Letters

To the Editor: Growing revenue from the sale of products for nicotine-replacement therapy (NRT), such as nicotine patches, has fuelled media interest in the likelihood that “reformed smokers” are “getting hooked on nicotine replacement”.1 While there may be anecdotal evidence of long-term use, there are no current population-based data to indicate whether this is the case in Australia. Overseas data suggest long-term use of NRT is low.2,3 For example, a United States study found the median duration of patch use decreased from 30 days to 21 days following over-the-counter NRT availability.2 Another study found that more than 75% of NRT purchases were for 1 month, while only 5% of smokers purchased NRT for more than 3 consecutive months and less than 1% of purchases continued to 24 months.3 An Australian survey conducted in 2000 suggested that most NRT use (61%) was short-term, lasting less than 2 weeks.4 More recently, our 2004 telephone survey of smoking-related perceptions and practices included an item on length of NRT use. The survey involved households selected at random from the New South Wales electronic white pages, with quotas applied to the sample based on NSW census proportions. The study was approved by the University of Newcastle Human Research Ethics Committee. Of the 3503 participants (response rate, 43%), all 539 current smokers and 1013 former smokers were asked about NRT use. Those who had made their most recent quit attempt in the previous 2 years reported on their NRT use during that quit attempt. Of the 138 who had used NRT on their most recent quit attempt, only three (2%) used an NRT product for 12 weeks (the recommended length of use). Only four NRT users (3%) reported using the product for more than 3 months, and none reported using NRT for more than 6 months. It appears that fears of widespread addiction to NRT products are probably unfounded. In fact, lack of compliance with use recommendations, resulting in inappropriately short episodes of use, is probably a bigger problem, and one that may help explain the disappointing effectiveness of NRT under “real world” over-the-counter conditions.5 Data on frequent repeated short-term use of NRT products would be useful to round out the picture on NRT use in the over-the-counter environment.

Christine L Paul · Flora Tzelepis · Raoul A Walsh · Billie Bonevski

To the Editor: In the 4 February issue of the Journal, Playford and colleagues highlighted that clinical schools are encouraging interns and postgraduate year 2 (PGY2) trainees to complete some training in rural locations,1 a good strategy considering the link between living in a rural area and working there later.2 Prevocational training in New South Wales and the Australian Capital Territory is undertaken in 15 training networks administered by the NSW Institute of Medical Education and Training (IMET). Networks typically include a city tertiary referral hospital, a metropolitan district hospital and a rural hospital. Until now, all trainees were allocated to a network by an “optimised-preference” algorithm that maximises trainees’ preference for a particular network but does not guarantee their first choice. Intern and PGY2 rotations occur in the hospitals throughout the network, including rural sites. Over the past few years, IMET has received requests to expand the number of rural sites accredited to provide trainees with all or most of their prevocational training in a rural site because: graduates with an interest in rural medicine want more opportunities for rural-based training; rural hospitals associated with a rural clinical school want to “retain” their rural students after graduation; and investment in rural clinical schools and the expanding service roles of rural hospitals has increased the attractiveness and viability of rural postgraduate training. In 2006, as part of its review into the delivery of prevocational training in NSW, IMET piloted the Rural Preferential Recruitment (RPR) process: Accredited rural hospitals advertise positions under RPR. Interested trainees apply directly to these hospitals while applying for network optimised-preference allocation. These hospitals run a merit-based selection process before the main allocation process. Trainees who receive and accept an offer from a rural hospital are removed from the main allocation list. Trainees who do not gain a position from the RPR process remain in the main allocation process. In 2006, four rural hospitals were involved in RPR and recruited 15 interns for the 2007 clinical year. In 2007, 11 rural hospitals attracted 122 applications from 58 applicants, and 35 doctors began a rural internship in January 2008. IMET recently evaluated the RPR scheme, and there is clear demand for quality prevocational training in rural areas, particularly when applicants can choose their hospitals. We hope this increase in rural exposure during the prevocational years will result in more doctors spending all or part of their careers in rural practice.

Louise Rice · Marie-Louise Stokes · Mark A Brown · Kirsten A Campbell · Cassandra Smith

To the Editor: Cunningham and colleagues discussed the rationale for using a live attenuated vaccine against varicella zoster virus (VZV) in preventing herpes zoster (HZ) in an older population.1 They also noted the difficulties in using a live vaccine in immunocompromised adults. Although generally considered less immunogenic than its live counterpart, an inactivated VZV vaccine would be ideal for vaccinating immunocompromised hosts. There is little information in the medical literature on inactivated VZV vaccines. However, the studies that do exist tested inactive vaccine on adult populations and showed favourable performance when compared with a live vaccine.2,3 Despite these promising results, the inactivated vaccine seems to have gone out of favour. Furthermore, if an inactivated VZV vaccine was used in the childhood vaccination programs against varicella, then it would simultaneously solve two problems caused by the vaccine strain of the virus, namely the development of infectious varicella and the reactivation of the vaccine strain as HZ.4 Cunningham and colleagues discussed the benefits of vaccinating an older population with VZV vaccine,1 but did not raise the intriguing possibility that the vaccination program might reduce rates of listeriosis in older people.4 A recent study examined the T-cell response in mice to latent herpesvirus infection, and found that it led to activation of macrophages that, surprisingly, protected the host against subsequent infection with other pathogens such as Listeria monocytogenes.5 Given that protection from HZ through vaccination is achieved by stimulating T-cell numbers above a critical threshold for HZ,6 it could be hypothesised that VZV vaccinees may be protected against listeriosis, an infection to which older people are more susceptible. The basis of this hypothesis is that macrophage activity would be stimulated by the T-cell response to the VZV vaccine, thereby providing cross-protection against L. monocytogenes. Prospective follow-up of vaccinees in Australia over time could refute or confirm this hypothesis.

Sanjaya N Senanayake

To the Editor: Spriggs and Gillam1 recently evaluated the updated guidance on ethical conduct in human research from the National Health and Medical Research Council (NHMRC),2 with particular reference to paediatric consent. The introduction in 2007 of the National Ethics Application Form (NEAF; http://www.neaf.gov.au) represented an attempt to streamline the process of obtaining ethics approval from multiple human research ethics committees (HRECs) for multicentre research. In 2007, just prior to mandatory introduction of the NEAF, we submitted identical NEAFs to 13 HRECs, covering all Australian states and territories, for an epidemiological study into childhood empyema. All but one HREC accepted the NEAF, but, despite use of the same form by the majority, we identified a variety of inconsistencies. With regard to child consent or assent, 11 HRECs required a single child information sheet and consent form; one required two separate age-appropriate forms; and one questioned the planned involvement of children in the consent/assent process and did not require a child’s consent. This latter response arguably contravenes the United Nations Convention on the Rights of the Child, which provides for a child’s right to information in a form they can comprehend, whether or not they have the ability to make decisions.3 Other inconsistencies included the time taken to obtain approval, which ranged from 1 day to 197 days (median, 31 days). One HREC defined a child as being aged less than 18 years; the others used a cut-off of 16 years. One HREC responded that the application did not specifically address local Aboriginal and Torres Strait Islander peoples’ issues, which suggests that the NEAF may not be sufficient to cover such site-specific requirements. One HREC required plain-language translation of consent and information sheets, and another required Aboriginal translation. Also of concern, the NEAF requires justification for the inclusion of Aboriginal or Torres Strait Islander children and other groups where ethical considerations may be different, such as children with intellectual impairment or mental illness. This approach places the wrong emphasis on the desired outcome, which is to give due consideration to cultural, social, health, psychological and local issues that may introduce ethical concerns that are not the same for all children, and it risks exclusion of some children from research that is relevant to them. We suggest the NEAF should instead include a justification for exclusion of any children as a result of cultural or religious background or social or psychological problems. This would provide an alternative way of gathering information about ethically relevant issues, to ensure best practice in ethical conduct or research. Clearly, there is a lack of consistency across Australia in engaging children in research, including the consent/assent process. We believe that use of the NEAF alone is insufficient to rectify these inconsistencies, and now is the time to consider a single national ethics committee for Australia, similar to the National Research Ethics Service recently introduced in the United Kingdom (http://www.nres.npsa.nhs.uk).

Adam Jaffe · Roxanne E Strachan · Katrina J Williams

To the Editor: I read with interest the letter by Lim and colleagues on anorexia nervosa and senna misuse.1 I have seen abnormal whole body bone scans in patients with severe eating disorders of exactly the same pattern (except for the avid bilateral apical lung and gastric uptake) as the case described. However, I disagree with the interpretation of the bone scan. There was increased periarticular tracer uptake involving long bones. The pattern was not that of hypertrophic osteoarthropathy (HOA). The pattern in HOA is linear tracer uptake by the periosteum, particularly along the distal ends of long bones.2 The scan in the case reported did not show uptake of this pattern, despite radiological evidence showing periosteal reaction and new bone formation of the tibia and fibula at the ankle. The pattern exhibited in this patient was more consistent with metabolic bone disease (increased tracer uptake by the ends of long bones periarticularly, the axial skeleton, calvaria, mandible, sternum and “beading” of costochondral junctions, with faint, or absent, renal uptake),3 although not all of these features were present in this case. Metastatic calcification of the gastric wall (not mentioned by the authors) and upper lobes of the lung was present in this patient. Metastatic calcification of the lungs can be diffuse4 or localised (most commonly) to the upper lobes, as in this case.5 With regard to the bone mineral density results in this case, the authors state that the lumbar and femoral neck T scores were elevated (1.2 and 1.3, respectively). The normal range of the T scores is ± 1.0 standard deviation of young adult normal values.6 Elevated bone mineral density measurements are generally not of pathological significance and are therefore clinically not relevant. In my experience they are usually decreased, and are often osteoporotic, in patients with severe eating disorders.

Andrew F McLaughlin

To the Editor: We share the sentiments of Murphy’s article in the 7 April issue of the Journal.1 As intensive care physicians, the issue of futile care is an almost daily consideration. We agree with his assertion that “the community looks to the (senior) medical practitioners for the security they need to accept decisions of great moment, such as withholding futile treatment”.1 It is common for a referral to an intensive care unit to be made because “We asked the family, and they want everything done”. This is the least confrontational manner of “sorting out the resuscitation status” with the next of kin. Unfortunately, it shifts end-of-life decision making to others, particularly the family in crisis. This places additional stress on an already stressful situation. It often results in undignified, ultimately futile medical interventions and prolongation of dying. It is also a potential pastoral and mental health disaster for families. It is our duty of care to such patients to minimise the iatrogenic damage to their families by having senior clinicians communicate which therapies are appropriate, and thereby help families accept the likely prognosis. Ethically, we believe doctors should not harm families in crisis. Establishing when treatment is futile is difficult. The decision is often qualitative, with differing thresholds for futility. Personal and religious beliefs and anecdotal experience all affect the ability of a clinician to determine when a therapy is futile. We believe it is the duty of the clinician who performs an intervention, not the referring clinician, to determine its utility. A patient should not be referred to an intensive care unit if the intensivist believes the multitude of life-supporting therapies are not of clear benefit. If initiated, the intensivist should determine when such therapies are no longer of benefit. A framework for debate and review of contentious cases should be established within institutions as a matter of process. Sadly, intensive care units are increasingly seen as locations for palliative care. When a patient dies, it is unreasonable for referring clinicians to claim a clear conscience by saying “we did everything we could”, when the outcome is a prolonged, undignified death in an intensive care unit. Such deaths are not just wasteful of resources, but cause unnecessary distress to patients, their families and staff who care for them. We must not mistake “treating” our patients for “caring” for them. Doctors should be part of the solution, not part of the problem.

Thomas R Solano · James D Fratzia

To the Editor: Congratulations to Murphy1 for raising the important and sensitive issue of when to stop trying. This is an issue that needs to be discussed more widely in the community and in hospitals, and presented sensitively to all health students. We know that a significant proportion of the health dollar is spent on the last 12 months of life,2 but, more importantly (as Murphy points out), a clear decision, discussed openly with patients and their families, can save significant pain — both physical and emotional — to all concerned. Advance treatment orders can aid decision making in these situations, but need to be backed up with support for patients’ families when they are to be followed. This issue is with us now but will become more widespread in the future. Health professionals need to be well schooled in this important area of caring. We have to understand when to cease the desire to keep a patient alive. Modern health care has provided incredible advances but we are still not good at knowing and being “strong” in our beliefs and behaviour about when to stop.

Peter M Brooks

To the Editor: In the 7 April issue of the Journal, Murphy encouraged the medical profession to be more proactive about discussing end-of-life care options with family members (or next of kin) with a view to withholding care that may be considered futile by the clinical team.1 While we agree that it is important to offer advice about what course of action the clinical team recommends in a particular case, it is equally important that this advice be based on good evidence and sound clinical judgement. This can be difficult, even for experienced clinicians. Further, it is unwise to leave the family without any alternative but to accept that advice, because this can lead to distrust and disagreement between the family and the treating team. This is not a matter of acquiescing to a family’s unrealistic expectations — often the prognosis is not clear-cut, and there are times when a planned but limited trial of therapy is warranted. In complex situations, the prognosis often becomes obvious, and families can and do draw comfort from the fact that every effort was made, and are then more willing to accept limitation or withdrawal of therapy. In the case of withholding cardiopulmonary resuscitation, the treating team has sole responsibility for the medical opinion, but the family should be involved in the final decision and not have it enforced unilaterally.

Mathew Piercy · Graeme Duke

To the Editor: We support the conclusions reached by Parker and colleagues in their study on the attitudes of Australian medical practitioners to end-of-life decisions.1 They recommend the inclusion of decision-making theory and practice within medical ethics curricula, and highlight the need “to facilitate more discussion between specialties about medical decisions at the end of life”.1 An investigation commissioned to the Australian Institute for Suicide Research and Prevention by the Australian Government Department of Health and Ageing in 2006 aimed to verify receptivity towards, and possible ways of implementing, suicide prevention education in the medical curricula of Australian universities. This mandate also provided the opportunity to assess potential interest in and feasibility for education on end-of-life decisions.2 Our exploratory investigation included interviews of key academics in curriculum or accreditation committees of 10 out of 15 Australian medical schools, 24 general practitioners from six Australian states, and 373 medical students from the University of Queensland.2 Representatives of the medical schools considered it a “very high priority” to implement adequate education on end-of-life issues, including euthanasia, in medical curricula. Most of the interviewed GPs (21/24) and 80% of medical students agreed with this sentiment. Common themes that emerged from the study were the need for good preparedness in coping with difficult situations, and the desired capacity in competently handling decisions that are perceived to be requested with increasing frequency in clinical scenarios.2 End-of-life issues nearly always involve aspects that go beyond the treatment of somatic conditions. Moral convictions, religious beliefs, and self-identification processes (with the patient) all compound the challenge physicians face in their practice. The very complexity of the challenge should push towards more knowledge, and this should be obtained through modern medical curricula.

Diego De Leo · Jacinta L Hawgood

To the Editor: In their recent “Clinical Update” on adrenal insufficiency, Jung and Inder1 state: In patients with adrenal insufficiency who are fasting before procedures, glucocorticoid therapy must be continued, by parenteral routes if necessary. A recent case report has highlighted the adverse consequences of omitting oral steroid therapy in a patient who was fasting before a surgical procedure. The patient developed hypotension and acute renal failure. The patient described in the case report2 was admitted with septic arthritis. His usual cortisone dose of 12.5 mg had been omitted that evening, and his morning dose of 25 mg was not given the next day until after he had returned from the operating theatre. Over the next 3 days, he became overtly septic, and returned to theatre for another knee washout. Cortisone was not given during this time. When he developed acute renal failure on Day 5, dehydration and gentamicin toxicity were listed as possible causes. The article by Jung and Inder does not make it clear that the case report contains nothing of relevance to the management of patients with adrenal insufficiency who are fasting for routine surgical procedures, as this man’s hypotension and acute renal failure actually developed over 5 days in the context of sepsis, dehydration and possible gentamicin toxicity, in addition to prolonged withholding of cortisone and two operations.

Ian J Woodforth

To the Editor: The recent article by Jung and Inder1 provides sensible advice for the safe management of adults with adrenal insufficiency (AI) during illness and surgery, without risking adrenal crisis or excessive steroid dosing. However, the authors make no reference to paediatric practice and no guidelines have been provided for the body-size-related steroid doses required in paediatric patients with AI, either for routine steroid replacement or during illness and surgery. It is important that doctors be aware that the doses recommended by Jung and Inder are not suitable for children with AI. In keeping with recent studies of daily cortisol production, daily hydrocortisone replacement doses of 6–8 mg/m2/day are now recommended for children with secondary AI (eg, due to adrenocorticotropic hormone deficiency), provided the patient has no hypoglycaemia or symptoms of cortisol deficiency.2 In children with primary AI, higher hydrocortisone doses are often necessary (up to 10–15 mg/m2/day) — for example, to minimise adrenal androgen secretion in children with congenital adrenal hyperplasia.3 During minor illness (as defined in Box 3 of Jung and Inder’s article1), a child’s usual daily oral dose of glucocorticoid should be doubled or tripled until recovery.3,4 However, for children with secondary AI who are on the lower doses of daily hydrocortisone (about 6–8 mg/m2/day), these multiples may not constitute adequate doses during stress. In these patients, per-m2 dosing is more accurate (ie, 30–40 mg/m2/day for minor illnesses). During moderate-to-severe illness, for patients who are vomiting, those who have experienced trauma and those undergoing anaesthesia and surgery, the following doses of intravenous hydrocortisone are recommended: For children aged < 3 years: 25 mg initial dose then 25–30 mg/day; For children aged 3–12 years: 50 mg initial dose then 50–60 mg/day; and For adolescents and adults: 100 mg initial dose then 100 mg/day. These doses are in keeping with national4 and international3 recommendations, and equate to doses of 60–100 mg/m2/day of hydrocortisone. The more accurate per-m2 dosing should be used for children who are not within the normal weight range for their age. These recommendations for children are extrapolated from adult studies and also based on expert consensus. Attention to the specific body-size dose adjustments required in paediatric prescribing can provide safe levels of steroid cover while avoiding exposure to excessive steroid doses.

Ann M Maguire · Maria E Craig · Christopher T Cowell

To the Editor: The excellent article by Jung and Inder1 in a recent issue of the Journal contains a detailed discussion of different regimens proposed for glucocorticoid supplementation in the perioperative period and makes recommendations for the use of hydrocortisone therapy according to the degree of “surgical stress”. It is worth noting that, in many cases, these recommendations and the detailed advice of endocrinologists regarding individual patients are rendered moot by the changes in routine perioperative antiemetic therapy that have occurred in the past decade. The use of intravenous dexamethasone as an antiemetic has been the subject of much clinical research. The IMPACT study2 showed that it has an antiemetic efficacy similar to that of ondansetron or droperidol when given prophylactically. Dexamethasone is less expensive than either of these drugs and is ineffective as rescue therapy in the setting of postoperative nausea and vomiting (PONV), unlike the alternative drugs. As a result, it is used routinely on induction of anaesthesia in many cases of surgery associated with an increased risk of PONV or where PONV would pose a risk of injury or delayed discharge. A range of doses of dexamethasone for antiemetic prophylaxis has been investigated without finding superior efficacy from higher doses (of up to 1.0 mg/kg).3 The dose typically used in clinical anaesthesia practice is 0.05–0.1 mg/kg. This is equivalent in glucocorticoid activity to more than the highest dose of hydrocortisone described in the guidelines of Jung and Inder1 and should provide a self-tapering effect over 2–3 days, consistent with their recommendations for hydrocortisone dosing.

James A Mitchell

In reply: We thank Woodforth for his interest in our article.1 The cited case report2 involved a patient with panhypopituitarism who had septic arthritis following a total knee replacement, requiring knee washout. As stated by Woodforth, the patient was without glucocorticoid replacement for 5 days, during which time he underwent two surgical procedures. Symptoms of cortisol deficiency were described on Days 1 and 2 postoperatively, with overt sepsis not manifesting until Day 3. The absence of adequate glucocorticoid replacement while the patient was under a “nil oral” instruction and suffering sepsis was undoubtedly a contributory factor in his decline, given that his condition improved significantly after he had received 24 hours of intravenous hydrocortisone treatment and other supportive care. It appears that the cortisone acetate was withheld because of concerns about administering it without food, as other medications were in fact given. We stand by our assertion that patients with proven or suspected cortisol deficiency should receive adequate glucocorticoid replacement before and after surgery, according to the likely stress of the procedure. Often, for minor procedures, an oral route of administration will suffice. Doses of oral glucocorticoids given under these circumstances do not need to be taken with food. If there are sound clinical reasons for the patient not to have any medications orally, then parenteral administration is appropriate.1 Maguire and colleagues correctly point out that the glucocorticoid dosage recommendations in our article are suitable only for adults. They have made a significant contribution to the literature on the investigation and management of paediatric adrenal insufficiency and we would like to thank them for providing the appropriate glucocorticoid doses for paediatric patients under stress. We are aware of the use of dexamethasone as a perioperative antiemetic, as outlined by Mitchell, although it is not clear how widespread this practice is. He is correct in stating that in cases in which dexamethasone is used for this purpose, the glucocorticoid dose thereby provided is likely to be more than adequate for adrenal replacement. However, dexamethasone has no mineralocorticoid activity, and this must be taken into account when treating patients with primary adrenal insufficiency. Doses of hydrocortisone greater than 50–75 mg per 24 hours provide adequate mineralocorticoid replacement. If dexamethasone is used for patients with primary adrenal insufficiency undergoing surgery, it is imperative that the patient continue to take oral fludrocortisone throughout the perioperative period to provide mineralocorticoid replacement. This highlights the need for good communication between the patient’s general practitioner, endocrinologist, surgeon and anaesthetist to ensure the best patient outcome.

Caroline Jung · Warrick J Inder

To the Editor: We all privately seek statistics that enable us to put ourselves in perspective (even if we keep the results to ourselves!), but I am now unsure where my sexual performance stands.1 On the one hand, I am told premature ejaculation affects at least one, and from time to time two, of every three males (is that the < 2 minutes version?), and on the other that there is a skewed distribution with a median of 5.4 minutes and a range of 0.55–44.1 minutes. I’m impressed by the aerobic fitness, never mind the sex. It seems we have a continuously distributed, perhaps skewed, normal distribution of an apparently genetically determined variable, with which individual players (?70%) and their partners are dissatisfied at times. Is that not like height, or IQ? “Premature” ejaculation may not be caused by individual psychology, but it is defined by it: from our beginnings in the Garden of Eden we have always wanted more than we have! The early sperm may not get the bird but historically it got its share of the ovum and thus has persisted over millennia. There may be a role for medicine in some extreme cases (as for “constitutional” dwarfism and gigantism, where being very different carries a significant psychological disadvantage), but for the rest are we not colluding to some extent with an escape from the reality of our limitations? How much of this is treatment and how much is performance enhancement?

Paul T Dignam

In reply: Dignam queries the validity of treating early ejaculation that may simply be a variant of normal. However, if one in three men complain to us of premature ejaculation and how it affects their relationships, we listen. They may regard themselves as very different from other men and may become psychologically disadvantaged. In our article we detailed various presentations of premature ejaculation (PE), including that of a subjective perception of PE although the intravaginal ejaculatory time is normal.1 In such cases, reassurance is an appropriate response. However, for men with primary PE, for whom ejaculation consistently occurs within 1 minute or even before vaginal penetration, there is a problem. This problem can be treated successfully to improve a relationship that may have been foundering. And, yes, this may mean performance enhancement unrelated to aerobic fitness. If men are unsure where their sexual performance stands, they should ask their partner. After all, communication improves a loving relationship.

Neil R Palmer · Bronwyn G A Stuckey

To the Editor: Computed tomography (CT) of the chest is superior to chest x-ray as an imaging modality of the lungs, mediastinum, pleura and the chest wall,1 and its use is increasing for a range of diagnostic and therapeutic applications.2 There are clear indications for the appropriate use of chest CT, and adherence to these can reduce cost, workload, procedure-related complications and radiation exposure. Our group recently analysed referrals for chest CT from general practice, and found that the scan was clinically helpful in only 12%, and inappropriate in 68%.3 We thus examined the indications for ordering CT of the chest, and the associated outcomes in hospital inpatients, who had been referred for chest CT by general physicians. Two respiratory physicians retrospectively reviewed the clinical files, the CT request form, and previous and current imaging of 47 consecutive non-surgical patients admitted to Cairns Base Hospital between 1 January and 1 July 2005. One illustrative patient’s case is described in the Box. The impact of the chest CT on the patient’s clinical outcome was assessed. We used the imaging guidelines of the Royal Australian and New Zealand College of Radiologists (RANZCR) as the standard for evaluating appropriate ordering of chest CT.4 Overall, chest CT was appropriately ordered in 26 of 47 patients (55%). The correct type of scan (contrast, non-contrast or high resolution) was requested for 38 of the 47 patients (81%). In 25 of the 26 appropriately ordered scans (96%), the patient’s physicians had compared the CT scan with previous chest x-rays and recorded this in the file; this was done for only 11 of the 21 inappropriately ordered scans (52%; P = 0.001). Further useful information that had not been detected by other means was obtained from the CT scan (compared with chest x-ray alone) in 26 of 47 patients (55%, comprising 25 of 37 [68%] in the subgroup in whom the CT had been ordered appropriately and one of 10 [10%] in the group ordered inappropriately; P = 0.01). Management was changed as a result of CT scanning in 19 of 47 patients (40%): 18/26 (69%) in the appropriately ordered CT group and 1/21 (5%) in the inappropriately ordered CT group (P = 0.001). The correct type of CT scan led to a higher incidence of change in management (18 of 38 patients; 47%; P = 0.046). We encourage all doctors to use the RANZCR guidelines, or web-based imaging pathways such as those developed by Royal Perth Hospital <www.imagingpathways.health.wa.gov.au> to ensure better clinical practice. An illustrative case of acute respiratory illness from the study A 41-year-old woman with a past history of asthma was admitted to hospital with moderately severe right-lower-lobe pneumonia. She responded to antibiotic and bronchodilator therapy and was discharged on Day 6 with no complications. During her admission she had five chest x-rays and high-resolution computed tomography (HRCT) of the chest to rule out empyema; all of these showed consolidation with a small effusion. In outpatient follow-up, she had two further chest x-rays and HRCT of the chest repeated once during Week 3 because of “slowly resolving” shadows. Assessment and comment: The imaging guidelines of the Royal Australian and New Zealand College of Radiologists4 recommend that further imaging is indicated for clinical deterioration, complications, or slow recovery. Thus, this patient did not need computed tomography (CT) scanning, as none of these criteria were met. Had CT been indicated, conventional CT, and not HRCT, would have been the correct choice. A repeat chest x-ray with a lateral view at discharge and at 6 weeks would have been the appropriate management in this patient.

Askin Gunes · Lloyd J Ridley · Graham Simpson

To the Editor: Bethanechol is a parasympathomimetic agent similar to acetylcholine that is known to be a selective stimulant of smooth muscle in the gastrointestinal tract and urinary bladder. It is normally used to treat non-obstructive urinary retention and has not previously been known to have any effect on skeletal muscle. Adults with cerebral palsy usually slowly deteriorate over the years, with gradually increasing muscle tone, worsening speech, mobility difficulties and a loss of independence. There has been no change in their management for decades. While working in a residential facility for adults with cerebral palsy, we serendipitously found that bethanechol significantly reduced the muscle spasticity in a patient for whom it was initially used to treat micturition difficulty. Seven other patients who were wheelchair-bound with cerebral palsy were then progressively given bethanechol in increasing doses. All patients and/or their carers were advised that the medication was being used experimentally, and all consented to participate in a clinical trial. The results are summarised in the Box. In all patients, bethanechol treatment was ceased for a week once the clinical benefits had been established, and all deteriorated during that week. None of the patients suffered any detectable side effects from the use of bethanechol, but many were already taking a proton-pump inhibitor that may have protected them from any gastrointestinal adverse effects. A synergistic interaction between bethanechol and another medication (eg, diazepam) was excluded as an explanation for the results obtained, as no other medication was common to all patients. Bethanechol’s effect seems to be long-lasting, as the first patient has now been using it for 6 months with no deterioration in his improved muscle tone. A Medline search revealed no studies in which bethanechol had been used as a treatment for cerebral palsy. Although our sample was very small, the fact that every patient improved indicates that a larger trial of bethanechol for cerebral palsy is warranted. Clinical outcomes for eight patients with cerebral palsy after treatment with bethanechol Sex (age in years) Diagnosis Final daily dose of bethanechol* Clinical effects M (41) Ataxic and spastic quadriplegia 60 mg Reduced muscle spasm, improved joint movement and speech, improved sense of wellbeing F (53) Ataxic and spastic quadriplegia 60 mg Improved arm movement and speech, looser muscle tone, more relaxed F (47) Spastic quadriplegia, kyphoscoliosis 60 mg Able to abduct legs from previously clamped closed position, loss of leg spasm pain, improved speech, muscle spasm induced by touch eliminated M (68) Spastic quadriplegia, dysphagia 60 mg Less stiffness, speech clearer, easier for carers to move, improved sense of wellbeing M (58) Rigid spastic quadriplegia 60 mg Less limb muscle spasm, improved arm and trunk movement, markedly improved speech F (44) Spastic quadriplegia, epilepsy 60 mg Improved arm and leg movement, easier to roll M (49) Spastic quadriplegia, athetosis 30 mg Chronic spasmodic jerks ceased completely, speech better, able to play carpet bowls better, back extension improved M (68) Spastic quadriplegia, kyphoscoliosis 60 mg Less muscle pain, less back spasm, easier for carers to lift, felt happier and more relaxed * Given orally in three divided doses.

Warwick J Carter

To the Editor: It has been well established that traditional inhalational anaesthetic agents can cause mild and sometimes fulminant liver failure.1 However, while newer inhalational agents are a theoretical cause of hepatotoxicity, such cases have rarely been reported.2,3 We describe desflurane-induced acute liver failure in a 53-year-old woman with achalasia, hypertension, type 2 diabetes mellitus and hyperlipidaemia. She underwent a Heller myotomy for treatment of the achalasia in late 2004. During anaesthesia, desflurane was administered (1.2 minimum alveolar concentration [MAC]) via a Datex–Ohmeda Aestiva/5 anaesthesia delivery system (GE Healthcare, Sydney, NSW). After the operation, her serum alanine aminotransferase (ALT) concentration peaked at 943 U/L (reference range, < 35 U/L). This was attributed to antibiotic toxicity. As the initial myotomy was inadequate, the surgery was repeated 10 days later with desflurane (0.9 MAC) anaesthesia. The patient developed acute liver failure 96 hours after surgery (serum ALT level, 11 600 U/L; pH, 7.06; international normalised ratio, 3.7) and died despite supportive management. A postmortem examination confirmed massive hepatic necrosis and significantly elevated trifluoroacetyl chloride-specific IgG4 antibodies (optical density, 0.585; reference range, < 0.233) — consistent with an inhalational agent being the cause of the necrosis. There are few similar cases of desflurane-induced acute liver failure in the literature to date2,3 and none, to our knowledge, in Australia. Fulminant hepatic necrosis induced by halothane, the original offending agent, occurs in about one in 35 000 adults. This is thought to be immune-mediated and appears to be directly correlated with the metabolism of the anaesthetic, catalysed by cytochrome P450 2E1, to trifluoroacetylated hepatic proteins. The altered protein is seen as “non-self”, generating an immune response that, on re-exposure, leads to inflammation and cellular death.4 Desflurane is metabolised to inorganic fluoride and trifluoroacetyl chloride. However, due to a lower blood : gas partition coefficient and its resistance to degradation (as a result of replacement of chlorine by fluorine at the α-carbon position), desflurane is metabolised by hepatic enzymes to a lesser extent than halothane, enflurane and isoflurane.4 Thus, the degree of hepatic metabolism appears to be related to the potential for hepatic injury, as seen clinically. Evidence for immune-mediated, allergic sensitisation continues to emerge. Identification of IgG4 antibodies, the rarest and most IgE-like immunoglobulins, strongly suggests an allergic component in the pathophysiology of this disease.5 Although hepatotoxicity is a rare complication of the newer inhaled volatile agents, it may have devastating consequences. Anaesthetic agents should be considered in the differential diagnosis of hepatotoxicity, especially in the context of extreme elevation of serum transaminases, suggesting the presence of massive hepatic necrosis. In this case, postoperative ALT elevation was attributed to antibiotic — rather than desflurane — toxicity, with disastrous results following re-exposure, a scenario that might have been prevented if recognised earlier. A full incident report was made at the tertiary hospital involved, and the death was reported to (and examined by) the coroner. The main recommendation made from the case was that inhalational agents should be avoided in the setting of hepatitis.

Marcus W Chin · Dolores B Njoku · Gerard MacQuillan · Wendy S Cheng · Nickolas Kontorinis

To the Editor: Gastric volvulus is rare but has been reported increasingly due to greater frequency of upper gastrointestinal tract investigations. Depending on the rotation axis, gastric volvulus can be classified as organoaxial, mesenteroaxial or mixed type. We report a case of laparoscopic mesh repair of a mesenteroaxial gastric volvulus secondary to a transverse colon diaphragmatic hernia. A 50-year-old woman presented with a 10-year history of intermittent epigastric pain and vomiting. Symptoms persisted despite multiple investigations over the years and treatment with proton-pump inhibitors and prokinetic agents. She described weight loss and intolerance to solid food, but her medical history was unremarkable. Gastroscopy revealed an unusual stomach configuration and difficulty was experienced in intubating the pylorus. A barium x-ray showed no gastric herniation, but the stomach had an unusual appearance (Box, A). Manometry studies showed normal gastric muscle activity. The patient underwent a laparoscopy, which revealed a mesenteroaxial intra-abdominal gastric volvulus secondary to the presence of a section of transverse colon caught in a diaphragmatic hernia adjacent to the oesophagus (Box, B). The colon was reduced and the hernia sac excised (Box, C). The defect in the diaphragm was subsequently closed, and a dual-layered prosthetic mesh was laid over the repaired area. The stomach was repositioned by anterior gastropexy. The patient’s recovery was uneventful and she was discharged on a fluid diet 3 days after surgery. At 4-month review, she was well and a follow-up abdominal computed tomography scan showed no abnormalities. Reports of isolated colonic hiatal hernia are rare.1,2 This case was interesting as it was associated with an intra-abdominal gastric volvulus that presented with chronic symptoms, despite most cases of mesenteroaxial volvulus presenting acutely. Barium studies from 19 patients with colonic herniation through the oesophageal hiatus showed that these hernias were invariably associated with herniation of the stomach, which was partially volvulated in many cases.3 These patients were mostly older women, and did not present in an emergency setting. With growing use of laparoscopic surgery, patients benefit from a minimally invasive approach, decreased pulmonary and wound complications, and faster postoperative recovery. Several authors have reported favourable outcomes after performing laparoscopic diaphragmatic hernia repairs and gastropexy.2,4,5 Our case demonstrates the feasibility of laparoscopic repair of a gastric volvulus secondary to a transverse colon diaphragmatic hernia. Diagnosis and repair of a gastric volvulus A: Barium x-ray of stomach, showing two air–fluid levels that give the impression of an “upside-down” stomach of mesenteroaxial rotation; pylorus (P) and diaphragm (D) are shown. B: Herniated transverse colon (TC) tracking under the liver (L) and into a hernia of the diaphragm. C: Diaphragmatic sac adjacent to the oesophagus, revealed by reducing the colon; oesophagus (O) and stomach (S) are shown.

Kevin Ooi · Christophe Berney

To the Editor: In bicycle accidents, direct impact with the bicycle handlebar can cause serious abdominal injuries. These injuries occur not only in high-speed collisions, where the rider is thrown from the bicycle, but also in low-speed crashes, where the bicycle handlebar strikes the rider in the abdomen or pelvic region.1 We retrospectively reviewed all children who presented to Princess Margaret Hospital for Children with abdominal bicycle handlebar injuries from January 2002 to July 2007. The patients were identified from the emergency department trauma database; 60 boys and 10 girls were identified, aged 5–15 years. Significant injuries (defined as injuries to the liver, spleen, kidney, pancreas, small bowel, stomach or urinary bladder) were noted in 25 of the 70 patients (36%), and 15 of the 70 patients (21%) required surgery. Twenty-one patients (30%) had handlebar imprints on the abdomen (Box, A), and 17 of them (81%) had significant injuries. Traumatic abdominal wall hernia (TAWH) was present in three patients (Box, B). The odds of a significant injury were 21.8 times higher (95% CI, 5.8–82.1) for patients with handlebar imprints than for those with no handlebar imprints. Computed tomography (CT) was the main method of diagnosis of significant injury, and there was a statistically significant association between handlebar imprints and a positive CT scan result, defined as evidence of a solid or hollow viscus injury (2-sided Fisher’s exact test, P = 0.01). Of those patients who underwent CT scanning, 89% of those with handlebar imprints (16/18) had a positive CT scan, compared with 36% of those with no handlebar imprints (4/11). The odds of a positive CT scan were 14 times higher (95% CI, 2.1–95.1) for patients with handlebar imprints than for those with no handlebar imprints. Similar rates of significant injury resulting from impact with handlebars have been reported previously.2 TAWH was first described in 1906,3 and 31 cases of handlebar-related TAWH in children have been reported to date, excluding our cases.4,5 TAWH is produced by sudden application of blunt force to the abdomen that does not penetrate the skin, but is strong enough to disrupt muscle and fascia. Surgical repair is usually required to prevent complications.5 Children with handlebar imprints should be observed closely, and assessed by CT scan and treated surgically as indicated. They should be encouraged to use protective gear, such as handlebar padding, helmets and protective clothing, when riding bicycles. Injuries caused by bicycle handlebars in children A: Handlebar imprint on abdomen. B: Traumatic abdominal wall hernia, caused by handlebar injury, with omentum protruding through the defect.

Parshotam K Gera · Andrew P Barker · Ian Gollow · Jillian Orford · Sue Wicks · Liz Whan

To the Editor: We read with interest Rey’s interpretation of the Multimodal Treatment Study of Children with Attention Deficit Hyperactivity Disorder (MTA).1 The MTA was a large randomised study comparing the impact of stimulant medication, behavioural treatment, a combination of the two, and standard community care on attention deficit hyperactivity disorder (ADHD).2 The treatment phase lasted 14 months, during which the children taking medication showed more improvement than the other groups. Participants were then allowed to change their treatment and, at 36-month follow-up, the outcomes in all groups were similar. Rey concluded that, if stimulant medication is not associated with sustained improvement, its place in the treatment of ADHD is limited. This conclusion overlooks two important points. First, the greater initial improvement in symptoms of ADHD associated with stimulant medication might be important both clinically and socially. The second point is the expected impact of a relatively brief intervention: is it really plausible that an independent effect of 14 months of controlled treatment will be detectable after a further 22 months of self-selected management? The observation that the 14-month treatment phase becomes progressively less relevant as time passes is perhaps not altogether unexpected. In the unmedicated group, the 23% non-compliance rate during the 14-month treatment phase indicated greater dissatisfaction with treatment than the 10% non-compliance in the medication groups (P < 0.005, χ2 test). This could imply a parental preference for more immediate relief of symptoms, even if it involves their child taking medication. Parental preference can be accommodated if the family and treating physician discuss and agree on a treatment plan, adjusted to optimise functioning. Far from indicating a diminished role for medication, the evidence from the MTA study suggests that the clinical approach would involve most individuals with ADHD being treated with stimulant medication at some stage. Stimulant medication treats symptoms; it is not curative. It is likely that the role of stimulant medication in the treatment of ADHD decreases as children mature. However, temporary relief of symptoms can be highly valuable for affected children and their families.

Alison Poulton · Ralph K H Nanan

In reply: Poulton and Nanan question my statement that the role of psychostimulant medication in attention deficit hyperactivity disorder (ADHD) becomes less prominent when the 3-year results of the Multimodal Treatment Study of Children with Attention Deficit Hyperactivity Disorder (MTA) are taken into account.1 Studies such as the MTA that report dramatic short- to medium-term improvement have, in my experience, increased practitioners’ expectations and reliance on these medications. Their clinical use has gradually widened to preschool-aged children and to the, so far, poorly validated inattentive and impulsive–hyperactive subtypes of ADHD. I observe this increasing the pressure on parents — not necessarily from clinicians — to use stimulants through an emphasis on the consequences of non-treatment, such as underachievement and conduct problems. The 3-year follow-up of the MTA brings the early findings into perspective: a carefully titrated medication regimen produces no better results 3 years later than behavioural treatment and standard community care.2 In that sense, the role of stimulants versus other interventions has shrunk, and conscientious practitioners will inform parents and children of these findings when examining treatment options. My editorial did not query the many short-term benefits of stimulants but raised questions about when, and for how long, they should be used. Poulton and Nanan rightly emphasise that stimulants are a “symptomatic” treatment. Further, stimulants increase the ability to concentrate and be on task whether or not individuals meet criteria for ADHD.3 This is further compounded because ADHD, like intellectual disability in the case of intelligence, represents the extreme of a dimension of behaviour.4 The boundary between illness and non-illness depends on where you draw the line, not on qualitative differences. However, there is no good tool to measure ADHD, unlike intelligence, and asessment depends on clinicians’ thoroughness and skill, and on informants, who may or may not be reliable. The situation with ADHD is also similar to that for nocturnal enuresis, another disorder that lessens with increasing age, although it may persist. While behavioural treatment (the bell and pad alarm) is effective for enuresis, families and clinicians prefer using medication, even though the latter is “symptomatic” treatment and potentially harmful.5 This may be an alternative explanation for the higher non-compliance rate in the non-medicated group: behavioural treatments place more demands on parents, children and schools than a pill.

Joseph M Rey

To the Editor: We describe our experience of using community consultative strategies at a family planning clinic in Dubbo, central-west New South Wales, to increase recruitment of Indigenous women to a human papillomavirus (HPV) prevalence study — WHINURS (Women, Human papillomavirus, Indigenous, Non-Indigenous, Urban, Rural Study).1 The strategies also resulted in a sustained increase in the number of Indigenous women attending the clinic for cervical screening. The Family Planning NSW research team committed to recruit 50 Indigenous and 100 non-Indigenous women from January 2006 to WHINURS. The researchers worked collaboratively with, among others, the National Indigenous Immunisation Coordinator of the National Centre for Immunisation Research and Surveillance and the Dubbo Aboriginal Women’s Advisory Group. The study was approved by the Aboriginal Health and Medical Research Council of NSW Ethics Committee. Non-Indigenous women were recruited within a few months but, despite the clinic team’s efforts, only one Indigenous woman was recruited over 12 months. Strategies to increase recruitment were then developed with input from one of us (C J O, a Wiradjuri Health Promotion Officer). Key strategies included street walks with a family planning nurse in Dubbo’s main street, attendance at community forums (including mothers’ groups and playgroups), and provision of drop-in clinics and transport assistance. As a result, an additional 42 Indigenous women aged 18–40 years were recruited between January and April 2007 for HPV and Pap tests. There are many barriers to Indigenous women participating in cervical screening programs.2,3 An added benefit of our recruitment approach was that the number of Indigenous women attending the clinic for Pap tests increased from 29 in 2006 to 81 in 2007, suggesting that the strategies had a sustained effect on cervical screening rates. The involvement of a respected and trusted Wiradjuri woman (C J O), known in the region as an advocate for Indigenous women’s health, appeared critical to the success of the recruitment intervention. The street walks and community visits with family planning nurses were a strategy to ensure that Indigenous women who are “very skilled at observing people and reading the unspoken word” felt safe and comfortable about undergoing the sensitive examination (C J O). The women were able to discuss their fear of finding an abnormality and balance this against their desire to do the right thing by their children by having a health check. Given that the age-standardised mortality rate for cervical cancer from 2001 to 2004 was 4.7 times higher for Indigenous women than for non-Indigenous women,4 we suggest that lessons learned from our study could help facilitate continued participation of Indigenous women in the national cervical screening program.

Christine M Read · Deborah J Bateson · Christine J Ohrin

To the Editor: We read with interest the article by Rosenfeld and Duggan,1 who speculate on the possible psychological downsides of colorectal cancer (CRC) screening with faecal occult blood testing, and possible barriers preventing women accessing screening. We are concerned that the article has multiple limitations, and would like to report prospective data on CRC screening in Australia. While not mentioning three studies showing no long-term psychological harm from CRC screening,2 the authors have chosen to quote anecdotes from breast cancer screening, and a study of diagnostic testing for hepatitis C in a high-risk population, which is not a population screening test. Further, in the quoted study by Mant et al,3 an example they give of anxiety after a screening test, they neglected to mention that 98% of participants with false positive results felt the test worthwhile, and almost 40% were more likely to take part in other screening. The quoted reduction of 16% in CRC mortality is from one trial only, and potentially misleading as, overall, the studies have shown a 15%–33% reduction in mortality.2 Benefit also goes well beyond reduced mortality, as the 20% reduction in incidence2 with early detection averts some of the physical and financial costs of surgery, radiation therapy and chemotherapy. Further, there are the definite negative impacts of dealing with the consequences of surgical management of a more advanced-stage symptomatic cancer (such as colostomy bags), compared with a screen-detected cancer managed by simple polypectomy. The additional negative effects of diagnosis of a potentially terminal illness are also relevant. Data on participation in CRC screening are available from two sources. The National Bowel Cancer Screening Program evaluations to date have shown that significantly more women participate in the screening offer than men.4 Data from a multicentre Australian prospective CRC database5 reveal 56 of 619 cases in women (9.0%) and 65 of 759 cases in men (8.6%) were detected by screening. Australia has been slow to adopt CRC screening despite the almost 5000 deaths annually, and the major potential benefits. Unlike Rosenfeld and Duggan, we argue that studies specific to CRC screening show no clear negative impact, and that the negative impacts of not screening are undisputed. Also, the available data indicate that women are participating in CRC screening to a greater extent than men.

Suzanne Kosmider · Kathryn M Field · Finlay A Macrae · Peter Gibbs

To the Editor: We read the article by Bunting and colleagues1 with interest, as it attempted to address the important question of whether agitation and aggression are more commonly seen with methamphetamine toxicity. However, we have several concerns about the results presented in this study and the conclusions drawn by the authors. First, while they have shown that methamphetamine users were more likely to be agitated and aggressive than patients in other “toxicology-related presentations”, this is not surprising. The most common “toxicology-related presentations” to emergency departments are deliberate self-poisonings with drugs like paracetamol, non-steroidal anti-inflammatory drugs, and benzodiazepines,2 and these agents do not cause significant agitation. The control group in the study by Bunting and colleagues should have been patients presenting with toxicity associated with other recreational drugs. Second, the real issue is whether agitation and aggression are more common with methamphetamine than with other sympathomimetic agents, such as cocaine, amphetamine and methylenedioxy-methamphetamine, as well as ketamine. The authors should therefore have compared patients in methamphetamine-related presentations with those presenting with toxicological symptoms related to this group of drugs, which have also been shown to be associated with significant aggression.3,4 Third, the authors have not stated how they determined whether the presentation was related to methamphetamine or other drugs. It must be assumed that this was on the basis of patients’ self-report. Patients could potentially have been miscategorised without appropriate confirmatory toxicological screening. Fourth, the authors made no comment on the effect of ethanol co-ingestion and the risk that this can precipitate violence and aggression, which could be a considerable confounding factor. Previous authors have reported that violence and aggression are more commonly associated with ethanol ingestion than with use of other recreational drugs.4 Finally, we are concerned that the conclusion of their abstract is not backed up by the results of their study, as there are no data presented to support their statement that “methamphetamine appeared to be used consistently, rather than as an episodic ‘party drug’”. We therefore urge that clinicians interpret the results of this study with caution.

Paul I Dargan · David M Wood