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Ovid: Oxford Handbook of Psychiatry

Editors: Semple, David; Smyth, Roger; Burns, Jonathan; Darjee, Rajan; McIntosh, Andrew Title: Oxford Handbook of Psychiatry, 1st Edition Copyright ©2005 Oxford University Press > Table of Contents > Chapter 13 – Substance misuse Chapter 13 Substance misuse P.496
The psychiatry of substance misuse The sub-specialty of substance misuse is concerned with the assessment and treatment of patients with problems arising from the misuse of harmful or addictive substances. These include: 1) alcohol, 2) illegal or ‘street’ drugs, 3) prescription and over-the-counter medicines, and 4) volatile chemicals. The resultant problems include both mental and physical illnesses and family, housing, employment, and legal difficulties. In treatments, both psychological and pharmacological interventions are used; these may include detoxification and substitute prescribing. The majority of interventions in patients with substance use problems are undertaken by GPs. In areas where there are no substance misuse specialists the majority of more complex cases are seen by general psychiatrists, with management of the acute medical problems, including overdose and withdrawals, treated in the general hospital. All psychiatrists will have ample opportunity to see patients whose problems derive from substance use. Around the UK there is variable provision of services for drug and alcohol abusers. Drug and alcohol problems may be dealt with within a combined ‘addiction service’, or may be managed separately. Some services will restrict themselves to the primary substance misuse and its problems, while others will address all mental health needs. In the field of treatment services for those with substance use problems, specialists will work alongside voluntary and non-medical treatment agencies, many of which provide a good and very vital service. Strong links between psychiatry/ substance use services and the non-medical agencies should be fostered. Drug treatment services within the health care system make up only one part of the wider range of centrally and locally funded and volunteer services for problem drug users. Within the health service sector most of drug user contact and service provision is with GPs who will have a variable degree of experience of, and enthusiasm for, such work. The availability of specialist services will vary by area and setting (e.g. rural/urban) and may range from the special interest of an individual psychiatrist or GP, to a specialist service with support staff and dedicated facilities. Local pharmacists can also be a useful resource in supervising consumption of substitute drugs. Non-health care provision will also vary by setting but may include: advice shops offering leaflets and education about drugs and harm reduction strategies; self-help groups, some adhering to an AA style ‘twelve-step approach’, usually involving peer support from ex-users; residential facilities offering detoxification and abstinence programs. The practitioner working in the field of drug misuse should develop an awareness of these services and their referral criteria and encourage a collaborative approach to client management. The skills required for those working in the field of substance misuse are:

  • Knowledge of the psychiatric syndromes associated with misused substances Both knowledge of the patterns of physical and mental disorders associated with substance misuse and the presentations of mental disorder when there is comorbid substance use.
  • P.497

  • Experience of interviewing and counselling methods Skills at interviewing and motivating patients who may have very ambivalent feelings about changing behaviour.
  • Experience of the pharmacological and psychological treatment methods An area undergoing constant development where there is a need to keep abreast of changes in guidelines over time.
  • Awareness of the pattern of drug use within a community Patterns of drug use change over time, and the types and strengths of drugs available in a community will also change. Information from police and the voluntary sector can be helpful here.
  • Willingness to be involved with other agencies Valuable work in the field of substance misuse is done by agencies outside the health-care system. Practitioners should attempt to understand the work of these agencies and refer to them where appropriate.
  • Ability to take a long-term view Substance misuse disorders can be chronic, some would say lifelong, conditions and patients may relapse many times before showing improvement.
  • Ability to consider health in its wider context Substance misuse gives rise to health risks beyond the effect of the drug, (e.g. drink driving deaths, HIV infection). In addition, substance misuse is a community problem leading to lost productivity, crime, road accidents, violence, and family break-up.
  • Consider change beyond change in an individual patient Patterns of substance misuse in a society are susceptible to political manipulation (e.g. licensing hours, decriminalisation, legalisation, availability of treatment services). One role of substance misuse specialists is to understand these factors and to present the case for political change.

Sometimes there is a perception that drug or alcohol users are difficult or unrewarding patients to treat. It should be noted that GMC guidelines direct that it is ‘unethical for a doctor to withhold treatment from any patient on the basis of a moral judgement that the patient’s activities or lifestyle may have contributed to the conditions for which treatment was being sought’. N.B. For the purposes of this chapter, we refer to alcohol misuse and drug misuse separately and refer to them collectively as substance misuse. Alcohol is of course a drug and should be thought of as such, but we believe this terminology to be clearer and more understandable to patients. P.498
Substance use and misuse ‘Mankind cannot bear very much reality’ — T.S. Eliot ‘The urge to escape, the longing to transcend themselves, if only for a few minutes, is and always has been one of the principal appetites of the soul’ — Aldous Huxley People in all cultures, at all times through history, have sought out mood-or perception-altering substances. 25% of adults smoke; 90% drink alcohol; 33% have lifetime experience of one illegal drug (mostly cannabis). Society’s attitude to substance use and to those with substance use problems has varied from prohibition and condemnation to tolerance and treatment. Within British society at the moment caffeine use is legal and accepted; alcohol and tobacco use are accepted with legal limitations; and other substances have severe legal limitations—some available only on prescription, others not at all. Despite this, the harmful effects of alcohol dwarf those of other drugs. Many of the abused substances subsequently described have been used in their naturally occurring form throughout history (e.g. the chewing of coca leaves by Peruvian Indians). There has been a tendency for the development of more potent drug preparations which contain a higher concentration of the active ingredient (e.g. freebase cocaine), and the development of routes of administration which produce more rapid and intense effects (e.g. IV use). This has generally been associated with an increase in the attendant problems. Patients presenting with drug misuse problems represent only a small percentage of those who take drugs. Little is known about the non- presenting drug users. Their numbers may be revealed by community surveys but they are otherwise poorly studied. It is clear, however, that the normal route from use of to abstinence from a substance is the individual deciding to discontinue use and then doing so, without medical consultation or help. The reasons for substance use are varied, may be mixed, and may change over the course of a patient’s life. They include: a search for a ‘high’; a search for a repeat of initial pleasurable effects; cultural norm in some sub-cultures; self-medication for anxiety, social phobia, insomnia etc; self-medication for negative symptoms of psychotic illness; and to prevent development of withdrawal symptoms. The pattern of risks associated with substance use varies with the substance taken, the dose and route of administration, and the setting. They include: acute toxicity; behavioural toxicity (e.g. jumping from height due to believing one can fly); toxic effects of drug contaminants; secondary medical problems; secondary psychiatric problems; risk of development of dependency; and negative social, occupational, marital, and forensic consequences. P.499
P.500
Substance misuse disorders Acute intoxication The pattern of reversible physical and mental abnormalities caused by the direct effects of the substance. These are specific and characteristic for each substance, (e.g. disinhibition and ataxia for alcohol, euphoria and visual sensory distortions for LSD). Most substances have both pleasurable and unpleasant acute effects; for some, the balance of positive and negative effects is situation-, dose- and route-dependent. At-risk use A pattern of substance use where the person is at increased risk of harming their physical or mental health. This is not a discrete point but shades into both normal consumption and harmful use. At-risk use depends not only on absolute amounts taken but the situations and associated behaviours, (e.g. any alcohol use is risky if associated with driving). Harmful use The continuation of substance use despite evidence of damage to the user’s physical or mental health or to their social, occupational, and familial well-being. This damage may be denied or minimised by the individual concerned. Dependence The layman’s ‘addiction’. Encompasses a range of features initially described in connection with alcohol abuse (p. 502), now recognised as a syndrome associated with a range of substances. Dependence includes both physical dependence (the physical adaptations to chronic, regular use) and psychological dependence (the behavioural adaptations). In some drugs (e.g. hallucinogens), no physical dependence features are seen. Withdrawal Where there is physical dependence on a drug, abstinence will generally lead to features of withdrawal. These are characteristic for each drug. Some drugs are not associated with any withdrawals; some with mild symptoms only; and some with significant withdrawal syndromes. Clinically significant withdrawals are recognised in dependence on alcohol, opiates, nicotine, benzodiazepines, amphetamines, and cocaine. Symptoms of withdrawal are often the ‘opposite’ of the acute effects of the drug, (e.g. agitation and insomnia on benzodiazepine withdrawal). Complicated withdrawal Withdrawals can be simple, as above or complicated by the development of seizures, delirium, or psychotic features. Substance-induced psychotic disorder Illness characterised by hallucinations and/or delusions occurring as a direct result of substance-induced neurotoxicity. Psychotic features may occur during intoxication and withdrawal states, or develop on a background of harmful or dependent use. There may be diagnostic confusion between these patients and those with primary psychotic illness and comorbid substance misuse. Substance-induced illnesses will be associated in time with episodes of substance misuse and may have atypical clinical features, (e.g. late first presentation with psychosis, prominence of non-auditory hallucinations). Cognitive impairment syndromes Reversible cognitive deficits occur during intoxication. Persisting impairment (in some cases amounting to dementia) caused by chronic substance use is recognised for alcohol, P.501
volatile chemicals, benzodiazepines, and, debatably, cannabis. Cognitive impairment is associated with heavy chronic harmful use/dependence and shows gradual deterioration with continued use and either a halt in the rate of decline or gradual improvement on abstinence. Residual disorders Several conditions exist (e.g. alcoholic hallucinosis, p. 526; persisting drug-induced psychosis, p. 560; LSD flashbacks, (p. 92) where there are continuing symptoms despite continuing abstinence from the drug. Exacerbation of pre-existing disorder All other psychiatric illnesses, especially anxiety and panic disorders, mood disorders, and psychotic illnesses may be associated with comorbid substance use. Although this may result in exacerbation of the patient’s symptoms and a decline in treatment effectiveness, it can be understood as a desire to self-medicate (e.g. alcohol taken as a hypnotic in depressive illness) or escape unpleasant symptoms (e.g. opiates taken to ‘blot out’ derogatory auditory hallucinations). Sometimes there is debate about whether there is, for example, a primary mood disorder with secondary alcohol use or vice versa. Careful examination of the time course of the illness may reveal the answer. In any case, it is advisable to address substance misuse problems first as this may produce secondary mood improvements and continuing substance misuse will limit antidepressant treatment effectiveness. P.502
The dependence syndrome This is a clinical syndrome describing the features of substance dependence. It was described initially by Edwards & Gross1 as a provisional description of alcohol dependence but may be applied to the description of drug dependence. These features form the core of both ICD-10 and DSM-IV descriptions of substance dependence.

  • Primacy of drug-seeking behaviour Also called ‘salience’ of drug use. The drug and the need to obtain it become the most important things in the person’s life, taking priority over all other activities and interests. Thus drug use becomes more important than retaining job or relationships, remaining financially solvent, and in good physical health and may diminish moral sense leading to criminal activity and fraud. This diminishes the ‘holds’ on a person’s continued use. If he rates drug use above health, then stern warnings about impending illness are likely to mean little.
  • Narrowing of the drug-taking repertoire The user moves from a range of drugs to a single drug taken in preference to all others. The setting of drug use, the route of use, and the individuals with whom the drug is taken may also become stereotyped.
  • Increased tolerance to the effects of the drug The user finds that more of the drug must be taken to achieve the same effects. They may also attempt to combat increasing tolerance by choosing a more rapidly acting route of administration, (e.g. IV rather than smoked), or by choosing a more rapidly acting form, (e.g. freebase cocaine rather than cocaine hydrochloride). In advanced dependence there may be a sudden loss of previous tolerance; the mechanism for this is unknown. Clinically, tolerance is exhibited by individuals who are able to display no or few signs of intoxication while at a blood level in which intoxication would be evident in a non-dependent individual.
  • Loss of control of consumption A subjective sense of inability to restrict further consumption once the drug is taken.
  • Signs of withdrawal on attempted abstinence A withdrawal syndrome, characteristic for each drug, may develop. This may be only regularly experienced in the mornings because at all other times the blood level is kept above the required level.
  • Drug taking to avoid development of withdrawal symptoms The user learns to anticipate and avoid withdrawals, (e.g. having the drug available on waking).
  • Continued drug use despite negative consequences The user persists in drug use even when threatened with significant losses as a direct consequence of continued use, (e.g. marital break-up, prison term, loss of job).
  • Rapid reinstatement of previous pattern of drug use after abstinence Characteristically, when the user relapses to drug use after a period of abstinence, they are at risk of a return to the dependent pattern in a much shorter period than the time initially taken to reach dependent use.

References 1 Edwards G and Gross MM (1976) Alcohol dependence: provisional description of a clinical syndrome. BMJ 1, 1058–61. P.503
Stages of change and harm reduction Stages of change A model for understanding motivation and action towards change in harmful patterns of drug use proposed by Prochaska and DiClemente1. Motivation is regarded as a prerequisite for and a precursor to action towards abstinence or more controlled drug use.

  • Pre-contemplation The user does not recognise that problem use exists, although this may be increasingly obvious to those around them.
  • Contemplation The user may accept that there is a problem and begins to look at both the positive and negative aspects of continued drug use.
  • Decision The point at which the user decides on whether to continue drug use or attempt change.
  • Action The point of motivation, where the user attempts change. A variety of routes exist by which change may be attempted, which may or may not include medical services.
  • Maintenance A stage of maintaining gains made and attempting to improve those areas of life harmed by drug use.
  • Relapse A return to previous behaviour but with the possibility of gaining useful strategies to extend the maintenance period on the user’s next attempt.

Harm reduction Harm reduction is a method of managing drug users in which it is accepted that steps can be taken to reduce the mortality and morbidity for the user without necessarily insisting on abstinence from drugs. This approach gained currency during the 80s in an attempt to halt the projected AIDS epidemic. Perhaps the majority of patients will present before abstinence is a realistic or achievable goal for them. Optimum care for this group of patients will involve engaging them with the service, exploring and encouraging motivation to change, and suggesting harm reduction strategies. Examples of such strategies include:

  • Advice directed at use of safer drugs or safer routes of administration.
  • Advice regarding safer injecting practice (p. 539).
  • Advice regarding safe sex.
  • Prescription of maintenance opiates or benzodiazepines.
  • Assessment and treatment of comorbid physical or mental illness.
  • Engagement with other sources of help, (e.g. social work, housing).

Drug misuse is a community problem and some aspects of harm reduction include consideration of reduction of morbidity to the community more generally. Prescription of methadone may reduce criminality in a dependent individual, with consequent community benefit. Equally, there is a responsibility with the prescriber to consider the potential for community harm via leakage and accidental overdose when monitoring the prescription of any drug. References 1 Prochaska JO and DiClemente CC (1986) Towards a comprehensive model of change. In Miller WR and Heather N pp3–27 (eds) Treating addictive behaviours: processes of change, Plenun Press, New York. P.504
Alcohol misuse In the UK, roughly 93% of men and 87% of women drink alcohol. Minimal alcohol consumption can of course be pleasurable, socially enjoyable, and associated with health benefits (reduction in deaths from coronary artery disease). There is a tendency to view most people as normal drinkers and a subset as vulnerable to the development of alcohol problems. In fact on a population level, increasing the overall alcohol consumption (e.g. by reducing the real price of alcohol) tends to increase the total number of problem drinkers. Alcohol consumption in the community is roughly normally distributed with a long ‘tail’ to the right. The distinction between normal and heavy drinking is arbitrary. On both a population and individual level, increased consumption is associated with increased risk of harm of all kinds. However, the fact that normal drinkers heavily outnumber heavy drinkers means that, despite their lower rates of problems, greater numbers of alcohol-related problems occur in normal rather than heavy drinkers. This gives rise to the so-called ‘prevention paradox’—that to significantly reduce overall alcohol related morbidity we must look to reduce problems in normal rather than heavy drinkers. This applies more to problems such as drink driving and drink-related trauma rather than to medical complications of heavy use such as cirrhosis. The term ‘alcoholic’ is often used by patients themselves and is the preferred term of Alcoholics Anonymous. It has unfortunately acquired a pejorative meaning to the general public, and images of the ‘down and out’ or ‘skid row’ alcoholic, drinking strong drink from brown paper bags, have damaged this word’s use in clinical contexts. It is not used in DSM-IV or ICD-10 where the preference is to make the diagnosis of alcohol dependence or harmful use (abuse in DSM-IV). A history of alcohol use Alcohol has been used in all societies throughout recorded history, with documentary evidence of brewing and wine making as early as 3000 B.C. The intoxicating effects of alcohol were most probably discovered independently in many cultures around the time of the evolution of agriculture, possibly on noting fermentation in fruit. Ancient peoples produced alcoholic beverages from a wide variety of materials including fruits, berries, honey, corn, barley, wheat, sugar cane, and potatoes. The use of alcohol by individuals has been variously regarded, from complete tolerance through to outright prohibition. Alcohol has always had a place in the lifestyles and formal rituals of many peoples around the world. It was used as an intoxicant in religious rituals, as a celebration, as a gift, as a greeting, and to mark births and deaths. For almost as long as alcohol use is recorded there are recorded attempts at control on its use by the authorities. In AD 92 The Roman emperor, Domitian, attempted to restrict wine production and its distribution and sale. Similar restrictions were attempted at various times by other leaders, sometimes accompanied by moral disapproval of drinking or drunkenness in particular. In Medieval Britain, ale was a staple part of the diet and was consumed in huge quantities, while drunkenness, particularly among the clergy was frowned upon by the Christian churches. Consumption of wine P.505
is of course the centrepiece of Christian worship. After initially preaching moderation, Mohammed later forbade the use of alcohol to followers of his religion, possibly as a way of differentiating his converts from the Christians around them. The process of natural fermentation of alcohol by yeasts can produce beverages of up to 13% proof: above this concentration the yeast dies. Stronger concentrations of alcohol are produced by the process of distillation which was discovered in the Middle East in 1000 AD. Public consumption of distilled liquor became prevalent in the 18th Century and the accompanying social problems together with the conservative attitudes of the emerging Protestant clergy led to a developing moral disapproval of alcohol consumption. In the mid 18th Century, as part of a continuing military and trade dispute with France, the British government imposed heavy taxes on French wine imports and encouraged the distillation of cheap domestic spirits—in particular, gin. This change in the drinking practice in the general population from low- to high-strength alcohol produced significant alcohol-related problems in the general public, immortalised in the lithographs of the ‘gin palaces’ by George Cruikshank. In an effort to control the problem the government passed laws to restrict the time and place at which alcohol could be sold and began to levy increasing taxes on distilled spirits. This had the positive effect of reducing consumption but the negative effect of introducing a government interest in continuing consumption. The late 18th Century writings of Benjamin Rush describe habitual drunkenness as a ‘disease of the mind’. 18th-century America saw the development of an increasingly widespread temperance movement (those signing a pledge ‘TA’ for total abstinence becoming known as teetotalers). The temperance movement lobbied for a complete ban on alcohol consumption, and succeeded in 1921 following the passing of the 18th amendment to the US Constitution which provided for prohibition. The period of 11 years until the repeal of prohibition in the 21st amendment did indeed see a reduction in social problems and mortality; however, its unpopularity, widespread flouting of the law, and the flourishing of illegal activity in gangsterism led to its repeal. Today, in most western countries, alcohol use is widely tolerated and socially accepted. Interestingly though, moral disapproval of drinking during pregnancy and drinking while driving a motor vehicle has resulted in substantial decreases in these activities. Despite improvement in these limited areas, most western countries have seen an increase in absolute consumption and alcohol-related medical harm compounded by an increasing passion for drug misuse. P.506
Alcohol as a drug Preparations The active ingredient in alcoholic drinks is ethyl alcohol which makes up a variable percentage of the volume. The flavour of drinks comes from ‘congeners’—the additional organic substances derived from the brewing materials. Pattern of use Of all drugs, alcohol has the widest range of patterns of use, ranging from yearly light consumption to continuous consumption throughout the waking hours. Drug actions The effects of alcohol on the CNS were traditionally described as being due to non-specific effects on neuronal cell wall fluidity and permeability. It is now believed that in addition to these general effects there are neurotransmitter-specific effects, including: enhancement of GABA-A transmission (anxiolytic effects), release of dopamine in the mesolimbic system (euphoriant effects), and inhibition of NMDA-mediated glutaminergic transmission (amnesic effects). Ethyl alcohol is oxidised by alcohol dehydrogenase (ADH) to acetaldehyde, which in turn is oxidised by acetaldehyde dehydrogenase (ALDH) to carbon dioxide and water. 98% of alcohol metabolism takes place in the liver. Approximately one unit, (or 8 g), of alcohol can be metabolised per hour. Illicitly brewed alcohol may contain methanol, which is broken down to formaldehyde, which has marked toxic effects in the retina. Acute effects Alcohol is absorbed rapidly from mouth, stomach, and small intestine, and from a single consumption maximum blood levels are obtained in -60 minutes. Absorption is slowed by the presence of food in the stomach and is speeded-up by taking effervescent drinks. Alcohol is hydrophilic and is widely distributed throughout the body organs including the brain, placenta, lungs, and kidneys. Blood alcohol concentration (BAC) is consistent throughout the body with the exception of fat and can be estimated from breath samples. In normal drinkers BAC correlates with the subjective and the observable CNS effects of alcohol. Heavy drinkers may have high BAC with limited outward signs of intoxication due to the development of tolerance. Because of their different body fat distribution, women will have a higher BAC than men following the same oral intake. Initial symptoms of alcohol intoxication are subjective elevation of mood, increased socialisation, and disinhibition. Continuing consumption, intended to prolong these effects, can lead to lability of mood, impaired judgement, aggressiveness, slurred speech, unsteady gait, and ataxia. Societal factors The prevalence of alcohol-related harm increases with the mean population consumption. This mean consumption is increased by increased availability of alcohol, increased societal tolerance of drinking, decreased restrictions on the sale of alcohol, and a decreased ‘real price’ of alcohol. Price is the most influential factor in demand, the real price of a pint of beer or bottle of whiskey having dropped considerably since the war. Where societies forbid all alcohol consumption (e.g. prohibition America, Islamic counties), there is a decrease in alcohol related problems but an increase in the level of personality abnormality in those who continue to drink. P.507
Risk factors Heavy drinking is more common in men, in lower socio-economic groups, in those with lower educational levels, and in the young. Some professions are also associated with heavy drinking and drink-related harm. These include drinks industry workers (easy availability and effect of heavy drinkers seeking out jobs here); travelling salesmen (boredom, periods away from home, acceptance of drinking on the job); doctors (stress, freedom from direct supervision, reluctance to seek help with incipient problems). Genetics First-degree relatives of alcoholics have double the risk of alcohol problems themselves. Significantly higher rates in identical compared with fraternal twins (although not 100% concordance). Children of alcoholics have increased risk of development of alcohol problems themselves even when adopted into families without alcohol problems. A metabolically relatively inactive form of ALDH is common in oriental people, leading to accumulation of acetaldehyde and an unpleasant ‘flushing’ reaction in affected individuals who take alcohol. This may account for the significantly lower rate of alcohol problems found in affected individuals. No causative genes for alcoholism have been identified and it is expected that it will show polygenic inheritance. Problem drinkers contain a significant sub-group of individuals with dissocial personality traits which predisposes to alcoholism and is itself heritable. Medical complications Acute toxicity occurs at levels over 300 mg% (see p. 524), with clouding of consciousness and coma, risk of aspiration, hypoglycaemia, and acute renal failure. Associated with a wide range of chronic medical problems (pp. 532, 533). Psychiatric complications Harmful use and dependent use (p. 524) distinguished by the presence of withdrawals on abstinence; withdrawals may be complicated by seizures and development of acute confusional state—delirium tremens (p. 516); acute alcohol induced amnesia; alcoholic hallucinosis, (p. 526); alcohol-induced delusional disorder, (p. 526); Wernicke-Korsakoff syndrome (p. 530–1); pathological jealousy, (p. 526); alcohol-related cognitive impairment and alcoholic dementia, (p. 526); alcohol misuse also associated with development of or exacerbation of anxiety/depressive symptoms and with deliberate self-harm and suicidal behaviour. Interventions Advice regarding safer drinking patterns in those with ‘at risk’ or harmful use, (p. 512); strategies towards encouraging and maintaining abstinence in those with dependency and those with established medical or psychiatric damage; medically managed detox, (p. 518); Psychological and pharmacological support of abstinence or changed drinking pattern, (pp. 520, 521, 522, 523.) P.508
Screening for alcohol problems Diseases related to alcohol abuse are common, significant, and amenable to improvement by early intervention. They are therefore suitable for screening. There are low rates of detection in primary care and hospital settings which may be improved by increased vigilance, increased awareness of alcohol problems, awareness of routes of referral, asking routine alcohol-screening questions (e.g. CAGE—see opposite), and paying special attention to at-risk groups. Many patients give reasonably accurate drinking histories if asked, although some may underestimate consumption. Disorders suggesting occult alcohol problem Hepatitis; cryptogenic (i.e. medically unexplained) cirrhosis; seizures—particularly late onset; gastritis; anaemia; unexplained raised MCV or deranged LFTs; cardiomyopathy; accidents, particularly repeated and poorly explained; TB; head injury; hypertension persisting despite apparently adequate treatment; treatment resistance in other psychiatric conditions; impotence in men. Breath testing Blood alcohol concentration (BAC) is a measure of recent alcohol consumption. Measured in mg alcohol per 100 ml blood (mg%). Correlates well with breath alcohol measured by breathalyser (see opposite). Useful in assessing recent drinking, (e.g. in supervised detox regimes) and as objective measure of intoxication, (e.g. in A&E). Discrepancy between high BAC and lack of apparent intoxication suggests the development of tolerance. Blood tests Elevated red cell mean corpuscular volume (MCV), gamma glutamyl transferase (γGT), and carbohydrate deficient transferrin (CDT) act as markers for excess alcohol consumption. They are best used to monitor consumption in patients in follow-up. Not sensitive/specific enough for routine screening purposes.

  • MCV Sensitivity 20–50%, specificity 55–100%. Remains raised for 3–6 months due to 120-day lifespan of RBC. False positive in B12 and folate deficiency
  • γGT Sensitivity 20–90%, specificity 55–100%. Raised for 2–4 weeks Other LFTs are less specific for alcoholic-related. liver damage. False positive in liver diseases of other cause and may remain raised in chronic alcoholic liver disease despite abstinence.
  • CDT Sensitivity 70%, specificity 95%. Increased levels in response to heavy drinking. More expensive than γGT and not available in all areas.

P.509
Cage questionnaire A brief screening questionnaire for identification of at-risk drinking: C: Have you ever felt you should Cut back on your drinking? A: Has anyone ever Annoyed you by criticising your drinking? G: Have you ever felt Guilty about your drinking? E: Have you ever had a drink early in the morning as an Eye-opener? More than two positive responses suggests possible at-risk drinking and should prompt further assessment. NB The ‘Cage + 2’ adds two additional questions:

  • What is the most alcohol you have drunk in a single day?
  • What is the most alcohol you have drunk in a single week?

Breath and blood alcohol levels

Breath alcohol reading (mcg%) BAC (mg%)
0.35 80
0.52 120
0.70 160
0.87 200
1.05 240
1.40 320
1.75 400
A breathalyser allows an objective measurement of the breath alcohol and hence an approximation of the BAC. Breath alcohol reading should form part of the routine assessment of a patient presenting with alcohol problems and of patients in follow-up (e.g. supervised detox), rather than being prompted by suspicion of inaccuracy of oral report.

P.510
Assessment of the patient with alcohol problems Patients with a primary alcohol problem, or where it is thought that alcohol consumption is a contributory factor in their presentation, should have a more detailed assessment of their alcohol use, in addition to standard psychiatric history and MSE. Lifetime pattern of alcohol consumption Age at first alcoholic drink. Age when first drinking regularly. Age when first drinking most weekends. Age when first drinking most days. When did they first begin to drink more than their peers? When (if ever) did they first feel they had an alcohol problem? Pattern of drinking throughout life until present—describe periods of abstinence and more heavy drinking and the reasons for these. Current alcohol consumption Describe a current day’s drinking. When is the first drink taken? What types of drink are taken and in what setting? What is the total number and volume of drinks taken in a day? Some patients find it hard to describe a typical day or easy to over-rationalise recent heavy consumption. Ask them to describe the previous day’s drinking, then the day before that etc., until a pattern emerges. Describe a typical and a ‘heavy’ day’s drinking. Signs of dependence Do they experience withdrawals in the morning or when unable to get alcohol? Have they ever drunk more alcohol as way of relieving withdrawals? Are they having to drink more to get the same intoxicating effect? Do they no longer get ‘drunk’ at all? Do they find it difficult to stop drinking once started? Have they tried and failed to give up, and if so why? Do they have episodes of ‘lost’ memory? Physical/mental health Have they been told of any physical health problems due to drinking? Have they previously been told to stop drinking by a doctor? Any previous or current psychiatric diagnoses. Problems related to alcohol Have they missed days at work, or had warnings about poor performance, or lost a job as a result of alcohol? Are there relationship difficulties or a relationship breakdown due to drinking? Are there financial problems? Have they been in trouble with the police or have outstanding charges against them? Previous treatment attempts Describe the nature and type of previous treatments. Describe the subsequent return to drinking. Describe any periods of abstinence since the development of the drinking problem. How were they maintained and what ended them? Family history Drinking problems in parents and extended family. Quality of relationships in past and present. Childhood environment. Attitude to referral Why have they attended the appointment today? Do they feel they have an alcohol problem and if so will they accept help for it? What sort of help do they want and are there types of treatment they will not accept? P.511
Patient goals What (if anything) do they want to change about their drinking? What pattern of drinking do they aspire to? Physical examination Note general condition; evidence of withdrawals including tremor in hands or protruded tongue; degree of facial capilliarisation; stigmata of liver disease (palpable liver edge, jaundice, spider naevi, ascites, palmar erythema); evidence of peripheral neuropathy; ataxia of gait; breath alcohol reading. Blood testing FBC, LFTs, other blood tests as indicated on history/ examination. P.512
Giving drinking advice There are a variety of situations where the doctor will be called on to give ‘safe drinking’ advice: individuals whose histories reveal evolving risky drinking patterns; patients with comorbid psychiatric illness; and individuals with alcohol problems who are attempting controlled drinking rather than abstinence. There are a wide variety of types of alcoholic drink, each of a different ‘strength’, (i.e. percentage alcohol by volume). It is the amount of alcohol taken rather than the type of drink which contributes to physical/mental health effects—avoiding spirits or other drinks perceived as ‘strong’ will not protect from health risks if the absolute amount of alcohol is above safe limits. Sensible drinking Men should drink no more than 21 and women no more than 14 units of alcohol per week. There should be at least two non-drinking days per week. The amounts should be spread over several days, not drunk all at once. Amounts should not be ‘saved up’ from a light week and drunk on top of the following week’s allowance. The amounts quoted are not ‘safe’ amounts but represent levels of drinking not associated with significant risks to health. In some situations (e.g. driving, operating machinery) the ‘safe amount’ is zero. Some individuals (e.g. previously alcohol-dependent, chronic medical conditions, pregnant) should not drink at all. Techniques of controlled drinking Patients who are seeking advice about avoiding potential alcohol problems and those individuals who are seeking to change from ‘at risk’ or harmful drinking patterns to controlled drinking patterns may find a selection of the following strategies helpful:

  • Set a weekly and daily alcohol limit and keep to it.
  • Do not drink alone.
  • Do not drink with individuals who drink heavily themselves.
  • Pace drinking, matching the consumption of a light or slow drinker.
  • Don’t buy rounds.
  • Alternate soft and alcoholic drinks. Drink with a meal.
  • Rehearse what to say if offered a drink that you don’t want.
  • Plan alternative, enjoyable non-drinking activities to replace drinking periods, (e.g. cinema, sports).

P.513
Amounts of alcohol in common drinks The amount of alcohol in drinks is measured in units. One unit contains -8 grams of alcohol. In alcoholic drinks where the percentage of alcohol by volume is given, the number of units = volume in litres × % alcohol. Numbers of units in common drinks are given below. In calculating numbers of units in an alcohol history, remember that home measures of drinks are usually more generous than those in pubs.

Drink Alcohol % by volume Measure Alcohol units
Beer and stout 4.0 Pint 2.0
Continental lager 5.0 440 ml can 2.2
Strong lager 9.0 440 ml can 4.0
Normal cider 4.5 Pint 2.5
1 litre 4.5
Strong cider 8.4 1 litre 8.4
Wine 9–14 125 ml glass 1.5
750 ml bottle 6.8–10.5
Gin/vodka/rum 37.5 25 ml measure 1
700 ml bottle 26.3

P.514
Planning treatment in alcohol misuse Patients presenting with alcohol problems often display marked ambivalence about whether there is even a problem, let alone about the need for change. This reflects both the perceived positive as well as negative roles alcohol plays in their lives and the memory of previous failure or difficulties in attempting change. The aim in counselling such patients is to guide them in making their own decision towards change, or if change is not likely or possible now, to guide them towards harm reduction and considering the possibility of future change. Motivational interviewing This is a technique aimed at enabling a patient to move through the stages of change (p. 503) to the point where action can be contemplated. It is based on the principle that: ‘people believe what they hear themselves say’. The interviewer aims to aid the patient in explaining why they should change their behaviour and how this will be achieved.

  • Therapist does not take a directive or prescriptive role but expresses interest and concern for the patient’s problems and explores the consequences of their behaviour.
  • Uses open-ended questions, reflective listening and summarising with identification of discrepancy between individual statements.
  • Aids the assessment of the pros and cons of current behaviour, avoiding confrontation or direct challenge.
  • Emphasises patient’s own perceptions of degree of risk rather than telling them about risks which they may not believe.
  • Encourages personal responsibility and patient’s choice of treatment options.

Planning interventions The initial assessment interview forms the beginning of intervention. Its aims are to gather and impart information, promote the possibility of positive action, and to plan treatment. The ongoing therapeutic relationship aims to maintain purpose, monitor progress, aid self-monitoring and self-awareness. The process of planning treatment should proceed along the following lines:

  • Make diagnosis (alcohol dependence, harmful, or ‘at-risk’ use).
  • Assess stage of change, (p. 503).
  • Decide with patient the goal of intervention:
    • Continue current drinking pattern In some patients there will be no need for change at all. In others there will be a clear history of alcohol problems but the patient presents as ‘pre-contemplative’ regarding change. In these cases give harm-reduction advice and ‘leave the door open’ to further assessment and help rather than alienating the patient.
    • Change to safer drinking pattern Many individuals will be able to modify risky or harmful drinking patterns given appropriate advice and help (perhaps monitored by a ‘drinking diary’, which is later reviewed).
    • Attempt abstinence from alcohol In some individuals the only safe course is to aim to abstain from alcohol completely.
  • For abstinence in a dependent drinker, consider the need for and setting of detox (p. 518).
  • P.515

  • Plan support methods and follow-up (pp. 520, 521).
  • At follow-up contact, review progress, emphasise changes made, review mental health.
  • Anticipate and deal with relapse if it occurs.

Abstinence vs. controlled drinking The decision to try for controlled drinking rather than abstinence is one for individual patient choice. The doctor should offer suitable advice.

  • Factors suggesting possibility of success of controlled drinking: previous prolonged periods of controlled drinking, alcohol misuse primarily in context of other mental disorder which has responded to treatment, otherwise stable lifestyle, absence of drinking problem in family and friends.
  • Factors against controlled drinking: previously alcohol-dependent, previous failure at controlled drinking, comorbid mental illness, comorbid drug use, established organ damage, risk of job loss/ marriage loss.

Relapse Alcohol misuse is a chronic illness and many patients will ‘fall off the wagon’ several times before achieving long-standing change. The possibility of relapse should be anticipated with the patient and appropriate strategies should be in place to deal with it (e.g. early OP review). Causes of relapse: ambivalent motivation, insufficient support, novel events, overconfidence, new mental illness. Counselling families The family of a patient with alcohol problems may contact you directly to ask for advice regarding their relative.

  • Patient’s relatives sometimes request that their relative be detained in hospital ‘to stop them drinking’. The MHA in the UK specifically does not allow detention of patients solely for reason of drug or alcohol dependency.
  • Aim to encourage and reward moves by the drinker to achieve change in their drinking pattern, while avoiding rewarding and hence reinforcing drinking, but avoiding confrontation or ultimatums.
  • Sometimes continued family involvement, despite their best intentions, serves only to support the drinker in their chosen lifestyle. In this case the family may have to be aided to step back, (AA call this ‘disengaging with love’).

Prognostic factors There is -3.6-fold excess mortality cf. age-matched controls. Of 100 45-year-old patients at 20 years follow-up: 40% dead, 30% abstinent, 30% problem drinking. Positive factors Motivated to change; supportive family or relationship; in employment; treatable comorbid illness (e.g. anxiety disorder, social phobia); accepting of appropriate treatment goal; AA involvement. Negative factors Ambivalent to change; unstable accommodation or homeless; drinking embedded into lifestyle (e.g. limited pursuits outside alcohol, all friends are drinkers); repeated treatment failures; cognitive impairment. P.516
Alcohol withdrawal syndromes In a patient with alcohol dependence, stopping alcohol completely or substantially reducing the usual amount taken causes the development of characteristic withdrawal syndromes. These syndromes should be anticipated and prophylaxis considered in any patient:

  • With a history of dependence.
  • Who has previously experienced withdrawal syndromes.
  • Who has consumed more than 10 units of alcohol on a daily basis for the previous 10 days.
  • Currently experiencing withdrawals.

Uncomplicated alcohol withdrawal syndrome

  • Occurs 4–12 hours after the last alcoholic drink.
  • Features—coarse tremor, sweating, insomnia, tachycardia (pulse > 100), nausea and vomiting, psychomotor agitation, and generalised anxiety.
  • Occasionally, transitory visual, tactile, or auditory hallucinations or illusions.
  • There may be increasing craving for alcohol both in itself and as a relief from the withdrawal symptoms.
  • Symptoms increase in severity in rough proportion to the habitual alcohol consumption, peaking at 48 hours and lasting 2–5 days, with more severe symptoms being more prolonged.

Alcohol withdrawal syndrome with seizures

  • In 5–15% of cases withdrawals are complicated by grand mal seizures occurring 6–48 hours after the last drink.
  • If seizures occur only during withdrawal they do not signify the development of idiopathic epilepsy.
  • Predisposing factors: previous history of withdrawal seizures, idiopathic epilepsy, history of head injury, hypokalaemia.

Delirium tremens Acute confusional state (p. 534) secondary to alcohol withdrawal. A medical emergency requiring inpatient medical care.

  • Occurs in 5% of episodes of withdrawal. Onset 1–7 days after the last drink with a peak incidence at 48 hours.
  • Risk is increased by severe dependence, comorbid infection, and pre-existing liver damage.
  • In addition to the features of uncomplicated withdrawal there is:
    • Clouding of consciousness
    • Disorientation
    • Amnesia for recent events
    • Marked psychomotor agitation
    • Visual, auditory, and tactile hallucinations (characteristically of diminutive people or animals—‘Lilliputian’ hallucinations).
    • Marked fluctuations in severity hour by hour, usually worse at night.
    • In severe cases: heavy sweating, fear, paranoid delusions, agitation, suggestibility, raised temperature, sudden cardiovascular collapse.
  • P.517

  • Reported mortality of 5–10%. It is most risky when it develops unexpectedly and its initial manifestations are misinterpreted (e.g. in a patient not known to be alcohol-dependent developing symptoms post-operatively).
  • Differential diagnosis—hepatic encephalopathy, head injury, pneumonia, acute psychotic illness, acute confusional state with other primary cause.

P.518
Management of alcohol withdrawal Detoxification (detox) is the medical management of withdrawal symptoms in a patient with substance dependence. Alcohol detox involves: psychological support; medication to relieve withdrawal symptoms (usually via a reducing benzodiazepine regime); observation for development of features of complicated withdrawal; nutritional supplementation; and integration with follow-up. Detox may be carried out as inpatient or, with support, in the community. The need to medically manage the complications of alcohol withdrawal can also arise in an unplanned fashion, (e.g. in an alcohol-dependant patient in police custody or following emergency surgery). Most of the problems of alcohol use are related to inability to maintain abstinence rather than to the initial problems of withdrawal. Detox procedure

  • Decide on setting.
  • Assess need for benzodiazepine-reducing regime.
  • Consider need for other medications.
  • Provide verbal and written advice.
  • Inform GP of the plans.
  • Give the patient a contact in case of emergency.
  • Decide on explicit follow-up after detox.

Setting Outpatient detox

  • Treatment of choice for most uncomplicated alcohol-dependent patients, with comparable completion rates to inpatient detoxification and comparable percentage remaining abstinent at 6 months.
  • Where there are doubts about compliance or concerns about drinking ‘on top of’ the prescribed drug, the patient should be seen daily in the morning and breathalysed before dispensing that day’s and the following morning’s supply of the drug.

Indications for inpatient detox

  • Past history of complicated withdrawals (seizures or delirium).
  • Current symptoms of confusion or delirium.
  • Comorbid mental/physical illness, polydrug misuse, or risk of suicide.
  • Symptoms of Wernicke-Korsakoff syndrome (pp. 530, 531).
  • Severe nausea/vomiting; severe malnutrition.
  • Lack of stable home environment.

Reducing regime Benzodiazepines are prescribed in alcohol withdrawal to ameliorate unpleasant withdrawal symptoms (e.g. tremor, anxiety) and to reduce the risk of withdrawal seizures. They are prescribed in a rapidly reducing regime in order to avoid the development of secondary, iatrogenic dependence, while covering the period of maximum risk.

  • Many units prefer chlordiazepoxide to diazepam for outpatient use as it has a lower abuse potential.
  • Diazepam is often preferred for inpatient use as it is faster acting, allowing dose titration against effect, and can be given parenterally.

P.519
Indications for prescribing a reducing regime

  • Clinical symptoms of withdrawal.
  • History of alcohol dependence syndrome.
  • Consumption is greater than 10 units/day over the previous 10 days.

Not required if

  • <10 units daily.
  • No history of withdrawals/drinking to avoid anticipated withdrawals.
  • BAC = 0 and no withdrawal features.

Symptom monitoring Review patients regularly to assess withdrawals. Continuing symptoms should be managed by increasing the next day’s planned dosages, rather than increasing the length of the course or relying on ‘prn’ dosage. Benzodiazepine withdrawal regime

  On waking Midday Early evening At bedtime
Day 1 — 30 mg 30 mg 30 mg
Day 2 20 mg 20 mg 20 mg 20 mg
Day 3 20 mg 10 mg 10 mg 10 mg
Day 4 10 mg 10 mg — 20 mg
Day 5 10 mg — — 10 mg

Other medications

  • Anticonvulsants Benzodiazepines in sufficient dosage are the most effective anticonvulsants in alcohol withdrawal. Other oral drugs (e.g. phenytoin, carbamazepine) do not reach therapeutic level until after the time of maximal risk.
  • Antipsychotics Where hallucinations or delusions develop they can usually be managed by temporarily increasing the benzodiazepine dose. The addition of an antipsychotic (e.g. haloperidol 5–10mg orally up to tds) should be considered if this fails. Antipsychotics do reduce the seizure threshold, but given sufficient benzodiazepine cover this should not be a concern.
  • Supplementary vitamins Where there are symptoms suggestive of Wernicke-Korsakoff syndrome or evidence of malnourishment give parenteral B vitamins (p. 530). In other patients give a 4-week course of 100mg thiamine, tds.
  • Other psychotropics While many patients withdrawing from alcohol complain of anxiety and/or depressive symptoms, many will be directly secondary to alcohol use/withdrawal. They should not be treated with psychotropics until they have been assessed when abstinent from alcohol. Generally speaking, do not start new psychotropics at this time.

P.520
Maintenance interventions in alcohol misuse (1)—psychological methods In planning treatment in alcohol problems, attention should be focused not only on achieving, but on maintaining change. Many patients find the initial change (e.g. moving to abstinence or controlled drinking) surprisingly easy, but find it difficult to maintain change in the longer term. Alcohol misuse is a chronic illness characterised by relapse and in dependent drinkers there is the tendency for dependent drinking patterns to recur rapidly on abstinence. For this reason, maintenance interventions should support change, and in every patient, relapse should be anticipated and strategies to deal with it should be in place. Individual counselling In addition to monitoring agreed change, individual counselling can address the following:

  • Social skills training (e.g. ‘saying no’).
  • Problem-solving skills.
  • Relaxation training.
  • Anger management.
  • Cognitive restructuring.
  • Relapse prevention.

In selected patients there may be a role for more formal psychotherapies. Group support Variety of group methods both within the health service and in the voluntary sector. Variable local provision. Most widespread and best known is AA (see opposite). Pharmacological support (pp. 522, 523). Residential abstinence In selected patients, time in a residential facility may offer a period of abstinence which is unachievable ‘outside’, allowing interventions in physical and mental health and a chance to plan social change to permit continued abstinence on discharge. A variety of facilities exist, usually outside health care provision; some offer detoxification, while others will only accept patients following detox. Used in patients where home environment is unsupportive of abstinence and there has been failure of previous treatment options. Advice to all patients regarding relapse Returning to drinking is the most common outcome in patients. The stages of change model (p. 503) considers relapse to be at the beginning of a further process of change, but with increased knowledge as to future strategies to combat relapse. A relapse can be motivated by overconfidence or forgetting gains. A ‘slip’ does not mean a full-blown relapse is inevitable and all patients should have strategies to deal with relapse discussed and agreed ‘ahead of time’. P.521
Alcoholics anonymous (AA) Alcoholics Anonymous (AA) is the best known and the most widespread of the voluntary self-help organisations for problem drinkers. It was founded in 1935 in the USA by Bill Wilson and Dr Bob Smith, themselves both problem drinkers. Currently there are -3000 groups in the UK and -88 000 groups worldwide. Associated organisations are Al-anon (for relatives of problem drinkers); Al-Ateen (for teenage children of problem drinkers); and Narcotics Anonymous (NA) (for addicts of illicit drugs). AA views alcoholism as a lifelong, incurable disease whose symptoms can be arrested by lifelong abstinence. Many other groups will use a variant of the AA model—‘12-step’ programme. AA is a useful and effective intervention in many problem drinkers and all patients should be informed about AA and encouraged to consider attendance. An AA meeting will generally follow a standard routine: there will be 10–20 people in each group, only first names are used; a rotating chairman will introduce himself with ‘my name is X, and I am an alcoholic’, then will read the AA preamble; a number of speakers are called from the floor who give an account of their stories and recovery if possible, leading to general discussion; the meeting ends with a prayer and is followed by informal discussions and contact between new members and sponsors who may offer emotional and practical support and perhaps a phone number. Open meetings are held where friends, family and interested professionals can attend. Closed meetings are for AA members only. (See ‘Useful addresses’ for AA contacts in the UK and Ireland—p. 916.) The ‘12 steps’

  • We admitted we were powerless over alcohol—that our lives had become unmanageable.
  • Came to believe that a power higher than ourselves could restore us to sanity.
  • Made a decision to turn our will and our lives over to the care of God as we understood him.
  • Made a searching and fearless moral inventory of ourselves.
  • Admitted to God, to ourselves, and to another human being the exact nature of our wrongs.
  • Were entirely ready to have God remove these defects of character.
  • Humbly asked Him to remove our shortcomings.
  • Made a list of the persons we had harmed, and became willing to make amends to them all.
  • Made direct amends to such people wherever possible, except when to do so would injure them or others.
  • Continued to take personal inventory, and when we were wrong promptly to admit it.
  • Sought through prayer and meditation to improve our conscious contact with God as we understood Him, praying only for knowledge of His will for us and the power to carry that out.
  • Having had a spiritual awakening as a result of these steps, we tried to carry this message to alcoholics and to practice these principles in our affairs.

P.522
Maintenance interventions in alcohol misuse (2)—pharmacological methods Aversive drugs Disulfiram Action Irreversible inhibition of acetaldehyde dehydrogenase (ALDH) which converts alcohol to carbon dioxide and water. If alcohol is taken, there is a build-up of acetaldehyde in the bloodstream causing unpleasant symptoms of flushing, headache, nausea and vomiting, and tachycardia. Indication Can act as a helpful adjunct to therapy and allow the patient’s relatives/employers regain confidence in their ability to remain abstinent. Dose Prescribe once abstinence achieved. Starting dose: give 5 day’s loading dose of 800 mg daily. Maintenance dose: 200 mg daily or 400 mg on alternate days (or 3 days/wk). Side-effects Halitosis and headache. Rare reports of psychotic reactions and hepatotoxicity. Notes:

  • Patients should be counselled as to the nature and purpose of the drug and the likely side-effects if they drink.
  • It is no longer recommended to give an alcohol ‘challenge’ to a patient newly started on disulfiram.
  • Compliance is increased if the taking of the drug is monitored by another person (e.g. spouse).

Anti-craving drugs Acamprosate Action Believed to act through enhancing GABA transmission in the brain. Has been found to reduce alcohol consumption in animal models of alcohol addiction and patients taking it report diminished alcohol craving. In RCT, cohort treated with acamprosate showed an increased percentage remaining abstinent and a doubling of time to first relapse. Indications Patients who wish to remain abstinent from alcohol. Dose Once abstinence achieved: 666 mg tds. Side effects GI upset, pruritis, rash, altered libido. Notes:

  • Discontinue if patient returns to regular drinking or relapses more than once while on the drug.
  • Has no role in assisting with controlled drinking.
  • Has no aversive action if alcohol is taken.
  • Has no addictive potential itself.

Naltrexone Action Antagonises the effects of endogenous endorphins released by alcohol consumption. It is believed that this diminishes both the desirable ‘high’ experienced on taking alcohol and the loss of control reported by most dependent drinkers. Indications In motivated sub-groups of alcohol-dependent patients it appears to be effective in reducing total alcohol consumed and number of drinking days. P.523
Dose Once abstinence achieved, give 50 mg od. Side effects GI upset, feeling anxious/‘on edge’, headache, fatigue, sleep disturbance, ‘flu-like’ symptoms. Notes:

  • Does not have an aversive or dependence-producing effect.
  • Not currently licensed in the UK for treatment of alcohol dependence.

P.524
Alcohol misuse disorders (1) Acute intoxication The symptoms of alcohol intoxication will vary depending on the blood alcohol concentration (BAC), individual alcohol tolerance, and to some extent the setting in which the alcohol is taken. In general, as BAC rises from mild intoxication (BAC < 100 mg%) to moderate intoxication (BAC 100–200 mg%) to severe intoxication(BAC > 200 mg%) a characteristic syndrome of acute intoxication is observed. Initial symptoms are elevated mood, disinhibition and impaired judgement, followed by slurred speech, unsteady gait, nystagmus, ataxia, aggressiveness, lability of mood and impaired concentration, and eventually sopor and coma. ‘At-risk drinking’ There are reported benefits to health (lowered risk of coronary artery disease and strokes) associated with low levels of alcohol consumption as compared with those who are abstinent (the ‘j-shaped curve’). Above this low level, health risks increase with increasing alcohol consumption. It is therefore arbitrary at which point drinking is considered ‘at risk’. Patient and situational factors are important (e.g. any alcohol consumption while driving or in pregnancy carries increased risks; for patients with established alcohol-related organ damage any consumption is risky). Harmful drinking (DSM-IV—alcohol abuse) Non-dependent drinking which continues despite established harm to the patient’s physical or mental health secondary to the alcohol consumption. ICD-10 diagnosis considers only physical and mental health harm, not harm related to social sanction. Alcohol dependence Harmful use of alcohol + established dependence syndrome (p. 502). Usually daily, stereotyped drinking pattern with increased tolerance, withdrawal features on abstinence, and ‘relief drinking’, (i.e. further drinking to alleviate the effects of withdrawals). Pathological intoxication (‘mania à potu’) This is a medically and legally disputed syndrome which was not included in DSM-IV due to lack of empirical evidence. It is described as an idiosyncratic reaction to a small amount of alcohol characterised by severe agitation, belligerence, and violent behaviour followed by collapse, profoundly deep sleep, and amnesia for the events which followed the alcohol consumption. It is a very dubious diagnosis which is mainly sought after by defence lawyers, as most legal systems do not regard normal self-induced intoxication as a valid defence. There is of course a strong association between alcohol and violent crime. Careful re-examination of the history will usually demonstrate significant quantities of alcohol have been consumed. Alcohol-induced amnesia (‘blackouts’) This term refers to transient amnesic episodes related to periods of intoxication. Characteristically the patient will report a ‘gap’ in their memory lasting several hours with global or partial amnesia for their actions during that time. The patient’s behaviour as reported by witnesses is usually characteristic of their normal behaviour when intoxicated. This amnesia seems to be a failure of recall rather than initial registration and represents a reversible form of brain P.525
damage. Its occurrence is not predictive of longer-term cognitive impairment. It occurs in the later stages of a drinking career, if at all, and tends to recur once established. Two forms are described:

  • ‘En bloc’—dense amnesia with well demarcated start and finish points.
  • Partial—episodes with indistinct start and end point with islands of preserved memory and variable degrees of recall.

There is some degree of state-dependent recall in blackouts and a return to intoxication may aid recall. Because of the potential confusion of the term blackout with periods of LOC, the term ‘alcoholic palimpsest’ is to be preferred. P.526
Alcohol misuse disorders (2) Alcoholic hallucinosis This is a substance-induced psychotic illness which is a rare complication of prolonged heavy alcohol abuse. The sufferer experiences hallucinations—usually auditory—in clear consciousness and while sober. The auditory hallucinations may begin as elemental hallucinations (e.g. bangs or murmurings) before, with continued alcohol use, being experienced as formed voices, most usually derogatory in nature. There may be secondary delusional elaboration.

  • Differential diagnosis Transitory hallucinatory or illusionary experiences while intoxicated, delirium tremens, psychotic illnesses.
  • Course In -95% of patients there is rapid resolution of these symptoms on ceasing alcohol consumption but the symptoms rapidly recur on restarting drinking. In -5% there are prolonged symptoms (<6 months after abstinence) and an emergence of more typical schizophrenic symptomatology.
  • Management Persisting symptoms may be treated with anti-psychotic medication.

Alcohol-induced psychotic disorder with delusions Long recognised but only recently included in DSM-IV. Development of persecutory or grandiose delusions after long history of heavy drinking. No other features of delirium tremens. Resolves on abstinence. Delirium tremens p. 516). Alcohol-related cognitive impairment The majority (50–60%) of heavy drinkers display some degree of cognitive impairment on cognitive testing while sober. There is impairment in short-term memory, long-term memory recall, new skill acquisition, ability to ‘task-shift’ and a decline in visuospatial ability greater than decline in language ability. CT/MRI examination of the brains of heavy drinkers reveals cortical atrophy (mainly white matter loss), and ventricular enlargement. Degree of structural abnormality is poorly correlated with degree of functional impairment. Alcoholic dementia A potentially reversible, generalised dementia in which there is progression with continued drinking and arrest of decline and possible functional improvement on abstinence. There is cortical atrophy and ventricular enlargement (predominantly white matter loss). The changes correlate with total lifetime drinking and length of drinking history and occur earlier in women than men. Mechanism is believed to be a direct toxic effect of alcohol on neuronal tissue, with head injury, episodes of hypoglycaemia, and nutritional deficits contributing factors in some cases. Wernicke-Korsakoff syndrome (pp. 530, 531) Pathological jealousy (Othello syndrome) This is a monosymtomatic delusional disorder (see p. 231) seen most commonly secondary to current or previous alcohol abuse. The form is a primary delusion in which the content is that the patient’s spouse or partner has been or is being unfaithful. Delusional evidence may be provided to back up this P.527
belief and the patient may go to great lengths to obtain ‘evidence’ (e.g. following her, planting tape recorders, examining discarded clothing). There is a significant association with violence and even homicide towards the supposedly unfaithful partner. Management

  • Abstinence from alcohol with addition of anti-psychotic medication.
  • It may be necessary for the couple to separate and advice to this effect may have to be given to the at-risk partner.

P.528
Psychiatric comorbidity Anxiety and depressive disorders Symptoms such as generalised anxiety, panic attacks, and low mood are very frequently reported in alcohol abusers. Many patients with alcohol problems also merit diagnoses of depressive illness (-50%) or anxiety disorder (-75%). The phenomenology of these disorders is similar to that found when the disorders occur in isolation. The difficulty is deciding the sequence of events, as in some cases the alcohol problem is secondary to the patient ‘self-medicating’ with alcohol in order to relieve primary anxiety or depressive symptoms. Nonetheless, chronic alcohol use will act as a direct depressant, its secondary effects will produce depressogenic life events (e.g. loss of job) and alcohol-related effects such as 4 a.m. waking due to withdrawals or weight loss related to nausea may masquerade as, or mask, biological depressive features. Patients may emphasise the primacy of the mood or anxiety features and seek their resolution before tackling the alcohol problem. Generally a primary mood or anxiety disorder diagnosis should not be made in the presence of continuing alcohol misuse and psychological or pharmacological treatment for mood disorder is unlikely to be effective. The correct course is to initiate detox if indicated and to reassess mood/anxiety symptoms after 4 weeks of abstinence, treating residual symptoms at this point. Only a minority will require formal treatment. An undiagnosed depressive illness preceding the alcohol problem is more common in women. Alcohol problems can also arise as a result of self-medication of agoraphobia and social phobia. Suicide Classically quoted as lifetime risk of 10–15% in dependent drinkers. Now estimated at -4% lifetime risk of suicide in those with alcohol problems. Psychiatric comorbidity is important, as is social isolation, physical ill health, and repeated failed attempts at abstinence. Schizophrenia High rates of alcohol and substance use found in schizophrenic patients (-20%). Increased risk of violence and TD development. Alcohol is an easily available temporary treatment for some of the distressing symptoms of psychotic illness Drug misuse Comorbid alcohol and drug misuse can be to enhance effects (e.g. euphoriant effect of alcohol and cocaine combined) or to minimise unpleasant side-effects (e.g. alcohol to relax after taking stimulants), or as a substitute when the primary drug is unavailable. Comorbid drug misuse is associated with poorer outcome. Some comorbidity can have an iatrogenic component where there is mixed abuse or substitution of benzodiazepines for alcohol. This can result from inappropriate prescribing of anxiolytics, misdiagnosis of alcohol problems as anxiety disorders, and repeated unsupervised withdrawals with hoarding of tablets. Aim to limit new prescriptions, review diagnosis in patients with treatment-resistance anxiety disorders, and avoid short-acting benzodiazepines (e.g. lorazepam). P.529
P.530
Wernicke-Korsakoff syndrome Wernicke encephalopathy and Korsakoff psychosis represent the acute and chronic phases of a single disease process—Wernicke-Korsakoff syndrome—which is caused by neuronal degeneration secondary to thiamine deficiency, most commonly seen in heavy drinkers. Wernicke encephalopathy Clinical features Acute onset of tetrad of: 1) acute confusional state; 2) ophthalmoplegia; 3) nystagmus; 4) ataxic gait. Associated features of: peripheral neuropathy, resting tachycardia, and evidence of nutritional deficiency. Ophthalmoplegia is most commonly 6th nerve palsy (paralysis of lateral gaze). The classical tetrad may not all be present in an undoubted case. Aetiology Occurs secondary to thiamine (vitamin B1) deficiency. Heavy drinkers are especially vulnerable due to poor intake (alcohol is calorie rich but vitamin poor), reduced absorption, and impaired hepatic storage. Other rare causes of thiamine deficiency are starvation, post-gastric resection, anorexia nervosa, and hyperemesis gravidarum. Pathology Haemorrhages and secondary gliosis in periventricular and periaqueductal grey matter involving the mammiliary bodies, hypothalamus, mediodorsal thalamic nucleus, colliculi and tegmentum of midbrain. Treatment

  • Give high potency parenteral B1 replacement—intramuscular Pabrinex®, 2 ampoules twice daily for 3–7 days. (N.B. Associated with allergic reactions: facilities for treatment of anaphylaxis must be available.) Avoid carbohydrate load until thiamine replacement is complete (e.g. do not rehydrate with glucose solutions).
  • Treat immediately diagnosis is made or strongly suspected. In addition, consider treating all those at high risk (alcohol-dependent patients with poor nutrition) prophylactically with parenteral vitamins.
  • All patients with symptoms of Wernicke encephalopathy and those at high risk should have parenteral vitamins as above. All other patients undergoing detox, or being assessed for alcohol problems should receive oral replacement—thiamine 100 mg tds for one month.
  • Assess and treat for alcohol withdrawal syndrome pp. (518, 519).

Prognosis

  • Untreated the acute phase lasts -2 weeks with 84% of cases developing features of Korsakoff psychosis. Mortality of -15% in untreated cases.
  • With treatment, the ophthalmoplegia and confusion resolve within days, but the ataxia, neuropathy, and nystagmus may be prolonged or permanent.

Korsakoff psychosis Clinical features Absence or significant impairment in the ability to lay down new memories, together with a variable length of retrograde amnesia. Working memory (e.g. ability to remember a sequence of numbers) is unimpaired as is procedural and ‘emotional’ memory. Thus the affected individual may be able to go with a psychologist to an interview room, perform adequately on working memory testing, show evidence of P.531
a new skill (e.g. mirror writing) they practised the day before, and yet later have no memory of ever having been in that room or having seen that psychologist before (although, on returning to the room, they may be more relaxed on subsequent occasions, due to state-related emotional memories). Confabulation for the episodes of amnesia may be prominent. Aetiology Most commonly due to thiamine deficiency secondary to heavy alcohol use. Rarer causes are head injury, post-anaesthesia, basal/temporal lobe encephalitis, carbon monoxide poisoning, and thiamine deficiency secondary to other causes. Pathology Pathological features are those of Wernicke encephalopathy. The presumed mechanism is disconnection of a mammillothalamic pathway crucial for memory formation. Treatment

  • Continue oral thiamine replacement for up to 2 years.

Prognosis

  • 25% of cases show some degree of memory improvement over time with the remainder largely unchanged.
  • The degree of impairment is directly related to the degree of memory impairment which may be incompatible with independent living.

P.532
Medical complications of alcohol misuse Hepatic

  • Alcoholic liver disease (ALD) is the most common cause of liver damage in the developed world. Presents as fatty change, alcoholic hepatis, and, finally, as cirrhosis.
    • Fatty change seen in >90% of heavy drinkers, can emerge after single heavy bout, may be asymptomatic, or may present as lethargy, malaise, painful, swollen liver, and obstructive jaundice. Reverses with abstinence.
    • Alcoholic hepatitis—40% of heavy drinkers.
    • Cirrhosis—up to 30% of heavy drinkers after 10–30 years. Predisposed to by genetic variation (reduced alcohol oxidation and increased acetaldehyde accumulation), female sex (less first pass metabolism and lower body water content for alcohol dispersal), comorbid hepatitis B or C infection.

Gastro-intestinal

  • Gastritis/gastric erosions with consequent haematemesis.
  • Metaplasia of lower third of the oesophagus (Barrett’s oesophagus).
  • Mallory-Weiss oesophageal tears secondary to vomiting.
  • Peptic ulceration.
  • Chronic diarrhoea.
  • Chronic pancreatitis (alcohol is most common cause) with chronic fluctuating abdominal pain and steatorrhoea.

Cancers

  • Hepatocellular, oesophagus, stomach, mouth, tongue, and pharynx.

Cardiovascular

  • Hypertension.
  • Dilated cardiomyopathy.
  • Cardiac arrhythmias (esp. atrial fibrillation).
  • CVA.
  • Non- or very light drinkers have higher risk than light drinkers even after controlling for smoking, hypertension, etc. (i.e. ‘the J shaped curve’ for mortality); no specific drink type (i.e. not red wine); mechanism may be increase in protective HDL and reduced platelet adhesion.

Respiratory

  • Tuberculosis.
  • Klebsiella and streptococcal pneumonia.
  • Increased vulnerability is related to decreased immunity, poor nutrition, and self neglect.

Neurological

  • Wernicke-Korsakoff syndrome (pp. 530, 531).
  • Peripheral neuropathy.
  • Central pontine myelinolysis (pseudobulbar palsy + quadriplegia).
  • Marchiafava-Bignami disease (corpus callosum degeneration).
  • Cerebellar degeneration.
  • P.533

  • Optic atrophy.
  • Alcoholic myopathy.

Genito-urinary

  • Erectile problems.
  • Hypogonadismin men.

Other

  • Foetal alcohol syndrome (p. 710).
  • Gout.
  • Osteoporosis.
  • Impaired absorption and diminished intake of specific vitamins and food overall.
  • Contribution to accidents particularly RTA.
  • Exacerbating factor in violent crime and assaults.
  • Diminished compliance with treatment for other medical and psychiatric disorders.

P.534
Illegal drugs In the UK, community surveys indicate that one third of adults have tried illegal drugs in their lifetime, with 10% having used them in the previous year. The rates for those aged under 25 are higher, with 50% lifetime use and 33% in the previous year. At all ages males have higher rates of drug use than females (♂:♀ = 3–4:1). Cannabis is the most commonly used illegal drug, while community rates for the other drugs of abuse are low. Users show a variable pattern of consumption with episodic and situational use for drugs with low dependence potential and a tendency to continuous dependent use for more ‘addictive’ drugs. Among some users, particularly those in the dance scene, polydrug use is the norm with individuals consuming more than 10 different drugs. Use of illegal drugs is commoner in the young, in the lower socio-economic classes, and in those with psychiatric illness. At any one time <33% of dependent users will be in contact with treatment services; mean length of dependent use before seeking help is 9 years. There are as many patterns of drug use as drug user and individual patient assessment is mandatory; nonetheless a number of patterns of use of illegal drugs can be recognised:

  • Experimental use Use of drug in order to explore effects. Common among young and heavily driven by drug availability and drug use among peers. Very common for ‘softer’ drugs, (e.g. cannabis, volatile chemicals), rarer for more ‘hard’ drugs, (e.g. heroin).
  • Situational use Drug use limited to certain situations, (e.g. parties, raves). Mainly drugs with stimulant/hallucinogenic properties.
  • Recreational use Regular but non-dependent use. May be limited in time by period of life (e.g. ending at the end of university life) or may progress to dependent use.
  • Polydrug use Non-dependent use of variety of drugs. One drug may be taken to potentiate the effects of another or to manage unpleasant after effects of drug use. Risks can be additive or multiplicative.
  • Dependent use Use of a drug for which a dependence syndrome (p. 502) has developed. Continued use may be motivated more by the desire to avoid withdrawals than by positive drug effects which may have diminished due to the development of tolerance. Tendency is for the use of the dependent drug to predominate, with other drugs being taken only if the primary drug is unavailable.
  • Dual diagnosis use Drug users who also suffer from a major mental illness. An important group for therapeutic intervention.

Categories of drugs of abuse

  • Opiates e.g. heroin, dihydrocodeine, methadone, codeine, buprenorphine, pethidine.
  • Depressants e.g. benzodiazepines barbiturates, alcohol, GHB.
  • Stimulants e.g. amphetamine, cocaine, MDMA.
  • Hallucinogens e.g. LSD, PCP, mushrooms, ketamine.
  • Others e.g. cannabis, volatile substances, anabolic steroids.

P.535
P.536
Street slang associated with drug misuse

Street drug name Conventional name
Acid LSD
Adam MDMA
Angel dust PCP
Billy Amphetamine
Blow Cannabis
Brown Heroin
C, Charlie, Coke Cocaine
Crack Freebase cocaine
Dope Cannabis
Downers Depressant drugs
E, Ecstasy, Eccies MDMA
GBH, Grievous bodily harm GHB (gammahydroxybutyrate)
Gear Heroin
Grass, Hash Cannabis
Jellies Temazepam
Marijuana Cannabis
Mushies Psilocybin mushrooms
Poppers Volatile nitrates
Roids Anabolic steroids
Roofies Rohypnol
Skag Heroin
Skunk Potent form of cannabis
Smack Heroin
Snow Cocaine
Special K Ketamine
Speed Amphetamine
Sulph Amphetamine
Uppers Stimulant drugs
Vallies Diazepam
Vitamin K Ketamine
Whizz Amphetamine

P.537

Slang term Meaning
Backtrack Allow blood to flow back into IV syringe and then reinject
Chasing Consume heroin by heating on foil and inhaling the fumes
Cold turkey Withdrawal symptoms (referring to the piloerection)
Cooking up Melting down heroin prior to injection
Fix The required regular dose of drug in a dependent user
Gouching Apparent somnolence following heroin use
Jag up To inject drugs IV
Juggling Selling drugs to finance one’s own dependency
Junkie An individual dependent on a drug
Mainline To inject drugs IV
Nodding, On the nod Apparent somnolence following heroin use
Rattling Suffering from withdrawals
Score Obtain drugs
Script Legitimate prescription for drugs
Shooting gallery Place where individuals meet to use drugs IV
Skin popping To inject drugs sub-dermally
Sorted Having obtained sufficient drug for one’s own needs
Spliff Cannabis cigarette
Tab Dose of LSD impregnated onto paper
Works Syringe and needles

P.538
Opiates The opiates are a group of chemicals derived from the opium poppy (papaver somniferum); synthetic compounds with similar properties are called opioids. They have potent analgesic properties and as such have wide legitimate uses in medicine. They are widely abused for their euphoriant and anxiolytic properties. Heroin is the most frequently abused opiate. Heroin Illicit heroin is sold as a brown or white powder in ‘bags’ or ‘wraps’, costing £50–£100 per gram, with a typical dependent user taking 0.25–2.0 g per day. It is most commonly consumed by smoking (‘chasing’), but is also taken orally, occasionally snorted, and parenterally by IV, IM, or subcutaneous routes. Street supplies are of variable purity (25–50% by volume); occasionally, a particularly pure batch is associated with a series of deaths and ODs from users used to a less concentrated form. In common with other opiates, heroin binds to specific receptors for which there are endogenous ligands (endorphins). There are overall cortical inhibitory effects with diminished pain sensation. After consumption effects are virtually immediate with euphoria amounting to ecstasy, intense relaxation, and untethering from worries and cares. Although recreational use is not unknown, the tendency is for progression to dependent use and this is the most usual pattern by the time of presentation to treatment services. An established dependent user may move from smoking to occasional or regular IV use to potentiate effects. Users develop tolerance with regular use and there is cross-tolerance to other opiates. Dependent patients may describe limited euphoriant effects, with the drug being mainly taken to avoid unpleasant withdrawals. Acute medical problems associated with heroin use by any route include nausea and vomiting, constipation, respiratory depression, and loss of consciousness with aspiration (the cause of many fatalities). Injected use adds risks of local abscesses, cellulitis, osteomyelitis, bacterial endocarditis, septicaemia, and the transmission of viral infections (Hepatitis B and C, HIV). Opiate dependency develops after weeks of regular use and is associated with an unpleasant (but not generally medically dangerous) withdrawal syndrome (p. 500). Interventions Give harm reduction advice to users who continue to use opiates: do not use opiates while alone; do not use in combination with other drugs; avoid IV route; if injecting, give safe injecting advice (opposite). Consider managed detox (p. 554) or transfer to maintenance prescribing (pp. 554, 555) in established dependence. Other opiates These include dihydrocodeine, morphine, methadone, pethidine, buprenorphine, and codeine. They may be taken in their pre-prepared tablet or liquid form or prepared for injection. Their acute and chronic risks are similar to heroin. P.539
Safer injecting advice If using heroin it is safest to avoid IV use which has the greatest risk of overdose and other complications. If using heroin IV:

  • Use new sterile needles and syringes on each occasion (give details of local needle exchange services if available)
  • Use sterile water (water from running cold kitchen tap is closest)
  • Never share needles, syringes, spoons, or filters with another user
  • Rotate injection sites
  • Avoid injecting into neck, groin, or breast
  • Avoid injection into infected areas
  • Ensure that the drug is completely dissolved before injecting
  • Always inject with, not against the blood flow
  • Do not take heroin while alone

It is safest to use new sterile needles and syringe on each occasion. Failing this, rather than use dirty equipment, flush both needles and syringes several times with thin bleach, then several times with clean water. P.540
Depressants Drugs of this group produce their effects by generalised or specific cortical depression. They include the benzodiazepines, alcohol, and the barbiturates. They can be taken for their pleasurable anxiolytic and relaxant properties alone, or as a way of counteracting unpleasant side-effects of other drugs of abuse (e.g. to ‘come down’ after stimulant use). Benzodiazepines A class of chemicals initially synthesised in the 1950s. Largely replaced barbiturates in clinical practice as they did not cause fatal respiratory depression. They have therapeutic uses as anxiolytics, hypnotics, anti-convulsants, and muscle relaxants. Problems of dependency arising from long-term use became recognised in the 1980s leading to a fall in their legitimate prescription, but did nothing to diminish their popularity as drugs of abuse. All benzodiazepines have similar effects and are distinguished by their length of action: short-acting (e.g. temazepam, oxazepam), medium-acting (e.g. lorazepam, alprazolam), long-acting (e.g. diazepam, nitrazepam, chlordiazepoxide). Benzodiazepines are taken orally, or less commonly by injection. There is hepatic metabolism to active compounds, some with long half-lives. They enhance GABA transmission and produce marked anxiolytic and euphoriant effects. Tolerance develops rapidly (with cross tolerance to all drugs in the benzodiazepine group), so requiring increasing doses to achieve similar effects. Acutely they cause forgetfulness, drowsiness, and impaired concentration and coordination with consequent risk of accidents. Use by injection is associated with the same infective risks as IV heroin (p. 538). An additional problem seen in IV benzodiazepine users is limb ischaemia secondary to intravenous use of melted tablet contents. Chronic use is associated with impaired concentration and memory and depressed mood, all of which are more severe in the elderly. Benzodiazepine dependency develops after 3–6 weeks of regular use. There is a withdrawal syndrome (p. 500) which can be complicated by seizures and delirium. Interventions Harm reduction advice to user as for opiates (p. 538), specifying safe injecting advice (p. 539) if using via IV route. Consider managed detox or transfer to maintenance prescribing (p. 556) in established dependence. Flunitrazepam (Rohypnol) A short-acting potent benzodiazepine seen particularly in dance settings with intoxicant and (probably apocryphal) aphrodisiac effects. As it can produce impaired judgement and anterograde amnesia and is tasteless in solution it has been implicated in cases of ‘date rape’. Gamma-hydroxy-butyrate (GHB) A synthetic compound originally developed as an anaesthetic which is a probable intrinsic neurotransmitter. Particularly seen in dance settings usually in combination with other drugs or alcohol. Produces a sense of dissociation, euphoria, and intoxication. Taken as liquid, 5–10 mg dosage with effects coming on in 15–30 minutes and lasting several hours. Side-effects of nausea and vomiting, seizures, and respiratory depression. Dependence rare but reported. P.541
Barbiturates Group of compounds used as hypnotics/anxiolytics in clinical practice prior to the introduction of the benzodiazepines. Now rarely prescribed and rarely seen as drugs of abuse. They act by facilitating GABA neuro-transmission. There is rapidly increasing tolerance to their anxiolytic effects in regular use but not to the associated respiratory depression. P.542
Stimulants These drugs potentiate neuro-transmission and increase cortical excitability producing effects of increased alertness and endurance, diminished need for sleep, and a subjective sense of well-being. They include cocaine (and crack cocaine), amphetamines, 3,4, methylenedioxymethamphetamine (MDMA or ecstasy), and caffeine. Cocaine The mild stimulant/euphoriant effects of the chewed leaves of the coca shrub have been known to the people of South American for thousands of years, but in its refined form cocaine is a potent and highly addictive drug. Cocaine hydrochloride is refined to a white powder which may be inhaled (‘snorted’) or dissolved and injected. The main route of intake is by inhalation as it undergoes rapid ‘first pass’ liver metabolism. The user forms the powder into ‘lines’ and inhales via rolled paper tube (classically, a high denomination banknote). Each line contains -25 mg cocaine. Freebase (‘crack’) cocaine (produced by alkalinisation, which produces the hydrochloride-free ion form) has a lower vaporisation temperature than the hydrochloride and can be smoked. In terms of rapidity of action and peak blood levels this compares with IV use. Cocaine acts as a local anaesthetic at the mucous membranes. It has widespread effects in potentiating dopaminergic, serotinergic, and noradrenalinergic neurotransmission by blocking neuro-transmitter reuptake. Its actions begin a few minutes after consumption. There is increased energy, increased confidence, euphoria, and diminished need for sleep but with rapid fall-off in effects due to rapid metabolism, leading to repeated use. There are very intense effects from freebase cocaine use with rapid and intense ‘high’ with subsequent dysphoria. Cocaine is usually taken in an opportunistic way, sometimes in association with other stimulant drugs. Acute harmful effects include arrhythmias, intense anxiety, hypertension → CVA, acute impulsivity, and impaired judgement. Chronic harmful effects include necrosis of nasal septum, foetal damage (‘crack babies’), panic and anxiety disorders, persecutory delusions, and psychosis. It is not associated with classical dependence but a minority of users will consume in a regular ‘compulsive’ pattern. Interventions Harm reduction advice (including safe injecting advice, p. 539, if appropriate). No role for substitute prescribing in managing withdrawal or for maintenance prescribing. Amphetamines A group of compounds synthesised in the late 19th Century with current legitimate uses in child psychiatry (p. 578) and in narcolepsy (p. 402). Sold as 5 mg tablets or as white powder (-£10 per gram). The powder may be swallowed, inhaled, or dissolved and injected. Use is usually situational or recreational, although very regular use with dependence is recognised. There is chemical similarity to noradrenaline and dopamine, producing similar pharmacological effects to cocaine, but its slower metabolism gives a longer duration of action. Acute harmful effects include tachycardia, arrhythmias, hyperpyrexia. irritability, post-use depression, and quasi-psychotic state with visual, auditory, and tactile hallucinations. Dependency is not seen but marked psychological addiction occurs, particularly in situations associated with drug P.543
use. Anxiety and depressive symptoms are frequently seen in users; their proper assessment requires a period of abstinence. Interventions Harm reduction advice (including safe injecting advice, p. 539, if appropriate). No role for substitute prescribing in managing withdrawals. Very limited role for maintenance prescribing of dexamphetamine sulphate in the management of chronic, primary, heavy IV users (specialist instigation only). MDMA (Ecstasy) This compound was synthesised in 1914. and initially was occasionally used as a adjunct to psychotherapy. Initially legal, it became widely used in the mid 1980s in association with house, rave, and techno music. It is taken orally as 50–200 mg tablet. A typical pattern of use is two or more tablets taken at weekends. MDMA causes serotonin release and blocks reuptake. It has structural similarities to mescaline and amphetamine, therefore has both hallucinogenic and stimulant properties, these effects appearing -30 minutes after ingestion. The initial ‘rush’ period of intoxication lasts -3 hours and is characterised by a feeling of increased camaraderie and ‘closeness’ to others, a pleasurable agitation relieved by dancing, and decreased fatigue. Acute harmful effects include increased sweating, nausea and vomiting, and diminished potency despite increased libido. Deaths have occurred associated with dehydration and hyperthermia (a toxic reaction similar to serotonin syndrome appears to exist (p. 870)). Chronic harmful effects include possible neuro-toxicity, hepatotoxicity, and possible chronic cognitive impairment. There is tolerance to its effects but dependence does not occur. ‘Hangover’ effects develop 24–48 hours after ingestion including fatigue, anorexia, and depressed mood (which may be severe). Interventions Harm reduction advice regarding maintaining hydration and avoiding overheating during use. No role for substitute prescribing in managing withdrawal or for maintenance prescribing. For all stimulant drugs there may be a problem of assessing other aspects of mental state, particularly affective and psychotic features while chaotic use continues. In selected patients, inpatient assessment will be indicated to allow this. P.544
Hallucinogens Hallucinogens (or psychedelics) are a heterogeneous group of natural and synthetic substances which produce altered sensory and perceptual experiences. They include: lysergic acid diethylamide (LSD), phenylcyclidine (PCP), magic mushrooms, ketamine, mescaline, 2,5-di-methoxy 4-methylamphetamine (DOM), and dimethyltriptamine (DMT). Lysergic acid diethylamide (LSD) A compound synthesised by Hofman while working at Sandoz pharmaceuticals in 1944. He reported the hallucinatory experiences which followed his initial, accidental ingestion. The drug also occurs naturally in seeds of the ‘Morning Glory’ plant. It became strongly associated with 1960s culture when its use was at its peak. There was early experimentation with its role in psychotherapy but there is no current legitimate use. It is very soluble and intensely potent (effective dose -250 micrograms). It is sold impregnated onto paper, in tablets, or as a powder. LSD is a indolealkylamine with structural similarity to serotonin. There are direct and indirect effects on serotinergic and dopaminergic transmitter systems. It is not now thought to provide a good model for endogenous psychosis. Its actions are very markedly situation-and expectation-dependent. Effects develop 15–30 minutes after ingestion and last up to 6 hours. There is initial euphoria; a sense of detachment; a sense of novelty in the familiar and a sense of wonder at the normal; visual distortions and misperceptions; synaethesia; and distorted body image. Somatic effects include dizziness and tremors. Acute harmful effects are behavioural toxicity (i.e. harm related to acting on beliefs such as having the ability to fly) and ‘bad trips’ (i.e. dissociation, fear of incipient madness, frightening perceptions). There is no risk of overdose and physiological dependence and withdrawals do not occur. Chronic harmful effects include flashbacks (p. 92) even many years after consumption, post-hallucinogenic perceptual disorder, persistent psychosis, and persistent anxiety/depressive symptoms. Interventions Harm-reduction advice directed towards maintaining a safe environment during use and avoiding behavioural toxicity—do not use alone, use accompanied by non-user if possible. For all hallucinogens, acute psychotic features should in general be managed by admission, maintenance of a safe environment, symptomatic treatment of agitation (e.g. with benzodiazepine), with expectation of resolution. Continuing psychotic features should be managed as for acute schizophrenia, (p. 198). Phenylcyclidine (PCP) A hallucinogen rarely seen in the UK except as a contaminant of other drugs. May be smoked, snorted, taken orally, or more, rarely, parenterally. There is direct binding to opioid and aspartate excitatory receptors as well as serotinergic and cholinergic effects producing acute effects of confusion, visual sensory distortions, aggression, and sudden violence (which may be severe). Intoxication may give way to longer psychotic states. Magic mushrooms About a dozen varieties of hallucinogenic mushrooms grow in the UK, the best known being the ‘Liberty Cap’ (Psilocybe semilanceata). They may be eaten raw or cooked, dried or prepared as a P.545
drink. Possession and consumption of mushrooms is not an offence unless they have been processed or prepared for illicit use. Small doses cause euphoria, while larger doses (>25 mushrooms) cause perceptual abnormalities similar to LSD. They are not associated with dependence or withdrawal features and tolerance develops quickly making continuous use unlikely. Harmful effects include nausea and vomiting, dizziness, diarrhoea and abdominal cramps, behavioural toxicity, and risk of accidental consumption of toxic fungi. Ketamine A compound structurally similar to phencyclidine used as veterinary anaesthetic and in battlefield surgery. It is a unique anaesthetic as it does not produce RAS depression, instead it prevents cortical awareness of painful stimuli. It is taken illicitly as a sniffed powder, mean dose -100 mg. Small amounts lead to a sense of dissociation, larger amounts to LSD-like synaesthesia and hallucinations, associated with nausea, ataxia, and slurred speech. Rare late effects are flashbacks, psychosis, and amnesic syndromes. P.546
Other drugs Cannabis This is the most commonly used illegal drug, with only a small minority of its users ever using another illegal drug. It has been used for centuries as a pleasurable mind-altering substance and as a medication for a wide variety of ailments. Clinical trials are underway to clarify its role in the treatment of chronic pain. Its illegal use is of interest to psychiatrists because of its association with other drugs of abuse (as a ‘gateway drug’) and because of its exacerbating effect on chronic psychotic illnesses. Cannabis is produced from the dried leaves, flowers, stems, and seeds of the weed Cannabis Sativa. It may be distributed as herbal material (‘grass’ or marijuana), as a resin (‘hash’), or as cannabis oil. Cannabis may be smoked in cigarettes, alone, or mixed with tobacco; the resin form may be eaten directly or incorporated into foodstuffs (e.g. cakes). These various forms contain at least 60 psychoactive cannaboids, the most important of which is 9-delta-tetrahydrocannibinol (THC). The dried herb contains -5% THC by weight; resin -10%; and cannabis oil -15%. A particularly potent form of cannabis (‘skunk’) is becoming increasingly available. Usage pattern is very variable, from infrequent situational use to daily heavy use; the latter at highest risk of harmful effects and most likely to take other drugs. There is a specific cannaboid receptor and a naturally occurring agonist at this receptor—‘anandamide’. The role of this endogenous system has yet to be defined. In addition, cannabis shows both weak opiate-like and weak barbiturate-like effects. The drug is metabolised to both active and inactive metabolites and absorption of cannabis metabolites into fat mean that urine tests remain positive for up to 4 weeks after regular use has ceased. The effects of intoxication are apparent within minutes if the drug is smoked, peaking in -30 minutes and lasting 2–5 hours. The effects of orally consumed cannabis are slower to begin and more prolonged. The immediate effects include mild euphoria (‘the giggles’), a sense of enhanced well-being, subjective sense of enhanced sensation, relaxation, altered time sense, and increased appetite (‘the munchies’). Physically there is mild tachycardia and variable dysarthria and ataxia. Acute harmful effects include mild paranoia, panic attacks, and accidents associated with delayed reaction time. Cannabis is normally smoked with tobacco, therefore all of the health risks associated with tobacco will also apply. The tendency of cannabis smokers to inhale deeply and to retain the smoke in the lungs for as long as possible will exacerbate this risk. There are no reports of fatal overdose. Chronic harmful effects include dysthymia, anxiety/depressive illnesses, the disputed amotivational syndrome (possibly representing a combination of chronic intoxication in a heavy user and a long half-life). The drug is not usually associated with physical dependency but there is a mild but characteristic withdrawal syndrome in the previously heavy regular user who stops suddenly, consisting of insomnia, anxiety, and irritability. Cannabis use can precipitate an episode of or relapse of schizophrenia. In addition, in regular users it is associated with dose-related paranoid ideation and other psychotic features. Interventions As an illegal drug there are no set guidelines on safe use. Clinical experience suggests that irregular use can be free from major P.547
problems. Abstinence is indicated in those with major mental illness and continuing cannabis use may expose those recovering from more serious drug problems to dealers and the drugs sub-culture. Volatile substances Simple hydrocarbons such as acetone, toluene, xylene, and butane have intoxicant properties. These chemicals are found in a variety of common products including glue, solvents, lighter fuel, paint stripper, fire extinguishers, aerosols, paints, petrol, typewriter correcting fluid, and nail varnish remover. They are rapidly absorbed when deeply inhaled or by sniffing propellant gases or aerosols. They cause non-specific increased permeability of nerve cell membranes and produce euphoriant effects, disinhibition, slurred speech and blurred vision, and visual misperceptions. Acute harmful effects include local irritation, headache, cardiac arrhythmias, acute suffocation by bag or laryngeal oedema, unconsciousness, aspiration, and sudden death. Chronic harmful effects include liver and kidney damage, memory/concentration impairment, and probable long-term cognitive impairment. There is a withdrawal syndrome similar to alcohol in very heavy regular users. Interventions Education of users and ‘at risk’ groups. Most use will be experimental with few going on to regular use. Legal controls on substance availability. Anabolic steroids These prescription-only medicines (e.g. nandrolone and stanozolol) have limited legitimate uses in the treatment of aplastic anaemia and osteoporosis. They can be abused by athletes and body builders seeking competitive advantage or, more rarely, for their euphoriant effects alone. They produce increased muscle mass and strength, with increased training time and reduced recovery time as well as euphoriant effects and a sense of increased energy levels. (Other drugs misused by athletes include thyroxine, growth hormone, diuretics, erythropoietin, and amphetamine.) Use of anabolic steroids is associated with physical health problems including hypertension, hypogonadism, gynaecomastia, amenorrhoea, liver damage, impotence, and male pattern baldness; and with mental health problems including acute emotional instability (sometimes known as ‘roid rage’), increased aggressiveness, persecutory/grandiose delusions, depressive illness, and chronic fatigue. If injected they can also be associated with infection risks (p. 538). There is no withdrawal syndrome. Interventions Education of risks through coaches, teachers, etc. Effective monitoring of individual sports with out-of-season testing. P.548
Assessment of the drug user In most cases an assessment of a patient’s history of drug use will form part of a routine psychiatric interview. In addition, all doctors should consider the possibility of, and be prepared to ask about, comorbid drug misuse when interviewing patients for other reasons. The more detailed assessment described here is appropriate for patients in whom drug use is the primary focus of clinical concern and who are being assessed for entry into a treatment programme. The detailed assessment of a patient with drug use problems will usually be carried out over more than one consultation. There are only a few circumstances (such as an opiate-dependent patient presenting as an acute medical emergency), where treatment should be considered before full assessment. History should cover the following topics: Background information Name, address, next of kin, GP, names of other professionals involved (e.g. social worker, probation officer). Reasons for consultation now Why has the drug user presented now, (e.g. pressure from family, pending conviction, ‘had enough’, increasing difficulty injecting)?. What does the user seek from the program? In females, is there a possibility of pregnancy? Current drug use Enquire about each drug taken over the previous 4 weeks. Describe the frequency of use (e.g. daily, most days, at weekends); and the number of times taken each day. Record the amount taken and the route. Ask the user about episodes of withdrawal. Include alcohol, tobacco, and cannabis. If there is IV use, inquire about needle or other equipment sharing. Lifetime drug use Record the age at first use of drugs and the changing pattern of drug use until the most recent consultation. Enquire about periods of abstinence or stability and the reasons for this (e.g. prison, relationship, treatment programme). Complications of drug use Overdoses—deliberate or accidental. History of cellulitis, abscesses, or phlebitis. Hepatitis B and C and HIV status if known. Previous treatment episodes Timing, locus, and type of previous drug treatment. How did the treatment attempt end? Was the treatment helpful? Medical and psychiatric history All episodes of medical or psychiatric inpatient care. Contact with hospital specialists. Current health problems. Relationship with GP. Family history Are there other family members with drug or alcohol problems? Family history of medical or psychiatric problems. Social history Current accommodation. How stable is this accommodation? Sexual orientation and number of sexual partners. Enquire about safe sex precautions. Describe the user’s relationships—sexual, personal, and family. Note how many of these individuals currently use drugs. P.549
Forensic history Previous or pending convictions. Periods of imprisonment. Enquire about continuing criminal activity to support drug use (remind the patient about confidentiality). Patient’s aims in seeking treatment What is the patient’s attitude to drug use? What treatment options do they favour? MSE Observe for history or objective signs of depressed mood or suicidal thoughts or plans. Inquire directly about generalised anxiety and panic attacks (a benzodiazepine user may be self medicating a neurotic condition). Inquire directly about paranoid ideas and hallucinatory experiences and the directness or otherwise of their relationship with drug use. Physical examination General condition. Weight. Condition of teeth. Signs of IV use (examine particularly arms for signs of phlebitis, abscess, or old scarring). Examine for enlarged liver. Signs of withdrawals on assessment. Urine screening This is essential. Several specimens should be taken over several weeks. Repeated absence of evidence of a drug on screening make its dependent use unlikely. Occasionally, testing errors do occur so do not take action (e.g. stopping maintenance prescription) on the basis of the results of a single sample. Blood testing FBC, LFT, discuss with patient the need for HIV and Hepatitis screening. Urine drug testing

Substance Duration of detectability
Amphetamines 48 hours
Benzodiazepines
Ultra-short-acting (e.g. Midazolam) 12 hrs
Short-acting (e.g. Triazolam) 24 hrs
Intermediate-acting (e.g. Temazepam) 40–80 hrs
Long-acting (e.g. Diazepam) 7 days
Cocaine metabolites 2–3 days
Methadone (maintenance-dosing) 7–9 days (approximate)
Codeine/morphine 48 hrs
(Heroin is detected in urine as the metabolite morphine)
Cannabis
Single use 3 days
Moderate use (4 times per week) 4 days
Heavy use (daily) 10 days
Chronic heavy use 21–27 days
Phencyclidine (PCP) 8 days (approximate)

P.550
Planning treatment in drug misuse The longer-term goal of treatment will be eventual abstinence from drugs, but this may not be an achievable short-or medium-term goal in an individual case. Immediate treatment aims are therefore: to reduce drug related mortality and morbidity; to reduce community infection rates; to reduce criminal activity, including the need for drug users to sell to others to finance their own habit; to optimise the patient’s physical and mental health; and to stabilise where appropriate on an alternative substitute drug. Make diagnosis Confirm drug use (history, signs of withdrawals, urine testing). Assess presence and extent of dependence. Assess severity of current problems and risk of future complications. Explore social, relationship, and medical problems. Assess stage of change (p. 503) and motivation. What are the short-term and medium-term aims of treatment? Consider need for emergency treatment Where there is evidence of psychotic illness or severe depressive illness the patient may require inpatient assessment. Engage in service Treatment of drug misuse cannot be carried out through ‘one off’ interventions. Patients should be engaged in the service by empathic and non-judgemental interviewing, availability of the service close to the point of need, and ability of the service to respond to change in a previously ambivalent patient. Substitute prescribing will be a strong motivator for engagement in some patients but should always also have a role in helping the patient achieve some worthwhile change. Decide treatment goals and methods After assessment and diagnosis the doctor should discuss with the patient their thoughts about treatment options given the patient’s drug history and local treatment availability. The doctor may have strong feelings about the appropriateness of a certain treatment but this will not be successful unless the patient agrees. Plans may include:

  • Return to dependent use as previously Where individuals present in withdrawals, without other medical surgical or psychiatric reasons for admission, and where there is no history of complicated withdrawal, and where there has been no previous involvement in treatment services, it is inappropriate to prescribe. The individual should not receive replacement medication. They should be offered the opportunity to attend for further assessment.
  • Counselling and support For non-dependent drug use particularly episodic use this may be the appropriate course. Give drug information and harm-reduction advice, possibly coupled with referral to a community resource.
  • Detoxification (pp. 554, 556) Where there is drug dependence and the patient wishes abstinence, then a plan for detox is considered. This may be community-based, with psychological support, symptomatic medication, or reducing substitute medication, or as an inpatient. Consideration should be given to support after detox. How is abstinence to be maintained? P.551
    • Supported detox without prescription Some individuals can withdraw from drugs of dependence without use of a prescription. This may occur particularly where other changes in a person’s life (e.g. change of area, break from dependent partner) facilitate abstinence. Unsupported detox without any medical help is frequently reported by users.
    • Supported detox with symptomatic medication Here, in addition to the support mentioned above, the individual is prescribed other, non-replacement drugs to ameliorate withdrawal symptoms (e.g. lofexidine in opiate withdrawal).
    • Conversion to substitute drug with aim of detox Here the aim is to convert the individual’s drug use from street-bought to prescribed, Then, from a period of stability, attempt supervised reduction in dose, aiming towards abstinence.
  • Conversion to substitute drug with aim of maintenance Here the aim again is to convert from street to prescribed drugs, with stabilisation via maintenance prescribing in the medium term. In a dependent user who does not feel that they can move to abstinence in the short term, maintenance prescribing to suitably selected patients is useful and associated with overall health benefits.

Address other needs The drug treatment service should consider part of its role as being a gateway to other services which the drug user may require but be reluctant or unable to approach independently. Patients with social, financial, or physical health needs should have these explored and the need for referral considered. Do not make such referrals without the knowledge and agreement of the patient. Review psychiatric symptoms which have been attributed to drug use to assess their resolution. Consider ‘in-house’ or specialist psychiatric treatment of residual anxiety/ depressive symptoms. P.552
Substitute prescribing (1)—principles Withdrawal syndromes Any drug consumed regularly and heavily can be associated with withdrawal phenomena on stopping, even if not a classical withdrawal syndrome. The severity of withdrawal symptoms experienced by individual patients does not correlate well with their reported previous consumption and so it is best to rely on objective evidence of withdrawal severity. Clinically significant withdrawal phenomena occur in dependence on alcohol, opiates, and benzodiazepines and are occasionally seen in cannabis, cocaine, and amphetamine use. In general, drugs with short half-lives will give rise to more rapid but more transient withdrawals. Detoxification refers to the process of managed withdrawal from drugs of dependence which can be aided by psychological support, symptomatic prescribing, or by prescription of reducing doses of the same or similar drug. Substitute prescribing In many circumstances the management of a drug user will include prescription of substitute medication. This may be to enable detoxification from a dependent drug, or maintenance prescribing—a move from unstable street use to prescribed dependent use to facilitate change now with abstinence later. The prescription of a drug should not occur in isolation but should be part of a comprehensive management plan, previously agreed with the patient and with relevant members of the multidisciplinary team. Prescribing for drug users should be guided by local procedures and practice, by the Home Office document ‘Drug misuse and dependence—guidelines on clinical management’ and by the British National Formulary. Substitute prescribing may have the following indications

  • To acutely reduce or prevent withdrawal symptoms. Where detoxification is planned, a first step can be the conversion of all opiate or benzodiazepine use to a single prescribed drug, which can then be reduced in a planned manner. Short-term prescription of a substitute drug may also be indicated to alleviate symptoms of withdrawal complicating the assessment of a dependent patient presenting with a medical or surgical emergency.
  • To stabilise drug intake and reduce secondary harm associated with street drug use. In patients who are not considering detox in the short term, substitute prescribing can be a means of harm reduction (e.g. by reducing risk of accidental OD or by changing from IV to prescribed oral use). In addition, having a stable, legitimate supply can reduce the need to resort to criminal activity to fund drug use, reducing the secondary, wider social harms of drug use.
  • To begin a process of change in drug-taking behaviour. A major aim in substitute prescribing is to fully supply the dependent drug and to move the patient away from extra, recreational drug use and chaotic, polydrug misuse. After stabilisation, the user should be encouraged to discontinue contact with dealers and friends who continue to use drugs in a chaotic fashion.
  • To provide an incentive to continued patient contact and involvement with treatment services.

P.553
Substitute prescribing should only be considered where:

  • There is objective evidence of current dependence. This should include a history of daily consumption, description of withdrawal symptoms, history of drug seeking to relieve or prevent withdrawals, and consistent presence of the drug on urine screening.
  • The patient displays realistic motivation to change their drug use in a way which would be aided by prescription, (e.g. to cease IV heroin use on instigation of oral methadone prescription).
  • The doctor believes the patient will cooperate with the prescription and that circumstances exist to allow adequate monitoring.

Assessing need for substitute medication Before prescribing substitute medication for detoxification or maintenance the treating doctor should positively confirm dependence via:

  • Positive history of daily use with features of dependence syndrome.
  • Presence of drug in two urine specimens at least 1 week apart.
  • Objective evidence of withdrawal features at assessment.

Writing a controlled drug prescription

  • In doctor’s own handwriting (some specialists have local exemption to this regulation but hand signature is always required).
  • Patient’s name, age, and current address.
  • Name, concentration, and type of preparation required (e.g. methadone, 1 mg in 1 ml, sugar-free suspension).
  • Dose and frequency.
  • Total quantity of drug to be dispensed in both words and figures (not required for temazepam).
  • Signed and dated.

P.554
Substitute prescribing (2)—opiates Opiate detoxification Opiate withdrawal In an opiate dependent individual, withdrawal symptoms appear 6–24 hours after the last dose and typically last 5–7 days, peaking on the 2nd or 3rd day. The withdrawal following discontinuation of the longer-acting methadone is more prolonged with symptoms peaking on the 7th day or so and lasting up to 14 days. Symptoms of opiate withdrawal: sweating; dilated pupils; tachycardia; hypertension; piloerection (‘goose flesh’); watering eyes and nose; yawning; abdominal cramping; nausea and vomiting; diarrhoea; tremor; joint pains; muscle cramps. Symptomatic medication Several non-opiate, oral medications are effective in ameliorating symptoms of opiate withdrawal. Unlike opiates, they are not liable to abuse or diversion to the black market.

  • Lofexidine Alpha-adrenergic agonist. Starting dose: 200 micrograms bd, increased in 200–400 microgram steps up to maximum of 2.4 mg daily given in 2–4 divided doses. Measure baseline BP and monitor BP while raising dose (risk of symptomatic hypotension). 10 day course, withdraw over 2–4 days.
  • Loperamide For treatment of diarrhoea. 4 mg initial dose with 2 mg taken after each loose stool. Maximum daily dose:16 mg.
  • Metoclopramide For nausea and vomiting. 10 mg dose, up to maximum of 30 mg daily
  • Ibuprofen For headaches and muscle pains. 400 mg dose, up to maximum of 1600 mg daily.

Substitute prescribing Several opiates are used in detoxification regimes. Where it is planned to continue prescribing on a maintenance basis, currently methadone is the drug of choice.

  • Methadone Long-acting synthetic opiate. Its half-life is 24 hours and it is therefore suitable for daily dosing (which can be supervised). At daily dose >80 mg it produces near saturation of opiate receptors, minimising the ‘reward’ of further consumption. It is prescribed as a coloured liquid, unsuitable for IV use, at concentration 1 mg/1 ml. A sugar-free form is available. Licensed for use in opiate withdrawal and maintenance.
  • Buprenorphine A partial opiate agonist. Licensed for treatment of drug dependence. Available in once-daily sublingual preparation. 8 mg – = 30 mg methadone. Believed to produce less euphoria at higher doses than methadone. Abuse potential as tablet can be prepared for injection.
  • Dihydrocodeine Short-acting opiate. Not licensed for use in drug dependence. Occasional use in reduction regimes in patients already on a stable dose of street dihydrocodeine or in final stages of dose reduction in patients on doses of methadone <15 mg daily. Need for 2–4 times daily doses means that all dosage cannot be supervised.

Opiate maintenance In maintenance prescribing, the aim is to prevent under-dosing (risk of use of street opiates, withdrawal symptoms) and overdosing (sedation, more drug available than required with diversion to the black market). There is P.555
research evidence1 that a methadone script reduces street usage, criminality, and drug-related mortality. For outpatient initiation of methadone maintenance, arrange to review the patient in the morning with them having consumed no opiates for the previous 24 hours. Assess withdrawals and dispense methadone as follows:

  • None or mild → no prescription. Review following day.
  • Moderate (aches, dilated pupils, yawning) →10–20 mg methadone.
  • Severe (vomiting, piloerection, hypertension) → 20–30 mg methadone.

Review after 4 hours and repeat dose if severe withdrawals continue, up to 30 mg. Review daily over the first week with dose increments of 5–10 mg daily if indicated. Methadone reaches a steady state 5 days after the last dose change. Arrange regular review after first week, making subsequent increases by 10 mg on each review up to -120 mg. Stabilisation may take up to 6 weeks to achieve. For maintenance monitoring, see p. 558. Dose reduction After stabilisation and complete abstinence from street opiates, a decision should be made as to whether the aim is dose reduction or maintenance prescribing. Rapid reduction regimes reduce the dose over 14–21 days (perhaps using the above symptomatic drugs as adjuncts). Usually reduction is more gradual. Slow reduction is over 4–6 months, reducing by -5–10 mg each fortnight. In reduction regimes, make the largest absolute cuts at the beginning and make smaller, more gradual cuts as the total dose falls (i.e. aim to keep the percentage drop in dose similar). In general do not carry out reduction against the wishes of the patient as it is better to carry on a maintenance script rather than return to street use. Occasionally ‘tread water’ then restart reduction. Opiate relapse prevention In previously dependent opiate users who have successfully completed detox, the opiate antagonist naltrexone may be used as an aid to relapse prevention. Taken regularly it will prevent the rewarding, euphoriant effect of opiate consumption. Naltrexone Prescribed to aid abstinence in formerly dependent patients who have been drug free for >7 days. Starting dose 25 mg, increased to 50 mg daily. Total weekly dose may be given 3 days per week (e.g. to aid compliance, or to enable supervision), give 100 mg Monday and Wednesday and 150 mg on Friday. Naltrexone is also used in specialist inpatient facilities to facilitate rapid detox over 5–7 days. Converting opiate dose to methadone dose

Drug Daily dose Methadone equivalent
Street heroin 0.5 mg–1g 50–80 mg
Morphine 10 mg 10 mg
Dipipanone (Diconal) 10 mg 4 mg
Dihydrocodeine (DF118) 30 mg 3 mg
Pethidine 50 mg 5 mg
Codeine phosphate 30 mg 2 mg

References 1 Ward J Mattick R. Hall W (1997) Maintenance treatment and other opioid replacement therapies. Harwood Academic Press. P.556
Substitute prescribing (3)—benzodiazepines Benzodiazepine detoxification Benzodiazepine withdrawal Chronic benzodiazepine use leads to development of dependence, with a characteristic withdrawal syndrome. The symptoms appear within 24 hours of discontinuing a short-acting benzodiazepine, but may be delayed for up to 3 weeks for the longer-acting preparations. Symptoms of benzodiazepine withdrawal: anxiety; insomnia; tremor; agitation; headache; nausea; sweating; depersonalisation; seizures; delirium. Substitute prescribing As for opiates, benzodiazepine substitute prescribing should only be undertaken where there is clinical evidence of dependence, a clear treatment plan, and suitable patient monitoring in place. Substitute prescribing in benzodiazepine dependency uses the long-acting diazepam. In prescribing for patients with benzodiazepine dependency, convert all benzodiazepine doses to diazepam using the table opposite. The aim is to find the lowest dose which will prevent withdrawal symptoms (which may be well below the amount the patient has been taking). Divide the daily dose to avoid over sedation. Benzodiazepine maintenance Unlike methadone maintenance in opiate dependency, there is no evidence that long-term benzodiazepine prescription reduces overall morbidity. There is evidence that long term prescription of >30 mg diazepam daily is associated with harm. New prescriptions should be for 30 mg or less with patients already on higher doses reduced to this amount. Dose reduction Cut dose by -1/8th of total dose each fortnight. For low dose 2.5 mg fortnightly; for high dose 5 mg fortnightly. Review and halt or temporarily increase if substantial symptoms re-emerge. If patient is also opiate-dependent and on methadone, keep methadone stable while reducing benzodiazepine. P.557
Conversion to equivalent diazepam dose

Drug Dose
Diazepam 5 mg
Nitrazepam 5 mg
Temazepam 10 mg
Chlordiazepoxide 15 mg
Oxazepam 15 mg
Loprazolam 500 micrograms
Lorazepam 500 micrograms
Lormetazepam 500–1000 micrograms

P.558
Monitoring of maintenance prescribing Detoxification and stabilisation on maintenance medication are often followed by rapid relapse despite successful completion. It is important to build monitoring of compliance into treatment strategies from the beginning. Review Regular review of all patients on maintenance prescription is indicated at least monthly. At each review:

  • Is dose sufficient? Is there evidence of withdrawals? Obtain feedback from pharmacist /community nurse.
  • If dose insufficient? Consider small weekly increases in dose. Stop if evidence of intoxication.
  • Confirm use of illegal drugs via history, urine testing, and observation of evidence of IV use.
  • Plan movement towards goals.
  • Consider intervention in mental health/other issues.
  • Consider need for period of increased supervision.

Supervision of substitute prescribing The aim of supervised consumption is to ensure that the drug is being used as prescribed.

  • Supervised consumption usually for initial minimum period of three months, taking into account work and child care issues.
  • Consider ongoing supervised consumption (e.g. in pharmacy).
  • Once-daily dosing with daily pick-up of drugs.
  • No more than one week’s prescription at a time.
  • Advice re. children and methadone.
  • Close liaison with pharmacist and GP.
  • Thorough and clear records should be kept.
  • No replacement of ‘lost’ prescriptions

Discontinuing a failing treatment Where there is persistent non-compliance with treatment and where attempts to improve compliance or modify treatment goals have failed then the maintenance should be discontinued.

  • Discontinue via reduction regime
  • Offer involvement with other services
  • Inform GP and pharmacist

P.559
P.560
Psychotic illnesses and substance misuse The association of substance misuse and psychotic features is a common and problematic one in clinical practice. The key to management is accurate diagnosis. Psychotic symptoms represent underlying psychiatric abnormality in this group of patients as in any other. There is not a general finding of ‘low-grade’ psychotic features in substance users and apparent psychotic features should not be attributed to effects of substance use without further inquiry. Psychotic features during drug intoxication Substances with hallucinogenic or stimulant activity can produce psychotic features during acute intoxication. This is not consistent and varies by drug dose and setting. These are characterised by a rapidly changing pattern of symptom type and severity and include visual and other hallucinations, sensory distortions/illusions, and persecutory and referential thinking. They are characteristically rapidly fluctuating hour by hour and show resolution as the drug level falls. Psychotic features during withdrawal In patients with physiological dependency on alcohol, benzodiazepines, or cocaine, withdrawals may be complicated by delirium in which variable psychotic features may be prominent. These will occur in the context of the general features of delirium (p. 734). There may be fluctuating visual or tactile hallucinations and poorly formed persecutory delusional ideas. Residual psychotic illness (drug-induced psychosis) In some individuals, psychotic features continue after the period of acute intoxication and withdrawals has passed. These may be symptomatically more typical of primary psychotic illness and, once established, should be treated as for acute episodes of schizophrenia (p. 198). Genuine comorbidity Many individuals with primary psychotic illnesses will misuse substances. In addition to the intrinsic risks of substance misuse, this carries risks in this group of diminished treatment compliance, risk of disinhibition leading to violence, and exacerbation of the primary illness. In view of the sometimes obvious (to others) causal link between drug use and relapse it is worth asking why patients persist in substance use. Reasons include:

  • Endemic drug use within patient’s environment, (e.g. home or social setting) or within other individuals with mental health problems.
  • As means of self medicating distressing positive and negative symptoms (which may be improved by addressing these symptoms directly).

P.561
P.562
Legal issues related to drug and alcohol misuse Fitness to drive It is the patient’s responsibility to inform the DVLA of any ‘disability likely to affect safe driving’. The DVLA regard drug misuse as a disability in this context. Group 1 licences cover motor cars and motor cycles, group 2 licences cover HGVs and buses. Decisions regarding licensing are made on a case-by-case basis; however, the DVLA’s current guidelines are as follows:

  • Alcohol misuse: loss of licence until 6-months (group 1) or 1-year (group 2) period of abstinence or controlled drinking has been achieved with normalisation of blood parameters.
  • Alcohol dependence: loss of licence until 1-year (group 1) or 3-year (group 2) period of abstinence, with normalisation of blood parameters. Consultant referral and support may be required.
  • Dependency/persistent use of cannabis, amphetamines, MDMA, LSD and hallucinogens: loss of licence until 6-months (group 1) or 1-year (group 2) period of abstinence. Medical assessment and urine screening may be required.
  • Dependency/persistent use of heroin, morphine, cocaine, methadone: loss of licence until 1-year (group 1) or 3-year (group 2) period of abstinence. Independent medical assessment and urine screening prior to relicensing. A favourable consultant report may be required for group 1 and will be required for group 2. Subject to annual review and favourable assessment, drivers complying fully with a consultant-supervised methadone maintenance programme may be licensed.

Travel abroad Patients receiving a methadone prescription can travel abroad with a supply. Amounts up to 500 mg do not need a licence; amounts above 500 mg require a Home Office licence, obtained by application by the prescriber to the Home Office stating the patient’s name and address, the strength, form, quantity, and daily amount of the drug prescribed, and the date of departure and return. In both cases the Home Office advises patients to carry a ‘To whom it may concern’ letter, indicating that the drug has been legitimately prescribed. This advice applies only to the right to take the drug out of the UK and return with any surplus. Travellers are advised to contact the embassy or consulate of the destination country prior to travel to ensure that import of methadone is allowed under local laws: countries’ regulations vary widely. Registration of drug addicts Compulsory registration of all drug addicts to the Home Office register of addicts ceased in 1997. Since then data have been collected on a regional basis via the anonymised regional drug misuse databases. Details regarding supply of forms in each area can be found in the BNF. P.563
Drug testing and treatment orders (DTTOs) A form of community sentence introduced in the UK in 2000. The court makes an order requiring offenders with drug problems to undergo treatment and follow-up with a drug treatment service. This may be part of another community order or a sentence in its own right. The sentencing court monitors compliance via mandatory urine testing. Sentence plans may change in response to individual progress or problems. May last 6 months to 3 years.

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