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Toxicity, heroin
Toxicity, Heroin
Rania Habal, MD, Assistant Professor, Department of Emergency Medicine, New York
Medical College
Updated: Dec 11, 2009
Introduction
Background
Heroin (diacetylmorphine) is a semisynthetic narcotic that was first synthesized in
1874. It was originally marketed
as a safer, nonaddictive substitute to morphine. Soon after its introduction, heroin
was realized to be clearly as
addictive as morphine, prompting the US government to institute measures to control
its use. By 1914, the Harrison
Narcotics Act prohibited the use of heroin without a prescription. In 1920, the
Dangerous Drugs Act prohibited the
use of heroin altogether, thus driving it underground. In the United States, heroin
remains one of the most frequently
abused narcotics.
In its pure form, heroin is a white powder with a bitter taste. Street heroin
samples are frequently mixed with other
substances so dealers may maximize their profits. Because of these impurities and
additives, street heroin may
appear in various hues and colors, ranging from white to dark brown. Heroin is
occasionally sold as a black, tarry
substance, especially when crude processing methods are used to manufacture it.
The presence of impurities and additives also limits heroin absorption through
mucous membranes, thus limiting its
"rush" and "high" when it is sniffed or snorted. In patients who are dependent on
heroin, intravenous injection
("mainlining") becomes the only effective method of heroin use. During the 1990s,
the purity of US street heroin
increased significantly, and its price sharply dropped. In 1980, for example, the
average street sample (100-mg bag)
contained 3.6% heroin (3.6 mg of heroin) and cost $3.90, compared with 1999, when
the average street sample
contained 38.2% heroin and cost $0.80.
Samples from South America appeared to have the highest purity, reaching the 90%
range. Not surprisingly, this
dramatic increase in heroin purity, coupled with the well-publicized dangers of
intravenous drug use, led to a change
in the pattern of use. Snorting and smoking became the methods of choice and were
especially favored by the
younger users and new users. Recent samples, however, have demonstrated a rise in
impurities. Analysis of heroin
powder seized by the US Food and Drug Administration (FDA) in 2005 revealed a heroin
content that ranged from
7.3-75%.
Heroin poisoning occurs when an individual accidentally or intentionally overdoses
on the drug or when an ingested
heroin packet ruptures in the GI tract of a "body packer" or "body stuffer."
Pathophysiology
Heroin is a highly addictive semisynthetic opioid that is derived from morphine.
When used intravenously, it is 3-5
times more potent than its parent compound and is able to modulate pain perception
and cause euphoria. Similar to
morphine, heroin and its metabolites have mu, kappa, and delta receptor activity. In
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Toxicity, heroin
general, stimulation of the mu
receptors results in analgesia, euphoria, CNS depression, respiratory depression,
and miosis. Stimulation of the
delta and kappa receptors also results in analgesia, but the kappa receptors are
mostly involved in spinal analgesia.
Heroin, like morphine and other narcotics, reduces the brain's responsiveness to
changes in PCO2 and hypoxia,
thus resulting in respiratory depression. It also reduces peripheral vascular
resistance (resulting in mild
hypotension), causes mild vasodilation of the cutaneous blood vessels (resulting in
flushing), and stimulates
histamine release (resulting in pruritus).
Heroin's inhibitory effects on baroreceptor reflexes results in bradycardia, even in
the face of hypotension.
Finally, heroin decreases gastric motility, inhibits the effect of acetylcholine on
the small intestine, and diminishes
the colonic propulsive waves, resulting in gastric-emptying time that is prolonged
by as much as 12 hours and
constipation.
The onset of action, peak effects, and duration of action vary with the different
methods of use. Patients experience
heroin's effect within 1-2 minutes when injected intravenously and within 15-30
minutes when injected
intramuscularly. Heroin's peak therapeutic and toxic effects are generally reached
within 10 minutes when injected
intravenously, within 30 minutes when injected intramuscularly or when snorted, and
within 90 minutes when
injected subcutaneously. Analgesic effects generally last 3-5 hours.
Intravenously injected heroin creates a "rush" or a sensation of intense pleasure
that begins within one minute of the
injection and lasts from one to a few minutes. This "rush" is followed by a period
of sedation that lasts about an hour.
The initial "rush" is likely due to heroin's high lipid solubility and rapid
penetration to the brain. The half-life of heroin
is 15-30 minutes.
Heroin is rapidly converted to 6-monoacetylmorphine (6-MAM) by the liver, brain,
heart, and kidney and may not be
detected in the blood at the time of blood draw. 6-MAM is then converted to
morphine. Morphine is metabolized by
the liver and excreted as a glucuronide product or in its free form by the kidneys.
Morphine's half-life is considerably
longer than heroin's, ie, 2-3 hours. A small amount of unchanged 6-MAM is excreted
in the urine for up to 24 hours
after heroin use. Because 6-MAM can originate only from heroin, its detection in the
urine can mean only that the
patient used either heroin or 6-MAM.
Frequency
United States
The true prevalence of heroin use is probably much higher than reported in surveys
because surveys depend on self
-reporting and may not reach some of the persons who use heroin the heaviest.
Results from the SAMHSA 's 2008
National Survey on Drug Use and Health (NSDUH) revealed that the number of current
heroin users increased from
136,000 in 2005 to 338,000 and then decreased to 213,000 in 2008. In 2008, 114,000
persons aged 12 or older had
used heroin for the first time within the past 12 months. The average age at first
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use among recent initiates aged 1249 years was 23.4 years in 2008.[1 ]
Additionally, for 2005 the Drug Abuse Warning Network (DAWN) estimated that heroin
was involved in 164,572
Emergency Department patient visits.
International
According to the 2009 report of the United Nations Office on Drug and Crime (UNODC),
Afghanistan produced most
of the world's opium supply in 2008.[2 ]
The European Monitoring Centre for Drugs and Drug Addiction (EMCDDA) estimates the
average prevalence of
problem opioid use in the European Union and Norway to be between 3.6-4.6 cases per
1,000 population aged 15–
64 years (1.2–1.5 million users).[3 ]
Mortality/Morbidity
According to the American Association of Poison Control Centers' National Poison
Data System annual report in
2007, 1688 case mentions of heroin exposure were documented. Nine deaths were
reported.[4 ]
About 3-7% of patients treated for heroin overdose require hospital admission
because of complications such as
pneumonia, noncardiogenic pulmonary edema (NCPE), and infectious complications.
Most fatalities from heroin overdose occur in long-term users, usually early in
their third decade of life. Fatality rates
are higher in patients who use alcohol and other drugs such as benzodiazepines and
cocaine. Death is most
commonly due to respiratory failure or asphyxiation.
Race
Although heroin addiction has traditionally been viewed as a disease of the
economically disadvantaged population,
addiction among the affluent is grossly underreported. According to the National
Institute on Drug Addiction (NIDA),
little difference exists in lifetime heroin use among races and ethnic
backgrounds.[5 ]
Sex
Although heroin addiction has traditionally been viewed as a disease of males,
addiction among females is grossly
underreported. According to NIDA, males were more likely than females to report
heroin use during their lifetime.[5 ]
Age
The National Survey on Drug Use and Health reports stability at low levels of heroin
use among young people.
According to the American Association of Poison Control Centers' National Poison
Data System annual report in
2007, 124 heroin poisonings occurred in those younger than 19 years.[4 ]
Clinical
History
In general, when it is the sole agent used, the clinical presentation of heroin
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poisoning and its diagnosis hold little
challenge for the experienced health care practitioner. The diagnosis of heroin
poisoning should be suspected in all
comatose patients, especially in the presence of respiratory depression and miosis.
Symptoms generally develop within 10 minutes of intravenous heroin injection.
Patients who survive heroin
poisoning commonly admit to having used more than their usual dose, having used
heroin again after a prolonged
period of abstinence, or having used a more concentrated street sample.
Heroin toxicity shares common clinical characteristics with other medical or
toxicologic conditions. For example,
clonidine administration in a patient with pontine hemorrhage may cause coma,
respiratory depression, and miosis
similar to opioid intoxication. Phencyclidine, certain phenothiazines, and
organophosphates may also cause miosis
with altered mental status.
The clinical presentation of heroin poisoning may be altered by a number of the
following factors:
Concomitant conditions: The presence of CNS disease, traumatic injuries, hypoxia,
hypoglycemia,
hypovolemia, acidosis, or metabolic disease may alter the clinical presentation of
heroin poisoning.
•
Co-ingestions: The most commonly co-ingested substance is alcohol, followed by
benzodiazepines, cocaine,
and amphetamines.
•
Contaminants: Street heroin samples are often contaminated with agents that have
their own toxicity profile,
eg, sedative hypnotics, amphetamines, local anesthetics, anticholinergic agents,
quinine, strychnine, arsenic,
and, most recently, clenbuterol[6 ].
•
Physical
Coma, respiratory depression, and miosis are the hallmarks of opioid overdose.
According to Hoffman and
colleagues, the presence of these hallmarks (ie, coma, respiratory depression,
miosis) has a 92% sensitivity and
76% specificity for heroin overdose.
The clinical presentation and depth of coma may be altered in patients with
co-ingestions and in the presence of
concomitant medical conditions such as hypoxia, trauma, hypoglycemia, and shock or
with concomitant ingestion of
other toxins such as amphetamines, cocaine, and anticholinergics. In these
circumstances, patients may exhibit
delirium, tachypnea, and mydriasis. Delirium may also be noted in overdoses with
prescription narcotics such as
dextromethorphan, meperidine, and codeine. Convulsions occur with overdoses of
meperidine, fentanyl,
pentazocine, or propoxyphene.
Mild hypotension and mild bradycardia are commonly observed with heroin use. These
are attributable to peripheral
vasodilation, reduced peripheral resistance and histamine release, and inhibition of
baroreceptor reflexes. In the
setting of heroin poisoning, hypotension remains mild. The presence of severe
hypotension should prompt a search
for other causes of hypotension, such as hemorrhage, hypovolemia, sepsis, pulmonary
emboli and other causes of
shock.
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Respiratory depression, due to heroin's effect on the brain's respiratory centers is
a hallmark. However, the
presence of tachypnea should prompt the search for complications of heroin use such
as pneumonia, pulmonary
edema, pneumothorax; or an alternative diagnosis such as shock, acidosis or CNS
injury. Tachypnea may also be
seen in overdoses of pentazocine or meperidine.
Examination of the skin may also reveal patterns of heroin use such as track marks,
fresh puncture wounds, and "skin-popping" marks.
Causes
The most common scenarios for a significant heroin overdose are the use of a higher
dose, the accidental injection
of highly concentrated solution in the unsuspecting user, or the use of heroin after
a prolonged period of abstinence.
Intentional (ie, suicidal) overdoses are rare. Other scenarios include body packing
and body stuffing.
"Body packers," also called "mules," are people who pack their GI tract with bags of
heroin in order to smuggle the
illegal drug from one country to another. In these persons, the drugs are carefully
packaged for safe passage.
Persons may become symptomatic when a heroin-containing package ruptures or when the
packages cause GI
obstruction or rupture. Body packing should be suspected in persons who are found
unconscious at airports, during
international flights, or soon after a trip to endemic countries.
"Body stuffers," on the other hand, are people who ingest all the drugs in their
possession in order to conceal the
evidence from the police. Because these packages are typically not designed for safe
GI transport, they easily
rupture and frequently cause poisoning. The clinical presentation is often atypical
because multiple substances may
have been ingested.
Differential Diagnoses
Acute Respiratory Distress Syndrome Metabolic Acidosis
Diabetic Ketoacidosis Respiratory Failure
Head Trauma Toxicity, Alcohols
Hypercalcemia Toxicity, Barbiturate
Hypernatremia Toxicity, Benzodiazepine
Hyperosmolar Coma Toxicity, Clonidine
Hypoglycemia Toxicity, Gamma-Hydroxybutyrate
Hypothermia Toxicity, Phencyclidine
Injecting Drug Use
Lactic Acidosis
Other Problems to Be Considered
Clonidine Overdose
Phenothiazine toxicity
Pontine Hemorrhage
Workup
Laboratory Studies
The diagnosis of heroin poisoning is usually made clinically, and laboratory
analysis does not alter therapy in
the emergent setting. Additional tests and further workup are indicated if the
patient's condition does not
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respond to naloxone or if the patient's course of treatment is complicated.
•
Qualitative analysis may be helpful in confirming heroin use, as well as concomitant
use of other drugs. Coingestion
of alcohol, benzodiazepines, cocaine, and amphetamines is common and may contribute
to
morbidity and mortality. Therapeutic drug levels should be obtained if the patient
is taking prescription
narcotics, as these drug levels commonly contain acetaminophen or aspirin.
•
Heroin is quickly metabolized to 6-MAM and morphine. Most qualitative toxicologic
studies screen for
morphine only and use the presence of morphine in the urine as a surrogate for
heroin use. In criminal and
legal cases, however, testing for specific compounds is necessary, and, because
6-MAM can be generated
only from heroin metabolism, the presence of 6-MAM on a drug screen is taken as
evidence for heroin use.
•
Arterial blood gas analysis: In mild-to-moderate heroin overdoses, arterial blood
gas (ABG) analysis reveals
respiratory acidosis. In more severe overdoses, tissue hypoxia is common, leading to
mixed respiratory and
metabolic acidosis. The presence of unexplained metabolic acidosis should prompt a
search for a coingestion
or contamination with poisonous substances such as cyanide and clenbuterol.
•
Metabolic panel: Hypoglycemia must be diagnosed at the bedside and treated
immediately. A complete
metabolic panel is indicated if the patient's coma persists despite the infusion of
naloxone (Narcan), dextrose,
and thiamine (the coma protocol).
•
Liver function tests (LFTs) and coagulation studies are indicated if hepatitis is
suspected and can determine
ammonia levels if hepatic encephalopathy is suspected.
•
Renal function tests: Renal function should be monitored in patients with
rhabdomyolysis, shock, or
prolonged coma and in the setting of sepsis, severe hypertension (HTN), and
preexisting renal insufficiency.
•
Complete blood cell (CBC) count: A CBC count is indicated if infection, blood loss,
or immunodeficiency is
suspected.
•
Creatine kinase (CK): Determination of the CK level is indicated when rhabdomyolysis
or compartment
syndrome is suspected. An elevated CK level may denote cardiac injury in comatose
patients.
•
A pregnancy test should be considered • in women of childbearing age.
• Cerebrospinal fluid (CSF) analysis is indicated when an infectious process is
suspected.
Imaging Studies
Chest radiography: Chest radiography is indicated if the patient remains hypoxic. A
chest radiograph may
help diagnose many of the pulmonary complications of heroin poisoning, including
noncardiogenic pulmonary
edema (NCPE) (depicted in the radiograph below), aspiration pneumonitis,
atelectasis, and other
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Toxicity, heroin
complications of drug use such as pneumothorax, pneumomediastinum, pneumoperitoneum,
septic
pulmonary emboli, fungal infections, and aspiration pneumonia. Adulterants may also
cause pulmonary
abnormalities. Talc, for example, causes granulomatosis and thrombosis of small
pulmonary vessels and
may appear as a reticulonodular pattern. Long-term talc exposure may also result in
pulmonary hypertension.
•
Heroin-related noncardiogenic pulmonary edema.
Abdominal radiography: Abdominal radiographs are helpful in demonstrating the
presence of radiopaque
substances in the GI tract, as well as vials or bags of heroin.
•
Computerized tomography (CT) scan: CT scan of the brain is indicated in the presence
of focal neurologic
findings or when coma persists. A CT scan may reveal space-occupying lesions such as
brain abscesses,
intracerebral or extracerebral hematomas, and stroke.
•
Magnetic resonance imaging (MRI): MRI of the brain is helpful in establishing the
diagnosis of heroin-induced
leukoencephalopathy. Findings include white-matter abnormalities in the cerebellum
and posterior limb of the
internal capsule.
•
Other Tests
Electrocardiogram: An electrocardiogram (ECG) may show abnormalities in rhythm and
rate, which are rare
in pure opioid overdoses but common to some co-ingestants and adulterants of street
drugs. An ECG may
also reveal evidence of myocardial ischemia.
•
Echocardiography (ECHO): An ECHO is indicated if endocarditis is suspected. An ECHO
may also help
diagnose acute pulmonary hypertension secondary to embolic disease.
•
Procedures
Endotracheal intubation: Endotracheal intubation is indicated for airway protection
and may be required in the
management of hypoxia due to NCPE. Endotracheal intubation with ventilation may also
be required in the
management of increased intracranial pressure and shock.
•
Pulmonary artery catheterization: NCPE secondary to opioid overdose is characterized
by a normal
pulmonary capillary wedge pressure and mildly increased pulmonary arterial pressure.
•
Lumbar puncture: In the absence of signs of increased intracranial pressure, a
lumbar puncture is indicated
in comatose patients who have evidence of meningitis or fever without a source. In
cases in which bacterial
meningitis is suspected, antibiotic therapy should not be delayed by the lumbar
puncture.
•
Treatment
Medical Care
The direct effects of heroin on the CNS are quickly reversible with naloxone.
Naloxone may be given intravenously,
intramuscularly, subcutaneously, or through the endotracheal tube. A response should
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be expected within 5
minutes. The effects from naloxone generally last 20-40 minutes. Resedation occurs
when large doses of heroin are
used, when continuous absorption from a ruptured transport bag occurs, or in the
presence of a long-acting narcotic
agent. The absence of a response to naloxone should prompt a search for another
cause of the clinical
presentation, such as hypoglycemia. Respiratory support should be instituted early,
when necessary.
Gastric lavage in the setting of oral heroin overdose is generally not recommended
because it has no documented
value. Furthermore, gastric lavage is contraindicated in "body packers" and "body
stuffers" because the procedure
may rupture a package.
Activated charcoal, which is indicated for orally ingested narcotics, especially
those with large enterohepatic
circulation (eg, propoxyphene, diphenoxylate) is of no value in pure heroin
overdose.
"Body packers" and "body stuffers" also generally require whole-bowel irrigation,
except in the presence of intestinal
obstruction or perforation. Whole-bowel irrigation may be accomplished with an oral
polyethylene glycol (GoLytely)
solution at a rate of 2 L/h until stools are watery and clear.
Admission to the hospital is rarely necessary and generally limited to complications
of heroin overdose and
intravenous drug use. Admission to the intensive care unit is also rarely required
and is indicated for patients who
require respiratory support and those with life-threatening arrhythmias, shock, and
recurrent convulsions, as well as
those who require continuous naloxone infusions (rebound coma, respiratory
depression).
• Pulmonary edema
NCPE affects 0.3-2.4% of heroin overdoses and generally becomes clinically apparent
within 2-4
hours of the overdose. NCPE is heralded by the onset of hypoxia, increased
respiratory rate, and a
cough that produces frothy pink sputum. Chest radiography generally reveals
bilateral infiltrates.
Heroin-related NCPE generally lasts 24-48 hours and responds to supportive care. In
most instances,
hypoxia improves with mask oxygen ventilation only, but NIPPV and endotracheal
intubation may be
required. Endotracheal intubation is indicated for airway protection, severe
hypoxia, acidosis, and
cardiovascular instability.
◦
While the cause of NCPE remains uncertain, hypoxia-induced lung damage is likely to
play a major
role in the development of pulmonary edema. Other causes that have been suggested
include acute
anaphylaxis, neurogenic effects, humoral effects, immune-complex deposition, and
depressed
myocardial contractility.
◦
• Convulsions
The presence of recurrent convulsions in a patient with heroin overdose should
prompt a search for
causes of seizures, such as hypoxia, CNS injury, adulterants, or co-ingestions (eg,
tricyclic
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Toxicity, heroin
antidepressants, cocaine, amphetamines).
◦
Some narcotics, such as meperidine (Demerol), pentazocine (Talwin), propoxyphene
(Darvon),
diphenoxylate, and fentanyl (Actiq), may cause seizures. Seizures caused by these
narcotics,
excluding diphenoxylate and atropine (Lomotil), are usually of short duration and do
not progress to
status epilepticus.
◦
◦ Heroin and narcotic-related convulsions respond to conventional benzodiazepine
therapy.
• Rhabdomyolysis
Prolonged coma and convulsions may contribute to the development of rhabdomyolysis,
which is
treated conventionally, with large amounts of crystalloid solutions, alkalinization
of the urine, and
forced diuresis.
◦
Infusion of large amounts of crystalloids in patients with narcotic overdose may
require close
monitoring of hemodynamic parameters because these patients are also at risk for
pulmonary edema.
◦
Consultations
Consultation with a toxicologist or the regional poison control center may be
indicated if multiple ingestions have
occurred.
Consultation with a surgeon is indicated when heroin packets cause a "body packer"
or "body stuffer" to
experience a bowel obstruction, intestinal rupture, and peritonitis and when
compartment syndrome is
suspected.
Consultation with a psychiatrist is indicated for patients with an intentional
suicidal overdose (extremely rare).
Diet
Patients with ileus and GI obstruction should be kept on a nothing by mouth status.
Medication
The goals of pharmacotherapy are to reduce absorption of the drug, to prevent
complications, and to reduce
morbidity.
Narcotic antagonists
Naloxone is a pure opioid antagonist that has been in use since the 1970s. Naloxone
has an ultrarapid onset of
action (1 min) and a short half-life (20 min). Duration of action is 20-60 minutes.
Nalmefene is a new narcotic antagonist that is effective in the termination of
respiratory and CNS depression
associated with heroin overdose. Has a considerably longer duration of action (lasts
4-8 h after IV injection) than
naloxone. Duration of action makes it ideal in patients who are not dependent on
opiates and who present with
respiratory depression, thus reducing the incidence of resedation.
Naloxone has an excellent safety record, especially when used appropriately. Doses
of up to 100 mg have been
administered to patients with spinal injury, without untoward effects.
Naloxone reverses the characteristic respiratory depression and the analgesia, coma,
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and miosis that occur with
heroin overdose. It may also reverse the cardiovascular effects of an overdose and
reduce immediate and delayed
mortality of patients.
Reports that link the use of naloxone to the development of NCPE, convulsions, and
death have not been
substantiated because these complications have also been noted in patients with
other opiates in the absence of
naloxone and may be due to hypoxia.
Naloxone use in patients who are dependent on narcotics may precipitate withdrawal
syndrome (33% of cases)
characterized by abdominal discomfort, vomiting, diarrhea, lacrimation, rhinorrhea,
yawning, and piloerection. In
patients with polydrug overdose, naloxone may unmask the effects of other substances
(eg, cocaine), leading to
confusion and restlessness in up to 32% of cases, and, rarely, more serious events.
Naloxone (Narcan)
In suspected narcotic overdose, small increments (0.1 mg) may be used IV until the
desired effect is obtained or
until 10 mg have been administered with no response. Small increments are used
rather than a large bolus injection
in order to prevent narcotic withdrawal in the patient who is dependent on opioids.
Large bolus injections of
naloxone may also unmask adverse effects of co-ingestants (eg, scopolamine,
amphetamines, cocaine), resulting in
a sympathetic or an anticholinergic crisis. When desired effect is obtained and
patient requires continuous infusion,
a drip solution is mixed so that two thirds of the originally effective dose is
administered qh. To prepare drip, add 40
mg naloxone to 1 L D5W or NS and infuse at 10 mL/h (0.4 mg/h).
Dosing
Adult
0.2-2 mg IV/IM q2-3min until desired effect or total of 10 mg reached
Pediatric
<20 kg: 0.1 mg/kg IV/IM q2-3min as needed based on response
>20 kg: Administer as in adults
Interactions
Decreases analgesic effects of narcotics; may reduce efficacy of clonidine
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies
in animals
Precautions
Caution in cardiovascular disease; may precipitate withdrawal symptoms in patients
dependent on opiates; caution
in co-ingestions of sympathomimetics and anticholinergics
Nalmefene (Revex)
Prevents or reverses opioid effects (eg, hypotension, respiratory depression,
sedation), possibly by displacing
opiates from their receptors.
Dosing
Adult
0.1 mg IV q2-3min until desired effect or total of 1.5 mg reached
Pediatric
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Toxicity, heroin
0.25 mcg/kg IV q2-5min until desired effect
Interactions
Decreases analgesic effects of narcotics
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies
in animals
Precautions
Caution in cardiovascular disease and co-ingestions of sympathomimetics or
anticholinergics
GI decontaminants
These agents are used to minimize systemic absorption of the toxin.
Activated charcoal (Liqui-Char)
Emerging as the decontamination method of choice. Emergency treatment in poisoning
caused by drugs and
chemicals. Network of pores present in activated charcoal absorbs 100-1000 mg of
drug per gram of charcoal.
Indicated for orally ingested narcotics and co-ingestions, but no benefit exists in
pure heroin overdose.
Dosing
Adult
25-100 g PO, 1 g/kg or 10 times amount of poison ingested as a suspension in 4-8 oz
of water
Pediatric
<1 year: Not recommended
>1 year: 1 g/kg PO or 10 times amount of poison ingested as a suspension in 2-4 oz
of water
Interactions
May inactivate syrup of ipecac if used concomitantly; effectiveness of other
medications decrease with
coadministration; do not mix charcoal with sherbet, milk, or ice cream (decreases
absorptive properties of activated
charcoal)
Contraindications
Documented hypersensitivity; poisoning or overdosage of mineral acids and alkalies
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in
humans; may use if benefits
outweigh risk to fetus
Precautions
Not very effective in poisonings of ethanol, methanol, and iron salts; induce emesis
before administering activated
charcoal; after emesis with ipecac, patient may not tolerate activated charcoal for
1-2 h; can administer in early
stages of gastric lavage; without sorbitol gastric lavage, returns will be black
Polyethylene glycol (GoLytely, Colyte)
Laxative with strong electrolyte and osmotic effects that has cathartic actions in
GI tract. Accomplished whole-bowel
irrigation.
Dosing
Adult
2 L/h until rectal effluent clear
Pediatric
Not established
Interactions
Reduces effectiveness and absorption of oral medications
Contraindications
Documented hypersensitivity; colitis; megacolon; bowel perforation; gastric
retention; GI obstruction
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Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in
humans; may use if benefits
outweigh risk to fetus
Precautions
Caution in ulcerative colitis and hot loop polypectomy
Follow-up
Further Inpatient Care
Further inpatient care may be needed for patients with medical complications that
require prolonged
specialist care (eg, development of pneumonia, septic emboli, endocarditis,
cellulitis, osteomyelitis, subdural
abscess, compartment syndrome, cerebrovascular accident).
•
• Monitor patients for opioid withdrawal symptoms.
Psychiatric support and therapy must be provided concomitantly with medical therapy
for all intentional
overdoses.
•
Further Outpatient Care
• Psychiatric support and therapy for all intentional overdoses
• Social support for addiction (eg, Narcotics Anonymous, detoxification programs)
• Methadone maintenance programs
Inpatient & Outpatient Medications
• Consider methadone programs.
• Long-term antibiotics may be required for certain infections such as
osteomyelitis.
Transfer
Transfer to a nonmonitored bed is indicated when the patient's condition is stable
and requires further
medical therapy.
•
• Transfer to a psychiatric service may be indicated for intentional overdoses.
Deterrence/Prevention
Enrollment in deterrence programs (eg, Narcotics Anonymous, detoxification programs)
may be beneficial for
some patients.
•
Reduction in supply has been shown to reduce heroin use and heroin-related deaths in
Australia and other
countries.
•
Heroin overdose deaths may be prevented by training users and those close to them to
respond quickly to
the overdose. In as many as 32% of heroin-related deaths, the patients were not
alone, and the others who
were present failed to recognize the seriousness of the overdose or were reluctant
to respond because of
legal repercussions.
•
Complications
About 3-10% of patients treated for heroin overdose require admission to the
hospital because of complications
such as pneumonia, noncardiogenic pulmonary edema (NCPE), persistent
hypoxia/hypoventilation, persistent
altered mental status, trauma, rhabdomyolysis, compartment syndrome, and infectious
complications.
NCPE affects 0.3-2.4% of heroin overdose cases and has been reported in 50-90% of
autopsies performed on
patients who overdosed on heroin and were found dead at the scene. NCPE may occur
with any narcotic but is
Page 12
Toxicity, heroin
encountered most commonly in cases that involve overdoses of heroin, methadone,
propoxyphene, or codeine.
Typically, heroin-related NCPE occurs in males with a Glasgow Coma Scale of less
than 5 and severe respiratory
depression that requires naloxone.
In a retrospective chart review, Sporer and Dorn reported that 74% of patients
ultimately diagnosed with heroin induced
NCPE were hypoxic upon presentation to the ED, 22% of patients developed severe
hypoxia during the first
hour, and 4% of patients developed hypoxia in the 4 hours following the overdose.[7
]None of these patients was
hypoventilating upon arrival to the ED; the average respiratory rate was 24 breaths
per minute (range, 16-44 breaths
per min). The patients' average initial oxygen saturation level on room air was 76%
(range, 47-89%).
Most patients (66%) responded to oxygen via nonrebreather face mask and to
observation only. Mechanical
ventilation was required to achieve adequate oxygenation in 33% of patients. Hypoxia
resolved in most patients
(74%) within 24 hours, several within 8 hours. In the remainder of patients (22%),
hypoxia resolved over the next 48
hours. Most intubated patients were extubated within 24 hours.
Although the cause of NCPE remains uncertain, hypoxia-induced lung damage likely
plays a major role in the
development of pulmonary edema. Other mechanisms that have been suggested as causes
of pulmonary edema
include acute anaphylaxis, neurogenic effects, humoral effects, immune-complex
deposition, and depressed
myocardial contractility.
Long-term use of narcotics leads to narcotic addiction, a condition marked by a
constant craving for narcotics and an
extremely uncomfortable withdrawal syndrome. This syndrome is characterized by
yawning, piloerection,
lacrimation, salivation, nasal congestion, vomiting, diarrhea, and general body
aches. Clonidine may be used to
control the symptoms of opiate withdrawal.
Complications that relate to the intravenous injection of heroin and other drugs
include the following:
• Septic emboli
• Foreign body embolization
• Endocarditis, shown in the image below
•
Endocarditis-related septic pulmonary emboli in a heroin user.
• Valvular insufficiency
Skin and soft tissue infections (eg, abscesses, cellulitis, suppurative
thrombophlebitis, necrotizing fasciitis,
shown in the image below)
•
•
Necrotizing fasciitis in a heroin user.
• Wound botulism
• Sepsis
• Osteomyelitis
• Subdural abscess
• Cerebrovascular accident
• Mycotic aneurysm
• AIDS
• Hepatitis
Page 13
Toxicity, heroin
• Fungal infections
• Tuberculosis
Complications that relate to inhalation include pneumothorax, pneumomediastinum, and
toxic
leukoencephalopathy.
•
Patients may present with complications related to adulterants of street drugs.
Street drugs are combined with inert
or toxic substances to increase the mass and street value of the original product.
Common heroin adulterants
include talc, sugars, quinine, local anesthetics, flour, sodium bicarbonate,
amphetamines, lysergic acid diethylamide
(LSD), phencyclidine, cocaine, and scopolamine. Recently, a number of deaths due to
clenbuterol toxicity were
reported in patients who used heroin in the northeastern United States. Talc may
cause pulmonary injury. Quinine,
local anesthetics, amphetamines, and cocaine may be cardiotoxic and cause cardiac
arrhythmias.
Prognosis
Prognosis is directly related to the duration of hypoxia and the rapid
identification and management of
complications. Survival after cardiac arrest is limited.
Patient Education
For excellent patient education resources, visit eMedicine's Substance Abuse Center
and Mental Health and
Behavior Center. Also, see eMedicine's patient education articles Substance Abuse,
Drug Dependence & Abuse,
Club Drugs, Narcotic Abuse, Substance Abuse, and Activated Charcoal.
Miscellaneous
Medicolegal Pitfalls
Failure to consider co-ingestions (eg, acetaminophen, aspirin) in the evaluation and
management of any
overdose
•
Failure to consider other diagnoses (eg, CNS infection or bleed, hypoglycemia,
carbon monoxide poisoning)
in the evaluation and treatment of presumed narcotic overdoses
•
• Failure to consider concomitant trauma
• Failure to identify and treat complications
• Failure to evaluate efficacy and complications of therapy
Special Concerns
• Pregnant patients
◦ Heroin addiction in the pregnant patient is grossly underestimated.
Heroin readily crosses the placenta and the blood-brain barrier of the fetus,
leading to narcotic
dependence in the fetus.
◦
Heroin overdose results in hypoxia, which, in turn, causes placental
vasoconstriction, thus causing
further injury to the fetus.
◦
Complications in the mother can lead ◦ to additional and similar complications in
the fetus.
Childhood heroin overdose: This is rare and does not differ clinically from an adult
overdose. Similarly,
treatment of pediatric heroin overdose would not differ from that of an adult. In
Page 14
Toxicity, heroin
all cases of pediatric heroin
overdose, social services should be involved.
•
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Keywords
heroin toxicity, heroin overdose symptoms, heroin overdose treatment, heroin, heroin
poisoning, heroin overdose,
heroin addiction, heroin use, heroin dependence, dope, smack, body stuffers, body
packers, intravenous drug use,
intravenous drug abusers, IVDA, skin-popping, diacetylmorphine, narcotic,
mainlining, opioid
Contributor Information and Disclosures
Author
Rania Habal, MD, Assistant Professor, Department of Emergency Medicine, New York
Medical College
Disclosure: Nothing to disclose.
Medical Editor
Laurie Robin Grier, MD, Medical Director of MICU, Associate Professor of Medicine,
Section of Pulmonary and
Critical Care Medicine, Louisiana State University Health Science Center at
Shreveport
Laurie Robin Grier, MD is a member of the following medical societies: American
College of Chest Physicians,
American College of Physicians, American Society for Parenteral and Enteral
Nutrition, and Society of Critical Care
Medicine
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Managing Editor
Daniel R Ouellette, MD, FCCP, Associate Professor of Medicine, Wayne State
Page 18
Toxicity, heroin
University School of Medicine;
Consulting Staff, Pulmonary Disease and Critical Care Medicine Service, Henry Ford
Health System
Daniel R Ouellette, MD, FCCP is a member of the following medical societies:
American College of Chest
Physicians and American Thoracic Society
Disclosure: Boehringer Ingleheim Honoraria Speaking and teaching; Pfizer Honoraria
Speaking and teaching
CME Editor
Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and
Pediatrics and Adolescent
Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy
of Pediatrics and American
College of Physicians
Disclosure: Nothing to disclose.
Chief Editor
Michael R Pinsky, MD, CM, FCCP, FCCM, Professor of Critical Care Medicine,
Bioengineering, Cardiovascular
Disease and Anesthesiology, Vice-Chair, Academic Affairs, University of Pittsburgh
School of Medicine, University
of Pittsburgh Medical Center
Michael R Pinsky, MD, CM, FCCP, FCCM is a member of the following medical societies:
American College of
Chest Physicians, American College of Critical Care Medicine, American Heart
Association, American Thoracic
Society, Association of University Anesthetists, Shock Society, and Society of
Critical Care Medicine
Disclosure: LiDCO Ltd Honoraria Consulting; iNTELOMED Intellectual property rights
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