Volume 176 Issue 9

Communication overload may well lead to errors, but this is yet to be firmly established Although stories of misunderstandings, ambiguity, amnesia and lack of cooperation abound, there have been few studies of communication between healthcare professionals. Recently, the topic has been given new impetus as communication problems have been identified as a major contributory factor to the occurrence of errors and adverse events.1 In this issue of the Journal, Coiera and colleagues (page 415) report a study of communication in two Australian emergency departments,2 extending earlier work carried out in the United Kingdom.3 The "communication load" was high, occupying about 80% of clinicians' time. As in other studies,4 almost a third of communications were interruptions, and about 10% of the time two or more conversations were occurring simultaneously (multitasking). Synchronous communication (face-to-face or telephone conversations) accounted for almost 90% of communications traffic. The authors argue that the combination of interruptions, multitasking, and sheer volume of information (much of it unwanted or irrelevant) may produce clinical errors by disrupting memory processes. Communication problems may take a number of different forms and it is important to distinguish between them, as both the contribution to error or adverse outcome and the appropriate remedy vary considerably. Communications may simply be omitted, as when a surgeon fails to inform the anaesthetist of a drug being administered, thus not preparing him or her for a fall in blood pressure. A common cause of omitted communication is an excessively deferential and hierarchical workplace social structure. The classic examples derive from copilots being reluctant to inform senior pilots of potentially dangerous situations.5,6 There is evidence that medical hierarchies and attitudes are even more entrenched than those in aviation.7 Communications may be ambiguous in a variety of ways. Semantic ambiguity occurs when the same phrase is correctly sent and received, but assigned different meanings by the parties. For example, in a child with a right forearm fracture of both the ulna and radius and a dislocation of the right elbow, a plan to reduce "both injuries" might refer to the two fractures, or to the forearm injury (taken as a whole) and the dislocation. Phonetic or lexical ambiguity (eg, aortic stenosis confused with atherosclerosis8) underlies the problem of sound-alike or look-alike drugs. And finally, message ambiguity can occur because the channel is noisy and the message received does not match the one transmitted. Emergency departments, in particular, are literally noisy channels, with high levels of ambient noise from patients, staff, telephones, alarms, pagers and equipment. Ironically, the natural response to noise interfering with communication is to speak more loudly, creating a positive-feedback loop and an ever-increasing din. Communication may also become problematic because the sheer volume of information overwhelms short-term memory, causing some of the information to be lost before processing is completed.9 In addition, the incoming information may be distracting, interrupting and disrupting complex procedures and decision-making. When levels of interruption are high, clinicians may react by ignoring pagers and messages, or waiting until they are paged twice before responding, to separate the trivial from the truly urgent, which, paradoxically, increases the volume of communications still further. A particularly interesting insight arising from previous studies by Coiera and colleagues is that, despite their own disinclination to be interrupted, clinicians often initiate communication or request information without any thought of the impact of their request on the other person.3,10 This is a form of suboptimisation, in which trying to increase one's own performance results in a net decrement in performance over the entire organisation. Solutions to communication difficulties are often couched in terms of training — "we must learn to communicate better". In a sense this will always be true, in that, ultimately, most improvements in communication will require a change in human behaviour. However, depending on the nature of the problem, the key intervention may be individual training, or involve technical aids, or be team oriented. Training of individuals might focus on giving precise information according to a standard format and considering the impact of the information on the other person. More thought might also be given to how clinicians could be trained to maintain focus and concentration in the face of multiple demands and a constantly changing environment; Technical aids might be simply the introduction of a white board in the emergency department, cutting down the need for multiple face-to-face interactions; and Team-based interventions might include restrictions on interruptions and face-to-face interactions (when information might be easily available in written form), or restrictions on communication and interruption at certain critical phases of procedures, analogous to the "sterile cockpit" rules prohibiting extraneous conversation during takeoff and landing. Human beings are immersed in a sea of communications for much of their waking life, and are well equipped for interpreting ambiguous messages when using information-rich channels such as face-to-face conversation. While communication overload may well lead to errors, this is yet to be firmly established and further studies of the nature of communication between clinicians may be needed first. It is important to realise that safety in high-risk environments relies heavily on continuous communication and rapid updating of information. The task for researchers is to begin to separate out the irrelevant and ambiguous communication from the necessary, if sometimes burdensome, flow of important information.11 Until this issue is clearer, any interventions to reduce communication overload should be implemented with caution. There is a risk that attempts to reduce the communication burden in healthcare by shifting it to progressively terser, more impoverished channels might inadvertently increase miscommunication, or result in even greater demand for synchronous communication. Coiera rightly points out in another article that the benefits of technical solutions may be limited unless they are well understood and carefully targeted.12 Observational studies of the many factors which affect human performance in complex environments have a long history, going back at least to World War II.7 However, in medicine, with a few notable exceptions,13 such studies have been infrequent. The approach taken by Coiera and colleagues2 to the understanding of error and adverse events is important in that it involves direct observation and study of work and workers "in the wild".14 While many valuable studies of error and adverse events have been conducted from records or other documents, it is clear that the full range of factors involved in the genesis of adverse events15 can never be captured completely by such methods. The fluidity and complexity of the clinical environment16 and the need to appreciate clinicians' decision making and cognitive load require studies in which interviews and verbal protocols are combined with observation or video recordings. These methods are not familiar to medicine, and will require collaboration with psychology and engineering.17 Future studies will also have to tackle the difficult topic of linking the details of communication to the occurrence of error or some more general aspect of clinical performance or outcome.

Charles A Vincent PhD · Robert L Wears MD, MS, FACEP

Neurosurgery is now an effective treatment option for some patients with epilepsy When a seizure disorder persists despite optimum drug therapy and significantly affects quality of life, surgical treatment should be considered. Many patients with severe refractory epilepsy can benefit from appropriate surgery and should be given this option by timely referral and investigation. Extrapolating US studies,1 there are probably several thousand eligible people in Australia. In the past, operations were confined to removal of obvious structural causes of seizure, such as tumours or post-traumatic scars. Over the past 50 years, it has become increasingly apparent that there are many patients with persisting epilepsy who could benefit from surgical resection of foci previously difficult to define. The development of increasingly precise methods of anatomical and functional seizure localisation has expanded this group. The evidence for effectiveness of surgery for epilepsy can be seen by outcome studies comparing patients who have had surgery with patients who have had long-term medical therapy. An important recent Canadian study2 of 80 patients refractory to at least two anticonvulsants who were randomly assigned to either undergo temporal lobe surgery or receive further drug treatment showed clear statistical evidence of the success of surgery. At one year, 58% of patients in the surgical group and 8% in the medical group were free of seizures. It should be noted that four patients had adverse effects of surgery, including one small thalamic infarct, one wound infection, and reduced verbal memory in two cases. One patient in the medical group died. Not all patients with refractory epilepsy can be treated surgically. A prerequisite for successful surgery for epilepsy is the precise definition of a discrete seizure focus involving an area of cortex amenable to safe excision. Psychiatric and social factors must also be taken into account. The sequence of events leading to surgery will usually include a period of video electroencephalography (EEG) to define and localise the seizure syndrome, magnetic resonance imaging (MRI), and localisation of eloquent cortex (ie, functional [speech or motor] cortex) by neuropsychological or functional testing. Intraictal single-photon emission computed tomography (SPECT) scanning of regional blood-flow changes is an extremely useful tool for confirmation of a seizure focus. Where available, positron emission tomography is helpful to correlate abnormal glucose metabolism with areas of anatomical abnormality. Anterior temporal lobectomy with hippocampectomy is the most commonly performed surgical procedure for treating epilepsy (see Box). This is because the procedure has a high rate of cure or significant reduction of seizures in patients with complex partial seizures due to hippocampal sclerosis, the largest group of suitable patients. The long-term result of this operation, performed on appropriately selected patients, is that about 70% of patients will become seizure-free.3 Resection of areas of cortical dysplasia has been performed more frequently in recent years, as this condition can now usually be defined with MRI. Where cortical dysplasia occurs close to motor or language areas of the cortex, surgery is often performed under local anaesthesia so that motor function or speech can be monitored by cortical stimulation, reducing the risks of postoperative paresis or dysphasia. In addition, electrocorticography (EEG recorded directly from the cortex), performed either acutely, during surgery, or electively, after placement of subdural electrodes, can further define the boundary between functional and non-functional cortex. Image-guided surgery linked to MRI has enhanced the accuracy and safety of cortical excision. Hemispherectomy is the most successful form of excisional surgery. This major procedure is occasionally indicated for young patients with developmental or acquired affections of one hemisphere leading to catastrophic and continued seizure patterns, although it constitutes a high-risk procedure. Many of these patients make a good recovery once their seizures are eliminated. Corpus callostomy or vagotomy are palliative procedures that may benefit some patients with severe generalised seizure patterns. The former may also be helpful (although rarely curative) in some patients with atonic seizures or drop attacks. Chronic stimulation of the left vagal nerve via a subcutaneous stimulator linked to electrodes placed in the cervical region is a low-risk, albeit expensive, procedure that reduces seizure frequency in about 50% of patients with otherwise untreatable severe epilepsy. A small group of patients with hypothalamic hamartomas leading to the syndrome of gelastic ("laughing") epilepsy may now be treated successfully surgically using an image-guided technique via the third ventricle.4 Postoperatively, adequate support systems are extremely important. Most patients will require ongoing anticonvulsant treatment for two or more years. Mortality and major morbidity after surgery for epilepsy are nowadays low: mortality is less than 0.5% and hemiparesis and hemianopia occur in less than 2% of cases.5 Devastating memory disorders following temporal lobectomy can be avoided by appropriate patient selection and preoperative neuropsychological testing. For example, verbal memory deficits suggesting a left or dominant hippocampal lesion would contraindicate a right hippocampal resection. Considering the poor long-term prognosis for patients with refractory seizures, appropriate surgery has unequivocal advantages. In addition to the social and psychological benefits to the individual, cost–benefit analysis has demonstrated the advantages of surgical treatment compared with life-long medical management.6 The requirements for input from various specialists and the need for particular investigative techniques means that such patients should be assessed in Comprehensive Epilepsy Centres. Some notable contributions to the development of surgery for epilepsy have come from Australia and New Zealand.7-9 There are many more Australians who could benefit from surgical treatment, and this option should be considered by those caring for patients whose seizures continue to be disabling despite best medical treatment.

Gavin C A Fabinyi FRACS

To avoid confusion, the term "autistic spectrum disorders" should only be used as the collective term for a group of defined disorders Autism is a severe neurodevelopmental disorder associated with considerable personal suffering, parental burden and community cost. In recent reports, the prevalence of autism has varied widely from five to 67 cases per 10 000 children, an increase compared with the 3.5–4.5 cases per 10 000 children reported in the 1970s.1,2 This apparent prevalence increase has raised considerable public concern, particularly as it has been temporally linked to the introduction of the measles–mumps–rubella (MMR) vaccine. However, recent epidemiological investigations found no causal link between autism and the MMR vaccine.3,4 The increase in prevalence might indicate a true increase in incidence, but most of the increase can be accounted for by changes in case-finding methods and diagnostic criteria, and by differences in sample sizes, and the age range and intellectual ability of the populations studied.3 The increase in numbers identified has led to a corresponding increase in demand for services. The predominant international approach to diagnosis used by the ICD-10 classification of mental and behavioural disorders5 and the Diagnostic and statistical manual of mental disorders, 4th edition [DSM-IV],6 groups autistic conditions in the category pervasive developmental disorder (PDD) and specifies criteria for the subtypes autistic disorder, Asperger's disorder and atypical autism (PDD – not otherwise specified [PDD-NOS]) (Box). Recently, some confusion has been introduced, as there is a general move away from the term PDD towards the term autistic spectrum disorder (ASD), which has been used in at least four different ways. 1. To refer to a broader group of conditions sharing a "triad of impairments" in social interaction, verbal and non-verbal communication and imagination. Wing7 introduced the term ASD for this purpose. These conditions include the PDDs, but also disorders of empathy and deficits in attention, motor control and perception.8 The term ASD implies a continuum of disturbance in each of these three domains and has led to empirical studies of the continuum of social reciprocity which has implications for testing the clinical validity of categorical diagnostic subtypes of ASD.9,10 Contemporary genetic studies of autism provide evidence of a broad phenotype of social disability, anxiety, depression and unusual personality traits, and a complex interaction of several genes.11 It is not known whether specific patterns of genetic abnormality or the interaction of other risk factors with a common genetic predisposition operate to produce different developmental outcomes, such as severe language disability. Ultimately, genetic studies will determine the validity of categorical diagnoses. In the meantime, for this broad phenotype construct of ASD to have better research and clinical utility each subtype requires international consensus on the discriminating diagnostic criteria, and reliable methods to measure the continuum of each domain. 2. To describe a continuum of intellectual ability among children with PDD — from normal IQ levels (functioning at a high level) through to severe levels of intellectual disability. Some argue that autism is a single-spectrum condition, with the observed differences resulting from different levels of intellectual ability, and that subtypes (eg, Asperger's disorder) are not empirically justified.12 Other studies have used the criterion of significant delay in language development to differentiate children with autism who function at a high level from those with Asperger's disorder. They have found higher levels of psychopathology in children with Asperger's disorder,13 and significant differences in executive function and motor planning between these two groups.14 3. As a description of symptom severity. For example, the Department of Education and Training in Victoria uses the Childhood Autism Rating Scale15 completed by clinicians to provide a cumulative score on the severity of some autistic symptoms to assist in determining funding for education aides. Applying the concept of severity to a disorder that has multiple diagnostic criteria is problematic. For example, a child with autism might have relatively better developed language skills and only a few untroublesome rituals, but may have severe social withdrawal. Can a concept of overall severity be meaningfully applied to such a child and might it overshadow the recognition of a potentially treatable comorbid condition such as anxiety, depression, or attention deficit hyperactivity symptoms? Children with autism who function at a high level are referred to by some as having mild symptoms,12 even though there is evidence that they are often handicapped by high levels of psychopathology.13 4. As a developmental concept. Autistic spectrum is used to describe how skills, such as language, might improve relatively over time so that some children with autism might move from being less able to being more able.16 Use of the term ASD is likely to persist, but to avoid confusion it should be confined to the collective term for a group of defined disorders. Wing used it to promote access to services otherwise denied to young people with autism functioning at a high level.7 This problem still exists, for example in Victoria. Such children do not meet the criteria for funding for an education aide, even though they have a range of severe social, emotional and behavioural problems. Should the inclusion criteria for services be broadened to include the full range of social, emotional and behavioural needs, or, to contain costs, should they be confined to intellectual ability? Behavioural and educational approaches to treatment have received the best empirical support.17 Therefore, allocation of increased funding to support a flexible range of behavioural, educational and family support programs, based on a comprehensive assessment of the diagnostic and cognitive profile and the emotional and behavioural needs of all young people with a PDD, is likely to prove the most economical use of resources in the long term. Pervasive developmental disorders: broad diagnostic criteria Autistic disorder (DSM-IV) Childhood autism (ICD-10) Asperger's disorder (DSM-IV) Asperger's syndrome (ICD-10) Social interaction disability Social interaction disability (as for autistic disorder) Language delay and communication disability No delay in language Restricted, stereotyped behaviour Restricted stereotyped behaviour (as for autistic disorder) Onset before age 3 No delay in cognitive development (DSM-IV only) Other subtypes: Rett's disorder, childhood disintegrative disorder, atypical autism (PDD-NOS). DSM-IV = Diagnostic and statistical manual of mental disorders, 4th edition.6 ICD-10 = ICD-10 Classification of mental and behavioural disorders.5

Bruce J Tonge MD, FRANZCP

The latest triennial review of maternal deaths showed a rise in the maternal death ratio. Whether this represents a new trend or just a statistical fluctuation remains to be seen. The Report on maternal deaths in Australia, 1994–961 was released in September 2001. It is the eleventh in a series of triennial reports that detail maternal deaths in a case summary format. The principal aim of the Report is to improve the quality and safety of healthcare during pregnancy and the puerperium through the education of obstetric practitioners. The Report defines a "maternal death" as the death of a woman while pregnant or within 42 days of the pregnancy being delivered or terminated, and classifies maternal deaths occurring in Australia into three categories: Direct deaths, resulting from obstetric complications of the pregnant state; Indirect deaths, resulting from pre-existing disease or disease that developed during pregnancy and was not due to obstetric causes, but which may have been aggravated by the physiological effects of pregnancy; and Incidental deaths, due to condition(s) occurring in pregnancy, in cases where the pregnancy is unlikely to have contributed significantly to the death. The current Report documents the first rise in the maternal death ratio in Australia since the 1988–1990 triennium — a rise from 10.9 deaths per 100 000 confinements in 1991–1993 (total number of deaths, 84) to 13.0 deaths per 100 000 confinements in 1994–1996 (total number of deaths, 100). Of particular concern is the finding that the rise in the number of deaths was almost exclusively in the "direct deaths" category (see Box). However, as the rise was non-significant in a statistical sense, we will not know, until the next two triennial maternal death reviews are completed, whether this represents the beginning of a new trend or just a statistical fluctuation in very rare events. Although a high proportion of the direct deaths (22/46 [48%]) involved the presence of avoidable or preventable factors, the lack of uniform assessment of avoidable factors across all States and Territories, and the absence of any single factor that could account for the rise in deaths, suggests the apparent increase in avoidable factors should be interpreted with caution. The disparity between Indigenous and non-Indigenous maternal mortality rates has previously been observed2 and remains an issue of concern. The Indigenous maternal mortality rate did decline, from 41.4 to 34.8 deaths per 100 000 confinements, between the 1991–1993 and 1994–1996 reviews. However, changes in ascertainment of Indigenous status over the past nine triennia make it difficult to determine whether there has been a consistent decline, particularly among direct Indigenous maternal deaths. A number of factors may have contributed to the increase in deaths in the most recent triennium. In other countries,3 improved ascertainment of maternal deaths through the use of multiple data sources, including vital statistics and hospital morbidity collections, has resulted in the identification of more deaths. However, in the latest Australian Report, only three of the 12 deaths identified using additional data sources were direct deaths. The changing risk profile of women becoming pregnant may account for some of the increase in deaths. Many women are delaying child-bearing,4 leading to an older cohort of women being pregnant and at increased risk of maternal death.5 Furthermore, with advances in technology an increasing number of women who previously were unable to have children because of infertility or complex medical problems are now having children. Also to be considered is the largely unevaluated impact on maternal death rates of the implementation of multiple models of delivery of obstetric care as well as the larger structural changes in healthcare delivery. Both require further investigation. Despite recent publicity to the contrary, the rise in maternal deaths does not appear to be attributable to the increasing caesarean section rate. The proportion of maternal deaths associated with caesarean section has remained higher than the proportion of all caesarean births over the past four triennia. However, despite rising caesarean section rates (18.4% of all births in 1991–1993 and 19.4% in 1994–1996), maternal deaths associated with caesarean section, excluding those on recently dead or moribund women, fell from 29.8% of deaths in 1991–1993 to 24.0% in 1994–1996. There are no data causally relating the rising caesearan section rate with the increase in the number of maternal deaths. With a small number of deaths from a range of very different causes, it is difficult to draw meaningful conclusions about the impact of the many factors purported to relate to maternal death in Australia. Furthermore, without the availability of the 1997–1999 and probably the 2000–2002 results, it cannot be determined whether the increase in deaths represents a new trend or merely an aberration. Overall, the risk of maternal death during pregnancy and the puerperium remains small. Although differences in definition and collection procedures make international comparisons difficult, Australia appears to compare well with other developed countries, having a similar adjusted maternal mortality ratio to Canada, and a lower ratio than New Zealand, the United States and the United Kingdom.6 With improved general health status and family planning and increased access to general and specialised healthcare, maternal mortality declined considerably in the 20th century. Nevertheless, life-threatening complications still occur, often unpredictably and relatively more often among Indigenous women. It is therefore important that we closely monitor and review all maternal deaths and develop a surveillance system for severe maternal morbidity to ensure the health and safety of all women during pregnancy and the puerperium. The inclusion of pregnancy tick-boxes on Australian death certificates and the use of a standardised national maternal death reporting form should facilitate more accurate reporting of maternal deaths in the future. Summary of key findings from the Report on maternal deaths in Australia, 1994–961 The 1994–1996 Australian maternal mortality ratio was 13.0 per 100 000 confinements, compared with the 1991–1993 ratio of 10.9 per 100 000 confinements. In the 1994–1996 triennium, there were 100 maternal deaths, of which 46 (46%) were direct deaths, 20 (20%) were indirect deaths and 34 (34%) were incidental in nature. This represented an increase of 19% in the number of deaths compared with the 1991–1993 triennium. The increase in deaths occurred almost exclusively in the direct deaths category: 27 (32%) direct deaths were reported in the 1991–1993 triennium, compared with 46 (46%) direct deaths in 1994–1996. There was an increase in the proportion of direct maternal deaths in which avoidable factors were considered to be possibly or certainly present from 7 (26%) of 27 deaths in 1991–1993 to 22 (48%) of 46 deaths in 1994–1996. The principal causes of direct maternal deaths remained pulmonary embolism (8 deaths [17%]), amniotic fluid embolism (8 deaths [17%]) and pre-eclampsia (6 deaths [13%]). Cardiorespiratory disease was the most common cause of indirect maternal death, with 10 (50%) indirect deaths falling into this category, while the leading causes of incidental death were injuries (16 deaths [47%]), neoplasms (5 deaths [15%]) and cerebrovascular disease (4 deaths [12%]). The Indigenous maternal mortality ratio (34.8 deaths per 100 000 confinements) remains about three times that of the non-Indigenous maternal mortality ratio (10.1 deaths per 100 000 confinements).

William AW Walters FRCOG FRANZCOG PhD · Jane B Ford BA (Hons) PhD · Elizabeth A Sullivan MPH FAFPHM · James F King

Objective: To measure communication loads on clinical staff in an acute clinical setting, and to describe the pattern of informal and formal communication events.Design: Observational study.Setting: Two emergency departments, one rural and one urban, in New South Wales hospitals, between June and July 1999.Participants: Twelve clinical staff members, comprising six nurses and six doctors.Main outcome measures: Time involved in communication; number of communication events, interruptions, and overlapping communications; choice of communication channel; purpose of communication.Results: 35 hours and 13 minutes were observed, and 1286 distinct communication events were identified, representing 36.5 events per person per hour (95% CI, 34.5–38.5). A third of communication events (30.6%) were classified as interruptions, giving a rate of 11.15 interruptions per hour for all subjects; 10% of communication time involved two or more concurrent conversations; and 12.7% of all events involved formal information sources such as patients' medical records. Face-to-face conversation accounted for 82%. While medical staff asked for information slightly less frequently than nursing staff (25.4% v 30.9%), they received information much less frequently (6.6% v 16.2%).Conclusion: Our results support the need for communication training in emergency departments and other similar workplaces. The combination of interruptions and multiple concurrent tasks may produce clinical errors by disrupting memory processes. About 90% of the information transactions observed involved interpersonal exchanges rather than interaction with formal information sources. This may put a low upper limit on the potential for improving information processes by introducing electronic medical records.

Enrico W Coiera PhD, FACMI · Rohan A Jayasuriya MPH, MBA, MD · Jennifer Hardy RN, CM, ICU(Cert), BSc, MHP Ed · Aiveen Bannan MB BS, DTM · Max E C Thorpe MD, FRACP

Objectives: To derive indicators of quality prescribing by Australian general practitioners based on Health Insurance Commission (HIC) data and assess the influence of incomplete capture of data on under-copayment drugs on the validity of these indicators.Design: Two expert groups proposed prescribing indicators that can be derived from aggregate prescribing data, and which reflect important clinical or cost-effectiveness issues. Indicators were examined using HIC data and compared with national prescribing trends over time using Australian Statistics on Medicines. The effect of incomplete data capture on indicator interpretation was examined by stratifying GPs into five strata based on the proportion of concession card holders in their practice.Participants: Approximately 14 000 Australian GPs providing ≥ 1500 Medicare services per year.Main outcome measures: Measures of prescribing for individual GPs (based on HIC data 1993–1997).Results: Forty-three potentially useful indicators were identified. These covered a fairly narrow range of prescribing activities and many required additional clinical information for interpretation. Indicators based on prescribing rates gave a misleading picture of prescribing trends where the extent of HIC data capture changed over time. Indicators expressed as ratios that reflected choice of agent within a drug class were less affected by incomplete data capture.Conclusions: Indicators of quality prescribing can be derived from HIC data. However, indicators for under-copayment drugs that represent prescribing rates may unfairly classify doctors practising in areas of socioeconomic disadvantage or high morbidity as "high prescribers". Ratio indicators are more robust, and may be more valid prescribing measures. If HIC data are to be used to monitor the quality of prescribing, data on all prescriptions dispensed will be needed.

Jane Robertson BPharm, MMedSc · Jayne L Fryer BMaths, GradDipMedStat · Dianne L O'Connell BMaths(Hons), PhD · Anthony J Smith DM, FRCP · David A Henry MB, FRCP

Objectives: To assess the intentions of Australia's specialist obstetricians to cease practice and their reasons for abandoning this specialty.Design: A structured questionnaire posted to Fellows of the Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG), issued 11 July 2001 with a return date of 31 July 2001 (in practice, responses were accepted up to 31 August 2001).Participants: Australian specialists holding a Fellowship of the RANZCOG.Main outcome measures: Demographic data (eg, age, sex); type and location of practice; past, current and intended future obstetric practice; reasons for stopping practice; cost of indemnity premiums; experience of litigation and its influence on practice; and experience in giving medicolegal opinion.Results: The response rate was 74% (829/1116), with 826 responses fulfilling our selection criteria. The median number of years since admission as a Fellow was 17 (range, 1–47 years), and 19% (158/817) of respondents were women (9 people did not specify their sex). Of the 826 respondents, 596 (72%) were currently practising obstetrics, 548 (66%) intended to still be practising after one year, 365 (44%) intended to be practising after five years, and 196 (24%) intended to be practising after 10 years. The median indemnity premium in 2001–02 was $35 515 (range, nil to $156 000) for practising obstetricians. The main reasons given for ceasing obstetrics were intention to specialise in gynaecology, fear of litigation, high indemnity costs, family disruption, and long working hours. About two-thirds of respondents (557/818) had experienced the threat of litigation, and almost all (768/803) desired some type of "no-fault" indemnity scheme. Thirty-three of the 314 respondents who had given medicolegal opinions accounted for 71% of the total number of opinions. Many of these were non-practising obstetricians who were not accredited RANZCOG expert witnesses.Conclusion: There will soon be a shortage of experienced practising obstetricians in Australia.

Alastair H MacLennan MD, FRANZCOG · Michael K Spencer BSc(Hons), LLB(Hons)

Non-sedating antihistamines are available as "over-the-counter" preparations and have been widely promoted in public advertisements. However, two such antihistamines, terfenadine and astemizole, have been withdrawn in Australia and overseas. Their use was associated with ventricular arrhythmias — QT-interval prolongation on the surface electrocardiogram (ECG) and polymorphic ventricular tachycardia ("torsade de pointes").1-3 We report a case of ventricular tachycardia (VT) which was probably "torsade de pointes" following ingestion of a single tablet of loratadine. Clinical recordA 43-year-old woman presented after her identical twin died suddenly, presumably from cardiac arrhythmia. The patient was asymptomatic, had no other risk factors and was not taking any regular medication. Clinical examination showed evidence of mitral valve prolapse, with normal left ventricular function and trivial mitral regurgitation on echocardiography. Several ECGs (Box 1a) and her biochemical profile were normal. An electrophysiological study did not show inducible ventricular arrhythmias with standard stimulation testing or adrenaline provocation. Atrial fibrillation was induced during catheter introduction into the right atrium, with ventricular rate less than 130/minute. A prophylactic automatic implantable defibrillator (Medtronic Micro Jewel 7221) was subsequently inserted. Transient prolongation of the QT interval was noted on ECG monitoring in association with non-sustained VT (Box 1b) within 48 hours of the implant. Two years later, the patient had an episode of presyncope, interrupted by a spontaneous defibrillator shock, about 90 minutes after taking a single 10 mg tablet of loratadine for minor symptoms of nasal congestion; this was the patient's first exposure to this drug. She was reviewed on the following day, when the defibrillator device history revealed a rapid ventricular rhythm with changing axis of the intracardiac ventricular electrogram, with a cycle length of 320–230 ms (average rate, 250/minute; Box 2), successfully terminated by a 31-Joule biphasic discharge. The patient was not taking other medications at the time. DiscussionThe term "torsade de pointes" describes polymorphic ventricular tachycardia where the QRS axis appears to be twisting around a baseline. It is associated with prolongation of the QT interval, usually greater than 500 ms (normal is less than 440 ms). A pattern of long–short cycle length in the beats immediately before tachycardia is typical of torsade de pointes (Box 3). It is only possible to diagnose probable "torsade de pointes" in our case, as the defibrillator placed in the patient recorded only a brief snapshot after the device had made the diagnosis of a treatable arryhthmia, so the initiating beats were not recorded. Further, the tracing that the device makes is a ventricular electrocardiogram without any atrial tracing, and the intracardiac QT is not generally accepted as a valid measure of the QT interval. However, the rate of the arrhythmia and its twisting morphology, together with the previous brief episode of prolonged QT interval, make any other diagnosis unlikely. If we could have made a definite diagnosis, this would be the first documented case of torsade de pointes following ingestion of the non-sedating antihistamine loratadine. In this patient's case, the family history of sudden death and the prior history of transient QT-interval prolongation suggests a possible congenital predisposition to the deleterious effects of a drug with potential to prolong the QT interval. Prolongation of the QT interval and torsade de pointes can result from a variety of drug therapies. The likelihood of developing deleterious cardiac reactions to drugs that can prolong the QT interval can be enhanced under certain conditions (Box 4).4-6 Two non-sedating antihistamines (terfenadine and astemizole) were withdrawn after reports of sudden cardiac death.7,8 They were found to block the channels that regulate entry of potassium into cardiac cells during the repolarisation phase of the action potential. Blockade of these channels produces lengthening of the action potential duration.1,2 This is expressed as QT prolongation on ECG and is associated with the development of early after-depolarisations which can give rise to polymorphic VT and, in turn, degenerate into ventricular fibrillation. Loratadine has been retained because of favourable laboratory and clinical data.7 Although cardiac deaths have been reported in relation to this drug,3 no life-threatening arrhythmias have been documented. However, a mechanism for susceptibility to ventricular arrhythmias is suggested by a recent report demonstrating blockade of the human ether-a-go-go-related potassium channel in a similar manner to terfenadine in an animal preparation.9 ConclusionThis case suggests the need for caution in administering loratadine in patients with a predisposition to arrhythmias. Patients should be cautioned to report symptoms such as palpitations, presyncope or syncope after exposure to this drug. As QT-interval prolongation may be intermittent, routine ECG screening may not accurately identify susceptible patients. 1: Electrocardiograms from the patient before (a) and after (b) implantation of an automatic implantable defibrillator (a) ECG strip showing sinus bradycardia (rate, 50/min) and a normal QT interval (420 ms). (b) ECG monitor strip showing QT prolongation (560 ms) and a run of non-sustained ventricular tachycardia (arrow). 2: Intracardiac electrogram obtained following spontaneous discharge of the implanted defibrillator VS = ventricular sensed beat; FS = ventricular beat within the fibrillation zone. Numbers at the bottom denote the tachycardia cycle length in milliseconds. 3: Electrocardiogram rhythm strip illustrating torsade des pointes (not from this patient) ECG shows classical torsade de pointes with long QT interval (a), long–short initiating cycles and twisting QRS complexes (b). 4: Factors predisposing to QT-interval prolongation Electrolyte abnormalities: hypokalaemia, hypocalcaemia, hypomagnesaemia Metabolic disturbance: hypothyroidism, hypothermia, anorexia Drugs: class I and class III antiarrhythmics, antihistamines (eg, astemizole, terfenadine), psychiatric drugs (eg, tricyclic antidepressants, haloperidol, lithium, prochlorperazine, sertindole), antimicrobials (eg, macrolides, ketoconazole, chloroquine, halofantrine), cisapride Structural heart disease: left ventricular hypertrophy or failure Severe renal or hepatic dysfunction Congenital long-QT syndrome

Dennis L Kuchar MD, FRACP · Bruce D Walker MB BS, PhD, FRACP · Charles W Thorburn BM, FRACP, MA

The use of biological agents as weapons of war is not new. In the 14th-century siege of Kaffa, on the Black Sea, the attacking Tartars catapulted bodies of plague victims at the defending Genoese, who contracted the disease and abandoned the city. Over the past century, many countries have developed the capacity to use biological agents to produce casualties in humans and domestic animals and to damage crops and environmental systems. Some biowarfare programs are known to have continued despite the adoption by 144 countries of the 1972 Biological Weapons Convention, which prohibited development or acquisition of such weapons. Early recognition of unusual clinical illness by physicians is an integral part of the public health response to a biological attack. We review the features of four biological agents of greatest concern. In this article, we discuss smallpox, a disease not seen in the world for the past two decades, and botulism. A subsequent article will discuss anthrax and plague. SmallpoxEpidemiologyIn a world declared free of smallpox in May 1980,1 this disease has characteristics that make it particularly suitable for biological warfare. It can be spread person-to-person. With the cessation of vaccination programs over 20 years ago, immunity has waned among those who have been vaccinated, while those born since 1980 are unvaccinated. The virus spreads by the respiratory route (primarily by droplet nuclei or aerosols expelled from the nasopharynx of infected people) or by direct contact (being released from ulcers on the oral mucosa from the time lesions appear on the skin and two to three days after onset of fever). It has also been transmitted by soiled clothing and blankets used by patients. Smallpox spreads rapidly between close family contacts2 and within hospitals when no special precautions are taken.3 Smallpox as a weaponOther features of smallpox that contribute to its suitability as a weapon are the stability of the virus in aerosol form and the likely small infective dose.4 Smallpox virus was added to the biowarfare program of the Soviet Union in 1980. Successful methods of stockpiling large amounts of this virus and delivering it from aircraft or ballistic missiles have been developed.5 With the discontinuation of the Soviet civilian biowarfare program in 1992, hundreds of experienced scientists became available to sell their services and take smallpox virus to other countries.5 The Indian strain of smallpox virus, used in the Soviet biowarfare program, causes a mortality of about 30% in unvaccinated people. Clinical features and diagnosisThe incubation period of 10–14 days ends with sudden onset of fever, headache and backache, usually severe enough to confine the patient to bed. Fever usually continues as the rash develops, with pain associated with pustule growth. Scabs develop and gradually separate, leaving pitted scars. The rash is the most important feature allowing early recognition of smallpox (Box 1). Most cases have been "ordinary type" smallpox, which has pustular lesions, but variant forms ("flat" and "haemorrhagic type" smallpox) occurred rarely and were almost always fatal. Modified smallpox occurred in people with waning immunity after vaccination and those who were vaccinated very early in the incubation period, and comprised a few skin lesions, which evolved more rapidly than those in unvaccinated people. Clinical diagnosis can be confirmed by electron microscopy of vesicular or pustular fluid or scabs, which should be collected and processed under maximum containment conditions. Management and preventionThe only proven effective treatment for smallpox is vaccination before or within three days of exposure, which may abort or modify the severity of an attack. Other treatment is supportive only, plus antibiotic therapy if secondary bacterial infection develops. Strict quarantine with respiratory isolation for 17 days is required of all cases and direct contacts of index cases. Vaccination with vaccinia virus is effective in preventing smallpox for at least five years and may prevent or modify infection for a much longer period, but this varies greatly from person to person. However, very few doses of vaccine are available worldwide at present. Furthermore, smallpox vaccination is associated with more severe adverse effects than any other type of vaccination: for example, encephalitis occurs at a rate of one per 300 000 primary vaccine doses and a quarter of cases are fatal, with some survivors having permanent neurological deficits.4 Therefore, both the World Health Organization and the United States Centers for Disease Control and Prevention have recommended that it should be used only to contain suspected cases and not for mass vaccination.6 BotulismEpidemiologyBotulism is extremely rare in Australia, with no reported foodborne cases since 1991.7 The causative organism, Clostridium botulinum, is an anaerobic, spore-forming, gram-positive rod found in soil (Box 2). It produces a potent neurotoxin that causes paralysis of skeletal and smooth muscle by interfering with acetylcholine release at the neuromuscular junction. Botulism as a weaponBotulinum toxin was first developed as a biological weapon over 60 years ago; it can be aerosolised, or used to contaminate food,8 and the estimated lethal oral dose is 70 µg. The Aum Shinrikyo cult released aerosolised toxin in Japan in the 1990s, but fortunately no cases of botulism resulted. The Soviet Union and Iraq have produced large amounts of botulinum toxin, and Iraq loaded toxin into missiles and bombs.8 Clinical featuresTwo forms of botulism could arise from deliberate release of botulinum toxin — foodborne and inhalational botulism. In contrast, gastrointestinal (infant) and wound botulism arise from infection with C. botulinum, rather than ingestion or inhalation of toxin, and are unlikely to occur in a biological attack. Foodborne botulism, the most common natural form of the disease, results from ingestion of preformed toxin that is produced when food contaminated with C. botulinum has been stored under anaerobic conditions. Cases are mostly associated with improperly home-bottled or preserved foods, but could potentially result from intentional addition of toxin to food. Botulism after inhalation of aerosolised toxin is an unnatural, man-made form of the disease, and would be the intended result of toxin delivery by missiles, bombs or aerosolisation devices. Only one instance of inhalational botulism has been reported, involving accidental exposure of three veterinary personnel to toxin re-aerosolised from animal fur.8 The incubation period for gastrointestinal botulism and probably also inhalational botulism (based on animal studies) is usually 12 to 72 hours. All forms of botulism have identical clinical features, with the exception that foodborne botulism may be preceded by gastrointestinal symptoms (nausea, vomiting, diarrhoea, abdominal cramps).8 The pattern of illness is characteristic: onset with cranial nerve palsies of bulbar distribution, followed by descending motor weakness (from head and chest muscles to upper, then lower, limbs) in a patient with a normal conscious state and no fever.9 Absence of sensory changes is another important negative feature. Reflexes are preserved early, but may be lost with time. Dilated pupils, blurred vision, dry mouth and constipation indicate parasympathetic involvement. Severity of the weakness and its rate of progression vary, depending on the amount of toxin ingested. With modern medical therapy, mortality of foodborne botulism is less than 10%. DiagnosisDiagnosis is initially clinical. The principal differential diagnoses are the Miller–Fisher variant of Guillain–Barré syndrome (a demyelinating condition causing cranial nerve palsies and absent deep tendon reflexes) and disorders of the neuromuscular junction, such as myasthenia gravis. These and other conditions can be differentiated from botulism on the basis of clinical signs (eg, impaired consciousness in brainstem stroke or infection), analysis of the cerebrospinal fluid (infection and Guillain–Barré syndrome), neuroimaging (stroke) and electromyography (myasthenia gravis). Laboratory testing for botulism is complicated and time consuming and is available only through selected public health laboratories. To detect toxin, mice are inoculated with serum, faeces or vomitus; the organism, if present, can also be cultured from these specimens. Results are not available soon enough to assist initial diagnosis or management. Management and preventionPrompt administration of botulinum antitoxin, available in the US but not Australia, lessens disease severity. As the toxin is an equine preparation, serum-sickness-like reactions may occur in some recipients, but anaphylaxis is rare. Otherwise, treatment is supportive. Close respiratory monitoring is essential, and patients should be admitted to an intensive care or high-dependency unit. In one foodborne outbreak, 20% of patients required mechanical ventilation. An investigational toxoid vaccine has been given to laboratory and military personnel in the United States but is not available for more widespread use. 1: Smallpox lesions in an unvaccinated child Evolution of smallpox lesions from papules (top left; three days after onset of fever) to vesicles and pustules (bottom right; nine days after onset of fever). For the first two to three days, the rash of smallpox resembles that of chickenpox, but the two can be differentiated by the following: Smallpox lesions appear after two to three days of prominent prodromal symptoms (fever, headache and backache) and develop slowly (over nine to 10 days). Chickenpox lesions develop rapidly after a one- to two-day prodrome (fever and malaise). All smallpox lesions develop at the same pace and, on any part of the body, appear identical. Chickenpox lesions are much more superficial and develop in crops over a two- to four-day period, with scabs, vesicles and pustules seen simultaneously on adjacent areas of skin. Smallpox lesions are most concentrated on the face, arms and legs, and may occur on the palms or soles. Chickenpox lesions are most dense over the trunk and almost never found on the palms or soles. 2: Clostridium botulinum Gram-positive rods with characteristic subterminal spores (Gram stain; original magnification x 1000). (Picture courtesy Microbiological Diagnostic Unit, Public Health Laboratory, University of Melbourne, VIC.)

Michael Whitby FRACP, FRCPA · Alan C Street FRACP · Tilman A Ruff FRACP · Frank Fenner MD, FRS

The United Kingdom National Health Service (NHS) has experienced 10 years of primary care budget holding in a variety of forms. Half of all general practitioners had joined the GP fundholding scheme by 1997, and many others had joined broader GP commissioning groups, but fundholders controlled only about 20% of the budget for hospital and community health services. Research on fundholding and commissioning groups suggests that delegation of budgets produced some gains in the range and effectiveness of services, but also had significant management costs and inequities. From 1999, all primary care professionals joined Primary Care Groups, which are now becoming Primary Care Trusts (PCTs). PCTs will control three-quarters of the healthcare budget and provide all primary and community services as well as commissioning hospital care. Control of a unified healthcare budget presents opportunities to improve quality, increase integration of services, reduce inequities and improve health. However, PCTs are threatened by a growing gap between capacity and expectations, and by continuing tension between devolution of power and increasingly prescriptive management by central government.

David Wilkin MSc, PhD

1: Clinical records Case 1: A 46-year-old Indian man required lumbosacral (Steffee) fusion1 for chronic low-back pain after a successful laminectomy for disc herniation sciatica. Good pain relief was obtained for four weeks after the operation, and then his back pain recurred. After a brief period of symptomatic treatment, he was re-operated on at six weeks, and the metal screws and plates, which were found to be loose in the bone, were removed. The bone was noted to be softer than normal and the fusion was not sound. Swabs for infection were sterile. The patient gave a history of long-term adherence to a vegetarian diet, as well as continuous night-shift work for 10 years with minimal sunlight exposure. He had never smoked. His 25-hydroxyvitamin D (25OHD) concentration was < 12 nmol/L (reference range, 35–155 nmol/L). The results of laboratory tests were calcium, 2.27 mmol/L; albumin, 38 g/L; phosphate, 1.33 mmol/L; alkaline phosphatase, 179 U/L (reference, < 120 U/L); and γ-glutamyltransferase, 195 U/L (< 65 U/L). The patient was taking carbamazepine, which may account for the liver function abnormalities. Vitamin D supplementation (ergocalciferol, 2000 units daily) was commenced. Dietary calcium intake was assessed as at least 800 mg/day. Physiotherapy, initiated because of his back problems, was continued and his work was transferred to day-time shifts only. After eight weeks of treatment and sunlight exposure, the results of laboratory tests were calcium, 2.44 mmol/L; albumin, 45 g/L; alkaline phosphatase, 117 U/L; γ-glutamyltransferase, 102 U/L; and 25OHD, 125 nmol/L. Plain x-ray and computed tomography scan showed his fusion to be sound at 12 months and his symptoms to be much improved. Case 2: A 49-year-old white woman was admitted for elective removal of metal plates (Steffee) from L2–L3 fusion two years previously. Before x-ray films were obtained, it was hoped that her fusion was sound. However, imaging had suggested the pedicle screws had loosened, contributing to ongoing low-back pain and sciatica (Figure 1). Furthermore, x-ray of the lumbar spine in flexion showed narrowing of the angle between the end-plates of L2 and L3, indicating movement posteriorly (Figure 2). At operation, all screws were grossly loose, and a bone graft placed posterolaterally had not joined to the vertebral bodies. Further bone chips were inserted, and a bone biopsy was taken. Swabs for infection were sterile. Areas of woven bone were present and the appearance of the osteoid suggested a mineralisation defect, although undecalcified sections were not available. This patient had a four-year history of insulin-requiring diabetes mellitus, for which she also took metformin, glibenclamide and pioglitazone. Other medical problems included obesity (body mass index, 44 kg/m2), hypertension and bronchospasm, treated without long-term inhaled or systemic corticosteroids. She had never smoked. Her 25OHD concentration was < 12 nmol/L. Ergocalciferol 3000 units daily was commenced. The serum alkaline phosphatase level was normal (79 U/L). Dietary calcium intake was considered adequate. Specific questioning revealed a history of "hating the sun", and avoiding exposure to sunlight throughout her adult life. One month later, her 25OHD concentration was 27 nmol/L and the dose of ergocalciferol was increased to 4000 units daily. Six months after operation, imaging suggested that the new bone graft had become incorporated into the spine. Figure 1: Lateral x-ray of the lumbar spine in extension. Arrow denotes a radiolucent zone at the margin of the upper screw, indicating loosening. Figure 2: Lateral x-ray of the lumbar spine in flexion, showing significant narrowing of the angle between the endplates of lumbar vertebrae 2 and 3, compared with Figure 1. Recently, attention has again been drawn to the high prevalence of severe vitamin D deficiency in certain population groups in Australia, including veiled and dark-skinned women and their children.2,3 Another group at high risk are the elderly: 67% of older patients admitted to a short-stay geriatric rehabilitation unit were found to have vitamin D deficiency.4 A similar prevalence has been found in residents of nursing homes.5 However, it is not widely appreciated that moderate to severe vitamin D deficiency may also occur in middle-aged people. Our two patients were in their late 40s when severe vitamin D deficiency became apparent. In the first patient, recurrent pain a short time after surgery was of such severity that internal fixation plates had to be removed. The screws were loose, and, in the absence of infection, the profound vitamin D deficiency can be assumed to have resulted in failure of mineralisation of osteoid and hence failure of the surgical procedure, with resulting increased morbidity. This patient had multiple risk factors for vitamin D deficiency (pigmented skin, habitual night-shift work and a vegetarian diet). Although he now exercises regularly, including during daylight hours, and works day-time shifts, he has required ongoing vitamin D supplementation to maintain satisfactory 25-hydroxyvitamin D (25OHD) concentrations. The second patient's bone had an abnormal histological appearance, and, despite an omnivorous diet, her choice to avoid direct sunlight for many years had resulted in profound vitamin D deficiency. Vitamin D deficiency of the severity reported here is extremely uncommon in younger Australian adults. However, patients with long-standing orthopaedic or spinal disorders who become housebound may be particularly at risk, irrespective of their age. The functions of vitamin D in bone metabolism are well known and its deficiency may be reconciled with the failure of spinal fusion, as described in these patients. This report highlights the need for attending surgeons and physicians to be aware of the potential for vitamin D deficiency in their patients, since failure to recognise this easily reversible problem may result in complications of treatment, including failure of spinal fusion surgery, additional morbidity and the substantial costs of further surgery and hospitalisation. Lessons from practice Persistence or recurrence of low back pain and sciatica after spinal fusion surgery may indicate failure of the operation. Risk factors include infection, smoking and vitamin D deficiency. Patients at any age who actively avoid exposure to sunlight are at risk of vitamin D deficiency. Vitamin D deficiency is readily identified and corrected and should be considered in patients who may require spinal fusion surgery.

Walter E Plehwe FRACP, PhD · Roy PL Carey MB BS, FRACS

To the Editor: Consensus exists that the provision of medical advice must be based on the correct interpretation of the evidence base. It is logical to assume that consideration should also apply to the provision of medical opinion in cases of medical litigation. The recent article on Sharp v Port Kembla RSL Club1 raises concerns which require wider debate. It is not our purpose to discuss legal niceties nor to contest the epidemiological evidence of an increased incidence, in active smokers, of cancers at several sites, including the head and neck. Rather, we wish to concentrate on a central conclusion in the report, namely the assertion that ". . . a relationship between exposure to ETS [environmental tobacco smoke] and an increased risk of head and neck cancer . . . is supported by the available epidemiology". The larger2 of the two studies quoted showed a crude odds ratio of 2.4 (95% CI, 0.9–6.8). This result is statistically non-significant. The authors also claimed a dose response between "moderate" and "heavy" exposure of 1.8 (95% CI, 0.5–7.3) and 4.3 (95% CI, 0.8–23.5) for non-smokers and 2.5 (95% CI, 0.9–6.9) and 5.3 (95% CI, 1.8–16.1) for smokers. Statistical interpretation of these results leads to a conclusion of no evidence of an increased risk compared with people who were "never" exposed to ETS. Leaving aside our considerable reservations regarding the overall design and analysis of this case–control study, the data as presented are at best suggestive. Significant doubt must remain regarding the role of ETS in head and neck cancer. That being so, two disturbing issues emerge which merit further debate. Firstly, there is an ethical issue as to whether the requirements for the correct interpretation of the evidence base for medical opinion should be any different in the clinic or the courtroom. Secondly, the judgment in this case highlights a dilemma in clinical practice. A clinician is not expected to practise according to non-significant differences in outcome. But, in the event of litigation, will the courts decide, as in this case, that bigger is better?

Allan O Langlands FRACR, FRACS · Val J Gebski BA, MStat

In reply: Our article1 outlined evidence presented to the Supreme Court of New South Wales. The paucity of epidemiological evidence concerning an association between exposure to environmental tobacco smoke (ETS) and laryngeal cancer (two studies available) was offset by biological plausibility concerning the carcinogenicity of tobacco smoke. To that extent, the epidemiological evidence in question "supported" a clear inference of causality from other data. The views offered by Langlands and Gebski do not alter this consideration, and are otherwise without merit for several reasons. To restrict the inference reasonably drawn from epidemiological data to whether or not statistical significance is achieved is inadequate. To offer an overall conclusion other than one based on all the data (in this instance, both studies) is unsound. To publish imputations concerning a specific study in a context denying right of reply by the authors concerned is unfortunate. To identify an ethical problem predicated only on a perceived discontinuity between evidence accepted by a court and evidence accepted by the medico-scientific community is spurious. The Court in Sharp v Port Kembla RSL Club was provided with vigorous criticism of the epidemiological data. Most of the eight weeks of court time was occupied by a painstaking analysis of this and other causative issues. The Court then made a determination consistent with the medico-scientific evidence. Stewart BW, Semmler PCB. Sharp v Port Kembla RSL Club: establishing causation of laryngeal cancer by environmental tobacco smoke. Med J Aust 2002: 176; 113-116. (Received 18 Mar 2002, accepted 21 Mar 2002) South East Sydney Public Health Unit, Randwick, NSW. Bernard W Stewart, PhD, FRACP, Head, Cancer Control Program, and Professor, UNSW School of Paediatrics. Sir James Martin Chambers, Sydney, NSW. Peter C B Semmler, MA, QC, Senior Counsel. Correspondence: Professor B W Stewart, South East Sydney Public Health Unit, Locked Bag 88, Randwick, NSW 2031. stewartbATsesahs.nsw.gov.au AntiSpam note: To avoid spam, authors' email addresses are written with AT in place of the usual symbol, and we have removed "mail to" links. Replace AT with the correct symbol to get a valid address.

Bernard W Stewart · Peter C B Semmler

To the Editor: Donovan and colleagues bring attention to the restrictions placed by the Health Insurance Commission via the Medicare system on clinicians investigating patients for sexually transmitted infections (STIs).1 In their study of Sydney general practitioners, they suggested that reform was required to the three-test pathology testing rule to improve gonorrhoea screening in high-risk individuals living in a region of epidemic gonorrhoea. In the Kimberley region of Western Australia, where we practise, syphilis, gonorrhoea and chlamydia continue to be endemic. Best-practice guidelines for primary healthcare providers in WA state that investigation for other possible STIs is essential to the care of patients with STIs or HIV infection.2 Health policy should be based on best-practice standards. For patients with confirmed or suspected STIs, this means that Medicare funding should meet the full costs of all tests for suspected STIs (as indicated by clinical need and best-practice guidelines) to enable and facilitate effective control of these infections at the population health level. An Australian legal precedent exists for medical practitioners regarding testing for STIs. In the New South Wales Supreme Court case of BT v Oei, it was found that a doctor has a duty of care to offer testing for other STIs to a patient with one STI or a suspected STI.3 In that case, a sexual partner of an HIV-positive patient brought successful legal action against her partner's doctor for failing to diagnose HIV infection in her partner. The doctor was found negligent in failing to offer an HIV test to a patient with ongoing symptoms who had been found to be infected with hepatitis B virus and whose only risk factor for this infection was unprotected sex. The doctor's duty of care was found to extend to the patient's sexual partner, who became infected with HIV after unprotected sex with her partner. Given that best-practice guidelines and a legal precedent exist which confirm that a medical practitioner should offer testing for other STIs to a patient with one STI or a suspected STI, what are the medicolegal implications of the Health Insurance Commission's three-test rule? Comment: The Journal sought a comment from the Commonwealth Department of Health and Ageing, but after three months had yet to receive a response.

Graeme H Johnson MB BS (Hons), BMedSci(Hons) · Donna B Mak FAFPHM, FACRRM

In reply: We disagree with Wodak and colleagues in a number of respects. If the results of a hydromorphone trial were as good as Wodak et al claim a heroin trial would be, then a heroin trial would be unnecessary. We accept, as did the Dutch and Swiss, that politicians have the authority to make decisions about what medical research is permitted. The heroin trials in Switzerland and the Netherlands were approved by parliament and supported by referenda in cantons and cities in Switzerland. The Australian survey data cited by Wodak and colleagues indicate that a heroin trial would not have been approved if a referendum had been held in 2001. Nor do we think it would be supported by a free vote in Federal Parliament, as it was not supported by a similar vote at the NSW Drug Summit in 1999. Wodak et al present no evidence to support their claim that the delivery of a treatment that costs between A$25 000 and A$45 000 per patient per year in the Netherlands1 to less than 5% of the heroin-dependent population would have a detectable impact at the population level. A hydromorphone trial would provide a way of evaluating the role of injectable opioids in the treatment of heroin dependence. It would not prevent Wodak and colleagues from convincing the community that injectable heroin is the drug of choice to treat refractory heroin dependence.

Wayne D Hall PhD · Richard P Mattick PhD · Jo Kimber BSc (Hons)

To the Editor: Lamberth stated in his case report that Antarctic tourist ships should be equipped to provide life support, as well as better screening and education of Antarctic tourists.1 I recently travelled to both the Arctic and Antarctic as a medical officer on small ships, caring for seven passengers injured in a helicopter crash in the remote Russian Arctic and a 12-year-old with diabetic ketoacidosis in the Drake Passage, as well as numerous people with minor ailments. To compare these ships with large tropical cruise liners is unrealistic. Ships' medical supplies are selected with an appreciation of the casemix. A study of 16 Antarctic trips in 1997 and 1998 found that most problems were respiratory tract complaints, acute soft tissue injuries and complaints, sea sickness and dermatological problems.2 Few major incidents have been reported, and equipment for advanced life support is tailored to this. Paralysing agents and ventilators are not supplied. A single doctor with no nursing staff cannot safely care for a ventilated patient for 72 hours, as suggested by Lamberth, and the additional staff needed for this would be a huge additional expense for a very rare occurrence. While some ingenuity and adaptability may be required, the equipment supplied is adequate for the vast majority of events. Safety and preventive medicine are very much part of the ship's doctor's role. Most doctors give a brief lecture as part of the initial briefing of passengers. Seasickness, appropriate medication and safety on the ship are usually part of this. The passengers are predominantly elderly and, in my experience, many are fulfilling a long-held ambition to travel to the polar regions. Reputable companies require a fitness-to-travel assessment from passengers' general practitioners before the trip is confirmed. This assessment is tailored to potential problems in remote regions. I believe that excluding people from the wonders of polar travel on the basis of age or previous coronary artery disease would be a terrible shame, while accepting that there will always be a risk in travelling to remote locations. Having shared in the 90th birthday celebration of a woman with chronic obstructive pulmonary disease in the Arctic, I hope that I will still be able to enjoy such experiences at that age.

Eve R Merfield FACEM

To the Editor: Lamberth raised some worthwhile issues about small-ship adventure tourism to Antarctica in his recent case report describing the death of an 82-year-old tourist.1 This occurred in 1999, the season I started as medical director for the leading polar adventure tour company that chartered the vessel involved. I have some comments and an update. The former Soviet oceanographic research vessel was converted in the 1990s to carry 78 passengers. She had a two-bed infirmary and a procedure room with Russian and German medical supplies for passengers and crew, and carried a German- and English-speaking Russian doctor experienced with passenger ship medicine. The tour operator provided additional medical supplies and an emergency physician. Ventilatory support could have been provided, although not to the standard of a contemporary Australian intensive care unit. Polar adventure operations are very different from "tropical" cruise lines, which generally operate their own ships from home ports and cater for up to 3000 passengers with very different expectations.2 Operators require that prospective passengers submit a medical information form and a declaration from their personal physician that they are fit for the journey. The 82-year-old who died was a retired physician who did not declare the extent of his limitations, and who acted as his own medical advisor. His is the only death I am aware of after seven years' involvement in the industry. The medical declaration form has been modified and now addresses the risk factors identified by Lamberth. Prospective clients with questionable health are referred to the medical director. However, operators cannot verify declarations of good health, and physicians have been known to collude with passengers to avoid risk of rejection. Furthermore, "ageism" is as unacceptable as sexism and racism. I was present on the first passenger-circumnavigation of Antarctica in the company of several octogenarians and a 90-year-old, and on the first circumnavigation of the Arctic Ocean, with other octogenarians and a 92-year-old. Short trips to the Antarctic Peninsula are very different from scientific expeditions; Lamberth's suggestion that advising doctors should consider scientific expedition criteria is inappropriate. The International Association of Antarctic Tour Operators (<www.iaato.org>) is a voluntary association of competing adventure eco-tour operators whose purpose is to self-regulate the industry and to develop good standards. Standards for provision of medical supplies and capabilities are under development by this association.

Chris H Curry

In reply: I welcome Curry and Merfield's interest and comments. The patient described in my case report1 was not, as Curry states, "a retired physician". Nor did he provide his own health assessment, but had his assessment form filled out by another physician. Unfortunately, this form, along with those of 60 other passengers, was not made available to any doctor before embarkation. Curry confirms that many older passengers are travelling to Antarctica.2 Merfield's experiences attest to the potential for serious (including multiple casualty) incidents in this remote location. I agree that ageism per se is unacceptable. Rather, the issue is the provision of adequate facilities to deal with potential problems or, alternatively, warning as to the hazards. Advertising for Antarctic cruises emphasises the medical facilities provided. The public may not realise that a doctor with minimal equipment cannot deliver the same care available in a First World hospital. Curry's assertion that ventilation could have been provided illustrates this. Ventilation is more than placement of an endotracheal tube. It is ludicrous to suggest that, without oxygen, paralysing drugs, positive end-expiratory pressure or means to suction the copious thick secretions, hand-bagging for 36 hours while crossing the heavy seas of the Drake Passage might have altered the tragic outcome for this patient. I recommend a book by Levinson, a seasoned polar physician, and Ger on health aspects of polar tourism.3 They have collated the findings of a conference held on this topic at Cambridge in the United Kingdom in 1995. The book addresses what Levinson describes as "the often inadequate medical care which exists in these regions". He notes "major concerns . . . expressed by travel experts, the American Medical Association, the American College of Emergency Physicians, and other professional organisations."3 The survey by Curry and Johnston found that illnesses among their company's Antarctic tourists in 1997 and 1998 included cardiac arrest, acute myocardial infarction, severe pneumonia, diabetic ketoacidosis due to seasickness, haematemesis, anaphylaxis, ruptured ectopic pregnancy and acute appendicitis. The fact that polar trips are short does not seem to protect against potentially lethal diseases. Given the stress of this travel and the nature of the population involved, maybe the contrary applies.

Paul G Lamberth FACEM

To the Editor: The experience described by Jones on books as carriers of disease in a recent issue of the Journal,1 following Ferson's article in the Christmas issue,2 reminded me of my experience in about 1933 at the Coast Hospital (now Prince Henry Hospital) at Little Bay, Sydney. My mother was a medical resident at the Coast, which was the infectious diseases hospital for NSW. She developed acute diphtheria and was admitted. I (aged five) and my sister had been immunised and were not sick. However, we were throat swabbed, and the swabs were positive for Corynebacterium diphtheriae. We spent three weeks in the hospital with no treatment until we returned negative throat swabs. While waiting to be admitted to the "blocks", we saw children with shaven heads through glass doors, and I've always assumed they were the ones with scarlet fever, as did Jones.1 I was given The Anzac book, on Gallipoli, to browse through. This is now a collector's item and very valuable. Then, much to my chagrin, I was not allowed to take it home. Later, in 1953, I was to return to my old ward as a resident medical officer, although I was never to find out what happened to all those books!

John V Roche MB BS, FRACGP, D(Obs), RCOG, DRACOG

Henry Oliver Lancaster was born in Sydney on 1 February 1913, but spent his early years in Kempsey, NSW, where his father had a medical practice. His father died when Oliver was almost nine, and he boarded in Kempsey through his primary and West Kempsey Intermediate High School years. After a year studying economics/arts at Sydney University, he enrolled in medicine in 1931 and graduated in 1937. In that year he worked as a Resident Medical Officer at Sydney Hospital, and in 1938 as a pathologist and Senior Medical Officer. Lancaster joined the Australian Imperial Force as a Medical Officer in 1940, and later served as a pathologist in the Middle East and New Guinea. His first two papers (jointly with T E Lowe), on worm infestations in troops, were published in the Medical Journal of Australia in 1944. The same year, a secondment to the Australian New Guinea Administrative Unit awakened his interest in demography and sparked his return to the serious study of mathematics. From 1946 to 1948, while on a temporary appointment to the School of Public Health and Tropical Medicine (SPHTM) (affiliated with Sydney University), he took the opportunity to study advanced mathematics and read the work of the English and American medical statisticians/epidemiologists. In 1948, he left to spend a year as Rockefeller Fellow in Medicine at the London School of Hygiene. After returning to work at the SPHTM, Lancaster was involved with statistical and epidemiological studies of disease in Australia, including diabetes, cancer (notably melanoma and its association with latitude) and tuberculosis. In 1941, the ophthalmologist Norman Gregg had observed that many cases of cataract were the result of maternal rubella in the first month of pregnancy. This was to lead to Lancaster's landmark discovery that "ordinary" rubella infection of pregnant women (rather than a new, highly virulent strain, as Gregg had thought) was linked with congenital deafness of offspring.1 In 1959, Lancaster was appointed to the Foundation Chair of Mathematical Statistics at the University of Sydney, a position he held until his retirement in 1978. He was elected a Fellow of the Australian Academy of Science in 1961, and awarded its Thomas Ranken Lyle Medal for Physics and Mathematics in the same year. He was awarded an MD in 1967, and in his retirement returned to intensive writing in medical statistics. His publications included Expectations of life (1990), a massive study of world mortality, and Quantitative methods in biological and medical sciences. A historical essay (1994). Oliver was made an Officer of the Order of Australia in 1992 for services to science. An account of his career, Some recollections of Henry Oliver Lancaster (1996), edited by his brother Richard, is in the Sydney University archives. He died in Sydney on 2 December 2001 of coronary heart disease.

Eugene Seneta

Longer lives People with Down syndrome are now living much longer. In the United States, median age at death increased from 25 years in 1983 to 49 years in 1997, with a substantial decrease in deaths before age five years. Data on all deaths for persons with Down syndrome (n = 17 897) were selected from officially compiled, multiple-cause mortality files for all deaths from 1983 to 1997, then compared with a random sample of 25% of all deaths. Standardised mortality odds ratios (SMORs) were calculated, adjusted for age, sex, race and year of birth. Death certificates for people with Down syndrome were significantly more likely to list congenital heart defects (peaking at age 20–29 years, SMOR 85.5 [95% CI, 75.9–96.4]), dementia (SMOR, 116.0 [95% CI, 93.6–143.8] at age 40–49 years), hypothyroidism, seizure disorder, aspiration pneumonia, influenza, viral hepatitis, or leukaemia. Lancet 2002; 359: 1019-1025 New neurones Californian researchers have demonstrated that new cells in the adult mouse hippocampus mature into functional neurones. The structure of the cells could be seen by electron microscopy after they were labelled with a retroviral vector expressing green fluorescent protein (GFP), which only labels dividing cells. In mice killed after 48 hours, the GFP-positive cells were immature neurones. In those killed at four weeks, dendrites and an axon were observed, and by four months the cells were larger with more dendrites and spines, and resembled mature neurones. Electrophysiological recordings of GFP cells made after 4–8 weeks showed that the neurones were functional. New brain cells have also been observed in the adult human hippocampus. As this region of the brain is important in memory and learning, an understanding of the functional significance of these newly developed cells is keenly awaited. Nature 2002; 415: 1030-1034 Get moving A study from Stanford University confirms the importance of fitness to survival. Peak exercise capacity was estimated during symptom-limited testing on a treadmill in 6213 men referred for clinical reasons. At age 59 years (SD, 11), 3679 men had either a history of cardiovascular or pulmonary disease or abnormal results on this test (CVS group), while 2534 were considered normal. During 6.2 years’ (SD, 3.7) follow-up, 1256 of the men died. In both groups, subjects with lower exercise capacity had a higher risk of death (for lowest v highest quintiles of exercise capacity, the age-adjusted relative risk was 4.5 for the normal group and 4.1 for the CVS group). Peak exercise capacity was the best predictor of an increased risk of death in both groups. In the normal group this was followed by pack-years of smoking and, in the CVS group, by histories of congestive cardiac failure and myocardial infarction, then pack-years of smoking. N Engl J Med 2002; 346: 793-801 Start early A British study suggests that the prevention of insulin resistance and its consequences may need to begin before adult life. Blood samples were collected from 73 South Asian children (mostly from Pakistan) and 1287 white children, aged 10–11 years, as part of a cross-sectional comparison of primary school children from 10 towns. Observations included height, weight, blood pressure, heart rate and waist and hip measurements. Despite similar glucose levels, insulin levels were higher in South Asian children than white children, both fasting (47.8 v 31.2 pmol/L) and 30 minutes after glucose (459.8 v 298.7; adjusted difference, 54% [95% CI, 19%–99%]). As these differences were not associated with corresponding differences in adiposity, the causes of increased insulin resistance in these South Asian children remain unclear. BMJ 2002; 324: 1-6 Take half an aspirin An Israeli study of acute myocardial infarction (AMI) found improved survival when aspirin was given early. In an RCT, 1200 patients with AMI were commenced on thrombolytic therapy within six hours of onset of symptoms, receiving either recombinant tissue plasminogen activator or streptokinase, plus either heparin or argotroban. There were no differences in outcome between the groups. Aspirin 160 mg was to be given within one hour of starting thrombolytic therapy, then daily for 30 days. However, 364 subjects had received aspirin significantly earlier, before starting thrombolysis (1.6 v 3.5 hours). This early- aspirin group was found to have significantly lower mortality than the other patients at 7 days (2.5% v 6%), 30 days (3.3% v 7.3%) and one year (5.0% v 10.6%). In further analysis, early aspirin treatment emerged as an independent variable associated with improved survival. Am J Cardiol 2002; 89: 381-385

Med J Aust 2002; 176 (9 Suppl).