Volume 170 Issue 2

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

Review Vascular dementia: diagnosis, management and possible prevention There has been a recent upsurge of interest in the clinical features of and risk factors for vascular dementia, and consensus is emerging on its diagnostic characteristics. We discuss these features and risk factors and the main intervention strategies, both for treatment and prevention. Perminder S Sachdev, Henry Brodaty and Jeffrey C L Looi MJA 1999; 170: 81-85 Introduction - Definition - Epidemiology - Clinical-pathological correlates and pathogenesis - Clinical features and diagnosis - Prognosis - Prevention and treatment - Acknowledgements - References - Authors' details - - More articles on Geriatrics Introduction Developments in the past three decades have led to a radical rethinking of the association between cerebrovascular disease (CVD) and dementia, and set the stage for a reconceptualisation of dementia from vascular causes. We will review recent developments in the concept of vascular dementia (VaD), and discuss its importance as a common, and potentially preventable, form of dementia. Definition There are two obvious steps in the diagnosis of VaD -- diagnosis of dementia per se and establishment of its vascular aetiology. Dementia is defined as a multifaceted decline in cognitive functioning causing impaired functioning in daily life.1,2 Impairment of memory is generally regarded as a necessary aspect, but decline in one or more other cognitive domains (ie, language, praxis, gnosis, visuoconstructive function, frontal-executive functions) must also be demonstrated.1,2 VaD is diagnosed if significant CVD is present and is judged to be causally relevant to the cognitive impairment.1-4What constitutes significant vascular aetiology is not always easy to establish. Minor cerebrovascular pathology is common in healthy elderly people5 and in association with other dementias, notably Alzheimer's disease (AD).6 Recent studies using magnetic resonance imaging (MRI) of the brain have reported periventricular hyperintensities on T2-weighted images, arguably vascular in origin, in up to 93% of healthy elderly individuals,5 so guidelines for determining the significance of cerebral vascular lesions are needed. An early approach was to base the diagnosis on the score obtained on an ischaemia scale,7 which comprises a list of historical and clinical examination items known to discriminate multi-infarct dementia (MID) from AD. On a 13-item scale (maximum score 18), a score of seven or more suggested MID and four or less suggested AD.7 This approach has limitations as it is based on a concept that VaD is caused by multiple strokes (hence, MID), now recognised to be only one vascular pathway to dementia. In addition, it uses only some of the relevant clinical information, and it excludes neuroimaging from consideration. More recent efforts have attempted to address these deficiencies. According to the NINDS-AIREN criteria (developed at an international workshop involving 54 neurologists and neuroscientists),4 a diagnosis of probable VaD is made if dementia is associated with focal neurological signs and imaging evidence of CVD is present. On computed tomography (CT) or MRI this could comprise multiple or strategic single infarcts, multiple lacunae, extensive white matter lesions (WMLs), or combinations of these. Like other dementias, VaD requires histopathological confirmation and is a postmortem diagnosis. Some investigators have argued that the emphasis on dementia in patients with CVD may be inappropriate for several reasons: (i) the diagnosis of dementia is contentious in many patients because a qualitative judgement is involved; (ii) it imposes a categorical distinction on the continuous construct of cognitive impairment; and (iii) it is important to recognise cognitive impairment before it has reached the stage of dementia, especially if prevention strategies are to be introduced. Thus, the term "vascular cognitive impairment" has been proposed, in which "vascular" refers to all causes of ischaemic CVD, and "cognitive impairment" encompasses all levels of cognitive decline, which may fall well short of dementia.8 Epidemiology Prevalences of VaD have varied across studies because of methodological differences, but point to VaD being the second most common dementia after AD in Western societies. A quantitative integration of studies published between 1945 and 1985 suggested an overall prevalence of dementia of 5.6% in people older than 60 years.9 AD was more prevalent than MID by a relative factor of 1.05 to 1.43 in Western societies. VaD had an increasing prevalence with age (a doubling every 5.3 years). It also found an excess of VaD in men, and a cross-national effect, with AD being more common in Western countries and VaD being much more common in Japan, China and Russia.9 A Swedish study estimated the lifetime risk of VaD as 34.5% for men and 19.4% for women.10 In community-based studies, the incidence of VaD has ranged from 0.17 to 0.71 per 100 person-years.10,11 In a sample of hospitalised ischaemic stroke patients, the incidence of VaD was estimated to be 8.4 per 100 person-years.12 Dementia was diagnosed in 26.3% and 31.8% of patients, respectively, in two studies at three months after an acute stroke.12,13Risk factors for VaD (summarised in Box 1) are incompletely understood.14 As stroke is a major determinant of VaD, it is reasonable to expect that risk factors for stroke would also increase the risk of VaD. While hypertension increases the risk of VaD, high systolic blood pressure may serve a protective role once dementia has set in.15 In one study, although subjects with VaD were more likely to have been hypertensive in the past, they currently had lower blood pressure values and more orthostatic hypotension than stroke patients without dementia.13 Genetic factors for CVD, and consequently VaD, are not well understood. Exceptions are rare disorders such as cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy (CADASIL) and autosomal dominant hereditary cerebral haemorrhage with amyloidosis -- Dutch type. The role of apolipoprotein E polymorphism in VaD is unclear; there is conflicting evidence for a link with the e4 allele.14 Not all stroke patients develop dementia, suggesting the nature and extent of strokes and their interaction with host factors are important. Left hemisphere strokes are more likely to produce severe cognitive impairment, and the infarction of certain strategic areas may be crucial (eg, deep frontal white matter, dominant thalamus and angular gyrus).12,13 VaD may occur in the absence of strokes, and this is usually associated with periventricular WMLs or lacunae and silent infarcts.4 Clinical-pathological correlates and pathogenesis Brain parenchymal lesions of vascular origin may be produced through ischaemia, haemorrhage or oedema. VaD may therefore be caused by multiple mechanisms, individually or in combination (Box 2). The resulting neuropathology will vary according to the dominant mechanisms and will comprise combinations of multiple large infarcts, single strategic infarcts, lacunae and WMLs. Multiple large infarcts may result in summative damage to widespread regions causing a heterogeneous pattern of deficits, overwhelming compensatory mechanisms. Single infarcts, when strategically placed and large, may affect a critical cortical or subcortical region to disrupt multiple cognitive functions. Lacunae (or lacunar infarcts) are small cavities, up to 1.5 cm in diameter, that usually occur in the basal ganglia, thalamus, pons, internal capsule and deep white matter areas irrigated by the superficial and deep penetrating arteries and arterioles. WMLs are commonly seen on CT and especially on T2-weighted MRI. As they are present in otherwise healthy elderly individuals, their pathological significance has been greatly debated.5 When their severity was considered, periventricular WMLs were reported in VaD to be 11.6 times greater than in AD and 3.5 times greater than in healthy people, and subcortical WMLs were 2.6 and 13.5 times greater, respectively.16 A threshold effect has been suggested, with cognitive impairment resulting when WMLs reach a certain severity. WMLs must nevertheless be distinguished from Binswanger's disease,17 a rare clinicopathological entity characterised by slowly progressive dementia, usually beginning in the fifth or sixth decade, and associated with hypertension, psychiatric features, gait disturbance, parkinsonism, corticobulbar features and incontinence. The vascular pathology in VaD is varied; atherosclerosis, arteriosclerosis, lipohyalinosis, amyloid angiopathy, senile arteriolar sclerosis and other angiopathies have been described.4 Systemic causes of thromboembolism are important in some cases: inflammatory diseases (eg, systemic lupus erythematosus, polyarteritis nodosa, sarcoidosis), hyperviscosity syndromes (eg, polycythaemia vera, sickle cell anaemia) and embolic disorders (eg, atrial fibrillation, myocardial infarction with mural thrombus, congenital heart disease, as well as septic, air or fat emboli). VaD and Alzheimer-type changes not uncommonly co-occur, and 10%-20% of patients with dementia are classified clinically and pathologically as having both AD and VaD. VaD is known to promote the clinical expression of AD;6 the relationship between these two dementias needs further study. Clinical features and diagnosis The onset of VaD is often sudden, with a transient ischaemic attack (TIA) or a stroke, after which the clinical course may be static, remitting or progressive, often with a fluctuating or stepwise deterioration. Predominantly subcortical lesions may produce cognitive impairment of gradual onset and slow progression. Other features that distinguish VaD from AD are nocturnal confusion and wandering, relative preservation of emotional responsiveness and personality until the later stages of the disease, and the presence of depression, emotional lability, incontinence and somatic symptoms.4 A history of risk factors for CVD should alert the clinician to the possibility of VaD, and the presence of focal neurological symptoms (such as visual disturbances, brainstem abnormalities, sensory or motor symptoms) and signs (hemiparesis, visual field defects, pseudobulbar palsy, extrapyramidal signs) will provide further support. The cognitive deficits in VaD are multifocal and therefore more varied than generally seen in AD. Memory deficit may not be as marked; discrepancies between verbal and non-verbal memory performance are often notable. Other common elements are visuospatial dysfunction, dysphasia, cognitive slowing and impairment of executive function.4 Impairment in frontal lobe functioning is usually more severe for VaD than AD. Language impairment in patients with left hemispheric strokes may impede the assessment of abnormalities in other cognitive domains. Assessment of a patient with possible VaD should include establishment of the diagnosis of dementia; documentation of evidence for CVD; determination of the aetiological role of CVD; evaluation of functional status of the individual and his or her disability, and the interpersonal and community supports available; and determination of risk and protective factors that could be modified (Box 3). Absence of vascular lesions on CT and, in particular, MRI is strong evidence against vascular aetiology. As CVD is commonly present in otherwise healthy individuals, guidelines are available for the topography and severity of lesions to be considered significant.4 At least a quarter of all white matter would need to be involved for the lesions to be clearly significant (Figure). Prognosis While not totally consistent, longitudinal studies of VaD suggest mortality rates greater than for AD and rates of admission to nursing homes comparable in the two. One study reported a five-year mortality rate of 63.6% (compared with 31.8% for AD) and a nursing home admission rate of 31.8% (compared with 20.6% for AD).19 Cognitive impairment in patients with stroke has adverse functional consequences, independent of any physical impairments. The prognosis may be improved by better treatment and preventive strategies. Prevention and treatment The management of risk factors for VaD offers the opportunity to reduce its incidence significantly, or, if dementia has already been diagnosed, halt its progression and sometimes achieve partial improvement. Some strategies for primary prevention of VaD are listed in Box 4. One of the more established interventions is control of hypertension. Treatment of patients with diastolic blood pressure (BP) greater than 110 mmHg is universally accepted, and there is evidence that treatment of those with diastolic BP of 90-110 mmHg and systolic BP greater than 160 mmHg is beneficial.20 While antihypertensive drugs are often indicated, lifestyle changes which lower BP are advisable at all levels of BP. In controlling hypertension, avoidance of hypotension is strongly advocated, as poor autoregulation in VaD patients increases its deleterious effects on cerebral blood flow. The control of risk factors such as hyperlipidaemia and diabetes mellitus may also have a stabilising effect, although evidence is lacking.21 Other modifiable factors include cigarette smoking, excessive alcohol consumption, obesity, and lack of exercise. Non-atherogenic risk factors that may be modifiable include atrial fibrillation and carotid artery stenosis. Warfarin is clearly beneficial in reducing the risk of stroke in patients with atrial fibrillation, with aspirin being less effective.22 In those with a past TIA or non-haemorrhagic stroke, antiplatelet therapy is helpful in reducing the risk of further such events. The optimal dose of aspirin to be used is not known, and doses between 75 mg and 325 mg are recommended.22 For those "failing" aspirin therapy, other antiplatelet agents, such as ticlopidine, may be indicated. Current evidence is insufficient to recommend aspirin for the primary prevention of stroke and VaD in low-risk individuals; there may be a slight increase in the risk of haemorrhagic stroke with such treatment.23 In stroke or TIA patients with a severe carotid artery stenosis (> 70% occlusion), carotid endarterectomy is an effective procedure. The role of such surgery in the presence of moderate stenosis or for asymptomatic individuals is uncertain.23 Many drugs have been investigated for treating VaD, but with limited success, and no drug can be positively recommended at present. Vasodilators (eg, hydergine [co-dergocrine mesylate; Sandoz], other alkaloids and cyclandelate) have some positive effects, and modest gains in cognition have been reported with an orally active haemorheological agent (pentoxifylline).22 A related drug, propentofylline, may exert an additional neuroprotective effect and has shown some promise in clinical trials.24 Other drugs that have been tried include the vinca alkaloids, calcium channel antagonists, nootropics, and extracts of Ginkgo biloba, with no convincing successes.25 Some of the drugs that improve memory in some AD patients (eg, cholinergic drugs such as tacrine and donepezil) may find a role in VaD. Other drugs may serve a neuroprotective role (eg, propentofylline, calcium channel antagonists and N-methyl-D-aspartate receptor antagonists). The mainstay of treatment is preventive and supportive. Supportive measures should include rigorous treatment of psychiatric complications such as depression, measures to facilitate independence, community or institutional care, and support for the carer. Specific neuropsychological rehabilitative measures may have a role in particular cases. Self-help groups such as the Alzheimer's (and Related Disorders) Association and the Stroke Society play an important supportive and educational role. Acknowledgements The assistance of Barbara Brierley and Agata Wachala in literature search is gratefully acknowledged. References World Health Organization. The ICD-10 classification of mental and behavioural disorders. Diagnostic criteria for research. Geneva: World Health Organization, 1993. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington DC: American Psychiatric Association, 1994. Chui HC, Victoroff JI, Margolin MD, et al. Criteria for the diagnosis of ischemic vascular dementia proposed by the State of California Alzheimer's Disease Diagnostic and Treatment Centers. Neurology 1992; 42: 473-480. Roman GC, Tatemichi TK, Erkinjuntti T, et al. Vascular dementia: diagnostic criteria for research studies. Report of the NINDS-AIREN international workshop. Neurology 1993; 43: 250-260. Kertesz A, Black SE, Tokar G, et al. Periventricular and subcortical hyperintensities on magnetic resonance imaging. "Rims, caps and unidentified bright objects." Arch Neurol 1988; 45: 404-408. Snowdon DA, Greiner LH, Mortimer JA, et al. Brain infarction and the clinical expression of Alzheimer disease: the nun study. JAMA 1997; 277: 813-817. Hachinski VC, Iliff LD, Zilkha E, et al. Cerebral blood flow in dementia. Arch Neurol 1975; 32: 632-637. Hachinski VC, Bowler JV. Vascular dementia. Neurology 1993; 43: 2159-2160. Jorm AF, Korten AE, Henderson AS. The prevalence of dementia: a quantitative integration of the literature. Acta Psychiatr Scand 1987; 76: 465-479. Hagnell O, Franck A, Grasbeck A, et al. Vascular dementia in the Lundby study: 1. A prospective, epidemiological study of incidence and risk from 1957-1972. Neuropsychobiology 1992; 26: 43-49. Schoenberg BS, Kokmen E, Okazaki H. Alzheimer's disease and other dementing illnesses in a defined United States population: incidence rates and clinical features. Ann Neurol 1987; 22: 724-729. Tatemichi TK, Paik M, Bagiella E, et al. Risk of dementia in a hospitalized cohort: results of a longitudinal study. Neurology 1994; 44: 1885-1892. Pohjasvaara T, Erkinjuntti T, Ylikoski R, et al. Clinical determinants of poststroke dementia. Stroke 1998; 29: 75-81. Gorelick PB. Status of risk factors for dementia associated with stroke. Stroke 1997; 28: 459-463. Gorelick PB, Brody JA, Cohen DC, et al. Risk factors for dementia associated with multiple cerebral infarcts: a case-control analysis in predominantly African-American hospital-based patients. Arch Neurol 1993; 50: 714-720. Boone BK, Miller BL, Lesser IM, et al. Neuropathological correlates of white matter lesions in healthy elderly subjects: a threshold effect. Arch Neurol 1992; 49: 546-554. Binswanger O. Die abgrenzung der allgemeined progressiven paralyse, I-III. Berl Klin Wochenschr 1884; 48: 1103-1105, 1137-1139, 1180-1186. Folstein M, Folstein S, McHugh PR. Mini-Mental State: a practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 1975; 12: 189-198. Brodaty H, McGilchrist C, Harris L, Peters KE. Time until institutionalization and death in patients with dementia: role of caregiver training and risk factors. Arch Neurol 1993; 50: 643-650. Lawrence M, Cruickshank K. Hypertension. In: Lawrence M, Neil A, Mant D, Fowler G, editors. Prevention of cardiovascular disease. Oxford: Oxford University Press, 1996; 18-34. Atkins D, Psaty BM, Koepsell TD, et al. Cholesterol reduction and the risk for stroke in men: a meta-analysis of randomized controlled trials. Ann Intern Med 1993; 119: 136-145. Black RS, Barclay LL, Nolan KA, et al. Pentoxifylline in cerebrovascular dementia. J Am Geriatr Soc 1992; 40: 237-244. Mant J. Prevention of stroke. In: Lawrence M, Neil A, Mant D, Fowler G, editors. Prevention of cardiovascular disease. Oxford: Oxford University Press, 1996; 162-174. Marcusson J, and European Propentofylline Study Group. HWA 285 for the treatment of dementia: results of a 12 months clinical trial. J Cerebr Blood Flow Metab 1995; 15 Suppl 1: S107. Wong AHC, Smith M, Boon HS. Herbal remedies in psychiatric practice [review]. Arch Gen Psychiatry 1998; 55: 1033-1044. (Received 21 Apr, accepted 30 Jul, 1998) Authors' details School of Psychiatry, University of New South Wales, NSW. Perminder S Sachdev, MD, PhD, Professor of Neuropsychiatry, and Neuropsychiatric Institute, The Prince Henry Hospital, NSW; Henry Brodaty, MD, FRANZCP, Professor of Psychogeriatrics, and Academic Department of Psychogeriatrics, The Prince Henry Hospital, NSW. Neuropsychiatric Institute, The Prince Henry Hospital, NSW. Jeffrey C L Looi, MB BS, NSW Institute of Psychiatry Fellow. Reprints will not be available from the authors. Correspondence: Dr P S Sachdev, NPI, The Prince Henry Hospital, Little Bay, NSW 2036. Email: P. SachdevATunsw.edu.au Two magnetic resonance imaging proton-density transaxial cuts from the brain of a hypertensive patient with vascular dementia. Note extensive involvement of white matter, which appears as hyperintense signals. The patient's computed tomography brain scan showed minor periventricular hypodensity. Back to text 1: Risk factors for vascular dementiaSociodemographicAgeIncreasing incidence with age, especially after 60 yearsRace/ethnicHigher rates in Asian and black populations15SexHigher rates in menEducationMay have a protective effect12-15Atherogenic12-15HypertensionMajor risk factorCoronary artery disease Increases stroke riskDiabetes mellitusRisk factor for strokeCigarette smokingRisk factor for strokeHypercholesterolaemiaRisk factor for strokeFibrinogen, obesityEvidence lackingOther cardiovascularAtrial fibrillationRisk of cerebral embolismMitral valve prolapseCerebral embolismPeripheral vascular disease Inconsistent evidenceOther factorsGeneticWeak; CADASIL an exceptionApolipoprotein E polymorphism Evidence inconsistentAnticardiolipin antibodies Evidence inconsistentAlcoholismEvidence inconsistentStroke-relatedNumber, volume, location of stroke12,13Strategic silent infarctsPre-existent atrophyPresence of abnormal periventricular signal on magnetic resonance imaging, or (especially) on computed tomographyCADASIL = cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy Back to text 2: Pathogenetic mechanisms of vascular dementiaI. Infarct (single or multiple)A. Arterial territory infarct Multiple infarcts Single strategic infarcts B. Watershed infarction C. Lacunar infarctionII. Non-infarction ischaemiaA. Subcortical leukoencephalopathy (Binswanger's) B. Laminar necrosis C. Granular atrophy D. Gliosis or sclerosisIII. HaemorrhageA. Subdural B. Subarachnoid C. Intracerebral Back to text 3: Clinical assessment for vascular dementia History should include onset, course and nature of cognitive deficits, and information from the carer or other person close to the patient on subtle personality and behavioural changes that may have been noticed. Full neuropsychological evaluation is required at some stage, although the Mini-Mental State Examination,18 supplemented by clock-drawing and clinical assessment of frontal lobe functioning, may be useful for screening. Assessment of functional losses. This may be aided by administration of scales for activities of daily living and instrumental activities of daily living, and assessment at home by an occupational therapist. Psychiatric evaluation is important, as depressive disorder is common in patients with cerebrovascular disease and depression may produce a syndrome resembling dementia. Anxiety disorders and psychotic symptoms may also occur in people with vascular dementia. General physical examination, including pulse irregularity, cardiovascular status, carotid bruits, fundus examination, peripheral vascular disease and hypertension (multiple blood pressure measurements). Examination for focal neurological signs, in particular gait abnormality, visual field defects, pseudobulbar palsy (dysarthria, dysphagia, spastic tongue, brisk jaw jerk), brisk reflexes, extensor-plantar responses and spasticity in the limbs. Routine investigations, including full blood count, erythrocyte sedimentation rate, blood glucose, serum cholesterol and triglyceride level, syphilis serology, electrocardiogram, and chest x-ray. Investigations are directed towards providing evidence for CVD and its risk factors. Structural brain imaging (computed tomography or magnetic resonance imaging) is essential to provide information on the extent, type and distribution of vascular lesions and to exclude other potential causes of dementia, such as subdural haematoma or tumour. Functional imaging, such as single photon emission tomography, positron emission tomography and functional magnetic resonance imaging, may provide further information on the functional significance of any observed lesions or detect abnormalities not apparent on structural imaging. Other specialised investigations may include echocardiography, carotid doppler, antinuclear antibodies, antiphospholipid antibodies, lupus anticoagulant, serum protein electrophoresis and cerebrospinal fluid examination. Back to text 4: Some strategies for primary prevention of vascular dementia Target high risk groups. These include elderly people; people with hypertension, diabetes, atrial fibrillation, or past transient ischaemic attack or stroke; and smokers. Treat hypertension optimally. Treat diabetes. Control hyperlipidaemia. Persuade patients to cease smoking and decrease alcohol intake. Prescribe anticoagulants for atrial fibrillation. Provide antiplatelet therapy for high risk patients. Perform carotid endarterectomy for severe (> 70%) carotid stenosis. Use dietary control for diabetes, obesity and hyperlipidaemia. Recommend lifestyle changes (eg, weight loss, exercise, reduce stress, decrease salt intake). Intervene early for stroke and transient ischaemic attacks with neuroprotective agents (eg, propentofylline, calcium channel antagonists, N-methyl-D-aspartate receptor antagonists, antioxidants). Provide intensive rehabilitation after stroke. Back to text

Perminder S Sachdev · Henry Brodaty