Letters

To the Editor: Prescribing and dispensing generic medicines is an option to reduce costs in the community and is also common practice in public hospitals. In addition to the issues discussed by McLachlan,1 we have noted a concerning trend in the “branding” of many new generic medicines that has the potential to add to the confusion for patients, prescribers and pharmacists. Medicines with special release properties are branded with suffixes as a reminder of their longer duration of action, such as Sustained Release (eg, Tramal SR; CSL Limited) or eXtended Release (eg, Efexor-XR; Wyeth Australia). Different formulations may also use a suffix to indicate distinguishing properties, such as “dispersible” in Rulide D (Sanofi-Aventis) or “osmotic release oral system” in Adalat OROS (Bayer Schering). However, these suffixes, while meaningful, can be a source of misunderstanding about dosing intervals and length of action, leading to errors.2 A standard nomenclature does not exist, even for formulation descriptors. Adding to this confusion, generic medicine manufacturers are now marketing products with prefixes or suffixes, not to denote a modified formulation but to place their “brand” on the medicine. Ascent Pharmaceuticals has three different suffixes/prefixes for its generic products, reflecting the names of previous manufacturers (eg, Quinapril-GA, GN-Carvedilol), and two suffixes for simvastatin (GA and DP). Spirit Pharmaceuticals adds its name to some products (eg, Simvastatin-Spirit). Taking an oral medication history becomes challenging when patients state they use “Spirit” medication for their cholesterol, “GN” tablets for their heart and “GA” tablets for their high blood pressure. With the many generic “brands” now available (eg, 22 simvastatin products), packs with similar labelling lined up on the pharmacy or patient’s shelves increase the risk of wrong selection. Although no reports have been published to date, similarities in brand prefixes may cause medication errors in electronic prescribing and dispensing systems, when an incorrect medication is selected from a dropdown menu. Entering “Apo” in some systems selects more than 40 products manufactured by Apotex, which uses a naming pattern of the generic drug prefixed by Apo (eg, Apo-Alendronate), as well as APO-go (Hospira), which is apomorphine (and does not contain “go”). This situation could be avoided in future if the National E-Health Transition Authority’s Australian Medicines Terminology and its editorial principles are adopted in systems. These rules require that all medicines are represented by descriptions that list the generic name first, with the sponsor’s name following in parentheses (Paul Frosdick, Chief Terminologist, National E-Health Transition Authority, personal communication, 25 August 2010). The Food and Drug Administration in the United States and the Therapeutic Goods Administration in Australia have developed documents outlining approved medicines terminology,2,3 but there are no official lists of approved suffixes or prefixes. The Institute for Safe Medication Practices, a non-profit US-certified patient safety organisation internationally regarded as an expert in medication safety, has recognised this problem and maintains a list of products with drug name suffixes and their meanings.4 With more generic options available, good communication between medical and pharmacy clinicians and patients is essential to clarify the indication, along with the specific name, of medications prescribed. Pharmaceutical manufacturers need to consider the impact of meaningless prefixes and suffixes, which add to the confusion and potentially contribute to medication errors. National authorities should improve overall governance of labelling of generic medicines, to prevent errors reaching patients.

Linda V Graudins · Michael J Dooley

To the Editor: In recent years, medical school selection criteria have continued to evolve as new information and evidence have come to light.1,2 Increasingly, data are becoming available that shed light on local selection processes, and we commend Laurence and colleagues for their contribution to this.3 Diversity in selection processes is desirable because of the varying educational cultures and emphases between medical schools, and for maintaining variety among students who gain entry. The pursuit of “ideal” evidence-based selection criteria ought to continue, although the effect that a single, standard national selection process would have on the diversity of students entering medicine is unknown. However, a national approach to offering places for medical school could have considerable advantages. Mutual recognition of admission processes by medical schools is one approach suggested by Laurence et al.3 This may not have as significant an impact on student diversity as might a single selection process, and it could reduce the substantial financial burden that the application process places on both applicants and medical schools.3 Students from low socioeconomic backgrounds are often unable to apply to interstate medical schools due to the travel costs associated with attending interviews. This both reduces the number of opportunities they have of gaining a place at a medical school, and prevents them from gaining valuable interview experience, further reducing the likelihood of a successful application.3,4 Mutual recognition of and sharing of selection information would potentially level the playing field for applicants who cannot afford to attend multiple interviews. Students commonly receive medical school offers as late as midway through the first semester — a consequence of students receiving offers from multiple universities, and universities having to make a number of rounds of offers until their quotas are complete. Universities already rank their applicants, and, if students were able to submit their medical school preferences, applications could be coordinated nationally through a centralised admissions system. This would result in fewer rounds of offers and a shorter admission process, reducing the cost for universities and enabling students to enrol earlier, with greater certainty. This may avoid the need for students to relocate and miss out on vital parts of their first year of study.

Christopher X J Wong · Adam J Nelson · Ross L Roberts-Thomson

To the Editor: In their recent editorial, Bower and colleagues effectively summarised the problem of apparent governmental indifference to congenital anomalies.1 This is not unique to Australia and probably exists worldwide. National systems to collect congenital anomalies data were set up in many countries in the mid 1960s, including the National Congenital Anomaly System in the United Kingdom and the Canadian Congenital Anomalies Surveillance System. This followed the thalidomide tragedy and exemplified that it often takes an acute crisis to stimulate politicians into action. However, due to a lack of leadership, foresight and finances,2-4 these systems gradually declined to the extent that they became of very little value, lacking in accurate ascertainment and pregnancy termination data. As a result, regional registries were set up in England and Wales, and Canada was left with only two provinces (British Columbia and Alberta) collecting data. Prevention is one of the new driving forces for collecting good data, and the advent of using folic acid to effectively reduce neural tube defects brought a new urgency to the need for comprehensive useable data. Accordingly, the Canadian government set up a task force and formed a new entity in 2002, the Canadian Congenital Anomalies Surveillance Network, with a mandate to provide logistical and financial help to all 10 provinces and three territories. While progress has been slow, it has been very encouraging, with three additional provinces and one territory developing new surveillance systems this fiscal year (April 2010 – March 2011). The Network has set up guidelines and standards to enable all provinces and territories to collect data in a comparable format,5 which can then be forwarded to a central database in the national capital, Ottawa. The quality of the data should be improved because they are gathered at a local level. This model could be adapted for use in Australia because, according to Bower et al,1 a nucleus of good data from at least three states already exists.

R Brian Lowry

To the Editor: I agree with Emery and colleagues1 that family history can add much to downstream clinical interventions that provide tangible benefits to the presenting patient and his or her kin. The pedigree chart has some advantages over simple narrative recording of the same details, including the ability to instantly visualise relationships between individuals and the ease with which the chart can be updated and annotated.2 There is a familial aggregation (commonly an affected first-degree relative) in up to 25% of presenting cancer patients, while around 5% will harbour a highly penetrant genetic predisposition to cancer. In the cancer clinic, an acceptably detailed family cancer pedigree can typically be obtained in even less time than the 30 minutes suggested by Emery et al.1 Steps in drawing pedigrees have been outlined elsewhere2,3 and typically involve collecting information such as simple demographics, naming and symbolising different cancer types, and recording age of onset and age of death (if relevant) for the different individuals, starting with the presenting patient. The time required to construct a three-generation pedigree would typically be around 10 minutes, making it an attractive addition to routine history taking. If a cancer pattern emerges, the pedigree should be extended as far as possible. Of course, diagnosis verification (through death registries, etc) would be required before surveillance, prophylaxis and therapy decisions are addressed in the familial cancer setting. A convenient refresher for doctors who do not routinely draw pedigrees might be to first construct their own family tree, with reference to the symbols and relationship illustrators commonly used.2,3 It is likely that pedigrees in most clinics will be drawn by hand, at least initially, although there are software programs for pedigree creation available (eg, Family Tree Builder; <http://www.myheritage.com/family-tree-builder>). Over the years, I have informally asked my specialist oncology trainees to routinely construct family pedigrees. I do not recall, among these highly clinically skilled doctors, one that was able to correctly draw a family pedigree until we had worked on it together. Given the benefits of family pedigree analysis across many disease categories, a little practice in pedigree drawing may be a useful exercise for many of us. Even without the requisite confirmation of disease status of the individuals represented, a simple pedigree chart, combined with quick reference to information on the potential clinical significance of any patterns it shows (eg, by consulting National Health and Medical Research Council guidelines),4 can help prioritise referrals to busy familial cancer clinics.

Michael J McKay

To the Editor: Langlands and colleagues show that family history is poorly taken in patients presenting to an acute medical unit at a major tertiary hospital.1 However, their article and its companion editorials2,3 do not adequately stress the settings in which family history taking may be both easily achievable and most cost-effective. The nihilism that Thomas and Thompson2 convey about recording family history in the acute setting is of more concern, given that a tertiary hospital may offer the best opportunity to initiate the process of case detection for a number of heritable and lethal diseases, such as autosomal dominant familial hypercholesterolaemia (FH), the most common monogenic cause of premature coronary artery disease (CAD). We previously demonstrated that a family history of cardiovascular disease was almost never recorded by coronary care unit medical staff at Royal Perth Hospital.4 For 509 patients aged < 60 years presenting with symptomatic CAD to the coronary care unit, we found that 70% had insufficient clinical data documented in the medical records to enable a diagnosis of FH. In a follow-up study of 103 patients with premature CAD admitted to the coronary care unit, a nurse practitioner was able to record a positive family history of premature cardiovascular disease in a primary relative for 43% of patients, of whom 95% had phenotypic FH based on a recognised clinical diagnostic tool (the Dutch Lipid Clinic Network score).5 Patients detected in this way in Western Australia are now referred to a statewide FH program run by staff from a lipid clinic.5 In this program, where detailed pedigree drawing and family tracing is performed by trained nurses, we have found a causative mutation for FH in up to 85% of patients with a clinical phenotype strongly suggestive of FH. Additionally, we find that for every index case so detected, we can additionally diagnose at least three new cases of FH in the patient’s relatives, many of whom are young. This method of case detection and subsequent treatment with cholesterol-lowering therapies is highly cost-effective and, more importantly, enables therapy to be targeted at younger patients, thereby maximising the potential for preventing CAD. Our experience illustrates that for a lethal condition such as FH, an accurate family history recorded by a nurse can spark a cascade of action that leads to a definitive diagnosis of FH in the index patient and the subsequent detection of otherwise undiagnosed FH in the community, with significant associated cost savings.6 Hence, we propose that nursing staff can efficiently bridge this gap in medical care while we are getting our house in order by training medical staff to effectively take a family history.

Timothy R Bates · Elissa B Poulter · Frank M van Bockxmeer · Gerald F Watts

To the Editor: I read the article by Langlands and colleagues1 with some dismay, and a sinking heart. Their report is further evidence of the dangers of moving away from the basic skills of comprehensive history taking and performing a detailed physical examination. Interestingly, in the United States, the debate regarding performing a physical examination has come full circle, from virtually ignoring its importance to now telling us how vital it is and how to perform it.2 But it is the taking of a comprehensive history that, as one of my mentors told me, “is where the money is”, and a detailed family history is an integral part of this. Eliciting a detailed family history is arguably more important for paediatric patients, who have a longer potential life span and hence have more to gain from this information. In my paediatric practice, for example, I see numerous overweight children, some of whom have a strong family history of hypercholesterolaemia, vascular disease or type 2 diabetes mellitus, which places them at considerable risk of cardiovascular disease in their adult years. A detailed family history may also “unmask” the genetic contribution to a child’s history of deafness or learning disability. Time constraint is the main impediment to taking a comprehensive family history, but it is worth keeping in mind that it is time well spent and that, in the paediatric population, it may make a significant contribution to the long-term health of the child. With the impending advent of personalised genomic screening, there will be an even greater imperative to formalise the gathering of family history details.3,4

Simon E P Hauser

To the Editor: Pridmore1 describes a case in which a man’s recent actions suggested suicidal intent. The man told police he had no ongoing suicidal plans and they took his words at face value. He subsequently killed himself. The High Court exonerated the police of any responsibility, a decision that seemed based on two premises: that suicide does not presuppose mental disorder; and that “There is no general common law duty of care to rescue a person from harm, including self-harm”.2 There is sufficient grey in both those inter-related premises to make a black-and-white judgment suspect. I share Pridmore’s position that suicide does not always equal mental disorder, although one wonders whether situational crises in individuals with subtle vulnerabilities could be subsumed under such a label. More important is the question of individual autonomy. The reason we have no common law requiring us to “rescue” another adult is because we set such a high value on autonomy. Although we assume a person’s competence, our curiosity about it should be aroused when people behave in unexpected ways. When the behaviour is strikingly different, and has potential for serious harm, are we not obliged to intervene or procure assessment? This is, I would have thought, a moral rather than legal or medical concern. This is what we would do for a child wandering on the road or a demented person lost at night. We might be free of legal or medical censure for ignoring them, but we would be embarrassed to publicly admit our failure to act if we might have done something useful at the time. Making serious preparation to kill yourself is strikingly different behaviour, and should raise questions about both your competence and autonomy. Perhaps not 100% but surely more than 50% of such people have a disorder. A person preparing to suicide is “more likely than not” mentally ill, and that is how the “common person” would surely see it: “guilty”, as it were, till proven innocent. Expertise is called for to make that final determination. The police certainly do not have the expertise. Why, then, would they not seek it? Furthermore, if the “rational, cooperative and responsible” man in this case had indicated his plans to “rationally” commit suicide to escape an intolerable predicament, it is hard to believe the police would have walked away, even though he may have been competent to make such a decision!

Paul T Dignam

To the Editor: The editorial on the Human Variome Project by Cotton and Macrae1 neatly lays out the reasons for government funding for gene mutation databases for inherited diseases. Most of these diseases are rare, but collectively, they are common. The article highlights the key principles of detecting gene mutations and establishing pathogenicity in order to offer individuals (or couples) relevant health information for themselves and/or their (future) offspring. Cotton and Macrae mention a number of specific diseases, but do not mention the commonest life-shortening inherited disease affecting Australian children — cystic fibrosis (CF). Far from being theoretical, nearly all of the principles outlined by Cotton and Macrae are already in place for CF, including clinical databases (in Australia, the Australian Cystic Fibrosis Data Registry), an international gene mutation database (at http://www.sickkids.on.ca, which is contributed to by Australian genetics laboratories) and programs to offer carrier screening to the population. Unfortunately there is very little government funding for these initiatives, so they are not coordinated. In particular, screening for CF carriers in the population, which is of considerable clinical utility, has only small, fee-for-service programs that reach very few people.2,3 These programs are inequitable in that many people are unaware of the existence of such screening programs and, of those who are, many cannot afford the cost of testing. CF provides an excellent model for the development of a coordinated approach to inherited disease screening and, given that 800 000 Australians are carriers of CF mutations, funding CF screening should be a major government priority.

R John Massie · Martin B Delatycki

To the Editor: Costello and Murphy’s lament1 about the discoverer of prostate-specific antigen (PSA), Richard Ablin, describing PSA testing as a “hugely expensive public health disaster”2 contains several egregious claims that require correction. They write that “since the introduction of PSA testing in the 1980s, we have seen a 25% reduction in mortality” from the disease. Thirty years ago (in 1980), before PSA testing was possible, the age-adjusted mortality rate from prostate cancer in Australia was 33.4/100 000. In 2007, it was 31.0/100 000, a decline of 7.2%. Over the same period, prostate cancer incidence rose 110%, from 80.8/100 000 to 170/100 000,3 thanks to the aggressive promotion of PSA testing. Recent New South Wales data show that 3 years after radical prostatectomy, 77.4% of men are impotent and 12.3% have urinary incontinence, compared with 22.3% and 1.0%, respectively, of controls.4 Many of these men are, to use Costello and Murphy’s word, “overtreated”1 — they underwent unnecessary surgery and now live with the consequences. From a 2009 European trial,5 the take-home message for a man being tested today is: There is a one in 50 chance that, in 2019 or later, he will be spared death from a cancer that would otherwise have killed him. And there is a 49 in 50 chance that he will have been treated unnecessarily for a cancer that was never a threat to his life.6 This is what Ablin called a public health disaster. With reference to this European trial,5 Costello and Murphy claim that “PSA testing has led to greatly reduced mortality”. This “great reduction” was from 4.2 to 3.3 deaths per 10 000 person-years. Costello and Murphy propose that “those with a PSA level well below the median for men in their 40s . . . (the vast majority at this stage) could be reassured . . .”, but below the median lie half the men, not the vast majority. This policy would mean that the other half of men aged 40 (not the small minority, as implied by Costello and Murphy) would be above the threshold. They would not be reassured; presumably they would be offered more frequent testing and follow-up. Labelling half the population of men aged 40 as higher risk has enormous implications for the men (anxiety, inconvenience, cost) and the health system that would be called on to fund more appointments and tests. Such a proposal does indeed sound like a public health disaster.

Simon Chapman · Alexandra Barratt

In reply: Chapman and Barratt’s statements about prostate cancer highlight the dramatic difference between the views of sociologists and the views of clinicians who deal daily with the burden of prostate cancer diagnosis, treatment and mortality. In 1851, prostate cancer was considered a rare disease.1 Chapman and Barratt’s views seem to remain consistent with this thesis. However, in 2010 in Australia, prostate cancer is the most common cancer diagnosed in men, and the most common cancer causing death in men. Our own data do not support the contention that treatment for prostate cancer produces dreadful outcomes. We can reassure men that there is a high likelihood of cure through early treatment for prostate cancer, with a less than 5% chance of becoming incontinent and a 70% chance of retaining erectile function.2 Clearly, Chapman and Barratt have not taken into account a recently reported Swedish study which showed that in 20 000 men randomly allocated to prostate-specific antigen (PSA) screening or a control group between 1994 and 2008, there was a 50% reduction in mortality from prostate cancer for men in the screened arm.3 The numbers needed to screen (293) and treat (12) from this study are almost exactly the same as those from breast cancer screening studies. We repeat our recommendation for the early use of a single PSA test4 in men aged in their 40s. This is most beneficial because the background noise from benign prostatic hyperplasia development does not occur, and PSA level is very discriminatory for detecting those who go on to develop significant prostate cancer.

Anthony J Costello · Declan Murphy

To the Editor: The long-term functional outcomes in the three cases of swimming pool filter-induced transrectal evisceration described by Price and colleagues1 are excellent and significantly better than many other cases described in the literature. However, it may be possible to improve further on such results, or at least decrease short-term morbidity, by expediting the reduction of the eviscerated bowel. In all three cases described,1 the children presented initially to a local hospital and were subsequently transferred to a tertiary care facility before operative reduction was initiated. It is likely that earlier operative reduction of the eviscerated bowel would decrease secondary venous congestion of the prolapsed segment, thus minimising further ischaemic changes already initiated by the mesenteric arterial and/or venous tear. This in turn may improve the perfusion of the affected segment; lessen the development of hypothermia, hypovolaemia and sepsis; and possibly increase the final length of viable bowel. A “damage control” laparotomy2,3 performed at an appropriate hospital of initial presentation (one with a surgeon and anaesthetist available), with the principal aim of early reduction of the prolapsed bowel into the abdominal cavity, may improve outcomes in such cases.

Phillip J Carson

To the Editor: We read with interest the recent meta-analysis of rates and methods of suicide in Australia by Large and Nielssen.1 Previous research has shown a marked increase in hanging suicides in women in South Australia over the 15-year period 1986 to 2000,2 which concurs with the findings of Large and Nielssen at a national level between 1988 and 2007.1 One of the features of this increase in hanging suicides, which was not specifically addressed in their excellent overview, relates to trends in specific age groups such as the young. A previous analysis of suicides in individuals aged 16 years and under and for whom autopsies were performed at the Forensic Science Centre (now Forensic Science South Australia; FSSA), in Adelaide,3 included a total of 19 cases of suicide for the 5 years 1985 to 1989, of which seven deaths (37%) were from hanging. The age range of the hanging victims was 14–16 years (mean age, 15 years), with a male to female ratio of 6:1. This compares with a total of 10 suicides among young people, recorded in FSSA files for the 5 years 2005 to 2009, of which nine (90%) were by hanging. The age range of the hanging victims in this group was 10–16 years (mean age, 14.7 years), with a male to female ratio of 4:5. The difference between these two periods was statistically significant (P < 0.005).3 Thus, although suicide in those aged 16 years and under remains an uncommon event,3 developments in deliberate self-harm among the general population may also be reflected in the young. While there was a fall in the total number of young suicide victims, from 19 to 10, between the two periods in the SA study, this has not been matched by a decline in hanging suicides (ie, a significantly greater percentage of suicides in the young in SA now involve self-suspension).3 This finding may be of use to those studying specific issues and trends in youth suicide.

Roger W Byard · Amy Austin · Corinna van den Heuvel

To the Editor: I would like to correct some inaccuracies in an article by Jelinek and Gawler in the December 2008 issue of the Journal about a survivor of disseminated osteosarcoma.1 The article describes a 58-year-old man who was diagnosed in 1974, at the age of 24 years, with histologically confirmed high-grade osteosarcoma of the right femur. He underwent a full leg amputation in January 1975, but metastases recurred 11 months later, in December 1975. The authors of the article misreported a sequence of medically significant events, altering the patient’s actual history. (The correct chronology and early clinical history of the case have been published elsewhere.2,3) The errors and omissions in the article by Jelinek and Gawler, together with the correct sequence of events and relevant inclusions, are outlined in Box 1. In summary, the major errors in the article were as follows: Timeline errors. The authors stated that the patient first saw Dr Meares in September 1976, after chemotherapy had failed. In fact, the patient consulted Meares as a first-line treatment approach on 12 December 1975, and did not consider chemotherapeutic options until September 1976. The authors also stated that the patient had palliative radiotherapy in September 1976. In fact, the patient had only one course of palliative radiotherapy treatment, in February 1976. Vegan diet. The patient never followed a vegan diet. Date of photographs. The photographs in Figures B and C of the article by Jelinek and Gawler were taken on 7 July 1977 (Box 2), not at the time of first contact with Meares, as implied in the article. An appraisal of the patient’s symptoms, combined with an accurate clinical history, reveals a more plausible scientific hypothesis for his remission than the effects of diet and meditation. Although diet and meditation may be adjuncts to a patient’s wellbeing, it is unlikely in this case that they were curative, and certainly veganism was not a relevant factor. Immunotherapy with BCG vaccine treatments, the timing of symptoms and the patient’s eventual diagnosis of tuberculosis could be associated with his remission, as postulated by his radiation oncologist in 1978.6 There is extensive scientific literature about remission of cancer, including osteosarcoma, associated with febrile conditions.5,8-15 The patient’s sporadic visits to doctors meant that metastases were not diagnosed histologically and much of the information reported on his case is anecdotal. Clearly, in this and other cases, unbiased investigative scientific research needs to be undertaken before reporting anecdotes and extrapolations as if they were fact. Teasing apart the errors in Jelinek and Gawler’s story, now on the public record and almost medical myth, is an enormous task, but one that must be done, because correctly reporting the patient’s clinical timeline is crucial in any discussion about the causes of his remission and the flow-on effect to cancer patients and their treating doctors.16 1 Corrections to errors in the article by Jelinek and Gawler1 Errors and omissions in the article Facts, corrections and inclusions December 1975: widespread bony and pulmonary metastases were diagnosed. December 1975: an isolated metastasis in an inguinal node was diagnosed. The patient undertook the Gerson dietary regimen,4 immunotherapy with BCG vaccine,5 and the Meares intensive meditation program.6 September 1976: “[the patient] underwent three cycles of palliative chemotherapy with vincristine, adriamycin, cyclophosphamide and darcarbazine, as well as brief palliative radiation therapy”. September–October 1976: growth of tumours on the sternum increased, and metastases were detected in the left lung. Coughing and haemoptysis were present.6 Experimental chemotherapy (with adriamycin, vincristine and methotrexate)2 was ceased at 10 weeks after December 1976. No radiation therapy was given at this time. Palliative radiotherapy was administered in February 1976, not September 1976. September 1976: “He elected to discontinue these therapies as his condition deteriorated further.” “The patient then consulted prominent psychiatrist and hypnotherapist Dr Ainslie Meares ...”. December 1975: the patient first consulted Meares. In February 1976, he abandoned the Meares meditation program. The 10-month discrepancy between December 1975 and Jelinek and Gawler’s stated date of September 1976 (actual date, October 1976) alters the patient’s medical timeline, implying that it was only after other treatments had failed that meditation began and played a key role in his recovery. Dates of photographs shown in the article: “When Meares first saw the patient, he had visible bony tumours protruding from his ribs, sternum (Figure B) and iliac crest, and was coughing up blood containing small spicules of bone (Figure C).” The article by Jelinek and Gawler implies that the photographs in their Figures B and C were taken around the time when the patient first contacted Meares. The photograph in Figure B was actually taken on 7 July 1977, 19 months after his first contact with Meares. Tumours were not protruding from the sternum when Meares first saw the patient to begin meditation in December 1975, and there were no visible metastases. The coughing up of blood containing bone spicules (Figure C) began in mid 1977, not in the period between December 1975 and February 1976. Vegan diet: “[the patient] adhered faithfully to a vegan diet”. The patient never followed a vegan diet. Veganism involves exclusion of all animal products. The Gerson regimen4 includes dairy foods and calf liver juices. For the following 22 years, the patient’s diet included seafood, dairy products and eggs. First appearance of tuberculosis: “Presumably related to immunosuppression from chemotherapy, he developed pulmonary tuberculosis in June 1978, and was treated for this condition for 12 months.” In 1978, an oncologist diagnosed advanced tuberculosis (TB) dating back to early 1976. (Previous x-rays were examined, showing evidence that TB had been present and undiagnosed for at least 2 years. The patient had very advanced TB by June 1978.6) The suspected cause was BCG vaccine treatments administered in December 1975, possibly exacerbated by chemotherapy and associated immunosuppression in late 1976. 2 Original photographs of patient’s chest taken on 7 July 1977 I am in possession of these original photographs (left), which were dated 7 July 1977 (date enlarged in inset). A copy of page 227 from the original edition of You can conquer cancer7 also confirms the accurate date of the photographs as 7 July 1977 (date enlarged in inset)

Grace O Gawler

In reply: In conjunction with the patient’s memory, and teasing out details, where available, from medical records and investigations of over 30 years ago, we sought to piece together our follow-up story of a remarkable recovery from cancer as accurately as possible.1 We did not attempt to reproduce the original case report in the Journal,2 but rather were highlighting the long-term issues that can be associated with such recoveries. We thank Ms Gawler for attempting to clarify the original timelines. However, based on the medical records and published data, as well as checking further with the patient himself, it seems her letter does little more than muddy the waters in this case. Ms Gawler claims the patient abandoned the Meares meditation program in February 1976. This is factually incorrect and misleading. The patient continued to use Meares’ methods to meditate for 3 hours daily until he recovered, and has meditated at least 1 hour daily since then. The timelines quoted around the photographs in Figures B and C in our original article1 were based on information from Meares’ 1978 article.2 He was somewhat inaccurate, as is Ms Gawler, who claims the photos were taken in July 1977. This is incorrect. Figure B was photographed in July 1976 as chemotherapy was commenced. Figure C was photographed in 2008 and documents bony spicules coughed up during the first half of 1977, collected and retained by the patient. Regarding the use of BCG vaccine treatments, the patient reports that none of the three tuberculosis (TB) specialists whom he consulted gave credence to Ms Gawler’s suggestion that the onset of TB was related to the BCG vaccine. Ms Gawler further postulates that the remission could be linked to a febrile condition associated with TB. The patient did have severe night sweats (which may or may not have been accompanied by fever) over a period of 2–3 weeks in February and March 1976, at a time when he almost certainly had not yet contracted TB, and after which the metastases continued to grow rapidly. After this time, the patient never reported fevers that would make sense of this claim. Ms Gawler claims that the patient’s metastases were not diagnosed histologically and that much of the reported evidence is anecdotal. This is misleading and would surely surprise the involved surgeon, oncologist and other physicians, who used the best available medical evidence at the time and cooperated in the preparation of our original article. The case is documented with a thorough medical history, the patient’s surgeon and other specialists were consulted regularly, and accurate records were retained. Full details confirming the report are available in the patient’s biography.3 The metastases were thoroughly investigated and confirmed by the Peter MacCallum Cancer Centre in Melbourne and regularly tracked via x-ray. The original lesion seen on x-ray was diagnostic for osteosarcoma and the diagnosis was confirmed histologically by biopsy, and again after amputation. The case history is certainly complex and compelling. The message is clear: unexpected recovery from disseminated cancer remains a possibility, and is likely to be influenced by lifestyle factors.

George A Jelinek · Ruth H Gawler

To the Editor: The Between the Flags project of the Clinical Excellence Commission (CEC) is designed to establish a “safety net” in all New South Wales public hospitals, to enable early identification and management of deteriorating hospital inpatients.1 A paediatric advisory group within of the program is currently developing five age-group-specific paediatric observation charts to account for the changes in normal physiological parameters that occur with age in children, and these have been distributed for comment before finalisation. Each chart has specific physiological calling criteria defining when a clinical review or rapid response is required from medical staff (Box). If one or more criteria fall in the “red” zone, the patient requires an immediate, rapid response; if criteria fall in the “yellow” zone, the patient needs a clinical review within 30 minutes. A paucity of data on what represents an abnormal parameter for each age group has also led to a lack of clear triage guidelines for emergency department nurses. For example, the paediatric physiological discriminators of the Australasian Triage Scale include terms such as “mild tachycardia” as a guide for allocating patients to triage Category 3 and “moderate tachycardia” for Category 2.2 We trialled the CEC paediatric inpatient calling criteria to determine whether they could also be used for emergency department triage purposes. We carried out a retrospective review of patients presenting to triage at the emergency department of the Children’s Hospital at Westmead between 1 and 14 March 2010. We assumed that patients who met the CEC’s yellow criteria should be allocated to triage Category 3 (“urgent: review within 30 minutes”) and those who met the CEC’s red criteria should be allocated to at least triage Category 2 (“emergency: review within 10 minutes”). Patient outcomes were classified as “admitted”, “discharged” or “did not wait”. From 1968 presentations, 1885 patients had observations at triage available for review. The numbers of patients in each triage category were: Category 1 (5); 2 (41); 3 (403); 4 (422); and 5 (1014). Only 10 of the 46 patients in Category 1 and 2 would have been flagged by the CEC parameters as needing a rapid response (ie, review within 10 minutes), and none of the three patients admitted to the paediatric intensive care unit would have been identified by the CEC parameters. Of the 403 patients in Category 3 (needing review within 30 minutes), 32 would have been uptriaged to Category 2 by the CEC criteria. Twelve of these 32 patients were in fact discharged home, indicating that the CEC criteria are unsuitable for triage purposes. Of the 1436 patients in Category 4 and 5, 30 would have been uptriaged to Category 2 according to the CEC parameters and, of these, only three were admitted. A further 271 patients would have been uptriaged to Category 3 (181 of these were discharged and 54 did not wait). Of particular note is that 151 of the 271 patients met the yellow criteria because of low respiratory rates that were flagged by the charts but were normal for the patient. At present, the physiological parameters defined in the new CEC paediatric inpatient observation charts are not suitable as a triage tool in the paediatric emergency department, do not replace an experienced triage nurse, and are a poor predictor of disposition. CEC calling criteria* and physiological parameters for children, by age group Calling criteria, by age group Call Physiological parameter < 30 days 1–12 months 1–4 years 5–11 years ≥ 12 years Red† Heart rate (beats/min) Above 180 190 170 160 150 Below 80 80 70 60 40 Respiratory rate (breaths/min) Above 100 65 60 50 40 Below 20 15 15 10 5 Systolic blood pressure (mmHg) Above — — — — — Below 60 50 70 70 80 Oxygen saturation (%) Below 85 85 85 85 85 Temperature (°C) Above 38 — — — — Yellow‡ Heart rate (beats/min) Above 160 170 150 140 130 Below 90 100 80 70 50 Respiratory rate (breaths/min) Above 60 50 50 35 30 Below — 30 20 15 10 Systolic blood pressure (mmHg) Above — 120 120 130 160 Below 70 80 80 80 90 Oxygen saturation (%) Below 95 90 90 90 90 Temperature (°C) Above 37.5 — — — — CEC = Clinical Excellence Commission. * Calling criteria as of March 2010 at the time of this study (the CEC has subsequently revised some of these criteria). Only one “flag” was required to meet a calling criterion. Other calling criteria such as pain, work of breathing and level of consciousness were not measured in our study but will also generate a call. Where no values are present, there are no calling criteria for the parameter. † Red call requires immediate, rapid response. ‡ Yellow call requires review within 30 minutes.

Fenton M O’Leary · Jennifer I Major

To the Editor: Chen and colleagues1 published a risk assessment tool for type 2 diabetes (AUSDRISK) based on the Australian Diabetes, Obesity and Lifestyle Study (AusDiab).2 We tested AUSDRISK’s performance in an independent cohort of 1494 women enrolled in the Geelong Osteoporosis Study (1994–1997; 77% participation),3 comprising an age-stratified sample of women randomly selected from the Barwon Statistical Division and followed prospectively over a decade.4 In 2004–2008, of 1015 surviving study participants aged 25 years or older at enrolment, 800 (79%) returned for follow-up assessment. We excluded 261 women who did not have a fasting plasma glucose (FPG) test result at both baseline and follow-up assessments, and 33 with baseline diabetes. The remaining 506 women formed the cohort on which the AUSDRISK tool was tested. Diabetes was defined by one or more of three criteria: FPG level ≥ 7.0 mmol/L, treatment with insulin or oral hypoglycaemic agents, or self-report. Demographics, ethnicity and lifestyle factors were documented by questionnaire. Participants were described as “active” if they described their mobility as “moves, walks and works energetically, and participates in vigorous activity”; otherwise, they were considered “inactive”. As our baseline questionnaire did not document a history of high glucose levels, we performed two analyses: one assuming no participants had this history, and a second identifying participants with baseline impaired fasting glycaemia (FPG level, 6.1–6.9 mmol/L). The study was approved by the Human Research Ethics Committee, Barwon Health. Using the final AUSDRISK model,1 we allocated points for baseline characteristics according to sex, age, ethnic background, parental history of diabetes, history of high blood glucose (FPG level, ≥ 6.1 mmol/L), use of antihypertensive medications, current smoker status, physical inactivity, and waist circumference. The predictive power of AUSDRISK was determined using the area under the receiver operating characteristic curve (AROC). Using a total AUSDRISK score ≥ 12 as the criterion for prediction of diabetes, we evaluated the performance of AUSDRISK by calculating its sensitivity, specificity and positive predictive value (PPV) in our cohort. Ninety-eight participants had an AUSDRISK score ≥ 12 (or 106 if those with impaired fasting glycaemia were scored for a history of high blood glucose). Statistical analyses were performed using Stata software, version 9 (StataCorp, College Station, Tex, USA). Twenty-eight participants (5.6%) developed incident diabetes during the period of follow-up (13 with FPG ≥ 7.0 mmol/L, 14 receiving treatment with insulin or hypoglycaemic agents, and seven self-reporting the condition). If we assumed that none of the participants had a history of high blood glucose levels, the AROC for AUSDRISK in the Geelong cohort (0.78 [95% CI, 0.72–0.85]) was comparable with that in the AusDiab cohort (0.78 [95% CI, 0.76–0.81]).1 In our study, the sensitivity of the AUSDRISK tool was 50.0% (95% CI, 30.6%–69.4%), specificity was 82.4% (95% CI, 78.7%–85.7%) and PPV was 14.3% (95% CI, 8.0%–22.8%). Recognising baseline impaired fasting glycaemia increased AUSDRISK’s predictive power (AROC, 0.81 [95% CI, 0.74–0.88]; sensitivity, 60.7% [95% CI, 40.6%–78.5%]; specificity, 81.4% [95% CI, 77.6%–84.8%]; and PPV, 16.0% [95% CI, 9.6%–24.4%]). Study limitations were that we only evaluated women, we did not collect data on a history of high blood glucose levels, diabetes was diagnosed in the absence of an oral glucose tolerance test, and criteria for inactivity differed from those used in the AusDiab study. Our population was older than that of the AusDiab study and would probably have had a higher prevalence of diabetes, influencing our PPV result. Not surprisingly, including individuals with impaired fasting glycaemia increased the point estimates for AROC, sensitivity and PPV. In conclusion, our data independently demonstrate the limited predictive value of AUSDRISK for women over a 10-year period.

Julie A Pasco · Mark A Kotowicz · Margaret J Henry · Geoffrey C Nicholson

To the Editor: Evidence is beginning to accumulate on the effectiveness of the low-density lipoprotein (LDL) cholesterol-lowering medicine ezetimibe. While there are no completed trials investigating ezetimibe’s effect on clinically important end points, two recent trials investigating its effect on carotid intima media thickness (CIMT) have both reported disappointing results.1,2 After each of these trials, the Journal has published editorials by Hamilton-Craig, who offers reassurance about ezetimibe and encourages ongoing prescription of this drug to patients who have elevated LDL levels despite maximum-tolerated statin therapy.3,4 Such a sanguine opinion seems at odds with the negative trial evidence, and therefore worthy of debate. Briefly, the ENHANCE (Ezetimibe and Simvastatin in Hypercholesterolemia Enhances Atherosclerosis Regression) trial, which compared ezetimibe plus simvastatin with simvastatin treatment alone in 720 patients with familial hypercholesterolaemia, found no significant difference (and a trend in the direction of harm) with respect to the primary end point of CIMT.1 The ARBITER 6-HALTS (Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol 6 — HDL and LDL Treatment Strategies in Atherosclerosis) trial compared ezetimibe with extended-release niacin in statin-treated patients with coronary heart disease.2 Among 315 patients with available results, the group taking niacin showed a statistically significant reduction in CIMT, but the group taking ezetimibe showed no such reduction. Of concern, increased cumulative exposure to ezetimibe was associated with progression of CIMT (P = 0.05). Although far from definitive, the results of these two trials offer no reassurance of benefit from ezetimibe and, in my view, may portend harm. It may seem counterintuitive that ezetimibe, which significantly lowers LDL cholesterol levels,1,2 could be ineffective or harmful. However, the history of medicine is replete with examples of interventions that improve numerical disease measures without benefit to patients. One recent example was torcetrapib, which, despite increasing high-density lipoprotein cholesterol and reducing LDL cholesterol levels in a promising manner, was found to cause serious adverse events, including death.5 I agree with Hamilton-Craig that we require trials measuring major cardiovascular events to really understand the effects of ezetimibe. Where we disagree is how to manage our patients during the period of uncertainty until publication of the results of these trials. While he argues for continued prescribing of ezetimibe, I suggest we should explicitly share our uncertainty about the safety and efficacy of this drug with our patients by discussing the existing research. Some patients will, like Hamilton-Craig, place their faith in the cholesterol hypothesis and be reassured by an assumption of cardiovascular protection as their LDL falls. Others will choose to wait until we have more robust evidence that ezetimibe is safe and effective. I would wait.

Brett D Montgomery

In reply: I agree with Montgomery that cardiovascular disease (CVD) outcomes are required to determine the role of ezetimibe. The Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) trial (in which patients with aortic stenosis were treated for 52.2 months with statin plus ezetimibe or statin plus placebo) showed a 4.7% reduction in ischaemic CVD events in the ezetimibe group (P = 0.02; number needed to treat, 23), driven by a reduced need for coronary artery bypass grafting.1 In contrast to previous trials showing regression of atherosclerosis in response to statin therapy, baseline carotid intima media thickness (CIMT) levels in the ENHANCE (Ezetimibe and Simvastatin in Hypercholesterolemia Enhances Atherosclerosis Regression) trial were normal, due to previous statin therapy. This is likely to account for the lack of change in CIMT with ezetimibe treatment in the ENHANCE trial.2 As no placebo group was included, neither lack of benefit nor harm from ezetimibe therapy can be inferred.2 Data from animal studies have shown atherosclerosis regression after ezetimibe treatment through multiple mechanisms.3-5 Prospective randomised controlled trials with statins, resins or surgery have independently shown an approximate 1% reduction in CVD per 1% reduction in low-density lipoprotein cholesterol (LDL-C) level. Evidence for the benefits of lowering LDL-C is among the most robust in medicine. Pending the outcomes of IMPROVE-IT (the Improved Reduction of Outcomes: Vytorin Efficacy International Trial, a multicentre study of ezetimibe plus simvastatin versus simvastatin treatment of patients with acute coronary syndrome [http://clinicaltrials.gov/ct2/show/NCT00202878]), or clinical outcome data confirming those of the ARBITER 6-HALTS (Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol 6 — HDL and LDL Treatment Strategies in Atherosclerosis) trial,6 it seems reasonable to continue to use ezetimibe to lower LDL-C levels in patients who are not achieving LDL-C targets despite statin therapy or who are intolerant to statins. Extended-release nicotinic acid (Niaspan [Abbott Laboratories, Chicago, Ill, USA]) may be an appropriate alternative to statins as second-line therapy, and should be made available under the Pharmaceutical Benefits Scheme for treating patients with dyslipidaemia. (Niaspan has approval from the Therapeutic Goods Administration for marketing in Australia, but is not being imported into Australia at this stage.)

Ian R Hamilton-Craig

To the Editor: National best practice guidelines recognise that accurate data on the health of Indigenous Australians are crucial to improving health service delivery.1 The draft revision of the RACGP Standards for general practices acknowledges the need for improvement and requires that a practice demonstrates how it routinely records, in active patient health records, self-identified Aboriginal and Torres Strait Islander status.2 This is a commendable improvement but should be further strengthened, requiring that Indigenous status be recorded for at least 90% of active patients, the level required for a history of allergies. Improved record keeping in general practice has resulted in the potential to improve Indigenous identification among patients notified with a communicable disease. This enables the documentation of health disadvantage, and allows evaluation of measures aimed at closing the gap in health outcomes between Indigenous and non-Indigenous people. Demographic data in the NSW notifiable diseases database (NDD) were audited for all 258 Hunter New England (HNE) Salmonella infection notifications in 2007 by interviewing patients and their referring general practitioners. Interviews were completed for 83% of patients. Indigenous status was poorly recorded. The NDD listed three patients with salmonellosis as Aboriginal, but showed an unknown status for 87%. Among patients who had attended a GP during their illness (66%), practice records listed two as Aboriginal, but Indigenous status was unknown for 70%. Most GPs (95%) reported using electronic medical records, and 89% completed pathology requests with practice software. Many GPs (60%) requested information on how to appropriately ask about a patient’s Indigenous status. Interviews with patients who had been notified as having had salmonellosis identified 13 as Aboriginal, and no resistance to identification was encountered. The crude salmonellosis notification rates per 100 000 population were 42.2 (95% CI, 19.3–65.1) for Aboriginal HNE residents and 25.5 (95% CI, 21.7–28.6) for non-Aboriginal HNE residents which, while not statistically significant for this small sample, suggests a differential salmonellosis burden, consistent with studies elsewhere.3 The true burden of disease was likely to have been substantially higher, as many infections are not notified.4 The differential burden may also be an underestimate if Aboriginal HNE residents were less likely to be notified than non-Aboriginal residents due to, for example, reduced access to health services. The widespread availability of electronic practice software for generating pathology requests provides a new opportunity to substantially improve Indigenous identification in communicable disease notifications.3 Indigenous status should be routinely recorded by GPs and automatically included on their pathology request forms and subsequent laboratory notifications. There is now a need for a coordinated national approach to ensure consistent inclusion of Indigenous status on all laboratory notification data.

Anthony D Merritt · April R Roberts-Witteveen · David N Durrheim

To the Editor: I refer to the article by Gallego and colleagues in the 19 April 2010 issue of the Journal,1 which stated that (as at the time of writing, in July 2009) Australia had no formal policies for iodine supplementation in pregnant and lactating women. In January 2010, the National Health and Medical Research Council (NHMRC) released a public statement, Iodine supplementation for pregnant and breastfeeding women.2 The NHMRC recommends that women who are pregnant, breastfeeding or considering pregnancy take an iodine supplement of 150 μg each day; and women with pre-existing thyroid conditions should seek advice from their medical practitioner before taking a supplement. The public statement also provides information on the increased need for iodine during pre-pregnancy, pregnancy and breastfeeding, the risks of not having enough iodine and the types of supplement that should and should not be used. The statement was developed in consultation with an expert reference group and was based on a review of recent international scientific literature for the efficacy of iodine supplementation in increasing iodine levels in pregnant and breastfeeding women to levels that mitigate the risks associated with iodine deficiency.3 The public statement and supporting literature review can be found on the NHMRC website.2,3

Warwick P Anderson

To the Editor: We disagree with the opinion expressed by Gallego and colleagues that Australian “women planning a pregnancy and pregnant and lactating women should be advised to take an iodine supplement”,1 and offer two reasons to support our view. First, the data suggesting mild iodine deficiency in Australian women were collected from opportunistic samples of women not representative of the population at large and were obtained before the introduction of mandatory iodine fortification of bread in October 2009. We believe that recommending iodine supplementation in pregnancy without evaluating the effect of mandatory iodine fortification on iodine intake and status of pregnant women in Australia is premature.2 This is supported by a recent report, developed by the Dietitians Association of Australia on behalf of the National Health and Medical Research Council (NHMRC).3 The report clearly shows that the recommended iodine intake for pregnant women (recommended dietary allowance, 220 μg/day) is achievable from foods alone, together with iodine fortification of bread. Second, there are no randomised controlled trials (RCTs) that have examined the effect of iodine supplementation of pregnant women from regions of mild iodine deficiency (as in Australia) on neurodevelopment of the offspring or any other clinical outcomes. Gallego et al state that “iodine-containing supplements consistently benefit the iodine and thyroid status of both mother and newborn”, citing a review of iodine supplementation of pregnant women from populations with mild-to-moderate iodine deficiency.4 In fact, none of the six RCTs included in that review showed a clear effect of supplementation on maternal and newborn thyroid hormone concentrations, which suggests that the maternal thyroid is able to adapt to meet the increased thyroid hormone requirements of pregnancy in areas of mild-to-moderate iodine deficiency.5 Furthermore, Gallego et al cite no evidence to support their statement “Even subclinical hypothyroidism in the mother, occurring as a consequence of iodine deficiency, can cause irreversible brain damage in the fetus . . .”. In our view, major public health recommendations advising routine iodine supplementation for women planning a pregnancy, as well as pregnant and lactating women, should await the results of current RCTs6-8 examining the effect of maternal iodine supplementation on longer-term maternal health and neurodevelopmental outcome of children in regions with mild-to-moderate iodine deficiency, including Australia and New Zealand.

Shao J Zhou · Sheila A Skeaff · Philip Ryan · Maria Makrides

In reply: While Zhou and colleagues disagree with our viewpoint that Australian “women planning a pregnancy and pregnant and lactating women should be advised to take an iodine supplement”,1 we note that they suggest any such recommendation should await the results of their planned randomised controlled trial (RCT) examining the effects of maternal iodine supplementation on maternal health and neurodevelopmental outcome of the offspring. They neglect to mention that the National Health and Medical Research Council (NHMRC) issued a public statement in January this year, with supporting evidence attached, stating that: “The NHMRC recommends that all women who are pregnant, breastfeeding or considering pregnancy take an iodine supplement of 150 μg each day”.2 Similar recommendations, based upon available scientific evidence, have been issued by the World Health Organization, International Council for Control of Iodine Deficiency Disorders, American Thyroid Association and American Endocrine Society. We agree that there is a paucity of RCT evidence examining the effect of iodine supplementation of pregnant women living in mildly iodine-deficient areas, and this is regrettable. Given the overwhelming animal and human evidence that maternal iodine deficiency causes brain damage in the offspring of deficient mothers, we consider there are major ethical issues in conducting such trials where pregnant women would be deprived of iodine and their babies put at risk of brain damage. Zhou and colleagues imply that mild-to-moderate iodine deficiency is not widely prevalent in Australia. This statement ignores the evidence from several clinical studies of pregnant women in New South Wales, Victoria and Tasmania, all showing that mild-to-moderate iodine deficiency is widespread in the majority of the Australian population. Analysis of the data in some of these studies shows between 20% and 40% of women tested are moderately to severely iodine deficient.3 Furthermore, food modelling studies by Food Standards Australia New Zealand (FSANZ) predict between 45% and 75% of Australian women will continue to be iodine deficient after the mandatory use of iodised salt in bread that commenced in October 2009.4 Finally, we disagree with their assertion that the recommended iodine intake for pregnant women can be achieved by the majority of women from foods alone, together with iodine fortification of bread. A trial of bread fortification in Tasmania showed this was not achievable.5 If this were achievable, it is questionable why Zhou and colleagues would even consider conducting an RCT of maternal iodine supplementation in pregnant women in Australia and NZ.

Gisselle Gallego · Stephen Goodall · Creswell J Eastman

In reply: I thank Mountain and colleagues from the Australasian College for Emergency Medicine for their letter.1 Despite their interpretation of our article,2 I think we share many points of agreement. Having worked extensively as a clinician, I agree that patient harm is occurring because of insufficient capacity to treat, and that patients will benefit from more capacity to treat. I also agree that this is an important issue and that approaches to dealing with it should not be subverted. Most importantly, I would also agree that the number of available hospital beds is critical — the unanswered questions are about how many beds, and where they should be provided. I also thank the authors for their acknowledgement that “clinical modelling” is a fundamental driver for their position. Our industry would do well to take its direction in the use of queuing theory from internationally recognised experts in the area, rather than from within the ranks of my fellow doctors. In response to Mountain et al’s call for an 85% bed-occupancy limit as a solution, my call is for more detail about the practicalities of how we would implement this limit, which could start with the provision of clear answers to the following questions: How would compliance with the 85% occupancy limit be monitored? What are the practical measures that bed managers, nurse unit managers, executives and others could use to ensure that compliance occurs? If patient throughput in acute inpatient areas increased, what downstream effects could we expect? How would the application of resources in fixing “access block” compare with the application of the same resources in fixing “exit block”? (And an obvious sub-question: what is the relationship between the two phenomena?) Has a consensus been reached with all specialist groups as to which clinical units in hospitals should have access to extra beds when they become available? Or is it intended that an 85% limit would be applied across the board, irrespective of the differences between patient care needs, lengths of stay, rates of arrival and staffing mixes in different wards? How and when would the effectiveness of such an initiative be assessed? Perhaps another occupancy figure would appear even more efficacious through the lessons learned. I believe these are reasonable questions that ought to be answered by anyone calling for this change. I repeat my group’s call for more, and more informed, investment in health system capacity given this huge problem and the solution being proffered.

Christopher A Bain

To the Editor: In his letter1 regarding Heeley et al’s article on cardiovascular risk perception and evidence–practice gaps in Australian general practice,2 Radford quotes, “no [automated blood pressure-measuring machines] were accurate enough to ... replac[e] a manual sphygmomanometer”. The citation dates from 1973, when oscillometric blood pressure monitors such as the Omron HEM-907 — distributed by the High Blood Pressure Research Council of Australia (HBPRCA) with support from the Servier Foundation — did not exist. In defence of digital blood pressure devices, a cluster randomised controlled trial conducted in Australian general practice has demonstrated their superiority compared with existing manual devices.3

Mark R Nelson

To the Editor: The recent MJA supplement provides an excellent summary of internet interventions for a range of psychiatric conditions, including anxiety, depression and substance misuse.1 However, in highlighting the positive uses of the internet, it is important to remember other aspects of online engagement that can have a negative impact on patients’ mental health. It is useful to ask patients specifically about their internet activities, as they will not necessarily volunteer this information. For example, people can spend a large amount of time accessing pornography online. Negative effects of this may include the impact on existing real-world relationships, the cost, and the risks associated with participation in illegal activities. Some patients may go further, arranging to meet people they have encountered on the internet in person, which entails a risk of physical or sexual assault. The internet provides an opportunity for discreet gambling and, as with other forms of gambling, the effects can be destructive. Excessive participation in online games such as World of Warcraft, to the extent that people spend virtually all their waking hours engrossed in playing games, can also be a problem. Bullying and socially destructive behaviour occurring on widely used social networking sites such as Facebook can cause considerable distress to the victim. Such sites can be used to deliver unwelcome information (eg, ending a relationship by changing one’s Facebook status to “single” and “de-friending” the partner). Privacy can also be an issue, and Facebook provides much information to potential stalkers if users fail to adequately protect their data. Some medical practitioners have allowed patients to become their “friends” on Facebook, which can involve inappropriate access to the doctor’s personal life and a risk of blurring professional boundaries.2 Finally, the internet is increasingly being incorporated into delusions expressed by people with psychotic disorders.3 For example, patients with schizophrenia may have paranoid beliefs that derogatory material about them is being distributed via the internet. Enquiring about patients’ internet activities is therefore a useful addition to the standard mental health assessment.

Cherrie A Galletly