Respiratory disease

Re: "The effectiveness of coordinated care for people with chronic respiratory disease", by Smith BJ, McElroy HJ, Ruffin RE, Frith PA, Heard AR, Battersby MW, Esterman AJ, Del Fante P and McDonald PJ, published in the 4 November issue of the Journal (Med J Aust 2002; 177: 481–485). The correct credentials and title for Peter A Frith are MB BS, FRACP, Director, Respiratory Medicine, Repatriation General Hospital, Daw Park, SA 5041. The web version of the article was corrected on 18 December 2002.

Brian J Smith MB BS, PhD · Heather J McElroy BSc(Hons) · Richard E Ruffin MD, FRACP · Adrian R Heard MPH, BSocAdmin · Peter A Frith MB BS FRACP · Malcolm W Battersby MB BS, PhD · Adrian J Esterman BSc(Hons), MSc · Peter Del Fante MB BS(Hons), MSc(Public Health) · Peter J McDonald MB BS, FRACP

To the Editor: "Chop-chop" tobacco is illicit tobacco that has been grown and clandestinely distributed by farmers and wholesalers and sold on without government intervention or taxation. There is no quality control over this illicit substance, which may be adulterated or "bulked up". It is sold illegally "under the counter" by weight for rolled cigarettes by unscrupulous tobacconists and grocers. This type of tobacco, which has been roughly chopped up (hence "chop-chop"), is very cheap compared with legally produced manufactured cigarettes. The prevalence of the use of chop-chop in the smoking community is unknown. However, the Australian Taxation Office (ATO) has a keen interest in the distribution of this substance, and estimates that many millions of dollars are lost in revenue from the illegal sale of chop-chop. Arrests and fines initiated by the ATO have so far occurred primarily in Queensland and Victoria. Results of analysis of chop-chop vary from batch to batch, but samples have been shown to contain nicotine (Professor G Starmer, Department of Pharmacology, and Mr B Tattam, Mass Spectrometry Unit, Department of Pharmacy, University of Sydney, personal communication). It may also be fumigated with bleach and may be bulked up to add weight (M Rushton, ATO, personal communication). Although most people smoke it because it is cheap, many have misguided beliefs, for which there is no evidence, that it is "better" than other forms of tobacco. Results of a survey of 44 consecutive patients attending the Smokers' Clinics of the Central Sydney Area Health Service 43% currently using "chop-chop" 84% smoke it because it is cheaper 58% believe it is better for you 74% believe it has no additives 16% believe it has no nicotine 63% know it is not legal A retrospective survey was carried out to assess the prevalence of and attitudes towards illicit tobacco smoking among patients attending the Smokers' Clinics of the Central Sydney Area Health Service (approved by the CSAHS Ethics Committee, June 2002). Patients were routinely asked the type of tobacco they smoked and their beliefs regarding this type of tobacco. The results are shown in the Box. Many of the patients attending the Smokers' Clinics (dedicated exclusively to patients who smoke and have chronic obstructive pulmonary disease [COPD]) smoke this type of illegal tobacco. Several patients volunteered that smoking chop-chop precipitated an acute exacerbation of their COPD. Four patients have recently presented to a hospital emergency department for exacerbation of COPD after smoking chop-chop. Although smokers are loath to volunteer their use of this illegal tobacco, smokers and clinicians should be warned that smoking chop-chop does not constitute a positive health move, is not less harmful, and may be quite dangerous. Quitting smoking altogether is the best health move.

Renee Bittoun

Clinical record In 2001, an outbreak of Bordetella pertussis infection occurred in a hospital special care nursery. The index case, Parent A, had a two- to three-week history of non-productive cough without paroxysms, whooping or vomiting. She was admitted to hospital in labour and gave birth to Baby A on Day 0 in early January 2001. The baby was born four weeks prematurely and remained in the special care nursery for 15 days. The mother spent several hours there each day handling her infant and occasionally assisted with the care of infants in adjoining cots. Serum taken 19 days after she developed cough was negative for Bordetella pertussis IgA and IgM and equivocal for IgG (Figure) by enzyme-linked immunosorbent assay (ELISA). On Day 15, Baby B (in the cot adjacent to Baby A) developed a cough and respiratory distress. Initial investigations did not reveal a cause. A nasopharyngeal aspirate collected on Day 23 was positive for B. pertussis by direct fluorescent antigen testing. On Day 18, a nurse who had cared for Baby A developed a cough. Her serum was positive for B. pertussis IgA on Day 31 by ELISA; she commenced roxithromycin therapy. On Day 31, serum collected from Parent A was positive for B. pertussis IgA. On Day 39, Baby A developed a respiratory illness despite a seven-day prophylactic course of erythromycin. A nasopharyngeal aspirate was positive for B. pertussis by polymerase chain reaction (PCR) on Day 43. Both received erythromycin. On Day 41, a nasopharyngeal aspirate collected during contact tracing from Baby C (in the nursery from Day 0 to 6) grew B. pertussis. She had not received chemoprophylaxis and had a mild cough. She was treated with erythromycin. Contact tracing Contact tracing of infants, parents and staff was undertaken. The incubation period of pertussis is six to 21 days, and is generally less than 10 days.1 The parents of all 19 babies who had been in cots adjoining Baby A were notified, and erythromycin prophylaxis was recommended. Eleven babies received prophylaxis. Parents of other babies in the nursery were contacted and advised to notify the hospital if they or their babies developed a cough over the following 21 days. No further cases were identified. Fifty-three staff with close contact with the cases were screened using direct fluorescent antigen testing of nasopharyngeal aspirates and serum IgA testing. Thirty-three received antibiotic prophylaxis. No staff had illness consistent with acute pertussis or developed infection, as shown by nasopharyngeal and serum IgA tests. There were 10 339 notifications of pertussis in 1999– 2000 in Australia.2 People aged 15 years and over comprised 62% of these notifications.2 Studies indicate that 12% to 32% of cases of prolonged cough (over two weeks' duration) in adolescents and adults are due to B. pertussis.3 Recent articles highlight reasons for the apparent shift in disease burden.3-6 Although adolescents and adults are the primary reservoir of the disease and the main source of infection in infants and unvaccinated children, pertussis often goes unsuspected in these age groups.3,4,7 Pertussis in adults is difficult to detect clinically. Delays and errors in diagnosis occur because the presentation is commonly mild or atypical, and may be asymptomatic.7 This may be a result of immunological recall. As past vaccination or illness does not confer lifelong immunity to pertussis, reinfection is common.8 Detection in adults is further impeded by the poor sensitivity of culture and serological tests,1 particularly if performed several weeks after onset of cough.6 Polymerase chain reaction of nasopharyngeal swabs or aspirates improves detection.6 Deaths from pertussis average one per year in Australia, and almost all involve neonates and unvaccinated infants.2 These groups acquire pertussis in a range of settings, including hospitals;9,10 parents, visitors and healthcare staff are a source of nosocomial outbreaks.7 During the events described here, there was no concurrent epidemic of pertussis in the community (Dr B McCall, Director, Brisbane Southside Public Health Centre, personal communication). Hospitalised infants exposed to pertussis are at high risk of morbidity and mortality, as maternal antibodies provide inadequate protection, while infants less than four weeks old are too young to commence vaccination.11 While erythromycin is the prophylaxis of choice,11 it has been associated with hypertrophic pyloric stenosis in neonates.12 Preventing nosocomial transmissionB. pertussis is spread via mucosal contact with infectious respiratory droplets and secretions.13 We suggest the following standard and transmission-based infection control precautions to protect hospitalised infants: limit access of staff and visitors to nurseries; provide adequate space between open cots (at least one metre); discourage parents from contact with infants other than their own; and perform hand antisepsis before entering the nursery and before and after patient contact. Surgical masks are chiefly designed to protect the wearer from exposure to blood and body fluids; it is suggested that they may also reduce the opportunity for onward transmission of infections spread via large droplets.13 Other important measures include educating staff and visitors to report coughs, diagnosing their aetiology, and providing treatment and prophylaxis. A diagnosis of pertussis can be confirmed by nasopharyngeal aspirate (culture, direct fluorescent antigen testing or PCR) or serological testing (IgA).7 Erythromycin is the treatment and prophylaxis of choice at all ages.11 Targeted booster vaccination of parents and healthcare workers in contact with infants has been recommended, although not universally adopted.3-6 An acellular pertussis vaccine is available for this purpose, but its efficacy and duration of protection remain to be determined.3-5 Australia's pertussis immunisation schedule is restricted to infants and young children.11 Infection control measures are important because of the difficulty in prohibiting all people with coughs from entering hospital nurseries, and the cost implications of vaccinating all adults in contact with infants. Lessons from practice Pertussis should be considered in adults and older children with a cough lasting over two weeks regardless of a past history of pertussis vaccination or infection. If pertussis is suspected, a nasopharyngeal aspirate or swab should be tested by polymerase chain reaction. Serological testing may also be useful when symptoms have been established for longer than two weeks. Adolescents and adults are the primary reservoir of the disease and the main source of infection in infants and unvaccinated children. Hospitalised infants are at high risk for morbidity and mortality from pertussis. Infection control measures are paramount, and targeted vaccination of adults should be considered.

Natalie M Spearing BSN, MBA · Robert L Horvath FRACP · Joseph G McCormack FRCP, MD, FRACP

Objectives: To evaluate the effectiveness of coordinated care for chronic respiratory disease.Design and setting: Community-based geographical control study, in western (intervention) and northern (comparison) metropolitan Adelaide (SA).Participants: 377 adults (223 intervention; 154 comparison) with chronic obstructive pulmonary disease, asthma or other chronic respiratory condition, July 1997 to December 1999.Intervention: Coordinated care (includes care coordinator, care guidelines, service coordinator and care mentor).Main outcome measures: Hospital admissions (any, unplanned and respiratory), functionality (activities of daily living) and quality of life (SF-36 and Dartmouth COOP).Results: At entry to the study, intervention and comparison subjects were dissimilar. The intervention group was 10 years older (P < 0.001), less likely to smoke (P = 0.014), had higher rates of hospitalisation in the previous 12 months (P < 0.001) and had worse self-reported quality of life (SF-36 physical component summary score [P < 0.001] and four of nine COOP domains [P = 0.002–0.013]). After adjustment for relevant baseline characteristics, coordinated care was not associated with any difference in hospitalisation, but was associated with some improvements in quality of life (SF-36 mental component summary score [P = 0.023] and three of nine COOP domains [P = 0.008–0.031]) compared with the comparison group.Conclusions: Coordinated care given to patients with chronic respiratory disease did not affect hospitalisation, but it was associated with an improvement in some quality-of-life measures.

Brian J Smith MB BS, PhD · Heather J McElroy BSc(Hons) · Richard E Ruffin MD, FRACP · Adrian R Heard MPH, BSocAdmin · Peter A Frith MD, FRACP · Malcolm W Battersby MB BS, PhD · Adrian J Esterman BSc(Hons), MSc · Peter Del Fante MB BS(Hons), MSc(Public Health) · Peter J McDonald MB BS, FRACP

To the Editor: Comprehensive care has been shown to improve outcome in asthma management when it has four components — asthma education, self-monitoring, written self-management plans, and regular medical review.1,2 A recent Cochrane Review has explored the role of one of these components — written self-management plans — and concluded that there is "no consistent evidence that written plans produced better patient outcomes".3 Should this cause us to change our management strategies in Australian general practice? Does this mean that our patients are not able to care for their own asthma without our intensive assistance? These findings update a 1998 review of the role of written asthma management plans as part of comprehensive care in 1998: "In five studies which compared subjects who managed their asthma by self-adjustment according to individualised written plan with those whose medications were adjusted by the doctor, lung function data (FEV1 [forced expiratory volume in one second] and PEF [peak expiratory flow]) were significantly higher in the self-managed group."1 In Australian general practice, between 30% and 50% of patients are given a written asthma management plan.4 These plans form part of known beneficial comprehensive asthma care plans, such as the Six-Step Asthma Management Plan5 or the Asthma 3+ Visit Plan.4 The small number of available high quality trials for this most recent review led the authors to say, "Available trials are too small and the results too inconsistent to form any firm conclusions", and suggests that more trials are needed to produce a conclusive result.3 We should be careful not to lose the positive effects of improved chronic disease management in asthma by over-responding to this one review of one component of comprehensive care.

Andrew M Thornett · Jonathan W Newbury · Andre J Duszynski

Comment: A Cochrane systematic review identified the beneficial effects of planned asthma management and education that includes a written action plan.1 These findings have now been adapted for primary care and implemented as the Asthma 3+ Visit Plan. This involves a systematic assessment of asthma symptoms, lung function, and current treatment at each visit. Treatment and management skills are optimised and the patient is given written instructions on how and when to increase treatment when asthma deteriorates (a written action plan). A recent Cochrane review asked whether one can get the same benefits by doing less — by simply supplying a patient with a written action plan.2 The review found that the literature was inconclusive. This doesn't mean that written action plans are not effective; it means that there is not enough evidence to be able to answer the question. The result of "no evidence of effect" is completely different to "evidence of no effect".3,4 This is a crucial distinction, as many systematic reviews find insufficient evidence to be able to assess a treatment. This is a statement about our ignorance rather than a statement about whether a treatment works or not. The review also highlights the need to carefully evaluate the control intervention. For example, the control groups in two studies in the systematic review2 received regular medical review, with assessment of severity and optimisation of inhaled steroid therapy. It is not surprising that these studies found it difficult to identify any additional effect of an action plan. Cochrane systematic reviews conclude with recommendations for clinical practice that highlight effective treatments,1 and with recommendations for research that indicate where more information is needed.2 The review looking at just supplying patients with written action plans2 exemplifies the latter.

Peter G Gibson

To the Editor: The recent article by Johnston et al is an important contribution to the small but growing body of literature on the health effects of particulate matter (PM) pollution derived from bush or forest fire.1 The authors studied an important wood smoke PM exposure in Australia and showed consistent associations between higher concentrations of PM and emergency department presentations for asthma. Most research on the effects of PM has focused on motor-vehicle-derived PM pollution.2,3 However, Johnston et al do not appear to have accounted for serial correlation in their data. Measurements connected in time, such as repeated measurements of the same population, are likely to be correlated and not independent.4 Further, school holidays have been shown to influence hospital admission rates.5 The major Northern Territory school holidays in June and July are in the middle of the study period. Johnston et al adjusted for some important confounders in their analysis (acute respiratory infections and weekdays/weekends).1 However, in time-series data, especially those dealing with asthma, serial correlation, as well as other potentially important confounders such as school holidays and temperature and humidity, should also be assessed. It may be that, even after appropriate adjustments for serial correlation and potential confounders, the rate ratios found by Johnston et al may not alter appreciably. However, it would have been useful for the investigators to have at least discussed any effects that controlling for serial correlation and other potential confounders might have had on their findings.

Bin B Jalaludin · Guy B Marks · Geoffrey G Morgan

In reply: Jalaludin and colleagues query the potential effects that serial correlation and confounding by school holiday time periods may have had on our finding of an association between particulates derived from bushfire smoke and asthma presentations.1 As previously discussed by Schwartz, time series analyses are important to control for serial correlations, particularly those due to the effects of seasonality and weather fluctuations.2 Our study did not cover a number of seasons. It was conducted during one tropical dry season, a period characterised by remarkably stable day-to-day weather conditions.3 For this reason, we believe that the effects of any autocorrelation would have been negligible. It is of interest that the development of statistical methods for analysing time series of count data during the 1990s, and analysis of large studies of particulate pollution using these methods, did not have an important effect on the conclusions reached by earlier studies.4 There is evidence that hospital admissions for asthma fall during school holidays.5 Anecdotal reports of more regional fires suggest that, if anything, particulate concentrations over Darwin might increase at these times. A reanalysis of our data including school holiday periods as a potential confounding factor did not appreciably alter our results in either the continuous (revised incidence rate ratio [IRR],1.26; 95% CI, 1.12–1.41, compared with original IRR, 1.20; 95% CI, 1.09–1.34) or categorical analysis (see Table). Asthma presentations and exposure levels of PM10* (μg/m3) Rate ratio for asthma presentations (95% CI) Same-day PM10 category (μg/m3) Original analysis† Revised analysis‡ < 10 1.0 1.0 10–< 20 0.90 (0.60–1.35) 0.84 (0.43–1.63) 20–< 30 1.11 (0.74–1.69) 1.13 (0.58–2.18) 30–< 40 1.18 (0.72–1.97) 1.21 (0.58–2.50) ≥ 40 2.38 (1.46–3.90) 2.47 (1.21–5.01) * Particles of 10 microns or less in aerodynamic diameter per cubic metre. † Adjusted for influenza-like illness and weekday. ‡ Adjusted for influenza-like illness, weekday and school holiday periods.

Fay H Johnston · Anne Kavanagh · David MJS Bowman · Randall K Scott

Asthma is, quite literally, a household word in Australia, a disease so commonplace that there is a tendency within our community to understate the seriousness of it. But when you have a disease that affects one in four primary-school-aged children, with no known cure, there must be unceasing vigilance in the fight against it. Clearly, we need to know more about asthma and its causes — ...

David Clarke

While we have learnt much of the molecular and immunological basis of childhood asthma and treatment has changed dramatically, the impact on lifestyle, especially in early childhood, has not moved forward as rapidly. This is predominantly due to the difficulty of collecting objective data on the very young. To understand the causes of asthma and improve outcomes, with particular emphasis on primary prevention, it is ...

Craig M Mellis MD, MPH · Louis I Landau MD, FRACP

What we knowWhat we need to know

Louis I Landau MD FRACP

What we knowWhat we need to know

Peter N Le Souëf MD FRACP

What we knowWhat we need to know

Colin F Robertson MD, FRACP

Over the past 20 years, inhaled corticosteroids have become established as cornerstone therapy in the treatment of obstructive pulmonary disorders, ranging from asthma and chronic obstructive pulmonary disease to cystic fibrosis. The appropriate use of inhaled corticosteroids has transformed the management of asthma in children, improving the quality of life of children and their families, improving exercise tolerance, and reducing hospitalisation and mortality rates. Asthma mortality rates in Australia have fallen by more than 50% over the past 12 years, in parallel with our increased use of inhaled corticosteroids and the development of clinical guidelines.1 We have gained confidence in the safety of inhaled steroids at recommended doses, supported by national guidelines and extensive reviews.2 Local side effects, including oropharyngeal candidiasis and laryngeal dysfunction, can usually be controlled with the use of spacer devices. Further, at recommended doses, initial concerns about growth failure and impaired bone mineralisation have not been realised.2 In recent years, with the advent of more potent steroids and more efficient delivery systems, the relative doses commonly used have increased. There have been several reports of serious adverse events resulting from doses of inhaled corticosteroids in excess of those recommended. These include growth failure,3 and suppression of the hypothalamic–pituitary–adrenal axis4-6 — resulting in acute hypoglycaemia, altered consciousness and coma, convulsions7,8 and death.9 While the majority of these effects have been reported at higher doses, some have occurred at a dose within the recommended range, suggesting that individual susceptibility may also be important. These effects are more commonly associated with one potent inhaled corticosteroid, but this is probably a result of over-representation of that drug in the higher dosage range. Comparative studies would suggest that this is a class effect of inhaled corticosteroids.4 Are we overusing inhaled corticosteroids? New evidence-based National Asthma Council guidelines define the need for inhaled corticosteroids in asthma. They recommend an upper limit of 500 μg per day of fluticasone propionate (or equivalent) in children, and 1000 μg per day in adults with severe asthma. In support, a recent meta-analysis, examining the dose response to inhaled corticosteroids in adolescents and young adults, reported that 90% of the maximum benefit was achieved at a daily dose equivalent to 250 μg fluticasone propionate.10 Minimal further improvement resulted from increases up to 600 μg/day. The introduction of long-acting β-agonists at low doses of inhaled corticosteroids can achieve improved asthma control, avoiding the need for higher doses of inhaled corticosteroids. When asthma is not controlled by a dose of inhaled corticosteroids equivalent to 500 μg/day fluticasone propionate and long-acting β-agonists, consideration should be given to issues of adherence to the treatment regimen, inhaler technique or an alternative diagnosis. In the UK survey of adrenal crisis due to inhaled corticosteroids,9 three of the 28 children did not have asthma and, in five, asthma did not account for all the respiratory symptoms. Inhaled steroids have been shown to be ineffective in children with recurrent cough and those with episodic viral-associated wheeze. Clinicians should be alert to the clinical features of hypoadrenalism, particularly when precipitated at a time of metabolic stress, perhaps indicating adrenal crisis. Children taking excessive doses of inhaled corticosteroids (> 500 μg/day fluticasone propionate) should have their hypothalamic–pituitary–adrenal axis assessed, and their parents should be informed of the risks and the potential need for systemic corticosteroid cover during intercurrent illness and surgery. The National Asthma Council recommends the introduction of inhaled corticosteroids (alone or in combination) to gain control of symptoms. On clinical review, there should be a reduction (ie, back-titration) to an appropriate dose to optimise symptom control and reduce the likelihood of adverse effects. By comparison with their United States and European counterparts, Australian prescribers have used higher doses of inhaled corticosteroids, but there is now a clear incentive to reverse this trend. The availability of effective anti-inflammatory therapy, useful and well-publicised guidelines, as well as incentive payments to general practitioners for the treatment of moderate to severe asthma under the 3+ Visit Plan (http://www.health.gov.au/pq/asthma/3plusgp.htm), should pave the way for greater improvements in the management of asthma. The goal of asthma management is to achieve optimal control of asthma symptoms with the lowest effective medication dose, allowing children to enjoy a normal quality of life neither burdened by, nor at risk of, serious adverse events. Inhaled corticosteroids remain the cornerstone of asthma management. Responsible use of inhaled corticosteroids will reinforce confidence in the consumer, whereas irresponsible use will promote steroid phobia — a significant barrier to adherence.

John W Wilson PhD, FRACP · Colin F Robertson MD, FRACP

What we knowWhat we need to know

Karen O McKay LLB, PhD · James C Hogg MD, PhD

What do we know?What do we need to know?

Gary P Anderson PhD

Objectives: To explore the burden of asthma on the lives of people presenting to hospital emergency departments for asthma treatment.Design: A qualitative study. Consenting individuals with asthma who presented to emergency departments were interviewed in-depth, and interviews were taped, transcribed and thematically analysed. Questionnaire data on medication use, respiratory health and asthma knowledge were also collected. Asthma severity was determined from the medical records.Setting: A tertiary teaching hospital and a suburban hospital during March and April 2000, and a rural hospital during July and August 2000.Participants: Sixty-two participants (19 male and 43 female), aged 18–70 years.Results: The burden of asthma was broad, affecting social life, personal relationships, employment and finances. The cost of asthma medication was an issue for nearly two-thirds of participants. Individuals performed their own "cost–benefit analysis" for medication use, weighing up expense, perceived side effects and potential benefits. As a consequence, several participants chose to alter their medication dose, or not to take prescribed medications. For some participants, asthma directly contributed to diminished employment opportunities.Conclusions: To achieve a therapeutic partnership, doctors need to be aware of the substantial social, personal and financial burden of asthma for their patients. They should also recognise that patients' perceptions of treatment cost may compromise treatment adherence.

Dianne P Goeman MA, PostgradDipSoc · Francis C K Thien MD, FRACP · Michael J Abramson PhD, FRACP · Jo A Douglass MD, FRACP · Rosalie A Aroni PhD · Susan M Sawyer MD, FRACP · Kay Stewart PhD, BPharm(Hons)

What we knowWhat we need to know

David Isaacs MD, FRACP, FRCPCH · Preeti Joshi PhD, FRACP

What we knowWhat we need to know

Andrew S Kemp PhD, FRACP

What we knowWhat we need to know

Stephen M Stick MD, PhD, FRACP

What we knowWhat we need to know

Richard L Henry MD, FRACP

What we know What we need to know

Stephen M Stick MD, PhD, FRACP

What we knowWhat we need to know

Sandra D Anderson PhD, DSc

What we knowWhat we need to know

Peter P Van Asperen MD, FRACP

What we knowWhat we need to know

Gary P Anderson PhD