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Individuals who abuse substances often have comorbid psychiatric disorders—80% of alcoholics have another axis I disorder1—and the reverse also is true. More than one-half of schizophrenia patients and 30% of anxiety and affective disorder patients abuse substances.1
In addition to worsening psychiatric illnesses and interfering with proper treatment, alcohol and other substances can lead to serious cardiac, neurologic, pulmonary, or gastrointestinal complications that can linger even after your patient stops abusing drugs. This article provides an overview of common medical complications related to using alcohol, marijuana, cocaine, methamphetamines, and opioids.
Alcohol
Because some consequences of alcohol abuse (Table 1) are thought to be dose-dependent, ask about your patient’s alcohol consumption. Moderate drinking is defined as up to 2 drinks/day for men and 1 drink/day for women.2 Heavy drinking is ≥5 drinks/day (or ≥15 drinks/week) for men and ≥4/day (or ≥8/week) for women.3 A drink contains 12.5 grams of ethanol and is defined as:
- 12 oz (360 mL) of beer or wine cooler
- 5 oz (150 mL) of wine
- 1.5 oz (45 mL) of 80-proof distilled spirits.3
Gastrointestinal effects. Chronic heavy alcohol consumption can lead to fatty liver (steatosis), alcoholic hepatitis, and cirrhosis. Steatosis—the first stage of alcoholic liver disease—can occur from heavy drinking for just a few days but can be reversed with abstinence from alcohol. Prolonged use can lead to alcoholic hepatitis. Symptoms include nausea, lack of appetite, vomiting, fatigue, abdominal pain and tenderness, spider-like blood vessels, and increased bleeding times.
Abstinence might not reverse liver damage from alcoholic hepatitis, and cirrhosis can still develop. Up to 70% of patients with alcoholic hepatitis will develop cirrhosis.4,5 Common physical manifestations of cirrhosis include generalized weakness, fatigue, malaise, anorexia with signs of malnutrition, and increased bleeding.
Laboratory findings of elevated aspartate aminotransferase/alanine aminotransferase, gamma-glutamyltransferase, and carbohydrate-deficient transferrin also point to heavy alcohol use.6
Acute pancreatitis—the most common cause of hospitalization from alcohol-related GI complications—is seen more often than liver disease.7
Cardiovascular effects. Light to moderate drinking may be cardioprotective, but heavy alcohol consumption increases the risk of hypertension and ischemic heart disease.8 Incidence of hypertension is two-fold greater in individuals who have >2 drinks/day and highest in those who have >5 drinks/day.9
Prolonged excessive alcohol consumption is the leading cause of nonischemic dilated cardiomyopathy. Symptoms of alcoholic cardiomyopathy include fatigue; dyspnea, including paroxysmal nocturnal dyspnea and orthopnea; loss of appetite; irregular pulse; productive cough with pink/frothy material; lower extremity edema; and nocturia.10 Cardiac function can recover with early diagnosis and alcohol abstinence.11
Cognitive decline. The effects of light drinking on cognitive function are controversial, but heavy consumption—especially at ≥30 drinks/week—is known to cause impairment.12 Alcohol-dependent individuals have been shown to have impaired verbal fluency, working memory, and frontal function as is seen in Alzheimer’s disease.13 One possible factor contributing to cognitive dysfunction is cortical volume loss in chronic alcoholics.12
To read how nicotine plus alcohol increases the risk of heart disease and brain atrophy, click here.
To read about the medical complications of nicotine, click here.
Table 1
Medical complications of alcohol abuse
| Cardiovascular: Cardiomyopathy; hypertension; ischemic heart disease; acute myocardial infarction |
| Gastrointestinal: Alcohol hepatitis; cirrhosis of the liver; pancreatitis; cancer of the mouth, larynx, pharynx, esophagus, liver, and colon/rectum/appendix |
| Neurologic: Wernicke’s encephalopathy; Korsakoff’s syndrome; decline in cognitive abilities; decreased gray and white matter; increased ventricular and sulcal volume; peripheral neuropathy |
| Other: Renal dysfunction; osteoporosis; breast cancer |
Marijuana
Marijuana is the most commonly abused illicit substance worldwide, and data show an increasing prevalence of marijuana abuse and dependence (32% of U.S. 12th graders endorsed its use in 2007).14
In many populations marijuana use seems to precede use of cocaine, opioids, or other substances.15 Although the concept of marijuana as a “gateway drug” is still debated, consider the possibility that your patients who use marijuana also are using other illicit substances. In a 2004 survey, 19% of marijuana users admitted to use of other illicit drugs.16 Although many people consider marijuana a “safe” drug, it can cause adverse effects (Table 2).
Pulmonary complications. Even infrequent marijuana use can lead to burning and stinging of the mouth and throat, usually accompanied by a heavy cough. Regular users may develop complications similar to chronic tobacco use: daily cough, chronic phlegm production, susceptibility to lung infections (such as acute bronchitis), and potential for airway obstruction.17,18
Marijuana use can double or triple the risk of cancer of the respiratory tract and lungs.19 Tetrahydrocannabinol—the active chemical in marijuana—might contribute to this risk because it can augment oxidative stress, lead to mitochondrial dysfunction, and inhibit apoptosis.19
Cardiac complications. Acute marijuana use causes tachycardia, increases supine blood pressure, and decreases standing blood pressure, resulting in dizziness, syncope, falls, and possible injuries.20,21 Increased cardiac output and cardiac work—coupled with a decreased capacity to carry oxygen—can lead to angina or acute coronary syndrome, especially in older adults with preexisting cardiovascular disease.21 Growing evidence shows that marijuana use could lead to cardiac arrhythmias, such as atrial fibrillation.20 Long-term heavy users seem to develop tolerance to some cardiovascular effects, but blood volume overall increases, heart rate slows, and circulatory responses to exercise are diminished.18
Cognitive impairment. Chronic marijuana users might experience cognitive impairment—particularly on memory of word lists and attention tasks22—but there is debate as to whether these deficits are stable or temporary. Some studies show persistent cognitive impairments in longer-term cannabis users, even after 2 years of abstinence.22 However, most studies suggest that marijuana-associated cognitive deficits are reversible and related to recent exposure.18
Table 2
Medical complications of marijuana use
| Cardiovascular: Tachycardia; increased supine blood pressure; increased risk of myocardial infarction; atrial fibrillation |
| Pulmonary: Stinging of mouth/throat; chronic/heavy cough; increased lung infections; obstructed airways; lung cancer |
| Neurologic: Decreased performance on cognitive tasks (word lists, attention); diminished reaction times |
| Other: Decreased serum testosterone, sperm count, and sperm motility; shorter menstrual cycles; increased prolactin; suppressed activity of macrophages and natural killer cell |
Cocaine
Cocaine is the most frequent cause of drug-related death, particularly when combined with alcohol.23
Chronic nasal insufflations can cause loss of sense of smell, nosebleeds, dysphagia, hoarseness, and overall irritation of the nasal septum, which in turn can lead to chronic mucosal inflammation and rhinorrhea.24 Intravenous users often have puncture marks or “tracks,” usually on the forearms, and are predisposed to infectious diseases such as human immunodeficiency virus (HIV) and other blood-borne infections.24,25 Regular cocaine ingestion can lead to bowel gangrene because of reduced blood flow and orofacial complications.24 Asking about how your patient ingests cocaine will guide your evaluation of possible medical complications (Table 3).
Cardiac complications. Recent cocaine use is a common cause of chest pain. A 2002 survey reported that 25% of patients in urban hospitals and 13% in rural settings presenting with nontraumatic chest pain tested positive for cocaine use.26 Although cocaine can lead to ventricular fibrillation, tachycardia, and increased blood pressure, its main mechanism for inducing chest pain and myocardial infarction (MI) is coronary vasospasm, especially of diseased vessels. The acute risk of MI is increased by a factor of 24 in the first 60 minutes after cocaine use.23 Chronic use promotes thrombus formation, leading to atherosclerotic disease.23 Recurrent chest pain in a young, otherwise healthy individual could indicate cocaine abuse.
Neurologic complications. Headache is the most common neurologic complication of cocaine use. Although usually associated with intoxication or withdrawal, headaches can become chronic with chronic use.25 Reduced seizure threshold also has been reported with cocaine use, particularly in patients with cerebral lesions, and most seizures occur with first-time use. Isolated events might not require anticonvulsant therapy, although referral to a neurologist is recommended.27
Cocaine use puts individuals at higher risk for subarachnoid hemorrhage, intracerebral bleed, ischemic stroke, and transient ischemic attacks. The route of cocaine ingestion seems to influence the type of stroke: IV and intranasal use are associated with hemorrhagic stroke, and inhalation with ischemic stroke.25
Table 3
Medical complications of cocaine use
| Cardiovascular: Chest pain; 24-fold increased risk of myocardial infarction; coronary vasospasm; ventricular fibrillation; tachycardia; hypertension |
| Pulmonary: Pleuritic chest pain; chronic cough; wheezing; hemoptysis; melanoptysis (black sputum); ‘crack lung’ (fever, cough, difficulty breathing, and chest pain) |
| Gastrointestinal: Xerostomia; bruxism; decreased gastric motility; ischemic colitis; bowel ulceration, infarction, and perforation |
| Neurologic: Seizures; headaches; cerebral vasoconstriction; hemorrhagic/ischemic stroke; cerebral gray matter atrophy (especially frontotemporal lobes); dystonic reactions; akathisia; choreoathetosis (‘crack dancers’) |
| Other: Acute renal failure via rhabdomyolysis; nephrosclerosis; impaired sexual function (chronic use) |
Methamphetamine
Like many illicit substances, methamphetamine can be taken in many forms.
- “Speed,” a powder form, can be snorted or injected.
- “Base” is a powder with higher purity.
- “Ice,” also known as “crystal,” has very high purity and can be smoked, “chased” (cooked on aluminum foil and smoked), mixed with marijuana, or injected.28
Evaluate meth-abusing patients for many of the same medical complications associated with cocaine and other stimulants. Acute effects include hypertension, tachycardia, and arrhythmias; chronic effects include stroke and cardiac valve sclerosis. Pulmonary hypertension can occur when the drug is smoked (Table 4).28
Dental complications. Originally believed to result from the acidity of methamphetamine, advanced tooth decay or “meth mouth” is thought to be caused by decreased production of saliva—a consequence of increased sympathetic activity—combined with overall decreased oral intake, sugar and soft drink consumption, and poor oral hygiene. Methamphetamine abusers often experience bruxism, which exacerbates tooth decay.29
Neurologic changes. Chronic methamphetamine use is characterized by poor cognitive functioning and emotional changes such as paranoia and depression.29 These are believed to be caused by neuropathologic changes in the cortex, striatum, and hippocampus.
Table 4
Medical complications of methamphetamine abuse
| Cardiovascular: Arrhythmias; hypertensive crisis; myocardial infarction; cardiomyopathy; tachycardia |
| Pulmonary: Pneumomediastinum respiratory failure |
| Gastrointestinal: Tooth decay (‘Meth mouth’); xerostomia; bruxism; hepatitis infection; hepatotoxicity |
| Neurologic: Cerebral infarct; seizures; blurred vision; obtundation |
| Other: Jaw clenching; excessive sweating; aplastic anemia; hyperthermia; muscle cramping |
Opioids
Prescriptions of opioid analgesics for chronic pain—and their subsequent diversion—are the main conduit to nonmedical use.30 IV heroin use is the most common cause of illicit drug overdose.31 Opioids are used by:
- ingestion, usually of synthetic analgesics (prescription drugs)
- parenteral administration, often IV heroin
- inhalation, a pure form that is heated and burned.
Infectious complications. Injection drug use—especially with unsterilized shared needles—is an efficient vector for blood-borne infections. Needle sharing is the most common cause of new HIV and viral hepatitis infections.32 All IV drug users should be routinely tested for these viral infections. Chronic IV drug use can cause vein sclerosis, leading to visible “track marks” and, rarely, thromboembolic events. Be alert for integumentary infections—especially in patients who “skin pop” drugs by injecting them under the skin—or systemic infectious diseases, such as skin abscesses, cellulitis, septicemia, botulism, or bacterial endocarditis (Table 5).33
Pulmonary complications. Overstimulation of opioid receptors in the brainstem and carotid bodies can cause slow and irregular respiration and decreased gag and coughing reflex during acute intoxication. The rate of opioid intake appears to play a role; a gradual increase in opioid blood levels leads to progressive respiratory depression by causing gradual hypercapnia, and a quick rise in receptor occupancy can lead to rapid apnea. Therefore opioids with slow receptor binding, such as buprenorphine, may be safer than those that bind more quickly, such as fentanyl. However, all opioids can cause this dangerous side effect.34 Inhaled forms of heroin have also been shown to lead to status asthmaticus.35
Table 5
Medical complications of opioid abuse
| Cardiovascular: Prolonged QTc interval (methadone) |
| Pulmonary: Respiratory suppression |
| Gastrointestinal: Hepatitis C infection; hepatotoxicity; nausea; constipation |
| Neurologic: Drowsiness; lightheadedness; confusion; myoclonus; hyperalgesia; miosis |
| Other: Urinary retention; pruritus |
Cardiac and neurologic complications. Methadone use could prolong the QTc interval, leading to dysrhythmias such as torsades de pointes. Higher doses increase the incidence of syncope.36 Ongoing monitoring of the QTc interval is warranted for all patients on methadone.
Neurologic effects of opioids include:
- delayed leukoencephalopathy with IV overdose and inhaled preheated heroin, known as ”chasing the dragon”
- widespread cortical dysfunction (abulia, lack of volition, hemineglect,37 and deficits in executive functioning and emotional processing) leading to impaired decision-making.38
Related resources
- National Institute on Drug Abuse. www.nida.nih.gov.
- Substance Abuse and Mental Health Services Administration. www.samhsa.gov.
- National Institute on Alcohol Abuse and Alcoholism. www.niaaa.nih.gov.
- Johnston LD, O’Malley PM, Bachman JG, et al. Monitoring the Future national survey results on drug use, 1975-2008. Volume I: Secondary school students. Bethesda, MD: National Institute on Drug Abuse; 2009. NIH Publication No. 09-7402.
Drug brand names
- Buprenorphine • Subutex
- Fentanyl • Actiq, Duragesic, others
- Methadone • Dolophine, Methadose
Disclosures
Drs. Khan and Morrow report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Dr. McCarron is a consultant to Eli Lilly and Company.
1. Brady KT. Comorbidity of substance use and Axis I psychiatric disorders. Medscape Psychiatry and Mental Health eJournal [serial online]. March 25, 2002. Available at: http://www.medscape.com/viewarticle/430610. Accessed September 28, 2009.
2. Dietary guidelines for Americans, 2005. Chapter 9 alcoholic beverages. Washington, DC: United States Department of Agriculture; 2005. Available at: http://www.health.gov/dietaryguidelines/dga2005/document/html/chapter9.htm. Accessed September 15, 2008.
3. National Institute on Alcohol Abuse and Alcoholism. How to screen for heavy drinking. Bethesda, MD: National Institute on Alcohol Abuse and Alcoholism; 2005. Available at: http://pubs.niaaa.nih.gov/publications/Practitioner/PocketGuide/pocket_guide5.htm. Accessed September 15, 2008.
4. Zakhari S, Li TK. Determinants of alcohol use and abuse: impact of quantity and frequency patterns on liver disease. Hepatology. 2007;46(6):2032-2039.
5. National Institute on Alcohol Abuse and Alcoholism. Alcohol alert. Alcoholic liver disease. Washington, DC: US Department of Health and Human Services; 2005. Available at: http://pubs.niaaa.nih.gov/publications/aa64/aa64.htm. Accessed August 23, 2009.
6. Spiegel DR, Dhadwal N, Gill F. ‘I’m sober, doctor, really’: best biomarkers for underreported alcohol use. Current Psychiatry. 2008;7(9):15-27.
7. Yang AL, Vadhavkar S, Singh G, et al. Epidemiology of alcohol-related liver and pancreatic disease in the United States. Arch Intern Med. 2008;168(6):649-656.
8. Hvidtfeldt UA, Frederiksen ME, Thysesen LC, et al. Incidence of cardiovascular and cerebrovascular disease in Danish men and women with a prolonged heavy alcohol intake. Alcohol Clin Exp Res. 2008;32(11):1920-1924.
9. Fuchs FD, Chambless LE, Whelton PK, et al. Alcohol consumption and the incidence of hypertension: the Athersclerosis Risk in Communities Study. Hypertension. 2001;37(5):1242-1250.
10. Alcoholic cardiomyopathy. The New York Times Health Guide. Available at: http://health.nytimes.com/health/guides/disease/alcoholic-cardiomyopathy/overview.html. Accessed September 28, 2009.
11. McKenna CJ, Codd MB, McCann HA, et al. Alcohol consumption and idiopathic dilated cardiomyopathy: a case control study. Am Heart J. 1998;135(5 pt 1):833-837.
12. Meyerhoff DJ, Bode C, Nixon SJ, et al. Health risks of chronic moderate and heavy alcohol consumption: how much is too much? Alcohol Clin Exp Res. 2005;29(7):1334-1340.
13. Liappas I, Theotoka I, Kapaki E, et al. Neuropsychological assessment of cognitive function in chronic alcohol-dependent patients and patients with Alzheimer’s disease. In Vivo. 2007;21(6):1115-1118.
14. Johnston LD, O’Malley PM, Bachman JG, et al. Monitoring the Future. National Results on Adolescent Drug Use. Overview of Key Findings, 2007. Bethesda, MD: National Institute on Drug Abuse; 2008. Available at: http://www.monitoringthefuture.org/pubs/monographs/overview2007.pdf. Accessed August 20, 2008.
15. Hales RE, Yudofsky SC, Gabbard GO. The American Psychiatric Publishing textbook of psychiatry. 5th ed. Arlington, VA: American Psychiatric Publishing, Inc.; 2008.
16. Substance Abuse and Mental Health Services Administration. Results from the 2004 National Survey on Drug Use and Health: National Findings. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2005. NSDUH Series H-28, DHHS Publication No. SMA 05-4062.
17. National Institute on Drug Abuse. Research report series—marijuana abuse. Bethesda, MD: National Institute on Drug Abuse; 2005. Available at: http://www.nida.nih.gov/ResearchReports/Marijuana. Accessed September 1, 2008.
18. Khalsa JH, Genser S, Francis H, et al. Clinical consequences of marijuana. J Clin Pharmacol. 2002;42(suppl 11):7S-10S.
19. Tashkin DP. Smoked marijuana as a cause of lung injury. Monaldi Arch Chest Dis. 2005;63(2):93-100.
20. Korantzopoulos P, Liou T, Papaioannides D, et al. Atrial fibrillation and marijuana smoking. Int J Clin Pract. 2008;62(2):308-313.
21. Jones RT. Cardiovascular system effects of marijuana. J Clin Pharmacol. 2002;42(suppl 11):58S-63S.
22. Harrison GP, Jr, Gruber AJ, Hudson JI, et al. Cognitive measures in long-term cannabis users. J Clin Pharmacol. 2002;42(suppl 11):41S-47S.
23. Lange RA, Hillis LD. Cardiovascular complications of cocaine use. N Engl J Med. 2001;345(5):351-358.
24. National Institute on Drug Abuse. What are the long-term effects of cocaine use? Bethesda, MD: National Institute on Drug Abuse; 1999. Available at: http://www.nida.nih.gov/PDF/RRCocaine.pdf Accessed September 1, 2008.
25. Wang CM, Huang CL, Hu CTS, et al. Medical complications of cocaine abuse. Medical Update for Psychiatrists. 1997;2(2):34-38.
26. Hollander JE, Todd KH, Green G, et al. Chest pain associated with cocaine: an assessment of prevalence in suburban and urban emergency departments. Ann Emerg Med. 1995;26:671-676.
27. Agarwal P, Sen S. Cocaine. e-medicine [serial online]. February 21, 2007. Available at: http://www.emedicine.com/neuro/TOPIC72.HTM. Accessed September 27, 2008.
28. Maxwell JC. Emerging research on methamphetamine. Curr Opin Psychiatry. 2005;18(3):235-242.
29. Goodchild JH, Donaldson M, Mangini DJ. Methamphetamine abuse and the impact on dental health. Dent Today. 2007;26(5):124-131.
30. Substance Abuse and Mental Health Services Administration. Results from the 2007 National Survey on Drug Use and Health: National Findings. Rockville, MD: Substance Abuse and Mental Health Services Administration. Available at: http://www.oas.samhsa.gov/nsduh/2k7nsduh/2k7Results.cfm#TOC. Accessed January 21, 2009.
31. Schuckit MA. Drug and alcohol abuse. 5th ed. New York, NY: Kluwer Academic/Plenum Publishers; 2000:114-119.
32. National Institute for Drug Addiction. Research on the nature and extent of drug use in the United States. Bethesda, MD: National Institute for Drug Addiction; 1999. Available at: http://www.drugabuse.gov/STRC/Data.html. Accessed January 21, 2009.
33. Galanter M, Kleber H. The American Psychiatric Publishing textbook of substance abuse treatment. 4th ed. Arlington, VA: American Psychiatric Publishing, Inc.; 2008.
34. Pattinson KT. Opioids and the control of respiration. Br J Anesth. 2008;100(6):747-758.
35. Cygan J, Trunsky M, Corbridge T. Inhaled heroin-induced status asthmaticus: five cases and a review of the literature. Chest. 2000;117(1):272-275.
36. Fanoe S, Hvidt C, Ege P, et al. Syncope and QT prolongation among patients treated with methadone for heroin dependence in the city of Copenhagen. Heart. 2006;93(9):1051-1055.
37. Barnett MH, Miller LA, Reddel SW, et al. Reversible delayed leukoencephalopathy following intravenous heroin overdose. J Clin Neurosci. 2001;8(2):165-167.
38. Brand M, Roth-Bauer M, Driessen M, et al. Executive functions and risky decision-making in patients with opiate dependence. Drug Alcohol Depend. 2008;97(1-2):64-72.
Individuals who abuse substances often have comorbid psychiatric disorders—80% of alcoholics have another axis I disorder1—and the reverse also is true. More than one-half of schizophrenia patients and 30% of anxiety and affective disorder patients abuse substances.1
In addition to worsening psychiatric illnesses and interfering with proper treatment, alcohol and other substances can lead to serious cardiac, neurologic, pulmonary, or gastrointestinal complications that can linger even after your patient stops abusing drugs. This article provides an overview of common medical complications related to using alcohol, marijuana, cocaine, methamphetamines, and opioids.
Alcohol
Because some consequences of alcohol abuse (Table 1) are thought to be dose-dependent, ask about your patient’s alcohol consumption. Moderate drinking is defined as up to 2 drinks/day for men and 1 drink/day for women.2 Heavy drinking is ≥5 drinks/day (or ≥15 drinks/week) for men and ≥4/day (or ≥8/week) for women.3 A drink contains 12.5 grams of ethanol and is defined as:
- 12 oz (360 mL) of beer or wine cooler
- 5 oz (150 mL) of wine
- 1.5 oz (45 mL) of 80-proof distilled spirits.3
Gastrointestinal effects. Chronic heavy alcohol consumption can lead to fatty liver (steatosis), alcoholic hepatitis, and cirrhosis. Steatosis—the first stage of alcoholic liver disease—can occur from heavy drinking for just a few days but can be reversed with abstinence from alcohol. Prolonged use can lead to alcoholic hepatitis. Symptoms include nausea, lack of appetite, vomiting, fatigue, abdominal pain and tenderness, spider-like blood vessels, and increased bleeding times.
Abstinence might not reverse liver damage from alcoholic hepatitis, and cirrhosis can still develop. Up to 70% of patients with alcoholic hepatitis will develop cirrhosis.4,5 Common physical manifestations of cirrhosis include generalized weakness, fatigue, malaise, anorexia with signs of malnutrition, and increased bleeding.
Laboratory findings of elevated aspartate aminotransferase/alanine aminotransferase, gamma-glutamyltransferase, and carbohydrate-deficient transferrin also point to heavy alcohol use.6
Acute pancreatitis—the most common cause of hospitalization from alcohol-related GI complications—is seen more often than liver disease.7
Cardiovascular effects. Light to moderate drinking may be cardioprotective, but heavy alcohol consumption increases the risk of hypertension and ischemic heart disease.8 Incidence of hypertension is two-fold greater in individuals who have >2 drinks/day and highest in those who have >5 drinks/day.9
Prolonged excessive alcohol consumption is the leading cause of nonischemic dilated cardiomyopathy. Symptoms of alcoholic cardiomyopathy include fatigue; dyspnea, including paroxysmal nocturnal dyspnea and orthopnea; loss of appetite; irregular pulse; productive cough with pink/frothy material; lower extremity edema; and nocturia.10 Cardiac function can recover with early diagnosis and alcohol abstinence.11
Cognitive decline. The effects of light drinking on cognitive function are controversial, but heavy consumption—especially at ≥30 drinks/week—is known to cause impairment.12 Alcohol-dependent individuals have been shown to have impaired verbal fluency, working memory, and frontal function as is seen in Alzheimer’s disease.13 One possible factor contributing to cognitive dysfunction is cortical volume loss in chronic alcoholics.12
To read how nicotine plus alcohol increases the risk of heart disease and brain atrophy, click here.
To read about the medical complications of nicotine, click here.
Table 1
Medical complications of alcohol abuse
| Cardiovascular: Cardiomyopathy; hypertension; ischemic heart disease; acute myocardial infarction |
| Gastrointestinal: Alcohol hepatitis; cirrhosis of the liver; pancreatitis; cancer of the mouth, larynx, pharynx, esophagus, liver, and colon/rectum/appendix |
| Neurologic: Wernicke’s encephalopathy; Korsakoff’s syndrome; decline in cognitive abilities; decreased gray and white matter; increased ventricular and sulcal volume; peripheral neuropathy |
| Other: Renal dysfunction; osteoporosis; breast cancer |
Marijuana
Marijuana is the most commonly abused illicit substance worldwide, and data show an increasing prevalence of marijuana abuse and dependence (32% of U.S. 12th graders endorsed its use in 2007).14
In many populations marijuana use seems to precede use of cocaine, opioids, or other substances.15 Although the concept of marijuana as a “gateway drug” is still debated, consider the possibility that your patients who use marijuana also are using other illicit substances. In a 2004 survey, 19% of marijuana users admitted to use of other illicit drugs.16 Although many people consider marijuana a “safe” drug, it can cause adverse effects (Table 2).
Pulmonary complications. Even infrequent marijuana use can lead to burning and stinging of the mouth and throat, usually accompanied by a heavy cough. Regular users may develop complications similar to chronic tobacco use: daily cough, chronic phlegm production, susceptibility to lung infections (such as acute bronchitis), and potential for airway obstruction.17,18
Marijuana use can double or triple the risk of cancer of the respiratory tract and lungs.19 Tetrahydrocannabinol—the active chemical in marijuana—might contribute to this risk because it can augment oxidative stress, lead to mitochondrial dysfunction, and inhibit apoptosis.19
Cardiac complications. Acute marijuana use causes tachycardia, increases supine blood pressure, and decreases standing blood pressure, resulting in dizziness, syncope, falls, and possible injuries.20,21 Increased cardiac output and cardiac work—coupled with a decreased capacity to carry oxygen—can lead to angina or acute coronary syndrome, especially in older adults with preexisting cardiovascular disease.21 Growing evidence shows that marijuana use could lead to cardiac arrhythmias, such as atrial fibrillation.20 Long-term heavy users seem to develop tolerance to some cardiovascular effects, but blood volume overall increases, heart rate slows, and circulatory responses to exercise are diminished.18
Cognitive impairment. Chronic marijuana users might experience cognitive impairment—particularly on memory of word lists and attention tasks22—but there is debate as to whether these deficits are stable or temporary. Some studies show persistent cognitive impairments in longer-term cannabis users, even after 2 years of abstinence.22 However, most studies suggest that marijuana-associated cognitive deficits are reversible and related to recent exposure.18
Table 2
Medical complications of marijuana use
| Cardiovascular: Tachycardia; increased supine blood pressure; increased risk of myocardial infarction; atrial fibrillation |
| Pulmonary: Stinging of mouth/throat; chronic/heavy cough; increased lung infections; obstructed airways; lung cancer |
| Neurologic: Decreased performance on cognitive tasks (word lists, attention); diminished reaction times |
| Other: Decreased serum testosterone, sperm count, and sperm motility; shorter menstrual cycles; increased prolactin; suppressed activity of macrophages and natural killer cell |
Cocaine
Cocaine is the most frequent cause of drug-related death, particularly when combined with alcohol.23
Chronic nasal insufflations can cause loss of sense of smell, nosebleeds, dysphagia, hoarseness, and overall irritation of the nasal septum, which in turn can lead to chronic mucosal inflammation and rhinorrhea.24 Intravenous users often have puncture marks or “tracks,” usually on the forearms, and are predisposed to infectious diseases such as human immunodeficiency virus (HIV) and other blood-borne infections.24,25 Regular cocaine ingestion can lead to bowel gangrene because of reduced blood flow and orofacial complications.24 Asking about how your patient ingests cocaine will guide your evaluation of possible medical complications (Table 3).
Cardiac complications. Recent cocaine use is a common cause of chest pain. A 2002 survey reported that 25% of patients in urban hospitals and 13% in rural settings presenting with nontraumatic chest pain tested positive for cocaine use.26 Although cocaine can lead to ventricular fibrillation, tachycardia, and increased blood pressure, its main mechanism for inducing chest pain and myocardial infarction (MI) is coronary vasospasm, especially of diseased vessels. The acute risk of MI is increased by a factor of 24 in the first 60 minutes after cocaine use.23 Chronic use promotes thrombus formation, leading to atherosclerotic disease.23 Recurrent chest pain in a young, otherwise healthy individual could indicate cocaine abuse.
Neurologic complications. Headache is the most common neurologic complication of cocaine use. Although usually associated with intoxication or withdrawal, headaches can become chronic with chronic use.25 Reduced seizure threshold also has been reported with cocaine use, particularly in patients with cerebral lesions, and most seizures occur with first-time use. Isolated events might not require anticonvulsant therapy, although referral to a neurologist is recommended.27
Cocaine use puts individuals at higher risk for subarachnoid hemorrhage, intracerebral bleed, ischemic stroke, and transient ischemic attacks. The route of cocaine ingestion seems to influence the type of stroke: IV and intranasal use are associated with hemorrhagic stroke, and inhalation with ischemic stroke.25
Table 3
Medical complications of cocaine use
| Cardiovascular: Chest pain; 24-fold increased risk of myocardial infarction; coronary vasospasm; ventricular fibrillation; tachycardia; hypertension |
| Pulmonary: Pleuritic chest pain; chronic cough; wheezing; hemoptysis; melanoptysis (black sputum); ‘crack lung’ (fever, cough, difficulty breathing, and chest pain) |
| Gastrointestinal: Xerostomia; bruxism; decreased gastric motility; ischemic colitis; bowel ulceration, infarction, and perforation |
| Neurologic: Seizures; headaches; cerebral vasoconstriction; hemorrhagic/ischemic stroke; cerebral gray matter atrophy (especially frontotemporal lobes); dystonic reactions; akathisia; choreoathetosis (‘crack dancers’) |
| Other: Acute renal failure via rhabdomyolysis; nephrosclerosis; impaired sexual function (chronic use) |
Methamphetamine
Like many illicit substances, methamphetamine can be taken in many forms.
- “Speed,” a powder form, can be snorted or injected.
- “Base” is a powder with higher purity.
- “Ice,” also known as “crystal,” has very high purity and can be smoked, “chased” (cooked on aluminum foil and smoked), mixed with marijuana, or injected.28
Evaluate meth-abusing patients for many of the same medical complications associated with cocaine and other stimulants. Acute effects include hypertension, tachycardia, and arrhythmias; chronic effects include stroke and cardiac valve sclerosis. Pulmonary hypertension can occur when the drug is smoked (Table 4).28
Dental complications. Originally believed to result from the acidity of methamphetamine, advanced tooth decay or “meth mouth” is thought to be caused by decreased production of saliva—a consequence of increased sympathetic activity—combined with overall decreased oral intake, sugar and soft drink consumption, and poor oral hygiene. Methamphetamine abusers often experience bruxism, which exacerbates tooth decay.29
Neurologic changes. Chronic methamphetamine use is characterized by poor cognitive functioning and emotional changes such as paranoia and depression.29 These are believed to be caused by neuropathologic changes in the cortex, striatum, and hippocampus.
Table 4
Medical complications of methamphetamine abuse
| Cardiovascular: Arrhythmias; hypertensive crisis; myocardial infarction; cardiomyopathy; tachycardia |
| Pulmonary: Pneumomediastinum respiratory failure |
| Gastrointestinal: Tooth decay (‘Meth mouth’); xerostomia; bruxism; hepatitis infection; hepatotoxicity |
| Neurologic: Cerebral infarct; seizures; blurred vision; obtundation |
| Other: Jaw clenching; excessive sweating; aplastic anemia; hyperthermia; muscle cramping |
Opioids
Prescriptions of opioid analgesics for chronic pain—and their subsequent diversion—are the main conduit to nonmedical use.30 IV heroin use is the most common cause of illicit drug overdose.31 Opioids are used by:
- ingestion, usually of synthetic analgesics (prescription drugs)
- parenteral administration, often IV heroin
- inhalation, a pure form that is heated and burned.
Infectious complications. Injection drug use—especially with unsterilized shared needles—is an efficient vector for blood-borne infections. Needle sharing is the most common cause of new HIV and viral hepatitis infections.32 All IV drug users should be routinely tested for these viral infections. Chronic IV drug use can cause vein sclerosis, leading to visible “track marks” and, rarely, thromboembolic events. Be alert for integumentary infections—especially in patients who “skin pop” drugs by injecting them under the skin—or systemic infectious diseases, such as skin abscesses, cellulitis, septicemia, botulism, or bacterial endocarditis (Table 5).33
Pulmonary complications. Overstimulation of opioid receptors in the brainstem and carotid bodies can cause slow and irregular respiration and decreased gag and coughing reflex during acute intoxication. The rate of opioid intake appears to play a role; a gradual increase in opioid blood levels leads to progressive respiratory depression by causing gradual hypercapnia, and a quick rise in receptor occupancy can lead to rapid apnea. Therefore opioids with slow receptor binding, such as buprenorphine, may be safer than those that bind more quickly, such as fentanyl. However, all opioids can cause this dangerous side effect.34 Inhaled forms of heroin have also been shown to lead to status asthmaticus.35
Table 5
Medical complications of opioid abuse
| Cardiovascular: Prolonged QTc interval (methadone) |
| Pulmonary: Respiratory suppression |
| Gastrointestinal: Hepatitis C infection; hepatotoxicity; nausea; constipation |
| Neurologic: Drowsiness; lightheadedness; confusion; myoclonus; hyperalgesia; miosis |
| Other: Urinary retention; pruritus |
Cardiac and neurologic complications. Methadone use could prolong the QTc interval, leading to dysrhythmias such as torsades de pointes. Higher doses increase the incidence of syncope.36 Ongoing monitoring of the QTc interval is warranted for all patients on methadone.
Neurologic effects of opioids include:
- delayed leukoencephalopathy with IV overdose and inhaled preheated heroin, known as ”chasing the dragon”
- widespread cortical dysfunction (abulia, lack of volition, hemineglect,37 and deficits in executive functioning and emotional processing) leading to impaired decision-making.38
Related resources
- National Institute on Drug Abuse. www.nida.nih.gov.
- Substance Abuse and Mental Health Services Administration. www.samhsa.gov.
- National Institute on Alcohol Abuse and Alcoholism. www.niaaa.nih.gov.
- Johnston LD, O’Malley PM, Bachman JG, et al. Monitoring the Future national survey results on drug use, 1975-2008. Volume I: Secondary school students. Bethesda, MD: National Institute on Drug Abuse; 2009. NIH Publication No. 09-7402.
Drug brand names
- Buprenorphine • Subutex
- Fentanyl • Actiq, Duragesic, others
- Methadone • Dolophine, Methadose
Disclosures
Drs. Khan and Morrow report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Dr. McCarron is a consultant to Eli Lilly and Company.
Individuals who abuse substances often have comorbid psychiatric disorders—80% of alcoholics have another axis I disorder1—and the reverse also is true. More than one-half of schizophrenia patients and 30% of anxiety and affective disorder patients abuse substances.1
In addition to worsening psychiatric illnesses and interfering with proper treatment, alcohol and other substances can lead to serious cardiac, neurologic, pulmonary, or gastrointestinal complications that can linger even after your patient stops abusing drugs. This article provides an overview of common medical complications related to using alcohol, marijuana, cocaine, methamphetamines, and opioids.
Alcohol
Because some consequences of alcohol abuse (Table 1) are thought to be dose-dependent, ask about your patient’s alcohol consumption. Moderate drinking is defined as up to 2 drinks/day for men and 1 drink/day for women.2 Heavy drinking is ≥5 drinks/day (or ≥15 drinks/week) for men and ≥4/day (or ≥8/week) for women.3 A drink contains 12.5 grams of ethanol and is defined as:
- 12 oz (360 mL) of beer or wine cooler
- 5 oz (150 mL) of wine
- 1.5 oz (45 mL) of 80-proof distilled spirits.3
Gastrointestinal effects. Chronic heavy alcohol consumption can lead to fatty liver (steatosis), alcoholic hepatitis, and cirrhosis. Steatosis—the first stage of alcoholic liver disease—can occur from heavy drinking for just a few days but can be reversed with abstinence from alcohol. Prolonged use can lead to alcoholic hepatitis. Symptoms include nausea, lack of appetite, vomiting, fatigue, abdominal pain and tenderness, spider-like blood vessels, and increased bleeding times.
Abstinence might not reverse liver damage from alcoholic hepatitis, and cirrhosis can still develop. Up to 70% of patients with alcoholic hepatitis will develop cirrhosis.4,5 Common physical manifestations of cirrhosis include generalized weakness, fatigue, malaise, anorexia with signs of malnutrition, and increased bleeding.
Laboratory findings of elevated aspartate aminotransferase/alanine aminotransferase, gamma-glutamyltransferase, and carbohydrate-deficient transferrin also point to heavy alcohol use.6
Acute pancreatitis—the most common cause of hospitalization from alcohol-related GI complications—is seen more often than liver disease.7
Cardiovascular effects. Light to moderate drinking may be cardioprotective, but heavy alcohol consumption increases the risk of hypertension and ischemic heart disease.8 Incidence of hypertension is two-fold greater in individuals who have >2 drinks/day and highest in those who have >5 drinks/day.9
Prolonged excessive alcohol consumption is the leading cause of nonischemic dilated cardiomyopathy. Symptoms of alcoholic cardiomyopathy include fatigue; dyspnea, including paroxysmal nocturnal dyspnea and orthopnea; loss of appetite; irregular pulse; productive cough with pink/frothy material; lower extremity edema; and nocturia.10 Cardiac function can recover with early diagnosis and alcohol abstinence.11
Cognitive decline. The effects of light drinking on cognitive function are controversial, but heavy consumption—especially at ≥30 drinks/week—is known to cause impairment.12 Alcohol-dependent individuals have been shown to have impaired verbal fluency, working memory, and frontal function as is seen in Alzheimer’s disease.13 One possible factor contributing to cognitive dysfunction is cortical volume loss in chronic alcoholics.12
To read how nicotine plus alcohol increases the risk of heart disease and brain atrophy, click here.
To read about the medical complications of nicotine, click here.
Table 1
Medical complications of alcohol abuse
| Cardiovascular: Cardiomyopathy; hypertension; ischemic heart disease; acute myocardial infarction |
| Gastrointestinal: Alcohol hepatitis; cirrhosis of the liver; pancreatitis; cancer of the mouth, larynx, pharynx, esophagus, liver, and colon/rectum/appendix |
| Neurologic: Wernicke’s encephalopathy; Korsakoff’s syndrome; decline in cognitive abilities; decreased gray and white matter; increased ventricular and sulcal volume; peripheral neuropathy |
| Other: Renal dysfunction; osteoporosis; breast cancer |
Marijuana
Marijuana is the most commonly abused illicit substance worldwide, and data show an increasing prevalence of marijuana abuse and dependence (32% of U.S. 12th graders endorsed its use in 2007).14
In many populations marijuana use seems to precede use of cocaine, opioids, or other substances.15 Although the concept of marijuana as a “gateway drug” is still debated, consider the possibility that your patients who use marijuana also are using other illicit substances. In a 2004 survey, 19% of marijuana users admitted to use of other illicit drugs.16 Although many people consider marijuana a “safe” drug, it can cause adverse effects (Table 2).
Pulmonary complications. Even infrequent marijuana use can lead to burning and stinging of the mouth and throat, usually accompanied by a heavy cough. Regular users may develop complications similar to chronic tobacco use: daily cough, chronic phlegm production, susceptibility to lung infections (such as acute bronchitis), and potential for airway obstruction.17,18
Marijuana use can double or triple the risk of cancer of the respiratory tract and lungs.19 Tetrahydrocannabinol—the active chemical in marijuana—might contribute to this risk because it can augment oxidative stress, lead to mitochondrial dysfunction, and inhibit apoptosis.19
Cardiac complications. Acute marijuana use causes tachycardia, increases supine blood pressure, and decreases standing blood pressure, resulting in dizziness, syncope, falls, and possible injuries.20,21 Increased cardiac output and cardiac work—coupled with a decreased capacity to carry oxygen—can lead to angina or acute coronary syndrome, especially in older adults with preexisting cardiovascular disease.21 Growing evidence shows that marijuana use could lead to cardiac arrhythmias, such as atrial fibrillation.20 Long-term heavy users seem to develop tolerance to some cardiovascular effects, but blood volume overall increases, heart rate slows, and circulatory responses to exercise are diminished.18
Cognitive impairment. Chronic marijuana users might experience cognitive impairment—particularly on memory of word lists and attention tasks22—but there is debate as to whether these deficits are stable or temporary. Some studies show persistent cognitive impairments in longer-term cannabis users, even after 2 years of abstinence.22 However, most studies suggest that marijuana-associated cognitive deficits are reversible and related to recent exposure.18
Table 2
Medical complications of marijuana use
| Cardiovascular: Tachycardia; increased supine blood pressure; increased risk of myocardial infarction; atrial fibrillation |
| Pulmonary: Stinging of mouth/throat; chronic/heavy cough; increased lung infections; obstructed airways; lung cancer |
| Neurologic: Decreased performance on cognitive tasks (word lists, attention); diminished reaction times |
| Other: Decreased serum testosterone, sperm count, and sperm motility; shorter menstrual cycles; increased prolactin; suppressed activity of macrophages and natural killer cell |
Cocaine
Cocaine is the most frequent cause of drug-related death, particularly when combined with alcohol.23
Chronic nasal insufflations can cause loss of sense of smell, nosebleeds, dysphagia, hoarseness, and overall irritation of the nasal septum, which in turn can lead to chronic mucosal inflammation and rhinorrhea.24 Intravenous users often have puncture marks or “tracks,” usually on the forearms, and are predisposed to infectious diseases such as human immunodeficiency virus (HIV) and other blood-borne infections.24,25 Regular cocaine ingestion can lead to bowel gangrene because of reduced blood flow and orofacial complications.24 Asking about how your patient ingests cocaine will guide your evaluation of possible medical complications (Table 3).
Cardiac complications. Recent cocaine use is a common cause of chest pain. A 2002 survey reported that 25% of patients in urban hospitals and 13% in rural settings presenting with nontraumatic chest pain tested positive for cocaine use.26 Although cocaine can lead to ventricular fibrillation, tachycardia, and increased blood pressure, its main mechanism for inducing chest pain and myocardial infarction (MI) is coronary vasospasm, especially of diseased vessels. The acute risk of MI is increased by a factor of 24 in the first 60 minutes after cocaine use.23 Chronic use promotes thrombus formation, leading to atherosclerotic disease.23 Recurrent chest pain in a young, otherwise healthy individual could indicate cocaine abuse.
Neurologic complications. Headache is the most common neurologic complication of cocaine use. Although usually associated with intoxication or withdrawal, headaches can become chronic with chronic use.25 Reduced seizure threshold also has been reported with cocaine use, particularly in patients with cerebral lesions, and most seizures occur with first-time use. Isolated events might not require anticonvulsant therapy, although referral to a neurologist is recommended.27
Cocaine use puts individuals at higher risk for subarachnoid hemorrhage, intracerebral bleed, ischemic stroke, and transient ischemic attacks. The route of cocaine ingestion seems to influence the type of stroke: IV and intranasal use are associated with hemorrhagic stroke, and inhalation with ischemic stroke.25
Table 3
Medical complications of cocaine use
| Cardiovascular: Chest pain; 24-fold increased risk of myocardial infarction; coronary vasospasm; ventricular fibrillation; tachycardia; hypertension |
| Pulmonary: Pleuritic chest pain; chronic cough; wheezing; hemoptysis; melanoptysis (black sputum); ‘crack lung’ (fever, cough, difficulty breathing, and chest pain) |
| Gastrointestinal: Xerostomia; bruxism; decreased gastric motility; ischemic colitis; bowel ulceration, infarction, and perforation |
| Neurologic: Seizures; headaches; cerebral vasoconstriction; hemorrhagic/ischemic stroke; cerebral gray matter atrophy (especially frontotemporal lobes); dystonic reactions; akathisia; choreoathetosis (‘crack dancers’) |
| Other: Acute renal failure via rhabdomyolysis; nephrosclerosis; impaired sexual function (chronic use) |
Methamphetamine
Like many illicit substances, methamphetamine can be taken in many forms.
- “Speed,” a powder form, can be snorted or injected.
- “Base” is a powder with higher purity.
- “Ice,” also known as “crystal,” has very high purity and can be smoked, “chased” (cooked on aluminum foil and smoked), mixed with marijuana, or injected.28
Evaluate meth-abusing patients for many of the same medical complications associated with cocaine and other stimulants. Acute effects include hypertension, tachycardia, and arrhythmias; chronic effects include stroke and cardiac valve sclerosis. Pulmonary hypertension can occur when the drug is smoked (Table 4).28
Dental complications. Originally believed to result from the acidity of methamphetamine, advanced tooth decay or “meth mouth” is thought to be caused by decreased production of saliva—a consequence of increased sympathetic activity—combined with overall decreased oral intake, sugar and soft drink consumption, and poor oral hygiene. Methamphetamine abusers often experience bruxism, which exacerbates tooth decay.29
Neurologic changes. Chronic methamphetamine use is characterized by poor cognitive functioning and emotional changes such as paranoia and depression.29 These are believed to be caused by neuropathologic changes in the cortex, striatum, and hippocampus.
Table 4
Medical complications of methamphetamine abuse
| Cardiovascular: Arrhythmias; hypertensive crisis; myocardial infarction; cardiomyopathy; tachycardia |
| Pulmonary: Pneumomediastinum respiratory failure |
| Gastrointestinal: Tooth decay (‘Meth mouth’); xerostomia; bruxism; hepatitis infection; hepatotoxicity |
| Neurologic: Cerebral infarct; seizures; blurred vision; obtundation |
| Other: Jaw clenching; excessive sweating; aplastic anemia; hyperthermia; muscle cramping |
Opioids
Prescriptions of opioid analgesics for chronic pain—and their subsequent diversion—are the main conduit to nonmedical use.30 IV heroin use is the most common cause of illicit drug overdose.31 Opioids are used by:
- ingestion, usually of synthetic analgesics (prescription drugs)
- parenteral administration, often IV heroin
- inhalation, a pure form that is heated and burned.
Infectious complications. Injection drug use—especially with unsterilized shared needles—is an efficient vector for blood-borne infections. Needle sharing is the most common cause of new HIV and viral hepatitis infections.32 All IV drug users should be routinely tested for these viral infections. Chronic IV drug use can cause vein sclerosis, leading to visible “track marks” and, rarely, thromboembolic events. Be alert for integumentary infections—especially in patients who “skin pop” drugs by injecting them under the skin—or systemic infectious diseases, such as skin abscesses, cellulitis, septicemia, botulism, or bacterial endocarditis (Table 5).33
Pulmonary complications. Overstimulation of opioid receptors in the brainstem and carotid bodies can cause slow and irregular respiration and decreased gag and coughing reflex during acute intoxication. The rate of opioid intake appears to play a role; a gradual increase in opioid blood levels leads to progressive respiratory depression by causing gradual hypercapnia, and a quick rise in receptor occupancy can lead to rapid apnea. Therefore opioids with slow receptor binding, such as buprenorphine, may be safer than those that bind more quickly, such as fentanyl. However, all opioids can cause this dangerous side effect.34 Inhaled forms of heroin have also been shown to lead to status asthmaticus.35
Table 5
Medical complications of opioid abuse
| Cardiovascular: Prolonged QTc interval (methadone) |
| Pulmonary: Respiratory suppression |
| Gastrointestinal: Hepatitis C infection; hepatotoxicity; nausea; constipation |
| Neurologic: Drowsiness; lightheadedness; confusion; myoclonus; hyperalgesia; miosis |
| Other: Urinary retention; pruritus |
Cardiac and neurologic complications. Methadone use could prolong the QTc interval, leading to dysrhythmias such as torsades de pointes. Higher doses increase the incidence of syncope.36 Ongoing monitoring of the QTc interval is warranted for all patients on methadone.
Neurologic effects of opioids include:
- delayed leukoencephalopathy with IV overdose and inhaled preheated heroin, known as ”chasing the dragon”
- widespread cortical dysfunction (abulia, lack of volition, hemineglect,37 and deficits in executive functioning and emotional processing) leading to impaired decision-making.38
Related resources
- National Institute on Drug Abuse. www.nida.nih.gov.
- Substance Abuse and Mental Health Services Administration. www.samhsa.gov.
- National Institute on Alcohol Abuse and Alcoholism. www.niaaa.nih.gov.
- Johnston LD, O’Malley PM, Bachman JG, et al. Monitoring the Future national survey results on drug use, 1975-2008. Volume I: Secondary school students. Bethesda, MD: National Institute on Drug Abuse; 2009. NIH Publication No. 09-7402.
Drug brand names
- Buprenorphine • Subutex
- Fentanyl • Actiq, Duragesic, others
- Methadone • Dolophine, Methadose
Disclosures
Drs. Khan and Morrow report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Dr. McCarron is a consultant to Eli Lilly and Company.
1. Brady KT. Comorbidity of substance use and Axis I psychiatric disorders. Medscape Psychiatry and Mental Health eJournal [serial online]. March 25, 2002. Available at: http://www.medscape.com/viewarticle/430610. Accessed September 28, 2009.
2. Dietary guidelines for Americans, 2005. Chapter 9 alcoholic beverages. Washington, DC: United States Department of Agriculture; 2005. Available at: http://www.health.gov/dietaryguidelines/dga2005/document/html/chapter9.htm. Accessed September 15, 2008.
3. National Institute on Alcohol Abuse and Alcoholism. How to screen for heavy drinking. Bethesda, MD: National Institute on Alcohol Abuse and Alcoholism; 2005. Available at: http://pubs.niaaa.nih.gov/publications/Practitioner/PocketGuide/pocket_guide5.htm. Accessed September 15, 2008.
4. Zakhari S, Li TK. Determinants of alcohol use and abuse: impact of quantity and frequency patterns on liver disease. Hepatology. 2007;46(6):2032-2039.
5. National Institute on Alcohol Abuse and Alcoholism. Alcohol alert. Alcoholic liver disease. Washington, DC: US Department of Health and Human Services; 2005. Available at: http://pubs.niaaa.nih.gov/publications/aa64/aa64.htm. Accessed August 23, 2009.
6. Spiegel DR, Dhadwal N, Gill F. ‘I’m sober, doctor, really’: best biomarkers for underreported alcohol use. Current Psychiatry. 2008;7(9):15-27.
7. Yang AL, Vadhavkar S, Singh G, et al. Epidemiology of alcohol-related liver and pancreatic disease in the United States. Arch Intern Med. 2008;168(6):649-656.
8. Hvidtfeldt UA, Frederiksen ME, Thysesen LC, et al. Incidence of cardiovascular and cerebrovascular disease in Danish men and women with a prolonged heavy alcohol intake. Alcohol Clin Exp Res. 2008;32(11):1920-1924.
9. Fuchs FD, Chambless LE, Whelton PK, et al. Alcohol consumption and the incidence of hypertension: the Athersclerosis Risk in Communities Study. Hypertension. 2001;37(5):1242-1250.
10. Alcoholic cardiomyopathy. The New York Times Health Guide. Available at: http://health.nytimes.com/health/guides/disease/alcoholic-cardiomyopathy/overview.html. Accessed September 28, 2009.
11. McKenna CJ, Codd MB, McCann HA, et al. Alcohol consumption and idiopathic dilated cardiomyopathy: a case control study. Am Heart J. 1998;135(5 pt 1):833-837.
12. Meyerhoff DJ, Bode C, Nixon SJ, et al. Health risks of chronic moderate and heavy alcohol consumption: how much is too much? Alcohol Clin Exp Res. 2005;29(7):1334-1340.
13. Liappas I, Theotoka I, Kapaki E, et al. Neuropsychological assessment of cognitive function in chronic alcohol-dependent patients and patients with Alzheimer’s disease. In Vivo. 2007;21(6):1115-1118.
14. Johnston LD, O’Malley PM, Bachman JG, et al. Monitoring the Future. National Results on Adolescent Drug Use. Overview of Key Findings, 2007. Bethesda, MD: National Institute on Drug Abuse; 2008. Available at: http://www.monitoringthefuture.org/pubs/monographs/overview2007.pdf. Accessed August 20, 2008.
15. Hales RE, Yudofsky SC, Gabbard GO. The American Psychiatric Publishing textbook of psychiatry. 5th ed. Arlington, VA: American Psychiatric Publishing, Inc.; 2008.
16. Substance Abuse and Mental Health Services Administration. Results from the 2004 National Survey on Drug Use and Health: National Findings. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2005. NSDUH Series H-28, DHHS Publication No. SMA 05-4062.
17. National Institute on Drug Abuse. Research report series—marijuana abuse. Bethesda, MD: National Institute on Drug Abuse; 2005. Available at: http://www.nida.nih.gov/ResearchReports/Marijuana. Accessed September 1, 2008.
18. Khalsa JH, Genser S, Francis H, et al. Clinical consequences of marijuana. J Clin Pharmacol. 2002;42(suppl 11):7S-10S.
19. Tashkin DP. Smoked marijuana as a cause of lung injury. Monaldi Arch Chest Dis. 2005;63(2):93-100.
20. Korantzopoulos P, Liou T, Papaioannides D, et al. Atrial fibrillation and marijuana smoking. Int J Clin Pract. 2008;62(2):308-313.
21. Jones RT. Cardiovascular system effects of marijuana. J Clin Pharmacol. 2002;42(suppl 11):58S-63S.
22. Harrison GP, Jr, Gruber AJ, Hudson JI, et al. Cognitive measures in long-term cannabis users. J Clin Pharmacol. 2002;42(suppl 11):41S-47S.
23. Lange RA, Hillis LD. Cardiovascular complications of cocaine use. N Engl J Med. 2001;345(5):351-358.
24. National Institute on Drug Abuse. What are the long-term effects of cocaine use? Bethesda, MD: National Institute on Drug Abuse; 1999. Available at: http://www.nida.nih.gov/PDF/RRCocaine.pdf Accessed September 1, 2008.
25. Wang CM, Huang CL, Hu CTS, et al. Medical complications of cocaine abuse. Medical Update for Psychiatrists. 1997;2(2):34-38.
26. Hollander JE, Todd KH, Green G, et al. Chest pain associated with cocaine: an assessment of prevalence in suburban and urban emergency departments. Ann Emerg Med. 1995;26:671-676.
27. Agarwal P, Sen S. Cocaine. e-medicine [serial online]. February 21, 2007. Available at: http://www.emedicine.com/neuro/TOPIC72.HTM. Accessed September 27, 2008.
28. Maxwell JC. Emerging research on methamphetamine. Curr Opin Psychiatry. 2005;18(3):235-242.
29. Goodchild JH, Donaldson M, Mangini DJ. Methamphetamine abuse and the impact on dental health. Dent Today. 2007;26(5):124-131.
30. Substance Abuse and Mental Health Services Administration. Results from the 2007 National Survey on Drug Use and Health: National Findings. Rockville, MD: Substance Abuse and Mental Health Services Administration. Available at: http://www.oas.samhsa.gov/nsduh/2k7nsduh/2k7Results.cfm#TOC. Accessed January 21, 2009.
31. Schuckit MA. Drug and alcohol abuse. 5th ed. New York, NY: Kluwer Academic/Plenum Publishers; 2000:114-119.
32. National Institute for Drug Addiction. Research on the nature and extent of drug use in the United States. Bethesda, MD: National Institute for Drug Addiction; 1999. Available at: http://www.drugabuse.gov/STRC/Data.html. Accessed January 21, 2009.
33. Galanter M, Kleber H. The American Psychiatric Publishing textbook of substance abuse treatment. 4th ed. Arlington, VA: American Psychiatric Publishing, Inc.; 2008.
34. Pattinson KT. Opioids and the control of respiration. Br J Anesth. 2008;100(6):747-758.
35. Cygan J, Trunsky M, Corbridge T. Inhaled heroin-induced status asthmaticus: five cases and a review of the literature. Chest. 2000;117(1):272-275.
36. Fanoe S, Hvidt C, Ege P, et al. Syncope and QT prolongation among patients treated with methadone for heroin dependence in the city of Copenhagen. Heart. 2006;93(9):1051-1055.
37. Barnett MH, Miller LA, Reddel SW, et al. Reversible delayed leukoencephalopathy following intravenous heroin overdose. J Clin Neurosci. 2001;8(2):165-167.
38. Brand M, Roth-Bauer M, Driessen M, et al. Executive functions and risky decision-making in patients with opiate dependence. Drug Alcohol Depend. 2008;97(1-2):64-72.
1. Brady KT. Comorbidity of substance use and Axis I psychiatric disorders. Medscape Psychiatry and Mental Health eJournal [serial online]. March 25, 2002. Available at: http://www.medscape.com/viewarticle/430610. Accessed September 28, 2009.
2. Dietary guidelines for Americans, 2005. Chapter 9 alcoholic beverages. Washington, DC: United States Department of Agriculture; 2005. Available at: http://www.health.gov/dietaryguidelines/dga2005/document/html/chapter9.htm. Accessed September 15, 2008.
3. National Institute on Alcohol Abuse and Alcoholism. How to screen for heavy drinking. Bethesda, MD: National Institute on Alcohol Abuse and Alcoholism; 2005. Available at: http://pubs.niaaa.nih.gov/publications/Practitioner/PocketGuide/pocket_guide5.htm. Accessed September 15, 2008.
4. Zakhari S, Li TK. Determinants of alcohol use and abuse: impact of quantity and frequency patterns on liver disease. Hepatology. 2007;46(6):2032-2039.
5. National Institute on Alcohol Abuse and Alcoholism. Alcohol alert. Alcoholic liver disease. Washington, DC: US Department of Health and Human Services; 2005. Available at: http://pubs.niaaa.nih.gov/publications/aa64/aa64.htm. Accessed August 23, 2009.
6. Spiegel DR, Dhadwal N, Gill F. ‘I’m sober, doctor, really’: best biomarkers for underreported alcohol use. Current Psychiatry. 2008;7(9):15-27.
7. Yang AL, Vadhavkar S, Singh G, et al. Epidemiology of alcohol-related liver and pancreatic disease in the United States. Arch Intern Med. 2008;168(6):649-656.
8. Hvidtfeldt UA, Frederiksen ME, Thysesen LC, et al. Incidence of cardiovascular and cerebrovascular disease in Danish men and women with a prolonged heavy alcohol intake. Alcohol Clin Exp Res. 2008;32(11):1920-1924.
9. Fuchs FD, Chambless LE, Whelton PK, et al. Alcohol consumption and the incidence of hypertension: the Athersclerosis Risk in Communities Study. Hypertension. 2001;37(5):1242-1250.
10. Alcoholic cardiomyopathy. The New York Times Health Guide. Available at: http://health.nytimes.com/health/guides/disease/alcoholic-cardiomyopathy/overview.html. Accessed September 28, 2009.
11. McKenna CJ, Codd MB, McCann HA, et al. Alcohol consumption and idiopathic dilated cardiomyopathy: a case control study. Am Heart J. 1998;135(5 pt 1):833-837.
12. Meyerhoff DJ, Bode C, Nixon SJ, et al. Health risks of chronic moderate and heavy alcohol consumption: how much is too much? Alcohol Clin Exp Res. 2005;29(7):1334-1340.
13. Liappas I, Theotoka I, Kapaki E, et al. Neuropsychological assessment of cognitive function in chronic alcohol-dependent patients and patients with Alzheimer’s disease. In Vivo. 2007;21(6):1115-1118.
14. Johnston LD, O’Malley PM, Bachman JG, et al. Monitoring the Future. National Results on Adolescent Drug Use. Overview of Key Findings, 2007. Bethesda, MD: National Institute on Drug Abuse; 2008. Available at: http://www.monitoringthefuture.org/pubs/monographs/overview2007.pdf. Accessed August 20, 2008.
15. Hales RE, Yudofsky SC, Gabbard GO. The American Psychiatric Publishing textbook of psychiatry. 5th ed. Arlington, VA: American Psychiatric Publishing, Inc.; 2008.
16. Substance Abuse and Mental Health Services Administration. Results from the 2004 National Survey on Drug Use and Health: National Findings. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2005. NSDUH Series H-28, DHHS Publication No. SMA 05-4062.
17. National Institute on Drug Abuse. Research report series—marijuana abuse. Bethesda, MD: National Institute on Drug Abuse; 2005. Available at: http://www.nida.nih.gov/ResearchReports/Marijuana. Accessed September 1, 2008.
18. Khalsa JH, Genser S, Francis H, et al. Clinical consequences of marijuana. J Clin Pharmacol. 2002;42(suppl 11):7S-10S.
19. Tashkin DP. Smoked marijuana as a cause of lung injury. Monaldi Arch Chest Dis. 2005;63(2):93-100.
20. Korantzopoulos P, Liou T, Papaioannides D, et al. Atrial fibrillation and marijuana smoking. Int J Clin Pract. 2008;62(2):308-313.
21. Jones RT. Cardiovascular system effects of marijuana. J Clin Pharmacol. 2002;42(suppl 11):58S-63S.
22. Harrison GP, Jr, Gruber AJ, Hudson JI, et al. Cognitive measures in long-term cannabis users. J Clin Pharmacol. 2002;42(suppl 11):41S-47S.
23. Lange RA, Hillis LD. Cardiovascular complications of cocaine use. N Engl J Med. 2001;345(5):351-358.
24. National Institute on Drug Abuse. What are the long-term effects of cocaine use? Bethesda, MD: National Institute on Drug Abuse; 1999. Available at: http://www.nida.nih.gov/PDF/RRCocaine.pdf Accessed September 1, 2008.
25. Wang CM, Huang CL, Hu CTS, et al. Medical complications of cocaine abuse. Medical Update for Psychiatrists. 1997;2(2):34-38.
26. Hollander JE, Todd KH, Green G, et al. Chest pain associated with cocaine: an assessment of prevalence in suburban and urban emergency departments. Ann Emerg Med. 1995;26:671-676.
27. Agarwal P, Sen S. Cocaine. e-medicine [serial online]. February 21, 2007. Available at: http://www.emedicine.com/neuro/TOPIC72.HTM. Accessed September 27, 2008.
28. Maxwell JC. Emerging research on methamphetamine. Curr Opin Psychiatry. 2005;18(3):235-242.
29. Goodchild JH, Donaldson M, Mangini DJ. Methamphetamine abuse and the impact on dental health. Dent Today. 2007;26(5):124-131.
30. Substance Abuse and Mental Health Services Administration. Results from the 2007 National Survey on Drug Use and Health: National Findings. Rockville, MD: Substance Abuse and Mental Health Services Administration. Available at: http://www.oas.samhsa.gov/nsduh/2k7nsduh/2k7Results.cfm#TOC. Accessed January 21, 2009.
31. Schuckit MA. Drug and alcohol abuse. 5th ed. New York, NY: Kluwer Academic/Plenum Publishers; 2000:114-119.
32. National Institute for Drug Addiction. Research on the nature and extent of drug use in the United States. Bethesda, MD: National Institute for Drug Addiction; 1999. Available at: http://www.drugabuse.gov/STRC/Data.html. Accessed January 21, 2009.
33. Galanter M, Kleber H. The American Psychiatric Publishing textbook of substance abuse treatment. 4th ed. Arlington, VA: American Psychiatric Publishing, Inc.; 2008.
34. Pattinson KT. Opioids and the control of respiration. Br J Anesth. 2008;100(6):747-758.
35. Cygan J, Trunsky M, Corbridge T. Inhaled heroin-induced status asthmaticus: five cases and a review of the literature. Chest. 2000;117(1):272-275.
36. Fanoe S, Hvidt C, Ege P, et al. Syncope and QT prolongation among patients treated with methadone for heroin dependence in the city of Copenhagen. Heart. 2006;93(9):1051-1055.
37. Barnett MH, Miller LA, Reddel SW, et al. Reversible delayed leukoencephalopathy following intravenous heroin overdose. J Clin Neurosci. 2001;8(2):165-167.
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