Substance‐related disorders

To the Editor: Cannabis use is implicated in serious social disruption in many Northern Territory Aboriginal communities.1 Rising levels of cannabis use were first reported in Aboriginal communities in Arnhem Land in 2002, along with associated concerns about escalating social impacts and mental health effects compounded by other substance use.2 A random sample of 164 people in Arnhem Land initially interviewed and assessed in 2004 were followed up between October 2005 and June 2006. Their cannabis use was measured using health worker assessments and self-reports from interviews. Ethical approval was granted by the NT Health Department, Menzies School of Health Research, and James Cook University. Despite a modest decline in cannabis use in this population between 2002 and 2004,3 the 2005–2006 data indicate persisting high rates, with 61% of males and 58% of females (aged 13–34 years) using cannabis at least weekly. In a subsample of 60 cannabis users opportunistically recruited for in-depth interviews in 2005–2006 (37 male and 23 female, aged 13–42 years), 92% of males and 78% of females used cannabis daily; 88% reported cannabis dependence symptoms. These figures appear to be far higher than national rates, although national data for similar age groups are not available.4,5 Research has found that, nationally, 6% of males and 3% of females (aged ≥ 14 years) reported using cannabis in the past week; 18% of males and 13% of females smoked cannabis daily;4 and 21% of adults (aged ≥ 18 years) using cannabis were dependent.5 Beyond high rates of cannabis use in Arnhem Land communities, we also found local characteristics and perceptions that illustrate the drug’s distinctive context of use (Box). Quantities of cannabis used appear to be higher than in the general population; unemployment among users is higher; and violence related to diminished supply is common. One Indigenous community leader described attitudes to cannabis use: “... if there’s a bowl of it on the table, it is smoked until gone, morning to night”. Interestingly, some respondents reported that using cannabis prevents them from engaging in criminal activity (Box). While key community members may believe that cannabis is a tool for social control — “good for calming down people” — they are increasingly recognising the significant social and mental health problems it causes: People get chained by [cannabis], they don’t go hunting with family ... lots of fights when they can’t get any ... [Cannabis] becomes the boss. Continued concerns about adverse mental health consequences for Aboriginal people in Arnhem Land who use cannabis seem to be warranted. Cannabis appears to be firmly entwined in these isolated communities in a manner not seen nationally. High levels of concurrent drug use, particularly tobacco, raise additional health concerns. Resources are urgently needed for prevention programs and targeted interventions for chronic cannabis users and those with psychiatric comorbidity. If these patterns of use continue, the implications for compounding of pre-existing mental illness and the potential mental health burden are disturbing. Characteristics and perceptions of cannabis use in Arnhem Land Aboriginal communities (57 males and 49 females, aged 13–42 years*) in 2005–2006 compared with available national data from 1997† and 2004‡ National4,5 Arnhem Land* National4,5 Arnhem Land* Number of cones smoked Per cent unemployed current users / daily users 3.2 (average per day)‡ 7.4 (average per occasion) 25.6%† / nd 60% / Males, 41%; females, 94% Concurrent drug use Motivations for use Alcohol (86.2%); stimulants§ (8.2%–27.9%); none (10.8%); analgesics (6.6%); antidepressants (5.7%); tranquillisers/sleeping pills (4.4%); other (3.9%)‡ Tobacco (100%); alcohol, restricted access (40%); kava (15%); petrol (5%)¶ nd Socialisation (tempted, lonely, copying friends); mood altering (“calms me down”, “gets me going in the morning”, “makes my mind straight”); drug substitution (from alcohol or petrol); prevents criminal activity (stealing or other trouble) Drug substitution (when cannabis unavailable) Motivations for ceasing/moderating use Alcohol (60.4%); no substitution (34.2%); ecstasy/designer drugs (1.3%); painkillers/ analgesics (0.8%); tranquillisers/sleeping pills (0.5%); heroin (0.3%); antidepressants (0.2%); cocaine/crack (0.1%); other (1.1%)‡ No substitution (83%); kava (7%); alcohol (5%); petrol (5%)¶ nd Limited supply; starting a family (females); “sick of fighting when cannabis runs out”; “made me sick”; “mind not straight”; expenses and time spent looking for cannabis; employment (males) * Self-report interview data from an opportunistically recruited sample (using age and sex quotas) of respondents, including people who had never used cannabis as well as current and former cannabis users. † People aged ≥ 18 years.5 ‡ People aged ≥ 14 years.4 § Including ecstasy. ¶ There have been no reliable reports of stimulant, benzodiazepine or barbiturate use in these communities. nd = data not available.

K S Kylie Lee · Alan R Clough · Katherine M Conigrave

Objective: To ascertain the beliefs of young people and their parents about the role of alcohol, tobacco and marijuana in the prevention and treatment of mental disorders.Design, setting and participants: Between May and August 2006, a national computer-assisted telephone survey was conducted on a representative sample of Australian youths aged 12–25 years. 3746 young people and 2005 of their parents were presented with a case vignette portraying psychosis, depression, depression with alcohol misuse, or social phobia in a young person.Main outcome measures: Participants’ beliefs regarding the role of substance use in preventing or dealing with mental disorders in young people.Results: Over 85% of participants agreed that alcohol, tobacco and marijuana were harmful for the young people in the vignettes, and over 80% of youths agreed that not using marijuana or drinking alcohol in excess would reduce the risk of developing a similar problem.Conclusion: Young people and their parents are fully aware of the negative impact of substance use on mental disorders. Translating this knowledge into behavioural change will be a major challenge for future public health campaigns.

Dan I Lubman PhD, FRANZCP, FAChAM · Leanne Hides BBehSc(Hons), PhD(Clin) · Anthony F Jorm PhD, DSc

Although early studies of hepatitis C indicated this is a serious disease, more recent evidence shows it can be relatively benign. A major determinant of hepatitis C prognosis is alcohol consumption. Promotion of alcohol abstinence among people with hepatitis C could result in substantial reductions in morbidity, mortality and treatment costs.

John M Duggan FRACP, FRCP, FRACMA · Anne E Duggan FRACP, MHP, PhD

To the Editor: Gibson et al provide us with five cases of fatal drug overdose in an article titled “Opioid overdose deaths can occur in patients with naltrexone implants”.1 Three of these people did not have an active naltrexone implant — two of the deaths occurred 6 months after implant insertion (which is the outer limit of the longest duration implant available), and the implant had been removed from the third person. This leaves only two cases. In one of these, the cause of death was combined non-opioid drug toxicity, including amphetamine and a cocktail of other drugs, where opioids were not present. Obviously, naltrexone, an opioid antagonist, will not protect against non-opioid drug overdose. Clearly these four cases should never have been included under the title “Opioid overdose deaths can occur in patients with naltrexone implants” (our italics). That leaves a single fatal opioid overdose in a patient who had an active implant, and in which the cause of death was acute narcotism, where the individual had injected heroin. Here at last is a case study that should be included, and the authors note that the effects of naltrexone can be overcome, and alert us to the danger of using excess heroin to overcome naltrexone blockade. However, this information is less than new. MIMS annual notes under “Attempts to overcome [naltrexone] blockade”: While . . . [naltrexone] is a potent . . . [opioid] antagonist . . . the blockade produced . . . is surmountable . . . [and] poses a potential risk to individuals who attempt, on their own, to overcome the blockade by administering large amounts of exogenous opioids. Indeed, any attempt by a patient to overcome the antagonism by taking opioids is very dangerous and may lead to a fatal overdose . . . Patients should be told of the serious consequences of trying to overcome the opiate blockade.2 It is also surprising that no denominator is attempted on the number of patients who may have received treatment by implanted naltrexone between 2000 and 2004. This information is available through the Therapeutic Goods Administration, and would have given the reader a clearer ability to evaluate the significance of this single case study. For example, one of the articles they cite reports one fatality in nearly 600 person-years of follow-up,3 giving a very different impression of risk compared with the article by Gibson and colleagues.

Gary K Hulse · Robert J Tait

To the Editor: I read with interest the article by Gibson and colleagues,1 who purport to have evaluated the claim that naltrexone “prevent[s] relapse to opioid use and therefore fatal opioid overdose”. The article fails in its stated intent, as it neglects to provide adequate context and comparison in its evaluation of the five deaths between 2000 and 2004 identified through Australia’s National Coroners Information System. The significance of the data cannot be assessed, as the authors omitted the number of naltrexone implants made available through the Therapeutic Goods Administration Special Access Scheme and comparison with other opioid users. This is extraordinary, given the high risk of death in this group both in and out of treatment.2 Of the five cases identified, three people no longer had active naltrexone implants and therefore could not be used to support the title “Opioid overdose deaths can occur in patients with naltrexone implants” any more than recurrence of depression can be attributed to previous antidepressant treatment. The remaining two deaths involved polydrug use, a known risk factor in overdoses;3 naltrexone did not prevent death, but no clear causation was established. In summary, this article was about two deaths among an unspecified number of naltrexone implant users across Australia over a period of 4–5 years, and it overlooked comparison with other opioid users, including those in the accepted gold-standard treatment, methadone maintenance. From the data presented, it is impossible to determine if the implant was associated with an increased or decreased risk of fatal overdose. A previously raised valid concern is the risk of overdose following all abstinence-based treatments.4 Post-treatment outcomes from randomised controlled trials with naltrexone implants are needed to quantify this risk. Despite the inadequacies described above, this article was published in a prestigious Australian medical journal, with a title linking opioid overdose with naltrexone, yet lacking the scientific basis for this association. Medical practitioners have limited time, frequently scan titles and abstracts, and rely on editors to provide summarised information based on scientific rigour.5 Perhaps a more accurate title would have been “Two cases with naltrexone implants among X number of opioid-related deaths between 2000 and 2004”.

Moira G-B Sim

To the Editor: As one of the first clinicians to use naltrexone implants (in 1997) and author of two references cited by Gibson et al,1 I wish to comment on their article. In writing that “Treatment with implanted naltrexone has been claimed to prevent . . . fatal opioid overdose”, Gibson et al imply that this claim is untrue, or that anything less than total prevention is not useful. Lowest conventionally effective blood naltrexone levels (1–2 ng/mL) may indeed fail to block opioids, but such instances are extremely uncommon. (In any case, even after 100 mg of supervised oral naltrexone, trough naltrexone levels after 24 hours can be no higher than that.2,3) An article describing three cases of implant breakthrough is in preparation; 4.3 ng/mL was insufficient to prevent obvious opioid effects after one patient smoked about 80 mg of diamorphine equivalent.4 The other cases involve much bigger opioid doses. However, higher naltrexone levels would almost certainly provide adequate blockade. Many patients test out the blockade soon after implantation5 and while “pseudo-breakthrough” is occasionally seen,2 true breakthrough with heroin or methadone is, I must stress, very rare. Gibson et al cite my report that modest naltrexone levels can block 500 mg of pure diamorphine (an enormous dose).3 They cite no reports of opioid receptor immunity to blockade by naltrexone. Therefore, unlike many drugs, naltrexone probably always does what it says on the packet. Accordingly, it follows that naltrexone implants can indeed prevent opioid overdose deaths, in the same sense that thyroxine prevents hypothyroidism. In all cases, adequate blood levels are important, and some patients, for various reasons, need more than average doses to achieve them. Gibson et al’s article may be an argument for therapeutic drug monitoring or opioid challenge,3,4 but not for therapeutic gloom. Finally, details of all known coroner-linked “active” implant deaths in Western Australia have already been presented.6 None appeared to be opioid-related; suicide, homicide, medical conditions and non-opioid overdoses caused them. Gibson et al report one apparently certain opioid overdose death despite an unprecedentedly high blood naltrexone level. This is puzzling, but postmortem opiate levels are notoriously misleading,7,8 and the same may be true for naltrexone. Little is known about naltrexone disposition after death, perhaps because, unlike opioids, naltrexone is very rarely found in dead heroin addicts. In contrast, of the small proportion (27%) of patients actually completing a 28-day British inpatient opioid withdrawal program and thus losing their opioid tolerance, 10% died within a few months from resuming heroin.9

Colin L Brewer

To the Editor: Gibson and colleagues recently reported opioid overdose deaths occurring in patients with naltrexone implants.1 The article is of great clinical significance, identifying that patients can override the effect of naltrexone and experience fatal opioid toxicity. However, it fails to address some important clinical and forensic issues that the five deaths highlight. Firstly, it is disappointing that patients could be known to have been on naltrexone and not had naltrexone levels measured during the postmortem examination process. The absence of data compromises a full understanding of the circumstances leading to death. In an “evidence-based medicine” society, it should no longer be acceptable that drug screening in coronial cases be restricted to drugs that have been measured for many years. Given the increasing use of a much wider range of drugs than has previously been the case, I suggest that all postmortem examinations on drug-using patients now include the measurement of naltrexone, if there is any history of naltrexone use, and buprenorphine, whether the patient is known to be on buprenorphine treatment or not. To this could be added the need to test for para-methoxyamphetamine and ecstasy. The article also fails to comment on the level of clinical care provided to these patients. That a patient can be found to have, as well as naltrexone in their bloodstream, a variable combination of codeine, alprazolam, methamphetamine, propranolol, diazepam, amisulpride and morphine suggests that these patients were not necessarily being monitored or managed as well as they might have been. This point is stressed because the role of naltrexone in the treatment of opioid dependence is often questioned based on a higher rate of death in patients on this drug compared with those on methadone or buprenorphine.2 If used as recommended by national and state guidelines in a program of abstinence maintenance with appropriate monitoring, acceptable outcomes can be achieved.3 Patients who use other drugs while on naltrexone are demonstrating a degree of instability requiring active clinical intervention. Perhaps the more important point this article raises is the need for close supervision and appropriate clinical response to instability, rather than the fact that heroin can override the effects of naltrexone at the opioid receptor.

Robert G Batey

To the Editor: On the basis of five coroners’ reports, Gibson et al warn of dangers connected to the use of naltrexone implants.1 Two of the deaths occurred after the expected lifetime of the implant, a third after the implant had been removed, and a fourth was partially attributed to naltrexone by the coroner without detailing any physical evidence. Only the fifth case had the potential to support the authors’ claims, with both a relatively high level of naltrexone and opioids present in the blood at the time of death. Still, as toxicological tests showed not only a high level of heroin, but also stimulants and benzodiazepines, the cause of death in this case is open to debate. Some further comments seem appropriate. First, despite 30 years of scrutiny, systematic reviews find no support for claims of lethal side effects of naltrexone.2 One coroner claiming otherwise in one death does not constitute evidence to the contrary, especially as no further physical evidence was presented. Second, any discontinuation of a lifesaving medication is followed by a period of increased vulnerability. This is a problem naltrexone treatment shares with all treatments for this group,3 and indeed with most other medications designed to protect against premature death. In opioid addiction, patients die from overdose, and if their medication is discontinued, a larger proportion will do so. If prospective studies prove that opioid overdose can occur during naltrexone implant treatment, it would only be advisable to restrict the use of implants if the death rate proved higher than similar rates in maintenance treatment. Third, in the absence of high-quality evidence, authors will have to make logical arguments as to why they prefer one explanation over the alternatives. However, Gibson et al did neither, even though alternatives are readily available in the literature; for example, it is well known that sudden and unexpected death can occur as a consequence of the use of recreational doses of non-opioid drugs.4 We agree that great care needs to be taken to prevent overdose after the discontinuation of naltrexone medication, and agree that there is insufficient documentation to conclude on the safe lower limit for a protective naltrexone serum level. But to draw valid conclusions beyond that requires the direct and prospective observation of a large number of implant patients, or a review of such studies.

Nikolaj Kunøe · Helge Waal

To the Editor: Gibson et al confidently conclude that the “clinical implications are clear: patients can die from an opioid overdose while undergoing naltrexone implant treatment”.1 The obvious implication from this statement and the general tone of the article encourages the reader to believe that naltrexone implants are somehow directly associated with opioid deaths. However, more questions than answers are raised by the article. Five deaths were listed involving implantable naltrexone. Male 1 died of “acute narcotism”, but do the authors believe this case demonstrates that the naltrexone implant used was implicated in the death? In the female case, the authors state that “Naltrexone was viewed by the coroner as playing a causal role in the death”, but did the “numerous medications” and her “depression” also make a causal contribution to this death from a “combined drug effect”? The authors freely admit that the deaths of Males 3 and 4 “cannot be definitively linked to the naltrexone implant treatment” and their causes of death were “multiple drug toxicity”, so why were these cases included? In addition, these men had their naltrexone implants removed 6 months previously. Male 2 had his naltrexone implant removed 2 weeks before his death. Of the five cases cited, it seems that only one actually died of an opioid overdose in the presence of a naltrexone implant. Readers will agree with the authors that a risk of fatal opioid overdose exists in heroin or opioid users with and without treatment, regardless of the type of treatment chosen, and that medical professionals should provide balanced information to their patients. The community has strong feelings about the philosophy of treatments available for substance misuse. Therefore, as health professionals, it is important to ensure that what we write is not based upon personal beliefs and that facts are presented in an objective and independent manner. However, it seems that Gibson et al are providing, at best, poorly interpreted science and, at worst, speculation and alarmist rhetoric.

Eric Khong · Winston Choy

In reply: We agree with Hulse and Tait, Brewer, Kunøe and Waal, and Sim that we need comparisons of mortality between naltrexone, other therapies such as methadone and buprenorphine, and heroin users outside of treatment. We have such a study in press.1 The point of our article was made simply in our title: opioid overdose deaths can occur during naltrexone implant treatment. This is important information because some doctors have advocated the coerced use of these implants on the unproven assumption that overdose deaths cannot occur in patients with these implants.2,3 Our cases were obtained from the National Coroners Information System (NCIS), and Khong and Choy, and Hulse and Tait are correct: only two deaths occurred during naltrexone implant treatment. Cause of death was reported exactly as recorded by experienced professionals: the pathologist who conducted the autopsy in one case, and a pathologist and the coroner in the second case. Both deaths were attributed in part to naltrexone. We agree with Kunøe and Waal that care needs to be taken to avoid deaths occurring after naltrexone discontinuation: the three deaths out of treatment were included to highlight this period of increased risk after naltrexone implant cessation, as has been documented after cessation of oral naltrexone.4 Batey is correct when he points out the importance of good clinical care accompanying naltrexone implant treatment. As naltrexone implants are not currently registered, we lack clinical guidelines regarding their use. Unfortunately, the NCIS does not routinely report clinical information, so we could not ascertain the level of psychosocial support being provided to the patients who died. We agree with Sim, Batey, and Brewer that Australia needs therapeutic drug monitoring and studies of in-treatment and post-treatment mortality outcomes from randomised controlled trials of naltrexone implants. Indeed, in publishing these cases, it was our intention to highlight the need for such studies. We think it unacceptable that more than 1000 Australians have been given these implants5 with little evidence of their safety and efficacy from randomised controlled trials or any systematic monitoring of their safety. Naltrexone has been implanted using special provisions under the Therapeutic Goods Administration on the grounds that the implants allegedly prevent fatal opioid overdoses. There is little evidence to support this claim, and the cases that we reported show that such deaths can occur. Scheduling of naltrexone, routine postmortem testing for naltrexone in suspected patients, and maintenance of national databases of naltrexone recipients would assist in investigating the full extent of the risks associated with naltrexone implant treatment.

Amy E Gibson · Louisa J Degenhardt · Wayne D Hall

Australian prisons have been identified as a focus of the ongoing hepatitis C epidemic. Harm minimisation is the major strategy directed to community-based public health measures to control hepatitis C. Harm-minimisation strategies to protect inmates and workers are incompletely and inconsistently applied in Australian prisons. Overseas experience has demonstrated that introducing injecting-equipment exchange programs and professional tattoo parlours in prisons could at least partially reduce the risks of ongoing hepatitis C transmission, and would support prevention and treatment programs. A two-stage approach is suggested: firstly, implementing programs of proven effectiveness consistently across the eight Australian jurisdictions, and, secondly, expanding current initiatives in the light of international “best practice”.

Michael H Levy MB BS, MPH, FAFPHM · Carla Treloar BSc(Hons), PhD · Rodney M McDonald BAppSc · Norman Booker GradDipAdultEd

To the Editor: Single case reports of “meth mouth”, similar to that recently published in the Journal,1 exaggerate the dental problems surrounding the use of methamphetamines. Evidence that methamphetamines cause grinding and wear of teeth,2 xerostomia,3 and cravings for sweet drinks is weak. The drug use reported by Shetty was intravenous or intranasal, not oral. While systemic effects may contribute to dental problems, local oral effects associated with acidity of methamphetamines would be minimal with intravenous or intranasal drug use. A more plausible explanation for dental disease may be the years of neglect, trauma and poor diet experienced by many people who use drugs.4 Many drug users begin using as early as 14 years of age and consume multiple illegal psychoactive and legal antipsychotic and antidepressant medications associated with xerostomia. A comprehensive drug-use history is required before dental problems are attributed to one drug. Advising treating dentists to avoid the use of analgesics is misinformed and potentially leaves patients in severe pain unnecessarily. People affected by methamphetamines are unlikely to seek dental or medical treatment. A more likely scenario is presentation because of pain between methamphetamine binges, or presentation when they are taking stock of their health problems. At such times, they are unlikely to be affected by methamphetamines, which generally have short half-lives. At these times, non-steroidal anti-inflammatory drugs, nitrous oxides, narcotics (including codeine) or increases in methadone dose may be needed to manage pain. Analgesic depressants are not contraindicated unless other illicit or licit depressants are being used concurrently, as depressants work on different receptors and areas of the brain than amphetamine-type stimulants. Careful discussion with the patient and the patient’s general practitioner or alcohol and drug specialist is critical in balancing the need for pain relief with the potential for drug interactions and even overdose, if the patient is taking other depressants (legal or otherwise). Practitioners can contact a 24-hour drug information line for health professionals for information of this kind in most Australian states and territories (Box). Drug information contact numbers Service Contact number DACAS (VIC) 1800 812 804 DACAS (TAS) 1800 630 093 DACAS (NT) 1800 111 092 DASAS (NSW) 1800 023 687 or (02) 9361 8006 ADIS (SA) 1300 131 340* CAS (WA) 1800 688 847 or (08) 9442 5042 ADIS = Alcohol and Drug Information Service. CAS = Clinical Advisory Service. DACAS = Drug and Alcohol Clinical Advisory Service. DASAS = Drug and Alcohol Specialist Advisory Service. * Clinicians should ask to be put through to the duty doctor service.

Anne-Marie L Laslett · John N Crofts

It is well accepted that heavy alcohol consumption during pregnancy is a risk factor for fetal alcohol spectrum disorder, but research findings for exposure to low to moderate alcohol levels during pregnancy are equivocal, allowing a range of interpretations. The 2001 guideline from the National Health and Medical Research Council (NHMRC) for low-risk drinking for “women who are pregnant or might soon become pregnant” recommends fewer than seven standard drinks per week, and no more than two standard drinks on any one day. This position has polarised health professional and consumer opinion in Australia. The NHMRC guidelines on alcohol are scheduled for review in 2007. We surveyed the alcohol and pregnancy policies and clinical practice guidelines of Australia and six other English-speaking countries to identify current policy. Documents were obtained through Internet searches and direct contact with the relevant organisations. The policies and guidelines varied both across and within countries, and the NHMRC guideline, while not universally supported in Australia, is in step with the policies of the United Kingdom and Canada. Research is needed to elucidate the true association between low to moderate alcohol consumption and fetal harm, the impact of different policies on rates of maternal alcohol consumption during pregnancy, and any untoward outcomes of an abstinence message, to inform and underpin future policy development in Australia.

Colleen M O'Leary BSc, MPH · Louise Heuzenroeder BN, MBA, MPH, MHlthSc · Elizabeth J Elliott MD, FRACP, FRCP, FRCPCH · Carol Bower PhD, FAFPHM, DLSHTM

Objective: To describe the prevalence, characteristics and outcomes of amphetamine-related presentations to a tertiary hospital emergency department (ED).Design, setting and participants: Prospective observational study of amphetamine-related presentations to the ED of the Royal Perth Hospital (RPH), an adult, inner-city, tertiary referral hospital, between 3 August and 2 November 2005. For all patients presenting to the ED, the treating doctors were automatically prompted by the computerised data entry system to consider amphetamine use.Main outcome measures: Proportion of ED presentations related to amphetamine use; demographic features and usage practices of amphetamine users; characteristics of presentations and admissions; associated psychiatric illnesses and use of other drugs.Results: Over the study period, there were 13 125 presentations, of which 156 (1.2%) were judged to be causally related to amphetamine use. Of those 156 patients, over half were habitual drug users (89 [57.1%] used amphetamines at least weekly), and the majority were men (111 [71.2%]). The mean age was 28 years (range, 16–55 years). Presentations were of high acuity: 104 patients [66.7%] were rated 1, 2 or 3 on the Australasian Triage Scale; 50 (32.1%) arrived by ambulance; and 25 (16.0%) arrived with police. The mean time spent in the ED was 6 h (range, 0.5–24 h). Fifty patients (32.1%) required sedation, and the likelihood of requiring sedation increased almost threefold if the heart rate was over 100 beats/min on presentation. Sixty-two patients (39.7%) were admitted and 58 (37.2%) required psychiatric evaluation. Repeat attendance was common, with 71 patients (45.5%) having previous amphetamine-related presentations to the RPH ED.Conclusions: Amphetamine-related presentations comprise 1.2% of all ED attendances and have a major impact on hospital EDs. Patients are often agitated and aggressive, require extensive resources, and frequently re-attend. The burden of amphetamine-related illnesses on EDs is likely to increase in the future.

Suzanne D Gray MB BS · Daniel M Fatovich MB BS, FACEM · David L McCoubrie MB BS, FACEM · Frank F Daly MB BS, FACEM

Objective: To examine trends in hospital separations related to “drug-induced” psychosis for cannabis and methamphetamine, in the context of patterns of cannabis and methamphetamine use in the Australian population.Design and setting: Analysis of prospectively collected data from the National Hospital Morbidity Database on hospital separations primarily attributed to drug-induced psychosis (July 1993 – June 2004), and specifically for cannabis and amphetamines (1999–2004). Calculation of Australian population-adjusted rates of drug-induced psychosis hospital separations using estimated resident population data from the Australian Bureau of Statistics (at 30 June each year) and data on cannabis and methamphetamine use from the 2004 National Drug Strategy Household Survey.Main outcome measures: Number of hospital separations due to drug-induced psychosis, and standardised (age-specific) rates per million population and per million users.Results: There have been notable increases in hospital separations due to drug-induced psychosis, which appear to have been driven by amphetamine-related rather than cannabis-related episodes. The rate of hospital separations was higher for amphetamine users than for cannabis users in all age groups, and the rate increased among older amphetamine users.Conclusions: The risk of hospitalisation for a drug-induced psychotic episode associated with amphetamine use appears to be greater than that for cannabis use in all age groups.

Louisa Degenhardt PhD, MPsych(Clinical) · Amanda Roxburgh BA(Hons)Psych, MCrim · Rebecca McKetin PhD

Objective: To review homicides committed during psychotic illness in New South Wales over 10 years from 1993 to 2002.Design and setting: Case series of all known homicides committed during psychotic illness in NSW, taken from reports of psychiatrists submitted in proceedings in the Supreme Court of NSW.Main outcome measures: Demographic and clinical features of perpetrators; estimated frequency of homicide during psychotic illness.Results: In the 10 years from 1993 to 2002, there were at least 88 people charged with 93 homicide offences committed during the acute phase of mental illness. High rates of drug misuse, especially of drugs known to induce psychotic illness and brain injury, were reported. Evolving auditory hallucinations and delusional beliefs that led the person to believe they were in danger were the symptoms strongly associated with lethal assault. The victims were mostly family members or close associates. Only nine of the victims were strangers, including three fellow patients. Most lethal assaults (69%) occurred during the first year of illness, and the first episode of psychotic illness was found to carry the greatest risk of committing homicide.Conclusions: People in their first episodes of mental illness should be considered to be at greater risk of committing serious violence than those in subsequent episodes. Illicit drug use, a history of brain injury, auditory hallucinations and delusional beliefs of immediate danger were particularly associated with lethal assault.

Olav B Nielssen MB BS, MCrim, FRANZCP · Bruce D Westmore MCrim, FACLM, FRANZCP · Matthew M B Large BSc(Med), MB BS, FRANZCP · Robert A Hayes LLB, PhD

From Australian coronial records, we identified five deaths involving implantable naltrexone between 2000 and 2004. One man died from acute narcotism with a naltrexone implant in place and a blood naltrexone level of 0.3 mg/L. A woman died of combined drug effect (including naltrexone) accompanied by severe pain from a naltrexone implant site. These cases indicate that patients can die from opioid overdose with a naltrexone implant and blood naltrexone levels higher than reported blockade levels. Clinical recordsTreatment with implanted naltrexone has been claimed to prevent relapse to opioid use1-3 and therefore fatal opioid overdose.4,5 We evaluated this claim by examining a series of deaths related to implanted naltrexone in the treatment of opioid dependence identified through Australia’s National Coroners Information System (NCIS). This research was approved by the University of New South Wales Human Research Ethics Committee and the Monash University National Centre for Coronial Information. The NCIS database provides access to all coronial cases in Australia, and is likely to capture most opioid-related deaths. Each database record is linked to available documents, including coronial finding, autopsy, toxicology and police reports. Naltrexone-related deaths were determined by searching for the keyword “naltrexone”. All closed cases were searched in December 2005 for deaths occurring between 2000 and 2004 inclusive. Ninety-one records were identified containing the keyword, of which five involved an implantable form of naltrexone (Box). The average age of the five people was 26 years (range, 22–32 years). Naltrexone was detected at autopsy in two and not tested for in the remaining three. All five deaths were related to the use of drugs. Two deaths occurred while undergoing naltrexone implant treatment, one shortly after naltrexone implant removal, and two about 6 months after insertion of an implant. In these last two cases, it is not known whether these people received an implant designed to last 6 months, or if shorter-acting implants were used. Both types are available in Australia.5 Blood concentrations of naltrexone were quantified in two cases. Male 1 died of acute narcotism with 0.3 mg/L total (0.2 mg/L free) naltrexone and 0.05 mg/L total (0.03 mg/L free) naltrexol detected. Heroin (as morphine and codeine) was the only other drug detected in toxic levels, and the autopsy report specifically highlights the danger of using excess heroin to overcome the blockade given by the active naltrexone implant. The only woman among the five people died of a combined drug effect, including naltrexone. Soon after the insertion of a naltrexone implant and 2 days before her death, she began to experience strong pain from the implant site (abdomen). She used methamphetamine the day before her death and was discovered by her carer to be delirious, in severe pain and clutching her abdomen on the morning of her death. Her blood levels of free naltrexone and naltrexol were 0.004 mg/L and 0.035 mg/L respectively, close to reported “therapeutic” levels.6 Naltrexone was viewed by the coroner as playing a causal role in the death. DiscussionNaltrexone is an opioid antagonist that acts to inhibit the effects of opioids,7 and is used for treating opioid dependence. Non-compliance with naltrexone is common, and is usually followed by relapse to heroin use,8 with a substantially increased risk of fatal overdose.9 Implanted forms of naltrexone have been advocated to reduce non-compliance.1,10 These devices are not currently registered in Australia, but can be accessed through the Therapeutic Goods Administration Special Access Scheme.2,4 In this series of deaths in people treated with naltrexone implants, we have identified a case of fatal opioid overdose with detectable post-mortem levels of naltrexone. The blood level of naltrexone (0.3 mg/L = 300 ng/mL) was several orders of magnitude higher than the 2.8 ng/mL previously reported to block 500 mg doses of pure diamorphine11 or the 2.4 ng/mL reported to completely antagonise 25 mg of heroin.12 Blood naltrexone levels of 1–2 ng/mL are commonly quoted as being sufficient to offer protection from fatal opioid overdose.6,13 The case of Male 2 highlights the risks of opioid overdose after chronic naltrexone treatment. The deaths of Males 3 and 4 by multiple drug toxicity 6 months after insertion of their naltrexone implants cannot be definitively linked to the naltrexone implant treatment, as it is not known if they were using long-acting (6-month) implants. In Male 4, the possible relationship between the naltrexone implant and the subject’s higher risk of opioid overdose death was noted by his doctor in the coronial finding. The likely under-detection of oral naltrexone-related death through the NCIS database has been previously reported,14 and naltrexone implant-related deaths might be even more under-reported. Naltrexone implants are highly likely to be overlooked at autopsy, unless the pathologist had prior knowledge of their presence (Associate Professor J Duflou, Chief Forensic Pathologist, New South Wales Department of Forensic Medicine, Sydney, personal communication). For this reason, this case study should not be used to estimate the naltrexone implant-related death rate in Australia. The clinical implications are clear: patients can die from an opioid overdose while undergoing naltrexone implant treatment with blood naltrexone levels higher than reported “blockade” levels. Although the risk of fatal overdose is probably reduced in naltrexone implant treatment, a risk still exists. Medical professionals have a duty to consider the risks of naltrexone implant treatment and to warn patients of the possibility of opioid overdose death during compliant naltrexone implant treatment as well as after treatment cessation. Details of deaths in people with naltrexone implants listed in the National Coroners Information System, 2000–2004 Case Cause of death* Substances detected post mortem† Comments Male 1 Acute narcotism Naltrexone 0.3 mg/L total (0.2 mg/L free), naltrexol 0.05 mg/L total (0.03 mg/L free), morphine 1.9 mg/L, codeine 0.2 mg/L, alprazolam < 0.1 mg/L, methamphetamine < 0.1 mg/L, benzoylecgonine 0.09 mg/L Autopsy reports the danger of using excess heroin to overcome naltrexone blockade. Had a current naltrexone implant (small scar and 10 naltrexone tablets in left groin). Female Combined drug effect (amphetamine, naltrexone, propranolol, doxepin, diazepam, paracetamol) Naltrexone 0.004 mg/L free, naltrexol 0.035 mg/L free, methamphetamine 1.2 mg/L, amphetamine 0.07 mg/L, propanolol 0.7 mg/L, doxepin 1.1 mg/L, desmethyldoxepin 0.7 mg/L Worsening stomach pain near recent naltrexone implant site for 2 days before death. Also had depression and had been prescribed numerous medications. Male 2 Multiple drug toxicity (heroin, diazepam) Naltrexone not tested, morphine 1.9 mg/L, codeine 0.2 mg/L, diazepam 0.3 mg/L, nordiazepam 0.5 mg/L, amisulpride 0.5 mg/L Naltrexone implant was removed 2 weeks before death for unknown reasons. Male 3 Mixed drug toxicity (heroin, codeine, diazepam) Naltrexone not tested, morphine > 15 mg/L (urine), codeine 11.2 mg/L (urine), diazepam trace, nordiazepam 0.1 mg/L Naltrexone implant 6 months previously.‡ Male 4 Combined drug toxicity (heroin, alcohol and diazepam) Naltrexone not tested, ethanol 0.04 g/100 mL, morphine 0.2 mg/L free, codeine 0.06 mg/L free, diazepam 0.4 mg/L, nordiazepam 0.5 mg/L Naltrexone implant approximately 6 months earlier with scar.‡ Doctor who inserted implant noted that after implant his opioid tolerance would have been low and the risk of opioid overdose high. * Causes of death were recorded directly from findings or autopsy documents. † Substances were detected in blood unless otherwise specified. ‡ Some naltrexone implants available in Australia are claimed to provide “effective” blood naltrexone levels up to 6 months after implanting.4 Without reported blood naltrexone levels we cannot be certain of the duration of action of these implants, as shorter-acting implants may have been used.

Amy E Gibson MPH, BSc(Hons), BA · Louisa J Degenhardt PhD, MPsychol(Clinical), BA(Hons) · Wayne D Hall PhD, BSc

Getting the message right will help the public reduce their risk of mental illness In the 2006–07 budget, the Australian Government announced expenditure of $21.6 million over 4 years to improve community awareness of the link between using illicit drugs and the development of mental disorders. Community awareness programs to reduce the prevalence of unhealthy behaviours are nothing new; they have been around for decades for cancer, heart disease and infectious diseases. While campaigns focusing on the negative effects of drug misuse have already been delivered, this initiative breaks new ground. It will be the first large-scale campaign in Australia to tell the public what actions they can take to reduce their risk of developing mental disorders. Australia is not alone in this area, with both France and the United States launching campaigns in 2005 to alert the public to the potential link.1,2 However, it is too early to know whether these campaigns have had any effect. Probably the main reason that there have not been earlier campaigns on how to reduce the risk of mental disorders is a lack of evidence for causal links. How good then is the evidence that illicit drugs cause mental disorders? First, there is substantial agreement that an association exists between early onset of cannabis use and later psychotic symptoms or disorder,3 but there is ongoing disagreement regarding the causal basis of this association.4 Clearly, cannabis use is “neither a sufficient nor necessary cause for psychosis”,3 but it may “unmask” psychotic disorders in individuals who are vulnerable. The timing of drug exposure may be particularly critical here, especially given recent evidence that a specific polymorphism of the COMT (catechol-O-methyltransferase) gene conveyed increased risk of later psychosis only if cannabis was consumed during adolescence.5 Second, a number of studies have reported a modest association between early onset of regular cannabis use and later depression, although further research is required to determine whether this relates to a direct causal role or common psychosocial factors.6 The evidence implicating other illicit drugs is more limited. Methamphetamine, which is rapidly growing in popularity in Australia, has been consistently associated with a transient psychotic state that is more common in people dependent on this drug.7 A growing body of literature suggests that a significant minority of those regularly using methamphetamine are also at risk of more entrenched patterns of psychosis.8 While there is currently limited evidence of a direct causal relationship between illicit drug use and mental disorders, the issue becomes whether we can afford to wait and see if increasing early use of illicit drugs actually does lead to a rise in the incidence of mental disorders. If a community awareness campaign is to be effective, it needs to be appropriately targeted. Initiation of illicit drug use typically starts in adolescence, and the evidence points to those with the earliest onset of drug use as being at greatest risk of subsequent mental disorders. A campaign targeting an early adolescent audience requires clear, coherent and credible evidence-based messages that are balanced and free from political dogma. The messages must also be delivered in a format that is appealing and meaningful to adolescents and informed by current trends in media and information technology. This might include web-based campaigns and the development of related Internet sites. Whether the campaign also focuses on providing information for parents will need to be determined, as this would require a complementary set of relevant information and materials. Mass media campaigns in other areas of health have typically had very little effect, including when drug misuse prevention has been the goal.9 In many cases, the weak effect has been due to campaigns being insufficient in intensity. Nevertheless, there are lessons that can be learned from earlier campaigns and these need to be applied (see Box). Given that the campaign discussed here will be the first to address risk of mental disorders, it needs to be well evaluated, either through a staggered roll-out in which some regions serve as controls, or through a time-series analysis in which there are repeated measurements over time — before, during, and after the campaign. As the first of its kind in Australia, it is important that this campaign is done well. A bad start could set back a field with considerable potential. Reducing the prevalence of risky behaviours, like illicit drug use, is not the only approach. It is also possible to promote positive actions that all individuals can take to reduce their risk of mental disorders.12 Campaigns that focus on educating the public about other effective preventive strategies (eg, exercise) should also be a clear priority, similar to other areas of health policy. Indeed, we have good evidence regarding psychosocial factors that increase risk for both substance misuse and mental disorders, and we need to communicate this information to the wider community. We envisage a future in which the public will know as much about how to reduce their risk of mental disorders as they currently do about how to reduce their risk of cancer and heart disease. Principles of effective mass media campaigns9 and possible applications to a campaign promoting awareness of illicit drugs as a risk factor for mental disorders Carry out preliminary research with the target audience Carry out qualitative research with young people to help design the campaign and to get feedback about the effectiveness of messages. Use a theory to give the campaign a conceptual foundation There are several relevant theories of behaviour change, including the transtheoretical model (which specifies how to communicate with people who are at various stages of readiness to change)10 and the theory of planned behaviour (which looks at how behaviour is influenced by a person’s attitudes and those of the people closest to them, and whether the person believes that the behaviour is under volitional control).11 Segment the audience into subgroups of people whose message preferences are similar to one another Potential audience subgroups might include: young people currently using illicit drugs, adolescents not using drugs, people with a personal or family history of mental disorders, and parents. Design messages that are targeted to the audience subgroups Messages need to appeal to each group. For example, messages for young people might need to avoid preaching, use suitable role models, and include features such as humour, novelty and a fast pace. Place messages through appropriate media that are widely used by the audience The appropriate media may be quite different for each group (eg, the Internet or youth radio might be more appropriate for young people than for parents). Conduct a process evaluation to see that the messages reach the audience Surveys should be conducted to ensure that the messages have reached the target audiences with a high frequency of exposure. The approach should be changed if an audience is not being reached. Evaluate outcomes to find out whether the campaign caused any changes in target audience behaviour Measure changes in attitudes towards the link between drug use and mental disorders, as well as changes in drug use. Evaluate the effects using a staggered roll-out, with some regions used as controls, or a time-series design, which involves multiple measures before, during, and after the campaign.

Anthony F Jorm MPsychol, PhD, DSc · Dan I Lubman PhD, FRANZCP, FAChAM

New national guidelines recommend that women who choose to drink alcohol during pregnancy “should have less than seven standard drinks” in any week and “no more than two standard drinks” on any one day, and that they should never become intoxicated. Exposure to alcohol at these recommended levels has been shown to affect brain development and certain behaviours in animals. Some longitudinal studies in human children have detected detrimental affects from exposure to low levels of alcohol. Normal public health standards for exposure to environmental toxins should be applied for the unborn baby. We do not know what level of alcohol exposure is safe and pregnant women can only be advised to abstain.

John S Whitehall FRACP, MRCP, DCH

Will DrinkWise truly act independently to reduce alcohol-related harm? The Australian Government recently awarded $5 million to “DrinkWise” to educate the public about responsible drinking.1 DrinkWise is a putatively independent body that was originally funded by the alcohol industry, whose representatives occupy six of its 12 board positions.2 DrinkWise’s stated mission is to change the “drinking culture” of Australia; its slogan is: “Moderation is always in good taste”. According to its Chairman, Emeritus Professor of Medicine John Dwyer, DrinkWise will produce policy by consensus. Given the alcohol industry’s representation on its board, will DrinkWise be able to advocate policies that the industry finds unacceptable? There is reason to be concerned, because the alcohol industry does not have a distinguished track record in reducing alcohol-related harm in Australia. It strenuously opposed the introduction of random breath testing in the 1970s and 1980s,3 because it would reduce alcohol consumption — which it did, and in the process reduced road crash fatalities and injuries. In the early 1990s, the brewers and distillers opposed the innocuous and basic policy of including standard drink labelling on alcohol beverage containers4 so that consumers could assess their own alcohol intake. DrinkWise is the Australian incarnation of a series of similar alcohol industry-funded “policy” groups that have been established in North America and the United Kingdom in recent decades — the industry’s term for them is “social aspects organisations”.3 The policies that these groups have advocated provide a reasonable guide to what we may expect from DrinkWise. These are alcohol policies that are apparently plausible and have a high media profile, but are likely to have little effect on problem alcohol use or alcohol-related problems: namely, school-based education and mass media campaigns about “responsible drinking”, the “self-regulation” of alcohol advertising and promotion, and 24-hour alcohol trading as a way of reducing alcohol-related harm.5 The evidence is clear that these are ineffective ways of reducing alcohol-related harm.6 School-based education on alcohol has been extensively investigated. At best, it has very modest effects on alcohol use; at worst, it can encourage experimentation.6 Youth are a favourite focus for the industry, because young people are their future (and best) customers. In 2002, for example, underage Australian adolescent drinkers were estimated to have consumed $217 million worth of alcoholic beverages.7 Educational messages that portray drinking as an activity only for adults are double-edged when delivered to teenagers who often are in a hurry to assume adult status. Industry-funded advocacy groups have attempted to circumvent the inconvenient lack of evidence for the efficacy of their preferred policies by using some of the same tactics as the tobacco industry — trying to manufacture spurious controversies about the effectiveness of policies of which they disapprove while producing apparently authoritative but biased reviews of evidence in favour of the polices that they advocate. In the early 1990s, for example, The Portman Group in the UK tried to covertly commission critical reviews of a World Health Organization report on alcohol policy from academics it assumed would be hostile to the report.8 More recently, the International Center for Alcohol Policies has been accused of commissioning a selective review of the evidence on the effectiveness of school-based alcohol education, while ignoring critical peer review comments that it solicited on the document.9 Alcohol industry advocacy groups also like to emphasise the protective health effects of alcohol consumption in older adults.2 These benefits have been contested,10 and even if they exist, they are small, at best, and far smaller than the overall harm. Any such health benefits largely accrue to middle-aged men at risk of cardiovascular disease who drink in moderation, rather than to the many more numerous young adults who drink in risky ways.6 None of this should be surprising. The alcohol industry cannot afford to reduce the risky alcohol consumption that generates most of its profits. Conservatively estimated, two-thirds of all alcohol consumed in Australia (and 90% of that consumed by young men) is consumed in ways that put drinkers’ and others’ health and wellbeing at risk.11 Nor should we be surprised, given the $5.5 billion in tax revenue that alcohol generated in 2004–05,12 that the Australian Government supports policies that purport to reduce alcohol-related harm without reducing per capita alcohol consumption. How will we be able to tell if DrinkWise lives up to its claim of being an independent organisation that reduces alcohol-related harm in Australia? First, we would see DrinkWise advocating public health policies that are supported by evidence, rather than the plausible but ineffective ones favoured by the alcohol beverage industry (Box).6 These will include (but not be limited to) policies such as increasing taxation on the most misused forms of alcohol in Australia (namely, cheap cask wine); more effective enforcement of licensing laws that penalise hotels for selling alcohol to intoxicated customers; and reductions in the hours of alcohol trading in areas where drinking causes public disorder and violence.6,12 Second, over the next half decade we should see a reduction in per capita alcohol consumption and reductions in key indicators of alcohol-related harm. These would include a lower proportion of fatal and non-fatal road crashes in which alcohol is a contributory cause; fewer hospitalisations for alcohol-related accidents, injuries, and suicides, especially among young adults; and fewer liver cirrhosis deaths and hospitalisations. If instead we see high profile media and school-based education campaigns urging us to drink responsibly, and no reductions in any of these indicators of alcohol-related harm, then DrinkWise will prove to have been what many in the alcohol field fear it will be — an attempt by the alcohol industry to avert serious consideration of public health policies that will adversely affect their bottom line. Evidential support for strategies to reduce alcohol-related harm6 Strong evidence of effectiveness and cost-effectiveness Alcohol taxation: higher taxes for higher alcohol beverages Availability restrictions: Raising the minimum drinking age to 21 years Reducing outlet density Reducing trading hours Enforcement: Random breath testing with blood alcohol concentration < 0.05 g/dL Enforcing licensing laws Penalties for serving intoxicated customers Medium evidence of effectiveness and cost-effectiveness Screening for at-risk drinking in primary care Early intervention for problem drinkers Weak evidence of effectiveness School-based education Public service messages

Wayne D Hall BSc, PhD · Robin Room

Early adolescence is associated with high rates of experimental inhalant misuse, but only a minority continue to inhale on a regular basis. Inhalant misuse is associated with a range of adverse outcomes, including reports of increased morbidity and mortality. Research into inhalant use among adolescents is lacking, with limited data available on long-term outcomes or evidence-based approaches to treatment. Legislative and supply-reduction strategies have been introduced by a number of states and territories over recent years, but direct funding for specific targeted interventions is lacking. Investment and commitment to a national research framework, as well as coordination of local services, is urgently required.

Dan I Lubman PhD, FRANZCP, FAChAM · Leanne Hides BBehSc(Hons), PhD(Clin) · Murat Yücel BA(Hons), ClinPhD(Npsych)

Intraoral examination revealed rampant dental caries (a), enamel erosion (b) and generalised calculus deposits (c). A 22-year-old man presented with badly decayed teeth and generalised dental pain. Intraoral examination revealed rampant dental caries, enamel erosion and generalised calculus deposits (Box). The patient had a 2-year history of daily use of crystal methamphetamine, administered intravenously or via snorting. He complained of a dry mouth, which led him to consume 2–3 litres of carbonated beverages a day, and reported periods of jaw clenching and temporomandibular joint discomfort on waking. This clinical syndrome in methamphetamine users, which has been referred to as “meth mouth”,1 can be attributed to several factors: the acidic nature of the drug, its xerostomic effect and propensity to cause cravings for sweetened carbonated beverages; drug-related tooth grinding and clenching; and extended periods of poor oral hygiene. Treating dentists should avoid the use of nitrous oxide, narcotics and vasoconstrictors. Early interventions, such as dietary counselling, application of fluoride varnish and dental plaque control, can prevent significant damage to the teeth.

Kishore Shetty

To the Editor: There has been much public discussion recently about comorbidity between substance misuse and psychiatric disorders.1,2 Drug and alcohol misuse can precipitate, exacerbate and prolong psychiatric disorders, and is often accompanied by a range of social problems. Here we report on the prevalence of substance misuse in an unselected group of patients admitted to the 20-bed acute psychiatric facility at Lyell McEwin Health Service, situated in an underprivileged region of northern Adelaide. The facility has five closed beds and 15 open beds. In October 2005, 45 patients (23 men, 22 women; mean age, 39 years) were admitted to the unit, of whom 28 (62%) were detained involuntarily. Semi-structured interviews, clinical history taking and collateral information gathering revealed that 27 patients (60%) had a comorbid substance misuse disorder. The most common substance misused was cannabis (20 patients [44%]), followed by alcohol (16 patients [36%]), amphetamines (15 patients [33%]), opiates (6 patients [13%]) and benzodiazepines (5 patients [11%]). Misuse of more than one substance was common — for example, all 15 patients diagnosed with amphetamine misuse also misused cannabis. Patients who misused cannabis were younger (mean age, 33 years) than those who did not (mean age, 44 years) (t43 = 0.23; P = 0.023) and were more likely to be male (61% of male patients misused cannabis compared with 27% of female patients; χ2 = 5.14; P = 0.036). Of 19 patients with psychotic disorders, 11 misused cannabis. These results indicate high rates of substance misuse in patients admitted to a psychiatric facility. Cannabis misuse by young men is a particular concern. It is apparent that more than half of inpatients with acute psychiatric conditions could benefit from interventions to address their substance misuse. The extent of cooperation between drug and alcohol services and mental health services varies between different localities and between the private and public sectors. In states such as South Australia, where there is a historical separation between drug and alcohol services and mental health services, the treatment of these disorders is regarded as outside the role of mental health services. Patients considered to have a primary problem with substance misuse are treated by specialised drug and alcohol services. This service divide does not reflect clinical reality. Patients with comorbidity can “fall through the cracks”, each service regarding them as someone else’s responsibility. Postgraduate training in psychiatry includes both academic input and the submission of case logs describing 10 patients with addiction disorders, but this aspect of training may need to be expanded in response to changes in the pattern of disorders in the patient population. Mental health clinicians, along with general practitioners and doctors working in settings such as emergency departments, will increasingly need to be highly skilled in diagnosing and managing comorbid drug and alcohol and psychiatric disorders.

Cherrie Ann Galletly DPM, FRANZCP, PhD · Darryl P Watson MB BS, FRANZCP

Objectives: To identify the prevalence of blood-borne viruses (BBVs) testing, counselling and vaccination services by drug and alcohol services for injecting drug users in Australia.Design, setting and participants: Cross-sectional survey of drug and alcohol agencies throughout Australia.Outcome measures: Current availability of testing, counselling and vaccination services for hepatitis B virus (HBV), hepatitis C virus (HCV) and HIV; availability of medical coverage; and barriers to greater provision of services.Results: Survey responses were provided by 222 agencies nationally (61% response rate). About three-quarters of agencies provided some access to HIV, HBV, and HCV testing and HBV vaccinations, but only a third offered these services routinely on site. HBV vaccination availability differed depending on the primary function of the agency, with drug dependence units and needle and syringe programs more likely to provide vaccination on site. The major barriers preventing agencies from providing routine on-site BBV services are lack of access to medical staff and trained personnel; the cost of providing these services; and a lack of facilities.Conclusions: The restricted provision of BBV services represents missed opportunities to reduce individual and community morbidity and to maximise the potential savings from preventable disease in relation to HBV infection. To address key barriers and patient retention issues, it is necessary to expand the role of non-medical staff, increase the use of shorter HBV vaccination schedules, and identify and maintain local clinical partnerships between public and private service providers.

Adam R Winstock MSc, MRCPsych, FAChAM · Caroline M Anderson GradDipSc(Psych), BA · Janie Sheridan PhD, MRPharmS, MPS(NZ)

Alan R Clough,* Bart J Currie,† Maymuna W Yunupingu,‡ Katherine M Conigrave§ * Postdoctoral Fellow, Institute of Advanced Studies, Menzies School of Health Research, Charles Darwin University, PO Box 1479, Nhulunbuy, NT 0881; † Professor, and Head, Tropical and Emerging Infectious Diseases Division, Menzies School of Health Research, Charles Darwin University, and Northern Territory Clinical School, Flinders University, Royal Darwin Hospital, Darwin, NT; ‡ Senior Aboriginal Health Worker, NT Department of Health and Community Services, Yirrkala, NT; § Specialist in Drug Health Services, Royal Prince Alfred Hospital and University of Sydney, Sydney, NSW. Alan. CloughATbigpond.com To the Editor: We are concerned that the Northern Territory’s regulations on kava have not succeeded in controlling its availability in Arnhem Land (the north-eastern region of the NT). Under the Kava Management Act 1998 (NT), one wholesaler is licensed to supply kava (Piper methysticum Forst. f.) to four licensed retailers in Arnhem Land Aboriginal communities.1 “Kava Management Plans” in “Kava Licence Areas” permit retailers to supply 600–800 g per week of kava powder to each purchaser1 — more than double the known harmful consumption levels (240–440 g per week).2 Legal kava supplied will reach 26 tonnes in 2005 (worth $3.6 million), with a persistent illegal trade adding 8 tonnes, worth perhaps $2 million (Box). Two proposed additional retail licences1 will increase kava’s availability. Kava’s social and economic effects remain an ongoing concern. The region’s community-controlled health service attributes to kava abuse an accelerated decline in participation in traditional ceremonies and mortuary rites in some localities. Kava is the psychoactive substance with greatest impact on the financial resources of communities and individuals in Arnhem Land.2 Kava’s health effects include seizures and extreme weight loss in heavy users (up to 20% of body mass), similar to that seen in anorexia nervosa.4 Extreme weight loss, evident during the 1980s, has re-emerged in the region’s kava users (M W Yunupingu, unpublished observations). Raised total and low-density lipoprotein (LDL) cholesterol levels4 add to unresolved concerns that heavy kava use may be a risk factor for cardiovascular disease and sudden cardiac deaths. Potential immunosuppressive effects are suggested by relative lymphocytopenia in heavy kava users4 and by increased risk of melioidosis.5 Raised levels of liver enzymes (alkaline phosphatase and γ-glutamyltransferase), which reverse after ceasing moderate kava use, should be monitored because of fatal hepatotoxicity documented in users of manufactured kava products available as natural therapies.6 Given the scarcity of substance misuse treatment services in the region, with no effective treatments for kava misuse, controlling supply is the only practical measure to reduce kava-related harms. Tighter controls on kava supply are urgently required while licensees implement promised demand-reduction and harm-minimisation strategies.1 We recommend that: no further retail licences be granted until kava supply is reduced; retail licensees supply no more than 440 g per week to individual kava consumers; quantities permitted to be imported by the wholesaler and supplied to retailers be limited; kava selling prices be reviewed in the light of trade-offs between higher prices to reduce demand and minimal financial drains on communities; rigorous enforcement be continued to eliminate illegal kava dealing; and the Kava Management Act be reviewed to facilitate these changes. History of kava use and retail value ($ million) on the legal and black markets in Arnhem Land, Northern Territory, since 1982, extrapolated to the end of 2005* * Data on kava supplied were obtained from d'Abbs (for 1982–1993);3 were estimated from population surveys of kava use (for 1994–1997); were estimated from kava seized by Police and Licensing Inspectors (for illegal use, 1998–2005) (seizures were estimated to account for 14% of the illegal kava supplied, based on correlation with population surveys in 1999 and 2000); and were based on the licensed wholesaler’s monthly figures, extrapolated to the end of 2005 (for legal use from May 2002). Retail value was calculated from data on kava supplied and regulated values of $100 per kg (1990–1993), $140 per kg (2002–2004) and $150 per kg (2005), or a black market value of $250 per kg.2 † Approval required from Minister for communities to supply kava. pa = per annum.

Alan R Clough · Bart J Currie · Maymuna W Yunupingu · Katherine M Conigrave