Letters

Faith healing or Russian roulette? MJA 1997; 167: 649 To the Editor: In 1995, a Brisbane woman visited a renowned faith healer in Manila for treatment of chronic tinnitus. The treatment involved the removal of what appeared to be a clot of blood from below her left ear and also one from her abdomen. The operation was performed seemingly by way of incisions at those sites without instruments or anaesthetic and using bare hands. During both procedures, blood was released which spilled onto her skin and stained her clothing. The woman's husband and brother-in-law, who witnessed and photographed the proceedings in close proximity, were convinced that what they had seen was genuine. However, following treatment her condition remained unchanged. To explore the facts more closely, the woman brought her bloodstained clothing to the Forensic Biology Laboratory in Brisbane. Examination of the clothing confirmed the presence of splashes and stains of human blood, but most appeared diluted. These findings were corroborated by photographs which showed the blood to be far less viscous than usual (Figure). Blood samples taken from her clothing were examined using three independent genetic tests: HLA DQA1, D1S80, and HUMTH01. These tests are commonly used in forensic practice to identify the origins of biological materials and stains such as blood, hair, saliva and semen; they distinguish individuals based on their genetic make-up. The results unequivocally showed that the blood on her clothing was not her own but a mixture of blood from at least two other individuals. As a precaution, she was tested for HIV and hepatitis B antibodies, both of which were negative after three months. Hundreds of people are treated by this faith healer every day. He is revered in the Philippines and people travel from all over the world to attend his "clinic". He also claims to travel frequently to other countries to perform his services. His healing power appears to be based on illusion. No doubt, the wellbeing of patients can be influenced by their confidence in their physician ("the placebo effect"). Judging by this man's reputation, it would seem that many have felt that they benefited from his treatment. However, it is a serious health concern that he uses blood to "convince" people that his practice is authentic, considering the number of people that he treats and the diversity of their backgrounds. The possible transmission of diseases such as hepatitis B and HIV to Australian citizens during these procedures would be of interest to Australian health authorities. Paul E Roffey Formerly, Forensic Scientist, Queensland Health Department; now Lecturer, School of Biomedical Sciences, Charles Sturt University, PO Box 588, Wagga Wagga, NSW 2678 E-mail: proffey AT csu.edu.au Leo C Freney Supervising Scientist Anthony J Ansford Director, John Tonge Centre for Forensic Sciences, Queensland Health Scientific Services, Brisbane, QLD - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Paul E Roffey · Leo C Freney · Anthony J Ansford

"Irukandji" syndrome: a risk for divers in tropical waters MJA 1997; 167: 649 To the Editor: Envenomation by the cubozoan jellyfish Carukia barnesi causes "Irukandji" syndrome (named by Dr Hugo Flecker after an Aboriginal tribe near Cairns).1 I report a case of Irukandji syndrome in a scuba diver for whom appropriate therapy was delayed because it was not initially considered as a possible cause of the patient's symptoms. A 28-year-old experienced diver was diving off Brampton Island in Queensland. During his second dive, at a depth of 6 m, he had a feeling of disequilibrium and so made a controlled ascent and removed his gear. His vague malaise was accompanied by aching pain in the groin and thighs, with numbness in the fingers and toes. This rapidly progressed to severe pain in the skin, muscles, face, jaw, testes and lumbar region, with profuse sweating and agitation. By the time he presented to the emergency department (after a delay of six hours because of transport difficulties), he was in great pain, with tachycardia (90 beats/min) and hypertension (170/100 mmHg). He was treated with 100% oxygen and pethidine (intramuscular and intravenous). At this stage, there were no diagnostic clues, except that symptoms had developed rapidly within minutes of his ascent. Decompression sickness was therefore considered, but after two conversations with the consultant at the Townsville General Hospital Hyperbaric Unit, an interview with the dive buddy, and in view of the patient's diving experience and the dive history, this diagnosis was dismissed. Irukandji syndrome was suggested and, when prompted, the patient recalled seeing a small jellyfish while descending and feeling a slight irritation on his right arm. A 3 cm x 4 cm oval inflamed area was evident on his right antecubital fossa and the patient provided a sketch of the jellyfish (Figure). He was commenced on an intravenous morphine infusion over 10 hours. Although a dull chest pain and lower-limb pain persisted, he did not require further analgesia. His serum creatine phosphokinase level peaked at 7317 IU/L (normal range, 10-60 IU/L) and his serum lactate dehydrogenase level reached 349 IU/L (normal range, 120-300 IU/L). Echocardiography after two days showed mild mitral valve regurgitation. Fortunately, the patient escaped the more sinister complications of Carukia envenomation (myocardial failure and pulmonary oedema).2-4 This is the first reported case where a patient with Irukandji syndrome identified the jellyfish. It has been reported that the syndrome may be mistaken for decompression sickness,5,6 thus evading rapid diagnosis and triggering costly evacuation and recompression procedures (J Williamson, Director of Hyperbaric Medicine, Royal Adelaide Hospital, personal communication). This case is a reminder that Irukandji syndrome can be a "diving-related illness", and should always be considered in the differential diagnoses of an ill diver in tropical waters. John C Hadok Senior Medical Officer, Emergency Department, Mackay Base Hospital PO Box 5580, Mackay, QLD 4740 E-mail: jchadokAThealth.qld.gov.au Fenner PJ, Williamson J, Callanan VI, Anderley I. Further understanding of, and a new treatment for, "Irukandji" (Carukia barnesi) stings. Med J Aust 1986; 145: 569-574. Fenner PJ, Williamson JA, Burnett JW, et al. The "Irukandji syndrome" and acute pulmonary oedema. Med J Aust 1988; 149: 150-156. Martin JC, Audley I. Cardiac failure following Irukandji envenomation. Med J Aust 1990; 153: 164-166. Herceg I. Pulmonary oedema following an Irukandji sting. SPUMS J (South Pacific Underwater Medicine Society Journal) 1987; 17: 95-97. Williamson J. Scuba diving perspective. In: Williamson JA, Fenner PJ, Burnett JW, Rifkin JF, editors. Venomous and poisonous marine animals. Sydney: University of New South Wales Press, 1996: 423-427. Williamson J. "Irukandji" syndrome or decompression sickness or cerebral arterial gas embolism? A differential diagnostic trap for practitioners of diving medicine in north Queensland. SPUMS J 1985; 15: 38-39. My thanks to Drs Bruce Todd, Bert Sadleir and Associate Professor John Williamson. - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

John C Hadok

Papilloedema and coma in a child: undescribed symptoms of the "Irukandji" syndrome MJA 1997; 167: 650 To the Editor: The "Irukandji" syndrome, so named in 1952,1 refers to the severe systemic symptoms that follow envenomation by the jellyfish Carukia barnesi,2,3 named by Dr Jack Barnes in 1964.4 Here, we report papilloedema and coma in a seven-year-old child who developed Irukandji syndrome after a jellyfish sting in the tropical waters of Cairns, in far north Queensland. The child was treated by one of us (R J H) in 1981, but not reported at the time and only recently described to colleagues. The boy was admitted to hospital with the severe systemic symptoms of Irukandji syndrome, including generalised muscle cramps, anxiety and sweating. Ten hours later, he was confused, disoriented, tachycardic and tachypnoeic, and had several episodes of profound sweating, cyanosis and agitation. Bilateral crepitations (more marked on the left) were heard on chest auscultation, and a chest x-ray showed increased interstitial markings consistent with pulmonary oedema. He had 4+ glycosuria, Dextrostix of 130 mg/100 mL (normal range, 80-120 mg/100 mL), and periodic auditory and visual hallucinations. The boy was pale and in obvious respiratory distress, requiring oxygen 6 L/min via facemask to maintain his central colour. Examination of his fundi showed blurring of the disc margins. Initial management consisted of an intravenous dexamethasone infusion and intermittent intravenous frusemide (exact doses not known). His symptoms persisted through the first 24 hours of admission, and by the second evening he was more disoriented and unresponsive to commands. He was given 100 mL of 20% mannitol intravenously and within two hours had a huge diuresis with a wet bed. Three hours later, he was answering questions with a grunt, and shortly after was obeying commands and was easily rousable. Ten hours later, he was talking freely and answering questions, and subsequently made a complete recovery with no neurological sequelae. To our knowledge, this is the first reported case of papilloedema and unconsciousness associated with the Irukandji syndrome. We believe this indicates cerebral oedema, but no cerebral scan was done to confirm this. Recently, a case of cerebral oedema was reported after a chirodropid (multitentacled box jellyfish) sting.5 We suggest that the patient's level of consciousness be carefully monitored in all serious jellyfish envenomations, and that any deterioration of consciousness be appropriately investigated. Peter J Fenner Honorary Medical Officer, Surf Life Saving Association, PO Box 3080, Mackay, QLD 4740 RJ Heazlewood Visiting Medical Officer, Cairns Base Hospital, QLD Flecker H. "Irukandji" sting to north Queensland bathers without production of wheals but with severe general symptoms. Med J Aust 1952; 1: 89-91. Fenner PJ, Williamson JAM, Callanan V, Audley I. Further understanding of, and a new treatment for, "Irukandji" (Carukia barnesi) stings. Med J Aust 1986; 145: 569-574. Fenner PJ, Williamson JA. World wide deaths and severe envenomation from jellyfish stings. Med J Aust 1996; 165: 658-661. Barnes JH. Cause and effect in Irukandji stingings. Med J Aust 1964; 1: 897-904. Fenner PJ, Williamson JA, Burnett JW, et al. The "Irukandji syndrome" and acute pulmonary oedema. Med J Aust 1988; 149: 150-156. - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Peter J Fenner · RJ Heazlewood

European wasps: an emerging hazard in Australia MJA 1997; 167: 650 To the Editor: The Victorian Department of Natural Resources and Environment has predicted a surge in European wasp (Vespula germanica) numbers this summer (6 August 1997, press release).1 This is expected to result in an increase in serious and potentially life-threatening injuries from wasp stings.2 Since arriving in mainland Australia in 1977, the European wasp has spread dramatically,3 and is now found in all States and Norfolk Island. It has so far resisted biological and chemical control measures, and the wasp population is expected to explode.3 The toxicity of wasp venom, their multiple stinging capacity, aggressiveness and tendency to build hidden subterranean nests2,3 mean that increased morbidity from wasp stings is likely. According to the Victorian Minimum Inpatient Dataset, hospitalisations as a result of wasp stings have increased in Victoria in recent years (1992-1996),4 and wasp stings were among the top 10 poisons exposure inquiries in Victoria for 1996.4 Fatalities have been reported in other countries.5 The current paradigm is that most serious reactions to wasp stings are allergic in nature, so that only a small percentage of the population is at risk. However, as in the case of a Melbourne child who disturbed a wasp nest,2 the large number of stings sustained from an attack by a swarm of wasps (often 30 to 200 stings) can result in a massive life-threatening envenomation. Therefore, not only those with wasp allergy are at risk. Unfortunately, this issue has not been studied, despite the important implications for patient management. Allergic effects, which may be managed by immunotherapy and early administration of adrenaline, need to be distinguished from the toxic effects of envenomation, which require alternative management. We support the initiative of the Victorian Conservation Minister to develop a national European wasp strategy and recommend that it include a national surveillance system, through the Australian Venom Research Unit (AVRU), to monitor the health impact of the growing wasp population. We also encourage doctors to report serious wasp-related injuries to the AVRU: telephone (03) 9344 7753 or facsimile (03) 9348 2048. Interdisciplinary collaborative research involving entomological, toxicological, public health and emergency medicine professionals is needed to address this increasing threat to our health and enjoyment of the great outdoors. Nadine R Levick Faculty, Division Pediatric Emergency Medicine, Johns Hopkins Medical Institutions 600 North Wolfe Street, CMSC 144, Baltimore, MD, USA 21287-3144 E-mail: nlevickATwelchlink.welch.jhu.edu Ken D Winkel Deputy Director, Australian Venom Research Unit, Department of Pharmacology University of Melbourne, VIC Gordon Smith Associate Professor, Center for Injury Research and Policy, School of Hygiene and Public Health Johns Hopkins University, Baltimore, MD, USA Alexander C. Wasp plague on the way. Herald Sun 1997 Aug 8. Levick N, Braitburg G. Massive European wasp envenomation of a child. Emerg Med 1996; 8: 239-245. Spradbery JP, Maywald GF. The distribution of the European or German wasp in Australia, past, present and future. Aust J Zool 1992; 40: 495-510. Royal Children's Hospital, Pharmacy Department. Keeping tabs. Newsletter. Melbourne: Royal Children's Hospital, 1997; 3: 1. Man dies after attack by wasps. The Washington Post 1997 Aug 29: D06. - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Nadine R Levick · Ken D Winkel · Gordon Smith

Choking after inhaling a foreign body through a Ventolin puffer MJA 1997; 167: 651 To the Editor: A 10-year-old boy awoke with asthma. His mother, also an asthmatic, took her salbutamol inhaler from her purse and gave the boy a puff. The boy immediately became extremely distressed and was unable to speak. He mouthed to his mother, "I cannot breathe". His mother performed the Heimlich manoeuvre, during which a white object was expelled from the boy's mouth, immediately relieving his distress. The object was a cigarette filter. His mother is a cigarette smoker and rolls her own cigarettes. Loose cigarette filters and uncapped asthma inhalers were found in the clutter at the bottom of her purse (Figure). As she had previously propelled a filter into her own airway from an inhaler, with less severe consequences, she recognised the likely cause of her son's sudden inability to breathe. This frightening and potentially lethal episode illustrates the importance of keeping caps on asthma aerosol inhalers when not in use, so preventing objects from lodging in the aerosol mouthpieces. Michael J Mackay Senior Medical Officer, Emergency Department, Mackay Base Hospital Bridge Road, Mackay, QLD 4741 - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Michael J Mackay

Out of the blue and into the pink A new litmus test for chlorine gas exposure MJA 1997; 167: 651 To the Editor: A 40-year-old man arrived at the emergency department by ambulance in respiratory distress. In his duties as a hotel maintenance worker, he had been mixing swimming pool chemicals in a dark, confined space. Inadvertently, he had mixed liquid pool "chlorine" (sodium hypochlorite) with a hydrochloric acid solution, forming an irritating yellow-green gas. Despite a brief exposure, he rapidly developed eye irritation, burning in his oropharynx, cough and chest pain. He noticed that the keys in his pocket had turned a dull colour. On arrival, about 20 minutes after the exposure, he had an irritating cough, but his vital signs were normal, oxygen saturation was 99%, and his chest was clear to auscultation. His clothing smelt of chlorine and was removed to prevent skin irritation. On removing his white overalls, it was noticed that his blue underpants had changed colour to a pink-mauve hue. Although he suffered acute embarrassment, he developed no acute clinical or radiographic signs and was discharged well after several hours' observation. Chlorine gas exposure is not an uncommon hazard of mixing household cleaners or pool chemicals. The addition of an acid to a chloride-containing base releases chlorine gas in an exothermic reaction. Chlorine gas is highly water soluble and on moist surfaces is transformed into hydrochloric acid and an oxygen radical. This mechanism explains the clinical manifestations, with the hydrochloric acid causing immediate irritation to mucosal surfaces, leading to lacrimation, burning sensations and cough. These symptoms usually serve as a warning to the victim to move away from the gas to prevent the more serious sequelae of laryngeal oedema, bronchospasm and adult respiratory distress syndrome. Presumably in this case, the elaboration of acid in the sweaty confines of his true-blue Y-fronts mimicked the classic pH indicator reaction of litmus paper. Perhaps he should have worn his underpants on the outside! Tim C Green Staff Specialist, Emergency Department, Royal Prince Alfred Hospital Missenden Road, Camperdown, NSW 2050. E-mail: timgreenATmpx.com.au Reference: Hoffman RS. Toxic inhalations. In: Rosen P, Barkin R, et al., editors. Emergency medicine -- concepts and clinical practice. 3rd ed. 1992: 2673-2682. - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Tim C Green

A sad stool MJA 1997; 167: 654 To the Editor: With greater attention being given to improving communication between healthcare professionals and the public, the following incident is a simple yet worthy reminder that effective communication depends not only on the information that is transmitted but, more importantly, on the information that is received. A young woman came into my pharmacy with a prescription for Ferro-Gradumet (ferrous sulfate, Abbott), and it was obvious that she was reluctant to have it dispensed. During our conversation, she remarked that she was very concerned about becoming depressed because the doctor had told her that while taking this medicine her emotions would be black. This certainly wasn't the message that the doctor intended to transmit (viz. her motions would be black), and it could have led her to abandon the treatment. How can we ensure that the correct message is received? Failures in communication like this can be avoided if plain, straightforward words are used instead of outdated euphemisms. In this instance, the more direct word "faeces" is less likely to be misinterpreted and, if not understood, is more likely to prompt the question, "What do you mean by that?". Richard M Worrell Pharmacist, PO Box 274, Rose Bay, NSW 2029 - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Richard M Worrell

"Hale-Bopp" and "Knocking on Heaven's Gate" Hits of the Net, 1997 MJA 1997; 167: 654 "If anyone comes to Me and does not hate his father and mother and his wife and children and brothers and sisters -- and even his own life also -- he cannot be My disciple". Luke 14:261 To the Editor: This Christmas, as we renew old family quarrels, we should remember we are celebrating the birth of Christ, who, according to the Heaven's Gate cult, was the first visitor from TELAH -- The Evolutionary Level Above Human.1 On 22 March 1997, when the Hale-Bopp comet was nearest to Earth, 39 members of this cult left earth to link up with the comet's "companion spaceship" bound for TELAH,2 wearing black Nike sneakers. Their transport to TELAH began with deliberate self-poisoning. Although we previously found no relationship between self-poisoning and celestial or occult events,3 this event combined both and suggested that we might have overlooked a synergistic mechanism. We also examined the possibility that traffic was going in the opposite direction that day, with ancient astronauts escaping their spaceship to appear on earth as newborn babies. We used two databases to test our hypothesis: a register of births in the Canberra Hospital (which we felt would closely resemble the sterile environment of a spaceship) and the Hunter Area Toxicology Service database of presentations to hospital with self-poisoning in the Lower Hunter Valley of New South Wales. To examine for evidence of massive successful and attempted soul migrations, we compared the number of births and self-poisonings between 21 and 23 March with those for the rest of the month. There did not appear to be any significant surge in self-poisonings or births at this time. On those three days, there were eight self-poisonings, compared with 51 on all the other days in March (P = 0.24, Mann-Whitney test), and 13 births compared with 141 (P = 0.61). However, we did note a surprisingly strong correlation between self-poisonings and the Nike share price4 (P = 0.005, Spearman) (Figure). In the three months after the Heaven's Gate tragedy, the share price of Nike fell by 20%, despite a 15% increase in the market index and a 28% increase in sales.4 This could either be a suicide prevention strategy or evidence that people are reducing their Nike stocks to invest in futures. When surfing the Internet, it is quickly apparent that data-dredging is not confined to medicine and there is no statistical refereeing. Significance can be found everywhere on the Net: a place to publish and perish. Nicholas A Buckley Visiting Fellow,National Centre for Epidemiology and Population Health The Australian National University, Canberra, ACT 0200 E-mail: mdnabATcc.newcastle.edu.au Janelle A McDonald Obstetric Registrar, National Centre for Epidemiology and Population Health The Australian National University, Canberra, ACT 0200 Do, Ti, et al. How and when Heaven's Gate may be entered (The door to the Physical Kingdom Level Above Human). Phoenix (Ariz): TELAH Services, 1997. On the Internet: http://www5.zdnet.com/yil/higher/heavensgate/ http://www.neosoft.com/~cshramek/comet.htm Buckley NA, Whyte IM, Dawson AH. There are days . . . and moons. Self-poisoning is not lunacy. Med J Aust 1993; 159 (11/12): 786-789. http://quote.yahoo.com/ - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Nicholas A Buckley · Janelle A McDonald

Effect of postgraduate exams on putting performance MJA 1997; 167: 655 Objective: To test the hypothesis that examination stress adversely affects golf putting performance. Participant: An advanced trainee of a learned specialist college, with moderate golfing skills and about to undertake final fellowship examinations. Methods: A week before the exams, the subject was asked to perform 50 consecutive 60 cm putts on the practice putting green, under standard conditions. The hole was cut on a flat portion of the green, with negligible borrow or irregularities. The number of successful putts was recorded. Two weeks after successfully completing the exams, the subject was asked to repeat the test. The hole and the weather conditions were similar. Results: Test one. Successful putts: 40 (including three mulligans); unsuccessful putts: 10. Test two. Successful putts: 46 (including one mulligan); unsuccessful putts: 4. Mulligans were putts that, while not successfully "holed", were deemed by the subject to have been so close that they were considered "holed". Reasons included: "The wind changed direction at the last minute" and "The hole moved after I had putted". Statistical analysis: Two new techniques relevant to golfing data were used. The Norman Index of the sum of rank performances (n value) was multiplied by the Tiger Woods covariant of superior performances (t value). The resulting score was divided by the square root of the subject's handicap, giving a dubious value (d) which was statistically feasible (d < 0.05). Like all golfing data, these values need to be treated with suspicion. Discussion: The adverse affects of examination stress on putting performance could be a result of physical impairment (tremors and sleep deprivation) and psychological impairment (distraction and fear of failure). As putting is a vital component of a golfer's repertoire, it is reasonable to extrapolate that examination stress would be detrimental to overall golfing performance. It may be that poor golfing performances adversely impact upon examination performances. This requires further testing, preferably over a long period of time (several months would be fine), at a suitable golf course (perhaps Port Douglas in far north Queensland) and with appropriate funding (to cover travel expenses!). Conclusion: Examination stress adversely affects putting performance. Postgraduate examinations should be scheduled to avoid significant golfing fixtures, such as club championships. (Disclosure: Any resemblance between the author and subject is purely coincidental.) Craig T Hore Clinical Fellow, CareFlight, NSW Medical Retrieval Services PO Box 159, Westmead, NSW 2145 - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Craig T Hore

Letter Ultrarapid opiate detoxification. What's all the fuss about? MJA 1997; 167: 393 To the Editor: In the past few months, the Australian electronic and print media have hailed ultrarapid opiate detoxification (UROD) as being able to "cure" 60%-100% of heroin addicts. These claims were initially made as part of a professionally organised media campaign by CITA/ATT, a Spanish-Israeli organisation, but have been repeated by opponents of harm-minimisation addiction treatments.1 While there is no conclusive evidence as to the efficacy of UROD, CITA/ATT has attempted to patent and franchise what it considers to be "its" treatment. In UROD, opioid addicts are anaesthetised for several hours and given naltrexone to precipitate withdrawals. Naltrexone is a long-acting, opioid antagonist with little or no agonist activity that is effective orally. It has not been approved for use in Australia. While there are benefits in terms of speed and reduced suffering, there are no published reports comparing the long-term outcome after UROD with other methods of rapid opioid detoxification. UROD is expensive and has obvious risks; a patient died during treatment in the United Kingdom.2 After UROD, patients are given up to a year's maintenance treatment with naltrexone, usually 100 mg on Mondays and Wednesdays and 150 mg on Fridays. While the available evidence is contradictory, there is a suggestion that socially stable addicts with no psychiatric comorbidity may benefit from postdetoxification naltrexone treatment. In two randomised, placebo-controlled, double-blind trials the treated group tended to use less heroin, but the differences were not statistically significant.3,4 CITA claimed UROD was discovered by a Spanish psychologist, Dr Juan Legarda.5 However, rapid opiate detoxification was first described by researchers working at Vienna University in a series of papers published in the international peer-reviewed literature between 1988 and 1991.6 Dr Legarda's first and only published account dates from 1994 and refers to the work of the Vienna group and others.7 CITA/ATT sought to franchise "its" treatment (international patent application PCT/ES94/100108),5 and has threatened to sue a British and American physician who offer patients similar services. CITA/ATT has also attempted to issue national franchises for the "CITA Method". A United Kingdom version of the franchise agreement stipulated "the Method" must remain secret. A minimum 240 detoxifications had to be performed in the first six months and one-quarter of all payments were to be paid to the parent company. The British licensee would have been obliged to spend no less than US$50 000 in the first year and US$25 000 in subsequent years marketing and advertising "the Method".2 The CITA/ATT marketing campaign represents a corruption of the scientific process and is unethical. The profession should condemn this and similar attempts to use the mass media to bypass the peer-reviewed literature. However, despite the concerns raised by the CITA/ATT media campaign, a local, randomised trial of UROD versus another form of rapid, antagonist-assisted detoxification is warranted.5 Such a study should include a double-blind, placebo-controlled trial of postdetoxification naltrexone maintenance. John R M Caplehorn PhD Student, Department of Public Health and Community Medicine University of Sydney, NSW 2006 E-mail: johncATpub.health.su.oz.au Ackerman P. Aim must be abstinence when it comes to drugs. Sunday Telegraph 1997 March 23; 143. Tyaransen O. The strange and terrible saga of Brendan Woolhead. Hot Press (Dublin) 1997 May 14; 12, 13, 62. National Research Council Committee on Clinical Evaluation of Narcotic Antagonists. Clinical evaluation of naltrexone treatment of opiate-dependent individuals. Arch Gen Psychiatry 1978; 35: 335-340. Shufman EN, Porat S, Witzum E, et al. The efficacy of naltrexone in preventing reabuse of heroin after detoxification. Biol Psychiatry 1994; 35: 935-945. Brewer C. Ultra-rapid, antagonist-precipitated opiate detoxification under general anaesthesia or sedation. Addiction Biol 1997; 2: 291-302. Loimer N, Schmid R, Presslich Q, Lenz K. Continuous naloxone administration suppresses opiate withdrawal symptoms in human opiate addicts during detoxification treatment. J Psychiatr Res 1988; 23: 81-96. Legarda J, Gossop M. A 24-h inpatient detoxification treatment for heroin addicts: a preliminary investigation. Drug Alcohol Depend 1994; 35: 91-93.