Table of Contents

Drug Dependence

Epidemiology

The only satisfactory way of estimating the number of persons misusing drugs requires large-scale representative and confidential surveys, nothing such have yet been done.

MORBIDITY

Psychic and social effects: Society tends to ostracize the addict - this further aggravates feelings of inadequacy, isolation and general resentment.

Physical Effects: Parenteral administration of any drug may cause hepatitis C due to sharing needles, abscesses (heroin, barbiturates), septicaemia , endocarditis and AIDS .

DRUG ABUSER DEATHS

Overdoses (by mistake/deliberate) of various drugs are the main cause of death in 'known' addict group (about 60% of the deaths). Large number of what seems to be 'natural causes' like renal failure, septicaemia, malnutrition, are possibly all drug related. Likewise, those due to accidents (fire, drowning) in drug addicts are related to the drug misuse. Death may occur due to an overdose of opioids and in the past Barbiturates.

INDIVIDUAL DRUGS OF MISUSE:

LSD

Lysergic acid Diethylamide (LSD) is psychotomometic. It produce symptoms similar to mental illness and therefore has to be considered in the differential diagnosis of any psychosis. Hoffman, manufactured it by chance in his laboratory. He experienced marked perceptual changes after accidentally inhaling the dust.

Chemistry:

All Ergot compound contain LYSERGIC ACID AMIDE and some natural compounds has similar pharmacological effects. Morning Glory has some of the potency of L.S.D - Lysergic Acid diethyl amide. The dose to produce subjective effects in human is as low as 1 microgram.

Fate of L.S.D

LSD is rapidly absorbed and distributed throughout tissues with highest concentration in the gut and liver and lower concentration in the brain.

Action:

LSD constricts peripheral blood vessels and thus potentiates the response to adrenaline by increasing blood Pressure. It also increases temperature and dilates the pupil - in the human (the degree of pupillary dilation correlates with the degree of psychological arousal). EEG and other studies suggest it increases SENSORY input to the RECTICULAR formation.

Psychological Effects include impaired concentration, hallucinations . LSD antagonises 5-HT (serotonin) both centrally and peripherally. This could cause hallucinations. However, several other 5-HT antagonists do not cause hallucinations, also we may find hallucinogenic action of a compound not dependent on 5-HT antagonism. It can only regarded that the mental state effects of L.S.D. are due to complex biochemical and physiological effects.

LSD users also experience 'Flash backs' in the form of recurrence of psychotic episodes which may persist for several months following L.S.D. use. LSD can be detected in urine by immunoassay.

Cannabis

Pharmacokinetics:-

Tetrahydrocannabinol (THC) the active substance in cannabis is absorbed and stay for some time in body stores. It is then converted into a psychically active metabolite. Further metabolism varies with species and there is no established animal model. In Humans, chronic use causes accumulation and the effects persist several weeks after cessation of consumption. Cannabis interferes with other drug metabolism and vice versa.

Effects:-

Cardiovascular effects: Cannabis use lead to increase in pulse rate and electrical functions of heart are changed. Carbon monoxide during smoking of cannabis decreases oxygen carrying capacity of the blood (as with tobacco smoking). Blood Pressure is lowered on standing, but this is not of therapeutic significance. Dilation of conjunction of blood vessels leads to a red eye.

Respiratory

Acute cannabis smoking may constrict bronchi on inhalation. There is no convincing evidence of short and medium term harm. In animal studies there are similar effects from tobacco and cannabis, but extrapolation to man is difficult.

Reproduction and Immunology

There is evidence of effect fertility in males.[1] This is based on Animal studies which have been inadequate in methodological control procedures. However, there is evidence of adverse effects.

Brain damage

Cerebral atrophy is not confirmed. Cannabis can lead to localised disturbance of electricity activity (in man and experimental animals). In animals:- ultramicroscopic changes in the brain were reported.

Psychiatric effects

Cannabis use can cause tolerance and withdrawal symptoms. The evidence is vague, although dependence syndrome may exist. Cannabis Psychosis is acute short lived psychoses which is reported with moderate dosage.

Chronic continuous cannabis use causes psychotic illness. Prolonged depersonalisation following Cannabis use. Experimental studies in normal volunteers and from clinical studies show acute cannabis intoxication which causes depersonalization and derealization.

Prolonged depersonalization is also reported with preservation of insight. Symptoms have temporal relationship to cannabis in absence of other psychiatric illness/drug abuse. Flashbacks occurs.

Cannabis is excreted over several weeks but that alone cannot explain persistence of flashbacks for over 1 year. Hence, we have to consider residual neurotoxic effects. Psychiatric sequelae following cannabis so far remain under-recognised.

BARBITURATES

Rarely used nowadays. They cause cause both physical and psychic dependence, Tolerance due to enzyme induction (leading to increased rate of metabolism of the drug) and cross tolerance for example with alcohol.

Withdrawal effects:

Anxiety, irritability, agitation, tremor, twitching, convulsions (in the absence of any underlying epilepsy), delirium, vomiting and nausea. Blood pressure is reduced (which may be slightly orthostatic) and pulse is increased in rate, sweating.

Prolonged heavy dosage lead to personality changes, persistent intoxication, labile effect, poor concentration, impaired judgement and motor in-coordination.

Overdose is dangerous. It may accidently happen when addicts attempt to prepare oral preparations for intravenous use (as with amphetamines).

Acute intoxication: leads to drowsiness which may progress to coma in particular when barbiturates are taken with alcohol. Temperature, pulse and heart rates are all decreased. Muscle flaccidity, nystagmus, ataxia, incoordination and dysarthria.

In chronic Intoxication (as with Alcohol), mood is variable, grasp impaired, with irritability and impaired judgment.

Treatment of Barbiturate Addiction:-

(a) Slow reduction of dosage to prevent fits

(b) Epanutin 100 mg. t.d.s.

(c) Valium

In order to withdraw an addict effectively from barbiturates, in-patient programme is required.

AMPHETAMINES

Under the Drugs Prevention of Misuse Act 1964, Possession of amphetamines is unlawful without prescription. By law, amphetamines are a class B drug (Schedule 2) but move up to class A if they are prepared for injection.

Amphetamines produce tolerance and psychic dependence, without physical dependence - some people can be withdrawn from large IV dosage of methylamphetamine (Methedrine) without physical withdrawal symptoms.

Stimulant activity on reticular activating system causes arousal. When the person is fatigued, performance may be improved under the influence of amphetamines. Mood is elevated and the person feels euphoric. When the effect wears off, the user develops unpleasant 'let down' feelings. It is the desire to relieve this let down feeling that leads to abuse.

Interactions:

Tricyclic and MAOI's potentiate amphetamines, barbiturates are nullified as regard hypnotic effects.

There is no indications to use amphetamines except in the following conditions: * Narcolepsy * Hyperkinetic hyperactive child (paradoxically, and again there is real risk of promoting adolescent dependence) * Nocturnal enuresis

There is a dangers of drug dependence and developing Amphetamine paranoid psychosis (consider this along with LSD as possible causes of organic psychosis). Amphetamine psychosis remits when the drug is withdrawn.

Apart from Indications mentioned above, there is no place for amphetamine prescription. GP’s are sometimes coaxed to prescribe for obesity, but this is contra-indicated.

AMPHETAMINE DEPENDENCE

When taken with barbiturates amphetamines produce euphoria, the same occurs with alcohol. The pre-morbid personality of user is characterised by instability and psychopathy. However, Dependence may follow prescription for depression or obesity. Overdose produce restlessness which may progress to delirium.

Amphetamine misuse should be differentiated from Mania or Hypomania. Dependence may result in organic psychosis with paranoid delusions and auditory hallucination. An important condition in the differential diagnosis is paranoid schizophrenia

Irresponsible and aggressive behaviour may occur under the influence of this drug and withdrawal may aggravate the paranoid features, or the depression.

KHAT (alkaloid cathinone)

The fresh leaves of khat bush have stimulating effect. They are grown in East Africa and Arabian peninsula. These leaves are chewed habitually, may be compulsively addictive. The risk is of some impairment of health and there is a possible economic loss in the form of cultivating the plant instead of crops for food and also the economic loss due lack of productivity of involved population in the countries concerned. Due to rapid air travel, the plant may be obtained fresh in UK by habitual users.

CNS stimulation is mainly due to the alkaloid cathinone, which is a 'natural amphetamine', with similar effects resembling those caused by amphetamines. Compulsive use lead to constipation (due to tannin effect), anorexia, mydriasis (dilatation of the pupils), insomnia, hypertension. On the other side, there is excessive energy, arrhythmias, excitation, euphoria, hyperthermia, and increased respiration. Cathinone is pharmacologically and chemically similar to amphetamine of which it is an analogue but it is more difficult to synthesise because it is a labile substance.

Animal experiments (in vitro) shows that it has the same mechanism of action as amphetamine. This is the dependence producing constituent of khat leaves. Monkey experiments show that its reinforcing effects equate with those of cocaine. Currently, UK use including trading is not illegal.

CAFFEINE

Caffeine along with alcohol and nicotine are the 3 most widely used psychoactive substances. Caffeine use may occur from childhood onwards. 80-200 mg may produce pharmacological effects which include mood elevation, alertness and clarity of thought, increased productivity and intellectual effort. It is also induce diuresis, increased gastric secretion, pulse rate and blood pressure.

Caffeine in Beverages:-

An average cup of tea or coffee contains 80-150 mg of caffeine which varies with brewing. There is a significant amounts of caffeine in cocoa, chocolate, soft drinks, over counter analgesics, common cold remedies, diuretics and patent stimulants. The caffeine content of some analgesic combinations and cold remedies is sometimes equivalent to that of patent stimulants.

Metabolism:-

Caffeine is absorbed from gastrointestinal tract and is rapidly distributed throughout tissues. Peak blood level is reached in 15-45 minutes. The plasma half-life varies between 3-10 hours and is reduced by smoking and increased by oral contraceptives and pregnancy up to twice the normal. In the Neonate, the half-life of caffeine is up to 80 hours as it has no enzymes responsible for metabolism.

Caffeinism:-

Caffeine intoxication may occur from 250 mg (DSM III, 1980). The picture simulates acute anxiety and is characterised by nausea, agitation and restlessness. euphoria is replaced by dysphoria when intake exceeds 600-700 mg per 24 hours (there is a wide individual variation). Features of intoxication include anxiety, mood disturbance and sleep impairment

Withdrawal features:

Withdrawal from caffeine causes restless, irritability and dizziness. There is diuresis and gastro-intestinal disturbance. The person complains of headache and insomnia. There is also arrhythmias and flushing. The anxiety state cannot be differentiated from caffeinism and may co-exist with it. Identification of Caffeine abuse is essential for accurate diagnosis of anxiety states, depressive illness, sleep disorder, anorexia and even psychotic disorder.

Interaction of caffeine and benzodiazepine:

Caffeine antagonises diazepam at electrophysiological and behavioural levels. Diazepam induced performance impairment is antagonised by caffeine at a dose of 250 mg. The anxiolytic effect of diazepam 10 mg is counteracted by 500 mg caffeine. Benzodiazepine sedative hypnotic effects is also antagonised by caffeine.

Summary

Excessive amounts of caffeine produce unpleasant symptoms. If over 600 mg is consumed daily, there is withdrawal period when caffeine us is suddenly stopped. Sources to be considered in diagnosis of caffeinism include coffee, tea, soft drinks and over counter medication for pain or headaches.

Caffeine withdrawal (from 600-1000 mg or more) causes severe headache, running nose, irritability, nervousness, drowsiness, depression, poor work performance. It is counterproductive to use caffeine containing analgesics for caffeine withdrawal headaches.

Caffeinism is considered in the differential diagnosis with anxiety, atypical depression, sleep disturbance, headache, poor response to minor tranquilisers and hypnotics. Diagnosis is confirmed by significant reduction of intake and return when challenged with caffeine.

COCAINE DEPENDENCE

Cocaine is a stimulating drug with sympathomimetic activity. Morphine and heroin addicts use it as an adjuvant. Cocaine is sniffed (hence nasal ulceration associated with peripheral vasoconstriction) or self-injected (Free basing). Its effects on the mental state include elation, increased energy excitement and hallucinations in the form of tactile hallucinations of insects crawling on the skin (formication). There is also signs of restlessness. Withdrawal effects are usually mild. Following the introduction of 1968 legislation, cocaine was very much less used. Recently, there is evidence for increase in its use, particularly in upper social classes and business world. 'Yuppies.

OPIATE DEPENDENCE

Opiates include a group of substances extracted from opium. Heroin (diacetylmorphine) is easily synthesized from morphine by a simple chemical process, while other opiate are industrially produced such as synthetic agents, for example methadone.

People particularly at risk are workers in medical, dental and nursing professions. Psychopathic and unstable personalities are also vulnerable. Opiates are administered by intravenous injection (the fastest route of drug administration), followed by smoking (heroin), suppository (anal or vaginal insertion), insufflation (snorting), and ingestion (swallowing). Analgesic and euphoriant properties predispose to dependence. Opiates lead to tolerance, physical and psychological dependence.

Coincidental hospitalisation of an addict may result in onset of withdrawal symptoms 12-48 hours later.

The Abstinence Syndrome

Onset of symptoms occur within a few hours of the last dose and peak in 24-48 hours, subsiding in 7-10 days. Clinical features appear in the form of anxiety, yawning, dilated pupils, restlessness, sweating, gooseflesh, tension, lacrimation, abdominal cramps, and running nose. Abstinence symptoms increase in degree over first 18-26 hours, during which time, sleeplessness, vomiting, respiratory rate increases, accompanied by twitching of muscles and anorexia. These effects are due to continued sympathetic and parasympathetic over-activity (release phenomenon). There is cross-tolerance within the opiate group.

Chronic use of opiate shows features such as chronic malaise, constipation, tremors, weakness, small pupils, impotence. Opiate dependence is often associated with amphetamine misuse, occasionally with cocaine nowadays.

Management of Opiate dependence:

This depends on motivation of the person. After hospitalisation which allow assessment of true degree of dependence, medication is useful during withdrawing from the opiate. The addict needs intensive support and group work.

Maintenance Methadone is used in the community. The interests and support of the caring person are considered. Role of the family, accommodation and rehabilitation is most important.

BENZODIAZEPHINE DEPENDENCE

1.25 million of UK population use benzodiazepines for more than 1 year. There is no evidence of long term effectiveness and they lead to psychological impairment and neurological changes. Normal maximum doses are between 30-45 mg in 24 hrs. A specific physical withdrawal syndrome appears following withdrawal of a normal therapeutic dose. For example using chlordiazepoxide 45 mg/24 hours (in divided doses) for 20 weeks followed by sudden withdrawal produces feelings of anxiety, tension, trembling, decreased appetite, faintness and dizziness. Withdrawal syndrome after cessation of normal dosage had the same clinical features as that following high dosage cessation. 15-45% of long term benzodiazepine users experience withdrawal syndrome.

Withdrawal features:-

There is increased sensory perception in the form of oversensitivity to sounds (hyperacusis), light (photophobia), pins and needles (paraesthesiae), sleepiness (hyperosmia) and hypersensitivity to pain. Sleep disturbance, headache, pain, muscle spasm and gastro intestinal symptoms occur. Anxiety withdrawal symptoms including choking sensation, dry mouth, hot and cold flushes, irritability, depersonalisation and derealisation also emerge. There is also insomnia (less than 3 hours of sleep) for up to 4 days then the sleep rhythm return to normal after 2 weeks.

Less common features of withdrawal are hand tremor, profuse perspiration, and headaches. Depression - if it occurs, is not prolonged. Psychological performance may suffer although motor co-ordination, which is ususally impaired before withdrawal will show improvement later.

Incidence of Benzodiazepine dependence and tolerance

Dependence: This is uncertain as some 12-20% of those commenced on benzodiazepines remain on them for some 6 months. Withdrawal symptoms appear at 6 months in 15-25% and after 1 year in 25-40%. After 7 years, the majority are physically dependent.

Tolerance: is uncommon. It occurs when a steady maintenance dose is used. Special stress may cause increase in the dose used which is not reduced later. Any signs of development of tolerance or increased dosage indicate dependence.

Withdrawal can be done on an outpatient or in-patient basis. It is better to try at the Drug Detox Unit or on out-patient basis or by GP. There is inadequate research to say which withdrawal procedure is optimal.

Out-patient detoxification is safe for most even long-standing normal-dose patients provided adequate medical supervision is available. The dose is reduced over 4 weeks. Relaxation and anxiety management, cognitive therapy and self help groups are useful, provided anticipation of problems is not augmented.

Pharmacology :-

Withdrawal symptoms are related to the rate at which circulating benzodiazepines and active metabolites are metabolised and excreted. Gradual withdrawal reduces the severity of withdrawal symptoms.

Long-term prospects of gradual withdrawal - (over one year)

One third of patients reported feeling well and no problems since completing withdrawal. One third expereinced some anxiety and depression and responded to anti-depressent. Overall, most patients were relieved. One third remained chronically anxious and they use alternative anxiolytics or returned to benzodiazepine. Abrupt withdrawal lead to a higher dropout rate.

Rate of withdrawal -

abrupt cessation is more likely to cause severe symptoms, including fits and confusional states. Tapering is more effective (Diazepam 0.5-2.5 mg). Opinions vary as to size of dosage decrement and duration of each stage. A 4-16 week programmes are described. Ideally, the practitioner titrates the dose against withdrawal symptoms by weekly reduction until first withdrawal signs appear, then delay the rate. Next decrement occurs when withdrawal signs are abated. Psychological aspects of dependence may respond in final stages to a placebo or taking final minuscule dose on alternate days/even less frequently. Sometimes withdrawal features do not occur until the final withdrawal.

Other medication are substituted. As long acting benzodiazepine is associated with less marked withdrawal features, It is used as a substitute for short acting benzodiazepine before starting withdrawal. Onset of withdrawal features is delayed by 2-5 days. However, incomplete cross tolerance by a substitute can itself cause withdrawal signs. Drugs used in withdrawal include clonidine (alpha 2 adrenoceptor agonist); propranolol which may reduce somatic symptoms, not psychological ones and antidepressant in cases of severe depressive episodes and as their sedative effects are helpful.

Prevention of Benzodiazepine dependency

Careful prescribing is essential. Lorazepam is responsible for 3 times the problems due to all other benzodiazepine combined, based on recent GP survey of 1500 NHS GPs. Duration of benzodiazepine prescription should be the shortest possible and the lowest possible dose used. Intermittent use is safer. Brief counselling by GP for minor affective problems is preferable to benzodiazepine use. Benzodiazepines should not be used for acute stress associated with traumatic life events, such as death, bereavement, and marital breakdown.

ANALGESIC ABUSE

Non opiate analgesic consumption has risen progressively since the late 1940's. Surveys in Australia and Western Scotland show that the majority of those taking analgesics infrequently use single drugs, e.g. aspirin or paracetemol. These are taken appropriately for pain or colds. Some 60-70% taking daily analgesics use compound tablets containing caffeine or codeine. These compound preparations are frequently taken inappropriately for insomnia, agitation and depression.

Analgesic nephropathy

Misuse of analgesics may cause kidney impairment. The pathological changes are papillary necrosis and chronic interstitial nephritis. This change is associated with the use of phenacetin, phenazone, caffeine and aspirin. It is controversial whether phenacetin or aspirin is most toxic in this respect. Both are potentially dangerous and nephrotoxicity is increased by their combination. More than 90% of those with analgesic nephropathy have used compound preparations. Self medicators always under estimate their intake. Analgesic nephropathy is a feature of dependence as is alcoholic cirrhosis.

Evidence of dependence is supported by continued consumption despite known medical risks and warnings and the use of caffeine and codeine containing preparations. Caffeine, codeine and phenacetin all have psychotropic effects potentiated in mixture or powder form. The development of dependence occurs gradually over several years in association with the analgesic effect, as well as the invigorating, stimulating and enhanced performance effects ensued. These secondary effects become obligatory. Attempts to stop may cause caffeine withdrawal symptoms such as headaches. Progressive anaemia and uraemia make the psychotropic effects more necessary in the abusers coping efforts.

Background of Analgesic Abusers

Those with analgesic nephropathy due to analgesic abuse were found to come from have disturbed families. They tend to smoke excessively; abuse alcohol; abuse other psychotropic drugs and have a high psychiatric morbidity. Their personality is characterised by passive, neurotic and introvert traits more than controls. Female psychiatric patients with chronic neurotic disorders, reactive depression and inadequate personality are prone to abuse analgesics.

Preventive Policies against Minor Analgesic Abuse:

Phenacetin is the common constituent of most nephrotoxic analgesic mixtures. Withdrawal of phenacetin from analgeisc combinations led to an apparent decline of analgesic nephropathy, but, renal function continued to deteriorate from non phenacetin containing analgesics. Paracetomol was substituted for phanacetin, although paracetemol is the major metabolite of phanacetin. Other manufacturers increased the dose of aspirin. Both paracetemol and aspirin are nephrotoxic in very large quantities. In animals, they potentiate each other's toxicity. The increased caffeine/codeine content stimulated the users's desire for continued and increased use.

SOLVENT SNIFFING

Solvent abuse can be fatal from indirect effects, either asphyxiation or inhaled vomit. Many substances are taken in solvent abuse such as dry cleaning fluids, petrol, aerosols. Sniffing is not a criminal offence.

CHIEF TOXIC CONSTITUENTS IN SOLVENT SNIFFING

  • Plastic (Styrene) Cements
  • Toluene, Benzene, Acetone
  • Model Cements
  • Toluene, Nephtha, Acetone
  • Nail Polish Remover
  • Acetone, Benzene, Alcohol
  • Lighter/Cleaning Fluid
  • Naphtha, Trichioroethane, Perchlorethylene

CHARACTERISTICS OF SNIFFERS

They are usually children and adolescents (8-17), mostly males rather than females (10:1). It is sometimes a group activity associated with truancy and rebellious behaviour.

SOLVENT SNIFFING

Polystyrene plastic glue vapours are inhaled in sufficient quantities to intoxicate. Vapours affect the brain causing dizziness, euphoria, grandiosity, recklessness and impaired consciousness

TREATMENT OF DRUG ABUSE

DRUG DEPENDENCE CLINICS

The management and treatment of Drug Abusers comprise a range of different approaches. Assessment of the patient is the first part of the process. Although not the most important element of treatment, prescribing a reducing or maintenance dose of drugs may be highly controversial and is undoubtedly a decision which should not be taken lightly or before careful review of the individual patient. Prescribing is initiated if thought appropriate. Some control drugs need to be notified.

Support and rehabilitation is provided by a community specialist nurse or a social worker, and sometimes a key caring person. Treatment programmes vary and include detoxification, methadone maintenance, drug free regimes and Narcotics Anonymous.

The overall problem of Drug Dependence must be considered in the context of general psychiatry and medicine and not regarded as being dealt with exclusively in Drug Dependence Clinics. Primary care must be closely involved together with statutory and voluntary community agencies.

In-patient treatment for Drug Abuse

Usually, those too severely dependent are unsuitable for out-patient care. One indication of severity is re-admissions. In the treatment of opiate dependence, Ghodse showed that 74% of opiate detoxification programmes were completed. This finding is similar to that of Gossop.

The Pattern of addiction has been altered. Benzodiazepine abuse replaced barbiturates. Benzodiazepines identified in urine of 60% of Drug dependence clinic outpatients and 76% of these were illegally obtained. A very high proportion of those admitted for sedative detoxification (benzodiazepines and a barbiturates) were dependent on opiates. Only some 25% of those describing regular benzodiazepine usage showed physical dependence. Some units insist on completion of sedative withdrawal programme because of the risk of fits.

In-patient programme goes into two phases:

(i) Drug withdrawal - mainly dealing with symptoms of withdrawal and physical illness.

(ii) Recovery, rehabilitation and future planning including the community links and back-up.

Due to inadequate facilities, self discharges occur during this phase due to resentment of restrictions such as being nursed on a closed ward. A high proportion of patients are successfully stabilised after withdrawal from the drug. However, this is only very much the first step as it is the case with alcohol detoxification for alcohol abusers. While community projects require support to the patient, so do inpatient programmes for the severely disturbed and physically ill.

Education on Drug Abuse

Rehabilitation programmes require a stated objective. Realistically, it has to be accepted that eradication of drug abuse through primary prevention is impossible to achieve. Therefore minimization of harm is sensible goal, that is to modify styles of drug use. While recognising ethical and valid objections, by clarifying treasonable use' the programme may be more effective by avoiding blanket rejection.

Reduction of harm is achieved by reducing frequency of use, changing to 'safer' substances, and change of route of intake. This is now highly relevant because of AIDS and the prevalence among drug users of sharing same syringes and needles. It is essential to assist people to develop the attitude necessary to handle 'factual information. That is to tackle deficiencies within the individual which predispose to drug abuse such as low self esteem, lack of personal skills, and interpersonal problems predisposing to peer group pressure. It is important to ensure development of drug free environment.

Relationship between IV drug abuse and high AIDS risk is complex. The rapid increase in intravenous drug abusers has been linked to cases infected with HTL V - III virus. Those who are not concerned regarding risk of infection are very few.

Some request screening despite fairly comprehensive self-acquired knowledge and some have avoided sharing needles. Others have changed their use to smoking or 'chasing'. The provision of disposable syringes is important. Intravenous drug abusers are the second highest risk group. Four strategies were suggested to manage this problem. The first is avoid starting the habit of misuse itself, however, this may be unrealistic.

Counselling and screening of existing addicts for HIV. Distributing free disposable syringes and offering treatment for dependence or HIV. Apparently, being sero-positive does not dissuade some patients from continuing IV abuse. Life style is not changed by counselling alone. At a drug advisory and treatment centre where seeing a doctor is not mandatory, the fear of contracting AIDS is not a motivating factor in seeking rehabilitation help. Addicts denial of seriousness of situation is reflected by a series reported by O'Connor with 43% seropositive patients attending a special programme for pregnant addicts becoming pregnant again despite counselling regarding dangers to health of further conception.