Research

Research Vancomycin and teicoplanin use in Victorian hospitals Marion B Robertson, Jonathan G A Dartnell and Tony M Korman, on behalf of the Victorian Drug Usage Evaluation Group MJA 1999; 171: 127-131 See also Ferguson, Grayson et al & Collignon Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Pharmacology Abstract Objective: To determine patterns of prescribing of glycopeptide antibiotics (vancomycin and teicoplanin) in Victorian hospitals and identify areas for targeted intervention. Design: A concurrent, observational, multisite evaluation of drug use. Setting: Thirty-five Victorian hospitals, 1-14 September 1997. Study population: Patients commencing a glycopeptide antibiotic course. Main outcome measures: Rate of glycopeptide antibiotic use; indications; duration of use; main hospitals using glycopeptide antibiotics. Results: 293 patients (269 adults and 24 neonates) commenced on 302 glycopeptide antibiotic courses: 296 intravenous (IV) vancomycin courses and three each of oral vancomycin and parenteral teicoplanin. The overall rate of use was 10.3 courses per 1000 inpatient separations. Of 271 IV vancomycin courses for adults, 176 (65%) were for treatment -- 120 empirically. The median duration of treatment courses was 4.7 days (interquartile range, 2.0-8.2 days). A flucloxacillin-resistant organism was confirmed for 44% of treatment courses. Ninety-five IV vancomycin courses were for prophylaxis, including for cardiac (54%) and vascular surgery (21%); 82% of prophylactic courses were administered for less than 24 hours. Of all the glycopeptide antibiotic courses, 69% were administered at five major metropolitan hospitals. Conclusions: Glycopeptide antibiotic use in Victoria is concentrated in the major metropolitan hospitals. Prolonged durations of vancomycin therapy, including for surgical prophylaxis and empirical therapy not subsequently confirmed by microbiology findings, would be suitable targets for interventional strategies. Introduction The emergence of resistant strains of Staphylococcus aureus and coagulase-negative staphylococci has resulted in increased use of the glycopeptide antibiotics vancomycin and teicoplanin.1 These antibiotics are the only effective treatments for infections with these pathogens, but the emergence of vancomycin-resistant enterococci (VRE) threatens their utility.1,2 VRE can cause serious life-threatening infections, and can transfer their resistance in vitro to other pathogens, such as Staphylococcus, rendering the bacteria resistant to currently available antimicrobials.3,4The emergence of VRE has been linked to both overuse and inappropriate use of antibiotics such as vancomycin, teicoplanin and extended-spectrum cephalosporins.2,4 There is also a strong relationship with the use of glycopeptide antibiotics in animals.5 Australian studies have reported inappropriate use of vancomycin ranging from 42% to 65% in individual hospitals.6,7 Responding to these concerns, consensus guidelines have been disseminated to all Victorian hospitals.8 The aim of this study was to examine patterns of prescribing vancomycin and teicoplanin in Victorian hospitals in order to identify potential areas for targeted intervention to improve use of these antibiotics. Methods This study was conducted by the Victorian Drug Usage Evaluation Group, a multidisciplinary group that aims to promote and improve coordination of drug use evaluation activities as a means to improve drug use. All Victorian public and private hospital pharmacy departments listed in the Society of Hospital Pharmacists of Australia directory9 were invited to participate. All patients at participating hospitals who commenced a course (Box 1) of oral or intravenous (IV) vancomycin or teicoplanin between 1-14 September 1997 inclusive were enrolled. Pharmacists at each hospital collected data concerning: demographic details, the indication for antibiotic therapy as determined from the medical record or by consultation with the prescriber, site and source of infection, beta-lactam hypersensitivity, and past history of methicillin-resistant S. aureus (MRSA) or methicillin-resistant S. epidermidis (MRSE), microbiology results of specimens taken up to seven days before or concurrent with vancomycin or teicoplanin therapy, administration of antibiotics before, during and immediately after vancomycin or teicoplanin therapy, and specialist consultation and advice. Prescription data were collected until the end of the course, until the day of discharge or death, or until 28 September 1997. Each hospital provided details of the number of inpatient separations between 1-14 September 1997. This was used to estimate the number of glycopeptide antibiotic courses commenced per 1000 inpatient separations. Data were evaluated by the Mann-Whitney rank sum test of the equivalence of medians of samples not drawn from a normally distributed population. Proportions were compared using the χ2 test. Data are presented as proportions, medians and interquartile ranges. Results Hospitals: Thirty-five hospitals participated in the study: 33 of 58 public and two of 14 private hospitals invited to participate. Twenty hospitals were in the Melbourne metropolitan area and 15 in regional areas. Patients: In the study period, 293 patients (mean age, 54 years; range, 0-90 years; 112 females) commenced a course of vancomycin or teicoplanin. The 293 patients received 302 courses of glycopeptide antibiotics -- three teicoplanin, three oral vancomycin, and 296 intravenous vancomycin (Box 2). Five of Melbourne's six major metropolitan hospitals participated and administered 209 (69%) of the 302 courses. Twenty hospitals enrolled between one and 11 patients and contributed the remaining 93 courses. Glycopeptide antibiotic use in neonates: Four hospitals enrolled 24 neonates who were prescribed 25 courses of IV vancomycin, with a median duration of 2.3 days (interquartile range, 2.0-4.6 days). One course was for prophylaxis for abdominal surgery; the other 24 courses were for empirical treatment. One treatment course was for respiratory infection and the others were for an unknown site of infection. Flucloxacillin-resistant organisms were isolated for six courses (two MRSA, four coagulase-negative staphylococci). Glycopeptide antibiotic use in adults: Twenty-five hospitals enrolled 269 adults who commenced 277 glycopeptide antibiotic courses; 143 (53%) patients were treated by a medical unit and 126 (47%) by a surgical unit; 73 (27%) of the patients were in an intensive care unit at some stage during the glycopeptide antibiotic course. Of the 269 patients, 235 (87%) were discharged, 30 (11%) died, and 4 (1%) were still in hospital three months after the study. For 94 courses (34%), specialist consultation for the use of vancomycin and teicoplanin was noted in the records. More than 80% of these consultations were with infectious disease/microbiology specialists. There were 263 patients who received 271 courses of IV vancomycin -- 176 (65%) for treatment and 95 for prophylaxis (Box 3). Of the 176 IV vancomycin treatment courses, 120 (68%) were for empirical treatment and 56 (32%) as specific treatment. Empirical courses were shorter than specific courses (P < 0.02). Patients being treated empirically had been in hospital for fewer days before the course commenced than patients receiving specific treatment (P < 0.001). The duration of empirical courses for which a flucloxacillin-resistant organism was subsequently identified was significantly greater than that of the unconfirmed courses (P < 0.05). Of the other six patients, three received a course of oral vancomycin for the treatment of confirmed (two cases) or suspected (one case) Clostridium difficile diarrhoea, and three received IV teicoplanin for treatment of wound infections (2 patients) or cellulitis (1 patient), commenced on the advice of infectious diseases clinicians. Other antibiotic use in adults: In the seven days before IV vancomycin treatment courses, the most frequently prescribed antibiotics were ceftriaxone and cefotaxime (28% of courses), metronidazole (16%), flucloxacillin (15%), and gentamicin (15%). The most frequently prescribed concurrent antibiotics were ceftriaxone and cefotaxime (11% of vancomycin courses), gentamicin (11%), ceftazidime (9%), imipenem (7%), ciprofloxacin (6%) and metronidazole (6%). For 14 treatment courses, vancomycin was continued beyond the close of the study. Immediately following the 162 completed courses (in 162 patients), other antibiotic therapy was commenced for 57 patients (35%), concurrent antibiotic therapy continued for 35 patients (22%), and there was no antibiotic therapy for 50 patients (31%). On-going therapy was not recorded for nine patients (6%), and the remaining 11 patients (7%) died. The antibiotics most frequently commenced immediately after vancomycin were oral flucloxacillin (12 courses), oral fusidic acid and oral rifampicin (12 courses), and oral ciprofloxacin (eight courses). For the 95 IV vancomycin prophylaxis courses, other antibiotics were given concurrently for 46 (48%) courses, most frequently gentamicin (14% of vancomycin courses), ceftriaxone (14%), cephazolin (6%) and ticarcillin/clavulanate (5%). Comparison of five main vancomycin users: The five hospitals that used most vancomycin were major metropolitan university teaching hospitals where use was restricted by protocols and consultations. Use by number of courses was greatest in Hospital 1 but the total quantity used was less than half that used at Hospital 2 (Box 4). Rate of use was significantly lower in Hospital 4 than in the other four hospitals. Surgical use of vancomycin predominated in Hospital 1, while medical use predominated in Hospital 4. Hospitals 2, 3 and 5 had a significantly smaller proportion of single doses for prophylaxis than Hospitals 1 and 4. Discussion We have examined the pattern of use of vancomycin in a large sample of Victorian hospitals. We found that use of teicoplanin and oral vancomycin was low, and that intravenous vancomycin was used predominantly for empirical treatment or prophylaxis. Our study is the first to capture a statewide picture of hospital drug use linked to indication, and we are not aware of any published comparable multihospital pharmacoepidemiological data. Based on the number of inpatient separations for Victorian public hospitals in 1996-97 (about 890 000),10 we reviewed an estimated 82% of public hospital inpatient separations in the two-week study period. We estimated the overall rate of glycopeptide antibiotic use to be 10.3 courses per 1000 inpatient separations, which suggests about 9160 courses are used annually in Victorian public hospitals. The main limitation of our study was that vancomycin courses were not individually compared against explicit criteria to determine the proportion of appropriate use on the basis of indication, dosage and duration. We chose not to compare against criteria because of the variety of prescribing restrictions in participating hospitals. The most frequent indications for empirical IV vancomycin were febrile neutropenia, pneumonia and wound infections. The indications for and duration of empirical therapy could be targets for intervention. For pneumonia, IV vancomycin use may be reasonable for hospital-acquired infections in institutions with a high prevalence of MRSA. For febrile neutropenia, IV vancomycin may be best restricted to patients with suspected associated IV line sepsis. For wound infections, unless there is a high prevalence of MRSA, IV vancomycin treatment should wait until after microbiological confirmation. Oral vancomycin should be restricted to the treatment of antibiotic-associated colitis due to toxigenic C. difficile unresponsive to or relapsing after an adequate course of metronidazole (or bacitracin), or for patients with severe colitis.11 Clinicians should be encouraged to regularly review the need for ongoing drug therapy; however, to improve the current situation, we need effective decision support tools to facilitate timely attention to important test findings.12 Almost half the treatment courses were sanctioned or recommended by infectious diseases/microbiology specialists, who should be familiar with relevant guidelines for vancomycin use. Surgical prophylaxis consumed 35% of IV vancomycin courses, with cardiac and vascular surgery accounting for 75% of prophylactic courses. The duration of vancomycin prophylaxis was generally according to recommendations, with 72% of courses given as single doses and 82% of courses given for less than 24 hours. However, there was considerable interhospital variation in the duration of surgical prophylaxis. The implementation of hospital policies on duration of surgical prophylaxis would be an important target for intervention. Glycopeptide antibiotic use was concentrated in five major metropolitan teaching hospitals. Although these five hospitals all had policies in place, vancomycin use varied substantially. It is of critical importance for patient care and resource management that there is a conscious effort to preserve the utility of vancomycin and teicoplanin. This should be founded on good infection control practice, but there is also a need for all hospitals to implement effective interventional strategies to improve the use of the glycopeptide antibiotics. Acknowledgements Financial support for the employment of the Project Coordinator was provided by the Victorian Drug Usage Advisory Committee and the Victorian Standing Committee on Infection Control. The project was also reliant on the voluntary work of pharmacists at the participating hospitals who undertook all the data collection. We acknowledge the assistance of the other members of the Victorian Drug Usage Evaluation Group in the planning and execution of the study and the preparation of this manuscript: Stephanie J Alvarez, Drug Utilisation Evaluation Pharmacist, Monash Medical Centre; Dr Jo-anne Brien, Senior Lecturer, Department of Pharmacy Practice, Monash University (Parkville Campus); Dr Lisa L Ioannides-Demos, Senior Research Fellow, Department of Epidemiology and Preventative Medicine, Monash University, and Senior Research Officer, Victorian Centre for Ambulatory Care Innovation, Alfred Hospital; Sam Koroneos, Senior Drug Utilisation Pharmacist, Pharmacy Department, Austin and Repatriation Medical Centre; Anne Leversha, Senior Lecturer, Monash University, Faculty of Medicine, and Victorian College of Pharmacy, and Deputy Manager Pharmacy Services, Latrobe Regional Hospital, Traralgon West; Julie A V Lord, Senior Drug Information and Clinical Research Pharmacist, St Vincent's Hospital, Melbourne; Heather J Lyall, Deputy Director of Pharmacy, Geelong Hospital; Roslyn I McKinnon, Executive Officer, Victorian Drug Usage Advisory Committee; Associate Professor R Moulds, Director, Department of Clinical Pharmacology and Therapeutics, Royal Melbourne Hospital; Susan G Poole, Deputy Director, Peter MacCallum Cancer Institute; Dr Gail J Ware, Drug Usage Evaluation Pharmacist, Alfred Hospital. References Ena J, Dick RW, Jones RN, Wenzel RP. The epidemiology of intravenous vancomycin usage in a university hospital: a 10 year study. JAMA 1993; 269: 598-602. Heath CH, Blackmore TK, Gordon DL. Emerging resistance in Enterococcus spp. Med J Aust 1996; 164: 116-120. Reduced susceptibility of Staphylococcus aureus to vancomycin -- Japan, 1996. MMWR Morb Mortal Wkly Rep 1997; 46: 624-626. Quale J, Landman D, Atwood E, et al. Experience with a hospital-wide outbreak of vancomycin-resistant enterococci. Am J Infect Control 1996; 24: 372-379. Witte W. Medical consequences of antibiotic use in agriculture. Science 1998; 279: 996-997. Misan GMH, Martin ED, Smith ER, et al. Drug utilisation review in a teaching hospital: experience with vancomycin. Eur J Clin Pharmacol 1990; 39: 457-461. Radford JM, Whitby RM, Looke DFM, Coombes JA. Vancomycin usage review in the era of vancomycin-resistant enterococci (VRE). Aust J Hosp Pharm 1997; 27: 1410-1413. Guidelines for preventing emergence of vancomycin-resistant enterococci. Melbourne: Victorian Drug Usage Advisory Committee and the Standing Committee on Infection Control in collaboration with the Writing Group for the Therapeutic Guidelines: Antibiotic, 1997. Vernon G, Thomson W, editors. Directory of hospital pharmacy and pharmaceutical organisations. Melbourne: Society of Hospital Pharmacists of Australia, 1996. Department of Human Services Annual Report 1996-97. Melbourne: Department of Human Services, Victoria, 1997. Therapeutic Guidelines: Antibiotic, 10th ed. Melbourne: Therapeutic Guidelines Limited, 1998. Schiff GD, Rucker D. Computerized prescribing. Building the electronic infrastructure for better medication usage. JAMA 1998; 279: 1024-1029. (Received 21 Dec 1998, accepted 17 May 1999) Authors' details Victorian Drug Usage Evaluation Group, Melbourne, VIC. Marion B Robertson, BPharm, MSc, Project Coordinator. Royal Melbourne Hospital, Melbourne, VIC. Jonathan G A Dartnell, BPharm, MPS, Senior Pharmacist, Department of Clinical Pharmacology and Therapeutics. Monash Medical Centre, Melbourne, VIC. Tony M Korman, FRACP, Infectious Diseases Physician. Reprints will not be available from the authors. Correspondence: Mr J G A Dartnell, Department of Clinical Pharmacology and Therapeutics, c/- Post Office, Royal Melbourne Hospital, VIC 3050. Email: Jonathan. DartnellATnwhcn.org.au 1: Definitions Course: The administration to a patient of at least one dose of vancomycin or teicoplanin. If a dose was administered more than 24 hours after a previous dose (and the drug was re-prescribed), this was considered a new course. Patients with renal impairment on regimens with dosing intervals longer than 24 hours were considered to have received a continuous course. Prophylaxis: Antibiotic administration commenced perioperatively to prevent postoperative infection. Empirical treatment: Antibiotic administration commenced before or without identification of flucloxacillin-resistant bacterial pathogens. Specific treatment: Antibiotic administration commenced after identification of flucloxacillin-resistant bacterial pathogens. Duration: Durations of courses were calculated by subtracting the date and time of the first dose from the date and time of the last dose. The duration of a single dose was considered to be 0 hours. Back to text 2: Glycopeptide antibiotic courses commenced in participating hospitals during study period*Hospital locationNumber of courses † (patients)Number of inpatient separationsCourses per 1000 separationsMelbourne52 (51)‡235622.0Melbourne49 (48)245520.0Melbourne38 (37)194319.6Melbourne37 (37)299712.3Melbourne33 (30)§141623.3Regional11 (11)14777.4Melbourne10 (9)53818.6Melbourne10 (10)14776.7Melbourne9 (9)10718.4Melbourne8 (8)10897.3Melbourne8 (7)13575.9Melbourne7 (7)42316.5Regional5 (5)8086.2Melbourne5 (5)10554.7Melbourne3 (3)15002.0Melbourne3 (2)27111.1Regional3 (3)3748.0Regional2 (2)§14613.7Melbourne2 (2)8772.3Melbourne2 (2)4694.3Melbourne1 (1)6681.5Regional1 (1)7251.4Regional1 (1)§2663.8Melbourne1 (1)6361.6Melbourne1 (1)5102.0Overall*302 (293)2944510.3*Another 9 regional and 1 Melbourne hospital accounted for 2785 inpatient separations but did not use glycopeptide antibiotics during the study period. †Intravenous vancomycin except where indicated. ‡Includes 3 courses of teicoplanin. §Includes 1 course of oral vancomycin. Private hospital. Back to text 3: Intravenous vancomycin courses commenced in adultsAll treatment courses 176 treatment courses median duration, 4.7 days (interquartile range, 2.0-8.2 days) indications: wound infections33 (18.8%)pneumonia29 (16.5%)febrile neutropenia21 (11.9%)septicaemia12 (6.8%)intravenous catheter-associated sepsis11 (6.3%)cellulitis9 (5.1%)infected prosthesis9 (5.1%)peritonitis/CAPD8 (4.5%)meningitis3 (1.7%)other16 (9.1%)not recorded25 (14.2%)Gram-positive bacteria, including Staphylococcus, Streptococcus, Enterococcus and Bacillus species isolated for 113 (64%) courses Isolated organism confirmed flucloxacillin-resistant in 78 courses; organism was MRSA in 67 coursesEmpirical treatment courses 120 empirical treatment courses (68% of all treatment courses) median duration, 4.4 days (interquartile range, 1.5-8.0 days) patients in hospital for median 4.0 days (interquartile range, 1-12 days) before course commenced most frequent indications: febrile neutropenia (18%), pneumonia (16%) and wound infections (12%) 32 (26%) of patients had history of beta-lactam antibiotic hypersensitivity or a previous infection with MRSA or MRSE. Two patients had a history of severe hypersensitivity that may have necessitated use of vancomycin rather than beta-lactam antibiotics. flucloxacillin-resistant organism subsequently identified in 24 (20%) empirical courses duration of courses with confirmed resistant organism was 6.9 days (interquartile range, 2.0-13.8 days) compared with 3.9 days (interquartile range, 1.3-6.7 days) for unconfirmed courses (P<0.05) Specific treatment courses 56 specific treatment courses (32% of all treatment courses) median duration, 6.1 days (interquartile range, 3.0-11.6 days) patients in hospital for median 12 days (interquartile range, 4-22 days) before course commenced Surgical prophylaxis courses95 surgical prophylaxis courses 68 (72%) single-dose courses, 78 (82%) less than one day, 12 (12%) one to three days, 5 (5%) more than three days 12 (13%) were for patients with history of beta-lactam hypersensitivity, including four severe cases, and 5 (5%) were for patients with history of MRSA or MRSE infection 51 (54%) used in cardiac surgery; 31 single doses, 12 (24%) lasted more than 36 hours 20 (21%) used in vascular surgery; all were single dosesCAPD=chronic ambulatory peritoneal dialysis. MRSA=methicillin-resistant Staphylococcus aureus. MRSE=methicillin-resistant S. epidermidis. Back to text 4: Comparison of intravenous vancomycin in adults in the major teaching hospitalsHospital 1Hospital 2Hospital 3Number of courses494938Number of patients484837Courses per 1000 separations*20.820.019.6Vancomycin used (g)177371280Median length of stay (days)121816Courses given in intensive care9 (18%)9 (18%) 17 (45%)Courses prescribed by medical unit12 (24%)28 (57%)20 (53%)Indication: prophylaxisNumber of courses (%)28 (57%)15 (31%)15 (39%)Number (%) as single doses †28 (100%)7 (47%)9 (60%)Surgery type (number of courses) cardiac2476 vascular241 other248Indication: treatmentNumber (%) empirical13 (62%)30 (88%) 19 (83%)Median duration of courses (days) empirical3.73.64.8 specific3.04.511.0Indications (number of courses) pneumonia724 wound infection436 febrile neutropenia181 other92112 Hospital 4Hospital 5Number of courses3332Number of patients3229Courses per 1000 separations*12.322.6Vancomycin used (g)299118Median length of stay (days)209Courses given in intensive care6 (18%)9 (28%)Courses prescribed bymedical unit30 (91%)17 (53%)Indication: prophylaxisNumber of courses (%)8 (24%) 16 (50%)Number (%) as single doses †8 (100%)11 (69%)Surgery type (number of courses) cardiac18 vascular63 other15Indication: treatmentNumber (%) empirical18 (72%)10 (62%)Median duration of courses (days) empirical5.51.5 specific3.02.0Indications (number of courses) pneumonia60 wound infection33 febrile neutropenia24 other149* Hospital 4 significantly less than Hospitals 1, 2, 3 and 5 (P<0.02). †Hospitals 2, 3, and 5 significantly less than Hospital 1 (P<0.01) and Hospital 4 (P<0.1). 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Marion B Robertson

Research Outcome of a screening program for vancomycin-resistant enterococci in a hospital in Victoria M Lindsay Grayson, Elizabeth A Grabsch, Paul D R Johnson, Dianne Olden, Melissa Aberline, H Y Li, Geoffrey Hogg, Marguerite Abbott and Peter G Kerr MJA 1999; 171: 133-136 See also Ferguson, Robertson et al & Collignon Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Infectious diseases and parasitology Abstract Objective: To screen for faecal colonisation with vancomycin-resistant enterococci (VRE) among potentially at-risk patients. Design: Infection control screening program. Setting: Monash Medical Centre (a tertiary care hospital), Melbourne, Victoria, in the seven months from June 1997. Patients: Patients in the Renal, Oncology and Intensive Care (ICU) Units. Main outcome measures: Presence of VRE in a rectal swab or faecal specimen taken at admission and at regular intervals during inpatient stay; presence of vancomycin-resistance genes (vanA, vanB and vanC) assessed by polymerase chain reaction (PCR); genetic clonality of isolates assessed by pulsed-field gel electrophoresis (PFGE). Results: 574 patients (356 renal, 134 ICU and 84 oncology) were screened; 12 were colonised with VRE -- nine renal inpatients, two having peritoneal dialysis or in-centre haemodialysis, and one ICU patient. Nine isolates were Enterococcus faecalis (seven positive for vanB and two negative for all three resistance genes) and three were Enterococcus faecium (all positive for vanB). Eight were high-level gentamicin resistant. PFGE suggested genetic clonality between the index isolate and five other isolates from renal patients. No specific clinical practice was associated with VRE colonisation. Attempts to clear rectal carriage with oral ampicillin/amoxycillin or bacitracin were of limited success. Although antibiotic prescribing in the Renal Unit was generally consistent with defined protocols, use of vancomycin and third-generation cephalosporins has been further restricted. Conclusions: Renal inpatients in our institution appear most at risk of VRE colonisation (4.6% overall) and therefore of VRE infection. Routine screening, especially of potentially high-risk patients, should be considered in major Australian hospitals. Introduction Vancomycin-resistant enterococci (VRE) were first reported in the United Kingdom, Europe and the United States in 1988,1-6 and in Australia in 1994.7 In the United States, VRE have become common and potentially fatal nosocomial pathogens; they account for 14% of enterococcal bacteraemias in intensive care patients, while VRE bacteraemia has an attributable mortality of 30%-46%.4,8 In Australia, cases of VRE infection have now been reported from hospitals in all States and Territories except the Australian Capital Territory and Tasmania.9,10In May 1997, a patient receiving renal haemodialysis at Monash Medical Centre, Melbourne, developed a VRE urinary tract infection (see Box 1). This was the first identified case of VRE infection at this institution. As the patient had had close contact with other patients and had suffered diarrhoea, we were concerned about a significant nosocomial outbreak of VRE infection. Clinical infection is almost always associated with faecal colonisation with this organism. We therefore assessed the extent of faecal VRE colonisation among renal and other high-risk patients by active screening, and isolated infected or colonised patients. We describe the results of this screening program and our infection control measures, and highlight some of the clinical issues. Methods An infection control screening program for faecal colonisation with VRE was implemented in the Renal, Oncology and Intensive Care Units at Monash Medical Centre, Melbourne, Victoria, for the seven months from June 1997. These patients were chosen as experience (local, US and European) suggested they were at greatest risk of VRE infection.4-6,8,10 Patients In the Renal Unit, screening was planned for all patients receiving care in the renal ward and in-centre haemodialysis or continuous ambulatory peritoneal dialysis and, when possible, for dialysis patients managed at home. In the Oncology and Intensive Care Units (ICU), screening was planned for an arbitrary number of 100 consecutive patients admitted to each unit. All inpatients were screened on admission and discharge. In the renal ward this was later modified to on admission and a regular day of the week (Tuesday). Patients managed by the in-centre haemodialysis unit were screened every three months, and other outpatients were screened at least once. Screening Rectal swabs were obtained using standard cotton-alginate-tipped sterile swabs from all patients except neutropenic oncology patients. In these, a perianal swab or faecal specimen was substituted for a rectal swab because of their increased risk of septicaemia after rectal trauma.13 Specimens were plated on media specifically selective for vancomycin-resistant enterococci (bile esculin azide agar with 6 µg/mL vancomycin) and cultured for up to 72 hours. Esculin-positive isolates with possible resistance to vancomycin were identified, and single colonies of each morphology type were assessed to identify Enterococcus faecalis and Enterococcus faecium (the pathogenic enterococcal species most commonly associated with vancomycin resistance). Assessment included Gram stain, tests of motility and pigment production, the pyrrolidonyl arylamidase test (Murex Diagnostics Ltd, Dartford, UK) and streptococcal latex grouping.14 VRE assessment VRE isolates were tested further for antibiotic susceptibility. Minimum inhibitory concentrations (MICs) were determined for vancomycin, teicoplanin and ampicillin and high-level gentamicin (MIC > 500 µg/mL) using the E test (AB Biodisk, Dalvagen, Sweden). Production of β-lactamase was assesssed by nitrocephin disc (Becton Dickinson Microbiology Systems, Cockeysville, MD, USA). Enterococcal species was confirmed and presence of vancomycin-resistance genes vanA, vanB or vanC was assessed by polymerase chain reaction (PCR) genetic probe using a modification of techniques described previously.10,15 Genetic similarity (ie, potential clonality) of VRE isolates was assessed by pulsed-field gel electrophoresis (PFGE) using a method modified after Miranda et al.16 Factors that were potentially associated with VRE colonisation were assessed retrospectively.6,8 Statistical analyses were by χ2 or t test. Results Patients Screening was undertaken on 574 patients -- 356 renal, 134 ICU and 84 oncology patients. Renal patients comprised: 194 of 238 inpatients in the renal ward (82%); 66 of 82 peritoneal dialysis and in-centre haemodialysis patients (80%); 94 outpatients (mostly satellite and home haemodialysis patients); and 2 of 180 renal transplantation patients. In general, consecutive oncology and ICU patients were screened; none refused screening. In the Oncology Unit, the target number (100 patients) was not attained because of a protocol lapse. VRE colonisation Faecal colonisation with VRE was found in 12 patients, including the index patient -- 11 renal patients (3% of renal patients tested) and one ICU patient (0.7% of ICU patients tested). Their characteristics are shown in Box 2. No VRE colonisation was found in oncology patients. The 11 renal patients with VRE colonisation comprised nine inpatients (9/194 [5%]) and two having peritoneal dialysis or in-centre haemodialysis (2/66 [3%]). No non-dialysis renal outpatients were colonised. VRE colonisation was found on the initial rectal swab for seven patients and after a series of negative cultures for the remaining five patients. Characteristics of VRE isolates Characteristics of the 12 VRE isolates are shown in Box 2. Nine of the 12 were E. faecalis -- seven testing positive for vanB, including the index isolate (vancomycin MICs, 12-32 µg/mL), and two testing negative for vanA, vanB and vanC (vancomycin MICs, 6 and 8 µg/mL, respectively). The other three isolates were E. faecium -- all testing positive for vanB (vancomycin MICs, 16, 64 and > 256 µg/mL, respectively). All isolates were susceptible to teicoplanin. While all E. faecalis isolates were susceptible to ampicillin, all E. faecium isolates were resistant (MICs > 256 µg/mL). Six of the nine E. faecalis isolates and two of the three E. faecium isolates had high-level resistance to gentamicin. None of the 12 produced detectable β-lactamase. Eleven isolates were assessed by PFGE. Results are shown in the Figure. Six of the seven vanB E. faecalis isolates, including the index isolate, appeared genetically similar (lanes 4-8 and index isolate in lane 9). Three of these similar isolates, plus one dissimilar vanB E. faecalis isolate (not shown), were isolated from patients who had been nursed together in a four-bed area. One of these patients (with vanB E. faecalis) had been nursed with the index patient six months before screening positive. The three E. faecium isolates and the non-ABC E. faecalis isolate (lanes 1-3 and 10, respectively) showed a variety of electrophoretic patterns on PFGE, suggesting they were genetically dissimilar from each other. Factors potentially associated with VRE Among the 12 patients with VRE colonisation, nine had received vancomycin in the previous month, four of whom had also received a third-generation cephalosporin (ceftriaxone). Information on previous antibiotics was not available for patients without VRE colonisation. Among the six renal patients found to have VRE colonisation on their initial swab (including the index case), five had been inpatients during the previous three months, compared with 127 of the 350 non-colonised patients (36%). Mean duration of preswab inpatient stay for these six colonised patients was 17.5 days (range, 0-62), compared with 2.6 days (range, 0-43) for non-colonised patients (P < 0.001). VRE control measures All patients identified with faecal VRE colonisation were nursed in a single room according to infection control guidelines.11 In January 1998, an eight-bed VRE isolation facility was established. Continued, less rigorous screening of renal inpatients identified four new cases of VRE colonisation in the following three months (not described here), but these VRE strains were dissimilar on PFGE to the previous 12 strains. Antibiotic usage patterns were also reviewed. Most antibiotic use in the Renal Unit was found to be consistent with the unit's protocols. These were amended to further restrict use of third-generation cephalosporins and glycopeptides to specific situations, such as nosocomial pneumonia and serious staphylococcal infections. In seven patients, an attempt was made to "clear" faecal VRE colonisation with either ampicillin or amoxycillin (variable doses, depending on renal function) or oral bacitracin (25 000 units four times a day for 7-14 days).17,18 In four of these patients, follow-up rectal swabs were taken, and in two (one taking ampicillin and one bacitracin) VRE was no longer detected 18 and 13 days, respectively, after therapy. At completion of the study, nine of the 12 patients with VRE colonisation had died, although, other than the index patient, none had developed VRE infection. Discussion A screening program introduced at Monash Medical Centre after identification of VRE infection in a renal patient found faecal VRE colonisation in another 10 renal patients (3% of renal patients overall) and one ICU patient (0.7%). Isolates from six of the renal patients, including the index patient, were genetically similar and probably clonal. No patients except the index patient developed VRE infection. VRE is now a major nosocomial pathogen in many US and European centres, but until recently relatively few clinical VRE infections had been reported in Australia.6,8-10 To our knowledge, this is the first Australian report of a systematic screening program for VRE among potentially at-risk patients. Our results were consistent with those of previous studies, which suggested that 10-20 patients are likely to have faecal colonisation for every case of clinical VRE infection.6,8,19,20 Although risk factors for VRE infection have been identified by US and European investigators,6,8the factors associated with VRE colonisation are less clear and may vary depending on the epidemiology of VRE in different countries. Antibiotic prescribing patterns, nosocomial transmission and use of antibiotics (eg, avoparcin) in the veterinary industry appear of varying importance in different regions.8,10 Our study did not allow valid assessment of all factors potentially associated with VRE colonisation in our patients. Nevertheless, the fact that renal patients with VRE colonisation spent significantly more days in hospital in the previous three months than patients without colonisation raises the possibility that the hospital environment or illness-related factors influenced the likelihood of VRE colonisation. Resistance to vancomycin among enterococci is generally due to presence of one of four resistance genes -- vanA, vanB, vanC and vanD. These genes result in synthesis of abnormal precursors in the peptidoglycan layer of the bacterial cell wall, thereby reducing the affinity with which vancomycin binds to this target site.8VanA is associated phenotypically with resistance to vancomycin (MIC > 64 µg/mL) and teicoplanin (MIC > 16 µg/mL), and is the most common genotype found in Europe and some centres in the US.8VanB is associated with medium-level resistance to vancomycin (MIC > 4 µg/mL) but susceptibility to teicoplanin. Consistent with our findings, it is the predominant genotype noted in Australia.9,10VanC is associated with naturally occurring low-level resistance to vancomycin and susceptibility to teicoplanin among less pathogenic enterococcal species, while vanD, which is phenotypically similar, has been occasionally noted in some E. faecium isolates.8,21,22 It is possible that our two non-ABC E. faecalis isolates contain vanD, but we are currently unable to test for this gene. Presence of faecal VRE colonisation among 5% of renal inpatients at our institution (3% of renal patients overall) was higher than expected, but suggested that nosocomial transmission of VRE was not yet a widespread problem. Nevertheless, our PFGE data suggested that six of the seven vanB E. faecalis strains were clonal, raising infection control issues for the Renal Unit. As reported previously,17,18 we found attempts to clear faecal VRE carriage with antibiotic therapy were unsuccessful and not worthwhile. The screening program and establishment of VRE isolation facilities to readily cohort and barrier-nurse patients with VRE colonisation appeared to assist in limiting nosocomial VRE transmission, while continuing to provide medical care for patients in a compassionate manner. The incidence of faecal VRE colonisation that we found among high-risk patients at our institution suggests that routine screening for faecal VRE colonisation should now be considered by other similar Australian hospitals. Acknowledgements We wish to acknowledge the contribution of the nursing staff of the Renal, Oncology and Intensive Care Units and the Outpatient Department in obtaining rectal cultures. References Leclercq R, Derlot E, Duval J, Courvalin P. Plasmid-mediated resistance to vancomycin and teicoplanin in Enterococcus faecium. N Engl J Med 1988; 319: 157-161. Uttley AHC, Collins CH, Naidoo J, George RC. Vancomycin-resistant enterococci. Lancet 1988; 1: 57-58. Clark NC, Cooksey RC, Hill BC, et al. Characterization of glycopeptide-resistant enterococci from U. S. hospitals. Antimicrob Agents Chemother 1993; 37: 2311-2317. Centers for Disease Control. Nosocomial enterococci resistant to vancomycin -- United States, 1989-1993. MMWR Morb Mortal Wkly Rep 1993; 42: 597-599. Frieden TR, Munsiff SS, Low DE, et al. Emergence of vancomycin-resistant enterococci in New York City. Lancet 1993; 342: 76-79. Boyce JM. Vancomycin-resistant enterococcus. Detection, epidemiology, and control measures. Infect Dis Clin North Am 1997; 11: 367-384. Kamarulzaman A, Tosolini FA, Boquest AL, et al. Vancomycin resistant Enterococcus faecium infection in a liver transplant recipient [abstract]. Aust N Z J Med 1995; 25: 560. Eliopoulos GM. Vancomycin-resistant enterococci. Mechanism and clinical relevance. Infect Dis Clin North Am 1997; 11: 851-865. Bell J, Turnidge J, Coombs G, O'Brien F. Emergence and epidemiology of vancomycin-resistant enterococci in Australia. Commun Dis Intell 1998; 22: 249-252. Bell JM, Paton JC, Turnidge J. Emergence of vancomycin-resistant enterococci in Australia: phenotypic and genotypic characteristics of isolates. J Clin Microbiol 1998; 36: 2187-2190. Standing Committee on Infection Control (SCIC), Department of Human Services, Victoria. Guidelines for the management of patients with confirmed vancomycin-resistant enterococci (VRE) infection/colonisation. Melbourne: Department of Human Services, 1996. Moellering RC Jr. The Garrod lecture. The enterococcus: a classic example of the impact of antimicrobial resistance on therapeutic options. J Antimicrob Chemother 1991; 28: 1-12. Weinstein JW, Tallapragada S, Farrel P, Dembry L-M. Comparison of rectal and perirectal swabs for detection of colonisation with vancomycin-resistant enterococci. J Clin Microbiol 1996; 34: 210-212. Facklam RR, Sahm DF. Enterococcus. In: Murray PR, Baron EJ, Pfaller MA, et al, editors. Manual of clinical microbiology. 6th ed. Washington: ASM Press, 1995: 308-314. Dutka-Malen A, Evers S, Courvalin P. Detection of glycopeptide resistance genotypes and identification to the species level of clinically relevant enterococci by PCR. J Clin Microbiol 1995; 33: 24-27. Miranda AG, Singh KV, Murray BE. A fingerprinting of Enterococcus faecium by pulsed-field gel electrophoresis may be a useful epidemiologic tool. J Clin Microbiol 1991; 29: 2752-2757. O'Donovan CA, Fan-Havard P, Tecson-Tumang FT, et al. Enteric eradication of vancomycin-resistant Enterococcus faecium with oral bacitracin. Diagn Microbiol Infect Dis 1994; 18: 105-109. Chia JKS, Nakata MM, Park SS, et al. Use of bacitracin therapy for infection due to vancomycin-resistant Enterococcus faecium. Clin Infect Dis 1995; 21: 1520. Jordens JZ, Bates J, Griffith DT. Faecal carriage and nosocomial spread of vancomycin-resistant Enterococcus faecium. J Antmicrob Chemother 1994; 34: 515-528. Montecalvo MA, deLaencastre H, Carraher M, et al. Natural history of colonization with vancomycin-resistant Enterococcus faecium. Infect Control Hosp Epidemiol 1995; 16: 680-685. Leclercq R, Courvalin P. Resistance to glycopeptides in enterococci. Clin Infect Dis 1997; 24: 545-556. Perichon B, Reynolds P, Courvalin P. VanD-type glycopeptide-resistant Enterococcus faecium BM4339. Antimicrob Agents Chemother 1997; 41: 2016-2018. (Received 15 Dec 1998, accepted 23 Apr 1999) Authors' details Infectious Disease and Clinical Epidemiology Department, Monash Medical Centre, Melbourne, VIC. M Lindsay Grayson, MD, FRACP, Director, and Professor of Epidemiology and Preventive Medicine, Monash University, Melbourne, VIC; Elizabeth A Grabsch, BSc, GradDipClinEpid, Infection Control Scientist; Paul D R Johnson, PhD, FRACP, Infectious Disease Physician, and Senior Lecturer, Microbiology Department, Monash University, Melbourne, VIC; Dianne Olden, PhD, Research Scientist. Infection Control Unit, Monash Medical Centre, Melbourne, VIC. Melissa Aberline, RN, BSc, Infection Control Nurse. Microbiological Diagnostic Unit, Melbourne University, Melbourne, VIC. H Y Li, MMed, Scientist; Geoffrey Hogg, FRACP, FRCPA, Director. Nephrology Department, Monash Medical Centre, Melbourne, VIC. Marguerite Abbott, RN, BAppSci, Nurse Director; Peter G Kerr, PhD, FRACP, Deputy Director. Reprints will not be available from the authors. Correspondence: Professor M L Grayson, Infectious Diseases and Clinical Epidemiology Department, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168. Email: Lindsay. GraysonATmed.monash.edu.au Pulsed-field gel electrophoresis of vancomycin-resistant enterococcal isolates. Lanes 1-3: E. faecium (vanB) isolates from renal patients. Lanes 4-9: E. faecalis (vanB) isolates from renal patients, including index isolate (lane 9). Lane M: Molecular weight markers. Lane 10: E. faecalis (non-ABC) isolate from renal patient. Back to text 1: Case history of the index patient In May 1997, a 26-year-old woman presented to Monash Medical Centre with a fever and urinary tract infection caused by vancomycin-resistant enterococci (VRE). She had faecal colonisation with the same VRE strain. She had endstage renal failure requiring in-centre haemodialysis three times a week. Ten days later, the patient presented in status epilepticus with faecal incontinence that led to substantial faecal contamination of the Emergency Department and the in-centre Haemodialysis Unit. Appropriate cleaning protocols11 were implemented in each area, and limited environmental cultures suggested no contamination. Five months later, the patient developed symptomatic VRE bacteraemia after surgical insertion of a femoral Goretex arteriovenous fistula. The VRE isolate was phenotypically identical to the initial urinary isolate. As it had high-level gentamicin resistance, she was treated with continuous-infusion ampicillin, continuing for 10 weeks because of the possibility of graft sepsis.12 The patient continued to show faecal VRE colonisation until her death (not related to VRE) in September 1998. Back to text

Elizabeth A Grabsch · Dianne Olden · Melissa Aberline · H Y Li · Geoffrey Hogg · Marguerite Abbott · Peter G Kerr

Research Australian suicide trends 1964-1997: youth and beyond? Christopher H Cantor, Kerryn Neulinger and Diego De Leo MJA 1999; 171: 137-141 Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Psychiatry Abstract Objective: To examine Australian suicide rates across all ages, and compare Australian rates with those of other Western nations. Design: Australian Bureau of Statistics data were used to examine Australian suicide trends, 1964-1997, by age and sex. For comparison, suicide rates of 22 other Western nations, 1990-1994, were obtained from the World Health Organization. Results: Australian suicide rates for males 15-24 years and 25-34 years rose from 1964-1997. Comparable rates for females showed no significant change. Suicide rates for several of the older age and sex groups declined over this period. Comparison with suicide rates of other Western nations showed that, while Australian youth suicide rates are relatively high, this is not the case for older age groups. Australian suicide rates are higher than those in the European nations of origin of our major migrant groups, but similar to those of other Western nations also recently colonised by Europeans (Canada, the United States and New Zealand). Conclusions: Priorities for suicide prevention in Australia are correctly concentrated on youth, but the targeted age range should be extended to include men aged 25-34 years. A comprehensive policy should also not neglect the needs of other age groups. Further epidemiological study of national and international data may suggest new approaches to suicide prevention. Introduction It is well known that there is a high suicide rate in Australian males aged 15-24 years, and previous and present governments have instituted committees to address youth suicide rates.1 There have been only sporadic reports of suicide rates in other age groups,2 including suggestions of high rates in elderly people.2,3We present suicide rates and trends across all ages, placing them in context by comparing them with rates from other Western nations. The national focus on youth suicide to the relative exclusion of older age groups is examined in the light of these data. Methods Australian suicide and population data for 1964-1997 were obtained from the Australian Bureau of Statistics (ABS) and annual suicide rates (per 100 000 estimated mean resident population) were calculated (see Appendix). These were plotted by 10-year age groups and sex over time. Change over time was examined by comparing the suicide rate in 1964-1966 (rates were averaged to smooth out random fluctuations within one-year periods) with the suicide rate in 1995-1997; 95% confidence intervals were calculated for these two time periods to assess the significance of change. Variations in suicide rate trends over this 34-year period were assessed by calculating the series autocorrelation suicide rates and the values of Pearson's correlation coefficient. Years of potential life lost (YPLL) were calculated for 10-year age and sex groups for the most recent year (1997). The formula used was adapted from that used by the Australian Bureau of Statistics4 in order to incorporate age groups (Box 1). The Australian population at 30 June 1991 was chosen as the standard population, as suggested by the Australian Bureau of Statistics. International data were obtained from the World Health Organization (WHO)5-8 and Lester and Yang.9 Mean suicide rates were calculated for 23 Western countries (including Australia), averaged over 1990-1994, for 10-year age and sex groups. These 10-year age and sex rates were then ranked to compare Australia with other nations. Results Figures 1-8 show suicide rates over time for sex and 10-year age groups, as well as all ages combined. Males Suicide rates overall and for those aged 15-24 and 25-34 years increased significantly over time (1964-1966 to 1995-1997). The rise in suicide rates from 1973-1997 for men aged 25-34 years was of similar magnitude to the rise for those aged 15-24 years (Figures 2 and 3). Suicide rates in the older age groups (35 to 75 years and over) declined (for men aged 35-44 years and 75 years and over these declines were not statistically significant). Significant autocorrelations (P < 0.01) were found in each age group and for all ages combined. Females Suicide rates overall and for each age group from 25 to 75 years and over declined significantly (1964-1966 to 1995-1997). There was no change in suicide rates for females aged 15-24 years. Significant autocorrelations (P < 0.01) were found for all ages combined and for most age groups (the exceptions were those aged 15-24 years and 75 and over). Years of potential life lost by suicide in 1997 are shown in Box 2. Boxes 3a and 3b list the mean suicide rates (per 100 000 population) by age group and sex for 23 Western nations, including Australia. Discussion The priority accorded to youth suicide prevention by successive Australian governments is supported by our data. In the last three decades, when overall suicide rates were falling, the suicide rate of males 15-24 years more than doubled. Suggestions of a plateauing of this rate since 1989 are not supported by the latest figures for 1997, although it is premature to draw conclusions either way. (It should also be noted that at the time of submission of this article there were significant concerns about the validity of the 1997 suicide rate figures. For example, major rises in rates in New South Wales and Victoria were absent from Queensland -- the next most populous State -- suggesting the possibility of interstate data collection influences.) From a policy perspective, the most important finding is that suicide rate increases since 1973 for men aged 25-34 years have paralleled those of 15-24 year olds, with even less evidence of a recent plateau. Despite having shorter life expectancies, the toll in potential years of life lost (in 1997) was greatest for 25-34 year olds. These years are also the peak years for early parenthood, making the likelihood of there being bereaved offspring greater than in the younger group. These findings suggest that priority initiatives for youth suicide prevention should be extended to those aged 15-34 years, if not further (the high level of potential years of life lost continues to 44 years). The Federal Government's recently announced National Suicide Prevention Policy provides for ages beyond youth, by recognising that rising rates are not confined to the age group 15-24 years and that high suicide rates in the elderly should not be overlooked. It is unclear whether or to what extent the suicide phenomenon in boys and young men might be a cohort effect -- a "damaged" generation. The later commencement of the rise in suicide rate in men aged 25-34 years and the, as yet, absence in this age group of the possible 1990s plateau could be seen as consistent with this. Rates in females aged 15-24 years showed no convincing rise. It has previously been noted that suicide rates in females aged 15-19 years rose modestly between 1960 and 1989, while rates for those aged 20-24 years showed no overall change over this period.10 However, much of the rise in females aged 15-19 years was in the early 1960s, predating the rise in rates of 15-19-year-old males, but coinciding with a general, transient rise in suicide rates in females of all ages. Perhaps the most important observation regarding young females in the present study is that their suicide rates remained relatively static at a time when rates for most other female age groups declined. Suicide rates in children under 15 years of age have not significantly altered over time, although the small numbers involved do not lend confidence to rate estimates. The recording of suicide in children under the age of 10 years is affected by the different criteria used by the Australian Bureau of Statistics for determining suicide: it is considered that children have a limited ability to form an intent to suicide. Hence, more explicit evidence of suicidal intent is required,11 usually a coroner having stated explicitly that suicide was the cause of death. As most State and Territory Coroners' Acts discourage if not prohibit such findings (for all ages), such explicit statements are unlikely.11 Beyond 35 years in women, and 45 years in men, and up to 75 years and over for both sexes, Australian suicide trends are striking. In both sexes there have been major declines, and for much of the period these declining male and female rates have been parallel, quite unlike the trends for 15-24 year olds. It is unclear whether these declining rates have as yet plateaued. Even if this were not the case, it is inevitable that these declining rates will shortly level out and increase again (from the trends over the complete period a number of these age rates would reach zero in the early decades of the next century). In the early 1960s, suicide rates, particularly in women and in older age groups, rose in association with an epidemic of barbiturate poisoning, subsequently to fall in the late 1960s, reaching rates in the early 1970s similar to those before this epidemic.12,13 The causal factors determining the subsequent decline in rates of those between 35 and 74 years are yet to be determined. It is possible that such determination might yield valuable clues as to the causes and possible methods of preventing suicide in young people. International comparisons should be interpreted conservatively, as variations in data collection systems will account for some of the variations. With these reservations in mind, among 23 Western nations, Australian suicide rates for 15-24 year olds ranked fourth for males and eighth for females (Boxes 3a and 3b). Australian rates for both sexes between the ages of 35 and 74 years, as well as declining, compared favourably internationally (ranking in the middle of or below those of other Western nations). Although Australian suicide rates for those over 75 years were not declining, they nevertheless again compared favourably from an international perspective. Whereas the Australian suicide rate for 15-24-year-old males was over half that of the highest-placed nation (Finland), the corresponding ratio for males 75 years and over was about one-sixth. For females, these comparisons were even more marked. Nevertheless, a comprehensive policy should not overlook the needs of men over 75 years, especially as, in Australia, suicide rates in this age group surpass those of all other age groups. The Western nations with lower suicide rates include those that provided most of the early immigrants to Australia: Greece, Italy (except in the elderly), the United Kingdom and Ireland. The highest suicide rates were in mainland Western Europe (especially Hungary) and Scandinavia (especially Finland). Some of these nations, for example Denmark, have profiles radically different from that of Australia, with lower youth suicide rates but much higher rates in those over 35 years of age. Canada and, to a lesser extent, the United States and New Zealand are the nations with suicide rate profiles most similar to Australia's. All four of these nations have common characteristics of European migration, a comparatively short history (apart from their indigenous populations), geographical isolation, climatic extremes and more.10 They serve as potentially valuable nations to study shared characteristics that may affect suicide rates. Studies have yet to provide explanations for these similarities and differences which have often been overlooked, largely as a consequence of the worldwide lack of epidemiological mental health data. While differences in prevalence of psychiatric disorders are potentially relevant, the magnitude of the different international rates suggests other factors may operate. Hungary and Finland share common cultural origins and high suicide rates. It has been suggested that Finland's high suicide rates in young men may relate to cultural expectations that men should be tough and resilient14 -- a suggestion that might be equally relevant in Australia, New Zealand, the United States and Canada. It is possible that a better understanding of cultural influences and how to positively modify them might be relevant to suicide prevention. Acknowledgements The study was funded by Griffith University and Queensland Health through their co-funding of the Australian Institute for Suicide Research and Prevention. We thank the Australian Bureau of Statistics for providing information on suicide and population numbers. References Commonwealth Department of Health and Family Services. Youth suicide in Australia: a background monograph. 2nd edition. Canberra: AGPS, 1997. Snowdon J. Suicide rates and methods in different age groups: Australian data and perceptions. Int J Geriat Psychiatry 1997; 12: 253-258. Hassan R, Carr J. Changing patterns of suicide in Australia. Aust N Z J Psychiatry 1989; 23: 226-234. Australian Bureau of Statistics. Causes of death, Australia, 1996: 73. (Catalogue No. 3303.0.) World Health Organization. World Health Statistics Annual 1992. Geneva: WHO, 1993. World Health Organization. World Health Statistics Annual 1993. Geneva: WHO, 1994. World Health Organization. World Health Statistics Annual 1994. Geneva: WHO, 1995. World Health Organization. World Health Statistics Annual 1995. Geneva: WHO, 1996. Lester D, Yang B. Suicide and homicide in the twentieth century: Changes over time. Commack, NY: Nova Science, 1998: 165-204. Cantor CH, Leenaars AA, Lester D, et al. Suicide trends in eight predominantly English-speaking countries 1960-1989. Soc Psychiatry Psychiatr Epidemiol 1996; 31: 364-373. Cantor CH, Neulinger K, Roth J, Spinks D. The epidemiology of suicide and attempted suicide among young Australians: a report to the National Health and Medical Research Council: Australian Institute for Suicide Research and Prevention. In press. Oliver G, Hetzel BS. An analysis of recent trends in suicide rates in Australia. Int J Epidemiol 1973; 2: 91-101. Whitlock FA. Suicide in Brisbane, 1956-1973: The drug-death epidemic. Med J Aust 1975; 1: 737-743. Retterstol N. Suicide in the Nordic countries. Psychopathology 1992; 25: 254-265. (Received 14 Jan, accepted 7 Jun, 1999) Authors' details Australian Institute for Suicide Research and Prevention, Griffith University, Nathan, QLD. Christopher H Cantor, FRANZCP, MRCPsych, Senior Research Psychiatrist; Kerryn Neulinger, BBehSc, GradDipPsych, Research Assistant; Diego De Leo, MD, PhD, Director. Reprints will not be available from the authors. Correspondence: Dr C H Cantor, Australian Institute for Suicide Research and Prevention, Griffith University, Nathan, QLD 4111. Email: C. CantorATmailbox.gu.edu.au Back to textBack to text Back to text 3a: Mean male suicide rates (per 100000 population) for 23 Western countries by 10-year age groups, 1990-199415-24 yearsFinland 41.4 New Zealand 39.0 Switzerland 25.8 Australia 25.7 Canada 25.2 Norway 24.9 Austria 24.3 USA 21.9 Hungary 20.1 Scotland 19.0 Ireland 18.3 N Ireland 17.6Belgium 15.7 France 15.3 Germany 14.0 Sweden 13.4 Denmark 13.0 Engl/Wales 11.1 Netherlands 9.3 Spain 7.0 Italy 6.1 Portugal 5.8 Greece 4.0 25-34 yearsFinland 60.7 Hungary 54.4 Switzerland 32.7 New Zealand 32.0 France 32.0 Belgium 30.5 Austria 30.3 Australia 29.0 Canada 29.0 Ireland 27.1 Denmark 26.4 Norway 26.1Scotland 26.1 USA 24.6 Sweden 23.9 N Ireland 22.4 Germany 21.3 Engl/Wales 16.3 Netherlands 15.9 Portugal 13.2 Spain 10.6 Italy 10.3 Greece 5.635-44 yearsHungary 82.0 Finland 67.8 France 40.1 Denmark 38.1 Austria 37.2 Belgium 35.6 Switzerland 33.0 Sweden 29.3 Canada 27.3 Norway 26.9 Scotland 26.2 Germany 26.0Australia 25.2 New Zealand 23.9 USA 23.5 Ireland 22.9 Netherlands 17.7 Engl/Wales 17.4 N Ireland 15.5 Portugal 11.8 Italy 10.6 Spain 9.4 Greece 5.945-54 yearsHungary 95.1 Finland 64.1 Denmark 47.5 Austria 41.5 France 40.1 Switzerland 39.8 Belgium 36.2 Sweden 31.9 Germany 31.1 Norway 28.8 Canada 25.6 Scotland 24.2Australia 24.2 New Zealand 24.2 USA 23.1 Ireland 19.6 Netherlands 16.7 Engl/Wales 16.2 N Ireland 15.1 Portugal 14.6 Italy 12.6 Spain 11.9 Greece 6.755-64 yearsHungary 84.6 Finland 57.3 Austria 46.7 Denmark 42.6 Switzerland 41.9 belgium 38.9 France 38.1 Germany 32.2 Sweden 30.7 Norway 28.8 Ireland 25.9 USA 25.0 Canada 24.2 New Zealand 23.2 Australia 22.9 Portugal 21.5 Netherlands 18.6 Scotland 18.1 N Ireland 17.4 Spain 17.4 Italy 17.1 Engl/Wales 12.8 Greece 7.865-74 yearsHungary 92.5 Austria 61.1 Belgium 50.4 Switzerland 47.4 France 47.1 Denmark 46.4 Finland 45.9 Germany 35.9 Sweden 33.7 USA 30.9 Norway 30.7 Portugal 30.1 Australia 24.4 Spain 23.2 Italy 22.9 Canada 22.1 New Zealand 21.2 Netherlands 19.7 Ireland 18.3 Scotland 14.3 N Ireland 12.8 Engl/Wales 11.9 Greece 10.175+ yearsHungary 183.0 Austria 118.0 France 103.0 Belgium 98.6 Switzerland 89.8Germany 86.1 Denmark 74.9 Finland 71.9 Portugal 59.1 USA 55.4Sweden 51.9 Spain 47.8 Italy 44.3 Netherlands 35.4 Australia 32.8 Norway 31.8 New Zealand 29.8 Canada 28.9 Engl/Wales 17.1 Scotland 16.0Greece 15.8 Ireland 13.8 N Ireland 13.3Back to text Appendix: Identifying suicide deaths in Australia11 Coding deaths as suicide relies on an interaction between the Australian Bureau of Statistics (ABS) and State and Territory coroners and government medical officers. The six States and two Territories of Australia each have different Coroners' Acts. Most States and Territories discourage coroners from making formal pronouncements about suicide. Western Australia and New South Wales are the only States that routinely use suicide verdicts. ABS receives information from coroners that is generally sufficient for coding in most cases. Deaths that were in reality suicides, but were not deemed as such by coroners or the ABS, will most likely be coded as undetermined deaths or accidents, and involve similar causes as suicide deaths (eg, poisoning). There has been a rise in both undetermined and accidental deaths in recent years. However, the impact of these uncertainties is unlikely to be sufficient to greatly alter our overall study findings. Back to text 3b: Mean female suicide rates (per 100000 population) for 23 Western countries by 10-year age groups, 1990-199415-24 yearsFinland 7.5 Austria 6.2 Hungary 6.2 New Zealand 6.2 Sweden 5.9 Switzerland 5.8 Norway 5.5 Australia 5.1 Belgium 5.1 Canada 4.9 France 4.5 USA 3.8Netherlands 3.7 Scotland 3.7 Germany 3.5 Denmark 3.3 Ireland 2.5 N Ireland 2.4 Portugal 2.2 Engl/Wales 2.1 Italy 1.8 Spain 1.7 Greece 0.725-34 yearsFinland 12.0 Belgium 11.8 Hungary 11.6 Sweden 10.1 Switzerland 9.0 France 9.0 Scotland 8.3 Austria 8.0 Denmark 7.7 New Zealand 7.3 Netherlands 7.2 Norway 7.1Ireland 6.7 Australia 6.6 Canada 6.4 Germany 5.7 Germany 5.7 N Ireland 3.9 Portugal 3.5 Engl/Wales 3.5 Italy 2.9 Spain 2.6 Greece 1.435-44 yearsHungary 20.3 Finland 17.4 Denmark 15.7 Belgium 14.5 Switzerland 13.5 France 13.0 Austria 12.1 Sweden 11.8 Norway 9.8 Netherlands 9.6 Canada 8.1 Germany 7.7New Zealand 6.9 Scotland 6.8 N Ireland 6.8 Australia 6.6 USA 6.6 Ireland 4.8 Engl/Wales 3.9 Italy 3.9 Portugal 3.8 Spain 3.0 Greece 1.3 45-54 yearsHungary 26.5 Denmark 25.5 Finland 20.4 Belgium 18.2 Austria 17.1 Switzerland 16.7 France 16.5 Sweden 15.0 Germany 12.1 Norway 11.5 Netherlands 9.5 N Ireland 9.4New Zealand 8.9 Canada 8.1 USA 7.3 Scotland 7.2 Australia 7.0 Ireland 6.8 Portugal 5.0 Italy 4.9 Engl/Wales 4.7 Spain 3.9 Greece 2.355-64 yearsDenmark 28.5 Hungary 28.0 Belgium 17.9 France 17.6 Finland 17.5 Austria 17.4 Switzerland 17.0 Sweden 15.4 Germany 12.9 Norway 12.0 Netherlands 10.9 New Zealand 7.7Ireland 7.7 Australia 6.9 USA 6.8 Italy 6.8 Scotland 6.7 Canada 6.4 Portugal 6.2 Spain 6.0 N Ireland 4.8 Engl/Wales 4.7 Greece 2.4 65-74 yearsHungary 37.6 Denmark 31.5 Belgium 23.5 Switzerland 19.8 Austria 18.5 France 17.9 Germany 16.7 Sweden 13.5 Finland 13.3 Norway 12.4 Netherlands 10.4 Spain 8.8Portugal 8.1 Italy 8.0 New Zealand 6.6 Australia 6.6 Ireland 6.4 Scotland 6.4 USA 6.2 Canada 6.1 Engl/Wales 5.2 N Ireland 3.9 Greece 2.875+ yearsHungary 67.3 Denmark 30.2 Austria 28.5 Germany 26.4 France 25.3Belgium 24.2 Switzerland 23.0 Sweden 14.2 Portugal 12.2 Netherlands 12.1Spain 11.9 Finland 9.6 Italy 9.3 Norway 9.2 Australia 8.0Scotland 6.0 USA 6.0 Engl/Wales 5.9 Canada 4.7 New Zealand 4.3 Greece 3.4 Ireland 3.0 N Ireland 2.5Back to text

Christopher H Cantor · Kerryn Neulinger

Editorial Asthma in general practice: action plans or planned actions There's more than one way to implement effective asthma management in general practice Peter G Gibson MJA 1999; 171: 67 Good general practice is integral to effective asthma management. Asthma prevalence and hospitalisations are high, and, although we don't yet know how to reverse the rise in asthma prevalence, we know that severe exacerbations can be reduced by inhaled corticosteroid therapy and by effective education that involves an individualised, written action plan and regular medical review.1The burden of illness from asthma is concentrated in general practice, but studies of asthma education have mainly been conducted in hospitals. We need to transfer the improvements seen in these randomised trials to Australian general practice. Several approaches have been tried, including public health initiatives conducted by the National Asthma Campaign (NAC), practice audit,2,3 and nurse-run asthma clinics.4 In this issue of the Journal, Abdulwadud et al provide data showing just how different asthma can be in general practice to asthma in a specialist setting.5 Predictably, asthma is less severe in general practice.5 Medication use and understanding about asthma are similar, but fewer general practice patients have a written action plan and understand how to respond to an asthma emergency. Thus, for Australia, where inhaled corticosteroid use is already high, educational interventions in general practice should focus on the early management of exacerbations using written action plans and on smoking cessation. Also in this issue, Heard et al report their trial of a combined nurse educator/general practitioner asthma clinic.6 As part of the intervention, patients attending the asthma clinic received action plans and education about asthma. Patients in the control group also received action plans from their doctors, so that by the end of the study about 70% of patients had a written action plan and 80% were taking inhaled preventer medication. Asthma morbidity was reduced in both groups, and the asthma clinic did not prove to be any better than regular review of asthma by a general practitioner. Presumably outcomes in the control group improved because the participating general practitioners, who were caring for patients in both intervention and control groups, modified their behaviour by appropriately following proven guidelines. This problem is common in studies of asthma education, where blinding is seldom used and participation in the study is enough to improve management. Thus, this article compares asthma clinics to enhanced medical care, and a direct comparison with usual medical practice is lacking. What can we learn from this? Firstly, that the improvements in asthma mordibity that follow education and medical review can be achieved in general practice in Australia, and can be achieved in several ways. Regular review of asthma control and issuing an action plan by a general practitioner can be as effective as a special asthma clinic. General practitioners can now be confident that modifying their practice will improve asthma control. We know that this is needed, as surveys indicate that, although more people use action plans since the NAC, their use is still unacceptably low.7 General practitioners can choose between setting up an asthma clinic or implementing a structured program of regular review in their practices. The NAC and asthma liaison officers within the divisions of general practice are implementing suggested schemes at present. Regular review could turn into complacency, where a general practitioner feels that his or her current practice is satisfactory and that people with asthma are well managed. The best way to avoid this is to conduct regular quality control of asthma management. There are some simple interventions with asthma audit that do reap rewards for patients and doctors alike.2,3 Special asthma clinics also need to conduct regular quality control of their services, as when they provide asthma education without general practitioner consultations and action plans there is no benefit to patients.8 Structured asthma management programs, whether by systematic regular review or a special asthma clinic, will need to be adapted to the organisational structure of the practice. This can be done fairly simply in practices with several doctors. It is more difficult to do so in solo practices, but here it is even more important, as patients from small practices have a higher admission rate for asthma than those from larger practices.9 General practitioners need to adapt the National Asthma Campaign's six-point asthma management plan to their practices and ensure that all patients with asthma understand their disease, have a set of written instructions about when and how to treat exacerbations (all people with asthma are at risk of exacerbations), and are prescribed optimal therapy to control symptoms and exacerbations. Special asthma clinics or a system of regular education and review will suffice, provided that the processes and outcomes are monitored to ensure success. Organising the process of care for asthma in general practice and defining how to do it may be just as important as educating the doctor about what to do. Most general practitioners understand asthma management. Effective implementation is the issue. Peter G Gibson Staff Specialist, Respiratory Medicine John Hunter Hospital, Newcastle, NSW Gibson PG, Wilson AJ, Coughlan J, et al. The effects of self-management asthma education and regular practitioner review in adults with asthma. In: Cates C, DuCharme F, Gibson PG, et al. Airways module. Cochrane database of systematic reviews, issue 4. Oxford, UK: Update Software, 1998. Bryce FP, Neville RG, Crombie IK, et al. Controlled trial of an audit facilitator in diagnosis and treatment of childhood asthma in general practice. BMJ 1995; 310: 838-842. Feder G, Griffiths C, Highton C, et al. Do clinical guidelines introduced with practice based education improve care of asthmatic and diabetic patients? A randomised controlled trial in general practices in east London. BMJ 1995; 311: 1473-1478. Charlton I, Charlton G, Bloomfield J, et al. Audit of the effect of a nurse-run asthma clinic on workload and patient morbidity in general practice. Br J Gen Pract 1991; 41: 227-231. Abdulwadud OA, Abramson MJ, Light L, et al. Comparison of patients with asthma managed in general practice and in a hospital clinic. Med J Aust 1999; 171: 72-75. Heard AR, Richards IJ, Alpers JH, et al. Randomised controlled trial of general practice based asthma clinics. Med J Aust 1999; 171: 68-71. Comino EJ, Mitchell CA, Bauman A, et al. Asthma management in eastern Australia, 1990 and 1993. Med J Aust 1996; 164: 403-406. Premaratne UN, Sterne JAC, Marks GB, et al. Clustered randomised trial of an intervention to improve the management of asthma: Greenwich asthma study. BMJ 1999; 318: 1251-1255. Griffiths C, Sturdy P, Naish J, et al. Hospital admissions for asthma in East London: associations with characteristics of local general practices, prescribing, and population. BMJ 1997; 314: 482-486.

Peter G Gibson

Research Randomised controlled trial of general practice based asthma clinics Adrian R Heard, Ian J Richards, John H Alpers, Louis S Pilotto, Brian J Smith and Julie A Black MJA 1999; 171: 68-71 See also Gibson & Abdulwadud et al Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on General practice and primary care Abstract Objective: To compare the effects on asthma morbidity of asthma clinics based in general practice with standard general practice care. Design and setting: A randomised controlled trial in eight general practices. Patients, general practitioners and outcomes assessors were not blinded to treatment allocation. Participants: 195 patients with asthma aged 5-64 years; 191 completed the trial. Intervention: Three asthma clinic sessions over six months involving nurse counselling, education about asthma management, spirometry and consultation with the general practitioner. Main outcome measures: Patients reporting days lost from work or school, number of days lost, the presence of morning or nocturnal asthma symptoms, use of an action plan, medication use, current smoking, hospitalisation, and emergency visits. Results: Asthma clinics were associated with a greater reduction in nocturnal symptoms, an increase in the ownership of peak flow meters and an increase in the number of patients commencing or resuming smoking. Both control and intervention groups showed similar improvement in days lost from work or school, the presence of symptoms, use of an action plan and taking reliever medication. Conclusion: Our study does not show that asthma clinics are more effective than standard general practice care in reducing asthma morbidity. It is uncertain how much of the improvement in outcomes was due to the asthma clinic, the influence of the study itself upon patients and practitioners, or other factors, such as the tendency for a patient's asthma management to improve over time. Introduction Asthma is the most common chronic disease in children and a leading cause of morbidity in adults in Australia.1,2 Asthma clinics may be a way of improving comanagement practices between health professionals and people with asthma. They involve trained nurses conducting asthma education, peak flow readings and spirometry with asthma patients, combined with a brief general practitioner review. Asthma clinics are an integral part of general practice in the United Kingdom, but have yet to gain acceptance in Australia.3 One reason for this might be that studies have not provided conclusive evidence that these clinics reduce morbidity.4-9 This may be because regular general practitioner review10 and/or asthma education11 is the key element in reducing asthma morbidity, and therefore only studies comparing asthma clinics with patients receiving irregular reviews are likely to show significant differences in outcomes. In this study, we used a randomised controlled trial design to test whether asthma clinics (intervention) were more effective in reducing morbidity from asthma than standard medical treatment (control). The clinics used the Patient Management System, a recognised model for operating asthma clinics.12 Methods Ethical approval Ethics approval for the study was obtained through the Royal Australian College of General Practitioners' ethics committee at the RACGP national office. Recruitment A previous major study of asthma self-management found a 50% reduction in the number of people reporting at least one day lost from work.6 We calculated that to detect a similar reduction in a study with 80% power and a 95% confidence interval a sample size of 170 was required. Patients were recruited from eight general practices staffed by 42 general practitioners. Consent was sought from all people with asthma aged 5-64 years attending these practices during three months of 1997. Subjects were individually randomised within practices into intervention and control groups. This meant that each participating general practitioner potentially saw both intervention and control patients. A randomisation chart was set up for each participating practice at Asthma South Australia, and general practitioners and the asthma educators were informed of a subject's treatment allocation before the baseline interview. Thus, patients, doctors and outcome assessors were not blinded as to who had received the intervention and who were controls. Intervention Each general practice operated one three-hour asthma clinic session per week. The asthma educators in the trial were practising registered nurses with extensive experience in respiratory care. Their component of the clinic session involved education in asthma management strategies, including a written asthma management plan, spirometry and instruction on using peak flow meters, inhalers and an asthma diary card. The session ended with a consultation by the general practitioner. Each asthma clinic patient was asked to attend three asthma clinic sessions within the six months of the study. Gathering outcomes data We conducted a telephone interview using adapted questions from the Southampton Morbidity Index13 and questions relating to clinical practice14 at the beginning and end of the study. Our outcome measures included number of patients reporting days lost from work or school, number of days lost, use of an action plan, medication use, current smoking, the level of morning or nocturnal asthma symptoms, hospitalisation, emergency visits, and number of home visits by the general practitioner. Data analysis All data were analysed on an intention-to-treat basis. For analysis, we categorised morning and nocturnal symptoms as "at least weekly" or "less frequently/never" to distinguish regular from irregular symptoms and to maintain adequate numbers of participants in each of the two categories. We analysed the number of days lost from work with both linear and logistic regression. Linear regression was conducted on the difference in the number of days lost from work between baseline and six months, and was adjusted for clustering by doctor. For logistic regression, also adjusted for clustering by doctor, the variable was divided into two categories (two or fewer days lost and three or more days lost), representing better-controlled and less well controlled asthma, respectively. The statistical analyses for all other study factors used logistic regression, adjusted for baseline measurements and clustering by treating doctor. We also conducted a longitudinal analysis using χ2 tests to examine changes in the intervention and control groups over the six months of the trial. Odds ratios and 95% confidence intervals (95% CIs) were calculated for all outcome measures. All tests were conducted using the Stata statistical software package.15 Results Patients Over the three-month recruitment period, 195 people entered the study, and 191 (97 in the clinic group and 94 controls) completed both interviews (Box 1). The demographic profile of the control group (mean age, 26.3 years, 95% CI, 22.3-30.2; proportion of males, 45%, 95% CI, 34%-55%) was similar to the intervention group (mean age, 27.5 years, 95% CI, 23.6-31.4; proportion of males, 42%, 95% CI 32%-52%). Although there were no records of the number of eligible subjects across all participating practices, an audit of all patients seeing general practitioners at two of the eight practices showed a participation rate of 45.1% of all asthmatics. The main reasons for non-participation were either the general practitioner's failing to ask the patient for consent or the patient's refusing consent. The average age of non-participants (mean age, 20.8 years, 95% CI 17.1-24.5) was not significantly different from that of participants (mean age, 21.4 years, 95% CI 17.1-25.7) in the two audited practices. Of the 97 people in the clinic group, 67 completed the three planned clinic sessions, 17 attended only one or two sessions, and 13 failed to attend any sessions. Outcomes There was no difference between the clinic and control groups at baseline for dichotomous study variables (Box 2), which provided evidence for effective randomisation. There was a low incidence of hospitalisation and emergency department attendance in both groups. At six months, however, waking at night at least weekly due to asthma and current smoking were significantly different between the two groups, as was ownership of a peak flow meter (Box 3). There were no differences reported at six months in patients' having discussed trigger factors with their general practitioner or receiving an action plan from their general practitioner. Unlike the dichotomous outcome variables, the mean number of days lost from work was significantly different between the treatment groups at baseline, with a high level of variability in the control data (intervention group mean, 2.62, 95% CI 1.84-3.40; control group mean, 5.37; 95% CI 3.46-7.29). There was no difference in the number of days lost from work at six months in the intervention group compared with the control group (intervention group mean, 2.09, 95% CI 0.91-3.27; control group mean, 2.66; 95% CI 1.66-3.66). Linear regression to compare the number of days lost at six months minus those at baseline between intervention and control participants showed a significant reduction in number of days lost in the control group compared with the intervention group (P = 0.04). Logistic regression comparing two or fewer days lost with three or more days lost showed a non-significant trend towards fewer days lost from work at six months in the intervention group (odds ratio, 0.50; 95% CI 0.24-1.03). Longitudinal analyses within the clinic and control groups showed a trend towards decreasing morbidity over the six-month period, with a 13% decrease in the number of people reporting days lost from work, school or usual activities in both groups (intervention group odds ratio, 0.57, 95% CI 0.31-1.06; control group odds ratio, 0.57, 95% CI 0.31-1.06). Longitudinal analyses also showed that the reported issuing of action plans increased significantly in both groups (intervention group odds ratio, 11.25, 95% CI 3.07-41.21; control group odds ratio, 3.94, 95% CI 1.53-10.10). An increase in the discussion of trigger factors was only significant for the control group (intervention group odds ratio, 2.6, 95% CI 0.84-8.02; control group odds ratio, 3.72, 95% CI 1.36-10.21). Discussion Our study does not show that asthma clinics are more effective than standard general practice care in reducing asthma morbidity. We observed an improvement in most of the outcome measures in both the intervention and control groups. Outcomes for patients who attended an asthma clinic had few differences from those in the control group. The intervention group was less likely to be woken "at least weekly" at night due to asthma. This may signal better home management of asthma in the intervention group, an outcome that is anticipated by guidelines16 but challenged in recent studies.17 Ownership of peak flow meters increased among the intervention group during the course of the study, probably because the asthma educators promoted the use of peak flow readings for asthma self-management. More people in the intervention group either adopted or recommenced smoking during the study. Smoking cessation advice was not included as part of the study intervention. In intensive interventions such as asthma clinics, smokers should be identified to ensure that smoking cessation is achieved or maintained if possible. In this study there were few reports of hospitalisations and emergency department visits at baseline, reflecting our broad inclusion criteria, which did not focus on severe asthmatics. Outcomes which were infrequent in this study may be significant in much larger studies. In relation to days lost from work or school, the significant difference between the intervention and control groups at baseline, the high variability at baseline in the control group and the different findings between the logistic and linear regressions at six months do not allow an adequate understanding of the effect of the intervention. The lack of difference between groups in the proportion of participants who had discussed trigger factors with their doctor and who had received an asthma action plan raises one of the possible explanations for the limited differences observed in this study. Baseline levels of both these clinical practice indicators are usually around 40%-60%,14 and were within that range at baseline in our study. Yet the frequency of both indicators increased substantially over the six months for both groups, which might suggest that clinical practice for the control subjects was contaminated as a result of general practitioners' seeing both intervention and control subjects. Other explanations may be: The asthma clinic in itself makes no difference to the outcomes being measured, and that a simpler intervention, such as regular general practitioner review, is the critical factor. The results of a review of asthma education support this.10 Whether the presence of an asthma clinic in a general practice increases the rate of general practitioner review is unknown. A possible Hawthorne effect.18 With general practitioners and patients being unblinded to the study, it is possible that both increased behaviours which led to better asthma self-management outcomes. People with asthma tend to show improved outcomes over time. This effect is likely to be enhanced after a visit to a general practitioner where management decisions are made. The data showing that the number of people reporting days lost from work or school decreased in both intervention and control groups support this explanation. Baseline data may have been biased because subjects were randomised into treatment groups before the baseline interview, and some subjects may have been aware of their treatment status at the baseline interview. Whatever reasons led to the apparent improvement in outcomes, a factor that may have contributed to the lack of difference between intervention and control groups may be the poor compliance with the intervention regimen. Nearly one-third of patients from the intervention group did not comply with the required three clinic visits, and 13% did not attend any visits. The outcome of this study holds some lessons for future randomised controlled trials in general practice. The major limitation of the study was the randomisation by patient rather than practice, which may lead to modification of general practitioner behaviour towards the control group as well as the intervention group, thus increasing the chance of contamination of controls and the Hawthorne effect. The inability to blind general practitioners and patients to the patient's treatment allocation also limited the study. The participation rate of less than 50% is lower than the rate considered desirable for randomised controlled trials, but compares favourably with other community-based studies.6,19 This study also demonstrates that, in general practice, larger, longer-term or more targeted studies (such as to more severe asthmatics) are required to show differences, especially for variables such as hospitalisation for asthma, which have a relatively low incidence among most general practice patients. Conducting this study for a longer period would also have allowed it to run over the full range of seasons, which is preferable for studies of seasonal diseases such as asthma. Acknowledgements We would like to thank the two nurses who conducted the asthma clinics, and Kieran McCaul from the Department of Human Services, South Australia, for statistical advice on the final drafts of the article. Thanks also go to the doctors and staff at the following participating practices: Angaston Medical Centre, Brooker Clinic, Greenwith Medical Centre, Golden Grove Medical Centre, Flinders Clinic, Nuriootpa Medical Centre, North Plympton Medical Centre and Tanunda Medical Centre. This study was made possible through a grant from the Department of Human Services, Adelaide, South Australia. References Abramson M, Kutin J, Czarny D, et al. The prevalence of asthma and respiratory symptoms among young adults: Is it increasing in Australia? J Asthma 1996; 33: 189-196. Peat JK, Toelle BG, Gray EJ, et al. Prevalence and severity of childhood asthma and allergic sensitisation in seven climatic regions of New South Wales. Med J Aust 1995; 163: 22-26. Barnes G, Partridge MR. Community asthma clinics: 1993 survey of primary care by the National Asthma Task Force. Qual Health Care 1994; 3: 133-136. Jones KP, Mullee MA. Proactive, nurse-run asthma care in general practice reduces asthma morbidity: scientific fact or medical assumption? Br J Gen Pract 1995; 45: 497-499. Lahdensuo A, Haahtela T, Herrala J, et al. Randomised comparison of guided self-management and traditional treatment of asthma over one year. BMJ 1996; 312: 748-752. Mayo PH, Richman J, Harris HW. Results of a program to reduce admissions for adult asthma. Ann Intern Med 1990; 112: 864-871. Martys C. Asthma care in Darley Dale: general practitioner audit. BMJ 1992; 304: 758-760. Evans D, Mellins R, Lobach K, et al. Improving care for minority children with asthma: Professional education in public health clinics. Paediatrics 1997; 99: 157-164. Charlton I, Charlton G, Broomfield J, et al. Audit of the effect of a nurse run asthma clinic on workload and patient morbidity in a general practice. Br J Gen Pract 1991; 41: 227-231. Gibson P, Coughlan J, Abramson M, et al. The effects of self-management education and regular practitioner review in adults with asthma. (Cochrane Review). In: The Cochrane Library, Issue 2. Oxford: Update Software; 1998. Bauman A. Effects of asthma patient education upon psychological and behavioural outcomes. Int Rev Health Psych 1993; 2: 199-212. Charlton I, Antoniou AG, Atkinson J, et al. Asthma at the interface: bridging the gap between general practice and a district general hospital. Arch Dis Child 1994; 70: 313-318. Jones K, Charlton I, Middleton M, et al. Targeting asthma care in general practice using a morbidity index. BMJ 1992; 304: 1353-1356. Beilby J, Wakefield M, Ruffin R. Reported use of asthma management plans in South Australia. Med J Aust 1997; 166: 298-301. StataCorp. Stata Statistical Software: Release 5.0. [computer program]. College Station, Texas: Stata Corporation, 1997. The Thoracic Society of Australia and New Zealand. Peak flow meter use in asthma management. Med J Aust 1996; 164: 727-730. Garrett J, Fenwick J, Taylor G, et al. Peak expiratory flow meters (PEFMs): who uses them and how does education affect the pattern of utilisation? Aust N Z J Med 1994; 24: 521-528. Rice B. The Hawthorne effect: persistence of a flawed theory. Psychol Today 1982; 16: 71-74. Garrett J, Fenwick J, Taylor G, et al. Prospective controlled evaluation of the effect of a community based asthma education centre in a multiracial working class neighbourhood. Thorax 1994; 49: 976-983. (Received 4 May 1998, accepted 31 May 1999) Authors' details SA HealthPlus, Department of Human Services, Adelaide, SA. Adrian R Heard, BSocAdmin, MPH, Senior Project Officer. Centre for Health Care Evaluation, Bedford Park, SA. Ian J Richards, BApplSc, MPH, Project Officer. Flinders Medical Centre, Bedford Park, SA. John H Alpers, MD, FRACP, Director, Respiratory Unit. North Western Adelaide Health Service, Woodville South, SA. Louis S Pilotto, FAFPHM, PhD, Senior Consultant. Brian J Smith, FRACP, PhD, Senior Lecturer, Department of Medicine. Asthma SA, Royston Park, SA. Julie A Black, BNG, Chief Executive Officer. Reprints will not be available from the authors. Correspondence: Mr A R Heard, SA HealthPlus, PO Box 65, Rundle Mall, SA 5000. Email: Adrian. HeardaATdhs.sa.gov.au Back to textBack to textBack to text

Adrian R Heard · Ian J Richards · John H Alpers · Louis S Pilotto · Brian J Smith · Julie A Black

Research Comparison of patients with asthma managed in general practice and in a hospital clinic Omar A Abdulwadud, Michael J Abramson, Larry Light, Francis C K Thien and E Haydn Walters MJA 1999; 171: 72-75 See also Heard et al & Gibson Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Respiratory medicine Abstract Objectives: To compare knowledge and attitudes about asthma, self-management skills and impact of asthma on quality of life between patients managed in general practice (GP) and in a hospital clinic. Design: Cross-sectional survey with six months' follow-up. Patients and setting: 105 adults with asthma: 61 from the Alfred Hospital Asthma and Allergy Clinic, Melbourne, and 44 from nearby general practices, in 1994-1995. Main outcome measures: Patient sociodemographic and clinical characteristics; patient knowledge, attitudes and beliefs about asthma; self-management skills; and impact of asthma on quality of life. Results: GP patients were more educated (P = 0.04) and more likely to smoke (P = 0.04) and to have mild asthma (P = 0.04) than hospital patients; they were less likely to use theophylline (P = 0.006) and to have exercise limitation (P = 0.03), and had fewer previous hospital admissions (P = 0.01). Impact of asthma on quality of life was greater in the hospital group than in the GP group. At baseline, the GP group were less likely to have written asthma action plans (P = 0.018), and were less able to manage rapid onset attacks than the hospital group (P = 0.02). More subjects in the hospital group than the GP group felt their asthma was severe (P = 0.02) and were optimistic about their asthma improving (P = 0.03). GP patients increased their knowledge about asthma significantly (P = 0.002) over six months. Conclusions: Patients with asthma managed in general practice and in hospital differ in clinical parameters, quality of life and attitudes to asthma. Future educational initiatives should take such differences into account. Introduction Asthma is the third most common reason for consultations with general practitioners (GPs) in Australia,1 but is both under-recognised and undertreated.2 The finding that GPs were the usual source of routine asthma treatment for 89% of the people who died of asthma3 demonstrates that GPs have the primary management role even in severe asthma.4To guide both doctors and patients, in 1989 the Thoracic Society of Australia and New Zealand developed the "six-point" Australian Asthma Management Plan (AMP).5 This was adopted by the National Asthma Campaign (NAC) at its inception in 1990. While the Royal Australian College of General Practitioners is a partner in the NAC, the plan was originally drawn up by hospital-based specialists. There is concern among GPs that they do not have sufficient time and knowledge to devise action plans and counsel patients about asthma management,4 as suggested in the AMP. The effectiveness of patient education about asthma as proposed in the AMP has not been widely evaluated in general practice. Only one such study has been reported,6 and only one nationwide survey of selected GPs was conducted before the launch of the NAC intervention.7 We aimed to examine patient knowledge about asthma and its management, self-management skills, impact of asthma on quality of life, and attitudes to asthma. We compared these between patients managed in general practice and in a hospital clinic over a six-month period that coincided with widespread advertising and dissemination of the AMP. Methods Design and setting The study was a cross-sectional survey with six months' longitudinal follow-up during 1994-1995. There was no intervention, and patients received their usual care from their GPs or hospital specialists. The study was conducted at the Alfred Hospital Asthma and Allergy Clinic, Melbourne, Victoria, and at 13 general practices near the hospital. Fourteen GPs were recruited by a practising GP (L L). The study was approved by the Ethics Review Committee at the Alfred Hospital. Subjects Consecutive patients being seen for asthma at the participating general practices were nominated by their GPs. Of 54 patients invited to participate, 44 were recruited (nine refused or did not respond and one died). Sixty-one patients were recruited from the Alfred Clinic. Inclusion and exclusion criteria were reported previously.8 All patients gave written informed consent. Diagnosis of asthma was based on American Thoracic Society criteria.9 Assessments Clinical and demographic characteristics of patients were determined by questionnaire. The term "priority asthmatic" was given to asthmatics who had severe and precipitately acute attacks of asthma; they had usually (but not necessarily) been admitted to an intensive care unit. Forced expiratory volume in 1 second (FEV1) was obtained from the records of the lung function laboratory, and predicted FEV1 at baseline was calculated for males and females separately, as suggested by Gibson et al.10 The mean daily peak expiratory flow (PEF) variability was estimated from patient diaries.5 Severity of asthma was classified as mild, moderate or severe based on medication use, as reported previously.8 Medication was grouped into generic categories. Outcome measures Patients completed the Asthma General Knowledge,11 Quality of Life,12 Self-Management Skills,13 and Attitudes and Beliefs14 questionnaires on entry and six months later. Selection of these outcomes was based on the asthma education targets and outcome measures proposed by the National Asthma Campaign.15 Statistical analysis Data were analysed with the SAS for Windows statistical package.16 Categorical variables were summarised as percentages, and associations were tested in contingency tables by χ2 tests. For continuous variables that were normally distributed, differences in mean scores were assessed by Student's t test. For continuous variables that were not normally distributed, the Wilcoxon signed rank and rank sum tests were used. Results Participation Follow-up questionnaires were returned by 39 of the 44 (87%) GP patients (with five of those with the most severe asthma lost to follow-up) and by 47 of the 61 (77%) hospital patients (with the remaining 14 either lost to follow-up or not responding). Subject characteristics Characteristics of the two patient groups are shown in Box 1. They were similar in age and sociodemographic characteristics, including occupation (data not shown), except that the GP group had a significantly higher proportion of tertiary-educated people and of current smokers than the hospital group. GP patients had less exercise limitation and milder asthma than the hospital patients, and were less likely to have been admitted to hospital and to have priority asthma. There was no significant difference in lung function or other clinical parameters (data not shown). GP patients were significantly less likely to use theophylline and to have a written asthma action plan than hospital patients. Proportions using β-agonists, anticholinergics, and inhaled or oral steroids and owning peak flow meters were not significantly different in the two groups. Asthma outcome measures Asthma knowledge: Asthma General Knowledge scores did not differ significantly between the GP and hospital groups either at baseline (means, 20.2 and 20.5 out of 31, respectively) or six months later. Scores increased in both groups over the six months, but the increase was significant only in the GP group (P = 0.002), which had a mean score increase of 1.66 (95% confidence interval [CI], 0.58 to 2.76) compared with 0.83 (95% CI, 20.39 to 2.03) in the hospital group. Quality of life: Scores for impact of asthma on quality of life are shown in Box 2. Impact at baseline was significantly greater in the hospital group than in the GP group for total quality of life and the subcategories of breathlessness, social disruption, and concern for health, but not mood disturbance. After six months, impact had significantly decreased in the hospital group for all these parameters except mood disturbance, but there was no significant change in the GP group. Despite the significant decrease in the hospital group, impact was still significantly greater than in the GP group for total quality of life (P = 0.03), social disruption (P = 0.008) and concern for health (P = 0.04). None of the improvements in quality of life differed significantly between the two groups over six months. Self-management skills: At baseline, the hospital group had a significantly higher median score for knowledge about self-management of a rapid onset asthma attack than the GP group (P = 0.02), but the two groups had similar scores for a slow onset attack (Box 3). After six months, the hospital group had significantly improved its slow onset scenario score (P = 0.02), but the GP group had not. Overall, there was no difference in the median change over six months in scores for either scenario between the two groups. Attitudes and beliefs about asthma: Patients' attitudes and beliefs about their asthma are shown in Box 4. At baseline, hospital patients were significantly more likely than GP patients to believe that their asthma was severe, but also that it would improve in the future. After six months, hospital patients were significantly less optimistic (P = 0.03), and the difference in this parameter between the two groups was no longer significant. The proportion of patients who said they could do everything they wanted regardless of the effect it might have on their asthma did not differ significantly between the two groups at baseline, but at follow-up hospital patients were significantly less likely to say this than GP patients. More hospital than GP patients wished their doctor would talk more to them about their asthma at both baseline and six-month follow-up, but the difference was significant only at follow-up. Concomitantly, fewer hospital patients than GP patients felt that their doctor had told them everything they wanted to know about their asthma; the difference was significant at both baseline and follow-up. Discussion We found that our samples of GP and hospital patients with asthma differed in sociodemographic and clinical parameters, quality of life, self-management skills and attitudes and knowledge about asthma. Some of our findings about the GP sample were more positive than reported previously. Use of inhaled steroids was significantly higher than found in random community samples,17,18 possibly because our sample of GP patients had more severe asthma, or because of industry promotion of these drugs.18 It is also possible that this form of treatment has become more acceptable in our group of GPs, many of whom had a particular interest in asthma. Use of peak flow meters and prevalence of written action plans in the GP patients were also higher than previously reported,17,18 but, once again, this finding may be confounded by the group of GPs studied. Actual prevalence of peak flow meter use and written action plans may be substantially lower in more typical general practices. There was some evidence from our study that implementation of the AMP may have improved, especially in general practice, over the period of our study. However, despite NAC recommendations, half of the hospital patients and three-quarters of the GP patients had no written asthma action plans; and about a third of the hospital patients and half of the GP patients did not have access to a peak flow meter. While our study sheds no light on the reasons for these findings, it demonstrates that there was room for improvement in asthma management in both settings, but particularly in general practice. Asthma knowledge among the GP patients was similar to that among the hospital patients at baseline, but improved more over the six months to follow-up. This was possibly due to the GP patients' higher educational level, our interaction with them during the study or better than average care from their doctors. As doctors had recruited the patients to the study, they may have put more effort into educating them before follow-up, although we have no evidence for this. The absence of any significant improvement in quality of life among the GP patients after six months suggests that insufficient attention may be given to this aspect of asthma. Furthermore, the potential selection bias towards milder disease and the loss to follow-up of five of those with more severe asthma from the GP group may have biased the results away from detecting improvement. Overall, the general practice group had better quality of life than the hospital group. This would be expected, as the GP group had milder disease with fewer hospital admissions. It is surprising that mood disturbance was the only category which did not differ between the two groups at baseline. Possibly moods such as sadness, depression and frustration are similar in all patients regardless of the severity of asthma. At baseline, the GP group was less able to manage the rapid onset attack, perhaps because they were likely to have experienced fewer such attacks. The hospital group improved their ability to manage slow onset attacks significantly over six months. Maybe their doctors educated them informally, although they did not have access to the results of the questionnaires. Alternatively, participants may have improved their answers with practice, but as this did not happen in the GP group it is unlikely. There was little difference in attitudes and beliefs about asthma between groups. However, at six months, the hospital group was significantly less optimistic about their asthma improving in the future than the GP group. This could result from the difference in asthma severity between the two groups, which resulted in hospital patients having a more realistic appreciation of their poor prognosis after education. At six months, more of the hospital patients than GP patients also wished that their doctors would tell them more about their asthma. Perhaps this reflects a low level of communication between doctors and patients in the hospital asthma clinic compared with general practice and requires further study. This study has some limitations. The GP patients may not be representative of the total general practice population, and recruiting interested GPs may have biased results. In the absence of any viable alternative strategy, evaluation focused on patients rather than GPs. Despite potential sampling and selection biases, the results highlight the impact of patient education among patients attending general practices and the differences between GP and hospital patients. Future educational initiatives should take such differences into account. The type and scope of patient education in general practice and hospitals should be thoroughly evaluated to identify areas in which GPs and specialists could be trained and supported more effectively. Continued dissemination and implementation of the Australian AMP is required to improve the self-management skills of patients in general practice. Acknowledgements We acknowledge a public health postgraduate research scholarship from the National Health and Medical Research Council. Dr Andrew Forbes, Jan Driver and Michael Bailey provided statistical support. We are grateful to the general practitioners who participated in the study. Drs Guy Marks, Rae Allen and Bonnie Sibbald gave permission to use their questionnaires. Dr John Kolbe gave permission to use his scoring system for the asthma attack scenarios. References Bridges-Webb C, Britt H, Miles DA, et al. Morbidity and treatment in general practices in Australia 1990-1991. Med J Aust 1992; 157 Suppl: 1-56. Tse M, Cooper C, Bridges-Webb C, Bauman A. Asthma in general practice. Opportunities for recognition and management. Aust Fam Phys 1993; 22: 736-741. Robertson CF, Rubinfeld AR, Bowes G. Deaths from asthma in Victoria: a 12 month survey. Med J Aust 1990; 152: 511-517. Antic R. Asthma in Australia: the current understanding. Overview of a national series of interactive meetings for general practitioners. Sydney: Excerpta Medica, 1993. Woolcock A, Rubinfeld AR, Seale JP, et al. Asthma management plan, 1989. Med J Aust 1989; 151: 650-653. Byrne DM, Drury J, Mackay RC, et al. Evaluation of the efficacy of an instructional program in the self-management of patients with asthma. J Adv Nursing 1993; 18: 637-646. Tse M, Bauman A, Bridges-Webb C. Asthma management in general practice. Aust Fam Phys 1991; 20: 1085-1092. Abdulwadud O, Abramson M, Forbes A, et al. Evaluation of a randomized controlled trial of adult asthma education in a hospital setting. Thorax 1999; 54: 493-500. American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease (COPD) and asthma. Am Rev Respir Dis 1987; 136: 225-244. Gibson J, Gallagher H, Johansen A, Webster I. Lung function in an Australian population: spirometric standards for non-smoking adults. Med J Aust 1979; 1: 292-295. Allen RM, Jones MP. The validity and reliability of an asthma knowledge questionnaire used in the evaluation of a group asthma education self-management program for adults with asthma. J Asthma 1998; 35: 537-545. Marks GB, Dunn SM, Woolcock AJ. A scale for the measurement of quality of life in adults with asthma. J Clin Epidemiol 1992; 45: 461-472. Sibbald B. Patient self care in acute asthma. Thorax 1989; 44: 97-101. Sibbald B, Collier J, D'Souza M. Questionnaire assessment of patients' attitudes and beliefs about asthma. Fam Pract 1986; 3: 37-40. National Asthma Campaign (NAC) National Asthma Strategy. Goals and targets. Melbourne: National Asthma Campaign, 1994. SAS Institute Inc. SAS language guide for personal computers, the SAS system for Microsoft Windows. Release 6.10. Cary, NC: SAS Institute Inc, 1994. Abramson MJ, Kutin JJ, Rosier MJ, Bowes G. Morbidity, medication and trigger factors in a community sample of adults with asthma. Med J Aust 1995; 162: 78-81. Comino EJ, Mitchell CA, Bauman A, et al. Asthma management in eastern Australia, 1990 and 1993. Med J Aust 1996; 164: 403-406. (Received 28 Sep 1998, accepted 7 Jun 1999) Authors' details Department of Epidemiology and Preventive Medicine, Monash Medical School, The Alfred Hospital, Melbourne, VIC. Omar A Abdulwadud, PhD, Postdoctoral Fellow; Michael J Abramson, PhD, FRACP, Associate Professor. Department of Allergy and Clinical Immunology, Monash Medical School, The Alfred Hospital, Melbourne, VIC. Larry Light, MB BS, Clinical Assistant; Francis C K Thien, MD, FRACP, Staff Physician. Department of Respiratory Medicine, Monash Medical School, The Alfred Hospital, Melbourne, VIC. E Haydn Walters, DM, FRACP, Professor, and Director of Respiratory Medicine. Reprints: Associate Professor M J Abramson, Department of Epidemiology and Preventive Medicine, Monash Medical School, The Alfred Hospital, Prahran, VIC 3181. Email: Michael. AbramsonATmed.monash.edu.au Back to textBack to textBack to text Back to text

Omar A Abdulwadud · Michael J Abramson · Larry Light

Abstract Objective: To investigate possible HIV transmission among prison inmates. Setting: A prison system in an Australian State. Participants: 13 ex-prisoners and their prison contacts. Methods: Ex-prisoners who claimed to have been infected with HIV in prison and their prison contacts were interviewed about HIV risk behaviour. Entries in prison and community medical records were used by a three-member expert panel to establish the likelihood of primary HIV infection and its possible timing and location. Main outcome measures: Determination of whether HIV infection probably occurred in prison. Results: There was a very high probability that at least four of 13 ex-prisoners investigated acquired HIV in prison from shared injection equipment. Another two ex-prisoners most probably acquired HIV infection outside prison. The location of infection for the remaining seven could not be determined. Conclusions: HIV transmission in prison has substantial public health implications as most drug-using prisoners soon return to the community. HIV prevention strategies known to be effective in community settings, such as methadone maintenance treatment and syringe exchange schemes, should be considered for prisoners. Introduction HIV transmission in prison has been reported in the United States,1 Scotland2 and Australia.3 The infrequency of these reports has led to a belief that HIV transmission occurs rarely among inmates. A more likely explanation is that confirmation of HIV transmission is more difficult in prisons than community settings.4 Multiple and powerful factors conducive to high HIV incidence are found in prisons. These include that: HIV prevalence is generally several times higher in prisons than in surrounding communities because of the considerable over-representation of injecting drug users (IDUs) among prisoners;5 reports of syringe sharing with multiple injectors are still common in prisons but now rare in community settings;6 HIV infection has been associated with imprisonment in France7 and Spain;8 and incidence of hepatitis C among IDUs incarcerated twice within a 12-month period was double that among IDUs who remained at liberty.9 Furthermore, HIV prevention measures, such as provision of sterile injecting equipment, condoms and methadone maintenance, are uncommon in prisons.10 Although several estimates of HIV prevalence have been conducted in correctional institutions,1,11,12 assessing the incidence of HIV transmission within a prison system poses considerably greater challenges.4 Most drug users serve short, repeated sentences. This hampers the investigation of infection outbreaks and identification of transmission location. In an earlier Australian study,13 several IDUs claimed to have become infected with HIV in prison. Some reported symptoms indicative of primary HIV infection while incarcerated. The aim of this study was to assess, using epidemiological data, whether these IDUs or their contacts had become infected in prison. A similar approach has been used to investigate an HIV outbreak in a Scottish prison.2 Methods Index cases The investigation took place between 1993 and 1994. Seven IDUs from an earlier study13 who claimed to have acquired HIV infection in prison were recontacted. In the earlier study, respondents who had injected drugs and had recently been released from prison were recruited from methadone units, hostels for ex-prisoners or drug injectors, probation offices, syringe exchange schemes, local media advertisements, AIDS organisations and via street networking.13 Prison contacts We traced prison contacts nominated by these seven people through the state methadone registry, AIDS services, drug users' organisations, HIV physicians and the State Registry of Deaths. The contacts were inmates with whom the seven index inmates had engaged in syringe sharing, anal sex or tattooing while in prison. Assessment of HIV infection HIV infection was assessed by an expert panel of three HIV physicians. The experts were provided with dates of entry to and exit from prison, HIV test results, symptoms recorded at the time the prisoner believed infection occurred, self-reported symptoms and self-reported risk behaviour. All dates were referenced in months from the year before the first detected case had last tested HIV negative. Each expert independently assessed whether the recorded symptoms indicated an HIV seroconversion illness and whether the infection occurred in prison, in the community, or if the location was indeterminate. We then accepted the majority decision in each assessment. Ethical approval Relevant ethics committees approved the study on condition that study participants' contacts in the community following their release from prison were not traced. We were also required to alert potential study participants to the possibility of legal or other consequences of admitting drug use in prison or transmitting HIV to another person. Participation in the study required signed, informed consent. Information which would identify the exact time and location of these possible infections has not been included, in accordance with requirements of one ethics committee. Results Contact tracing Between 1993 and 1994, seven male IDUs described in a previous study13 were recontacted (subjects A, B, C, D, E, F, G). They identified 20 prison contacts: six of these contacts could not be located, six had died of AIDS (according to death certificates), and two declined to participate for fear of repercussions for transmitting HIV. The six remaining contacts (H, I, J, K, L, M) plus the seven index cases made a total of 13 ex-prisoners available for investigation (Figure). Prison clusters Prison records revealed two clusters (C1, C2) of six subjects in one or two prison wings. Subjects B, E, I, K and M were held in Prison 1 (population about 250 inmates) in months 22 and 23, during which time index subject B seroconverted. Subjects B, D, I, K and M were held in Prison 2 (population about 300 inmates) in months 29 and 30, during which time contact subject K seroconverted. Index participant A was not part of either cluster, but another participant reported sharing syringes with him. Of the six deceased potential respondents, two had been part of C1 and another two had been part of C2. According to death certificates, two deceased potential respondents became infected with HIV in the year when they were held with the clusters. Cluster analysis was not possible because of the lack of records being kept on the total number of inmates held in the prison wings during the crucial times. Self-reported risk behaviour Eleven participants (A, B, C, E, I, K, M, D, F, G, L) reported syringe sharing in prison, with the first seven nominating another person in this series as a sharing partner. Contact participants I and M also reported receiving a tattoo in prison, and index subject C reported unprotected anal sex. All six deceased prison contacts wereidentified by one or more participants as having shared syringes with them around the crucial periods of months 22 and 23 and months 29 and 30. Assessment of HIV infection Medical file entries for 10 subjects (A, B, C, E, F, G, I, K, L, M) were reviewed by the expert panel. The experts concluded that five participants (A, B, C, G, K) had experienced primary HIV infection and that the most likely location of transmission for individuals A, B and C was in prison (Box 1). Overall, it was concluded that infection occurred in prison for four subjects and in the community for two (Box 2). Discussion The epidemiological evidence that individual A was infected in prison is beyond doubt: he tested negative and then positive for HIV infection after years of confinement in prison. There was strong epidemiological evidence that individuals B, C and J were also infected in prison. Individuals D and G were infected with HIV in the community. The location of infection for the remaining seven subjects (and the six deceased potential respondents) could not be determined. Thus, on epidemiological grounds, at least four of the 13 people investigated were infected with HIV while in an Australian prison system. The most likely route of HIV transmission was shared injection equipment. These are both conservative and probabilistic assessments. It is likely that a prospective investigation of these 13 people, or even a retrospective investigation closer to the events, would have yielded a larger number of confirmed HIV transmissions in prison. However, the strength of evidence for this network and the multitude of factors conducive to HIV infection in prisons suggest that the extent of HIV transmission occurring in prisons through shared injection equipment is underestimated. A mathematical model of HIV transmission in an Australian prison system14 using values derived from empirical studies also suggests that transmission is occurring within correctional centres. This study illustrates some of the difficulties of confirming HIV transmission in prison. We became aware of a possible outbreak by chance. Obtaining ethical approval for the study was an extremely protracted process requiring the assistance of a legal expert. Inmates were understandably wary of admitting risk behaviour because of the potentially serious consequences (as outlined in the consent form). Apart from the logistical and ethical problems of this type of research, the incubation period for HIV infection is almost as long as the average duration of a prison sentence served for drug-related offences in Australia. Consequently, many HIV infections occurring in prisons will not be detected by conventional surveillance. These factors may help to explain why so few cases of HIV transmission among inmates have been reported. Our study differed from previous reports10 in the extent of transmission detected and the type of prisoners studied. Previous studies have investigated long term, high security prisoners, who have less opportunity to associate with other inmates and visitors to obtain drugs and consequently become infected with HIV.15 Our study found a relatively large number of incident cases considering the small sample size, the extremely low prevalence of HIV infection in the Australian prison population16 and the rapid turnover of inmates. All these factors militate against detection of HIV transmission in prison. A limitation of the study was reliance on self-reported risk behaviour. However, we accepted self-reported data only if corroborated by another external source. Moreover, symptoms reported by informants coincided closely with medical records, supporting the validity of self-reported data. We were precluded by ethics committee requirements from determining whether any sexual partners (and their children) were infected with HIV by participants following release from prison. This restriction prevented investigation of possible HIV transmission beyond prison to the community. However, medical files indicated that four subjects had each had an HIV-positive female sexual partner following release from prison. Two of these women, and an additional HIV-negative partner, became pregnant, with at least two pregnancies reaching full term. Medical files also indicated that at the time of the investigation two former inmates had been engaging in unprotected sex with two HIV-negative women, against the advice of their counsellors. Existing evidence of HIV transmission among prisoners has persuaded prison authorities in few countries to implement effective prevention strategies for inmates. Confirmation of HIV infection from prison to the community may be more persuasive for authorities. Syringe exchange, methadone and bleach programs reduce the spread of HIV in community settings,16-18 and preliminary results from these programs in prison appear promising.19-21 The paucity of data confirming HIV transmission in prison should not be regarded as adequate justification for the lack of effective HIV prevention measures within prisons. There is already sufficient information on HIV transmission between prisoners to justify rapid implementation in correctional institutions of prevention measures shown to be effective in community settings. Improved methods of monitoring the spread of HIV within prisons and from inmates to community members following release are required urgently. Acknowledgements We are grateful to the NSW Department of Health for funding this study. We also wish to thank David Buchanan, Andrew Carr, Ying Chun Ge, David Cooper, Anthony Cunningham, Basil Donovan, John Dwyer, Tania Sorrell and Dominic Dwyer. Results of tracing 20 prison contacts of seven index cases for recruitment into the study. References Brewer TF, Vlahov D, Taylor E, et al. Transmission of HIV-1 within a statewide prison system. AIDS 1988; 2: 363-367. Taylor A, Goldberg D, Emslie J, et al. Outbreak of HIV infection in a Scottish prison. BMJ 1995; 310: 289-292. Dolan K. AIDS, drugs and risk behaviour in prison: state of the art. Int J Drug Policy 1997; 8: 5-17. Dolan K. Why is there conflicting evidence of HIV transmission in prison? In: O'Brien O, editor. Report of the 3rd European Conference on Drug and HIV/AIDS Services in Prison. London: Cranstoun Drug Services, 1997; 19-21. Gaughwin MD, Douglas RM, Wodak AD. Behind bars -- risk behaviours for HIV transmission in prisons, a review. In: Norberry J, Gerull SA, Gaughwin MD, editors. HIV/AIDS and prisons conference proceedings. Canberra: Australian Institute of Criminology, 1991; 89-107. Crofts N, Webb-Pullman J, Dolan K. An analysis of trends over time in social and behavioural factors related to the transmission of HIV among IDUs and prison inmates. Evaluation of the National HIV/AIDS Strategy. Technical Appendix 4. Canberra: AGPS, 1996. Richardson C, Ancelle-Park R, Papaevangelou G. Factors associated with HIV seropositivity in European injecting drug users. AIDS 1993; 7: 1485-1491. Granados A, Miranda MJ, Martin L. HIV seropositivity in Spanish prisons. Presented at the VIth International AIDS Conference, San Francisco. Abstract no Th. D.116, 1990. Crofts N, Stewart T, Hearne P, et al. Spread of blood-borne viruses among Australian prison entrants. BMJ 1995; 310: 285-288. Dolan K, Wodak A, Penny R. AIDS behind bars: preventing HIV spread among incarcerated drug injectors. AIDS 1995; 9: 825-832. Vlahov D, Brewer TF, Castro KG, et al. Prevalence of antibody to HIV-1 among entrants to US correctional facilities. JAMA 1991; 265: 1129-1132. Bird AG, Gore SM, Jolliffe DW, Burns SM. Anonymous HIV surveillance in Saughton Prison, Edinburgh. AIDS 1992; 6: 725-733. Dolan K, Wodak A, Hall W, et al. Risk behaviour of IDUs before, during and after imprisonment. Addict Res 1996; 4: 151-160. Dolan K, Wodak A, Hall W, Kaplan E. A mathematical model of HIV transmission in NSW prisons. Drug Alcohol Depend 1998; 50: 197-202. Dye S, Isaacs C. Intravenous drug misuse among prison inmates: implications for spread of HIV. BMJ 1991; 302: 1506. Feachem R. Valuing the past . . . investing in the future. Evaluation of the National HIV/AIDS Strategy. 1993-94 to 1995-96. Canberra: AGPS, 1996. Ward J, Mattick R, Hall W. Methadone maintenance treatment and other opioid replacement therapies. Amsterdam: Harwood Academic Publishers, 1998. Normand J, Vlahov D, Moses LE. Preventing HIV transmission: the role of sterile needles and bleach. Washington: National Academy Press, 1995. Nelles J, Harding T. Preventing HIV transmission in prison: a tale of medical disobedience and Swiss pragmatism. Lancet 1995; 346: 1507-1508. Dolan K, Wodak A, Hall W. Methadone maintenance treatment reduces heroin injection in NSW prisons. Drug Alcohol Rev 1998; 17: 153-158. Dolan K, Wodak A, Hall W. A bleach program for inmates in NSW: an HIV prevention strategy. Aust N Z J Public Health 1998; 22: 838-840. Authors' details National Drug and Alcohol Research Centre, University of New South Wales, Sydney, NSW. Kate A Dolan, BSc, PhD, Research Fellow. Alcohol and Drug Services, St Vincent's Hospital, Sydney, NSW. Alex Wodak, FRACP, FAFPHM, Director. Reprints: Dr K A Dolan, Research Fellow, National Drug and Alcohol Research Centre, University of New South Wales, Sydney, NSW 2052. Email: ndarc8@unsw.edu.au

Kate A Dolan · Alex Wodak

Research Women's role and satisfaction in the decision to have a caesarean section Deborah A Turnbull, Chris Wilkinson, Anisa Yaser, Vanessa Carty, John M Svigos and Jeffrey S Robinson MJA 1999; 170: 580-583 For editorial comment, see "de Costa" Rapid reader response (with authors' reply) added 28/6/99: see Chung Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Obstetrics & gynaecology and women's health Abstract Objective: To examine women's role in the decision to perform caesarean section (CS). Design: Cross-sectional survey. Written questionnaires were completed seven weeks after giving birth by CS. Setting: An obstetric tertiary referral hospital (Women's and Children's Hospital, Adelaide, South Australia), July to December 1996. Participants: A consecutive sample of women who underwent CS over a six-month period. To be eligible, women had to be at least 18 years old, able to complete a questionnaire in English and well enough to consent to study participation. Main outcome measures: Women's involvement in decision making, stated preference for CS, and satisfaction with obstetric care. Results: 278 women (76.4%) returned questionnaires: 171 women (61.5%; 95% confidence interval [CI], 55.8%-67.2%) reported being involved in the decision to have a CS. Factors influencing their decision were physical duress and partner's reaction during labour (emergency CS), considerations about recovery, planning for the event and pain (elective CS), and information from the doctor (both groups). Half the women "strongly agreed" that they were satisfied with the decision to have a CS, but 40.9% only "agreed" and 4.7% were "not sure". About 20% reported they needed more information on other options, and only 28.8% "strongly agreed" that they had been given good information to prepare for the possibility of CS. 27.9% of women (95% CI, 22.5%-33.2%) "agreed" or "strongly agreed" that they had "insisted on a CS" and 21.3% (95% CI, 16.4%-26.2%) that they had told the staff they were "keen to have a CS". Given the option of a vaginal delivery, 37.8% of women (95% CI, 22.5%-55.2%) with a breech presentation, and 34% of women (95% CI, 21.2%-48.8%) who had had a previous CS, chose a CS. Conclusions: It is of concern that over a third of women felt they had not been involved in the decision to have a CS; others were very positive about CS, but an appreciable proportion may not have received sufficient information. A broad-based strategy of providing more information to women and their partners could be one way of ensuring appropriate CS rates and should be tested in a randomised controlled trial. Introduction Despite national policy documents calling for a reduction in medical interventions in birth,1 Australia now has one of the highest caesarean section (CS) rates among First World countries.2 At the same time, it is recognised that the "ideal" or "correct" rate is difficult to derive,3 given the varying risk profiles of women attending different institutions. A range of strategies aimed at obstetricians4,5 have had limited success in reducing CS rates. The assumption is often made that the decision to perform a CS is made on clinical grounds only.6 The role of maternal request in decision-making has been raised,7 but so far studies from the woman's perspective have tended to use small samples with unique characteristics.8,9Our study examines the role of women in the decision to have a CS in an effort to identify an alternative approach to lowering the rates. Methods Setting The study was conducted at the Women's and Children's Hospital in Adelaide, South Australia. In 1996, this State had the highest CS rate of any State in Australia (23.1% v. national average of 19.5%).10 The Women's and Children's Hospital is a major obstetric tertiary referral centre for South Australia and much of the Northern Territory. In 1996, 23% (811/3536) of the women giving birth at the hospital were considered to have very high risk pregnancies and the CS rate for high risk pregnancies at the Women's and Children's Hospital was 43.9% (356/811).11 During that year, the overall CS rate was 25.4% (898/3536). Sample Over a six-month period (July to December 1996) questionnaires were sent to consecutive women who underwent CS. To be eligible for our study, the women had to be at least 18 years old, able to complete a questionnaire in English, and well enough to give consent to participate in the study (as decided by the senior midwife on the postnatal ward). We aimed to receive responses from about 288 women having a CS. This would provide a true population proportion of 60% (to within 5%) of women stating they had a say in the decision. To obtain this sample, we allowed for a non-eligibility, non-response rate of about 25% and thus sampled from a consecutive population of 375 women. Questionnaire The questionnaire was developed on the basis of a review of published reports, a review of existing questionnaires, and interviews with women, obstetricians, midwives and perinatal epidemiologists. It consisted of a combination of questions with forced-choice responses (mainly presented as a complete statement with a five-point response scale ranging from "strongly agree" to "strongly disagree"), open-ended questions and questions on demographic characteristics. (The questionnaire is available from the authors.) Procedure Ethical approval was obtained from the Hospital Ethics Committee, and, with the Committee's permission, a member of the research team (A Y), not involved in providing care, approached women on the postnatal ward between the second and fourth day and sought written consent for participation in the study. Questionnaires were sent to the participating women's homes seven weeks after the birth, to give women time to recover and to minimise biases such as the "halo" effect and social desirability (ie, the effect on respondents of the intensity of labour; and their tendency soon after the event to be uncritical of healthcare providers, particularly if they think their comments can be attributed to them).12 Follow-up of non-respondents included the mailing of a second questionnaire and a telephone call. A summary of the results was sent to participating women at the conclusion of the study. Data analysis The data were analysed using SPSS for Windows13 and Epi Info 6.14 We assessed whether variables such as age, language spoken at home, age left school, type of care, and type of CS distinguished between those who reported involvement in the decision and those who reported no involvement. Categorical data were analysed by χ2 tests. Point estimates and odds ratios are presented with 95% confidence intervals (CI). Results Sample Our sample consisted of 375 women having a CS over a six-month period. Of these, 11 (2.9%) women were not eligible, and 16 (4.3%) were "missed" by the researcher (mainly because they were discharged before contact). Thus, there was a defined sample of 364 women (taking the conservative view that all of the 16 missed women were in fact eligible and thus could be included in the sample). Completed questionnaires were obtained from 278 women (76.4% of our defined sample). The sample included women from a range of sociodemographic backgrounds receiving a diversity of care, including private obstetric care, hospital clinic care and different models of publicly funded midwifery care. About a third of the sample had an elective CS. Women's involvement in decision to have a caesarean section 171 women (61.5% of the study group; 95% CI, 55.8%-67.2%) reported that they were involved in the decision to have a CS. 81.4% (70/86) of those having an elective CS reported involvement in the decision, compared with 53.2% (100/188) of those having an emergency CS (odds ratio [OR] = 3.85; 95% CI, 2.01-7.47). Women cared for by a private obstetrician were less likely to report involvement in the decision (51.9%; 40/77) compared with women receiving other models of care (67.0%; 120/179) (OR, 0.53; 95% CI, 0.30-0.95). Reasons for the decision to have a caesarean section The 171 women who reported involvement in the decision were asked an open-ended question: "What led you to make the decision to have a CS?". A content analysis of the 164 responses to this question indicated that women framed their responses in terms of medical risks and benefits and not in terms of non-clinical personal issues. The questions with forced-choice responses gave women the opportunity to reveal that other factors were also important (Table 1). All women were very likely to have been influenced in their decision by information from their doctor. Women who had an elective CS were influenced by factors such as their recovery and the ability to plan. In contrast, women who had an emergency CS were influenced by the physical stress of labour ("I just couldn't go on any longer"), as well their partner's reaction in the labour ward. Other issues which distinguished the two groups were considerations about pain and previous negative experiences of childbirth: and in each of these about twice as many women with an elective CS agreed or strongly agreed that these issues had influenced their decision. In addition, about four times as many women with an elective CS reported that they had been influenced by family and friends during their pregnancy. Rejecting alternative options to caesarean section We examined women's responses to: Vaginal delivery after previous CS (women who had had one previous CS) Fifty of 209 women (23.9%) for whom these data were available reported one previous CS; 17 of these women (34.0%; 95% CI, 21.2%-48.8%) reported that their doctor talked to them about the possibility of having a vaginal delivery, but they did not subsequently try to have the baby vaginally. Vaginal breech delivery Of the total sample, 62 women (22.3%) reported that they had a breech presentation, and were asked "Did the doctor suggest that it would be possible to have the baby vaginally even though it was positioned bottom first?". In 14 of 37 women (37.8%; 95% CI, 22.5%-55.2%) with whom the doctor had discussed this option, the women reported "I decided against it". External cephalic version The women with a breech presentation were also asked "Did the doctor talk to you about the possibility of turning your baby while it was still in the womb?". In 12 of 39 women (30.8%; 95% CI, 17.0%-47.6%) with whom the doctor had discussed this option, the woman reported "I decided against it". Reporting preference for caesarean section "I insisted on a CS" Women having an emergency CS were less likely to agree with this statement. Demographic factors did not affect the response. Agreement: 27.9% of 269 women (95% CI, 22.5%-33.2%) (including 13.8% who strongly agreed); 18.8% of 181 women having emergency CS v. 46.4% of 84 women having elective CS (OR, 0.27; 95% CI, 0.15-0.49). "I told the staff at the very start that I was keen to have a CS" Women having an emergency CS were less likely to agree with this statement, and the only demographic factor affecting the response was educational level, with women in an intermediate category for education being more likely to agree. Agreement: 21.3% of 268 women (95% CI, 16.4%-26.2%) (including 11.6% who strongly agreed); 13.3% of 181 women having an emergency CS v. 38.5% of 83 women having an elective CS (OR, 0.24; 95% CI, 0.13-0.47), and 29.2% of 106 women in an intermediate education category v. 16% of 159 women in lower and higher education categories (χ2 = 6.31, df = 2, P = 0.04). "At the beginning of my pregnancy, I really wanted to have this baby vaginally" Agreement was not affected by demographic factors, but fewer women attending a private obstetrician agreed (non-significant difference), and fewer women having an elective CS agreed. Agreement: 64.6% of 274 women (95% CI, 58.9%-70.3%) (agreed or strongly agreed); 57.3% of 75 women in private obstetric care v. 68.0% of 178 women in other care (OR, 0.63; 95% CI, 0.35-1.15), and 52.4% of 84 women having elective CS v. 71.0% of 186 women having emergency CS (OR, 0.45; 95% CI, 0.26-0.79). Satisfaction Interpretation of the results for satisfaction is based on the assumption that women who answered anything other than "strongly agree" to positively worded items were not entirely satisfied or may have experienced problems with their care. This approach has been recommended in previous research15 and has been applied to other Australian studies examining satisfaction in childbirth.16 An appreciable number of women were only able to "agree" to such items or were "not sure" about their care (Table 2). For example, while half the women were satisfied with the decision to have a CS (as judged by indicating "strongly agree"), a further 40.9% only "agreed" and 4.7% were "not sure". Similarly, about a third and a half of women, respectively, were unable to "strongly agree" that they were "confident in the final decision" and "believe that caesarean section was the only alternative". More than two-thirds of women were unable to "strongly agree" that they had been "given good information to prepare for the possibility of a CS". Using the related assumption that we should pay attention to any level of affirmative responses (ie, "strongly agree", "agree", or "not sure") to negatively worded items, it can be seen that about 20% of women reported that they "needed more information on other options". Similarly, between about one in 10 and one in four women expressed some degree of dissatisfaction with the decision-making process. Discussion Over a third of the women in our study felt that they were not involved in the decision to have a CS, and an appreciable proportion expressed some degree of dissatisfaction with the decision, or may not have been given sufficient information. The strengths of our study include the good response rate and the fact that we used a hospital-based sample of women, including those with private health insurance. This is an important consideration given that about one-third of childbearing women are privately insured.10 The study also avoided some of the pitfalls of recently published research which relied on women giving feedback to the clinicians involved in their care.17 A shortcoming of our study was that it was conducted in only one hospital and may not be representative of women attending other Australian centres. For example, the average age of women in our study was 30 years, compared with a mean age for childbearing women in Australia of 28.6 years.10 The broader implications of the findings need to be considered, and should be the subject of further research. Clearly, there would be public health benefits in increasing the proportion of women who feel that they have been involved in the decision to have a CS, to avoid the possibility of psychological sequelae.18 While this may not be possible for the 50% of women who felt uninvolved in the decision to have an emergency CS, there may be scope for addressing the one in five women who felt uninvolved in the decision to have an elective CS. There are, of course, some absolute indications for CS (eg, major placenta praevia, massive placental abruption where the baby is still alive, transverse lie with shoulder presentation, and cord prolapse before full dilatation), and alternatives in these instances would not be discussed. These defined reasons may comprise up to 5%-8% of all births,19 and may account for a proportion of those who felt uninvolved in the decision-making process. Our study findings suggest that an informational package would be worth testing in a randomised controlled trial. This package should be broad based, rather than targeted to specific sociodemographic groups. In addition, it should be aimed not only at women, but also their partners, and families and friends. The package, which would include videos, posters and pamphlets, should address issues such as recovery after a CS and the risks and benefits of alternatives to CS. Evaluation of outcomes could be stratified for type of CS (elective or emergency), as it is possible that education would have a more substantial impact on elective CS rates, which appear to be influenced by non-clinical issues outside the labour ward experience. Any such intervention should aim to provide women with balanced information for making a truly informed choice. It is imperative that health messages are not framed in a way that makes women feel inadequate, or that they have failed in some aspect of their pregnancy. To this end, any evaluation of interventions should include outcome data examining not only intervention rates and associated morbidity, but also looking at psychosocial outcomes, such as maternal well-being and satisfaction. The need for information is well recognised in countries such as Britain, where there has been a major drive to develop evidence-based information pamphlets for pregnant women on issues such as ultrasound scans.20 This is not to suggest that information alone will address the high rates of CS,21 which relate to a multiplicity of factors. However, this strategy may help to create a different clinical climate and would at least partially meet the needs of the almost one in five women who agreed that they needed (or were unsure whether they needed) more information on other options. Acknowledgements We wish to thank the women who participated in the study. We would also like to thank the obstetricians and the postnatal ward midwives of the Women's and Children's Hospital for their support. This study was funded by a grant from the Women's and Children's Hospital Foundation and was supported by the Department of Public Health, University of Adelaide. Dr Yaser's position was funded by the Commonwealth Government Jobskills Participation Scheme. References Commonwealth Department of Health, Housing and Community Services. Goals and targets for Australia's health in the year 2000 and beyond. Canberra: AGPS, 1993. National Health and Medical Research Council. Options for effective care in childbirth. Canberra: AGPS, 1996. What is the right number of caesarean sections [editorial]? Lancet 1997; 349: 815. Wilkinson C, McIlwaine G, Boulton-Jones C, Cole S. Is a rising caesarean section rate inevitable? Br J Obstet Gynaecol 1998; 105: 45-52. Molloy D, Richardson P. Caesarean section -- public versus private. Why the differential? A reply to "Obstetric intervention and the economic imperative". Br J Obstet Gynaecol 1993; 101: 88-90. Spurrett B, Cook CM. Why we choose caesarean section: a prospective study. Aust N Z J Obstet Gynaecol 1997; 37: 297-300. Controversies in management. Should doctors perform an elective caesarean on request? BMJ 1998; 317: 462-465. Shepherd McCC. Patent decision making: the case of delivery method after a previous caesarean section. Culture Med Soc 1987; 11: 495-508. Ryding EL. Investigation of 33 women who demand a caesarean section for personal reasons. Acta Obstet Gynaecol Scand 1993; 72: 280-285. Day P, Sullivan EA, Lancaster P. Australia's mothers and babies 1996. Sydney: Australian Institute of Health and Welfare National Perinatal Statistics Unit, 1999. (Perinatal Statistics Series No. 7.) Computerised Maternity Database. Adelaide: Women's and Children's Hospital, Clinical Information Services Database, 1998. Lumley J. Assessing satisfaction with childbirth. Birth 1985; 12 (3): 141-145. SPSS (Statistical package for the social sciences) [computer program], standard version. Chicago, Ill: SPSS Inc, 1997. Epi Info (Word processing, database and statistical program for public health) [computer program], version 6.03. Atlanta, Ga: Centers for Disease Control and Prevention, 1996. Carey RG, Posavac EJ. Using patient information to identify areas for service improvement. Health Care Manage Rev 1982; 7(2): 43-48. Brown S, Lumley J. Satisfaction with care in labour and birth. A survey of 790 Australian women. Birth 1994; 21(1): 4-13. Mould TA, Chong S, Spencer JAD, Gallivan S. Women's involvement with the decision preceding their caesarean section and their degree of satisfaction. Br J Obstet Gynaecol 1996; 103: 1074-1077. Astbury J, Brown S, Lumley J, Small R. Birth events, birth experiences and social differences in postnatal depression. Aust J Public Health 1994; 18: 176-184. Francome C, Savage W. Caesarean section in Britain and the United States -- 12% or 24%: is either the right rate? Soc Sci Med 1993; 37: 1199-218. Oliver S, Rajan L, Turner H, et al. Informed choice for users of health services: views of ultrasonography leaflets on women in early pregnancy, midwives, and ultrasonographers. BMJ 1996; 313: 1251-1253. Fraser W, Maunsell E, Hodnett E, Moutquin J. Randomised controlled trial of a prenatal vaginal birth after cesarean education and support programme. Am J Obstet Gynecol 1997; 176: 419-425. (Received 21 Sep 1998, accepted 30 Apr 1999) Authors' details University of Adelaide, Adelaide, SA. Deborah A Turnbull, MPsych(Clin), PhD, Senior Lecturer in Public Health (Epidemiology), Department of General Practice; Anisa Yaser, MB BS, Research Officer, Department of Public Health; Vanessa Carty, MPsych, Research Student, Department of Public Health; Jeffrey S Robinson, FRCOG, FRACOG, Professor, and Head, Department of Obstetrics and Gynaecology. Department of Perinatal Medicine, Women's and Children's Hospital, Adelaide, SA. Chris Wilkinson, MPH, FRACOG, Staff Specialist Obstetrician Gynaecologist. John M Svigos, FRCOG, FRACOG, Senior Visiting Medical Officer. Reprints will not be available from the authors. Correspondence: Dr D A Turnbull, Department of General Practice, University of Adelaide, SA 5005. Email: dturnbull@medicine.adelaide.edu.au 1: Reasons women give for deciding to have a caesarean section (CS)* Elective Emergency†OR (95% CI)Information from doctor 75.7% (53/70)77.4% (79/102)0.91 (0.42-1.98)Considerations about recovery60.0% (42/70)36.3% (37/102)2.64 (1.35-5.18)Partner's attitude in general44.3% (31/70)35.3% (36/102)1.46 (0.75-2.85)Couldn't go on any longer21.2% (14/66)44.5% (45/101)0.34 (0.15-0.72)Could plan what was going to happen38.6% (27/70)16.0% (16/100)3.30 (1.52-7.22)Considerations about pain30.4% (21/69)15.7% (16/102)2.35 (1.06-5.26)Previous pregnancy/labour awful26.5% (18/68) 12.0% (12/100)2.64 (1.10-6.41)Partner's reaction in the labour room8.8% (6/68)23.8% (24/101)0.31 (0.10-0.85)Influence of family/friends during pregnancy15.7% (11/70)3.9% (4/102)4.57 (1.27-20.39)Felt too old4.5% (3/67)2.0% (2/102)2.34 (0.26-28.63)Previous infertility4.3% (3/69)2.0% (2/101) 2.25 (0.25-27.48)Medical risks/benefits not that important21.4% (15/70)27.0% (27/100) 0.74 (0.34-1.61)*Missing data are excluded. †Some totals exceed 100 (= number of women with emergency CS who indicated that they were involved in the decision-making process), because two additional women answered some of these questions, but denied involvement in the decision. Back to text 2: Women's satisfaction with decision to have a caesarean section (CS)*StronglyNotStronglyItemagreeAgreesureDisagreedisagreeSatisfaction with the decision itselfSatisfied with the decision (n = 274)50.4%40.9%4.7%2.9%1.1%Confident in the final decision (n = 276)62.3%31.2%2.9%2.9%0.7%Believe that a CS was the only alternative (n = 276)53.3%26.8%12.3%5.4%2.2%Now feel a bit cheated (n = 274)5.1%10.9%9.1%28.5%46.4%Believe that CS may not have been necessary (n = 275)2.2%2.5%14.2%31.3%49.8%Satisfaction with information provisionGiven good information about why CS was necessary (n = 275)58.2%33.1%4.7%3.3%0.7%Needed more information on otheroptions (n = 272)2.9%4.4%11.8%48.5%32.4%Given good information to prepare for possibility of CS (n = 274)28.8%40.1%10.2%12.8%8.0%Satisfaction with decision-making processFelt pressured to try to have the baby vaginally (n = 272)4.0%7.4%5.1%34.9%48.5%Unhappy about the amount of say in the decision (n = 275)5.5%6.5%5.8%45.1%37.1%Took too long to make decision (n = 274)7.7%9.9%8.4%38.7%35.4%Felt pressured by staff to have a CS (n = 272)1.8%3.3%3.3%36.8%54.8%* Missing data are excluded. Back to text Reader response to: Women's role and satisfaction in the decision to have a caesarean section I commend the authors for this paper. However I wonder if the contention that unless the respondents "strongly agree" or "strongly disagree", the response is mixed is debatable. Patient satisfaction is multidimensional and to focus on patient's response to assess whether for example the information given has been adequate may be unnecessarily harsh on the care givers. Almost all major decisions are accompanied by a degree of regret and doubt by a proportion of people. To infer, unless the patient is entirely satisfied with something, that the care given was somehow less than satisfactory is to demand too much of a complex human relationship, that of a technically dependent patient and a care giver. I note that only 61.5% felt that they were involved in the decision to have a caesarean section, and only 81.4% in the elective cases where presumably there was ample time to ask for further information. I presume that they had in fact legally consented to the decision. What would have been interesting is a personality study on all the respondents. It may be that information are not the issue but the inherent psychological characteristics of the study subjects. Information packs may be useful but the decision to consent to a caesarean section rests with the woman alone. Packs aimed at her partner, family and friends may do more harm than good where there are conflicting opinions. One only has to look at the diverse response in this study itself to confidently predict that there will be such conflict amongst any group and an already potentially emotional decision may be further complicated. Tony Chung Associate Professor Department of Obstetrics & Gynaecology The Prince of Wales Hospital Shatin, NT Hong Kong SAR, China Submitted by email 24/6/99, posted online with author response 28/6/99. Reply by the authors We would like to thank Dr Chung for his thoughtful reply to our paper. The use of 'strongly agree' and 'strongly disagree' as markers of satisfaction has a precedence in the literature on satisfaction with hospital care.1 Importantly, it has been used in relation to maternity service provision.2 Although this approach may seem unnecessarily critical, it avoids over-simplistic interpretations, as demonstrated in a British report into this issue which concluded (after using disputed methodology) that attempts to reduce caeasrean section rates may be futile, because of women's preferences.3-5 Dr Chung's second point relates to the issue of legal consent. In contrast, our paper examines participation in decision making, for which the signing of informed consent is only one part of a broader process. The paper does not intend to infer that the requirements for informed consent for a procedure have been neglected. The point about measuring women's personalities is an interesting one. There is research which finds increased psychological morbidity in women demanding caesarean section in the absolute absence of clinical indications.6 In contrast to this somewhat rare individual,6 our study examines a cross-section representing about one quarter of the women at the study hospital. Dr Chung's point implies that the problem rests with these women. This seems an unreasonable assumption to make of such a large proportion of childbearing women. It is imperative that we avoid 'blaming' the women. Finally Dr Chung is concerned that the provision of information to the broader community may lead to conflict. Our research suggests that there is already an involvement of family and friends in the decision making process. It is for this very reason that we hypothesize that providing evidenced based information may lead to a more beneficial outcome. To this end any randomized controlled trial evaluating such a strategy should include not only clinical outcomes but also psychosocial variables such as anxiety, feelings of failure and reassurance. Deborah Turnbull Chris Wilkinson Submitted by email 28/6/99, posted online 28/6/99. 1. Carey RG, Posavac EJ. Using patient information to identify areas for service improvement. Health Care Manage Rev 1982; 7(2): 43-48. 2. Brown S, Lumley J. Satisfaction with care in labour and birth. A survey of 790 Australian women. Birth 1994; 21(1): 4-13. 3. Mould TA, Chong S, Spencer JAD, Gallivan S. Women's involvement with the decision preceding their caesarean section and their degree of involvement. Br J Obstet Gynaecol 1996; 103: 1074-1077. 4. Grant JM, Women are satisfied with caesarean section [editorial; comment]. Br J Obstet Gynaecol 1996; 103 (11): 7-8. 5. Hemminki E. Cesarean Sections: Women's choice at giving birth? Birth 1997; 24: 124-125. 6. Ryding EL. Investigation of 33 women who demanded a cesarean section for personal reasons. Acta Obstet Gynecol Scand 1993; 72: 280-285. Back to top of article Back to reader response

Deborah A Turnbull · Chris Wilkinson · Anisa Yaser · Vanessa Carty · John M Svigos · Jeffrey S Robinson

Research Why do preterm infants die in the 1990s? Lex W Doyle, Sheryle Rogerson, Shu-Ling Chuang, Matthew James, Ellen D Bowman and Peter G Davis MJA 1999; 170: 528-532 Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - Articles on similar material Abstract Objectives: To describe the mortality rate for preterm infants (born 23-36 completed weeks' gestational age) and to determine the causes of death, focusing on avoidable causes. Design and setting: Prospective cohort study of preterm infants born at Royal Women's Hospital, Melbourne (a tertiary referral hospital with a neonatal intensive care unit and a special care nursery) from January 1994 to December 1996. Subjects: 2475 consecutive liveborn infants with gestational ages from 23 to 36 weeks. Main outcome measures: Mortality rate during the primary hospitalisation, and causes of death. Results: The total mortality rate was 4.8% (118/2475). The mortality rate declined with increasing maturity. The decrease in mortality was rapid between 23 and 28 weeks' gestational age, from 64.5% at 23 weeks to 4.0% at 28 weeks, then slower, falling to 0.4% at 36 weeks. Fifty of the 118 infants who died had lethal congenital anomalies. Lethal anomalies accounted for three-quarters of deaths in infants aged 28-36 weeks. The mortality rate in infants free of lethal anomalies was 2.8% (68/2425) and only 0.2% (4/1759) for infants aged 32-36 weeks. In the 68 infants without lethal anomalies who died, few obvious preventable causes were identified. Conclusions: Mortality rates fell rapidly between 23 and 28 weeks' gestational age. Survival rates for preterm infants born after 31 weeks' gestational age approached the survival rates of term infants. Lethal congenital anomalies were the most common cause of death; preventable causes of death were rare. Introduction The survival rate for very preterm infants (born at 23-27 weeks' gestational age) has improved dramatically with advances in perinatal care,1 particularly efforts to reduce neonatal respiratory distress syndrome (hyaline membrane disease), such as administering corticosteroids to the mother before delivery,2 administering exogenous surfactant to preterm infants,3 and assisted ventilation.4 However, mortality rates and causes of death for more mature but still preterm infants (28-36 weeks' gestational age) have received little attention, especially since the advent of exogenous surfactant in Australia in 1991. As hyaline membrane disease has diminished as a cause of death of preterm infants, other causes of death, some of which may be preventable, have assumed more prominence. The aim of this study of preterm infants 23-36 weeks' gestational age born in 1994-1996 in a hospital with neonatal intensive care facilities was to describe the variation with gestational age in the mortality rate and the causes of death, focusing on avoidable causes. Methods Setting This was a prospective cohort study of consecutive livebirths between 23 and 36 completed weeks of gestational age in the Royal Women's Hospital, Melbourne, over the three years from 1 January 1994 to 31 December 1996. Data collection Data have been collected prospectively since 1977 on all infants admitted to the neonatal intensive care unit (NICU), all infants of birthweight below 1500 g, and all infants below 32 weeks' gestational age, whether admitted to the NICU or not. Data on infants 32 to 36 weeks were collected from the special care nursery (SCN) admissions book, and the hospital's main computer database was checked to obtain data on those not admitted to either the NICU or SCN. Data collected included gestational age, birthweight, and mortality during the primary hospitalisation, whether during the neonatal period (first 28 days after birth) or later. Data were included for infants transferred from our hospital to another. Gestational age in completed weeks was assigned according to the first antenatal ultrasound scan, or maternal dates if no ultrasound report was available. Birthweight ratio was calculated by dividing the infant's birthweight by the expected gender-specific median birthweight for that gestational age.5 Causes of death For infants who died, the major causes of death were determined after the regular monthly clinicopathological conference at which the deaths of all livebirths within the hospital were discussed, and which was chaired by one of the authors ( LW D), who retained all records from the meeting. Causes of death included lethal congenital anomalies, complications of prematurity, perinatal asphyxia, or sepsis (Box 1). Preventable causes of death For each infant who died, avoidable factors included whether antenatal corticosteroids or surfactant had been given to infants who died from respiratory causes, whether intramuscular vitamin K had been given to those who died from pulmonary haemorrhage, whether appropriate anti-infective therapies were given to those who died from infection, and whether antenatal corticosteroids had been given to those who died from cerebroventricular haemorrhage or cystic periventricular leukomalacia. Data analysis Mortality data for preterm births at the Royal Women's Hospital were compared with published data for livebirths in Victoria in 1994,7 1995,8 and 1996,9 and for admissions to neonatal intensive care units in Australia and New Zealand in 1994.10Data were edited and analysed with SPSS for Windows.11 Dichotomous variables were contrasted by 2 analysis, and continuous variables were compared by Mann-Whitney U test,12 as most data were skewed. Results Causes of death There were 2475 infants of 23-36 weeks' gestational age born during the study period, of whom 118 died (4.8%). The mortality rate diminished rapidly between 23 and 28 weeks' gestational age (from 64.5% at 23 weeks to 4.0% at 28 weeks), then more slowly, to reach 0.4% at 36 weeks (Box 2). The autopsy rate in the infants who died was 51.8% (59/114), with no data on autopsies for four infants who died after transfer to other hospitals. Fifty infants died of lethal anomalies, all but two within 28 days of birth (Box 3). Lethal anomalies accounted for 11 of 67 deaths (16.4%) in infants born at 23-27 weeks' gestational age, 16 of 24 deaths (66.7%) in infants born at 28-31 weeks' gestational age, and 23 of 27 deaths (85.2%) in those born at 32-36 weeks' gestational age. Sixty-eight infants died who were without lethal anomalies: 2.8% of the 2425 livebirths, but only 0.2% of infants of 32-36 weeks' gestational age (4/1759) (Box 4). Sixty-one died within 28 days of birth and seven (10.3%) died later during the primary hospitalisation. In the Australian and New Zealand Neonatal Network, 35 of 256 deaths (13.7%) of infants of less than 32 weeks' gestational age without lethal anomalies died during the primary hospitalisation but after 28 days of age.10 Preventable causes of death Respiratory problems: The mothers of 23 of the 30 infants who died from HMD or BPD had received antenatal corticosteroids. In the remaining seven cases, the gestational ages were 23 or 24 weeks. In six cases there was not enough time to give corticosteroids, five mothers presenting in advanced preterm labour and one with eclampsia. In the seventh case, the gestational age was 23 weeks and before birth the infant was considered incapable of surviving, yet was given full intensive care postnatally. All 30 infants who died from HMD or BPD received exogenous surfactant after birth. The one infant who died from pulmonary haemorrhage without HMD received antenatal corticosteroids and did not have respiratory distress after birth and therefore did not re- ceive exogenous surfactant; the fatal pulmonary haemorrhage occurred at three days of age. The two infants who had HMD and pulmonary haemorrhage also received antenatal corticosteroids. All three infants who died from pulmonary haemorrhage had received intramuscular vitamin K at birth. None had clinical signs of heart failure or a patent ductus arteriosus before the haemorrhage. None had clinical indications for an echocardiogram, hence subclinical cardiac dysfunction cannot be excluded. Considering the 12 infants in the gestational age range 28-36 weeks who died without lethal anomalies, six died from sepsis, two from asphyxia, two from BPD, one from pulmonary haemorrhage, and one from SIDS. None died acutely from HMD. Infections: In the 22 infants who died from sepsis without NEC, there were only two in whom the management might have been different. In one infant of 30 weeks' gestational age the mother ignored the antenatal signs of sepsis for several days before presenting to hospital and delivering a moribund infant who died at 11 hours of age from E. coli pneumonia, despite full treatment, including appropriate antibiotics. In the other infant, of 33 weeks' gestation, who died of herpes simplex, the clinical presentation was that of sepsis several days before death, but, in the absence of other features of herpes in the mother or infant, no antiviral therapy was given. CVH and CPVL: Antenatal corticosteroids were given to the mothers of all nine infants in whom CVH or CPVL were major contributing causes of death. In addition to the five infants in whom CVH was a major cause of death, another 12 infants who died had a grade 3 or 4 CVH that was thought not to contribute substantially to their deaths. Comparison with regional outcomes The neonatal survival rate for infants of 24-31 weeks' gestational age at our hospital was similar to that reported in regional data from Victoria for the same three years7-9 (Box 5). In livebirths of less than 2500 g birthweight in Victoria in 1994-1996, 377 infants died within 28 days; 33.4% with lethal anomalies (compared with 44.0% in our hospital cohort; 2 = 3.7, not significant) and 5.6% died from infections (compared with 24.8% in our hospital; 2 = 32.9, P < 0.0001). The neonatal mortality rate in livebirths free of lethal malformations with birthweights greater than 2499 g was 0.45 per 1000 (81/178834) in Victoria in 1994-1996,7-9 compared with 2.27 per 1000 (4/1735) in infants of 32-36 weeks' gestational age in our hospital. The survival rate to hospital discharge in 1994 for infants free of lethal malformations cared for in neonatal nurseries at 23-31 weeks' gestational age was higher in our hospital than in reported data from the Australian and New Zealand Neonatal Network (Box 6). Discussion Comparing our data with regional data in Australia is difficult. States and territories provide data to the Australian Institute of Health and Welfare (AIHW), which then produces an annual report.13 However, the denominator in the AIHW report is predominantly determined by birthweight; gestational age is reported for confinements (ie, mothers), or for births, but not for all livebirths. Regional reports from Victoria provide data for births, including stillbirths and livebirths, by gestational age, but in two-week intervals, and only up to 31 weeks' gestational age.7-9 Moreover, the numerator in both of these regional data sets is usually limited to the neonatal period, rather than the primary hospitalisation. The Australian and New Zealand Neonatal Network collects data from all the Australian and New Zealand Neonatal Intensive Care Units.10 In this data set, the denominator is limited to admissions to neonatal units, eliminating livebirths who die outside the neonatal unit, and hence augmenting the reported survival rates. Moreover, this data set is limited to infants up to 31 weeks' gestation and excludes those with lethal malformations. The numerator, however, includes deaths in the neonatal period and those beyond 28 days of age that occur during the primary hospitalisation. Comparing data on cause of death is also difficult. Most government data collection sources, such as those in Victoria7-9 and other States, rely on confidential reports. They may not obtain enough data to classify the cause of death, and rarely can they confirm the gestational age. The final report includes an individual infant under only one cause of death, even though there may be several equally contributing causes of death, such as the common combination of HMD and airleak, which caused 25% of deaths from non-lethal causes in our study. Our system of clinicopathological conferences for each death, although not perfect, provided more detailed information about causes of death. As regional data sources do not provide complete data on deaths during the primary hospitalisation at all gestational ages, we cannot compare survival rates for preterm infants (32-36 weeks) with those of term infants (37-42 weeks). However, we have calculated rates of neonatal survival in Victoria for livebirths free of lethal malformations with birthweight greater than 2499 g, assuming that the results would be similar for infants of 37-42 weeks' gestation. In our hospital, the neonatal survival rate for infants of 32-36 weeks' gestational age (99.77%) approached the neonatal survival rate expected of term infants in Victoria (99.95%). The commonest causes of death were lethal anomalies, sepsis, and HMD. Deaths from lethal anomalies are over-represented in our hospital compared with Victoria as a whole as most have been diagnosed antenatally, and, in many cases, the mother has been transferred before birth from another hospital for management because of the fetal anomaly. The death rate from infection is higher in our hospital than for Victoria, but this is probably because infants in our hospital live longer, and hence acquire infections, rather than dying soon after birth from other problems related to prematurity. E. coli and Group B streptococci remain the chief cause of septic deaths, particularly soon after birth, consistent with the observations of Isaacs et al.14 Staphylococcus species are an increasingly frequent cause of late infections,15 and of late deaths in our study. HMD remains a leading cause of death for very preterm infants despite the fact that most mothers receive antenatal corticosteroid therapy and all infants receive exogenous surfactant. Improvements in exogenous surfactant offer hope of reducing mortality further, but other antenatal interventions, such as thyrotropin stimulating hormone,16 have been disappointing in large randomised controlled trials. HMD did not cause any deaths in our hospital in more mature preterm infants (28-36 weeks). Within the infants who died from HMD, the observation that those who also had an airleak were not as growth restricted as those who had no airleak might reflect some structural change within the lung or with use of pulmonary surfactant that is associated with growth restriction. The problem of extreme intrauterine growth restriction is highlighted by the deaths from pulmonary haemorrhage in three infants, all with birthweight ratios below 0.55. The pulmonary haemorrhage was not caused by failure to give intramuscular vitamin K at birth.17 The mechanism for fatal pulmonary haemorrhage is unclear, but may represent acute left heart failure, contributed to by a patent ductus arteriosus. The association of pulmonary haemorrhage and fetal growth restriction is well known and may be related to histological changes in the ductus arteriosus in growth-restricted fetuses.18 Pulmonary haemorrhage is also seen more frequently with exogenous surfactant therapy,19 which was given to two of the three infants in our study who died of pulmonary haemorrhage. Preventing prematurity, an obvious solution to the problem of higher death rates in preterm infants, remains an elusive goal. In all infants who died, few obvious preventable factors, apart from avoiding preterm birth, were evident. The Annual Report from the Victorian Consultative Council on Obstetric and Paediatric Mortality and Morbidity consistently identifies more avoidable factors in stillbirths than neonatal deaths.7-9 In summary, mortality rates fell sharply between 23 and 28 weeks' gestational age, and few infants of more than 28 weeks' gestational age without lethal anomalies died. Survival rates for preterm infants of more than 31 weeks' gestational age approached the survival rates expected of term infants. There were few obvious avoidable factors in the deaths of any of the infants who died, either in the very preterm infants of 23-27 weeks' gestational age, or the more numerous preterm infants of 28-36 weeks' gestational age. References The Victorian Infant Collaborative Study Group. Outcome at 2 years of children 23-27 weeks' gestation born in Victoria in 1991-92. J Paediatr Child Health 1997; 33: 161-165. Crowley P. Corticosteroids before preterm delivery (Cochrane Review). In: The Cochrane Library, Issue 2. Oxford: Update Software, 1998. [Updated quarterly.] Soll RF. Natural surfactant extract vs synthetic surfactant in the treatment of established respiratory distress syndrome (Cochrane Review). In: The Cochrane Library, Issue 2. Oxford: Update Software, 1998. [Updated quarterly.] Doyle LW, Davis P, Dharmalingam A, Bowman E. Assisted ventilation and survival of extremely low birthweight infants. J Paediatr Child Health 1996; 32:138-142. Beeby PJ, Bhutap (sic) T, Taylor LK. New South Wales population-based birthweight percentile charts. J Paediatr Child Health 1996; 32: 512-518. Northway WH Jr, Rosan RC, Porter DY. Pulmonary disease following respirator therapy of hyaline- membrane disease: bronchopulmonary dysplasia. N Engl J Med 1967; 276: 357-368. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Annual report for the year 1994. Melbourne: Department of Human Services, 1995. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Annual Report for the Year 1995: Incorporating the 34th Survey of Perinatal Deaths in Victoria. Melbourne: Department of Human Services, 1996. <http://hna.ffh.vic.gov.au/phb/hce/peri/ob95/index.htm> Accessed 11 May 1999. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Annual report for the year 1996. Melbourne: Department of Human Services, 1997. <http://hna.ffh.vic.gov.au/phb/hce/peri/rep_96/contents.htm> Accessed 11 May 1999. Donoghue DA. Australian and New Zealand Neonatal Network, 1994. Sydney: AIHW National Perinatal Statistics Unit, 1996. [Neonatal Network Series no. 1.] SPSS for Windows version 6.1 [computer program]. Chicago: SPSS Inc, 1994. Moses LE, Emerson JD, Hosseini H. Analyzing data from ordered categories. N Engl J Med 1984; 311: 442-448. Lancaster P, Huang J, Lin M. Australia's mothers and babies 1993. Sydney: AIHW National Perinatal Statistics Unit, 1996. [Perinatal Statistics Series No. 3.] Isaacs D, Barfield C, Clothier T, et al. Early-onset group B streptococcal infections in Aboriginal and non- Aboriginal infants. Med J Aust 1995; 163: 302-306. Isaacs D, Barfield C, Clothier T, et al. Late-onset infections of infants in neonatal units. J Paediatr Child Health 1996; 32:158-161. Actobat Study Group. Australian collaborative trial of antenatal thyrotropin-releasing hormone (ACTOBAT) for prevention of neonatal respiratory disease. Lancet 1995; 345: 877-882. Loughnan PM, McDougall PN, Balvin H, et al. Late onset haemorrhagic disease in premature infants who received intravenous vitamin K1. J Paediatr Child Health 1996; 32: 268-269. Ibara S, Tokunaga M, Ikenoue T, et al. Histologic observation of the ductus arteriosus in premature infants with intrauterine growth retardation. J Perinatol 1994; 14: 411-416. Raju TN, Langenberg P. Pulmonary hemorrhage and exogenous surfactant therapy: a metaanalysis. J Pediatr 1996; 123: 603-610. (Received 29 Jun 1998, accepted 25 Mar 1999) Authors' details Division of Paediatrics, The Royal Women's Hospital, Melbourne, VIC. Lex W Doyle, MD, MSc, FRACP, Paediatrician, and Associate Professor, Department of Obstetrics and Gynaecology, University of Melbourne; Sheryle Rogerson, MB BS, Paediatric Fellow; Shu-Ling Chuang, MB BCh, MRCP, Paediatric Fellow; Matthew James, MB ChB, MRCP, Paediatric Fellow; Ellen D Bowman, MB BS, FRACP, Paediatrician; Peter G Davis, MD, BS, FRACP, Paediatrician. Reprints will not be available from the authors. Correspondence: Associate Professor Lex Doyle, Department of Obstetrics and Gynaecology, University of Melbourne, Parkville, VIC 3052. Email: l.doyle@obgyn-rwh.unimelb.edu.au ©MJA 1999 Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1999 Medical Journal of Australia. 1: Causes of death defined Lethal congenital anomalies: Any infants with major malformations that were considered untreatable or who died despite attempts at surgical correction, and infants with untreatable inborn errors of metabolism, chromosomal abnormalities, or overwhelming congenital infection acquired early in pregnancy. Complications of prematurity: Hyaline membrane disease (HMD), with or without an airleak: clinical signs of respiratory distress in the first days after birth, supported by radiological and/or autopsy evidence. Airleak comprised any air not confined to normal airspaces, such as pulmonary interstitial emphysema or pneumothorax. Bronchopulmonary dysplasia (BPD): respiratory distress beyond four weeks of age requiring oxygen therapy, and radiographic changes typical of bronchopulmonary dysplasia,6 or a pathological diagnosis of bronchopulmonary dysplasia at autopsy. Necrotising enterocolitis (NEC): confirmed by definite radiological, operative, or autopsy evidence. Cerebroventricular haemorrhage (CVH): included any evidence of haemorrhage of any degree identified by ultrasound examination or autopsy. Cerebroventricular haemorrhage was considered a substantial contributor to death when knowledge of an intracerebral haemorrhage (grade 4) led to withdrawal of intensive care and the infant subsequently died. Cystic periventricular leukomalacia (CPVL): included any cystic degeneration within the cerebral cortex. Cystic periventricular leukomalacia was considered the cause of death when it was severe enough to lead to the withdrawal of intensive care. Ultrasound scanning was routine within the first three days after birth, at the end of the first week, then monthly until discharge as a minimum. Pulmonary haemorrhage was diagnosed in infants with frothy, blood-stained tracheal fluid and clinical deterioration in respiratory function, or at autopsy. Perinatal asphyxia: Infants who were liveborn but failed to respond adequately to resuscitation at birth. Neonatal sepsis: Infants who died with clinical signs of sepsis supported by positive blood or cerebrospinal fluid (CSF) culture, but also included the occasional infant in whom sepsis was considered likely, but in whom blood or CSF cultures were sterile because of prior treatment with antibiotics, most commonly via the mother before birth. Pneumonia was diagnosed in infants with respiratory distress, signs of sepsis and a chest x-ray consistent with pneumonia, or at autopsy. Back to textBack to textBack to text 4: Causes of death in 68 preterm infants without lethal anomalies born at Royal Women's Hospital, Melbourne, January 1994-December 1996Median gestationalMedianMajorNumberage in weeksbirthweightcause*(%)(range)(range)Not offered intensive care7 (10.3%)23 (23-23)580 (545-725)Perinatal asphyxia5 (7.6%)26 (24-28.5)725 (630-1322)Sepsis27 (39.7%)25 (23-26)751 (606-896)NEC5 (7.4%)24 (23-29.5)756 (610-916)HMD23 (33.8%)24 (23-26)600 (522-750)HMD with airleak17 (25.0%)24 (23-25.5)670 (561-853)HMD without airleak6 (8.8%)25.5 (23-27) 509 (371-582)BPD7 (10.3%)26 (24-28)711 (640-751)CPVL4 (5.9%)25 (24-27)765 (568-858)Pulmonary haemorrhage3 (4.4%)27 (27-30)¶390 (315-756)¶Other**5 (7.4%)Total6825 (23-27)721 (590-856)MedianMedian days ofMajorbirthweight ratioage at deathcause*(range)(range)Not offered intensive care1.03 (0.94-1.23)1 (1-1)Perinatal asphyxia0.96 (0.83-1.13)1 (1-1)Sepsis1.00 (0.90-1.09)8 (1-15)NEC1.02 (0.68-1.16)14 (10-22.5)HMD0.92 (0.82-1.07)2 (1-4)HMD with airleak0.99 (0.89-1.13)2 (1-3.5)HMD without airleak0.66 (0.36-0.92)1.5 (1-5)BPH0.80 (0.66-0.92)38 (19-141)CPVL0.82 (0.76-1.13)49 (22-55)Pulmonary haemorrhage0.37 (0.30-0.54)¶5 (3-5)¶Other**Total0.95 (0.82-1.07)* Some infants had more than one major cause of death. Range = interquartile range. BPD = bronchopulmonary dysplasia Includes five infants who died with NEC. Six also had HMD, two had both HMD and CVH, and two had CVH. CPVL = cystic periventricular leukomalacia Three infants also had CVH and two had pulmonary haemorrhage. CVH = cerebroventricular haemorrhage¶ Range = complete range. HMD = Hyaline membrane disease** Two with cardiomyopathy following twin-twin transfusion syndrome, one spontaneous gut perforation, one neuroblastoma, one sudden infant death syndrome. NEC = necrotising enterocolitisInfants not offered intensive care were significantly less mature than those who died after intensive care (median gestational age 23, interquartile range 23-23 v. median gestational age 25, interquartile range 24-27; z = 3.0, P < 0.01). Excluding those with lethal anomalies and those not offered intensive care, children dying with HMD were less mature than those dying without HMD (median gestational age 24, interquartile range 23-26 v. median gestational age 26, interquartile range 24-28; z = 2.9, P < 0.01) and lighter at birth (median birthweight 600 g, interquartile range 522-750 g v. median birthweight 758 g, interquartile range 683-888 g; z = 3.0, P < 0.01), but had similar birthweight ratios (median 0.92, interquartile range 0.82-1.07 v. median 0.96, interquartile range 0.81-1.05, not significant). Within the group of infants who died of HMD, those who also had airleak were not significantly different in maturity, but were significantly heavier (z = 2.7, P < 0.01) and had higher birthweight ratios (z = 2.5, P < 0.02). The three infants who died of pulmonary haemorrhage were particularly growth restricted, with birthweight ratios of 0.30, 0.37, and 0.54, respectively; their median birthweight ratio of 0.37 was substantially below that of the infants who died of other causes (median birthweight ratio 0.96, interquartile range 0.85-1.07; z = 2.8, P < 0.01). Most infants who died did so soon after birth, except those who died of sepsis, BPD, or CPVL. Infants who died of sepsis were generally quite immature and small at birth, but were not particularly growth restricted. In infants without NEC who died of sepsis, the infectious organisms were Escherichia coli (8), Group B streptococci (3), Staphylococcus aureus(5), S epidermidis (1), Haemophilus influenzae (1), Klebsiella and Pseudomonas spp. combined (1), Streptococcus viridans (1), Candida albicans (1) and herpes simplex (1). E. coli and Group B streptococci were the predominant organisms causing early infections, and Staphylococcus species, later infections. Back to textBack to textBack to text

Lex W Doyle · Sheryle Rogerson · Shu-Ling Chuang · Matthew James · Ellen D Bowman · Peter G Davis

Research Health burden of hip and other fractures in Australia beyond 2000 Projections based on the Geelong Osteoporosis Study Kerrie M Sanders, Geoffrey C Nicholson, Antony M Ugoni, Julie A Pasco, Ego Seeman, and Mark A Kotowicz MJA 1999; 170: 467-470 For editorial comment, see Morris et al; see also Pocock et al. Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Author's Detials - - More articles on Public and environmental health Abstract Objective: To calculate the expected increase in the number of fractures in adults attributable to the predicted increase in the number of elderly Australians. Data sources: All fractures in adult residents (> 35 years) of the Barwon Statistical Division (total population, 218 000) were identified from radiological reports from February 1994 to February 1996. The Australian Bureau of Statistics supplied predictions of Australia's population (1996 to 2051). Main outcome measure: The projected annual number of fractures in Australian adults up to 2051 (based on stable rates of fracture in each age group). Results: The number of fractures per year is projected to increase 25% from 1996 to 2006 (from 83 000 fractures to 104 000). Hip fractures are projected to increase 36% (from 15 000 to 21 000) because of a substantial rise in the number of elderly aged 85 years and over. Hip fractures are expected to double by 2026 and increase fourfold by 2051. Conclusions: In contrast to Europe and North America, where numbers of hip fractures are expected to double by 2026 and then stabilise, in Australia hip fractures will continue to place a growing demand on healthcare resources for many decades. These projections can be used for setting goals and evaluating the costs and benefits of interventions in Australia. Introduction Australia's population is ageing. Thus, diseases such as osteoporosis are affecting a greater proportion of the population. Cost-effective prevention and treatment of fractures will become increasingly important, as the proportion of the "prime working" population (aged 15 to 64 years) is expected to decrease by 7% between 1996 and 2051.1 Estimations of the annual number of fractures will facilitate effective allocation of limited healthcare resources. Previously, fracture rates in Australia have been extrapolated from rates in Dubbo and Busselton,2,3 populations that may not be representative of the national population as they are both fairly isolated towns with small numbers of men and women in the oldest age groups. Lord et al investigated changes in hip fracture admissions in New South Wales between 1979 and 1990 using International Classification of Diseases hospital discharge codes.4 Although frequently used for ascertaining hip fractures, the limitations of this method are well documented.5,6 The Geelong Osteoporosis Study is a population-based study of age-, sex- and site-specific fracture rate(s) within a well-defined geographic region sufficiently large to establish reliable rates of fracture. It is the largest Australian epidemiological study of adult fractures, identifying 2184 fractures over two years in people aged 35 years and over. Data from the 1996 national census confirm the findings of an earlier study7 that the regional population is typical of the nation in age distribution and socioeconomic range. The Australian Bureau of Statistics publishes projections of the size, structure and distribution of Australia's population into the next century.1 Assuming stable age- and sex-specific rates of fracture, we have projected annual numbers of fractures by anatomical site in adults over the next 50 years. Methods Population The Barwon Statistical Division is a region of southern Victoria7 defined by the Australian Bureau of Statistics which includes urban, semi-urban and rural residents and has a population of 218 000 (109 923 aged 35 years and over). Fracture ascertainment Using radiological reports from the two medical imaging practices in the region, we identified all fractures in adults (aged 35 years and over) residing within the Barwon Statistical Division over the two-year ascertainment period (17 February 1994 to 16 February 1996). Fractures were identified by a weekly computerised keyword search of all radiological reports. Although radiological services are available at several sites throughout the region, these sites are under the auspices of two medical imaging practices. Only reports of definite fractures were included as "cases". Reports referring to "likely" or "possible" fracture were not included unless radiologically confirmed at a later date. Vertebral fractures were included in the study on the basis of the radiological report, provided there was no previous record of a fracture at that level. The initial x-ray demonstrating each fracture was sought and the date of fracture was the date of the radiological diagnosis. As the region is well provided with medical facilities, few fractures would not have been assessed or followed up by services within the region. The standing orders for the ambulance service are to transport patients from residences within the study region to The Geelong Hospital. The study was well advertised and adults who may have sustained fracture(s) while outside the region were asked to contact study coordinators. Non-residents and patients with pathological fractures (metastatic cancer, Paget's disease and multiple myeloma) were excluded. We have previously reported that the exclusion of high trauma fractures may underestimate the prevalence of bone-fragility fractures in the community,8 so we did not exclude fractures on the basis of trauma classification. The method of fracture ascertainment has been previously described9 and validated, using hip fracture as a model.10 The study was approved by The Geelong Hospital Human Research and Ethics Advisory Committee. Projections We calculated the predicted number of fractures in each five-year age group for men and women as: Predicted number of fractures = Number of fractures in the study region Study region population X Projected Australian population X 0.5 (2 year ascertainment) The study region population was determined from the 1996 Australian Bureau of Statistics census. Annual population projections were also provided by the Australian Bureau of Statistics.1 This method of projection assumes that the fracture rate in each age group will remain unchanged over time. Confidence intervals around the projections were calculated by the bootstrap method.11 Results The number of fractures identified in the study population is shown in Table 1. Projections for all fractures During the ascertainment period, 2184 adults sustained fractures, producing an age- and sex-adjusted incidence of 102 per 10 000 person-years. In 1996, we estimate that about 83 000 Australians aged 35 years and over sustained fractures. We predict that by 2006 the total number of fractures per year will increase by 25%, to 104 000 (Figure 1). Projections for hip fractures Over the two-year ascertainment period, 428 people sustained hip fractures, producing an age- and sex-adjusted incidence in people aged 35 years and over of 17.2. The number of hip fractures in Australian women is projected to increase from 11 300 per year in 1996 to 44 700 in 2051. In men, the number is projected to rise from 4 000 to 15 300. Figure 2 shows the projection for all people aged 35 years or over. The number of Australians sustaining hip fractures each year is projected to increase by 15% every five years until 2036, then by about 10% every five years until 2051. A fourfold increase in hip fractures is expected by 2051, when about 23% of Australia's projected population will be aged 65 years and over (compared with 12% in 1996) and over 8% of the population will be aged 85 years and over (compared with 2% in 1996). Hip fractures are likely to increase more than fractures at other sites because the greatest population growth is expected in the oldest age groups, where the hip is the most common site of fracture.9 Projections for fractures at sites other than the hip During the ascertainment period, 1756 adults aged 35 years and over sustained fractures at sites other than the hip, producing an age- and sex-adjusted incidence of 77 per 10 000 person-years. We estimate that in 1996 about 68 000 Australians aged 35 years and over sustained fractures at sites other than the hip, and that the number of non-hip fractures is likely to increase by 9% every five years until 2036, and then by 4% every five years until 2051 (to 147 645 non-hip fractures per year). Projections for vertebral, Colles, humeral and pelvic fractures (the most common sites of fracture after the hip) are shown in Figure 3. Fractures at these sites are likely to increase more than fractures at other sites where fracture rates do not increase substantially with age.9 Population projections suggest that vertebral, humeral and pelvic fractures will increase by 12% every five years to 2036, then by 6% every five years to 2051. Colles fracture rates increase with age in women, but not in men,8 and the overall number of adults sustaining a Colles fracture will increase by 10% every five years until 2036, then by 5% every five years until 2051. Fractures other than hip, vertebral, Colles, humeral and pelvic fractures are predicted to increase at about half the rate predicted for these sites (6% every five years until 2036, then 3% every five years until 2051). Projection of fracture numbers by age group The number of fractures in adults aged 35 to 59 years is not predicted to change substantially over the projection period, as only a small population increase in this age group is anticipated. By contrast, among those aged 60 years and over, the number of fractures is predicted to increase by at least 10% every five years, and by almost 20% every five years among those aged 85 years and over (Table 2). Figure 4 shows the projected distribution of hip fractures across age groups for selected years from 1996 to 2051. Discussion The ageing of the Australian population is increasing the demand for health resources. Health expenditure per person aged 65 years and over is nearly four times higher than for younger individuals ($4900 v $1300).12It is likely that hip fracture, which becomes increasingly common with advancing age, contributes significantly to this higher expenditure. Almost all people with a fractured hip are hospitalised, with an average length of stay of 13 days.13 Studies in other white populations suggest that 50% of patients who survive hip fracture are discharged to nursing homes, and 25% remain institutionalised one year later.14,15 Comparable Australian data are not available, although the increased mortality after hip fracture has been confirmed.16 We estimate that hip fractures accounted for 0.9% of total government health services expenditure for 1995/96.12 Based on the number of Australian salary earners in 1998 (Australian Bureau of Statistics) and an average cost of $16 000 per hip fracture,17 treatment alone costs salary earners an average of $28 per year. In current dollar terms, this may escalate to $120 per salary earner per year by 2051 if the projected increase is realised. The number of adults sustaining a hip fracture is likely to more than double from 15 000 in 1996 to 34 000 in 2026, then almost double again by 2051. Fractures at other sites are expected to increase by 70% from 1996 to 2026, then by a further 26% to 2051. These rates of increase are far above the expected growth in total healthcare costs due to the ageing of the Australian population, which is estimated to be 4% every five years for the next 30 to 40 years.18 For the number of hip fractures to remain stable, their incidence (per 10 000 population per year) would need to decline from 17.2 in 19969 to 15.6 in 2001, 14.3 in 2006 and 11.3 in 2026. In the United States, an 18% reduction in hip fracture rates between 1988 to 2000 has been targeted by public health strategists.19 Current therapies (such as hormone replacement therapy and bisphosphonates) may reduce fracture rates by 50%, but their cost-effectiveness remains controversial.20,21 In most white populations the number of hip fractures is predicted to double between 1990 and 2025, and then plateau as the growth in the aged population ceases.22 However, in contrast with Europe and North America, the aged population and the number of hip fractures in Australia and New Zealand are likely to continue to increase from 2025 to 2050.22 Current trends suggest that almost three times as many women as men will sustain a hip fracture (Table 1). Largely for this reason, efforts to prevent hip fracture have focused on osteoporosis in women. However, mortality and rate of institutionalisation after hip fracture is higher in men,23 and increasing hip fracture rates among men, but not women, have been reported.24,25 The projected increased longevity in men suggests that osteoporosis will affect a growing number of Australian men, yet there are no data concerning efficacy of any drug treatment to prevent hip or vertebral fractures in men.26 Our projected number of vertebral fractures is likely to be an underestimate because our ascertainment relied on clinical indications for medical imaging. Between 50% and 75% of vertebral fractures do not come to medical attention.27,28 However, our data are likely to include some previously undiagnosed vertebral fractures that occurred before the ascertainment period. Nevertheless, the predicted number of vertebral fractures represents the number likely to come to medical attention each year. Excluding vertebral fractures does not alter the projected rate increase of all fractures. The validity of these projections is dependent upon reliable and stable incidence rates and accurate population projections. The major strength of our study was the comprehensive ascertainment of all fractures among adult residents of a defined region representative of Australia.9 A decline in hip fracture rates has recently been reported,19 but other studies have pointed to stable age-specific rates in women and younger men and increasing rates in older men.24,25,29,30 These projections highlight the need to decrease fracture rates among the elderly and can be used for setting goals and evaluating the costs and benefits of interventions in Australia. Acknowledgements This study was supported by the Victorian Health Promotion Foundation. We acknowledge the invaluable contributions of the radiologists (D Barry, JM Cameron, PJ Carman, WP Holloway, V Mercuri, PM Motterdam and DB Robertson) and staff at the Geelong Radiological Clinic, as well as the radiologists (NJ Ferris, DO Lun, CB Styles) and staff of the Medical Imaging Department at the Geelong and Colac hospitals. We also wish to thank Biljana Skoric and Soheila Panahi. References McLennan W. Projections of the populations of Australia, States and Territories, 1995-2051. Canberra: Australian Bureau of Statistics, 1996: 128. (Catalogue no. 3222.0.) Jones G, Nguyen T, Sambrook PN, Kelly PJ, Gilbert C, Eisman JA. Symptomatic fracture incidence in elderly men and women: The Dubbo osteoporosis study (DOES). Osteoporos Int 1994; 4: 277-282. Prince RL, Knuiman MW, Gulland L. Fracture prevalence in an Australian population. Aust J Public Health 1993; 17: 124-128. Lord SR. Hip fractures: changing patterns in hospital bed use in NSW between 1979 and 1990. Aust N Z Surg 1993; 63: 352-355. Bacon W, Maggi S, Looker A, et al. International comparison of hip fracture rates in 1988-89. Osteoporos Int 1996; 6: 69-75. Maggi S, Kelsey JL, Litvak J, Heyse SP. Incidence of hip fractures in the elderly: a cross national analysis. Osteoporos Int 1991; 1: 232-241. Ross KN. The development of the 1984 "Indicator of Disadvantage" and its application to resource allocation decisions for the "Disadvantaged Schools Program" in Australia. Geelong: School of Education, Deakin University, 1984. Sanders K, Pasco J, Ugoni A, et al. The exclusion of high trauma fractures may underestimate the prevalence of bone fragility fractures in the community: The Geelong Osteoporosis Study. J Bone Mineral Res 1998; 13: 1337-1342. Sanders K, Seeman E, Ugoni A, et al. The age- and gender-specific rate of fractures in Australia: a population based study. Osteoporos Int 1999. In press. Pasco JA, Henry MJ, Gaudry TM, et al. Identification of incident fractures: Geelong Osteoporosis Study. Aust N Z J Med 1999; 29: 203-206. Efron B, Tibshirani R. The introduction to the bootstrap. New York: Chapman & Hall, 1993. Australia's health 1998: the sixth biennial health report of the Australian Institute of Health and Welfare. Canberra: AGPS, 1998. Abraham B, d'Espaignet E, Stevenson C. Australian health trends 1995. Canberra: Australian Institute of Health and Welfare, 1995. Orwoll ES. The special problem of hip fracture. In: Favus MJ, editor. Primer on the metabolic bone diseases and disorders of mineral metabolism. 3rd ed. Philadelphia: Lippincott-Raven, 1996: 272-282. Keene G, Parker M, Pryor G. Mortality and morbidity after hip fractures. BMJ 1993; 307: 1248-1250. Center J, Nguyen TV, Schneider D, et al. Mortality after all major types of osteoporotic fracture in men and women: an observational study. Lancet 1999; 353: 878-882. Randell A, Sambrook P, Nguyen T, et al. Direct clinical and welfare costs of osteoporotic fractures in elderly men and women. Osteoporos Int 1995; 5: 427-432. Gray R. Insurance: the long term funding of aged care. National Healthcare 1998; 8(4): 32-33. Melton L, Atkinson EJ, Madhok R. Downturn in hip fracture incidence. Public Health Rep 1996; 111 (March/April): 146-150. Black DM, Cummings SR, Karpf DB, et al. Randomised trial of effect of alendronate on risk of fracture in women with existing vertebral fractures. Fracture Intervention Trial Research Group. Lancet 1996; 348: 1535-1541. Jonsson B, Christiansen C, Johnell O, Hedbrandt J. Cost-effectiveness of fracture prevention in established osteoporosis. Osteoporos Int 1995; 5: 136-142. Cooper C, Campion G, Melton LJ III. Hip fractures in the elderly: A world-wide projection. Osteoporos Int 1992; 2: 285-289. Sernbo I, Johnell O. Consequences of a hip fracture: A prospective study over 1 year. Osteoporos Int 1993; 3: 148-153. Melton LJI, O'Fallon WM, Riggs BL. Secular trends in the incidence of hip fractures. Calcif Tissue Int 1987; 41: 57-64. Bacon W. Secular trends in hip fracture occurrence and survival: Age and sex differences. J Aging Health 1996; 8: 538-553. Seeman E. Osteoporosis: trials and tribulations. Am J Med 1997; 103 (2A): 74S-87S. Kanis JA, McCloskey EV. Epidemiology of vertebral osteoporosis. Bone 1992; 13 Suppl 2: S1-S10. Cooper C, Atkinson EJ, O'Fallon M, Melton L. Incidence of clinically diagnosed vertebral fractures: a population-based study in Rochester, Minnesota, 1985-1989. J Bone Min Res 1992; 7: 221-227. Falch JA, Kaastad TS, Bohler G, et al. Secular increase and geograpical differences in hip fracture incidence in Norway. Bone 1993; 14: 643-645. Agnusdei D, Camporeale A, Gerardi D, et al. Trends in the incidence of hip fracture in Siena, Italy, from 1980 to 1991. Bone 1993; 14: S31-S34. (Received 13 Nov 1998, accepted 13 Apr 1999) Author's Detials University of Melbourne Department of Medicine, Barwon Health-The Geelong Hospital, Geelong, VIC Kerrie M Sanders, MNutrition, PhD, Research Fellow; Geoffrey C Nicholson, PhD, FRACP, Professor of Medicine; Julie A Pasco, PhD, Study Coordinator; Mark A Kotowicz, FRACP, Senior Lecturer in Medicine. Department of General Practice and Public Health, The University of Melbourne, Melbourne, VIC. Antony M Ugoni, BSc(Hons), Lecturer in Biostatistics. Austin and Repatriation Medical Centre, Melbourne, VIC. Ego Seeman, MD, FRACP, Associate Professor of Medicine, The University of Melbourne. Reprints will not be available from the authors. Correspondence: Dr M A Kotowicz, University Department of Medicine, Barwon Health-Geelong Hospital, PO Box 281, Geelong, VIC 3220. Email: m.kotowiczATmedicine.unimelb.edu.au Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> Back to textBack to textBack to textBack to textBack to textBack to text

Kerrie M Sanders · Geoffrey C Nicholson · Antony M Ugoni · Julie A Pasco · Ego Seeman · Mark A Kotowicz

Research An analysis of the causes of adverse events from the Quality in Australian Health Care Study Ross McL Wilson, Bernadette T Harrison, Robert W Gibberd and John D Hamilton MJA 1999; 170: 411-415 For editorial comment, see Vincent Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Administration and health services The Quality in Australian Health Care Study (QAHCS), published in the Journal in 1995,1 reported that 16.6% of hospital admissions were associated with an iatrogenic patient injury, termed an adverse event (AE) (see Box 1). This compares with the rate of 3.7% for AEs in the Harvard Medical Practice Study (HMPS),2 and a rate of 17% in a more recent study with an alternative observational method of determining AEs.3 Fifty per cent of the AEs in the QAHCS were judged to have a high preventability score (4 or more on a scale of 1-6 of increasing likelihood of preventability).1 The disability caused by these adverse events ranged from temporary disability (fully resolved in one month) in 46.6% of AEs, to death in 4.9% of AEs. Although recording AEs emphasises only the "complications" of rather than the benefits derived from healthcare, AEs are of great significance to individual patients as well as to the whole healthcare system. Abstract Objective: To examine the causes of adverse events (AEs) resulting from healthcare to assist in developing strategies to minimise preventable patient injury. Design: Descriptions of the 2353 AEs previously reported by the Quality in Australian Health Care Study (QAHCS) were reviewed. A qualitative approach was used to develop categories for human error and for prevention strategies to minimise these errors. These categories were then used to classify the AEs identified in the QAHCS, and the results were analysed with previously reported preventability and outcome data. Results: 34.6% of the causes of AEs were categorised as "a complication of, or the failure in, the technical performance of an indicated procedure or operation", 15.8% as "the failure to synthesise, decide and/or act on available information", 11.8% as "the failure to request or arrange an investigation, procedure or consultation", and 10.9% as "a lack of care and attention or failure to attend the patient". AEs in which the cause was cognitive failure were associated with higher preventability scores than those involving technical performance. The main prevention strategies identified were "new, better, or better implemented policies or protocols" (23.7% of strategies), "more or better formal quality monitoring or assurance processes" (21.2%), "better education and training" (19.2%), and "more consultation with other specialists or peers" (10.2%). Conclusion: The causes of AEs or errors leading to AEs can be characterised, and human error is a prominent cause. Our study emphasises the need for designing safer systems for care which protect the patient from the inevitability of human error. These systems should provide new policies and protocols and technological support to aid the cognitive activities of clinicians. Introduction An additional analysis of data from the Quality in Australian Health Care Study (QAHCS)1 was undertaken in order to understand more fully the causes of the adverse events (AEs) identified and to assist in developing prevention strategies. Here, we describe the error or errors in the delivery of healthcare which led to the AEs. This contrasts with our previous report,1 which focused on the patient characteristics associated with AEs and the nature and consequences of the AEs. Methods The method of determining AEs in the QAHCS has been described previously.1 The AEs were re-examined with the specific goals of determining the causes for, or the underlying errors leading to, each AE. In addition, strategies that were judged to have the potential to prevent AEs were recorded. To obtain this information the first and subsequent review forms (RF1 and RF2 forms1) collected during the QAHCS were re-examined. The source material for these forms had been the hospital medical records, but neither the hospitals nor the medical records were revisited in this analysis. Categories for the causes of the AEs were devised by an iterative process during a three-day workshop. For this, we sought additional expertise in clinical epidemiology and qualitative research methods. Using these categories, the AEs recorded on the review forms were assessed by three of the senior medical specialists who had originally reviewed the medical records in the QAHCS. All the material from each AE was reviewed by only one reviewer, as the agreement between the medical reviewers in determining the presence or absence of an AE during the QAHCS was 80% (kappa, 0.55). A proforma was completed which asked the reviewer to identify the error and then classify it by human cause and preventive strategy. All AEs were also categorised into some of the processes of clinical care. Results for the "delay", "treatment" and "investigation" categories are presented. The categories were not mutually exclusive. These data were then entered into a database, merged with the original data from the QAHCS for each case and analysed. Two of the original total of 2353 AEs were missed in this review; thus, results are given for 2351 AEs. Our analysis provides the frequency of occurrence of each of the categories of causes of AEs, together with the proportion in each category resulting in permanent disability (including death) and the proportion with high preventability. Results Human error categories Box 2 shows the frequency of occurrence of each of the human error categories, and the proportion of the AEs in each category judged to have permanent disability and high preventability. Of the 2351 AEs, 1922 (81.8%) were associated with one or more human error categories. As the error categories were not mutually exclusive, the 1922 AEs were associated with 2940 causes. "Complication of, or failure in, the technical performance of an indicated procedure/operation" was the most frequent cause of AEs; examples of this category are shown in Box 3A. Human errors associated with categories of failure of cognitive function were the next most frequent cause of AEs (Box 2). These included "Failure to synthesise, decide and/or act on available information", "Failure to request or arrange investigation, procedure or consultation", and "Misapplication of, or failure to apply, a rule; or use of a bad or inadequate rule". The most frequent error category, "complication of, or failure in, the technical performance of an indicated procedure/operation", had a lower proportion of AEs with permanent disability (14.2%). The next five most frequent human error categories all had a high proportion of AEs with permanent disability (25% or more) (Box 2). This pattern was also seen in the proportions of AEs with death as the outcome: 2.2% in the first category, and 8% or more in each of the next five categories. Of the 1201 AEs having high preventability, 9 (0.7%) were not associated with a human error category; for the remaining 1192 AEs, 2051 causes were identified (Box 2). Delay categories The importance of timeliness to the quality of healthcare led to further analysis of all AEs to ascertain the nature and role of delay in their causation (Box 4A). Delays contributed to 20.0% of AEs: of these, delays in diagnosis accounted for 56.8% and treatment delays for 40.6%. Diagnostic delay was usually the failure to make, or attempt to make, a diagnosis of a patient's condition rather than just providing symptomatic or even no treatment. Treatment delay was when the diagnosis had been made but there was a delay in initiating specific therapy. Examples of AEs in the delay category are included in Box 3B. The AEs with delay categories were judged to have very high preventability (86%-90%) compared with the average (51.2%) for all AEs (Box 4A). Treatment categories AEs categorised as caused by a treatment error were also analysed (Box 4B). In 19.6% of all AEs, treatment error contributed to the cause. The majority of AEs in this group fell into the categories of "no or inadequate treatment" (51.5%), or "wrong or inappropriate treatment" (27.4%). As with AEs caused by delay, these AEs were judged to have much higher preventability than the average for all AEs. Examples of AEs involving treatment errors are shown in Box 3C. Investigation categories Analysis of the AEs caused by patient investigation issues is shown in Box 4C, and examples are given in Box 3D. There was a problem with clinical investigation in 10.7% of AEs. Paralleling the results in the treatment category, most (78.6%) of these AEs were in this category because an investigation was not done, rather than the investigation being inappropriate (3.6%), or not acted upon (15.5%). Consistent with other AEs that are attributed to cognitive failure, there was a very high percentage of these AEs rated as high preventability. Strategies for preventing AEs When describing AEs, preventability refers to the identification of an avoidable error that led to the adverse event. This is not to say that the error could be avoided on every occasion, and that the adverse event would not occur. Rather, it implies that, with the current state of knowledge and technology, it is possible to identify and avoid that particular error, and hence reduce the probability of an AE. The reviewers were making a judgement, having identified the error, on the particular strategy for a change in the healthcare system that could have prevented the AE. The outcomes of these judgements are given in Box 5. Nineteen (1.6%) of the 1201 high preventability AEs did not have a prevention strategy category. Of the 2613 prevention strategies identified in the 1182 AEs with high preventability, 24.7% (646) were for "better education and training", 20.9% (545) were for "new or better implemented policies or protocols" and 18.6% (486) were for "more or better formal quality monitoring or assurance processes". Discussion AEs are important to patients, healthcare providers and to the custodians and funders of health services. One estimate of the national cost to the Australian healthcare system of just the additional hospital bed-days (as a result of the AEs identified in 19921) is in excess of $800 million dollars per year.4 This estimate ignores any subsequent hospital admissions and out-of-hospital healthcare expenses, loss of productivity of the patients involved, and long term community costs of permanent disability from AEs. It also ignores the benefits received from healthcare. Providing insights into how AEs occur can help in developing prevention strategies to reduce the frequency and severity of patient injuries during healthcare. Our review and analysis of the AE data from the QAHCS have shown that the causes of AEs or errors leading to AEs can be characterised, and that human error is a prominent cause. It is important to recognise that human error is inevitable for even the best-trained and best-qualified healthcare providers. Weed has recently pointed out that the unaided human mind is incapable of performing consistently at the necessary level to provide optimal healthcare.5 However, other studies6 have noted that the label "human error" is prejudicial and non-specific; it may retard rather than advance our understanding of how complex systems fail. It is postulated that within complex systems error is a symptom of organisational problems, and this is likely to apply to healthcare. Therefore, we need a healthcare-system response to error that moves the system towards being as "failsafe" as possible rather than one that blames the clinician who may have erred. Examples from the more frequently studied area of adverse drug events7 would be decision-support technology for antibiotic prescribing,8 with its demonstrated benefits, and electronic prescribing to reduce prescribing and transcription errors in hospital.9 Our analysis identified broad functional categories that are linked to the processes that make up the system of healthcare delivery and hence cut across specialties, diagnosis-related groups (DRGs) and particular patient groups. The sample size is large enough to provide useful information even when several AEs could not be classified into the categories chosen, or insufficient information was available to indicate cause. On the other hand, several factors bias the information available for assessing AEs because of an emphasis on procedures and short term outcomes and possible under-reporting of the contribution of the supporting systems to the cause of the AEs. Firstly, because the original data source was the hospital medical record, the information available about AEs is biased towards the patient involved and away from other potentially important contextual events at the time. Further, the medical record often focuses more on the actions of clinicians involved in direct or procedural patient intervention, and less on the actions of other staff or systems with a more supportive role. These and other factors will lead to an emphasis on procedures and short term outcomes, and a possible under-reporting of the contribution of supporting systems in causing AEs. Finally, information about subsequent or prior hospitalisations is usually only available if the patient attended the same hospital on all occasions. Having acknowledged these potential limitations, cognitive failure (Box 2) appears to have a role in 57% of all the causes of AEs, and most of the AEs involved were judged to be of high preventability and to have caused significant disability. These AEs were largely associated with errors of omission rather than commission. Does this represent a minimum "obligatory" error rate resulting from a combination of human error and our healthcare system, and hence which cannot be improved? Our data are not able to answer this question unequivocally, but we believe they show sufficient opportunities for moving the system towards a failsafe mode to suggest that the answer is no. Until recently there has been an under-recognition of the role and responsibilities of the healthcare system and its custodians in providing a "safe environment" using systems-improvement tools.10 One response to these data should be to look at the factors in healthcare delivery that may interfere with the cognitive or technical performance of healthcare providers. Insufficient use of information technology to assemble the necessary information at the time of decision-making may increase error. Another important factor is fatigue, which has already been shown to increase error in doctors.11 Sleep deprivation may have a much more significant role in human error in healthcare than the current work-load patterns pay heed to, but more research is needed. Other factors that may be important include the level of supervision provided to junior staff, and the pervasive effect of the culture of medical practice, which can unhelpfully portray error as individual failure or deviation from perfection.12 Our study method does not provide direct information about the role of these factors. The high proportion of causes of AEs involving cognitive failure must represent a manifestation of human error occurring in a system that is not patient protective, if one accepts that these practitioners are appropriately trained and competent by international standards. Our study provides clear guidance on methods for improvement, with "new, better, or better implemented policies or protocols" accounting for 24% of prevention strategies identified for the AEs, "quality monitoring and assurance processes" accounting for 21%, and "better education and training" for a further 19%. In summary, improvement is needed in the agreed processes of care, supported by information systems that allow general dissemination of current knowledge of diseases or treatments, and information on outcomes of care for each patient, through appropriate quality processes. Simple examples are the availability of practice guidelines and protocols at the point-of-care, and the use of automated reminders for patients and practitioners when a particular test or follow-up is required. In addition, having adequate patient "outcome" information in a form that can be benchmarked is a powerful tool in identifying unacceptable variation. Acknowledgements We acknowledge the contributions of Professor B Armstrong, Professor W R Runciman, Professor R Holland, Dr T Robertson and Dr A Hobbes. References Wilson RMcL, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. <eMJA pdf> Brennan TA, Leape LL, Laird N, et al. Incidence of adverse events and negligence in hospitalised patients: results of the Harvard Medical Practice Study I. N Engl J Med 1991; 324: 377-384. Andrews LB, Stocking C, Krizek T, et al. An alternative strategy for studying adverse events in medical care. Lancet 1997; 349: 309-313. The Final Report of the Taskforce on Quality in Australian Health Care. Appendix 7. Canberra: AGPS, June 1996. <http://www.health.gov.au/pubs/hlthcare/toc.htm> Weed LL. New connections between medical knowledge and patient care. BMJ 1997; 315: 231-235. Cook RI, Woods DD. Operating at the sharp end: the complexity of human error. Human performance in anaesthesia: a corpus of cases. Report to the Anaesthesia Patient Safety Foundation, 1991. Columbus, Ohio: The Ohio State University: 255-307. Classen DC, Pestonick SL, Evans RS, et al. Adverse drug events in hospitalised patients: excess length of stay, extra costs and attributable mortality. JAMA 1997; 227: 301-306. Evans RS, Pestonick SL, Classen DC, et al. A computer-assisted management program for antibiotics and other anti-infective agents. N Engl J Med 1997; 338: 231-238. Bates DW, Boyle DL, Vander Vliet MB, et al. Relationship between medication errors and adverse drug events. J Gen Intern Med 1995; 10: 199-205. Leape LL. A systems analysis approach to medical error. J Eval Clin Pract 1997; 3: 213-222. Nocera A, Khursandi DS. Doctors' working hours: can the profession afford to let the courts decide what is reasonable. Med J Aust 1998; 168: 616-618. Leape LL. Error in medicine. JAMA 1994; 272: 1851-1857. (Received 4 May 1998, accepted 20 Jan 1999) Authors' details Royal North Shore Hospital, Sydney, NSW 2065. Ross McL Wilson, MB BS, FRACP, Senior Specialist in Intensive Care; Director of QARNS (Quality Assurance Royal North Shore); Bernadette T Harrison, RN RM, Manager QARNS. University of Newcastle, Newcastle, NSW 2308. Robert W Gibberd, PhD, Associate Professor, Department of Statistics; and Director of Health Services Research Group. John D Hamilton, MB BS, FRCP, Professor of Medicine, Faculty of Medicine and Health Sciences. Reprints: Dr R McL Wilson, Director of QARNS, Royal North Shore Hospital, Pacific Highway, St Leonards, NSW 2065. Email: rwilsonATdoh.health.nsw.gov.au Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> 1: Terms and definitions Adverse event (AE): An AE was defined as an injury or complication which resulted in disability or prolongation of hospital stay and was caused by the healthcare received rather than by the disease from which the patient suffered. The AE either occurred during the hospital admission, or during an earlier contact with healthcare services, and was responsible for all or part of the hospital admission. Error: An act of commission or omission that caused, or contributed to the cause of, the unintended injury. for errors of commission this will usually be the immediate morbid consequences of the error for errors of omission this will usually be the continuation of, and consequences of, an existing morbid state that could have been cut short, or had a better outcome, if the error had not occurred. Prevention strategy: Changes in the system in which an error occurred that mayreduce the probability of the error occurring increase the probability that the error would be remedied before an unintentional injury occurredPreventability: Preventability of an AE was assessed by the detection of "an error in management due to the failure to follow accepted practice at an individual or system level"; accepted practice was taken to be "the current level of expected performance for the average practitioner or system that manages the condition in question". Back to textBack to text 3. Examples of categories of causes of adverse events and preventability scoresA. Human error categories Example 1: A 50-year-old man sustained a bowel perforation from colonoscopy for investigation of abdominal pain. Laparotomy required. Category: "Technical performance". Preventability score: 3. Example 2: A 71-year-old man required six operations for femoral hernia repair. Category: "Technical performance". Preventability score: 2. Example 3: A 32-year-old woman had persisting severe back pain after two laminectomies, three myelograms, one decompression/fusion, and three thecal/epidural injections over 18 months. In pelvic traction at the time of review. Category: "Technical performance". Preventability score: 4. Example 4: A failed attempt at percutaneous endoscopic gastrostomy on a 32-year-old woman was followed by an open procedure. The patient died 9 days later. Autopsy revealed acute peritonitis, subphrenic abscess and bilateral pneumonia. There did not appear to have been an antemortem diagnosis of intra-abdominal sepsis, or any specific treatment for it. Category: "Technical performance". Preventability score: 6. B. Delay in diagnosis and/or treatment categories Example 1: Diagnosis of cancer of the colon was delayed until the patient, a 62-year-old woman, presented with a ruptured caecum and peritonitis from an obstructing tumour. In hospital 3 months earlier with a history suggestive of cancer of the colon and iron-deficiency anaemia, but no investigation performed. Categories: Diagnosis delay, violation of protocol or rule; failure to synthesise, decide or act on available information; lack of care/attention. Preventability score: 5.5. Example 2: A 28-year-old man with abdominal pain was treated with cholecystectomy. Gallbladder was macroscopically and histologically normal. Small bowel lymphoma was eventually diagnosed and treated, with resolution of the presenting symptoms. Categories: Diagnosis delay; failure to synthesise, decide or act on available information; failure to request or arrange an investigation, procedure or consultation. Preventability score: 5. C. Treatment categories Example 1: A 52-year-old man with known asthma was prescribed a beta-blocker for hypertension. This resulted in acute respiratory failure leading to artifical ventilation and tracheostomy. Categories: Wrong or inappropriate treatment; misapplication of or failure to apply a rule; failure to synthesise, decide or act on information. Preventability score: 6. Example 2: A 54-year-old man developed gastrointestinal bleeding (haemoglobin level, 45 g/L) while receiving non-steroidal anti-inflammatory drugs and steroids for rheumatoid arthritis. This required hospital admission and blood transfusion, at which time the correct diagnosis of osteoarthritis was made. Categories: Wrong or inappropriate treatment; acting on insufficient information; failure to request or arrange an investigation, procedure or consultation. Preventability score: 5.5. Example 3: Hospitalisation and surgical intervention for septic arthritis that followed steroid injection into a joint. Categories: Unclassified treatment; technical; lack of care/attention. Preventability score: 4.5. D. Investigation categories Example 1: A 75-year-old woman died from acute renal failure after developing gentamicin toxicity. Gentamicin was used to treat an infected pleural effusion, and drug levels were not measured. Categories: Investigation not performed; failure to request or arrange an investigation, procedure or consultation; lack of care/attention. Preventability score: 5. Example 2: A 58-year-old woman had recurrent hospital admissions for chest pain and impaired cardiac function without specific investigation, and hence a reduction in treatment options. Categories: Investigation; violation of protocol or rule; failure to synthesise, decide and/or act on available information. Preventability score: 5. Back to text 4: Contribution of delay, treatment and investigation categories to adverse events (AEs). Values are number (%) of AEsPermanentHighA. Delay categoryFrequencydisabilitypreventabilityDiagnostic delay267 (56.8%)93 (34.8%)231 (86.5%)Treatment delay191 (40.6%)53 (27.7%)172 (90.1%)Administrativedelay12 (2.6%)3 (25.0%)11 (91.7%)Total470 (100%)149 (31.7%)414 (87.9%) B. Treatment categoryNo or inadequatetreatment237 (51.5%)72 (30.4%)176 (74.3%)Wrong/inappropriatetreatment126 (27.4%)35 (27.8%)96 (76.2%)No or inadequateprophylaxis41 (8.9%)9 (22.0%)34 (82.9%)Treatmentunclassified36 (7.8%)7 (19.4%)28 (77.8%)Missed treatment20 (4.4%)4 (20.0%) 16 (80.0%)Total460 (100%) 127 (27.6%)350 (76.1%) C. Investigation categoryInvestigationnot performed198 (78.6%)81 (40.9%)171 (86.4%)Investigationnot acted on39 (15.5%)13 (33.3%)36 (92.3%)Investigationinappropriate9 (3.6%)2 (22.2%)9 (100.0%)Investigationunclassified6 (2.4%)2 (33.3%)5 (83.3%)Total252 (100%)98 (38.9%)221 (87.7%)Back to text 5: Frequency of occurrence of categories of prevention strategies and the proportion of adverse events (AEs) judged as causing permanent disability or having high preventability. Values are number (%) of AEsPermanentHighCategoryFrequencydisabilitypreventabilityNew, better, or better implementedpolicies or protocols884 (23.7%)206 (23.3%)545 (61.7%)More or better formal quality monitoringor assurance processes790 (21.2%)186 (23.5%)486 (61.5%)Better education and training715 (19.2%)160 (22.4%)646 (90.3%)Consultation with other specialistsor peers391 (10.5%)133 (34.0%)294 (75.2%)Don't know341 (9.2%)51 (15.0%)186 (54.5%)Better access to, or transfer of, information135 (3.6%)40 (29.6%)100 (74.1%)Discharge procedures and protocols122 (3.3%)27 (22.1%)100 (82.0%)Other89 (2.4%)22 (24.7%)46 (51.7%)Changes in organisation management88 (2.4%)22 (25.0%)75 (85.2%)Changes in organisation culture77 (2.1%)26 (33.8%)66 (85.7%)More or better personnel72 (1.9%)29 (40.3%)53 (73.6%)More or better equipment or otherphysical resources22 (0.6%)8 (36.4%) 16 (72.7%)Total3726 (100%)*910 (24.4%)2613 (70.1%) * Total is greater than the number of AEs (2351) as the categories were not mutually exclusive. Back to text

Bernadette T Harrison · Robert W Gibberd · John D Hamilton

Research Consultants in cases of intended euthanasia or assisted suicide in the Netherlands Bregje D Onwuteaka-Philipsen, Gerrit van der Wal, Piet J Kostense and Paul J van der Maas MJA 1999; 170: 360-363 For editorial comment, see Hendin Abstract - Introduction - Methods - Results - Discussion - Acknowledgement - References - Authors' details - - More articles on Ethics Abstract Objective: To investigate how often physicians act as a consultant in the review of intended euthanasia and assisted suicide (EAS), by whom physicians are asked to act as a consultant, and the consultant's reasons for not agreeing with the intended performance of EAS. Design: A retrospective descriptive study. Setting: The Netherlands. Participants: A stratified random sample of 405 Dutch physicians. Main outcome measures: Number of times the physician has been a consultant; how often a physician had previously been asked to be a consultant by the same treating physician; why consultants advised against EAS. Results: 42% of interviewed physicians had acted as a consultant for EAS and 11% had been a consultant more than three times. Half the physicians who acted as a consultant more than once were invited to do so by the same attending physician, and 41% of consultants had previously consulted the attending physician. The main reasons consultants advised against EAS were because treatment options were still available, the patient's request was not well-considered or persistent, and the patient's suffering was not unbearable and hopeless. Conclusions: Many physicians have at some time been a consultant in a case of intended EAS, but only very few have been able to gain experience in consultancy. To guarantee high standards of consultation, it may be advisable to appoint and train specific consultants for EAS. Introduction In the Netherlands, physicians can be involved in euthanasia or assisted suicide (EAS) either by performing or by being consulted by another physician who intends to perform EAS. Consultation is considered to be an important aspect in the review of cases of EAS,1 and is a requirement that must be met to avoid prosecution for performing EAS. Consultation takes place in about 99% of reported cases of EAS (41% of cases are reported) and in about 37% of unreported cases. In 88% of cases of EAS in which consultation took place the consultant had seen the patient.2,3 In a consultation, a physician formally confers with an independent colleague in considering whether to grant a request for EAS. The consultant determines whether the patient's physician has acted according to the requirements for prudent practice: the patient's request is voluntary, well-considered and persistent, the patient's suffering is unbearable and hopeless, and there are no alternatives for treatment remaining. A consultant should be competent and independent of both the attending physician and the patient, and should visit the patient.1,4 Consultation for EAS is a relatively new task for physicians, and is not part of general medical training. Physicians generally are not used to pronouncing formal judgement on the decision-making process of their colleagues and are not used to seeing patients in a consultancy role. Moreover, consultants need to have knowledge relevant to EAS, such as the possibilities of palliative care.5 Gaining experience as a consultant seems to be important for a physician to become comfortable in this role. As part of a nationwide study on EAS and other practices involving the end of life in the Netherlands,3,6 we set out to determine how often physicians act as a consultant, whether physicians frequently consult the same colleague (or vice versa), whether groups of physicians are asked to be a consultant more often than other groups, the reasons why consultants do not agree with the intended performance of EAS, and the extent to which the consultant feels responsible for the attending physician's final decision to grant or refuse a request for EAS. Methods Study population For this retrospective, descriptive study, we interviewed a stratified random sample of Dutch physicians.2 Participants were stratified according to specialty. The physicians in each stratum were ordered by postal code of their work address and every nth physician was selected. The stratum size was based on the frequencies of medical decisions concerning the end of life and the homogeneity of the patient population (morbidity and age) per stratum. To interview the desired number of physicians, 559 were included in the sample; 83 did not meet the selection criteria and 21 had a chronic illness or could not be located. Of the remaining 455, 50 (11%) did not respond. The final sample of 405 physicians included 124 general practitioners, 74 nursing home physicians (nursing homes in the Netherlands are multifunctional institutions which care for predominantly elderly patients with chronic diseases and physical and/or mental disorders and handicaps) and 207 specialists in cardiology, surgery, internal medicine, respiratory medicine and neurology (oncology and palliative care are not distinct specialties in the Netherlands, but are practised by specialists in other disciplines, such as internal medicine). Physicians in the above-listed specialties attend 87% of all deaths occurring in hospitals. Together with the general practitioners and nursing home physicians, they attend about 95% of all deaths in the Netherlands. Physicians who were not practising in their registered specialty in the same institution since 1 January 1994 were excluded. Measuring instruments The interviews were conducted from November 1995 to February 1996 by 30 experienced physicians who were specially trained for the study. The questionnaire consisted mainly of open-ended questions for the respondents, with prestructured response categories for the interviewers. In the interviews, the definitions of euthanasia, assisted suicide and consultation (Box 1) were explicitly described to the respondents. The interviews took about 2-3 hours. For this study we predominantly used data on how often the respondents had been consultant ever and in 1994 and 1995, and data on the most recent case (all 108 cases occurred between 1994 and 1996) in which the respondent had been a consultant. Analysis To make the data of the stratified samples representative for all deaths in the Netherlands, we weighted the data per stratum. We calculated weights based on the proportion of the various types of physicians in the sample. In addition, the weights of the five specialties were corrected for the 13% of in-hospital deaths that were attended by other medical specialists. Proportions and 95% confidence intervals for these proportions were obtained by direct standardisation7 to adjust for marked variation among the different types of physicians. The normal approximation to the binomial distribution was used. Estimates of the number of consultations in 1995 were based on the (weighted) data on how often each physician had acted as consultant in 1994 and 1995. Multiple logistic regression analyses were used to obtain insight into determinants of whether physicians had ever been a consultant. Because of the stratification according to specialty, the variable "specialty" was included in all analyses. To deal with this categorical variable we used indicator variables, choosing the general practitioners as the reference category. Results In 1995, in the Netherlands, we estimate that almost 4000 consultations took place in cases of intended EAS. In most of these, the consultant was a general practitioner; nursing home physicians rarely acted as a consultant (Box 2). Physicians who had been a consultant Of the 405 physicians in the sample, 42% at some time had been a consultant in intended EAS (Table 1). In 1994 (the year in which the notification procedure was legally enforced) or 1995, 32% of physicians had been a consultant -- general practitioners more often than medical specialists, and specialists more often than nursing home physicians (Box 2). Eight physicians had refused to act as a consultant, for various reasons: lack of time (2), not independent of the attending physician or the patient (2), doubt whether requirements for prudent practice had been met (2), disagreement with notification procedure (1), or the attending physician did not intend to perform euthanasia (1). Eleven per cent of the physicians had been a consultant more than three times (Box 3), and in 1995, 3% had been a consultant three or more times. Previous consultations between consultant and consulting physician Half of the physicians who had been a consultant more than once had previously been consulted by the same physician who consulted them in their most recent case. In 24% of these cases, the treating physician and the consultant had previously acted as consultants for each other (Box 4). Physicians who previously consulted or had been consulted by the same physician agreed more often with the intended EAS than physicians who did not (90% v. 80%), but this difference was not significant. Reasons for advising against EAS The 28 physicians who had at some time advised against the performance of EAS were each asked to describe up to three such cases. Together, they described 48 cases in which they had given this advice. In 42 cases EAS was not carried out, in three it was, and in three instances the consultant did not know the outcome. The consultants gave the following reasons for advising against EAS: there were still alternative treatment options (20 cases), the patient's request was not well-considered or persistent (12 cases), the patient's suffering was not unbearable and hopeless (nine cases), the request was made under pressure of the family (five cases), the patient was already dying (five cases), and the attending physician felt manipulated by the patient (one case). The consultant's responsibility Sixty-five per cent of consultants considered that they had joint responsibility only in those cases in which the attending physician acted according to their judgement, and 30% did not consider that they had any joint responsibility. Medical specialists felt that they had joint responsibility more often than general practitioners (80% [95% CI, 68.6%-91.3%] v. 61% [95% CI, 47.7%-74.6%]). Determinants of having been a consultant With univariate analyses corrected for specialty, physician's age, sex, religion, region in which the physician lives, belief that every case of EAS should be reviewed and belief that consultation should take place in every case of EAS were not significantly related to whether the physician had been a consultant. The results of multiple logistic regression analysis for those determinants that were predictive in the univariate analysis are shown in Box 5. Male physicians had more often been a consultant than female physicians. The strongest association was found for the variable "ever performed EAS". Physicians who had performed EAS had been a consultant more frequently than physicians who had never performed EAS. Discussion We estimate that consultation with another physician in cases of intended EAS took place almost 4000 times in the Netherlands in 1995 (see Box 6). In about 60% of consultations, the consultant was a general practitioner. Overall, 42% of Dutch physicians had been a consultant; 11% had been a consultant more than three times. The most common reason why consultants advised against the performance of EAS was the availability of alternative treatment options. Most consultants considered that they have joint responsibility for the final decision to grant or refuse a request for EAS. Male physicians, general practitioners and physicians who had performed EAS had more frequently been a consultant. The forming of "pairs" of consultants suggests that familiarity is very important in the choice of consultant. An earlier study found that an important reason for choosing a consultant is accessibility and that physicians mainly consult physicians of their own specialty.2 A problem with these consultations may be that the independence of the consultant with regard to the attending physician might be threatened. This is suggested by the fact that "consultants of a pair" more often agree with the intended performance of EAS than other consultants, although this difference is not statistically significant. A possible way of assuring independence of the consultant while safeguarding the consultant's accessibility would be to appoint independent trained consultants who could be contacted by all physicians in a region. Such a system was implemented for general practitioners in Amsterdam in 1997.8 It might also be useful in increasing the frequency of consultation, and possibly the reporting of EAS. The reasons given by consultants for advising against EAS all related to the requirements for prudent practice; the fact that physicians very rarely carry out EAS when the consultant advises against it suggests that consultation can have an important function in assuring the quality of this kind of medical practice. However, our results do not show how often consultants agreed with EAS in cases in which not all the requirements for prudent practice were met. Nursing home physicians, neurologists, surgeons and cardiologists are less likely than general practitioners to have been a consultant. A possible explanation is that, for being asked to act as a consultant, it is not only important to have carried out EAS, but also to have done so relatively frequently: general practitioners, respiratory specialists and specialists in internal medicine carry out EAS more frequently than other physicians.6 In general, Dutch physicians do not have much experience in acting as a consultant in cases of intended EAS. Of the 42% of physicians who have been a consultant, only 27% had been a consultant more than three times, and only 3% more than 10 times. Because acting as a consultant differs greatly from a physician's normal working relationship with colleagues and patients, and because the consultation concerns a matter of life and death, it is important that consultants are experienced and specifically trained. A training program for consultants, in which the skills needed, knowledge about the requirements for prudent practice, palliative care and medicotechnical aspects of EAS are addressed, has been developed by the Royal Dutch Medical Association. In the future it might be advisable to permit only specifically trained physicians to act as a consultant. Acknowledgement This study was funded by the Dutch Ministry of Health, Welfare and Sports and the Ministry of Justice. We are indebted to Professor J Th M van Eijk for his comments on previous versions of this manuscript. References Board of the Royal Dutch Medical Association. Vision on euthanasia. In: Euthanasia in the Netherlands. 5th ed. Utrecht 1996. 24-56. Van der Wal G, van der Maas PJ. Euthanasia and other medical decisions concerning the end of life. The Hague, the Netherlands: Staatsuitgeverij, 1996 (in Dutch). Van der Wal G, van der Maas PJ, Bosma JM, et al. Evaluation of the notification procedure for physician-assisted death in the Netherlands. N Engl J Med 1996; 335: 1706-1711. Van der Wal G, Dillmann RJM. Euthanasia in the Netherlands. BMJ 1994; 308: 1346-1349. Onwuteaka-Philipsen BD. The role of the consultant. In: Legemaate J, Dillmann RJM, editors. Physician-assisted death: between norm and practice. 105-114. Bohn Stafleu Van Loghum, Houten 1998 (in Dutch). Van der Maas PJ, van der Wal G, Haverkate I, et al. Euthanasia, physician-assisted suicide, and other medical practices involving the end of life in the Netherlands, 1990-1995. N Engl J Med 1996; 335: 1699-1705. Armitage P, Berry G. Statistical methods in medical research. 3rd ed. Oxford: Blackwell, 1994; 436-440. Dillman RJM, Krug CHM, Onwuteaka-Philipsen B, et al. Support and consultation in cases of euthanasia in Amsterdam. Med Contact 1997; 52: 743-745 (in Dutch). (Received 7 Jul, accepted 21 Dec, 1998) Authors' details Institute for Research in Extramural Medicine, Vrije Universiteit, Amsterdam, The Netherlands. Bregje D Onwuteaka-Philipsen, MSc, Researcher, and Department of General Practice, Nursing Home Medicine and Social Medicine; Gerrit van der Wal, MD, PhD, Professor, and Department of General Practice, Nursing Home Medicine and Social Medicine; Piet J Kostense, PhD, Epidemiologist/Statistician, and Department of Epidemiology and Biostatistics. Department of Public Health, Erasmus University, Rotterdam, The Netherlands. Paul J van der Maas, MD, PhD, Professor. Reprints will not be available from the authors. Correspondence: B D Onwuteaka-Philipsen, Vrije Universiteit, Institute for Research in Extramural Medicine, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands. Email: B. Philipsen. EMGOATmed.vu.nl Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> 1: Definitions Euthanasia was defined as the administration of drugs with the explicit intention of ending the patient's life, at the patient's explicit request. Assisted suicide was defined as the prescription or supply of drugs with the explicit intention of enabling the patient to end his or her own life. Consultation was defined as consultation of a colleague, as stipulated in the notification procedure for EAS. Back to text 2: Physicians consulted in cases of intended EAS, and number of consultations in 1995 in the NetherlandsGeneral practitioners Medical specialists (n=124)* (n=207)† Proportion§ (95% CI) Proportion§ (95% CI) Physicians consultedEver consulted49% (40.2%-58.1%) 30% (23.9%-36.6%) Consulted in 1994 or 199540% (31.3%-49.1%) 22% (16.5%-28.2%) Number (95% CI) Number (95% CI) Consultations in 19952502 (2004-3086) 1424 (1217-1631) Nursing home physicians Total (n=74)‡ (n=405) Proportion§ (95% CI) Proportion§ (95% CI) Physicians consultedEver consulted19% (10.9%-30.1%) 42% (35.6%-47.7%) Consulted in 1994 or 199514% (6.77%-23.7%) 32% (25.1%-40.4%) Number (95% CI) Number (95% CI) Consultations in 199559 (33-98) 3985 (3419-4551) * 4 missing observations; †1 missing observation; ‡ 6 missing observations; § Calculated by direct standardisation.7 Back to text 3: Number of consultations (ever and in 1995) by physiciansGeneral practitioners (n=124)* Specialists (n=207)* Total (n=405)* Proportion‡ (95% CI) Proportion‡ (95% CI) Proportion‡ (95% CI) Number of consultations everno consultation51% (41.9%-59.8%) 69% (62.3%-75.5%) 58% 1 consultation15% (8.61%-21.4%) 10% (5.9%-14.7%) 13% more than one34% (25.7%-42.7%) 21% (15.1%-26.4%) 29% 2 or 323% 7% 18% 4 or 5 5% 4% 5% 6 to 10 5% 7% 5% more than 101% 2% 1% Number of consultations in 1995no consultation54% (70.0%-85.0%) 83% (77.3%-88.1%) 80% one or more46% (36.9%-54.7%) 17% (11.9%-22.7%) 20% 1 consultation32% 9% 13% 2 consultations9% 3% 4% more than 25% 5% 3% * General practitioners: 4 missing observations; medical specialists: 2 missing observations; total: 7 missing observations. †Includes 74 nursing home physicians. ‡ Calculated by direct standardisation.7 Back to text4: Previous consultations between attending physician and consultant*General practitioners (n=40) Specialists (n=39) Total (n=80) Proportion‡ (95% CI) Proportion‡ Proportion‡ Attending physician previously consulted the consultant§53% (36.1%-68.5%) 40% 50% Consultant previously consultedthe attending physician¶46% (30.1%-62.8%) 22% 41% Attending physician and consultantpreviously consulted each other§28% (14.6%-43.9%) 11% 24% CI = confidence interval. * Analysis is restricted to those physicians who had been a consultant twice or more and described their most recent consultation for EAS. †Numbers are too small for calculating confidence intervals. ‡ Calculated by direct standardisation. § Medical specialists: 4 missing observations; total: 4 missing observations. ¶General practitioners: 1 missing observation; medical specialists: 3 missing observations; total: 4 missing observations. Back to text5: Determinants of having ever been a consultant (n = 405)*Number Odds ratio (95% CI) Specialtygeneral practice119 1 nursing homemedicine72 0.42 (0.20-0.87) neurology34 0.36 (0.15-0.89) respiratorymedicine35 0.96 (0.43-2.12) surgery35 0.36 (0.15-0.90) cardiology32 0.21 (0.07-0.65) internal medicine64 0.78 (0.41-1.49) Male327 2.14 (1.08-4.85) Ever carried outEAS166 3.04 (1.91-4.85) * 14 missing observations. CI = confidence interval. EAS = euthanasia or assisted suicide. Back to text6: Confirmation of our estimate of number of consultations From our data on how often physicians had acted as a consultant in 1994 and 1995, we estimated that almost 4000 consultations took place in 1995. This estimate is reasonably consistent with the estimate we can make based on other data. There were 3600 granted requests for EAS, and 44% of 6100 refused requests. Consultation occurs in 63% of acceded requests (in 10%, the attending physician consults two, and in 2% three or more, colleagues) and in 16% of refused requests.2,3 Number of consultations = 0.63 x 3600 + 0.63 x 0.1 x 3600 + 0.63 x 0.02 x 3600 x 2 + 0.16 x 0.44 x 6100 = 3015 consultations. This estimate does not take into account the (unknown) frequency of consultation in the approximately 2625 (0.43 x 6100) requests for EAS that were not carried out because the patient died.6 Back to text

Bregje D Onwuteaka-Philipsen · Piet J Kostense

Research Rainfall, evaporation and the risk of non-contact anterior cruciate ligament injury in the Australian Football League John Orchard, Hugh Seward, Jeanne McGivern and Simon Hood MJA 1999; 170: 304-306 Abstract - Introduction - Methods - Results - Discussion - Acknowledgement - References - Authors' details - - More articles on Emergency medicine Abstract Objective: To determine if weather conditions affect the risk of anterior cruciate ligament (ACL) tear in Australian Football. Design: Prospective observational analytic study of football matches. Setting: The Australian Football League (AFL), a professional competition. Participants: All players in 2280 matches from 1992-1998. Main outcome measures: Surgically-proven ACL injury, not involving a direct contact mechanism, during a match; rainfall; water evaporation. Results: 59 ACL injuries not involving direct contact occurred during the study period, more commonly in cities north of Melbourne (χ2 = 17.0; df = 1; P < 0.001). Senior grade matches (relative risk [RR], 3.03; 95% confidence interval [CI], 1.52-6.03), high water evaporation in the month before the match (RR, 2.80; 95% CI, 1.53-5.10) and low rainfall in the year before the match (RR, 1.93; 95% CI, 1.12-3.34) were significantly associated with these injuries. Conclusion: Low water evaporation and high rainfall significantly lower the risk of ACL injuries in AFL footballers. The likely mechanism is a softening of the ground, which lowers shoe-surface traction. Consistent extra watering and covering of grounds during periods of high water evaporation may lower the rate of ACL injuries. Introduction Anterior cruciate ligament (ACL) injuries of the knee are the most costly injuries in football at both professional and amateur levels. Of the commonly occurring injuries, they are the most devastating for the player, as they usually require reconstruction and long term rehabilitation in order to retain normal knee function. In the Australian Football League (AFL), ACL injuries account for 12% of all missed playing time,1 which costs the competition over $1 million annually in injury payments alone. The rate of ACL injury in the AFL competition has increased over recent years.2 The exact numbers and costs of ACL injuries in amateur football are unknown. One report that tried to estimate the cost of sports injuries in Australia3 suggested that the cost of ACL injuries in all grades and codes of football was at least 10% of the nation's entire bill for sports injuries. It estimated 5000 football-related ACL injuries in Australia annually, directly costing $5000 each (not including lost work time and the increased susceptibility to later knee problems caused by these injuries).4 Recent studies have noted that there have been relatively more ACL injuries in the early months of the AFL season, in non-Victorian games, and in recent seasons of dry weather.2,5 Our aim was to examine the strength of the relationship of weather conditions to ACL injury. Methods We studied 2280 matches (all AFL home and away season, finals, reserve grade and Ansett Cup matches which occurred from 1992-1998 in the cities of Adelaide, Brisbane, Canberra, Darwin, Geelong, Hobart, Melbourne, Perth and Sydney), involving 2239 individual players. Approximately 75% of the matches were held in Melbourne, 5% to the south (Geelong and Hobart) and the remaining 20% in the northern cities. The occurrence of ACL injuries was determined by an ongoing injury surveillance program, which has attempted to determine the cause of every game missed through injury of listed players. The accuracy of this survey in determining the cause of missed games reached 100% in 1997, and has been greater than 90% in every year.1 In addition, a separate register for ACL injuries is held by the AFL. ACL injuries in the AFL are managed surgically and have the diagnosis proven at the time of simultaneous arthroscopy and reconstruction. The mechanism of injury was recorded by team doctors and divided into the categories of direct contact (where the player's knee or leg was contacted by another player) and no direct contact (which was subdivided into indirect contact and no contact). Daily weather variables were measured prospectively (but obtained by us retrospectively) by the Bureau of Meteorology at central locations in each city studied. No differentiation was made between rainfall in the differing suburbs of any city, except for Waverley Park (30 km from the centre of Melbourne), for which rainfall data were taken from the nearest centre (Moorabbin). Maximum and minimum temperature of the day of the match, rainfall, water evaporation and maximum wind gust were the raw weather variables considered. Water evaporation is a meteorological variable measuring the change of surface water into water vapour -- it is affected by temperature, sunshine, humidity and wind.6 Composite rainfall and evaporation variables were created (measuring the totals for the previous 7, 14, 28, 90 and 365 days), which were considered to have had potentially more effect on ground conditions than the weather only on the day of the match. Statistical analysis was carried out using SPSS for Windows.7 Chi-square and t tests (after variances assessed using Levene's test) were performed in the initial stages of the analysis. Multivariate analysis was performed using a logistic regression forward stepwise technique, with a significance of 0.05 to enter the equation. Continuous variables in the logistic regression were redefined into binary variables based on group median values, to calculate risk ratios adjusted for confounding. Results There were 111 surgically-proven ACL tears recorded in AFL players during the study period. Excluded from analysis were 33 injuries that did not occur in AFL matches (13 occurred during practice matches, 14 during training sessions and six in other league matches). Of the 78 injuries in AFL matches, 19 occurred through direct contact, 15 involved indirect contact (to another part of the body than the leg) and there was no contact involved in 44. Overall, games played north of Melbourne had a significantly higher rate of all ACL injuries (Table). However, injuries involving contact were not significantly associated with being north of Melbourne, although indirect-contact injuries were more common north of Melbourne. For the 59 ACL injuries that did not involve direct contact, the most predictive rainfall and evaporation variables for ACL injury were 28-day evaporation (t = - 3.8; df = 59; P < 0.001) and 365-day rainfall (t = 1.34; df = 2278; P = 0.18). Other significant associations were higher grade of match (t = 4.8; df = 59; P < 0.001), lower minimum temperature (t = - 3.7; df = 59; P < 0.001) and month (fewer injuries in winter) (t = 3.1; df = 2278; P = 0.002). Non-significant associations were night games (t = - 1.7; df = 59; P = 0.09) and wind speed (t = - 0.18; df = 2278; P = 0.86). Although 365-day rainfall was not significant according to the t test, this variable was entered into the logistic regression equation as significant. This is because of the confounding effect of evaporation -- venues with high evaporation also tend to have high rainfall. In a multivariate analysis including evaporation, variance in rainfall is more significant than when rainfall is considered alone. In contrast, night games and minimum temperature had less significance in the logistic regression model. All variables were considered in a logistic regression model with match grade, 28-day evaporation and 365-day rainfall qualifying to be entered into the equation. Senior grade matches had a 3.03-times risk of injury compared with reserve grade matches (95% confidence interval [CI], 1.52-6.03). Matches with high evaporation in the previous 28 days (> 48 mm) had a 2.80-times greater risk of injury (95% CI, 1.52-6.03). Matches with low rainfall (< 449 mm) in the previous year had a 1.93-times greater risk of injury (95% CI, 1.12-6.03). Figures 1 and 2 illustrate a strong association between the rate of ACL injuries not involving direct contact and 28-day evaporation and 365-day rainfall, respectively, for the matches in Melbourne over the study period. Discussion Risk factors for injury can be divided into intrinsic (personal) and extrinsic (environmental). Two intrinsic risk factors for ACL injury have been established: female sex8-11 and narrowed intercondylar notch.12-14 In a recent study, both factors were prospectively followed, and it was concluded that narrow intercondylar notch accounts for the increased number of ACL tears seen in female athletes. At this stage, narrowed intercondylar notch is not a reversible risk factor, but it can be measured at the time of injury and used to counsel athletes on the risk of recurrence, particularly to the contralateral knee. The most promising extrinsic risk factors postulated relate to the shoe-surface interface. It has been hypothesised for many years that increasing traction between a football boot and the playing surface would cause an increase in the rate of knee injuries.15 A recent study showed that American football boots, with a greater number of cleats and higher torsional resistance, were prospectively associated with an increased number of ACL injuries.16 Our results show that high water evaporation in the month before and low rainfall in the year before an AFL match confer an increased risk of ACL injury. This relationship is strong for most injuries not involving contact, but may not apply when the mechanism of injury involves a direct blow to the knee. The mechanism of this association is almost certainly through ground-related factors (either soil moisture content or amount and/or quality of grass). Increased speed of the game on dry grounds may also be relevant. These results are in keeping with the theory that excessive shoe-surface traction is a risk factor for ACL injury. Friction and torsional resistance from football boots has been shown to be higher in dry conditions on natural grass compared with wet conditions.17 In a recent review of non-contact ACL injuries in American Football, it was noted that almost all injuries on natural grass occurred in dry conditions,18 but that review did not measure or control for conditions on days when injury did not occur. We found that the long term effects of rainfall and water evaporation (over a period of months) are more relevant than the amount of rainfall and evaporation on the day or in the days leading up to a match. Further studies are required to determine the exact mechanism by which this relationship occurs and what the effects of intervention would be. The AFL has embarked on a study, beginning with the 1998 season, where matches have ground hardness readings taken with a Penetrometer, a device used in horse racing to measure track hardness. Penetrometer results are reliable and correlate with the speed of races.19 The preliminary results of the AFL study confirm that low rainfall and high evaporation are associated with hard (low) Penetrometer readings (< 4.7 cm).20 We did not study differences between ground conditions in coastal and inland locations, as (except for Canberra) all the major AFL venues are currently in coastal cities. Further study could include inland cities, which may experience different ground conditions due to much colder and drier winters. Irrespective of their mechanism of action, the effects of high water evaporation and low rainfall could be reversed on football grounds by consistently watering grounds during times of lower rainfall and covering them during times of increased sunshine. If grounds were prepared in this way to simulate the ground conditions typically experienced in a Melbourne winter, the number of ACL injuries would almost certainly be reduced. This is unlikely to lead to an increase in injuries of other types, as overall injury rates are consistently higher outside Victoria than in Victoria.1,5 In rugby league in the United Kingdom, injury rates increased across the board when the season was changed from winter to summer,21,22 suggesting harder grounds may be a universal risk factor for football injuries. In AFL, the main competing concern would be whether games played on consistently softer grounds would be a lesser spectacle for the attending and television public. In amateur football, similar reductions in ACL injuries could probably be achieved, without the standard of spectacle being an issue. The cost of manipulating ground conditions might seem initially prohibitive in this environment, but when the massive cost of ACL injury is considered, great overall savings could be made. In conclusion, low water evaporation and high rainfall significantly lower the risk of non-contact ACL injuries in AFL footballers. The mechanism is likely to be a softer surface, with lower shoe-surface traction and consequently less force transferred to the knee in movements such as pivoting. Consistent extra watering and covering of grounds during times of high water evaporation (sunny, windy periods with no rain) is likely to lower the rate of these devastating and costly injuries. Acknowledgement The Australian Football League funds the AFL Injury Surveillance System from which data for this study were derived. References Orchard J, Wood T, Seward H. AFL injury report 1997. Football Record 1998; 87: 54-61. Seward H. Can ACL injuries be prevented? In: Australian Conference of Science and Medicine in Sport. Canberra: Sports Medicine Australia, 1997. Egger G. Sports injuries in Australia: causes, costs and prevention. Sydney: National Better Health Program, 1990. Deacon A, Bennell K, Kiss ZS, et al. Osteoarthritis of the knee in retired, elite Australian Rules footballers. Med J Aust 1997; 166: 187-190. Orchard J, Seward H, Garlick D. Ground conditions and AFL injuries. In: Australian Conference of Science and Medicine in Sport. Canberra: Sports Medicine Australia, 1997. Lewis R, editor. Meteorological glossary. 6th ed. London: HMSO Publications, 1991. SPSS for Windows [computer program]. Version 6.0. Chicago, Ill: SPSS Inc, 1992. Arendt E, Dick R. Knee injury patterns among men and women in collegiate basketball and soccer. NCAA data and review of the literature. Am J Sports Med 1995; 23: 694-701. Ferretti A, Papandrea P, Conteduca F. Knee ligament injuries in volleyball players. Am J Sports Med 1992; 20: 203-207. Gray J, Taunton J, McKenzie D. A survey of injuries to the anterior cruciate ligament of the knee in female basketball players. Int J Sports Med 1985; 6: 314-316. Bjordal J, Arnoy F, Hannestad B, Strand T. Epidemiology of anterior cruciate ligament injuries in soccer. Am J Sports Med 1997; 25: 341-345. Souryal T, Moore H, Evans J. Bilaterality in anterior cruciate ligament injuries: associated intercondylar notch stenosis. Am J Sports Med 1988; 16: 449-454. Shelbourne K, Facibene W, Hunt J. Radiographic and intraoperative intercondylar notch width measurements in men and women with unilateral and bilateral anterior cruciate ligament tears. Knee Surg Sports Traumatol Arthrosc 1997; 5: 229-233. Shelbourne K, Davis T, Klootwyk T. The relationship between intercondylar notch width of the femur and the incidence of anterior cruciate ligament tears: a prospective study. Am J Sports Med 1998; 26: 402-408. Torg J, Quendenfeld T, Landau B. The shoe-surface interface and its relationship to football knee injuries. J Sports Med 1974; 2: 261-269. Lambson R, Barnhill B, Higgins R. Football cleat design and its effect on anterior cruciate ligament injuries: a three year prospective study. Am J Sports Med 1996; 24: 155-159. Heidt R, Dormer S, Cawley P, et al. Differences in friction and torsional resistance in athletic shoe-turf surface interfaces. Am J Sports Med 1996; 24: 834-842. Scranton P, Whitesel J, Powell J, et al. A review of selected noncontact anterior cruciate ligament injuries in the National Football League. Foot Ankle Int 1997; 18: 772-776. Neylan J, Stubbs A. Assessing racetrack conditions: a review of available devices. Canberra: Rural Industries Research & Development Corporation, 1998. Orchard J. Measurement of football ground hardness using the racetrack Penetrometer [abstract]. Med Sci Sports Exer. In press, 1999. Hodgson Phillips L, Standen P, Batt M. Effects of seasonal change in rugby league on the incidence of injury. Br J Sports Med 1998; 32: 144-148. Gissane C, Jennings D, White J, Cumine A. Injury in summer rugby league football: the experiences of one club. Br J Sports Med 1998; 32: 149-152. (Received 30 Jul, accepted 28 Nov, 1998) Authors' details Sports Medicine Unit, University of New South Wales, Kensington, NSW. John Orchard, MB BS, FACSP, Visiting Fellow. Australian Football League Medical Officers Association, Melbourne, VIC. Hugh Seward, MB BS, FACSP, President; Jeanne McGivern, MB BS, FRCS, Club Medical Officer; Simon Hood, BAppSci(PE), Research Officer. Reprints: Dr J Orchard, South Sydney Sports Medicine, 111 Anzac Parade, Kensington, NSW 2033. Email: johnorchardATmsn.com.au Make a comment Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> Back to text Back to text Back to text

John Orchard · Hugh Seward · Jeanne McGivern · Simon Hood

Research Colorectal cancer after open-access colonoscopy: a community and case survey John Croese MJA 1999; 170: 251-254 For editorial comment, see Bolin & Korman Abstract - Introduction - Methods - Results - Discussion - References - Author's Details - - More articles on Gastroenterology Abstract Objective: To evaluate whether colonoscopy protects against subsequent colorectal cancer (CRC). Design: Case and population survey. Setting: Townsville region in northern Queensland, between mid 1985 and January 1998. Subjects: All 8430 patients who underwent 11 148 colonoscopies performed by the author at the Mater Private Hospital (a community-based open-access colonoscopy service) between July 1985 and December 1996; those who were subsequently diagnosed with CRC, to January 1998; and all 476 residents diagnosed with colorectal cancer between 1994 and 1997. Main outcome measures: Age-standardised CRC incidence for 1994-1997 for patients who had had a previous colonoscopy and for the remaining community; Dukes' grade of CRCs. Results: For people aged 50 years and over, the incidence of CRC was significantly lower among those who had had a previous colonoscopy than in the remaining community (1.14 versus 2.31 per 1000 patient-years; P = 0.0046). For people aged 35-49 years, the incidence was 0.35 versus 0.31 per 1000 patient-years (P = 0.86). Thirty-one CRCs developed in 29 people who had had previous colonoscopy; only five of these CRCs were graded Dukes C, with none graded Dukes D. In contrast, almost half the CRCs in the rest of the community were graded Dukes C or D (P < 0.001). All but one of those diagnosed with CRC on repeat colonoscopy had risk factors (personal or family history), and 23 of the CRCs were subclinical, with 20 being diagnosed during surveillance colonoscopy. Conclusions: Patients aged over 50 years who had previously undergone a colonoscopy and ensuing treatment were less likely to be diagnosed with CRC than otherwise expected. Surveillance colonoscopy led to diagnosis of CRCs with lower Dukes grades. Introduction Colorectal cancer (CRC) is the most common internal malignancy and the second most common cause of death from cancer in Australia. CRC incidence in Australia is similar to that in other developed countries,1 but in the US both incidence and mortality are now decreasing.2 This change has been attributed to removal of premalignant polyps, detection of proportionally more early lesions by colonoscopy, and more effective treatment.3 Strategies based on colonoscopic surveillance and targeting people at increased risk of developing CRC are being promoted.3-5 However, colonoscopy, particularly in community-based, open-access practice, has not been shown to reduce CRC mortality. Indeed, although the rate of colonoscopies in Australia has increased fourfold since 1984, the incidence of CRC in New South Wales between 1973 to 1992 continued to increase by 2% per year in men and 0.9% per year in women.6This study aimed to evaluate whether colonoscopy protects against subsequent CRC by comparing CRC incidence and pathological grading between people who have had a previous colonoscopy and the rest of the population in a geographically isolated area. Methods Setting The study was set in Townsville and the surrounding region (defined by the postcodes 4804-4822, 4849 and 4850; Figure 1). Townsville is a regional centre in northern Queensland that provides centralised health services, including colonoscopy, for a population of 198 000 dispersed over 200 000 km2. The nearest alternative colonoscopy services are located at Cairns and Mackay, 400 km distant. Colonoscopy patients Subjects were patients who underwent colonoscopy performed by myself at the Mater Private Hospital, Townsville. All patients who underwent colonoscopy between July 1985 and December 1996 were identified, most from the hospital's detailed computerised records, but some of those examined between 1985 and 1990 from a hospital work ledger which gave only surname and given name. In addition, detailed demographic and clinical information was collected prospectively in a procedural database for all colonoscopy patients from April 1994 to December 1997. Similar information was obtained retrospectively from the case records of 600 randomly chosen patients who underwent colonoscopy between 1986 and 1990. Colonoscopic procedures and surveillance Colonoscopies were performed on patients referred by a general practitioner or specialist either for surveillance or for investigation of symptoms. Through concessions available until mid 1996, the service was equally available to all patients irrespective of financial resources. Fibreoptic colonoscopes were used before 1990, and video colonoscopes after then. Patients were lightly sedated with fentanyl (100 µg) and midazolam (2.5-5 mg). Treatment (eg, polypectomy, CRC resection) was given as necessary. Surveillance recommendations were mostly included in procedure reports and passed to both the patient and the referring doctor. While these recommendations changed over time consistent with published guidelines,3,7 a general summary is: Annual surveillance for either active ulcerative pancolitis of seven years' duration or longer or a previous malignancy plus a family history of hereditary non-polyposis colorectal cancer (HNPCC);3,7 One- to two-yearly surveillance for a previous CRC before 50 years and for those older than 25-40 years with either CRC developing in a first-degree relative before 50 years or a family history of HNPCC; Two- to five-yearly surveillance for longstanding quiescent pancolitis or active limited colitis, CRC or polyps in a first-degree relative, previous CRC, or large (>1 cm diameter) or multiple colonic polyps; and Five- to 10-yearly surveillance, depending on age, for a small adenomatous polyp. Colorectal cancer diagnoses All patients diagnosed with CRC in Townsville between January 1994 and December 1997 were identified retrospectively by searching the computerised databases of all three pathology services, three hospitals, three endoscopy services, three colonoscopists (including myself) and one oncology service provider in Townsville, and from the CRC audits maintained by the six surgeons in Townsville. From 1995, patients diagnosed with CRC were also identified prospectively by clinicians and institutions. Patients diagnosed with CRC who had had a previous colonoscopy performed by myself at the Mater Private Hospital were identified to January 1998. Clinical records of all patients diagnosed with CRC were audited by myself. A modified Dukes classification (A, B, C or D) was used for staging cancer spread.8,9 A malignant polyp was classified separately if colonoscopic resection was regarded as the definitive treatment. In cases of synchronous lesions, the lesion with the most invasive grading was registered. Incidence of CRC Colonoscopy population: The incidence of CRC was calculated as the number of cases per thousand patient-years for the period 1994-1997 for patients who had had a previous colonoscopy and still lived in the region in 1997 (colonoscopy population). Residence was determined from the electoral register current in January 1997,10 which is considered reliable as voter registration is compulsory in Australia. To reduce mismatch errors caused by individuals with identical names, only patients with a known middle name (duplication rate, 0.3%) were cross-referenced against voters who also had a recorded middle name (duplication rate, 1.3%). The number of patients without a middle name who were still resident was estimated and added to the above on the assumption that the proportion still resident would be the same in the groups with and without a known middle name. CRC incidence in each year was calculated for patients who had undergone previous colonoscopy up until the previous calendar year. For example, the incidence of CRC in 1994 was calculated for patients who had undergone previous colonoscopy up to 1993. Age of colonoscopy patients was determined for the year of incidence. The number of patient-years was the total for all patients in a given age range who had previously had a colonoscopy up to 1993, 1994, 1995 and 1996. Community: The incidence of CRC in the remaining population (community) was determined from the number of cases that occurred between 1994 and 1997 in people not registered as a colonoscopy patient per the region's population less the colonoscopy population. Population data were obtained from the August 1996 census undertaken by the Australian Bureau of Statistics.9 Statistical analyses Binary data were compared in two by two contingency tables using chi-squared analyses.12 The age-standardised incidences of CRC in colonoscopy patients versus the community were tested for the hypothesis that the ratios were equal to one.13 Results Colonoscopies From mid 1985 to the end of 1996, I performed 11 148 colonoscopies on 8430 patients (Figure 2). The number increased steadily, from 590 in the 18 months 1985-1986 to 2708 in the two years 1995-1996. The number of repeat colonoscopies increased from 12 (2.0%) in 1985-1986 to 875 (32.3%) in 1995-1996. Clinical and procedural characteristics are summarised in Box 1. Slightly more women than men had colonoscopies. Patients undergoing repeat colonoscopies were an average six years older than those newly referred and were more likely to have had surveillance for increased CRC risk as the primary indication (50.7% of repeat colonoscopies versus 15.0% of first colonoscopies; P < 0.0001). Primary indication also varied with time. For example, an abnormal barium enema was a common indication before 1991 (7.0%), but accounted for few after 1994 (0.3%; P < 0.0001). In contrast, a family history of polyps or CRC accounted for a greater proportion of colonoscopies after 1994 (10.6% of first and 11.2% of repeat colonoscopies) than before 1991 (6.3%; P < 0.0001). From the outset, the caecal completion rate exceeded 95%, and from 1994 it was 98.9% overall and 99.5% in those without a malignant obstruction. Polyps were diagnosed (and removed) in a greater proportion of repeat than first colonoscopies (36.1% versus 29.8%; P < 0.0001). Both these rates were higher than for colonoscopies performed before 1991 (24.5%; P < 0.0001). However, CRC was diagnosed less often in repeat than in first colonoscopies (0.6% versus 2.2%; P = 0.001). Resident populations Complete details, including a middle name, were recorded for 5762 of the 8430 colonoscopy patients (68.4%), and 4200 of these (72.9%) were registered voters and residents of the Townsville region in 1997. A surname and one given name only were recorded for the remaining 2668 patients -- 1913 from the hospital's computer register and 755 from the work ledger. This gave an estimated total number of resident colonoscopy patients of 6195 in 1997. Colorectal cancers Between 1994 and 1997, 476 new CRCs were diagnosed in residents of the Townsville region, with 474 in people aged over 35 years. Eighteen were in patients who had had a previous colonoscopy; each of these was diagnosed per colonoscopy by myself, nine at the study hospital (registered in the procedural database and shown in Box 1), and the remainder elsewhere. Incidences of CRC between 1994 and 1997 are shown in Box 2. In people aged over 50 years, the annual incidence of CRC in the colonoscopy population (1.14) was just less than half that in the remaining community (2.31; P = 0.0046). Between July 1985 and January 1998, I diagnosed 31 CRCs in 29 patients who had had a previous colonoscopy (two patients had a second CRC diagnosed two years after the first in each case). All but one of these patients had a personal or family history that warranted surveillance, and 21 had been enrolled in surveillance programs, with 20 (65%) having had multiple previous colonoscopies (mean, 3.4; range, 2-9). For 20 of the CRCs, planned surveillance was the indication for the repeat colonoscopy. Among the 11 people with symptoms as the primary indication, these symptoms were considered unrelated to the CRC in at least three. The time between most recent previous colonoscopy and diagnosis averaged 37 months (range, 3-136 months). Staging of CRCs is shown in Box 3. Metastatic spread from CRCs was less common in patients who had had a previous colonoscopy than in the community; only five of the 31 cases in colonoscopy patients were graded C, and none were graded D, while 219 of the 458 community cases (48%) were graded C or D (P < 0.001). Among the five colonoscopy patients with metastatic spread (Dukes C), the time between most recent previous colonoscopy and diagnosis was 19, 24, 29, 32 and 70 months, respectively. Discussion The study evaluated a colonoscopic service that followed and promoted contemporary surveillance guidelines similar to those currently recommended by professional cancer and gastroenterological societies.3 The incidence data suggest, but do not prove, that colonoscopic surveillance confers a benefit. Age-standardised incidence of CRC among people aged 50 years and over in the Townsville region was lower among those who had had a previous colonoscopy, along with any treatment considered necessary (eg, polypectomy or bowel resection), than in the community. This was despite the fact that many of those who had had a previous colonoscopy had a personal or family history likely to increase their risk of developing CRC. Furthermore, the CRCs that occurred in those who had had a previous colonoscopy were of a lower Dukes grade than those occurring in the community. The difference in incidence suggests but does not prove that colonoscopy is protective against CRC. CRC incidence for 1994-1997 in those who had had a previous colonoscopy may have been reduced, at least partly, by detection of subclinical CRCs during their pre-1994 colonoscopies. On the other hand, selection bias suggests that these people would develop more CRCs than the general population. The impact of each of these factors could not be measured, and there is no historical benchmark or matched population for comparison of outcomes. However, the result does suggest that colonoscopy confers a benefit, possibly because of removal of polyps and certainly because of detection and treatment of subclinical CRCs. In people aged 35-49 years, CRC incidence in those who had had a previous colonoscopy was similar to that in the community. Without a control group, a benefit of colonoscopy cannot be dismissed, as the colonoscopy group was expected to have higher CRC incidence. However, it is evident that, because of the large number of people aged 35 to 49 years and the low incidence of CRC, surveillance must be targeted to be effective. Polypectomy rate was high, and higher in repeat than in first colonoscopies. This also implies that patients having repeat colonoscopies had increased risk of developing CRC.14 While the high polyp rate may have been due to their older average age,15 the latter would also be expected to increase the CRC rate, which did not occur. Given an expectation that all lesions seen at the previous colonoscopy had been dealt with, this outcome (high polyp versus low CRC rate) validates the selection criteria for surveillance. The higher polypectomy rate after 1994 compared with that before 1990 probably relates to other circumstances, such as a higher caecal completion rate, while both indices probably reflect improved instrument technology. Thirty-one new primary cancers developed in 29 colonoscopy patients, with two-thirds diagnosed by planned surveillance colonoscopy. Metastatic spread occurred in only five of these patients. These findings confirm, firstly, that new CRCs will develop and, secondly, that outcome can be improved through early (subclinical) diagnosis.3,16 The number of cancers diagnosed in patients who had had a previous colonoscopy was of concern and suggested lesions might have been missed in the earlier examination. Colonoscopy, even when performed by an expert, does not identify all small lesions, while adverse conditions sometimes obscure gross pathology.17 Colon morphology, quality of the bowel preparation, instrument capabilities and operator proficiency may also impose limitations.3,18 However, substandard colonoscopy is unlikely to have been responsible. The caecum was reached at a rate exceeding the accepted standard (95%),3 and CRCs were observed in all parts of the bowel, arguing against an operator-dependent blind spot. Possibly, the comparatively large number of CRCs found in people undergoing colonoscopic surveillance was simply the outcome of increasing enlistment of an appropriate, at-risk cohort. Although most sporadic CRCs evolve slowly through malignant transition in a polyp, this sequence is truncated or absent for some sporadic CRCs and for CRCs developing in patients with ulcerative colitis or a genetic predisposition.19 It is unrealistic to imagine that surveillance colonoscopy with polypectomy as necessary will much reduce CRC incidence in such at-risk populations. Indeed, it might conceivably increase apparent incidence by uncovering subclinical CRCs. The results support the current practice of targeting individuals with recognised risk factors for surveillance colonoscopy. However, it is important to explain to patients that surveillance does not provide complete protection and that new CRCs are inevitable. Early diagnosis through repeated testing is the essential component of surveillance-derived protection. References Parkin DM, Pisani P, Ferlay J. Estimates of the world-wide incidence of eighteen major cancers in 1985. Int J Cancer 1993; 54: 594-606. SEER Program (National Cancer Institute). Surveillance, epidemiology, and end results (SEER) program. Bethesda, Md: National Cancer Institute, 1973-1992. Winawer SJ, Fletcher RH, Miller L, et al. Colorectal cancer screening: clinical guidelines and rationale. Gastroenterology 1997; 112: 594-642. Bolin TD, Korman MG. How can we reduce the incidence and mortality of colorectal cancer [editorial]? Med J Aust 1997; 166: 175-176. Macrae FA. Screening for colorectal cancer, 1996 [editorial]. Med J Aust 1996; 165: 102-105. Bell JC, McCredie M, Coates MS, Armstrong BK. Trends in colorectal cancer incidence and mortality in New South Wales, 1973-1992. Med J Aust 1997; 166: 178-181. Mecklin J-P, Jarvinen HJ, Peltokallio P. Cancer family syndrome. Genetic analysis of 22 Finnish kindreds. Gastroenterology 1986; 90: 328-333. Astler VB, Coller FA. The prognostic significance of direct extension of carcinoma of the colon and rectum. Ann Surg 1954; 139: 846-851. Dunlop MG. Polyps and carcinoma. In: Shearman DJC, Finlayson N, Camillieri, Carter D, editors. Diseases of the gastrointestinal tract and liver. 3rd ed. New York: Churchill Livingstone, 1997: 1399-1448. Australian Electoral Commission. Elector information access system. Electoral roll information for Queensland. Canberra: Australian Electoral Commission, 1997. Australian Bureau of Statistics. 1996 census of population and housing. Community profile, Canberra: ABS, 1996 (Cat. no. 2020.0). Approximate significance for contingency tables. In: Matthews DE, Farewell VT. Using and understanding medical statistics. 2nd ed. Basel: Karger, 1988: 20-66. The binomial distribution. In: Snedecor GW, Cochran WG. Statistical methods. 8th ed. Ames: Iowa State University Press, 1989: 107-134. Atkin WS, Morson BC, Cuzick J. Long-term risk of colorectal cancer after excision of rectosigmoid adenomas. N Engl J Med 1992; 326: 658-662. Williams AR, Balasooriya BAW, Day DW. Polyps and cancer of the large bowel: a necropsy study in Liverpool. Gut 1982; 123: 835-842. Mandel JS, Bond JH, Church TR, et al. Reducing mortality from colorectal cancer by screening for fecal occult blood. Minnesota Colon Cancer Control Study. N Engl J Med 1993; 328: 1365-1371. (Published erratum appears in N Engl J Med 1993; 329: 672.) Rex RK, Cutler CS, Lemmel GT, et al. Colonoscopic miss rates of adenomas determined by back-to-back colonoscopies. Gastroenterology 1997; 112: 24-28. Baille J, Ravich WJ. On endoscopic training and procedural competence. Ann Intern Med 1993; 118: 73-74. Kuramoto S, Oohara T. Flat early cancers of the large intestine. Cancer 1989; 64: 950-955. (Received 1 May, accepted 21 Dec, 1998) Author's Details 42 Ross River Road, Townsville, QLD. John Croese, MD, FRACP, Gastroenterologist. Reprints will not be available from the author. Correspondence: Dr J Croese, 42 Ross River Road, Townsville, QLD 4812. Email: jcroeseATmedeserv.com.au Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> Back to text Back to text Back to text Back to text Back to text

John Croese

Research Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial Carlos D Scheinkestel, Michael Bailey, Paul S Myles, Kerry Jones, D James Cooper, Ian L Millar and David V Tuxen MJA 1999; 170: 203-210 For editorial comment, see Moon & DeLong Abstract - Introduction - Methods - Results - Discussion - Conclusion - References - Authors' details - - More articles on Anaesthesia and intensive care Abstract Objective: To assess neurological sequelae in patients with all grades of carbon monoxide (CO) poisoning after treatment with hyperbaric oxygen (HBO) and normobaric oxygen (NBO). Design: Randomised controlled double-blind trial, including an extended series of neuropsychological tests and sham treatments in a multiplace hyperbaric chamber for patients treated with NBO. Setting: The multiplace hyperbaric chamber at the Alfred Hospital, a university-attached quarternary referral centre in Melbourne providing the only hyperbaric service in the State of Victoria. Patients: All patients referred with CO poisoning between 1 September 1993 and 30 December 1995, irrespective of severity of poisoning. Pregnant women, children, burns victims and those refusing consent were excluded. Intervention: Daily 100-minute treatments with 100% oxygen in a hyperbaric chamber -- 60 minutes at 2.8 atmospheres absolute for the HBO group and at 1.0 atmosphere absolute for the NBO group -- for three days (or for six days for patients who were clinically abnormal or had poor neuropsychological outcome after three treatments). Both groups received continuous high flow oxygen between treatments. Main outcome measures: Neuropsychological performance at completion of treatment, and at one month where possible. Results: More patients in the HBO group required additional treatments (28% v. 15%, P = 0.01 for all patients; 35% v. 13%, P = 0.001 for severely poisoned patients). HBO patients had a worse outcome in the learning test at completion of treatment (P = 0.01 for all patients; P = 0.005 for severely poisoned patients) and a greater number of abnormal test results at completion of treatment (P = 0.02 for all patients; P = 0.008 for severely poisoned patients). A greater percentage of severely poisoned patients in the HBO group had a poor outcome at completion of treatment (P = 0.03). Delayed neurological sequelae were restricted to HBO patients (P = 0.03). No outcome measure was worse in the NBO group. Conclusion: In this trial, in which both groups received high doses of oxygen, HBO therapy did not benefit, and may have worsened, the outcome. We cannot recommend its use in CO poisoning. Introduction Carbon monoxide (CO) poisoning is one of the most common lethal poisonings,1 with neurological or psychiatric sequelae occurring in up to 67% of survivors.2Treatment with hyperbaric oxygen (HBO) is recommended because it reduces carboxyhaemoglobin (COHb) dissociation half-life from more than four hours at room air or 45 minutes on 100% oxygen to 23 minutes at 2.5 atmospheres absolute (ATA).3 Carbon monoxide also inhibits cellular respiration by binding to cytochrome oxidase, a component of the mitochondrial electron transport chain.4 Hyperbaric oxygen enhances the dissociation of CO from this enzyme.5 Despite these physiological effects, it has not been established in humans that HBO either improves survival or decreases neuropsychological deficits. Much of the evidence that HBO is more efficacious than normobaric oxygen (NBO) therapy in humans arises from isolated case reports,6-8 uncontrolled clinical observations,9-11 small,12 non-randomised13 and unblinded series9,11,13-20 and incomplete assessment of outcome (no neuropsychological testing).9,11,15-18 All reported non-randomised studies have suggested benefit from HBO. Of the four published randomised studies, two report benefit from HBO12,14 and two report no benefit15,17 (Box 1). Three restricted entry to mildly poisoned patients, while the fourth15 included severely poisoned patients, but did not allocate any to NBO treatment. None of the randomised studies blinded patients by using sham treatments for NBO, only one blinded outcome assessment12 and only one used neuropsychological tests to assess outcome.14 Hence, the benefit of HBO in CO poisoning has been questioned1,2,21-27 and remains unproven. We therefore performed a randomised double-blind trial in patients with all grades of CO poisoning, comparing HBO and NBO (with sham treatments for the NBO group), and using an extended series of neuropsychological tests to assess both persistent and delayed neurological sequelae (PNS and DNS). Methods The multiplace chamber at the Alfred Hospital, a university-attached quarternary referral centre, provides the only hyperbaric service in the State of Victoria (population, 4.5 million; area, 228 000 km2). Between 1 September 1993 and 30 December 1995, most CO-poisoned and all severely poisoned patients were referred for treatment. We included all referred patients, irrespective of severity of poisoning. Patients were excluded if they were pregnant, children, burns victims or if they did not consent. Informed consent to enter the trial was requested from patients with a Mini-mental score >2428 and from the next of kin for those obtunded or with a score ≤24. The Alfred Hospital's Ethics Committee approved the trial, conditional on an independent blinded interim analysis after recruitment of 50 patients (using a stopping rule of P < 0.001); this allowed continuation of enrolment to completion. Randomisation and blinding Patients were randomly allocated to HBO or NBO treatment. To ensure a similar distribution of causes and severity of poisoning in both groups, patients were first stratified into four groups (suicide versus accidental, then mechanically ventilated versus non-ventilated). A hyperbaric technician then allocated patients to treatment groups by opening envelopes chosen from random blocks, each with equal numbers of HBO and NBO selections. To minimise the impact of the trial on daily practice, we used cluster randomisation for patients who presented simultaneously from the same CO exposure, allocating them all to the same treatment group. Cluster randomisation accounted for the difference in numbers between HBO and NBO groups. As patients presenting simultaneously could be uniquely identified by having identical measurements for three continuous baseline severity measurements (exposure time, time to COHb measurement and time to treatment), any effects due to cluster randomisation could be controlled and adjusted for by including these variables in the generalised linear model. The hyperbaric technicians and nursing staff had knowledge of the treatment group but patients and outcome assessor did not. Interventions Before arrival at Alfred Hospital, non-intubated patients received high flow oxygen by non-occlusive facemask and intubated patients received 100% oxygen. All patients were admitted to hospital, received three treatments on a once-daily basis and continuous oxygen by non-occlusive facemask at 14 L/min (100% oxygen for ventilated patients) between treatments. Patients randomised to NBO therapy were treated for 100 minutes in the multiplace chamber with 100% oxygen at 1.0 atmosphere absolute (ATA). Non-ventilated patients used an occlusive facemask attached via a non-rebreathing valve to a Laerdal adult ventilation bag (1.6 L) with an oxygen reservoir (2.6 L; Armund S Laerdal, Stavanger, Norway). The chamber door was closed and the chamber flushed with air regularly to simulate pressurisation, but the chamber was not pressurised (sham treatment). HBO patients received 100% oxygen by hood, occlusive facemask or mechanical ventilator in the hyperbaric chamber for 100 minutes (60 minutes at 2.8 ATA). After the third treatment, patients were reassessed medically and underwent full neuropsychological assessment. Patients who were clinically abnormal or had poor neuropsychological outcome received three further treatments and received high flow oxygen between treatments. Outcome measures Patient assessment at entry included length of CO exposure, COHb level, time from end of exposure to COHb measurement and to treatment, Mini-mental score and clinical effects of poisoning (Box 2). We then assessed patients at completion of treatment (three or six treatments), and, wherever possible, at one month. We attempted to quantify deficits known to occur in CO poisoning by assessing attention, information processing, memory and learning. A clinical psychologist trained in neuropsychological assessment of brain-injured patients performed all tests at completion of treatment and at follow-up. Computerised testing was used to standardise administration and data-recording procedures and increase objectivity. The tests used were the digit span subtest of the Wechsler Adult Intelligence Scale -- Revised,29 comprising (i) Digit span forward and (ii) Digit span backwards (in which patients are asked to repeat a series of numbers read to them), which measures immediate auditory-verbal memory span, working memory and attention; computerised reaction-time tests,30 consisting of (iii) Simple reaction time (in which subjects are requested to press the space bar on a computer keyboard as soon as they see anything appear on the screen) to give a basal measure of alertness or arousal, and (iv) Choice reaction time (which requires subjects to ignore stimuli in a centre box and to respond selectively to the word "SEVEN" as it appears around the periphery of the computer screen) to test selective attention (reaction time was tested because it can show diffuse cerebral dysfunction, and because processing speed is considered to underlie attention deficits31); (v) a score on the Rey auditory verbal learning test, in which a 15-word list (List A) is presented over five learning trials, followed by an interference trial (List B), after which (vi) Short term free recall is tested without any further presentation of the word list, and (vii) Long term free recall is tested 20 minutes later (this provides a measure of learning across trials, and retention of information following short and long delay periods32). Raw scores of these seven neuropsychological tests were converted to z scores ([score - mean in normal population] / standard deviation), and then t scores (McCall's T; an adjusted z score so that the mean is 50 and the standard deviation is 10).33 Age-based and education-based norms were used where available to calculate t scores. A t score more than one standard deviation below the mean was considered abnormal, and two or more abnormal scores constituted a poor outcome. Patients with poor outcome at hospital discharge were considered to have persistent neurological sequelae (PNS). Delayed neurological sequelae (DNS) were defined as morbidity found at follow-up that was not obvious at hospital discharge, or deterioration of neuropsychological subtest scores by more than one standard deviation. Statistical analyses Statistical analyses were made using mixed linear models to adjust for all baseline covariants (age, sex, suicide attempt, COHb level, time to COHb level, duration of exposure, time to treatment, and presence of other drugs). Data were presented as mean and SD, median and interquartile range (IQR) or number and per cent. Continuous data were first assessed for normality and then analysed by unpaired two-tailed Student's t-test, or Wilcoxon rank sum test. Proportions were compared with chi-squared tests (with Yates' correction), or Fisher's exact test, as appropriate, with multiple logistic regression being used to adjust for confounding factors. We calculated odds ratios and 95% confidence intervals (95% CI) for the difference between proportions. The 95% CI for the difference between means and P values were calculated after adjustment for baseline covariants. All statistical analyses were performed using SAS.34 Results Two hundred and thirty patients with CO poisoning were referred for treatment. Thirty-nine were excluded (one child, eight burns victims, and 30 who refused consent) and treated with HBO. Thus, 191 patients entered the trial (Box 2). Based on the most sensitive neuropsychological test (Short reaction time), with 191 patients and a significance level of 0.05, we had greater than 99% power to detect a 10% difference between groups (ie, 408 seconds v. 450 seconds; SD, 63 seconds) (Clinical Trials Design Program, Biosoft, Cambridge, UK). The groups (104 HBO patients, 87 NBO patients) were comparable in age, sex, incidence of suicide attempt, mechanical ventilation, Mini-mental score, and other markers of severity, including loss of consciousness (coma). Forty-four per cent of patients who had attempted suicide (44% HBO and 44% NBO) also had evidence of self-administration of drugs or alcohol. Most of our patients (73%) had severe CO poisoning, defined by any of the following before or on arrival at Alfred Hospital: a Mini-mental score ≤24, COHb level >30%, confusion, focal neurological deficits, loss of consciousness, electrocardiogram abnormalities, arrhythmias, pulmonary oedema, metabolic acidosis, hypotension, convulsions, and cardiac arrest. All mechanically ventilated patients met the criteria of severe poisoning. Overall mortality was 3%, and the incidence of PNS was 71% at hospital discharge and 62% at follow-up, with no significant differences between the HBO and NBO groups (Box 3). A smaller proportion of NBO patients than HBO patients were considered to be medically or neuropsychologically impaired after three treatments and thus received additional treatments (all patients, 15% v. 28%, P = 0.01; severely poisoned patients, 13% v. 35%, P = 0.001). The only statistically significant difference between groups in neuropsychological performance was in the learning test at completion of treatment (Boxes 3 and 4); this was in favour of the NBO group for both all patients (P = 0.01) and severely poisoned patients (P = 0.005). NBO patients had a significantly lower number of abnormal test results at completion of treatment (all patients, 3.4 v. 2.7, P = 0.02; severely poisoned patients, 3.7 v. 2.6, P = 0.008) and, for those severely poisoned, there were fewer NBO patients with a poor outcome (85% v. 65%; P = 0.03). All five relapses (DNS) occurred in HBO patients (P = 0.03) at a median of 40 days (IQR, 29-81 days) after initial treatment; these patients then received a mean 4.5 (SD, 2.5) additional treatments. Although three of these patients improved with further treatments, all DNS patients had a poor outcome after re-treatment, with a mean 6.3 (SD, 1.2) abnormal test results. The evaluation at completion of treatment showed no difference in outcome between the HBO and NBO groups for patients: treated within four hours of exposure; with severe poisoning and treated within four hours of exposure; who required ventilation; and who were accidentally poisoned (as opposed to those who attempted suicide). Only 46% of patients attended the one-month follow-up. Thus, the numbers in subgroups of interest at one month were small, but showed no difference in any test between HBO and NBO groups. Ten patients had chamber-related complications; seven HBO patients experienced ear barotrauma, one HBO patient developed oxygen toxicity (convulsions) and two patients (one HBO and one NBO) developed severe claustrophobia. The incidence of such complications was thus 9% for HBO and 1% for NBO treatment. Discussion In patients with acute CO poisoning, we found no benefit and possible adverse effects of HBO therapy compared with three days of high-flow NBO. Our multiple comparisons between groups may have produced type 1 errors, and some differences may be spurious. However, differences were consistent and all suggested a more detrimental outcome in the HBO group. Despite multiple comparisons, we found no evidence to support HBO therapy. Our findings thus contrast with those of all other published studies, which have suggested benefit or lack of benefit, but never detriment, from HBO therapy (Box 1). To explain this, careful comparison with previous studies is required. Baseline severity No previous study has compared HBO with NBO in severely poisoned patients. Unlike the non-randomised studies (Box 1) which used HBO for all severely poisoned patients and NBO only for mildly poisoned patients,9,13,16,18-20 all patients in our study were randomised. Of the randomised studies (Box 1), three included patients with mild CO poisoning only12,14,17 (two showing benefit and one no benefit from HBO),17 while the fourth compared one versus two HBO treatments for severely poisoned patients.15Whereas most CO poisoning in the northern hemisphere occurs as a result of heating accidents, in Australia most results from suicide attempts. Not only had a high proportion of our patients (69%) attempted suicide, but, as in other studies,9,35 many (44%) had ingested other drugs. Stratified randomisation equalised this factor between groups and hence could not account for lack of benefit in the HBO group. Further, the six potential factors thought to influence baseline severity (listed in the Methods) were subsequently adjusted for in the generalised linear modelling process. This adjustment also accounted for the small imbalances in the data resulting from cluster randomisation. Carboxyhaemoglobin level Although COHb level is often used as an indicator of the severity of CO poisoning and to determine need for HBO,12-16,20 our findings and other reviews9,14,18,24,36-40 have shown no relationship between COHb level and outcome. COHb level depends on CO exposure, time elapsed to measurement and whether or not oxygen has been given. The low COHb levels in our study (HBO 20.5%; NBO 22%) reflect the delay to the measurement and use of high flow oxygen before measurement. Most previous studies did not report time to measurement and used isolated COHb levels to compare severity of poisoning between groups.12-16,20 Our multivariate analysis showed no correlation between outcome and COHb level even when taking the time to measurement into account. The low COHb levels do not explain the lack of benefit of HBO. Treatment delay Animal studies5 reporting beneficial effects of HBO given immediately after CO exposure cannot readily be extrapolated to clinical practice because treatment delay is to be expected in all clinical scenarios. Our study had a geometric mean treatment delay of 7.1 hours (95% CI, 1.9-26.5 hours), which is longer than in others,14,16,20 but well within entry criteria limits of most studies that report treatment delay15,17,39 (Box 1). Some authors have suggested that the benefits of HBO diminish with treatment delay,12,41 that more than six hours' delay increases DNS and mortality,9 and that treatment delay is associated with increased neuropsychological sequelae.13 Other studies have found treatment delay to be unimportant,42 while some case studies43 and small case series7 report HBO benefit regardless of treatment delays ranging from days to months. Most North American hyperbaric facilities surveyed in 1995 treated CO-poisoned patients who had neurological deficits despite presentation delays ranging from six hours to 56 days,44 and HBO has been advocated for DNS occurring weeks after initial exposure.20,44 In our study, analysis of patients commencing treatment within four hours (all patients or severely poisoned only) showed no differences in outcome between HBO and NBO. We also analysed time to treatment in quartiles (<3, 3-6, 6-12 and >12 hours) and found no difference in outcome between HBO and NBO. Further, multivariate regression analysis did not identify delay in treatment as a predictor of poor outcome. Thus, there was no evidence that delay to treatment might explain the lack of benefit from HBO. Oxygen dose There are no universally accepted recommendations for depth of pressurisation or duration of hyperbaric treatment for CO poisoning (Box 1). The only studies of the benefit of multiple treatments reached contradictory conclusions.13,15,38 Raphael et al15 found no difference in recovery at one month among 286 patients with transient loss of consciousness who received either one or two HBO treatments 12 hours apart. Gorman and Runciman reviewed 13 case series involving 3441 patients and concluded that HBO at 2-3 ATA for 1-2 hours on three or more occasions achieved the lowest mortality, PNS and DNS.38Based on the conclusions of Gorman and Runciman, our study was designed to provide maximum advantage for HBO, with a daily 60-minute treatment at 2.8 ATA on three consecutive days. Because the required dose of NBO for treating CO poisoning is unknown, to ensure we did not undertreat patients, and to maximise similarity of treatment in HBO and NBO groups, all our patients received a treatment on at least three consecutive days and continuous oxygen by non-occlusive facemask at 14 L/min between treatments. Compared with most previous studies, we performed more treatments, of longer duration, at higher ATA and in conjunction with prolonged high flow oxygen therapy between treatments (Box 1). Our HBO group received oxygen therapy equating to approximately 35.7 COHb-dissociation half-lives, while the NBO group received the equivalent of 28.5 COHb-dissociation half-lives. Most other studies have used total oxygen doses of less than 7.0 COHb-dissociation half-lives,9,12,14,15,17 with two series using up to 18 COHb-dissociation half-lives.13,16 It is possible that some of the reported beneficial effects of HBO are purely oxygen-dose related, and that adequate NBO, as given in our study, may achieve the same result. This is supported by an uncontrolled study in which a single HBO treatment had no benefit over NBO, but two or more HBO treatments of 60 minutes at 2.8 ATA resulted in significantly less PNS at hospital discharge and DNS at one month (P < 0.005).13 The apparent worse outcome in our HBO group may also be oxygen-dose related, with higher doses of oxygen adding no further benefit and possibly causing adverse effects. Hampson et al45 (discussing seizures rather than neuropsychological sequelae) have suggested that CO-poisoned patients are at greater risk of brain injury because of the higher ATA used in treatment, concomitant use of other drugs and toxins (particularly in patients who have attempted suicide), as well as the underlying CO poisoning. Assessment of outcome Abnormalities of the basal ganglia, subcortical white matter and hippocampus are the most consistent neuropathological findings in victims of CO poisoning42,46 and are associated with deficits of attention, information processing and memory.47 These deficits can be easily missed on casual assessment or simple neurological examination unless specifically targeted. Studies that did not use neuropsychological assessments9,12,15 reported a lower incidence of PNS than those that did,48 including our study. Appropriately targeted neuropsychological assessment provides the most objective, reliable and sensitive evaluation of outcome after CO poisoning,24,49,50 and in studies that did not report these data9,12,15-17 it is possible that significant adverse effects were missed, making resulting conclusions unreliable. The Carbon monoxide neuropsychological screening battery (CONSB)50 does not adequately measure memory, which may be impaired following CO poisoning.47 The neuropsychological tests we used were therefore more comprehensive than the CONSB, very sensitive to the deficits known to occur in CO poisoning and were computerised (thus increasing objectivity). Further, as one clinical psychologist performed all our testing, interviewer bias was eliminated. Because a full pretreatment neuropsychological assessment was not practical, a Mini-mental examination was used as our baseline neuropsychological assessment, as it gives a global assessment of severity of cerebral injury. Although not ideal, it had the advantages that (i) it could readily be performed by the assessing doctor and quantified, (ii) it enabled us to determine which patients were capable of giving informed consent, and (iii) as it was tested on presentation, completion of treatment and at follow-up, patients served as their own "controls". Our definition of an abnormal test result (>1 SD below the mean) would have included 16% of normal patients. This definition was deliberately chosen to be sensitive to small group differences. We defined a poor outcome as at least two test scores more than one standard deviation below the mean, which would have included less than 2.6% of normal patients. While it is possible that the true incidence of poor outcome or PNS may therefore be slightly lower than we report, the important analyses in making the group comparisons were based on the raw data. Non-randomised studies (Box 1) suggest beneficial effects of HBO, but only two13,20 used neuropsychological tests. One used extensive neuropsychometric evaluation at the one-month review,13 but no evaluation before or at completion of treatment. The other used the CONSB before treatment whenever possible,20 but not after treatment. Of the randomised studies (Box 1), one supplemented clinical assessments with electroencephalogram and cerebral blood flow reactivity to acetazolamide,12 but the clinical relevance of these is uncertain, as the abnormal results were found in patients who were clinically normal. Another used the CONSB, but only after completion of treatment and if patients were "fatigued", the tests were performed in the patients' homes within 12 hours, and a three-month review was only a telephone interview. The lack of baseline assessment, the variable circumstances of immediate outcome assessment and the restricted assessment of delayed outcome greatly limit the interpretation of the findings. Insensitive assessments and lack of blinding may also have missed important differences and created bias in these randomised studies. Study outcomes Our high rate of PNS (compared with previous studies) is probably attributable to our high proportion of severe poisonings (73%) and suicide attempts (69%, likely to be associated with depression and possibly a poor outcome on neuropsychological testing), as well as the comprehensive neuropsychological testing we employed. A type 1 error resulting from multiple testing may have contributed, as well as our cautious definition of PNS (≥2 test scores <1 SD below the mean). The rate of DNS in our study (2.6%) is lower than in most previous reports9,13,16,17,51 (especially given our higher proportion of severe poisonings) and possibly the result of effective treatment with higher doses of oxygen. Our findings differ from those of most published series (Box 1). Although all the non-randomised studies9,11,13,16,18-20 have reported benefit from HBO, none had a control group of matching severity, most had no neuropsychological assessment, and all had low doses of oxygen (brief treatment times) in the NBO groups. With these significant limitations, it is not possible to rely on the conclusions of these studies nor to compare them with adequately conducted randomised trials. None of the four randomised trials included pretreatment or follow-up neuropsychological assessments or sham treatment of the NBO group (our study is unique in doing this). Three did not have blinded outcome assessments. Both randomised trials that concluded there was benefit from HBO12,14 studied only patients with mild CO poisoning, thereby excluding the patients in whom the effects of HBO might be most important. The other two found no benefit in HBO and support our findings.15,17 Mathieu et al found a significantly different incidence of neurological sequelae between HBO and NBO at three-month review (9.5% v. 15%; P = 0.016), but not at completion of treatment, one month, six months or 12 months.17 Raphael et al randomised only mildly poisoned patients,15 and both treatment regimens used (HBO and NBO) have been criticised.38 Interim results (61 patients) of a United States randomised controlled trial enrolling all patients, irrespective of severity of poisoning and also using sham normobaric treatments, found no difference in PNS between NBO and HBO.52 Of the four published randomised studies, the two small ones12,14 reported a benefit from HBO, whereas the two larger studies15,17 did not. If our study is included, three studies involving 1395 patients have now shown no benefit for HBO, compared with two studies involving 91 patients which showed a benefit. Thus, it appears that much of the evidence supporting HBO for CO poisoning is flawed. Although our multiple tests increased the likelihood of a type 1 error, as the main outcome measures (the number of abnormal tests and a "poor outcome") were based on combining all tests we have minimised the chance of a spurious result. Delayed review Despite repeated efforts, only 46% of patients attended for follow-up. This low rate was probably affected by many of our patients having characteristics associated with suicide attempts and depression, many being referred from distant locations, and lack of incentive. However, the follow-up rate was equal in both groups, and evenly distributed across subgroups. Our follow-up assessment was more comprehensive than in all but one other study,13 but failed to show benefit for HBO. Others studies have had significant non-attendance rates at delayed review of 11%-47%.12-15,19,48 Most studies do not quote the "drop-out" rate.9,16-18,20 Conclusion Our prospective, randomised controlled trial of CO-poisoned patients of all severities attempted to address the shortcomings of previous studies by incorporating sham treatments for the NBO group, blinded outcome assessment and extensive neuropsychological assessment. Our HBO protocol was designed to provide the maximum potential advantage for HBO therapy based on currently available knowledge. When compared with three days of normobaric oxygen, we could find no evidence that treatment with HBO was beneficial to outcome and therefore do not recommend its use. References Meredith T, Vale A. Carbon monoxide poisoning. BMJ 1988; 2 96(6615): 77-79. Tibbles PM, Perrotta PL. Treatment of carbon monoxide poisoning: a critical review of human outcome studies comparing normobaric oxygen with hyperbaric oxygen. Ann Emerg Med 1994; 24: 269-276. Pace N, Strajman E, Walker EL. Acceleration of carbon monoxide elimination in man by high pressure oxygen. Science 1950; 111: 652-654. Tibbles PM, Edelsberg JS. Hyperbaric-oxygen therapy. N Engl J Med 1996; 334: 1642-1648. Brown SD, Piantadossi CA. In vivo binding of carbon monoxide to cytochrome c oxidase in rat brain. J App Physiol 1990; 68: 604-610. Dean BS, Verdile VP, Krenzelok EP. Coma reversal with cerebral dysfunction recovery after repetitive hyperbaric oxygen therapy for severe carbon monoxide poisoning. Am J Emerg Med 1993; 11: 616-618. Myers RAM, Snyder SK, Linberg S, Adams Cowley R. Value of hyperbaric oxygen in suspected carbon monoxide poisoning. JAMA 1981; 246: 2478-2480. Thomson LF, Mardel SN, Jack A, Shields TG. Management of the moribund carbon monoxide victim. Arch Emerg Med 1992; 9: 208-213. Goulon M, Barois A, Rapin M, et al. Carbon monoxide poisoning and acute anoxia due to breathing coal gas and hydrocarbons. J Hyperbar Med 1986; 1: 23-41. Yang ZD, Sun CQ, Cao XL. Clinical analysis of the effect with hyperbaric oxygen therapy on 672 cases with acute carbon monoxide poisoning. J Hyperbar Med 1986; 1: 188. Roche L, Bertoye A, Vincent P. Comparison de deux groupes de vingt intoxications oxycarbonees traitees par oxygenenormobare et hyperbare. Lyon Med 1968; 49: 1483-1499. Ducasse JL, Celsis P, Marc-Vergnes JP. Non-comatose patients with acute carbon monoxide poisoning: hyperbaric or normobaric oxygenation? Undersea Hyperb Med 1995; 22: 9-15. Gorman DF, Clayton D, Gilligan JE, Webb RK. A longitudinal study of 100 consecutive admissions for carbon monoxide poisoning to The Royal Adelaide Hospital. Anaes Intens Care 1992; 20: 311-316. Thom SR, Taber RL, Mendiguren II, et al. Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Ann Emerg Med 1995; 25: 474-480. Raphael J, Elkharrat D, Jars-Guincestre M, et al. Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication. Lancet 1989; 2: 414-419. Mathieu D, Nolf M, Durocher A, et al. Acute carbon monoxide poisoning: risk of late sequelae and treatment by hyperbaric oxygen. J Toxicol Clin Toxicol 1985; 23: 315-324. Mathieu D, Wattel F, Mathieu-Nolf M, et al. Randomized prospective study comparing the effect of HBO versus 12 hours NBO in non-comatose CO poisoned patients: results of the interim analysis. Undersea Hyperb Med 1996; 23 Suppl: 7. Willms SJ, Turner F, Kerr J. Carbon monoxide or smoke inhalations treated with oxygen (hyperbaric vs normobaric): 118 reviewed. Undersea Biomed Res 1985; 12 Suppl: S56. Ely EW, Moorehead B, Haponik EF. Warehouse workers' headache: emergency evaluation and management of 30 patients with carbon monoxide poisoning. Am J Med 1995; 98: 145-155. Myers RAM, Snyder SK, Emhoff TA. Subacute sequelae of carbon monoxide poisoning. Ann Emerg Med 1985; 14: 1163-1167. Weaver LK, Hopkins RO, Larson-Lohr V. Hyperbaric oxygen and carbon monoxide poisoning. Ann Emerg Med 1995; 26: 390-391. Mitchell CA, Carroll PA. Acute toxicity of inhaled gases and particulates. Med J Aust 1989; 150: 717-720. Seger D. The science (or lack thereof) in the treatment of carbon monoxide poisoning. Am J Emerg Med 1994; 12: 389. Seger D, Welch L. Carbon monoxide controversies: neuropsychological testing, mechanism of toxicity, and hyperbaric oxygen. Ann Emerg Med 1994; 24: 242-248. Olson KR, Seger D. Hyperbaric oxygen for carbon monoxide poisoning: does it really work? Ann Emerg Med 1995; 25: 535-537. Van Meter KW, Weiss L, Harch PG, et al. Should the pressure be off or on in the use of oxygen in the treatment of carbon monoxide-poisoned patients. Ann Emerg Med 1994; 24: 283-288. Weaver LK. Randomized clinical trial in carbon monoxide poisoning needed. Am J Emerg Med 1994; 12: 685. Folstein MF, Folstein SE, McHugh PR. Minimental state. J Psychiatr Res 1975; 12: 189-198. Wechsler D. Wais-R manual. New York: Psychological Corporation, 1981. Miller EN, Satz P. The Californian computerised assessment package (Calcap). Los Angeles, CA: Miller EN & Satz P, 1987. Van Zomeren AH, Brouwer WB. Clinical neuropsychology of attention. New York: Oxford University Press, 1994. Lezak MD. Neuropsychological assessment. New York: Oxford University Press, 1995. Howell DC. Statistical methods for psychology. 2nd ed. Boston: Duxbury Press, 1987. Littell RC, Milliken GA, Stroup WW, Wolfinger RD. SAS [computer program]. Version 6.12. Cary, NC: SAS Institute Inc, 1996. Power BM, Prentice DA. Carbon monoxide poisonings at The Royal Perth Hospital. Anaesth Intens Care 1991. 19: 149. Myers RAM. Planning an effective strategy for carbon monoxide poisoning. Emerg Med Rep 1987; 8: 193-201. Runciman WW, Gorman DF. Carbon monoxide poisoning: from old dogma to new uncertainties. Med J Aust 1993; 158: 439-440. Gorman DF, Runciman WB. Carbon monoxide poisoning. Anaesth Intens Care 1991; 19: 506-511. Norkool DM, Kirkpatrick JN. Treatment of acute carbon monoxide poisoning with hyperbaric oxygen: a review of 115 cases. Ann Emerg Med 1985; 14: 1168-1171. Choi IS. Delayed neurologic sequelae in carbon monoxide intoxication. Arch Neurol 1983; 40: 433-435. Origani G, Michael M, Tuscano R, Arghetti S. Outcome of patients suffering from CO poisoning. Undersea Hyperb Med 1996. 23 Suppl: 83. Pracyk JB, Stolp BW, Fife CE, et al. Brain computerized tomography after hyperbaric oxygen therapy for carbon monoxide poisoning. Undersea Hyperb Med 1996; 22: 1-7. Samuels AH, Vamos MJ, Taikato MR. Carbon monoxide, amnesia and hyperbaric oxygen therapy. Aust N Z J Psychiatry 1992; 26: 316-319. Hampson NB, Dunford RG, Kramer CC, Norkool DM. Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning. J Emerg Med 1995. 13: 227-231. Hampson NB, Simonson SG, Kramer CC, Piantadosi CA. Central nervous system oxygen toxicity during hyperbaric treatment of patients with carbon monoxide poisoning. Undersea Hyperb Med 1996; 23: 215-219. Miura T, Mitoma M, Kawai R, Harada K. CT of the brain in acute carbon monoxide intoxication: characteristic features and prognosis. Am J Neuroradiol 1985; 6: 739-742. La Plane D, Baulac M, Widlocher D, Dubois B. Pure psychic akinesia with bilateral lesions of basal ganglia. J Neurol Neurosurg Psychiatry 1984; 47: 377-385. Hopkins RO, Weaver LK. Long-term outcome in subjects with carbon monoxide poisoning. Undersea Hyperb Med 1994; 21 Suppl: 17. Starkstein SE, Berthier ML, Leigurada R. Psychic akinesia following bilateral pallidal lesions. Int J Psychiatry Med 1989; 19: 155-164. Messier LD, Myers RAM. A neuropsychological screening battery for emergency assessment of carbon monoxide-poisoned patients. J Clin Psychol 1991; 47: 675-684. Hopkins RO, Weaver LK. Does late repetitive hyperbaric oxygen improve delayed neurologic sequelae associated with carbon monoxide poisoning? Undersea Biomed Res 1991; 18 Suppl: 34. Weaver LK, Hopkins RO, Larson-Lohr V, et al. Double-blind, controlled, prospective, randomized clinical trial (rct) in patients with acute carbon monoxide (CO) poisoning: outcome of patients treated with normobaric oxygen or hyperbaric oxygen -- an interim report. Undersea Hyperb Med 1995; 22 Suppl: 14. (Received 25 Mar, accepted 1 Dec, 1998) Authors' details Alfred Hospital, Melbourne, VIC. Carlos D Scheinkestel, FRACP, DipDHM, Deputy Director, Department of Intensive Care and Hyperbaric Medicine, and Head, General Intensive Care Unit; Paul S Myles, MD, FANZCA, Head of Research, Department of Anaesthesia and Pain Management; D James Cooper, MD, FRACP, Head, Trauma Intensive Care Unit; Ian L Millar, FAFOM, DipDHM, Head, Hyperbaric Medicine; David V Tuxen, MD, FRACP, Director, Department of Intensive Care and Hyperbaric Medicine. Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, VIC. Michael Bailey, BSc, MSc(Stat), Statistical Consultant. School of Psychological Science, La Trobe University, Melbourne, VIC. Kerry Jones, BBSc(Hons), MPsych, Psychologist, and PhD student. Reprints: Dr C D Scheinkestel, Department of Intensive Care and Hyperbaric Medicine, Alfred Hospital, Commercial Road, Prahran, Melbourne, VIC 3181. Email: cdschATozemail.com.au Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> 1: Published trials of carbon monoxide poisoning treated with hyperbaric oxygen (HBO) and normobaric oxygen (NBO)StudyPatients includedNo. HBO patientsNo. NBO patientsBlindedNeuropsychological testsNon-randomised Roche et al11All2020NoNo Mathieu et al16All20327NoNo Myers et al20All13182NoYes Willms et al18All7246NoNo Goulon et al9All27329NoNo Gorman et al13All928NoYes Ely et al19All426NoNoRandomised Raphael et al15Non-comatose Severely poisoned173 145170 141No NoNo No Thom et al14Mildly poisoned3332NoYes Ducasse et al12Non-comatose1313YesNo Mathieu et al17Non-comatose299276NoNo This study*All10487YesYesStudyNumber of treatmentsMaximum ATATime at maximum ATA (min)Entry criteria time to treatment (h)Actual time to treatment (h)HBO benefit reportedNon-randomised Roche et al111-102.560??Yes Mathieu et al161-52.590?~4Yes Myers et al20?1.8-2.046?1-1.5Yes Willms et al1832.5???Yes Goulon et al92290??Yes Gorman et al131, 2, >22.860??Yes Ely et al1912.5120??YesRandomised Raphael et al151 1 v. 22 2120 12012 12? ?No No Thom et al141 2.8 230 90 <6 ~1 Ducasse et al121???~1Yes Mathieu et al1712.59012?No This study*≥32.860<247.1 (95% CI, 1.9-26.5)NoATA = atmospheres absolute; HBO = hyperbaric oxygen; NBO = normobaric oxygen; ? = not reported; ~ = approximately. * Our study was the only one listed in which there were sham treatments for NBO patients. 2: Patient characteristics and description of severity of carbon monoxide poisoning for patients treated with hyperbaric oxygen (HBO) and normobaric oxygen (NBO)HBO (n = 104)NBO (n = 87)PDemographic characteristics Age37.8 (35.1-40.5)34.8 (32.0-37.6)0.13+ Male89 (86%)67 (77%)0.13++ Suicide attempt68 (65%)63 (72%)0.3++Baseline severity Ventilated20 (19%)16 (18%)0.88++ Exposure time (h)2.6 (2.0-3.2)2.5 (1.9-3.1)0.87+ Time to carboxyhaemoglobin level (h)*3.2 (2.6-3.8)2.6 (2.1-3.1)0.11+ Carboxyhaemoglobin level (%)20.5 (18.0-23.0)22.0 (19.6-24.4)0.39+ Time to treatment (h)*7.5 (6.6-8.6)6.6 (5.7-7.5)0.16+ Mini-mental score27.0 (26.1-27.9)26.4 (25.4-27.4)0.27+ No. with criteria for severe poisoning72 (69%)67 (77%)0.23++Signs Coma53 (51%)49 (56%) Acidosis11 (11%)13 (15%) Focal neurological deficits9 (9%)6 (7%) Electroencephalogram changes7 (7%)9 (10%) Hypotension3 (3%)2 (2%) Arrhythmias2 (2%)7 (8%) Pulmonary oedema2 (2%)1 (1%) Convulsions1 (1%)3 (3%) Cardiac arrest1 (1%)1 (1%)Symptoms Headache55 (53%)38 (44%) Fatigue47 (45%)38 (44%) Difficulty in thinking46 (44%)37 (43%) Dizziness38 (37%)21 (24%) Nausea38 (37%)25 (29%) Acute confusional state20 (19%)10 (11%) Paraesthesiae11 (11%)6 (7%) Visual disturbance9 (9%)4 (5%) Palpitations8 (8%)3 (3%) Chest pain7 (7%)3 (3%) Tinnitus4 (4%)2 (2%) Abdominal pain3 (3%)0 Diarrhoea2 (2%)2 (2%)Figures are number (%) or mean (95% CI). HBO = hyperbaric oxygen; NOB = normobaric oxygen. *Geometric mean; +t test; ++chi-squared test. 3: Neuropsychological outcome for all patients treated with hyperbaric oxygen (HBO) and normobaric oxygen (NBO)HBO (n = 104)NBO (n = 87)Difference (95% CI) in favour of HBO*PAt end of treatment No. requiring >3 treatments29 (28%)13 (15%)OR 2.8 (1.3-6.2)++0.01++ Deaths3 (3%)3 (3.4%)0.96++Average neuropsychological test results+ Simple reaction time (s)385375-10 (-50 to 30)0.63s Choice reaction time (s)10.411.1-0.7 (-1.9 to 0.5)0.25s Digit span forward (no. digits recalled)8.28.10.1 (-9 to 1.1)0.87s Digit span backwards (no. digits recalled)5.35.6-0.3 (-1.1 to 0.5)0.55s Rey auditory verbal learning test (score)42.247.7-5.5 (-9.8 to -1.2)0.01s Short term free recall (no. objects)3.23-0.2 (-1.1 to 0.7)0.54s Long term free recall (no. objects)4.44.2-0.2 (-1.5 to 1.1)0.76s Improvement in Mini-mental score00.7-0.7 (-2.7 to 1.3)0.53sAverage number of abnormal tests 3.42.7-0.7 (-1.3 to -0.1)0.02sPoor outcome (PNS)0.740.68OR 1.7 (0.8-4.0)++0.19++Relapse (DNS)5 (4.8%)00.03**Figures are number (%) or mean (95% CI). HBO = hyperbaric oxygen; NBO = normobaric oxygen; OR = odds ratio; PNS = persistent neurological sequelae (>2 abnormal test results); DNS = delayed neurological sequelae. *After adjustment for age, sex, suicide attempt, carboxyhaemoglobin (COHb) level, time to measurement of COHb level, duration of exposure, time to treatment, presence of other drugs; +See Methods section for description of neuropsychological tests; ++chi-squared test; sF-test; **Fisher's exact test. 4: Characteristics of 139 patients with severe carbon monoxide poisoning, and the neurophysiological outcome for this subgroupHBO (n = 72)NBO (n = 67)Difference (95% CI) in favour of HBO*P*Demographic characteristics Age38.6 (35.2-42.0)36.7 (33.5-39.9)0.42** Male60 (83%)55 (82%)0.99s Suicide55 (76%)54 (81%)0.69++Baseline severity Ventilated20 (28%)16 (24%)0.74s Exposure time (h)2.5 (1.9-3.1)2.2 (1.6-2.8)0.45** Time to carboxyhaemoglobin level (h)+2.9 (2.3-3.7)2.2 (1.9-2.7)0.07** Carboxyhaemoglobin level (%)+23.0 (19.8-26.2)22.9 (22.0-25.8)0.94** Time to treatment (hours)7.3 (6.3-8.5)6.1 (5.4-6.9)0.08** Mini-mental score25.6 (24.3-26.9)25.8 (24.5-27.1)0.8**At end of treatment No. requiring >3 treatments25 (35%)9 (13%)OR 5.4 (2.0-14.8)0.001s Deaths3 (4.2%)3 (4.5%)OR 1.0 (0.2-6.0)0.97sAverage neuropsychological test results+ Simple reaction time (s)410377-33 (-72 to 6.0)0.01ss Choice reaction time (s)9.910.7-0.8 (-2.4 to 0.8)0.32ss Digit span forward (no. digits recalled)7.98-0.1 (-1.3 to 1.1)0.91ss Digit span backwards (no. digits recalled)55.5-0.5 (-1.6 to 0.6)0.35ss Rey auditory verbal learning test (score)4249.2-7.2 (-12.2 to -2.2)0.005ss Short term free recall (no. objects)43.5-0.5 (-1.7 to 0.7)0.43ss Long term free recall (no. objects)4.65.20.6 (-1.1 to 2.3)0.47ss Improvement in Mini-mental score21.60.4 (-0.2 to 2.8)0.71ssAverage number of abnormal tests3.72.6-1.1 (-1.9 to -0.3)0.008ssPoor outcome (PNS)0.850.65OR 3.6 (1.1-11.9)0.03sFigures are number (%) or mean (95% CI). HBO = hyperbaric oxygen; NBO = normobaric oxygen; OR = odds ratio; PNS = persistent neurological sequelae (>2 abnormal test results); DNS = delayed neurological sequelae. *After adjustment for age, sex, suicide attempt, carboxyhaemoglobin (COHb) level, time to measurement of COHb level, duration of exposure, time to treatment, presence of other drugs; +Geometric mean (95% CI); ++See Methods section for description of neuropsychological tests; schi-squared test; **t-test; ssF-test.

Carlos D Scheinkestel · Michael Bailey · Paul S Myles · Kerry Jones · Ian L Millar · David V Tuxen

Research Hospital in the home: a randomised controlled trial Gideon A Caplan, John A Ward, Nicholas J Brennan, Janis Coconis, Neville Board and Ann Brown MJA 1999; 170: 156-160 For editorial comment, see Montalto Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Administration and health services Abstract Objectives: To compare treatment of acute illness at home and in hospital, assessing safety, effect on geriatric complications, and patient/carer satisfaction. Design: Randomised controlled trial. Setting: A tertiary referral hospital affiliated with the University of New South Wales. Participants: 100 patients (69% older than 65 years) with a variety of acute conditions, who were assessed in the emergency department as requiring admission to hospital. Interventions: Patients were allocated at random to be treated by a hospital-in-the-home (HIH) service in their usual residence or to be admitted to hospital. Main outcome measures: Geriatric complications (confusion, falls, urinary incontinence or retention, faecal incontinence or constipation, phlebitis and pressure areas), patient/carer satisfaction, adverse events, and death. Results: There was a lower incidence of confusion (0 v. 20.4% [95% CI, 9.1%-31.7%]; P = 0.0005), urinary complications (incontinence or retention) (2.0% [95% CI, -1.8%, 5.8%] v. 16.3% [95% CI, 6.0%, 26.6%]; P = 0.01), and bowel complications (incontinence or constipation) (0 v. 22.5% [95% CI, 10.7%, 34.1%]; P =0.0003) among HIH-treated patients. No significant difference in number of adverse events and deaths (to 28 days after discharge) in the two groups was found (although numbers were small). Patient and carer satisfaction was significantly higher in the HIH group. Conclusions: Home treatment appears to provide a safe alternative to hospitalisation for selected patients, and may be preferable for some older patients. We found high levels of both patient and carer satisfaction with home treatment. Introduction Acute care of patients at home is one of the fastest-growing healthcare sectors in the United States1-3 and is gaining acceptance in many countries.4 Although there have been randomised controlled trials of patients receiving home versus hospital treatment for deep venous thrombosis,5 there are few data from trials involving other conditions, or assessing the safety of acute care at home, especially for older patients. It is these patients who occupy an increasing proportion of hospital beds and may derive most benefit from home treatment.6,7Recent studies characterising hospital-associated adverse events8,9 make home treatment more attractive,10 especially for elderly patients who are known to suffer a higher incidence of complications in hospital.11 When treated at home, patients do not have to change their environment or routine, they are not exposed to nosocomial infection, and they do not need to adapt to the sociological culture of the hospital. On the other hand, the incidence and severity of intrinsic complications in older patients can be minimised by round-the-clock supervision by expert staff in hospital. However, there is inadequate evidence to support the popular belief that programs which transfer care to the home result in a worse outcome for the patients.12,13 We have conducted a randomised controlled trial of a hospital-in-the-home (HIH) program targeting older patients. We selected conditions which were amenable to home treatment, but tried to include a variety of diagnostic groups. To accentuate the difference between the two groups, the HIH patients were taken home on the day of presentation to the emergency department, or on the following morning if they presented at night. We studied the safety, efficacy and patient/carer satisfaction of home treatment compared with hospital treatment. Methods Patients and randomisation One hundred patients requiring admission to hospital and meeting criteria for study inclusion were randomised to HIH treatment (intervention group) or treatment in hospital (control group). We targeted patients older than 65 years, including those living in nursing homes, but also accepted younger patients. Patients were accepted only if they had been assessed as requiring admission by the relevant medical or surgical team. The medical, surgical and emergency department staff were encouraged to refer patients with acute (pneumonia, urinary tract infections and cellulitis) and subacute (endocarditis and osteomyelitis) infections requiring treatment with intravenous antibiotics, deep venous thrombosis (DVT), minor cerebrovascular accidents (not affecting mobility or swallowing), and cardiac failure. Patients were excluded from the study if they had evidence of shock (systolic blood pressure < 100 mmHg); if they required oxygen (Pao2 < 60 mmHg); if they were judged too unwell by the study team; if they had no available carer; if they lived outside the local area; or if their home was unsuitable for home treatment (lack of running water, electricity or an inside toilet, concerns about safety, or dangerous pets). If any doubts about home suitability arose during the emergency department assessment, a study nurse visited the home before randomisation. After informed consent was obtained from the patient (written) and the patient's carer (verbal), randomisation (stratified according to whether the patient lived at home or in a nursing home, or had DVT) was achieved by computer-generated random numbers coded into sealed envelopes. The study protocol required that patients in the HIH group be discharged from hospital within 24 hours of diagnosis. HIH patients receiving intravenous antibiotics were given the first dose in hospital. The study protocol was approved by the hospital's Research Ethics Committee. Data collection For all study patients, study nurses completed a Barthel Index of Activities of Daily Living,14 a modified Instrumental Activities of Daily Living Index15 and a Mental Status Questionnaire16 on admission and discharge. Baseline demographic data on current medical diagnoses, a detailed social history, physical function, medications and allergies were also recorded. Hospital treatment Hospital patients (control group) were admitted under the appropriate physician or surgeon of the day and treated in accordance with standard regimens without the intervention of the study team. The hospital team treating the patient was notified that the patient had been included in the trial. HIH treatment HIH patients (intervention group) were treated according to the presenting diagnosis by the hospital community outreach team. The range of treatments in the study protocol included administration of parenteral antibiotics and other medications, and blood transfusions. Infections were generally treated with once-daily intravenous antibiotics such as ceftriaxone, gentamicin or vancomycin, as appropriate, according to the result of bacteriological tests (if positive) or by diagnosis. Intravenous access was usually via cannulas inserted by study nurses. Owing to safety concerns, some patients with dementia did not have cannulas left in situ, and were cannulated daily with butterfly cannulas. Patients requiring long term treatment or with difficult venous access were treated via a peripherally inserted central cannula. Patients with DVT were treated with daily subcutaneous enoxaparin injections (1.5 mg/kg) and oral warfarin until their international normalised ratio was 2.0 or above. GP involvement Before the study, we conducted an educational program consisting of an evening lecture and a question-and-answer session for the local division of general practice. Study nurses also visited general practitioners (GPs) and nursing homes to explain the program. Our preference was for the patient's own GP to be the primary medical manager, and we therefore sought the agreement of the patient's GP before entering the patient in the trial. If GPs declined to participate, the hospital provided medical support. Follow-up After discharge, an unmarked satisfaction survey based on the principles outlined by Draper and Hill,17 colour coded to differentiate between responses from HIH and hospital treatment, was sent to patients, carers and GPs. This was followed by a phone call to encourage response. Patients were asked "How would you rate your treatment overall?" and offered a four-point scale of answers: excellent (1), good (2), fair (3), and poor (4). A similar question about satisfaction with the patient's care was asked of the carer and GP. Patients were recontacted by telephone at one and six months after discharge to ascertain their health status. Complications Complications were assessed by two methods. Study personnel performed a systematic medical record review, focusing on the more common geriatric syndromes, as recorded in the patients' notes. The geriatric syndromes18 include confusion, falls, incontinence of bladder and bowel, constipation, urinary retention, and pressure ulcers. These are not specific to older patients, but occur more commonly in frail elderly patients (geriatric patients). The medical records were also assessed according to the validated method of counting adverse events developed for the Harvard Medical Practice Study8 and refined in the Quality in Australian Health Care Study (QAHCS). This was done by independent reviewers engaged from the team of the Australian study.9 This method records an adverse event -- unintended injury or complication -- only if it results in disability, death or prolonged hospital stay and is caused by healthcare management. The reviewers were a doctor and a nurse with extensive experience of QAHCS procedures. Reliability assessments were undertaken by a senior member of the QAHCS study team. The only difference from the standard technique was that the reviewers were instructed only to seek adverse events arising after randomisation, whereas the original study also sought those which had caused the admission. Statistical analyses The study had a power of 80%, assuming = 0.05, to find a difference of about 20% in the occurrence of complications. All analyses were performed on the basis of intention to treat, using the SPSS for Windows and Epi Info statistical packages.19,20 Continuous data are expressed as means and 95% confidence intervals (95% CI) and were compared by t tests. Satisfaction scores were compared by the Mann-Whitney U test. Fisher's exact test was used to compare proportions. All statistical tests were two-tailed. Results Between October 1995 and February 1997, 129 patients requiring admission to hospital were assessed for participation in the study. Reasons for exclusion before randomisation were: patient too unwell for home treatment (12 patients), patient declined (6), carer refused or no carer available (9), and patient lived too far from the hospital (2). One hundred patients were enrolled; 51 were allocated at random to HIH treatment and 49 to hospital treatment. The two groups were comparable in characteristics and diagnoses (Tables 1 and 2). A quarter of the patients lived in nursing homes and 69% were 65 years of age or older. For 92 of the patients their GP agreed before randomisation to assist in their care. Four patients had no GP, one GP was not interested and three patients' GPs could not be contacted before randomisation. Adverse events and complications The proportion of adverse events was similar in the HIH group and the control (hospital) group (11.8% [95% CI, 3.0%, 20.6%] v. 16.3% [95% CI, 6.0%, 26.6%]). However, there was a significantly lower occurrence in the HIH group of confusion, urinary (either incontinence or retention) complications, and bowel (either constipation or faecal incontinence) complications (Table 3). Home visits On average, patients in the HIH group were seen, at home, on 9.0 occasions by the study nurse, 0.8 times by their GP, 0.9 times by a doctor from the hospital, 0.2 times by a physiotherapist, and 0.1 times by an occupational therapist. This translates to one visit per day by the nurse, given that each patient was also seen by a study nurse in the emergency department. Outcomes Treatment failed in four of the 51 patients in the HIH group and they were admitted to hospital. Three and five patients in the HIH group and the hospital-treated group, respectively, were recorded as having an unplanned readmision within 28 days of discharge. There was one death in each of the HIH- and hospital-treated groups during the admission. Total deaths up to 28 days after discharge were three in the HIH group and four in the hospital-treated group, and at six months after discharge six and seven deaths, respectively, had occurred. There were no significant differences between the two groups in these outcomes. Patient, carer and GP satisfaction The response rates for the satisfaction surveys were (HIH v. control): patients 78% v. 40%, carers 55% v. 27%, and GPs 63% v. 37%. There was significantly greater satisfaction with overall HIH treatment among both patients (P < 0.0001) and their carers (P = 0.0001). Despite the increased workload and despite having to deal with more severely ill patients than usual, GPs were equally satisfied by home and hospital treatment (Table 4). Discussion In our study, treatment of a range of acute infections and other diseases at home was as safe as treatment in hospital. Previous studies which claimed to have demonstrated safety documented so few complications that risk appeared to have been eliminated by patient selection.1-3 Our study group's 7% mortality up to 28 days after discharge (compared with zero mortality in previous studies1-3) establishes our patients' illness severity. The most significant finding resulting from our inclusion of geriatric complications was the higher incidence of confusion in hospital-treated patients. The role of the hospital environment in the aetiology of delirium has long been recognised,21 although this is not universally accepted.22 For some of the patients in our study recorded as having confusion, all of the features of delirium according to the Diagnostic and statistical manual of mental disorders (DSM-IV)23 were not present. Our aim was to be as inclusive as possible of geriatric complications, so that if a problem was noted by ward staff or carers it was included even if study personnel had not observed it. These complications were not always serious clinically and often did not have a great impact, but we valued the perspective of patients, families and hospital staff. Similarly, the occurrence of urinary and bowel complications reflects the difficulty of caring for frail elderly patients24 (especially those from nursing homes) in an acute hospital ward. Patients with mobility or communication problems require carers attuned to their routines and signals to maintain continence. Because of small numbers our study was limited in its power to draw conclusions about the difference between HIH and hospital treatment as far as adverse events and deaths were concerned. As there have been no previous studies addressing this question, it was not possible to estimate the size of the expected difference. Another limitation of our study was that, although we did not directly inform the adverse event reviewers about which patients were in each group, we were not able to completely blind them to the status of each group because of stylistic differences between the patient records of the hospital- and the HIH-treated patients. Few similar comparative studies have been published. As reports and discussions entitled "home hospitalisation" or "hospital at home", for example, may include few or no acute patients, the home treatment of acute illness is obscured in the medical literature.25,26 Our study included only patients who met the criterion of requiring admission to hospital because of illness. By bringing the hospital care to the patient's home, we substituted completely for hospital facilities. There is a need for more studies of patients with illness of this severity treated at home. A number of factors may explain the greater satisfaction with treatment at home. In their own homes, patients are in their familiar environment, their privacy is protected, their sleep less interrupted, and they can eat their usual food.27,28 As an example, for an elderly patient with limited cognitive function and/or decreased visual acuity, finding the bathroom at night in hospital may be impossible. Moreover, elderly patients may be unable to get out of bed because of rails on the sides of the bed. These difficulties may have contributed to the higher incidence of incontinence in our hospital-treated group. At home, patients are more active participants, often partners, in their care. All these factors invariably translate into greater satisfaction with home treatment.29 Frail, older patients -- because of their atypical disease presentations, more rapid deterioration when ill and greater prevalence of disease -- need hospital-level services more frequently than younger patients. However, admission to hospital, like any medical intervention, has side effects as well as benefits.8 Elderly patients have more to gain from many treatments (eg, thrombolytic therapy) because of their higher underlying mortality rates,30 but they also suffer from a much greater occurrence of iatrogenic complications.10 Although many of these complications may be explained by an interaction between their underlying frailty and their disease process,8 we were able to detect a measurable effect attributable to a change of environment. The results of this study do not imply that older patients should never be admitted to hospital. On the contrary, the elderly as a group have more need for the technical expertise of the acute hospital than younger people. However, if such technical expertise can be delivered at home, this alternative should at least be evaluated. On the other hand, our study does not imply that treatment which can be delivered at home should always be delivered at home. Successful home treatment depends on careful patient and home selection, as the necessary minimum level of sanitation, facilities and support from carers is not universally available.4 However, where it is feasible, we have demonstrated that home treatment of acute illness, even for frail elderly patients, can be effective, safe and more satisfying for the patient and their families. Acknowledgements We would like to acknowledge the invaluable assistance of the staff of Post Acute Care Services and the Emergency Department at Prince of Wales Hospital and Ms Bernie Harrison and Dr Ross Wilson from QARNS at Royal North Shore Hospital. This study was supported by a grant from the Commonwealth Department of Health and Family Services - Hospital Access (National Projects) Program. References Antoniskis A, Anderson BC, Von Volkinburg EJ, et al. Feasibility of outpatient self-administration of parenteral antibiotics. West J Med 1978; 128: 203-206. Kind AC, Williams DN, Persons G, et al. Intravenous antibiotic therapy at home. Arch Intern Med 1979; 139: 413-415. Stiver HG, Telford GO, Mossey JM, et al. Intravenous antibiotic therapy at home. Ann Intern Med 1978; 89: 690-693. Tice AD. Outpatient parenteral antibiotic therapy in different countries. Int J Infect Dis 1996; 1: 102-106. Levine M, Gent M, Hirsh J, et al. A comparison of low-molecular-weight heparin administered primarily at home with unfractionated heparin administered in the hospital for proximal deep-vein thrombosis. N Engl J Med 1996; 334: 677-681. Balinsky W, Nesbitt S. Cost-effectiveness of outpatient parenteral antibiotics: a review of the literature. Am J Med 1989; 87: 301-305. Poretz DM, Eron LJ, Goldenberg RI, et al. Intravenous antibiotic therapy in an outpatient setting. JAMA 1982; 248: 336-339. Leape LL, Brennan TA, Laird N, et al. The nature of adverse events in hospitalised patients: results of the Harvard Medical Practice Study II. N Engl J Med 1991; 324: 377-384. Wilson RM, Runciman WB, Gibberd RW, et al. The quality in Australian health care study. Med J Aust 1995; 163: 458-471. Caplan GA, Brown A. Post acute care: can hospitals do better with less? Aust Health Rev 1997; 20: 43-54. Fretwell MD. Acute hospital care for frail older patients. In: Hazzard WR, Andres R, Bierman EL, Blass JP, editors. Principles of geriatric medicine and gerontology, 2nd ed. New York: McGraw-Hill, 1990: 247-253. Maxwell RJ. Why rationing is on the agenda. Br Med Bull 1995; 51: 761-768. Larkins RG, Martin TJ, Johnston CI. The boundaryless hospital -- a commentary. Aust N Z J Med 1995; 25: 169-170. Mahoney FI, Barthel DW. Functional evaluation: the Barthel index. Md Med J 1965; 14: 61-65. Lawton MP, Brody EM. Assessment of older people: self-maintaining and instrumental activities of daily living. Gerontologist 1969; 9: 179-186. Pfeiffer E. A short portable mental status questionnaire for the assessment of organic brain deficit in elderly patients. J Am Geriatr Soc 1975; 23: 433-441. Draper M, Hill S. The role of patient satisfaction surveys in a national approach to hospital quality management. Canberra: AGPS, 1996. Hazzard WR, Andres R, Biermen EL, Blass JP, editors. Principles of geriatric medicine and gerontology. 2nd ed. Section 4 -- geriatric syndromes and special problems. New York: McGraw-Hill, 1990: 1055-1222. SPSS for Windows [computer program], version 6.0. Chicago: SPSS Inc, 1993. Dean AG, Dean JA, Burton AH, Dicker RC. Epi-Info [computer program], version 5. Stone Mountain, Ga: USD Inc, 1990. Wahl CW, Golden JS, Liston EH, et al. Toxic and functional psychoses: diagnosis and treatment in a medical setting. Ann Intern Med 1967; 66: 989-1007. Lipowski ZJ. Delirium and impaired consciousness. In: Evan JG, Williams TF, editors. Oxford textbook of geriatric medicine. Oxford: Oxford University Press, 1992: 490-495. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (DSM-IV). Washington, DC: APA, 1994. Caplan GA, Brown A, Croker WD, Doolan J. Risk of admission within four weeks of discharge of elderly from the emergency department -- the DEED study. Age Ageing. In press. Stressman J, Ginsberg G, Hammerman-Rozenberg R, et al. Decreased hospital utilization by older adults attributable to a home hospitalization program. J Am Geriatr Soc 1996; 44: 591-598. Donald IP, Baldwin RN, Bannerjee M. Gloucester hospital-at-home: a randomized controlled trial. Age Ageing 1995; 24: 434-439. Consumer reports of hospital experiences. In: Draper M, Hill S, editors. The role of patient satisfaction surveys in a national approach to hospital quality management. Canberra: AGPS, 1996: 12-20. Cruse PJE, Foord R. The epidemiology of wound infection: a 10-year prospective study of 62,939 wounds. Surg Clin North Am 1980; 60: 27-40. Brown RB. Selecting the patient. Hosp Pract 1993; 28(Suppl 1): 11-15. Fibrinolytic Therapy Trialists' (FTT) Collaborative Group. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Lancet 1994; 343: 311-322. (Received 17 Jun, accepted 22 Oct, 1998) Authors' details Post Acute Care Services, Prince of Wales Hospital, Sydney, NSW. Gideon A Caplan, MB BS, FRACP, Director; and Lecturer, University of New South Wales, Sydney, NSW; Nicholas J Brennan, MB BS, FRACP, Senior Registrar; Janis Coconis, RN, Clinical Nurse Specialist; Neville Board, RN, BA, Research Assistant; Ann Brown, RN, Nurse Manager. Community Health Services and Programs, South Eastern Sydney Area Health Service, Sydney, NSW. John A Ward, MB BS, MSc, FRACP, Community Geriatrician; and Lecturer, University of New South Wales, Sydney, NSW. Reprints: Dr G A Caplan, Post Acute Care Services, Prince of Wales Hospital, Randwick, NSW 2031. Email: g.caplanATunsw.edu.au Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> Back to text Back to text Back to text Back to text

Gideon A Caplan · John A Ward · Nicholas J Brennan · Janis Coconis · Neville Board · Ann Brown

Research Mortality associated with New South Wales methadone programs in 1994: lives lost and saved John R M Caplehorn and Olaf H Drummer MJA 1999; 170: 104-109 For editorial comment, see Ali & Quigley Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Drugs and alcohol Abstract Objectives: To estimate the effects of methadone programs in New South Wales on mortality. Design and cases: Retrospective, cross-sectional study of all 1994 New South Wales coronial cases in which methadone was detected in postmortem specimens taken from the deceased. Cases were people we identified as patients in NSW methadone maintenance programs or those whose deaths involved methadone syrup diverted from maintenance programs. Outcome measures: Relative risks of fatal, accidental drug toxicity in the first two weeks of treatment and later; the number of lives lost as a result of maintenance treatment; preadmission risks and the number of lives saved by maintenance programs, calculated from data from a previous study. Results: There was very close agreement between this study's classifications and official pathology reports of accidental drug toxicity. The relative risk (RR) of fatal accidental drug toxicity for patients in the first two weeks of methadone maintenance was 6.7 times that of heroin addicts not in treatment (95% CI RR, 3.3-13.9) and 97.8 times that of patients who had been in maintenance more than two weeks (95% CI RR, 36.7-260.5). Despite 10 people dying from iatrogenic methadone toxicity and diverted methadone syrup being involved in 26 fatalities, in 1994 NSW maintenance programs are estimated to have saved 68 lives (adjusted 95% CI, 29-128). Conclusions: In 1994, untoward events associated with NSW methadone programs cost 36 lives in NSW. To reduce this mortality, doctors should carefully assess and closely monitor patients being admitted to methadone maintenance and limit the use of takeaway doses of methadone. Introduction Methadone maintenance greatly reduces heroin addicts' risk of death.1 A 15-year follow-up of patients in New South Wales showed methadone maintenance saved lives by reducing addicts' risk of fatal heroin overdose.1 When combined in a meta-analysis with the results of overseas cohort studies, the relative risk of death in methadone maintenance was a quarter that of addicts not in treatment (95% CI, 0.19-0.33).1 However, methadone maintenance is also a cause of death. Patients are at risk of fatal iatrogenic toxicity and other drug users may die from taking methadone syrup diverted from maintenance programs.2-6Mortality associated with NSW maintenance programs was independently investigated. The first report from this project presented the case histories of the 13 patients who died in the first two weeks of treatment.7 It identified 10 probable cases of fatal iatrogenic methadone toxicity (ie, where prescribed doses of methadone either caused or contributed to fatal accidental drug toxicity).7 This, the second report, presents an estimate of the relative risk of fatal accidental drug toxicity in the first two weeks and later maintenance. It also presents estimates of the effect of admission to methadone maintenance on the risk of fatal accidental drug toxicity and of the number of lives saved by NSW maintenance programs in 1994. Methods This study was approved by the Human Research Ethics Committee of the Western Sydney Area Health Service and the NSW State Coroner. In late 1995 the database at the NSW Health Department's Division of Analytical Laboratories was searched to identify 1994 coronial cases in which methadone was detected in postmortem specimens. These analytical laboratories receive specimens for toxicological analysis in all cases of sudden death referred to the NSW State Coroner. Autopsy, toxicology and police reports and the statements of family and friends, prescribers and other witnesses were collected from coronial files. The methadone treatment histories of the deceased were extracted from data held by the NSW Health Department's Pharmaceutical Services Section. The Department also provided data on the number of people admitted to and treated with methadone maintenance in NSW in 1994. Cases were grouped according to the source of the methadone: methadone syrup given as maintenance treatment; methadone syrup diverted from the maintenance program; and methadone tablets (Physeptone; Glaxo Wellcome, Boronia, Vic.) prescribed for pain relief. As the Sydney black market consists almost entirely of methadone syrup diverted from maintenance programs,8 illicit drug users who obtained methadone from an unknown source were classified as having taken diverted syrup. We used two parallel classifications of cause of death -- that on the official pathologist's report, and our own. In our classification, we initially established cause of death independently of one another, with one of us (O H D) blind to the official cause of death. Cases were first categorised as "accidental drug toxicity" and "other". The "other" category included suicides, deaths from natural causes and trauma, and deaths in which drug toxicity was considered to have contributed to a death from natural causes. The "accidental drug toxicity" cases were further categorised into "methadone" and "other drug or drugs" on the basis of whether or not methadone was considered to have either caused or made a significant contribution to the death. There were no simple criteria for establishing the contribution of methadone to deaths involving other drugs. However, as deaths to which methadone contributed closely resembled cases of fatal methadone toxicity,2,3,7 a relatively confident decision could be made after a thorough examination of the documentary and toxicological evidence and the autopsy report.2,7,9-12 Police statements and photographs of the deceased at the scene of death provided some assistance. A brownish, frothy oedema fluid was often observed coming from the deceased's mouth or nose (see Box 1).7 Witnesses' statements provided a guide to likely tolerance and chronologies of ingestion and of the development of symptoms and signs of toxicity.2,7 These statements were particularly useful in cases involving methadone as death usually occurred some hours after the drug was taken,14 and some time after the development of coma (see Box 1).2,3,7,10,11 Postmortem blood methadone concentration was helpful but not definitive, as fatal concentration varies widely with tolerance11,12 and the blood concentration of methadone increases after death.15 Moreover, the postmortem increase in blood methadone concentration varies unpredictably from one part of a cadaver to another.16 The autopsy findings were remarkably consistent in cases of fatal drug toxicity involving methadone, with the immediate cause of death being pulmonary oedema secondary to hypoventilation.2,7,10,11 As methadone toxicity usually causes a gradually worsening hypoventilation, the hypoxia and resulting pulmonary hypertension are generally prolonged and severe, and significant quantities of water and electrolytes, large proteins and red blood cells leak from the pulmonary capillaries into the air spaces. Consequently, brownish oedema fluid was often observed in the large airways and the lungs were unusually heavy (see Box 1). Microscopic examination of lung specimens often showed areas of patchy bronchopneumonia and other evidence of prolonged hypoventilation and suppression of the cough reflex.2,7,10 Statistical analysis We used published estimates of NSW methadone patients' risks of death after leaving treatment as approximations of 1994 NSW methadone patients' risks before admission to treatment.1Rates were adjusted for age, as the risk of death was significantly higher for those aged 20-29 years compared with those aged 30-39 years.1 Weighted average risks were calculated in the knowledge that, in 1994, 68% of NSW maintenance patients were at least 30 years of age.17 We assumed half of those admitted to maintenance were aged 20-29 years and half 30-40 years. The 95% confidence intervals of mortality rates were calculated by dividing the estimates by significance factors taken from a published table.18 The standard errors of the relative risks were estimated using the binomial approximation of the Poisson distribution.19 Results Methadone was detected in postmortem material from 89 NSW coronial cases in 1994. These cases comprised 41 methadone maintenance patients (38 registered with the NSW Health Department and three with the Queensland Health Department), one neonate being breastfed by a NSW methadone maintenance patient, 29 cases considered to have involved methadone syrup diverted from the NSW methadone program, and 18 cases considered to have involved methadone tablets. In 18 of the 29 cases involving diverted methadone syrup, either a bottle used to dispense methadone syrup (5 cases), a statement from a witness (10 cases), or both (3 cases), indicated that the maintenance program was the source of the methadone. In the remaining 11 cases, it was assumed methadone syrup was obtained from the black market.8 In 16 of the 18 cases involving methadone tablets, either a statement from the prescribing doctor (8 cases), a tablet bottle (4 cases), or both (4 cases), indicated the source of the methadone. The remaining two people had professional access to methadone tablets and committed suicide. We excluded the three Queensland maintenance patients, the neonate and all cases involving methadone tablets, leaving 67 cases in the study. Methadone maintenance patients Box 2 shows that, of the 38 NSW maintenance patients, 13 died in the first two weeks after admission, and 25 died later in treatment. We and the official pathologists concluded that 12 of the 13 fatalities in the first two weeks of maintenance and six of the 25 deaths later in treatment were caused by accidental toxicity. Three of six deaths from accidental drug toxicity among established maintenance patients were caused by heroin, one by dextromoramide, one by the combined effects of heroin and dextroproxyphene, and one involved injected methadone syrup. Diverted methadone syrup Box 2 shows that, for the 29 cases involving diverted methadone, we concluded methadone contributed to 26 of 27 deaths from accidental drug toxicity compared with 24 of 26 on the official pathologists' reports. One death which we classified as accidental drug toxicity was officially attributed to bronchopneumonia with methadone intoxication as a contributing factor. In another case, we concluded injected, diverted methadone contributed to a death which was officially attributed to acute heroin poisoning. Witnesses' statements or autopsy reports indicated that methadone syrup was injected in 16 of the 26 cases we classified as accidental drug toxicity to which diverted methadone contributed. One of the 10 cases involving oral ingestion of diverted methadone was that of an infant who either took or was given some of his mother's syrup. Relative risks of accidental drug toxicity We concurred with official pathologists' conclusions that 12 patients died of accidental drug toxicity during the first two weeks of maintenance treatment in NSW in 1994 (see Box 2). To calculate the rate of fatal accidental drug toxicity, we estimated the total time patients spent in the first two weeks of maintenance treatment. In 1994, 4449 people were admitted to methadone maintenance in NSW. Assuming all new admissions stayed at least two weeks in treatment,20,21 patients spent approximately 170.5 person-years in the first two weeks of maintenance. Using this estimate as the denominator, the rate of fatal accidental drug toxicity in the first two weeks of maintenance was 70.4 deaths per thousand per year (Box 3). We also agreed with official pathologists' conclusions that six NSW methadone patients died from accidental drug toxicity after being in maintenance treatment for at least two weeks (Box 2). An approximation of the total time methadone patients spent in treatment in NSW in 1994 was derived from the average of the number in treatment at the beginning and end of the year (7975 and 9038, respectively).22 The 170.5 person-years spent in the first two weeks' maintenance were subtracted from the average of the totals, 8506.5, to estimate the total time spent in later maintenance -- 8336 person-years. When this was used as the denominator, the rate of fatal accidental drug toxicity in later maintenance was 0.72 deaths per thousand per year (Box 3). When combined with the previous estimate, the risk of fatal accidental drug toxicity in the first two weeks of treatment in NSW in 1994 was estimated to have been 97.8 times the risk later in maintenance (95% CI RR, 36.7-260.5 times). Based on the results of a previous study,1 the rate of fatal accidental drug toxicity for addicts on the street was estimated to be 10.4 per thousand per year. Using this estimate, the risk of fatal accidental drug toxicity in the first two weeks of methadone maintenance in NSW in 1994 was 6.7 times the risk before admission (95% CI RR, 3.3-13.9 times). Lives saved by NSW maintenance programs The age-adjusted approximation of the expected mortality from all causes among heroin addicts was 15.5 deaths per thousand per year (95% CI, 11.0-21.9 deaths).1 Using this estimate, 132 deaths would have been expected to occur in 8506.5 person-years (95% CI, 93-187 deaths). As 64 people either died while receiving maintenance (38) or from the toxic effects of diverted methadone (26), NSW methadone programs are estimated to have saved 68 lives in 1994 (95% CI, 29-123 lives saved). To save one life approximately 125 patients needed to be given methadone maintenance for a year (95% CI, 69-293 patients). To adjust for possible bias, we assumed that up to three of the 11 cases classified as involving diverted methadone syrup may have actually involved methadone tablets. When added to the two cases involving diverted methadone syrup in which there were differences in the official and study classifications of cause of death (Box 2), the number of lives saved may increase by up to five. Consequently, the upper limit of the confidence interval increased to give an adjusted 95% CI of 29 to 128 lives saved. If all 10 cases of fatal iatrogenic methadone toxicity7 and 26 deaths to which diverted syrup contributed had been avoided, NSW maintenance programs would have saved 104 lives in 1994 (adjusted 95% CI, 65-164 lives saved), making them up to 53% more effective at saving lives (adjusted 95% CI, 37%-124%). Discussion We found that, in NSW in 1994, the risk of fatal accidental drug toxicity in the first two weeks of methadone maintenance was nearly seven times the risk before admission to treatment. A previous report suggested that this excess mortality was primarily the result of iatrogenic methadone toxicity.7 However, the risk of fatal accidental drug toxicity later in maintenance was approximately one-hundredth the risk in the first two weeks of treatment and less than one-tenth the risk before admission. As there was complete agreement between our classification and that of official pathologists, our estimate of the relative risk of fatal accidental toxicity in the first two weeks and later maintenance is unlikely to have been significantly affected by misclassification of causes of death. Further, in estimating that NSW methadone programs saved 68 lives in 1994, we allowed for the difference between our opinion and that of the official report on the role of diverted methadone in two cases when calculating the upper limit of the adjusted 95% confidence interval (29-128) for the number of lives saved by NSW maintenance programs. Another consideration in estimating the number of lives saved is that mortality among patients discharged from maintenance is only an approximation of preadmission risk. If the real risk on the streets was higher than our estimate, NSW methadone programs would have saved more lives and admission to maintenance would not have caused such a dramatic increase in the risk of fatal accidental drug toxicity. Conversely, if the real risk was lower, the reverse applies. Our estimates of the number of lives saved and the increase in the risk of fatal accidental drug toxicity associated with admission to maintenance are approximations only. However, as our estimated 71% reduction in mortality is very similar to that observed in the US during the early 1970s, in Sweden during the 1980s, in Germany in the 1990s and Australia during the 1970s and 1980s,1 they are probably reasonably accurate. Previous Australian studies have also identified mortality associated with methadone programs. Eighteen people died from methadone toxicity in Western Australia in the years 1975 to 1980. However, there were virtually no such deaths after WA maintenance patients were required to take their methadone under supervision.23 In South Australia, nine maintenance patients died from drug toxicity in the years 1984 to 1994, while 12 other people died from the toxic effects of diverted methadone syrup.22 The number of deaths per 1000 SA maintenance patients was approximately 75% of that observed in our study. Our finding that diverted methadone syrup contributed to 26 deaths in NSW in 1994 is supported by the results of a previous investigation which suggested that diverted methadone syrup was involved in up to 100 deaths between July 1990 and December 1995.6 The WA experience23 suggests the number of deaths from diverted methadone syrup is related to the number of takeaway doses dispensed to maintenance patients for consumption on subsequent days. In 1994, two-thirds of private sector patients received four takeaway doses a week, with some programs giving five or six a week to newly admitted patients.24 Although the NSW Health Department argued against such practices, there was no policy enforcement.24 To minimise the diversion of methadone syrup from maintenance programs, the NSW Health Department should monitor and ensure compliance with its current policy which strictly limits the number of takeaway doses available to recent admissions while giving stable, long-term patients access to generous takeaway privileges. A serious problem with iatrogenic methadone toxicity was identified in Victoria, where 10 deaths occurred among newly admitted methadone patients in the last six months of 1989.2 As Victorian methadone programs treated fewer than 1200 maintenance patients in this period, the rate of iatrogenic methadone toxicity was many times that observed in our study. It is noteworthy that, during 1989, the number of Victorian maintenance patients and programs increased rapidly and a number of inexperienced and poorly trained prescribers entered the field.2,3 Persons with minimal or no tolerance were prescribed initial, daily methadone doses of 50-70 mg, with fatal results.2 Two recent British studies, from Sheffield and Manchester, have similarly identified significant numbers of deaths from iatrogenic methadone toxicity early in maintenance treatment.4,5 These problems also arose after the relaxation of admission criteria and during a period of rapid increase in the numbers of maintenance patients and the involvement of new, inexperienced prescribers.4,5 While the official criteria for admission to methadone maintenance in NSW have not changed since 1988,25 they were not being implemented in 1994.26 Statements made by its Chairman in 1996 indicate that the NSW Medical Committee had not been applying the official admission criteria for some time.26 This is significant because, under the NSW Poisons Act, the Medical Committee advises the NSW Health Department on applications from doctors to prescribe methadone maintenance to addicts. There were also problems with prescriber training. Since 1993, the NSW Methadone Prescribers' Accreditation Program has used the Methadone prescribers' manual as its course material.27 Contrary to NSW Health Department policy,25 the "Manual" states heroin users need not have a history of physiological dependence on opioids to be eligible for maintenance treatment.26,27 We urge the NSW Health Department to revise its Methadone prescribers' manual,27 review prescriber training and to ensure compliance with its current admission criteria for maintenance treatment.25,26 In 1994, Victorian and Queensland methadone prescribers were required to examine new patients during the first days of maintenance for signs of toxicity.28,29 Unfortunately, the NSW Health Department did not, and still does not, have a similar policy. Indeed, many private practitioners in NSW are only available to see maintenance patients one day a week (see Box 1), and the day-to-day supervision of patients attending public clinics is left to nurses working in busy dispensaries. The first two weeks of methadone maintenance will always be the "danger period" owing to the difficulty in determining a safe and effective starting dose. There is wide variation in opioid-na•ve individuals' response to and ability to metabolise and excrete methadone,30 and applicants' self-reports of recent drug use are an unreliable measure of tolerance.7 Given this uncertainty and variability, it is not possible to define safe, effective starting doses of methadone. We recommend prescribers be made aware of the risks, signs and symptoms of methadone toxicity and be required to examine newly admitted patients every day for the first one to two weeks of maintenance. People seeking methadone maintenance should be required to give written consent after being warned about the dangers of misleading their doctor and of the use of other drugs, particularly benzodiazepines.7,31 We believe that the forthcoming NSW methadone maintenance treatment clinical practice guidelines will address these issues. We strongly recommend the establishment of independent, expert committees to investigate methadone-related deaths in States and Territories with maintenance programs. These committees should be modelled on those used to monitor anaesthesia-related deaths. Acknowledgements For their advice and generous assistance, we thank the NSW State Coroner at Glebe, the Westmead Court, the Division of Analytical Laboratories, and the Pharmaceutical Services Branch of the NSW Health Department, and the Drugs of Dependence Unit, Queensland Health Department. We also thank Professor Geoffrey Berry of the Department of Public Health and Community Medicine, University of Sydney, who assisted with the statistics and presentation of results. References Caplehorn JRM, Dalton MSYN, Haldar F, et al. Methadone maintenance and addicts' risk of fatal heroin overdose. Substance Use Misuse 1996; 31: 177-196. Drummer OH, Opeskin K, Syrjanen SM, Cordner M. Methadone toxicity causing death in ten subjects starting on a methadone maintenance program. Am J Forensic Med Pathology 1992; 13: 346-350. McPherson CJ. Coronial inquiry into methadone related deaths. Melbourne: State Coroner Victoria, 1996. Clark JC, Milroy CM, Forrest ARW. Deaths from methadone use. J Clin Forensic Med 1995; 2: 143-144. Cairns A, Roberts ISD, Benbow EW. Characteristics of fatal methadone overdose in Manchester, 1985-94. BMJ 1996; 313: 264-265. Sunjic S, Zador D. Methadone-related deaths in New South Wales, Australia, 1990-1995. Euro-Methwork Newsletter 1998; issue 13: 11. Caplehorn JRM. Deaths in the first two weeks of maintenance treatment in NSW in 1994: identifying cases of iatrogenic methadone toxicity. Drug Alcohol Rev 1998; 17: 9-17. Darke S, Ross J, Hall W. The injection of methadone syrup in Sydney, Australia. Sydney: National Drug and Alcohol Research Centre, 1995. (Technical Report No. 23). Helpern M, Rho Y-M. Deaths from narcotism in New York City: incidence, circumstances and postmortem findings. NY State J Med 1966; 66: 2391-2408. Siegel H, Helpern M, Ehrenreich T. The diagnosis of death from intravenous narcotism. J Forensic Sci 1966; 11: 1-16. Segal RJ, Catherman RL. Methadone -- a cause of death. J Forensic Sci 1974; 19: 64-74. Worm K, Steentoft A, Kringsholm B. Methadone and drug addicts. Int J Leg Med 1993; 106: 119-123. Transcript of Proceedings, Case 011 0487/95. New South Wales Coroner's Court Westmead. Ruigrok M, Caplehorn J. A case of near-fatal methadone toxicity following repeated injections of methadone [letter]. Drug Alcohol Rev 1997; 16: 433. Pounder DJ, Jones GR. Post-mortem drug redistribution -- a toxicological nightmare. Forensic Sci Int 1990; 45: 253-263. Levine B, Wu SC, Dixon A, Smialek JE. Site dependence of postmortem blood methadone concentrations. Am J Forensic Med Path 1995; 16: 97-100. Drug and Alcohol Directorate. NSW methadone program 1993/94: annual statistical report. Sydney: NSW Health Department, 1995. Bailar JC, Ederer F. Significance factors for the ratio of a Poisson variable to its expectation. Biometrics 1964; 20: 639-643. Armitage P, Berry G. Statistical methods in medical research. 3rd ed. Oxford: Blackwell Scientific, 1994: 131. Caplehorn JRM, McNeil DR, Kleinbaum DG. Clinic policy and retention in methadone maintenance. Int J Addict 1993; 28: 73-89. Caplehorn JRM, Irwig L, Saunders JB. Physicians' attitudes and retention of patients in their methadone maintenance programs. Substance Use Misuse 1996; 31: 663-677. Williamson PA, Foreman KJ, White JM, Anderson G. Methadone-related overdose deaths in South Australia, 1984-1994. Med J Aust 1997; 166: 302-305. Swensen G. Opioid drug deaths in Western Australia: 1974-1984. Aust Drug Alcohol Rev 1988; 7: 181-185. Transcript of Proceedings, Case 010 1924/94. New South Wales Coroner's Court Glebe, Thursday 15th June 1995: 31-37. Directorate of the Drug Offensive. Policies and Procedures for the Methadone Treatment of Opioid Dependence in NSW. Sydney: New South Wales Department of Health, undated: 15, pars 4.3.1 and 4.3.2. Caplehorn JRM. Official and de facto admission criteria for methadone maintenance in New South Wales, Australia [letter]. Drug Alcohol Rev 1998; 17: 121-122. Bell J, O'Connor D. Methadone prescribers' manual. Sydney: NSW Health Department, 1993: 11, 23. Public Health Branch. Victorian methadone program guidelines for providers. Melbourne: Department of Health and Community Services, 1995: 7, par 3.5.2. (No. 93/0388). Bolton M, Reynolds A, Biggs L. Queensland methadone program: policy and procedures and treatment manual. Brisbane: Queensland Health, 1995: 35, par 4.14. Wolff K, Sanderson M, Hay AWM, Ralstrick D. Methadone concentrations in plasma and their relationship to drug dosage. Clin Chem 1991; 37: 205-209. Caplehorn JRM. More on iatrogenic methadone toxicity [letter]. Drug Alcohol Rev 1998; 17: 467-468. (Received 22 Sep 1997, accepted 18 Oct 1998) Authors' details Department of Public Health and Community Medicine, University of Sydney, NSW. John R M Caplehorn, MB BS, MPH, PhD Student. Victorian Institute of Forensic Medicine, Melbourne, VIC. Olaf H Drummer, PhD, Head of Scientific Services, and Associate Professor, Department of Forensic Medicine, Monash University. Reprints: Dr J R M Caplehorn, Department of Public Health and Community Medicine, Building A27, University of Sydney, Sydney, NSW 2006. Email: johnc@dph1.health.usyd.edu.au 1: A case of fatal iatrogenic methadone toxicity This 1995 NSW case highlights the danger of daily doses of 30-40mg methadone in non-tolerant individuals and presents a classic history of fatal iatrogenic toxicity. The deceased had clear, early signs of methadone toxicity: somnolence; unsteady gait; vomiting; and a general feeling of being unwell. The terminal events were also typical: prolonged coma following sleep; very slow, deep, irregular, noisy breathing; brown pulmonary oedema fluid coming from the mouth or nose. Six weeks before his death, the 19-year-old man was admitted to hospital with hypothermia, pneumonia, right brachial plexus neurapraxia, rhabdomyolysis and acute renal failure after a heroin overdose. He reported using amphetamines for six months and heroin for two weeks. Liver function test and echocardiogram findings were normal, and at discharge three days later his serum creatinine level had fallen from 0.18mmol/L to 0.10mmol/L (upper normal limit, 0.12mmol/L). He was referred to a short-stay, residential program and told the admitting officer he had had problems with alcohol for five years, cannabis for seven years and amphetamines for one year, but had only used heroin six times. While he was considered suitable for admission to a drug-free rehabilitation program, this was delayed pending full recovery of his arm. However, he was advised not to wait to enter this program as he was facing trial for a criminal offence. Soon after, the deceased apparently told a general practitioner and a methadone prescriber he had been using heroin daily for a year. He was prescribed 30mg methadone, with the dose to be increased by 5mg every day for six days and then reviewed. The deceased vomited several times after receiving his second dose (35mg). The next morning, he was difficult to rouse, had trouble walking and urinating and kept falling asleep. His father was unable to contact the methadone prescriber, who was on holiday, and the nurses at the private methadone clinic did not seem to have recognised the seriousness of the situation. By late afternoon he felt much better and travelled by public transport to receive his last dose of methadone (35mg) at 1830. That evening he seemed well, was in a very good mood and ate a large dinner. However, he was still having difficulty urinating. He went to bed at 2245. Around 0645 the next morning his father was unable to wake him, he was breathing deeply, noisily and irregularly and had brown fluid coming from his mouth. After about fifteen minutes he stopped breathing and died. At autopsy, the body weighed 72kg. No "track" or recent injection marks could be identified. The lungs weighed 960g (right) and 860g (left) and were described as "very oedematous and congested". The heart and liver were macroscopically and microscopically normal. The postmortem blood methadone concentration was 0.32mg/L. No other drugs were detected in blood, bile or urine samples. The investigating pathologist determined the cause of death was methadone toxicity. The Deputy NSW State Coroner determined the fatal toxicity was caused by the administration of three daily doses of methadone (30mg, 35mg and 35mg).13 At the inquest, the deceased's methadone prescriber said he did not physically examine methadone patients and had not rejected an applicant for maintenance in the past two years. He routinely saw methadone patients only one day a week at a private methadone clinic.13 Back to text 2: Causes of death determined in this study and in official pathologists' reports for 38 patients in New South Wales methadone maintenance programs and 29 people whose deaths involved methadone diverted from maintenance programs Accidental drug toxicityMethadone*Other drug(s)Other causes of deathMethadone maintenance patientsDeath in first two weeksThis study11 1 1 Official report10 2 1 Death after two weeksThis study1 5 19 Official report1 5 19 Diverted methadoneThis study26 1 2 Official report24 2 3 TotalsThis study38 7 22 Official report 35 9 23 *Methadone either caused or contributed to the death. Back to text 3: Rates of fatal accidental drug toxicity and relative risks of fatal accidental drug toxicity and sudden death from all causes for patients in New South Wales methadone maintenance programs in 1994Rate Relative (Deaths/1000/yr) risk 95%CI Deaths from accidental drug toxicityIn first two weeks' maintenance70.4 36.3-122.8 after two weeks' maintenance0.72 0.26-1.57 First two weeks' maintenance v.out of treatment* 6.7 3.3-13.9 First two weeks' maintenance v.after two weeks' maintenance 97.8 36.7-260.5 Out of treatment* v.after two weeks' maintenance 12.2 4.8-30.6 Deaths from all causesOut of treatment* v.all maintenance 3.5 2.2-5.6 Out of treatment* v.after two weeks' maintenance 5.2 3.1-8.7 *Calculated from approximations derived from previously published data. Back to text

Olaf H Drummer · John R M Caplehorn

Research Australian general practitioners' views and use of colorectal cancer screening tests Michael J Sladden and Jeanette E Ward MJA 1999; 170: 110-113 For editorial comment, see Young Abstract - Introduction - Method - Results - Discussion - Acknowledgements - References - Author's details - - More articles on Gastroenterology Abstract Objectives: To determine general practitioners' (GPs) current beliefs, knowledge and self-reported practices of screening for colorectal cancer. Design and setting: Postal survey of national random sample of 1271 GPs in 1996. Outcome measures: GP views on effectiveness of faecal occult blood testing (FOBT) and flexible sigmoidoscopy in reducing premature death from colorectal cancer in "average-risk" patients (asymptomatic with no family history); views on frequency of tests and target group; use of these tests; and independent predictors of views and use. Results: Response rate was 67%. FOBT and flexible sigmoidoscopy were said to be effective as screening tests by 38% and 61% of GPs, respectively, but 30% and 25% were unsure. Independent predictors of belief in screening effectiveness were State of practice (for FOBT), male sex and awareness of Gut Foundation guidelines (for flexible sigmoidoscopy) and increasing age (for both). Most often chosen screening frequencies were every year for FOBT (29%), and five-yearly for flexible sigmoidoscopy (24%), although 19% and 26%, respectively, were unsure of the appropriate screening interval. Most often cited target group was people aged over 40 years with first-degree relatives with colorectal cancer: 63% of GPs would offer FOBT and 74%, flexible sigmoidoscopy. Fewer than 3% of GPs were likely to adopt an opportunistic approach to screening, yet 15% would be highly likely to recommend FOBT during a dedicated health check-up for a 58-year-old male patient, and 9% for a female patient. Conclusion: The absence to date of a coherent national policy on colorectal cancer screening is associated with wide variations in views and practice that are inconsistent with the available evidence. If GPs are to be involved in implementing population screening, national policy must be widely and effectively promulgated. Introduction The past decade has seen a saga of unfinished policy initiatives on screening for colorectal cancer in Australia. As early as 1990, screening by faecal occult blood test (FOBT) was being promoted for people with "average risk" of colorectal cancer, in the absence of convincing evidence or national policy.1 Since then, a range of bodies have produced guidelines with quite different recommendations, particularly for this "average risk" group.2-8 Examples are shown in Box 1. More recent among these was the 1997 report of the Australian Health Technology Advisory Committee (AHTAC) Working Party on Colorectal Cancer Screening. This working party was formed after a 1994 call for a national symposium to develop "recommendations about early detection of colorectal cancer" as part of Australia's national health goals and targets,9 and a 1995 deputation to the Commonwealth from the Australian Cancer Network. The Network recommended pilot projects of screening and, if these were successful, implementation of national screening. AHTAC found that FOBT was effective in reducing mortality from colorectal cancer in the average-risk population (defined as the "well population aged over 50") and recommended studies to determine the effectiveness of different screening strategies, particularly how best to involve general practitioners (GPs). Meanwhile, in 1998, another set of draft guidelines, not yet nationally endorsed, was circulated by the Clinical Oncological Society of Australia and the Australian Cancer Network.8 Despite the unresolved status of national policy, research has continued to involve Australian GPs overtly or covertly in colorectal cancer screening.10-14 Most recently, a survey of Perth GPs reported high uptake of this screening.15 As no national studies have been conducted, we designed a postal survey to assess GPs' perceptions of the effectiveness of screening for colorectal cancer and self-reported levels of screening. Method GP sample and survey administration A covering letter, questionnaire and reply-paid envelope were mailed in May 1996 to a national random sample of 1271 GPs, as described elsewhere.16 Standardised response-aiding strategies were used to follow up non-respondents.16 Questionnaire Questions on colorectal cancer screening were part of a larger questionnaire on current status of cancer screening in general practice. Respondents were asked to tick the response that matched their views on: Effectiveness of FOBT and flexible sigmoidoscopy in reducing premature deaths from colorectal cancer in "average risk" patients (ie, asymptomatic patients with no family history); Frequency of screening; Who should be screened; Likelihood of their initiating a discussion about FOBT or flexible sigmoidoscopy with a well 58-year-old male, and next female, patient during non-urgent consultations for ear syringing as well as during scheduled health check-ups; and Usefulness of three guidelines available at the time of the surveys (first three items in Box 1). The final section of the questionnaire included eight sociodemographic questions. Data analysis Descriptive, cross-tabulation and logistic regression analyses were performed with SPSS for Windows 7.17 Logistic regression analyses were performed to determine independent predictors of knowledge and practice outcomes. Fourteen potential predictors were considered: GP's sex; age; State; full- or part-time practice; practice type (solo or group); membership of a Division of General Practice; Royal Australian College of General Practitioners (RACGP) affiliation; membership of the Australian Medical Association; personal history of cancer; family history of cancer; awareness of RACGP guidelines; Australian Gastroenterology Institute/Australian Cancer Society guidelines; and Gut Foundation of Australia (GFA) guidelines; and practice location (metropolitan or other18). All independent variables were included in the full model. A further variable -- belief that FOBT/flexible sigmoidoscopy is an effective screening test -- was included in the model to predict behaviour. A backwards stepwise modelling strategy was used to identify significant independent variables, whereby all dependent variables were initially included and non-significant terms were progressively eliminated. Significance was assessed using the Wald chi-squared statistic. Results We received 855 usable questionnaires from 1271 eligible GPs (67% response rate). The response rate for women (75%) was significantly higher than that for men (63%) (chi-squared = 15.4, 1 df, P < 0.001), but did not vary with age, vocational registration status, RACGP affiliation, or practice size and location. GP views about screening GP views about the effectiveness of screening for colorectal cancer in preventing premature deaths are shown in Box 2. More GPs believed flexible sigmoidoscopy to be effective (61%) than believed FOBT to be effective (38%), but there was substantial uncertainty about both screening tests, with 25% and 30% of GPs unsure. Independent predictors of believing either test to be effective are summarised in Figure 1. For FOBT, these comprised increasing GP age and State of practice (specifically, South Australia). For flexible sigmoidoscopy, they comprised increasing GP age, male sex, and awareness of the Gut Foundation guidelines (which favour screening). GPs' views on appropriate screening frequencies and target groups are shown in Box 2. Most often chosen frequencies were every year for FOBT (29%), and five-yearly for flexible sigmoidoscopy (24%). However, 19% and 26%, respectively, were unsure of the appropriate screening interval. The most often cited target group was people aged over 40 years with first-degree relatives with colorectal cancer: 63% of GPs would offer FOBT and 74%, flexible sigmoidoscopy. Self-reported practice Likelihood of suggesting colorectal cancer screening is shown in Box 3. Fewer than 3% of GPs were "highly likely" to adopt an opportunistic approach to colorectal cancer screening for a 58-year-old patient (by either test) or to recommend flexible sigmoidoscopy screening during a dedicated health check-up. More would be "highly likely" to recommend FOBT during a dedicated health check -- 15% if the patient was a man and 9% if a woman. This sex difference was significant (McNemar's chi-squared = 43.7, 1 df, P < 0.0001). Independent predictors of being "highly likely" to include FOBT in a health check-up are shown in Figure 2. They comprised increasing GP age, State of practice, and belief in the effectiveness of the tests. Usefulness ratings of guidelines available at the time of the survey are shown in Box 4. While RACGP, AGI/ACS and GFA guidelines were rated as "very" or "somewhat" useful by 33%, 50% and 45% of respondents, respectively, they were unable to be recalled by 52%, 35% and 41%. Discussion Our study suggests considerable confusion about colorectal cancer screening at the "front line" of general practice. About a third of respondents believed that FOBT was an effective screening test in average-risk individuals, while two-thirds believed this of flexible sigmoidoscopy. These beliefs are inconsistent with the evidence available at the time of our study: level II (randomised controlled trial) evidence19 that FOBT reduced colorectal cancer mortality, but only level III (case-control study) evidence20 supporting flexible sigmoidoscopy. A wide range of responses were given about appropriate screening frequency. This is not surprising, as the three guidelines available at the time offered different and contradictory advice, and none met the criteria for being systematically evidence-based. Further confusion is likely if yet more guidelines8 are published that contradict the evidence-based AHTAC guidelines.7Far fewer GPs reported using the screening tests than reported they were effective; most respondents did not use the tests. This discordance was greater for sigmoidoscopy than for FOBT. Again, it is likely that the lack of clarity and the variation between guidelines, as well as availability of conflicting information and educational material, have caused uncertainty among GPs, with concomitant inconsistency in their behaviour. Perhaps FOBT is used more often than sigmoidoscopy because it is easier to arrange. Increasing GP age and physician belief in screening effectiveness independently predicted self-reported provision of screening. South Australian GPs were more likely to advocate screening, perhaps because of research studies and community-based initiatives in that State.10 GPs also favoured screening men rather than women for colorectal cancer. Sex bias not been reported previously in colorectal cancer screening, and may reflect the higher incidence of colorectal cancer among men.21 Alternatively, perhaps GPs place a lower priority on colorectal cancer screening in women, for whom cervical and breast cancer screening are widely performed, but a higher priority in men, for whom there is, as yet, no "male cancer" screening of proven benefit. National levels of self-reported use of screening tests were less than previously reported,15,22,23 although the higher levels in South Australia were consistent with earlier data.10 GPs' wider endorsement of screening for "above-average-risk" individuals with first-degree relatives with colorectal cancer (63%-74%) was similar to the levels found in recent studies (80%-94% GP support),10,15 but considerably higher than in a similar 1982 study (23% GP support).22 Screening of relatives is apparently becoming more acceptable. Usefulness and recall of guidelines was low, similar to other recent findings.15 Our results suggest an urgent need for a national colorectal cancer screening policy. As GPs remain the most respected source of health information,24 it is vital they have access to timely and accurate information. The AHTAC report, released in 1998, was necessary but insufficient. If GPs are to be involved in implementation of colorectal cancer population screening (which, by definition, will target average-risk individuals), strategies are needed to inform them of the importance of screening and to facilitate appropriate changes in behaviour. When there has been a concerted effort to communicate agreed policy to Australian GPs (eg, about mammographic screening), uniformity of GP views has been achieved.25 However, when evidence is lacking (eg, for clinical breast examination),25 or State-based initiatives are patchy,26 it appears that GPs differ considerably in their views of screening effectiveness and self-reported behaviour. Our study concentrated on screening average-risk individuals, for which previous guidelines have been confusing, non-evidence based and at variance with each other. Most guidelines distinguish between screening for average-risk and above-average-risk individuals, generally recommending colonoscopic screening for above-average-risk groups (eg, those with familial adenomatous polyposis and hereditary non-polyposis colorectal cancer). Clearly, strategies for effective evidence-based screening of above-average-risk groups must also be promoted. Thus, our results reveal our failings to date as an organised healthcare system to provide GPs with timely, consistent and evidence-based health policy, as they and their patients deserve. Our study provides a baseline against which the effectiveness of future dissemination of colorectal cancer screening policy may be measured. Acknowledgements A Commonwealth General Practice Evaluation Program seeding grant funded this study. We thank the GPs who participated in our research with no financial incentive, Phoebe Holt for contributing to questionnaire design, and Tracey Bruce for diligent survey administration. The study was approved by the Ethics Committee of the Royal Prince Alfred Hospital, Sydney, NSW. References Woodward A, Weller D. Colorectal cancer: implications of mass screening for public health. Med J Aust 1990; 153: 81-88. Guidelines for screening for colorectal cancer. Sydney: Australian Gastroenterology Institute, 1991. Australian Cancer Society. National cancer prevention policy, 1993. Sydney: Australian Cancer Society, 1993. Bolin T, Collopy B, Cowen A, et al. Colorectal cancer: prevention, diagnosis and treatment. Sydney: The Gut Foundation and Colorectal Surgical Society of Australia, 1993. Goulston K, St John DJ, Bokey L, et al. Guidelines for early detection, screening and surveillance for colorectal cancer. 2nd ed. Sydney: Australian Gastroenterology Institute and Australian Cancer Society, 1994. Guidelines for preventive activities in general practice. 3rd ed. Sydney: Royal Australian College of General Practitioners, 1994. Australian Health Technology Advisory Committee (Standing Committee of the National Health and Medical Research Council). Colorectal cancer screening. Canberra: Commonwealth Department of Health and Family Services, 1997. Clinical Oncological Society of Australia and Australian Cancer Network. Guidelines for the prevention, early detection and management of colorectal cancer. Draft 3. June 1998. Better health outcomes for Australians. Canberra: National Health Goals and Targets Section, Department of Human Services and Health, 1994. Cockburn J, Thomas R, McLaughlin S, et al. Acceptance of screening for colorectal cancer by flexible sigmoidoscopy. J Med Screen 1995; 2: 79-83. Rae L. Community screening for colorectal cancer in north-eastern New South Wales, 1987-1996. Med J Aust 1998; 168: 382-385. King J, Fairbrother G, Thompson C, Morris D. Colorectal cancer screening: optimal compliance with postal faecal occult blood test. Aust N Z J Surg 1992; 62: 714-719. King J, Fairbrother G, Thompson C, Morris D. Influence of socioeconomic status, ethnicity and an educational brochure on compliance with a postal faecal occult blood test. Aust N Z J Public Health 1994; 18: 87-92. Olynyk J, Aquilia S, Fletcher D, Dickinson J. Flexible sigmoidoscopy screening for colorectal cancer in average-risk subjects: a community-based pilot project. Med J Aust 1996; 165: 74-76. Olynyk J, Aquilia S, Platell C, et al. Colorectal cancer screening by general practitioners: comparison with national guidelines. Med J Aust 1998; 168: 331-334. Ward J, Bruce T, Holt P, et al. Labour-saving strategies to increase response rates in general practice surveys. Aust N Z J Public Health 1998; 22: 394-396. Statistical Package for the Social Sciences. SPSS for Windows 7.5.1. Chicago (Ill): SPSS Inc, 1996. Commonwealth Department of Primary Industries and Energy and Commonwealth Department of Human Services and Health. Rural, Remote and Metropolitan Areas Classification: 1991 Census edition. AGPS, Canberra: 1994. Mandel J, Bond J, Church T, et al. Reducing mortality from colorectal cancer by screening for fecal occult blood. N Engl J Med 1993; 328: 1365-1371. Selby J, Friedman G, Quesenberry C, Weiss N. A case-control study of screening sigmoidoscopy and mortality from colorectal cancer. N Engl J Med 1992; 326: 653-657. Jelfs P, Coates M, Giles G, et al. 1996 Cancer in Australia 1989-1990 (with projections to 1995). Canberra: Australian Institute of Health and Welfare (Cancer Series No. 5). Macrae FA, Hill DJ, Dent O, et al. Colorectal cancer: knowledge and attitudes of doctors in Victoria. Aust N Z J Med 1982; 12: 278-283. Rolfe I, Pearson S. Screening recommendations in general practice: a survey of graduates from different medical schools. Med J Aust 1996; 165: 14-17. Cumming R, Barton G, Fahey P, et al. Medical practitioners and health promotion: results from a community survey in Sydney's western suburbs. Community Health Stud 1989; 13: 294-301. Young J, Ward J, Holt P. Breast cancer screening in Australian general practice: results of a national survey. Med J Aust 1998; 169: 364-368. Ward J, Donnelly N, Holt P. Impact in general practice of the policies of the organised approach to preventing cancer of the cervix. Aust N Z J Public Health 1998; 22: 336-341. (Received 25 Jun, accepted 28 Oct, 1998) Author's details Division of Community and Rural Health, University of Tasmania, Hobart, TAS. Michael J Sladden,FRACGP, MAppEpid, Honorary Senior Lecturer. Needs Assessment and Health Outcomes Unit, Central Sydney Area Health Service, Sydney, NSW. Jeanette E Ward, PhD, FAFPHM, Director. Reprints will not be available from the authors. Correspondence: Dr M J Sladden, Division of Community and Rural Health, PO Box 252-33, University of Tasmania, Hobart, TAS 7001. Email: M. Sladden@utas.edu.au Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> Figure 1 : Independent predictors of general practitioners (GPs) reporting that faecal occult blood testing or flexible sigmoidoscopy is effective in reducing premature deaths from colorectal cancer. Back to text Figure 2 : Independent predictors of general practioners (GPs) reporting they would be "highly likely" to discuss faecal occult blood testing during a deicated health check-up with a 58-year-old patient. (Adjusted odds ratios with 95% confidence intervals are available from the authors.)Back to text 1: Recommendations about colorectal cancer screening for average-risk* people Gut Foundation of Australia (1993)4 Screening by annual FOBT; consider 3-5-yearly flexible sigmoidoscopy Australian Gastroenterology Institute/Australian Cancer Society (1994) 5 Routine screening not recommended; can be performed at patient request Royal Australian College of General Practitioners (1994)6 Screening not recommended Australian Health Technology Advisory Committee (1997)7 Screening by FOBT; research required to determine method and frequency Clinical Oncological Society of Australia/Australian Cancer Network (draft 1998)8 Screening by annual FOBT; consider 5-yearly flexible sigmoidoscopy FOBT=faecal occult blood test. *Asymptomatic people aged over 50 years with no family history Back to text Back to text Back to text Back to text

Michael J Sladden · Jeanette E Ward

Research General practitioners' use of evidence databases Jane M Young and Jeanette E Ward MJA 1999; 170: 56-58 For editorial comment, see Van Der Weyden Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on General practice and primary care Abstract Objective: To determine the awareness and use of the Cochrane Library and access to the Internet by general practitioners in New South Wales. Design: Cross-sectional postal survey in September 1997. Participants: 311 of 428 (73% response rate) randomly selected general practitioners in New South Wales. Main outcome measures: Proportion of respondents with access to the Internet at home or at work; proportion of respondents aware of, with access to, and ever using the Cochrane Library; independent predictors of awareness of the Cochrane Library. Results: 134 respondents (43%) had access to the Internet either at home or at work; 42 (14%) were "on line" at their workplace. Seventy (22%) were aware of the Cochrane Library, although only 20 (6%) had access to it and 13 (4%) had ever used it. Those in group practice and members of Divisions were independently more likely to be aware of the Cochrane Library. Conclusions: As patient outcomes will improve with systematic implementation of evidence-based treatments, these low rates of access to useful evidence databases raise issues regarding the best ways to support general practitioners with information technology. Introduction There has been increasing interest in the use by clinicians of evidence databases and other resources, such as systematic reviews, meta-analyses and evidence-based guidelines, as aids for clinical decision-making. The first report of Australian clinicians' use of evidence databases was recently published in the Journal.1 In that study, 72% of neonatologists and 44% of obstetricians reported using evidence databases, with higher rates of use among those familiar with computers. Although lack of awareness of evidence databases does not preclude evidence-based practice,2 the inability of practitioners to access research findings readily at the time of decision-making is a major impediment to best practice.3Because of the breadth of their work, general practitioners have diverse needs for evidence to inform their practice.4 Accessible evidence databases potentially represent an essential resource to meet these needs. The Cochrane Library, which includes the Cochrane Database of Systematic Reviews and the Database of Abstracts of Reviews of Effectiveness (Box 1), is recognised as one of the best resources for evidence. General practitioners can use it on CD-ROM or through the Internet. Research from other countries suggests that general practitioners are reluctant to embrace information technology to support evidence-based clinical decision-making. Two recent surveys both reported that, at most, 40% of British general practitioners were aware of the Cochrane Database of Systematic Reviews.5,6 Furthermore, despite positive attitudes towards evidence-based medicine, general practitioners reported low levels of use of either printed or electronic summaries of evidence, even among those who were aware of these resources.6 In 1995, it was reported that a quarter of a national random sample of Australian general practitioners had access to a computer with a modem but less than 10% had access to the Internet.7 No reports have been published more recently to assess the uptake of information technology by general practitioners. The aim of our study was to determine New South Wales general practitioners' current awareness of, access to, and use of the Cochrane Library, and their access to the Internet both at home and at work. Methods Survey content and administration We added the following questions to a statewide random postal survey of general practitioners in NSW conducted in September 1997:Are you aware of the Cochrane Library? Do you have access to the Cochrane Library? Have you ever used the Cochrane Library? Do you have access to the Internet at your practice? Do you have access to the Internet at home? Respondents could indicate "Yes", "No" or "Unsure" to each of these questions. Respondents also completed eight standard sociodemographic questions. A copy of the questionnaire is available from the authors on request. Four hundred and twenty-eight eligible general practitioners in NSW, randomly selected from a commercial list, were contacted by telephone in advance of our survey. Two mail reminders and a telephone prompt were used to maximise the response rate. Data analysis Proportions and 95% confidence intervals were calculated for responses to questions about the Cochrane Library and Internet. The univariate association between awareness of and access to the Cochrane Library and personal and professional characteristics of respondents were assessed using c2 tests, or Fisher's exact test where expected cell frequencies were less than five. Logistic regression using a backwards stepwise modelling strategy was then carried out to identify factors that significantly and independently predicted positive responses to these questions. All analyses were conducted using SAS for Windows.8 Ethics approval This study was approved by the Central Sydney Area Health Service Ethics Review Committee and the Human Ethics Committee of Sydney University. Results We received completed questionnaires from 311 general practitioners (73% response rate). Although the response rate for women (80%) was significantly higher than for men (70%) (chi-squared = 4.5; df = 1; P = 0.03), respondent characteristics were similar to those of general practitioners in NSW.9 Respondents ranged in age from 24 to 72 years (mean, 45 years), 96 (31%) were women, 236 (76%) worked full time, and 202 (65%) were in group practice. Professional characteristics of respondents included RACGP affiliation (141; 45%), AMA membership (109; 35%), and membership of a Division of General Practice (242; 78%). A third of respondents (107; 34%) had trained with the Family Medicine Program. Responses to the questions about the Cochrane Library and Internet are shown in Box 2. Less than a quarter of respondents were aware of the Cochrane Library and only 13 (4%) had used it. Nearly one in five respondents were unsure if they had access to this resource. One hundred and thirty-four respondents (43%) had access to the Internet either at home or work, significantly higher than the 9% reported previously (chi-squared = 86.6; df = 1; P < 0.001).7 Awareness of the Cochrane Library was unrelated to age (t = -1.1; df = 298; P = 0.2) or sex (chi-squared = 0.6; df = 1; P = 0.4). The only significant associations were with general practice Divisional membership and working in group practice. These variables remained independently predictive of awareness of the Cochrane Library following logistic regression analysis (Box 3). The number of respondents who had actually used the Cochrane Library were too few for further analysis. Discussion Overall, 22% of respondents were aware of the Cochrane Library. As awareness was greater among those in group practice and members of their local Division, peer contact appears to be an important mechanism to promote evidence databases. Nonetheless, the level of awareness in our study was considerably lower than that reported in the United Kingdom,5,6 where the Cochrane Database of Systematic Reviews has been available since 1992.10 However, our finding that only 4% of respondents had ever used the Cochrane Library is comparable. Our finding of a marked uptake since 1995 of Internet access by general practitioners is reassuring. Nearly half had Internet access either at home or at their practice. However, only 14% were "on-line" at their practices, where clinical decisions are likely to be made. Evaluation of strategies to support the uptake of information technology for desktop Internet access will be an immediate challenge in ensuring evidence databases are used in general practice. Access to evidence databases is crucial to support the scientific paradigm now advocated in healthcare.11 Having accessed an evidence database, general practitioners can focus on treatments for which there is Level I (meta-analysis of randomised controlled trials) or Level II (randomised controlled trials) evidence of effectiveness. By ensuring treatments with such compelling evidence are used, GPs can confidently anticipate that their patient outcomes will positively and predictably improve. Less confidence can be placed on interventions for which only Level IV (descriptive case reports) evidence exists. Measurement and improvement of care based on Level I or II evidence of effectiveness should also be emphasised in quality assurance activities.12 Three years ago it was argued that "the health care system needs an infrastructure for the dissemination of evidence-based medicine into clinical practice".13 Subsequently, some people have suggested that general practitioners need mediated search services.14 Other problems to overcome include training general practitioners to appraise evidence4 and to incorporate research findings into their daily consultations with patients.15 Our findings suggest we have a long road ahead. Since June 1998, members of the Royal Australian College of General Practitioners (RACGP) have had access to the Cochrane Library through the RACGP Virtual Resource Centre. Evaluation of the impact of electronic evidence resources, including evidence databases or Web-based guidelines, on decision-making in general practice is the next step. Initiatives to encourage evidence-based decision-making in general practice are likely to generate dissatisfaction with the limitations of currently available evidence.16 We are optimistic this will accelerate the quality and quantity of research conducted in general practice. Syntheses of current knowledge prevent the reinvention of wheels or repetition of past mistakes, minimising expenditure on populist strategies without strong evidence of effectiveness. Gaps in current knowledge of effective interventions in clinical practice are tellingly revealed in evidence databases, inviting a responsive academic research agenda. General practitioners adopting an evidence-based approach may be more inclined to participate in research which is relevant, rigorous and responsive to gaps in evidence sorely felt in clinical decision-making. Acknowledgements The participation of general practitioners in our research, without financial incentive, is acknowledged gratefully. We thank Nancy Harding for organisational support and Leonie Cambage for data entry. J M Y is supported by an NHMRC research scholarship. References Jordens CFC, Hawe P, Irwig LM, et al. Use of systematic reviews of randomised trials by Australian neonatologists and obstetricians. Med J Aust 1998; 168: 267-270. Phillips PA. Disseminating and applying best evidence. Med J Aust 1998; 168: 260-261. Haines A, Jones R. Implementing findings of research. BMJ 1994; 308: 1488-1492. Ridsdale L. Evidence-based learning for general practice. Br J Gen Pract 1996; 46: 503-504. Prescott K, Lloyd M, Douglas HD, et al. Promoting clinically effective practice: general practitioners' awareness of sources of research evidence. Fam Pract 1997; 14: 320-323. McColl A, Smith H, White P, Field J. General practitioners' perceptions of the route to evidence based medicine: a questionnaire survey. BMJ 1998; 316: 361-365. Gupta L, Ward J, Hayward RSA. Future directions for clinical practice guidelines: needs, lead agencies and potential dissemination strategies identified by Australian general practitioners. Aust N Z J Public Health 1997; 21: 495-499. SAS for Windows [computer program]. Version 6.11. Cary, North Carolina: SAS Institute, 1995. Commonwealth Department of Health and Family Services. General practice in Australia: 1996. Canberra: Commonwealth of Australia, 1996. Silagy C. Randomised controlled trials: the challenge of Archie Cochrane. Med J Aust 1993; 158: 656-657. Risdale L. How do you know? The process of scientific reasoning. In: Evidence-based general practice: a critical reader. London: WB Saunders, 1995; 160-169. Ward J, Del Mar C, Colmer P, O'Connell D. Quality and outcomes in general practice. In: General practice in Australia: 1996. Canberra: Commonwealth of Australia, 1996; 169-199. Ahmed T, Silagy C. The move towards evidence-based medicine. Med J Aust 1995; 163: 60-61. Fowler C. Evidence-based learning in general practice. Br J Gen Pract 1996; 46: 754-755. Jacobson LD, Edwards AGK, Granier SK, Butler CC. Evidence-based medicine and general practice. Br J Gen Pract 1997; 47: 449-452. Campion-Smith C. Evidence-based general practice. Br J Gen Pract 1997; 47: 462. (Received 18 May, accepted 15 Sep, 1998) Authors' details Needs Assessment and Health Outcomes Unit, Central Sydney Area Health Service, Newtown, NSW. Jane M Young, MB BS, MPH, Postgraduate Fellow; Jeanette E Ward, PhD, FAFPHM, Director. Reprints: Associate Professor J E Ward, Needs Assessment and Health Outcomes Unit, Central Sydney Area Health Service, Locked Bag 8, Newtown, NSW 2042. Email: jwardATnah.rpa.cs.nsw.gov.au Make a comment Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Jane M Young · Jeanette E Ward

Abstract Objective: To ascertain the effectiveness of clinical pathways for improving patient outcomes and decreasing lengths of stay after hip and knee arthroplasty. Design and setting: Twelve-month randomised prospective trial comparing patients treated through a clinical pathway with those treated by an established standard of care at a single tertiary referral university hospital. Participants: 163 patients (56 men and 107 women; mean age, 66 years) undergoing primary hip or knee arthroplasty, and randomly allocated to the clinical pathway (92 patients) and the control group (71 patients). Main outcome measures: Time to sitting out of bed and walking; rates of complications and readmissions; match to planned discharge destination; and length of hospital stay. Results: Clinical pathway patients had a shorter mean length of stay (P = 0.011), earlier ambulation(P = 0.001), a lower readmission rate (P = 0.06) and closer matching of discharge destination. There were beneficial effects of attending patient seminars and preadmission clinics for both pathway and control patients. Conclusion: Clinical pathway is an effective method of improving patient outcomes and decreasing length of stay following hip and knee arthroplasty. Introduction The past two decades have seen an 85% rise in Australian health costs to 36.6 billion dollars, with the largest proportion of this expended in acute hospital care.1 Newer health policies now incorporate measures to rationalise and improve the efficiency of many services. Such policies, however, are economically driven and frequently fail to consider the optimum level of service required by the community.2 Treatment protocols, variously known as clinical pathways, critical pathways and care paths, that aim to streamline and standardise management through a systematic approach so that high quality care may be provided in a timely and cost effective manner3,4 have been developed. Clinical pathways describe the course of hospitalisation for patients with a specified illness and encompass a predetermined plan of treatment. The use of clinical pathways is now well established and their successes are widely reported.5-7 Joint arthroplasty is a common and costly procedure associated with high resource use that is frequently performed in the elderly who may have many coexisting morbidities. These characteristics suggest that joint arthroplasty may be a suitable procedure to incorporate into a clinical pathway.8 As part of a "best practice" initiative in line with quality assurance activities at St Vincent's Hospital, the hospital's Orthopaedic Service has developed clinical pathways for hip and knee joint arthroplasty for treating osteoarthritis which aim to maximise the use of all available resources and minimise negative patient outcomes, thereby improving patient care. To this end, we report the effects of introducing clinical pathways at our hospital on quality indicators such as mobilisation, complication rates, discharge planning and readmission rates while also exploring the impact on length of stay. Methods We used a prospective randomised control group design to compare the outcomes of patients who underwent hip or knee joint arthroplasty at St Vincent's Hospital, Melbourne (a tertiary referral hospital affiliated with the University of Melbourne), between 1 January 1996 and 30 December 1997. All such patients were randomly allocated to either the control or clinical pathway group by a clerical assistant who was blinded to their demographic and clinical profiles. Diagnostic category and comorbidities had no bearing on the allocation of patients to either the pathway or control groups, but patients were excluded from the study after randomisation if they were having revision arthroplasty, simultaneous bilateral joint arthroplasty, arthroplasty for acute trauma or complex tumour surgery. The management of patients undergoing joint arthroplasty at St Vincent's Hospital, Melbourne, is outlined in Box 1. Outcome measures Length of stay (calculated from the time of the patient's admission to the time of discharge and expressed in days); Time to sitting out of bed and ambulation (time between surgery and the patient's first day of sitting out of bed or walking with assistance); Complications (wound infections, including all wound erythema lasting more than 24 hours, chest infections, deep vein thrombosis [DVT] as diagnosed by clinical features and confirmed by ultrasonography, joint dislocation, decubitus pressure areas, failure to cope at home and a decreased range of motion after discharge); Readmission (for complications during a follow-up period of three months from discharge); and Discharge matching (between the presumptive discharge destination given at the preadmission clinic and the patient's postdischarge destination). Clinical pathway and control patients Patients randomly allocated to the clinical pathway received proactive treatment whereby specific goals were set each day for the patient and treating team. Their hospital records included a special written protocol which listed milestones to be achieved, identified tests that should be ordered, set daily tasks for patients and members of the treating team, and provided space for documenting any variation in treatment or patient response. Each intervention was signed by the treating health professional and the discharge plan was re-evaluated daily to ensure it remained realistic and appropriate to the patient's needs. The clinical pathway formalised in writing the participation of the various members of the treating team. Patients not allocated to the pathway received "reactive" treatment whereby the treating team responded to the will and condition of the patient in providing postoperative care. Statistical analysis Results were analysed with SigmaStat V2 software.9 Data were compared using t tests for independent groups and multiple linear regression where appropriate. We used the z test for comparisons of proportions between groups. As the data for length of stay (LOS), time to sitting out of bed and time to ambulation were not normally distributed, these data were transformed using a logarithmic transformation before analysis with t tests. We calculated the sample size for this study after reviewing all hip and knee arthroplasty patient data for 1995, which showed a mean LOS of 13 days (range, 5.8-43.3; SD, 5.3). We believed that a 20% reduction in LOS (2.6 days) would represent a clinically significant outcome. Therefore, we calculated that to detect a reduction of 2.6 days in LOS at a significance level of 0.05 with a power of 0.8 would require two groups with a minimum of 65 subjects in each group. Results During the study period 175 patients underwent hip or knee joint arthroplasty and were randomly allocated to the pathway (94 patients) and control (81 patients) groups. Twelve patients were then excluded by the crtiteria listed in the methods, leaving 163 patients -- 92 in the clinical pathway group and 71 in the control group. The sample comprised 56 men and 107 women, with a mean age of 66 years (range, 67-93 years). All patients were followed for a minimum of three months and none were lost to follow-up. Our findings are summarised in Box 2. There was no significant difference between control and pathway patients in terms of age or weight. Although the clinical pathway group included more patients with premorbid conditions than the control group, this difference was not statistically significant (95% CI, - 0.03 to 0.21). Length of stay (LOS) was significantly shorter for the pathway group than for the control group (t = 2.585; P = 0.011). When LOS was analysed for the subgroups of patients in each group with premorbid conditions, this was still significantly shorter for the pathway group than the control group (t = 3.152; P = 0.001) despite the larger number of patients with premorbid conditions in the pathway group. Patients in the clinical pathway group sat out of bed and walked earlier after surgery than control patients. Multiple linear regression for each group showed that time to ambulation was the only significant contributor to reduction in log LOS in the clinical pathway group (time to ambulation -- coeff = 19.6, standard error [SE] = 9.6, P = 0.04; time to sitting out of bed -- coeff = - 4.35, SE = 9.3, P = 0.64, R2 = 0.127). Neither time to ambulation nor time to sit out of bed was significantly associated with reduced log LOS in the control group (time to ambulation -- coeff = 21.05; SE = 26.28, P = 0.42; time to sit out of bed -- coeff = - 4.13, SE = 28.54, P = 0.88, R2 = 0.0251). Patients from both the clinical pathway and control groups who attended either the preadmission clinic (n = 122) or the patient information seminar (n = 61) had a shorter LOS (7.22 days and 6.84 days, respectively) than patients who attended neither (n = 36; LOS, 8.55 days). The 54 patients who attended both the clinic and seminar had the shortest LOS at 6.6 days, and t tests showed that the shorter LOS for these patients relative to those who attended neither the clinic nor seminar was significant (t = 2.66; P = 0.009). Post-hoc t tests showed that the shorter LOS for patients who had attended both preadmission clinics and information seminars relative to those who had attended neither was significant (t = 2.66; P = 0.009). Box 2 shows that a greater proportion of clinical pathway patients were discharged to their planned discharge destination than control patients (95% CI, - 0.05 to 0.23), and that there were fewer readmissions in clinical pathway patients (95% CI, 0.006-0.174), although neither result was statistically significant. However, there were significantly fewer complications in clinical pathway patients (95% CI, 0.036-0.27). Discussion We found that a clinical pathway for hip and knee joint arthroplasty had a beneficial impact on the duration of admission, with patients on the pathway having a 1.5-day shorter stay than control patients. The seven-day LOS for our pathway patients compared favourably with that of Gregor et al,10 who showed a reduction in LOS from 12 to nine days for pathway patients. Length of stay was significantly shorter for the pathway group than the control group despite the larger proportion of pathway patients with premorbid conditions. This result should be interpreted cautiously, as the small overall number of patients with premorbid conditions meant that the test had less than optimal power (0.45). However, we conclude that comorbidities per se should not exclude patients from clinical pathways. Patients with comorbid conditions may actually be better served because of the greater fastidiousness and vigilance imposed by the daily protocol. While our findings that there were fewer complications and readmissions in clinical pathway patients were not significant, we believe that given the appropriate number of subjects in future studies both of these areas may approach significance. We noted that reducing the length of stay did not increase the complication rate, a finding corroborated by others.11 In addition, the readmission rate for complications for pathway patients was one-third that of controls. This contrasts with some studies which have reported an inverse relationship between length of stay and readmission rates.11 We, like other authors,12 believe that it is a lower quality of care and not length of stay per se that increases the risk of unplanned readmission. Discharge planning is an important part of the clinical pathway which appears to be closely linked with the length of stay. Appropriate matching of predetermined discharge destinations is a correlate of shorter admissions. If we are able to improve on our destination matching rate of 70%, we may be able to further reduce our length of stay, thereby making more resources available for other patients. Education of patients and their relatives appeared to have a positive influence on the patients' recovery after joint arthroplasty, with earlier mobilisation and discharge from hospital. Attending information seminars and preadmission clinics assisted in reducing the length of stay by almost two days. Patients and their relatives who understand the disease and the necessary treatment may be in a better position to assist with care and rehabilitation. Attendances for our information seminar and preadmission clinic were 38% and 74%, respectively, and we are endeavouring to increase these. First introduced by the New England Medical Center, clinical pathways are now incorporated into the management philosophy of many hospitals worldwide.13,14 Pathways involve input from medical, nursing, paramedical and administrative staff, and reflect the expertise of all members of the healthcare team while highlighting the interdependent nature of these roles in achieving positive outcomes for patients.15 A valuable subsidiary purpose of pathways is in providing information from which the financial cost of care may also be derived.16 Accurate costing of treatment is fundamental to the operation of institutions where prospective payments are made in accordance with diagnosis-related groups (DRGs), standardised lengths of stay and fixed reimbursement for care. Clinical pathways thus provide an important tool for coordinating and managing clinical resources. However, the driving force behind clinical pathways must remain the need to improve the quality of care and patient outcomes, and not their utility as a tool to ensure that budgetary demands are met. We are encouraged by our findings, which indicate substantial improvements for patients on a clinical pathway. To our knowledge, no other study has investigated the effect of clinical pathways on joint arthroplasty using a contemporaneous control group. 1 Management of joint arthroplasty patients at St Vincent's Hospital, Melbourne Preadmission clinics Preoperative review for patients undergoing elective joint replacement involves a multidisciplinary approach and includes medical, nursing, physiotherapy and occupational therapy consultation and anaesthetic and social work screening. Preexisting conditions are identified and testing and treatment are undertaken to achieve an optimum level of preoperative health. A discharge destination is determined based on medical and projected rehabilitation needs. Appropriate referrals are initiated. Patient information seminars Groups of patients and their families are invited to attend an information seminar about the surgery. The surgeon explains the aetiology of the disease, principles of management, nature of potential risks and their prevention. The nursing staff discuss acute postoperative care, including pain relief, pressure and wound care, intravenous therapy, and prophylaxis for deep venous thrombosis. The physiotherapist discusses the regimen of postoperative exercises, cautions and mobilisation. The occupational therapist describes the availability and use of various personal aids which assist the patient in preventing complications such as falls, injury or dislocation. Patients are able to raise any questions related to their surgery. Patients and their families are encouraged to take an active role in the postoperative management, and are acquainted with their very important role in the postdischarge phase. All members of the team stress the philosophy that the primary intention is to return patients home in preference to a rehabilitation hospital after the surgery. Discharge Patients are discharged home or to a rehabilitation unit. For those discharged home, community nursing care is provided at regular intervals for the first three weeks after discharge. Community nurses pay special attention to the nature of the patient's wounds, their exercise regimen and general medical condition. Any concerns are immediately related to the medical staff for further attention. Patients are followed up on a regular basis in the outpatient department. 2 References MacIntyre CR, Brook CW, Chandraraj E, Plant AJ. Changes in bed resources and admission patterns in acute public hospitals in Victoria, 1987-95. Med J Aust 1997; 167: 186-189. Parry TG. Health expenditure in Australia -- the current dilemma. Med J Aust 1992; 156: 592-594. Wigfield A, Boon E. Critical care pathway development: the way forward. Br J Nursing 1996; 5: 732-735. Grudich G. The critical path system. AORN J 1991; 53: 705-714. Gouveia WA, Massaro FJ. Critical pathway experience at New England Medical Center. Am J Health-Syst Pharm 1995; 52: 1068-1070. Saltiel E. Critical pathway experience at Cedars-Sinai Medical Center. Am J Health-Syst Pharm 1995; 52: 1063-1068. Stevenson LL. Critical pathway experience at Saratosa Memorial Hospital. Am J Health-Syst Pharm 1995; 52: 1071-1073. Leininger SM. Tools for building a successful orthopaedic pathway. Orthop Nurs 1996; 15: 11-19. SigmaStat [computer program]. Version 2. San Rafael, CA: Jandel Scientific Software, 1995. Gregor C, Pope S, Werry D, Dodek P. Reduced length of stay and improved appropriateness of care with a clinical path for total knee or hip arthroplasty. Joint Commiss J Qual Improv 1996; 22: 617-628. Rushworth RL, Rob MI. Readmissions to hospital: the contribution of morbidity data to the evaluation of asthma management. Aust J Public Health 1995; 19: 363-367. Ashton CM, Kuykendall DH, Johnson ML, et al. The association between the quality of inpatient care and early readmission. Ann Intern Med 1995; 122: 415-421. Zander K. Managed care within acute care settings: design and implementation via nursing case management. Health Care Supervisor 1988; 6: 27-43. Bower KA. Managed care: controlling costs, guaranteeing outcomes. Definition 1988; 3: 14. Heacock D, Brobst RA. A multidisciplinary approach to critical path development: a valuable CQI tool. J Nurs Care Qual 1994; 8: 38-41. Weilitz PB, Potter PA. A managed care system. Financial and clinical evaluation. J Nurs Admin 1993; 23: 51-7. (Received 27 Jan, accepted 20 Aug, 1998) Authors' details Department of Orthopaedics, St Vincent's Hospital, Melbourne, VIC. Michelle M Dowsey, BN, GradCertOrth, Clinical Nurse Specialist; Meredith L Kilgour, BN, GradDipAdvClinPrac, Nurse Unit Manager; Nick M Santamaria, BAppSc, PhD, Director of Nursing Research; Peter F M Choong, MD, FRACS, Professor, and Director of Orthopaedics. Reprints: Professor P F M Choong, Department of Orthopaedics, St Vincent's Hospital, 41 Victoria Parade, Fitzroy, VIC 3065. Email: PeterChoongATc031.aone.net.au

Michelle M Dowsey · Meredith L Kilgour · Nick M Santamaria

MJA 1999; 170: 11-14 For editorial comment, see Conyers Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Author's details Abstract Objective: To assess the effect of a total quality management (TQM) approach on the appropriateness of clinical laboratory testing of patients with acute myocardial infarction. Design: Retrospective, control-group, quasi-experimental study. Setting: Two metropolitan teaching hospitals: one involved in the intervention (TQM experimental group); the other had no intervention (control group). Intervention: A multidisciplinary team involved in the development of improvement strategies, including laboratory testing guidelines, education programs, data collection, monitoring and feedback. Outcome measures: Total number of requested clinically indicated and non-clinically indicated tests. Results: The proportion of clinically indicated tests that were requested increased from 77.5% to 88.2% (P < 0.01) and the number of non-clinically indicated tests was reduced by 81.7% with the introduction of the TQM strategies (P < 0.01). Conclusions: The introduction of a TQM approach has improved the appropriateness of test ordering in acute myocardial infarction. The reduction in non-clinically indicated tests could produce substantial savings in hospital pathology costs, and the increase in clinically indicated tests provides better patient care. Introduction The determination of plasma creatine kinase (CK) and creatine kinase-MB fraction (CK-MB) is pivotal in the diagnosis of acute myocardial infarction (AMI).1 However, the inappropriate use of these and other laboratory tests has increased markedly during the past 10-15 years, contributing to escalating healthcare costs2 and undesirable clinical consequences because of false positive results in AMI, often leading to unnecessary further investigations.3A number of reports have indicated an excessive use of laboratory tests in patients admitted to hospital with AMI or other clinical disorders. One Australian study found that at one hospital up to 20% of all laboratory tests were unnecessary.4 Another found that there were three times as many clinical chemistry tests ordered as were appropriate for patients admitted with chest pain.5 Similarly, a recent study found inappropriate testing of calcium, phosphate and magnesium in the emergency department of a United States teaching hospital.6 The conventional approach to address inappropriate laboratory testing has been to target doctors through education,7 feedback8 and providing information on laboratory testing costs.9 Such measures have had limited success, and in most cases have had limited input from clinicians.10 I have examined the effect of a total quality management (TQM) approach (that was developed and introduced by clinicians and other healthcare professionals) on the appropriateness of clinical laboratory test use in the management of patients with AMI. Total quality management refers to the overall approach of managing the total aspects of an organisation's quality. In my study, this involves changing the way quality in test use is viewed, focusing on the customer and including everyone involved in its provision and use in the process of continuous improvement. The specific TQM model I used was the FOCUS-PDCA approach to quality improvement (Box 1).11 Methods Setting and patient groups The study was conducted from March 1993 to August 1995 at two teaching hospitals in Sydney. Patients at Bankstown-Lidcombe Hospital were designated the "experimental" group, and those at Nepean Hospital were the "control" group. Only the experimental group was subjected to the TQM intervention. At the time of the study, Bankstown-Lidcombe Hospital was a 454-bed hospital with 21 724 annual admissions from the Emergency Department and 2355 admissions to the Coronary Care Unit (CCU). Nepean Hospital was a 415-bed hospital with 20 485 annual admissions from the emergency department and 1891 admissions to the CCU. Within the study groups, two subgroups of AMI patients were identified: "suspected AMI" and "confirmed AMI". The suspected AMI group included all patients who were admitted to the CCU via the emergency department with chest pain and electrocardiographic (ECG) signs suggesting AMI: these were greater than 0.1 mV of ST-segment elevation in two or more limb leads or greater than 0.2 mV in two or more contiguous precordial leads, and the Minnesota code was used to classify Q-wave changes.12 Not all the cases of suspected AMI did in fact progress to AMI. Patients were included in the confirmed AMI group if they had a primary discharge diagnosis in accordance with the World Health Organization criteria.13 The diagnosis was confirmed if the patient had at least two of the following three findings: the presence of a typical history of characteristic chest pain, new ECG changes of pathological Q waves, and an elevation of serum CK to 390 U/L or above during the first 72 hours of admission. Improvement process A quasi-experimental design involving a pre-intervention and post-intervention phase with a concurrent control was used to test the effect of the TQM approach. The study was conducted in two 15-month stages. The first stage involved the collection of pre-intervention data. In the second stage the TQM intervention took place. Using the FOCUS-PDCA TQM model, a multidisciplinary team was empowered to make the necessary improvements, which were introduced during the intervention period as they were developed. The team included representatives from all clinical areas involved in the process of laboratory testing. These included the Emergency Department (Director of Emergency, Assistant Director of Nursing, Clinical Nurse Specialist and Senior Medical Officer), CCU (Director of Cardiology, Nurse Unit Manager, Clinical Nurse Specialist), Pathology Department (Director of Pathology, Senior Technologist), and Administration (Deputy Director of Medical Services). The hospital's Quality Assurance Officer was appointed the Quality Advisor for the TQM team. TQM team meetings were held weekly over the first two months of the 15-month intervention period, and then monthly. The TQM team established an overall review and improvement of the total systems and processes involved in test ordering. The team's mission statement was To ensure that the pathology services used are appropriate, effective and efficient for supporting clinical care in AMI. Practice guidelines were introduced for laboratory testing in the management of AMI. Clinicians in the team were actively encouraged to participate in the improvement process. Draft copies of the guidelines were circulated widely to other clinicians for comment. Suggestions for change were considered and incorporated into the guidelines as determined by the team. The guidelines provided details of all recommended laboratory tests during the 72-hour period following the admission of a patient with suspected AMI into hospital. Strategies were developed for education and training programs, feedback mechanisms and ongoing monitoring of performance through data collection and analysis. To implement the changes, the TQM team assigned responsibility to motivated individuals to accomplish specified tasks. Progress reports were provided at subsequent meetings. Medical staff requesting laboratory tests for suspected AMI patients were issued with pre-stamped pathology request forms that listed the recommended tests from the guidelines. Clinically indicated tests Requested laboratory tests were designated as "clinically indicated" if the ordered tests matched those listed in the AMI practice guidelines devised by the team, or if the tests were found to be justified when the patient's records were checked by one of the study's hospital medical officers. Conversely, "non-clinically indicated" tests were all requested tests found to be outside the recommendations of the AMI practice guidelines that could not be justified for inclusion when checked by one of the study's hospital medical officers. Data collection and statistical analysis Once the suspected AMI patients were transferred to the CCU of the experimental group hospital, an audit was undertaken of the laboratory tests requested and the time and date of each blood collection. The data were collected by me in collaboration with the Senior Technologist of the Pathology Department. The findings on the appropriateness of test use were reported to the Emergency Department and CCU staff, and at the team meetings. For each of the confirmed AMI groups, the number of clinically and non-clinically indicated tests were retrospectively determined. Group equivalency between the pre-TQM and post-TQM groups was determined using the t test. Only the results for the confirmed AMI groups are presented here. All data were coded, entered and analysed using SPSS for Windows.14 Ethical approval The study was approved by the Ethics Committees of both the South Western Sydney Area Health Service and the Nepean Health Service. Results The experimental and control groups did not differ in age, sex ratio or length of stay in hospital (Box 2). The proportion of clinically indicated tests that were requested for the experimental group increased from 77.5% before the TQM intervention to 88.2% in the intervention period (Box 3). For the control group, the proportion of clinically indicated tests that were requested did not change significantly (Box 4A). For the experimental group, the number of non-clinically indicated tests per admission was reduced by 81.7% in the intervention period (Box 4B), whereas for the control group this number did not change significantly. Overall, the total number of tests requested at the experimental hospital was approximately halved in the intervention period, whereas there was no change at the control hospital (Box 5). Discussion The introduction of TQM strategies achieved statistically highly significant improvements to the appropriateness of laboratory test ordering in AMI. The findings were sustained over the 15-month intervention period and were not replicated within the concurrently monitored control group hospital. The findings have a number of potentially important economic and patient care implications. Firstly, the 81.7% reduction of unnecessary tests may provide a substantial reduction in the overall cost of hospital inpatient pathology services if the TQM strategies were to be successfully introduced to more clinical situations. Such potential savings remain the challenge for future investigations. Secondly, there was an overall benefit to patient care through the increased use of clinically indicated laboratory tests. In addition, although not reported here, there was a statistically significant improvement to the clinically recommended timing of the blood collections for cardiac enzyme testing. I have not been able to find any study published in medical and health sciences journals during the past 15 years that has used TQM specifically to improve the appropriateness of clinical laboratory use in AMI. However, the FOCUS-PDCA model has had widespread and successful application within the healthcare system.15-16 As the model is process driven, it is likely to be adaptable to other test-ordering processes. My study supports the recent findings by Nardella et al of significant cost reductions and increased appropriateness of testing through the use of continuous quality improvement strategies.17 Although Nardella et al did not specifically use the FOCUS-PDCA model, they adopted a similar improvement approach. Methodologically, however, my study provided several strengths, with the inclusion of a pre-test and a concurrent control group to enable substantial control over threats to internal and external validity. The introduction of the TQM intervention was accompanied by additional staff time spent undertaking activities such as training, meetings, data collection and analysis. There was also medical, nursing and clerical staff time saved as a result of the accompanying improvements to the clerical systems used in test ordering. Although such costs and benefits were not quantified, I suspect that any savings made in staffing time were expended in establishing and maintaining the intervention. Following the 15-month intervention and the disbandment of the formal TQM team, the AMI laboratory testing guidelines remain in operation. However, recent discussions with key personnel from the original team reveal that the pre-stamped pathology request forms are no longer in use and that compliance with the testing guidelines has generally declined. These observations are consistent with those of other studies where improvements have failed to be sustained once improvement strategies had been completed.18-19 In view of the important economic and patient care implications, further investigations should be undertaken on the effects of the TQM approach in a variety of other clinical laboratory testing situations. Acknowledgements This research formed part of a major doctoral study undertaken by the author under the supervision of Professor Graeme Rawson, former Dean of the Faculty of Health, University of Western Sydney, Macarthur, NSW. Thanks also to Ms Margaret Gehrig, Quality Advisor to the study. I also acknowledge the contribution of the staff of the Bankstown-Lidcombe Hospital, particularly the Emergency Departments, Coronary Care Units, Pathology and Clinical Information Departments. Similarly, thanks also to the Clinical Information Department of the Nepean Hospital. References Hamm CW. New serum markers for acute myocardial infarction. N Engl J Med 1994; 331: 607-608. Deeble J, Lewis-Hughes P. Directions for pathology. Background Paper No. 6. Melbourne: National Health Strategy, 1991; 7. Gama R, Swain DG, Nightingale PG, et al. The effective use of cardiac enzymes and electrocardiograms in the diagnosis of acute myocardial infarction in the elderly. Postgrad Med J 1990; 66: 375-377. Grantham P, Weinstein S. Reducing pathology test misuse. Aust Health Rev 1993; 16: 16-23. Ratnaike D, Hunt D, Eilermann R, et al. The investigation of chest pain: audit and intervention. Med J Aust 1993; 159: 666-671. Rose WD, Martin JE, Abraham FM, et al. Calcium, magnesium and phosphorus: emergency department testing yield. Acad Emerg Med 1997; 4: 559-563. Hindmarsh JT, Lyon AW. Strategies to promote rational clinical chemistry test utilization. Clin Biochem 1996; 29: 291-299. Mugford M, Banfield P, O'Hanlon M. Effects of feedback of information on clinical practice: a review. BMJ 1991; 303: 398-402. Winkens RA, Ament AJ, Pop P, et al. Routine individual feedback on requests for diagnostic tests: an economic evaluation. Med Decis Making 1996; 16: 309-314. Goldman L. Changing physicians' behavior -- the pot and the kettle. N Engl J Med 1990; 322: 1524-1525. Hospital Corporation of America. Hospitalwide quality improvement process, strategy for improvement: FOCUS-PDCA. Nashville: Hospital Corporation of America, 1989. Rose GA, Blackburn H. In: Cardiovascular survey methods. WHO Monograph Series No. 56. Geneva: World Health Organization, 1968; 137-153. World Health Organization criteria for the diagnosis of acute myocardial infarction. Geneva: World Health Organization Cardiovascular Disease Unit, 1981. SPSS Inc. SPSS for Windows [computer program]. Version 6.0. Chicago Ill: SPSS Inc, 1992. Rhew E. Quality improvement project reviews: a tool to accelerate the transformation. Jt Comm J Qual Improv 1994; 20: 79-89. Schneider PD. FOCUS-PDCA ensures continuous quality improvement in the outpatient setting. Oncol Nurs Forum 1997; 24: 966-969. Nardella A, Farrell M, Pechet L, et al. Continuous improvement, quality control, and cost containment in clinical laboratory testing. Arch Pathol Lab Med 1994; 118: 965-968. Reeves CA, Bednar DA. What prevents TQM implementation in health care organisation? Qual Prog 1993; 26: 41-44. Chan YCL, Ho SJK. Continuous quality improvement -- a survey of American and Canadian healthcare executives. Hosp Health Serv Adm 1997; 42: 525-544. (Received 24 Oct 1997, accepted 3 Aug 1998) Author's details Division of Public Health, University of Western Sydney, Macarthur, NSW. Godfrey Isouard, BSc, PhD, Lecturer. Reprints will not be available from the author. Correspondence: Dr G Isouard, Division of Public Health, University of Western Sydney, Macarthur, PO Box 555, Campbelltown, NSW 2560. E-mail: g.isouardATuws.edu.au 1: The FOCUS-PDCA model Find a process to improve Organise a total quality management team select team members team building Clarify laboratory test-requesting process flow charts of test-requesting process identify problems customer requirements Uncover causes of poor quality test use causes of variation collect data Select process improvement determine proposed improvements prioritise Plan process improvement develop improvement strategies education and training development Do the improvement pilot test implement strategies collect and analyse data Check results check lessons learnt determine how effort could be improved Act to hold the gain standardise procedures establish monitoring and feedback processes plan continuous improvement 2: Comparison of characteristics of patients with confirmed acute myocardial infarction, before and during the total quality management intervention Experimental group Control group Pre-TQM intervention periodn=252n=203 Mean age in years (95% CI)60.3 (48.6-74.4)59.2 (47.5-71.8) Men:women (%)71.8:28.277.1:22.9 Median LOS in days (95% CI)8.8 (7.2-12.6)8.0 (6.8-11.4) TQM intervention periodn=253n=211 Mean age in years (95% CI)61.0 (49.1-77.3)59.6 (47.8-72.6) Men:women (%)74.7:25.370.8:29.2 Median LOS in days (95% CI)8.0 (6.3-11.4)7.3 (5.4-10.5) TQM=total quality management. CI=confidence interval. LOS=length of stay in hospital. 3: Changes in the use of clinically indicated tests for the experimental confirmed acute myocardial infarction group Pre-TQM intervention period TQM intervention periodPercentage point increase Number of testsNumber of testsin indicated tests Requested*Indicated†Ratio A‡Requested*Indicated†Ratio B§requested (B-A)P Sodium, potassium, chloride2193339464.6%2631318082.7%18.1<0.01 Urea00--00------ Creatinine17532953.2%28129495.6%42.4<0.01 Glucose31052958.6%37552271.8%13.2<0.01 Calcium, magnesium, phosphate758192.6%242885.7%-6.9<0.01 Cardiac enzyme profile§§1860201692.3%1962202496.9%4.70.18 Liver function tests#14715495.5%778491.7%-3.8<0.01 Cholesterol/triglyceride47950495.0%43850686.6%-8.5<0.01 Free thryoxine, thyrotropin304271.4%202676.9%5.5<0.01 Miscellaneous clinical chemical tests116116100.0%8686100.0%0-- All clinical chemical tests5385716575.2%5894675087.3%12.2<0.01 Automated blood count**1136130487.1%1028114889.6%2.40.20 Prothrombin index252252100.0%253253100.0%0-- Miscellaneous haematology tests2424100.0%4545100.0%0-- All haematology tests1412158089.4%1326144691.7%2.30.15 Urine microexamination1111100.0%1414100.0%0-- Miscellaneous microbiology tests1616100.0%2828100.0%0-- All microbiology tests2727100.0%4242100.0%0-- All tests6800877277.5%7262823888.2%10.6<0.01 TQM=total quality management. *Clinically indicated tests that were requested. †Total number of tests that were clinically indicated but not necessarily requested. ‡Pre-TQM tests requested/pre-TQM tests indicated. §TQM tests requested/TQM tests indicated. §§Creatine kinase and creatine kinase-MB. #Total bilirubin, aspartate aminotransferase, alanine aminotransferase, gamma glutamyltransferase, alkaline phosphatase, protein, albumin. **Haemoglobin, white cell count, red cell count, platelets. 4: Comparison of the changes in the use of clinically indicated tests (A) and non-clinically indicated tests (B) for the experimental and control confirmed AMI groups APre-TQM intervention period TQM intervention periodPercentage point increase Number of testsNumber of testsin indicated tests Requested*Indicated†Ratio A‡Requested*Indicated†Ratio B§requested (B-A)P Experimental group6800877277.5%7262823888.2%10.6<0.01 Control group7340893382.2%7399920080.4%-1.80.19 BPre-TQM intervention period TQM intervention periodReduction in Total number of tests requestedNumber of tests per admissionTotal number of tests requestedNumber of tests per admissionnon-clinically indicated tests per admissionP Experimental group966738.417767.081.7%<0.01 Control group489024.1484823.04.6%0.48 AMI=acute myocardial infarction. TQM=total quality management. *Clinically indicated tests that were requested. †Total number of tests that were clinically indicated but not necessarily requested. ‡Pre-TQM tests requested/pre-TQM tests indicated. §TQM tests requested/TQM tests indicated. 5: Total number of tests requested in the experimental and control confirmed acute myocardial infarction groups Pre-TQM intervention period TQM intervention period TotalIndicated*Not indicated†TotalIndicated*Not indicated† Experimental group1646768009667903872621776 Control group12230734048901224773994848 TQM=total quality management. *Number of clinically indicated tests requested. †Number of non-clinically indicated tests requested.

Godfrey Isouard

Outdoor air pollution and children's respiratory symptoms in the steel cities of New South Wales Peter R Lewis, Michael J Hensley, John Wlodarczyk, Ruth C Toneguzzi, Victoria J Westley-Wise, Trevor Dunn and Dennis Calvert MJA 1998; 169: 459-463 For editorial comment, see Abramson & Beer Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Public and environmental health - ©MJA1998 Abstract Objective: To investigate the relationship between outdoor air pollution and the respiratory health of children aged 8 to 10 years. Design: A cross-sectional survey (between October 1993 and December 1993) of children's health and home environment. Summary measures of particulate pollution (levels of particles with an aerodynamic diameter less than 10 µm [PM10] each 6th day) and SO2 (daily mean and maximum hourly values) were estimated for each area (using air quality monitoring station data from July 1993 to June 1994). Setting and survey participants: Parents of 3023 primary school children (Years 3, 4 and 5) from industrial and non-industrial areas with air quality monitoring stations in the Hunter and Illawarra regions of New South Wales. Main outcome measures: Reported occurrence of four or more chest colds, four or more attacks of wheezing, and night-time cough without a cold for more than two weeks, all within the previous 12 months. Results: 77% response rate, ranging by area from 66% to 88%. The average annual outdoor air pollution for the nine areas was 18.6-43.7 µg/m3 for PM10 and 0.16-0.90 parts per hundred million for SO2. The proportion of children reported to have the main outcome symptoms were: chest colds, 3.0%-9.7%; night cough, 12.3%-30.5%; and wheeze, 3.4%-11.3%. There was no significant association with SO2, but a significant increase in the odds of symptoms per 10 µg/m3 increase in PM10 on chest colds (odds ratio [OR], 1.43; 95% confidence interval [CI], 1.12-1.82) and night-time cough (OR, 1.34; 95% CI, 1.19-1.53), but not wheeze. Passive smoking was significantly associated with chest colds but not with the other symptoms. Maternal allergy was associated with all three respiratory symptoms, most strongly with wheeze. Conclusion: These results provide evidence of health effects at lower than expected levels of outdoor air pollution in the Australian setting. They also suggest differences in contributions of environmental and hereditary factors to cough and chest colds compared with wheeze. Introduction The effect of outdoor air pollution on the respiratory system has been investigated and reviewed often.1,2 Various health outcomes have been studied; for example, the relationship between exposure to elevated sulfur dioxide, total suspended particulates (TSP) and respiratory symptoms;3 the association between increased air pollution and hospital admissions for asthma;4,5 and studies of air pollution and mortality.6,7 These studies consistently report associations between air pollution and health outcomes, and illustrate the coherence of effects8 across the range of outcomes. There have been few studies of the relationship between air quality and health in Australia. Studies of asthma in school children living near power stations in the Hunter region of New South Wales had very low levels of exposure and lacked the power to detect small associations.9,10 Other studies in south-eastern Australia confirmed the high prevalence of asthma in Australia but had no exposure measures.11-13 The lower Hunter and Illawarra regions of New South Wales are on the coast, about 150 km north and 80 km south of Sydney, respectively. The main cities are Newcastle, in the Hunter region, and Wollongong, in the Illawarra region. The estimated resident populations in 1993 for Newcastle and Wollongong were 451 100 and 248 700, respectively.14 Both regions have fully integrated steelworks, combining coke ovens, blast furnaces, steel-making vessels and rolling mills, and the main pollutants are coke oven gases, blast furnace gases and particulates. In addition, lead smelting occurs in the Hunter region, and copper smelting in the Illawarra region. The Hunter Illawarra Study of Airways and Air Pollution (HISAAP) arose out of longstanding community concerns about the health effects of air pollution near heavy industry in Newcastle and Wollongong. The generalisability of overseas studies to Australia was not known, because of differences in climate, geography, population and pollution sources. Public health workers need local data to initiate action on air quality at the community level and to formulate air quality guidelines. This study, the first part of HISAAP, investigated the association between outdoor air quality, as particulates and sulfur dioxide, and respiratory symptoms among primary school children. Methods The study was a cross-sectional survey to measure the prevalence of respiratory and atopic symptoms among primary school children and relate these to measures of ambient air quality. Study areas To make best use of resources, study areas were selected on the basis of existing or proposed air quality monitoring stations. In the lower Hunter region, the study areas close to industrial sources of air pollution were North Lake Macquarie, Mayfield and Stockton, and distant areas were Beresfield and Wallsend (Figure 1a). In the Illawarra region, we estimated that there would be an increasing gradient of exposure to air pollution, from Wollongong, to Albion Park, Kembla Grange and Port Kembla (Figure 1b). Wallsend, Beresfield, Wollongong and Albion Park were expected to have background levels of air pollution. We were able to compare these multiple control areas with those areas close to point sources of air pollution. Sampling strategy All primary schools within a three-kilometre radius of the air quality monitoring sites were approached to be involved in the study. The sampling frame included all children in Years 3 and 4, aged 8 to 10 years, whose parents or guardians approved their child's participation. In areas that had small numbers of children, children in Year 5 were included. We aimed to enrol about 300 children in each of the nine areas. Questionnaire Our questionnaire incorporated features used by previous investigators in the Hunter region and NSW,9,11,12 the International Study of Asthma and Allergies in Childhood,15 the American Thoracic Society questionnaire16 and the Six Cities study.17 It addressed demographic data and parental education; child's health (cough, chest colds, wheeze) and atopic symptoms (hayfever, eczema); child's use of respiratory medications; family's symptoms; and home environmental factors (indoor smoking, heating, cooking, carpets, cats). The questionnaire was piloted in both regions.18The primary health outcomes were night-time cough, chest colds and frequent wheeze. They were the responses to the following questions: In the last 12 months has your child had a dry cough at night, apart from a cough with a cold or chest infection? If yes, has this cough lasted for more than 2 weeks? In the last 12 months how many chest colds did your child have? . . . 4 or more chest colds. How many attacks of wheezing has your child had in the last 12 months? . . . 4 or more attacks. Exposure to indoor tobacco smoke was assessed by asking whether the respondent, other adult or any other person smoked cigarettes inside the home. The survey was conducted from October 1993 to December 1993. Children received consent forms and questionnaires at school. Parents completed the questionnaires, and children returned them to their teachers. If a questionnaire was not returned after two weeks, a copy was posted to the parents for completion and return by reply-paid post. Exposure measurement The lower Hunter and Illawarra Air Pollution Monitoring Networks19 consist of sites operated by the Environment Protection Authority (EPA) and industry self-monitoring sites audited by the EPA. Particulate and sulfur dioxide measures were collected for all study areas, from January 1993 to December 1994. As air pollution data were incomplete for some sites in 1993, the goal was to have representative data for 12 consecutive months close to the reference period of the questionnaire (the 1993 calendar year). The most complete data were found to be from July 1993 to June 1994. Sensitivity analyses using data from adjacent 12-month periods showed very little effect on the results. Particulate pollution as PM10 (particles with an aerodynamic diameter less than 10 µm) was measured for 24 hours every sixth day using high volume air samplers with a size-selective inlet, and these measures were averaged over the 12 months. North Lake Macquarie, Mayfield and Stockton measured only TSP, so local data in which both TSP and PM10 were measured for shorter periods20,21 were used to derive a conversion factor to PM10. In North Lake Macquarie, PM10 was estimated to be 60% of TSP, close to the value used by others.22 In Mayfield and Stockton, PM10 was estimated to be 45% of TSP. Sulfur dioxide measurements were obtained hourly using pulsed fluorescent spectrophotometry. Twelve-month averages of the daily maximum values and of the daily mean values were calculated. There were no major trends in air pollution during this time. Seasonal changes did not affect the relative ranking of the areas in terms of air pollution. Analysis We used SAS software for the analysis.23 Descriptive statistics were produced for participation rates, health measures and environmental measures for each of the nine study areas. Logistic regression analysis using generalised estimating equations (GEEs) was used to model the reported symptom (outcome variable) on the following explanatory variables: PM10 and sulfur dioxide measures, unflued gas heating, adults smoking inside the home, indoor cats, age, sex, and maternal allergy.24 The level of clustering for this analysis was the school (ie, clusters of children within schools), with 35 schools in the study. Although schools were also clustered within study areas, area was not chosen as the clustering level because of the allocation of exposure measure by area. Ethical approval The study received ethical approval from the NSW Education Department, the Regional Catholic Education Office, and the Ethics Committees of the Hunter Area Health Service, the University of Newcastle, the Illawarra Area Health Service, and the University of Wollongong. Results Subjects Questionnaires were given to 3023 primary school children -- 1554 children (from 18 schools) in the Hunter region, and 1469 (from 17 schools) in the Illawarra region. In the Hunter region, 1284 (82%) questionnaires were returned, and in the Illawarra region 1056 (72%) were returned. There were no significant differences in age and sex profiles across the study areas (Table 1). Respiratory symptoms About a quarter of the children were reported to have had at least one of the primary respiratory symptoms in the preceding 12 months (Table 2). While some areas with high proportions of children with symptoms were close to industry (Mayfield and Stockton with children having chest colds), this was not a consistent pattern (Beresfield and children with night cough). The proportion of children who had ever been diagnosed with asthma ranged from 17.4% to 38.4%. Home environment and outdoor air pollution Depending on the study area, a third to half of the children lived in homes where one or more adults smoked cigarettes in the home (Table 3). The proportion of children in homes with gas heating that did not have a flue to the outside varied greatly between the areas. The levels of particulate pollution in Mayfield and Stockton approached the US EPA standard for PM10 of 50 µg/m3 (annual mean) (Table 3) and the Australian standard, at that time set for TSP at 90 µg/m3 (annual mean). The annual mean sulfur dioxide levels (daily means) were below the Australian standard of 2 parts per hundred million (annual mean).19 Within study areas, particulate levels were not necessarily high in high sulfur dioxide areas, and vice-versa. Scatter plots of primary health outcomes by air quality measures suggested some positive associations between PM10 and both night cough and chest colds (Figure 2). Generalised estimating equation analysis For each 10 µg/m3 increase in annual mean PM10, children were 43% more likely to be reported as having four or more chest colds (odds ratio [OR], 1.43; 95% confidence interval [CI], 1.12-1.82). The approximate difference in particulate pollution between the area with the highest PM10 level and the area with the lowest was 25 µg/m3, and children were 144% more likely to be reported to have frequent chest colds per 25 µg/m3 increase in annual mean PM10 (OR, 2.44; 95% CI, 1.33-4.49). There was a consistent significant association between particulate pollution and symptoms of night cough and chest colds (Table 4). No association was found between sulfur dioxide and the three respiratory symptoms. An adult smoking in the home was associated with chest colds, and unflued gas heating was associated with frequent wheeze. Boys were more likely to experience frequent wheeze, and there was a significant association between increasing age and likelihood of frequent wheeze. Maternal allergy was consistently associated with an increased risk for all health outcomes, but strongest for wheeze. To estimate the possible impact of the two areas with the largest particulate pollution (Mayfield and Stockton, in the Hunter region), the GEE analysis was repeated excluding those areas. There was little change in the coefficients for most variables, including maternal allergy, for each outcome. However, the odds ratio for chest colds per 10 µg/m3 increase in annual mean PM10 increased substantially -- with Mayfield and Stockton excluded, the odds ratio was 2.05 (95% CI, 1.46-2.87), compared with 1.43 for the full dataset. Discussion This cross-sectional study of primary school children has shown an important association between relatively low levels of particulate air pollution and respiratory symptoms. The importance is reflected in the finding that the odds ratios for particulates were of the same order as for exposure to indoor tobacco smoke. We found an association with maternal allergy across all three symptom outcomes, but strongest for wheeze. The prevalence estimates of respiratory symptoms are similar to those found in other Australian and New Zealand studies.11-13,25 The association between air pollution and respiratory symptoms in children is also consistent with similar cross-sectional studies from other countries. An Italian study found that children living in polluted areas experienced more cough, rhinitis, pneumonia and early respiratory infections than control subjects,26 but that study did not measure actual air pollution exposure. A British study found that children were more likely to miss school because of respiratory symptoms of cough and wheeze if their school was exposed to a higher coal dust burden (OR, 1.55; 95% CI, 1.17-2.06).27 Our results are directly comparable with those of the Six Cities and 24 Communities studies in North America;17,28,29 effects of particulate pollution on respiratory symptoms and effects of indoor smoking were of the same order in those studies and ours. Two results of particular note are the relationship between frequent wheeze and age, and the effect of removing from the analysis the areas with the highest particulate pollution. The increase in wheeze with age is quite large (OR, 1.38 per year). Stratified analysis revealed similar coefficients for younger and older age groups, suggesting that a sampling bias may explain the strength of the relationship. The substantial increase in the odds ratio of particulate pollution and chest colds after removal of the areas with highest PM10 suggests that the dose-response curve for particulate pollution and chest colds is curvilinear and much steeper at lower pollution levels. Potential limitations of our study include possible reporting bias by residents of industrial areas and the variability in the measurement methods for particulate air pollution. It is not possible to estimate the level of possible reporting bias, but its effect may be reduced by selection bias in that families with children with lung disease may not come to, or may leave, polluted areas. The difference in measurement of particulates was unavoidable. A subsequent diary study obtained comparisons of TSP and PM10 which provided evidence on which to convert the measures for local conditions.20,21 Particularly striking are the results which show differences in the determinants of wheeze compared with coughs and colds. While maternal allergy played a part in all, passive smoking was restricted to colds, and particulates to coughs and colds. This suggests differences in underlying pathology which deserve further exploration. Our data lead us to question the current air quality standards, which are based on the premise that levels at or below recommended ambient levels are not likely to produce a clinically important effect. In particular, recommended levels do not consider increased individual sensitivity caused by a disease such as asthma. While this study cannot infer causation, it adds to other local and overseas work that increasingly indicates the role of air pollution in respiratory health -- alone and synergistically with other aeroallergens.30 This information contributes to the review of Australian air quality guidelines, and to the broader societal debate about lifestyle, transport and energy consumption. Individuals, communities, industry and organisations need to reassess their environmental performance not only for the environment, but also for health. Acknowledgements Our thanks to members of the following organisations which supported the study: Newcastle Environmental Toxicology Research Unit (especially Randall Robertson and Julie Holt), University of Newcastle, Hunter Public Health Unit, Hunter Area Pathology Service, Newcastle City Council, Lake Macquarie Council, Illawarra Public Health Unit, University of Wollongong, NSW Health Department, NSW Environment Protection Authority, Australian Nuclear Science and Technology Organisation, BHP (Newcastle and Port Kembla), Incitec, Pasminco Metals Sulphide, Southern Copper. We are grateful to the schools, parents, and children who participated in this study. HISAAP was partly funded by the NSW Health Department as part of its Health and Air Research Program. Dr P Lewis received an NHMRC Public Health Fellowship for two years. References Committee on the Medical Effects of Air Pollution. Asthma and outdoor air pollution. London: HMSO, 1995. Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society. Health effects of outdoor air pollution. Am J Respir Crit Care Med 1996; 153: 3-50. Lunn FE, Knowelden J, Handyside AJ. Patterns of respiratory illness in Sheffield infant schoolchildren. Br J Prev Soc Med 1967; 21: 7-16. Pope CA III. Respiratory admissions associated with PM10 pollution in Utah, Salt Lake and Cache Valleys. Arch Environ Health 1991; 46: 90-97. Bates DV, Baker-Anderson M, Sizto R. Asthma attack periodicity: a study of hospital emergency visits in Vancouver. Environ Res 1990; 51: 51-70. Anderson HR, Ponce de Leon A, Bland JM, et al. Air pollution and daily mortality in London: 1987-92. BMJ 1996; 312: 665-669. Dockery DW, Pope CA III, Xu X, et al. An association between air pollution and mortality in six US cities. N Engl J Med 1993; 329: 1753-1759. Bates DV. Health indices of the adverse effects of air pollution: the question of coherence. Environ Res 1992; 59: 336-349. Henry RL, Abramson R, Adler JA, et al. Asthma in the vicinity of power stations: I. A prevalence study. Pediatr Pulmonol 1991; 11: 127-133. Henry RL, Bridgman HA, Wlodarczyk J, et al. Asthma in the vicinity of power stations: II. Outdoor air quality and symptoms. Pediatr Pulmonol 1991; 11: 134-140. Bauman A, Mitchell CA, Henry RL, et al. Asthma morbidity in Australia: an epidemiological study. Med J Aust 1992; 156: 827-831. Peat JK, Toelle BG, Gray EJ, et al. Prevalence and severity of childhood asthma and allergic sensitisation in seven climatic regions of New South Wales. Med J Aust 1995; 163: 22-26. Robertson CF, Bishop J, Dalton M, et al. Prevalence of asthma in regional Victorian schoolchildren. Med J Aust 1992; 156: 831-833. Australian Bureau of Statistics. Regional population growth 1991 and 1996. Canberra: ABS, 1997. (Catalogue No. 3218.0.) Asher M, Keil U, Anderson H. International study of asthma and allergies in childhood (ISAAC): rationale and methods. Eur Respir J 1995; 8: 483-491. Ferris BG. Epidemiology standardisation project. Part II. Am Rev Respir Dis 1978; 118: 1-53. Ware JH, Dockery DW, Spiro A III, et al. Passive smoking, gas cooking and respiratory health of children living in six cities. Am Rev Respir Dis 1984; 129: 366-374. Lewis PR, Toneguzzi R, Long K, et al. The Hunter Illawarra study of airways and air pollution: refining the process. NSW Public Health Bulletin 1995; 6: 110-112. State Pollution Control Commission. Quarterly air quality monitoring report No 4, 1990. Sydney: SPCC, 1992. Lewis P, Holt J, Fryer J. Daily particulate monitoring in the Speers Point/Boolaroo area -- Lake Macquarie Research Grant 94-9. Newcastle: University of Newcastle, Newcastle Environmental Toxicology Research Unit, 1997. Environment Section, BHP. Mayfield quality control: measures of particulate pollution. BHP, 1995. Dockery DW, Pope CA III. Acute respiratory effects of particulate air pollution. Annu Rev Public Health 1994; 15: 107-132. SAS for Windows [computer program]. Version 6.03. Cary, North Carolina: SAS Institute, 1988. Karim MR. PC version of GEE1 [computer program]. Baltimore: Department of Biostatistics, The Johns Hopkins University, 1989. Moyes CD, Waldon J, Ramadas D, et al. Respiratory symptoms and environmental factors in schoolchildren in the Bay of Plenty. N Z Med J 1995; 108: 358-361. Corbo GM, Forastiere F, Dell'Orco V, et al. Effects of environment on atopic status and respiratory disorders in children. J Allergy Clin Immunol 1993; 92: 616-623. Brabin B, Smith M, Milligan P, et al. Respiratory morbidity in Merseyside schoolchildren exposed to coal dust and air pollution. Arch Dis Child 1994; 70: 305-312. Cunningham J, O'Connor GT, Dockery DW, Speizer FE. Environmental tobacco smoke, wheezing and asthma in children in 24 communities. Am J Respir Crit Care Med 1996; 153: 218-224. Dockery DW, Speizer FE, Stram DO, et al. Effects of inhalable particles on respiratory health of children. Am Rev Respir Dis 1989; 139: 587-594. Devalia JL, Rusznak C, Herdman MJ, et al. Effect of nitrogen dioxide and sulphur dioxide on airway response of mild asthmatic patients to allergen inhalation. Lancet 1994; 344: 1668-1671. (Received 29 Oct 1997, accepted 21 Jul, 1998) Authors' details Newcastle Environmental Toxicology Research Unit, University of Newcastle, Newcastle, NSW. Peter R Lewis, MPH, FAFPHM, Public Health Research Fellow; Michael J Hensley, MB BS, PhD, Director and Professor of Medicine; John Wlodarczyk, BEc, PhD, Statistician; Ruth C Toneguzzi, RN, DipClinEpi, Clinical Nurse Specialist. Illawarra Public Health Unit, Wollongong, NSW. Victoria Westley-Wise, MPH, FAFPHM, Director; Trevor Dunn, GdDipSc(Nursing), MPH(Occ Health), Project Manager. University of Wollongong, Wollongong, NSW. Dennis Calvert, MD, FRACP, Professor in Medicine and Public Health. Reprints will not be available from the authors. Correspondence: Dr P R Lewis, Newcastle Environmental Toxicology Research Unit, Division of Medicine, John Hunter Hospital, Locked Bag 1, Hunter Regional Mail Centre, NSW 2310. E-mail: plewiATdoh.health.nsw.gov.au - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Peter R Lewis · Michael J Hensley · John Wlodarczyk · Ruth C Toneguzzi · Victoria J Westley-Wise · Trevor Dunn · Dennis Calvert

HIV disease progression in Australia in the time of combination antiretroviral therapies Patricia K Correll, Matthew G Law, Ann M McDonald, David A Cooper and John M Kaldor MJA 1998; 169: 469-472 For editorial comment, see Stewart Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Infectious diseases and parasitology - ©MJA1998 Abstract Objective: To examine the effect of recent developments in antiretroviral therapy on HIV disease progression and survival. Design: Retrospective cohort study. Participants and setting: Two cohorts of people with HIV were defined retrospectively from the records of a large immunology laboratory. The first cohort were subjects whose CD4+ T cell counts had dropped to 200 x 106/L during 1990, and the second were subjects whose CD4+ T cell counts had dropped to 200 x 106/L in 1994. Main outcome measures: HIV disease progression and survival was determined over a minimum three years of follow-up for each cohort (ie, 1990-1993; 1994-1997). Results: 346 subjects were included in the analysis (193 subjects from 1990 and 153 from 1994). The relative risk of progression to AIDS in the 1994 cohort compared with the 1990 cohort was 0.57 (95% confidence interval, 0.35-0.91; P = 0.018) and the relative risk of death was 0.20 (95% confidence interval, 0.08-0.49; P < 0.001). Conclusions: There were 43% fewer AIDS cases and 80% fewer deaths in the time following the increased availability of combination antiretroviral therapy in Australia. Introduction In recent years there have been major advances in antiretroviral treatments for people with HIV infection. Evidence from clinical trials (DELTA and ACTG 175)1,2 first defined the superiority of combination therapy over monotherapy in delaying progression to AIDS and prolonging survival. Since that time more potent antiretroviral agents have been approved, including lamivudine (widely available in Australia since early 1995) and protease inhibitors (available since late 1995). In clinical trials, these drugs have demonstrated significant ability to reduce disease progression and improve survival when added to existing regimens of antiretroviral treatments.3,4Although there has been anecdotal evidence in Australia suggesting that these treatments have reduced the overall number of AIDS cases and improved survival following AIDS, their effect has not been systematically studied. We therefore decided to compare the rates of progression to AIDS and survival in two cohorts of people between 1990-1993 and 1994-1997, with CD4+ T cell counts of 200 x 106/L (CD4 cell count 200/µL) at entry to the study, as a basis for assessing the impact of new treatments. Methods Subject identification Two cohorts of subjects in this study with CD4 cell counts of 200/µL were defined retrospectively from records of routine CD4 cell counts undertaken at the Centre for Immunology, St Vincent's Hospital, Sydney. St Vincent's Hospital has been responsible for the care of about 25% of people with AIDS in Australia, and its immunology laboratory is used by St Vincent's Hospital inpatient and outpatient services, and by several general practitioner clinics that specialise in managing people with HIV infection. Subjects whose CD4 cell counts fell below 200/µL in 1990 would not have had access to combination therapies, whereas the 1994 cohort was under follow-up when combination therapies with more potent drugs were becoming available in Australia. A CD4 cell count of 200/µL was used as the starting point for follow-up because at this point individuals have not usually developed AIDS-defining illnesses,5 but are considered to be at a point of immune decline where the probability of developing AIDS in the near future has greatly increased.6,7 Subjects included were HIV-positive but without AIDS at entry to the study, with CD4 cell counts declining through 200/µL in the index year (1990 or 1994) or with a single CD4 cell count in the range 180-220/µL. All eligible subjects were included, except subjects from two large clinics which had used the Centre for Immunology laboratory in 1990 but not in 1994. Where available, two or more CD4 cell count results from the period beginning in the middle of the year before the index year and ending at the middle of the following year were recorded so that the rate of CD4 cell change could be estimated. Subjects with multiple CD4 cell counts entered the study on the date of the first test in the index year that was below 200/µL. For subjects with a single CD4 cell count only, entry to the study was on the date of this test, provided the result fell between 180-220/µL. Follow-up Analysis was based on a minimum of three (up to four) years' follow-up of both cohorts through linkage to the National AIDS Registry, which records AIDS diagnoses and deaths following AIDS in Australia. Testing records were linked to Registry data by matching name codes (first two letters of the surname and given name) and dates of birth from the reference laboratory database with the Registry. Because reporting of AIDS diagnoses and deaths to the Registry is subject to delay, subjects from the 1994 cohort who did not appear on the Registry were followed up through their referring doctors. The doctor was also contacted for follow-up information if a name code was not available with the CD4 count records. Information sought included name code, date of birth, whether the subject had progressed to AIDS or died with AIDS, and date of the doctor's most recent contact with the subject. Statistical methods All statistical analyses were performed using SAS.8 Decline of CD4 cells was estimated for subjects with two or more CD4 cell counts by linear regression. Baseline characteristics in the two cohorts were compared by means of Fisher's exact test for categorical variables and the Mann-Whitney rank sum test for continuous variables. We calculated AIDS-free survival and overall survival curves using Kaplan- Meier methods, and assessed the statistical significance of the difference in survival between the two cohorts by the log rank test. Proportional hazards regression was used to assess the effect of age, CD4 cell count at entry, and decline of CD4 counts on AIDS incidence and survival. In survival analysis, subjects without an AIDS diagnosis or death reported to the National AIDS Registry were assumed to be AIDS-free and alive at the end of follow-up. Secondary analyses were also performed based on confirmed AIDS-free and survival times by censoring at the date of last confirmed contact on the National AIDS Registry or with the referring doctor. Results After excluding 109 subjects in 1990 who had been referred from two clinics which did not use the Centre for Immunology laboratory in 1994, the database search identified 214 eligible subjects from 1990 and 169 from 1994, of whom 193 and 153, respectively, could be traced for follow-up and were included in the analysis (Box 1). As shown in Box 1, 60% of subjects who were followed up during 1990-1993 progressed to AIDS and 38% died, compared with 37% who progressed to AIDS and 13% who died during follow-up between 1994-1997. This corresponds to a 43% decrease in AIDS and an 80% reduction in death. As shown in Box 2, the median age at entry of the 1994 cohort was older than in the 1990 cohort, but sex, CD4 cell count at entry and CD4 cell decline were similar. The median age and sex of excluded subjects who came from the two clinics which did not use the Centre for Immunology laboratory in 1994 (age 37.5 years, 96% male) were similar to those included in the 1990 cohort (age 35 years, 98% male). Box 3 shows that progression to AIDS was slower and survival longer in the 1994 cohort than in the 1990 cohort, and that the improvement in both indices appeared to emerge after about one year of follow-up. Adjustment for age, CD4 count and CD4 slope at entry did not materially affect the differences between the two cohorts in progression time to AIDS and survival (Box 4). There were 52 subjects for whom only one CD4 cell count was recorded and rate of CD4 cell decline could not be estimated. A sensitivity analysis excluding these subjects gave very similar results to those for the full cohort (relative risk of AIDS and death in the 1994 group, 0.51 [P = 0.02] and 0.21 [P < 0.01], respectively). When follow-up was censored at the date of last confirmed contact, there remained a 28% decrease in progression to AIDS (P = 0.04) and a 45% reduction in death (P = 0.021). Discussion In this study, progression to AIDS was nearly halved and deaths fell by 80% among people with HIV infection whose CD4 cell count fell below 200/µL in 1994 compared with the corresponding 1990 cohort. The difference between the two groups emerged after about one year of follow-up, which in the 1994 cohort corresponded roughly to the introduction of lamivudine in early 1995, followed by protease inhibitors later in the same year. Although other differences between the cohorts cannot be entirely ruled out, the most likely explanation for the improved outcomes is advances in treatment strategies for people with HIV, including combination antiretroviral therapies. The benefit of combination therapy and new antiretroviral agents has been demonstrated so far largely through randomised controlled trials.9 Only recently has information started to emerge of the effectiveness of new therapies in a community-wide setting. The results of this study concur with recent cohort studies overseas, where substantial decreases in AIDS and deaths have been identified in patients followed up after the introduction of combination therapies compared with those under follow-up in earlier times.10,11 Although information on antiretroviral treatment was unavailable for the individuals in our cohorts, recent evidence suggests a dramatic change in the use of antiretroviral therapies in Australia over the time in which the two cohorts reported in our study were followed up. HIV-infected participants in the Sydney Men and Sexual Health Study (a prospective study of homosexually active men in Sydney) increased their uptake of combination antiretroviral therapy from about 2% in 1993 to more than 70% in 1997.12 Our study relied on the National AIDS Registry, which is subject to both reporting delay and underreporting. It is believed that about 70% of HIV diagnoses are reported to the Registry within six months (the minimum reporting time available in this study) and that nearly 100% are reported within three years.13 It is possible that incomplete reporting of AIDS and AIDS-related deaths to the National AIDS Registry may have resulted in underestimates of AIDS incidence or mortality in the later cohort. Results were similar, however, when analyses were censored at the date of last contact, suggesting that underreporting to the Registry was not in fact an important source of bias. One other potential source of bias is that changes in the natural history of the HIV epidemic may have resulted in a lower proportion of rapid progressors in more recent years, so that patients with CD4 counts of 200/µL in 1990 progressed more rapidly than those in 1994.14 In our analysis, there was little difference between the cohorts in CD4 cell decline (Box 2), and survival analysis adjusted for this gave very similar results. Furthermore, a sensitivity analysis excluding those subjects with only a single CD4 cell count also did not significantly affect the results. This analysis was based on CD4 cell counts collected over two years (mid year before the index year to mid year after), and is robust enough to suggest that both cohorts were subject to similar rates of progression. As the subjects were identified at two different times, it is possible that there were unidentifiable differences between the cohorts that may have influenced the outcomes in this study. However, the possibility of bias was substantially reduced by identifying all subjects from the same laboratory. This study contributes evidence to suggest that the rate of progression of HIV disease has decreased in Australia at the same time as new, more potent combination antiretroviral treatments have become available. It would be useful to study similar cohorts in the future to monitor the evolving pattern of the epidemic at a population level. Acknowledgements The National Centre in HIV Epidemiology and Clinical Research is funded by the Commonwealth Department of Health and Family Services through the Australian National Council on AIDS and Related Diseases. The help of the following medical practitioners in study follow-up is gratefully acknowledged: B Anderson, P Brooke, K Brown, A Carr, B Donovan, N Doong, C Duncombe, W Genn, J Kidd, A Mackie, M McMurchie, A McNulty, R Penny, A Pethebridge, M Robertson. We also thank John Zaunders at the St Vincent's Hospital Centre for Immunology for assistance in identifying the study sample. References Delta Coordinating Committee. Delta: a randomised double-blind controlled trial comparing combinations of zidovudine plus didanosine or zalcitabine with zidovudine alone in HIV-infected individuals. Lancet 1996; 348: 283-291. Hammer SM, Katzenstein DA, Hughes MD, et al. A trial comparing nucleoside monotherapy with combination therapy in HIV-infected adults with CD4+ cell counts from 200 to 500 per cubic millimeter. N Engl J Med 1996; 335: 1081-1090. CAESAR Coordinating Committee. Randomised trial of addition of lamivudine or lamivudine plus loviride-zidovudine-containing regimens for patients with HIV-1 infection: the CAESAR trial. Lancet 1997; 349: 1413-1421. Hammer SM, Squires KE, Hughes MD, et al. A controlled trial of two nucleoside analogues plus indinavir in persons with human immunodeficiency virus infection and CD4+ cell counts of 200 per cubic millimeter or less. N Engl J Med 1997; 337: 725-733. Centers for Disease Control. Conditions included in the 1993 AIDS surveillance case definition. MMWR Morb Mortal Wkly Rep 1992; 41: RR-17. Hoover DR, Rinaldo C, Yanhua H, et al. Long-term survival without clinical AIDS after CD4+ cell counts fall below 200 x 106/L. AIDS 1995; 9: 145-151. Tindall B, Swanson CE, Cooper DA. Development of AIDS in a cohort of HIV-seropositive homosexual men in Australia. Med J Aust 1990; 153: 260-265. SAS statistical software version 6.12. Carey, NC: SAS Institute Incorporated, 1994. HIV/AIDS Clinical Trials and Treatments Advisory Committee of the Australian National Council on AIDS and Related Diseases. Antiretroviral therapy for HIV infection: principles of use. Standard of care guidelines; October 1997. Sydney: HIV/AIDS Clinical Trials and Treatments Advisory Committee, 1997. Egger M, Hirschel B, Francioli P, et al. Impact of new antiretroviral combination therapies in HIV infected patients in Switzerland: prospective multicentre study. BMJ 1997; 315: 1194-1199. Palella F, Delaney K, Moorman A, et al. Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. New Engl J Med 1998, 338: 853-860. National Centre in HIV Epidemiology and Clinical Research. HIV/AIDS and related diseases in Australia: Annual Surveillance Report 1998. Sydney: National Centre in HIV Epidemiology and Clinical Research, 1998. National Centre in HIV Epidemiology and Clinical Research. An epidemiological assessment of the HIV epidemic in Australia. Evaluation of the National HIV/AIDS Strategy 1993-1994 to 1995-1996. Canberra: Commonwealth Department of Health and Family Services, 1996. Ioannidis JPA, Cappelleri JC, Schmid CH, Lau J. Impact of epidemic and individual heterogeneity on the population distribution of disease progression rates. Am J Epidemiol 1996; 144: 1074-1085. (Received 13 Jan, accepted 30 Apr, 1998) Authors' details National Centre in HIV Epidemiology and Clinical Research, Sydney, NSW. Patricia K Correll, BN, MPH, Research Assistant; Matthew G Law, MA, MSc, Statistician; Ann M McDonald, BSc, MPH, Senior Research Assistant; David A Cooper, DSc, MD, FRACP, Director; John M Kaldor, PhD, Deputy Director. Reprints will not be available from the authors. Correspondence: Patricia Correll, National Centre in HIV Epidemiology and Clinical Research, Level 2, 376 Victoria Street, Sydney, NSW 2010. Email: pcorrellATnchecr.unsw.edu.au - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Patricia K Correll · Matthew G Law · Ann M McDonald · David A Cooper · John M Kaldor

Factors involved in presentation of older people with thick melanoma Pauline F Hanrahan, Peter Hersey and Catherine A D'Este MJA 1998; 169: 410-414 For editorial comment, see Kelly Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Oncology - ©MJA1998 Abstract Objective: To examine whether presentation of older people with thick melanoma is a result of the site and histological type or of their reduced ability to identify melanoma. Design and setting: Retrospective analysis of the Newcastle Melanoma Unit patient database. Patients: 2154 patients with melanoma for whom complete data (histological type, thickness and site of melanoma) were available and who presented from February 1981 to April 1997. Main outcome measures: Histological type and site of melanoma in older (≥50 years) versus younger men and women; frequency with which these groups identified melanoma and the first changes of melanoma that were noticed. Results: Patients aged ≥50 years, particularly men, were more likely to present with thicker lesions. Older men and, to a lesser extent, older women were more likely to present with nodular melanoma, which were more frequent on the scalp and face in older, compared with younger, men, and scalp and back in older men compared with older women. Failure to identify melanoma was associated with older age, sites on the scalp and back and histological type of the lesion, but was independent of sex once histological type, age, site and thickness were taken into account. Multivariate analysis indicated that the association of older age of patients with failure to identify melanoma applied irrespective of the site, type and thickness of their melanoma. Conclusion:. The higher frequency of thick melanoma in older people is accounted for by an increased proportion of nodular melanoma and decreased ability to recognise the changes of melanoma. These findings have important implications for examination of older patients by doctors and for design of strategies for early detection of melanoma in this age group. Introduction Survival from melanoma is related to thickness of the tumour. Ninety-six per cent of patients whose lesions are detected early (< 0.75 mm thick) will survive to 10 years,1,2 but this decreases to 50% for patients with lesions 4 mm or greater.3,4 Previous studies have shown that most patients who present with thick lesions are men aged over 50 years.5-7 In New South Wales over 50% of deaths from melanoma involve men over 50, even though this group comprises only 12%-14% of the population.8 Clearly, strategies that facilitate early detection of melanoma in older men may markedly reduce the death rate from this cancer. We have previously investigated the ability of older men to distinguish between benign and malignant pigmented skin lesions in photographs and whether an educational brochure assists this ability;9 the brochure increased knowledge of melanoma, but did not help participants distinguish between benign and malignant pigmented skin lesions. We then investigated whether this age group had inherent difficulties in recognising the changes of melanoma and found that all age groups had difficulty in recognising the appearance of new pigmented lesions and changes in lesions over time.10,11 Older people were no less able than younger people to identify change, but falsely identified changes in unchanged lesions more frequently. In this study we sought to examine factors associated with failure of patients to identify their melanoma and the importance of this in presentation of older patients with thick melanoma. Methods Information for the study was obtained from the database in the Newcastle Melanoma Unit (NMU), which was established in 1981 and is a referral centre for patients from the Hunter region of New South Wales. Over 90% of patients with melanoma in the Hunter region attend the unit. The database contains information obtained by experienced oncology nurses who interview patients, asking questions about changes they had noticed leading to diagnosis of melanoma, for how long they had noticed the changes and whether these were in a pre-existing or new lesion. The age and sex of patients, site of their primary lesion, its histological type and thickness were also recorded. Histological investigation of the lesions was reviewed by at least two pathologists and reported as described previously.12 Patient clinical data were entered into a program developed jointly by the Sydney Melanoma Unit and the Macquarie University using Clinical Reporting Systems software (Brisbane Road, Castle Hill, NSW). We included data for all patients presenting to the NMU between February 1981 and April 1997. The data were categorised for statistical analysis as follows. Patients were divided into two groups by age (< 50 and ≥50). As in a previous study,5 thickness of primary lesions was categorised as < 3 mm, or ≥3 mm. Data on the site of the primary melanoma were divided into seven categories (scalp, face, neck, back, anterior trunk, arm and leg). Melanomas were categorised into seven histological types (superficial spreading melanoma [SSM], nodular melanoma [NM], lentigo maligna [LM], in-situ melanoma, desmoplastic melanoma, unknown, and unclassified) of which we included only the first three relatively common types. Categories for types of changes were: unidentified (including instances where patients were uncertain whether a change had occurred, or said that no change had occurred, but melanoma was detected by their general practitioners or other doctors); size and shape; colour; changes in sensation (eg, itching, tingling); and bleeding. Statistical analysis Data were analysed with SAS13 and STATA14 statistical software. Lesion characteristics (thickness, histological type and site of melanoma) were compared by age and by sex separately using chi-squared analyses. Lesion characteristics and age and sex were also compared for those who had, and had not, identified any changes. Logistic regression analyses were performed to examine factors associated with identification of any changes of melanoma, using any change versus no change, as the outcome variable. All five independent variables were tested for significance by forward stepwise regression analysis. After the final main effects model was obtained, all possible interactions were tested. The likelihood ratio statistic was used to assess statistical significance in the logistic regression analyses. We also tested (by chi-squared analysis) lesion characteristics, age and sex for association with type of changes noticed; 95% confidence intervals (CI) were calculated for each type of change. A significance level of 0.05 was used for all analyses. Subgroups were considered to differ significantly if 95% CIs did not overlap. Results The database included records for 3435 patients who attended the NMU during the study period. Exclusions included: 932 patients for whom there was incomplete data or for whom data could not be appropriately classified; 325 with uncommon, unknown, desmoplastic or unclassified histological types of melanoma; and 22 with melanoma at unusual sites (eg, mucosal regions, buttocks, groin). The final sample of 2154 patients comprised 1144 men (53%) and 1010 women (47%); 1142 patients (53%) were aged 50 years or over and 59% of the men in the study were in this age group, compared with 46% of the women. There were no significant differences in sex or age of patients excluded compared with those included (sex: chi-squared = 0.006, df = 1, P = 0.94; age: chi-squared = 1.7, df = 1, P = 0.18). The site and thickness of melanomas were similar in those excluded and included. Excluded patients had a different distribution of histological types (as this was part of the basis for their exclusion) and a higher proportion of unnoticed changes than those included. More detailed information about excluded patients is available from the authors. Lesion characteristics Thickness: Box 1 shows that patients aged 50 years or over (14.5%; 95% CI, 12%-16%) were significantly more likely to present with thick lesions than younger patients (4.7%; 95% CI, 3%-6%), and men (12%; 95% CI, 10%-14%) were more likely to have thick lesions than women (7%; 95% CI, 6%-9%). Site: Melanoma was found most often on the backs of male patients (47%; 95% CI, 45%-50% v. 24%; 95% CI, 22%-27% for women), whereas the leg was the predominant site in women (38%; 95% CI, 35%-41% v. 16%; 95% CI, 13%-18% for men). The incidence of melanoma on the scalp, face and neck was similar for men and women. Melanoma on the arms was more common in women (19%; 95% CI, 16%-21% v. 12%; 95% CI, 10%-13% for men), while melanoma on the face was more common in older patients and melanoma on the anterior trunk and leg was more common in younger men than older men. Melanomas were more common on the scalp and face in older, compared with younger, men and more common on the scalp and back of older men compared with older women (Box 1). Histological type: SSM was more common in younger patients of both sexes and NM was more common in older male patients. Most thin lesions (80%) were SSM and most thick lesions (72%) were NM. Thicknesses of the three histological types were: SSM, 0.02-10.5 mm (median, 0.63 mm; interquartile range [IQR], 0.4-1.0 mm); NM, 0.2-25 mm (median, 2.46 mm; IQR, 1.4-3.8 mm); and LM, 0.1-8.5 mm (median, 0.4 mm; IQR, 0.25-0.8 mm). Factors associated with failure to identify melanoma Many melanomas were not detected by patients, but were identified by their doctors. Sex and age: Men were more likely to fail to notice changes of melanoma than women (37%; 95% CI, 35%-49% v. 30%; 95% CI, 28%-32%) as were older, compared with younger, people (38%; 95% CI, 35%-41% v. 28%; 95% CI, 25%-31%). As shown in Box 2, a greater proportion of older men failed to identify changes in their lesions than younger men; the same trend was evident in women. Site: Patients most frequently failed to identify changes in lesions on the scalp (42%; 95% CI, 30%-52%) and back (41%; 95% CI, 37%-45%), but even among patients with a lesion on the face, 31% (95% CI, 26%-33%) did not identify it as melanoma. The anterior trunk was the least common site for unidentified change (24%; 95% CI, 20%-28%). Older patients failed to identify changes more often than younger patients for all sites except the face and scalp, where the reverse was the case (Box 2). However, numbers are very small for these groups and results should be interpreted with caution. Histological type: A greater proportion of patients with LM (47%; 95% CI, 40%-55%) failed to identify their melanoma than patients with SSM (33%; 95% CI, 31%-35%) or NM (29%; 95% CI, 25%-33%), although by the time they were detected the NM were much thicker. Older people were less likely than younger people to identify melanoma of all three histological types. Regression analyses: Age, thickness, histological type and site of lesion were significantly associated with identifying changes (Box 3). After these variables were included in the model, sex was no longer statistically significant. After adjustment for other variables in the model, the odds of older people identifying changes was two-thirds the odds of younger people identifying changes, and the odds of those with thicker lesions identifying changes was one-and-a-half times the odds of those with thinner lesions identifying changes. Those with LM had about half the odds of identifying changes as those with NM. As shown in Box 3, those with lesions on the face, arm, anterior trunk and leg had significantly higher odds of identifying changes than those with lesions on the back (reference group). Associations with thick melanoma (≥3 mm) As shown in Box 3, age and nodular melanoma were strongly associated with presentation with thick lesions. Changes of melanoma were more frequently identified in thick lesions, but as shown in Box 2, older people were less able to identify melanoma, irrespective of its thickness. It was also of interest that once the histological type of the lesion was taken into account, the site of the melanoma and sex of the patient were no longer related to thickness (ie, thick melanoma on the back and scalp in men appeared to result from the higher frequency of NM at these sites in men; see Box 3). Types of changes reported by patients Significantly fewer older than younger men reported changes in size and shape (21% v. 30%). The same was true for colour (20% v. 27%), and twice as many older men stated that the first change they were aware of in their skin lesion was bleeding (7% v. 3%). However, these differences were not statistically significant. Similarly, our findings that more younger than older women reported colour changes as the first change noticed (32% v. 25%) and (in contrast to men) older women reported changes in size and shape as the first change as frequently as younger women (30% v. 28%), were also not statistically significant. As shown in Box 4, patients with NM reported changes in colour significantly less frequently than those with SSM, change in sensation significantly more frequently than those with LM, and bleeding significantly more frequently than those with LM and SSM. Changes in size and shape were the most frequent changes reported in thick melanoma (34%), whereas changes in colour were more frequently reported in thin lesions (27%). Bleeding was reported as the first change significantly more frequently in thick than thin lesions (17% v. 4%). Reported changes in sensation were similar for thick or thin lesions. Discussion We excluded approximately one-third of the patients on the NMU database, mainly because of missing information about changes noticed or thickness measurements, or because they had melanoma of unusual histological type or location. However, the excluded patients appeared to have similar age and sex distribution, site and thickness measurements to patients in the study. Nonetheless, our results may not be generalisable to patients with the less common histological types of melanoma. Forty per cent of men and 34% of women aged over 50 failed to identify their melanoma. In contrast, younger patients of both sexes reported changes of melanoma in over 70% of cases. These findings were consistent with those of Koh et al15 who found that 38% of melanomas were not identified by men over the age of 60, compared with 23% in men less than 40 years of age. We also found that failure to detect melanoma was not only related to the age of the patient, but was associated with the site and type of the melanoma. Firstly, older men had lesions at sites which are more difficult to see, such as the back and scalp, with nearly 50% of melanoma in older men (compared with only 20% in older women) occurring on the back. Other series have reported similar differences in site distribution of melanoma between the sexes.16,17 Secondly, compared with younger people, older people, particularly men, had a higher proportion of NM, similar to that reported elsewhere.5,18 Patients also identified NMs when they were much thicker than SSMs (median, 2.46 mm v. 0.63 mm). The higher frequency of bleeding as the first change noted in patients with NM was consistent with this finding.19 The higher proportion of NM in older people and more frequent occurrence in "hard-to-see" sites could solely explain the presentation of older people with thicker melanomas. However, regression analysis indicated that for any given thickness and type of melanoma at a given site, older people were less able to recognise melanoma than younger people. In our examination of the first change that drew the attention of patients to their melanoma, we found that self-reporting of a change in colour was infrequent in patients with thick melanoma, and in patients with NM relative to those with SSM. These results were surprising, as previous studies have shown that changes in colour were one of the most frequent early changes of melanoma.20,21 Most of the thick melanoma were NM, which tend to be relatively homogeneous in colour compared with SSM. Thus, the different patterns of colour between NM and SSM may need to be emphasised in educational material directed at older patients. Bleeding was clearly associated with thick and nodular melanoma, but this is a late rather than an early sign.19 To the best of our knowledge this is the first study that has sought to identify reasons why older people present with thicker melanoma. The finding that older patients had lower ability to detect melanoma than younger people is consistent with our previous findings that older people had difficulty in discriminating early changes of melanoma in photographs of pigmented lesions.10,11 Previous studies have noted that younger people were more likely to rate change in skin lesions as extremely important in diagnosis of melanoma than older respondents.22 Older people may also not inspect their skin as frequently as younger people and this may contribute to their lower rate of detection of melanoma. Our findings raise questions about the likely effectiveness for older people of public health strategies that rely on self-detection of melanoma. It seems that that greater reliance will need to be placed on detection of melanoma in this age group by health professionals, who may need to be made aware of the high frequency of thick melanoma and characteristics of melanoma in this age group. Our previous studies have shown that recognition of change in existing lesions over time or the appearance of new pigmented skin lesions can be very difficult, but is assisted by whole-body photographs.10,11 The feasibility of using whole-body photographs to help general practitioners detect melanoma is currently under evaluation in a project funded by the National Health and Medical Research Council. Acknowledgements We thank the nursing sisters Sue Collins, Debbie Bradley, Donna Owens and Kathy Hall for collection of the data and Vicky Hunter for data entry. Dr Hanrahan was supported in part by the Hunter Melanoma Foundation. References Buttner P, Garbe C, Bertz J, et al. Primary cutaneous melanoma: optimized cutoff points of tumor thickness and importance of Clarks level for prognostic classification. Cancer 1995; 75: 2499-2506. Thorn M, Ponten F, Bergstrom R, et al. Clinical and histopathologic predictors of survival of patients with malignant melanoma: a population based study in Sweden. J Natl Cancer Inst 1994; 86: 761-769. Balch CM, Soong SJ, Shaw HM, et al. An analysis of prognostic factors in 8500 patients with cutaneous melanoma. In: Balch CM, Houghton AN, Milton GW, et al, editors. Cutaneous melanoma. Philadelphia: JB Lippincott Co.; 1992: 165-185. Breslow A. Tumor thickness, level of invasion and node dissection in stage 1 cutaneous melanoma. Ann Surg 1975; 182: 572-578. Hersey P, Sillar R, Howe CG, et al. Factors related to the presentation of patients with thick primary melanomas. Med J Aust 1991; 154: 583-587. McHenry PM, Hole DJ, Mackie RM. Melanoma in people aged over 65 in Scotland, 1979-89. BMJ 1992; 304: 746-749. Cohen HJ, Cox E, Manton K, Woodbury M. Malignant melanoma in the elderly. J Clin Oncol 1987; 5: 100-106. Coates M, Day P, McCredie M, Taylor R. NSW cancer incidence and mortality 1992. In: NSW Central Cancer Registry. Sydney: NSW Cancer Council; June 1995: 87, 97. Hanrahan P, Hersey P, Watson AB, Callaghan TM. The effect of an educational brochure on knowledge and early detection of melanoma. Aust J Public Health 1995; 19: 270-274. Hanrahan P, Hersey P, Menzies SW, et al. Examination of the ability of older people to identify early changes of melanoma in computer-altered pigmented skin lesions. Arch Dermatol 1997; 133: 301-311. Hanrahan P. Early detection of melanoma in older people [PhD thesis]. Sydney: University of NSW, 1998. McGovern VJ, Cochran AJ, Van Der Esch EP, et al. The classification of malignant melanoma, its histological reporting and registration: a revision of the 1972 Sydney classification. Pathology 1986; 18: 12-21. SAS for PC [computer program]. Version 6.11. Cary, NC: SAS Institute Inc., 1995. STATA [computer program]. Version 5.0. Houston, Tx: Stata Corp, 1997. Koh HK, Miller DR, Geler AC, et al. Who discovers melanoma? J Am Acad Dermatol 1992; 26: 914-919. Nguyen HL, Armstrong B, Coates M. Cutaneous melanoma in NSW 1983-1995. In: NSW Central Cancer Registry. Sydney: NSW Cancer Council; June 1997: 40. Green A, MacLennan R, Youl P, Martin N. Site distribution of cutaneous melanoma in Queensland. Int J Cancer 1993; 53: 232-236. Nguyen HL, Armstrong B, Coates M. Cutaneous melanoma in NSW 1983-1995. In: NSW Central Cancer Registry. Sydney: NSW Cancer Council; June 1997: 38. Fitzpatrick TB, Milton GW, Balch CM, et al. Clinical characteristics of primary melanoma. In: Balch CM, Houghton AN, Milton GW, et al, eds. Cutaneous melanoma. 2nd ed. Philadelphia: JB Lippincott Co.; 1992: 225-226. Mackie RM. Clinical recognition of early invasive melanoma. BMJ 1990; 301: 1005-1006. McGovern TW, Litaker MS. Clinical predictors of malignant pigmented lesions. J Dermatol Surg Oncol 1992; 18: 22-26. Baade PD, Balanda KP, Stanton WR, et al. Community perceptions about the important signs of early melanoma. J Am Acad Dermatol 1997; 36: 33-39. (Received 1 Sep 1997, accepted 14 May 1998) Authors' details John Hunter Hospital, Newcastle, NSW. Pauline F Hanrahan, BA, PhD, Research Officer, Newcastle Melanoma Unit and Division of Surgery; Peter Hersey, FRACP, D. Phil, Conjoint Professor of Oncology, Oncology and Immunology Unit, Division of Surgery. Centre for Clinical Epidemiology and Biostatistics, University of Newcastle, Newcastle, NSW. Catherine A D'Este, BMath, PhD, Lecturer in Biostatistics, Faculty of Medicine and Health Sciences. Reprints will not be available from the authors. Correspondence: Dr P Hersey, Room 443, David Maddison Clinical Sciences Building, Cnr King and Watt Streets, Newcastle, NSW 2300. - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Pauline F Hanrahan · Peter Hersey · Catherine A D'Este

Doctors detected self-administering opioids in New South Wales, 1985-1994: characteristics and outcomes Megan Cadman and James Bell MJA 1998; 169: 419-421 For editorial comment, see Breen & Court Abstract - Introduction - Methods - Results - Discussion - Acknowledgement - References - Authors' details - - More articles on Drugs and alcohol - ©MJA1998 Abstract Objective: To describe the characteristics and outcomes of doctors whose drug authorities were withdrawn as a result of self-administering opioids for non-medical purposes. Design: Retrospective review of New South Wales Health Department information relating to all doctors whose authorities to possess, supply, prescribe or administer drugs of addiction had been withdrawn in the period 1985 to 1994 as a result of confirmed self-administration of opioids. Outcome measures: Age, sex, geographical location and practice category at the time of intervention; drugs used; period of opioid use before authority withdrawal; means of detection; and registration status as at August 1995. Results: From 1985 to 1994, 79 doctors had their drug authorities withdrawn (0.4% of the NSW medical profession in 1994). The groups significantly over-represented were general practitioners and those aged 30-39 years. Pethidine was the main drug used (66 doctors; 84%). Drug use for more than two years before detection was reported by 34 (43%) doctors. Community pharmacists were the source of reports leading to detection of 28 (35%) doctors. As at August 1995, 27 (34%) of the study group were not practising; 10 (13%) had died. Conclusion: Outcomes for these doctors were poor. There was substantial attrition from practice and a high mortality rate. Introduction Medical practitioners have been shown to have a higher rate of drug abuse, mental illness and suicide than either matched controls or the general population.1-4 It is claimed that in the United States up to 10% of physicians at some time during their careers become dependent on psychoactive drugs or alcohol to an extent where their practice is impaired; about 1% become opioid-dependent.5 For these doctors, if placed in highly structured and strictly monitored programs, treatment outcomes are substantially better than for other opioid-dependent people.6,7Few data have been published on the prevalence of drug misuse among Australian healthcare professionals, and even less on the problems experienced by drug-dependent doctors and the extent of their professional impairment. Two studies of doctors with serious drug dependency brought to the attention of the Victorian Medical Board, in 1964-1984 and 1984-1990, indicated a prevalence of about 0.5%.8,9 By comparison, in a recent anonymous survey of 1125 doctors in New South Wales, 1% of those surveyed reported drug abuse problems, a figure closer to estimates from other countries.10 Accurate reporting of the prevalence of drug misuse in healthcare professionals is often undermined by the tendency of colleagues to either protect or ignore the impaired individual, and by treating doctors often anxious to avoid "labelling" a colleague with a potentially damaging diagnosis. Our study uses official records to examine the characteristics, and the limited information about outcomes, of those doctors in NSW whose opioid use had triggered official intervention. Methods Data collection The study group comprised all doctors whose authorities to possess, supply, prescribe or administer drugs of addiction (Schedule 8 authorities) were withdrawn by the NSW Health Department as a result of confirmed self-administration of opioids in the period 1985 to 1994, inclusive. The data for this study were obtained from files held by the Pharmaceutical Services Branch of the NSW Health Department. Information relating to sex, geographical location and main type of practice or specialty at the time of intervention, use of other drugs, period of opioid use before authority withdrawal, means of detection, and reports of psychiatric consultations, was collected from these files. Data relating to date of birth and registration status as at August 1995 were obtained from the NSW Medical Board, and data on the age, sex, specialty and geographical location of all medical practitioners in NSW were obtained from the Workforce Planning Unit of the NSW Health Department. Analysis To determine whether any groups were over-represented in the study group, demographic characteristics of the subjects were compared with those of the profession as a whole in NSW. Where available, data for 1990 were used in comparisons, as this represented a mid-point in the study period. For the number of medical practitioners and general practitioners in NSW, 1994 data were used. Confidence intervals and the χ2 test were used in the analysis of the data. Ethical approval The study was approved by the New South Wales Health Department. Strict confidentiality was maintained throughout the study. Results In the period 1985 to 1994, 79 doctors relinquished their Schedule 8 authorities as a result of confirmed self-administration of opioids. This represents 0.4% of the medical profession in NSW in 1994.11 Demographic characteristics The main characteristics of doctors in the study group at the time their Schedule 8 authorities were withdrawn are shown in Table 1. Ages of doctors in the study group at the time of authority withdrawal ranged from 26 to 69 years (mean, 39 years; 95% confidence interval, 36.8-41.2 years). Fifty-six per cent of the group were aged 30 to 39 years, a significant over-representation of this age group (Table 1). Rural practitioners were significantly over-represented in the group according to the chi-squared test (chi-squared, 4.67; P = 0.031) (Table 1). Four practice categories were identified in the study group: general practice (64; 81%), anaesthetics (3; 4%), psychiatry (3; 4%), and hospital salaried staff (9; 11%). Compared with the profession as a whole for 1994, general practitioners were significantly over-represented; anaesthetists and psychiatrists were not. Comparative data for hospital salaried staff in NSW were not available. Five of the nine doctors employed in salaried positions in hospitals were working in emergency departments. Drugs used Pethidine was the main drug used (66 doctors; 84%), with 31 (39%) apparently using nothing else. Commonly, doctors initially obtained pethidine, and to a lesser extent morphine, from their doctor's bag emergency supply, with prescriptions and surgery or hospital stock accessed as drug use escalated. Other drugs used included mixed opioids, barbiturates, ketamine and benzodiazepines. A concurrent alcohol problem was reported by 13 (16%) doctors, and eight (10%) admitted illicit drug use. All of the illicit drug users were men aged 30 to 43 years. Period of drug use Thirty-four (43%) doctors reported using opioids for more than two years before intervention, with four individuals admitting drug use for more than 10 years (Table 2). Two of these four also reported illicit drug use dating from their late teens. Means of detection Community pharmacists were the primary source of reports (Table 3), often alerted by a large number of opioid prescriptions written by a particular doctor. Common scenarios included prescriptions written for patients being either picked up personally from the pharmacy by the doctor, or requested to be delivered to the doctor's surgery, or patients being asked to collect opioids from the pharmacy and take them to the doctor's surgery, where one or two ampoules were administered to the patient and the balance retained by the doctor for personal use. Other reporting sources were routine inspections of community pharmacy records by departmental officers, and reports by colleagues and by the doctors themselves. Self-reports occurred in 14 cases (18%); most of these were due to the prompting of a treating psychiatrist or therapist as part of a rehabilitation program. Thirty-one doctors (39%) denied self-administration at first contact by the department. Of this group, 15 stated that the drugs were for use by others, usually relatives; 11 denied self-administration, with no other explanation offered; and five insisted that the drugs were used to treat a medical condition. At subsequent interviews, all admitted to self-administration for non-medical purposes and relinquished their drug authorities. Morbidity and mortality Twenty-eight (35%) doctors reported having consulted a psychiatrist before initial contact by the department. Twelve of these had consulted a psychiatrist for a drug abuse problem, the other 16 had consulted for non-drug related problems. Eight individuals in the study group reported that they had taken antidepressants. Ten (13%) of the doctors (nine men) are known to have died in the study period. Three of these are known to have committed suicide, one died of an overdose, two died in motor vehicle accidents, one died of a heart attack, and the cause of death of three individuals is not known. There were also five known suicide attempts by subjects during the study period. Registration status Only 54 (68%) of the subjects remained on the medical register as at August 1995 (Table 4). Two of these, although still on the register, were known to have left the profession. Including these two individuals, there was an overall loss from the medical profession in NSW of 27 (34%) individuals. Twenty-two doctors had continuing conditions placed on their registration by the Medical Board. These included, in addition to the continued withdrawal of the drug authority, requirements such as ongoing treatment by a psychiatrist, regular assessment and monitoring including urinalysis, supervised employment, and regular Board review, in line with the Board's Impairment Program protocols. Discussion From 1985 to 1994, 79 doctors had their authorities to possess, supply, prescribe or administer drugs of addiction withdrawn as a result of confirmed self-administration of opioids. Pethidine was the main drug used, and 43% of the doctors had been self-administering drugs for more than two years before detection. There are several limitations to the data in this study. The data were obtained from a retrospective review of file notes, which had been compiled by different interviewers, and did not follow a systematic data collection format. Data on several variables, including the extent of illicit drug use and period of drug use, relied on self-reporting and therefore introduced a "recall bias", either deliberate or inadvertent. A number of confounders may have influenced detection rates during the study period. These include the frequency and areas of prescription monitoring by the department, and changes in awareness and/or diligence of the reporting groups, such as community pharmacists and medical colleagues, who may have been influenced by articles in professional journals or by mailings by the Doctors' Health Advisory Service, as occurred in 1988. These factors may have varied between regions and over time. Another limitation of the study is that the subjects represent a subset of all drug-using doctors -- those who were detected. The data indicate that some doctors can self-administer drugs for prolonged periods without detection, and it is quite likely that sufficiently careful medical practitioners may self-administer opioids regularly and never be detected. Few doctors in the study sample surrendered their Schedule 8 drug authorities on their own instigation. Since detection of a problem was often based on observations by others, particularly community pharmacists, this could introduce systematic bias. Geographical isolation has been identified as a "marker" for substance abuse.12 However, the apparent correlation between rural practice and drug use may simply indicate that a doctor with a drug problem has a greatly increased chance of detection in a rural town than in the relative anonymity of the city. Among doctors detected self-administering opioids there is considerable attrition from medical practice. Of the 79 doctors in the sample, there was a loss of 27 individuals from the profession, with 10 of these known to have died in the study period. In recent years, the NSW Medical Board has adopted policies aimed at rehabilitating doctors who misuse drugs, while maintaining them in practice wherever possible. These policies include placing conditions on registration, such as supervised employment, restrictions on possessing and prescribing drugs of addiction, attendance for treatment and assessment, urine testing, and regular review by the Board. After a period of such supervision, practitioners who comply satisfactorily may return to full registration.11 There are no published data on the outcomes of these interventions. Attrition from the profession is taken as a poor outcome, but this may be an erroneous assumption. One hypothesis concerning medical practitioners who self-administer opioids is that they are ambivalent about medical practice,13 and this was confirmed by four subjects, two of whom had sought psychiatric treatment. It may be, therefore, that leaving practice was an appropriate decision for some individuals. The misuse of opioids described in this study should be seen within the wider context of the overall medical and psychological needs of medical practitioners. Acknowledgement The authors acknowledge the assistance of Pia Salmelainen, Policy Analyst (Research Officer), Pharmaceutical Services Branch, NSW Health. References Ball JRB. Alcohol and drug use and related problems in the medical profession. Aust Drug Alcohol Rev 1986; 5: 29-32. Murray RM. Psychiatric illness in male doctors and controls: an analysis of Scottish hospitals inpatient data. Br J Psych 1977; 131: 1-10. Preven DW. Physician suicide. In: Scheiber SB, Doyle BB, editors. The impaired physician. New York and London: Plenum Press, 1983; 39-47. Schlicht SM, Gordon IR, Ball JRB, Christies DGS. Suicide and related deaths in Victorian doctors. Med J Aust 1990; 153: 518-521. Webster TG. Problems of drug addiction and alcoholism among physicians. In: Scheiber SB, Doyle BB, editors. The impaired physician. New York and London: Plenum Press, 1983; 27-38. Centrelia M. Physician addiction and impairment -- current thinking: a review. J Addictive Diseases 1994; 13: 91-105. Morse RM, Martin MA, Swenson WM, Niven RG. Prognosis of physicians treated for alcoholism and drug dependence. JAMA 1984; 251: 743-746. Serry N, Ball JRB, Bloch S. Substance abuse among medical practitioners. Drug Alcohol Rev 1991; 10: 331-338. Serry N, Bloch S, Ball R, Anderson K. Drug and alcohol abuse by doctors. Med J Aust 1994; 160: 402-407. Pullen D, Cait EL, Lyle DM, et al. Medical care of doctors. Med J Aust 1995: 162: 481-484. New South Wales Medical Board. Annual report for the period ending 31 March 1994. Sydney: NSW Medical Board, 1994. Talbott GD, Gallegos KV, Wilson PO, Porter TL. The Medical Association of Georgia's impaired physician program, review of the first 1000 physicians: analysis of specialty. JAMA 1987; 257: 2927-2930. Modlin HC, Montes A. Narcotics addiction in physicians. Am J Psych 1964; 121: 358-363. (Received 11 Nov 1997, accepted 23 Jun 1998) Authors' details Pharmaceutical Services Branch, NSW Health, Gladesville, NSW. Megan Cadman, BPharm, MPH, Acting Deputy Chief Pharmacist. The Langton Centre, Surry Hills, NSW. James Bell, BA, FRACP, Director. Reprints will not be available from the authors. Correspondence: Ms M Cadman, Pharmaceutical Services Branch, NSW Health, PO Box 103, Gladesville, NSW 1675. E-mail: mcadmATdoh.health.nsw.gov.au - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Megan Cadman · James Bell