Updated: Aug 5, 2008
The hypodermic syringe was invented in the mid-1800s. By the late 1800s and early 1900s in the United States, the public could purchase hypodermic needles and syringes legally, and opiates and cocaine were widely available. The Harrison Act in 1914 allowed narcotics to be dispensed only by a prescription from physicians or dentists. Several states also developed legislation preventing the sale of hypodermic syringes and needles without a prescription.
Most individuals who use injection drugs inject their drugs intravenously, but subcutaneous injection (ie, "skin-popping") is also common, and intramuscular injection may occur intentionally or when the individual misses the vein or the subcutaneous space. Injecting drug use is associated with many local and systemic complications for the individual and is also associated with the transmission of infectious diseases via needle sharing and sexual activity. The most commonly injected drug is heroin, but amphetamines, buprenorphine, benzodiazepines, barbiturates, cocaine, and methamphetamine also are injected. Any water-soluble drug may be injected. Treatment of individuals who use injection drugs may be complicated by social and political barriers to treatment and by a lack of resources for public health approaches to treatment.
Both illegal drug production and injecting drug use have been globalized in recent years. Injecting drug use has diffused to countries that formerly had little problem with it. Both injecting drug use and HIV infection can spread rapidly within a community. Introduction of and rapid increase in injecting drug use is believed to be responsible for dramatic increases in HIV infection in some areas. In China, in Central Asia, and in several countries of Eastern Europe, injecting drug use is the primary risk factor for HIV infection.
See related Medscape CME activity, The Dark Side of Drug Addicition.
When injecting a drug intravenously, the individual introduces a bolus of the drug into the vein, producing a rapid and powerful drug high. The onset of drug effects is about 15-30 seconds for the intravenous route and 3-5 minutes for the intramuscular or subcutaneous route. Drug effects from inhaling (ie, smoking) a drug begin in 7-10 seconds, and drug effects from intranasal use (ie, transmucosal absorption) begin in 3-5 minutes.
Injecting drug use causes medical problems by introducing pathogens and other contaminants into the body via shared needles and a lack of sterile preparation and injection techniques. Medical problems also arise from damage caused by the drugs themselves (eg, morbidity and mortality associated with drug overdose). The injected drugs also may not be pure; they may be cut with irritants, such as talc, lactate, or quinine.
Death from the direct toxic effects of a heroin overdose itself is usually associated with respiratory depression, coma, and pulmonary edema. Death from the direct effects of cocaine is often associated with cardiac dysrhythmias and conduction disturbances, leading to myocardial infarction and stroke.
In 2003, the United Nations Office on Drugs and Crime estimated about 1.4 million people used injection drugs in North America.
The United Nations Office on Drugs and Crime reported that an approximate 13 million people used injection drugs worldwide in 2003, with 130 countries providing information and 78% residing in developing countries. About 8.8 million are in Eastern Europe and Central, South, and Southeast Asia. About 1 million are in Latin America.
Morbidity and mortality may result from infection secondary to injecting drug use, sequelae of injection with adulterants added to the drug mixture, sequelae of the drug use itself, drug overdose, or violence associated with drug use.
The National Survey on Drug Use and Health (NSDUH) found no differences in injection drug use reports by race or ethnicity in the United States in 2002 and 2003.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Individuals who have injected heroin or other opioids for long periods may need referral for opioid replacement therapy with methadone, buprenorphine, or buprenorphine/naloxone where such programs are available. In the United States, physicians who wish to prescribe buprenorphine must take a certification course. Levo-alpha-acetylmethadol (LAAM) has also been used for opioid replacement therapy, but use of LAAM has been less common because of concerns about severe QT prolongation secondary to LAAM.
Opioid replacement therapy reduces injecting drug use and thus reduces the mortality and morbidity associated with injecting drug use, including the transmission of HIV and HCV.
When individuals who are opioid dependent (including those who are on opioid replacement therapy) need analgesia, the clinician should be aware that these individuals may be tolerant to the analgesic effects of opioids; thus, they may require higher doses for pain control. Individuals taking naltrexone (an opioid antagonist) for opioid or alcohol dependence, also require higher doses of opioid analgesics to overcome the opioid blockade and provide pain relief.
Inhibits ascending pain pathways, diminishing the perception of and response to pain. In most countries, methadone is administered initially in the setting of a drug treatment program, both to prevent diversion (selling) of supply and to assure that counseling and other services also are provided.
Rate of dose increase and maximum dose often depend on program regulations and on federal and state regulations in the United States.
Patients who cannot take anything by mouth may be administered methadone IM, usually in a divided dose.
20-30 mg PO qd initially, gradually increase (depending on presence of opioid withdrawal symptoms) to 60-120 mg qd; higher doses may be used with the approval of the state authority within the United States
Not recommended
Phenytoin, rifampin, and pentazocine may decrease blood levels; phenothiazines, TCAs, MAOIs, and CNS depressants may increase toxicity
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in patients with severe liver disease; because of its relatively long half-life, titrate dose slowly
Mixed agonist-antagonist narcotic with central analgesic effects for moderate to severe pain. Used sublingually for the initial detoxification treatment of opioid addiction. Produces agonist/antagonist effects at the opioid mu receptor. The agonist effect is limited by a ceiling effect (ie, higher doses [>16 mg] do not produce more analgesia). The sublingual product is called Subutex.
12-16 mg/d SL as a single dose during induction (supervised) phase, then begin buprenorphine and naloxone SL (Suboxone) during maintenance (unsupervised) phase
<16 years: Not established
>16 years: Administer as in adults
Phenothiazines may antagonize analgesic effects of opiate agonists; TCAs, MAOIs, and other CNS depressants may potentiate adverse effects; metabolized to norbuprenorphine by CYP3A4; CYP3A4 inhibitors (eg, ketoconazole, erythromycin, ritonavir, indinavir) may increase serum levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in patients with hepatic or renal insufficiency, respiratory limitations (eg, bronchial asthma, obstructive respiratory conditions, cyanosis), neurologic injury, and Addison disease; causes respiratory depression; avoid use in patients with constipation and urinary retention; may precipitate abstinence syndrome in patients who are dependent on narcotics; may decrease pulse or blood pressure
Used sublingually for the maintenance detoxification treatment (unsupervised phase) of opioid dependence following induction with sublingual buprenorphine (Subutex). Contains both buprenorphine (an opiate agonist/antagonist) and the opiate antagonist naloxone. Naloxone has been added to guard against IV abuse of buprenorphine by individuals physically dependent on opiates.
Progressively adjust by increments/decrements of 2-4 mg/d SL to a target dose of 16 mg/d; adjust to the lowest dose that keeps patients in treatment while suppressing withdrawal effects; dosage may range from 4-24 mg/d
<16 years: Not established
>16 years: Administer as in adults
Increases toxicity of other CNS depressants (eg, barbiturates, benzodiazepines); metabolized to norbuprenorphine by CYP3A4; CYP3A4 inhibitors (eg, ketoconazole, erythromycin, ritonavir, indinavir) may increase serum levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hepatic or renal dysfunction, elderly patients, pulmonary diseases, biliary tract dysfunction, or neurologic injury; may precipitate abstinence syndrome in patients dependent on narcotics; may decrease pulse or blood pressure
Indicated for management of opioid dependence. No other recommended uses exist. In most countries, levomethadyl is administered initially in the setting of a drug treatment program, both to prevent diversion (selling) of supply and to assure that counseling and other services also are provided.
Patients with unknown tolerance to opioids: 20-40 mg PO 3 times qwk or qod initially, gradually increase by 5-10 mg if opioid withdrawal symptoms persist
Patients with known tolerance to opioids: Convert patients already on methadone maintenance to levomethadyl at 1.2-1.3 times the patient's dose of methadone; not to exceed 120 mg initially
Not recommended
Phenothiazines, TCAs, MAOIs, and other CNS depressants increase toxicity
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Peak activity is not immediate; use of other psychoactive drugs, including alcohol, may result in fatal overdose; may increase QT interval
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intravenous drug use, IV drug use, injecting drug user, IDU, heroin, opiate, opioid, methadone, syringes, needles, needle sharing, hypodermic syringe, hypodermic needle, cocaine, heroin, amphetamines, buprenorphine, benzodiazepines, barbiturates, methamphetamine, HIV infection, talc, lactate, quinine, respiratory depression, coma, pulmonary edema, cardiac dysrhythmias, conduction disturbances, myocardial infarction, stroke
Gloria J Baciewicz, MD, Director of Addiction Psychiatry Program, Clinical Associate Professor, Department of Psychiatry, Strong Memorial Hospital, University of Rochester
Gloria J Baciewicz, MD is a member of the following medical societies: American Academy of Addiction Psychiatry, American Psychiatric Association, and American Society of Addiction Medicine
Disclosure: Nothing to disclose.
Barry I Liskow, MD, Vice Chairman, Director Psychiatry Residency Program, Professor, Department of Psychiatry, University of Kansas Medical School
Barry I Liskow, MD is a member of the following medical societies: American Academy of Addiction Psychiatry
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Eduardo Dunayevich, MD, Adjunct Assistant Professor, Department of Psychiatry, University of Cincinnati; Clinical Research Physician, Neuroscience, Lilly Research Laboratories
Eduardo Dunayevich, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: Nothing to disclose.
Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; BMS Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Other; Northstar Grant/research funds Other; Novartis Other; Pfizer Honoraria Speaking and teaching
Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
Disclosure: Nothing to disclose.
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