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.”
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 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.
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 2006 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 in 2006, and the corresponding prevalence rate increased from 0.06% to 0.14%. In 2006, 91,000 persons aged 12 or older had used heroin for the first time within the past 12 months. The average age at first use among recent initiates aged 12 to 49 was 20.7 years in 2006.
Additionally, for 2005 the Drug Abuse Warning Network (DAWN) estimated that heroin was involved in 164,572 Emergency Department patient visits.
According to the 2008 report of the United Nations Office on Drug and Crime (UNODC), Afghanistan produced most of the world’s opium supply in 2007.
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 4-5 cases per 1,000 population aged 15–64 (1.3–1.7 million users).
In 2004, 1,730 heroin overdoses were reported to US Poison Control Centers, with 34 fatalities. Of those who survived, 772 developed moderate-to-severe morbidity.
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.
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.1
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.1
The National Survey on Drug Use and Health reports stability at low levels of heroin use among young people. Regarding pediatric heroin poisonings, 164 were reported to the US Poison Control Centers in 2004, of which 13 poisonings occurred in children less than 6 years of age.
In general, when it is the sole agent used, the clinical presentation of heroin 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.
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.
Respiratory depression, due to heroin’s effect on the brain’s respiratory centers is a hallmark. But 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.
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.