Heroin Toxicity

Back

Practice Essentials

Heroin remains one of the most frequently abused narcotics in the United States. It may be injected intravenously ("mainlining"), or subcutaneously (“skin-popping). It also can be ingested, snorted, or smoked. The presence of impurities may limit its absorption through mucous membranes, thus limiting its "rush" and "high" when sniffed or snorted.

Heroin poisoning occurs most commonly when an individual unintentionally overdoses on the drug. Poisoning may also occur in a "body packer," "body pusher," or "body stuffer." Body packers, also called "mules," are people who swallow and pack their GI tracts with bags of heroin in order to smuggle the illegal drug from one country to another. Body pushers conceal the drugs in their rectum and/or vagina. In both of these groups, the drugs are carefully packaged for safe passage, but poisoning occurs if the packages rupture. Body packing or pushing 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.

Background

Heroin (diacetylmorphine) is a semisynthetic narcotic derived from the opium poppy Papaver somniferum. It was first synthesized in 1874 and was originally marketed as a safer, nonaddictive substitute for 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.

Afghanistan remains the world's largest cultivator of opium, accounting for more than 60% of the world's opium poppy cultivation. Myanmar is the second largest, and Mexico is the third largest. Mexico, Colombia, Guatemala, and other Latin American countries are the main suppliers of opium products to North America.[1]

In its pure form, heroin is a white powder with a bitter taste. However, samples are frequently mixed with other substances so dealers can maximize their profits. Because of these impurities and additives, street heroin samples have different purities and may appear in various hues, 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. Heroin samples from South America appear to have the highest purity, reaching at times more than 70% purity.

Pathophysiology

Heroin is a highly addictive semisynthetic opioid that is derived from morphine. When used intravenously, it is three to five 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 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.[2]

Heroin, similar to morphine and other narcotics, reduces the brain's responsiveness to changes in carbon dioxide levels 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).[2]

Heroin's inhibitory effects on baroreceptor reflexes result in bradycardia, even in the face of hypotension.[2]

Finally, heroin decreases gastric motility, inhibits the effect of acetylcholine on the small intestine, and diminishes the colonic propulsive waves, resulting in prolongation of gastric emptying time by as much as 12 hours, with consequent constipation in habitual users.[2]

The onset of action, peak effects, and duration of action vary with the different methods of heroin use. Onset of action occurs within 1-2 minutes with intravenous injection and within 15-30 minutes with intramuscular injection. Heroin's peak therapeutic and toxic effects are generally reached within 10 minutes with intravenous injection, within 30 minutes with intramuscular injection or when snorted, and within 90 minutes when injected subcutaneously. Analgesic effects generally last 3-5 hours.[2]

Intravenously injected heroin creates a rush, or a sensation of intense pleasure, that begins within 1 minute of the injection and lasts from 1 minute 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.[2]

Heroin is rapidly converted to 6-monoacetylmorphine (6-MAM) by the liver, brain, heart, and kidneys 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 h). 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.[2]

Epidemiology

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. According to the US Substance Abuse and Mental Health Services Administration (SAMHSA) 2016 National Survey on Drug Use and Health (NSDUH), approximately 948,000 persons aged 12 years and older reported using heroin in the past year (about 0.4% of that age group); about 475,000 persons (about 0.2%) were current heroin users, and about 591,000 persons had a heroin use disorder.[3]

NSDUH estimates that the percentage of current heroin users in 2016 were higher than the percentages from 2002 to 2013, but was similar to the percentages in 2014 and 2015.[3]

International

According to the 2017 report of the United Nations Office on Drug and Crime (UNODC), the global prevalence of opiate (heroin and opium) use was estimated at 0.37% of the population, or 12.9-23.6 million people. Levels of opiate use were much higher than the global average in the Near and Middle East/Southwest Asia (1.40%), Central Asia (0.90%), and Eastern and Southeastern Europe (0.85%).[1]

In its 2018 annual report, the European Monitoring Centre for Drugs and Drug Addiction (EMCDDA) estimated that in 2016 there were 1.3 million high-risk opioid users in Europe, or 0.4 % of the adult population, with heroin being the most widely used opioid. The EMCDDA reported that although patterns and trends vary among countries, Europe may be witnessing a longer-term decline in heroin use, for reasons that may include reduced interest in the drug and reduced availability of it.[2]  The number of primary heroin users in Europe who entered drug treatment for the first time fell by more than half from a peak in 2007 to a low point in 2013, before stabilizing in subsequent years.[4]

Mortality/Morbidity

Most fatalities from heroin overdose occur in long-term users, usually early in their third decade of life.[5, 6] 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.[6, 7, 8]

The US National Center for Health Statistics reported that drug overdose deaths involving heroin more than tripled from 2011 to 2016, rising from 4,571 to 15,961 (from 11% to 25% of all drug overdose deaths). Of drug overdose deaths in which at least one specific drug was mentioned, heroin ranked first from 2012 to 2015, but was overtaken by fentanyl in 2016.[9]  From 2016 to 2017, the death rate from heroin overdose remained stable, at 4.9 deaths per 100,000 population.[10]

About 3-7% of patients treated for heroin overdose require hospital admission because of complications such as pneumonia, noncardiogenic pulmonary edema, and infectious complications.[5]

Demographics

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 CDC, heroin initiation rates generally increased across most demographic subgroups from 2002-2011. During that time, however, reported rates of heroin initiation were highest among males, persons aged 18–25 years, non-Hispanic whites, those with an annual household income of less than $20,000, and those residing in the Northeast. The racial/ethnic population with the highest previous-year heroin use was non-Hispanic whites.[11]

Sex

Although heroin addiction has traditionally been viewed as a disease of males, addiction among females is grossly underreported. According to the , CDC, the average rate of past-year heroin use per 1,000 population from 2011-2013 was 3.6 in males versus 1.6 in females.[11]  The death rate for heroin overdose in 2012 was almost four times higher in males than in females.[12]

Age

According to the American Association of Poison Control Centers' National Poison Data System, 3873 of the 4319 single exposures to heroin reported in 2016 were in persons 20 years of age and older; 20 were in those younger than 6 years, and 182 were in teenagers.[13] According to the CDC, in 2012 the heroin overdose death rate was highest in those aged 25–34 years.[12]

History

In general, when it is the sole agent used, the clinical presentation of heroin poisoning and its diagnosis hold little challenge for the experienced healthcare 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. Fluctuations in heroin purity have been moderately associated with an increased incidence of fatal heroin overdose.[14] Fentanyl or fentanyl analogues, which may be mixed with heroin, or sold as heroin, appear to be responsible for much of the increase in opioid overdoses seen in recent years.[15, 9]

Death from acute heroin overdose is due to respiratory arrest. The co-ingestion of other drugs such as alcohol, methadone, and cocaine and the presence of concomitant medical conditions increase the risk of death from a heroin overdose.[16, 17, 18]

Heroin toxicity shares common clinical characteristics with other medical or toxicologic conditions. For example, clonidine administration and 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.[2]

The clinical presentation of heroin poisoning may be altered by a number of the following factors:

Heroin body packers and body pushers pose a special problem, as they may present with symptoms unrelated to heroin overdose, such as bowel obstruction and bowel rupture. These patients may also present with symptoms of severe overdose, unresponsive to common therapy. Body packing and pushing should be suspected in persons who are found unconscious at airports, on international flights, or soon after a trip to endemic areas.

Noncardiac 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 noninvasive positive-pressure ventilation (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.

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.[23, 24]

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 can 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.

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, acute lung injury, and 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 (shown in the image below), fresh puncture wounds, and "skin-popping" marks.



View Image

Track marks in a heroin intravenous drug user.

Causes

The most common scenarios for a significant heroin overdose are as follows:

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 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. Co-ingestion of alcohol, benzodiazepines, cocaine, and amphetamines is common and may contribute to morbidity and mortality. If the patient is taking prescription narcotics, which commonly contain acetaminophen or aspirin, serum drug levels should be obtained.

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.

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 co-ingestion or contamination with poisonous substances such as cyanide and clenbuterol.[20]

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).

Other studies to consider include the following:

Imaging Studies

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 (depicted in the radiograph below), aspiration pneumonitis, atelectasis, and other complications of drug use such as pneumothorax, pneumomediastinum, pneumoperitoneum, septic pulmonary emboli, fungal infections, and aspiration pneumonia.



View Image

Heroin-related noncardiogenic pulmonary edema.

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.

Abdominal radiographs are helpful in demonstrating the presence of radiopaque substances in the gastrointestinal (GI) tract, such as vials or bags of heroin. The sensitivity of radiographs is only 85-90%.

A noncontrast computed tomography (CT) scan of the abdomen and pelvis has a higher sensitivity for foreign bodies in the GI tract than plain radiographs. CT scanning is also able to demonstrate lack of progression of the foreign body within the GI tract to help pinpoint the site of obstruction and the site of viscus perforation.

A 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) 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

An electrocardiogram (ECG) may show abnormalities in rhythm and rate, which are rare in pure opioid overdoses but common with toxicity from some co-ingestants and adulterants of street drugs. An ECG may also reveal evidence of myocardial ischemia.

Echocardiography is indicated if endocarditis is suspected. An echocardiogram may also help diagnose acute pulmonary hypertension secondary to embolic disease.

Procedures

Endotracheal intubation is indicated for airway protection and may be required in the management of hypoxia due to noncardiogenic pulmonary edema. Endotracheal intubation with ventilation may also be required in the management of increased intracranial pressure and shock.

Pulmonary artery catheterization may be indicated. Noncardiogenic pulmonary edema secondary to opioid overdose is characterized by a normal pulmonary capillary wedge pressure and mildly increased pulmonary arterial pressure.

Lumbar puncture may be indicated. 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.

Medical Care

The direct effects of heroin on the central nervous system (CNS) are quickly reversible with naloxone. Naloxone may be given intravenously, intramuscularly, subcutaneously, or via endotracheal tube; the newer intranasal formulation has proved especially convenient for first responders and laypersons.[26]

A response to naloxone should 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 a standard dose of naloxone should prompt a search for another cause of the clinical presentation, such as hypoglycemia. Alternatively, opioid-induced respiratory depression from fentanyl and acetyl fentanyl may require larger doses of naloxone, because of the higher potency of these drugs compared with heroin.[27] 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 is becoming increasingly controversial because of the risk of aspiration and charcoal pneumonitis. It may be indicated for orally ingested narcotics with large enterohepatic circulation (eg, propoxyphene, diphenoxylate) but 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 (eg, endocarditis, epidural abscess, cellulitis). 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

Noncardiogenic pulmonary edema (NCPE), which affects 0.3-2.4% of heroin overdoses, generally lasts 24-48 hours and responds to supportive care. In most instances, hypoxia improves with mask oxygen ventilation only, but noninvasive positive-pressure ventilation (NIPPV) and endotracheal intubation may be required. Endotracheal intubation is indicated for airway protection, severe hypoxia, acidosis, and cardiovascular instability.

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 antidepressants, cocaine, amphetamines).

Some narcotics, such as meperidine (Demerol), pentazocine (Talwin), diphenoxylate (Lomotil), 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.

Special considerations

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.[28] 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 all cases of pediatric heroin overdose, social services should be involved.

Surgical Care

Surgery is indicated for body packers with bowel obstruction or bowel perforation. Surgery is also indicated in patients with ruptured packets resulting in life-threatening symptoms not responding to naloxone infusions or when the ruptured packets contain cocaine and other life-threatening drugs. Unruptured heroin packages that remain in the stomach for longer than 48 hours without obstruction may be managed expectantly.

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.

Naloxone (Narcan)

Clinical Context:  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).

Polyethylene glycol (GoLYTELY, Colyte)

Clinical Context:  Polyethylene glycol is a laxative with strong electrolyte and osmotic effects that has cathartic actions in the GI tract. It is used in whole-bowel irrigation.

What is the difference between body packing and body stuffing of heroin?What is heroin?What is the pathophysiology of heroin toxicity?What is the prevalence of heroin toxicity in the US?What is the global prevalence of heroin use?What are the mortality rates of heroin toxicity?Which patient groups have the highest prevalence of heroin toxicity?What are the sexual predilections of heroin toxicity?Which age groups are at highest risk for heroin toxicity?Which clinical history findings are characteristic of heroin toxicity?Which factors may alter the clinical presentation of heroin toxicity?What are the signs and symptoms of heroin toxicity?Which physical findings are characteristic of heroin toxicity?What causes heroin toxicity?Which drugs should be considered in the differential diagnoses of heroin toxicity?What are the differential diagnoses for Heroin Toxicity?What is the role of lab testing in the workup of heroin toxicity?What is the role of imaging studies in the workup of heroin toxicity?What is the role of ECG in the workup of heroin toxicity?What is the role of intubation in the treatment of heroin toxicity?What is the role of pulmonary artery catheterization in the treatment of heroin toxicity?What is the role of lumbar puncture in the workup of heroin toxicity?How is heroin toxicity treated?How is pulmonary edema treated in heroin toxicity?How are convulsions treated in heroin toxicity?How is rhabdomyolysis treated in heroin toxicity?How is heroin toxicity treated during pregnancy?How is heroin toxicity treated in children?What is the role of surgery in the treatment of heroin toxicity?Which specialist consultations are beneficial to patients with heroin toxicity?Which dietary modifications are used in the treatment of heroin toxicity?Which medications in the drug class GI decontaminants are used in the treatment of Heroin Toxicity?Which medications in the drug class Narcotic antagonists are used in the treatment of Heroin Toxicity?

Author

Rania Habal, MD, Assistant Professor, Department of Emergency Medicine, New York Medical College

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Asim Tarabar, MD, Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Chief Editor

Jeter (Jay) Pritchard Taylor, III, MD, Assistant Professor, Department of Surgery, University of South Carolina School of Medicine; Attending Physician, Clinical Instructor, Compliance Officer, Department of Emergency Medicine, Palmetto Richland Hospital

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Employed contractor - Chief Editor for Medscape.

Additional Contributors

Daniel R Ouellette, MD, FCCP, Associate Professor of Medicine, Wayne State University School of Medicine; Medical Director, Pulmonary Medicine General Practice Unit (F2), Senior Staff and Attending Physician, Division of Pulmonary and Critical Care Medicine, Henry Ford Hospital

Disclosure: Nothing to disclose.

Laurie Robin Grier, MD, Medical Director of MICU, Professor of Medicine, Emergency Medicine, Anesthesiology and Obstetrics/Gynecology, Fellowship Director for Critical Care Medicine, Section of Pulmonary and Critical Care Medicine, Louisiana State University Health Science Center at Shreveport

Disclosure: Nothing to disclose.

References

  1. United Nations Office on Drugs and Crime. World Drug Report 2017. Available at https://www.unodc.org/wdr2017/. June 2017; Accessed: December 16, 2018.
  2. Yaksh TL, Wallace M. Opioids, Analgesia, and Pain Management. Brunten LL, Hilal-Dandan R, Knollmann BC, eds. Goodman & Gilman's The Pharmacological Basis of Therapeutics. 13th ed. New York, NY: McGraw Hill Medical; 2018. 35-37.
  3. US Substance Abuse and Mental Health Services Administration. Key substance use and mental health indicators in the United States: Results from the 2016 National Survey on Drug Use and Health. Substance Abuse and Mental Health Services Administration. Available at https://www.samhsa.gov/data/sites/default/files/NSDUH-FFR1-2016/NSDUH-FFR1-2016.htm#illicit9. 2017; Accessed: December 16, 2018.
  4. European Monitoring Centre for Drugs and Drug Addiction. European Drug Report. EMCDDA. Available at http://www.emcdda.europa.eu/edr2018_en#downloadReport. June 7, 2018; Accessed: December 16, 2018.
  5. Sporer KA, Dorn E. Heroin-related noncardiogenic pulmonary edema : a case series. Chest. 2001 Nov. 120(5):1628-32. [View Abstract]
  6. Centers for Disease Control and Prevention. Atypical reactions associated with heroin use--five states, January-April 2005. MMWR Morb Mortal Wkly Rep. 2005 Aug 19. 54(32):793-6. [View Abstract]
  7. Bikell WH, Benar O. Life-threatening opioid toxicity. Prob Crit Care. 1987. 1:106.
  8. Bryant WK, Galea S, Tracy M, Markham Piper T, Tardiff KJ, Vlahov D. Overdose deaths attributed to methadone and heroin in New York City, 1990-1998. Addiction. 2004 Jul. 99(7):846-54. [View Abstract]
  9. Hedegaard H, Bastian BA, Trinidad JP, Spencer M, Warner M. Drugs Most Frequently Involved in Drug Overdose Deaths: United States, 2011–2016. National Vital Statistics Reports. Available at https://www.cdc.gov/nchs/data/nvsr/nvsr67/nvsr67_09-508.pdf. December 12, 2018; Accessed: December 16, 2018.
  10. Hedegaard H, Miniño AM, Warner M. Drug Overdose Deaths in the United States, 1999–2017. NCHS Data Brief. November 2018. Available at https://www.cdc.gov/vitalsigns/pdf/2018-03-vitalsigns.pdf
  11. Jones CM, Logan J, Gladden RM, Bohm MK. Vital Signs: Demographic and Substance Use Trends Among Heroin Users - United States, 2002-2013. MMWR Morb Mortal Wkly Rep. 2015 Jul 10. 64 (26):719-25. [View Abstract]
  12. Rudd RA, Paulozzi LJ, Bauer MJ, Burleson RW, Carlson RE, et al. Increases in heroin overdose deaths - 28 States, 2010 to 2012. MMWR Morb Mortal Wkly Rep. 2014 Oct 3. 63 (39):849-54. [View Abstract]
  13. Gummin DD, Mowry JB, Spyker DA, Brooks DE, Fraser MO, Banner W. 2016 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 34th Annual Report. Clin Toxicol (Phila). 2017 Dec. 55 (10):1072-1252. [View Abstract]
  14. Darke S, Hall W, Weatherburn D, Lind B. Fluctuations in heroin purity and the incidence of fatal heroin overdose. Drug Alcohol Depend. 1999 Apr 1. 54(2):155-61. [View Abstract]
  15. Seelye KQ. Heroin Epidemic Is Yielding to a Deadlier Cousin: Fentanyl. NY Times. March 16, 2016. Available at http://www.nytimes.com/2016/03/26/us/heroin-fentanyl.html?_r=0
  16. Coffin PO, Galea S, Ahern J, Leon AC, Vlahov D, Tardiff K. Opiates, cocaine and alcohol combinations in accidental drug overdose deaths in New York City, 1990-98. Addiction. 2003 Jun. 98(6):739-47. [View Abstract]
  17. Darke S, Zador D. Fatal heroin 'overdose': a review. Addiction. 1996 Dec. 91(12):1765-72. [View Abstract]
  18. Davoli M, Perucci CA, Forastiere F, et al. Risk factors for overdose mortality: a case-control study within a cohort of intravenous drug users. Int J Epidemiol. 1993 Apr. 22(2):273-7. [View Abstract]
  19. Infante F, Domínguez E, Trujillo D, Luna A. Metal contamination in illicit samples of heroin. J Forensic Sci. 1999 Jan. 44(1):110-3. [View Abstract]
  20. Hoffman RS, Kirrane BM, Marcus SM. A descriptive study of an outbreak of clenbuterol-containing heroin. Ann Emerg Med. 2008 Nov. 52(5):548-53. [View Abstract]
  21. Vagi SJ, Sheikh S, Brackney M, Smolinske S, Warrick B, Reuter N, et al. Passive multistate surveillance for neutropenia after use of cocaine or heroin possibly contaminated with levamisole. Ann Emerg Med. 2013 Apr. 61 (4):468-74. [View Abstract]
  22. Centers for Disease Control and Prevention. Wound botulism among black tar heroin users--Washington, 2003. MMWR Morb Mortal Wkly Rep. 2003 Sep 19. 52(37):885-6. [View Abstract]
  23. Hoffman RS, Goldfrank LR. The poisoned patient with altered consciousness. Controversies in the use of a 'coma cocktail'. JAMA. 1995 Aug 16. 274(7):562-9. [View Abstract]
  24. Hoffman JR, Schriger DL, Luo JS. The empiric use of naloxone in patients with altered mental status: a reappraisal. Ann Emerg Med. 1991 Mar. 20(3):246-52. [View Abstract]
  25. Fentanyl and Fentanyl Analogs. National Drug Early Warning System. Available at http://pub.lucidpress.com/NDEWSFentanyl/#0uATvewBep_i. December 7, 2015; Accessed: December 21, 2017.
  26. Doyon S, Aks SE, Schaeffer S. Expanding access to naloxone in the United States. J Med Toxicol. 2014 Dec. 10 (4):431-4. [View Abstract]
  27. Centers for Disease Control and Prevention. Recommendations for Laboratory Testing for Acetyl Fentanyl and Patient Evaluation and Treatment for Overdose with Synthetic Opioids. CDC. Available at https://stacks.cdc.gov/view/cdc/25259. June 20, 2013; Accessed: December 21, 2017.
  28. ACOG Committee on Health Care for Underserved Women., American Society of Addiction Medicine. ACOG Committee Opinion No. 524: Opioid abuse, dependence, and addiction in pregnancy. Obstet Gynecol. 2012 May. 119 (5):1070-6. [View Abstract]
  29. Rudd RA, Aleshire N, Zibbell JE, Gladden RM. Increases in Drug and Opioid Overdose Deaths--United States, 2000-2014. MMWR Morb Mortal Wkly Rep. 2016 Jan 1. 64 (50-51):1378-82. [View Abstract]
  30. Centers for Disease Control and Prevention. Scopolamine poisoning among heroin users--New York City, Newark, Philadelphia, and Baltimore, 1995 and 1996. MMWR Morb Mortal Wkly Rep. 1996 Jun 7. 45(22):457-60. [View Abstract]
  31. Vagi SJ, Sheikh S, Brackney M, et al. Passive multistate surveillance for neutropenia after use of cocaine or heroin possibly contaminated with levamisole. Ann Emerg Med. 2013 Apr. 61(4):468-74. [View Abstract]

Track marks in a heroin intravenous drug user.

Heroin-related noncardiogenic pulmonary edema.

Heroin-related noncardiogenic pulmonary edema.

Track marks in a heroin intravenous drug user.

Necrotizing fasciitis in a heroin user.

Endocarditis-related septic pulmonary emboli in a heroin user.