment of seizures due to toxins or drugs and m
theophylline, or lindane. In such cases, levetiracetam, valproate, or phenobarbital should be used.
‡ With fosphenytoin administration, the rate of infusion should not exceed 2 mg PE/kg per minute (maximum
phenytoin may be used (20 mg/kg IV; do not exceed 1 mg/kg per minute; maximum rate: 50 mg per minute).
† When administering phenobarbital, the maximum infusion rate is 2 mg/kg per minute with a ceiling of 50 m
Rapid overview: Management of ST-elevation myocardial infarction

(STEMI) or non-ST-elevation acute coronary syndrome (NSTEACS)
Initial assessment:
Consider the diagnosis in patients with chest discomfort, shortness of breath, or other
suggestive symptoms. Women, older adults, and patients with diabetes may have "atypical"
presentations.
Obtain 12-lead ECG within 10 minutes of arrival; repeat every 10 to 15 minutes if initial ECG
is nondiagnostic but clinical suspicion remains high (initial ECG often not diagnostic).
1. STEMI: ST-segment elevations ≥1 mm (0.1 mV) in two anatomically contiguous leads or

≥2 mm (0.2 mV) in leads V2 and V3 or new left bundle branch block and presentation
consistent with ACS. If ECG suspicious but not diagnostic, consult cardiologist early.
2. Non-STEMI or unstable angina: ST-segment depressions or deep T-wave inversions

without Q waves or possibly no ECG changes.
Obtain emergency cardiology consultation for ACS patients with cardiogenic shock, left
heart failure, or sustained ventricular tachyarrhythmia.
Initial interventions:
Assess and stabilize airway, breathing, and circulation.
Attach cardiac and oxygen saturation monitors; provide supplemental oxygen as needed to
maintain O 2 saturation >90%. Establish IV access.
Treat sustained ventricular arrhythmia rapidly according to ACLS protocols.
Give aspirin 325 mg (nonenteric coated) to be chewed and swallowed (unless aortic
dissection is being considered). If oral administration is not feasible, give as rectal
suppository.
Perform focused history and examination: Look for signs of hemodynamic compromise and
left heart failure; determine baseline neurologic function, particularly if fibrinolytic therapy is
to be given.
Obtain blood for cardiac biomarkers (troponin preferred), electrolytes,

hematocrit/hemoglobin. Perform coagulation studies for patients taking anticoagulants or
as otherwise indicated (eg, known coagulopathy).
Give three sublingual nitroglycerin tablets (0.4 mg) one at a time, spaced five minutes apart,
or one aerosol spray under tongue every 5 minutes for 3 doses if patient has persistent
chest discomfort, hypertension, or signs of heart failure and there is no sign of
hemodynamic compromise (eg, right ventricular infarction) and no use of
phosphodiesterase inhibitors (eg, for erectile dysfunction); add IV nitroglycerin for persistent
symptoms.
Treat left heart failure if present: Give afterload-reducing agent (eg, nitroglycerin sublingual
tablet and/or IV drip at 40 mcg/minute provided no hypotension and no phosphodiesterase
inhibitors [eg, for erectile dysfunction]; titrate drip up quickly based on response); give loop
diuretic (eg, intravenous furosemide); administer noninvasive positive pressure ventilation
(eg, BLPAP) to appropriate patients.
Give beta blocker (eg, metoprolol tartrate 25 mg orally) if no signs of heart failure and not at
high risk for heart failure and no signs of hemodynamic compromise, bradycardia, or severe
reactive airway disease. If hypertensive, may initiate beta blocker IV instead (eg, metoprolol
tartrate 5 mg intravenous every 5 minutes for 3 doses as tolerated).
Give morphine sulfate (2 to 4 mg slow IV push every 5 to 15 minutes) for unacceptable,

persistent discomfort or anxiety related to myocardial ischemia.
Start 80 mg of atorvastatin as early as possible and preferably before PCI in patients not on
statin. If patient is taking a low- to moderate-intensity statin, switch to atorvastatin 80 mg.
Acute management STEMI:
Select reperfusion strategy: Primary PCI strongly preferred, especially for patients with
cardiogenic shock, heart failure, late presentation, or contraindications to fibrinolysis.
Activate cardiac catheterization team as indicated. For patients with symptoms of >12 hours,
fibrinolytic therapy is not indicated, but emergent PCI may be considered, particularly for
patients with evidence of ongoing ischemia or those at high risk of death.
Treat with fibrinolysis if PCI unavailable within 120 minutes of first medical contact,
symptoms <12 hours, and no contraindications.*
Give oral antiplatelet therapy (in addition to aspirin) to all patients:
1. Patients treated with fibrinolytic therapy: Give clopidogrel loading dose 300 mg if
age 75 years or less; if age over 75 years, give loading dose of 75 mg.
2. Patients treated with no reperfusion therapy: Give ticagrelor loading dose 180 mg.
3. Patients treated with primary PCI: Give ticagrelor loading dose of 180 mg or
prasugrel loading dose of 60 mg (if no contraindications: prior stroke or TIA, or relative
contraindications for prasugrel such as those age 75 years or older, weight less than 60
kg). For patients at high risk of bleeding or those for whom prasugrel or ticagrelor
cannot be used, we give clopidogrel 600 mg.
Give anticoagulant therapy to all patients:
1. For patients treated with primary PCI, we prefer UFH to bivalirudin. This
recommendation assumes that patients will receive a potent oral antiplatelet agent
(ticagrelor or prasugrel), which we prefer to clopidogrel. For those patients who receive
clopidogrel, we prefer bivalirudin.
Dosing of UFH: An initial IV bolus of 50 to 70 units/kg up to a maximum of 5000

units. Additional heparin may be given in the catheterization laboratory based on
the results of ACT monitoring.
Dosing of bivalirudin: Initial bolus of 0.75 mg/kg IV followed by IV infusion of 1.75
mg/kg per hour; can be discontinued after PCI.
2. For patients treated with fibrinolysis, we prefer enoxaparin for patients not at high
bleeding risk or fondaparinux for those at high bleeding risk. For those patients in
whom PCI is possible or likely after fibrinolytic therapy, UFH is reasonable.
Dosing of enoxaparin
Patients <75 years: Loading dose of 30 mg IV bolus followed by 1 mg/kg
subcutaneously every 12 hours; maximum of 100 mg for the first two
subcutaneous doses. The first subcutaneous dose should be administered with
the IV bolus.
Dose adjustment for renal impairment (CrCl <30 mL/minute)*: Loading
dose of 30 mg IV followed by 1 mg/kg subcutaneously every 24 hours. The
first subcutaneous dose should be administered with the IV bolus.
Patients ≥75 years: No IV loading dose. Administer 0.75 mg/kg subcutaneously
every 12 hours; maximum of 75 mg for the first two doses.
Dose adjustment for renal impairment (CrCl <30 mL/minute)*: No IV
loading dose. Administer 1 mg/kg subcutaneously every 24 hours.
Supplemental IV bolus dose for patients who will receive PCI after >1 dose of
therapeutic enoxaparin: 0.3 mg/kg if last enoxaparin dose was given 8 to 12
hours earlier; no supplemental IV dose if last enoxaparin dose was within 8
hours; use UFH if last enoxaparin dose was more than 12 hours ago.
Dosing of UFH: IV bolus of 60 to 100 units/kg to a maximum of 4000 units,
followed by an IV infusion of 12 units/kg per hour (maximum 1000 units per hour)
adjusted to achieve a goal aPTT of approximately 50 to 70 seconds (1.5 to 2 times
control).
Dosing of fondaparinux: 2.5 mg intravenously, followed by 2.5 mg

subcutaneously every 24 hours. This drug should be avoided in CrCl <30
mL/minute.
3. For patients not receiving reperfusion therapy, we use enoxaparin or UFH.
Dosing of enoxaparin: Dose same as for patients treated with fibrinolysis (refer to
section 2 above).
Dosing of UFH: IV bolus of 50 to 70 units/kg to a maximum of 5000 units, followed
by an IV infusion of 12 units/kg per hour adjusted to achieve a goal aPTT of
approximately 50 to 70 seconds (1.5 to 2 times control).
Acute management of unstable angina or non-STEMI:
Give antiplatelet therapy (in addition to aspirin) to all patients:
1. Patients not treated with an invasive approach: Give ticagrelor loading dose 180 mg.
For these patients who are at very high risk (eg, recurrent ischemic discomfort, dynamic
ECG changes, or hemodynamic instability), consider adding a GP IIb/IIIa inhibitor (either
eptifibatide or tirofiban).
2. For patients managed with an invasive approach: Give ticagrelor loading dose of 180
mg at presentation. Prasugrel loading dose of 60 mg may be used as an alternative if
given after diagnostic coronary angiography.
For patients age 75 years or older, who weigh less than 60 kg, or with past stroke or
TIA, ticagrelor or clopidogrel are preferred to prasugrel. Clopidogrel may be given in a
dose of 300 to 600 mg, but we prefer 600 mg. For patients otherwise at high risk for
bleeding due to prior hemorrhagic stroke, ongoing bleeding, bleeding diathesis, or
clinically relevant anemia or thrombocytopenia, clopidogrel 300 to 600 mg is an
option.
For patients treated with an invasive approach and who receive bivalirudin, we do not
recommend routinely giving a GP IIb/IIIa inhibitor; for those patients treated with
heparin and who are troponin-positive, we suggest adding a GP IIb/IIIa inhibitor
(either abciximab or eptifibatide) given after diagnostic angiography. For those
undergoing an invasive approach who are at very high risk (eg, recurrent ischemic
discomfort, dynamic ECG changes, or hemodynamic instability), we consider adding a
GP IIb/IIIa inhibitor prior to diagnostic angiography (either eptifibatide or tirofiban) or
after diagnostic angiography (abciximab or eptifibatide). Refer to text for dosing.
Give anticoagulant therapy in all patients:
1. For patients undergoing urgent catheterization (within four hours) or those
managed with an early invasive strategy (angiography within 4 to 48 hours), we

use either heparin or bivalirudin. We prefer initiation of heparin in the emergency
department and a switch to bivalirudin in the catheterization laboratory.
Dosing of UFH: IV bolus of 60 to 70 units/kg to a maximum of 5000 units, followed

by an IV infusion of 12 units/kg per hour adjusted to achieve a goal aPTT of
approximately 50 to 70 seconds (1.5 to 2 times control).
Dose of bivalirudin: If bivalirudin is given in the emergency department, IV bolus
of 0.1 mg/kg and an infusion of 0.25 mg/kg per hour before angiography. If PCI is
performed, an additional 0.5 mg/kg bolus is given and the infusion rate is
increased to 1.75 mg/kg per hour.
2. For patients receiving a noninvasive approach, we recommend either fondaparinux

or enoxaparin.
Enoxaparin is an alternative to UFH for patients not undergoing an early invasive

approach. No loading dose is necessary. Dosing is 1 mg/kg subcutaneously every
12 hours. Dose adjustment for renal impairment (CrCl <30 mL/minute)*: 1 mg/kg
subcutaneously every 24 hours.
Fondaparinux: 2.5 mg subcutaneously every 24 hours. This drug should be
avoided in patients with a CrCl <30 mL/minute.
Other important considerations:
Cocaine-related ACS: Give benzodiazepines (eg, lorazepam 2 to 4 mg IV every 15 minutes or

so) as needed to alleviate symptoms; Give standard therapies (eg, aspirin, nitroglycerin) but
do not give beta blockers.
Stop NSAID therapy if possible.
Correct any electrolyte abnormalities, especially hypokalemia and hypomagnesemia, which

often occur together.
ECG: electrocardiogram; STEMI: ST-elevation myocardial infarction; ACS: acute coronary

syndrome; IV: intravenous; ACLS: advanced cardiac life support; BLPAP: bilevel positive airway
pressure; PCI: percutaneous coronary intervention; TIA: transient ischemic attack; UFH:
unfractionated heparin; ACT: activated clotting time; CrCl: creatinine clearance estimated using
Cockcroft-Gault equation (a calculator is available in UpToDate); aPTT: activated partial
thromboplastin time; GP: glycoprotein; NSAID: nonsteroidal antiinflammatory drug.
* Repeated doses of low molecular weight heparin in patients with renal insufficiency may lead to
accumulation and increased risk of bleeding to varying degrees. By contrast, UFH is not
dependent primarily upon renal function for clearance and may be a preferred option for
patients with CrCl <20 mL/minute, kidney failure, or receiving dialysis.
Severe asthma exacerbation in adults: Rapid overview of emergency

management
Clinical danger signs
Use of accessory muscles of respiration; brief, fragmented speech; inability to lie supine;
profound diaphoresis; agitation; severe symptoms that fail to improve with initial emergency
treatment
Life-threatening airway obstruction can still occur when these signs are NOT present
Signs of imminent respiratory arrest: cyanosis, inability to maintain respiratory effort,

and depressed mental status
Assessment
Measurement of expiratory airflow (peak expiratory flow rate or PEFR) is the best measure of
severity; PEFR <40% predicted (or <200 L/minute in most adults) indicates severe obstruction;
patients in severe distress are often unable to perform peak flow tests
Severe hypoxemia (eg, SpO 2 ≤95% despite high flow O 2 treatment by nonrebreather mask)
portends imminent respiratory arrest or possibly severe complication (eg, pneumothorax);
continuous pulse oximetry monitoring should be performed
Patients in extremis should be managed clinically without waiting for arterial blood gases
(ABGs). ABGs can aid assessment of hypercapnia or impending respiratory failure: hypercapnia
usually does not occur unless PEF is <25% of normal (generally <100 to 150 L/min).
Chest radiograph is generally unhelpful; obtain if complications suspected (eg, pneumonia,

pneumothorax), diagnosis is in doubt, or patient is high-risk (eg, IV drug abuser,
immunosuppressed, chronic pulmonary disease, heart failure)
Standard treatments
Inhaled beta agonist: give albuterol 2.5 to 5 mg by nebulization every 20 minutes for three
doses, then 2.5 to 5 mg every one to four hours as needed, or give 4 to 8 puffs by metered dose
inhaler (MDI) with spacer every 20 minutes for three doses, then every one to four hours as
needed. Alternatively, for severe exacerbations, 10 to 15 mg can be administered by continuous
nebulization over one hour.
Oxygen: give sufficient oxygen to maintain SpO 2 ≥92% (>95% in pregnancy)
IV: establish intravenous access; give IV boluses of isotonic saline if patient is dehydrated due
to reduced intake and prolonged episode
Ipratropium bromide: give 500 mcg by nebulization every 20 minutes for 3 doses OR 4 to 8
puffs by MDI with spacer every 20 minutes for 3 doses; then may administer additional doses
hourly as needed for up to 3 hours
Systemic glucocorticoids: for patients with impending respiratory failure, give

methylprednisolone 60 to 125 mg IV. For the majority of less severe asthma exacerbations, give
prednisone 40 to 60 mg orally; alternatives include: dexamethasone 6 to 10 mg IV or
hydrocortisone 150 to 200 mg IV; glucocorticoids may be given IM or orally if IV access is
unavailable.
Magnesium sulfate: give 2 g (8 mmol) IV over 20 minutes for life-threatening exacerbations

and severe exacerbations that are unimproved after one hour of intensive bronchodilator
therapy
Additional treatments
Epinephrine: for patients suspected of having an anaphylactic reaction or unable to use inhaled
bronchodilators for severe asthma exacerbation, give epinephrine 0.3 to 0.5 mg IM (eg, 0.3 to
0.5 mL of 1 mg/mL [may be labeled 1:1000] solution) into the mid-outer thigh (vastus lateralis
muscle); if needed can repeat every 20 minutes for up to 3 doses; give epinephrine OR
terbutaline but not both
Terbutaline: may give 0.25 mg by SC injection every 20 minutes times 3 doses for patients
unable to use inhaled bronchodilators; give terbutaline OR epinephrine but not both
Endotracheal intubation and ventilation
The decision to intubate during the first few minutes of a severe asthma attack is clinical.
Slowing of the respiratory rate, depressed mental status, inability to maintain respiratory effort,
or severe hypoxemia suggests the patient requires intubation. In the absence of anticipated
intubation difficulty, rapid sequence intubation is preferred. Nasal intubation is not
recommended.
The goal of mechanical ventilation is to maintain adequate oxygenation and ventilation while
minimizing elevations in airway pressures. This is accomplished by using low tidal volumes (6 to
8 mL/kg), and low respiratory rates (10 to 12/minute). In some patients, elevations in PaCO 2
must be tolerated to avoid barotrauma (ie, permissive hypercapnia).*
IM: intramuscular; IV: intravenous; MDI: metered dose inhaler; PEFR: peak expiratory flow rate;
SC: subcutaneous; SpO 2 : pulse oxygen saturation.
* Please refer to the UpToDate topics on mechanical ventilation in adults with acute severe
asthma and permissive hypercapnia.
Contributor Disclosures
George Sam Wang, MD Grant/Research/Clinical Trial Support: National Institute on Drug Abuse [Impact
of marijuana legalization on opioid prescribing and poisonings in Colorado]. All of the relevant financial
relationships listed have been mitigated. Michele M Burns, MD, MPH No relevant financial relationship(s)
with ineligible companies to disclose. Stephen J Traub, MD No relevant financial relationship(s) with
ineligible companies to disclose. Michael Ganetsky, MD No relevant financial relationship(s) with
ineligible companies to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.
Conflict of interest policy

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Cannabis (marijuana): Acute intoxication

● (See "Synthetic cannabinoids: Acute intoxication".)

● (See "Cancer pain management: Role of adjuvant analgesics (coanalgesics)", section on

● (See "Symptom management of multiple sclerosis in adults", section on 'Cannabinoids'.)

● (See "Overview of the management of epilepsy in adults", section on 'Alternative

● (See "Cannabis use: Epidemiology, pharmacology, comorbidities, and adverse effects"

The public health impact of decriminalization or legalization of recreational cannabis use

● The impact of cannabis legalization on prevalence of use among youth is mixed. In

● Approximately 1 in 20 pregnant women report cannabis use some time during

PHARMACOLOGY AND TOXICITY

Site of action — The cannabinoid receptor is a G-protein-coupled receptor, which inhibits

Pharmacokinetics — Delta-9 tetrahydrocannabinol (THC) is the most psychoactive

● Inhaled cannabis – After inhalation of cannabis smoke, onset of psychoactive effects

Cannabis formulations — There are a variety of subspecies and strains of cannabis;

prognosis", section on 'Cannabidiol' and "Epilepsy syndromes in children", section on

In adolescents and adults, inhaled doses of 2 to 3 mg of THC and ingested doses of 5 to 20

The clinical manifestations of acute cannabis intoxication vary according to age.

Acute cannabis intoxication is an unusual primary complaint in adolescents and adults.

Children — In children, acute cannabis intoxication typically occurs after exploratory

Complications associated with inhalation use include:

● Pneumomediastinum and pneumothorax suggested by tachypnea, chest pain, and

● Mood, perception, thought content – Ingestion typically leads to feeling "high,"

machinery, such as automobiles, trains, and motorcycles. A meta-analysis of nine

Children — Diagnosis of cannabis intoxication in young children based solely on clinical

Adolescents and adults — Acute cannabis intoxication is a clinical diagnosis in adolescents

drug screen. (See 'Diagnosis' above.)

● Electrolyte imbalance (eg, hyponatremia or hypocalcemia) – Low serum sodium or

"Etiology of hypocalcemia in infants and children")

● Central nervous system infection (eg, meningitis or encephalitis) – Fever and/or

● Sedative/hypnotic agents – Cannabis toxicity typically causes more tachycardia or

● Antihistamines – Significant toxicity is often associated with anticholinergic findings

● Psychotropic agents (eg, antipsychotic or antidepressant agents) – These agents

● Cocaine (see "Cocaine: Acute intoxication", section on 'Clinical manifestations')

● Amphetamines and methcathinones (bath salts) (see "Acute amphetamine and

● MDMA (ecstasy) (see "MDMA (ecstasy) intoxication", section on 'Clinical features')

● Synthetic cannabinoids (see "Synthetic cannabinoids: Acute intoxication", section on

The management of cannabis intoxication consists of supportive care. Because of the

Treatment is supportive and consists of the following measures:

● Measure rapid blood glucose to exclude hypoglycemia ( table 3).

● Administer naloxone to patients presenting with features of opioid intoxication.

Agitation — Dysphoria with agitation is not a common presentation in pediatric cannabis

Adolescents and adults

Mild intoxication — Mild intoxication with dysphoria is a common presentation in either

(including cocaine, amphetamines, and phencyclidine) or coexisting mental illness. (See

Marked agitation or combativeness not responsive to reassurance and benzodiazepines may

● Acute coronary syndrome – Substernal squeezing chest pain suggestive of myocardial

● Pneumothorax or pneumomediastinum – Inhalation and breath-holding during

No specific treatment is necessary for uncomplicated pneumomediastinum. (See

(See "Acute exacerbations of asthma in adults: Emergency department and inpatient

Gastrointestinal decontamination — Activated charcoal has little efficacy in patients with

There is no role for gastrointestinal decontamination after toxicity caused by inhaled

Cannabis hyperemesis syndrome — Cannabis hyperemesis syndrome (CHS) is typically

● Clinical manifestations – Patients may complain of cyclic abdominal pain, vomiting, or

• Administer antiemetics (eg ondansetron [preferred] or metoclopramide). Give

• Perform evaluation to exclude other etiologies for the symptoms or potential

- Complete blood count with differential