Letters

Colleen T Bruce,* Paul S Thomas,† Deborah H Yates‡ * Research Assistant, † Associate Professor, Department of Respiratory Medicine, Prince of Wales Hospital, Randwick, NSW 2033. ‡ Respiratory Physician, St Vincent’s Hospital, Sydney, NSW. Paul. ThomasATunsw.edu.au To the Editor: The recent article by Willcock and colleagues on the high psychological morbidity and level of burnout that interns experience during their first year in hospital highlights an important topic.1 Willcock et al point out that there is an increase in psychiatric morbidity over the intern period in first-year medical graduates. This corroborates the findings of a larger study we conducted among interns during their first year, in which we showed that psychiatric morbidity rises, particularly during the middle of this first year as a doctor, but then decreases by the end of the year.2 The point made by Willcock et al1 is that psychiatric morbidity is not limited to first year graduates — senior doctors are also susceptible to psychological morbidity and burnout.3 Their article highlights the continuing need for workplace reform and support for the medical profession. In addition to reducing working hours, other interventions need to be considered to prepare medical students for their profession, and to reduce the factors which contribute to morbidity (eg, workload, multiple tasking, incessant paging). It should be feasible to test the efficacy of such interventions with the same instruments (such as the General Health Questionnaire) in future generations of interns, and to compare these results with the above studies. Showing that such interventions are effective will provide a strong platform from which to implement wider change in the workplace.

Colleen T Bruce · Paul S Thomas · Deborah H Yates

Simon M Willcock Director, Academic General Practice Unit, Hornsby Hospital, Palmerston Rd, Hornsby, NSW 2077. simonwATmed.usyd.edu.au In reply: Bruce and colleagues are correct to call for ongoing workplace reform and support for the medical profession in general. Our study, which followed medical students to the end of their intern year, did not show a significant fall in psychiatric morbidity towards the end of the intern year as theirs did. Our review of the recent literature suggests that any “improvement” in psychological morbidity after the mid-year peak during internship is likely to be transient, with the early postgraduate period representing a period of transition from normative population values of burnout and morbidity to levels which remain high throughout a medical career, when compared with the general population. The traditional interpretation of the internship as a “baptism by fire”, which tests and ultimately strengthens the new medical graduate, does not hold up to scrutiny. A realistic assessment of this period suggests that it is one where stress and distress often reach unhealthy levels, and where dysfunctional coping strategies may be developed which persist throughout a medical career. The development of mature personal coping strategies along with systemic changes to promote engagement with work have been identified as the most likely means of limiting burnout and its sequelae among medical practitioners.1

Simon M Willcock

Linsey S Hart,* Jane Vernon-Roberts† * AMC Liaison and Resource Officer, Postgraduate Medical Council South Australia, 71 Edward Street, Norwood, SA 5069. † Head of Clinical Studies, Royal Adelaide Hospital, Adelaide, SA. linseyATpmcsa.org.au To the Editor: McGrath’s article on integrating overseas-trained doctors (OTDs) into the Australian medical workforce noted that the areas of difficulty in this area have been well defined.1 McGrath challenged us to “get on with it”. We interpret this challenge to mean that there has been enough regurgitating and redefining of the problem, and it is time for some action. In South Australia, the difficulties of integrating overseas doctors into the workforce mirror those experienced by other states. The Department of Health Overseas Trained Doctor 2004 database listed 93 OTDs as eligible to work in SA. Seventy were employed. All of these doctors had only completed the Australian Medical Council (AMC) Multiple Choice Question (MCQ) examination. Since its inception in April 2003, the Postgraduate Medical Council of South Australia (PMCSA) AMC doctors subcommittee has worked to put in place a number of educational initiatives to support and assist OTDs to complete the Australian Medical Council Exams, and to advocate for their ongoing needs for better orientation to the workplace and protected education time at work. The programs initiated by the PMCSA are both Government-funded and self-funded. They are: culture and medical communication for doctors, MCQ tutorial program, ready for work program, hospital tutorials, objective structured clinical examination practice exam, clinical bridging program, and study groups. Examination results in 2004 for candidates undertaking the PMCSA programs bettered the national average. Of the 16 enrolled participants in the MCQ tutorial program, which ran from January to April 2004, nine sat the May AMC MCQ exam and seven deferred. Eight of the nine passed, giving a pass rate of 89% (AMC pass rate 56%; Australian Medical Council, personal communication). In the AMC clinical examinations, our candidates achieved an overall pass rate of 67%; 30 sat the exam, 20 passed and 10 were given a re-sit or a fail result. (AMC pass rate 59%; Examinations Officer Clinical, Australian Medical Council, personal communication). Twenty chose to defer after using the various programs and tutorials on offer to gauge their level of preparedness. These doctors are planning to undertake the exam in 2005. These programs constitute the South Australian Action Plan for OTD inclusion in the workforce. 2 All of these programs are available and appropriate for any OTD (permanent resident or temporary resident). To the best of our knowledge, no temporary resident wishing to work in “areas of need” has enrolled in our programs yet.

Linsey S Hart · Jane Vernon-Roberts

Barry P McGrath Professor of Medicine, Monash University; and Chair, Confederation of Postgraduate Medical Education Councils of Australia, Dandenong Hospital, Dandenong, VIC 3175. Barry.mcgrathATmed.monash.edu.au In reply: Hart and Vernon-Roberts outline the South Australian Action Plan by the Postgraduate Medical Council of South Australia Australian Medical Council (AMC) doctors subcommittee to support and assist overseas trained doctors (OTDs). Their worthy efforts are directed predominantly towards the many OTDs preparing for their AMC examinations, with associated bridging and “ready-for-work” programs to facilitate entry into the hospital medical workforce. However, the question that needs to be addressed, and which was the main thrust of my article,1 is why we don’t have a national coordinated approach to all elements of the pathway to integrating OTDs into the Australian health care system. This cannot be a largely political approach, as is the Australian Government’s Strengthening Medicare initiative, which is particularly weak in the areas of assessment for safe practice and support in training. A recent article has highlighted the need for a national approach to coordinated governance for postgraduate medical education in Australia and the unsatisfactory complexity of medical education and training systems in this country.2 This excellent article includes only very brief reference to OTDs, using the term “international medical graduates”, 2 which is becoming the more acceptable term and the one recognised by other countries. It does not address the many gaps and problems in the pathways for this group. The number of international medical graduates seeking employment and/or being actively recruited into the medical workforce in Australia each year is far greater than the number graduating from our own medical schools. Thus, there is a degree of urgency about the debate on postgraduate medical education in Australia. We need a national authoritative body, like the new United Kingdom Postgraduate Medical Education and Training Board.

Barry P McGrath

Deborah J Verran Senior Transplant Surgeon, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW 2050. deborahATemail.cs.nsw.gov.au To the Editor: A recent editorial by Mathew et al1 and an article by Kennedy et al2 tackle the issue of commercial kidney transplantation. In their editorial, Mathew and colleagues conclude that if the nationwide Australian deceased donor organ donation rate approached South Australian levels, dialysis patients would not travel overseas to purchase renal allografts.1 I believe that this statement oversimplifies the situation with respect to organ trafficking and the motives behind patients’ acceptance of this option. Organ trafficking is illegal under all state and territory laws within Australia and hence cannot occur. In a number of other countries around the world this is not the case. Although laws have been introduced in India, this has not necessarily led to cessation of trafficking in kidneys.3 Compounding this, the option of purchasing an organ is becoming more readily accessible by means of an increasing number of Internet sites.4,5 What motivates patients to go through with purchasing an organ overseas is not explored either in the editorial by Mathew et al1 or the article by Kennedy et al.2 Kennedy et al do not state whether any of the patients who travelled overseas for a kidney had been deemed not fit to be on the renal transplant waiting list in New South Wales. They also do not give the waiting time on dialysis for each patient before he or she decided to travel overseas. What is clear is that only patients who can afford to pay the US$70 000 or more currently quoted for a renal allograft will be the ones who end up travelling overseas. It would be nice to think that, with an increased organ donor rate in Australia, patients will no longer travel overseas to purchase organs. However, the ready availability of the commodity in not-too-distant countries and the increasing ease of access to this organ trade, combined with sufficient cash, will mean that there is no major barrier to some individuals.

Deborah J Verran

Sean E Kennedy,* Yvonne Shen,* John A Charlesworth,† James D Mackie,‡ John D Mahony,§ John J P Kelly,¶ Bruce A Pussell** * Renal Registrar, † Professor of Renal Medicine, Prince of Wales Hospital, Sydney, NSW. ‡ Renal Physician, Prince of Wales Hospital, Sydney, and Illawarra Regional Hospital, Wollongong, NSW. § Renal Physician, Royal North Shore Hospital, Sydney, NSW. ¶ Renal Physician, St George Hospital, Sydney, NSW. ** Professor of Medicine, Department of Nephrology, Prince of Wales Hospital, Sydney NSW 2031. b.pussellATunsw.edu.au In reply: We agree that the motives for organ trafficking are complex. The reasons that people choose to travel overseas to obtain an organ was not addressed in our article on this occasion, but some possible reasons may be self evident given the long waiting time, especially in New South Wales. Our aim was to alert our colleagues to the increased risks associated with overseas commercial transplant procedures so that they could ensure that their patients were fully informed when making a decision. Most of our patients were on the waiting list, and the time on dialysis was detailed in Box 2 in our article.1 However, two were not on the waiting list — one had a pre-emptive transplant and another was not on the list because of age-related medical problems.

Sean E Kennedy · Yvonne Shen · John A Charlesworth · James D Mackie · John D Mahony · John J P Kelly · Bruce A Pussell

To the Editor: We read with interest the recent cross-sectional survey of Helicobacter pylori infection in remote and urban Aboriginal populations in Western Australia.1 The prevalence of H. pylori was shown to be consistent with that in developing countries. This is not surprising, given the high prevalence of diseases such as chronic suppurative otitis media, rheumatic fever, scabies, and tuberculosis affecting Aboriginal peoples — all of which relate to poverty and overcrowding.2 Aboriginal and Torres Strait Islander people have a massively disproportionate share of the overcrowded households in Australia. In the 2001 Census, Aboriginal people in WA accounted for 53% and 93% of the two-bedroom and three-bedroom households that accommodated seven to nine and ten or more people, respectively (from 3% of the population).3 Windsor et al speculate that high H. pylori infection rates may be the result of children not wearing nappies and of poor personal hygiene — even though these matters (and housing standards, the presence of functional washing facilities and the degree of overcrowding) were not investigated. We are concerned that such conclusions reflect negatively on the Aboriginal population who took part in the survey in good faith with good will. Moreover, it is misleading to suggest that H. pylori is a cause of poor growth among Aboriginal children. There is insufficient evidence to support screening for H. pylori infection in children, as no studies have demonstrated that treating H. pylori infections improves their growth. It is expected that “some of the participants who tested positive for H. pylori have asked to be treated with antibiotics”. We assign considerable importance to research protocols that adhere to the criterion “no research proceeds without service”.4 Did those who were H. pylori positive with dyspepsia, a history of peptic ulcer complications, or a family history of gastric cancer5 receive treatment? Windsor et al do not describe what follow-up their survey participants received. Without clarity on this point (especially appropriate advice to those who were asymptomatic), we wonder what negative impacts a positive H. pylori finding had on participants’ social and emotional well-being. We are concerned by the authors’ anthropological musings: “Indigenous people may have their own H. pylori strains”. Given Australia’s heterogeneous Indigenous population, this potential research question is of no strategic relevance.4 The promotion of expanded testing for H. pylori is not supported by the evidence. Talley’s accompanying editorial prioritises a “randomised controlled trial to test the health benefits (and risks) of population-based screening and antibiotic treatment [for H. pylori] in Indigenous Australians”.5 In the absence of a clinical endpoint for an as-yet undefined health problem, there is no convincing argument for such a trial. Narrow medical answers to health problems that ignore economic and environmental solutions are not evidence-based. Both articles should have argued strongly for political commitment to these solutions to address a wide range of existing poverty-related diseases which currently affect Abori-ginal and Torres Strait Islander people on a massive scale.

Naomi R Mayers · Sophie Couzos · Richard Murray · John Daniels

In reply: We agree with Mayers and colleagues that the vexing issue of Indigenous health is a political one. We undertook this study because we thought it very strange that the prevalence of Helicobacter pylori was known in most populations on the globe, but not in Australian Indigenous people. Results from each participant in the study were forwarded to the clinicians at the test sites. These results were discussed with the participants and those who needed, or asked for, treatment received antibiotic therapy. In a previous editorial in the Journal, Mayers and Couzos state that “preventive health assessments are obviously needed earlier, given the occurrence of preventable chronic disease at younger ages and higher rates than in other Australians”.1 We agree with this, and it is to be hoped that our data will encourage further assessment and awareness of H. pylori infection in people of all ages in the Australian Indigenous community.

Barry J Marshall · Helen M Windsor

Laurelle J Burrell,* Elizabeth A Grabsch,† Alexander A Padiglione,‡ M Lindsay Grayson§ * Infectious Diseases Research Nurse, † Infection Control Scientist, § Director of Infectious Diseases, Austin Hospital, Studley Road, Heidelberg, VIC 3084; ‡ Infectious Diseases Physician, Department of Epidemiology and Preventive Medicine, Monash University (Alfred Hospital), Melbourne, VIC. Lindsay. GraysonATaustin.org.au To the Editor: Patients with end-stage renal failure are a key risk group for colonisation and infection with vancomycin-resistant enterococcus (VRE). Consequently, many renal units in Australia screen these patients regularly for VRE colonisation, to assist with infection control and treatment.1-3 Screening protocols are usually applied equally to inpatients and outpatients, even though the risk of VRE colonisation among outpatients (and therefore the cost–benefit of such screening) has not been clearly defined. To assess the prevalence of faecal VRE colonisation among haemodialysis outpatients, we conducted a cross-sectional survey of outpatients attending 12 Victorian in-centre haemodialysis units — Austin Health (four units), Southern Health (three units) and five regional haemodialysis units (Bendigo, West Gippsland, La Trobe Valley, Central Gippsland and Bairnsdale). Patients attending these units represent about a third of the state’s in-centre haemodialysis population. The study was approved by the ethics committee at each hospital, and written informed consent was obtained from all participants. All patients who attended the units between 1 October 2001 and 3 April 2002 were invited to participate. VRE faecal carriage was assessed by three rectal swabs and one faecal specimen taken on at least three separate occasions. Specimens were inoculated onto Enterococcosel agar (BBL, Sparks, USA) containing 6 μg/mL vancomycin. All cultures were processed by standard methods for VRE identification, as described previously.2,3 Of 345 available haemodialysis patients, 269 (78%) consented to participate in the study (205 [76%] metropolitan, and 64 [86%] regional; participation rate per centre, 70%–91%). The 269 patients represented approximately 30% of Victorian in-centre haemodialysis patients. Overall, 74% of participants had assessment of all three rectal swabs and a faecal specimen. VRE faecal colonisation was found in three of the 269 participants (1.1%) — two were from separate metropolitan hospitals, and one from a regional centre. All isolates were Enterococcus faecium vanB (the most common type of VRE in Australia).3 None of these three patients were known to be previously colonised. This 1.1% prevalence was substantially lower than the 3.0%–4.6% prevalence previously described in renal inpatients in Melbourne,2,3 and the 10% rate reported in the United States (where 33% of dialysis centres have one or more VRE-positive patients).1,4 Statistical comparisons of this study with our previous two Australian studies2,3 should be undertaken cautiously, as screening methods differed in specimen frequency, type and number. Bearing in mind this caveat, the rate of faecal VRE carriage was significantly lower among the haemodialysis outpatients in our current study compared with renal inpatients in a 1997 study by Grayson et al2 (3/269 v 9/194; P = 0.02 by χ2 test), but less definitely so when compared with renal inpatients in the 1998–1999 study of Padiglione et al3 (3/269 v 22/739; P = 0.09, by χ2 test). Since the outpatient study, screening surveys at our hospital have shown intermittent high rates of colonisation in renal inpatients and environmental contamination (unpublished data). Given our findings in outpatients, we believe future VRE screening protocols in Australian hospitals should focus primarily on inpatients, rather than faecally continent outpatients, who have both a low rate of colonisation and low potential risk for VRE transmission or acquisition. Good compliance with practical infection control guidelines remains important to avoid widespread dissemination of VRE in our haemodialysis centres.5

Laurelle J Burrell · Elizabeth A Grabsch · Alexander A Padiglione · M Lindsay Grayson

Adam P Morton,* H David McIntyre† * Endocrinologist, † Director, Endocrinology and Obstetric Medicine, Mater Hospital, Raymond Terrace, Sth Brisbane, QLD 4101. AmortonATmater.org.au To the Editor: We read with interest the article by Hussein and colleagues on their experience with thiazolidinediones (TZDs).1 These agents are only approved by the Pharmaceutical Benefits Scheme as part of dual therapy. We wish to present our experience of adding TZDs to metformin and sulfonylureas — hence, triple therapy — in patients with suboptimally controlled type 2 diabetes mellitus. The records of 28 patients (15 men, 13 women) with type 2 diabetes, for whom pioglitazone was added to maximal doses of metformin and sulfonylurea because of suboptimal control, were reviewed. Baseline patient characteristics are shown in . Mean follow-up was 9.6 months (range, 3–24 months); the average pioglitazone dose was 31.3 mg. The mean fall in the level of glycohaemoglobin (HbA1c) was 1.26% — 10 patients achieving an HbA1c level of less than 7% at last review. Four patients did not respond to therapy; none withdrew because of side effects. Eight patients whose HbA1c fell less than 0.5% after 3 months continued taking pioglitazone, achieving an average fall in HbA1c of 1.25% after a mean of 12 months follow-up. Mean weight gain was 3.35 kg (– 3.2 kg to 11.6 kg). Mean changes in HbA1c level and weight compared with baseline over 24 months are shown in . There was no correlation between these outcomes, and no baseline characteristic predicted glycaemic response. Six studies have reported the efficacy of TZDs in triple therapy (), and show a consistent fall in HbA1c level at the expense of weight gain, with a low rate of withdrawals because of adverse effects. Our findings were similar to those of these previous reports in terms of glycaemic response and low rate of side effects. The much higher rate of side effects reported by Hussein et al1 is likely to be the result of the coprescription of TZDs with insulin in 64% of patients in their study. While fluid retention has been reported in up to 5% of patients taking TZDs as monotherapy or in combination with oral hypoglycaemics, 15% of patients using TZDs with insulin may develop significant oedema. Most reports describing precipitation of cardiac failure with TZDs have been in patients using combination therapy with insulin. It would be interesting to know what proportion of the patients who developed peripheral and pulmonary oedema in the study by Hussein et al1 were also receiving insulin. One prospective randomised trial comparing the addition of pioglitazone and bedtime insulin to maximal metformin and sulfonylurea found similar efficacy in improving glucose control, but less hypoglycaemia and improved high density lipoprotein cholesterol levels with pioglitazone.3 A study of the long-term efficacy of triple therapy found 26 of 35 patients (74%) had good control after a mean follow-up of 37 months, their HbA1c level having fallen from 8.7% to 6.9%.8 In conclusion, the experience of our unit and the published literature is that TZDs are efficacious in improving suboptimal diabetic control in patients on maximal doses of metformin and sulfonylurea. Eight individuals in our group had a significant improvement in control subsequent to minimal response after the initial 3 months of treatment, suggesting a longer trial of TZDs should be employed before classifying patients as non-responders. It is to be hoped that the regulatory authorities will allow the use of TZDs in triple therapy. 1 Characteristics of our 28 patients at baseline Variable Mean (range) Age (years) 57.4 (31–74) Weight (kg) 96.3 (56–137) Body mass index (kg/m2) 34.6 (24–50.3) Duration of diabetes (years) 11 years (1–48) Glycohaemoglobin (HbA1c) level (%) 9.0 (7.1–10.4) 2 Changes in glycohaemoglobin (HbA1c) level and weight compared with baseline values 3 Studies of thiazolidinediones added to maximal dose metformin and sulfonylurea Variable Roy et al2 Aljabri et al3 Dailey et al4 Kiayias et al5 Kiayias et al5 Byrne et al6 Yale et al7 Thiazolidinedione Rosiglitazone Pioglitazone Rosiglitazone Rosiglitazone* Rosiglitazone† Rosiglitazone Troglitazone Duration (weeks) 16 16 24 20 20 nr 24 No. of patients 48 30 181 19 19 24 101 Baseline body mass index (kg/m2) nr 26 32 31 31 nr 30.1 Baseline HbA1c level (%) 9.3 9.7 8.1 8.9 9 9.6 9.6 Fall in HbA1c level (%) 1.8 1.9 0.9 1.1 1.4 1.2 1.3 Weight gain (kg) nr 2.6 3 4.2 4.6 0.7 0.9 % Patients withdrawn 4.2 0 5.5 0 0 0 2 % Patients with satisfactory control (HbA1c level) 65 (< 7.5) 23 (< 7) 42 (< 7) nr nr nr 43 (< 8) HbA1c = glycohaemoglobin. nr = not reported. * 4 mg/day; † 8 mg/day.

Adam P Morton · H David McIntyre

Nirusha Arnold,* Mark McLean,† David R Chipps,† N Wah Cheung† * Advanced Endocrinology Trainee, † Endocrinologist, Centre for Diabetes and Endocrinology Research, Westmead Hospital, Hawkesbury Road, Westmead, NSW 2145. nirusha_arnoldATozemail.com.au To the Editor: It was with interest that we read the recent article on real-life experience with thiazolidinediones by Hussein et al.1 The authors noted the absence of severe liver toxicity with the newer agents, rosiglitazone and pioglitazone, in contrast to troglitazone, which was withdrawn because of cases of hepatic failure.2 However, the sample was too small to conclude that these thiazolidinediones (TZDs) carry no hepatic risk, and they endorsed the current Pharmaceutical Benefits Scheme recommendations that liver function tests (LFTs) be monitored every 2 months. We have collected similar clinic data showing that the development of significant abnormalities in results of LFTs with TZD therapy is uncommon, and in fact, there are often improvements in LFT findings. We reviewed the files of 166 patients with type 2 diabetes treated with TZDs between 1 August 2000 and 30 November 2002, with the aim of assessing their long-term effect on LFT results. Therapy was discontinued within 3 months in 26 patients. The reasons were non-compliance (7), therapy ineffective (8), weight gain (5), dyspnoea (1), peripheral oedema (1), malaise (1), dizziness (1), angio-oedema (1), and pre-existing LFT abnormality (1). We analysed data on the remaining 140 patients (see Box) treated for a mean of 188 ± 4 days with either pioglitazone (109 patients) or rosiglitazone (31 patients). All LFT results improved significantly (Box). At baseline, 90 patients had abnormal findings on LFTs. These findings normalised in 43 of these patients (including one with steatohepatitis proven on biopsy); improved in 29 patients; and were unchanged in nine patients. LFT findings deteriorated in nine patients, leading to cessation of therapy in two. Most patients with normal LFT results at baseline experienced improvements of these parameters within the normal range. Three patients developed new abnormalities in their LFT findings, and therapy was stopped in one patient, leading to resolution of LFT abnormalitites. Changes in glycohaemoglobin (HbA1c) levels correlated positively with changes in activity of alkaline phosphatase (correlation coefficient [r], 0.33; P < 0.01), aspartate aminotransferase (r, 0.27; P < 0.01) and alanine aminotransferase (r, 0.29; P < 0.01). Our findings support those of Hussein et al, that TZD therapy is usually stopped for reasons other than hepatic dysfunction. In contradistinction to early concerns about their hepatic safety, the improvements in LFT findings seen in our patients suggest that TZDs may even benefit hepatic function. In patients with diabetes, abnormal findings on LFTs are often attributed to fatty liver, which predisposes to steatohepatitis. TZDs may well alleviate or prevent steatohepatitis,3 thereby providing benefits beyond that of improved glycaemic control, and mild abnormalities in LFTs should not discourage their use in patients with diabetes. Changes in liver function and glycohaemoglobin (HbA1c) level Variable Baseline 6-month follow-up Change P* Weight (kg) 93 ± 2 96 ± 2 3 ± 0.4 < 0.001 HbA1c (%) 8.9 ± 0.1 7.9 ± 0.1 – 1.0 ± 0.1 < 0.001 Albumin (g/L) 41 ± 0.2 41 ± 0.2 – 0.5 ± 0.2 < 0.02 Bilirubin (μmol/L) 9.4 ± 0.4 8.5 ± 0.3 – 0.9 ± 0.3 < 0.003 ALP (U/L) 92 ± 2 79 ± 2 – 13 ± 2 < 0.001 GGT (U/L) 44 ± 3 31 ± 2 – 13 ± 2 < 0.001 AST (U/L) 26 ± 1 22 ± 1 – 3 ± 1 < 0.001 ALT (U/L) 33 ± 2 25 ± 1 – 8 ± 2 < 0.001 ALP = alkaline phosphatase. GGT = γ-glutamyl transferase. AST = aspartate aminotransferase. ALT = alanine aminotransferase. * Paired t test.

Nirusha Arnold · Mark McLean · David R Chipps · N Wah Cheung

Huong V Nguyen,* Katherine B Ingram,† Jonathan Beilin‡ * Endocrinology Registrar, ‡ Endocrinologist, Royal Perth Hospital, Box X2213 GPO, Perth, WA 6847; † Geriatrician, Swan District Hospital, Middle Swan, WA Huong. NguyenAThealth.wa.gov.au To the Editor: Zoledronic acid is a new bisphosphonate treatment for hypercalcaemia of malignancy, multiple myeloma and documented bone metastases from solid tumours, in conjunction with standard chemotherapy.1 Transient hypocalcaemia, a side effect of bisphosphonate therapy, can occur with zoledronic acid.2 We describe a patient with transient severe hypocalcaemia after zoledronic acid treatment. An 88-year-old white woman with multiple myeloma presented with left hip pain. Imaging revealed multiple lytic lesions in the spine, pelvis and upper femurs. She was commenced on zoledronic acid 4 mg and a 5-day course of melphalan 10 mg/day and prednisolone 100 mg/day. At this stage, her serum calcium concentration was 2.38 mmol/L (normal, 2.15–2.55 mmol/L) and serum phosphate concentration was 0.8 mmol/L (normal, 0.8–1.5 mmol/L). She had renal impairment with reduced creatinine clearance of 35 mL/min. Nine days later, she underwent surgical repair of a duodenal ulcer. Post-operatively, she was found to be hypocalcaemic, with serum calcium concentration of 1.34 mmol/L and ionised calcium concentration of 0.78 mmol/L (normal, 1.14–1.29 mmol/L). Serum phosphate concentration was 0.4 mmol/L and magnesium concentration was 0.87 mmol/L (normal, 0.70–0.90 mmol/L). Her serum 25-hydroxyvitamin D concentration was 14 nmol/L (normal > 50 nmol/L) and her parathyroid hormone level was 44 pmol/L (normal, 1.5–8.0 pmol/L). The patient displayed no symptoms of hypocalcaemia and had negative Chvostek and Trousseau signs. Her QTc interval was normal. Her hypocalcaemia was managed with oral calcium carbonate 4.5 g/day and calcitriol 0.5 g/day. Ten days later, her total serum calcium concentration rose to 2.31 mmol/L and her phosphate concentration was 0.9 mmol/L. Bisphosphonates inhibit osteoclast-mediated bone resorption, thereby reducing serum calcium concentration. Compensatory secondary hyperparathyroidism prevents significant hypocalcaemia by enhancing renal calcium conservation, 1,25-hydroxyvitamin D production, and osteoclastic bone resorption.1,2 In our patient, the 1,25-hydroxyvitamin D concentration was not measured. However, in view of the low 25-hydroxyvitamin D and impaired renal function, this level may have been low, further exacerbating the hypocalcaemia. Transiently low phosphate concentration in this patient may be due to fasting and co-administration of 5% dextrose, as our patient was fasted for 3 days peri-operatively and given a combination of intravenous 5% dextrose and normal saline. Vitamin D insufficiency afflicts a large proportion of the elderly population,3 and its existence needs to be recognised before commencement of bisphosphonate therapy, so that adequate calcium and vitamin D supplementation can be given to reduce the occurrence of hypocalcaemia.

Huong V Nguyen · Katherine B Ingram · Jonathan Beilin

Peter A Frith Head of Southern Respiratory Services, Respiratory Unit, Flinders Medical Centre, Bedford Drive, Bedford Park, SA 5042. Peter.frithATrgh.sa.gov.au To the Editor: The informative study by Simons and colleagues1 has highlighted a major concern. Chronic obstructive pulmonary disease (COPD) is one of Australia’s top four causes of death and burden of illness,2 yet the authors have made no mention of COPD. Failure to recognise the importance of this disease is an endemic attitude in Australia and globally3-5 that results in under-representation of COPD in epidemiological surveys and in inadequate funding for effective treatments and research. The study found that peak expiratory flow (PEF) provides the highest hazard ratios for predicting time to death in women (and the second highest in men). There is even a “dose–response” effect. Using the term “impaired PEF” is a bit like saying “impaired ECG” without attributing a diagnosis. PEF is a measure of airway calibre, and impairment of PEF indicates airway disease — largely COPD in this population. Smoking accounts for about 85% of the risk of COPD, and about 50% of smokers develop airflow limitation,4-6 so it is not surprising that the interaction between PEF and smoking was the most important predictor of reduced survival in this large cohort. It’s time to stop hiding our heads in the ashtray! Smoking combined with low PEF is COPD. We must demand that our medical and epidemiological professions uncover people with undiagnosed COPD. Early diagnosis is simple.5 It’s not normal to be unable to keep up with friends at work or during recreation because of breathlessness, and a daily cough is really an airway disease. If symptoms are acknowledged, spirometry will confirm the diagnosis. We should help our patients to enunciate these hidden symptoms so their condition can be diagnosed accurately, and effective management begun, as highlighted in the “COPDX management guidelines”.5 Primary and secondary prevention must focus on reducing smoking among young people. Smoking cessation, the use of effective drugs, and pulmonary rehabilitation are the cornerstones of COPD therapy that lead to better quality survival. COPD is common and under-diagnosed. Simons et al have partly exposed this deadly condition. Their data, added to other Australian data,7 should trigger actions that facilitate earlier diagnosis throughout Australia and support delivery of effective treatment to the thousands “dying a slow death” from COPD. Australia’s illness burden from COPD is high. Its prevalence and burden in Australia are rising, especially in women. Globally, the World Health Organization expects COPD to rise from 12th to 5th as a cause of illness burden by 2020. We must acknowledge that PEF impairment is not simply a mysterious risk factor for early “all-cause mortality”, but is indicative of COPD being a major contributor to death in this population.

Peter A Frith

Leon A Simons,* Judith Simons† * Director, Dubbo Study of the elderly, † Data Manager, Lipid Department, St Vincent’s Hospital, Darlinghurst, NSW 2010. L. SimonsATnotes.med.unsw.edu.au In reply: The prospective Dubbo Study of the elderly has produced a series of publications in which reduced peak expiratory flow (PEF) has been shown to be associated with increased risk of death,1,2 as well as increased risk of heart attack,3 ischaemic stroke4 and admission to a nursing home. 5 We have employed a purely statistical definition of impaired PEF, namely the lowest third of our sex-specific population distribution. We agree that many subjects so defined with impaired PEF, and who are smokers, will have underlying and potentially undiagnosed chronic obstructive pulmonary disease (COPD). Epidemiological studies have highlighted the importance of impaired PEF. It is now time for health professionals to implement the COPDX management guidelines referred to by Frith6 in a still more effective manner and to devise better prevention programs.

Leon A Simons · Judith Simons

Bernard M Bourke Vascular Surgeon, Gosford Hospital, 4/213 Albany Street North, Gosford, NSW 2250. Dr. BourkeATgvs.com.au To the Editor: Up and coming surgical registrar, Ken Wong, presents a revolutionary plan to allow him to look after surgical patients in the operating theatre.1 The use of the telephone for communication has merit, but he won’t feel so smug when he gets to the chapter entitled “The management of surgical patients in NSW public hospitals in winter”. There will be nowhere for Dr Wong to “hide” when he realises our operating theatres are, in fact, solar powered and that, when the sun goes down in winter, the theatres conk out. Surely now, with the statewide mergers of health services, there will be enough excess “committee people” to form a collaboration with the western NSW farmers so that the mice plague can be harnessed and trained to run on the cogs and at least provide lighting during power shortages. I’m sure my daughter could lend a few cats to chase the mice. In the absence of the provision of more hospital beds, the substitution of cat-and-mouse power for solar power is the best “winter strategy” I’ve heard in the last 10 years. This concept will feature in our next chapter, “How to train surgeons without patients or operating time”.

Bernard M Bourke

Craig A Aboltins,* John R Daffy,† Penny Allen‡ * Infectious Diseases Registrar, † Infectious Diseases Physician, St Vincent’s Hospital, Victoria Parade, Fitzroy, VIC 3065; ‡ Ophthalmologist, Royal Victorian Eye and Ear Hospital, East Melbourne, VIC. craigaboltinsATnetspace.net.au To the Editor: Within the last 12 months, four injecting drug users (IDUs) who had been injecting buprenorphine presented to the Royal Victorian Eye and Ear Hospital with endogenous fungal endophthalmitis (EFE) involving Candida species. All four patients admitted that they had diverted or obtained diverted sublingual buprenorphine from the oral cavity after it was dispensed. They had dissolved the remaining drug in water and injected it intravenously. We present an illustrative case. A 28-year-old woman presented with a 4-week history of left eye pain and erythema. She had a 10-year history of intravenous drug use. Over the previous 6 months, she had been regularly injecting buprenorphine that was prescribed to a friend. The friend had been removing the partially dissolved buprenorphine from his mouth before giving it to our patient. On examination, the patient could only detect hand movement with her left eye. Fundoscopy showed vitritis with a “snow ball appearance” consistent with EFE. Treatment involved vitrectomy, intravitreal amphotericin and oral fluconazole. Candida albicans was cultured from vitreal specimens. Her visual acuity had improved to 1/60 at the time of discharge. Intravenous drug use is known to be a risk factor for EFE. Candida species are the usual causative organisms, but Aspergillus species have also been reported.1 In the 1980s, there were many reports of candida endophthalmitis in injecting drug users associated with the use of “brown” (or Iranian) heroin. The “brown” heroin required an acidic substance, often lemon juice, as a solvent. Lemon juice was shown to be the source of the candida.2 However, over the past 10 years, the heroin available in Australia has been water soluble, and sterile or tap water is usually used to dissolve the heroin before injection. None of the cases we report in this letter involved lemon juice to dissolve heroin or buprenorphine before injection. Buprenorphine has been available in Australia since 2001 for the treatment of opiate addiction. It is usually dispensed daily by pharmacies in a crushed tablet form. Pharmacists are required to watch patients place and dissolve the medication under the tongue before they leave the pharmacy. Contamination of injected buprenorphine with orally derived Candida species presents a recently recognised cause of fungal endophthalmitis in injecting drug users.3 Doctors, pharmacists and drug users need to be aware of the risk of this sight-threatening complication.

Craig A Aboltins · John R Daffy · Penny Allen

Ariella Glaser,* Dwight Arakaki,† Gar Ming Chan,‡ Robert S Hoffman§ * Resident, Mount Sinai Medical Center, New York City, NY, USA; † Resident, Beth Israel Medical Center, New York City, NY, USA; ‡ Fellow (and corresponding author), § Director, New York City Poison Control Center, New York City, NY, USA. garchanATpol.net To the Editor: Two aspects of the recent article by Kelly et al comparing intranasal with intramuscular naloxone in suspected opioid overdose1 make their study difficult to interpret. The methods allowed for a great deal of bias. There was no attempt to blind evaluators to therapy, and knowing which therapy is to be used a priori may influence both therapy selection and perceived outcome. The second flaw we noted was the use of the Glascow Coma Scale (GCS) in a non-trauma patient.2 An improvement in GCS score may represent increased wakefulness or even withdrawal. The use of the GCS does not make it possible to determine what degree of improvement or worsening the therapy resulted in. In the opioid-intoxicated patient, the “alert/verbal/pain/unresponsive” (AVPU) scale is more appropriate. We agree that the use of needles in a high-risk patient is dangerous. However, if these patients do not respond to painful stimuli, there should be no danger at all.

Ariella Glaser · Dwight Arakaki · Gar Ming Chan · Robert S Hoffman

Anne-Maree Kelly,* Debra Kerr,† Paul Dietze‡ * Director, † Deputy Director, Joseph Epstein Centre for Emergency Medicine Research, Western Hospital, Private Bag, Footscray, VIC 3011. ‡ Research Fellow, Turning Point Alcohol and Drug Centre, Fitzroy, VIC. Anne-Maree. KellyATwh.org.au In reply: The prehospital setting for research poses challenges that require some flexibility in study design. While it would have been preferable to have used blinded naloxone and placebo solutions for both routes of administration in our study, financial and operational constraints made this impossible, so some bias in evaluations is possible. However, this is not necessarily in favour of the intranasal route, as before the study many paramedics were very sceptical about the intranasal naloxone preparation. Therapy selection was by random allocation in sealed envelopes as described in our article. The Glasgow Coma Scale score was chosen as an outcome measure because it was the parameter used operationally for treatment and disposition decisions in the ambulance service within which our study was conducted. We acknowledge its limitations in non-trauma patients. The potential for needlestick injury in this situation is real. Patients with opioid intoxication may be in cramped locations and may be irritable on waking, increasing the risks involved with handling a “sharp”. Given the prevalence of blood-borne viruses in the injecting drug user population, strategies to reduce the risk of needlestick injury are highly desirable. Additionally, a strategy that has been suggested for preventing opioid-overdose-related deaths is to make naloxone more widely available in the community. 1 The intranasal formulation of naloxone may be appropriate for this, as it has significant advantages including reducing risks of blood-borne virus transmission and minimising the requirement for training and the secure storage of syringes and needles. 2

Anne-Maree Kelly · Debra Kerr · Paul Dietze

Roslyn G Poulos,* Anthony B Zwi† * Lecturer, † Professor and Head, School of Public Health and Community Medicine, University of New South Wales, Sydney, NSW 2052. r.poulosATunsw.edu.au To the Editor: With increasing attention focused on the need for evidence-based policy making in recent years, researchers have come to the realisation that research has, in fact, little impact on policy making. The literature abounds with theories on how to improve the appropriate use of research evidence in policy decisions. Researchers must shoulder a large proportion of the responsibility, having spent too much energy generating evidence and insufficient time “translating” this knowledge into a useful product for decision makers.1 Further, the failure of the two communities to communicate has allowed researchers to follow their own agendas, rather than those of the potential users of their research.2 Improved two-way communication between researchers and policy makers may improve the uptake of research evidence.3 This is best achieved by supporting policy makers to utilise evidence and researchers to become more policy-sensitive. However, even when evidence has been “translated” and acknowledged, it is still subject to other forces. There are numerous barriers to evidence-based policy making, not the least of which is politics. For example, Stevenson recently highlighted the fact that young drivers are disproportionately represented in road trauma statistics.4 He presented data on a number of interventions that have successfully reduced fatal and injurious crashes involving young drivers. Similar data were presented by the NSW Government in its options paper on improving safety for young drivers, which was put out for community consultation in late 2004.5 So far, a policy decision has been made on only two out of 11 options. One decision, which prohibits provisional (P1) licence holders from driving high-performance cars, has, by the Government’s own admission, no supporting evidence of effectiveness.5 The other decision places a limit of one passenger for 12 months for drivers who lose their provisional (P1 or P2) licence. However, this decision is a variant of a strategy that is supported by evidence, and consequently may have little or no effect. Researchers need to be aware that social, electoral, ethical, cultural and economic factors have a powerful influence on policy.6 While the literature on evidence-based policy exhorts researchers and policy makers to work on bridging the gap between evidence and policy, the role of other key players (such as the public) has tended to be overlooked.7 As part of a National Health and Medical Research Council capacity-building grant in population health research, a consortium of academic institutions is working on enhancing the interface between injury research and policy and on promoting evidence-informed policy in injury prevention. (Members of the consortium are the NSW Injury Risk Management Research Centre, the School of Public Health and Community Medicine, and the Prince of Wales Medical Research Institute [all of the University of NSW]; and the Rehabilitation Studies Unit and George Institute for International Health [of the University of Sydney]). The role of the public as an audience with which researchers might profitably interact to improve dissemination and uptake of evidence will be explored, as will the role of health journalists in facilitating this.

Roslyn G Poulos · Anthony B Zwi

Simon J Foote Professor, Senior Principal Research Fellow, and Joint Head, Genetics and Bioinformatics Division, The Walter and Eliza Hall Institute, 1G Royal Parade, Parkville, VIC 3050. footeATwehi.edu.au To the Editor: I am amazed by your assertion in your recent column in the Journal that many clinicians fail to equate advances in basic research to advances in clinical medicine. 1 I would therefore like to make some small contribution to your understanding of the work of Richard Axel and Linda Buck, 2004 Nobel laureates in Physiology or Medicine, 2 and why this was considered worthy of the Nobel Prize. Our understanding of the nervous system is still very primitive, and their almost complete description of the functioning of the odorant system — a small part of the nervous system — has laid down many of the principles pertinent to the more complex fundamentals for understanding neuronal signalling and signal processing. This is essential to an understanding of neurological and psychiatric diseases. The odorant receptors are also G-coupled protein kinases, and this is one of the most frequently targeted groups of compounds for novel small-molecular therapies. If anyone still believes that Nobel Prize-winning science, such as understanding neuronal circuitry, is irrelevant to clinical medicine, they might look at the 2003 recipients for the Nobel Prize in Physiology or Medicine, Paul Lauterbur and Peter Mansfield. They received the award for the discovery of magnetic resonance imaging, which clearly plays a role in “mainstream” medicine.

Simon J Foote

Martin B Van Der Weyden Editor, The Medical Journal of Australia, Locked Bag 3030, Strawberry Hills, NSW 2012. medjaustATampco.com.au In reply: I welcome Foote’s comments, but, to the contrary, I find it entirely credible that many clinicians “fail to equate advances in basic research to advances in clinical medicine.” The reasons are many, but include not only the tortuous language of research,1,2 but also the scepticism that inevitably follows research announcements of “cures” and “breakthroughs”, which prove to be patently premature or just peter out.3 However, I am amazed that Foote appears to have missed the point of my column — the “narrowness of the Nobel awards for physiology or medicine” with their recent predominance of basic research.4 While it must be admitted that the Nobel Prize is increasingly awarded for what is undoubtedly outstanding basic research that has the potential to be of “greatest benefit for mankind”, much of this potential remains unrealised. Indeed, it was the need for recognition of clinical and epidemiological research in the Nobel awards that moved the Lancet, in its Paper of the year 2004, to seek sponsorship for the clinical equivalent of the Lasker and Nobel awards.5 In summary, it is research’s exclusivity, the rise of its false prophets, and the irrelevance of most recent Nobel Awards to everyday practice that fuel disinterest among clinicians.

Martin B Van Der Weyden

Kevin L Forbes Head, Years 3 & 4 MB BS Program, School of Medicine, University of Queensland, Mayne Medical School, Herston, QLD 4006. k.forbesATuq.edu.au To the Editor: The personal perspective on continuous improvement outlined by Kilham succinctly documents the concerns surrounding the application of management tools to the practice of medicine.1 As Kilham says, continuous improvement has been around for a long time and “flowed from a particular attitude . . . [that of] a mind open enough to recognise better ways of doing things, or ways of doing better things”.1 However, I would argue that even history-taking does need to continually improve to include various communication skills appropriate to individual patients. Continuous improvement in history-taking skills, to enable each patient to express their major concerns and to feel more in control of the consultation, has significantly reduced my feelings of frustration provoked by previous patients. Adherence to the strict script of history-taking taught to me in my undergraduate training seemed to provoke a rejection of the expert advice I was giving them. Management does need to understand the importance of recognising good work already done and the current high achievements of medical practitioners. On the other hand, even the busiest of clinicians should understand the professional advantage of participation in a project to further improve or develop new ways of solving their patients’ problems. There are multiple strategies needed for the effective “change from the existing entrenched structure and culture of patient care to one based on patient- centred, evidence-based care”.2 However, management certainly needs to support the busy clinicians during the project. It is also better to avoid jargon and the constant renaming of programs. I would argue that the learning principle underlying the range of continuous improvement programs is the same. That principle is to question, accept challenges, explain, justify and seek further information as a continuous process.3 One essential feature of continuous improvement (whatever it is called) is that the practitioner needs to participate in the selection of the project for continuous improvement and the objective outcome measures that will prove the change to be advantageous or not advantageous. It is also important to recognise that successful continuous improvement programs in one context do not necessarily translate to another context. I agree that management must accept the same standards and accountability demanded of clinicians. In addition, all clinicians should participate in continuous improvement projects as well as being assured that we currently practise medicine at a high standard.

Kevin L Forbes

Bill Coote Medical Practitioner, 20 Ryrie St, Campbell, ACT 2612. billcooteATnetspeed.com.au To the Editor: Gordon, Director of the Centre for Medical Humanities at the University of Sydney, suggests that “the separation of clinical care from the ‘human sciences’ is a professional and social mistake”, and that “the arts, humanities and social sciences act as a counterbalance to the relentless reductionism of the biomedical sciences”. 1 Her university now offers a Masters in Medical Humanities and the opportunity to study subjects such as Medicine and war and Medicine and music. Gordon suggests that study of the medical humanities could result in “a more insightful view of the patient, the doctor and the health care system, and an enhanced capacity to cure, relieve and comfort”, and that “history, philosophy and sociology warn that the person with the disease is all too easily reduced to the non-hygienic, non-rational, disordered ‘other’ ”, while “the growth of medicine as an economic and rational profession has paradoxically contributed to the social diminution of the body, the very object of its focus”. 1 This warrants a response more elegant than the earthy Australian expletives that come to mind. That master of teasing irony, Jane Austen, makes gentle fun in Emma of educational establishments “which professed, in long sentences of refined nonsense, to combine liberal acquirements with elegant morality upon new principles and new systems”.2 In an article entitled Medicine and literature, UK medical historian Neve argues “there are numerous difficulties tracing the connections between two vast areas of human effort that may not be easily twinned” and that “the desire to twin them may be an ambition more attractive to medical practitioners than to writers and artists”.3 Doctors may yearn to counter a modern perception that they are mere technicians, some by seeking to reclaim a lost identity as the last of the humanists. Neve provocatively suggests that for many modern practitioners, often “their cases are routine, unglamorous, and socially explicable in matter-of-fact terms”.3 Maybe the best approach to the humanities for anyone, including doctors, lies somewhere between the sermonising of Gordon and the temptations of escapist fantasy, such as those offered by the master of ceremonies in the movie Cabaret with his excuse that “life is disappointing, forget it”.4

Bill Coote

Jill Gordon Director, Centre for Medical Humanities, University of Sydney, NSW 2006. jill.gordonATarts.usyd.edu.au In reply: It may be possible to identify an approach that lies “somewhere between the sermonising of Gordon”, as Coote puts it, and the world-weariness of the master of ceremonies at the Kit Kat Club. Research in the social sciences suggests that we derive more personal happiness from positive experiences, including our social and intellectual pursuits, than from material possessions. These findings are probably due to the fact that positive experiences generate pleasant memories and a richer sense of personal identity. Positive experiences also have greater social value than possessions, being more easily shared with others. Thinking and talking about new ideas provides a great deal of pleasure and satisfaction for students in the medical humanities. While mere “cases” may be, as Coote quotes, “routine, unglamorous, and socially explicable in matter-of-fact terms”, the doctor–patient relationship is not. Medicine provides a resource which can be used, as philosopher Martyn Evans has pointed out, to reflect on ourselves, express ourselves, develop ourselves, criticise ourselves and encounter ourselves.1 To do these things, we need tools constructed by the arts and humanities, as well as the sciences. Coote’s choice of reading material — the Companion encyclopedia of the history of medicine2 — is a great place to begin.

Jill Gordon

To the Editor: The disastrous events of Boxing Day, 2004 left hundreds of thousands dead, injured or homeless across large parts of Asia. Many aid teams dispatched to affected areas are grappling with the aftermath of this catastrophe. Here, I present one of many clinical observations of what we encountered in the field. It is a clinical anecdote, but one worth sharing, as it may guide future teams in similar situations. A 62-year-old woman was admitted to hospital with a history of vague ill-health for 12 months, and a subacute illness over the 4 weeks since immersion in the tsunami, with persistant cough, dyspnoea and weakness to the point of being largely bed-bound. She was cachectic, had a fever of 37.5°C and scattered crackles in both lower lung fields. Radiology facilities were not available and she was not producing sputum. She was treated empirically with antituberculous chemotherapy, as well as broad-spectrum antibiotics in the form of amoxycillin and ciprofloxacin orally, but her condition did not improve. X-ray facilities became available soon thereafter, and a chest x-ray showed changes more in keeping with a necrotising pneumonia than tuberculosis ( [a]). Her treatment was changed to intravenous meropenem (1 g every 8 hours) and her condition was slowly improving when we left. During our 2-week posting in Banda Aceh, we saw about 6–10 patients at three hospitals presenting about a month after their immersion, with fluctuating fever; chronic, non-productive cough; and radiological evidence of bilateral, asymmetric, necrotising pneumonia with cavitation. Some patients developed empyemas and pneumothoraces ( [b]). They failed to respond to broad-spectrum antibiotics including ampicillin/gentamicin/metronidazole and ticarcillin–clavulanate/cotrimoxazole. Burkholderia pseudomallei was cultured from the pleural fluid of two of these patients, and Nocardia sp. from the sputum of another. A notable feature of these patients was their subacute presentation weeks after immersion in the tsunami, the persistence of symptoms despite other broad spectrum antibiotic therapy, and the development of radiological and clinical manifestations of necrosis with pleural involvement. Many of our patients described the wave as being “black”. In view of the immersion in muddy water in a tropical environment, B. pseudomallei is likely to have been one of the causative organisms in many of these cases. However, it has not been possible to culture B. pseudomallei from all patients, and it is likely that their infections were polymicrobial given the circumstances of their injuries. A variety of bacterial organisms, as well as fungi, have been recognised in other such situations.1-3 When we were there, Fakinah hospital provided one of the few laboratory services in Banda Aceh, and the availability of these facilities were limited as they were focused on public health surveillance. Thus, collection of specimens for culture was not routine. Furthermore, when we arrived there were no nurses, no medical records and no medication or observation charts. While the situation improved rapidly during our stay, these limitations meant that recognition of emerging clinical patterns was important. Many of the antibiotics initially used for patients with immersion injuries were ineffective in this setting, and the use of carbapenems became our first-line, or early second-line, antibiotic in post-immersion respiratory infections in Banda Aceh. Chest x-rays of patients with subacute necrotising pneumonia (a) Bilateral consolidation with scarring and early cavitation in the lower lung fields (b) Bilateral necrotising pneumonia complicated by right pneumothorax

Anthony M Allworth