Substance‐related disorders

Experimentation with alcohol is a normal part of teenage psychosocial development. Society’s approach to adolescent alcohol consumption is ambiguous and sends young people mixed messages. Epidemiological data demonstrate disturbing trends in patterns of alcohol use by young people, including widespread early-onset, regular binge drinking. The acute harms of excess adolescent alcohol consumption are well documented, and data on long-term harms are now also emerging. As alcohol is an integral part of our culture, we urgently need to manage teenage drinking appropriately and comprehensively, and to guide young people to a “healthy norm” for adolescent alcohol consumption.

Yvonne A Bonomo FRACP, PhD, FAChAM

This case describes refeeding syndrome associated with volitional oral nutrition in a patient with chronic alcoholic abuse admitted for detoxification. Refeeding syndrome is an under-recognised and undertreated condition1-5 of severe, acute electrolyte, fluid-balance and metabolic abnormalities in chronically malnourished patients undergoing renutrition. Refeeding syndrome was first described in Japanese prisoners during World War II.6 Since then, it has been described in patients being refed after hunger strikes, starvation after being lost, chronic alcoholism, anorexia nervosa, malignancy, kwashiorkor and marasmus and in obese patients who have had duodenal switch operations.4,5 Reports conflict over whether it is more common following parenteral7 or enteral tube4 nutrition, but descriptions following volitional oral refeeding are less frequent. In people in a chronically starved state, insulin secretion is reduced in parallel with low carbohydrate intake. Fat catabolism predominates, and free fatty acids and ketone bodies replace glucose as the major energy source. If starvation is severe, body stores of phosphate, potassium and magnesium may be depleted, although serum levels are often maintained.3-5 With refeeding, there is a shift back to carbohydrate metabolism and an increase in insulin levels. Insulin stimulates the movement of phosphate, potassium and magnesium into the cells, leading to a fall in their serum concentrations.2 In addition, tissue anabolism increases cellular demand for phosphate, glucose, potassium and water.1 Hyperphosphaturia may occur with alcoholism,7,8 and thiamine, required for the intracellular transport of glucose, may be depleted.9 The principal biochemical hallmark of refeeding syndrome, as seen in this case, is severe, acute hypophosphataemia that usually occurs within 3–4 days of refeeding.2,3,10 This is often associated with hypokalaemia, hypomagnesaemia, sodium and fluid retention, thiamine deficiency and hyperglycaemia. Phosphate is the body’s major intracellular anion.4 Daily oral phosphate intake is about 1000–1400 mg, the major sources being meat, poultry, eggs, cereals and dairy products.4 Wine contains little phosphate.11 Phosphate is found in phospholipids, nucleic acids, adenosine triphosphate and 2,3-diphosphoglycerate in red blood cells. It is important for intracellular buffering, enzymatic phosphorylation, glucose metabolism, nervous system conduction and leucocyte function. Hypophosphataemia-induced depletion of 2,3-diphosphoglycerate in erythrocytes results in a left shift of the haemoglobin/oxygen dissociation curve, increasing haemoglobin affinity for oxygen and predisposing to local tissue hypoxia.1,2,4 However, the clinical manifestations of refeeding syndrome are varied and non-specific (Box 3). Potentially life-threatening sequelae include acute cardiac failure, respiratory failure, Wernicke’s encephalopathy, sepsis and acute renal failure. Sudden cardiac death has been reported in two chronically malnourished patients experiencing acute hypophosphataemia after initiation of total parenteral nutrition.12 Although non-specific, we believe the constellation of symptoms and signs observed in our patient is typical of refeeding syndrome. Most importantly, acute, severe hypophosphataemia not present on admission was noted 4 days after oral refeeding with a ward diet. The presence of a serum phosphate level of 0.15 mmol/L in our patient represents extreme hypophosphataemia. (The lowest published level we are aware of in a patient who survived is 0.07 mmol/L.11) Given the “low normal” value on admission and the patient’s risk factors for refeeding syndrome, the serum phosphate level should have been monitored more closely during the first few days of admission. We did consider several differential diagnoses. Although hypophosphataemia is commonly seen in sepsis,14 clinical and haematological evidence suggested that the patient’s respiratory infection had largely resolved by Day 4. Acute respiratory alkalosis may also cause hypophosphataemia,15 but was unlikely in this case, in view of the normal serum phosphate level on admission. Severe hypokalaemia was already being corrected by intravenous replacement from the day of admission. The development of paraesthesiae, myalgias, groin candidiasis, diarrhoea and sinus tachycardia (which may have indicated incipient cardiac failure4,9) was consistent with the diagnosis of refeeding syndrome.4 Unfortunately, the creatinine kinase level was not measured to exclude rhabdomyolysis. Cerebellar signs may have been secondary to alcoholic degeneration or mild Wernicke’s encephalopathy. Management of refeeding syndrome includes slowing of caloric intake, correcting electrolyte and metabolic abnormalities, monitoring fluid balance and treating complications. Thiamine and B-complex vitamins should be prescribed prophylactically before refeeding.4 Interestingly, the early administration of intramuscular thiamine for chronic alcoholism may have protected our patient against Wernicke’s encephalopathy secondary to refeeding syndrome. Ideally, patients at risk of developing refeeding syndrome should be identified and a prophylactic low-caloric low-carbohydrate dietary regimen implemented.3 Initially, 85 kJ per kilogram of body weight per day, with a generous protein allowance (1.2–1.5 g protein per kilogram of body weight per day), has been suggested.4,13 Caloric intake can then be gradually increased over the following 1–2 weeks, ensuring that clinical and biochemical parameters are closely monitored.4,12,13 It is important to note that most current recommendations are based on parenteral or enteral tube nutrition. Protocols are not well developed for volitional oral refeeding. However, “slow” refeeding in these patients could be achieved by providing a similar low daily caloric intake with reduced food portions. Ideally, an experienced dietitian should be consulted.4 In our case, a dietitian was not available on site, and, given the prompt correction of electrolyte abnormalities and absence of acute cardiac failure, no change to diet was made. Levels of serum electrolytes, urea and creatinine should be monitored at least daily in the acute phase. Prophylactic phosphate and potassium supplementation is often required at the time of refeeding in high-risk patients. Phosphate replacement is recommended if serum levels are below 0.3–0.5 mmol/L3,4,10 or if the patient is symptomatic. As oral replacement at these levels is often inadequate, intravenous replacement is advised.7,10 Complications of overzealous intravenous phosphate replacement may include hyperphosphataemia, hypocalcaemia, tetany, hypotension, hyperkalaemia, hypernatraemia, renal failure and metastatic calcification.2,10 Although successful intravenous regimens based on patient weight and serum phosphate levels in intensive care settings have been described,15 these are often complicated and impractical for ward patients. Terlevich et al10 described the use of 50 mmol intravenous phosphate over 24 hours in 30 ward patients with refeeding syndrome and normal renal function. Twenty-eight patients safely achieved a serum phosphate level above 0.5 mmol/L within 72 hours. We used 42 mmol intravenous phosphate over 36 hours to normalise serum levels in our patient. While less aggressive than the protocol described by Terlevich et al, it was deemed sufficient given that the patient was largely asymptomatic and that serum phosphate levels were improving. Intravenous phosphate was dispensed on site in 14 mmol aliquots, and prescribing this amount over 12 hours simplified the dosing regimen. Clinical diagnosis of refeeding syndrome requires a high index of suspicion.1 Its hallmark of acute, severe hypophosphataemia in chronically malnourished patients after refeeding may occur even in patients who are largely asymptomatic and orally fed. Prevention of morbidity and, in some cases, death requires careful management of diet, vitamin intake and electrolyte and fluid balance. Lessons from practice Refeeding syndrome is a potentially lethal condition in chronically malnourished patients undergoing renutrition. The syndrome is under-recognised and undertreated. Electrolyte levels should initially be monitored daily in at-risk patients, as acute, profound hypophosphataemia may develop even in asymptomatic patients. Regimens for volitional oral refeeding are not well developed, but a prophylactic low-caloric (85 kJ per kilogram of body weight per day), low-carbohydrate diet has been advised. Prophylactic thiamine, phosphate and potassium supplementation is often required for at-risk patients. Patients with serum phosphate levels below 0.3–0.5 mmol/L or symptoms of hypophosphataemia require intravenous phosphate replacement. 1 Serum electrolyte levels over the first 8 days after admission Day Electrolyte Reference range 1 4 8 Potassium (mmol/L) 3.6–5.1 2.4 3.5 3.9 Calcium (mmol/L) (corrected for serum albumin) 2.25–2.58 2.27 2.60 2.60 Magnesium (mmol/L) 0.74–1.03 0.71 0.69 0.70 Phosphate (mmol/L) 0.80–1.50 0.84 0.15 1.56 2 Serum phosphate levels over the first 8 days after admission* * Dotted line indicates the direction of change only (no data were available for Days 2 and 3). 3 Clinical features of refeeding syndrome4 Clinical feature Possible mechanisms Cardiovascular Acute cardiac failure Fluid retention (secondary to carbohydrate intake1,2,4 and hyperinsulinaemia9), arrhythmias, cardiomyopathy1,2,4 Arrhythmias, sudden cardiac death3,12 Electrolyte disturbance1,2 Respiratory Respiratory failure Diaphragmatic myopathy2,8 Neurological Seizures, paraesthesiae Electrolyte and/or metabolic disturbance,1,4 cellular hypoxia secondary to reduced 2,3-DPG and ATP Wernicke’s encephalopathy Thiamine deficiency1,2,13 Gastrointestinal Diarrhoea or constipation Electrolyte and/or metabolic disturbance,4 intestinal atrophy following malnutrition13 Haematological Sepsis Leukocyte dysfunction, hyperglycaemia, acid–base disturbance1,4 Haemorrhage Thrombocytopaenia,2,9 platelet dysfunction9 Haemolytic anaemia Depletion of erythrocyte ATP, resulting in increased cell membrane rigidity1 Metabolic Hyperglycaemia4 Glucose ingestion4 Acid–base disturbance1,4 Impaired phosphate renal buffering2,12 Renal Acute tubular necrosis Rhabdomyolysis4 Musculoskeletal Myopathy Depletion of muscle ATP,1,9 electrolyte disturbance1 Rhabdomyolysis Impaired production of phospholipid cell membranes causes sarcolemma dysfunction1,2 ATP = adenosine triphosphate. DPG = diphosphoglycerate.

Adrian T Fung MB BS · Janet Rimmer MB BS, MD, FRACP

To the Editor: The interesting case report by Currie and colleagues describes a variable cutaneous eruption of uncertain aetiology in a cluster of methadone-dependent patients.1 The rash was described as including pruritic, exanthematous, purpuric and eventually desquamative components, and typically as involving the trunk and extremities, particularly palms and soles. Secondary syphilis classically presents in a similar fashion, but no mention was made as to whether this had been excluded by serological testing. Indeed, the histology of the rash (perivascular inflammation, including plasma cell infiltrate, progressing to endarteritis) is similar to that seen in skin biopsies from methadone patients with secondary syphilis. However, an allergic or toxic cause appears to be implicated, in view of previous, well documented reports of hallucinogenic or other drug-related vasculitis published by ourselves2 and others.3-5

Vernon J Heazlewood

To the Editor: As a Victorian always on the lookout for something new, I read with interest the report by Currie and colleagues of a syndromic rash in patients attending methadone clinics in New South Wales.1 From the title I expected to read about a rash occurring as part of a syndrome, yet no group of concurrent symptoms was described. In fact, there was a long list with each patient of negative findings. I also had trouble deciding whether the four patients described indeed had the same rash. While the “lumpers” among us may consider it pedantic to split “rash” into more than one category, some doctors make an occupation of it quite successfully. For example, Patient 1 had petechiae and purpura, but no erythema and no involvement of the palms and soles. No photo, but nevertheless a nice description of vasculitis — common among intravenous drug users. Patient 2 had, from the look of the photo, a toxic erythema that resolved with desquamation of the palms and soles. No petechiae or purpura. Therefore, must be a different rash to Patient 1. Patient 3 is described as having “ a prominent purpuric rash involving both lower limbs”. However, the photo shows a macular erythema with some associated purpura that looks almost certainly to be an incidental manifestation of dependency. Difficult to say from a photo, as touch is so important in the diagnosis of true purpura. Of course, a 2 mm punch biopsy of the skin could resolve this almost instantly. Again, it is not clear whether this rash is similar to that seen in either Patient 1 or Patient 2. Patient 4 is described as having a red and itchy rash (erythematous and pruritic), but, from the photograph, we can clearly see that the rash is urticarial. This raises the possibility of urticaria, or urticarial vasculitis, or even erythema multiforme. Again, a skin biopsy would be very useful. The severe palmar peeling almost seems incongruous, but it does give me faith that buried in this report there might actually be a new desquamating rash associated with methadone use. In summary, I am still not clear whether the four patients described had the same rash, but I concur with the authors that several of these patients might warrant specialist assessment. Let’s hope they get it.

Rodney D Sinclair

In reply: The purpose of our report1 was to alert the wider medical community to the recent outbreak of a “syndrome” (“a group of symptoms and signs, which, when considered together, are known or presumed to characterise a disease or lesion”2) that included the development of various forms of rash in patients taking methadone syrup. Our report included four cases illustrating the different types of rash encountered to date. From October 2004, over 400 cases were reported from methadone clinics in New South Wales, although very few new cases have been reported since February 2005, presumably reflecting the success of preventive measures instituted by the NSW Health department. To date, the cause of this methadone-associated syndrome has not been elucidated. Skin biopsies of rash lesions have been performed in a number of our patients. All have shown chronic perivascular inflammation, with most demonstrating hyperkeratosis. A small number of patients have had a true leukocytoclastic vasculitis. As Heazlewood has commented, both secondary syphilis and illicit drugs such as amphetamines and cocaine have been reported to cause vasculitic rashes. However, none of the more than 50 patients in whom we have performed syphilis serological testing has had positive results, and few of our affected methadone patients have had urine drug-test results positive for amphetamine or cocaine use. We therefore believe that the syndrome we have described remains specific to the patients’ current use of methadone syrup. We are unaware of a rash that is “an incidental manifestation of dependency”, as suggested by Sinclair, but we would assure him that specialists from a wide variety of fields, including dermatology, immunology, immunopathology, infectious diseases, addiction medicine and epidemiology, have all been involved in the assessment and treatment of patients with this syndrome, and in the wider investigation of its pathogenesis.

Jon N Currie · Lisa Snell · Elizabeth M Benson

Craig A Aboltins,* John R Daffy,† Penny Allen‡ * Infectious Diseases Registrar, † Infectious Diseases Physician, St Vincent’s Hospital, Victoria Parade, Fitzroy, VIC 3065; ‡ Ophthalmologist, Royal Victorian Eye and Ear Hospital, East Melbourne, VIC. craigaboltinsATnetspace.net.au To the Editor: Within the last 12 months, four injecting drug users (IDUs) who had been injecting buprenorphine presented to the Royal Victorian Eye and Ear Hospital with endogenous fungal endophthalmitis (EFE) involving Candida species. All four patients admitted that they had diverted or obtained diverted sublingual buprenorphine from the oral cavity after it was dispensed. They had dissolved the remaining drug in water and injected it intravenously. We present an illustrative case. A 28-year-old woman presented with a 4-week history of left eye pain and erythema. She had a 10-year history of intravenous drug use. Over the previous 6 months, she had been regularly injecting buprenorphine that was prescribed to a friend. The friend had been removing the partially dissolved buprenorphine from his mouth before giving it to our patient. On examination, the patient could only detect hand movement with her left eye. Fundoscopy showed vitritis with a “snow ball appearance” consistent with EFE. Treatment involved vitrectomy, intravitreal amphotericin and oral fluconazole. Candida albicans was cultured from vitreal specimens. Her visual acuity had improved to 1/60 at the time of discharge. Intravenous drug use is known to be a risk factor for EFE. Candida species are the usual causative organisms, but Aspergillus species have also been reported.1 In the 1980s, there were many reports of candida endophthalmitis in injecting drug users associated with the use of “brown” (or Iranian) heroin. The “brown” heroin required an acidic substance, often lemon juice, as a solvent. Lemon juice was shown to be the source of the candida.2 However, over the past 10 years, the heroin available in Australia has been water soluble, and sterile or tap water is usually used to dissolve the heroin before injection. None of the cases we report in this letter involved lemon juice to dissolve heroin or buprenorphine before injection. Buprenorphine has been available in Australia since 2001 for the treatment of opiate addiction. It is usually dispensed daily by pharmacies in a crushed tablet form. Pharmacists are required to watch patients place and dissolve the medication under the tongue before they leave the pharmacy. Contamination of injected buprenorphine with orally derived Candida species presents a recently recognised cause of fungal endophthalmitis in injecting drug users.3 Doctors, pharmacists and drug users need to be aware of the risk of this sight-threatening complication.

Craig A Aboltins · John R Daffy · Penny Allen

Ariella Glaser,* Dwight Arakaki,† Gar Ming Chan,‡ Robert S Hoffman§ * Resident, Mount Sinai Medical Center, New York City, NY, USA; † Resident, Beth Israel Medical Center, New York City, NY, USA; ‡ Fellow (and corresponding author), § Director, New York City Poison Control Center, New York City, NY, USA. garchanATpol.net To the Editor: Two aspects of the recent article by Kelly et al comparing intranasal with intramuscular naloxone in suspected opioid overdose1 make their study difficult to interpret. The methods allowed for a great deal of bias. There was no attempt to blind evaluators to therapy, and knowing which therapy is to be used a priori may influence both therapy selection and perceived outcome. The second flaw we noted was the use of the Glascow Coma Scale (GCS) in a non-trauma patient.2 An improvement in GCS score may represent increased wakefulness or even withdrawal. The use of the GCS does not make it possible to determine what degree of improvement or worsening the therapy resulted in. In the opioid-intoxicated patient, the “alert/verbal/pain/unresponsive” (AVPU) scale is more appropriate. We agree that the use of needles in a high-risk patient is dangerous. However, if these patients do not respond to painful stimuli, there should be no danger at all.

Ariella Glaser · Dwight Arakaki · Gar Ming Chan · Robert S Hoffman

Anne-Maree Kelly,* Debra Kerr,† Paul Dietze‡ * Director, † Deputy Director, Joseph Epstein Centre for Emergency Medicine Research, Western Hospital, Private Bag, Footscray, VIC 3011. ‡ Research Fellow, Turning Point Alcohol and Drug Centre, Fitzroy, VIC. Anne-Maree. KellyATwh.org.au In reply: The prehospital setting for research poses challenges that require some flexibility in study design. While it would have been preferable to have used blinded naloxone and placebo solutions for both routes of administration in our study, financial and operational constraints made this impossible, so some bias in evaluations is possible. However, this is not necessarily in favour of the intranasal route, as before the study many paramedics were very sceptical about the intranasal naloxone preparation. Therapy selection was by random allocation in sealed envelopes as described in our article. The Glasgow Coma Scale score was chosen as an outcome measure because it was the parameter used operationally for treatment and disposition decisions in the ambulance service within which our study was conducted. We acknowledge its limitations in non-trauma patients. The potential for needlestick injury in this situation is real. Patients with opioid intoxication may be in cramped locations and may be irritable on waking, increasing the risks involved with handling a “sharp”. Given the prevalence of blood-borne viruses in the injecting drug user population, strategies to reduce the risk of needlestick injury are highly desirable. Additionally, a strategy that has been suggested for preventing opioid-overdose-related deaths is to make naloxone more widely available in the community. 1 The intranasal formulation of naloxone may be appropriate for this, as it has significant advantages including reducing risks of blood-borne virus transmission and minimising the requirement for training and the secure storage of syringes and needles. 2

Anne-Maree Kelly · Debra Kerr · Paul Dietze

Max Kamien Emeritus Professor, Senior Research Fellow, Discipline of General Practice, University of Western Australia, Perth, WA mkamienATcyllene.uwa.edu.au To the Editor: Over the past two years, the Journal has pointed out the health hazards and the lack of logic in the Health Insurance Commission’s closure of its previously cost-effective and successful “Doctor Shopping Hotline”.1-4 But it has taken the death of a 25-year-old “prescription shopper” in Cairns, his crusading mother, a scathing report by the Queensland Coroner5 and public exposure of these problems by Mark Bannerman on ABC TV (The 7.30 Report, 22 Dec 2004) for discernible action to occur. On that program, the Federal Minister of Health and Ageing promised that a “Prescription Shopper Line” would be up and running by the end of January 2005, and indeed it was activated on 31 January. This leaves two outstanding issues. The first is for the Health Insurance Commission to engage in an open exercise of mutual education by clearly reviewing its process of thinking in closing the previously successful Doctor Shopping Hotline and its lack of urgency in reinstituting its proposed better and broader successor.6 The second, and more important, issue is in understanding the underlying factors and thought processes of those doctors whom prescription shoppers describe as an “easy touch”. 7,8

Max Kamien

David G E Caldicott,* Cameron Duff† * Convener, Royal Adelaide Designer Drug Academic Research (RADAR) Unit, Emergency and Trauma Department, Royal Adelaide Hospital, Adelaide, SA; † Director, Centre for Youth Drug Studies, Australian Drug Foundation, Melbourne, VIC. dcaldicoATmail.rah.sa.gov.au To the Editor: Threatened with a surge of Athenian, one-eyed jingoism regarding Australian drug policy that the recent conference report by Ritter et al1 might have elicited, we offer a warning. Australia has achieved much to be proud of with its harm-reduction policies in recent decades. As Ritter et al attest, Australian researchers and practitioners are “leading the way” in generating political and community support for greater harm-reduction efforts. However, the implementation of real harm-reduction measures can hardly be described as “Olympian” under the current administration. Real Australian successes in the area of harm reduction have arguably occurred despite federal and state policy rather than because of it. Individual positions taken by clinicians such as Dr Alex Wodak, in the face of severe opposition and at times intimidation, account for much of this success. The sad reality is that the “Tough on drugs” approach currently pursued in Australia seems doomed to soon fuse with the Americans’ globally denounced “War on drugs”. Real harm reduction can hardly be said to have been given a “fair go” in the past decade, with 85% of the total drugs budget in Australia committed to law enforcement — the paltry remainder split between research and treatment.2 While harm reduction strategies have been widely implemented in response to the problems associated with injecting drug use, such strategies have not been nearly as popular in our responses to other types of drug use. Harm reduction is yet to be embraced as an effective response to the problems associated with the so-called “party drugs”, despite mounting evidence of its efficacy in Europe. Any premature triumphalism on the subject of harm reduction ought to be eschewed. Australia’s recent heritage is quietly being betrayed at a federal level. A little-publicised federal report recently called for a move away from harm minimisation and harm reduction.3 This is despite evidence indicating that functional drug use is emerging as “normal” rather than deviant behaviour among many Australians. 4 Clearly, we must redouble our efforts to ensure that harm reduction becomes a central part of Australia’s public policy stance. In an era in which it often seems easier to succumb to the whims of our larger neighbours than to resist them, it becomes even more important that doctors and health professionals, and particularly the younger generation of researchers, stand firm. We are, after all, standing on the shoulders of giants.

David G E Caldicott · Cameron Duff

Alison J Ritter,* Alex D Wodak,† J Nick Crofts‡ * Head of Research and Deputy Director, Turning Point Alcohol & Drug Centre, 54-62 Gertrude Street, Fitzroy, VIC 3065; † Director, Alcohol & Drug Service, St Vincent’s Hospital, Sydney, NSW; ‡ Deputy Director, and Director, The Centre for Harm Reduction, Macfarlane Burnet Institute for Medical Research and Public Health, Melbourne, VIC. alisonrATturningpoint.org.au In reply: Caldicott and Duff raise a very important question: is the federal government intending to soon terminate Australia’s national drug policy of harm minimisation? This view can be supported by numerous and recent unambiguous speeches by senior government ministers, including the Prime Minister. The government would like Australians to believe that it is implacably opposed to a harm-minimisation approach to illicit drugs. However, a different view appears when federal government funding allocations are examined. For example, the government allocated $215 million to the Illicit Drug Diversion Initiative over 4 years (in addition to a previous allocation of $221 million).1 The intention of this Initiative is to divert selected drug offenders from the criminal justice system to drug treatment. These efforts are, in our view, highly commendable, reducing the use of expensive and largely ineffective custodial punishment and increasing the use of less expensive and more effective drug treatment. They are, however, irreconcilable with a “zero tolerance” or “Tough on drugs” approach to illicit drugs. Another example is AusAID’s recent leadership in the introduction of harm-reduction measures to control HIV epidemics among injecting drug users in Asia. It is also worth noting that the Ministerial Council on Drug Strategy (Australia’s paramount official drug policy-making body since 1985) has repeatedly and recently endorsed a national drug policy of harm minimisation. The present federal government, unlike its predecessor, frequently and stridently attacks emotionally charged symbols of harm reduction, such as the proposed prescription heroin trial or the Medically Supervised Injecting Centre in Sydney. However, as the allocation of substantial funding to the Illicit Drug Diversion Initiative demonstrates, in most respects it is very much a case of business as usual.

Alison J Ritter · Alex D Wodak · J Nick Crofts

We report an outbreak of a “rash” syndrome in patients attending methadone clinics in New South Wales. It presents with a pruritic, exanthematous or purpuric rash involving the trunk, limbs, palms and soles, which develops over a week and proceeds in most patients to desquamation (mainly of palms and soles) persisting for 3–4 weeks. Mucosae are not involved, and patients are generally systemically well. To date, the rash has affected 22% of 316 patients attending one methadone clinic in western Sydney, as well as patients in clinics elsewhere in Sydney and rural NSW. The aetiology is as yet unknown. We report an outbreak of a “rash” syndrome in patients attending a number of methadone clinics across New South Wales during October and November 2004. The syndrome first came to our attention when, over a week, two patients presented to a methadone clinic in western Sydney and three to the Westmead Hospital emergency department with a distinctive rash. Subsequent enquiries and patient surveillance revealed that 70 of 316 patients (22%) at the methadone clinic had developed a similar “rash” syndrome in October and November. All were prescribed methadone syrup. Clusters of patients have also been increasingly reported at other methadone clinics across metropolitan Sydney and some regional and rural areas in NSW. To date, informal communication with interstate methadone clinics has identified small numbers of patients with the “rash” syndrome outside NSW. In the first western Sydney case reliably identified by history, symptoms developed in August 2004. The principal features of the “rash” syndrome are a pruritic, exanthematous or purpuric rash that typically develops over 2 to 4 days on the hands, feet, trunk and lower limbs and persists for up to 7 days. It is usually followed by a desquamative phase that particularly involves the hands and feet and lasts up to 3 to 4 weeks. Some patients develop only the desquamative phase. The condition appears relatively benign, with few, if any, systemic symptoms, although the palms and soles of the feet can become painful with pressure after desquamation. In several patients, the rapidly developing purpuric nature of the presenting rash raised initial concern about meningococcal disease or a systemic vasculitic syndrome sufficient to warrant referral for specialist assessment. We describe four illustrative cases. Clinical recordsPatient 1A man aged in his 30s presented to a hospital emergency department with a 3-day history of a petechial and purpuric rash. He was an intravenous drug user who had been in a methadone treatment program for 7 years. He intermittently injected his oral methadone intravenously, most recently 24 hours before onset of the rash. This initially involved the lower limbs, but spread over 24 hours to affect the buttocks, lower back and abdomen. Associated but relatively mild symptoms included malaise and nausea for a week before rash onset, followed by sore throat, myalgia, ankle arthralgia, abdominal and chest pain and vomiting. At presentation, the patient was afebrile. Blood pressure was 120/60 mmHg, and pulse 70 bpm. A sparse petechial and purpuric rash was present on lower limbs, feet, buttocks and lower abdomen. There was no pedal oedema, joint effusion or tenderness. There were no abnormalities on respiratory and cardiovascular examination, no clinical evidence of endocarditis, no lymphadenopathy, and mucosae were normal. The right upper abdominal quadrant was tender, but the liver and spleen were not enlarged, and no renal masses were palpable. Investigations were uninformative (Box 1). Inpatient progress was unremarkable, and, 10 days after presentation, all symptoms had resolved, despite ongoing oral and intravenous methadone use. Patient 2A middle-aged man presented with a 2-day history of an erythematous, pruritic rash over his trunk and limbs which was now beginning to desquamate. He was also an intravenous drug user in a methadone treatment program. In addition to taking prescribed oral methadone, he intermittently injected both methadone and stimulants, such as amphetamine, intravenously. There was no history of fever, oropharyngeal, genital, eye or systemic symptoms. On examination, he was afebrile, looked well and had a generalised exanthem, with erythema and significant desquamation of soles and palms (Box 2, A and B). There were no oral, mucosal or eye signs, and no lymphadenopathy or hepatosplenomegaly. Results of investigations were unremarkable (Box 1). He was treated for 2 days with oral prednisolone and an antihistamine, and then discharged. The rash settled over a week, although he continued to have desquamation of the soles and palms 2 weeks later. Patient 3A young man who was an intravenous drug user in a methadone treatment program presented to the same hospital with a 2-day history of a purpuric lower-limb rash. In addition to taking prescribed oral methadone, he intermittently injected both heroin and methadone intravenously. Five days before presentation, he developed bilateral calf pain and generalised myalgia. He was initially seen at another hospital, where he was treated with broad-spectrum intravenous antibiotics for presumed sepsis. He discharged himself after 24 hours and was admitted to our hospital about 12 hours later because of his concern about the rash. On admission, he was afebrile, with blood pressure of 115/65 mmHg and pulse of 75 bpm. He had a prominent purpuric rash involving both lower limbs (Box 2C), with sparse lesions on both forearms. Mucosae were normal, and there was no meningism, lymphadenopathy, hepatosplenomegaly, joint swelling or tenderness, no abnormalities on respiratory and cardiac examination, and no stigmata of endocarditis. Results of investigations were once again unremarkable (Box 1). The patient remained well despite the rash and was discharged from hospital 24 hours after admission. Patient 4A young woman who was an intravenous drug user in a methadone treatment program presented to the methadone clinic with a 4-day history of an erythematous, pruritic rash over her trunk, limbs and hands. Other than oral methadone, she was taking no drugs and was otherwise well. Examination revealed an extensive exanthem over her trunk, hands and legs. She had no fever, and blood pressure was normal. She was reviewed a week later and still had an extensive generalised erythematous exanthem, as well as finger and palm desquamation (Box 2, D and E). Results of investigations were unremarkable (Box 1). DiscussionThe aetiology of this “rash” syndrome is yet to be elucidated. Currently, it appears to be restricted to people using methadone syrup, with no reports of rash in over 100 patients in western Sydney prescribed buprenorphine for treatment of opioid dependence, nor among non-methadone-using family members of patients with the rash, nor among healthcare workers in contact with these patients. To date, all patients with the “rash” syndrome who have been assessed for hepatitis C exposure are seropositive, but not all are viraemic. Some patients with the “rash” syndrome smoke cannabis and intermittently inject methadone or other drugs. However, these characteristics are not universal among affected patients, nor more frequent than in unaffected patients on the methadone program, among whom they are also common. Similarly, the use of prescription or complementary medicines does not seem to be associated with the “rash” syndrome. Similar rashes and associated desquamation are common in staphylococcal and streptococcal toxin-induced illnesses, such as toxic shock syndrome and scalded skin syndrome,1-3 and in some viral illnesses, such as parvovirus infection and measles.4 However, the patients in the current outbreak did not give a history of bacterial or viral illness, and family members not taking methadone do not appear to have developed the syndrome. HIV antibody testing has been performed in some affected patients and has been negative. Throat swabs taken in some patients have grown only normal respiratory flora. Markers of streptococcal infection, such as antideoxyribonuclease B antibodies and anti-streptolysin O titre, are positive in some but not all patients. Skin biopsy performed in a number of patients has failed to help define the aetiology of the rash. Histological examination often shows focal and mild spongiosis with superficial perivascular chronic inflammation, while direct immunofluorescence examination shows deposition of IgM and complement 3 in dermal capillaries. These findings are consistent with an immunological reaction in the skin, but do not clarify whether it is the primary cause of the rash or a secondary phenomenon. A hypersensitivity reaction to a contaminant in the methadone syrup could present with such a picture. The fact that, to date, all the patients identified in western Sydney had been taking methadone syrup from a single manufacturer raises the possibility of batch contamination; however, batches are distributed nationally, so more widespread involvement would probably be expected if this was the basis of the syndrome. In addition, examination of the methadone syrup has failed to detect any contamination. The possibility of alternative sources of contamination, such as methadone storage or delivery devices, remains to be explored. We believe it is important for physicians to be aware of this newly emerging syndrome, both to assist with more accurate delineation of its epidemiology and pathogenesis, and to permit more effective investigation and treatment of affected patients. State public health units and the Therapeutic Goods Administration are investigating this outbreak to try to determine the cause of this new syndrome. 1 Results of investigations in four patients with rash Investigations Reference range Patient 1 Patient 2 Patient 3 Patient 4 Full blood count and film Normal; platelet aggregates on film Normal apart from WBC 10.8 x 109/L; occasional reactive lymphocytes Normal Normal, apart from Hb 107 g/L Haemoglobin (Hb) (g/L) 115–161 White blood cell count (WBC) (x 109/L) 3.7–9.5 ESR (mm/h) 0–15 4 11 5 38 C-reactive protein (mg/L) 0–11 20 27 22 15 Liver function tests Normal Abnormal Abnormal Normal γ-Glutamyltransferase (U/L) 8–43 47 48 Alanine aminotransferase (U/L) 10–47 88 157 Aspartate aminotransferase (U/L) 12–45 104 154 ANA, ANCA, ENAs, rheumatoid factor, complement C3 and C4 Normal nd Normal nd Cryoglobulins Absent nd Detected nd Prothrombin time (s) 11–18 Normal Normal Normal nd APTT (s) 25–36 Normal 39 Normal nd Hepatitis C virus IgG-positive; undetectable viral load (< 600 IU/mL) IgG-positive; viral load not assessed IgG-positive; viral load > 850 000 IU/mL IgG-positive; refused viral load assay HIV antibody Negative nd nd nd Urinalysis Trace protein (39 mg/24 h); no casts/red cells Normal Normal nd Blood culture Negative Negative Negative nd Throat swab Nd Normal flora nd nd Electrocardiogram Normal nd nd nd Chest x-ray Normal Normal Normal nd Echocardiogram Transthoracic normal; transoesophageal not tolerated by patient nd nd nd ESR = erythrocyte sedimentation rate. nd = not done. ANA = antinuclear antibody. ANCA = antineutrophil cytoplasmic antibody. ENAs = extractable nuclear antigen antibodies. APTT = activated partial thromboplastin time. 2 Features of the rash in four patients ↑A. Generalised exanthem on trunk and limbs in Patient 2. ↑B. Palm desquamation in Patient 2. ↑C. Purpuric rash involving lower limbs, with areas of confluence on the lower calf in Patient 3. ↓D. Extensive erythematous exanthem over trunk and limbs in Patient 4. ↑E. Palm desquamation in Patient 4.

Jon N Currie FRACP, FAChAM · Jimmy Chien BMed · Lisa Snell RN · Margaret Cluff RN · Karen Scrivener RN · Lucinda Wallman PhD, FRACP, FRCPA · Elizabeth M Benson FRACP, FRCPA

A man who had been taking prescribed methadone for many years presented with a desquamating rash (predominantly affecting the hands and feet) complicated by cellulitis of the right leg. There have now been multiple reports of a similar rash among methadone users in Sydney. The cause remains unknown. We report a man attending a methadone program in south-east Sydney who presented with a distinctive rash complicated by lower-leg cellulitis. This case adds to the widespread reports of a similar rash in methadone users around Sydney. The cause is under investigation by the New South Wales Department of Health. Clinical record In October 2004, a middle-aged man was referred to a hospital in south-east Sydney with a 14-day history of a painful, swollen, erythematous right lower leg and fever. Two days before onset of the leg symptoms, he had noticed a non-pruritic rash which started on his legs and feet and spread to abdomen and arms; it was accompanied by swelling, and then desquamation of the hands and feet. He had been diagnosed with cellulitis of the right lower leg 7 days before presentation and was prescribed oral flucloxacillin, but his condition did not improve significantly. Duplex ultrasound examination of the right leg 2 days before presentation excluded deep vein thrombosis. He was admitted to hospital for intravenous antibiotic treatment. The patient was a former intravenous heroin user and had been in a methadone program at a local pharmacy for the previous 8 years. He denied recreational drug use or injecting or sharing the oral methadone. His past medical history included previous right-leg deep vein thrombosis, chronic hepatitis B and C infection, gastro-oesophageal reflux, as well as melanoma excision several years before, and cholecystectomy a month previously. He had been taking griseofulvin for about 3 months for onychomycosis. He was taking methadone syrup (160 mg daily), griseofulvin (500 mg daily) and, when required, diazepam (5 mg three times daily), codeine/paracetamol (30/500 mg three times daily) and oxycodone (40 mg twice daily). He had recently started using, when required, cyproheptadine (4 mg at night), hyoscine (20 mg four times daily) and triamcinolone acetonide (0.02% cream topically) for the rash, and metoclopramide (10 mg three times daily) for mild nausea. On physical examination, the patient was haemodynamically stable and looked well. His temperature was 37.2°C. There was erythema, tenderness and warmth below the right knee, consistent with cellulitis. There was desquamation of the skin of both his lower legs, soles of feet (Box, a) and palms and fingers (Box, b), as well as non-pitting oedema of the feet and hands. There was hyperkeratosis of the soles, with xerosis and an erythematous maculopapular rash of the arms. The skin condition did not appear typical of disorders causing hyperkeratosis and desquamation, which usually do not present concurrently. He had no mucosal ulceration. Differential diagnoses included the early phase of an exfoliative erythroderma, psoriasis triggered by infection, early pityriasis rubra pilaris, bacterial toxin-mediated exfoliation, viral exanthem, sarcoidosis and syphilis. Rash in a patient who used oral methadone A: Hyperkeratosis and desquamation of the soles of the feet. B: Desquamation of the palms. C: Biopsy specimen from the maculopapular rash on the left arm, showing a slightly thickened epidermis with focal parakeratosis (P), and mild perivascular lymphocytic infiltrate (I). (Original magnification, × 20; haematoxylin–eosin stain.) Measurement of serum electrolyte, urea and creatinine levels and liver function tests all gave normal results. A full blood count revealed haemoglobin level of 125 g/L (reference range [RR], 130–180 g/L) and slight eosinophilia (0.48 × 10 9/L; RR, 0.04–0.44 × 10 9/L), but total white cell count was within the reference range (6.2 × 109/L; RR, 3.5–11.0 × 10 9 /L). Erythrocyte sedimentation rate was 10 mm/h (RR, 1–10 mm/h) and C-reactive protein level was 24 mg/L (RR, < 3 mg/L). Blood cultures showed no growth. A test for Treponema pallidum antibody was negative. Chest x-ray was normal, and HIV antibody test negative. Skin biopsy of the red macules on his left arm (Box, c) and the right-leg biopsy revealed non-specific histological changes, suggestive of chronic dermatitis. Periodic acid–Schiff staining for fungi was negative. Empirical treatment was begun with mometasone cream (0.1%), calcipotriol ointment (0.005%) and sorbolene cream twice daily to affected areas, and coal tar (5%) and salicylic acid (5%) in sorbolene base cream at night to the feet. Intravenous cephazolin (1 g three times daily) and oral clindamycin (300 mg four times daily) were begun for the cellulitis. The patient was discharged on Day 4 with the above topical preparations and oral cephalexin (500 mg three times daily), after both the rash and right-leg cellulitis abated significantly. He failed to attend a follow-up appointment, but reported by telephone that the rash had gradually resolved over several weeks. Discussion This case raises the alert to a possible adverse reaction to a methadone preparation. The cause may be methadone itself, another component of the preparation, or a contaminant. Previously reported cutaneous reactions to methadone include angioedema, facial oedema, flushing, pruritus, purpura, rash and urticaria.1 To our knowledge, no cases have been reported of a desquamating rash associated with methadone or other opioids. The cause of the rash in our patient did not appear infectious. He had no clinical evidence of staphylococcal toxic shock syndrome; he remained clinically well and did not develop the diffuse confluent erythema typical of this syndrome. Nor was the rash typical of a viral exanthem, in which a widespread morbilliform eruption predominates, without confluent erythema (as occurred on the lower legs), hyperkeratosis or desquamation. A reaction to a medication other than methadone seems less likely, as there had been no recent change. We are aware of other patients with a similar rash, oedema and desquamation of the hands and feet, all taking methadone: six patients in a methadone program at the same pharmacy as our patient, 20 from a local methadone clinic, and others at other methadone centres in Sydney (Mary Anne Ford, Registered Nurse, Bayside Clinic, Sydney, NSW, personal communication). We know of no patient with a similar rash who is not using methadone, and we believe all affected patients were taking the same brand and formulation of the drug. Most cases have been mild, and close contacts have not been affected. All patients appear to have continued using methadone from their usual dispensing clinic, and the rash has resolved over several weeks. The cause of the reaction remains unknown, and is possibly even an illicit drug available on the street. However, as all affected patients appear to have been taking methadone, this is perhaps the most likely agent. Marijuana has been reported, albeit rarely, to cause allergic reactions, and occasionally becomes contaminated with biological or chemical substances that might cause a reaction.2 -4 However, in that situation, one would expect cases to be more widely distributed outside the methadone-using population. In addition, at least one client with this rash from the local methadone clinic had a negative urine test for cannabinoids (Mary Anne Ford, as above, personal communication). Further investigation of these cases is required to determine the aetiology. Variables to be considered include the brand and batch of methadone used, storage, dose, mixing of batches in the dispensing pump, and other solutions included in the preparation to increase palatability. Pharmacists often mix batches of methadone and are not required to record the batch number dispensed to each patient, which makes tracing difficult. Also important to consider are any other prescription or non-prescription medications taken by patients, illicit drugs used, and sharing of methadone between patients from different methadone clinics. Many more cases may have been unreported and unrecognised, as most affected patients have had relatively mild and self-limiting symptoms. An investigation is now under way by the New South Wales Department of Health. Methadone clinics, pharmacists, dermatologists, general practitioners and emergency medicine staff need to be aware of the possibility of these reactions.

Natalie Kordjian BPharm, MB BS · Annabelle D Donaldson MB ChB · Steven A Krilis PhD, FRACP · Dedee F Murrell MA, BM BCh, FAAD(USA)

Objective: To examine the impact of a sudden and dramatic decrease in heroin availability, concomitant with increases in price and decreases in purity, on fatal and non-fatal drug overdoses in New South Wales, Australia.Design and setting: Time-series analysis was conducted where possible on data on overdoses collected from NSW hospital emergency departments, the NSW Ambulance Service, and all suspected drug-related deaths referred to the NSW Coroner’s court.Main outcome measures: The number of suspected drug-related deaths where heroin and other drugs were mentioned; ambulance calls to suspected opioid overdoses; and emergency department admissions for overdoses on heroin and other drugs.Results: Both fatal and non-fatal heroin overdoses decreased significantly after heroin supply reduced; the reductions were greater among younger age groups than older age groups. There were no clear increases in non-fatal overdoses with cocaine, methamphetamines or benzodiazepines recorded at hospital emergency departments after the reduction in heroin supply. Data on drug-related deaths suggested that heroin use was the predominant driver of drug-related deaths in NSW, and that when heroin supply was reduced overdose deaths were more likely to involve a wider combination of drugs.Conclusion: A reduction in heroin supply reduced heroin-related deaths, and did not result in a concomitant increase, to the same degree, in deaths relating to other drugs. Younger people were more affected by the reduction in supply.

Louisa J Degenhardt PhD, MPsych(Clinical) · Elizabeth Conroy BA · Stuart Gilmour BSc · Wayne D Hall PhD

Objective: To determine the effectiveness of intranasal (IN) naloxone compared with intramuscular (IM) naloxone for treatment of respiratory depression due to suspected opiate overdose in the prehospital setting.Design: Prospective, randomised, unblinded trial of either 2 mg naloxone injected intramuscularly or 2 mg naloxone delivered intranasally with a mucosal atomiser.Participants and setting: 155 patients (71 IM and 84 IN) requiring treatment for suspected opiate overdose and attended by paramedics of the Metropolitan Ambulance Service (MAS) and Rural Ambulance Victoria (RAV) in Victoria.Main outcome measures: Response time to regain a respiratory rate greater than 10 per minute. Secondary outcome measures were proportion of patients with respiratory rate greater than 10 per minute at 8 minutes and/or a GCS score over 11 at 8 minutes; proportion requiring rescue naloxone; rate of adverse events; proportion of the IN group for whom IN naloxone alone was sufficient treatment.Results: The IM group had more rapid response than the IN group, and were more likely to have more than 10 spontaneous respirations per minute within 8 minutes (82% v 63%; P = 0.0173). There was no statistically significant difference between the IM and IN groups for needing rescue naloxone (13% [IM group] v 26% [IN group]; P = 0.0558). There were no major adverse events. For patients treated with IN naloxone, this was sufficient to reverse opiate toxicity in 74%.Conclusion: IN naloxone is effective in treating opiate-induced respiratory depression, but is not as effective as IM naloxone. IN delivery of naxolone could reduce the risk of needlestick injury to ambulance officers and, being relatively safe to make more widely available, could increase access to life-saving treatment in the community.

Anne-Maree Kelly MD, MClinEd, FACEM · Debra Kerr RN, MBL · Zeff Koutsogiannis MB BS, FACEM · Paul Dietze PhD · Ian Patrick · Tony Walker

Re: “The hidden tragedy of offender deaths”, the editorial by Stuart Ross in the 1 November issue of the Journal (Med J Aust 2004; 181: 469-470). The reference numbering in the text is incorrect because of a computer error. In the first 3 paragraphs, references 12, 13, 14 and 15 should be references 1, 2, 3 and 4, respectively. All other references are correct, except for reference 13 in the last paragraph of the text, which, again, should be reference 2. The html and pdf versions of the article published in the eMJA were corrected on 17 December 2004.

Stuart Ross

Barbara A Hawkshaw,* Yeqin Zuo† * Planning and Evaluation Officer, Health Promotion Unit, Central Sydney Area Health Service, Level 9 North, King George V Building, RPAH, Missenden Rd, Camperdown, NSW 2050; † Currently Tobacco Control Program Coordinator, Cancer Institute NSW, Sydney, NSW barbara.hawkshawATemail.cs.nsw.gov.au To the Editor: The World Health Organization recommends that hospital staff ask about the smoking status of every patient, and offer brief quit advice and pharmacotherapy.1 These effective strategies2 underlie the Central Sydney Area Health Service (CSAHS) Smoke Free Environment Policy,3 which specifies the use of nicotine replacement therapy (NRT) in managing nicotine dependence of inpatients. Recording quit advice is yet to become a regular feature of medical records, but documentation of smoking status and NRT prescribing is evidence of compliance with the policy. To monitor the implementation of this policy in CSAHS, we examined the medical records of smokers for evidence of NRT prescribing in hospital or at discharge. A small sample was chosen to provide a “snapshot” of NRT use. First, we identified 2718 patients admitted to Royal Prince Alfred Hospital and Canterbury Hospital between 1 July 2001 and 30 June 2002 who were single admissions, stayed 48 hours or longer, and were current smokers (ICD-10 code Z720).4 Current smokers were defined as those who had smoked any tobacco in the past month.4 Sixty medical and 60 surgical patients from each hospital were selected randomly by random number generation (medical/surgical status was based on the specialty of the admitting doctor). After excluding 33 patients who were either ex-smokers or smokers who died during admission, the sample included 207 patients. Records were examined for smoking history, NRT prescribing during hospitalisation, and documentation of smoking status or NRT prescribing on discharge summary. NRT was prescribed to 13 patients (6.3%) during their hospitalisation (Box). All 13 received patches. A larger proportion of medical patients than surgical patients had NRT prescribed in hospital (8.1% v 4.6%) and at discharge (7.1% v 2.8%). In 8% of records, smoking was identified on the discharge summary. Most records (80%) provided numerical information about daily cigarette consumption. Seventy per cent of our sample smoked more than 10 cigarettes per day. Other records described consumption in subjective terms only, such as “heavy”. We believe that this is the first study in Australia to estimate the NRT prescribing rate for inpatients using medical record audit. Very few patients who were smokers were prescribed NRT. It is encouraging that most patients who were prescribed NRT were given a supply of patches at discharge. The NSW Health Department’s Guide for the management of nicotine dependent inpatients is a commitment to assisting people to quit.5 Implementation of the CSAHS Smoke Free Environment Policy3 by hospital staff requires a greater knowledge of the barriers to prescribing NRT and documenting quit activities at all levels of the hospital system. Nicotine replacement therapy (NRT) prescribing and smoking history Medical* Surgical* Total NRT prescribing (n = 99) (n = 108) (n = 207) During hospital stay 8 5 13 (6%) At discharge 7 3 10 (5%) Smoking history (n = 99) (n = 108) (n = 207) Number of cigarettes recorded 76 90 166 (80%) Years of smoking recorded 26 41 67 (32%) Cigarettes per day (n = 76) (n = 90) (n = 166)† 1–10 25 24 49 (30%) > 10 51 66 117 (70%) * Admission categorised according to specialty of admitting doctor. † Only 80% of total sample indicated number of cigarettes per day.

Barbara A Hawkshaw · Yeqin Zuo

The justice system could go further in supporting the needs of those it detains after they are returned to the community Nearly 20 years ago, public attention was drawn to the previously hidden tragedy of deaths in prison and police custody. Initially, attention was focused on deaths of Indigenous people. However, it quickly became apparent that the death rate for all people held in custody was much higher than that for the general population. The result was a detailed investigation into the causes of the problem, in the form of the Royal Commission into Aboriginal Deaths in Custody.1 The Royal Commission made over 300 recommendations on penal policy, cell design, custody management regimens, treatment programs, services to Indigenous offenders and a host of other topics. In addition, the Deaths in Custody Monitoring Program was established at the Australian Institute of Criminology (AIC) to scrutinise and report on deaths in prison or police custody.2 In parallel with the acknowledged problem of deaths in custody, there is an equally significant tragedy in the form of high death rates among released prisoners3-5 and offenders in the community.6,7 In the decade after the Royal Commission (1990 to 1999), the AIC monitoring program recorded 628 deaths in police or prison custody. Over the same period, in Victoria alone, 820 men and women who had been released from prison died unnatural deaths.4 The study by Coffey and colleagues in this issue of the Journal (page 473) shows that the problem is not confined to adult offenders but affects juveniles as well.8 The high rate of unnatural deaths among offenders living in the community is a major public health issue, but what can we do to reduce these rates? One of the groups at greatest risk is injecting drug users — over half of the unnatural deaths examined in the earlier Victorian study were heroin related,4 and drug-related offences were an indicator of high mortality risk in the study by Coffey et al.8 Drug treatment and maintenance (methadone) programs lower the risk of death by overdose.9 However, many of those at greatest risk are profoundly alienated from society, and we need to find ways to engage them. For example, heroin-dependent Indo-Chinese offenders frequently face rejection by their families and community, and are isolated from the mainstream community as well. Female offenders often come from backgrounds of extensive sexual and physical abuse, their heroin dependency is often supported by prostitution,5 and any interventions need to take account of their responsibilities as parents.10 Treatment and maintenance programs need to be delivered in ways that meet the material, social and cultural needs of those at risk. Overdose risk can be dramatically lowered by behaviour changes, like not using drugs by yourself, being aware of variations in the purity of heroin, and not taking heroin in conjunction with alcohol or benzodiazepines. Again, the problem is partly that those at greatest risk are also the most difficult to communicate with, and tend to be unrealistic in judging risks to themselves. Peer-based education and information dissemination programs have shown they can transmit the key messages about risk reduction to this group (eg, how to avoid overdose and recognise its signs),9 but, again, a range of approaches tailored to the needs of specific groups at risk is required. Such approaches could include maximising the effectiveness of needle and syringe program workers by having them provide standardised, evidence-based messages and materials on safe injecting, overdose prevention and support options.9 The importance of heroin as a cause of unnatural death should not obscure the other dangers that offenders face. Individuals who have the combination of mental disorder and drug and alcohol misuse experience much higher risks of both overdose and suicide and can find it difficult to obtain the kind of treatment and support services that might alleviate their problems. Older offenders are at increased risk of a variety of general health problems, such as diabetes, cancer and liver disease, and there need to be programs that link at-risk offenders with healthcare and support services.11 People who are released from custody are at greatly increased risk, in part because their tolerance for heroin is reduced, and also because return to the community can be a time of great emotional stress. Prisoner release support programs like the Victorian Bridging the Gap program have shown that the period before release can be an important “window of opportunity” when offenders are motivated to plan for their release.12 A key feature of this program is intensive, outreach-based support, with the support agency helping the releasee to identify his or her specific needs and brokering access to material support, healthcare and social services. Releasees who participated in Bridging the Gap had improved outcomes as measured by accommodation stability and engagement in drug-treatment programs, and these in turn translated into lower rates of reoffending.12 Finally, we need to attend to an important lesson from the Royal Commission. Despite real improvements in custodial management, the number of deaths of Indigenous people in custody has continued to increase because there are now more Indigenous people in custody.2 The high rate of unnatural deaths among offenders is a public health problem that requires changes in the way that healthcare services are delivered to this vulnerable population. However, we also need to recognise that the justice system has a key role to play in ensuring that its goals of punishing offenders and preventing crime are properly balanced by a consideration of the health and support needs of the people who are the subjects of its interventions.

Stuart Ross

Objective: To identify patterns of mental health, prescription drug use and personal circumstances associated with heroin overdose in young people.Design: Linkage of data on use of Pharmaceutical Benefits Scheme (PBS) prescription drugs with data from a self-report questionnaire.Setting: Inner metropolitan Melbourne, Australia.Subjects: 163 young people, 15–30 years, using heroin.Main outcome measures: Personal circumstances, mental health (as measured by various scales), and PBS-listed prescription drug use.Results: Young people using heroin reported high rates of feelings of hopelessness, depression, antisocial behaviour, self-harm and diagnosed mental illness. A prior history of overdose was associated with previous mental illness, which in turn was associated with being female, having poor social support, being dissatisfied with relationships, and living alone or in temporary accommodation. While feelings of hopelessness and antisocial behaviour were strongly associated with overdose history, the number of PBS prescription drugs used had a very strong relationship with overdose, particularly benzodiazepines, other opioids, tricyclic antidepressants and tranquillisers.Conclusions: Further research to explore causal relationships between prescription drugs and heroin overdose is warranted. Improved data linkage to PBS records for general practitioners may facilitate safer prescribing practices.

Jane M Burns BA (Hons), PhD · Raymond F Martyres MB BS, MMed, FRACGP · Danielle Clode BA(Hons), DPhil(Oxon) · Jennifer M Boldero MA, PhD

Addiction is a treatable disease and patients can enjoy rather than endure recovery My work is regarded in various ways by my colleagues. Some see me as a quixotic figure ranting futilely against the impregnable world of alcohol and other drugs, as in the cartoon. Others see me as a sort of medical Mother Teresa on Sydney’s North Shore, devoted to a life of cleaning others’ mess. I think most simply shake their heads, believing that I am delusional and beyond help. This article seeks to define and refine this “delusion”: that addiction is a disease, that it is treatable, and that patients enjoy rather than endure recovery. Do addicted doctors need special treatment?I sometimes feel that all the hard work and inconvenience of gaining a medical qualification is worth it for one short sentence: “Doctor is busy.” As doctors, we have a wealth of privileges not afforded other members of the community. Not only are we excused for lateness, we also have access to a wide range of medicines (many of them dangerous, even in prescribed doses), and are permitted, even expected, to examine people’s bodies and to ask intrusive questions. With these privileges come ethical dilemmas that are not new to the profession — abortion, euthanasia, inappropriate relationships with patients, confidentiality, and commitment to training the next generation of practitioners. All rate a mention in the Hippocratic Oath. However, Hippocrates did not have a protocol for addicted colleagues. The saying that addicts and alcoholics are just like other people except more so is attributed to Sylvester Minogue, a psychiatrist influential in the introduction of Alcoholics Anonymous to Australia. I believe that alcoholic and addict doctors are just like other alcoholics and addicts, except more so. The issues of shame and guilt, of inability to believe that an intelligent person could perform such irrational and obviously unintelligent actions, still abound. Furthermore, colleagues who are patients know and have opinions about many interventions, reducing any chance of a placebo effect and virtually eradicating the impact of medical advice. They’re in the club, and they look carefully for any hint of superficiality in explanations and advice. Are addicts simply adults behaving very badly?Understandably, the moral stance has been the traditional first response by families, communities and medical boards when learning of a doctor’s addiction. Attempts to keep the community safe from addicted doctors have traditionally involved the law and lawyers, in a process that selected out, then deregistered, the “bad apples”. The problem is that addiction also occurs in undeniably “good” colleagues, whose work and track record make it both unacceptable and unhelpful to deal with them punitively (Anecdote 1 and Anecdote 2). Addiction is not “like” a disease — it is oneThis is the heart of my fortifying “delusion” and a debate in which I participated in the Journal in 1992. 1,2 Then, as now, I believed that addiction is a disease because it has definable clinical features, a substantial genetic influence, a reasonably predictable natural history, effective treatments, and even potential biological markers. More recently, others have compared addiction with medical conditions like asthma, diabetes and hypertension. 3 These comparisons have yielded remarkable similarities in genetic heritability, pathophysiology, role of personal responsibility, and treatment response. The effectiveness of drugs such as naltrexone4 and acamprosate5 in the short- and medium-term course of alcohol dependence, and methadone in opiate dependence,6 also argues strongly for medical involvement. The issue of hopelessnessEven more important than whether addiction is a disease is the fact that prognoses are not nearly as hopeless as most medical colleagues believe. The natural history of alcohol addiction can include remission, mostly through long-term abstinence, and often associated with attendance at Alcoholics Anonymous (Anecdote 3). 7 However, the fact that psychosocial interventions work (as they do for many medical conditions) does not render addiction a “non-medical” problem, as some have argued. Sustained abstinence is not an end in itself. If prolonged abstinence merely resulted in a desert of joylessness, as so many people in active addiction fear, then my job would indeed be difficult. In fact, real recovery takes off once abstinence becomes comfortable. New relationships are formed or old ones improved. Central issues, such as what constitutes meaning in life, are addressed. That common core belief of self-inadequacy begins to wither. If addiction is a disease and resetting one’s neural “reward” pathway from the ventral tegmental area to the nucleus accumbens of the brain is a key feature,8 then the treatment is only complete when ego-syntonic activities are fully rewarding — that is, previously enjoyed experiences, such as the joy of relationships, work and recreation, are fully enjoyed once more. Patients of mine in longer-term recovery do not continue to mourn for the moments of pleasure experienced at the end of a needle or a drinking binge. Instead, they are grateful for each sober day. Often, they gladly provide me with assistance with newer patients. Rehabilitation: a more enlightened attitudeThe progress made in treating doctors’ addiction is obvious over my 20 years of practice. Medical or licensing boards worldwide have come to recognise that the safety of the community is enhanced by having a rehabilitative attitude to alcohol and drug dependence. 9 Unidentified doctors still drinking or using drugs pose a greater danger to the community than those who have been identified, are seeking treatment, and are supervised by a stringent medical board program. Medical boards have also come to recognise that monitoring impaired doctors in a process independent of the treatment process is likely to be more beneficial for both doctors and the community. Both treatment and monitoring are important and neither should interfere with the other. The NSW Medical Board was at the vanguard of this movement in developing the Impaired Registrants Program (IRP). Under this program, doctors identified as having breached laws or regulations (such as the NSW Poisons and Therapeutic Goods Act 1966 through self-prescribing of drugs of addiction) make certain voluntary undertakings, such as to attend for assessment by a Board-appointed psychiatrist (whose only role is to provide detailed feedback for the Board’s use). 10 One of the conditions imposed by the IRP is for the practitioner to concurrently undergo treatment. Soon after the establishment of the IRP, I decided that I would be a treating psychiatrist and never a Board-appointed one. I have become much more disposed to referring my medical colleague patients to the IRP, as I have found that assessments by independent psychiatric colleagues can augment and monitor my own assessments and treatment. My other (non-medical) patients do not have the back-up of an independent assessment every 6 or 12 months. My involvement in this process also means I receive regular reports from the Medical Board about my patients and any changes to their conditions. My own frisson of anxiety at receiving an unexpected piece of mail from the Board reminds me of just how trying this process is for my patients. Issues of concern for doctors on monitoring programsMany problems can loom larger than usual for doctors in medical board monitoring programs. For instance, confidentiality is absolutely paramount (Anecdote 4), a drug test result that has gone astray may be misconstrued as a deliberately missed test, and false-positive test results can be especially trying for someone in recovery and working hard to comply with every condition of the IRP (Anecdote 5). All NSW doctors in the IRP are identified as such on their medical registration cards, which bear the word “conditional”. This can be a great source of agitation, and, as some suspect, of prolonged unemployment. Lest I be seen as advocating greater freedoms for doctors on the IRP, let me also say that some doctors may show enough change to satisfy their supervisors, but seem to gain little real insight into their problems. The NSW program is unable, in its present form, to deal with this issue of reluctant compliance. The futureTrends in the United States are for programs that manage identified addict and alcoholic doctors to be handled by systems outside medical boards. These newer programs (including one in Victoria) are called “Doctors Health Programs” (DHP). Most of these are funded in much the same way as medical boards, by medical registration fees, but these programs are independently involved in monitoring, often at four levels (individual, group, workplace and pathology), leaving the medical board to perform disciplinary functions. These programs are probably more intrusive than the ones run by the medical boards, but, while disciplinary procedures may still be imminent if compliance with the DHP is found wanting, many find it an advantage that the term “conditional” is not emblazoned across the registration papers of a doctor in early recovery. Anecdote 1 Dr A was a trainee physician who had been practising in another jurisdiction. He returned to Sydney, unregistered, and was referred by a senior specialist. A had developed an addiction to pethidine in the context of major social upheaval while working, and had been found diverting some from the hospital. His registration was suspended for 9 months, but no treatment was offered. On his return to Sydney and referral to my care, he was only able to gain the benefit of the NSW Impaired Registrants Program (IRP) after his suspension elsewhere ended. He responded to a regimen including counselling, urine testing and regular review by the IRP. Initially, he worked in unfashionable posts, but later returned to his previous level, passed his specialist exams, married and had children. Anecdote 2 Dr B was an influential specialist who referred himself, saying that his principal problem was migraines, but he had begun to self-medicate with a variety of opiates, including pethidine. Representatives of the Pharmaceutical Services Section of the Department of Health (which monitors the dispensing of Schedule 8 drugs in New South Wales) had visited him and informed him that it would be best if he voluntarily surrendered his right to prescribe S8 drugs. On taking a history, I discovered that, some 20 years before, he had been identified as having misused opiates, been reprimanded by the Medical Board, and been sent for treatment, which was unconventional, unmonitored, and, as his current presentation showed, ineffective. Anecdote 3 A 22-year-old medical student’s drinking habits and poor exam results were a source of concern to his supervisors. He was called before the warden of the clinical school and reprimanded. He resentfully disregarded this advice, but soon after was serendipitously placed as a medical student at a drug and alcohol treatment facility, where he identified himself as an alcoholic. He became a member of Alcoholics Anonymous and has remained sober and happy for many years without treatment. I know of his story because he sometimes helps me in supporting my medical patients. Anecdote 4 Dr C, a Resident Medical Officer from another hospital, rang to say that he desperately needed inpatient treatment under my care. I agreed, not learning until later that he was due to commence a term at Royal North Shore Hospital in the 12 months after his discharge. Subsequently, a colleague and rival of C was found to have enquired about gaining access to C’s inpatient medical records. C’s initial distress was well managed, he became a dedicated Narcotics Anonymous member, and has now graduated from the Impaired Registrants Program and been drug-free for more than 5 years. Anecdote 5 A colleague referred his patient, Dr D, who had been self-injecting benzodiazepines and lying about his alcohol use. After a brief negotiation, D informed the Impaired Registrants Program. He began urine testing, attending the Doctors Recovery Group and Alcoholics Anonymous. D became distressed when, despite a month of abstinence, his urine was still testing positive for benzodiazepines. He sought detailed quantitative analysis of his urine benzodiazepine levels allowing for the urine concentration, which subsequently showed an exponential decline consistent with abstinence. After only a year, his work, marriage, parenting, physical health and leisure pursuits have all improved dramatically.

Stephen M Jurd MB BS, FRANZCP, FAChAM

Objective: To assess the effect of a restriction on publicly subsidised temazepam 10 mg capsules upon the injection of benzodiazepines by injecting drug users (IDUs).Design and participants: Cross-sectional study of regular IDUs targeting periods before and after the policy change. Analysis of prescription data, including time-series analysis.Setting: Drug services in the capital cities of New South Wales, Victoria, Tasmania, Queensland and the Northern Territory.Main outcome measures: Changes in prescriptions and patterns of benzodiazepine use; harms associated with benzodiazepine use.Results: There was a decrease in temazepam 10 mg capsule prescriptions and a corresponding increase in temazepam 10 mg tablet prescriptions after the policy change. IDU survey data suggested that IDUs continued to inject benzodiazepines and temazepam capsules. The frequency of the injection of capsules after the restriction appeared similar to that before the policy change. There was no change in the frequency of injection of tablets. Most IDUs reported obtaining their benzodiazepines from doctors, with substantial proportions obtaining capsules even after the restriction. About half the IDUs reported purchasing benzodiazepines on the street. Most IDUs who injected benzodiazepines reported injection-related problems.Conclusion: Limiting the prescribing of temazepam capsules may have reduced their injection by some IDUs, but additional strategies are needed to reduce the misuse among this group. These may include further restriction of capsule preparations, continued education of doctors and IDUs, and the examination of prescribing practices of individual doctors.

Courtney L Breen MPH(Hons), GradDipSc(Psych), BSc · Louisa J Degenhardt PhD, BSc(Hons) · Amanda D Roxburgh BAHons(Psych), MCrim · Raimondo B Bruno BSc(Hons) · Rebecca Jenkinson BEng(Geo), GradDipEpiBiostats

Objective: To identify deaths in Australasia associated with overdose of γ-hydroxybutyrate (GHB) and its precursors (γ-butyrolactone and 1,4-butanediol).Design: A retrospective search of medical and scientific information sources, as well as popular newsprint, for the period January 2000 – August 2003, with formal clinical, toxicological and forensic evaluation of retrieved data.Main outcome measure: Death associated with forensic data implicating GHB or its analogues.Results: Ten confirmed GHB-associated deaths were identified, with eight considered to be directly attributable to GHB. Only two of these eight cases were positive for ethanol toxicology.Conclusions: Our study supports the existing evidence that GHB overdose is associated with fatalities, and that fatal overdoses occur in the context of isolated use.

David G E Caldicott BSc(Hons), MB BS · Fiona Y Chow MB BS, FACEM · Brian J Burns MB BCh, BAO, MRCSEd(A · Peter D Felgate BSc(Hons) · Roger W Byard MB BS, MD, FRCPath

T C K Brown Former Director of Anaesthesia, Royal Children's Hospital, Flemington Road, Parkville, VIC 3052. tckbrownATnetspace.net.au To the Editor: The epidemic of recreational use of γ-hydroxybutyrate (GHB; also known as γ-OH) is a cause for concern, as it is a basal anaesthetic agent (ie, it renders the patient unconscious, with analgesic supplementation required for surgery). It is not surprising that people taking too much of it are becoming unconscious.1 GHB was introduced in France as a basal anaesthetic agent by Laborit about 1960. It has a slow onset of action (up to 10 minutes when given intravenously, thought to be due to conversion to an active metabolite, γ-butyrolactone).2 It causes bradycardia, sometimes requiring atropine administration to maintain cardiac output, and raises blood pressure. Respiration is slow and deep, so that alveolar ventilation is not reduced. Trials of GHB as an anaesthetic were conducted in Melbourne by Dr William Cole and myself in the late 1960s,3-5 and it was used for microlaryngeal surgery for several years. Its major problems were prolonged sleep (1–3 hours after 40–100 mg/kg in children) and a high incidence of postoperative vomiting, adding the danger of aspiration in unconscious patients. GHB was also tried as an anaesthetic in Dunedin, New Zealand, where it was found that the sleep time could be reduced by intravenous administration of physostigmine.6 The fact that this drug is a basal anaesthetic needs to be more widely publicised.

T C K Brown

Harm-reduction approaches are more easily embedded in policy when drugs are legally regulated “Harm reduction” in relation to drugs refers to policies and practices intended primarily to reduce the health, social and economic costs of mood-altering drugs without necessarily restricting their consumption. The recognition of AIDS in 1981, and the subsequent realisation of the magnitude of the threat of HIV spread among and from injecting drug users, has given increasing prominence to harm-reduction approaches. The 15th International Conference on the Reduction of Drug Related Harm was held in Melbourne from 20 to 24 April 2004. This is the third time this conference has been held in Australia, an indication of Australia’s leadership position in this field for nearly two decades. The goal of the conference is to bring together people representing the diverse aspects of harm reduction, and the conference’s theme was “Minimising the harm: maximising the impact”. As a reflection of the growing strength of the harm-reduction movement worldwide, the conference attracted over 1100 delegates from more than 40 countries. Delegates included researchers, clinicians, policy makers, law-enforcement officers, politicians, past and present drug users and private industry representatives. Cross-sectoral and interdisciplinary discussions and networking were a major feature of the conference. The 875 papers presented (including 450 posters) covered a diverse range of topics (see Box) and encompassed a wide range of approaches, including sophisticated science, complex policy analysis and activism. Research methods varied from quantitative epidemiology, qualitative ethnography, randomised clinical trials to economic analyses. Round-table discussion and other interactive forums were common, and the conference included the first international festival of films about drugs and harm reduction. Legal drugs (alcohol and tobacco), which account for 4% of the global burden of illness, were the subject of only 10% of papers, compared with illicit drugs, which account for 0.8% of the global burden of illness, but to which almost 90% of papers were devoted. This reflects the reality that harm-reduction approaches are much more easily embedded in policy when drugs are legally regulated. Public health and human rightsPublic health was the major framework for many conference speakers, who saw harm-reduction approaches as essential for improving the health status of drug users and their communities. Other speakers emphasised the important links between human rights and public health. This aspect dominated many discussions of HIV prevention among injecting drug users in countries where this population is savagely discriminated against and driven underground, reducing substantially the effectiveness of health and social interventions. Harm-reduction tensionsA fertile debate centred on the relationship between harm reduction and demand reduction. For some speakers, preventing drug use sat uncomfortably with harm reduction, while many others saw no conflict in simultaneous efforts to reduce both demand and harm. The observation that “what works in drug policy is unpopular and what’s popular doesn’t work” struck a chord with delegates from many countries familiar with official denigration of evidence-based interventions, such as needle and syringe and methadone programs, and the zealous promotion of law-enforcement efforts to restrict drug supply, notwithstanding limited evidence of benefit. A second area of controversy is in the relationship between harm-reduction and law-enforcement approaches. An important paper by Peter Reuter (School of Public Affairs and Department of Criminology, University of Maryland, USA), a world expert on organised crime and the impact of drug policy, concluded that there was “no evidence to support law enforcement efforts” to curtail the availability of illicit drugs. Two senior Russian law-enforcement representatives demonstrated for delegates — somewhat unintentionally — the conflict around harm reduction within conservative law-enforcement ranks in Russia, and the difficulties of establishing effective drug policy and HIV prevention in environments where authorities rely almost entirely on harsh law-enforcement measures to control illicit drugs. The first representative called for tougher measures against drug traffickers, and said that, although Russia needed harm reduction, its introduction was impossible because it was illegal. His colleague counselled “methadone is a therapy of despair . . . like a death sentence”. Attending delegates strongly refuted the claims, with representatives from the Central Eastern European harm-reduction network pointing to the lawful establishment of needle and syringe programs in Russia. Other papers emphasised the now extensive research evidence supporting methadone maintenance and needle and syringe programs as highly effective harm-reduction strategies. For example, new data were presented at the conference based on evidence that needle and syringe programs in Australia had meant 25 000 fewer cases of HIV and saved up to $7 billion.1 Collateral damageCollateral damage from the “War against drugs” was a popular theme, with numerous illustrations of the severe counterproductive effects of current prohibition policies. Some speakers provided ample grounds for pessimism: thousands of drug users and traffickers mysteriously murdered in Thailand in recent years after a government-inspired campaign; five million new cases of HIV infection globally in 2003; widespread and active discrimination against illicit drug users; entrenched negative attitudes opposing harm reduction among some UN organisations and in some countries and regions; and an epidemic of incarceration of drug users in many countries. Ernie Drucker (Director, Division of Public Health and Policy Research, Montefiore Medical Center, Albert Einstein College of Medicine, New York City, USA) estimated that the introduction of the draconian Rockefeller drug laws in New York State in 1973, requiring harsh prison terms for the possession or sale of relatively small quantities of drugs, had resulted in more years of life lost than had the 2900 deaths in the attack on the World Trade Center on 11 September 2001. Positive progressSome speakers saw abundant grounds for optimism: the growing strength of the evidence base for harm reduction and rational drug policy; revolutionary recent shifts in attitudes in Central and Eastern Europe; the success of the recent decriminalisation of use and possession of all drugs in Portugal; the remarkable adoption and implementation of harm reduction in Iran; and the active involvement of law-enforcement participants in the conference, and their growing involvement in harm reduction worldwide. The scientific and policy aspects of the conference were balanced by more personal views: some speakers referred to immense personal loss from drugs, while others argued from their individual perspective for more humane attitudes towards drug users. Conference highlightsThe 2004 Annual National Rolleston Award is granted at each conference to an individual from the host country who has contributed outstandingly to harm reduction. The award perpetuates the memory of an influential English physician who, in 1926, supported the lawful provision of morphine or heroin to selected drug-dependent people if this would assist their leading “a fairly normal and useful life”. It was awarded to Mr Tony Trimingham, founder and coordinator of Family Drug Support, Sydney, for his work in support of families and friends of those affected by heroin-related deaths. There was a strong presence of Indigenous Australians and Indigenous culture throughout the conference. This reflected the enormous toll, initially from licit and more recently also from illicit, drugs on the health and wellbeing of Indigenous Australians. A presentation by Tony McCartney (Chair of the National Aboriginal Community Controlled Health Organisation) highlighted the ineffectiveness of policy, attracting considerable attention and concern from national and international delegates. However, numerous delegates praised many other aspects of Australia’s response to illicit drugs in recent decades. Another of the conference highlights was the annual Rolleston Oration. Former Australian Minister for Health, Neal Blewett (currently President of the Alcohol and Other Drugs Council of Australia), delivered the 2004 Oration. He presented a magisterial review of the almost two decades since he, as the responsible minister, oversaw the introduction of harm reduction in Australia in 1985. This shifted the emphasis of drug policy from intent to consequences, enabling the rapid introduction and vigorous expansion of measures that successfully controlled HIV infection among injecting drug users, and allowed policy makers to encompass legal as well as illegal drugs in a pragmatic policy framework. The current Indonesian Minister for Health, Dr Achmad Sujudi, made a strong call for the wide-scale introduction of harm-reduction measures in his country to stem the tide of HIV infection. Ms Marina Mahathir, President of the Malaysian AIDS Council, echoed this call, urging the adoption of effective and pragmatic, human-rights-based measures to combat AIDS in Asia. ConclusionJudging by the breadth and confidence of the discussions and presentations at the conference, harm reduction now seems to be leaving behind a phase of marginalisation and conflict and entering an era of mainstream acceptance and understanding. The conference disseminated new evidence of the effectiveness of harm-reduction approaches to drug problems, stimulated collaboration between participants from diverse backgrounds, gave new energy and confidence to harm-reduction practitioners from far and wide, and helped focus attention on how much more needs to be accomplished, especially in the global battle to contain the AIDS epidemic. Distribution of the topics of the verbal presentations at the 15th International Conference on the Reduction of Drug Related Harm.

Alison J Ritter PhD, MA(ClinPsych), MAPS · Alex D Wodak FRACP, FAFPHM, FChAM · J Nick Crofts MB BS, FAFPHM, MPH

A Rod MacQueen Clinical Director, Drug and Alcohol Services, Mid Western Area Health Service, Bloomfield Hospital, Forest Road, Orange, NSW 2800 rod.macqueenATmwahs.nsw.gov.au To the Editor: The article by Martyres et al on drug-seeking behaviour by young heroin users,1 leading to the deaths of 202 people over 5 years, leads to an inescapable conclusion. Too often, the medical profession is part of the problem rather than the solution, and as a result young people die. Here is an issue where the admonition primum non nocere should be foremost in our practice. After working with drug users and prescribing methadone for 22 years in a variety of settings, my experience is that drug users use drugs! Whether it is logical, safe or appropriate, or not, this group seeks drugs to modify or modulate their state of being. They often have serious medical and mental health issues, but have sadly decided on their preferred treatment without much knowledge of the diagnosis or of alternative interventions. They are often very skilled in obtaining drugs. So, we must perform our role equally well. Doctors are not drug dealers. Our duty is not to promote or support intoxication, or even relaxed happiness if that increases the risk of misadventure. It is to promote and support health. It is difficult to see how a prescription for 50 benzodiazepines to a young person (or even an older person) can ever be construed as healthcare. To do it again next day, next week, on and on, is almost unbelievable, yet the data indicate that is exactly what is happening.1 Even publicans have rules prohibiting serving intoxicated patrons. That one was “offering the customer what he asked for”, a common excuse for this sort of prescribing practice, would not be a suitable defence in the Coroner’s Court if insulin, digitalis, or even vitamin A, had been prescribed on request. But appeals to good practice and commonsense, along with current regulatory strategies, are apparently not sufficient to protect this vulnerable group. Kamien points out that data from the HIC could be used to provide immediate information to doctors about whether a patient is a “doctor shopper”.2 The data are already collected and could easily be made available if the will existed. Potential prescribers could at least gain accurate and timely information on which to base their decisions. There would be less excuse for “convenience store” prescribing, and more chance of ethical behaviour. At present these data remain largely useless in preventing avoidable deaths. But, surely, learning nothing from the deaths of 202 young Australians is not an option?

A Rod MacQueen