Volume 190 Issue 1

Updated guidelines widen the definition of pre-eclampsia and highlight that hypertension in pregnancy has become a lifelong disorder The “political” enthusiasm for women to have more babies will not come without a downside. Complications such as pre-eclampsia — a major cause of premature delivery — are likely to become more prevalent as increasing numbers of women become pregnant when they are older or obese, and may affect up to 5% of these women. The reason why pre-eclampsia develops is an enigma. Although there have been no recent major advances in the clinical treatment of this diverse disorder, maternal and fetal outcomes in Australia and New Zealand are good.1 The big risk now is that obstetricians, physicians, general practitioners and midwives will become complacent about the management of these high-risk pregnancies. The institution of standardised surveillance guidelines for Canadian women with pre-eclampsia has been associated with a reduction in adverse maternal outcomes (from 5.1% to 0.7%), but not perinatal outcomes.2 For this reason, the updated Australian and New Zealand Guidelines for the management of hypertensive disorders of pregnancy,3 assuming they are adopted, should improve outcomes for women with hypertension in pregnancy. These guidelines, which were produced in 2008 by the Society of Obstetric Medicine of Australia and New Zealand (SOMANZ), highlight key aspects of these complex disorders. First, the traditional definition of pre-eclampsia — as only hypertension with proteinuria — fails to identify women who are at high risk by having other organ involvement (eg, hepatic, haematological or cerebral disease) without proteinuria.4 Second, a spot urine protein : creatinine ratio can be used to detect significant proteinuria, and 24-hourly urine collections are no longer necessary in routine clinical management.5 Third, although all women with pre-eclampsia should initially be admitted to hospital, many hospitals now have a day assessment unit where some patients with pre-eclampsia can be managed as outpatients — providing their initial assessment was as an inpatient. The treatment of these disorders is “supportive”, and does not ameliorate placental abnormalities or alter the pathophysiological sequelae of pre-eclampsia. Treatment of hypertension in pregnancy does not cure pre-eclampsia; it is intended to prevent cerebral haemorrhage and eclampsia (seizures), and may delay proteinuria.6 SOMANZ recommends antihypertensive treatment be commenced promptly in all pregnant women with a systolic blood pressure of 170 mmHg or higher, or a diastolic blood pressure of 110 mmHg or higher. Several rapidly acting agents are suitable for controlling severe hypertension, including oral nifedipine, intravenous labetalol and intravenous hydralazine.7 Treatment of mild to moderate hypertension in the systolic blood pressure range of 140–160 mmHg or diastolic blood pressure range of 90–100 mmHg is more controversial; however, most hospitals in Australia and New Zealand do implement treatment at these levels. At higher levels, treatment is mandatory, and several drug treatments are safe and efficacious: methyldopa, labetalol and oxprenolol are first-line options, and hydralazine, nifedipine and prazosin are second-line options. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are contraindicated in pregnancy. The drug of choice for the prevention and treatment of eclampsia is intravenous magnesium sulfate. However, eclampsia complicates only one in 200–300 cases of pre-eclampsia in Australia, and the case for its routine administration in women with pre-eclampsia in countries with low maternal and perinatal mortality rates is not compelling. SOMANZ recommends magnesium prophylaxis only for women considered at high risk of seizures. Some preterm cases are managed expectantly in units that treat patients at high risk, but delivery remains the definitive management. Many women with pre-eclampsia deteriorate for a few days after delivery, and they require close monitoring during this phase. When there is intense pressure to discharge patients quickly, this is an important point to remember. Women want to know their risk of developing recurrent pre-eclampsia or gestational hypertension, which is about 15% for each after pre-eclampsia in the index pregnancy.8 These rates are probably higher after early-onset pre-eclampsia. Low-dose aspirin and calcium supplementation have both been shown to reduce the risk of pre-eclampsia, and should be used in women at high risk of pre-eclampsia, such as those with a history of early-onset pre-eclampsia. It is apparent that women with either pre-eclampsia or gestational hypertension are at increased risk of cardiovascular morbidity in subsequent years, including hypertension, stroke, coronary heart disease, venous thromboembolism and overall mortality.9 These associations could reflect a common cause for pre-eclampsia and cardiovascular disease, or an effect of pre-eclampsia on vascular disease development, or both. A similar risk for later end-stage renal failure has been reported recently, however only 0.08% of women were affected.10 From a practical point of view, it is reasonable to counsel patients who develop hypertension in pregnancy that they will benefit from avoiding smoking, maintaining a healthy bodyweight, exercising regularly and eating a healthy diet. It is recommended that all women with previous pre-eclampsia or hypertension in pregnancy have an annual blood pressure check and regular (at least 5-yearly) assessment of other cardiovascular risk factors, including serum lipids and blood glucose. In other words, hypertension in pregnancy has become a lifelong disorder. Risks and practice recommendations for women with hypertensive disorders of pregnancy are summarised in the Box. Pre-eclampsia and other hypertensive disorders of pregnancy: risks and recommendations Hypertensive disorders of pregnancy are a leading cause of perinatal and maternal morbidity and mortality, even in developed countries. Management according to systematic guidelines3 improves outcomes. Proteinuria is not mandatory for the clinical diagnosis of pre-eclampsia; renal, cerebral, clotting and hepatic dysfunction also indicate severe disease. Prompt treatment of severe hypertension (systolic blood pressure of 170 mmHg or higher, or a diastolic blood pressure of 110 mmHg or higher) or seizures is mandatory; however, debate persists regarding treatment of mild to moderate hypertension in pregnancy and the selection of patients for magnesium sulfate prophylaxis. Several risk factors for pre-eclampsia are recognised, but accurate prediction of women at risk of pre-eclampsia is still developing. Pre-eclampsia is associated with increased risk of recurrence in the next pregnancy and future risk of cardiovascular and renal morbidity. Women who experience hypertension in pregnancy should adopt a healthy lifestyle, even more so than women who have normotensive pregnancies.

Mark A Brown MB BS, FRACP, MD · Sandra A Lowe MB BS, FRACP, MD

For Indigenous Australians, the “health of country” is inextricably linked with human health The impacts of climate change on human health are now being documented in Australia.1 Not surprisingly, these impacts are unequally distributed across our society, as vulnerability depends on a number of factors, including the degree of exposure, sensitivity and adaptive capacity. However, intranational heterogeneity of climate impacts on health has not been adequately documented to date.2 Using this lens, the vulnerability of Australia’s Indigenous people living in remote areas of the country is revealed. Their vulnerability to climate change is intensified by the social and economic disadvantage they already experience — the result of factors that include decades of inadequate housing and public services, and culturally inappropriate medical services. In addition, specific cultural ties between Indigenous people’s wellbeing and the “health” of their “country” create significant indirect impacts of climate change.3,4 We argue that it is vital to acknowledge the significance of this situation now, so that anticipatory adaptive policies can be implemented. Such policies should ensure that adequate resources are provided to mitigate some of the worst impacts of climate change on these communities, in a way that encourages community participation in decision making. We now know that, across northern Australia, climate change is expected to bring hotter day- and night-time temperatures.5 Elevated temperatures and increases in hot spells are expected to be a major problem for Indigenous health in remote areas, where cardiovascular and respiratory disease are more prevalent and there are many elderly people with inadequate facilities to cope with the increased heat stress. However, while the literature is not clear on the exact effects of increasing heat on people and communities, it does imply that these effects are likely to be less in regions where people are already acclimatised to hot conditions. Communicable diseases such as bacterial diarrhoea, which are more common in hot, dry conditions, may increase in incidence unless additional preventive action is taken. One study predicted that a 1.0–3.5oC increase in average temperature by the year 2050 would lead to an estimated 5%–18% increase in diarrhoea cases in Alice Springs.6 Dengue fever, spread by mosquitoes, also presents a climate-related risk to Indigenous communities. Although the virus is not currently endemic in Australia, there are sporadic epidemics, with occasional cycles over winter in the local mosquito populations in northern Queensland.7 The conceptual divide between Indigenous and non-Indigenous Australians about perceptions of “health” also needs to be recognised and accommodated.8 The Indigenous concept of health is broad and multifaceted, reflecting a different world view to that of the Western biomedical model. For many Indigenous people, a connection with “country” — a place of ancestry, identity, language, livelihood and community — is a key determinant of health.9 If community-owned country becomes “sick” through environmental degradation, climate impacts, or inability of the traditional owners to fulfil cultural obligations through ongoing management and habitation of their land, the people of that land will feel this “sickness” themselves. That is, the elements contributing to Indigenous health and wellbeing are often abstract and based on social interactions with people and the non-human landscape. Thus, as ecosystems change in response to biophysical impacts and extreme weather events, many traditional owners living in remote areas are likely to face increased physiological, psychological, economic and spiritual stress as it becomes more difficult to “look after their country”. At both international and national levels, there is some recognition of the specific needs of indigenous people in relation to the impact of climate change. The World Health Organization’s Commission on Social Determinants of Health and the United Nations Permanent Forum on Indigenous Issues have recently acknowledged the importance of tackling climate change, particularly with respect to health, for the world’s 350 million indigenous people. In Australia, the Garnaut Climate Change Review has recognised the importance of some non-quantifiable costs, including the specific intangible costs associated with improving Indigenous health.10 A challenge for medical practitioners dealing with this issue in the Australian context will be to look beyond the limitations of traditional epidemiology and scientific reductionism to embrace a more ecologically focused, social-determinants approach to health.11 This approach would enable the “health of country” and its inextricable links with human health to be considered in climate impact assessments. To address these different paradigms of health, the first step is to begin discussions with Indigenous people to prioritise activities. This process will certainly require a significant increase in the capacity of medical professionals and health systems in northern Australia, as well as increased education and training programs for Indigenous trainees and cross-cultural programs for nurses and local Indigenous support staff. Changes also need to be made in teaching practice across Australia. Currently, Indigenous health still occupies a peripheral place in many medical school curricula, with government funding and research disproportionally supporting high-cost, acute-care medicine at the expense of preventive and primary health care. In tandem with well planned, properly resourced programs that support strong livelihood activities in remote communities, there is the potential to begin to reduce the additional risk for many Indigenous communities from climate change. There are multiple co-benefits of this approach that would raise social and economic indicators. Ignoring the warning signs and failing to take action is no longer an option.

Donna Green PhD · Ursula King FACRRM, MPH · Joe Morrison MA

The Medical Journal of Australia (MJA) is published by the Australasian Medical Publishing Company (AMPCo), a wholly owned subsidiary of the Australian Medical Association (AMA). The Journal is available on subscription and is included as part of the membership package of the AMA. Since 2001, AMPCo has published an Internet version of the MJA (eMJA) to which readers have enjoyed free open access since its inception. The eMJA now contains 6350 pages of valuable information, which, while formidable, unfortunately comes with increasing production and maintenance costs. Because of these essential costs, the Board of AMPCo has decided that, commencing with the first MJA issue in 2009, access to certain content in the eMJA will require a subscription. In this move, the MJA will follow the steps taken by other prestigious medical journals, including the Journal of the American Medical Association (JAMA), the Annals of Internal Medicine (the journal of the American College of Physicians), the BMJ and The Lancet. Much information, including all previously published articles, current editions of In This Issue, plus guidelines, position statements and supplements, will remain on open access. Research articles will be freely accessible online for 2 weeks following publication, after which a subscription will be required. Twelve months after publication, all articles will revert to open access. This policy will be continually reviewed. Naturally, open access will be provided for any articles we consider to be of urgent public health importance. Importantly, all current AMA members will continue to enjoy free access to all content of the eMJA. Information about how to access the eMJA is available at http://www.mja.com.au/access_policy.html. The Medical Journal of Australia Martin B Van Der Weyden, Editor.

Martin B Van Der Weyden

Objective: To examine the circumstances of homicides of children in New South Wales from 1991 to 2005.Design and setting: Retrospective analysis of all identified child homicides in NSW from 1991 to 2005, based on data on offenders and victims obtained from crime statistics, documents located by systematic searches of legal databases and media reports, and medicolegal reports of offenders who committed child homicides during psychotic illness.Main outcome measures: Demographic characteristics of homicides and a history of prior psychiatric treatment among offenders with psychosis.Results: We located documents describing 165 homicides by 157 offenders. Fifty-nine deaths were a consequence of child abuse, including those of five children who died from methadone overdoses. Both the offenders and the victims in fatal child abuse were significantly younger than in other forms of child homicide. The courts found that 27 child homicides had been committed by 26 offenders during the acute phase of psychotic illness, and 15 of these offenders had never been treated with antipsychotic medication.Conclusions: Earlier identification and treatment of psychotic illness in mothers, and changes in the way methadone is provided to opiate-dependent parents, might result in a small overall reduction in the number of child deaths. More lives could be saved by measures that reduce the incidence of child abuse, including the prohibition of corporal punishment of children.

Olav B Nielssen MB BS, MCrim, FRANZCP · Matthew M Large BSc(Med), MB BS, FRANZCP · Bruce D Westmore MB BS, MCrim, FRANZCP · Steven M Lackersteen BPsych(Hons)

Objective: To document general baseline data on the patterns of childhood malignant tumours at a teaching hospital in south-western Nigeria.Design, setting and participants: A retrospective study of childhood malignancy at Olabisi Onabanjo University Teaching Hospital, Sagamu, Nigeria, during an 11-year period, from January 1996 to December 2006.Results: 77 children were diagnosed with malignant tumours (an average of seven diagnoses per year); 46 were boys (60%), giving a male-to-female ratio of 1.5 : 1. The age distribution of patients was 1–18 years. There were 42 diagnoses (55%) in the 1–5-year age group and 68 malignancies (88%) were diagnosed at ages of 12 years or younger. Lymphomas were the most prevalent malignancy identified, accounting for 31 diagnoses (40%). Burkitt’s lymphoma constituted the majority of malignancies (28 cases; 36%), followed by retinoblastoma (16 cases; 21%) and nephroblastoma (11 cases; 14%). Other malignancies included germ cell tumours (6), neuroblastomas (4), osteosarcomas (3), rhabdomyosarcomas (3) and non-Hodgkin’s lymphomas (3). One case each of medullary thyroid carcinoma, adenocarcinoma of the rectum, invasive mucinous carcinoma of the colon were also identified.Conclusion: These data suggest that Burkitt’s lymphoma is the most common childhood malignant tumour in our geographic area of south-western Nigeria. With the rising incidence of childhood malignancy in resource-poor countries, measuring the baseline occurrence of such tumours is imperative to provide much-needed resource allocation.

Ayodeji O J Agboola MB ChB, MSc · Folashade A Adekanmbi MB BS, FWACP · Adewale A Musa MB BS, FWACS · Adetoun S Sotimehin MB BS, FWACP · Anotu M Deji-Agboola BSc, MSc, PhD · Aderibigbe M O Shonubi MB BS, FWACS · Temitope Y Oyebadejo MB BS, FMCPath · Adekunbi A F Banjo MB BS, FMCPath

Telemedicine can help improve access to health care for people in rural and remote communities, but its uptake has been slow and fragmented. A telepaediatric service in Queensland, initiated in 2000, has made use of mobile “robot” videoconferencing systems. It has been cost-effective and well accepted by patients and clinicians. Telegeriatric services were instigated in Queensland in 2005, principally using videoconferencing. Telegeriatrics has been ideal for frail older patients in remote areas. For telemedicine to become a mainstream service, its focus must move beyond simply the provision of equipment and network connectivity. Telemedicine must be funded adequately if it is to be successful.

Anthony C Smith BNurs, MEd, PhD · Leonard C Gray MMed, PhD, FRACP

Rapid advances in communications and computing technology have opened up new opportunities for clinical teleradiology. The quality of teleradiology reporting, when carried out properly, is on par with onsite reporting, and offers the potential for increased accuracy and improved patient outcomes. Local and international industry organisations and professional bodies are creating standards, policies and protocols for every aspect of teleradiology in response to concerns about the use of this technology. The key factor for the long-term success of teleradiology has been identified as a commitment to ensuring duty of care to patients (encompassing high-quality service and patient safety) is the first priority. Evidence indicates that increased use of teleradiology will be a step forward if managed well, but requires a commitment to excellence, patience and perseverance.

Julian Adler MB BS(Hons), FRANZCR · Chris Yu MB BS, FRANZCR · Mineesh Datta MB BS, FRANZCR

There are well documented geographical, financial, social and professional barriers to continuing professional development (CPD) and peer support for rural medical practitioners, which significantly influence the recruitment and retention of health care professionals in rural areas. The Support Scheme for Rural Specialists (SSRS) provides a coordinated and collaborative framework to support the CPD and peer-support needs of medical specialists practising in rural and remote Australia. Since 2002, more than 80 CPD projects have been implemented by specialist medical colleges under the auspices of the SSRS. Projects have provided educational up-skilling or support for rural-specific clinical practice improvement initiatives aimed at strengthening clinician competence and capability, and workforce retention.

Belinda R Pond MPH, BA · Lauren G Dalton MPH, BSc(Hons) · Gary J Disher BBus, GradCertHSM, AAIM · Michael J Cousins MD, FANZCA, FAChPM

Objective: To investigate National Health and Medical Research Council (NHMRC) support over the decade to 2006 for researchers studying Indigenous health and researchers who self-identified as Indigenous.Design and setting: Review of data on all recipients of People Support awards and Capacity Building Grants in Population Health Research who were researching Indigenous health or who self-identified as Indigenous between 1996 and 2006.Main outcome measures: Annual People Support and Capacity Building grants and expenditure, by broad research area, state or territory, administering institution, and Indigenous status (as self-identified by award recipients in their applications).Results: Between 1996 and 2006, 134 People Support awards were made to researchers studying Indigenous health; of these, 27 (20%) were to researchers who self-identified as Aboriginal or Torres Strait Islander. In 2006, about 2.9% of the annual expenditure on all People Support funding was for Indigenous health research, representing a doubling in the proportion of funds since 2001. There was no increase in the number of self-identified Indigenous researchers funded under People Support, but Capacity Building Grants increased the number of people from Indigenous backgrounds supported by the NHMRC, with funds allocated to 36 Indigenous researchers from 2002 to 2006, compared with 14 funded by People Support during the same period.Conclusions: Funding to support Indigenous health research through the People Support scheme has increased since the NHMRC adopted policy changes in 2002, but it has not reached the targeted expenditure of at least 5% of agency allocations. The Capacity Building Grants have been a more effective vehicle for funding researchers from Indigenous backgrounds.

Sophia Leon de la Barra BA, MPH, MPhilPH · Sally Redman BA(Hons)(Psych), PhD · Sandra Eades BMed, PhD · Carey Lonsdale BSc, GradDip(Zool), MApplSci

The time has arrived to sort out the decades-long ADHD debate The Royal Australasian College of Physicians is currently revising the 1997 National Health and Medical Research Council (NHMRC) guidelines on attention deficit hyperactivity disorder (ADHD).1 Also, the American Psychiatric Association is working towards the fifth edition of the Diagnostic and statistical manual of mental disorders (DSM), with an expected publication date of 2012. These are valuable opportunities to review existing diagnostic criteria for ADHD and consider alternatives. Recent refinements in psychiatric classification and advances in neuroscience research have jointly contributed to a clearer understanding of some childhood psychiatric disorders. Paradoxically, these developments also raise doubts about the diagnostic validity of ADHD — the most common psychiatric clinical presentation in childhood. These doubts arise from difficulties in conceptualising ADHD as a “disorder”. They also exemplify the growing turmoil that is part of the larger disillusionment with psychiatry,2 reflecting fundamental changes both within and beyond the profession in many Western countries, including Australia. A central concern is the increasing tendency of psychiatry to transform what many regard as normal emotional responses to life’s stresses and traumas into psychiatric disorders. The nosological conundrum of ADHD was highlighted in the United States National Institutes of Health’s ADHD consensus statement; it concluded that there is evidence supporting the validity of the disorder, but did not provide a consensus regarding which ADHD patients should be treated with psychostimulants.3 A response to the statement noted that: ... [the] “unproven” status of the disorder should give pause to both researchers and clinicians who may have reified ADHD as a “thing” or “true entity” (rather than a working hypothesis that serves scientific, communication, and clinical decision-making purposes).4 In addition, it has been noted that discussion of the diagnostic validity of ADHD is far from stale or easily dismissed, and that a renewed sense of urgency arises when a: ... diagnostic concept is listed in an official nomenclature and provided with a precise, complex definition [which] tends to encourage ... insidious reification.5 Such unintentional reification by DSM-IV6 — where so-called core symptoms of ADHD (poor impulse control and lack of sustained attention) are construed as a disorder — is illustrated by tracing the DSM’s successive revisions of ADHD as a diagnostic entity. Antecedents for ADHD range from “motoric disinhibition” in DSM-II (categorised as hyperkinetic reaction) and “inattention” in DSM-III (categorised as attention deficit disorder) to attention deficit hyperactivity disorder (ADHD) in both DSM-III-R and DSM-IV.7 The fact that such conceptual changes are part of the DSM’s stated aim (ie, to identify clinical conditions that can be considered as genuine medical disorders and to distinguish them from problems of living) results in a catch-22 error that has been noted in relation to major depressive disorder.8 This flaw in logic also applies to ADHD. Beyond this flawed logic, Russell Barkley — a respected American authority on ADHD — reviewed the criteria for ADHD and concluded that “what is clear is that the current DSM-IV approach has little clinical or research merit”.9 Further disenchantment with the disease entity assumptions of the DSM revisions has arisen from the serial increase in numbers of diagnostic categories: from 60 in 1952 (DSM) to 145 in 1968 (DSM-II) and 410 in 1994 (DSM-III). This led one author to comment: ... particularly badly affected by this constantly creeping diagnostic expansion have been children, whose least oddity or not quite normal (frequently confused with average) quirk is now assigned to some syndrome or other and treated with behaviour therapy and drugs. The ethics of all this is rarely called into question.10 At the ideological level, some see a process of “psychotherapeutic revisionism” in mental health care in the US.11 I have discussed how such a revisionist ideology views ADHD in detail elsewhere.12 In summary, it fails to distinguish between psychology as “science” and as “scientism”. As a consequence, the former holds that ADHD symptoms arise from the interaction of genetic and developmental influences during pregnancy through childhood, whereas the latter focuses on symptoms as utilitarian targets for treatment. The DSM’s atheoretical approach, which perpetuates the continuing absence of a “developmentally sensitive, interactive or longitudinal perspective in the DSM system”,13 sits within such revisionist ideology. These contrasting conceptual and ideological views have resulted in divergent perspectives on the conceptualisation of ADHD, reliability and validity of ADHD diagnosis, and treatment options for behaviour labelled as ADHD.14,15 Ethical dimensions and other subjects for consideration in the ADHD debate include: diagnostic decision making; inappropriate (over- or under-) medication; “performance enhancement” arguments; the relationship between the psychiatric profession and the pharmaceutical industry, raising possible conflicts of interest; third-party reimbursement for ADHD as a disability; the lack of childhood safety and efficacy data leading children to be termed “therapeutic orphans”; and purported aetiologies based on genetics versus “toxic environments”.16 Importantly, these purported aetiologies have been recast into integrative models that include both genetics and environmental factors,17 a new direction that has immediate implications for clinicians and researchers. Global expenditure on drugs to treat ADHD rose ninefold to US$2.4 billion in the decade to 2003.18 It would be naïve to think that market pressure does not influence evidence-based protocols in resource-starved health services. The revised practice parameters from the American Psychiatric Association relied on the DSM-IV text revision definition of ADHD. The limitations of their recommendations were explicit: These parameters are not intended to define the standard of care, nor should they be deemed inclusive of all proper methods of care or exclusive of other methods of care directed at obtaining the desired results.19 Let us hope that the committee created by the Royal Australasian College of Physicians to define and describe the current conceptualisation of ADHD will have the scientific rigour, maturity and wisdom as they undertake the revision of the 1997 NHMRC guidelines on ADHD1 to emphasise the distinction between ADHD as a set of symptoms and a disease concept. As we approach the critical crossroads between the fourth and fifth revisions of the DSM’s ADHD criteria, a glimmer of hope has emerged, signalling that the time has arrived to sort out the decades-long ADHD debate. The Psychodynamic diagnostic manual (PDM)7 offers an alternative to the DSM construct of ADHD — a relief to what I believe to be shortcomings of the current DSM.9 The PDM’s inclusive approach to diagnosis integrates the subjective experiences of patients with their neuropsychological capacities for regulation of relationships, intimacy and emotional experiences, as well as attention and behaviour. Ideally, such an approach will enable the next generation of children to be spared prescription medications in the current quantities and combinations, based on dubious diagnostic criteria for behaviour labelled ADHD.

George Halasz MRCPsych, FRANZCP

The issue of “equal health” for Aboriginal and Torres Strait Islander peoples involves a broad range of social determinants, in addition to physical health. The formation of an Australian college of Aboriginal and Torres Strait Islander health would allow a continuing authoritative conference of broad expert opinion, including that of Aboriginal health workers, to address health and social inequality.

Robert M Parker BMed, AFACHSE, FRANZCP

There are controversies surrounding the indications, time and place for elective surgery, and role of multistage operations in the treatment of complicated diverticular disease. Most patients with uncomplicated diverticulitis can be managed non-operatively. Previous indications for elective surgery after two attacks of diverticulitis have been questioned. Evidence that patients are less likely to respond to medical therapy in subsequent attacks of diverticulitis is lacking. Decisions should be based on individual circumstances. The Hartmann procedure remains a safe option for patients with free perforation and generalised peritonitis. In experienced hands, a one-stage procedure can be as successful as a two-stage procedure in an emergency setting in selected patients. When possible, an operation should be converted from an emergency to a semi-elective one using techniques such as radiologically or laparoscopically guided drainage of collections.

Kevin Ooi BSc, MB BS · Shing W Wong MB BS, FRACS, MS(Colorectal)

An otherwise healthy 28-year-old man had a cardiac arrest after a day of motocross racing. He had consumed excessive amounts of a caffeinated “energy drink” throughout the day. We postulate that a combination of excessive ingestion of caffeine- and taurine-containing energy drinks and strenuous physical activity can produce myocardial ischaemia by inducing coronary vasospasm. Clinical recordA 28-year-old male amateur motocross rider was admitted to Port Macquarie Base Hospital in August 2007 after having an out-of-hospital cardiac arrest. He had collapsed shortly after participating in a motocross race. An off-duty paramedic and nurse had been on hand, and effective cardiopulmonary resuscitation was commenced promptly. Paramedics arrived after about 20 minutes of resuscitation. The patient’s initial cardiac rhythm was recorded as ventricular fibrillation (Box 1). He was restored to sinus rhythm after receiving two 150 J biphasic direct-current shocks. Adrenaline 1 mg and atropine 1 mg were both given as adjuvants. He was intubated by paramedics and transported to hospital. Later, the patient recalled feeling well earlier in the day, until after his second race, when he developed dull constant retrosternal chest pain. He described this as being mild in intensity, with no radiation or associated symptoms. It settled within 30 minutes of sitting down to rest. He went on to participate in (and win) one more race that afternoon. He collapsed at about 3 pm, approximately 20 minutes after the last race. There had been no symptoms immediately preceding the collapse that he could recall. The patient had been well in the week preceding these events. He denied having any previous episodes of chest pain or syncope. He had a large breakfast on the morning of the motocross race and had remained adequately hydrated throughout the day. Further, he had consumed 7–8 cans of a caffeinated “energy drink” between 8 am and his collapse 7 hours later. He was otherwise fit and well and taking no regular medication. There was no family history of premature coronary disease, sudden cardiac death or unexplained syncope. He was a smoker with a six pack-year history of smoking. He denied alcohol misuse or illicit drug use. On arrival at hospital, the patient was intubated and sedated. He was haemodynamically stable, and physical examination was unremarkable. An initial electrocardiograph (ECG) showed sinus rhythm and elevated anteroseptal ST segments with reciprocal inferior ST depression. Chest x-ray showed a normal cardiac silhouette and no signs of pulmonary venous congestion. Computed tomography scans of the chest and brain were unremarkable, specifically excluding aortic dissection. Abnormal findings from laboratory tests included an elevated level of troponin I (0.24 mmol/L; reference range [RR], < 0.05 mmol/L) and a lowered potassium level (3.0 mmol/L; RR, 3.6–5.4 mmol/L). Results of a urinary screen for drugs of misuse, including amphetamines and cocaine, were negative. Screening for anabolic steroids was not performed. The provisional diagnosis was of anteroseptal ST elevation myocardial infarction. The patient was given thrombolysis with 50 mg of tenecteplase and commenced on an infusion of intravenous heparin. He was given loading doses of 300 mg of both aspirin and clopidogrel, and 25 mg of metoprolol, all by nasogastric tube. Hypokalaemia was corrected via intravenous infusion. The patient was transferred to a tertiary referral centre for cardiac catheterisation. On arrival there, an ECG showed evolving ischaemic changes across the anterolateral leads (Box 2). A troponin I peak level of 12.2 mmol/L was measured; his potassium level had normalised at 4.0 mmol/L. Echocardiography showed mild left ventricular enlargement and low-normal systolic function with a hypokinetic anteroseptal segment. Coronary angiography, performed on the same day, gave normal results. No attempts were made during angiography to induce vasospasm. The patient was cooled for 24 hours and extubated without difficulty. He was discharged after 6 days. At discharge, he was taking atenolol 50 mg, aspirin 100 mg, spironolactone 25 mg and perindopril 2.5 mg. On follow-up 2 months later, the patient reported that he had remained well and symptom-free. Echocardiography showed preserved global left ventricular function with a limited residual area of akinesis of the anteroseptal wall. He continued taking aspirin, perindopril and atenolol (reduced to 25 mg). He was advised not to compete in motocross races for 6 months, after which a stress echocardiogram was performed; this was negative for exercise-induced ischaemia. DiscussionWe postulate a possible role of excessive consumption of caffeinated energy drinks in triggering the life-threatening cardiac events described in this case. Although sudden cardiac death is an uncommon occurrence in people under the age of 40 years, when it does happen it is most often associated with the presence of structural heart disease, most frequently premature coronary atherosclerosis. Other common associations are hypertrophic obstructive cardiomyopathy and myocarditis.1,2 However, autopsy review studies have found that some 10%–12% of subjects in this age group have no obvious cardiac abnormalities on postmortem examination.1,2 Of identified causes in this group, many are familial sudden cardiac deaths or disorders of conduction, such as Wolff–Parkinson–White syndrome.3 Our patient had electrocardiographic and echocardiographic features indicative of transmural ischaemia localised to the anterior territory. This is suggestive of a regional rather than a global process, and suggests an ischaemic event rather than a primary arrhythmia. However, the angiogram did not show any significant coronary lesions. Although non-stenotic atherosclerotic plaques may rupture or denude and cause infarction through the formation of superimposed thrombi, which may have then been dissolved by the administration of thrombolytics, we believe that — considering this man’s relative youth — there is a distinct possibility that the underlying abnormality was coronary vasospasm. An arrhythmia, possibly triggered by the ingestion of stimulants in the presence of hypokalaemia and physical exertion, was a differential diagnosis. However, this would not account for the regional abnormality seen. The cause of this patient’s hypokalaemia is unclear, but may have been related to electrolyte losses from excessive sweating during exertion. This effect may have been exacerbated by the diuretic effect of caffeine. The role of illicit stimulants, especially cocaine, in causing coronary vasospasm in young people is well established.4 However, this patient denied cocaine use and returned a negative result on his drug test, making this an unlikely cause. The energy drink consumed by our patient contains 80 mg of caffeine (equivalent to one cup of espresso) per can. He drank seven or eight cans within 7 hours — up to 640 mg of caffeine in total. The drink also contains high doses of taurine (an amino acid) and glucuronolactone (a glucose metabolite), neither of which are considered to have significant toxicity, although there is a paucity of data.5,6 Caffeine is a naturally occurring xanthine derivative related to theophylline; it has a number of potential pharmacological actions on the cardiovascular system. Its primary mechanism of action is thought to be through competitive inhibition of adenosine receptors.7 It also induces catecholamine release, and causes a rise in intracellular calcium in myocytes through release of calcium from the sarcoplasmic reticulum, leading variably to smooth muscle contraction and relaxation.8-10 The role of caffeine in triggering arrhythmia is well established.8 There have been a number of case reports on hospitalisations or deaths due to caffeine toxicity, although the mechanism usually seems to be tachyarrhythmia and involves far higher doses than in this case.11,12 The median lethal dose in rats is 200–400 mg/kg.13 A 1997 case report described a young woman who suffered a myocardial infarction due to caffeine toxicity; however, this involved an oral dose of 20 g.14 In-vitro studies have shown that taurine has an inotropic effect on cardiac muscle similar to that of caffeine, and potentiates caffeine-induced muscle contracture. Few taurine toxicity studies have been performed, and there are insufficient data to suggest what an unsafe level of taurine consumption might be, if any.9,14 Both taurine and caffeine have been shown in vitro to have physiological effects on intracellular calcium concentration within vascular smooth muscle, and they could conceivably induce coronary vasospasm. In-vivo studies have demonstrated a capacity for caffeine to decrease myocardial blood flow during exercise.15 We postulate that, in physiologically predisposed individuals, a combination of excessive ingestion of caffeine- and taurine-containing energy drinks and strenuous physical activity can induce myocardial ischaemia by coronary vasospasm, with potentially fatal results. Caffeine has been removed from the list of prohibited substances in sport but remains on a monitoring program run by the World Anti-Doping Agency.16 Anecdotal reports suggest that the many caffeinated energy drinks now on the market are widely used by amateur and professional athletes to enhance their performance. We are concerned that a combination of exercise and the caffeine contained in these drinks may have the potential to trigger serious cardiovascular events. We accept that this is a single case, which does not and cannot establish causality. However, in the context of concerns reported in the media in recent years relating to similar events overseas, and in the presence of a plausible pharmacological mechanism, we believe that the potential dangers of these caffeinated energy drinks should be highlighted, and monitoring for future adverse events should be conducted. 1 Patient’s initial cardiac rhythm, showing ventricular fibrillation 2 Patient’s electrocardiograph on arrival at tertiary referral centre, showing evolving ischaemic changes across the anterolateral leads

Adam J Berger MB BS, BSc(Med) · Kevin Alford MB BS, FRACP, DDU

After several years suffering from Parkinson disease, Ian Reid, a paediatric surgeon, died on 20 March 2008. Ian was born on 5 July 1926 at Port Vila, New Hebrides (now Vanuatu). The family returned to Australia in his early childhood. After service in the Royal Australian Air Force, Ian graduated in medicine from the University of Melbourne in 1953. Three years later, he returned to the New Hebrides as Mission Doctor on the island of Tanna. During his years in Tanna, Ian observed at close hand the infamous “cargo cult”. A rather dramatised account of his part in stopping the intrusion of cult members into his hospital was written by David Attenborough in his book The quest for paradise. And his ways are ways of gentleness and all his paths are peace In 1959, Ian went to Papua New Guinea (PNG) to work as a Medical Officer at the Port Moresby General Hospital. He became Foundation Dean of the Papuan Medical College, where he lectured from 1961 to 1969. In 1968, he was awarded a World Health Organization travelling fellowship in paediatric surgery, which took him to Philadelphia Children’s Hospital and other children’s hospitals throughout the United States. During his time in Philadelphia, he worked with “Chick” (C Everett) Koop, one of the first surgeons to successfully separate Siamese twins. On his return from PNG to Australia, Ian worked at the Royal Children’s Hospital, Melbourne, from 1970 to 1971. The following year, he became a James Fairfax Surgical Research Fellow at the Children’s Medical Research Foundation and a Consultant Surgeon at the Royal Alexandra Hospital for Children, Sydney. The award of a Sir Denis Browne Memorial Travelling Fellowship in Paediatric Surgery in 1975 took him to Great Ormond Street Hospital for Children, London, and to other hospitals in the United Kingdom and Ireland. In 1980, Ian was invited to take up a lectureship at the newly established Medical School at the University of Newcastle (New South Wales), where he would help plan the surgical contribution to the paediatric curriculum. In Newcastle he was involved with neonatal work and with children requiring particularly difficult surgical procedures. He also helped to establish neonatal paediatric surgery at the Newcastle Mater Misericordiae Hospital and had the distinction of performing the first neonatal operation at the John Hunter Hospital. Ian’s gentle sense of humour, matched by his courage, invariably won the day. In the somewhat stormy days during the establishment of the Medical School in Newcastle, he quietly retired from the academic arena, citing his reason as “preferring to deal with premature babies than immature professors”. After retirement, he helped in a voluntary capacity with the Hunter Orthopaedic School and the Tingira Centre for blind and deaf children.

Neville Wilmer was born in Townsville on 17 August 1918. He attended several state schools across North Queensland and was a border at All Souls School, Charters Towers, before studying medicine at the University of Queensland in Brisbane. During his undergraduate days, he excelled in swimming, boxing and rugby. After graduating in 1941, Neville worked as a Resident Medical Officer at the Royal Brisbane Hospital (RBH), then joined the Army and served with the 7th Division in Papua New Guinea. In 1945, he was sent to Timor to participate in the Japanese surrender. On his return to Australia, Neville worked for another year at the RBH before entering general practice in Gympie in 1947. He remained there until his retirement in 1988, providing full surgical and obstetric services as well as general practice. Neville was in the group of 16 doctors who sat the first Royal Australian College of General Practitioners (RACGP) examination in Queensland. He also made significant contributions to the RACGP in Queensland, being a member of the Faculty Board (1969–1982), the Research Committee (1970–1982), the Electives Advisory Sub-committee (1980–1982) and the Courses Approval Sub-committee (1979–1982), as well as a Supervisor for the Family Medicine Program (1980–1988). He also held positions as President and Secretary of the Gympie Local Medical Association and was a strong supporter of the Australian Medical Association (AMA). He was made a Fellow of the AMA in 1984. Neville performed the first exchange transfusion in Gympie (the first conducted outside Brisbane), and set up the Blood Bank in Gympie, which was later taken over by the Red Cross. For nearly 50 years, Neville served the people of Gympie, honouring the fine ideals of good patient care and making a positive commitment to civic welfare, for which he earned the high regard of the community. He was an Alderman on the Gympie City Council from 1961 to 1964 and was active in the local Returned Services League and many other community groups. A keen golfer, he played regularly at the Gympie Golf Club. Neville was awarded the Medal of the Order of Australia in the Queen’s Birthday Honours in 2008 for his services to medicine and the community of Gympie. He died in Gympie on 9 August 2008 and is survived by his children Neridah and Quentin and their families.

John A Comerford

To the Editor: A number of commentaries and articles have been published recently about the ability of doctors working in primary care skin cancer clinics to diagnose and manage skin cancer.1-3 However, limited information has been published comparing the patient populations that attend the different service providers (ie, “traditional” general practitioners versus doctors at skin cancer clinics). In 2005, we conducted a large population-based survey of Queensland residents aged 20–75 years to examine the prevalence of behavioural risk factors for cancer and current cancer screening practices.4 Using data from our study, we examined the prevalence of clinical skin examination and identified factors associated with choice of service provider. A total of 9419 respondents completed the interviews (response rate, 45.6%). Complete data for this analysis were available for 5499 of the respondents, of whom 48.2% were men. Thirty per cent of respondents reported they had had a general check of all or nearly all of their body in the previous 12 months. Factors associated with an increased likelihood of having a whole-body skin examination in the previous 12 months included being male (odds ratio [OR], 1.15 [95% CI, 1.00–1.31]), being 60–75 years of age (reference group, 20–39 years) (OR, 1.73 [95% CI, 1.45–2.07]) and having an annual gross income of ≥ $60 000 (reference group, < $20 000 annual gross income) (OR, 1.42 [95% CI, 1.18–1.71]). The strongest predictors were a self-reported history of melanoma (OR, 2.68 [95% CI, 2.01–3.57]) or non-melanoma skin cancer (OR, 2.01 [95% CI, 1.65–2.45]). No associations were seen between choice of service provider and any sociodemographic variables, including sex and age group. Additionally, skin cancer risk factors (such as having highly sensitive skin or a history of melanoma) did not make respondents any more or less likely to attend either a GP or a skin cancer clinic doctor. Various reasons were given by respondents for their choice of service provider (Box). Skin cancer clinics appeared to be chosen primarily because they offered bulk-billing or because respondents just wanted a general skin check. Traditional GPs were more likely to be chosen for convenience or because of concern about a specific spot or mole. Skin cancer is a major public health issue, and the provision of adequate and appropriate clinical services is a continuing and growing challenge. We found that a significant proportion of the Queensland population had undergone a whole-body skin examination by a doctor within the previous 12 months, and that those attending appeared to be the group most at risk of developing skin cancer. We did not find any significant differences in the profiles of those who chose a skin cancer clinic or a general practice for their skin examination. Reasons given for choice of service provider* by 2895 respondents who had had some type of skin check in the previous 12 months† * General practitioner or skin cancer clinic doctor. † Percentages do not total 100 due to multiple responses.

Philippa H Youl · Peter D Coxeter · David C Whiteman · Joanne F Aitken

To the Editor: Extended-spectrum-β-lactamases (ESBLs) are enzymes capable of hydrolysing penicillins, broad-spectrum cephalosporins and monobactams. Worldwide, ESBL-producing organisms are posing an increasing challenge for empirical antibiotic use and infection control. We recently carried out a review of microbiological isolates from clinical specimens taken from 2003 to 2007 at the Alfred Hospital, Melbourne. From 15 917 gram-negative bacilli, we identified 234 ESBL-producing organisms (1.5% of isolates) using double-disk synergy testing. Over the 5-year period, we noted three apparent changes in ESBL epidemiology relating to Escherichia coli isolates. First, E. coli became the most frequent organism in which ESBL production was observed, making up 55.6% of all ESBL-producing organisms in 2007 (up from 23.5% in 2003) (P = 0.03). Second, while the total number of E. coli isolates remained essentially constant over the study period, there was an increase in the proportion of E. coli isolates found to produce ESBLs: 1.8% of E. coli isolates in 2007 compared with 0.36% in 2003 (P < 0.001). The third and perhaps most striking change was in the epidemiology of ESBL-producing E. coli. In 2003, ESBL-producing E. coli infections were largely hospital-acquired, with 87.5% of isolates acquired after 48 hours in hospital or after a hospital admission in the previous 12 months. However, by 2007, ESBL-producing E. coli infections were found to be predominantly community-acquired, making up 62.2% of ESBL-producing E. coli isolates (P = 0.01). The increased proportion of community-acquired infections occurred despite a parallel increase in the frequency of hospital-acquired ESBL-producing E. coli infections (Box). Community-onset infections with ESBL-producing organisms have become increasingly recognised as important clinical entities.1 ESBL-producing E. coli bacteraemia is associated with higher mortality than bacteraemia caused by non-ESBL-producing organisms,2 a finding that has also been specifically demonstrated in the setting of community-acquired infections.3 Although local epidemiological data for infections with ESBL-producing organisms are not readily available, it appears that rates of community-associated infection vary greatly worldwide, with some regions of China reporting rates of ESBL-producing E. coli as high as 34% of all isolates.4 Although our study was limited by being a single-centre review, our findings are consistent with the emergence of multiresistant Enterobacteriaceae noted in Australian surveillance reports.5 It is not clear whether the change in our ESBL-producing isolates is reflective of local resistance patterns, or perhaps associated with travel to regions where ESBL-producing E. coli are known to be prevalent. Corroboration of these changes in other regions will be important for assessing the magnitude of this issue and responding appropriately, particularly in considering empirical antibiotic therapy for community-acquired gram-negative infections. Hospital-acquired (HA) versus community-acquired (CA) ESBL-producing E. coli isolates, Alfred Hospital, 2003–2007 E. coli = Escherichia coli. ESBL = extended-spectrum-β-lactamase.

Justin T Denholm · Michael Huysmans · Denis Spelman

To the Editor: Reported adverse reactions to food, which are common in many developed countries, can be produced by a wide variety of mechanisms. However, a low proportion of these are true food allergies.1 Recent Australian data show an increase in hospital presentations for food-induced anaphylaxis,2,3 but there are no Australian population data on the prevalence of either food allergies or adverse reactions to foods. Waiting lists for allergy services continue to remain long, and it is not known whether this is due to an increase in the prevalence of true food allergy or simply an increase in perceived food allergy. In October 2007, we undertook an Internet-based survey to assess the prevalence of self-reported perceived food allergies in Australian households. Participants were drawn from a consumer research panel of 8385 people (solicited through Internet-based marketing) who were proportionally representative of the Australian population with respect to age, sex and state. Cohort members were invited to participate in an Internet-based “health survey”, with no mention of food allergy during recruitment. Within 24 hours we had 1386 respondents and the required quota of participants was deemed to have been reached. Of the 1386 respondents, 406 (29.3%) reported at least one household member who believed he or she had a food allergy (Box). Of these, 250 (61.6%) reported at least one doctor-diagnosed allergy and 56 (13.8%) reported that the allergy was allergist-diagnosed. In addition, 42 respondents (3.0% of all respondents) reported that the person with the allergy had an EpiPen (Dey, LP, Napa, Calif, USA). Although there will be some selection bias in our sample because people without Internet access could not be sampled, we believe this bias is likely to be low, as at least 64% of the Australian population currently has home access to the Internet.4 Our questionnaire did not attempt to distinguish between true food allergy, sensitisation to foods, food intolerance or adverse reactions to food, although the majority of allergies had been diagnosed by a doctor or allergist, and foods such as peanut are more likely to be associated with allergies than intolerances. The high rate of perceived allergy to fruit and vegetables in an Australian context was surprising, although allergic reactions to fruit and vegetables are well documented.5 This may reflect either a rising prevalence of birch-pollen syndrome, as has been reported in Europe,6 or a community poorly informed about the true nature of food allergy reactions. Our data add to the evidence that there may be an increasing, largely unmet demand for health care information for patients with adverse reactions to food, including allergies. More formal evaluation should be undertaken to assess the type and prevalence of food allergy in the Australian context in order to facilitate future workforce planning and better community education. Proportion of Australian households in which at least one member believed they had a food allergy, and the individual foods nominated* Incidence of allergy (%) Food All households surveyed Households with perceived food allergy Cows milk 8.3 28.3 Peanut 6.9 23.4 Shellfish 5.9 20.2 Wheat 5.6 19.2 Fruit 5.3 20.9 Egg 3.4 11.6 Vegetables 2.7 6.7 Fish 2.5 8.4 Tree nuts 2.2 7.4 Soy 1.7 5.7 Other 6.3 21.4 * 40% had more than one food allergy.

Katrina J Allen · Jennifer J Koplin · Carmen Gould · Nicholas J Osborne

To the Editor: So a large proportion of women experience pelvic pain, often over years. What’s new? Of course they do. Pitts and colleagues1 fail to mention that virtually every normal, physiological event that occurs within a woman’s pelvis is associated with pain. Clearly, such pains vary in duration and intensity and are associated with events such as ovulation, menstruation, pregnancy, labour and childbirth. We men have it easy by comparison. But to conclude by saying that “only about a third of women who experience chronic pelvic pain seek advice from a health professional” gives the impression the authors are trying to medicalise yet another essentially normal event. One can get into long, philosophical discussions as to why such normal events should be so painful, but it remains a fact. I have spent my career urging general practitioners and fellow specialists to avoid surgery and “silver bullets” in most cases of pelvic pain and follow a conservative approach.2 It would have been more helpful if the authors had gone on to discuss what type of pain is suffered by what type of woman and who is treated by what type of doctor. This truly would have assisted in determining who would benefit from the attention of a health professional and who would not.

Jules S Black

To the Editor: We read the recent article by Pitts and colleagues1 with interest, given the rising trend of diagnosed chronic pelvic pain (CPP) in Australian women. The article identified three types of CPP, but did not differentiate pain into the two major categories of nociceptive (visceral and somatic) and neuropathic. In pain management settings it is considered essential, where possible, to make this differentiation, as it significantly alters management strategies, particularly in relation to medication. While the true incidence of neuropathic pain is unknown, it is believed to be underdiagnosed and inadequately treated. A 2008 French study based on a nationwide postal survey revealed a 6.9% prevalence of neuropathic pain in the general population, with 5.1% of respondents reporting pain levels as moderate to severe.2 Neuropathic pain results from damage to the nervous system. Specifically, this can be from damage to, or pathological changes in, the axons of peripheral nerves or from damage to the central nervous system, probably as a result of deafferentation. This is the process whereby neurones in the central nervous system lose their accustomed afferent input, either from a peripheral nerve or from an ascending sensory tract. Furthermore, neuropathic pain can and does cross neuroanatomical boundaries, often presenting viscerally as referred pain and eliciting pain descriptors such as burning, shooting, stabbing, and searing. For this reason, CPP is often wrongly assumed to be visceral in origin.3 In such cases, awareness that CPP may in fact be neuropathic may avoid inappropriate surgical interventions. Moreover, an association between CPP and neuropathy has been demonstrated in studies of sacral nerve and percutaneous tibial nerve stimulation in women presenting with CPP.4,5 Differential diagnosis of pain of neuropathic origin has been shown to be pertinent for the accurate implementation of pain management strategies.6 Therefore, we suggest that future studies on the epidemiology and/or prevalence of pain include tools to determine the proportion of pain of neuropathic, nociceptive and mixed origin. There are a number of tools available, including questionnaires such as painDETECT, DN4 (Douleur Neuropathique en 4), LANSS (Leeds Assessment of Neuropathic Symptoms and Signs) and NPS (Neuropathic Pain Scale). Some of these, such as the self-assessed LANSS (S-LANSS), do not require clinical examination and thus can be worked into population-based questionnaires. The ability to identify neuropathic pain should lead to individualised treatment, resulting in improved pain control for patients with CPP.

David Vivian · Adele Barnard

In reply: We are pleased to see our article about chronic pelvic pain in Australian women has provoked interest.1 Black’s suggestion that virtually every normal physiological event that occurs within a woman’s pelvis is associated with pain is surprising, and not supported by our evidence. Of the women in our sample, 23% were totally pain free, and most of the chronic pelvic pain reported was mild. A parallel study showed that men also suffered chronic pelvic pain — a smaller proportion than women, but still significant.2 We are not medicalising normal events; rather, we are alerting general practitioners to the normal range of pelvic pain experience to help them assess its clinical significance. A GP who says to a female patient “it’s normal, love, just grin and bear it” denies the psychosocial complexity of her experience. Vivian and Barnard suggest we might have differentiated between two major types of pain, nociceptive and neuropathic. It would not be practical to collect this information in a broad survey on sexual and reproductive health. Certainly, a study of the prevalence of neuropathic pain in the Australian population that mirrors recent studies overseas would be informative. However, our study concerned pelvic pain only. The pelvis is not a common site for neuropathic pain.3

Marian K Pitts · Jason A Ferris · Anthony M Smith · Julia M Shelley · Juliet Richters

Change surgeons mid-op? A change in surgeons may be necessary in very long operations, say UK researchers. Slack and colleagues studied the effect of operating time on surgeons’ muscular fatigue by collecting electromyographic signals from the deltoid (lateral head) and brachioradialis muscles in the dominant arms of eight surgeons while operating for a day. They found that the muscles fatigued during each operation, as well as over the course of the day; the longer the operation, the greater the fatigue. The researchers recommended that operations requiring high degrees of accuracy should be performed early in the day, that the more complex parts of each operation should be performed as early as possible, and that in the case of late complexity or very long operations, a change in surgeons may well be worth considering. Ann R Coll Surg Engl 2008; 90: 651-657 Forget ginkgo for dementia Ginkgo biloba cannot be recommended for preventing dementia, according to US researchers. Following early indications of possible effectiveness, the Ginkgo Evaluation of Memory (GEM) Study Investigators conducted a randomised controlled trial comparing a twice-daily dose of 120 mg extract of G. biloba with placebo in 3069 community volunteers.1 All the volunteers were aged 75 years or older; most had normal cognition, 482 had mild cognitive impairment. After an average of 6 years of this intervention, G. biloba was not effective in reducing either overall incidence rate of dementia or Alzheimer’s disease. Further, an accompanying editorial drew attention to the potential adverse effects of the G. biloba extract as an illustration of why it is untenable to recommend a drug or nutraceutical in the absence of efficacy evidence simply because it could possibly help and initially appears harmless.2 1 JAMA 2008; 300: 2253-2262 2 JAMA 2008; 300: 2306-2308 Presidential genetics? Would you vote for a prime ministerial (or presidential) candidate whose genetic information suggested an increased risk of cancer, Alzheimer’s disease or bipolar disorder? As voters, we may well have the right to know about a candidate’s risk of future disease as an indication of his or her fitness for office; however, US authors are concerned that genetic information is currently too easy to misinterpret and misrepresent. Further, it can simply be wrong by virtue of technical errors, low sequence coverage or low-complexity sequencing. As a result, Green and Annas say that we may be facing a future threat of “genetic McCarthyism”, whereby a candidate’s opponents may imply that his or her increased risk of disease is more substantial than it actually may be. To prevent such an era, they think future US presidential candidates should resist any calls to disclose their own genetic information. N Engl J Med 2008; 359: 2192-2193 Rising up after a fall Older people need training in strategies to get up from the floor after a fall, according to UK researchers. As part of the Cambridge City over-75s Cohort (CC75C) study, the researchers followed 110 participants — all aged over 90 years of age — for 1 year.1 They found that in a year, 60% of these generally frail nonagenarians had fallen at least once, and that among those who fell, 80% were unable to get up after at least one fall and 30% had lain on the floor for an hour or more. Nearly all of those who lay on the floor for a long time and had a call alarm system did not activate it. The CC75C researchers said preventive initiatives should include teaching older people how to get up if they fall. An editorialist advised planning, instruction and practice getting up from the floor in the person’s own home.2 This program might be presented to the person involved as being similar to the training of the professional athlete who adopts a positive mental attitude and “visualises” the event in preparation. 1 BMJ 2008; 337: a2227 2 BMJ 2008; 337: a2320

Ann Gregory