Research

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

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

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

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

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

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

Objective: To determine the prevalence of colorectal neoplasia detected by rescreening people with average risk five years after initial screening by flexible sigmoidoscopy.Design: Prospective survey of results of a colorectal cancer screening program.Participants: People aged 55–64 years with no symptoms or family history of colorectal cancer who were recruited from the community for flexible sigmoidoscopy screening five years previously (July 1995 to December 1996) and had no colorectal neoplasms detected.Setting: Fremantle Hospital, Western Australia, a community-based teaching hospital, December 2000 to June 2001.Main outcome measures: Number and size of colorectal neoplasms (adenomas or cancer) compared between rescreened patients and initial screening population (all 982 people screened between July 1995 and December 1996).Results: 803 people were eligible for rescreening; 138 were no longer at the recorded address, and 361 of the remaining 665 (54%) were rescreened. Rescreening found a significantly lower prevalence of colorectal adenomas than initial screening (8% [95% CI, 5%–11%] versus 14% [95% CI, 13%–15%]; P < 0.05) and also a lower percentage of adenomatous polyps over 5 mm in diameter (32% [95% CI, 15%–49%] versus 51% [95% CI, 46%–56%]; no significant difference).Conclusion: Average-risk people who have been screened for colorectal neoplasms, with none found, have a low prevalence of neoplastic lesions five years later. Longer rescreening intervals need to be considered.

Cameron F E Platell PhD, FRACS · Gillian Philpott EN · John K Olynyk MD, FRACP

Objectives: To identify approaches to and barriers associated with the management of patients with work-related stress by general practitioners (GPs).Design: Cross-sectional postal survey using a self-administered questionnaire which included a case vignette of a patient with work-related stress and questions ascertaining perceived barriers to the effective general practice management of work-related stress.Participants and setting: 450 Western Australian GPs on the mailing list of a GP journal. The survey was conducted between 22 March and 28 April 2000.Main outcome measures: Likelihood that GPs would (i) choose to open a workers compensation claim and (ii) provide time off work for the patient described in the vignette.Results: Response rate was 50.1%. Eighty-five per cent (95% CI, 79.6%–89.7%) of respondents advised the hypothetical patient to take time away from work; however, only 44.0% (95% CI, 37.2%–50.7%) chose to initiate a workers compensation claim. GPs with training or experience in occupational health were less likely to advise the patient to stay away from work (odds ratio [OR], 0.30; 95% CI, 0.12–0.73), but were just as likely to initiate a claim. GPs were reluctant to involve the employer in management decisions, because of concern about patient confidentiality and the potential to make matters worse for the patient. These, and the adversarial nature of the workers compensation system, were the strongest perceived barriers to effective management of the condition.Conclusions: Our findings indicate that general practitioners take a pragmatic and varied approach to the management of work-related stress. The perceived difficulties with contacting employers challenges the principles of injury management within a workers compensation system which is dependent on liaison between system stakeholders.

Grant M Russell FRACGP MFM (Monash) · Sally M Roach PhD, PostGradDip, BAppSc

Objectives: To determine the prevalence of stroke risk factors in a general practice population and to identify pharmacotherapies currently used in management of stroke risk factors.Design: Multicentre, observational study by 321 randomly selected general practitioners who each collected data on 50 consecutive patients attending their surgery.Patients and setting: 16 148 patients aged 30 years or older attending general practices across Australia during 2000.Outcome measures: Prevalence of hypertension, current smoking, diabetes, hypercholesterolaemia, atrial fibrillation, recent history of stroke or TIA; extent of pharmacotherapy use in risk-factor management.Results: 70% of patients had one or more risk factors and 34% had two or more. Hypertension was the risk factor with greatest prevalence (44%), followed by hypercholesterolaemia (43%) and current smoking (17%). The prevalence of risk factors generally increased with age, except for current smoking, where a decrease with age was seen. The most common pharmacotherapies were cardiovascular agents, followed by antiplatelet agents. Two-thirds of patients with hypertension were taking cardiovascular drugs, most commonly angiotensin-converting enzyme inhibitors.Conclusions: Stroke risk factors are highly prevalent in general practice patients and GPs are ideally placed for opportunistic case-finding. There is considerable scope for improving management of stroke risk factors. The Avoid Stroke as Soon as Possible (ASAP) general practice stroke audit provides a baseline against which progress in risk-factor management can be measured.

Jonathan W Sturm MB ChB, FRACP · Geoffrey A Donnan MD, FRACP · Stephen M Davis MD, FRACP · John G O'Sullivan MB BS, FRACGP · Miriam E Vedadhaghi BSc, PostGradDipNutr

Objective: To determine whether thyroid-stimulating hormone (TSH) concentrations in a large sample of neonates meet World Health Organization criteria for an iodine-replete population (< 3% of neonates with whole-blood TSH concentrations > 5 mIU/L), and, in a small subset of neonates, to examine the correlation between maternal urinary iodine and neonatal TSH concentrations.Design: Cross-sectional study of neonatal whole-blood TSH values obtained as part of a routine newborn screening program.Setting: Royal North Shore Hospital (RNSH) in northern Sydney.Participants: Two anonymous samples of neonates born at RNSH (1316 infants born between August 1998 and April 1999 and 1457 infants born between 1 March and 31 December 2000); and 84 infants whose mothers had attended RNSH between September 1998 and August 1999 and supplied a urine sample for iodine measurement.Main outcome measures: Iodine status of neonates (proportion with whole-blood TSH values > 5 mIU/L), and urine iodine concentrations of pregnant women.Results: In the two large population samples of neonates, 8.1% (95% CI, 6.6%–9.5%) and 5.4% (95% CI, 4.3%–6.6%), respectively, had whole-blood TSH values > 5 mIU/L (prevalence range for mild thyroid deficiency, 3%–19%). Comparing the TSH values of the 1316 anonymous infants and the 84 identified infants showed no difference between the proportions with TSH values > 5 mIU/L (8.1% v 10.7%, respectively; P = 0.39). Urine iodine concentrations in the 84 pregnant women indicated borderline mild iodine deficiency. TSH values in their 84 infants were positively correlated with maternal urine iodine concentrations.Conclusions: Our results suggest that the population of northern Sydney may have mild iodine deficiency. However, the expected relationship between maternal urine iodine levels and neonatal TSH concentrations was not found.

Aidan McElduff PhD, FRACP · Patrick McElduff BMath, PhD · Jenny E Gunton MB BS, FRACP · Graham Hams MAppSc · Veronica Wiley PhD · Bridget M Wilcken MB ChB, FRACP

Objective: To describe the variability and evidence base of recommendations in Australian protocols and national policies about six aspects of routine antenatal care.Design: Comparison of recommendations from local protocols, national guidelines and research about number of visits, screening for gestational diabetes (GDM), syphilis, hepatitis C (HCV), and HIV, and advice on smoking cessation.Setting: Australian public hospitals with more than 200 births/year, some smaller hospitals in each State and Territory, and all Divisions of General Practice were contacted in 1999 and 2000. We reviewed 107 protocols, which included 80% of those requested from hospitals and 92% of those requested from Divisions.Main outcome measures: Frequency and consistency of recommendations.Results: Recommendations about syphilis testing were notable in demonstrating consistency between local protocols, national policies and research evidence. Most protocols recommended screening for GDM, despite lack of good evidence of its effectiveness in improving outcomes. Specific approaches to screening for GDM varied widely. Coverage and specific recommendations about testing for HIV and HCV were also highly variable. Smoking-cessation information and advice was rarely included, despite good evidence of the effectiveness of interventions in improving outcomes. No national policies about the number of routine visits and smoking cessation could be identified. There were inconsistent national policies for both HIV and GDM screening.Conclusions: Antenatal care recommended in protocols used in Australia varies, and is not always consistent with national policies or research evidence. Producing and disseminating systematic reviews of research evidence and national guidelines might reduce this variability and improve the quality of Australian antenatal care.

Jennifer M Hunt MPH, FAFPHM · Judith Lumley PhD, FFPHM(UK)

Objectives: To study the incidence of and factors associated with single-vehicle rollover (SVRO) accidents in the "Top End" of the Northern Territory (NT); to identify factors associated with major injury and death from SVRO accidents.Design: Retrospective analysis of records from the NT Department of Transport and Works' police database, Royal Darwin Hospital's trauma database, coroner's records, and case notes from public hospitals in the Top End.Study population: All patients involved in SVRO accidents in the Top End between 1 January 1996 and 31 December 1997 whose accident was documented by the police, who attended a public hospital, or who died.Main outcome measures: Types and incidence of all accidents; details of the accident scene, vehicle features, and population groups associated with SVRO accidents; factors associated with major injury and death.Results: SVROs accounted for 30% of all accidents and 29% of all injuries and deaths (441 people) in the whole of the NT over the study period. Some of the factors associated significantly more frequently with SVRO accidents were (i) occurrence of the accident on a straight, dry, unsealed road; (ii) presence of a vehicle defect; (iii) travelling at excessive speed; and (iv) the person being male, aged 41–50 years, of Aboriginal descent. Among the 147 people who were admitted to hospital or died from SVRO accidents in the Top End, major injury occurred significantly more frequently if the person was under the influence of alcohol, was not wearing a seatbelt and was ejected; if the accident occurred in a rural area; and if the vehicle was speeding. Major injuries occurred in 21% (31/147), and death was more likely in those with head, chest and neck injuries.Conclusion: SVRO accidents are a major cause of morbidity and mortality in the Top End of the NT. Effective methods of limiting speeding, drink-driving and driver fatigue should be sought. Populations most at risk should be targeted.

P John Treacy MD, FRACS · Kerrie Jones BMBS, FACEM · Carole Mansfield RN

To fill a gap in knowledge about the effectiveness of brief intervention for hazardous alcohol use among Indigenous Australians, we attempted to implement a randomised controlled trial in an urban Aboriginal Medical Service (AMS) as a joint AMS–university partnership. Because of low numbers of potential participants being screened, the RCT was abandoned in favour of a two-part "demonstration project". Only 16 clients were recruited for ...

Beverly M Sibthorpe BA(Hons), PhD · Ross S Bailie MD, FAFPHM · Maggie A Brady MA, PhD · Sandra A Ball BCom, GradDip Public Administration · Polly Sumner-Dodd DipManagement · Wayne D Hall BSc, PhD

Aim: To survey the attitudes of a population of Australian men to potential use of male hormonal contraception (MHC). Design: Survey of male partners of women who had recently given birth. Men were approached while visiting their female partners on the ward. Participants: 118 out of 148 Australian-born English-speaking men who were approached. Setting: Postnatal ward of Monash Medical Centre (a public teaching hospital in Melbourne), between October 2000 and April 2001. Main outcome measure: Attitudes towards potential use of MHC, rated on a five-point scale. Results: 89/118 men surveyed (75.4%; 95% CI, 67.7%–83.2%) indicated that they would consider trying MHC if it were available. The three most popular choices for method of administration of MHC were (in descending order) an oral pill, a three-monthly injection, or a two-yearly injection. A statistically significant association was found between acceptability of vasectomy and acceptability of MHC (70.5% of men who indicated they would try MHC [MHC "triers"] found vasectomy acceptable versus 44.5% of MHC "non-triers"; P = 0.011). Triers reported a higher rate of approval of MHC by their female partners than non-triers (79.8% v 13.8%, respectively; P < 0.0001). Conclusions: MHC appears to be acceptable to a majority of Australian men when surveyed in a postpartum context. Attitudes of men towards existing male contraception, as well as the attitudes of their partners, appear to exert a strong influence on acceptability of MHC.

Gareth C Weston MB BS · Michelle L Schlipalius MB BS · Meabh Ni Bhuinneain MRCOG, MRCPI · Beverley J Vollenhoven PhD, FRANZCOG

Objectives: To determine the proportion of patients with established coronary heart disease (CHD) in two Australian studies (VIC-I in 1996–1998, and VIC-II in 1999–2000) who achieved their risk-factor targets as recommended by the National Heart Foundation of Australia, and to compare this proportion with those in studies from the United Kingdom (ASPIRE), Europe (EUROASPIRE I and II) and the United States (L-TAP).Design and setting: Prospective cohort study with VIC-I set in a single Melbourne university teaching hospital and VIC-II set in six university teaching hospitals in Melbourne, Victoria.Participants: 460 patients (112 in VIC-I, 348 in VIC-II) who completed follow-up in the control groups of two randomised controlled trials of a coaching intervention in patients with established CHD.Main outcome measures: The treatment gap (100%, minus the percentage of patients achieving the target level for a particular modifiable risk factor) at six months after hospitalisation.Results: The treatment gap declined from 96.4% (95% CI, 91%–99%) to 74.1% (95% CI, 69%–79%) for total cholesterol concentration (TC) < 4.0 mmol/L (P = 0.0001) and from 90.2% (95% CI, 83%–95%) to 54.0% (95% CI, 49%–59%) for TC < 4.5 mmol/L (P = 0.0001). This reduction in the treatment gap between VIC-I and VIC-II appears to be entirely explained by an increase in the number of patients prescribed lipid-lowering drugs. The treatment gaps in the UK and two European studies were substantially greater. The treatment gap for blood pressure (systolic ≥ 140 mmHg and/or diastolic ≥ 90 mmHg) in VIC-II was 39.5%, again less than corresponding European data. There were 8.1% of patients who had unrecognised diabetes in VIC-II (fasting glucose level ≥ 7 mmol/L), making a total of 25.6% of VIC-II patients with diabetes, self-reported or unrecognised. The proportion of patients in VIC-II who were obese (body mass index ≥ 30 kg/m2) was similar to the overseas studies, while fewer patients in VIC-II smoked compared with those in the UK and European studies.Conclusions: A substantial treatment gap exists in Victorian patients with established CHD. The treatment gap compares well with international surveys and, at least in the lipid area, is diminishing.

on behalf of the COACH study group

Objectives: To assess whether referrals for surveillance colonoscopy and subsequent follow-up recommendations for patients with a family history of colorectal cancer concurred with the published National Health and Medical Research Council (NHMRC) guidelines.Design: A prospective audit of patients with a family history of colorectal cancer referred for surveillance colonoscopy. Follow-up recommendations were assessed retrospectively.Setting and subjects: All patients referred to a major teaching hospital for surveillance colonoscopy on the basis of a family history of colorectal cancer from 2 January 2000 – 15 April 2001.Main outcome measures: Concurrence of referrals and recommendations with NHMRC guidelines.Results: Of 340 patients referred because of a family history of colorectal cancer, 202 (83 men, 119 women) were asymptomatic. Their mean age was 50 years (95% CI, 48.3–51.6 years). The family history of 95 (47%) of these patients satisfied the NHMRC criteria for colonoscopic surveillance. Another 20 patients (17%) satisfied the criteria, but were referred before the recommended age to commence surveillance. Analysis by referral source showed that the proportion of referrals meeting NHMRC guidelines was higher from specialists than from general practitioners (75% v 45%), and this difference was significant. Follow-up recommendations, when made, concurred with NHMRC guidelines in 81% of cases.Conclusions: Further education of the medical community is required to increase understanding of colorectal screening strategies and ensure appropriate resource allocation.

Ian F Yusoff MB BS, FRACP · Neville E Hoffman PhD, FRACP · Hooi C Ee PhD, FRACP

Objectives: To determine whether applying National Health and Medical Research Council (NHMRC) guidelines for colorectal cancer prevention would reduce the number of follow-up colonoscopies.Design: A prospective audit of colonoscopic surveillance decisions before and after the intervention.Setting: The endoscopy suite at a metropolitan tertiary hospital three months before and after January 2000. Intervention: Dissemination of NHMRC guidelines, and supervision of application of the guidelines by a nurse coordinator.Subjects: We compared colonoscopic surveillance decisions before and after the intervention in two groups of 100 consecutive patients after polypectomy and in two groups of 50 consecutive patients with a family history of colorectal cancer after a normal colonoscopy. Main outcome measures: Change in concordance of decisions with NHMRC guidelines; and effect on number of follow-up colonoscopies.Results: After the intervention, the proportion of postpolypectomy surveillance decisions matching the guidelines increased from 37% to 96% (P < 0.05). The mean time to repeat colonoscopy after polypectomy increased from 2.7 to 3.5 years (P < 0.005) (ie, a 23% reduction in the number of postpolypectomy surveillance colonoscopies performed per year). Likewise, the proportion of family-history surveillance decisions matching the guidelines increased from 63% to 96%. Adhering to the guidelines resulted in a 17% reduction in colonoscopies performed on the basis of a family history of colorectal cancer.Conclusions: Supervised application of evidence-based guidelines to a colorectal cancer surveillance program significantly reduces the number of surveillance colonoscopies performed.

Peter A Bampton FRACP · Jayne J Sandford BN · Graeme P Young MD, FRACP

Objective: To determine the incidence of adverse events related to an endoscopy sedation regimen that included propofol, delivered by general practitioner (GP) sedationists.Design: Audit of reports of sedation-related adverse events in patients undergoing endoscopy. A sample of 1000 patients' medical records was also reviewed to determine the drugs and dosages used and the proportion of sedations delivered by GPs.Setting and participants: All patients undergoing gastroscopy and/or colonoscopy from January 1996 to December 2000 in two private endoscopy centres in Canberra. Sedation was provided by GPs or a specialist anaesthetist, in most cases using a drug regimen that included propofol.Main outcome measures: Incidences of respiratory arrest, airway obstruction, hypoxia requiring intervention, hypotension, and death; number of interventions to correct these events, including extra airway management, bag-mask ventilation, intravenous fluid infusion, endotracheal intubation and the use of reversal agents, and admission to hospital.Results: 28 472 procedures were performed in the five years. There were 185 sedation-related adverse events (6.5/1000 procedures; 95% CI, 5.6–7.4): 107 for airway or ventilation problems (3.8/1000) and 77 hypotensive episodes (2.7/1000). Respiratory-related adverse events were more common in patients managed by GPs than anaesthetists, but this was not significant (P = 0.1). Interventions were recorded in 234 patients (8.2/1000; 95% CI, 7.2–9.3): 123 to maintain ventilation, and 111 intravenous infusions. GPs were more likely than anaesthetists to intervene to manage respiratory-related adverse events (P = 0.03). Four patients required transfer or admission to hospital. No patients required endotracheal intubation, and there were no deaths.Conclusions: The GP sedationists encountered a low incidence of adverse events, which they managed effectively. It appears that appropriately selected and trained GPs can safely use propofol for sedation during endoscopy.

Anthony C Clarke FRCP, FRACP · Louise Chiragakis MA · Lybus C Hillman MD, FRACP · Graham L Kaye FRACP

Objective: To determine the prevalence of faecal incontinence in the community and evaluate identifiable risk factors.Design and setting: Cross-sectional survey using a validated questionnaire. A short version of the questionnaire was sent to 220 subjects and a long version to 770 subjects, randomly selected from western Sydney, Australia.Main outcome measures: Self-reported faecal incontinence, defined as involuntary loss of anal sphincteric control leading to unwanted release of liquid or solid faeces (not flatus) at an inappropriate time or in an inappropriate place, within the past 12 months. The long questionnaire also sought information on bowel habit and potential risk factors for faecal incontinence.Results: The response rate was 66%. The prevalence of solid or liquid faecal incontinence was 2% and 9%, respectively. The mean age of subjects with faecal incontinence was 53 years; 55% were women. After adjusting for age and sex, there was a significant association between faecal incontinence and perianal injury (P = 0.03), perianal surgery (P < 0.001), feelings of incomplete defecation (P < 0.0001), loose or watery motions (P < 0.0001) and urgency (P < 0.0001). Seven of 48 subjects with faecal incontinence reported being asked by their physician about faecal incontinence and nine of 33 reported seeking medical advice for their incontinence. Subjects with faecal incontinence perceived their health to be significantly poorer than did other subjects (P = 0.02).Conclusion: There is a high burden of faecal incontinence in the community, and the prevalence in men may be greater than is usually appreciated. Despite significant associated morbidity, most cases of faecal incontinence were unrecognised by doctors.

Jamshid S Kalantar MB BS, FRACP · Stuart Howell BA(Hons) · Nicholas J Talley MD, PhD

Objectives: To determine whether hospital patients identified as Indigenous are less likely than other inpatients to have a principal procedure recorded, and the extent to which any disparity in procedure use can be explained by differences in patient, episode and hospital characteristics. Design: Retrospective analysis of routinely collected administrative data from the National Hospital Morbidity Database (NHMD). Setting: Australian public and private hospitals. Patients: All patients included in the NHMD whose episode type was recorded as acute and whose separation occurred between 1 July 1997 and 30 June 1998. Patients admitted for routine dialysis treatment were excluded. Main outcome measure: Whether a principal procedure was recorded. Results: In public hospitals, patients identified as Indigenous were significantly less likely than other patients to have a principal procedure recorded, even after adjusting for patient, episode and hospital characteristics (adjusted odds ratio [OR], 0.67; 95% CI, 0.66–0.68). This disparity was apparent for most diseases and conditions. In private hospitals, no significant difference was observed (adjusted OR, 0.94; 95% CI, 0.83–1.06). Conclusions: The disparity in procedure use after adjustment for relevant factors indicates that in Australian public hospitals there may be systematic differences in the treatment of patients identified as Indigenous.

Joan Cunningham ScD (Epidemiol)

Objectives: To describe the management of early-pregnancy bleeding and miscarriage reported by general practitioners in Victoria.Design, setting, and participants: Self-administered, mailed survey of a stratified random sample of GPs in Victoria. Responses weighted by strata to reflect GP population.Main outcome measures: Reported management in referral; investigation (especially ultrasound); expectant versus interventional management; and prevention of rhesus iso-immunisationResults: 382 of 621 eligible GPs responded (response rate, 62%). GPs' reported referral was more likely if the patient had painful bleeding (55%) or if the pregnancy was not viable (77%). Ultrasound strongly influenced the assessment of bleeding. Two-thirds of doctors (262/369; 66%) would routinely order ultrasound for painless bleeding, and 328/369 (84%) for painful bleeding. Expectant management was recommended by 15/353 (4%) for incomplete miscarriage with light bleeding and by 6/351 (2%) when bleeding was heavy. Some GPs are uncertain of the indications for anti-D prophylaxis, including instrumentation of the uterus, for which 261/337 (77%) said they would routinely offer anti-D. There was less agreement about anti-D after threatened miscarriage, for which 213/353 (57%) said they offered the injection.Conclusions: GPs need a working knowledge of the management of early-pregnancy bleeding, and can probably encourage more rational management. There are significant areas where GPs are uncertain, often reflecting uncertainty elsewhere, and some areas where a minority of GPs are not aware of essential requirements.

Bruce McLaren DRANZCOG, FRACGP, MPH · Julia M Shelley MPH, PhD

The research enterprise The Menzies Centre for Population Health Research A unique and supportive local population was a vital ingredient in the Centre's success Terence Dwyer MJA 2001; 175: 617-620 Early days: the Tasmanian Infant Health Survey and Sudden Infant Death Syndrome - The post-SIDS era: taking stock - New directions - Genomics - The future - References - Authors' details - - More articles on Psychiatry I ACCEPTED THE CHAIR IN COMMUNITY HEALTH at the University of Tasmania in 1985 with the intention of setting up a research centre that focused on epidemiological research into preventable causes of disease. While I did not know how the centre would be funded, I was certain that Tasmania would be a very competitive site for such research. Already, valuable epidemiological studies on iodine deficiency, hydatid disease and asthma had been conducted in the absence of significant research infrastructure.1 The "Island State" provided a perfect source population for unbiased selection of cases and comparison samples or controls. Further, the land area and population size (around 500 000 people) made follow-up of cohorts relatively easy. Thus, Tasmania had important advantages for the two major strategies used to search for environmental and lifestyle causes of disease — case-control and cohort studies. Funding from the Menzies Foundation came about through the input of three people — Basil Hetzel, then Chief of the Commonwealth Scientific and Industrial Research Organisation Division of Human Nutrition in Adelaide, who had a close association with the Menzies Foundation; Professor Ian Lewis, Dean of the Medical School at the University of Tasmania and a member of the Menzies Foundation Board; and Eric Wigglesworth, the Director of the Foundation. To determine the likely success of such a centre, the Foundation Board held a three-day workshop attended by representatives of State and Federal health departments and the World Health Organization, notable Australians in the field of public health, and distinguished British epidemiologist Sir Richard Doll. History of the Menzies Centre 1987 Workshop ("Towards a Centre for Population Health Research") in Hobart, Tasmania. 1988 Official opening in January. Collection of Tasmanian Infant Health Survey (TIHS) data began (prospective study on Sudden Infant Death Syndrome [SIDS]). 1990 Designated as a World Health Organisation Collaborating Centre for the Prevention of Cardiovascular Diseases. 1991 Provides prospective evidence confirming importance of prone sleeping position as a cause of SIDS (Lancet 1991; 337: 1244-1247). 1992 Evidence that SIDS death rate was falling after a national campaign on infant sleeping position. 1993 Research helps explain how prone position interacts with other factors to increase risk (N Engl J Med 1993; 329: 377-382). 1995 First follow-up of TIHS cohort searching for early life influences on childhood diseases. Shows that the major decline in SIDS deaths from 1991 onwards is the result of changes in infant sleeping position (JAMA 1995; 273: 783-789) 1997 Contract signed with AMRAD pharmaceutical company. Provides funding for Genetic Epidemiology Unit. 1997-2000 Follow-up of the Tasmanian Infant Health Survey cohort into childhood provides important evidence about early life determinants of risk for osteoporosis, blood pressure and asthma (J Clin Endocrinol Metab 1998; 83: 4274-4279; J Bone Miner Res 1999; 14: 146-151; BMJ 1999; 319: 1325-1329; Thorax 1999; 54: 664-669). 2000 Named "Tasmanian Icon" by State Premier. Core funding doubles. Key events Major scientific achievements. Subsequently, the Menzies Foundation Board decided to support the establishment of an epidemiology research centre, to be named the Menzies Centre for Population Health Research. The Foundation then met with the Tasmanian Premier and Minister for Health, who matched the Foundation's initial contribution of $100 000 per year. Early days: the Tasmanian Infant Health Survey and Sudden Infant Death Syndrome Before my departure from Sydney University, I had been reviewing the data on disease distribution in Tasmania. Sudden Infant Death Syndrome (SIDS), with an annual rate in Tasmania twice the national average, stood out. The head of neonatology at the Royal Hobart Hospital, Neville Newman, convinced me that this should be the subject of a major research effort. The cause had not been clearly identified, and epidemiological research had been limited. With helpful input from Geoffrey Berry, Professor of Biostatistics at Sydney University, we planned the first prospective cohort study on this condition. Preliminary work began just before the decision of the Menzies Foundation to support the establishment of the Centre. The epidemiology research group within the Medical School at the University of Tasmania consisted of one epidemiologist, the research fellow Trevor Beard, and limited support staff. Even with the extra $200 000 that the establishment of the new Centre brought, it would not have been realistic to work on a broad front. It was decided that we would focus most of our effort on the new SIDS research program. The next step was to build an appropriately skilled team. We advertised for another epidemiologist and a biostatistician, but it proved very difficult to attract qualified applicants. It seemed that Australian academics were either not interested in living in Tasmania, or were not confident their careers would flourish there. This problem was compensated for by a stroke of good luck when a young Tasmanian medical graduate, Anne-Louise Ponsonby, became our first postgraduate student, working on SIDS. She put an incredible amount of intelligently directed energy into the SIDS program, and together, with financial help from the Australian Rotary Health Research Fund, we were able to develop momentum in the project. In 1988, we initiated the first full data collection for the cohort study — a huge endeavour that involved measurements each year in 1500 infants and their mothers on three occasions in the first three months after birth. That we could get this work under way was pleasing, but we needed to find well-qualified biostatisticians. Given the previous lack of success with advertising in Australia, I decided to use our international network. Sir Richard Doll referred Michael Jones, a young Master of Science graduate from Oxford, who was recruited to our ranks, and then Laura Gibbons, from the University of Massachusetts, joined us. This relatively small and young team of investigators coordinated the conduct, data management and analysis of the SIDS program. They also assisted with less well resourced but developing areas in cancer and cardiovascular disease. In late 1990 evidence was accumulating from case-control studies that prone sleeping position might be a major cause of SIDS, but the research was retrospective, creating concerns that recall bias might explain the findings. We had the only prospective data in the world and were able to show that the association was equally strong prospectively, ruling out recall bias.2 A number of countries, including Australia, launched campaigns to encourage parents not to place babies on their stomachs in the cot, with astonishing results — the death rate from SIDS in Australia fell from 507 in 1990 to 139 in 1998, with similar falls in a number of other countries.3 While our work was not the only important contribution to the understanding of this major cause of SIDS, it provided an important piece of evidence needed for solving the puzzle. Later, in 1993, our team explained why prone sleeping position seemed to exert a different effect in winter than summer and a different effect across countries.4 Then, in 1995, we provided evidence that showed clearly that the fall in deaths could only be attributed to the changes in prevalence of prone sleeping position.5 This success will undoubtedly rank as one of the major contributions of the Centre in the years to come. It also established the organisation as one which, in its special location, could have a significant impact on international medical science. It was the much-needed platform that would underpin future recognition and opportunities. The post-SIDS era: taking stock The death rate from SIDS fell so rapidly after the prone sleeping position campaign that, by late 1991, it was clear there would eventually be insufficient cases occurring annually in Tasmania for epidemiological research (when we started the SIDS program, there had been an average of 27 cases a year for an extended period, and by 1998 there were only three). While this outcome was tremendously gratifying, it was clear that the research money to support our staff of now approximately 20 would dry up unless we repositioned our research program. This was confirmed by the National Health and Medical Research Council (NHMRC) Regional Grants Interview Committee's decision not to recommend refunding of our cohort study for 1992. We went from triumph to a period of considerable adversity. One of our first responses was to tell the Tasmanian public that we needed its financial and moral support. They responded generously. With a major public fundraising appeal, helped greatly by our Board and new Chairman John Tomlinson, and a timely decision by the United States National Institutes of Health, we were able to continue the study long enough to thoroughly evaluate the impact of the prone sleeping intervention campaign. In 1992, I took some time to review where we were going as an organisation and to think about where our future research opportunities might lie. I visited people like Richard Doll in Oxford, who had provided very helpful mentoring since 1987. I also had discussions with Ken Rothman (author of Modern epidemiology6), and Dimitris Trichopoulos at Harvard. These visits confirmed that, if we were to continue to conduct work of global significance, we would have to search even more thoroughly for gaps in knowledge that might be filled by an epidemiological approach. I was also convinced that we would need to develop stronger working relationships with basic scientists if we wished to use epidemiology to understand aetiology. These strategies were challenging, but all our team had learned a great deal from the SIDS research experience. While overseas, I also upgraded my skills in organisation and management by attending a management course in Salzburg, led by Peter Drucker, one of the world's most prominent management theorists. New directions The perspectives gained during my overseas visit were incorporated into planning from 1992 onwards. The major new strategy we decided on was to follow the Tasmanian Infant Health Survey (TIHS) cohort, now numbering 11 000 infants and children. The focus would be to search for links between early life exposures and later disease, using our extensive database of infant measurements that provided information on more than 450 variables measured during the first three months of life. One disease we looked at was asthma, an important disease for which preventable causes had not yet been identified and for which there was a shortage of good epidemiological data. This investigation would be coordinated by Anne-Louise Ponsonby, with help from David Couper, a biostatistician who had joined us from Seattle. We also increased our activity in research on the development in childhood of risk factors for cardiovascular disease and diabetes. Fitting into this theme was the new program started by a recent recruit from the Garvan Institute in Sydney, Graeme Jones (we were finally starting to see interest in work opportunities from well-qualified Australians outside Tasmania). He had a strong track record in osteoporosis in the elderly, and he used that background to focus on the impact of early-life factors on bone density in childhood. Fortuitously, interest in the "Barker hypothesis", which concerns the impact of fetal development on later disease, was gaining momentum. We were well placed to make an important contribution in this field, and our capacity was greatly enhanced by the addition of Ruth Morley, from the Institute of Child Health in London. Supplemented by smaller research efforts in cancer and adult cardiovascular disease, by 1994 we were able to see evidence that the research program was growing again. Between 1994 and 2000, the team was able to attract 17 new NHMRC grants from 38 applications submitted. This overall level of success was built on the tremendous preparedness of the Tasmanian public to be involved in the research. Response rates for case-control studies in this period were about 90% for cases and 80% for controls sampled from the electoral rolls, with comparable figures for cohort follow-up. In addition to our growing research effort we took on an important role in ensuring that knowledge was transferred to countries with less developed research capacity. The World Health Organization designated our institution as a Collaborating Centre for the Prevention of Cardiovascular Disease (CVD) a decade ago. That role has expanded steadily to the point where the Centre is assisting in studies on CVD in countries including Vietnam, Fiji and Samoa, where CVD and diabetes are producing an unexpectedly high disease burden. Genomics For the first seven years (1988-1995) the Centre focused solely on the environmental and lifestyle causes of disease. Meanwhile, others had been using the deep family pedigrees available in Tasmania to search for genetic causes of diseases following a Mendelian pattern of inheritance. Novel genes or linkages were discovered for several conditions, including multiple endocrine neoplasia and Huntington's disease. These successes were based on special features of Tasmania that are replicated in few other locations, namely (i) a population descended largely from identifiable founder families; (ii) comprehensive genealogical records; (iii) a modern healthcare system capable of identifying disease outcomes; (iv) a demonstrated capacity to involve the population in studies; and (v) organisational structures to facilitate the research. In 1995, David Mackey, a Tasmanian medical graduate and ophthalmologist at the Victorian Eye and Ear Hospital, approached us. He was undertaking important work in Tasmania on the more complex genetics of glaucoma. He wanted a base in Tasmania, and the Walter and Eliza Hall Institute, in Melbourne, was seeking a Tasmanian institution to manage new research and development syndicate funds to support his research. We accepted the role and our interest in the use of epidemiology to find genes for human diseases increased. Then, in 1996, the Australian pharmaceutical company AMRAD approached us about increasing its involvement in gene discovery in Tasmania through the Menzies Centre. We agreed, on the condition that the funding would be for a genetic unit that would employ people who could provide intellectual input to the work from a Tasmanian base. AMRAD signed a contract in 1997 for a five-year grant of $2.5 million, and, in 1998, we attracted Tasmanian molecular geneticist Michele Sale to coordinate the work. With financial and other help we were able to very quickly get projects under way in multiple sclerosis and osteoarthritis, and have continued to develop activity with Cerylid, a spin-off from AMRAD formed to operate its discovery arm. The genomics development has also led to an increase in postgraduate student training at the Centre, with five PhD students currently enrolled. The future During the past 12 months there have been several important developments for the Centre, driven by our very committed Board, chaired by Jean Trethewey, and strongly supported by the Dean of the Faculty of Health Science at the University of Tasmania, Allan Carmichael. The Tasmanian Government introduced an "Icons Program", which supports the Tasmanian Symphony Orchestra and our State cricket team. To this list Premier Jim Bacon added the Menzies Centre, with a commitment to provide $500 000 a year to help our organisation develop its capabilities. This, together with a large donation in 2000 from the United States-based Atlantic Philanthropies Inc, has placed us in a previously unimagined position to recruit more staff and drive our research program. To enable us to undertake these future developments with vigour, the University of Tasmania Council has established the Menzies Centre as an independent company limited by guarantee, remaining within the university structure. In 2002, the Centre will become the "Menzies Research Institute". Already, the Centre has grown to support a staff of 60. The new institute is likely to start 2002 with a budget of approximately $5 000 000 that will see staff numbers increase to more than 100, working on both environmental and genetic causes of disease. A major NHMRC grant of $2 290 000 over the next five years will enable us to study a cohort of Australians first measured as schoolchildren in 1985. They will be followed up for the emergence of adult disease, and it is anticipated this will provide the first direct evidence available on the impact of childhood lifestyle and biology on diseases such as coronary heart disease. A collaboration with similar cohorts in the US and Finland has already been established. A new director of the Cohort Studies Unit, Alison Venn, who has a strong background in this research strategy, has been recruited from the Centre for the Study of Mothers' and Children's Health at La Trobe University to coordinate developments. A large adult cohort study in Tasmania, with a focus on exposures that occur closer to the time of disease development, will also commence in 2002. Both studies will benefit from the input of a now-strong biostatistics group of three staff headed by one of our own PhD graduates, Leigh Blizzard. The level of genetic research activity will expand greatly. Tasmania presents opportunities as good as any in the world for gene discovery, and we intend to take up these opportunities. An increasing number of epidemiological studies at the Centre are focused on finding novel genes or validating candidate genes identified through animal or cell studies, or bioinformatic "data mining". This growth in activity reflects the recognition by commercial and government sources of the opportunities here, as well as the developing capacity of our genetic unit. Increasingly, our "environmental" epidemiologists and biostatisticians are developing their interests and skills in genetic research. This has not only led to the more rapid development of a critical mass for projects on gene discovery and validation, but has also opened up the possibility for in-depth investigation of gene-environment interaction. Projects with this focus are already under way in multiple sclerosis. There is great scope for us to contribute in an internationally significant way to the understanding of gene-environment interactions using Tasmania's unique population and our skill base. In the coming decade Australia will be relying more and more on its medical research institutes to maintain its competitive advantage in a knowledge-based global economy. We are confident that the new Menzies Research Institute will be making its contribution. References King H, editor. Epidemiology in Tasmania. Canberra: Brolga Press, 1987. Dwyer T, Ponsonby AL, Newman NM, Gibbons LE. Prospective cohort study of prone sleeping position and sudden infant death syndrome. Lancet 1991; 337: 1244-1247. Australian Bureau of Statistics. Deaths, Australia, 1990, 1998. Canberra: ABS, 1998. (Catalogue no. 3302.0/3303.0.) Ponsonby AL, Dwyer T, Gibbons LE, et al. Factors potentiating the risk of SIDS associated with the prone position. N Engl J Medicine 1993; 329: 377-382. Dwyer T, Ponsonby AL, Blizzard CL, et al. The contribution of changes in the prevalence of prone sleeping position to the decline in SIDS in Tasmania. JAMA 1995; 273: 783-789. Rothman K. Modern epidemiology. Boston: Little John and Co., 1986. Authors' details Menzies Centre for Population Health Research Terence Dwyer, MD, FAFPHM, Director. Reprints will not be available from the author. Correspondence: Professor T Dwyer, Menzies Centre for Population Health Research, 17 Liverpool Street, Hobart, 7000 TAS. t.dwyerATutas.edu.au Make a comment

Terence Dwyer

Research Mega-dose vitamin C in treatment of the common cold: a randomised controlled trial Carmen Audera, Roger V Patulny, Beate H Sander and Robert M Douglas MJA 2001; 175: 359-362 Abstract - Methods - Results - Discussion - Acknowledgements - Competing interests - Reference - Authors' details - - - More articles on Infectious diseases and parasitology Abstract Objective: To determine the effect of large doses of vitamin C in the treatment of the common cold. Study design: Double-blind, randomised clinical trial with four intervention arms: vitamin C at daily doses of 0.03 g ("placebo"), 1 g, 3 g, or 3 g with additives ("Bio-C") taken at onset of a cold and for the following two days. Participants and setting: 400 healthy volunteers were recruited from staff and students of the Australian National University, Canberra, ACT, between May 1998 and November 1999. The trial continued for 18 months. Interventions: Participants were instructed to commence medication when they had experienced early symptoms of a cold for four hours, and to record daily their symptoms, severity, doctor visits and use of other medications. Main outcome measures: Duration of symptoms and cold episodes; cumulative symptom severity scores after 7, 14 and 28 days; doctor visits; and whether participants guessed which medication they were taking. Results: 149 participants returned records for 184 cold episodes. No significant differences were observed in any measure of cold duration or severity between the four medication groups. Although differences were not significant, the placebo group had the shortest duration of nasal, systemic and overall symptoms, and the lowest mean severity score at 14 days, and the second lowest at 7 and 28 days. Conclusions: Doses of vitamin C in excess of 1g daily taken shortly after onset of a cold did not reduce the duration or severity of cold symptoms in healthy adult volunteers when compared with a vitamin C dose less than the minimum recommended daily intake. A recent Cochrane systematic review of the effects of vitamin C on the common cold concluded that large maintenance doses of vitamin C do not lower the incidence of colds in well-nourished subjects in Western countries.1 Nevertheless, the meta-analysis of 17 trials found that prophylactic doses of at least 1g per day were associated with a statistically significant weighted mean reduction in symptom days of about 0.45 days per cold (9% of symptom days).1 However, the authors of the Cochrane review could not draw conclusions about the therapeutic effects of vitamin C (ie, effects when taken at onset of a cold).1 Findings of four well-conducted trials of the effects of treating colds with a loading dose of vitamin C were inconclusive2-5(Box 1). This prompted us to design a study to answer the question "Would vitamin C, when used exclusively as a therapeutic agent in doses that greatly exceed the required daily intake, reduce the duration or severity of symptoms of the common cold in healthy Australian adults?". Methods Our study was a double-blind, randomised trial comparing the effects of different doses and formulations of vitamin C. We chose as "placebo" a dose of 0.03g per day of vitamin C (about half the recommended minimum daily intake), recognising that all participants would have some nutritional vitamin C intake. Ethics approval was obtained from the Human Ethics Committee of the Australian National University, Canberra. Participants Staff and students of the Australian National University, Canberra, ACT, were recruited between May 1998 and November 1999 through personal letters and emails, announcements at student gatherings and direct approach in university common areas. Volunteers were eligible for the study if they were aged over 18 years, not pregnant or planning to become pregnant, in good general health, and did not take vitamin supplements regularly or take vitamin C, echinacea, zinc or Chinese herbal preparations regularly at the onset of a cold. Volunteers were clearly informed about the objectives of the study and signed an informed consent form. They also completed a questionnaire about their current health and medication status, including respiratory infections in the previous year. An information letter was provided for their general practitioners. Participants who returned information on one respiratory event were eligible to re-enrol in the study. Interventions Participants were randomised to receive one of four interventions: vitamin C in a daily dose of 0.03 g, 1 g or 3 g, or "Bio-C" (containing vitamin C [3 g daily] plus bioflavenoids [75 mg], rutin [150 mg], hisperidin [150 mg], rose hip extract [750 mg] and acerola [150 mg]). They were to take the medication at onset of cold symptoms and on the following two days. The medications were prepared by Blackmores Ltd (Sydney, NSW) as compressed tablets with identical appearance and packaging. Dosage was confirmed by chemical analysis of unused tablets at the end of the study. A random number table was constructed to order the medications sequentially so that each sequence of four numbers comprised all four types of medication. The medications were issued to investigators in 400 sequentially numbered sets of three bottles, each bottle containing the daily dose in three tablets. As volunteers joined the study they were given a set of three bottles and a correspondingly numbered "respiratory event card" to record outcome. The code was retained by the manufacturer until we were ready to analyse the results. Participants were instructed that they must have at least two of the following symptoms for a minimum of four hours before commencing medication: sore or scratchy throat, nasal congestion or discharge, headache or stinging eyes, muscle aches, fever, or "four hours of certainty that a cold is coming on". On the first day of illness, they were to take the contents of one bottle (three tablets) as soon as possible. For the next two days, they were to take three tablets a day at intervals of at least four hours. Outcome measures The respiratory event card was designed to be carried in a wallet or purse. When a cold began, participants were instructed to score symptoms daily, noting presence and severity (1, mild; 2, moderate; or 3, severe) of cough, nasal, throat, and systemic symptoms, including fever, headache, aches, feeling unwell and "other symptoms". Recording was to cease either when all symptoms disappeared or 28 days after onset of the cold. Participants were also instructed to record hours between onset of symptoms and first dose of medication, use of other medication and whether they sought medical attention. They were also invited to guess to which medication group they had been assigned. Duration of the cold was measured from day of symptom onset to the last day of any symptom. Cold severity scores were the sum of daily individual symptom scores throughout the duration of the cold. Symptom days and severity scores for cough, nasal, throat and systemic symptoms were considered separately, and cumulative scores were considered at 7, 14, and 28 days. For any one day of symptoms, the maximum severity score was 12. Participants who did not return a respiratory event card were sent reminder letters after nine months and 15 months. The initial 12-month study period was extended by six months in an effort to increase the response rate. Statistical analysis We aimed to study 75 individuals in each intervention arm, in the expectation that the study would have an 80% power to detect a 30% difference between groups in duration or severity, which we considered clinically significant. Desired sample size was calculated assuming a mean duration of seven days and a standard deviation of four days. Statistical comparisons were carried out using the software package SPSS.6 Distribution, mean and median of duration and severity scores for each symptom were compared between the four groups by t-tests, analysis of variance and box plots. Results Study population Four hundred sets of medication were distributed to 323 volunteers. By November 1999, when the study was terminated, 149 people had returned completed respiratory event cards for 184 cold episodes. These 149 were significantly older than those who did not return cards (45.1 versus 40.9 years; P < 0.05), but the two groups did not differ significantly in sex distribution or previous cold history. Personal characteristics and previous cold history of those who returned cards are shown in Box 2, along with time from symptom onset to beginning medication. Participants in the four medication groups were comparable in sex distribution and time to beginning medication, but those who took Bio C were significantly older and had fewer colds in the previous year than those in the other three groups (P < 0.05). Cold duration and severity Duration and severity of symptoms are compared between the four medication groups in Box 2. There were no significant differences between the groups in either mean duration of symptoms or mean severity scores at Days 7, 14 or 28, although the placebo group (30 mg vitamin C daily) had the shortest duration of nasal, systemic and overall symptoms, and the lowest mean severity score at 14 days, and the second lowest at 7 and 28 days. A box plot of cumulative severity scores at Day 28 (Box 3) revealed that the distribution of values was more dispersed in the 1 g and 3 g vitamin C groups, with the lowest median values occurring in the placebo and Bio C groups. A box plot of cold duration showed a similar pattern (Box 3). Only 31 participants (17%) recorded a guess about the dose of vitamin C they had taken, and 14 guessed correctly that they had taken a high dose. Seventeen gussed incorrectly that they had taken either a high or low dose. Actual power of the study Because the mean cold duration for the whole group was 9.8 days with a standard deviation of 6.6 days, the number of completed cold episodes returned per group provided 80% power to detect a 40% difference in cold duration with a 95% level of confidence. Similarly, given that the mean severity score at Day 28 was 32 with a standard deviation of 32.3, the number of completed cold episodes provided 80% power to detect a 50% difference in severity at the 95% level of confidence. Discussion Our study found no significant differences in severity or duration of cold symptoms between groups who took low-dose (placebo) and high-dose vitamin C as treatment for the common cold. The lack of benefit from high-dose therapeutic vitamin C is consistent with the findings of four other randomised controlled trials2-5 (Box 1). The Cochrane and other reviews of the published evidence on high-dose vitamin C and the common cold have drawn attention to the relatively consistent trend for those taking prophylactic doses in excess of 1 g daily to experience some reduction in duration or severity of colds.1,7-9 Although high-dose prophylactic vitamin C was also found not to reduce the incidence of colds in well-nourished adult populations,1,7 Hemila has proposed that it may have an effect in groups who are physically stressed or have low nutritional intake.8-10 The main weakness of our study is that it necessarily relied on study participants to decide when the criteria for commencing medication were met and to provide all outcome data. In such a study, double-blindness must be rigorously preserved, and allocation to intervention arms must avoid selection bias. We are confident that our study met these requirements and that the few participants who correctly guessed their medication dose did so by chance. The focus on the university community meant a potential bias in socioeconomic and educational status of participants. The observed spectrum of cold experience may not have been representative of the cold experience of the rest of the Canberra community. Many potential volunteers in our study were ruled ineligible because of their regular use of vitamin C and other, non-traditional approaches for cold therapy and prophylaxis. A recent US study found that 67% of patients seeking medical care for cold episodes believed that vitamin C reduces cold symptoms.11 Our target of 75 colds in each treatment group was not reached, despite extension of the study and repeated reminder letters to participants. Fewer than half those enrolled returned a completed respiratory event card. As we expected most to suffer at least one cold during the 18 months of the study, based on their previous history, we assume that many did not use the medication as instructed. Although those who completed a respiratory event card were older than those who did not, both groups had similar previous cold experience. The double-blind nature of the study makes it unlikely that greater compliance would have changed the result. Our study had medication groups of comparable size, and for each medication group colds were found to have occurred across the entire study period. The Bio-C group was slightly older than the other groups and, probably in consequence, experienced fewer colds in the previous year, as the incidence of colds tends to decrease with age. However, these differences were not associated with significant differences in outcomes. The average time between symptom onset and medication use was 13 hours, although we encouraged participants to begin medication as soon as four hours after they were certain that a cold was developing. However, the time to beginning medication did not differ significantly between groups. The power of our study to detect a possible significant difference in symptom severity and duration after high-dose vitamin C treatment was limited by the smaller than expected participation rate. However, the non-significant trend that was observed was the reverse: symptoms tended to be less severe and of shorter duration in the placebo group. The lack of observed benefit in this trial is fully consistent with the observations from the four previous randomised controlled trials that have sought to evaluate this issue.2-5 It is time to question again the wisdom and utility of the wide practice of well nourished adults taking mega-doses of vitamin C to treat the common cold, a practice which has become prevalent worldwide since the advocacy of Linus Pauling in the early 1970s.12,13 Acknowledgements The project was supported by a grant from Blackmores Ltd, who also provided the study medications. We thank all those who participated in the study for their patience and compliance. Competing interests Blackmores Ltd were not involved in conduct or analysis of the trial or preparation of this article. References Douglas RM, Chalker EB, Treacy B. Vitamin C for preventing and treating the common cold (Cochrane Review). In: The Cochrane Library, 3, 2001. Oxford: Update Software. Anderson TN, Suranyi B, Beaton GW. The effect on winter illness of large doses of vitamin C. Can Med Assoc J 1974; 111: 31-38. Karlowski TR, Chalmers TC, Frenkel LD, et al. Ascorbic acid for the common cold. A prophylactic and therapeutic trial. JAMA 1975; 231: 1038-1042. Elwood PC, Hughes SJ, St Leger AS. A randomized controlled trial of the therapeutic effect of vitamin C in the common cold. Practitioner 1977; 218: 133-137. Tyrrell DA, Craig JW, Meada TW, White T. A trial of ascorbic acid in the treatment of the common cold. Br J Prev Soc Med 1977; 31: 189-191. SPSS [computer program]. Version 10.0 for Windows. Chicago, Ill: SPSS Inc, 1999. Hemila H. Vitamin C and the common cold. Br J Nutr 1992; 31: 3-16. Hemila H. Vitamin C supplementation and the common cold: was Linus Pauling right or wrong? Int J Vitam Nutr Res 1997; 67: 329-325. Hemila H. Vitamin C and common cold incidence: A review of studies with subjects under heavy physical stress. Int J Sports Med 1996; 17: 379-383. Hemila H, Douglas RM. Vitamin C and acute respiratory infections. Int J Tuberc Lung Dis 1999; 3: 756-761. Braun BL, Fowles JB, Solberg L, et al. Patient beliefs about the characteristics, causes, and care of the common cold: an update. J Fam Pract 2000; 49: 153-156. Pauling L. The significance of the evidence about ascorbic acid and the common cold. Proc Natl Acad Sci USA 1971; 68: 2678-2681. Pauling L. Vitamin C, the common cold, and the flu. San Francisco: Freeman, 1976. Authors' details National Centre for Epidemiology and Population Health, Australian National University, Canberra, ACT. Carmen Audera, MD, MPH, Lecturer; Roger V Patulny, BEc, BA (Hons), Research Assistant; Beate H Sander, BAppSc (Nursing), MEcDev, Research Assistant; Robert M Douglas, MD, FRACP, FAFPHM, Visiting Fellow. Reprints will not be available from the authors. Correspondence: Emeritus Professor R M Douglas, National Centre for Epidemiology and Population Health, Australian National University, Canberra, ACT 0200. Bob. DouglasATanu.edu.au Make a comment 1: Previous randomised controlled trials of the therapeutic effect of high-dose vitamin C on cold symptoms Study Participants and setting Interventions Outcomes Anderson et al2 (1974) Toronto, Canada Hospital and business employees (>275 per arm) 4 arms: 2 placebo, 2 therapeutic (4g or 8g vitamin C taken on day of symptom onset) The two placebo arms unfortunately differed in outcome. Mean days of respiratory symptoms over 3 months: placebo, 5.4 and 4.16 days (combined placebo mean, 4.77 days); intervention, 4.82 days (4g dose) and 4.52 days (8g) Karlowski et al3 (1975) Bethesda, USA National Institutes of Health employees (46 placebo, 43 therapy) 3g vitamin C daily or placebo for the first 5 days of a cold Problem in blinding, as over half the participants correctly guessed their medication through taste. Although mean duration of colds was longer in the placebo than therapy group (7.1 v 6.5 days), difference was confined to those who guessed their medication ("unblinded"). Unblinded group: 8.6 (placebo) v 4.7 days (therapy); blinded group: 6.3 (placebo) versus 6.7 days (therapy). Elwood et al,4 (1977) South Wales, UK Community volunteers (119 placebo, 145 therapy) 3g vitamin C daily or placebo for 3 days Vitamin C significantly reduced duration of "simple" colds in men (5.7 days [placebo] v 3.97 days [therapy]), but had no benefit in women (4.97 days [placebo] v 6.05 [therapy]), or in "chest" colds in either sex. Tyrrell et al5 (1977) Salisbury, UK 482 volunteers 4g of vitamin C or an identical-tasting placebo daily for 2.5 days No evidence that vitamin C alleviated or shortened upper respiratory or general constitutional symptoms. Back to text 2: Characteristics of participants and outcomes of a study of the effect of therapeutic vitamin C on the common cold Vitamin C formulation (daily dose) 0.03g (n=42)* 1g (n=47)* 3g (n=50)* Participant characteristics Mean age in years (95% CI) 38.6 (34.2-43.0) 40.1 (35.8-44.4) 39.9 (36.2-43.6) Male sex (95% CI) 45% (30%-61%) 38% (26%-54%) 50% (36%-65%) Cold history in previous year Mean number of colds (95% CI) 2.2 (1.7-2.7) (n=40) 2.25 (1.9-2.6) (n=46) 2.2 (1.8-2.7) (n=49) Mean number of days unwell from colds (95% CI) 8.0 (3.4-12.5) (n=39) 7.7 (6.2-9.3) (n=46) 7.7 (6.5-9.2) (n=49) Mean hours from symptom onset to medication (95% CI) 13.3 (9.4-17.2) (n=39) 11.6 (8.7-14.7) (n=44) 10.2 (8.2-12.3) (n=48) Outcome measures Mean days of symptom (95% CI) 8.5 (6.6-10.5) 10.1 (8.1-12.1) 10.4 (8.5-12.2) Cough 5.3 (3.0-7.6) 6.4 (4.1-8.6) 6.3 (4.4-8.3) Nasal symptoms 7.3 (5.4-9.1) 8.4 (6.7-10.1) 9.2 (7.4-11.1) Throat symptoms 5.4 (3.6-7.2) 6.1 (4.3-7.9) 6.3 (4.6-7.9) Systemic symptoms 3.5 (2.1-4.9) 3.7 (2.3-5.2) 3.8 (2.7-4.8) Mean severity score‡ (95% CI) Day 7 20.2 (16.5-24.0) 22.1 (18.1-26.0) 23.0 (19.3-26.6) Day 14 25.6 (19.0-32.1) 31.1 (23.5-38.8) 30.8 (24.9-36.6) Day 28 29.0 (19.5-38.6) 35.4 (23.4-47.5) 34.3 (26.6-42.1) Doctor visit (95% CI) 7% (2%-20%) 19% (8%-31%) 4% (0.5%-14%) Other medication taken for symptoms (95% CI) 57% (41%-72%) 55% (40%-70%) 55% (39%-68%) Vitamin C formulation (daily dose) "Bio C" (3g plus additives) (n=45)* Total (n=184)* Participant characteristics Mean age in years (95% CI) 45.1 (40.6-49.5)† 40.9 (38.8-43.0) Male sex (95% CI) 51% (36%-66%) 46% (39%-54%) Cold history in previous year Mean number of colds (95% CI) 1.5 (1.3-1.8)† (n=44) 2.1 (1.9-2.3) (n=179) Mean number of days unwell from colds (95% CI) 6.8 (5.4-8.2) (n=43) 7.5 (6.4-8.9) (n=177) Mean hours from symptom onset to medication (95% CI) 18.6 (11.2-26) (n=44) 13.4 (11.1-15.8) (n=175) Outcome measures Mean days of symptom (95% CI) 9.9 (7.9-11.9) 9.8 (8.8-10.7) Cough 4.4 (2.2-6.5) 5.6 (4.6-6.7) Nasal symptoms 8.1 (6.1-10.1) 8.3 (7.4-9.2) Throat symptoms 5.4 (3.8-6.9) 5.8 (5.0-6.7) Systemic symptoms 4.4 (3.2-5.6) 3.9 (3.2-4.5) Mean severity score‡ (95% CI) Day 7 19.2 (15.4-23.0) 21.2 (19.3-23.0) Day 14 25.9 (19.1-32.6) 28.5 (25.2-32.8) Day 28 28.6 (20.0-37.3) 32.0 (27.3-36.7) Doctor visit (95% CI) 9% (3%-21%) 9% (6%-14%) Other medication taken for symptoms (95% CI) 53% (38%-68%) 55% (47%-62%) *Number of completed cold episodes; 35 participants were counted twice, as they reported two medicated colds. For variables with missing data, numbers of participants who provided information are shown in parentheses. †P Back to text 3: Box plots of cold severity and duration in groups taking different vitamin C formulations Back to text

Carmen Audera · Roger V Patulny · Beate H Sander · Robert M Douglas

Abstract Objective: To examine the relationship between compensation claims for psychiatric injury after motor vehicle accidents and physical injuries sustained. Design: Audit of Compulsory Third Party (CTP) insurance claims. Subjects and setting: 559 consecutive CTP claims referred by NRMA Insurance Limited to its sole provider of CTP legal services during a three-month period in 1994 after the claimant had engaged legal representation. Main outcome measures: Claim for psychiatric injury (any psychiatric disorder excluding traumatic brain injury) supported by a medicolegal report from a psychiatrist, other medical practitioner or psychologist; pre-existing psychiatric disorders; Injury Severity Score; initial treatment setting; hospital stay; percentage of accidents involving loss of consciousness or a death. Results: 522 claims were eligible for the study; 19.5% (102/522) included a claim for psychiatric injury. A pre-existing depression or anxiety disorder was documented in 11 claims (2.1% of all claims and 3.9% of those claiming psychiatric injury). Only very severe injuries, particularly those involving loss of consciousness, were associated with an increased rate of claims for psychiatric injury. Conclusions: No association was found between claims for psychiatric injury and severity of physical injuries, except among those most severely injured. More than 25 000 people are injured in motor vehicle accidents in New South Wales each year.1 Data from the NSW Motor Accidents Authority from 1998 show that about 60% of people who made a claim after a motor vehicle accident obtained legal representation,2 and that the percentage of claims with a psychiatric component rose from 2.2% to 8% between 1990 and 1998.3 NSW Motor Accidents Authority data also show that minor physical injuries result in 54% of all claims, but 77% of claims for psychiatric injury.3Motor vehicle accidents are associated with post-traumatic stress disorder (PTSD), other anxiety disorders and depression,4,5 although most recent publications refer to PTSD rather than other syndromes.4-9 However, the true incidence of PTSD and other disorders after these accidents is unclear; most studies have sampling bias and other methodological problems.4 The extent to which motor vehicle accidents cause the observed psychiatric disorders is also uncertain. Factors associated with PTSD include those not directly related to the accident, such as past psychiatric history6-9 and involvement in litigation,6,7 and others that are difficult to assess objectively, such as victims' recollections of fear of death6-10 and self-reported loss of consciousness.6,7 The relationship between PTSD and severity of physical injuries has also been investigated,6-13 with one study finding a positive correlation.7 In this study, I examined the relationship between compensation claims for psychiatric injury after motor vehicle accidents and physical injuries sustained. Methods Sample The sample comprised 559 consecutive claims on Compulsory Third Party (CTP) insurance that were referred by NRMA Insurance Limited to its sole provider of CTP legal services in a three-month period in 1994 after the claimant had engaged legal representation. All claims arose from motor vehicle accidents that occurred in New South Wales between 1989 and 1994. In this period, 39.5% of NRMA CTP claimants had legal representation. Of the 559 claims, 37 were excluded from the study as files were missing (25), the claim was from bereaved relatives (10) or the claimant had died since the claim (2). A further 50 files had data missing on one or more of the following: injuries, demographic details, or setting of medical care. As these files did not to appear to include claims for psychiatric injuries, they were included in denominators for proportions with psychiatric injury but were excluded from further analysis. Data collection and analysis I collected de-identified data from the files on systematic forms. The dependent variable was a claim for psychiatric injury (defined as any psychiatric disorder, excluding traumatic brain injury) supported by a report from a psychiatrist, other medical practitioner or psychologist. I recorded the presence of one or more of these injuries or traumatic brain injury attributed to the accident by the claimant's experts, as well as any pre-existing psychiatric disorder noted by claimants' or defendants' experts. Independent variables recorded were age and sex, type of motor vehicle accident and whether fatal (ie, any person killed), Injury Severity Score (ISS)14(calculated from information in the injury summary document in each file), setting of initial medical care (most medically intensive setting in the week after the accident), length of hospital stay, loss of consciousness during or after the accident (self-reported or corroborated), and self-reported neck or back pain (irrespective of physical or radiological signs). Data were analysed using the computer program SPSS.15 Logistic regression was used to determine the influence of independent variables on the presence of a claim for psychiatric injury. Results Most claimants (380; 73%) were passengers or drivers, and the remainder were motorcyclists, cyclists or pedestrians (92; 18%). The status of another 50 (10%) was not known because of incomplete files. Mean age was 34 years (range, 2-82 years), and 49% were male. Claims for psychiatric injury Claims for psychiatric or traumatic brain injury are shown in Box 1. One hundred and two people (19.5%) claimed at least one psychiatric injury related to the accident, combined with traumatic brain injury in six cases (another 11 people claimed traumatic brain injury alone). Thirty-six people claimed more than one psychiatric injury. Pre-existing psychiatric disorders are also shown in Box 1. These were documented in 25 people (4.8%), and comprised a depressive or anxiety disorder in 11 (2.1% of all claimants, and 3.9% of those claiming psychiatric injury). The reports supporting the psychiatric injury claims came from psychiatrists (65), psychologists (28) and other medical practitioners (9); mean time between the accidents and report dates was over two years. Experts disagreed on many claims, with treating practitioners and claimants' experts using the diagnoses of PTSD and depression (15% of claimants) more often than defendants' experts (2.5% of claimants), as described elsewhere.16 Variables associated with psychiatric injury claims The group that claimed psychiatric or traumatic brain injury had significantly longer hospital stay and higher mean ISS and proportion of accidents involving loss of consciousness than the group who claimed neither type of injury (Box 2). The group that claimed psychiatric injury but not traumatic brain injury also had significantly more accidents involving loss of consciousness and fatal accidents compared with those who claimed neither type of injury. There were no significant differences between the groups in proportions with self-reported neck or back pain. For the 102 who claimed psychiatric injury, the most medically intensive treatment in the week after the accident was provided by a local medical officer (33), in an emergency department (35), as a general inpatient (25) or in an intensive care unit (9). Psychiatric injury claims and injury characteristics are shown in Box 3 by initial treatment setting. The percentage of people who claimed psychiatric injury was significantly higher in those treated initially in intensive care than in those treated elsewhere (χ2 = 6.74; df = 1; P = 0.009). The percentage who claimed for PTSD and traumatic brain injury was also higher in the intensive care group (PTSD: χ2 = 8.99; df = 1; P = 0.003; and traumatic brain injury: χ2 = 103; df = 1; P <0.001). Mean ISS, hospital stay and percentage who reported loss of consciousness were also greater in those treated in more medically intensive settings (inpatient and intensive care), supporting the use of initial treatment setting as an indicator of injury severity. However, claims for neck or back pain were lower in claimants who received inpatient or intensive care treatment (Box 3). The percentage of people who claimed for a psychiatric injury did not increase with increasing ISS over the first nine deciles (mean, 20%). However, the percentage was significantly higher (33%) in people in the tenth ISS decile (ie, the most severely injured 10%) compared with those in the lower nine deciles (χ2= 4.34; df = 1; P = 0.04). A logistic regression analysis was performed using variables found to be significantly related to claims for psychiatric or traumatic brain injury by previous analyses (Box 4). Loss of consciousness and a fatal accident were significant predictors of claims for psychiatric injury. Discussion A claim for psychiatric injury was made in 19.5% of the legally represented CTP claims in this study, which is higher than the 4.6% estimated by the NSW Motor Accidents Authority for all victims of motor vehicle accidents during the same period.3 This confirms the previously reported association between psychiatric injury and legal representation.6,7 PTSD and depression were reported more often in this sample than in a recent survey of the Australian population.17 Conversely, pre-existing psychiatric disorders were documented much less often than the estimated prevalence of all psychiatric conditions in Australia (4.7% v. 17.7%17). This suggests that medicolegal assessments may under-report pre-existing psychiatric disorders and may sometimes wrongly identify a motor vehicle accident as the cause of a depressive or anxiety disorder that was actually pre-existing. In contrast to findings of the NSW Motor Accidents Authority,3 my study found that minor injuries were no more likely to be associated with a psychiatric injury than more severe injuries. However, a third of psychiatric injury claims (33/102) were made by people with physical injuries that were not severe enough for them to attend an emergency department or be admitted to hospital at the time of the accident. The study did find a positive relationship between the severity of physical injuries and claims for psychiatric injury in people who were very seriously injured. The psychological trauma of being severely injured may cause PTSD.5,7 Severe physical injuries may also cause psychiatric symptoms because of disability, pain or financial loss.5 However, in my study, the higher rate of claims for psychiatric injury in severely injured claimants was associated with loss of consciousness and involvement in a fatal accident rather than with other measures of injury severity. Reported loss of consciousness may be difficult to distinguish from amnesia resulting from emotional stress,18 which may predispose to psychiatric injury.19 The use of insurance claimants as the sample in this study led to selection bias and may have influenced the psychiatric injuries diagnosed by experts. The incidence and prognosis of whiplash injury are influenced by the system of assessing eligibility for compensation,20 and psychiatric injury may be similarly affected. More severely injured claimants may under-report their psychiatric symptoms because they are more concerned about their physical injuries and because the grounds for compensation for physical injuries have been clearly established. Claimants who are not seriously injured but are hurt or upset and have received less initial medical care may report more psychiatric symptoms. The opinions of expert witnesses may, in turn, be influenced by their role in the adversarial legal system.16 Under the current NSW system, some claimants may exaggerate their disability or genuinely become disabled because "significant disability" is a requirement for compensation;21 claimants who have a psychiatric injury but are less disabled are not compensated. Reform of the rules on expert evidence designed to reduce bias22,23 and a move to more detailed assessment of the cause of psychiatric symptoms after motor vehicle accidents may reduce the pressure for the NSW government to further limit psychiatric injury claims. Acknowledgements I would like to acknowledge NRMA Insurance Limited and Mr Victor Kelly of Abbott Tout Solicitors, Sydney, NSW, for making claimants' files available; Dr Timothy Heath (Concord Repatriation and General Hospital, Sydney, NSW) for his help with data analysis; and Dr Olav Nielssen (Psychiatrist, Sydney, NSW) for his assistance with the manuscript. The study was not funded. References Motor Accidents Authority and Roads and Traffic Authority of New South Wales. Road safety statistics, 2000. Available at <http//www.maa.nsw.gov.au/proftest/statistics/injury/report05.htm> (last sighted Jul 2001). Motor Accidents Authority and Road Traffic Authority of New South Wales. Compulsory third party statistics, 1999. Available at <http//www.maa.nsw.gov. au/professionals/statistics/CTP_stats_98.htm> Suhood S. Claims involving psychological disturbance, September 2000. Sydney: Motor Accidents Authority and Road Traffic Authority of NSW, 2000. Blaszczynski A, Gordon K, Silove D, et al. Psychiatric morbidity following motor vehicle accidents: a review of methodological issues. Compr Psychiatry 1998; 39: 111-121. Mayou R. The psychiatry of road traffic accidents. In: Mitchell M, editor. The aftermath of road traffic accidents. London: Routledge Press, 1997: 33-48. Ehlers A, Mayou RA, Bryant B. Psychological predictors of chronic posttraumatic stress disorder after motor vehicle accidents. J Abnorm Psychol 1998; 107: 508-519. Blanchard EB, Hickling EJ, Taylor AE, et al. Who develops PTSD from motor vehicle accidents? Behav Res Ther 1996; 34: 1-10. Mayou R, Bryant B, Duthie R. Psychiatric consequences of road traffic accidents. BMJ 1993; 307: 647-651. Ursano RJ, Fullerton CS, Epstein RS, et al. Acute and chronic posttraumatic stress disorder in motor vehicle accident victims. Am J Psychiatry 1999; 156: 589-595. Green MM, McFarlane AC, Hunter CE, Griggs WM. Undiagnosed post-traumatic stress disorder following motor vehicle accidents. Med J Australia 1993; 159: 529-534. Feinstein A, Dolan R. Predictors of post traumatic stress disorder following physical trauma: an examination of the stressor criterion. Psychol Med 1991; 21: 85-91. Bryant RA, Harvey AG. Initial posttraumatic stress responses following motor vehicle accidents. J Trauma Stress 1996; 9: 223-234. Blanchard EB, Hickling EJ, Taylor AE, Loos W. Psychiatric morbidity associated with motor vehicle accidents. J Nerv Ment Dis 1995; 183: 495-503. Baker SP, O'Neill B, Haddon W, Long WB. The Injury Severity Score: a method for describing patients with multiple injuries and evaluating emergency care. J Trauma 1974; 14: 187-196. SPSS for Windows. Release 9.0.1. Chicago: SPSS Inc, 1999. Large M, Nielssen O. An audit of medico-legal reports prepared for claims of psychiatric injury following motor vehicle accidents. Aust N Z J Psychiatry. In press. Henderson S, Andrews G, Hall W. Australia's mental health: an overview of the general population survey. Aust N Z J Psychiatry 2000; 34: 197-205. Kopelman MD. Fear can interrupt the continuum of memory. J Neurol Neurosurg Psychiatry 2000; 69: 431-432. Mayou RA, Black J, Bryant B. Unconsciousness, amnesia and psychiatric symptoms following road traffic accident injury. Br J Psychiatry 2000; 177: 540-545. Cassidy JD, Carroll LJ, Cote P, et al. Effect of eliminating compensation for pain and suffering on the outcome of insurance claims for whiplash injury. N Engl J Med 2000; 342: 1179-1186. Motor Accidents Compensation Act (NSW) 1999. Friston M. New rules for expert witnesses: The last shots of the medico-legal hired gun. BMJ 1999; 318: 1365-1366. Federal Court of Australia. Practice direction: guidelines for expert witnesses. Canberra: Federal Court of Australia, 1998. Available at <http://www. fedcourt.gov.au/pracproc/practice_direct.html> last sighted Jul 2001. (Received 31 Jul 2000, accepted 3 May 2001) Authors' details Department of Psychiatry, Royal Prince Alfred Hospital, Sydney, NSW. Matthew M Large, FRANZCP, Staff Specialist Psychiatrist. Reprints will not be available from the author. Correspondence: Dr M M Large, Department of Psychiatry, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW 2050. mlargeATozemail.com.au Make a comment 1: Number of people claiming psychiatric or traumatic brain injuries and pre-existing psychiatric disorders among 522 insurance claimants Injury or disorder Injury claim Pre-existing disorder Traumatic brain injury (TBI) 17 (3.3%) 0 Post-traumatic stress disorder 48 (9.2%) 0 Depressive disorders 46 (8.8%) 8 (1.5%) Anxiety disorders 15 (2.9%) 3 (0.6%) Somatoform disorders 8 (1.5%) 3 (0.6%) Adjustment disorders 12 (2.3%) 0 Substance abuse 3 (0.6%) 4 (0.8%) Dementia or low IQ 0 3 (0.6%) Schizophrenia 0 2 (0.4%) Other 6 (1.1%) 2 (0.4%) Total* Psychiatric injury 102 (19.5%) 25 (4.7%) Psychiatric injury or TBI 113 (21.6%) 25 (4.7%) *36 people claimed more than one psychiatric injury. Back to text 2: Demographic, injury and accident characteristics among 472 insurance claimants* (95% CI) Variable No psychiatric or traumatic brain injury (n=359) Psychiatric injury (n=102) Psychiatric or traumatic brain injury (n=113) Age in years (95% CI) 33.4 (31.8-35.1) 36.4 (35.5-39.1) 35.7 (33.0-38.3) % Male 49% (44%-54%) 46% (36%-56%) 49% (39%-58%) Hospital stay in days 4 (3-5) 8 (4-12) 11 (6-16) Injury Severity Score† 11.7 (11.0-12.5) 14.0 (12.1-15.9) 16.1 (13.1-18.4) % With loss of consciousness 9% (6%-12%) 25% (16%-33%) 31% (23%-39%) % In fatal accident 1% (0-3%) 8% (3%-13%) 7% (2%-12%) % With neck or back pain 62% (57%-67%) 68% (59%-77%) 64% (55%-73%) Values in bold are significantly different from values for group with no psychiatric injury or TBI, as defined by non-overlapping 95% CIs. * 50 claimants were excluded from this analysis as no information was available on one or more of the following: nature of physical injuries, demographic details, or setting of medical care. † Maximum possible score, 75. Back to text 3: Psychiatric injury claims and injury characteristics among 472 insurance claimants,* according to initial treatment setting† (95% CI) Local medical officer (n=177) Emergency department (n=146) General inpatient (n=129) Intensive care unit (n=20) % With psychiatric injury 19% (13%-24%) 24% (17%-31%) 19% (12%-26%) 45% (26%-63%) % With post-traumatic stress disorder 10% (6%-14%) 10% (5%-15%) 8% (3%-12%) 30% (10%-50%) % With traumatic brain injury 0.6% (0-1.7%) 0.7% (0-2.0%) 5% (1%-8%) 45% (23%-67%) Mean Injury Severity Score 8.0 (7.5-8.5) 10.3 (9.5-11.0) 18.5 (17.0-20.0) 36.7 (31.3-42.0) Mean hospital stay (days) 0 1 13 (9-17) 40 (24-56) % With loss of consciousness 2% (0-4%) 12% (6%-18%) 27% (19%-35%) 60% (38%-82%) % With neck or back pain 81% (75%-87%) 71% (64%-78%) 33% (24%-41%) 20% (2%-38%) PTSD=Post-traumatic stress disorder. TBI=Traumatic brain injury. * 50 claimants were excluded from this analysis as no information was available on one or more of the following: nature of physical injuries, demographic details, or setting of medical care. † Most medically intensive treatment setting in the week after the accident. Back to text 4: Multivariate logistic regression analysis of variables potentially associated with psychiatric injury claims Odds ratio (95% CI) P Injury severity score* 0.98 (0.95-1.02) 0.29 ICU treatment 1.86 (0.80-4.35) 0.15 Hospital stay (days)* 1.00 (0.98-1.02) 0.45 Loss of consciousness 1.82 (1.20-2.88) 0.006 Fatal accident 3.47 (1.52-7.92) 0.003 ICU=Treatment in intensive care unit during first week. *Continuous variables. Back to text

Matthew M Large

MJA 2001; 175: 15-18 For editorial comment, see Hugh & Hugh Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Surgery Abstract Objective: To measure and describe changes in the incidence of appendicectomy in the population of Western Australia (WA) for 1981-1997. Design: Population-based incidence study using hospital discharge data. Setting: All hospitals in WA (1981-1997). Patients: All patients who underwent an appendicectomy in WA hospitals. Main outcome measures: Changes in the incidence of appendicectomy procedures over time; age-standardised rates and age-sex profiles of four appendicectomy subgroups: (1) acute emergency admission, (2) other emergency admission, (3) incidental appendicectomy and (4) other appendicectomy. Results: From 1981 to 1997, there were 59 749 appendicectomies in WA hospitals. The age-standardised rate of appendicectomy declined by 63% in metropolitan females, by 44% in non-metropolitan females, by 41% in metropolitan males and by 21% in non-metropolitan males. The rate of decline was significantly greater in females and in metropolitan patients. From 1988 to 1997, acute emergency admission for appendicectomy was the most common admission status and was more common in males than females (122 v 103 per 100 000 person-years) and in non-metropolitan areas. The rate of incidental appendicectomy was higher among females than males (20 v 7 per 100 000 person-years). From 1988 to 1997, recorded diagnosis coding for appendicitis became more specific, with a marked reduction in the use of the "unspecified" appendicitis code. Conclusions: The overall incidence of appendicectomy has declined markedly in WA and includes a decline in the practice of incidental appendicectomy. The trend was greatest in the metropolitan hospitals. Appendicectomy is one of the most common surgical procedures in adults and children.1-3 Increases in the incidence of appendicitis were reported during the early part of the 20th century, but a decline has been reported since about 1930.4-6 Significant advances in diagnostic and surgical technology may have influenced treatment options for patients and surgical outcomes.3 Linked hospital discharge data from Oxford (UK), 1970-1986, reported by Primatesta and Goldacre, showed falls in acute appendicitis and the prophylactic and incidental use of appendicectomy, but no decline in conditions that mimic the disease.7 The authors raised the concern that appendicectomy without acute appendicitis was much more common in women than men, questioning the appropriateness of the use of the procedure.7 Our study used data from the Quality of Surgical Care Project8 stored in the WA Health Services Linked Database (WA Linked Database)9 to assess trends in appendicectomy in Western Australia (WA) for 1981-1997. Methods The WA Linked Database provided hospital morbidity data for all patients who underwent appendicectomy for 1981-1997. Hospital morbidity records with a separation date before 1988 were selected using the ICPM procedure code 5-470,10 while ICD-9-CM procedure codes 47.0 and 47.1 were used for patients separated in 1988-1997.11 Data for incidental appendicectomy were evaluated only for the period 1988-1997, as there was no specific incidental appendicectomy procedure code before 1988. To allow comparison with the Oxford study,7 patients who underwent appendicectomy were classified into four subgroups based on procedure and diagnosis codes in conjunction with admission status (Box 1). Western Australia occupies the western third of the Australian continent. It is sparsely populated, except for the southwest corner of the State and some coastal settlements to the north. Seventy-three per cent of the total population of 1.9 million reside in the capital city of Perth. We used postcode data to classify patients as residing in Perth (metropolitan) or non-metropolitan areas, following the Health Zone classification system of the Health Department of Western Australia. We estimated annual rates of appendicectomy procedures per 100 000 person-years (PY) by the direct method,12 age standardised to the WA population.13 Population estimates were obtained from the Australian Bureau of Statistics.14 Men and women were analysed separately. We analysed descriptive statistics with the statistical program SPSS,15 and time trends in rates of admission by Poisson regression models using the SAS procedure GENMOD.16 These models included terms for "locality" (metropolitan/non-metropolitan), "time", "age-group" and "sex", and associated rate ratios are reported. Depending on goodness of fit, "time" was modelled either as a single term for linear trend or categorically. In our modelling, we also assessed whether trend effects differed by sex and/or locality by using appropriate higher-order interaction terms. Results Trends in appendicectomy rates, 1981-1997 Of the 59 749 appendicectomies performed in WA in 1981-1997, 33 352 (55.8%) were performed on female patients and 26 397 (44.2%) on males. There was a marked decline in the rate of appendicectomy during the study period (Box 2). The age-standardised rate declined by 63% (from 386 to 144 per 100 000 PY) in metropolitan females, by 44% (from 393 to 221 per 100 000 PY) in non-metropolitan females, by 41% (from 240 to 142 per 100 000 PY) in metropolitan males and by 21% (from 258 to 204 per 100 000 PY) in non-metropolitan males. The decline was more marked in females than males and was also greater in the metropolitan area. The adjusted rate ratio (RR) in metropolitan females fell by 6.2% per year (RR, 0.938; 95% CI, 0.933-0.943), compared with 3.2% per year (RR, 0.968; 95% CI, 0.959-0.976) in non-metropolitan females. For metropolitan males, the adjusted rate ratio declined by 3.9% per year (RR, 0.961; 95%CI, 0.955-0.967), compared with the 1.6% per year decline (RR, 0.984; 95% CI, 0.976-0.993) in non-metropolitan males. Trends in admission classification, 1988-1997 Of the 30 934 appendicectomies performed in WA during 1988-1997, 18 961 (61.3%) were acute emergency admissions, 3820 (12.3%) were other emergency admissions, 2192 (7.1%) were incidental procedures and 5961 (19.3%) were recorded as other appendicectomy admissions. The age-sex profiles for each group are presented in Box 3. Acute emergency admission appendicectomy was more common in males than females (122.2 v 102.9 per 100 000 PY). The highest rates were in males aged 10-14 years (300 per 100 000 PY) and females aged 15-19 years (289 per 100 000 PY). There was an asymptotic decrease in rates of acute emergency appendicectomy after the 20-24-years age group in both sexes. Rates were higher in non-metropolitan areas for males (149 v 111 per 100 000 PY) and females (131 v 93 per 100 000 PY). The difference between metropolitan and non-metropolitan areas remained significant after adjustment for age, sex and year of separation (RR, 1.37; 95% CI, 1.30-1.45). There was a modest increase in the rate ratio of 1.5% per year over time (95% CI, 0.6%-2.4%) for patients in this group, with no difference between metropolitan and non-metropolitan areas in the rate of acute emergency admissions. Rates of other emergency appendicectomies were higher in females than males (31 v 15 per 100 000 PY). In females, the rates were highest in those aged 15-19 years (108 per 100 000 PY) and declined sharply after the 20-24-years age group. Rates were higher in non-metropolitan areas for both females (44 v 26 per 100 000 PY) and males (21 v 13 per 100 000 PY) and this effect remained after adjustment for age, sex and year of separation (RR, 1.66; 95% CI, 1.53-1.80). The age-sex profile of incidental appendicectomies showed a very different pattern. The rate of incidental appendicectomy was higher in females than males (20 v 7 per 100 000 PY). The age profiles were also different, with a sharp, bell-shaped pattern of increase and decrease in women between the ages of 15 and 49 years, with the highest rate occurring in women aged 35-39 years (37 per 100 000 PY). Rates were higher in non-metropolitan areas, with this difference considerably more pronounced in females (29 v 17 per 100 000 PY) than in males (8 v 6 per 100 000 PY). There was a marked decline in the rate of incidental appendicectomies over time among females (Box 4), with a significantly more pronounced trend in metropolitan than non-metropolitan areas (P < 0.001). The primary surgical procedures with which incidental appendicectomies were performed varied by sex. Incidental appendicectomies in females were most frequent during admissions for operations of the uterus (57%) and ovary (24%), and for operations on the intestines (52%), and hernia and abdomen (20%) in males. Rates of other appendicectomy were higher in females than males (50 v 22 per 100 000 PY). The highest rate occurred in females aged 15-19 years (139 per 100 000 PY). Rates in this group were higher in non-metropolitan areas for both females (55 v 48 per 100 000 PY) and males (26 v 20 per 100 000 PY). This locality effect was significant after adjustment for age, sex and year of separation (RR, 1.19; 95% CI, 1.09-1.29). There was a strong linear decrease in the incidence of other appendicectomies, with the rate ratio declining 14.4% per year (95% CI, 13.2%-15.5%). This rate of decline was significantly greater for males (17.2%) than females (13.1%; P = 0.002). Changes in recorded diagnosis, 1988-1997 Changes in the diagnostic profiles of appendicectomy records, excluding incidental appendicectomies, are shown in Box 5. There was a 10-fold reduction in the use of the unspecified appendicitis diagnosis code, with an increase in the use of acute appendicitis diagnosis codes. To assess whether the increased use of acute appendicitis codes was more likely to reflect changes in recording practices rather than in true disease incidence, trends in appendicectomy rates were examined in males aged 10-24 years, as this group predominantly reflected acute emergency admissions. From 1981 to 1997, age-specific rates of appendicectomy in young males declined by 42% (from 692 to 399 per 100 000 PY) in those aged 10-14 years, by 45% (from 629 to 346 per 100 000 PY) in those aged 15-19 years and by 33% (from 373 to 251 per 100 000 PY) in those aged 20-24 years. Discussion The incidence rate of appendicectomy in WA hospitals declined markedly from 1981 to 1997, consistent with trends reported from other industrialised countries.5,6 The age-sex profiles of the four different classifications of appendicectomy defined in our study were similar to those found in the Oxford Record Linkage Study.7 These profiles were unaffected by the different procedure classifications employed, namely ICD-9-CM in our study and the Office of Population Censuses and Surveys Operations Codes in the Oxford study. Improvements in diagnostic technology during the past decade have resulted in a much greater use of compression ultrasonography, laparoscopic examination and scoring systems to verify acute appendicitis in patients with abdominal pain.17,18 These technical improvements may have contributed to the decline in appendicectomy and an improvement in coding practice. Further research is warranted here given a recent finding of no significant benefits from ultrasonography compared with clinical diagnosis alone, other than reduced time to operation.19 Our study found changes in the specificity of coding of recorded diagnoses of appendicitis from 1988 to 1997. In 1988, most diagnoses of appendicitis were recorded using the non-specific code 541.x. By 1997, relatively few diagnoses of appendicitis were assigned this code. There was an increase in the number of diagnoses coded as acute appendicitis either with peritonitis (540.0 or 540.1) or without peritonitis (540.9). This change could be taken to indicate that the incidence of acute appendicitis increased in WA during 1988-1997. However, our data show a fall in the number of appendicectomies in WA since 1981 and a fall among males aged 10-24 years, the group most likely to be admitted with acute appendicitis. A more likely explanation is that there was an improvement over time in the accuracy of coding in WA hospitals. There is now concern about the continued practice of incidental appendicectomy.20 While the physiological role of the appendix is unclear, it may have surgical potential in reconstructive urology and the management of faecal incontinence. The frequency of emergency (acute and other) appendicectomy peaks in the 15-19-years age group, the frequency of incidental appendicectomy peaks in the 35-39-years age group in women and at around 70 years in men. A retrospective review and meta-analysis of incidental appendicectomy by Snyder and Selanders supported incidental removal of the appendix in young patients (< 35 years), suggested that the patient's clinical condition should determine incidental removal between 35-50 years, and could not justify incidental appendicectomy in patients older than 50 years.21 To address the concerns that incidental appendicectomy is unjustified, further comparison of the risk of appendicectomy and the risk of complications (especially adhesion formation) for different age groups is needed. The decline in incidental appendicectomy has also seen a convergence of appendicectomy trends for males and females, which most likely reflects a change in attitude by surgeons. The rate of incidental appendicectomy was about five times higher in females than males in 1988, but had reduced to twice the magnitude by 1997. There was no indication of a parallel decline in other abdominal procedures to account for the decline in appendicectomy rates, although the increased use of laparoscopic procedures may have contributed to the decline in incidental appendicectomy. The decline in the incidence of appendicectomy in WA from 1981 to 1997 is consistent with trends in other industrialised countries and most likely reflects a change in attitude to the use of the procedure, coupled with improvements in diagnostic technology. The trend was most notable in young women in the metropolitan area. There was a fivefold decline in incidental appendicectomy in women in both the metropolitan and non-metropolitan areas. Incidental appendicectomy was more common in women in non-metropolitan areas, which raises questions about differences in practice between the metropolitan and non-metropolitan areas. While the decline in the rates of incidental appendicectomy reflects a change in clinical practice, the question still remains whether incidental appendicectomy is justified to prevent future appendicitis, and does the risk of additional problems and complications outweigh the potential benefit. Acknowledgements We thank the National Health and Medical Research Council for the funds that supported this study, and Dr John Bass and the Extramural Unit of the Western Australian Health Services Research Linked Database Project for the linkage of patient records. Mr Neil Donnelly was on secondment from the Needs Assessment and Health Outcomes Unit, Central Sydney Area Health Service, Sydney, NSW, Australia. References Pearl RH, Hale DA, Molloy M, et al. Pediatric appendectomy. J Pediatric Surg 1995; 30: 173-181. Reid RI, Dobbs BR, Frizelle FA. Risk factors for post-appendectomy intra-abdominal abscess. Aust N Z J Surg 1999; 69: 373-374. Wilcox RT, Traverso LW. Have the evaluation and treatment of acute appendicitis changed with new technology? Surg Clin North Am 1997; 77: 1355-1369. Raguveer-Saran MK, Keddie NC. The falling incidence of appendicitis. Br J Surg 1980; 67: 681. Bisset AF. Appendicectomy in Scotland: a 20-year epidemiological comparison. J Public Health Med 1997; 19: 213-218. Blomqvist P, Ljung H, Nyren O, Ekbom A. Appendectomy in Sweden 1989-1993 assessed by the Inpatient Registry. J Clin Epidemiol 1998; 51: 859-865. Primatesta P, Goldacre MJ. Appendectomy for acute appendicitis and for other conditions: an epidemiological study. Int J Epidemiol 1994; 23: 155-160. Semmens JB, Lawrence-Brown MMD, Fletcher DR, et al. The Quality of Surgical Care Project: a model to evaluate surgical outcomes in Western Australia using population-based record linkage. Aust N Z J Surg 1998; 68: 397-403. Holman CDJ, Bass AJ, Rouse IL, Hobbs MST. Population-based linkage of health records in Western Australia: development of a health services research linked database. Aust N Z J Public Health 1999; 23: 453-459. International classification of procedures in medicine. Geneva: World Health Organization, 1978. The official NCC Australian version of ICD-9-CM. Tabular list (annotated) and index of procedures. Sydney: National Coding Centre, Faculty of Health Sciences, University of Sydney, 1995. Rothman KJ. Modern epidemiology. Boston/Toronto: Little, Brown and Company, 1986. Muir C, Waterhouse J, Mack T, et al. Cancer incidence in five continents, Vol. V. Lyon: IARC Scientific Publications, International Agency for Research on Cancer, 1987. Australian Bureau of Statistics. Estimated resident population by age and sex in statistical local areas, Western Australia (Catalogue no. 3203.5). Canberra: ABS, 1995. SPSS for Windows, release 5.0 [computer program]. Chicago, Ill: SPSS Inc., 1992. SAS version 6.12 [computer program]. Cary, NC: SAS Institute, 1997. Calder JDF, Gajraj H. Recent advances in the diagnosis and treatment of acute appendicitis. Br J Hosp Med 1995; 54: 129-133. Beasley SW. Can we improve the diagnosis of acute appendicitis? [editorial]. BMJ 2000; 321: 907-908. Douglas CD, McPherson NE, Davidson PM, Gani JS. Randomised controlled trial of ultrasonography in diagnosis of acute appendicitis, incorporating the Alvarado score. BMJ 2000; 321: 1-6. Wheeler RA, Malone PS. Use of appendix in reconstructive surgery: a case against incidental appendicectomy. Br J Surg 1991; 78: 1283-1285. Snyder TE, Selanders JR. Incidental appendicectomy — yes or no? A retrospective case study and review of the literature. Infec Dis Obstet Gynecol 1998; 6: 30-37. (Received 20 Sep 2000, accepted 20 Mar 2001) Authors' details Needs Assessment and Health Outcomes Unit, Central Sydney Area Health Service, Sydney, NSW. Neil J Donnelly, BSc (Hons), MPH, Statistician. Centre for Health Services Research, Department of Public Health, The University of Western Australia, Nedlands, WA. James B Semmens, MSc, PhD, Research Fellow, Quality of Surgical Care Project. C D'Arcy J Holman, MB BS, MPH, PhD, Director. University Department of Surgery, Fremantle Hospital, Fremantle, WA. David R Fletcher, MB BS, MD, FRACS, Professor. Reprints will not be available from the authors. Correspondence: Dr James B Semmens, Quality of Surgical Care Project, Centre for Health Services Research, Department of Public Health, The University of Western Australia, Nedlands, WA, 6907. Make a comment 1: Four appendicectomy subgroups Definitions based on ICD-9-CM diagnosis and procedure codes in conjunction with recorded admission type status: Acute emergency admission appendicectomy Diagnosis code for acute appendicitis with or without rupture (540.0, 540.1 or 540.9) + procedure code for appendicectomy (47.0) or Diagnosis code for unspecified appendicitis (541.0 or 541.9) + procedure code for appendicectomy (47.0) + emergency admission type status. Other emergency admission appendicectomy Patients who were clinically hard to define: patients treated with appendicectomy where the diagnosis did not include either acute or unspecified appendicitis (540.x or 541.x) but who were admitted as an emergency case (procedure code for appendicectomy (47.0) + emergency admission type status + any diagnosis codes not including 540.0, 540.1, 540.9, 541.0 or 541.9). Incidental appendicectomy Incidental or prophylactic excision of a normal appendix during abdominal operations (procedure code 47.1). Other appendicectomy All patients with a procedure code for appendicectomy (47.0) not included in subgroups 1 and 2. Back to text Age-standardised total annual incidence rates for appendicectomy in men and women in the metropolitan and non-metropolitan areas of Western Australia for the period 1981-1997. Back to text A: Acute emergency appendicectomy in males and females, Western Australia, 1988-1997. B: Other emergency appendicectomy in males and females, Western Australia, 1988-1997. C: Incidental appendicectomy in males and females, Western Australia, 1988-1997. D: Other appendicectomy in males and females, Western Australia, 1988-1997. Back to text Age-standardised total annual incidence rates for incidental appendicectomy in males and females in the metropolitan and non-metropolitan areas of Western Australia for the period 1988-1997. Back to text 5: Diagnostic profiles of appendicectomy records excluding incidental appendicectomy in Western Australia, 1988-1997 Acute rupture (540.0, 540.1) Acute non-rupture (540.9) Unspecified appendicitis (541.x) Other appendix (542.x, 543.x) Abdominal pain (789.x) Other 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 157 230 215 316 318 311 388 386 469 527 943 988 922 1084 1265 1478 1396 1364 1559 1563 1436 1138 1016 658 448 369 225 195 167 157 102 169 179 219 306 289 296 263 201 213 273 228 248 282 341 378 297 243 206 161 153 167 211 258 246 277 233 207 183 225 Coding numbers used in this table are from ICD-9-CM.11 Back to text

Neil J Donnelly · James B Semmens · David R Fletcher

MJA 2001; 174: 621-625 For editorial comment, see Barraclough Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Administration and health services Abstract Objectives: To determine if an integrated clinical risk management program that detects adverse patient events in a hospital, analyses their risk and takes action can alter the rate of adverse events. Design: Longitudinal survey of adverse patient events over eight years of progressive implementation of the risk management program. Participants and setting: 49 834 inpatients (July 1991 to September 1999) and 20 050 emergency department patients (October 1997 to September 1999) at a rural base hospital in the Wimmera region of Victoria. Main outcome measures: Rates of adverse events detected by medical record review and clinical incident and general practitioner reporting. Results: The annual rate of inpatient adverse events decreased between the first and eighth years of the study from 1.35% of all patient discharges (69 events) to 0.74% (49 events) (P < 0.001). Absolute risk reduction was 0.61% (95% CI, 0.23%-0.99%), and relative risk reduction was 44.9% (95% CI, 16.9%-72.9%). The quarterly rate of emergency department adverse events decreased between the first and eighth quarters of monitoring from 3.26% of all attendances (84 events) to 0.48% (12 events) (P < 0.001). Absolute risk reduction was 2.78% (95% CI, 2.04%-3.52%), and relative risk reduction was 85.3% (95% CI, 62.7%-100%). Conclusions: Adverse patient events can be detected, and their frequency reduced, using multiple detection methods and clinical improvement strategies as part of an integrated clinical risk management program. Healthcare delivery in hospitals is associated with adverse patient events,1,2 and clinical risk management aims to reduce the probability of these events. One approach involves detecting adverse events, analysing their causes, estimating their likelihood and consequences and taking appropriate action to prevent the event recurring. Adverse events can be detected by medical record review3 and clinical incident reporting.4 However, after their detection, analysing the events and determining and taking appropriate action to reduce their rates are difficult tasks. Rates have been reduced in other complex industries, such as aviation, by analysing the systems of service delivery in which the events occurred and changing these systems to reduce their probability.5 This systems approach contrasts strongly with the blaming of individuals for errors in healthcare. In this study, we report the effect of an integrated clinical risk management program that used diverse methods to detect adverse patient events in a hospital and a systems approach to their analysis and action to reduce their rates. Methods Setting and patients The study was undertaken at Wimmera Base Hospital in Horsham, 300 km northwest of Melbourne, Victoria. The hospital provides services to 43 000 people in the Wimmera region, including 13 500 in Horsham. Eight specialists and 14 general practitioners live in the town. With the assistance of eight hospital medical officers, they treat about 6000 inpatients and 9000 emergency department patients annually. Another 14 specialists visit the town regularly to treat patients at the hospital. The components of the risk management program (Box 1) evolved over time. In 1989, the hospital medical staff chose four doctors to be medical reviewers and to form a surveillance committee. This committee was expanded to include a nurse in 1995 and a clinical risk manager in 1997. Detection of adverse events Inpatient medical record review: The medical records of all patients admitted to the hospital between July 1991 and September 1999 were reviewed shortly after discharge, using a process described previously.3 Briefly, each medical record was screened by medical records staff using eight general patient outcome criteria (Box 2). Records with at least one of these criteria were sent to one of the four nominated doctors to determine if an adverse event was present. This was defined as "an untoward patient event which, under optimal conditions, is not a consequence of the patient's disease or treatment".1 The reviewer independently completed an adverse event analysis form for discussion at bimonthly meetings of the surveillance committee. Recommendations for action relating to patient care were made by the committee and forwarded to medical and nursing staff groups in the hospital. When a clinical risk manager was appointed, the adverse event analysis forms were first forwarded to the manager to determine if immediate action was required. Emergency department medical record review: The medical records of all patients who attended the emergency department between October 1997 and September 1999 were reviewed. An administrative database of all inpatient admissions and emergency department attendances was screened for five general patient outcome criteria (Box 2), using software designed for the study. Attendances that screened positive were reviewed by the hospital's clinical risk manager and, if an adverse event was detected, by the director of medical services. If an event was confirmed, it was further analysed and recommendations to prevent its recurrence were made to relevant hospital staff, using the same committee review process as used for inpatient records. Clinical incident reporting: A clinical incident reporting system was developed in 1997 by the Australian Patient Safety Foundation, an independent organisation in Adelaide that promotes patient safety. Hospital staff in Horsham were educated about the system and encouraged to report clinical incidents and "near-misses". A clinical incident was defined as "any event that has caused harm, or has the potential to harm, a patient, visitor or staff member, or any event which involves malfunction, damage or loss of equipment or property, and any event which might lead to a complaint".5 Incident reporting forms developed by the Foundation were placed in all departments. These forms comprise two parts: the first provides details of actual or potential clinical incidents, while the second allows the incident to be reported anonymously to a national database. Staff members reporting incidents could identify themselves or remain anonymous. Completed forms for incidents reported between October 1997 and September 1999 were sent to the clinical risk manager for local analysis and were also reported to the national database. General practitioner reporting: As adverse events related to inpatient care may occur or be recognised after patient discharge from hospital, an adverse event reporting form was included in the inpatient summary routinely sent to each patient's general practitioner (GP). GPs were asked to attach the form to the patient's medical record for a month and to complete and return the form if they detected an adverse event. External sources: Some adverse events occur rarely in individual hospitals. Details about serious but infrequent adverse events at other hospitals were obtained from coronial and consultative committee reports, insurers, medical indemnity organisations, medical and nursing journals and the media. If the surveillance committee thought the event could occur locally, action was taken to reduce the risk. Patient satisfaction: Patient perspective on adverse events was sought through patient satisfaction surveys, focus groups and patient complaints. Satisfaction surveys were posted to every 10th patient who attended the emergency department or was admitted to the hospital. Event analysis and action When an adverse event was detected, its likelihood and consequences were estimated in accordance with the Australia/ New Zealand Risk Management Standard6 (Box 3). Events were ranked according to their risk severity (risk severity = consequence score x likelihood score) (Box 4). Events with high risk severity were given priority for analysis, and action was taken to reduce the risk, as described previously7 (Box 5). For adverse events with low risk priority, the surveillance committee decided whether to take action or to accept the risk and continue monitoring for that event. All data from the inpatient adverse event analysis forms were entered into a database program developed from the Clipper database compiler software package.8 Data from emergency department and GP reports were entered into access databases,9 and clinical incidents were entered into the Australian Patient Safety Foundation's database.4 Statistical analysis The χ2 test was used for categorical comparisons of data. A P value < 0.05 was considered to indicate statistical significance; all tests were two-tailed. Statistical analyses were performed using the statistical package GraphPad Instat.10 Confidence intervals were calculated using standard methods.11 Results \ Inpatient medical record review A total of 49 834 inpatients were discharged from the hospital between July 1991 and September 1999. The medical records of 4199 (8.43%) screened positive for one or more of eight general patient outcomes, and 386 (0.77%) contained an adverse event. These events were analysed and action was taken to reduce the probability of recurrence. The annual rate of adverse events decreased between the first and eighth years of the study from 1.35% of all patients discharged (69 events) to 0.74% (49 events) (χ2= 31.31; df = 7; P < 0.001). This trend was linear (χ2=11.52; df = 1; P < 0.001) (Box 6). The absolute risk reduction was 0.61% (95% CI, 0.23%-0.99%), and the relative risk reduction was 44.9% (95% CI, 16.9%-72.9%). Emergency department medical record review A total of 20 050 patients attended the emergency department between October 1997 and September 1999. The medical records of 544 screened positive for one or more of five general patient outcomes (2.71% of all patient attendances), and 250 (1.24%) contained an adverse event. Action was taken to reduce the probability of recurrence. The quarterly rate of adverse events decreased between the first and eighth quarters of monitoring from 3.26% of all attendances (84 events) to 0.48% (12 events) (χ2= 120.43; df = 7; P < 0.001). The trend was linear (χ2= 87.64; df = 1; P < 0.001) (Box 6). The absolute risk reduction was 2.78% (95% CI, 2.04%-3.52%), and the relative risk reduction was 85.3% (95% CI, 62.7%-100%). Clinical incident reporting Between October 1997 and September 1999, hospital staff completed 621 clinical incident forms, and 66 adverse events were found. The most common reported incidents were patient falls (280 incidents, 45% of all reported incidents) and medication errors (93; 15%). In response to the number of falls, a falls risk assessment tool was developed. Each patient over 65 years of age underwent a falls risk assessment on admission to hospital. Subsequently, the number of patient falls resulting in fractures while in hospital decreased. The 66 events detected by clinical incident reporting made up 16.3% of the total of 405 adverse events detected between October 1997 and September 1999 by clinical incident reporting and medical record review; 250 events (61.7%) were detected by emergency department medical record review and 89 (22.0%) by inpatient medical record review. Four adverse events were detected by more than one method; these were associated with failure of equipment in the operating room and an inpatient fall. For analysis, these four events were allocated to the first method by which they were detected. General practitioner reporting Between January and September 1999, 21 reports were made by general practitioners (0.25% of patients discharged). An adverse event was identified in 16 (76% of all reports). Events included discharge medication errors, postoperative wound infections and other surgical complications. Three patients required readmission. External sources Information about 12 adverse events at other hospitals in Victoria was obtained from the media and coronial reports. After analysis, preventive administrative and clinical changes were implemented in Horsham. These included the introduction of an organisation-wide policy on equipment service contracts, installation of thermostatic mixing valves in the hot water system to reduce burns, and development of an intercostal catheter insertion policy. Patient satisfaction Of the 69 formal complaints received by the hospital between October 1997 and September 1999, 11 (16%) related to clinical care. On review, four were associated with an adverse event. Complaints were analysed in the same way as adverse events from other sources. Discussion Our study has demonstrated that adverse events in hospitals can be detected using medical record review, clinical incident reporting and other methods. The rate of adverse events can then be reduced using a systems approach to event analysis, followed by appropriate action and continued monitoring for adverse events to evaluate the effectiveness of the action. As we found that few individual events were identified by more than one detection method, the use of multiple detection methods increased the total number of events identified. Scoring the risk associated with each event, using its likelihood and consequences, allowed events found by different methods to be ranked and prioritised for action to reduce risk. This allowed available resources to be directed to events with the greatest patient risk. To our knowledge, this is the first comparative study over time of a clinical risk management program that used diverse methods to detect adverse events and reduce their rate. Other studies have used a single detection method to measure adverse event rate at one point in time. For example, inpatient medical record review was used in the multihospital Harvard Medical Practice Study1 and the Quality in Australian Health Care Study.2 These studies detected adverse event rates of 3.7%1 and 16.6%2 of hospital admissions, respectively. Both used 18 screening criteria, including some that required clinical judgement, and neither measured the rate of adverse events over time after intervention. Our study found a lower rate of inpatient adverse events, but used only eight screening criteria, none requiring clinical judgement. We are not aware of any comparative studies that measured the adverse event rate in hospital emergency departments. The rate of adverse events found using clinical incident reporting depends on the rate of reporting. For example, an increase in reports of medication errors may reflect an increase in errors, the rate of reporting, or both. Reporting rates vary greatly between hospitals, making meaningful comparisons difficult. In a study in the United States comparing adverse events reported by resident medical staff and those found by medical record review, 30.8% of adverse events were found by both methods.12 This is a much greater proportion than the 0.9% of events found by both methods in our study. However, in our study, most events were reported by nursing staff, with medical staff reporting few events. Although we used multiple methods to detect adverse events, we did not find all adverse events that occurred in the hospital. Although we could have found more by using more screening criteria, our use of five to eight screening criteria for medical record review, rather than the 18 used in some other studies,1,2 meant that this would have required more resources. The study did not include a control hospital where adverse events were detected but no analysis was performed nor action taken. Also, adverse event rates were not adjusted for patient severity. Therefore, other factors may explain the reduction in adverse events. In our study, resource limitations meant that medical records identified by screening were reviewed by a single reviewer. In the Harvard Medical Practice Study and the Quality in Australian Health Care Study, each medical record identified by screening was reviewed by two reviewers and, if they disagreed, by a third. The resources for such intensive review of records are unlikely to be available in most hospitals. The strengths of our study included its eight-year duration and prospective nature. By keeping the method constant (eg, number and types of screening criteria and three of the four reviewers), the rate of adverse events could be meaningfully compared over a long period, and the effects of actions assessed. Further research is required to improve methods of detecting adverse events. A greater proportion of events might be detected with more effective and efficient screening criteria. A potentially effective criterion would be a code for external cause of injury13 to be assigned by medical records staff when coding diagnoses. Another potential screening device is clinical pathways that can detect adverse events by analysing deviations from the pathways. The development of electronic records may also assist in detecting adverse events. In addition, national databases of adverse events reported as clinical incidents or from coronial inquests would provide further information to reduce risk. Actions that are effective in changing clinical behaviour have been discussed in detail previously.7 Although some effective strategies are available, changing health delivery systems and clinical behaviour is frequently complex and difficult, and many strategies in use are not effective.14 More research is required to develop additional effective strategies. The components of the risk management program used in our study could be applied in hospitals of varying sizes. Hospitals or individual departments can decide which detection methods are appropriate for their services and available resources. For example, medical record screening does not need to use all outcome criteria, and further program components can be added over time. Finally, we believe that the risk management program has allowed our patients to receive better care with fewer adverse events and has been an effective use of resources. Acknowledgements We wish to thank the staff of the Wimmera Health Care Group for their enthusiastic participation in the program, especially Mrs Cathy Dooling, Manager Health Information Services, and staff, and previous members of the surveillance committee. This program was partly funded by a grant from the Victorian Department of Human Services. References Brennan TA, Leape LL, Laird NM, et al. Incidence of adverse events and negligence in hospitalised patients: results of the Harvard Medical Practice Study 1. N Engl J Med 1991; 324: 370-376. Wilson RM, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. Wolff AM. Limited adverse event screening: using record review to reduce hospital adverse patient events. Med J Aust 1996; 164: 458-461. <eMJA full text> Australian Patient Safety Foundation. What is incident monitoring? The Australian Incident Monitoring Study. Adelaide: The Foundation, 1997. Leape LL. Error in medicine. JAMA 1994; 272: 1851-1857. Standards Australia. Australian/New Zealand Standard 43:60. Sydney: Standards Association of Australia, 1999. Wolff AM, Bourke J. Reducing medical errors: a practical guide. Med J Aust 2000; 173: 247-251. Clipper. Version 5.0. Los Angeles, Calif: Nantucket Corporation, 1990. Microsoft access. Relational database management system for windows. Version 7.0. Seattle, Wash: Microsoft Corporation, 1999. GraphPad Instat. Version 2.0. San Diego, Calif: GraphPad Software, 1992. Sackett DL, Haynes RB, Guyatt GH, Tugwell P. Clinical epidemiology: a basic science for clinical medicine. 2nd ed. Boston: Little Brown and Co, 1991: 218. O'Neil AC, Peterson LA, Cook EF, et al. Physician reporting compared with medical-record review to identify adverse medical events. Ann Intern Med 1993; 119: 370-376. O'Hara DA, Carson NJ. Reporting of adverse events in hospitals in Victoria, 1994-1995. Med J Aust 1997; 166: 460-463. Oxman AD, Thomson MA, Davis DA, Hayes RB. No magic bullets: a systematic review of 102 trials of interventions to improve professional practice. CMAJ 1995; 153: 1423-1431. (Received 23 Oct 2000, accepted 6 Feb 2001) Authors' details Clinical Risk Management Unit, Wimmera Health Care Group, Horsham, VIC. Alan M Wolff, FRACGP, MBA, Director of Medical Services, and Director of Accident and Emergency Department; Jo Bourke, RN, GradDipCM, Clinical Risk Manager; Ian A Campbell, FRACS, Visiting General Surgeon; David W Leembruggen, FRACGP, Visiting General Practitioner, and Director of Postgraduate Education. Reprints: Dr A M Wolff, Medical Administration, Wimmera Health Care Group, Baillie Street, Horsham, VIC 3400. whcgmedATnetconnect.com.au Make a comment Back to text 2: General outcome criteria used for screening medical records Inpatient criteria Death Return to operating theatre within 7 days Transfer from general ward to intensive care Unplanned readmission within 21 days of discharge Cardiac arrest Transfer to another acute care facility Length of stay greater than 21 days Booked for theatre and cancelled Emergency department criteria Death Unplanned re-presentation to department within 48 hours for same condition Length of stay greater than 6 hours Transfer to another acute care facility Presentation to department for same condition within 28 days of hospital inpatient discharge Back to text 3: Qualitative measures used to determine risk severity of adverse events (modified from Australian/New Zealand Standard 43:606) Measures of consequence or impact 1 Insignificant No injuries, low financial loss 2 Minor Minor treatment required, no increase in length of stay or readmission, minor financial loss 3 Moderate Major temporary injury, increased length of stay or readmission, medium financial loss 4 Major Major permanent injury, increased length of stay or readmission, major financial loss 5 Catastrophic Death, huge financial loss or threat to goodwill Measures of likelihood 1 Rare May occur only in exceptional circumstances 2 Unlikely Could occur at some time 3 Possible Might occur at some time 4 Likely Will probably occur in most circumstances 5 Almost certain Is expected to occur in most circumstances Back to text 4: Examples of risk severity scores Adverse event Source Consequence score (C)* Likelihood score (L)* Risk severity score (C x L) Missed diagnosis (abdominal pain, fracture, myocardial infarction) Emergency Department record review 3 3 9 Drug administration errors Clinical incident reporting 2 3 6 Postoperative wound infection Inpatient record review 3 2 6 Failure to admit when indicated Emergency Department record review 3 2 6 * Scores are defined in Box 2. Back to text 5: Actions taken to reduce the frequency of adverse events Changes to clinical and administrative protocols Focused audits to investigate specific adverse events Discussion with staff involved Education (including presentation of adverse events at postgraduate education meetings and clinical risk management presentations) Creation of worksheets containing details of clinical policy, space to write clinical notes and a patient management checklist Developing checklists for complex procedures Increasing the supervision of junior hospital medical officers Introduction of patient risk assessment tools to determine risk of falling, developing a pressure ulcer or thromboembolus and difficulty with discharge home Regular feedback to clinical staff about adverse events and the results of actions taken to reduce risk Back to text Back to text

Alan M Wolff · Jo Bourke · Ian A Campbell · David W Leembruggen

CLASS="LinkBox"> Research Prevalence of overweight and obesity in Australian children and adolescents: reassessment of 1985 and 1995 data against new standard international definitions Anthea M Magarey, Lynne A Daniels and T John C Boulton MJA 2001; 174: 561-564 For editorial comment, see Baur; see also Eckersley Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Paediatrics Abstract Objective: To review the prevalence of overweight and ...

Anthea M Magarey · Lynne A Daniels

Henry Krum, Andrew M Tonkin, Robert Currie, Robert Djundjek and Colin I Johnston MJA 2001; 174: 439-444 For editorial comment, see Horowitz & Stewart; see also Krum Abstract - Methods - Results - Discussion - Acknowledgements - Reference - Authors' details - - More articles on Cardiology and cardiac surgery Abstract Objectives: To investigate the frequency and general practitioner awareness of patients with chronic heart failure (CHF), and to evaluate a cardiac algorithm and document cardiac investigations performed in establishing this diagnosis. Design and setting: Between March and August 1998, consecutive patients aged 60 years and older presenting to their GP were assessed. In patients previously diagnosed with CHF, aetiology and diagnostic assessments were documented. In patients with suspected CHF (by a standardised algorithm, based on World Health Organization guidelines), further investigations and GP diagnosis were recorded. Patients: 80 consecutive patients were assessed by each of 341 GPs throughout Australia, reflecting the Australian metropolitan/rural population mix of 1996. This provided a total of 22 060 evaluable patients. Main outcome measures: Estimated numbers of patients with CHF in general practice (previously and newly diagnosed); major aetiological factors; use of ancillary diagnostic tests; drugs prescribed. Results: CHF was diagnosed in 2905 of 22 060 patients (13.2%) (2485 previously diagnosed and 420 newly diagnosed). Major aetiological factors were ischaemic heart disease and hypertension. Echocardiography had been performed in 64% of previously diagnosed patients, but was performed in only 22% of possible CHF patients. Angiotensin-converting enzyme (ACE) inhibitors were prescribed in 58.1% of patients with CHF. Patients with evidence of left ventricular dysfunction were more likely to have received ACE inhibitors. Conclusions: CHF appears to be very common in the elderly, based on GP diagnosis of the condition. Of 100 patients aged 60 years and over presenting to their GP, two new cases of CHF will be detected using a simple clinical algorithm in conjunction with appropriate diagnostic tests. ACE inhibitors appear to be underutilised. Chronic heart failure (CHF) is a debilitating condition with high morbidity and mortality, and is a major public health burden. Its prevalence is increasing,1 despite a reduction in age-standardised mortality associated with cardiovascular diseases such as myocardial infarction and stroke.2 Factors implicated in this increased prevalence include the ageing of the population, decreased mortality rates following myocardial infarction, and more frequent diagnosis of CHF after investigations such as echocardiography.3The epidemiology of CHF in Australia has been assumed to be similar to that in the United States,4-6 the United Kingdom7-10 and Europe.11,12 However, substantive data have been lacking, and the approach taken to diagnosis of patients with suspected CHF in general practice in Australia is also unknown. Similarly, although international studies have suggested marked underutilisation of angiotensin-converting enzyme (ACE) inhibitors and β-blockers,4-11,13-17 no evaluation of use of drug therapies for CHF in Australia has been reported. Accordingly, the aims of the Cardiac Awareness Survey and Evaluation (CASE) Study were: to investigate the frequency, awareness, and aetiology of heart failure in general practice in Australia; to document cardiac investigations used by general practitioners in establishing the diagnosis of CHF; and to determine prescribing patterns in the treatment of CHF by Australian GPs. As the prevalence of heart failure increases steeply with age, the study focused on people aged 60 years and older. Methods Recruitment into the CASE study GPs were recruited solely on the basis of interest in participating in the study. Interest was first ascertained by the local pharmaceutical representative of the study sponsor (see Acknowledgements). The CASE steering committee then sent interested GPs a formal letter of invitation to participate in the study. GPs agreeing to participate attended a local education and information session. These sessions were spread across all Australian States and Territories with a mix of metropolitan, rural and remote regions in an effort to recruit a sample of GPs (and thus patients) representative of their distribution. Each GP was asked to assess 80 consecutive patients aged 60 years or older for the possibility of heart failure. GPs were recruited from March 1998, data were collected prospectively and the study was completed in August 1998. Assessment for CHF New patients: Patients not previously diagnosed as having CHF were assessed for that possibility using modified World Health Organization criteria (Box 1).18 Alternative conditions that may have contributed to these symptoms and signs were recorded. In patients suspected of having CHF based on the above criteria, further investigations (chest x-ray [CXR], electrocardiogram [ECG], and echocardiogram) were suggested (but not mandated). GPs were also asked to note any investigations that had been performed in the previous 12 months. For patients who had an echocardiogram, the GP was asked to indicate whether there was evidence of systolic or diastolic ventricular dysfunction (or both) from the echocardiogram report. At the conclusion of this process, the GPs assessed whether they thought the patient had CHF. Previously diagnosed patients: For patients who had previously been diagnosed as having CHF by their GP, records were retrospectively analysed for clinical and diagnostic criteria that contributed to that diagnosis. These included use of ECG, CXR and echocardiography, hospital admission for heart failure, and specialist referral for CHF. Pharmacotherapy For patients with previously diagnosed CHF, GPs were asked to document current drug therapy specifically prescribed for this condition (name of drug, daily dose, and frequency of administration). For patients with newly diagnosed CHF, GPs were asked whether they instituted pharmacotherapy immediately and what that pharmacotherapy comprised. A dosage equivalence table of commonly prescribed ACE inhibitors was compiled, and prescribing was divided into low, medium and high doses. To determine prescribing according to decade of life, prescribing was assessed in patients aged 60-69 years (n = 569), 70-79 years (n = 1360), and 80 years and older (n = 976). GP prescribing in patients with echocardiographic evidence of systolic or diastolic left ventricular dysfunction was specifically determined. Initial pharmacotherapy prescribed for patients diagnosed with CHF as part of the CASE study was evaluated. Because of the cross-sectional nature of the assessment in CASE, most of these patients did not have the opportunity to be up-titrated to target doses of drugs. For this reason, newly diagnosed patients were not included in the analysis of dose of ACE inhibitor prescribed. Results Of 523 GPs who originally expressed interest in participating, 341 completed the study. Their geographical distribution (78% metropolitan, 22% rural or remote) was similar to that observed for all Australian GPs (77% metropolitan, 23% rural or remote). In all, 23 845 patients were entered into the study. Of these, 1785 were excluded from analysis because of patient refusal or missing data, leaving 22 060 who made up the baseline population. Baseline demographics The distribution of the CASE patient population by area (capital city, 58.7%; metropolitan, 10.7%; rural, 21.4%; remote, 1.2%; 8% unclassified) was similar to the 1996 Australian population aged 60 years or older.19 However, there were fewer rural patients among the CASE cohort than in the census population. The total CASE study population comprised 45% men and 55% women; 8612 (39%) were aged 60-69 years (48% men), 9371 (42.5%) were aged 70-79 years (45% men) and 4077 (18.5%) were aged 80 years or older (39% men). Patients not previously diagnosed with CHF Box 2 shows the assessment process and results for the 22 060 patients. In the 4807 patients assessed as having possible CHF, at least one further investigation was performed in 2903 (60.4%). To determine whether the CASE audit itself may have prompted further investigation of these patients, the tests were divided into those ordered within the previous 12 months and those ordered subsequent to the CASE audit. Investigations ordered within the 12 months before the CASE audit were ECG in 1953 (40.6%), CXR in 1894 (39.4%), and echocardiogram in 366 patients (7.6%). Investigations subsequent to the CASE clinical assessment were performed in 488 patients who had ECGs (10.2%), 493 who had CXR (10.2%), and 466 who had echocardiograms (9.7%). The diagnosis of CHF was based on symptoms in 73%, signs in 66%, causative factors in 61%, and investigations in 49% (not mutually exclusive). Presence of at least one symptom and one causative factor had the highest sensitivity for detection of new heart failure (323 of the 420 [76.9%] new cases of heart failure). The sensitivity of the other diagnostic groupings for possible heart failure were > 2 symptoms, 68.6%; > 2 signs, 47.3%; > 1 symptom and > 1 sign, 68.6%; > 1 sign and > 1 causative factor, 66.9%. Possible false negative diagnoses: Of the 4807 patients who met diagnostic criteria for suspected CHF, 466 underwent echocardiography after the CASE audit (when systolic, diastolic or no dysfunction was specifically noted). Of these 466 patients, 108 had an echocardiographic report of left ventricular systolic or diastolic dysfunction. However, despite this objective evidence of ventricular dysfunction, GPs diagnosed CHF for only 77 of these 108 patients. Possible false positive diagnoses: Of the 420 patients newly diagnosed as having CHF, 162 underwent echocardiography. Nineteen of these 162 patients (11.7%) had no evidence of left ventricular systolic or diastolic dysfunction on this test, yet were still classified as having CHF by their GP. Patients previously diagnosed as having CHF CHF had been previously diagnosed in 2485 of the baseline population of 22 060 (11.3%). Both electrocardiograms and CXRs had been performed in 96% of the patients previously diagnosed as having heart failure, and 64% had had echocardiography performed. For these patients, in the previous 12 months: 1640 patients (66%) had been referred to a specialist; 1744 patients (70%) had either not been admitted to hospital with CHF or their hospitalisation status was unknown; and of the 741 patients admitted for CHF, 459 (62%) had one admission, 165 (22%) had two admissions, and 58 (8%) had three admissions. Six patients (1%) had been admitted 10 or more times for CHF. CHF patients in the CASE study At the end of the study, 2905 of the 22 060 baseline population (13.2%) were considered to have CHF: 2485 (11.2%) with a previous diagnosis, and 420 (1.9%) with a new diagnosis. The prevalence of CHF in these patients was closely related to age group (Box 3). The cardiovascular diagnoses that may be contributing to CHF in these patients are summarised in Box 4. Hypertension and ischaemic heart disease were major comorbidities and potential aetiological factors in both the new and previously diagnosed cohorts. Pharmacotherapy Specific CHF pharmacotherapy for the 2905 patients with CHF is summarised in Box 5. Most patients were receiving diuretics and ACE inhibitors. Alternatives to ACE inhibitors in patients who can not tolerate this medication include nitrates and hydralazine (prescribed for 0.6%) and/or angiotensin II receptor antagonists (prescribed for 4.3%). β-Blockers were prescribed for 12% of patients. Less than 50% of β-blocker prescribing was of the non-selective, vasodilating β-blocker carvedilol, approved for CHF in Australia. The dose of ACE inhibitor was determined in patients previously diagnosed as having CHF (Box 6). Based on our dosage equivalence table, prescribed doses were low in 60%, medium in 31%, and high in 9% of patients. Prescribing according to echocardiographic findings: Pharmacotherapy prescribed for CHF according to left ventricular (LV) systolic (found in 932 patients) or diastolic (found in 376 patients) dysfunction is summarised in Box 5. The presence of LV dysfunction on echocardiography resulted in higher prescribing of ACE inhibitors than in the overall patient cohort. However, the frequency of ACE inhibitor prescribing was not different between the systolic and diastolic LV dysfunction groups. Furthermore, there were very few differences among other agents in these groups according to systolic or diastolic LV dysfunction. Prescribing according to decade of life: Prescribing of drug therapy specifically for CHF according to decade of life is summarised in Box 5. ACE inhibitor prescribing was unaltered in the very elderly (≥ 80 years). Prescribing of β-blocker demonstrated an age-dependent decrease, whereas prescribing of digoxin and diuretics (thiazide and loop) demonstrated an age-dependent increase. Prescribing in patients with newly diagnosed CHF: Use of pharmacotherapy among newly diagnosed CHF patients was less than that observed in patients with previously diagnosed CHF. In particular, only 51% of newly diagnosed patients were prescribed ACE inhibitors, 37% diuretics, 17% received calcium-channel blockers, 10% digoxin and 8% β-blockers. Discussion We undertook a clinical algorithm approach to the possible diagnosis of CHF. By identifying possible CHF based on the grouping of symptoms, signs and causative factors, we demonstrated an 8.7% rate of identification of CHF (420 of 4807 patients). Although this approach resulted in a relatively low rate of successful diagnosis of CHF, the algorithm used was entirely clinical with a very simple screening process. Our results suggest that, of 100 patients aged 60 years or older presenting to a GP, two will have previously undetected CHF that can be simply diagnosed by attention to clinical symptoms and signs in conjunction with appropriate diagnostic tests. Prevalence of CHF We found somewhat higher rates of CHF patients (13.2%) than in earlier general practice based studies.4,7-9 Specifically, reported prevalence of CHF among patients aged 65 years or older in UK general practice ranged from 2.8%9 to 8.0%.7 The higher rate in the CASE study may reflect the differing methods by which the diagnosis of CHF was made (eg, patient file review,4,9 morbidity registry8), greater use of objective testing (ie, echocardiography in our patient cohort), or our study being a more representative sample of the true CHF population than previous geographically restricted studies performed in the US or UK. In contrast to the above assessments of CHF frequency, population studies where echocardiographic ventricular dysfunction was the main criterion for diagnosis detected fewer CHF patients within these age groups than in the CASE study.10,12 Numbers of CHF patients in the CASE Study increased dramatically with each decade of life — more than 20% of patients aged 80 years or older were diagnosed with CHF. Given the ageing of the population, these findings have important implications for resource allocation. Aetiology The aetiology of CHF was as expected, with a major contribution from ischaemic heart disease and previous myocardial infarction, as well as hypertension. Hypertension was a major contributor to CHF in the Framingham study,20,21 but less so in analysis of the Studies of Left Ventricular Dysfunction (SOLVD)22 and other, more recent data.23 The major contribution of hypertension in the CASE cohort may reflect the advanced age of the population studied, in which hypertension is a frequent comorbidity. Investigations Use of ECG and CXR was high, and echocardiography was used in more than half the patients. The lower use of echocardiography (despite recommendations by major organisations such as WHO)18 may reflect lack of full knowledge of the sensitivity and specificity of this diagnostic test, concerns regarding expense, and difficulty with access. Pharmacotherapy Use of ACE inhibitors: ACE inhibitor prescribing by Australian GPs ranges from 51%-71% of CHF patients, depending on the specific population studied. Prescribing of ACE inhibitor was more likely in patients in whom ventricular dysfunction had been objectively documented. These findings are consistent with international studies, in which prescribing of ACE inhibitors ranges from 10% to 60%.5,6,8-10,14-17 ACE inhibitors reduce morbidity and mortality across the entire spectrum of CHF severity, including in patients with asymptomatic systolic left ventricular dysfunction.24-26 Therefore, all patients with systolic left ventricular dysfunction should be receiving ACE inhibitors unless contraindicated or intolerant. Lack of compliance with these prescribing recommendations may relate to contraindications to ACE inhibitor therapy (ie, bilateral renal artery stenosis) or observed side effects such as hyperkalaemia or cough. Furthermore, ACE inhibitors are not of proven benefit in patients with diastolic CHF. Definitive diastolic dysfunction on echocardiography comprised only a small percentage in the CASE study, although the true percentage is undoubtedly considerably higher. Potential alternatives to ACE inhibitors in patients who are ACE intolerant or have contraindications include angiotensin II receptor antagonists and hydralazine (the latter as part of the hydralazine/nitrate combination). However, only 4.3% of patients were taking angiotensin II receptor antagonists and 0.6% were taking hydralazine. Our findings suggest that, despite the definitive data supporting the use of ACE inhibitors in CHF, these agents are still being underutilised. Dose of ACE inhibitors: Submaximal doses of ACE inhibitors were prescribed for those patients who are taking these drugs. The major clinical trials conducted in patients with CHF (SOLVD,24 CONSENSUS25) and LV dysfunction post-MI (SAVE27) used much higher doses (150 mg of captopril or 20-40 mg of enalapril) than the median and mean doses prescribed in this study. Doses prescribed by Australian GPs were generally lower than both the target and achieved ACE inhibitor doses used in these major trials. There are a number of reasons why the recommended target doses may not be achieved in general practice. First, patients may not tolerate the highest dosage because of hypotension, particularly if up-titration is rapid. Second, because these agents improve symptomatology, patients may become asymptomatic at lower doses of drug and the need to go to higher doses not be entertained in an asymptomatic patient. Finally, until recently, there has been no clear evidence that higher doses offer substantial clinical benefits over and above the use of ACE inhibitors at lower doses. The ATLAS study28 demonstrated a reduction in the combined endpoint of death/heart failure related hospitalisation with lisinopril 32.5-35 mg daily compared with lisinopril 2.5-5 mg daily. Mortality alone was reduced by 8% in the high-dose lisinopril subgroup. Although this reduction is modest, it does suggest that an attempt should be made to maximise ACE inhibitor dosage in every patient. β-Blockers: Prescribing of β-blockers was low, despite overwhelming evidence supporting the benefits of these agents in patients with New York Heart Association (NYHA) Class II-III symptoms.29-31 However, much of this evidence has only been published subsequent to the completion of the CASE study.30,31 Prescribing of the β-blocker vasodilator carvedilol occurred in fewer than half the patients receiving β-blockers. As carvedilol is the only β-blocker approved in Australia for CHF, this suggests that much of the prescribing of β-blockers for the CASE cohort was for indications other than CHF (eg, ischaemic heart disease and hypertension). As GPs in Australia are not permitted to prescribe carvedilol, our observed rate of use of β-blockers reflects specialist prescribing. Factors affecting prescribing: In patients with a definitive diagnosis of ventricular dysfunction by echocardiography, prescribing of ACE inhibitor therapy was higher than for the overall CASE CHF cohort. This may reflect more confidence with the cause of patient symptomatology as being related to CHF. Alternatively, it may be that a GP who is more likely to perform echocardiography to diagnose CHF is also more likely to prescribe best-practice pharmacotherapy. It was also noteworthy that the difference in overall prescribing for systolic versus diastolic dysfunction in these patients appeared similar, although many of the agents (eg, ACE inhibitors) are not of proven benefit in diastolic CHF. Furthermore, some drugs, such as non-dihydropyridine calcium-channel blockers, are relatively contraindicated in patients with systolic heart failure, yet prescribing rates were similar for the entire patient cohort. Conversely, these agents may be of particular benefit in diastolic heart failure, but again prescribing rates appeared similar to the entire patient cohort. There was no reduction in prescribing of ACE inhibitor with each decade of life, suggesting that GPs supported the use of these agents in CHF management in the very elderly (≥ 80 years). Very few data exist to support the use of ACE inhibitors in this group of patients, although studies are currently being conducted. In contrast, β-blocker use declined with each decade of life, suggesting less comfort in prescribing these agents for older patients. Increased digoxin and diuretic use with advanced age may reflect the need to increasingly prescribe these agents for comorbidities such as atrial fibrillation and oedema of other causes. Study limitations The CASE study had a number of potentially significant limitations. Selection of GPs was not random, but was based on interest in undertaking the study. This could introduce significant bias, and therefore we have not classified our evaluation as a prevalence or incidence study. Nevertheless, every effort was undertaken to ensure a representative distribution of general practices according to State, regional area and metropolitan versus rural practice. The study has also demonstrated the difficulty in making a clinical diagnosis of CHF. Diagnosis of CHF was left to the clinical judgement and decision of the GP. We noted a significant false positive and negative rate using documented left ventricular dysfunction on echocardiogram as the "gold standard" of CHF in conjunction with relevant signs, symptoms and causative factors. This is a limitation of many surveys of this type, in which the diagnosis is made based on subjective clinical criteria.4,9 A further limitation may have been the algorithm used to assist the GP in making the diagnosis. This clinical algorithm approach has not been used previously in the diagnosis of CHF. Therefore, the possibility exists of patients being wrongly assigned as having CHF using this approach. This is particularly true as echocardiography was not mandated for all patients. Nevertheless, this algorithm did yield an extra two new CHF patients for every 100 patients aged 60 years and older studied in this way. Acknowledgements The CASE study was supported by the National Heart Foundation of Australia and the Royal Australasian College of General Practitioners. The CASE Management Committee wish to thank all 341 GPs who participated in the CASE study and Servier Laboratories, Australia, who provided input into the study design as well as financial and logistical assistance in the conduct of the study. Servier Laboratories were not involved in the analysis of data. In addition, the Committee acknowledges the expert statistical assistance provided by Dr Chris Reid and Mr Stephen Lim (Baker Medical Research Institute, Prahran, VIC). References Bonneaux L, Barendregt J, Meeter K, et al. Estimating clinical morbidity due to ischemic heart disease and congestive heart failure: the future risk of heart failure. Am J Public Health 1994; 84: 20-28. Waters A-M, Bennett S. Mortality from cardiovascular disease in Australia. Cardiovascular Disease Series No. 3. Canberra: Australian Institute of Health and Welfare, 1995. McGovern PG, Pankow JS, Shahar E, et al. Recent trends in acute coronary heart disease. Mortality, morbidity, medical care and risk factors. N Engl J Med 1996; 334: 884-890. Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol 1993; 22: 6A-13A. Gardin JM, Siscovick D, AntonCulver H, et al. Sex, age and disease affect echocardiographic left ventricular mass and systolic function in the free-living elderly: the Cardiovascular Health Study. Circulation 1995; 91: 1739-1748. Lauer MS, Evans JC, Levy D. Prognostic implications of subclinical left ventricular dilatation and systolic dysfunction in men free of overt cardiovascular disease (the Framingham Heart Study). Am J Cardiol 1992; 70: 1180-1184. Mair FS, Crowley TS, Bundred P. Prevalence, aetiology and management of heart failure in general practice. Br J Gen Pract 1996; 46: 77-79. Morbidity statistics from general practice. 4th National Survey, 1991-92. Royal College of General Practitioners, Office of Population Census and Survey and Department of Health and Social Security. London: HMSO, 1995. Parameshwar J, Shackell MM, Richardson A, et al. Prevalence of heart failure in three general practices in west London. Br J Gen Pract 1992; 42: 287-289. McDonagh TA, Morrison CE, Lawrence A, et al. Symptomatic and asymptomatic left-ventricular systolic dysfunction in an urban population. Lancet 1997; 350: 829-833. Ambrosio GB, Riva LM, Casiglia E. Prevalence, clinical features and prognosis of congestive heart failure (CHF) in the elderly. A survey from a population in Veneto region. Acta Cardiologica 1994; 49: 324-325. Mosterd A, Bruijne de MC, Hoes AW, et al. Usefulness of echocardiography in detecting left ventricular systolic dysfunction in population based studies (The Rotterdam Study). Am J Cardiol 1997; 79: 103-104. Hillis GS, Trent RJ, Winton P, et al. Angiotensin-converting enzyme inhibitors in the management of congestive heart failure: are we ignoring the evidence? Q J M 1995; 89: 145-150. Mosterd A, Hoes AW, de Bruijne MC, et al. Prevalence of heart failure and (a) symptomatic left ventricular dysfunction in the general population. The Rotterdam Study. Eur Heart J 2001; in press. Bart BA, Gattis WA, Diem SJ, O'Connor CM. Reasons for underuse of angiotensin-converting enzyme inhibitors in patients with heart failure and left ventricular dysfunction. Am J Cardiol 1997; 79: 1118-1120. Newman J, Ahmed O, Hyngstrom T, et al. Heart failure treatment with angiotensin converting enzyme inhibitors in hospitalized Medicare patients in 10 large states. Arch Int Med 1997; 157: 1103-1108. Stafford RS, Saglam D, Blumenthal D. National patterns of angiotensin converting enzyme inhibitor use in congestive heart failure. Arch Intern Med 1997; 157: 2460-2464. World Health Organization/Council on Geriatric Cardiology Task Force on Heart Failure Education. Concise guide to the management of heart failure. Geneva: WHO/CGC, 1997; 6-9. Available at <http://www.who.int/ncd/cvd/concguid.pdf>. Rural, remote and metropolitan areas classification. 1991 Census Edition. Canberra: AGPS, 1994. McKee PA, Castelli WP, McNamara PM, Kannel WB. The natural history of congestive heart failure: the Framingham Study. N Engl J Med 1971; 285: 1441-1446. Kannel WB, Belanger JA. Epidemiology of heart failure. Am Heart J 1991; 121: 951-956. Bangdiwala SI, Weiner DH, Bourassa MG, et al. Studies of Left Ventricular Dysfunction (SOLVD) Registry: rationale, design, methods and description of baseline characteristics. Am J Cardiol 1992; 70: 347-353. Teerlink JR, Goldhaber SZ, Pfeffer MA. An overview of contemporary etiologies of congestive heart failure. Am Heart J 1991; 121: 1852-1853. The SOLVD Investigators. Effect of Enalapril on survival in patients with reduced left ventricular ejection fraction and congestive heart failure. N Engl J Med 1991; 325: 293-302. The CONSENSUS Trial Study Group. Effects of enalapril on mortality in severe congestive heart failure. Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). N Engl J Med 1987; 3161: 1429-1435. Nicklas JM, Pitt B, Timmis G, et al. Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med 1992; 327: 685-691. Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the Survival and Ventricular Enlargement Trial. N Engl J Med 1992; 327: 821-828. Packer M, Poole-Wilson PA, Armstrong PW, et al. Comparative effects of low and high doses of the angiotensin-converting enzyme inhibitor, lisinopril, on morbidity and mortality in chronic heart failure. ATLAS Study Group. Circulation 1999; 100: 2312-2318. Packer M, Bristow MR, Cohn JN, et al. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. N Engl J Med 1996; 334: 1349-1355. CIBIS II investigators and committees. The cardiac insufficiency bisoprolol study II (CIBIS II): a randomised trial. Lancet 1999; 353: 9-13. Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF). Lancet 1999; 353: 2001-2007. (Received 24 Dec 1999, accepted 28 Oct 2000) Authors' details Alfred Hospital, Melbourne, VIC. Henry Krum, PhD, FRACP, Associate Professor, Clinical Pharmacology Unit, Department of Epidemiology and Preventive Medicine, and Department of Medicine, Monash University. National Heart Foundation of Australia, Melbourne, VIC. Andrew M Tonkin, MD, FRACP, Director, Health, Medical and Scientific Affairs. North East Valley Division of General Practice, Melbourne, VIC. Robert Currie, MB BS, FRACGP, Director. Servier Laboratories, Melbourne, VIC. Robert Djundjek, BSc, Manager, Scientific Projects. Austin and Repatriation Medical Centre, Melbourne, VIC. Colin I Johnston, MD, FRACP, Professor and Head, Department of Medicine, University of Melbourne. Reprints will not be available from the authors. Correspondence: Professor C I Johnston, Baker Medical Research Institute, Prahran, VIC 3181. Make a comment 1: Modified World Health Organization18 criteria for assessment of possible chronic heart failure Symptoms: Dyspnoea, chronic fatigue, oedema, and exercise intolerance. Signs: Third or fourth heart sounds, heart murmur, cardiomegaly, pulmonary crackles, raised jugular venous pressure, and dependent oedema. Causative factors: Angina, previous myocardial infarction, hypertension, valvular heart disease/rheumatic fever, and cardiomyopathy. Patients were considered to have possible CHF if they had: > 2 symptoms, > 2 signs, > 1 symptom and > 1 sign, or > 1 symptom and > 1 causative factor. Back to text Back to text Back to text 4: Cardiovascular comorbidities that may be contributing to chronic heart failure Percentage of patients New CHF Previous CHF Hypertension 69.1% 63.6% Angina 44.2% 53.4% Previous MI 28.1% 39.3% Valve disease 15.2% 23.0% Cardiomyopathy 5.2% 11.8% MI = myocardial infarction. Back to text 5: Percentage (95% CI) of patients with chronic heart failure prescribed each class of drug, by evidence of left ventricular dysfunction, and by age group Left ventricular dysfunction* All patients (n = 2905) Systolic (n = 932) Diastolic (n = 376) Diuretics (thiazide, loop) 63.3 (62.4-64.2) 60.3 (58.7-61.9) 62.2 (59.7-64.7) ACE inhibitor 58.1 (57.2-59.0) 70.7 (69.2-72.2) 70.5 (68.1-72.9) Digoxin 31.3 (30.4-32.2) 35.0 (33.4-36.6) 33.2 (30.8-35.6) beta-Blocker 11.8 (11.2-12.4) 13.9 (12.8-15.0) 17.8 (15.8-19.8) CCB-DHP 10.1 (9.5-10.7) 11.1 (10.1-12.1) 12.0 (10.3-13.7) CCB-NDHP 10.0 (9.4-10.6) 10.3 (9.3-11.3) 11.2 (9.6-12.8) Aspirin 10.3 (9.7-10.8) 9.3 (8.3-10.3) 9.6 (8.1-11.1) Warfarin 7.7 (7.2-8.2) 8.2 (7.3-9.1) 8.8 (7.3-10.3) Spironolactone 8.1 (7.6-8.6) 6.9 (6.1-7.7) 1.0 (0.5-1.5) Hydralazine 0.6 (0.5-0.7) 0.2 (0.1-0.3) 0.0 (0.0-0.0) AIIA 4.3 (3.9-4.7) 6.4 (5.6-7.2) 7.7 (6.3-9.1) Age group (years) 60-69 (n = 569) 70-79 (n = 1360) ≥80 (n = 976) Diuretics (thiazide, loop) 57.1 (55.0-59.2) 62.1 (60.8-63.4) 68.4 (66.9-69.9) ACE inhibitor 58.7 (56.6-60.8) 58.0 (56.7-59.3) 58.1 (56.5-59.7) Digoxin 24.8 (23.0-26.6) 29.9 (28.7-31.1) 37.2 (35.7-38.7) beta-Blocker 14.1 (12.6-15.6) 13.2 (12.3-14.1) 8.4 (7.5-9.3) CCB-DHP 9.5 (8.3-10.7) 11.0 (10.2-11.8) 9.0 (8.1-9.9) CCB-NDHP 10.2 (8.9-11.5) 11.0 (10.2-11.8) 11.2 (10.2-12.2) Aspirin 10.0 (8.7-11.3) 11.4 (10.5-12.3) 8.9 (8.0-9.8) Warfarin 9.5 (8.3-10.7) 8.8 (8.0-9.6) 5.0 (4.3-5.7) Spironolactone 6.7 (5.7-7.7) 8.8 (8.0-9.6) 8.0 (7.1-8.9) Hydralazine 1.1 (0.7-1.5) 0.6 (0.4-0.8) 0.3 (0.1-0.5) AIIA 3.5 (2.7-4.3) 5.4 (4.8-6.0) 3.4 (2.8-4.0) * According to echocardiography. ACE = angiotensin-converting enzyme. CCB-DHP = calcium-channel blocker - dihydropyridine. CCB-NDHP = calcium-channel blocker - non-dihydropyridine. AIIA = angiotensin II receptor antagonist. Back to text 6: Dosage equivalence table for angiotensin-converting enzyme (ACE) inhibitors, and median and mean doses prescribed for patients with diagnosed chronic heart failure Dosage equivalence (mg) Low Medium High Captopril ≤ 50 ≤ 100 ≤ 150 Enalapril ≤ 10 ≤ 20 ≤ 40 Perindopril ≤ 2 ≤ 4 ≤ 8 Lisinopril ≤ 10 ≤ 20 ≤ 40 Ramipril ≤ 5 ≤ 10 ≤ 20 Fosinopril ≤ 10 ≤ 20 ≤ 40 Trandolopril ≤ 2 ≤ 4 ≤ 8 Quinapril ≤ 10 ≤ 20 ≤ 40 Dose (mg) Media Mean SD n Captopril 50 67.5 44.1 383 Enalapril 10 15.6 12.0 308 Perindopril 4 3.6 2.2 223 Lisinopril 10 12.6 9.7 218 Ramipril 5 5.1 4.3 98 Fosinopril 10 14.3 7.1 81 Trandolopril 1 1.9 1.8 76 Quinapril 10 11.6 9.1 74 Back to text

Henry Krum · Andrew M Tonkin · Robert Currie · Robert Djundjek · Colin I Johnston