Volume 192 Issue 12

Family history has a role, but who should be responsible for exploring and recording it? The increasing age, number and comorbidities of hospital inpatients has increased the load on emergency departments and necessitated significant redesign, including the introduction of short-stay and medical assessment units. These units are diverse in their casemix, but common factors include higher acuity of illness and expedited discharge. Obtaining a complete history of a patient’s acute illness and longstanding comorbidities, as well as his or her social and psychological issues, represents the ideal standard of care. Obviously, however, there are tensions between providing holistic care and continuity of care to the patient and achieving the rapid turnover required in such units. Genetic markers and tests are increasingly available for an expanding range of conditions. Genetic counselling has moved from specialised clinics into the mainstream practice of many disciplines. The inheritance of disease is rarely a simple algorithm, and these new genetic tools provide complexity rather than clear direction. Relevant guidelines are uncommon outside cancer medicine. Family history is a frequent criterion for determining further genetic testing. For example, the Amsterdam criteria for diagnosis of hereditary non-polyposis colorectal cancer (HNPCC) include a family history of at least three relatives with HNPCC-associated cancer.1 There can be harm in failing to interpret genetic tests correctly, and the complexity of many conditions demands a high level of knowledge. “Genetic literacy” is a term that has been used to describe competence in this area.2 However, it seems unreasonable to expect all doctors to be skilful at all times in eliciting and interpreting the family history and then appropriately counselling and testing each patient. Family history is an older tool than genetic testing and is poorly defined, applied and understood.3 Even now, there is not enough evidence to gauge its reliability and role.4 The family history can aid stratification of a patient’s risk of heritable conditions, and it has diagnostic utility for disorders with classic Mendelian inheritance, but it may be less useful in disorders with multifactorial inheritance or more complex genetic expression. In this issue of the Journal Langlands and colleagues report that family history is not recorded in the case notes of most medical short-stay patients.5 They argue that a family history offers potential health gains for the patient and relatives and suggest that there should be increased focus on this element of the medical history. However, this seems unrealistic in the context of increased workload and time pressures, particularly in a hospital short-stay unit. The acute admission is not an ideal setting for detailed and accurate history taking; patients are usually unwell and access to their family is compromised. The family history recorded is often inaccurate4 or misleading, not only because the level of health literacy among patients is variable but also because familial clustering is not distinguished from heritable disease. The accuracy of reporting of family history is rarely studied, but it has been shown that it can be poor in patients with cancer4 or cardiovascular disease.6 The primary care setting affords better opportunities to explore and record family history and to make adjustments after clarification with relatives. Certain conditions (eg, malignant hyperthermia, Huntington disease) drive consideration of genetic testing of the affected individual and sometimes lead to testing of family members. The counselling required should form part of an ongoing relationship with the patient and family. As Langlands and colleagues state,5 the family history may be a casualty of increasing numbers of acute hospital admissions. Perhaps it is a justifiable casualty in the acute health care environment, as long as information is elicited accurately afterwards. Ideally, a patient should have his or her acute illness diagnosed and managed within the acute admission, with a clear plan then delineated for follow-up, which includes notification of those who will be responsible for doing so. It is important to have a use for any family history information once it is accurately obtained. In future, the acquisition of a family history must embrace the developments in our understanding of genetic disease. Without diminishing the role of specialised genetic units, primary care clinicians and specialists in chronic care will need to assume greater responsibility for exploring family history. Screening assessments can identify those requiring a more comprehensive review. We would argue that, under present circumstances and with doubt hanging over its sensitivity, specificity and effect on health outcomes,3,4 the family history is a justifiable omission from many acute hospital admissions. The concept of holistic care is a noble one and, if we are to work within a new paradigm of shorter hospital inpatient stays, we will need to develop a strategy for preserving this concept. Certain diseases, such as unprovoked venous thromboembolism, should trigger an immediate focus on family history, but a routine family history is best ascertained when people are not acutely unwell. If we are serious about disease prevention and the role of genetics in modern medical management, more guidance is needed in terms of which patient groups will benefit from genetic testing and how any positive results will be managed. An integrated approach should include guidance for screening that is based on a better defined family history that has been obtained in the non-acute setting. This approach requires protocols for disease-specific genetic testing and specialist referrals for further assessment and management. A recent National Institutes of Health conference offers hope in this regard.3

Josephine S Thomas BM BS, FRACGP, FRACP · Campbell H Thompson DPhil, FRACP, MD

It is time to reconsider the clinical benefits arising from family history and start making better use of it A patient’s family history may aid clinical diagnosis and contribute to disease risk assessment and prediction. It frequently yields valuable social history, including information about family support structures and insights into individual beliefs about illness.1 Although taking family history is traditionally regarded as a routine part of the medical history, it is not used in a systematic way in clinical practice. In this issue of the Journal, Langlands and colleagues report the results of an audit in an Australian teaching hospital, which found that nearly three-quarters of patients admitted to a short-stay medical unit had no documentation of family history having been considered as part of the diagnostic assessment.2 A similar situation exists in primary care. Although there are no published comparable data from Australian general practice, a primary care study in the United States found that only 16% of subjects (n = 362) had any record of their family history in their clinical chart, including 15 individuals at high risk of an inherited cancer syndrome.3 Internationally, there is growing recognition that a family medical history can support tailored disease prevention, which may be more effective than existing approaches.4 This is also reflected in the Australian Medicare-funded adult health assessment for people aged 45–49 years at risk of developing chronic disease, which specifically includes assessment of the family history of chronic diseases such as diabetes and cardiovascular disease. Family history can also inform the formulation and weighting of differential diagnoses in presentations for a range of common conditions. The risk of many serious diseases is increased in the presence of a family history of the disorder, representing not only shared genetic factors but also environmental and behavioural exposures. For example, the relative risk of breast cancer is 1.4 times higher for women aged 60 years or older if they have a first-degree relative diagnosed with the disease after the age of 60 years; this risk is more than five times higher for women younger than 40 years with a first-degree relative diagnosed before the age of 40.5 Eleven per cent of women with breast cancer have a first-degree relative with the disease. The relative risk of colorectal cancer for a 50-year-old is increased from around twofold with one affected first-degree relative to almost fourfold in people with at least two affected first-degree relatives.6 About 15%–20% of people with colorectal cancer have an affected first-degree relative. In a US population-based study, 14% of the population had a family history of ischaemic heart disease, but these people accounted for 72% of early ischaemic heart disease and 48% of all cases of the disease.7 A parental history of type 2 diabetes is associated with a relative risk of 2.2 and a lifetime risk of 40%.8 These familial disease risks should be compared with other traditional risk factors that are routinely screened for in general practice. For instance, isolated hypertension is associated with a relative risk of 1.8 for ischaemic heart disease and is present in 14% of men and 5% of women with a coronary event.9 There are effective interventions for primary and secondary prevention of all these common diseases, ranging from disease surveillance to drug treatments and lifestyle management. There is some evidence that having knowledge of a family history of a specific condition is associated with improved uptake of a range of disease-preventive activities for breast, colorectal and skin cancer.10-12 Therefore, it is possible that identifying people with a family history of disease could act as an additional motivator for them to change their lifestyle or participate in disease screening. Why then do clinicians continue to neglect the family history as part of routine diagnostic assessment and disease prevention? The experienced clinician will know that recording a patient’s family history to assess disease risk ideally requires a three-generation pedigree, but this can take up to 30 minutes, which is unrealistic in most clinical settings. However, not all patients require such a detailed assessment. Simple, self-completed family history screening questionnaires could provide an answer. Several of these already exist, but many are disease-specific and few have been formally tested to determine their screening characteristics.13 Clinicians also cite patients’ uncertainty about their family history as a barrier. However, a systematic review of self-reported family history found high positive predictive values for cancer in first-degree relatives (breast, 93%; prostate, 85%; colon, 81%), although information was less accurate about second-degree relatives (breast, 91%; prostate, 80%; colon, 77%).14 Of course, sometimes the patient’s perception of his or her family history can be just as important as the reality in determining the patient’s risk perception, illness beliefs and likely response to medical advice. Better methods of recording family history are also required, particularly as we move towards an electronic health record in Australia. Tailored clinical software is potentially the most effective tool for recording and updating a patient’s family history, although current clinical software systems do not support the creation of pedigrees. Previous trials have demonstrated the capacity of computerised pedigree tools to improve the assessment of disease risk and identify those individuals who may benefit most from seeing a clinical geneticist.15 However, while clinicians continue to ignore the importance of the family history in diagnosis and risk assessment, software companies have little incentive to integrate family history tools into their systems. Raising awareness among consumers is an alternative approach that may drive clinicians to consider family history more often. A family health history campaign run in New South Wales in 2007 resulted in increased community awareness and discussions about family history within families and between patients and their general practitioners.16 While DNA-based disease risk prediction remains to be proven as an effective clinical tool, family history is a simple but potent tool that is available now for disease prevention. Langlands and colleagues audit findings show that this important element of the clinical history is seldom included in routine patient assessments.2 The family history should not be seen as a relic of medical school teaching; it is time to reconsider the clinical benefits arising from family history and start making better use of it in clinical practice.

Jon D Emery MB BCH, FRACGP, DPhil · Fiona M Walter MB BCh, FRCGP, MD · David Ravine MB BS, MD, FRCPath

Lowering the coffin, feeling its weight on the strap in my hands and glimpsing the darkness waiting at the bottom of the grave, my cheeks were wet with tears. Only later did I realise that those tears came not only from sorrow, but also from pride. Contrary to what Australians have been told about Aboriginal rules against mentioning the names of the deceased, we Noongar people of the south-west of Western Australia use names and images at our funerals. I was crying at the funeral of Lomas Roberts, a man so very important to me in the last decade of his life. In my memory, the photos shown at the funeral service flicker in the dark space into which the body is being lowered, and the old man’s name — the “s” sounds prolonged and blending together — is whispered by the old acacia trees at the cemetery. Kwel ngalak maya wanginy, Uncle Lomas would have said — “the trees are talking to us”. Only a few months previously, driving back from his sister’s funeral, he’d talked of joining her. “Soon”, he said, “not long now”. In fact, he’d missed the burial because I’d had to rush him to the local hospital almost as soon as the eulogy began. He’d had bypass surgery several months before, and the long drive to the funeral probably exacerbated his tension and stress. On the way back to the city, he tilted the car seat so that he could lie almost horizontal. He said it eased the pain in his chest and throat. So his death was really no surprise. When he was drinking, he’d show us the x-rays of his cloudy lungs, but, sober again the next day, he’d say it was all fixed and the cancer was gone because he’d had another visit from that old “bush blackfella” who came and went, as if from nowhere. We’d all nod. Wishing, hoping — none of us liked to see a strong man failing as he was. None of us ever saw this “Mabarn man” (traditional healer). Perhaps he didn’t exist. If he did, his efforts in this instance provided no more healing than the mainstream medical system, although at least the very idea gave Uncle Lomas hope and seemed to make him feel better for a while. Last time I saw Lomas Roberts alive, he was in a hospital bed, his son Geoffrey at his side. Uncle Lomas pulled away his oxygen mask and told us to get a wheelchair and take him home. Then he fell back exhausted, gripping our hands. The nurse adjusted the plastic mask and Uncle Lomas sucked at the oxygen, his eyes wide. He passed away the next day. Edward, a cousin, had taken him home the last time he had discharged himself. Ed said that when the old man got out of the car he thrust out his chest like in the days when he was still boxing, but by the time he got to the front door he was practically crawling. “What can you do?” we asked one another, “he doesn’t like hospital”. He would tell us the doctors were just “kids” — they were white and they were foreign and he couldn’t understand what they were saying. Then, changing the topic, he told us he’d sneaked into the toilets for a cigarette, but when he lit up and blew out that big blue cloud of smoke, the sprinklers on the ceiling came on and he got soaked. “It was a pretty nurse that told me off, too”, he added, enjoying our laughter. Uncle Lomas’s son, Troy, attended the funeral service handcuffed and chained to a prison guard. Wrists lifted in front of him and pulling on the chain, Troy dragged his reluctant, uniformed companion to the microphone. Locked up for years already and with years to go, Troy looked around the crowd that trembled with him, held the silence like a seasoned performer and spoke some of our names: Ed, Geoff, Graeme, Twinny, Iris, Roma ... “Dad loved what you were doing together”, he said, his voice not quite breaking. Troy was referring to a project we were running to retell stories in the old language and revisit the places where those stories belonged. Troy’s words and that project caused my proud tears at the funeral. Perhaps any pride was shameful in the middle of such sorrow and death, but the greatest shame was that we were all so late: the old people were falling away one by one, and Troy was probably not the only one there who understood how it felt to be restrained and isolated. Lomas Roberts, his sisters and some of their surviving cousins were the most important members of a group — an extended clan, a filial community that mostly only got together at funerals — who had gathered in the last couple of years around old pieces of paper returned from the collection of a long-ago linguist. The clash of paperwork and memory ignited stories, not only those carried on the paper, but also of the linguist’s “informants” and other tales they told. There were no welfare narratives in the picture books we developed and took into local schools, and there were no characters to feel sorry for. These stories were peopled by heroes and risk-takers. A few weeks before his death, we’d filmed Uncle Lomas and his remaining sister, Hazel, visiting the old camping grounds and places mentioned in the old stories that were burning within us. At times, on the audio track, you can hear the waves shushing in the background, trees whispering like they did at the cemetery, and even tongues of flame crackling fiercely. It is hard to make out what they might be trying to tell us, and in some of the audio, even the Elders’ voices are unclear because of the sound of the wind in the microphone. It’s as if voices are rushing in, all wanting to speak at once. Uncle Lomas and Aunty Hazel showed us the ruins of the tiny shed where the family had slept when he was a child. They showed us ancient dancing grounds and a whale-dreaming site, and we even went inland to find a granny’s grave not visited by these, her grandchildren, since the eldest was an infant. Uncle Lomas had never been there before. He and his sister thanked the farmer for allowing them on his land. Their respectful courtesy made me uncomfortable because it’s hard for me to reconcile the Elders’ courtesy to the farmer with the historical fact of land stolen from the Aboriginal people. They led us to another property. The farmer was a man with whom I knew Uncle Lomas loved to have a cup of tea and talk about their families. “Not the same today”, they said (as always), shaking their heads as they contemplated the younger generations. “It’s finished”, Uncle Lomas often said when we were talking — an old man feeling his own mortality, frustrated by what he couldn’t remember and what was right there at the tip of his tongue but seemingly unreachable. “All gone now.” Respectfully, I have to disagree. When we left the farmer, Uncle Lomas led us to what seemed to be just a bunch of rocks in a cleared paddock, but when we got up close we saw the circles in the rock of a moon waxing and waning and realised it was the site of one of the stories we’d read in the old paperwork and that Uncle Lomas had already known: an immortality story of how the moon never dies, but diminishes and then builds up again. He took us to another place that, by day, is a dry rock hole and yet, at night, holds the reflections of moon and starlight and cool, dark water. He took us to rocks beside the ocean where you might grind up crabs to lure the groper from his blue depths and then leap and drive your spear deep enough to bring the great fish ashore. Other rocks held the footprints of spirit creatures, creatures you might meet the other side of any tree. Always there is this other world, these other possibilities. So I don’t believe that Noongar heritage is “finished”. It may have diminished, and it’s true that we are a mostly ailing community. Only a minority of my Noongar ancestors survived the first few decades of colonisation, and we’ve had trouble ever since. If you only see skin colour and the like, we’re a truly mixed-up mob these days. We know the health statistics for Indigenous people, the sorry tale the social indicators tell. Very likely, many of you reading this are working yourselves thin and haggard trying to “close the gap” and improve Indigenous wellbeing. We need more efficient health service provision and new technologies, but we need other changes too. Relatively recent historical forces that have shaped Aboriginal heritage have rarely been nurturing, and neither are the ways of talking about that history. I’d like to reject the choice we’re usually offered between narratives simplistically titled either “stolen generations” or “continuity and native title”, because at my old mentor’s funeral I felt the power of some other story. Of course it was an ending. He was finished, he was gone. But my sons were with me, and there were many other young people who mostly only meet each other at funerals. In the tears and hugs, and in gathering around that hollow in the earth there was — there is — an element of “recovery” from grief and illness, and the consolidation of community and belonging. That’s the sort of recovery and consolidation Troy was interested in, and he wants to be part of the recovery and consolidation of old stories and knowledge in a home community. There’s a sense of belonging in that, and pride in one’s resilience, and also a sense of power that comes from sharing one’s Aboriginal heritage with widening circles of people who share the same geographical place. There’s a Noongar word, biirt, meaning “path”, but also “sinew” and “energy”. Biirdiya, from the same word, is most often translated as “boss”, or “leader”, being one who is very familiar with that path and its life-affirming sinews of energy. I don’t suppose such a path of energy can ever be walked in exactly the same way. As such, it’s a little like a river, but you can move along it in such a way as to resonate with that energy and let that life force move in you. I think there’s a many-layered recovery in the return to such old paths, and in the stories and sounds indigenous to that landscape. Many of us who care about social justice have retraced historical paths, noting how decisions were made and how people were forced to enter the unsafe territory they continue to inhabit. These are necessary journeys, but tend to only lead us into the deadends of victimhood and guilt. Biirt is a different kind of path. Some will insist there is no path from a precolonial past to a postmodern future. Indeed, it is often suggested that, in the interests of their own welfare, Aboriginal people must choose between a precolonial “utopian” past and a future as “economic citizens”, or between “assimilation” and “self-determination”. But these are false choices. Recent research suggests that the degree of connection with traditional culture correlates with improved Aboriginal wellbeing.1 If so, consolidating a traditional heritage in home communities is integral to improving Aboriginal health. Uncle Lomas certainly thought so. It made him feel powerful to be helping reconnect younger generations with their heritage, and made us all feel powerful to be sharing it. Closing the gap may require at least some of us to be walking old paths where we focus less on the choice between opposites or between simple alternatives of past and future, and more on where our journey resonates with the energy of a long-abiding culture. In this way, individuals alive to the rhythms of its spirituality may move together towards creating a respectful society in which even the most vulnerable individuals are safe.

Kim J Scott PhD

Objective: To retrospectively review the frequency and adequacy of family histories recorded from patients admitted to a short-stay medical unit in a tertiary teaching hospital.Design, setting and patients: A formal audit of the medical records of 300 randomly selected patients who were admitted to the Royal Perth Hospital short-stay medical unit between July and December 2007.Main outcome measure: Proportion of patient records with family history documents.Results: Of the 300 patient records, 48 (16.0%) contained a family history with specific details about the presence or absence of a medical condition in at least one relative. Overall, 221 records (73.7%) had no family history documented. There was a trend towards more frequent and detailed family histories being recorded from younger patients and those presenting with chest pain.Conclusions: Family history was seldom documented in patients admitted to a short-stay medical unit in a tertiary teaching hospital. An increased focus on family history taking among acutely ill patients offers potential health gains for patients and their high-risk relatives, particularly as preventive or risk-reducing health care strategies are emerging for a growing number of heritable disorders.

Andrew R Langlands MB BS · David A Prentice MB BS, FRACP · David Ravine FRACP, FRCPA

Objective: To compare the efficacy and safety of a 10-day, high-dose v a 3-month, continuous low-dose oral cholecalciferol course in a vitamin D deficient population. The primary end points were the change in serum 25-hydroxyvitamin D (25(OH)D) concentrations at 3 months and the development of hypercalcaemia and hypercalciuria. Design, setting and participants: Fifty-nine vitamin D deficient inpatients (serum 25(OH)D ≤ 50 nmol/L) were enrolled in a prospective, randomised, open-label trial. Participants were randomly assigned to a high-dose regimen of cholecalciferol 50 000 IU daily for 10 days or a 3-month, continuous low-dose cholecalciferol regimen of 3000 IU daily for 30 days, followed by 1000 IU daily for 60 days. Both groups received calcium citrate 500 mg daily. Results: Twenty-six patients completed the study within 3 ± 1 months. The mean increases in serum 25(OH)D were similar in both the high- and low-dose groups (to 55 v 51 nmol/L, respectively; P = 0.9). There was no significant difference in the proportion of subjects who attained serum 25(OH)D concentrations > 50 nmol/L between the high- and low-dose groups (9/10 v 13/14, respectively; P = 1.0). Hypercalciuria (urine calcium > 7.5 mmol/day) occurred in three patients (two low-dose, one high-dose), while renal impairment worsened in one patient. No patient developed hypercalcaemia (corrected calcium > 2.6 mmol/L), vitamin D toxicity (25(OH)D > 200 nmol/L) or nephrolithiasis during the study. Conclusion: Both the 10-day, high-dose and the 3-month, low-dose cholecalciferol regimens effectively increased serum 25(OH)D to within the normal range. The high-dose regimen may be an effective and cheap alternative for patients with vitamin D deficiency. Trial registration: Australian Clinical Trials Registry ACTRN 12607000338460.

Kathryn L Hackman MB BS · Claudia Gagnon MD, FRCPC · Roisin K Briscoe BSc(Hons) · Simon Lam MB BS, FRACP, MRCP(UK) · Mahesan Anpalahan MD, FRACP, MRCP(UK) · Peter R Ebeling MB BS, MD, FRACP

Objective: To assess women’s compliance with different Australian guidelines on alcohol intake during pregnancy and examine factors that might influence compliance.Design, setting and participants: We analysed prospective, population-based data on women aged 22–33 years who were pregnant before October 2001, when guidelines recommended zero alcohol (n = 419), or were first pregnant after October 2001, when guidelines recommended low alcohol intake (n = 829). Data were obtained from surveys conducted in 1996, 2000, 2003 and 2006 as part of the Australian Longitudinal Study on Women’s Health.Main outcome measures: Relative risks (RRs) for zero alcohol intake, low alcohol intake and compliance with alcohol guidelines, estimated by a modified Poisson regression model with robust error variance.Results: About 80% of women consumed alcohol during pregnancy under zero and low alcohol guidelines. Compliance with zero alcohol guidelines or low alcohol guidelines (up to two drinks per day and less than seven drinks per week) was the same for women who were pregnant before October 2001 and women who were first pregnant after October 2001 (20% v 17% for compliance with zero alcohol guidelines, P > 0.01; 75% v 80% for compliance with low alcohol guidelines, P > 0.01). Over 90% of women drank alcohol before pregnancy and prior alcohol intake had a strong effect on alcohol intake during pregnancy, even at low levels (RR for zero alcohol, 0.21 [95% CI, 0.16–0.28]; RR for low alcohol, 0.91 [95% CI, 0.86–0.96]). RR for compliance with guidelines was 3.54 (95% CI, 2.85–4.40) for women who were pregnant while low alcohol intake was recommended, compared with those who were pregnant while zero alcohol guidelines were in place.Conclusion: The October 2001 change in alcohol guidelines does not appear to have changed behaviour. Risks associated with different levels of alcohol intake during pregnancy need to be clearly established and communicated.

Jennifer R Powers BSc, MMedStat · Deborah J Loxton BPsych(Hons), PhD · Lucy A Burns MPH, PhD, GradCertHlthPol · Anthony Shakeshaft BA, MA, PhD · Elizabeth J Elliott MD, MPhil, FRACP · Adrian J Dunlop MB BS, PhD, FAChAM

Debating early invasive versus medical management When there is an apparent threat of myocardial damage from unstable angina or non-ST-elevation myocardial infarction (NSTEMI) (collectively referred to as the non-ST-elevation acute coronary syndromes, or NSTEACS), early opening of the culprit atherothrombotic coronary artery would seem logical. Clinical trials of early coronary intervention (the invasive approach) have shown variable results when applied to all patients with NSTEACS, but clear benefits when applied to high-risk patients.1,2 On this basis, the 2006 National Heart Foundation of Australia (NHFA) guidelines3 concluded that the evidence was strong enough to recommend that all high-risk patients with NSTEACS should be transferred urgently to a cardiac catheterisation facility to permit early coronary angiography and percutaneous coronary intervention or coronary artery bypass surgery, if appropriate. The advice is consistent with United States1 and European2 guidelines and has recently been reaffirmed and followed with recommendations for implementation in Australia.4 But does the invasive approach show true promise, or is it based on a false premise, as suggested by Forge in this issue of the Journal?5 Forge makes the point that the ICTUS (Invasive versus Conservative Treatment in Unstable Coronary Syndromes) trial, published in 2005,6 was overlooked in drawing up the NHFA guidelines and did not show any benefit of an invasive strategy in patients with NSTEACS. It is certainly a valid point that the ICTUS study was conducted with treatments that were more modern and effective than the earlier studies, which were conducted in the 1990s, before the widespread use of enoxaparin, clopidogrel and high-dose statins.7 However, several important points are relevant in analysing the results of the ICTUS study. Firstly, the 1-year mortality in the ICTUS study was 2.5%, which was lower than the 1-year mortality in typical Australian patients with NSTEACS (10.5% for NSTEMI and 3.3% for unstable angina),8 indicating that patients in the ICTUS trial were not high-risk patients. Secondly, the lack of difference in outcome between the conservative and the invasive approach in the ICTUS study was largely due to an apparent increase in minimal myocardial infarction in the interventional group, driven by small rises in creatine kinase MB levels that accompanied the interventional procedure. Such periprocedural infarctions have nowhere near the same long-term prognostic impact as spontaneous infarctions.9 Thirdly, despite the enhanced medical management, selection of a conservative approach in the ICTUS trial did not preclude subsequent coronary intervention. Forty per cent of patients in the conservative treatment arm of the trial required coronary intervention during the initial hospital course. Finally, the ICTUS study was conducted in hospitals with ready access to interventional procedures when they were thought to be necessary. This was not a study whose results can be readily applied to the management of patients in Australian regional hospitals. Forge’s suggestion that modern medical management could render invasive treatment irrelevant takes an unduly optimistic view of the power of medicines. There is no doubt that intensive therapy with statins and antiplatelet agents can significantly improve outcomes for patients with NSTEACS,10,11 but the conclusion that conservative management alone will remove the need to open a blocked artery is hardly justified based on the ICTUS study results, which comprise just over 10% of the evidence base.1-3,6,7 Nor is it valid for Forge to conclude that a strategy of early transfer of patients with NSTEACS to hospitals providing percutaneous coronary intervention is not in agreement with US guidelines. In the 2007 revision of the US guidelines for acute coronary syndromes,1 which considered the ICTUS results in detail, an initial conservative approach treatment option was accorded the status of only a Class IIB recommendation (ie, “may be considered”), whereas the early invasive approach was accorded Class IA status (“recommended”).1 The European guidelines2 concur with these recommendations. The Australian guidelines3 and the recommendations for implementing them4 are also consistent with these conclusions. In summary, the active use of evidence-based medical treatments for NSTEACS should be encouraged, as these are underutilised in patients with acute coronary syndromes in Australia.12 However, if a patient with an acute coronary syndrome with high-risk features presents to a regional hospital, guidelines based on sound evidence support early invasive treatment, and arrangements should be made for early transfer to a hospital that can provide coronary angiography and, if appropriate, percutaneous coronary intervention.

Peter L Thompson MD, FRACP, FACC

Recent National Heart Foundation of Australia (NHFA) guidelines for management of acute coronary syndromes (ACS) recommend increasing the rates of early invasive management of ACS and providing equal access for all Australians to percutaneous coronary intervention (PCI) facilities. For patients with ACS managed in regional hospitals without PCI facilities, review of the evidence does not show unequivocal benefit of early routine PCI over selective PCI for patients with non-ST-segment-elevation ACS or ST-elevation myocardial infarction. The current pattern of transfer based on the NHFA guidelines is expensive and disruptive of patient care, as well as undermining regional health care services. Further increase in transfer rates and increases in PCI facilities would divert resources away from supporting the regional infrastructure needed to provide evidence-based therapies, without any evidence that lives would be saved.

Brett H Forge MB BS, FRACP

Forge 1 has raised specific concerns about our recent position statement2 on implementing the National Heart Foundation of Australia (NHFA)/Cardiac Society of Australia and New Zealand (CSANZ) consensus recommendations for managing patients with acute coronary syndromes (ACS).3 In particular, he questions whether providing all patients with equal access to percutaneous coronary intervention (PCI) services is truly evidence-based. Abbreviations ACS Acute coronary syndromes CSANZ Cardiac Society of Australia and New Zealand ICTUS Invasive versus Conservative Treatment in Unstable Coronary Syndromes NHFA National Heart Foundation of Australia NSTEACS Non-ST-elevation acute coronary syndromes NSTEMI Non-ST-elevation myocardial infarction PCI Percutaneous coronary intervention STEMI ST-elevation myocardial infarction Transferring patients with non-ST-elevation acute coronary syndromes (NSTEACS)The 2006 NHFA/CSANZ guidelines recommend: High-risk patients with NSTEACS should be treated with aggressive medical management . . . and arrangements should be made for coronary angiography and revascularisation, except in those with severe comorbidities.3 Forge is disturbed by the lack of discussion in the 2006 NHFA/CSANZ guidelines around this recommendation. Detailed discussion about the evidence for early angiography and revascularisation was provided in the NHFA/CSANZ unstable angina guidelines produced in 2000.4 At that time, it was recognised that studies that reported the greatest benefit of an invasive strategy were those in which there was a large difference in intervention rates between the two treatment groups. With the completion of further trials, including the ICTUS (Invasive versus Conservative Treatment in Unstable Coronary Syndromes) study,5 this observation has been strengthened. When trials with the largest absolute differences in revascularisation rates are pooled, a significant reduction in death is seen. If the conservatively managed group has a high rate of intervention, as in the ICTUS study (in which 53% of the conservative management group underwent angiography in hospital, and 67% by one year), the differences between strategies diminish.6 A review of 2380 patients with chest pain admitted to 27 Australian hospitals between January 2003 and August 2005 found that only 20% of patients with ACS who were admitted to coronary care units in hospitals without angiographic services underwent coronary angiography.7 Low intervention rates such as these have consistently been shown to be associated with poorer outcomes, prompting our recommendation that access to catheterisation laboratories for high-risk patients with NSTEACS should be increased. We would have particular concern with Forge’s contention that the ICTUS study provides justification for a more conservative approach for these patients than is taken at present. Our recommendation is consistent with contemporary international guidelines.8,9 The American College of Cardiology/American Heart Association 2007 guidelines8 in fact offer a Class 1 recommendation, level of evidence A, for an early invasive strategy in initially stabilised patients with unstable angina or non-ST-elevation myocardial infarction (NSTEMI) who have an elevated risk of experiencing clinical events. The approach of choosing an initial conservative strategy for these patients, as cited by Forge, is afforded a Class 2B recommendation, level of evidence C — in other words, a weaker recommendation, supported by a less robust evidence base. Routine transfer of all patients with ST-elevation acute coronary syndromes (STEACS)The 2006 NHFA/CSANZ guidelines recommend: Patients who have had STEMI should be considered for early transfer to a tertiary cardiac centre with PCI facilities and links to cardiac surgical facilities (Grade B recommendation). If early transfer is not possible, all patients should be transferred or referred as soon as is practicable for assessment of the need for revascularisation (through PCI or coronary artery bypass grafting) (Grade D recommendation).3 Despite Forge’s concerns, we believe that the evidence supporting these recommendations is stronger than it was in 2005, when the guidelines were produced, particularly for anterior and large inferior STEMIs. The CARESS-in-AMI (Combined Abciximab Reteplase Stent Study in Acute Myocardial Infarction) trial demonstrated that a strategy of immediate PCI led to a significant reduction in death, reinfarction and refractory ischaemia compared with the standard care of rescue-only angioplasty after fibrinolysis.10 Importantly, only 30% of patients in the standard care arm underwent PCI during hospitalisation, compared with 97% in the immediate PCI arm. Thus, offering angiography to high-risk patients with STEMI receiving fibrinolysis during their admission contributes to a reduced event rate. Forge erroneously cites the TRANSFER-AMI (Trial of Routine Angioplasty and Stenting after Fibrinolysis to Enhance Reperfusion in Acute Myocardial Infarction) study11 as evidence against a strategy of routine transfer after fibrinolysis. In fact, most patients in the “standard treatment” arm were treated in this way: 88.7% underwent coronary angiography a median of 32.5 hours after fibrinolysis.11 Guideline implementation and future guideline developmentThe 2006 guidelines for managing ACS were developed by health professionals with different backgrounds through a consensus approach involving independent assessment of key clinical guidelines and scientific articles (acknowledged to be incomplete in some areas). The recommendations that emerged from the subsequent national acute coronary syndrome implementation forum arrived at a consensus view of the key priority interventions that, if applied Australia-wide, would result in improved clinical outcomes. The forum specifically addressed rural and remote settings, where one identified priority was to implement region-specific systems to facilitate reperfusion treatment and subsequent care, including transfer, if appropriate. We clearly do not accept Forge’s contention that our recommendations are based on flawed interpretation of the evidence, nor his inflammatory assertion that the authors had any pecuniary conflict of interest. Guidelines are becoming increasingly important in influencing clinical practice, and an understanding of the optimal processes for their development is evolving.12 We agree on the need for government support in this area. Australia needs a more formal and strategic approach to prioritising, developing and implementing clinical guidelines. To this end, the NHFA has accepted a commission from the Australian Department of Health and Ageing to work with stakeholders, including the National Health and Medical Research Council, to define potential components of an improved collaborative model for developing cardiovascular disease clinical guidelines in Australia.

David B Brieger MB BS, FRACP, PhD · Constantine N Aroney MD, FRACP · Derek P Chew MB BS, MPH, FRACP · Anne-Maree Kelly MD BS, MClinED, FACEM · Darren L Walters FRACP, FCSANZ, FSCAI · Carrie L Toohey RN, BN · Andrew N Boyden MPH, FRACGP

Objectives: To compare clinical outcomes between patients with ST-elevation myocardial infarction (STEMI) presenting to a hospital with facilities for primary percutaneous coronary intervention (PCI) and patients transferred from a non-PCI-capable unit, and to determine the success rate of meeting clinical guidelines for management of STEMI.Design, setting and participants: Prospective study of patients with STEMI who underwent PCI at Box Hill Hospital (BHH), Melbourne, between 1 July 2002 and 30 June 2008. We compared two patient groups: “BHH patients”, who were admitted directly to BHH (a hospital with PCI capability), and “SHIPEM (Shipping Infarcts for Primary Angioplasty in Eastern Melbourne Registry) patients”, who were transferred from other hospitals without PCI capability.Main outcome measures: Clinical outcomes; symptom-to-first-door time (time between symptom onset and arrival at first hospital); first-door-to-balloon time (time between arrival at the first hospital and inflation of the angioplasty balloon); compliance with Cardiac Society of Australia and New Zealand/National Heart Foundation of Australia (CSANZ/NHFA) guidelines for management of patients with STEMI.Results: There were 598 patients in the BHH group and 189 in the SHIPEM group. The median first-door-to-balloon time was 89 minutes (interquartile range [IQR], 69–107 minutes) for BHH patients and 128 minutes (IQR, 104–157 minutes) for SHIPEM patients. These figures did not vary significantly over the 6 years of the registry. In the BHH group, 180 patients (30.1%) had a symptom-to-first-door time of ≤ 60 minutes, with 32 (17.8%) receiving PCI in ≤ 60 minutes. The corresponding figure for the SHIPEM group was 48 patients (25.4%), with 1 (2.1%) receiving PCI within 60 minutes. In the BHH group, 304 patients (50.8%) had a symptom-to-first-door time of 61–180 minutes, with 166 (54.6%) receiving PCI in ≤ 90 minutes. In the SHIPEM group, 50 patients (26.5%) had a symptom-to-first-door time of > 180 minutes, with 21 (42.0%) receiving PCI in ≤ 120 minutes.Conclusion: Our study demonstrates that transfer for PCI is feasible and safe in selected patients, with outcomes comparable to those of patients presenting to a PCI-capable unit. However, the CSANZ/NHFA targets, predicated by symptom-to-first-door time, are not being met and have not improved over time, which suggests that strategies to improve symptom-to-first-door, first-door-to-balloon and transfer times need to be addressed.

Michael J Moore MB BCh BAO, MRCP, MD · Louise Roberts BSc, PhD · Houng-Bang Liew MB BCh BAO, FRCP · Esther M Briganti MB BS, FRACP, PhD · Gishel New MB BS, FRACP, PhD

Evidence is accruing of associations between male reproductive health disorders and chronic diseases such as coronary heart disease and type 2 diabetes. The links between reproductive health and general health are under-recognised by medical practitioners and the general public. Windows of opportunity exist for a more holistic approach to men’s health when men present with reproductive health symptoms (such as erectile dysfunction) or the reproductive implications of chronic disease are recognised. Further men’s health research is needed in Australia to guide policy, innovative health promotion, and clinical practice.

Carol A Holden PhD · Carolyn A Allan MB BS(Hons), PhD, DRCOG(UK), FRACP · Robert I McLachlan MB BS, FRACP, PhD

Recognising that brain and spinal cord injuries result in significant health and economic burdens for the affected individual and the community, the Victorian government committed $63 million towards neurotrauma research beginning in 2005. A survey of Victorian neurotrauma research units conducted in 2008 showed substantial increases in workforce capacity, collaborative activity and research output during the first 3 years of the funding program. Changes in economic and commercial activity, and research translation activity were also observed. The activity and output of the Victorian brain and spinal cord injury research sector increased substantially during a period coinciding with increased funding.

Alex Collie PhD

Cross-border importation of traditional and prescription medications is common, and many of these drugs are not approved by the Australian Therapeutic Goods Administration. Furthermore, counterfeit versions of prescription medications are also available (eg, weight-loss medications, anabolic steroids, and medications to enhance sexual performance). We describe a 54-year-old man with the first Australian case of severe hypoglycaemia induced by imported, laboratory-confirmed counterfeit Cialis. This serves to remind medical practitioners that counterfeit medication may be the cause of severe hypoglycaemia (or other unexplained illness). Clinical recordA 54-year-old male truck driver was admitted to a regional hospital with profuse sweating, slurred speech, ataxia and confusion. He had a history of heavy smoking and moderate alcohol consumption, but denied taking any medications or using recreational drugs. On the evening before his illness, he had four standard alcoholic drinks. On examination, his blood pressure was 150/97 mmHg, body mass index was 33.3 kg/m2, and his score on the Glasgow Coma Scale was 12/15 (eye response, 3; motor response, 6; and verbal response, 3). The rest of the general and systemic examination was unremarkable. In the emergency department, his blood glucose level indicated severe hypoglycaemia (1.1 mmol/L; reference range [RR], 3.0–6.0 mmol/L). After administering 50 mL of an intravenous infusion of 50% dextrose and giving an intramuscular injection of 1 mg glucagon, his Glasgow Coma Scale score improved to 15/15. Subsequently, apart from a high-carbohydrate diet, he required an intravenous infusion of 5% dextrose at a variable rate for 4 days to maintain euglycaemia. His glucose requirement decreased slowly over the following 4 days. He was extensively investigated for hypoglycaemia while in hospital. All other haematological and biochemical parameters, except β-hydroxybutyrate, insulin and C-peptide, were normal. His serum insulin and C-peptide levels, measured on Day 1 and Day 2, were abnormally elevated relative to his low blood glucose level (ie, for the low blood glucose level in this case, the serum insulin level would be expected to be lower). The serum insulin and C-peptide levels had normalised by Day 9 (Box). The serum β-hydroxybutyrate level, measured on Day 2, was particularly low at 0.05 mmol/L (RR, < 0.20 mmol/L), consistent with insulin excess. Magnetic resonance imaging of the pancreas gave negative results for insulinoma. A plasma sulfonylurea screening test, first done on Day 9, gave a negative result. No conclusive diagnosis about this self-limiting hypoglycaemic episode was made during admission. The patient was discharged after making a full recovery. He was advised to self-monitor his capillary blood glucose level and was referred to the endocrinology clinic at our hospital for further evaluation. He attended the endocrinology clinic 2 weeks after discharge. In view of his self-limiting hypoglycaemic episode, specific enquiry was made about the use of oral medication that may have caused the hypoglycaemia. He admitted that, an hour before developing the symptoms, he took a sexual performance-enhancing medication. This was the first time he had taken any medication of this type. The medication had been bought in Vietnam by a friend. This raised the suspicion of contaminated or counterfeit medicine as the cause of the hypoglycaemia. The medication from Vietnam was in a bottle labelled “Cialis 50”. When compared with Cialis manufactured by Eli Lilly, gross differences in packaging, labelling and dose strength were noticed. High-performance liquid chromatography performed by the Australian Therapeutic Goods Administration (TGA) confirmed that one tablet of counterfeit Cialis 50 contained 152.8 mg of glibenclamide and 0.5 mg of sildenafil. The TGA and Eli Lilly Australia were subsequently officially notified. DiscussionThis is the first report of a laboratory-confirmed counterfeit Cialis tablet in Australia. There have been recent warnings about this counterfeit drug and other similar sexual performance-enhancing medications on several health websites.1-4 Cialis (tadalafil), a phosphodiesterase-5 (PDE-5) inhibitor, is a pharmaceutical drug manufactured and marketed by Eli Lilly. It can be obtained only with a prescription, and is dispensed in 5 mg, 10 mg and 20 mg, but not 50 mg, doses. Our case reveals the poor quality-control measures used during the manufacturing process of counterfeit Cialis, which not only contained a lethal dose of a sulfonylurea, but also a subtherapeutic amount of a different agent from the PDE-5 inhibitor class. Glibenclamide is not known to have any sexual performance-enhancing effect, and hypoglycaemia is not a known adverse reaction of tadalafil. Consumption of counterfeit medicines may be harmful. As many countries have not yet enacted deterrent legislation, counterfeiters often do not need to fear prosecution.5 Medicines for erectile dysfunction or sexual enhancement have a huge global market, and this is not the first report of this adverse reaction. An outbreak of hypoglycaemia, secondary to ingestion of sexual performance-enhancing drugs, including counterfeit Cialis and other unlicensed drugs, was reported recently from South-East Asia.6 These drugs also contained high doses of glibenclamide and low doses of sildenafil. The World Health Organization estimates that up to 1% of medicines available in the industrialised countries, and 10% globally, may be counterfeit.7 In Australia, the TGA is an effective regulatory authority; however, despite the regulations, overseas travel and internet purchasing may allow counterfeit medicines to be imported. Under the “Personal import scheme”, many complementary medicines can be legally imported without import permits.8 Additionally, drugs from the PDE-5 inhibitor class, such as tadalafil, which are prescription-only medicines, are not listed under “Prohibited imports and exports (drugs and precursor chemicals)” and so can be purchased on the internet with a prescription from Australia.9 A universal cyberlaw or some other form of international convention is needed to regulate promotion and sales of these types of products on the internet. The WHO acknowledges that increasing international trade in pharmaceuticals, as well as sales via the internet, has further facilitated the entry of counterfeit products into the supply chain. To combat this, in 2006 the WHO helped to create the International Medical Products Anti-Counterfeiting Taskforce (IMPACT).5 Consumers are encouraged to use web sources like the TGA, Health on the Net Foundation, and the WHO to get useful and reliable online health information on medicinal products.10-12 Based on this case, we suggest that health warnings about counterfeit sexual performance-enhancing medications should be published on the TGA website. Glucose, insulin and C-peptide levels during admission Day 1 Day 2 Day 9 Glucose (RR, 3.0–6.0), mmol/L 2.4 2.8 4.7 Insulin (RR, 2–23), mU/L 17 11 0.3 C-peptide (RR, 0.3–1.4), nmol/L 2.6 Not done 0.7 RR = reference range.

Santosh K Chaubey MB BS, MD · Kunwarjit S Sangla MB BS, FRACP · Emershia N Suthaharan MB BS, MD · Yong M Tan MB BS, FRACP, FRCP(Edin)

A 90-year-old man presented to the emergency department with multiple symptoms including double vision, reduced mobility, dysphagia, recent rapid weight loss, ear discharge and deafness. He had diabetes and other chronic medical problems, including otitis media with mastoiditis. This case highlights the difficulty of investigating weight loss in older people, who may not show the usual clinical features of infection, and of distinguishing between infection and malignancy when radiological findings are inconclusive. His eventual diagnosis was osteomyelitis of the skull base with cranial nerve involvement. Clinical recordA 90-year-old, previously fit Estonian man was admitted to hospital from the emergency department (ED) with multiple symptoms including acute diplopia, difficulty with walking, several falls over 2 weeks, decreased taste sensation, dysphagia with solids over several months, a 10 kg weight loss over 5 months, and a 6-week history of otalgia, aural fullness, otorrhea, and deafness. Four months earlier, the patient had presented to the ED with acute onset of left facial nerve palsy, dysphonia and dysphagia. The facial nerve palsy had resolved spontaneously after 2 weeks without specific treatment. The patient had several significant background medical problems: late-onset diabetes mellitus of 17 years’ duration; peripheral neuropathy; chronic atrial fibrillation; hypertension; and chronic left otitis media with effusion and mastoiditis, for which he had been treated with insertion of a tympanostomy tube 5 months before admission, and a short course of a topical corticosteroid and an oral antibiotic 1 month before admission. The dysphagia was investigated before admission with a barium meal, oesophageal manometry and gastroscopy, which showed severe oesophageal dysmotility and no obstructive lesion. The patient was an ex-smoker with a 55 pack-year smoking history, regular moderate alcohol intake, and occasional salted fish but no areca (or “betel”) nut consumption (which have been linked to nasal and oral cancers, respectively). There was no family history of cancer. His regular medications included metformin, gliclazide, amiodarone, lercanidipine, frusemide and amitriptyline. The main findings on examination included failure of abduction (but no medial deviation) of the left eye consistent with abducens nerve palsy, bilateral haemoserous ear discharge, cachexia, and unsteady gait. No other localising neurological signs were found. The patient remained afebrile throughout the admission. A bedside swallowing assessment by a speech pathologist demonstrated moderate pharyngeal dysphagia. Communication with the patient was conducted through writing. The results of blood tests were unremarkable: his creatinine level was 100 μmol/L (reference range [RR], 70–110 μmol/L); leukocytes, 9.0 × 109/L (RR, 4.0–10.0 × 109/L); glycated haemoglobin, 7.1%; and C-reactive protein (CRP), 51 mg/L (RR, < 5.0 mg/L). One week later, the leukocyte count remained within the normal range and his CRP level had fallen to 35 mg/L, remaining at this level throughout the admission without any specific treatment. A computed tomography (CT) scan and magnetic resonance imaging (MRI) of the brain showed extensive skull base and prevertebral soft tissue thickening with contrast enhancement, bilateral mastoid air cell opacification, and bony destruction of the clivus and both petrous parts of the temporal bones (Box). Bone scintigraphy, performed using technetium-99m hydroxymethane diphosphonate, and a fluorodeoxyglucose positron emission tomography (FDG-PET) scan showed intense tracer uptake in the nasopharynx, base of the skull and mastoid air cells. There was no evidence on the FDG-PET scan of distant uptake. A culture of ear discharge grew a mixture of Staphylococcus aureus and Pseudomonas aeruginosa that were sensitive to flucloxacillin and ciprofloxacin, respectively. Nasopharyngeal carcinoma was strongly suspected by the treating medical team on the basis of radiological findings, significant weight loss (even though the weight loss could be partially attributed to dysphagia), and only a moderate rise in the CRP level. However, the treating ear, nose and throat (ENT) surgeon was of the strong opinion that the abnormalities were due to an infective process and that nasopharyngeal biopsy was not necessary. In view of the radically different nature of the treatments for the two conditions, the divergent opinions about the diagnosis, and the patient’s family wanting more certainty, the opinion of a second ENT surgeon was sought. Subsequent nasopharyngeal biopsy results showed only submucosal chronic inflammation. A diagnosis of skull base osteomyelitis complicating otitis media was made. The patient was started on oral ciprofloxacin 500 mg twice a day (to be continued long term), rehabilitated (practice in transfers, ambulation and self-care), and discharged after 31 days, having shown improvements in weight, mobility and other functional status. At 4-month follow-up, diplopia and abducens nerve palsy had resolved, the patient’s CRP level was 0.3 mg/L and he had gained 8 kg in weight. At 7-month follow-up, there was no ear discharge, the patient’s weight was stable, he felt well and had returned to his previous level of activity. Using hearing aids, the patient was able to converse. Cessation of ciprofloxacin would be considered at 1-year follow-up if there were signs of resolution of osteomyelitis on gallium imaging and repeat bone scan and MRI. DiscussionOsteomyelitis of the base of the skull is commonly associated with malignant otitis externa. However, this patient had chronic otitis media and mastoiditis. Involvement of lower cranial nerves (VI to X) is common in skull base osteomyelitis due to their anatomical proximity to the clivus.1,2 Accurate diagnosis of abnormalities in the base of the skull is important but difficult. Both infection and malignancy can result in severe disability and death, but a good clinical outcome can be achieved with the correct treatment.2 The difficulty of diagnosing either infection or malignancy in similar cases has been reported previously.3-5 However, this patient’s case is unique because of his advanced age, complete resolution of symptoms, attainment of his ideal body weight and full return to his previous level of functioning. The diagnosis at discharge relied on the negative biopsy result for malignancy, the history of complicated chronic otitis media with effusion, and the patient’s improvement after antibiotic treatment. Subsequent clinical improvement at follow-up gave further support to the diagnosis of infection. Although weight loss was the major sign raising suspicion of malignancy, it is not a common feature of nasopharyngeal carcinoma without distant metastases.6 As occurs in many older patients, this patient did not have the usual clinical features of infection. CT, MRI and bone scans demonstrated the extent and location of abnormalities but could not distinguish between infection and malignancy. The FDG-PET scan indicated there were no metastases. Ciprofloxacin was chosen on the basis of the ear discharge culture result and because P. aeruginosa has been implicated as the major pathogen causing skull base osteomyelitis related to ear infections — especially in people with diabetes who have otitis externa.7 S. aureus was thought likely to be a colonising organism rather than a copathogen; the clinical response to the ciprofloxacin was consistent with this. A challenging question with this patient was the optimal duration of ciprofloxacin treatment, especially when the ear discharge persisted for up to 7 months. The decision to stop treatment with the antibiotic would be a matter of judgement based on clinical features, persistently normal CRP levels and improvements on serial scans. After cessation of antibiotic treatment, the patient would require regular and prolonged follow-up to detect early relapse of infection. Magnetic resonance image showing skull base osteomyelitis and otitis media Axial T1 weighted, fat suppressed contrast enhanced scan showing extensive skull base enhancement (white region) with extension anteriorly to the retropharyngeal space (thin white arrow) and posteriorly to dura at the left cerebellopontine angle cistern (thick white arrow).

Jenson C S Mak MB BS, FRACP, FAFRM(RACP) · Lawrence H Kim MB ChB · Lawrence T C Ong BPsych(Hons), MB BS · Triet M Bui MB BS, FRACP, MPH

To the Editor: We describe here some of the difficulties in managing and investigating outbreaks of viral respiratory infection in aged care facilities (ACFs) in the context of an influenza pandemic. This adds to the previous report on logistics in a hospital setting.1 On 12 June 2009, NSW Health received a call from a surveillance officer in a remote town regarding a possible pandemic (H1N1) 2009 influenza outbreak in an ACF. On 9 June, a 77-year-old female resident had become unwell, without specific symptoms of influenza-like illness. From 7 to 10 June, nine of the other 27 residents developed influenza-like illness. On 10 June, nasal swabs were taken from the 10 unwell residents by the local general practitioner for influenza nucleic acid testing (NAT). On 12 June, the index case tested positive for pandemic influenza, while the other residents tested negative. Due to concern that there might be a pandemic influenza outbreak in the facility, the index case and the nine residents with influenza-like illness were given oseltamivir (75 mg twice a day for 5 days) from 13 June; the other 18 residents and the 27 staff were given oseltamivir prophylaxis (75 mg daily for 10 days). A formal outbreak investigation and further laboratory testing (NAT, serological testing) revealed a dual outbreak dominated by rhinovirus (10 cases), with two cases of pandemic influenza and one case of untyped influenza A. All 28 residents and 26 of the 27 staff had received seasonal influenza vaccine in early 2009. This outbreak illustrates that more than one respiratory virus may co-circulate in ACFs during winter outbreaks of respiratory infection. We followed Department of Health and Ageing policy guidelines for oseltamivir use in ACFs2 and the facility was closed to visitors from 12 to 18 June. However, as all residents had received seasonal influenza vaccination, and given that older people are generally at lower risk of pandemic (H1N1) 2009 influenza,3 we could have had a higher threshold for oseltamivir use. The total estimated cost of treatment and prophylaxis was $2750 (55 residents and staff at $50/person) for oseltamivir alone. Co-infection with respiratory viruses may be more common than thought in ACFs; a recent Canadian study found two and three different pathogens in 15% and 4% of respiratory infection outbreaks, respectively, from a total of 83 outbreaks (of which 91% occurred in long-term care facilities).4 If many ACF outbreaks have more than one respiratory virus involved, laboratory investigations should take a multiplex approach that covers common respiratory viruses. As many patients as practical (at least five) should be swabbed and tested to guide treatment, prophylaxis and other investigations. Community influenza surveillance should ideally include information on sensitivity to oseltamivir, and on other circulating respiratory viruses.

Gulam Khandaker · Bridget Doyle · Dominic E Dwyer · Robert Booy

To the Editor: It is a naïve public health physician who predicts ahead of time how many people will die in a disease outbreak. Such doctors have short careers. What Collignon calls the “wrong and exaggerated” expert predictions1 of mortality from the recent influenza pandemic are based on the numbers that the World Health Organization advised governments to use in planning for pandemics.2 They are derived from a sensible calculation: plan for a situation considerably better than the 1918–1919 pandemic but somewhat worse than the 1957 or 1968 pandemics. The problem in Australia is not so much the pandemic plans produced through the time-honoured process of ad-hoc, temporary federal government committees for implementation by multiple, variously organised state and territory authorities. The real problem is producing a consistent, flexible response to any developing national infectious disease emergency. No other nation tries to do that without having a national authority, made up of full-time professionals with a fair degree of independence from the political process. The United States has its Centers for Disease Control and Prevention (http://www.cdc.gov); the United Kingdom its Health Protection Agency (http://www.hpa.org.uk); and, perhaps the most pertinent example, Canada has its Public Health Agency (http://www.phac-aspc.gc.ca), established in the aftermath of the SARS (severe acute respiratory syndrome) outbreak. The European Union has set up a supranational European Centre for Disease Prevention and Control (http://www.ecdc.europa.eu). A plan can only ever hope to put in place all the resources needed for a response, but a flexible, consistent, science-based and targeted national response to infectious and other health emergencies requires a professional national authority.

Rodney C Givney

To the Editor: The recent clinical update by Chakera and colleagues highlights the problems and adverse patient outcomes that occur when current and prior diagnostic images are not accessible during the clinical care process.1 While the article describes a locally crafted, tactical, information technology (IT) solution, it fails to mention that much work has been done internationally to create a standards-based, scalable architecture for image and document exchange. This work has been done by Integrating the Healthcare Enterprise (IHE) (http://www.ihe.net), a global collaboration between health care equipment suppliers, IT experts and clinicians. The aim of the collaboration is “to improve the way computer systems in healthcare share information”. The profile for cross-enterprise document and image sharing is known as XDS-I. XDS-I defines how to use established health care and IT standards (eg, the Digital Imaging and Communications in Medicine [DICOM] and Health Level 7 [HL7] standards2,3) to facilitate secure exchange of health care information, including images, between health care institutions. Information exchange is independent of the hardware and software in place at the participating institutions, and system integration using XDS-I supports user needs, including security and privacy, while streamlining workflow. Using a single technical approach, implemented at a regional or state level, diagnostic images can be exchanged, along with documents such as radiology and laboratory reports, discharge summaries, and even general practitioner care plans. Providers can, with patient permission at the time of care, access such documents via secure internet connections. The solution developed by Chakera and colleagues covers Western Australian public hospitals and parts of the private sector. XDS-I is a platform that also allows image sharing between the public and private sectors, regardless of the picture archiving and communication system adopted by participating practices or hospitals. Many of the operational problems identified in the article by Chakera and colleagues (consent, staff time costs and manual processes) have been addressed in the IHE XDS-I profile. While projects such as the pilot program by Chakera and colleagues are useful learning exercises, locally crafted single-vendor solutions (even those using industry standards) are rarely scalable to broader usage. We strongly commend the IHE XDS-I model to everyone considering image exchange systems in Australia.

Nicholas J Ferris · Philip J Dubois · Christopher Lindop · Vincent B McCauley · Peter A MacIsaac

To the Editor: Alarm about the dangers of computed tomography (CT) scans1,2 is unjustified. The only hard facts about bio-harm from ionising radiation come from the 1945 atomic bomb explosions, which emitted very large amounts of radiation. Bio-harm from low-dose medical radiation has never been confirmed; the claim is based on backward extrapolation of data on radiation doses from the Japanese atomic bombs, which were orders of magnitude greater than doses in diagnostic radiation. The resultant linear no-threshold theory, which postulates that there is no safe radiation dose, remains unproven. Radiation protection authorities use this model because it is expedient, if unverified and overly conservative. Those who treat it as dogma forget that it remains a theory, and any derived calculations are subject to large uncertainties. Radiation scientists question its validity,3 and many regard the estimated risks as grossly exaggerated or negligible.4 The Health Physics Society has stated that the risks to health from radiation doses below 100 mSv are either too small to be observed or non-existent.5 The theory is also challenged by evidence that low-dose radiation is actually beneficial and protects against the effects of large-dose radiation by inducing DNA repair enzymes. A study of 407 000 nuclear shipyard workers and another of 7800 Russians exposed to low-level radiation from the 1957 Mayak nuclear facility accident showed that the exposed groups developed significantly less cancer than their unexposed controls.4 The lifespan of British radiologists over the past century has exceeded that of any other control group.6 Figures quoted in the media for cancer attributable to medical radiation are theoretical calculations and have never actually been observed. They are as “real” as estimated cancer rates due to mobile phones and power lines. Newspaper claims such as “More than 400 new cases of cancer a year in Australia are attributable to diagnostic radiology”2 are alarmist and misleading — they disguise the fact that their figures derive from an unproven theory, not from observations. Ironically, concern about the dangers of CT is rising even as the actual radiation doses involved are falling. A 2010 CT scanner emits 1/20th the radiation of its 5-year-old predecessor. CT coronary angiography can be accomplished today with a dose of less than 1 mSv — equivalent to six chest x-rays or 6 months of background radiation. Patients for whom a CT scan is medically indicated should not be denied one of modern medicine’s greatest benefits because of unfounded fears. The risks of delayed or missed diagnosis or wrong treatment far outweigh the theoretical risk of harm from a CT scan.

Carl M Blecher

To the Editor: We present a case of fatal cocaine overdose in which the drug was contaminated with levamisole, a therapeutic agent known to cause reversible agranulocytosis. The deceased, a previously well woman in her early 20s, was found dead in circumstances suspicious of a drug overdose. The death was reported to the coroner and the autopsy findings were unremarkable, with no evidence of injury or significant natural disease processes. Toxicological sampling of blood revealed a cocaine level in the blood of 4.9 mg/L, as well as the cocaine metabolite benzoylecgonine at a level of 3.4 mg/L. These are lethal levels for cocaine and benzoylecgonine.1 Cocaine was also detected in a nasal swab, and levamisole was detected in the nasal swab and in the blood, as well as in a quantity of white powder found near the woman’s body. The cause of death was given as cocaine toxicity. Illicit cocaine in Australia is generally diluted (“cut”) with a range of innocuous substances, including fructose and sucrose, and less commonly with other drugs, such as lignocaine.2 In this case, levamisole was detected as a contaminant. Levamisole is primarily used as a veterinary anthelmintic, and used uncommonly in humans for rheumatoid arthritis, and as adjuvant therapy to fluorouracil in the treatment of a variety of cancers.3,4 Agranulocytosis is a significant side effect of levamisole, and this has limited its use in humans. The clinical presentation of agranulocytosis is protean, presenting with a spectrum of abnormalities, ranging from a flu-like illness to leukopenia with a potentially fatal outcome.3-5 The mechanism whereby levamisole induces agranulocytosis is unknown, although a strong link with the human leukocyte antigen HLA-B27 and rheumatoid factor positivity suggests a likely genetic predisposition.4 Recent reports from the United States and Canada have highlighted the presence of levamisole in seized illicit cocaine entering these countries, with up to 69% of seized cocaine lots containing levamisole. There has been a subsequent clustering of fatal and nonfatal cases of agranulocytosis in a number of disparate locations.3-5 The reason for contaminating cocaine with levamisole is unknown, although there are indications that levamisole may promote the effects of cocaine by interfering with its reuptake at a synaptic level.4 Although there was no evidence of agranulocytosis in the present case, we highlight the apparent recent appearance of this contaminant in the cocaine supply in Australia, because it has the potential to induce reversible agranulocytosis in people not otherwise obviously at risk for this condition.

Johan A Duflou · Issabella G Brouwer · Shane Darke

To the Editor: The clinical justification for a medical intervention depends on absolute prevalence (p) of a disease or condition in a population and the relative risk reduction (R) that would result from the intervention. These variables determine the “number needed to treat” (NNT) to prevent one occurrence of a disease, according to the formula NNT = [100 ÷ (P × R)], where P and R are expressed as percentages. This principle applies to thromboprophylaxis in medical patients. However, the prevalence of venous thromboembolism (VTE) in hospitalised patients is uncertain. The main justification for medical thromboprophylaxis given on the National Institute of Clinical Studies (NICS) website1 is an unpublished report prepared by the University of Western Australia (UWA) on behalf of the NICS.2 The report noted that 40.8% of all hospital cases of VTE were “medical” rather than “surgical” or “idiopathic” (primary) cases, but the prevalence of VTE (overall or in each subgroup) was not stated. We obtained coded separation data for all multiday admissions to Royal Perth Hospital (RPH) for the most recent 2-year period with complete data (2005–2007). We searched for VTE events with a principal or secondary coding, and classified them as medical or surgical VTE cases according to the definitions used in the UWA report (for medical VTE, “admissions in which a diagnosis of VTE was recorded as a complication or in a diagnostic field other than the principal diagnosis OR admissions with VTE as the principal diagnosis within 3 months of a non-surgical [medical] admission”).2 We acknowledge that the use of prophylaxis during the index admission or any previous admission within 3 months (which we did not measure) may have meant that we underestimated the prevalence of VTE. Prevalence was calculated by dividing the event number by the total number of admissions or by the number of medical or surgical admissions, as required (expressed as a percentage). At RPH over the 2-year period, 805 VTE events (574 in medical and 231 in surgical patients) were observed in 72 991 medical and 29 177 surgical admissions (total, 102 168 admissions). These included 357 pulmonary emboli (44.3%), 207 of which were primary events. Of the 805 VTE events, 312 (38.8%) were medical, 209 (26.0%) surgical and 284 (35.3%) idiopathic (the corresponding proportions in the UWA report were 40.8%, 37.7% and 21.5%, respectively). The overall VTE rate in the medical patient population was 0.79%, but for “medical VTE” as defined in the UWA report,2 the rate was 0.43%. In surgical patients, the rate of VTE was 0.79% in our study, or 0.72% based on the UWA definition. Hence, according to the definitions used by the UWA report, “surgical VTE” is actually more frequent than “medical VTE”. Our study confirms that about 40% of VTE is in medical patients, but that the absolute prevalence is low (0.43%). This is similar to the rate of 0.4% reported in the PREVENT (Prevention of Recurrent Venous Thromboembolism) study.3 The 40% figure is not relevant for consideration of prophylaxis, as it depends on the number of non-medical events. The low prevalence is directly relevant, and weakens the case, as previously argued, for routine thromboprophylaxis.4 In summary, the NICS support for medical thromboprophylaxis may be biased by its reliance on the UWA report. The risk is of overuse of drugs that cause bleeding, and hence of doing more harm than good.5

J Alasdair Millar · Glenda E Lee · Rinaldo Ienco

To the Editor: The aim of the study by Kennare and colleagues1 was to establish data on home and hospital birth outcomes for the period 1991–2006, before the Policy for Planned Birth at Home in South Australia was introduced in 2007.2 One significant shortcoming of the study was the lack of data regarding the type of birth attendant, the degree of cooperation with the local hospital and the quality of transfer arrangements. Currently, there are virtually no home birth policies in Australia governing women’s access to qualified midwives with hospital visiting rights that enable appropriate transfer. Women who intend to have a home birth are forced to rely on the charity of midwives who provide care without professional indemnity insurance. Failing this, women are known to give birth without a midwife. Kennare et al1 suggested that the Bachelor of Midwifery program will increase the number of midwives planning to offer home birth. However, their study did not examine whether women were attended by registered midwives, non-registered midwives, doulas, untrained birth helpers or a professional of any capacity, and assumed that planned home birth equates to home birth under the care of a qualified registered midwife. This has been a weakness of previous Australian studies.3 Overseas studies which identify the status of the midwives have shown that, for low-risk pregnancies, births at home attended by competent registered midwives in a networked system have outcomes that are comparable to hospital births.4,5 We have previously detailed other limitations of the study, including the inclusion of women who planned a home birth at booking but subsequently developed risk factors and gave birth in hospital, as well as the difficulty of examining the rare outcome of intrapartum death or intrapartum asphyxia in such a sample, as the wide confidence intervals show.6 Kennare and colleagues1 provide useful recommendations about risk assessment, transfer to hospital and fetal monitoring, and rightly highlight that the system must be so terrible for some women that they choose to give birth outside of it, even with risk factors. Despite a malfunctioning system in Australia — where midwives are uninsured and have no visiting rights, and home birth is unfunded and often hard to access — the perinatal mortality rate was no different for home births compared with hospital births. Risk assessment, transfer to hospital and fetal monitoring will be improved when midwives are no longer excluded from mainstream services.

Hannah G Dahlen · Caroline S E Homer · Sally K Tracy · Andrew M Bisits

To the Editor: Kennare and colleagues are to be congratulated.1 Careful, systematic collection and analysis of data on planned home births and planned hospital births creates evidence that women need to make intelligent and safe choices about perinatal care. A central medical cause of concern in the article1 and accompanying editorial2 is a high relative risk of death caused by intrapartum asphyxia in the planned home birth group. But, on closer examination, the underlying cause appears more likely to be a lack of proper integration of home birth midwives into the health care system. Of the nine infant deaths in the study, five were, by definition, unrelated to the place of birth — three were antenatal deaths that occurred after transfer to hospital (all unrelated to type of antenatal care) and two occurred in cases where the baby was born at home but had a fatal congenital anomaly. Three of the other four deaths (two of them due to intrapartum asphyxia) occurred after the parents persisted in their home birth choice despite advice against it, resulting in delayed transfer to hospital, or declined intervention after transfer to hospital — factors thought to have contributed to the deaths. Thus, an underlying contributing cause of the higher risk of intrapartum asphyxia appears to be some parents’ perception that care in hospital was not best for them or their baby. This perception is not entirely baseless, given that the caesarean section rate for planned hospital births in South Australia was 27.1%, 3.7 times the risk associated with planned home births after factoring in differences in maternal characteristics and obstetric conditions between the two groups (adjusted odds ratio, 0.27; 95% CI, 0.22–0.34)1 and about double to triple the 10%–15% rates recommended by the World Health Organization.3 Furthermore, women had seven times the risk of episiotomy for planned hospital births compared with planned home births, and three times the risk of instrumental delivery.1 Recent large, high-quality studies of home birth in Canada4,5 and the Netherlands6 demonstrated that — when home birth midwives are an integral, accepted, insured and funded part of the health care system — home birth is safe and refusal of midwife-recommended care by patients does not appear to be an issue. We suggest that an evidence-based solution to the underlying causes of excess asphyxia and perinatal mortality highlighted in Kennare et al’s study would be to follow the lead of countries such as the Netherlands and Canada — provide state funding for independent home birth midwifery practice, provide professional indemnity insurance and provide home birth midwives with access to hospital privileges as autonomous caregivers. When women can depend on continuity of care during transport, they are less likely to refuse or delay necessary care or transfer to hospital.

Kenneth C Johnson · Betty-Anne Daviss

In reply: Dahlen and colleagues overlooked that we excluded births without professional antenatal care (n = 1217), ensuring that all 1141 planned home births in our study were cared for by registered midwives.1 Nonetheless, we appreciate their acknowledgement that our article contains useful recommendations. Yet, they failed to endorse these recommendations in their letter and in the earlier critique to which they refer. They instead draw attention to a lack of difference in total mortality, but dismiss large differences in intrapartum and asphyxia-attributed mortality through their misinterpretation of confidence intervals. Rare outcomes, such as these, inevitably have wide confidence intervals. However, it is wrong and misleading to use the lack of precision in how much more frequent they are as an argument to dismiss their significantly much higher frequency. We tend to agree with the above correspondents, though, that proper integration of home birth care in maternity services might prevent some avoidable deaths that are a recurrent feature in Australian home birth studies.1-3 Indeed, we postulated this too.1 However, it is fallacious to assume that differences in outcome between Australia and other countries, to which the correspondents refer, are merely an issue of funding and access to hospital privileges for autonomous practitioners. The Netherlands,4 for example, has more than 40 000 home births a year, but only three midwifery academies, with a 4-year curriculum. Australia has less than 1000 home births a year, fewer than it has midwifery students, most of whom learn both nursing and midwifery within 4 years. Midwives in the Netherlands are medical professionals and carefully select only low-risk pregnancies for home birth.4 In Australia, on the contrary, many independent midwives accept home birth for pregnancies that are not low risk.1,2 Adherence to approved policies for planned home birth5 and collaboration with hospital services must be a prerequisite to their integration into maternity services. Unless leaders and teachers of the midwifery profession in Australia unequivocally condemn home birth for women with substantial risks, such as twin pregnancy or previous caesarean section, babies will continue to die needlessly, irrespective of any funding models.

Marc J N C Keirse · Robyn M Kennare · Graeme R Tucker · Annabelle C Chan

To the Editor: Hudson and colleagues showed that rural patients are a willing teaching resource for medical students, but that there are problems in using this resource.1 My experience shows the problems and opportunities. I have long provided a consultant paediatric service to two rural hospitals and an Aboriginal community in south-east Queensland. Clinical demands are large; resources are minimal. Waiting time from referral to consultation is 4–12 months. Many children with schooling problems lose a year of education waiting for diagnosis and treatment, and many have physical and behavioural conditions seldom seen in city practice. Few families are insured; bulk-billing is the norm. I spend 4 days a month in the area. Hospital staff make the appointments, and I use hospital records for my clinical notes. Hospitals provide clinical and personal accommodation, but not a secretarial service or funds for travel. Facilities are poor by city standards and financial returns meagre. I finish my clinics early then spend 3–4 hours each day typing letters to referring doctors and other paperwork. This is wasteful use of skilled time. Several problems and opportunities regarding medical education in rural specialist practice are evident: The need for more clinical teaching for medical students is real and urgent. As rural patients are available and willing, we should use them. Lack of specialists to meet clinical needs and to meet teaching needs are two sides of the same problem. Specialist clinics and teaching should be done in local hospitals that already have basic facilities, but most rural hospitals are already stretched and cannot take on an extra load. Medical specialists must be used efficiently. Additional administrative staff are needed to organise appointments, type letters and do general paperwork. Suitable clinic space and nursing assistance are also needed. Payments to visiting specialists should be sessional rather than case based, so that teaching carries no financial penalty. Payments for clinical and teaching sessions, travel, and accommodation should be sufficient to attract specialists and consultants. Some costs could be recouped by bulk-billing. Ideally, the specialist or consultant would provide long-term continuity to patients and staff — in contrast to registrars, who tend to be transient. Rural specialist practice is an untapped resource for teaching. Given suitable conditions, senior medical staff could develop its potential while providing a much-needed clinical service.

Alan E Dugdale

Mental health across cultures. A practical guide for health professionals. Jill Benson, Jill Thistlethwaite. Oxford: Radcliffe Medical Press, 2008 (xiii + 208 pp). ISBN 9781846192197. In an increasingly multicultural Australia, a medical practitioner is called upon, on a daily basis, to treat patients from diverse cultural backgrounds: migrants, refugees, students from other cultures and Indigenous people. This cultural diversity extends to differences in social status, age, religion, sexual orientation and many other sociodemographic aspects. A medical consultation across the cultural divide is fraught with the risk of miscommunication. Jill Benson and Jill Thistlethwaite, in this small information-packed volume, provide an antidote to such a predicament. Both authors are doctors who have worked in diverse settings in Australia and overseas, have treated patients from many different cultural backgrounds, are knowledgeable about diverse cultures and sensitive to differences, recognise the importance of mental health consultations in general practice, and take a keen interest in their patients’ stories. The first call they make in the book is for physicians to become aware of cultural differences. They then present a model for working across the cultural divide, beginning with self-reflection, developing an understanding of another culture through networking and mentoring and, most importantly, listening to the patient’s story. The primary care physician is first and foremost a healer, and this book presents a succinct view of the issues that come up when psychotherapy, behaviour therapy or narrative therapy must bridge a cultural divide. Even pharmacotherapy is not immune to transcultural challenges as miscommunication can affect adherence and appropriate use of drugs, and ethnic or racial differences can influence drug kinetics and dynamics. The strength of this book lies in the distilled wisdom of two practitioners who teach through real-life examples and present practical solutions. It can therefore be recommended to all physicians and medical students. If you are an international medical graduate practising in Australia or an Australian graduate wishing to work overseas, you will find the case studies particularly appealing. The book fills a gap in the cross-cultural health literature.

Perminder S Sachdev

The pill and other forms of hormonal contraception. The facts. 7th ed. John Guillebaud, Anne MacGregor. Oxford: Oxford University Press, 2009 (xix + 193 pp). ISBN 9780199565764. Does life begin at fertilisation or implantation? At times, the sticky question about whether certain types of contraception are actually causing an abortion arises with patients or colleagues. This book helps by providing a discussion of some ethical aspects of contraception in one of the appendices, where the authors argue that one can write an equation for the definition of conception as follows: CONCEPTION = FERTILIZATION + IMPLANTATION (being with child) (crucial) (also crucial) This equation makes it possible to argue that methods of contraception which may block implantation are contraceptives, and not abortifacients. John Guillebaud is Emeritus Professor of Family Planning and Reproductive Health at University College London, and a guru in family planning. He first wrote this guidebook in 1980 as he is passionate about sharing his knowledge with women: “here are the facts, now you decide”. Anne MacGregor is an Instructing Doctor in Sexual and Reproductive Healthcare at the Royal College of Obstetricians and Gynaecologists, London. This “book about the Pill for a general readership” is a user-friendly explanation of the contraceptive pill and other hormonal contraceptive methods. There are plenty of diagrams, tables and flowcharts to assist the reader’s understanding of reproductive physiology, choice of pill and what to do about breakthrough bleeding and other management issues. Tables present the risks and side effects, but also the benefits of taking the Pill. Although many people regard the Pill as “unnatural”, one could argue that having regular menstrual cycles is an unnatural condition. Before contraception was available, women would have been pregnant or breastfeeding for most of their reproductive lives. Although the Pill is not suitable for all women, many women find that taking the Pill and being “a little bit pregnant” works well at one or more stages of their life, or “contraceptive ages” as this book puts it.

Lisa H Amir

Incorrect units: In “Impact of income management on store sales in the Northern Territory” in the 17 May 2010 issue of the Journal (Med J Aust 2010; 192: 549-554), there were errors in Box 2 under the column heading “Outcome measures”. The units for “Fruit and vegetable turnover” should have been kg, and the units for “Soft drink turnover” should have been L.

Julie K Brimblecombe · Joseph McDonnell · Adam Barnes · Joanne Garnggulkpuy Dhurrkay · David P Thomas · Ross S Bailie

Think tall Ever get that shrinking feeling? We tend to become shorter with age and this may be by as much as 4.5 cm by age 70, according to a recent observational study of about 8610 older French women. Since loss of height is considered as an indicator of osteoporosis and vertebral fracture, the researchers set out to determine how accurately the women reported their current height. Only 2% maintained the same height as reported or recalled from their younger days, while most overestimated their current height by 2.4 cm. Previous vertebral fracture and thoracic kyphosis were strong determinants of height loss. The authors recommend measuring actual height of postmenopausal women, rather than relying on reported estimates. CMAJ 2010; 182: 558-562 doi: 10.1503/cmaj.090710 All in the family Results from a Norwegian study support the belief that severe morning sickness tends to run in the family and that maternal, rather than fetal, genes are to blame. The population-based study analysed generational data spanning about 40 years and found that women were three times more likely to have hyperemesis if their mothers had experienced it. This was regardless of whether this had occurred in the pregnancy leading to the birth of the woman under study or in a previous or subsequent pregnancy. In contrast, the risk was not passed on to female partners of sons whose mothers had been affected, However, the authors acknowledge that the link between mothers and daughters may also be due to shared environmental factors. BMJ 2010; 340: c2050 doi: 10.1136/bmj.c2050 Running with scissors . . . Traumatic cataracts from eye trauma are not uncommon in Australia, according to a 15-year retrospective review of paediatric cases, during which time, 74 cases were reported. Offending objects included sharp pointed metal objects, scissors, rocks and, in one case, goggles. The mean age of injury was 7.5 years and males represented 75% of the cases. Best and worst case scenarios for visual acuity after cataract surgery were reported as 6/12 or better in about one third of children, and less than 6/60 in about 20%, including four with perception of light or worse. Clin Experiment Ophthalmol 2010; 38: 237-241 doi: 10.1111/j.1442-9071.2010.02236.x Being bullied Why are some children more likely to be bullied at school than others? A recent US study has shown that those who are obese are more likely to be bullied (OR 1.6; 95% CI, 1.18-2.25), regardless of their sex, race, socioeconomic status, social skills or academic achievement. The study included 821 school-aged children who had been recruited at birth as part of a study on child development and behaviour. The longitudinal nature of the study allowed the researchers to examine whether being obese was the cause of the bullying or whether being bullied actually led to excessive weight gain (due to stress-related overeating). They found that there was no significant increase in body mass index in the 2 years after reporting being bullied, indicating that obesity was probably the cause rather than the consequence of bullying. Pediatrics 2010, 3 May. doi: 10.1542/peds.2009-0774

Alison Williams