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Alcohol and Drug Abuse and Dependence
Clinical Vignette
A 73-year-old woman is seen in the emergency department after an unwitnessed fall at home in which her husband heard a crash and found her moments later on the ground in her bedroom. She was disoriented and bleeding from a head laceration that occurred when she fell and hit the corner of their bedroom dresser.
She has a past medical history of anxiety, obesity, gastroesophageal reflux, and chronic low back pain. She underwent a lumbar discectomy 10 years earlier with minimal improvement in her symptoms. Her medications include citalopram, lorazepam, oxycodone, and pantoprazole. She retired early from her job as an office manager because it was exceedingly stressful for her and she lives with her husband, daughter, and infant grandson. She reports “social” alcohol use and denies tobacco or other drug use.
On examination, she is sleepy but readily arouses to voice. She does not participate in the history or examination and tells healthcare team members that she is “just here to get stitches.” Her husband apologizes for her lack of cooperation. He explains that she tends to avoid medical care and is going through a lot of stress at home related to her daughter and grandchild. On mental status examination, she is oriented to year and city but not the name of the hospital or the date. She has moderate inattention but intact language and 3/5 recall at 5 min. Her remaining neurologic exam is significant for hyporeflexia, a distal, symmetric sensory neuropathy, and a slow, mildly ataxic gait with inability to tandem walk.
Urine toxicology screening was positive for benzodiazepines and opiates, and a blood alcohol concentration was 0.05%. A noncontrast head CT showed no hemorrhage or other sign of acute intracranial injury but was noted to have generalized mild atrophy.
Outside the room, the patient's husband expresses concern over his wife's use of pain and anxiety medications, noting that she frequently sleeps during the day. He has noticed that she has lost contact with her usual group of social contacts and that she gets extremely angry with him when he has asked her about cutting down on alcohol and pain killers. Upon further 1 : 1 questioning, the patient admits to drinking more than usual over the past several weeks and using higher doses of medication to treat “intolerable pain and anxiety.”
Most physicians are intimately familiar with the protean manifestations of alcohol abuse and dependence ( Fig. 43.1 ) and its characteristic clinical signs ( Fig. 43.2 ). Incidence rates vary widely depending on geography and social and cultural dynamics. In North America and Europe, the lifetime rate of alcohol abuse is estimated at 5%–10%. Therefore physicians who assert that they never see alcoholism are likely not recognizing the diagnosis. When obtaining the substance use history, it is critical to ask nonjudgmental, open-ended questions. “How much alcohol do you drink?” or “What do you find helpful for your pain/anxiety?” is more likely to elicit an honest reply than “Do you ever drink excessive amounts of alcohol?” Asking in a comfortable, relaxed setting, phrasing similar questions differently, as well as interviewing an individual by themselves rather than in front of family members or friends are all helpful ways to obtain a more accurate alcohol and drug use history. Patient denial poses a significant barrier in identifying and treating substance overuse. This denial has several sources. Admitting to a problem with alcohol or other drugs may be humiliating for patients. Furthermore, alcohol use, even at dangerous levels, is a culturally embedded and accepted, often pleasurable part of social life.
Alcohol Abuse.
Signs Suggestive of Alcohol Abuse.
The rubric of drug and alcohol abuse subsumes dozens of syndromes, but a few useful generalizations can be offered. Most drugs have safe and unsafe uses. Physicians routinely use opiates, sedative-hypnotics, psychostimulants, and dissociative anesthetics, all of which have abuse and addiction potential. Even over-the-counter drugs, including anticholinergics, pseudoephedrine, and dextromethorphan, can be abused.
Potentially abusable drugs cause dopamine release directly or indirectly in several forebrain structures. Beyond this, factors that may make a drug dangerous include the dosage, route of administration, and social context. High doses, routes of administration that rapidly deliver a drug to the brain (intranasal, injection, etc.), and ingestion beyond a stable social or religious context all predispose to abuse and addiction potential. These factors rather than, for example, the pharmacology of cocaine per se, explain why the Peruvian practice of chewing coca leaves rarely leads to addiction or neurologic injury, whereas smoking freebase cocaine is extremely addictive and risky.
Etiology
Liability to alcohol abuse and dependence, especially early-onset abuse, runs in families, but the mechanism of inheritance is not understood. Findings of a link between alcoholism and a particular dopamine DR-2 receptor allele remain controversial. Some Asian individuals are relatively protected from alcoholism because they possess a dysfunctional form of the enzyme alcohol dehydrogenase that leads to slow alcohol metabolism. This causes skin flushing and nausea with small amounts of alcohol ingestion. Conversely, young adults with a high alcohol tolerance, evaluated on measures of incoordination or subjectively, are at increased risk to develop alcoholism.
Alcohol is a central nervous system (CNS) depressant with cross-tolerance to benzodiazepines, barbiturates, and some other sedatives. It is distinguished within this group by its ease of manufacture, legal status, wide availability, rapid absorption, and exceptionally low therapeutic index. The lethal dose of alcohol is only a few times the intoxicating dose; one bottle of whiskey can be lethal to an individual who has not acquired tolerance. The dose at which tissue damage occurs is lower in this setting and falls within the range of commonly ingested doses. In adults, chemical signs of hepatic injury are detectable after consumption of three or more drinks within 24 hours. Alcohol is a potent fetal teratogen with no threshold dose and therefore contraindicated in pregnancy.
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