Substance (drug and alcohol) misuse

chapter 62 Substance (drug and alcohol) misuse



INTRODUCTION AND OVERVIEW


We define a drug (substance) as a chemical entity, self-administered (non-medically) for its psychoactive effect. The effect usually includes a change in mood, arousal or perception, thinking (cognition) and/or behaviour. It may vary according to which drug is used, the amount used, the route of administration, the mixture of drugs used, the expectations of effect by the user, the setting of use and the personal characteristics of the user such as weight, gender and previous drug experience.


Drugs can be classified according to their physiological effects:


• depressants—lower inhibitions and impair consciousness, coordination and concentration

• opioids—are strong analgesics with euphoric properties that impair consciousness

• cannabinoids—have a mixture of mild hallucinogenic and depressant properties

• stimulants—increase nervous energy and suppress sleep and appetite

• hallucinogens—distort perception of reality.

In this chapter we briefly consider the more important drugs in most of the categories, and for each we consider the drug and its mode of action, use and clinical effects, and current medical and integrative treatments.



WHY PEOPLE USE DRUGS


Although there is no easy explanation for why people use drugs, the aim of using drugs may be broadly considered to be the pleasurable alteration of consciousness. The neural circuits that underlie the experience of pleasure clearly have high evolutionary value, as there is powerful survival value in repeating adaptive behaviour associated with pleasure or the relief of suffering. The ‘reward centre’ is the brain pathway responsible for the subjective experience related to natural reinforcers such as sexual activity and eating. These cells arise in the midbrain and extend to the nucleus accumbens, the amygdaloid nucleus, hippocampus, olfactory bulb and parts of the prefrontal cortex. Dopamine is released in anticipation of reinforcing activity and it facilitates approach behaviour (that is, feeling drawn to the things we find attractive or pleasurable). Dopamine release is necessary for associative conditioning, essentially enabling emotionally tagged information to be acquired and retained efficiently—in essence, dopamine has distinct motivational properties and important survival value in signalling reinforcement and in facilitating incentive learning. Anticipatory release of dopamine may assume an attentional role and be the biological basis of drug-related craving. Drugs of abuse may be thought of as increasing dopamine release (e.g. amphetamines), inhibiting post-synaptic dopamine reuptake (e.g. cocaine) or interfering with interneuron inhibition of dopaminergic pathways (e.g. opioids).


Not all effects of drugs on brain function are due to dopamine: dopamine modulates the presynaptic release of glutamate (the major excitatory neurotransmitter) and gamma aminobutyric acid (GABA, the major inhibitory neurotransmitter), both of which are implicated in reward pathways. Generally, the more efficiently a drug alters neurochemical function, the stronger its potential reward or reinforcing effect. And vice versa—with opioids, for example, use of a partial agonist (e.g. buprenorphine) or an antagonist (e.g. naltrexone) that blocks opioid receptors can be beneficial in treatment.


The collective impact of drugs of abuse is that neurotransmitter release is occurring as a result of direct stimulation of brain pathways, rather than their stimulation by sensory input. The ease, reliability, intensity and rapidity of such effects go a large way towards explaining the potential for such drugs to lead to abuse. The underlying brain structures and processes responsible for drug-related reinforcement are at least partially under genetic control. For example, studies suggest that the heritability of liability to alcohol abuse is 50%.


Studies also suggest that there are a myriad psychosocial influences on drug use patterns. For example, risk factors for heavy adolescent substance abuse include social environmental factors (e.g. high unemployment and liberal, cultural norms of use), family factors (e.g. family disruption), peer factors (e.g. greater attachment to peers than to parents) and individual factors (e.g. low self-esteem and depression).


The influence of genes is not static and can be expressed differently in the presence of differing environmental conditions.



DRUG USE AND HEALTH


The health effects of tobacco and alcohol dwarf those of all illicit drugs combined. Up to 25% of hospital medical admissions are directly due to the effects of excessive alcohol consumption, and an estimated 15–20% of all general practice attendees consume harmful amounts of alcohol. Alcohol-related injuries account for 3–4% of the annual global burden of disease and injury, and tobacco smoking is the major cause of preventable death and disability worldwide.



DOCTORS AND SUBSTANCE ABUSE



• Medical practitioners are well placed to influence, assess, diagnose and treat people whose drug and alcohol consumption contributes to their health problems.

• Doctors are particularly prone to the excesses of alcohol and drugs, and this is the most common cause of disciplinary measures in the profession.

• Doctors are also a major source of street or illicit prescription drugs that can be misused.


MEDICAL AND PSYCHOSOCIAL PROBLEMS


Drug and alcohol use is not an all-or-nothing phenomenon. It exists as a spectrum extending from abstinence through intermittent non-hazardous and sometimes beneficial use to risky, hazardous use, or harmful use, to dependence. There are four core diagnoses.


• Hazardous or risky use is a repetitive pattern of use that confers a risk of harmful physical and psychological consequences. Hazardous substance abuse is also definable in terms of at-risk behaviours, such as bingeing to severe intoxication or sharing intravenous needles. Brief interventions that provide information and advice are effective in reducing many forms of hazardous use.

• Harmful use is use that is actually causing physical or psychological harm to the individual, e.g. over 40 grams of alcohol per day for women.

• Substance abuse is use that disrupts prevailing social norms, which vary with culture, gender and generation.

• Dependence is present when there are any three of the following features:
• impaired control over use of a psychoactive substance

• a strong desire or craving to take it

• a priority given to substance use over other activities

• a stereotyped or predicable pattern of use, tolerance and withdrawal

• continued use despite harm. Severe dependence is typically associated with drug withdrawal on cessation of use.


SPECIFIC SUBSTANCE ABUSE



ALCOHOL


Excessive alcohol consumption is a major risk factor for morbidity and mortality. The WHO estimates that, worldwide in 2002, alcohol caused 3.2% of deaths (1.8 million) and 4.0% of the burden of disease.1 In Australia, for example, it has been estimated that harm from alcohol was the cause of 5.3% of the burden of disease for males and 2.2% for females.2 In Australia in 1998–99, the total tangible cost attributed to alcohol consumption (which includes lost productivity, healthcare costs, road accident-related costs and crime-related costs) was estimated at $5.5 billion. Nevertheless, some benefits are thought to arise in the longer term from low to moderate alcohol consumption, largely through reduced risk of stroke and ischaemic heart disease. The net harm associated with alcohol consumption, after taking these benefits into account, was around 2.0% of the total burden of disease in Australia in 2003.3


In most developed countries, around 10% of the population drink at levels considered low risk for long-term harm. Around one-third of people drink above safe limits for short-term harm. Groups with higher than average consumption include young people, people in rural and remote areas and certain occupational groups such as miners and hospitality workers.


Alcoholic beverages are made by yeast fermentation of sugars from different plant sources to give a variety of drinks. The alcoholic strength (expressed by volume) varies from 2–5% for beers to 10–15% for table wines, to 35–55% for spirits. A standard drink contains approximately 10 g alcohol. Compared with most other drugs, alcohol has low potency, and large doses are required to produce its toxic effects.


The effects of alcohol on the central nervous system (CNS) vary according to the blood alcohol concentration, starting with mild euphoria, muscle relaxation and pleasure, possibly through release of noradrenaline, dopamine and endogenous opioids; then impairment of performance, especially of complex tasks; then ataxia and slurred speech, intellectual impairment and amnesia; and finally, profound depression and progressive loss of consciousness, respiratory failure and death.


Alcohol enhances the effects of the inhibitory neurotransmitter GABA at the GABA-A receptor to produce anxiolytic, muscle-relaxant and sedative effects. Alcohol also blocks the NMDA receptors (N-methyl d-aspartate receptors), probably causing the amnesic and cerebral depressant effects. Alcohol dilates blood vessels, irritates the gastrointestinal tract and damages the liver and other organs.


Regular intake of alcohol results in the development of tolerance, with larger amounts required to produce the same degree of intoxication. Tolerance develops in parallel with physical dependence.


A compulsive desire to use alcohol is attributed in part to its strong reinforcing properties—avoiding withdrawal symptoms and stimulation of the brain reward system with reduced anxiety and euphoria. Alcohol increases the firing of dopamine neurons in the ventral tegmental area and the release of dopamine in the nucleus accumbens. The alcohol-induced euphoria and stimulant effect in humans is antagonised, and craving for alcohol in chronic users is reduced by drugs that block the synthesis of catecholamines and deplete brain dopamine. Alcohol appears to increase endogenous opioid activity, and opioid receptor antagonists such as naltrexone decrease animal intake in both humans and animals and reduce the alcohol high and the number of relapses.



Clinical effects


Just as alcohol intake depresses the nervous system, its withdrawal produces over-excitation of the CNS. A mild acute withdrawal (hangover) can develop following a single intoxicating dose of alcohol or a short period of drinking, and manifests as headache, nausea, dehydration, tremulousness, lethargy and sleep disturbance.



Minor withdrawal syndrome


Minor withdrawal may cause symptoms within 24 hours of the last drink, including tremor, tachycardia, hypertension, sweating, nausea, diarrhoea, reduced appetite, anxiety, restlessness, headache, difficulty sleeping and bad dreams. The syndrome peaks on days 2–3 of abstinence and the major symptoms subside by day 4–5 or within a week. Fifteen per cent of withdrawing chronic alcohol users will experience withdrawal seizures 1–3 days after their last drink, and usually in the first 48 hours. These are usually grand mal in type, and between one and four seizures may occur.



Major withdrawal (delirium tremens)


Major withdrawal occurs 3–10 days after the last drink. Fewer than 5% of chronic alcohol patients (rarely under age 30 years) can suffer from agitation, disorientation, high fevers, sweating, paranoia and visual hallucinations. The patient gives a history of heavy alcohol use for at least 5 years and a recent episode of heavy drinking for two or more weeks.



Protracted withdrawal


Protracted withdrawal may be present, with symptoms of anxiety, irritability, hostility, depression, insomnia, fatigue and craving most severe in the first 5 days following the last drink. These may last for weeks or months following cessation of drinking and may be the major trigger for relapse.



Acute alcohol toxicity


The manifold manifestations of acute alcohol toxicity include acute alcohol hallucinosis or paranoia, pathological or idiosyncratic alcohol intoxication, blackouts, sleep disturbances, alcohol overdose, decreased myocardial contractility, peripheral vasodilatation with drop in blood pressure then systolic hypertension, atrial or ventricular arrythmias, oesophagitis, gastritis, subepithelial haemorrhages, increased small bowel motility and decreased water and electrolyte absorption, increased red cell volume, mild anaemia and leucopenia, hyperplasia of the bone marrow, mild thrombocytopenia and decreased platelet aggregation.



Chronic alcohol intoxication


Chronic alcohol use may affect almost every body system, and most of these effects are detrimental. Regular consumption of two drinks per day for men and one for women has been shown to be beneficial through decreased risk of atherosclerosis due to increased concentrations of circulating high-density lipoprotein cholesterol and inhibition of blood coagulation.


• Studies have linked high comorbidity of chronic alcohol dependence with mental disorders, especially anxiety disorders (25%), depression (20–40%) and alcohol-induced hallucinosis.

• Wernicke–Karsakoff syndrome is a neuropsychiatric condition found in the presence of ongoing carbohydrate load where thiamine is deficient.

Wernicke’s encephalopathy is an acute, reversible condition, seen in chronic alcohol-dependent individuals, characterised by ataxia, ophthalmoplegia and confusion. Not all of the classical triad of signs need be present for the diagnosis to be made. Indeed, it is underdiagnosed by up to a factor of 80% on this basis. Thiamine is required to act as an enzyme co-factor for pyruvate kinase, at the conclusion of glycolysis in the cytosol. It is mandatory for the production of high levels of ATP, produced via the Krebs cycle in mitochondria. Its absence causes significant under-utilisation of carbohydrates in the form of anaerobic over aerobic metabolism. Essentially the brain is starved of energy despite a high carbohydrate load. Despite the enormous variance of alcohol detoxification protocols and choice of detoxification agents used across the world, the single most important drug and the one common theme to all protocols is thiamine. In the absence of signs, parenteral (IV or IM) thiamine 100 mg q8h is thought to be sufficient prophylaxis.


Korsakoff syndrome (or Korsakoff’s psychosis) is the irreversible sequel to Wernicke’s, where thiamine is not administered quickly enough or in sufficient doses, and is characterised by inability to form new memories, loss of short-term memory and eventually long-term memory, confabulation and hallucinations. Treatment is with parenteral thiamine and is currently thought to require at least 500 mg per day, although resolution of symptoms is likely to be incomplete.


• Pancreatitis—inflammation of the pancreas (see Ch 30, Gastroenterology).

• Hepatic inflammation and cirrhosis (see Ch 30).

• Bones—chronic alcoholism is associated with other risk factors such as poor nutrition, leanness, liver disease, malabsorption, vitamin D deficiency, hypogonadism, haemosiderosis, parathyroid dysfunction and tobacco use, and these may contribute to the pathogenesis of bone disease related to alcoholism.4 Alcohol-related low bone density requires comprehensive lifestyle management in addition to alcohol reduction or abstinence in order to slow or prevent the development of osteoporosis.

• Poor immune function—alcohol has a deleterious effect on many immune system functions, and chronic alcoholism is associated with increased susceptibility to bacterial and viral infection. Assess immunisation status and arrange appropriate immunisation (e.g. influenza and pneumococcus, tuberculosis, hepatitis A and B).


Current guidelines5



• Low risk—less than 2 standard drinks per day on average for women and 4 per day for men, with 2 alcohol-free days per week in the long term. No more than 4 drinks for women and 6 for men on any one occasion, with consumption above long-term low-risk levels on more than 3 days per week. The guidelines suggest low-risk levels of < 25 g alcohol per day for women and up to 25–45 g per day for men.

• Hazardous—3–4 standard drinks for women and 5–6 for men per day in the long term. No more than 5–6 drinks per day for women and 7–10 for men on any one occasion.

• Harmful—5 or more standard drinks for women and 7 or more for men in the long term. More than 7 for women and 11 for men on any one occasion.

• No level is safe in pregnant women.

Without systematic screening, GPs are likely to miss up to 75% of risky drinking. A useful approach is to screen all patients annually and infrequent attenders opportunistically. The assessment should include:


• the level, frequency and pattern of alcohol consumption

• symptoms of alcohol dependence

• physical, psychological and social problems related to drinking.

Tools to assess alcohol intake:


• The WHO’s Alcohol Use Disorders Identification Test (AUDIT) is one of the most reliable to use.

• Another simple tool is the quantity–frequency index—on how many occasions in the past 30 days has the patient consumed more than 7 (women) or 10 (men) standard drinks?

• Physical examination and laboratory tests are not useful for identifying harmful drinking, and may be normal in alcohol dependence.


Management



1. Brief interventions—even as short as 5 minutes—have been shown to be effective. Compared to those receiving no intervention, those receiving any brief intervention show a 20–30% reduction in drinking and are at least twice as likely to modify their drinking. Brief interventions of 1–4 sessions can have an impact on drinking behaviour.

2. Follow-up is useful to reinforce changes and assess the need for further treatment.

3. Some patients find Alcoholics Anonymous (AA) helpful. A meta-analysis of AA and other 12-step programs found similar outcomes to other standard treatments including cognitive behaviour therapy (CBT).6

4. Motivational interviewing aims to motivate change in drinking behaviour by creating a discrepancy between the patient’s goals and their current actions. Evidence suggests that it is useful in risky and dependent drinkers.

5. Dependence and withdrawal management—patients who are physically dependent will require inpatient or outpatient withdrawal treatment, the latter being more common these days.
• Acamprosate (333 mg two tablets t.d.s. for patients < 60 kg and 4 tablets per day for patients > 60 kg) and naltrexone (50 mg daily) are generally well tolerated and can be continued if the patient is drinking. They are modestly effective in reducing relapse, delaying return to drinking and reducing drinking days.

• Disulphiram (Antabuse®) (200 mg daily) causes patients to become intensely unwell if they drink alcohol. It can be effective in patients when dosage is closely supervised. As reactions can be life threatening, it is not recommended as a first-line therapy.

• Psychosocial interventions have been shown to be effective in combination with anti-craving medications (acamprosate and naltrexone), and weekly follow-up may increase the effectiveness of pharmacotherapy.


Integrative approaches



Herbal medicines7


Herbal treatments such as St John’s wort (Hypericum perforatum), kudzu extracts (Pueraria lobata), panax ginseng, dried roots of S. militorrhiza (a Chinese medicine used for insomnia) and ibogaine (from a Central African root bark) may reduce alcohol consumption.8 While the mechanisms of action remain to be clarified, they probably act through several neurotransmitter systems. St John’s wort may provide some relief from comorbid depression.


Silybum marinarum (milk thistle)—silymarin, the flavonoid extracted from milk thistle, has been studied for treating all types of liver disease. Silymarin has the ability to block fibrosis, a process that contributes to the eventual development of cirrhosis in people with inflammatory liver conditions secondary to alcohol abuse.9



Nutrition


Nutritional deficiencies are common in people who chronically ingest excessive alcohol and may require dietary management and nutritional supplementation. Common deficiencies include vitamin B1, vitamin A, vitamin D, selenium, folate, riboflavin, zinc and vitamin B6.



Dietary advice



• Include foods high in B vitamins and iron, such as whole grains, dark leafy greens (such as spinach and kale) and sea vegetables.

• Include fruits (such as blueberries, cherries and tomatoes) and vegetables.

• Protein—alcohol causes both whole-body and tissue-specific changes in protein metabolism, resulting in loss of lean tissue mass. Clinical studies in alcoholic patients without overt liver disease show reduced rates of skeletal muscle protein synthesis. Ensure adequate protein with food sources (meat, chicken, fish, soy foods) and/or supplementation.

• Eliminate simple sugars and increase complex carbohydrates.

• Increase essential fatty acids, including omega-3 supplementation.

• Avoid caffeine.

• Recommend a multivitamin daily.


Acupuncture


Studies provide some evidence that acupuncture is more effective than placebo in:


• reducing alcohol intake over the subsequent 3 months and reducing the desire to drink

• reducing re-admissions for alcohol detoxification.

The studies have substantial methodological weaknesses, however, and there have been problems in finding appropriate control groups in blinded studies.7


It is claimed that complementary therapies may be effective in specific subgroups of alcohol abuse patients and that, in any case, acupuncture integrated with conventional treatment could represent a valid support treatment for some patients.


There are very few data on the effectiveness of homeopathy for alcohol dependence. Researchers generally agree on the need for more well-conducted studies.



TOBACCO


Smoking remains the most prevalent behavioural risk factor for disease and premature death. Daily smoking varies widely in different countries. For example, it is reported by nearly three-quarters of the male population in some Middle Eastern countries and by just over one-sixth of the population in Australia. A number of groups within the community, such as Indigenous Australians, those from specific ethnic groups, those with a mental health problem and those with other drug use problems have much higher rates. Nearly three-quarters of smokers report that they want to stop smoking, but the success rate of unaided attempts is low.


The process of drying, curing and ageing the tobacco leaf increases the concentration of the alkaloid nicotine and other constituents that contribute to the toxicity of tobacco. Substances added during manufacture to improve flavour, control burning and enhance nicotine delivery result in a complex cocktail of hundreds of biologically active substances in tobacco smoke.


Nicotine is selective for the nicotinic acetylcholine receptor. There are two major types of these receptors: at the skeletal neuromuscular junction, and at acetylcholine receptors in the brain and autonomic ganglia.


Nicotine increases arousal and attentiveness, and improves reaction time and psychomotor performance. It appears that nicotinic receptors have an important role in modulating higher brain functions; their effects on memory and learning are less clear. Nicotine can improve mood by relieving anxiety, and it reduces appetite. Autonomic effects include nausea and vomiting, tachycardia, vasoconstriction, increased blood pressure and cardiac output, and decreased gastrointestinal motility. It increases antidiuretic hormone secretion, reduces urine flow and suppresses the immune system via decreased T-cell activity. Smoking accelerates atherosclerosis and increases the risk of cardiovascular disease including angina, myocardial infarction and stroke.


The fastest route of absorption is by inhalation, which delivers a bolus of nicotine to the brain in about 10 seconds, leading to reinforcement. The rapid reinforcement probably contributes to the highly addictive nature of tobacco smoking. Absorption from nicotine gum is much slower, with a peak plasma level after 30 minutes of chewing compared with 5–10 minutes after smoking. Transdermal patches are even slower, with a peak level reached after 3–12 hours.


Smoking induces many liver enzymes responsible for the metabolism of nicotine itself and other drugs. There are therefore significant interactions, and nicotine seems to reduce the sedative effects of alcohol, possibly explaining their common consumption together.



Tolerance


Repeated exposure to nicotine results in neuronal adaptations that are reflected in tolerance, sensitisation and withdrawal. Tolerance of the cardiovascular and behavioural effects of nicotine develops during the course of one day, and smokers lose the tolerance overnight while sleeping and regain it the next day on resumption of smoking.



Dependence and withdrawal


Cessation of nicotine intake causes withdrawal: the symptoms can affect behaviour and provide strong motivation to continue smoking. Withdrawal symptoms start within a few hours of cessation and peak around 24–72 hours after the last cigarette. The DSM-IV criteria for nicotine withdrawal include four or more of eight symptoms and signs:


• dysphoria or depressed mood

• insomnia

• irritability, frustration, anger

• anxiety

• difficulty concentrating

• breathlessness

• decreased heart rate

• increased appetite or weight gain.

Craving, while not a diagnostic criterion, is an important element in withdrawal.


Smokers commonly maintain blood nicotine levels of 10–40 ng/mL. Withdrawal symptoms are believed to be mainly due to decreased nicotine concentration. Stress and anxiety affect nicotine tolerance and dependence because cortisol reduces the effect of nicotine. Elevated levels of cortisol mean that more nicotine needs to be consumed to achieve the same effect. Part of the reinforcement of smoking comes from relief of nicotine withdrawal (negative reinforcement). Nicotine also produces pleasurable effects that are important in positive reinforcement in that the smoker feels alert, yet relaxed. Nicotine activates the brain reward system with increased extracellular dopamine. Inhaled nicotine gets to the brain rapidly and each puff produces some discrete reinforcement.



Toxicity


The acute fatal dose of nicotine for an adult is about 60 mg of base. The average intake from a cigarette is 1–3 mg. The typical smoker obtains 20–40 mg nicotine per day. Acute tobacco poisoning results in symptoms of nausea, vomiting, dizziness and general weakness. Severe poisoning can result in convulsions, unconsciousness and possible death. Chronic tobacco exposure affects many organ systems. Nicotine, smoke tar and carbon monoxide play important roles in leading to atherosclerosis and cardiovascular disease, chronic obstructive airways disease, peptic ulceration, gastrointestinal tract cancers, impaired fertility, abortion, premature birth, low birth weight, SIDS, myopathy and osteoporosis.



Helping smokers to quit


There is good evidence that brief advice from healthcare providers to quit has a small effect: 2–3% of quitters one year later. This effect can be increased by adding other strategies including pharmacotherapy, active follow-up, and referral to quit-smoking services. The 5 A’s approach10 is recommended:


• Ask—being aware of who the smokers are in practice is important for effective management of chronic diseases. About one in three smokers attending their GP have not been correctly identified.

• Assess—assessment of interest in quitting is helpful in tailoring relevant advice to help motivate a quit attempt. Nicotine dependence can be rapidly assessed by asking about time to first cigarette after waking, the number of cigarettes smoked per day, and whether the patient had cravings or withdrawal symptoms in previous attempts to quit. Yes to any of these suggests nicotine dependence.

• Advise—brief assessment and advice to quit, often taking as little as three minutes, acts as a prompt to quit attempts and has a measurable effect on quit rates.

• Assist—all smokers interested in quitting should be given counselling and support by a GP or a trained practice nurse. A quit kit and referral to a Quitline should be provided.

• Arrange—a follow-up visit one week and one month after quit date to check for relapse has been shown to increase the likelihood of successful long-term abstinence.

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Jun 3, 2017 | Posted by in GENERAL SURGERY | Comments Off on Substance (drug and alcohol) misuse

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