Letters

To the Editor: Many of the arguments put forward by Bain and colleagues about modelling hospital occupancy1 are true in an academic sense. We agree that many acute care models use simplified inputs and outputs, without accounting for rapid daily fluctuations in occupancy. Occupancy definitions are often misleading and subject to gaming. We agree with the work by Bain, Taylor and others that highlights as a problem “the inability to move patients from the [emergency department] to a ward” and that hospitals should “engage procedures to free inpatient beds well in advance” of access block occurring.2 The capacity of a hospital must have flexibility to deal with demand fluctuations.1 However, we do not agree that the “85% occupancy” figure for optimal efficiency is a candidate for myth status. This threshold is used in various systems around the world. Efficiency is a well recognised concept in queuing theory and depends on setting the utilisation (occupancy) rate at a level where the costs of “underutilised” resources (beds, staff not fully used, etc) are shown to acceptably match the “costs” from delayed care (mortality, morbidity, economic, political, prolonged stay, etc). In particular, quoted occupancy figures often look better than reality because of unopened, unusable beds or data manipulation to improve reported occupancy. The more complex and variable the inputs into a system with multiple competing queues (such as hospitals, where acute admissions may be > 70% of the workload), the greater the need for additional capacity to avoid deferred service. Major acute care hospitals show dramatic daily fluctuations in bed use, with changes between low and high occupancy rates in the order of 15%–20%.3 As inputs and variation increase, the likelihood of marked performance deterioration increases exponentially. Real life (or “clinical modelling”) shows that reported occupancies around or above 85% routinely lead to loss of access to care. No benefits of emergency department or hospital overcrowding have been reported in the medical literature, only harm.4 Relying on developing complex mathematical models before accepting that we are already beyond the acceptable “efficient” occupancy of our current health systems is not a realistic way forward, when patients are dying due to the lack of available appropriate beds.4 Garling, in the overview of his report referred to by Bain and colleagues, states “my recommendations should make more beds available and reduce access block”, but that even with more efficient bed usage “the addition of 350 beds each year” will be required.5 Action is required now and shouldn’t be delayed or subverted by searching for perfect mathematical models. Our hospitals have demonstrably inadequate capacity, resulting in overcrowding with devastating effects. As we have repeatedly stated, it’s all about available beds.

David Mountain · Daniel Fatovich · Sally McCarthy

To the Editor: In her editorial, Christiansen states that the 2010 edition of Therapeutic guidelines: antibiotic (version 14) is very likely to recommend 24 hours of antibiotic prophylaxis for cardiac surgery,1 rather than the present regimen, which recommends that patients having routine cardiac surgery be given a large dose of cephazolin at induction, with a second dose if the operation is prolonged for more than 3 hours, and no doses after surgery.2 The only evidence presented in support of this proposed change is a single randomised controlled trial that purported to show a higher rate of surgical site infections after a single dose of cephazolin, than after a prolonged, multidose regimen.3 The study was flawed, for two reasons. First, cephazolin was not given until 20–30 minutes after induction of anaesthesia, which is likely to have been too late, because, as Christiansen points out, β-lactams should be given 30–60 minutes before incision.1 Second, the trial was analysed on a per-protocol, rather than an intention-to-treat basis, and 189 of the 1027 participants (18%) were excluded, so the findings may be seriously biased.4 Three other trials have compared one or two doses of a cephalosporin with multiple doses of the same antibiotic in patients having cardiac surgery; none found that multiple doses were superior, although all three were small studies with faults in their design.5-7 In 1998, McDonald and colleagues published a detailed review of single versus multiple doses of antimicrobial prophylaxis for major surgery. The analysis was in response to a suggestion by Christiansen and others that single-dose antibiotic prophylaxis may be inadequate for patients undergoing vascular surgery.8 McDonald and colleagues pointed out that the recommendation for single-dose surgical prophylaxis in Therapeutic guidelines: antibiotic (version 13),2 is based on microbiological first principles, published studies reporting efficacy, convenience of administration, reduced antibiotic resistance and toxicity, and relatively low cost. Their careful analysis of 28 randomised trials, in which the same antimicrobial was used in each arm, showed no advantage from the administration of multiple doses; the odds ratio for infection was 1.06 (95% CI, 0.89–1.25). There is no microbiological reason to suppose that the crucial interaction between contaminating bacteria and the prophylactic antibiotic in the heart is any different from that in the lung, biliary tree, uterus, bowel, prostate or bone.8 In the absence of such evidence, there is no sound reason to change the current, long-standing Therapeutic guidelines: antibiotic2 recommendation.

Frank Shann

In reply: Professor Shann raises three issues regarding the recommendation for 24 hours’ prophylaxis for cardiac surgery. First, he states that the trial1 on which this recommendation was made was flawed, because “cephazolin was not given until 20–30 minutes after induction of anaesthesia, which is likely to have been too late”. The trial included patients having coronary artery surgery and/or cardiac valve replacement, and, for these procedures, the time between induction of anaesthesia and surgical incision is about 60–75 minutes, as patients require the placement of intravenous lines and preparation for coronary artery bypass surgery. Antibiotic administration is recommended 30–60 minutes before incision, thus, administration 30 minutes after induction provides optimal serum concentrations at incision, in patients undergoing cardiac surgery. Second, the per-protocol analysis is perhaps less than ideal, but the demographics, clinical characteristics and operative data were comparable for the patients included in the analysis. Third, as stated by Professor Shann, the three earlier studies2-4 were either very small or flawed in design. The McDonald systematic review5 included 28 studies, only two of which were on cardiac surgery, both being the earlier flawed studies2,3 quoted above. The Therapeutic guidelines: antibiotic review process involves a rigorous, evidence-based assessment with input from experts in the field. The medical community of Australia can have every confidence that the recommendations made are current and evidence-based.

Keryn J Christiansen

To the Editor: I agree with the claim by Richardson that “the overlap between [primary care and emergency department (ED)] services is not as important as many have claimed” and that “‘primary care patients’ and ‘ED [Australasian Triage Scale] category 4 and 5’ patients are not interchangeable”.1 A review of the literature — especially from New Zealand — would show there are considerable differences between patients who attend the two types of services. For example, a comparison of patients with asthma attending either a Wellington after-hours medical centre or an ED service located only 800 metres away2 found that the after-hours medical centre was more likely to see younger patients who live further from the service, are given repeat medications, and are referred back to their general practitioner. In contrast, the ED patients were less likely to be referred by a GP and more likely to be admitted to hospital with asthma than patients attending the after-hours centre. Thus, the two services differed in terms of their clinical policies (repeat prescribing and referral) and patients’ demographic characteristics (age, place of residence). I applaud Richardson for highlighting the powerful effects of hospital policies on the behaviour of people outside hospital walls by saying, “it is not the so-called primary care patients who are blocking ambulances from offloading — it is the ‘access block’ patients waiting for beds on the inpatient wards who are inappropriately occupying ED space and staff time”. This claim has nothing to do with the kind of patients who attend primary care services, but more to do with the influence of management policies arising from within hospitals on patient flow from primary care. It confirms research in New Zealand demonstrating how hospital policies (on advertising their services) can have powerful contradictory effects on attendance at EDs. In some cases, people have been subjected to hospitals advertising the clear message that people should attend the ED when they should be seen in primary care instead; and in other cases, people are dissuaded from attending the ED when they are subjected to advertisements about the poor choices people make to attend a hospital. In each case, it is the hospital policy that determines the direction of flow, not the patients in primary care.3-5

Marjan Kljakovic

To the Editor: A recent commentary from the Editor of the Journal1 raises the health-funding dilemma facing current and future Australian governments. All stakeholders in the health industry need to dispassionately scrutinise the role of current models in perpetuating inefficient or socially discriminatory patterns of care. Health care economics is indivisible from the tendency of the broader economy to sustain growth or create disparities, and comparative analysis of systemic economic policies informs the divergent evolution of health systems. The United States, epitomising the free market paradigm, combines a high gross national product with a high poverty rate and significantly unequal income distribution.2 Per capita health care expenditure and its annual rate of increase are comparatively high.3 This is juxtaposed with one of the highest infant mortality rates in the developed world,3 as well as significant racially related variations in health indices. The Scandinavian societies, particularly Sweden, epitomise the benefits of a social welfare model that maintains low unemployment, relatively low income disparity, and advanced technology, while maintaining a healthy private sector.2 The Swedish health care system, which maintains best practice health indices, is characterised by administrative devolution, combined taxation and insurance-based funding, high equity of access, guaranteed maximum primary-care waiting times, and annually capped out-of-pocket expenses.4 Although it had one of the highest per capita health expenditures in the 1980s, its annual rate of increase is one of the lowest in the OECD.3 Since 1975, Australian economic and social policy has increasingly shifted towards a free-market orientated system, comparable with that of the US and United Kingdom rather than the more mixed economies of most European countries or the social welfare economies of Scandinavia. In this context, Medicare is an anomalous relic, which, because of inadequate funding, has struggled to contain patients’ out-of-pocket expenses and maintain equity. The most successful health care systems have a relatively small private sector, limited fee-for-service provisions, and smaller income disparities between health care workers. In contrast, Australia’s hybrid model has a significant private/entrepreneurial component based on a fee-for-service structure that is driven by market forces rather than needs analysis. As Medicare increasingly withers due to neglect, out-of-pocket expenses will continue to rise and health equity will diminish, but sections of private medicine, fuelled by demand from the more affluent, will continue to thrive. As we confront the unpalatable likelihood that the market-driven private sector is a major cause of increasing per capita expenditure, we shall have to justify the viability and equity of the dominant fee-for-service model.

Jeremy W Butler

To the Editor: Observing jugular venous pressure (JVP) is central to cardiovascular examination. Lewis, in 1930,1 was the first to report the use of the external jugular vein as a manometer for recording pressure in the right atrium. Unfortunately, some textbooks on clinical examination and many clinical teachers incorrectly state that the external jugular is unreliable for measuring JVP and that only the internal jugular should be used. The problem with this is that the internal jugular vein is located deep within the neck, where it is covered by the sternomastoid muscle and is therefore not usually visible. Lewis used the sternal angle as a reference point, presuming that it lay 5 cm above the centre of the right atrium in all positions of the patient between lying and sitting. A recent study using computed tomography to examine 160 patients noted that the median vertical distance between the sternal angle and the mid right atrium was 5.4 cm, thus confirming that Lewis’s estimate of the sternal angle in relation to the right atrium was correct (bearing in mind that adults are taller than they were in the 1920s).2 The mean right atrial pressure is the mean of the peak and trough of the external jugular wave above the sternal angle expressed in cm H2O. Over the past few decades, several studies have confirmed that the original findings of Lewis were correct: there is no significant difference in JVP whether it is measured using the internal or external jugular vein, and the external jugular pulse accurately reflects directly measured right atrial pressure.3 In a study of 52 patients with chronic congestive heart failure who had right heart catheterisation, elevation of the JVP showed 57% sensitivity for a raised pulmonary capillary wedge pressure (≥ 18 mmHg) and 93% specificity for non-elevation of JVP, corresponding with a capillary wedge pressure of ≤ 18 mmHg. If elevated JVP was inducible as well, sensitivity increased to 81% and specificity dropped to 80%, with a predicted accuracy of 81%.4 Generations of frustrated medical students and doctors who have stared intently at their patients’ necks awaiting that elusive flicker of the internal jugular pulse have been overlooking an accurate source of clinical information — namely the pulse in the external jugular vein. Lewis was right 80 years ago: measuring the external JVP is a valuable clinical tool and should be practised frequently.

David M Colquhoun · Glenn Jenkins

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

To the Editor: Treatment of critically ill pregnant women is challenging, and information on medication use during pregnancy is scant. We describe the case of a pregnant woman who required extracorporeal membrane oxygenation (ECMO), prolonged sedation and paralysis to treat acute respiratory distress syndrome secondary to pandemic (H1N1) 2009 influenza. A 34-year-old pregnant woman (G2P1) at 21 weeks’ gestation presented to a metropolitan hospital with level 1 intensive care unit facilities. She had known Grade 2 placenta praevia, a 5-day history of influenza-like symptoms, and no history of asthma, chronic disease or recent travel. On examination, she was severely hypoxic (PaO2, 27 mmHg on 15 L/min O2), conscious, tachypnoeic and speaking in single words. A chest x-ray showed extensive bilateral infiltrates (Box). She needed urgent endotracheal intubation but remained hypoxic despite maximal intensive mechanical ventilation. The patient was transferred to St Vincent’s Hospital, Sydney, where venovenous ECMO was commenced on arrival. Her oxygenation status improved and remained satisfactory. Mechanical ventilation was reduced (tidal volume, < 6 mL/kg; peak pressure, < 30 cm H2O) to avoid ventilator-induced lung injury. The patient required very high doses of morphine, fentanyl, midazolam, propofol, dexmedetomidine, cisatracurium and heparin during ventilation and ECMO. In addition, empirical treatment with oseltamivir (150 mg twice a day, Days 1–8), azithromycin and ceftriaxone was started on admission, before a bronchoalveolar lavage specimen tested positive for influenza A and pandemic influenza. Furthermore, a multiresistant Escherichia coli caused ventilator-associated pneumonia, which was treated with meropenem (1 g three times a day, Days 17–30). ECMO was discontinued on Day 19, when lung function had improved. No other organ failure developed. On Day 21, a tracheostomy was performed for severe weakness and weaning failure. The patient was weaned from the ventilator on Day 35 and was discharged home 2 weeks later, after making a full recovery. She gave birth by caesarean section at 35 weeks’ gestation. The baby was in good health and the patient recovered well — both left hospital 3 days after the birth. Information on the use of medication in pregnant women who require intensive care is limited, especially the use of neuraminidase inhibitors.1 We found little evidence on the safety of long-term use of neuromuscular blockers and sedation in pregnancy, with or without ECMO.2 Most literature on this topic describes short-term use of neuromuscular blockers and sedation. Dexmedetomidine has a short postmarketing history, and has therefore had limited use. Data from Australia and New Zealand indicate that 9% of patients admitted to an intensive care unit with pandemic influenza are pregnant. An estimated inhospital mortality rate of more than 16% in this population indicates the severity of the infection.3,4 Single-organ lung failure is a common feature of complicated pandemic influenza, and venovenous ECMO should be considered in these circumstances.2,4,5 Our case demonstrates that ECMO and the drugs necessary for its use can be used during pregnancy in a patient with influenza-associated acute respiratory distress syndrome, and that survival of the patient and fetus is possible. Chest x-ray of a pregnant woman with influenza-associated acute respiratory distress syndrome showing extensive bilateral infiltrates

Susan A Welch · Leone N Snowden · Hergen Buscher

To the Editor: Hydroxychloroquine is used infrequently (in less than 0.1% of Australians) for the long-term management of chronic conditions (eg, rheumatoid arthritis).1 Hydroxychloroquine retinopathy is a rare but sight-threatening side effect that is usually not reversible.2-5 Various eye screening recommendations for hydroxychloroquine toxicity have been proposed overseas,3-5 but there is no recommended consensus for eye screening in Australia. As a result, screening is currently not uniform or universal, and this sometimes leads to significant consequences. A 36-year-old woman with a longer than 10-year history of hydroxychloroquine therapy (400 mg/day; body weight, 62–67 kg) for rheumatoid arthritis presented to her general practitioner after a year of central visual disturbance and photopsias (a sensation of flashes of light). She was referred to the Medical Retinal Clinic at the Royal Victorian Eye and Ear Hospital in August 2009 with suspected hydroxychloroquine toxicity. She had undergone screening by her optometrist for an initial period, but had not been screened within the past 4 years because she failed to attend; she appeared unaware of the potential serious side effect of the medication on her vision. On examination, her visual acuity was 6/9 in the right eye and 6/12 + 2 letters in the left. Her colour vision (assessed by Ishihara plates for colour blindness) was normal. She had left vortex keratopathy (a whorl-like corneal epithelial deposit) and examination of her fundus revealed subtle macular pigment change and retinal arteriolar attenuation (Box, A). Fundus autofluorescence showed significant changes at the level of the retinal pigment epithelium (Box, B). Dense bilateral paracentral field defects were detected on visual field testing. The rheumatologist was notified of the hydroxychloroquine retinal toxicity, and therapy with the drug was ceased. At 6-month eye review, the patient’s vision was stable. Recommendations on the timing of eye screening vary.3 The manufacturer’s product information recommends quarterly ophthalmological examinations, but this is impractical and not cost-effective.3,5 The Royal College of Ophthalmologists (RCO) in the United Kingdom found no evidence-based justification for a systematic screening program.4 They recommend ophthalmological referral only when there are visual symptoms (eg, distorted or patchy central vision, reading difficulties), or eye disease is detected at baseline and confirmed by an optometrist. In contrast, the American Academy of Ophthalmology (AAO) suggests a systematic approach, determined by risk status, that is based on factors such as hydroxychloroquine dose and duration of intake.5 Despite their differences, these protocols both aim to detect toxicity early and minimise the degree of visual loss, rather than to prevent visual loss. This is because there are currently no established criteria to identify toxicity at a reversible stage.4 We recommend adoption of the AAO or RCO protocols and alerting patients to the symptoms of toxicity. Careful counselling of patients at commencement of hydroxychloroquine treatment and on an ongoing basis is essential to promote early presentation and minimise toxicity. Hydroxychloroquine toxicity, although rare, can lead to severe loss of vision if therapy is not stopped. By stopping treatment, the condition may stabilise, and further irreversible vision loss can potentially be avoided. Hydroxychloroquine retinopathy in a 36-year-old woman A: Subtle macular pigment change (black arrows) and some arteriolar narrowing (white arrows). B: Autofluorescence imaging showing symmetrical changes at the level of the retinal pigment epithelium. Mottled loss of autofluorescence (black arrows) indicates loss of retinal pigment epithelium cells, and the adjacent increased autoflourescence (white arrows) indicates cell abnormality.

Elvis Ojaimi · Robyn H Guymer · Tien Y Wong · C Alex Harper

To the Editor: In their letter in the 1 February 2010 issue of the Journal, Rashid and Grant reported the first Australian case of hepatotoxicity associated with the weight-loss product Hydroxycut.1 They noted that, in May 2009, the United States Food and Drug Administration (FDA) advised consumers to stop using Hydroxycut products on the basis of 23 reports linking them to serious injury, including one fatal case of liver failure. In response, the Australian sponsor, Export Corporation (Australia) Pty Ltd told the Therapeutic Goods Administration (TGA) that there were differences between the US and Australian formulations of Hydroxycut products. As the TGA had received no reports of adverse reactions similar to those reported in the US, they allowed local marketing to continue. The TGA website advised consumers to exercise caution when using Australian Hydroxycut products;2 however, no such warnings appeared in local promotional material. In contrast, despite also being told that products marketed in the United Kingdom had different formulations, the UK Food Standards Agency (FSA) said: The specific ingredient or dosage which might be causing health problems has not yet been identified. However, as a precautionary measure, the FSA is warning people not to take them. There are no reported illnesses in the UK related to these products. . . . Hydroxycut products have been withdrawn from sale in the USA, Finland and Canada. Ireland has also advised retailers to withdraw the product and consumers to discontinue use of the products.3 Meanwhile, there have been three complaints upheld about the promotion of Australian Hydroxycut products, with another in progress.4 In 2008, the Complaints Resolution Panel (CRP) requested that the sponsor, retailers and website publishers withdraw any representations that the advertised product(s) has benefits in relation to fat-burning, weight loss, or weight management. Regardless, these claims continue to be made by numerous Australian internet pharmacies, and supplement and health food sites. This highlights the impotence of the CRP (which lacks the power to impose sanctions), the ineffectiveness of the TGA (which can impose sanctions, but apparently declines to do so) and the need for regulatory reform.5 A reformulated Hydroxycut is back on the shelves in the US. An FDA spokesperson said: “The only ingredient left in from the original formulation is caffeine. We do not have any evidence that caffeine causes liver toxicity.”6 However, on 14 February 2010, I had no difficulty in purchasing Hydroxycut (AUST L 154243) from a local pharmacy. This product has a similar formulation to products withdrawn overseas. Rashid and Grant called on the TGA to re-examine the continued availability of these products in Australia.1 I reiterate their call. Why is the TGA out of step with other regulators? Why are these products still on the Australian market if their benefits are negligible or absent, if unethical promotion continues despite CRP determinations, and when the risks are clear?

Ken J Harvey

To the Editor: In the December 2009 issue of the MJA, I came across an interesting article by Dr Paul Zimmet, “A lifetime pursuit of diabetes through chance”.1 This is an account of his impressive achievements in medicine. However, I disagree with the statement that describes his father’s situation in 1930s Poland: “He returned to an unpaid position in the Tarnopol Hospital — unpaid because Jewish doctors could not be ‘officially’ employed in Poland.” I argue that, in Poland at that time, there was no discrimination against national minorities, and this applied to the Jewish minority as well.2 I have done some research on the subject. There were 3.5 million Jewish people in Poland before the war — 10% of the population. According to numerous historical sources, Jewish doctors represented 34% of doctors in Poland in 1938. In the Polish capital, Warszawa, this percentage was 66%. The same sources quote the percentage of lawyers of Jewish origin as 55%.3,4 These numbers are a tribute to the talents and assertiveness of Polish Jews; however, they do not support the statement by Zimmet that I am disputing. In Polish archives, I have discovered statistical documents containing alphabetical lists of all doctors registered in Poland between 1936 and 1938.5 According to these documents, there were two hospitals in Tarnopol at that time: the General Hospital and a Jewish hospital. In the official register of all Polish doctors practising between 1936 and 1938, I have not found the name of Dr Jacob Zimmet. He was not registered as a doctor, and therefore could not legally be employed as a doctor in Tarnopol or any other Polish hospital.

Wladyslaw W Smolilo

In reply: Dr Smolilo has challenged my claim that my father, the late Dr Jacob Zimmet, worked in a hospital in Tarnopol, Poland, and without salary, in the pre-World War II period.1 I am pleased to refute Smolilo’s inaccurate claims. Smolilo argues that “. . . in Poland at that time, there was no discrimination against national minorities, and this applied to the Jewish minority as well”. I accept his statement that there was not an official policy as such. There are, however, ample historical records of discrimination against Jews in many areas.2 Smolilo questions the specific instance relating to my late father. I have a letter in Polish from the Director of the Government Hospital in Tarnopol and its 1939 official translation by the Polish Consul-General in Sydney, copies of which I have provided to the Editor of the Journal. This letter not only confirms my father’s employment from 1935 to 1938, but also the fact that he was not paid. The very fact that Smolilo could not find my father in the official records also stands as confirmation! Clearly, there were many Jewish doctors and other professionals employed in Poland from earlier years who retained their positions during the period from 1935 to 1939. However, even before that time, a quota was imposed on Jewish students and many had to go overseas for medical training.3 On return, like my father, they were unable to find gainful employment and eventually left Poland, many emigrating to Australia. My father provided loving care to many Polish immigrants in his medical practice in South Australia.

Paul Z Zimmet

To the Editor: In your recent column, you drew attention to the “limitations of psychiatry’s scientific foundations for disorders of the mind”.1 This was despite psychiatry’s recent high profile, and the very large sums of money being thrown at the problem. The limiting factor for a scientific psychiatry is that there isn’t one. Extensive research has shown that orthodox psychiatry does not yet have a formal, articulated model of mental disorder to guide its practice, its teaching and its research.2,3 Moreover, not one of the models used today, including the biological approach, can be developed to the point where it would meet the minimum criteria for a scientific model. Confections such as the “biopsychosocial model” do nothing but conceal the problem under yet another layer of jargon. Releasing another Diagnostic and statistical manual of mental disorders (DSM) will achieve nothing because it does not address mental disorder within the framework of an agreed model. In the absence of science, there is scope for non-scientific pressures (such as politics and finance) to have an inordinate influence on the many DSM committees. Needless to say, this conclusion is most unpopular among many in the psychiatric establishment but, sooner or later, they will have to come to grips with the problem; otherwise, psychiatry as a profession will cease to exist.4

Niall McLaren

To the Editor: We read the article by Gibson and colleagues on the assessment and management of cough1 with some concern, specifically regarding the authors’ classification of levels of evidence for current therapies for allergic rhinitis. We would agree that a trial of antihistamines, intranasal corticosteroids and allergen immunotherapy is unlikely to help non-specific cough in the absence of allergic rhinitis. This consensus should be distinguished from the beneficial impact of these modalities on symptoms of allergic rhinitis, for which the authors misquote their main source of information2 and suggest that evidence of benefit from these is “weak”. Although evidence of benefit from allergen avoidance to help manage allergic respiratory disease is controversial,3 a large number of double-blind placebo-controlled trials of all other modalities show Level I evidence of benefit and category A strength of recommendation specifically for treatment of allergic rhinitis, as recently reviewed2,4-6 — evidence consistent with “strong” recommendations using the GRADE (Grading of Recommendations Assessment, Development and Evaluation) criteria.7 We do our patients and colleagues a disservice to suggest otherwise.

Raymond J Mullins · Constance H Katelaris · Janet Rimmer

To the Editor: We read with interest the Australian Cough Guidelines summary statement by the CICADA multidisciplinary group.1 However, we feel that the role of direct examination of the upper aerodigestive tract in assessing cough was underemphasised. Flexible nasal endoscopy (FNE) is a quick, relatively straightforward examination performed under topical anaesthesia as part of an ear, nose and throat (ENT) consultation. It allows direct visualisation of the nasal cavities, postnasal space, oropharynx and larynx, and can be performed on adults and older children and also some younger children.2 Nasal causes of cough, and hence the potential role of FNE, appear to have received more emphasis in previous chronic cough management strategies, including those proposed by the American College of Chest Physicians in 20063 and the European Respiratory Society task force in 2004.4 The diagnosis of chronic rhinosinusitis or upper airway cough syndrome (postnasal drip syndrome) is enhanced by direct examination. The presence of mucopus in the middle meatus of the nasal cavity is associated with a positive diagnosis of chronic rhinosinusitis.1 FNE can also provide direct evidence of the presence of gastro-oesophageal reflux affecting the larynx (laryngopharyngeal reflux), and plays a significant role in the clinical diagnosis of laryngopharyngeal reflux.5 FNE should be used in patients with alarm symptoms for serious underlying disease (as suggested by the CICADA group1), particularly those potentially related to laryngeal causes (hoarseness, haemoptysis, feeding difficulties, stridor or smoking). As part of a complete examination, FNE can help in targeting therapy for two of the three most common causes of cough in adults (gastro-oesophageal reflux and rhinosinusitis), and in excluding some of the significant causes of cough in both adults and children. It is particularly recommended in patients with a suspected nasal or laryngeal cause, in those with alarm symptoms, and in those for whom initial therapy fails.

Nicholas J Potter · Eduard I Pudel

In reply: The recently published CICADA cough guidelines1 draw attention to the important role of systematic assessment of chronic cough in children and adults, and provide an appraisal of the evidence that treating specific conditions will improve cough. Mullins and colleagues raise a key point that requires emphasis, and is relevant beyond the instance of allergic rhinitis that they cite. Chronic cough is associated with several common conditions, such as allergic rhinitis, asthma, gastro-oesophageal reflux disease and sleep apnoea. For each of these conditions, there are well established treatment guidelines that describe the effectiveness of treating that primary condition. However, in developing the CICADA guidelines we were considering the effect of the treatments on the symptom of cough, not on the primary condition. It was stated at the bottom of Box 1 (page 2661) that “The final GRADE recommendations were based on [the] votes [of committee members] and considered cough in the context of the respective conditions”. We agree that the evidence for treating symptoms of allergic rhinitis per se is strong, as published.2 But in the case of a patient presenting with cough and associated rhinitis, the CICADA group determined that the evidence that treating allergic rhinitis would resolve the cough was weak. It is often not possible to determine from successful trials of immunotherapy for rhinitis the outcome for cough. For example, trials of injectable or sublingual immunotherapy both mention cough only once, and it is not possible to determine the effect of the treatment on this symptom.3,4 We welcome the comments by Potter and Pudel giving more specific details of the role of FNE in assessing the upper airway in people with chronic cough. We agree that this is a quick and useful examination. We believe we have placed greater emphasis on upper airway disorders compared with other cough guidelines. Specifically, we have identified vocal cord dysfunction and sleep apnoea as relevant upper airway disorders that are associated with chronic cough. These conditions are not featured in previous guidelines, yet they respond well to specific therapy. We also devote comparatively more space to upper airway disorders that to lower airway disorders.

Peter G Gibson · Anne B Chang · Andrew S Kemp