Letters

Len C Gray,* Stephen J Duckett† * Professor in Geriatric Medicine, University of Queensland, Princess Alexandra Hospital, Ipswich Road, Woolloongabba, QLD 4102; † Professor of Health Policy, Latrobe University, Melbourne, VIC lgrayATsoms.uq.edu.au In reply: Mackay and Millard have raised some important issues in relation to our analysis. Our article was developed to encourage wider reflection and their response is thus welcomed. The primary criticism levelled by Mackay and Millard was that we underplayed the importance of supply of beds in our interpretation of the trends. We agree that bed supply is an important driver of utilisation patterns. We acknowledged this, in part, in the discussion as a possible explanation for rising separation and declining bed-utilisation rates in the older patient population. We are also sympathetic to the hypothesis that there may be a process of substitution of same-day separations for multi-day separations. However, data relating to bed availability are not readily available, and thus could not be included in our study. Our article was designed to highlight different trends between age groups, which have not previously been reported. Now that these trends have been identified, further research and analysis is required to fully explain them, with a view to supporting an intelligent strategy to prepare for future population ageing.

Len C Gray · Stephen J Duckett

Paddy A Dewan Head of Paediatric Surgery, Sunshine Hospital, PO Box 152, Parkville, VIC 3052. Paddy.dewanATwh.org.au To the Editor: Three recent articles in the MJA about complaints by patients attending hospital, 1 attitudes of hospital staff toward incident reporting2 and whistleblowing3 show that complaints are common, that cultural change is needed to allow staff to understand that a complaint from a patient or staff member should be viewed as an opportunity for change, and that quality assurance sometimes relies on whistleblowers but does not always appreciate their efforts. Faunce and Bolsin report on three whistleblower incidents,3 but fail to mention one at the Royal Children’s Hospital, Melbourne, in which I was involved. Attempts to highlight deficiencies in delivery of paediatric surgical care and concerns about the response to adverse events were managed with threatening tactics (of dismissal) by the division of surgery. This was followed by a hospital board investigation that, in my opinion, had neither the skill mix nor the terms of reference to adequately investigate the quality of care or the bullying. The subsequent investigation by the Department of Human Services involved narrowly focused terms of reference and failed to consider outcomes in some circumstances, thereby facilitating the “shooting of the messenger”. Current legislation does not effectively allow for dealing with threatening behaviour in the workplace, particularly when the refusal to look at complaints and adverse events in a productive manner goes well beyond the confines of the hospital involved. The Community Advisory Committee parliamentary enquiry was held in camera, with evidence being kept from the public. Worksafe legislation on bullying does not deal well with the complex situations that arise in the healthcare industry.4 The Colleges and other professional bodies, such as the AMA and the Medical Boards, need to take a proactive rather than a reactive role if further whistleblower incidents are to be avoided. I concur with the statement of Faunce and Bolsin that: “Even after substantiation of their allegations, the whistleblowers . . . received little respect and support from their institutions or professions”.3 From personal experience, I am very aware of the lack of support that stems from an ethos wary of public criticism, and the reactive bullying to which the whistleblower is often subjected. Until the culture of healthcare focuses on quality and caring, whistleblower sagas will continue to occur.

Paddy A Dewan

Luke R Bereznicki,* Shane L Jackson,† Gregory M Peterson‡ * PhD Candidate, † Research Fellow, ‡ Professor of Pharmacy, Unit for Medication Outcomes Research and Education, University of Tasmania, Private Bag 26, Hobart, Tasmania 7001. lberezniATutas.edu.au To the Editor: If a new drug such as ximelagatran is to be considered as a replacement for warfarin in preventing the thromboembolic complications associated with atrial fibrillation (AF), drug cost becomes an important issue. Brighton’s recent article in the Journal, 1 while comprehensive, does not discuss the cost-effectiveness of ximelagatran treatment. Ximelagatran was approved in several European countries for the prevention of venous thromboembolism associated with orthopaedic surgery. The cost of the drug for this indication (24 mg given twice daily) is 4.5 euros (A$7.7) per day.2 This represents the best available estimate of the cost of using ximelagatran for AF, although the dose is higher in AF (36 mg twice daily), and there are limitations in applying the drug cost in one country to another country. Routine monitoring of the antithrombotic effect of ximelagatran (ie, international normalised ratio [INR] testing) was not conducted in clinical trials. While this is potentially advantageous, frequent testing of alanine aminotransferase (ALT) levels is recommended at baseline and monthly for the first 6 months of therapy, every second month for the remainder of the first year, and every third month thereafter, for safety reasons.3 This is because some patients taking ximelagatran will develop elevated ALT levels (about 6.1% of patients to greater than threefold normal, and 3.4% to greater than fivefold normal) when ximelagatran therapy is commenced.3 The costs of INR and ALT tests are very similar (about $25 and $22, respectively). Although INR monitoring may be more frequent with warfarin than ALT testing with ximelagatran, the cost difference associated with therapeutic monitoring would remain far less than the likely cost of ximelagatran. We estimate the cost associated with treating 1000 patients with AF with ximelagatran instead of warfarin for 1 year, taking into account drug costs, monitoring costs and the slight difference in major bleeding rates, to be about $2.4 million (Box). A United States Food and Drug Administration advisory committee has recently raised concerns about the safety of ximelagatran (after episodes of severe liver damage), and has recommended that it not be granted any indication for use without further safety data. In particular, ALT monitoring did not prevent 3 deaths attributable to ximelagatran-associated hepatocellular necrosis.3 In light of the recent withdrawal of rofecoxib (Vioxx; Merck Sharp & Dohme), warfarin carries the intangible benefits of a long and proven track record. It certainly requires careful management and ongoing monitoring, but healthcare resources might be better spent on improving the use of warfarin rather than paying substantially increased costs for a drug with similar efficacy and an uncertain safety profile. Estimated costs of treating 1000 patients with atrial fibrillation (AF) with ximelagatran or warfarin for the first year of therapy. Ximelagatran* Warfarin† Total cost $2 803 821.00 $106 800.00 Cost per patient $2 803.82 $106.80 Monitoring Test (frequency/year) ALT (10)‡ INR (20)§ Total cost $217 000.00 $507 000.00 Cost per patient $217.00 $507.00 Major bleeding¶ Annual incidence** 1.6% 2.2% No. of expected events 16 22 Total cost $38 730.00 $53 253.00 Ischaemic stroke†† Annual incidence‡‡ 1.6% 1.6% No. of expected events 16 16 Total cost $101 936.00 $101 936.00 Overall cost Total $3 161 487.00 $768 989.00 Per patient $3 161.49 $768.99 Cost difference compared with warfarin Total $2 392 498.00 — Per patient $2 392.50 — ALT = Alanine aminotransferase. INR = International normalised ratio. * Cost of giving ximelagatran (24 mg twice-daily) to prevent venous thromboembolism post-surgery (German data; the dose for prevention of thromboembolism in AF is 36 mg twice-daily).3† Cost of warfarin taken from the Australian Pharmaceutical Benefits Scheme, December 2004. ‡ Monitoring cost derived from the cost of conducting ALT testing (Medicare Benefits Schedule, December 2004) according to the manufacturer’s directions (tests at baseline, monthly for the first 6 months, 2-monthly for remainder of the first year). § Cost derived from Medicare Benefits Schedule (December 2004) based on a frequency of 20 tests per annum. ¶ The cost of a hospital admission caused by a major bleed was $2420.60 in Australia for the years 2002–2003 (estimate based on 2002–2003 public hospital data).4 Intracranial haemorrhage may be associated with significant ongoing costs, but a smaller proportion of major bleeding incidents. ** No significant difference between warfarin and ximelagatran in either SPORTIF III5 or V;6 statistically significant when data from both trials were combined at P < 0.05. †† Cost ($6371) taken from the NEMESIS study7 and covers acute admission to an Australian hospital with ischaemic stroke only; this is an underestimate of the ongoing costs associated with ischaemic stroke. ‡‡ No significant difference between warfarin and ximelagatran in SPORTIF III5 and V;6 no significant difference when data from both trials were combined at P < 0.05.

Luke R Bereznicki · Shane L Jackson · Gregory M Peterson

Donald B Reid Co-convenor, Colleague of First Contact PO Box 896, Bridgetown, WA 6255 dbreidAThotlinks.net.au To the Editor: Thank you for your in-depth look at some of the concerns in doctors’ health in the October 2004 issue of the MJA. 1 I believe it would have been useful to include in the issue some practical information for doctors wanting to seek help, either for themselves or for a colleague. The attached table of contact phone numbers does not cover every state and territory, but it is a starting point. The services offered are confidential, and can be anonymous if desired. In Western Australia, the contact can include access to a list of doctors willing and able to be GPs for their colleagues. Further information is available on the Doctors’ Health Advisory Service website <www.doctorshealth.org.au>. Editor’s note: The AMA website also has a very useful “Doctors’ Health Database” at <www.ama.com.au/web.nsf/tag/doctors-health-database>. Australasian Association of Doctors’ Health Advisory Services (DHASs): helplines for doctors Victorian Doctors’ Health Programme (VIC) (03) 9495 6011 DHAS (SA) (08) 8273 4111 Colleague of First Contact (WA) (08) 9321 3098 DHAS (NSW) (02) 9437 6552 DHAS (New Zealand) (04) 471 2654 DHAS (QLD) (07) 3833 4352 DHAS (TAS) (03) 6223 2047 (in hours) (03) 6235 4165 (after hours)

Donald B Reid

Max Kamien Emeritus Professor, Senior Research Fellow, Discipline of General Practice, University of Western Australia, Perth, WA mkamienATcyllene.uwa.edu.au To the Editor: Over the past two years, the Journal has pointed out the health hazards and the lack of logic in the Health Insurance Commission’s closure of its previously cost-effective and successful “Doctor Shopping Hotline”.1-4 But it has taken the death of a 25-year-old “prescription shopper” in Cairns, his crusading mother, a scathing report by the Queensland Coroner5 and public exposure of these problems by Mark Bannerman on ABC TV (The 7.30 Report, 22 Dec 2004) for discernible action to occur. On that program, the Federal Minister of Health and Ageing promised that a “Prescription Shopper Line” would be up and running by the end of January 2005, and indeed it was activated on 31 January. This leaves two outstanding issues. The first is for the Health Insurance Commission to engage in an open exercise of mutual education by clearly reviewing its process of thinking in closing the previously successful Doctor Shopping Hotline and its lack of urgency in reinstituting its proposed better and broader successor.6 The second, and more important, issue is in understanding the underlying factors and thought processes of those doctors whom prescription shoppers describe as an “easy touch”. 7,8

Max Kamien

Ursula Bayliss,* Christopher Cowell,† James Hong,‡ Veronica Wiley,§ Bridget Wicken¶ * Clinical Nurse Consultant, §Principal Scientist, ¶ Clinical Director, NSW Newborn Screening Programme, † Head, Institute of Endocrinology & Diabetes, The Children's Hospital at Westmead, Westmead, NSW 2145; ‡ Paediatrician, North Gosford Medical Centre, North Gosford, NSW. bridgetwATchw.edu.au To the Editor: We report an acute presentation of congenital hypothyroidism in a child almost 6 years old. The condition was not detected by newborn screening. Screening of all neonates started in New South Wales in July 1977, with thyroid stimulating hormone (TSH) being measured in dried blood spots taken from a heel-prick blood sample (currently at 2–3 days of age). A whole-blood TSH level of 40 mIU/L or above triggers a request for full thyroid function testing, whereas with a level of 20–39 mIU/L a second sample is requested. We have screened over 2.3 million babies and detected 690 babies with congenital hypothyroidism. Ten babies with dyshormonogenesis or ectopic thyroid tissue had normal results and were missed by the screening test. Since screening started, “juvenile hypothyroidism” not associated with thyroid antibodies has all but disappeared. A healthy girl aged 5 years 11 months presented with acute dysphagia and drooling. There were no previous dysphagic symptoms. Initially, epiglottitis was suspected; however, at endoscopy a lingual thyroid was visualised at the base of her tongue, and this was confirmed by a technetium scan. She had normal growth and development, with both height and weight at the 50th centiles, a pulse rate of 90 beats/min, and normal deep tendon reflexes. The whole-blood TSH level at newborn screening on Day 3 was 40 mIU/L (reference range [RR], < 20 mIU/L). Thyroid function testing at another hospital on Day 10 showed a serum TSH level of 16.6 mIU/L and a serum free thyroxine (FT4) level within the normal range (12 pmol/L; RR, 11–30 pmol/L). These results were interpreted as normal, whereas, in fact, the TSH level was above the reference range for 10 days of age (< 10 mIU/L), although within the reference range for 2–7 days. On the patient’s admission for treatment of acute dysphagia, the TSH level was 10.9 mIU/L and the FT4 level was 18 pmol/L. A diagnosis was made of compensated hypothyroidism secondary to the ectopically placed lingual thyroid. Thyroxine treatment was commenced on diagnosis, and regular follow-up arranged. Three months after the start of treatment, the results of thyroid function tests (FT4, 17 pmol/L; TSH, 2.7 mIU/L) were within the normal range. Acute presentation of a lingual thyroid is most unusual.1 This case emphasises that further investigations must be performed when thyroid function test results are equivocal. Unfortunately, the thyroid status was considered normal because the FT4 value was within the normal range. All babies whose TSH results remain elevated while the FT4 levels are normal should have a thyroid scan, as we recommend when reporting results.

Ursula Bayliss · Christopher Cowell · James Hong · Veronica Wiley · Bridget Wicken

Emma J Best,* Monica M Lahra,† Pam Palasanthiran‡ * Paediatric Infectious Diseases Fellow, † Microbiology Registrar, Neonatal Medicine, Royal Prince Alfred Hospital, Sydney, NSW. ‡ Infectious Diseases Physician, Sydney Children’s Hospital, Level 4, High Street, Randwick, NSW 2031; PalasanthiranpATsesahs.nsw.gov.au To the Editor: Pasteurella multocida is an oral commensal of domestic pets known to be an opportunistic human pathogen after traumatic animal contact. The most common infections in humans are skin and pulmonary infections. This report outlines a case of P. multocida meningitis, which has not previously been reported in Australia. A 19-day-old girl presented with a 12-hour history of fever and poor feeding. Her temperature was 39.5°C, and she was irritable, with no localising signs or skin lesions. A full septic screen was performed. Cerebrospinal fluid (CSF) showed a neutrophilic pleocytosis and gram-negative coccobacilli. She was treated with intravenous cefotaxime and gentamicin. Within 24 hours both CSF and blood cultures showed growth of gram-negative bacilli. The initial Gram stain, growth on chocolate agar and positive oxidase and catalase tests were suggestive of a Haemophilus species. However, further biochemical tests revealed the organism to be P. multocida. The infant made an excellent clinical recovery, with normal neurological and growth assessments at 6 and 12 months. The family owned two cats but reported no contact between their baby and the pets. A single tonsillar swab performed on each cat by a veterinarian 10 days after the baby’s presentation failed to isolate Pasteurella species. The family elected to keep the pets. Pasteurella meningitis occurs at extremes of age, in the immunocompromised (associated with liver cirrhosis, renal disease and haematological malignancies) and after traumatic head injury.1 Infants aged under 1 year account for almost half the cases of P. multocida meningitis. On review of the literature, we found 37 reported cases of P. multocida infection in infants (Box).1-5 In more than three-quarters of these cases, there was known contact with household animals — in more than half of these contact was non-traumatic (licking or presumed handling of the pet). Molecular studies in one of the cases with no history of traumatic contact confirmed that P. multocida isolates from pet and infected child were indistinguishable.2 This infection is unusual, and, given the popularity of household pets, the risk appears low. However, this case highlights the relative immunocompromise of newborn infants, and is a reminder of the importance of hand hygiene and preventing contact between newborn infants and pets. Details of 38 case reports of invasive Pasteurella multocida infection in infants (including current case)1-5 Mean age (range) 2.6 months (1 day– 11 months) Type of infection Meningitis 30 (79%) Puerperal sepsis, chorioamnionitis 7 (18%) Bacteraemia (postnatal) 1 (3%) Nature of animal contact Traumatic (scratch, bite) 9 (24%) Non-traumatic 22 (58%) Unknown 7 (18%) Type of animal (n = 31) Cat 16 (52%) Dog 11 (35%) Both 4 (13%)

Emma J Best · Monica M Lahra · Pam Palasanthiran

Megan L Counahan,* Ross M Andrews,† Rick Speare‡ * Surveillance Manager, Communicable Diseases Section, Department of Human Services, Level 17/120 Spencer Street, Melbourne, VIC 3000; † Senior Research Fellow, Centre for International Child Health and Clinical Epidemiology and Biostatistics Unit, Murdoch Children’s Research Institute, Melbourne, VIC; ‡ Professor, School of Public Health and Tropical Medicine, James Cook University, Townsville, QLD. megan.counahanATdhs.vic.gov.au To the Editor: For parents to treat head lice (pediculosis) effectively in their children, it is necessary for them first to recognise it is present. We conducted a school-based screening program involving 1838 children from 16 randomly selected primary schools in Victoria between May and October 2001 (participation rate, 55.2%).1 As part of this program, we compared a written report from parents on their child’s pediculosis status against results of our examination (7–10 days later). We examined the scalp and hair of each child for lice (“crawlers”) or viable louse eggs (“active infestation”) and dead or hatched louse eggs (“inactive infestation”) using white hair conditioner, which makes lice and eggs easier to see with the naked eye, and a fine-toothed head lice comb. This is a validated, accurate and sensitive diagnostic technique.2 Parents were unaware of the proposed screening date, and the study team was unaware of the parents’ reports. We compared parental report about pediculosis against results of our screening for 1179 children who could be matched with completed questionnaires. Overall, 149 children (12.6%) had active pediculosis, but parents reported head lice in only 36 children (3.0%) (Box 1 and Box 2). These comprised 24 of the 149 children with confirmed pediculosis (16%), and another 12 children who did not have pediculosis when examined. The positive predictive value (PPV) of parental report was 66.6%, indicating that parental reporting was not a reliable indicator of pediculosis. An implication of the low PPV is that some children may have been unnecessarily treated with insecticide for an infestation they did not have. On the other hand, a substantial proportion of children with head lice had not been identified by their parents and could contribute to ongoing transmission within schools. While it was possible they were infected subsequent to completion of the questionnaire, this seemed unlikely, as 72% were found to have multiple louse eggs, indicating a longer duration of infestation than the 7–10 days since the questionnaire was completed. Our study clearly demonstrates that parental reporting of head lice in their children is unreliable. We suggest several possible reasons: parents did not see the head lice, did not recognise them, or used a diagnostic technique with a lower sensitivity than the method we chose, such as examining dry hair. It is also possible that parents were inhibited from reporting pediculosis by the possible repercussions, such as exclusion of the child from school. Indeed, children whose parents failed to answer the question about pediculosis had a higher prevalence of head lice than those whose parents answered. Nevertheless, parents’ management of pediculosis is likely to improve if a sensitive detection method is used. To improve the sensitivity of parental diagnosis and control of head lice we recommend that parents be instructed to screen their children weekly using hair conditioner and combing. 1 Screening results compared with parental report Pediculosis by parent report Pediculosis on examination Yes No Total Yes 24 12 36 No 99 969 1068 Unsure 26 49 75 Total 149 1030 1179 2 Sensitivity and specificity of parental report versus screening Pediculosis prevalence By parental report 3.0% (36/1179) By screening 12.6% (149/1179) Sensitivity 16.1% (24/149) Specificity* 98.8% (1018/1030) Positive predictive value 66.6% (24/36) Negative predictive value* 89.0% (1018/1143) * Specificity and negative predictive value were calculated after grouping “unsure” and “no” responses.

Megan L Counahan · Ross M Andrews · Rick Speare

Fiona M Wood,* Bess V Fowler,† Daniel McAullay,‡ Jocelyn R Jones§ * Plastic Surgeon and Director, † Epidemiologist, Burns Service of Western Australia, Royal Perth Hospital, GPO Box X2213, Perth, WA 6847; ‡ Senior Policy Officer, § Manager, Office of Aboriginal Health, Health Department of Western Australia, Perth, WA. FionawATmccomb.org.au To the Editor: People with major burn injuries (50% total body surface area or more) now have an improved likelihood of survival with the implementation of aggressive treatment regimens, including supportive therapy, nutrition, and advances in the control of sepsis. Technological developments and treatments, particularly expedient wound closure, early surgical debridement, covering of large burn wounds, early skin repair,1 use of cultured epithelial autograft2 and ventilation,3 have also contributed to improved outcomes for people with these injuries. In Australia, there are inequities in access to health services which may particularly affect Aboriginal people.4 We therefore undertook a retrospective, observational study to compare the incidence of major burn injuries, clinical and demographic characteristics of patients with burns, as well as treatment and outcomes between Aboriginal and non-Aboriginal children and adults in Western Australia between 1992 and 2002. Potential cases were identified using data linkage from the Western Australian Department of Health. Raw data came from clinical records. Of the 84 people identified with major burn injuries, nine were Aboriginal (11%) and 75 were non-Aboriginal (89%). The incidence of major burn injury among Aboriginal people is greater than expected, as data from 2001 show that 3.5% of the WA population are Aboriginal. Aboriginal people with major burn injuries were younger than non-Aboriginal people with those injuries (mean, 21 v 35 years). Eight of the nine Aboriginal people (89%) had flame-only burns, compared with 33 of 75 non-Aboriginal people (44%). No statistically significant difference was seen between the groups in the percentage of total body surface area affected, provision of treatment (including number of operative procedures, applications of cultured epithelial autografts, units of blood products used, nasogastric feeds, and antibiotic doses) or length of hospital stay. We found that, although a greater percentage of Aboriginal people sustained major burn injuries, after this group entered the hospital system they experienced comparable levels of service and outcomes to non-Aboriginal people. Further research into burn care is warranted, from culturally and environmentally appropriate prevention through to critical appraisal of outcomes.

Fiona M Wood · Bess V Fowler · Daniel McAullay · Jocelyn R Jones

Huy A Tran Director, Department of Clinical Chemistry, Hunter Area Pathology Service, John Hunter Hospital, Locked Bag No. 1, Hunter Region Mail Centre, New Lambton Heights, NSW 2310. huy.tranAThunter.health.nsw.gov.au To the Editor: I read with interest the recent review of Paget’s disease by Walsh.1 I would recommend that calcium and phosphate levels should be included in the initial biochemical assessment, as both tests are cheap and readily available. As Paget’s disease predominantly afflicts the older population, coexisting vitamin D deficiency is likely. Low (but within the normal range) calcium and phosphate levels may support this diagnosis. Conversely, hypercalcaemia, a rare event in Paget’s disease except in prolonged immobilisation,2 may indicate primary hyperparathyroidism, which is significantly associated with Paget’s disease,3 or, less commonly, metastatic bone disease. Both these conditions have prognoses and management distinctly different from those of Paget’s disease. Serum total alkaline phosphatase levels may not be elevated in 15% of active Paget’s disease.4 While bone-specific alkaline phosphatase level is more useful in these situations, this test is not readily available in some laboratories and, even among those in which it is available, some only provide qualitative results, making it less useful for monitoring Paget’s disease and the response to therapy. A suitable alternative test is urinary deoxypyridinoline/creatinine ratio, which can be done either on a random urine sample or a 24-hour urine collection. In addition, the serum total alkaline phosphatase level can be spuriously low in malnourishment, and specifically in zinc deficiency,5 a frequent occurrence in elderly people. I describe here a case highlighting such a problem. A 72-year-old socially isolated widower of 8 years presented with progressively worsening pain in his right hip in the preceding 3 months. He had poor appetite and had lost 6 kg in weight, but had no symptoms of malignancy. Clinical examination showed a thin man (body mass index, 20 kg/m2), who was otherwise normal with no features of zinc deficiency. A plain x-ray of the pelvis showed bilateral osteosclerosis. His total alkaline phosphatase level was 28 U/L (reference range, 35–110 U/L). Other investigations for metabolic bone disease gave normal results, including one for vitamin D level. Among other nutritional parameters, his zinc level was 5.2 mol/L (reference range, 10.0–18.0 mol/L). A computed tomography scan of the thorax and abdomen showed no evidence of malignancy, and a bone scan was consistent with Paget’s disease. A zinc supplement was prescribed and his diet optimised. At 6-week review, the serum zinc level had improved to 12.5 mol/L, but the serum total alkaline phosphatase level was 250 U/L. This confirmed that the patient’s acquired hypophosphatasia was secondary to zinc deficiency, with zinc being a critical cofactor for alkaline phosphatase activity.4 In light of the “correct” total alkaline phosphatase level, the patient was given intravenous pamidronate, with resulting marked resolution of his symptoms, including a 5-kg weight gain and normalisation of total alkaline phosphatase level. Although this case is unusual, it nevertheless highlights the need to consider occult and coexisting nutritional morbidities in an elderly population.

Huy A Tran

Stephen N Bolsin Director, Division of Perioperative Medicine, Anaesthesia and Pain Management, Geelong Hospital, Ryrie Street, Geelong, VIC 3220. stevebATbarwonhealth.org.au To the Editor: Two recent articles in the Journal highlight the need to re-evaluate the collection of performance data in Australian healthcare, as well as the uses and analysis of these data.1,2 Individual report cards are an extremely good and ethically mandated means of monitoring performance, especially when the information is given to patients as part of an informed-consent process.2 However, it is possible to provide more valuable analyses than simple crude complication or mortality rates. Cusum (cumulative summation) analysis was developed for industrial quality assurance to monitor production processes and detect subtle deviations from a preset, defined level of achievement. It can be applied to clinical practice to identify statistically significant improvements (or decrements) in performance, using agreed definitions of “acceptable” and “unacceptable” performance levels.3,4 It can be risk-adjusted if necessary. Cusum analyses are routinely undertaken by the Geelong Hospital Department of Anaesthesia for monitoring performance of College-accredited trainee anaesthetists, and have been suggested by surgeons as a method for monitoring performance of a series of procedures.5 Although cusum analysis may seem highly threatening to many senior professionals, the support it provides and the cultural change it achieves in trainee anaesthetists have already been well documented in a unique Australian initiative.4 Modern regulatory theory describes three levels of regulation: the individual (micro), organisational (meso), and state or national (macro) levels. The personal professional monitoring program based on personal digital assistants (PDAs) and cusum analysis that was introduced for accredited trainee anaesthetists by Geelong Hospital operates at all these levels. It encourages reflection on individual performance by accredited trainees in a supported environment; organisational review by the supervisor of training within a clinical governance framework; and College supervision, collation and endorsement as part of a national training program. The fact that the reporting structures inherent in this PDA-based model conform to these highest standards of regulatory theory and clinical governance confirms that the required professional change recommended by Irvine1 can be easily achieved through mechanisms already operating in Australian hospitals. The model also achieves cultural change in the trainees and the highest incident reporting rate in modern healthcare (96.7%–100% voluntary reporting of critical incidents occurring in their practice). 6 These two factors should mandate the wider introduction of the PDA-based program in Australian hospitals if the profession and the industry are to be taken seriously on this issue.

Stephen N Bolsin

David G E Caldicott,* Cameron Duff† * Convener, Royal Adelaide Designer Drug Academic Research (RADAR) Unit, Emergency and Trauma Department, Royal Adelaide Hospital, Adelaide, SA; † Director, Centre for Youth Drug Studies, Australian Drug Foundation, Melbourne, VIC. dcaldicoATmail.rah.sa.gov.au To the Editor: Threatened with a surge of Athenian, one-eyed jingoism regarding Australian drug policy that the recent conference report by Ritter et al1 might have elicited, we offer a warning. Australia has achieved much to be proud of with its harm-reduction policies in recent decades. As Ritter et al attest, Australian researchers and practitioners are “leading the way” in generating political and community support for greater harm-reduction efforts. However, the implementation of real harm-reduction measures can hardly be described as “Olympian” under the current administration. Real Australian successes in the area of harm reduction have arguably occurred despite federal and state policy rather than because of it. Individual positions taken by clinicians such as Dr Alex Wodak, in the face of severe opposition and at times intimidation, account for much of this success. The sad reality is that the “Tough on drugs” approach currently pursued in Australia seems doomed to soon fuse with the Americans’ globally denounced “War on drugs”. Real harm reduction can hardly be said to have been given a “fair go” in the past decade, with 85% of the total drugs budget in Australia committed to law enforcement — the paltry remainder split between research and treatment.2 While harm reduction strategies have been widely implemented in response to the problems associated with injecting drug use, such strategies have not been nearly as popular in our responses to other types of drug use. Harm reduction is yet to be embraced as an effective response to the problems associated with the so-called “party drugs”, despite mounting evidence of its efficacy in Europe. Any premature triumphalism on the subject of harm reduction ought to be eschewed. Australia’s recent heritage is quietly being betrayed at a federal level. A little-publicised federal report recently called for a move away from harm minimisation and harm reduction.3 This is despite evidence indicating that functional drug use is emerging as “normal” rather than deviant behaviour among many Australians. 4 Clearly, we must redouble our efforts to ensure that harm reduction becomes a central part of Australia’s public policy stance. In an era in which it often seems easier to succumb to the whims of our larger neighbours than to resist them, it becomes even more important that doctors and health professionals, and particularly the younger generation of researchers, stand firm. We are, after all, standing on the shoulders of giants.

David G E Caldicott · Cameron Duff

Alison J Ritter,* Alex D Wodak,† J Nick Crofts‡ * Head of Research and Deputy Director, Turning Point Alcohol & Drug Centre, 54-62 Gertrude Street, Fitzroy, VIC 3065; † Director, Alcohol & Drug Service, St Vincent’s Hospital, Sydney, NSW; ‡ Deputy Director, and Director, The Centre for Harm Reduction, Macfarlane Burnet Institute for Medical Research and Public Health, Melbourne, VIC. alisonrATturningpoint.org.au In reply: Caldicott and Duff raise a very important question: is the federal government intending to soon terminate Australia’s national drug policy of harm minimisation? This view can be supported by numerous and recent unambiguous speeches by senior government ministers, including the Prime Minister. The government would like Australians to believe that it is implacably opposed to a harm-minimisation approach to illicit drugs. However, a different view appears when federal government funding allocations are examined. For example, the government allocated $215 million to the Illicit Drug Diversion Initiative over 4 years (in addition to a previous allocation of $221 million).1 The intention of this Initiative is to divert selected drug offenders from the criminal justice system to drug treatment. These efforts are, in our view, highly commendable, reducing the use of expensive and largely ineffective custodial punishment and increasing the use of less expensive and more effective drug treatment. They are, however, irreconcilable with a “zero tolerance” or “Tough on drugs” approach to illicit drugs. Another example is AusAID’s recent leadership in the introduction of harm-reduction measures to control HIV epidemics among injecting drug users in Asia. It is also worth noting that the Ministerial Council on Drug Strategy (Australia’s paramount official drug policy-making body since 1985) has repeatedly and recently endorsed a national drug policy of harm minimisation. The present federal government, unlike its predecessor, frequently and stridently attacks emotionally charged symbols of harm reduction, such as the proposed prescription heroin trial or the Medically Supervised Injecting Centre in Sydney. However, as the allocation of substantial funding to the Illicit Drug Diversion Initiative demonstrates, in most respects it is very much a case of business as usual.

Alison J Ritter · Alex D Wodak · J Nick Crofts

Barry N J Walters,* Sivanthi Senaratne† * Physician in Obstetric Medicine, University of Western Australia, Subiaco, WA; † Registrar in Obstetric Medicine, Sir Charles Gairdner Hospital, Perth, WA. banjowATiinet.net.au To the Editor: The “Consensus statement on diabetes control in preparation for pregnancy”1 presents a counsel of perfection that is, regrettably, a cry in the wilderness in this most imperfect of all imperfect worlds. None will deny that the glycaemic target specified would represent a wonderful achievement in a woman attending in early pregnancy. Unfortunately, we are far from achieving this goal, for a variety of reasons. Firstly, and most importantly, “preparation for pregnancy” is unusual. At our clinic (King Edward Memorial Hospital, Perth), where we see up to 90 women each year whose diabetes (types 1 and 2) antedated pregnancy, fewer than 15% have been seen for preconceptional counselling, and a similar proportion have an HbA1c level below 7%. Moreover, at the same hospital, the rate of unplanned pregnancy in the general antenatal clinic exceeds 50%. Studies elsewhere have shown that the rate of unplanned pregnancy in women with diabetes is the same or greater,2 and this figure accords with our own observations. Finally, in many women of reproductive age with diabetes, glycaemic targets as recommended by the Diabetes Control and Complications Trial Research Group3 and the recent consensus statement1 are infrequently met. One study of young adults in a type 1 diabetes clinic4 revealed that “. . . only 3.4% . . . achieved an average HbA1c of less than 7% during 11 years of study . . . despite regular specialist physician, specialist diabetes nurse and dietitian input and repeatedly following up failed appointments”. Australian findings are probably not substantially better in this group. Unfortunately, levels espoused by the above authorities are difficult to attain outside the sequestered environment of a clinical trial. Thus, the realisation of the St Vincent declaration,5 which sought to normalise obstetric outcome for women with diabetes, has proven elusive. Statements that recommend ideal levels of glycaemic control before pregnancy, while laudable, are unlikely to improve the high rates of miscarriage, congenital abnormality, preterm birth and perinatal mortality that we observe. What, then, can we do? The most important intervention in the care of fertile women with diabetes is effective contraception, with the aim of preventing pregnancy until adequate control of diabetes has been achieved. Numerous studies have shown that women who plan their pregnancy and attend for preconceptional care demonstrate better periconceptional glycaemic control and, accordingly, lower rates of adverse events in pregnancy.6 Only by raising the matter of family planning repeatedly with all our younger female patients can we hope to avoid the disappointing observation of an unplanned pregnancy, with all its adverse consequences for the woman with diabetes and her baby.

Barry N J Walters · Sivanthi Senaratne

H David McIntyre,* Jeff R Flack† * Director, Endocrinology and Obstetric Medicine, Mater Health Services, South Brisbane, QLD; † Director, Diabetes Centre, Bankstown–Lidcombe Hospital, Bankstown, NSW. David. McIntyreATmater.org.au In reply: Walters and Senaratne raise two important points — that specific preparation for pregnancy is the exception rather than the rule, and that many people with diabetes (including women of childbearing age) demonstrate poor glycaemic control. As a first step to improving this situation, we believe it is reasonable to set a goal. We sought to alert clinicians, especially those with limited experience in this area, to the importance of optimal glycaemic control in preparation for pregnancy. We hope that the consensus statement represents a “signpost” rather than a forlorn “cry in the wilderness”. Many opinions were sought in developing the consensus statement. Some, for reasons similar to those given by Walters and Senaratne, thought the “HbA1c < 7%” goal too strict, while others believed it to be far too lax. In the end, we agreed to include this figure, with the proviso that the level of glycaemia should be the best achievable for each individual patient. We must educate women of childbearing potential with diabetes and their caring health professionals about the need for preconceptional diabetes control as part of their care. In some clinical circumstances, such as assisted reproduction, the timing of conception is actually determined by the treating doctor. In this setting, optimal glycaemic control should be a prerequisite for active treatment. Rather than taking a nihilistic view, clinicians should devote their combined talents and energy to providing optimal pre-pregnancy care to those women with diabetes who do plan their pregnancies, to promoting pre-pregnancy care (including contraception) for those who currently do not, and to assuming an advocacy role in promoting access to and funding for intensive treatment programs for all people with diabetes.

H David McIntyre · Jeff R Flack

Edzard Ernst Director, Department of Complementary Medicine, Peninsula Medical School, Universities of Exeter and Plymouth, 25 Victoria Park Road, Exeter, Devon EX2 4NT, UK. Edzard. ErnstATpms.ac.uk To the Editor: The article by Myers and Cheras1 is a good attempt to evaluate the safety of complementary therapies. However, I have one problem with it, which may be significant. The authors rightly state at the outset that “the critical issue in assessing any therapy is its risk to benefit”. At the end of their article they consider the “wider public safety issues” and point out that the risks of complementary and alternative medicine (CAM) are minimal compared with those of conventional therapies. I think this is not quite logical. Comparing risks of therapies does not make sense, because the “critical issue” is the risk–benefit profile. Comparing the risks and benefits of, for instance, acupuncture for severe pain versus opioids for the same type of pain would, I think, favour the latter over the former, even though the risks of acupuncture are minimal compared with those of opioids. In other words, comparing absolute risks of treatments is tempting, but meaningless.

Edzard Ernst

Stephen P Myers,* Phillip A Cheras† * Director, Australian Centre for Complementary Medicine Education and Research, Southern Cross University, PO Box 157, Lismore, NSW 2480; † Deputy Director, Australian Centre for Complementary Medicine Education and Research, University of Queensland, QLD. smyersATscu.edu.au In reply: We stand by our statement that “the critical issue in assessing any therapy is its risk to benefit”. 1 Ernst appears to miss the point made in the subsequent two sentences — that this assessment is available for conventional medicine, but not yet for complementary and alternative medicine (CAM) therapies and products. In the absence of such data, society must be able to make an assessment of health practices and medicines based on their overall risk. Ernst himself has made significant contributions to this literature, and in fact three of his articles2-4 were cited in our review. The second criterion of the Australian Health Ministers’ Advisory Council Criteria for Assessing the Need for Statutory Regulation of Unregulated Health Occupations asks the question: Do the activities of the occupation pose a significant risk of harm to the health and safety of the public? Answering this question for the currently unregulated CAM professions involves consideration of the “wider public safety issues”. This forms part of the determination about the appropriateness of occupational regulation. The two comments juxtaposed by Ernst to make his point are not mutually exclusive. While awaiting the risk–benefit analysis, society will need to make decisions about the absolute risks.

Stephen P Myers · Phillip A Cheras

Norman Shum Psychologist and Physician, Psychological Medicine, Eastwood, SA. menciusATsenet.com.au To the Editor: Patient arrogance definitely does exist and can complicate the process, described by Ellard, of “diagnosis, prognosis and therapeutics”.1 I believe this state of affairs has arisen for two reasons. Firstly, from the evolution of “informed consent” linked to “patients’ rights” — principles that need no elucidation. Secondly, as a consequence of the explosion of media and technology. Television has given us a surge of medical programs, especially of the so-called “reality” type, and technology has made information easily available on the Internet. Unfortunately, patients become Internet surfers and surfers become patients. When they then present with symptoms, it is often armed with some knowledge — albeit of dubious quality and veracity. If the doctor does not provide a very accepting ear to these proffered “medical data”, the patient often stops listening, becomes intransigent, and tends to prefer the media- or technology-generated opinion, including the suggested treatment for the semi-self-diagnosed disorder or illness. I am reminded of one of Groves’ subtypes of “hateful patients”, namely “entitled demanders”. He wrote, “. . . they use intimidation, devaluation and guilt induction. . . . The patient may try to control the physician. . . . Such patients often exude a repulsive sense of innate deservedness as if they were far superior to the physician.”2 In my own practice, I had one such patient who would arrive and immediately intimidate my secretary by literally throwing his Medicare card on the desk in front of her and ordering her to turn off the radio that was tuned quietly to ABC FM. She has now retired, but, even 2 years later, says she will always remember him! It takes considerable tact and skill to deflect and reduce the hostility of an arrogant patient so that he or she can ultimately benefit from the consultation. Perhaps it is best done by keeping in mind the fundamental principle primum non nocere.

Norman Shum

Zelman Freeman Retired Physician, 1/43 New South Head Road, Vaucluse, Sydney, NSW 2030. zelfreeATbigpond.net.au To the Editor: You recently commented on the closure of public hospital common medical dining rooms in the 1960s and 1970s.1 Traditionally, these common rooms were a place where residents and senior medical staff met. The closure of these facilities had more serious consequences than the loss of “breaking bread”, as you quaintly put it. The daily meeting between residents ending their shifts and those starting work allowed discussion about the sickest patients — after the dining room closure, such discussions became much less effective. Helpful comments and advice from senior staff were no longer available. New medical advances and the strengths and weaknesses of the system were previously subjected to keen analysis, but all this medical “shop talk” was lost. More importantly, the closure of medical dining rooms contributed greatly to the loss of hospital esprit de corps, which included a sense of belonging to a worthwhile institution to which most of the medical staff were sincerely dedicated. Medical dining rooms had a century-old history in the main state hospitals. I suspect that their closure had more to do with a Jacobin ideological mindset in health departments rather than being an “efficiency” move. Medical staff were not allowed to put tables together in the new refectory, as to do so might appear elitist. I remember going into the small staff room of my hospital at that time to have afternoon tea — a service provided to both lay and medical staff — only to be told by the medical administrator that “non-recoupable foodstuffs were no longer to be served to the medical staff”. Meanwhile, the cleaners in their room next door were enjoying their hospital biscuits! This was the beginning of the “doctor-bashing” era that only the older members of the public remember, and it is not unreasonable to claim that many of the public hospital problems in patient management stem from the actions of perverse individuals who undermined the cohesive and dedicated work of the medical staff, just as they did when they abolished the distinctive hospital uniforms and badges of the nurses, who had always taken pride in their own hospital traditions. A bland coloured gown was substituted to remind them that they were “health workers”. No wonder there is difficulty in recruiting new staff and building a sense of dedication to such an amorphous service. Administrators need to be reminded that good traditions should not be abolished without mature reflection on the consequences.

Zelman Freeman

William B Molloy Gynaecologist, Suite 10, Level 7, William Bland Centre, 229-231 Macquarie Street, Sydney, NSW 2000. drmolloyATbigpond.com To the Editor: I congratulate you on your column in the 1 November 2004 issue.1 For years, I have stated that it is a problem, not only in the public hospitals, but now creeping into the private hospitals, that there is no private room available for doctors to talk among themselves. This also includes the theatres, where only one room is available for both nurses and doctors, and I think this is a giant mistake. I remember that when I was a young doctor, consultations were arranged over lunch. Doctors talked to each other and everyone knew about the important cases in the hospital. It was a teaching and learning experience. In addition, in the afternoon, after one had finished work and was relaxing over the newspaper, again there was contact between doctors. At St Margaret’s Hospital, where I was the Medical Superintendent for fourteen-and-a-half years, between 1969 and 1984, I fought until the day I left to maintain these rooms. The dining room was lost, but at least there was a room where doctors could gather after they did their morning ward rounds. There was an enormous amount of work done and many opinions proffered in that room, and to this day many doctors tell me how much they miss that experience in the hospital they now attend. Isn’t there someone who can point out that, although the public health system is a shambles at present, we should not allow the private system to go down the same track? Sadly, it appears to be doing just that.

William B Molloy

Peter F Burke Surgeon, PO Box 84, Newborough, VIC 3825. burkeATvic.australis.com.au To the Editor: Somerset Maugham noted, “At a dinner party one should eat wisely but not too well, and talk well but not too wisely”.1 Your recent column lamenting the disappearance of doctors’ dining and common rooms2 precipitated a flood of warm memories of, in my case, St Vincent’s Hospital in Melbourne in the 1960s, 1970s and early 1980s. Now based in the Latrobe Valley, Victoria, I have witnessed first-hand, over almost 20 years, much grievous political and social engineering — the abject failure of the first “privatisation” of a public hospital in Victoria and, in the custom-designed “greenfields” hospital, the near-complete lack of provision of facilities for consultant medical staff, leading to their fleeting meeting in corridors and carparks. It is unlikely that C P Snow had this in mind when he wrote of “corridors of power”.3 Contemporary medical staff are indeed an amorphous lot. The clinical white coat is but a memory, and often the only way to recognise a doctor, usually dressed in a manner that would suggest forthcoming involvement in a “Clean up Australia” gathering, is the fashionably appropriate half-noose stethoscope, which, akin to a saint’s halo, confers immediate status on the bearer. Laennec, who invented the stethoscope in 1819, had surely not foreseen the commercial potential of his epochal invention.

Peter F Burke

Bruce P Waxman Medical Program Director, Surgery Program, Southern Health, PO Box 478, Dandenong, VIC 3125. b.waxmanATsouthernhealth.org.au To the Editor: Your recent experience in a staff cafeteria1 is clearly anecdotal, as are my own. I believe, however, the balance needs to be redressed. There is little point in campaigning for “return of the doctors’ common dining room”, as, at least in the public sector, there are no funds available for this campaign. I have been very impressed with the camaraderie that exists in the staff cafeteria at Dandenong Hospital, Southern Health, because medical care is now a team approach and I have the opportunity to meet with medical students, interns, house medical officers, registrars, nurses and administrators, either over a cup of coffee provided free by the Health Service, or a meal. The staff cafeteria has been a meeting place for the team, engendering a team approach to medical care which, I believe, is appropriate to champion for the future of healthcare delivery in Australia.

Bruce P Waxman

To the Editor: A recent editorial in the British Medical Journal reported advice from the UK Committee on Safety of Medicines that most types of selective serotonin-reuptake inhibitors (SSRIs) should not be used in the treatment of major depression in children.1 The editorial sparked interest in the Australian media, resulting in articles in large metropolitan newspapers with titles such as “Army of kids on antidepressants”.2 General practitioners were targeted as the cause of reported “over-prescribing”. Unfortunately, while the media drew data from the national BEACH program (Bettering the Evaluation and Care of Health; a continuing study of general practice activity3), the data presented were inflated: a “child” was defined as someone aged under 20 years (while the UK advice related to children under 18 years), and national figures were extrapolated from the upper confidence limit. Reliable estimates of GP prescribing of antidepressants to children in Australia are needed. We derived age-specific rates of antidepressants prescribed per encounter in Australian general practice for the period April 2001 to March 2004 from the BEACH data (Box 1). The data showed that children were prescribed antidepressants far less often than adults. Those aged under 12 years were rarely prescribed antidepressants. Most of those prescribed were tricyclics, which are more commonly used in management of enuresis than of depression. The media’s inclusion of 18–19-year-olds as “children” greatly increased the reported rate.2 The prescribing rate of antidepressants in children aged under 18 years was 0.47 per 100 encounters (5 per 1000 encounters), but was six times higher for 18–19-year-olds (2.82 per 100 encounters). Most antidepressants prescribed for 12–17-year-olds were SSRIs. Fluoxetine is the only SSRI currently approved for use in children in the UK.4 In Australia, caution is advised when prescribing any antidepressant to children, but venlafaxine and the SSRI paroxetine are specifically advised against.5 Nevertheless, venlafaxine and paroxetine were more often prescribed (accounting for 10% and 8%, respectively, of total antidepressants for children) than fluoxetine (5%). However, GPs provided concomitant counselling at almost 20% of contacts with children aged under 12 years where an antidepressant was prescribed, and at 40% with 12–18-year-olds (Box 2). GPs were also more likely to refer the children to a specialist than when prescribing antidepressants for adults. We do not know how many of these children have been referred to a specialist at a previous encounter, nor how often antidepressant medication is initiated by a specialist. However, it will be interesting to see whether the new advice reduces the current level of prescribing of antidepressants (SSRIs in particular) in children. 1 Antidepressant prescribing in Australian general practice, April 2001 to March 2004 Age-specific rate per 100 encounters (95% CI) Variable (ATC group)† <12 years (n = 31 869) 12–17 years (n = 11 576) 18–19 years (n = 5823) ≥ 20 years (n = 247 231) All antidepressants 0.11 (0.07–0.14) 1.48 (1.18–1.77) 2.82 (2.35–3.28) 4.18 (4.05–4.31) SSRIs (N06AB) 0.03 (0.01–0.05) 1.08 (0.82–1.34) 1.84 (1.49–2.19) 2.38 (2.29–2.46) Fluoxetine (N06AB03) 0.003 (–)* 0.08 (0.00–0.13) 0.07 (0.00–0.14) 0.28 (0.25–0.30) Paroxetine (N06AB05) 0.003 (–)* 0.13 (0.06–0.20) 0.22 (0.10–0.34) 0.48 (0.45–0.52) Other SSRIs 0.02 (0.01–0.04) 0.87 (0.63–1.12) 1.55 (1.22–1.87) 1.62 (1.55–1.69) Tricyclics (N06AA) 0.07 (0.04–0.10) 0.14 (0.07–0.21) 0.22 (0.09–0.35) 0.92 (0.87–0.97) Other antidepressants 0.006 (–)* 0.26 (0.16–0.36) 0.76 (0.49–1.02) 0.89 (0.83–0.94) Venlafaxine (N06AX16) 0 0.17 (0.09–0.25) 0.52 (0.29–0.74) 0.47 (0.43–0.51) * Insufficient observations for calculating 95% confidence intervals. † Drug group according to the World Health Organization Anatomic Therapeutic Chemical (ATC) classification. SSRIs = selective serotonin reuptake inhibitors. 2 Concomitant management provided at encounters where an antidepressant was prescribed in Australian general practice, April 2001 to March 2004 Concomitant management (% of encounters where at least one antidepressant was prescribed [95% CI]) Management <12 years (n = 34) 12–17 years (n = 171) 18–19 years (n = 164) ≥ 20 years (n = 10 137) Counselling 17.6% (4.8%–30.5%) 40.4% (32.8%–47.9%) 44.1% (36.1%–52.1%) 30.4% (29.0%–31.8%) Referral to specialist 5.9% (–)* 6.4% (2.7%–10.2%) 6.8% (2.7%–10.9%) 2.7% (2.4%–3.1%) * Insufficient observations for calculating 95% confidence intervals.

Christopher M Harrison BPsych(Hons), MSocHlth · Helena C Britt BA, PhD

To the Editor: I report a patient with splenic infarction associated with group A streptococcal sepsis that occurred post partum. Although spontaneous splenic infarcts have been associated with many types of infections, to my knowledge this is the first published report of an association with this organism. A 29-year-old woman had an unremarkable term labour and vaginal delivery of her third child. On Day 2, she felt feverish, but no abnormalities were detected on clinical examination or pelvic ultrasound examination. Over the next 24 hours, she developed abdominal pain and sweats, and appeared flushed. On Day 3, her temperature was 37.6°C, and she developed nausea and diarrhoea. Empirical treatment was begun with intravenous ampicillin and metronidazole. She developed hypotension (blood pressure, 90/60 mmHg) and an erythematous rash of the legs and diffuse erythema of the trunk, anterior thighs and face. Relevant results of laboratory investigations are summarised in Box 1. On Day 4, a vaginal swab was taken, and antibiotic therapy changed to ticarcillin–clavulanate and clindamycin on the basis of presumed toxic shock syndrome. The next day, the patient developed oedema of the hands and feet, a sore throat and sore ankles. Group A streptococcus grew from the vaginal swab. Blood cultures showed no growth, but the samples had been taken after antibiotic therapy was begun. Over the next few days, the patient’s condition improved, but on Day 9 again deteriorated, with recurrence of low-grade fever and the development of sharp, retrosternal chest pain. Computed tomography (CT) of the chest with a pulmonary angiogram revealed a small right lower-lobe opacity, suggestive of a pulmonary infarct. The CT scan also revealed multiple splenic infarcts (Box 2). Screening for thrombophilia gave normal results. She was treated initially with intravenous heparin, followed by oral warfarin for 3 months. Her clinical recovery was slow but complete. This patient had probable toxic shock syndrome caused by group A streptococcus.1 She had the non-specific features of toxic shock syndrome2 (fever, nausea, diarrhoea, rash, abnormal hepatic and renal function) and disproportionate abdominal pain as the initial symptom. The only criterion lacking for “definite” toxic shock syndrome was the isolation of group A streptococcus from a normally sterile site (it was isolated only from the vagina). Puerperal toxic shock syndrome caused by group A streptococcus is well reported,1,2 with mortality of 25%–50%.2 The patient’s clinical course was complicated by multiple splenic infarcts and a possible pulmonary infarct, thought to have developed in situ with no identifiable prothrombotic diathesis. Splenic infarction is not common and is usually associated with a haematological or rheumatological disorder.3,4 Spontaneous splenic infarcts have been associated with infections, but there is only one report of these infarcts in association with toxic shock syndrome, in that case caused by Staphylococcus aureus.5 The infarcts have been postulated to be caused by circulating endotoxin.5 1 Abnormal laboratory results Investigation Result RR White cell count (x 109/L) 11.07* 3.50–11.00 Platelet count (cells x 109/L) 63 150–450 Prothrombin time (s) 15.3 12–5 ESR (mm/h) 22 0–12 C-reactive protein (mg/L) 56 < 3 INR 1.2 0.8–1.1 Alkaline phosphatase (U/L) 298 38–126 γ-Glutamyltransferase (U/L) 95 0–30 Albumin (g/L) 18 33–48 Creatinine (μmol/L) 111 60–110 * 63% band forms. ESR = erythrocyte sedimentation rate. INR = international normalised ratio. RR = reference range. 2 Computed tomography of the abdomen Scan shows one of multiple splenic infarcts — in the lateral third of the spleen.

Adrienne Torda

To the Editor: Cokis and Faris describe an intraoperative complication detected by transoesophageal echocardiography (TOE).1 Their letter is interesting in that it describes a rare complication during aortic valve surgery, and it is provocative in that it is critical of the Department of Health and Ageing decision not to rebate TOE (except in valve repair or replacement) to anaesthetists. A rare complication is not an argument for routine monitoring. Justification for monitoring requires detailed analysis of complication rates. The number needed to monitor for this and other complications is not known. Cokis and Faris do not discuss the rate of complications from TOE, which could be similar to that of the rare complication they describe. That there is a link between efficacy and the likelihood of a Medicare rebate is yet to be shown, and the authors themselves allude to this. TOE can be performed without a rebate. This is good for patients and also for a healthcare service which is strapped for funds. There are arguably other pressing needs for Medicare funds in the healthcare system. Presumably, both doctors were remunerated for their presence at the operation. Eligibility for a Medicare rebate can be a “perverse incentive” leading to overservicing. I have seen this with monitoring with TOE. Procedures have a clinical and financial cost as well as perceived benefit. I have seen other diagnoses missed or misinterpreted because of routine use of TOE, and it has occasionally led to prolonged intensive care unit stays and other complications. None of my arguments should deny TOE a place as a useful monitoring tool. It may become as routine during cardiac surgery as central venous pressure and arterial pressure monitoring is now. Whether that happens should not depend on whether TOE is eligible for a Medicare rebate. The use of TOE during surgery should depend on whether there is evidence of a meaningful benefit, and it is well to remember that the routine use of any procedure is hard to justify and can sometimes be dangerous. Early in Australian cardiac surgery, it was argued that the rebate for coronary bypass surgery should be related to the number of grafts. This argument was rightly not accepted. Similarly, the rebates for cardiac anaesthesia should not be related to the number of monitors used. Cokis and Faris should be commended on their excellent care of the patient. However, their argument for a rebate is not compelling.

John W Stokes FANZCA, FJFICM