Ageing

Editorial Falls in the elderly: what can be done? We need to streamline referral to falls programs and coordinate services within and outside hospitals MJA 2000; 173: 176-177 Falls are often referred to as one of the "geriatric giants", generating diagnostic and rehabilitative dilemmas for a variety of specialists in a range of settings. In older people, falls are associated with significant mortality and morbidity and frequently lead to a decline in physical and/or psychological function, ultimately encroaching on independence and autonomy. In addition to the costs to the individual and immediate carers, falls consume significant resources in terms of hospital admissions, bed utilisation, and use of other health and allied services. With an ageing population, the problems associated with falls and injury will escalate unless there is a coordinated and effective approach to prevention and intervention. Given that most falls result from a dynamic interaction between intrinsic and extrinsic factors, a multidisciplinary approach to their management -- incorporating medical, functional, and environmental assessment -- is likely to be most rewarding. To date, there is limited evidence to support a population-based preventive strategy -- it thus becomes imperative to focus on high-risk groups with the potential to benefit. For any falls prevention strategy to be effective and of direct clinical relevance, it should: be acceptable and applicable to the affected population (applicability); alter outcome in terms of falls and fall-related injury (efficacy); be cost effective (cost-effectiveness); and be readily applicable to everyday practice (practicability). There is increasing evidence to support intervention in specific populations, although caution is advised when extrapolating results from one setting and population to another. Tinetti and colleagues' seminal article showed the benefits of undertaking risk factor modification in older people in the community with specific risk factors for falls,1 while Campbell et al have shown a reduction in risk of falling after individually tailored home exercise programs for women 80 years or older.2 T'ai chi undertaken in a group setting has also been shown to reduce the risk of recurrent falls.3 More recently, Campbell and colleagues reported a significant reduction in falls after withdrawal of psychotropic medication in older people.4 However, within a month of completion of the study, 47% of their patients had recommenced psychotropic medication, highlighting the need to provide continuing support. The role of the occupational therapist and home environment modification has not been established. A recently published study by Cumming et al showed a reduction in falls in patients having a home environment assessment by an occupational therapist on discharge from hospital.5 Interestingly, the observed reduction was for both indoor and outdoor falls, raising questions as to the mechanism of the observed effect. Perhaps modifying the home environment enhances safety awareness generally. It should be remembered that most people who fall do not sustain any injury and do not present to any medical service,6 despite increasing evidence supporting targeted intervention. Older people presenting to emergency departments are an easily identifiable, high-risk population. Studies have reported that, among older people discharged from emergency departments, up to half show an increase in dependency, usually secondary to trauma.7,8 A two-year follow-up of patients for whom a geriatric consultation was requested in the emergency department showed 34% had died and 52% were in a long term care facility.9 Falls contribute significantly to the emergency department workload, as highlighted by Bell and colleagues in this issue of the Journal.10 They report data on older people presenting after a fall to an inner-city teaching hospital in Sydney. Their results emphasise the multifactorial nature of falls. A UK inner-city teaching hospital with comparable baseline demographics has produced evidence of the benefits of a structured interdisciplinary assessment of such patients.11 The high rate of injury and admission reported by Bell et al is not surprising and reflects our own experience -- elderly people are four to five times more likely to be admitted to hospital than younger people -- and this must be taken into consideration in the context of demographic projections for the next 25-30 years. The emergency department represents a key interface between the hospital and the community and, as such, affords a unique opportunity for interdisciplinary and multiprofessional cooperation across health and social care sectors. However, assessment in the emergency department focuses largely on injury and limited time is available for investigating underlying causes or implementing preventive strategies. It is neither practical nor feasible for all older people who fall to undergo a detailed assessment in the emergency department, or to be assessed by geriatricians. However, using derived and easily identifiable predictors of risk, it is possible to streamline referrals to a falls program or clinic, which would be in keeping with an attainable level of service commitment. Predictors of future risk, as identified in the emergency department, include a history of one or more falls in the previous year, a fall occurring indoors, inability to get up from the floor after a fall, and polypharmacy (four or more regularly prescribed medications).12 Only through effective liaison with services within and outside hospital can we improve the outcome for older people presenting with falls. The increasing provision of falls programs fulfilling the effective intervention criteria provides the ideal opportunity to bring together existing, but frequently fragmented, services to enhance the care of older people. Jacqueline C T Close Physician Clinical Age Research Unit Department of Health Care of the Elderly King's College School of Medicine and Dentistry London, UK jacqueline.closeATkcl.ac.uk Ed Glucksman Physician, Department of Accident and Emergency Medicine King's College Hospital, London, UK Tinetti ME, Baker DI, McAvay G, et al. A multifactorial intervention to reduce the risk of falling among elderly people living in the community. N Engl J Med 1994; 331: 821-827. Campbell AJ, Robertson MC, Gardner MM, et al. Randomised controlled trial of a general practice programme of home based exercise to prevent falls in elderly women. BMJ 1997; 315: 1065-1069. Wolf SL, Barnhart HX, Kutner NG, et al. Reducing frailty and falls in older persons: an investigation of Tai Chi and computerized balance training. Atlanta FICSIT Group. Frailty and Injuries: Cooperative Studies of Intervention Techniques. J Am Geriatr Soc 1996; 44: 489-497. Campbell AJ, Robertson MC, Gardner MM, et al. Psychotropic medication withdrawal and a home-based exercise program to prevent falls: a randomized, controlled trial. J Am Geriatr Soc 1999; 47: 850-853. Cumming RG, Thomas M, Szonyi G, et al. Home visits by an occupational therapist for assessment and modification of environmental hazards: a randomized trial of falls prevention. J Am Geriatr Soc 1999; 47: 1397-1402. Graham HJ, Firth J. Home accidents in older people: role of primary health care team. BMJ 1992; 305: 30-32. Gerson LW, Rousseau EW, Hogan TM, et al. Multicenter study of case finding in elderly emergency department patients. Acad Emerg Med 1995; 2: 729-734. Khan SA, Miskelly FG, Platt JS, Bhattachryya BK. Missed diagnoses among elderly patients discharged from an accident and emergency department. J Accid Emerg Med 1996; 13: 256-257. Sinoff G, Clarfield AM, Bergman H, Beaudet M. A two-year follow-up of geriatric consults in the emergency department. J Am Geriatr Soc 1998; 46: 716-720. Bell AJ, Talbot-Stern JK, Hennessy A. Characteristics and outcomes of older patients presenting to the emergency department after a fall: a retrospective analysis. Med J Aust 2000; 173: 179-182. Close JCT, Ellis M, Hooper R, et al. Prevention of falls in the elderly trial (PROFET): a randomised controlled trial. Lancet 1999; 353: 93-97. Close JCT, Ellis M, Hooper R, et al. Predictors of falls -- results from Prevention of Falls in the Elderly Trial (PROFET). Age Ageing 1999, 28 Suppl 1: 14. Make a comment

Ed Glucksman

Research Characteristics and outcomes of older patients presenting to the emergency department after a fall: a retrospective analysis Anthony J Bell, Janet K Talbot-Stern and Annemarie Hennessy MJA 2000; 173: 179-182 For editorial comment, see Close & Glucksman Abstract - Methods - Results - Discussion - References - Authors' details - - More articles on Emergency medicine Abstract Objectives: To study older patients presenting to the emergency department after a fall -- factors associated with the fall, injuries sustained and outcome. Design: A retrospective analysis using the Emergency Department Information System (EDIS), the Trauma Registry and the patient information database (CCIS), in addition to the patient's emergency and inpatient medical records. Setting: Emergency department of a major inner city teaching hospital, 1 June - 30 November 1997. Patients: All patients over 65 years presenting to the emergency department (ED) after a fall, for whom complete medical records were available. Results: Of 803 patients over 65 years presenting to the ED after a fall, complete records were available for 733 (91.3%) (283 men and 450 women). Extrinsic (accidental) causes were implicated in more than a third of falls (313 patients [42.7%]). A high proportion of the patients were living at home (520; 70.9%) and walking unaided (389; 53.1%). Although absolute numbers of women increased with age, men were as likely as women to present after a fall. Many patients had fallen before -- 39% of the men (111/283) and 24% of the women (110/450). In 78 patients (10.6%), alcohol misuse may have been a direct cause of the fall. The overall injury rate was 70.5% (517/733 patients), the most common injury being an isolated fracture (269/517 patients; 52.0%). In all, 419 patients (57.2%) were admitted to hospital, 48% (200/419) with a fracture and 52% (219/419) for investigation of the medical cause of the fall. The median length of hospital stay was 6 days (mean, 10.4 days; range, 1-129 days); 35% (146/419) of patients were in hospital for more than 10 days. Conclusion: Older patients presenting to the ED after a fall had high injury rates, high admission rates and often prolonged hospitalisation. About a third had fallen before. Patients at risk can be identified in the ED and referred to falls prevention programs. Census data for 1996 show that 12.1% of Australians are aged 65 years or over.1 This proportion is expected to double in the next 40 years,2 with major implications for healthcare costs. Alone, the cost of falls in patients over 70 years in Australia was estimated to be $398 million in 1989.3In the United States, trauma causes a considerable proportion of presentations (and subsequent hospital admissions) of older patients. Falls account for most of these presentations.4 The annual incidence of all falls increases from 25% at age 70 years to 35% after the age of 75; the risk increases with age and is higher among those living in long-stay institutions.5 Up to 10%-15% of falls result in serious injury, of which at least half are fractures. Even falls not resulting in injury may have serious psychological consequences.5,6 The "postfall anxiety syndrome"7 and fear of falling leads to decreased activity,8 and ultimately an increased risk of future falls.9 Patients have reported continued disability two months after a fall.10 No Australian report has been published specifically about patients in this age group presenting to the emergency department (ED) after falls, although previous studies have looked at older people presenting to the ED.11,12 Our aim was therefore to focus on patients over 65 years who presented to our ED as a result of a fall. Several features were of interest: why the patients fell; what, if any, injuries were sustained; what proportion of patients required admission to hospital; and what morbidity and mortality resulted from the fall. Methods Royal Prince Alfred Hospital is a 700-bed tertiary referral centre with 60 000 admissions and 45 000 ED attendances per year. A retrospective review of attendances for the six-month period June - November 1997 was undertaken. All older patients who had fallen were eligible for the study. Patient data Data were obtained from the sources below and thereafter patients remained anonymous. EDIS: Patients eligible for the study were identified by a search of the EDIS (Emergency Department Information System) for "falls" in the age group chosen. EDIS is a computerised database in the ED with demographic information, presenting complaint, diagnosis and disposition for each patient. Medical records: A predetermined dataset was recorded from the medical record for each patient presenting to the ED. This included medical record number, age, sex, type of residence (home, hostel or nursing home), prefall mobility, nature of fall, alcohol misuse, recurrent fall, referral status, triage category, injury score, specific area of the body injured, fracture, admission, specialty, length of stay, mortality, and discharge disposition. Prefall mobility was further defined as unaided versus aided (use of a stick, frame, crutches, assistance by another person) versus unknown. Trauma Registry: Additional data were obtained from the hospital's Trauma Registry. An Injury Severity Score (ISS) is calculated for patients requiring admission after trauma. ISS is the sum of the squares of the highest Abbreviated Injury Scores (an anatomical system classifying injuries by body region on a scale of 1 [minor] to 6 [serious]) for the three most seriously injured body regions. ISS ranges from 1 (minor injury) to 75 (severe injury).13 CCIS: For patients transferred to an affiliated geriatric and rehabilitation hospital, the patient information database (CCIS [Central Sydney Area Health Service Clinical Information System]) was accessed for the length of stay. None of the patients in our study were transferred to non-affiliated geriatric and rehabilitation hospitals. Population data: The Australian Bureau of Statistics supplied population data for the hospital's catchment area.14 Definitions Fall: "Inadvertently coming to rest on the ground or other lower level with or without loss of consciousness."15 Extrinsic (accidental) causes: Environmental factors (eg, rugs, steps, uneven floors). Falls as a result of external trauma, such as motor vehicle accidents and violence, were excluded. Intrinsic (non-accidental) causes: Syncope, dizziness or vertigo, postural drop, central nervous system lesion (haemorrhage or infarct), drop attack, and balance or gait disturbance. Alcohol misuse: A history of alcohol misuse related temporally to the event, a record of alcohol on the breath, or a statement in the ED record about the patient's being intoxicated. Statistical analysis We used Minitab Statistical Software16 for statistical analysis and performed χ2 tests. Analysis was based on age group or sex and compared with a number of variables: presentation as a result of a fall, nature of the fall, outcome of a fracture, and admission status. A multivariate analysis was performed on four aspects of the falls considered to be related to place of residence or mobility: extrinsic cause, recurrent falls, fracture/no fracture and admission. Odds ratios (95% CI) were calculated for each of these groups. Multivariate analysis was also used to calculate odds ratios (95% CI) for whether alcohol use contributed to selected outcomes: admission (yes/no), extrinsic or recurrent falls versus other falls, and age under or over 80 years. Results Patient characteristics Of a total of 22 782 patients presenting to the ED during the six-month study period, 4489 (19.7%) were patients older than 65 years and 803 (17.8%) of these patients presented as a direct consequence of a fall. Of these patients, 733 (91.3%) had medical records available for review at the time of analysis and complete for the purposes of the dataset. Age and sex: The average age was 78.6 years (range, 65-101 years) and the median age was 79 years: 263 patients were aged 65-74 years, 279 were 75-84 years and 191 were 85 years or older. Increasing age of the patients was associated with presenting to the ED as a result of a fall (χ2 test for trend, P < 0.001) (Box 1). There were 283 men and 450 women. However, the number of men and women presenting to the ED after a fall reflected the age and sex distribution within the catchment population (Box 2). Thus, men were as likely as women to present as a result of a fall. Residence: At the time of the fall, 83% (211/253) of the 65-74 year olds, 74% (200/269) of the 75-84 year olds and 57% (109/191) of those over 85 years were living in their own homes. Thus, the proportion of those living in either a hostel or a nursing home increased with advancing age. In 20 patients residence could not be classified. Previous falls: 39% of the men (111/283) and 24% of the women (110/450) had fallen before. Mobility: Patients were classified according to mobility: walking aided or unaided. As expected, as the patients aged the use of a walking aid increased. Cause of fall Extrinsic or intrinsic: Overall, extrinsic causes for the fall accounted for 42.7% of patients presenting to the ED. In the age group 65-74 years extrinsic causes accounted for 49.4% of falls, which is more than expected when compared with the proportion in the older age groups (39.0% and 38.7%, respectively). Intrinsic causes were more likely with advancing age (χ2 test; P = 0.018) and accounted for 50.5% (95% CI, 45%-57%), 60.9% (95% CI, 55%-67%) and 64.2% (95% CI, 54%-68%) of falls in the respective age groups. The breakdown of all causes for falls presenting to the ED is shown in Box 3. Despite extensive review of the medical records we were unable to classify 23% of falls as either extrinsic or intrinsic. Alcohol misuse: This was documented in 78 patients (10.6%): 18% of the 65-74 year olds, 10% of the 75-84 year olds, and was not a factor in those over 85 years (χ2 test; P = 0.001). Sixty-five (83%) of these patients were living in their own homes. Multivariate analysis for alcohol misuse at the time of fall showed it to be significantly associated with an increased risk of both accidental and recurrent falls (Box 4). Outcomes Injury: 517 (70.5%) patients sustained an injury as a result of the fall: 73.3% (379/517) had an ISS of 4 or less (a score of 9 correlated with a femoral fracture); 13 patients had scores between 15 and 25, with all of these patients (except one with spinal cord compression) sustaining intracranial injury. The most common injuries were fractures (36.7%), soft tissue injuries (16%), lacerations and skin tears (14.5%). Fracture: 269 patients (36.7%) sustained a fracture: 36% (98/269) of which were neck-of-femur fractures, 16% fractured wrists, 12% fractured humeral neck and 5% pelvic fractures. The breakdown of fractures in each group is shown in Box 5. Women sustained both neck-of-femur and all fractures more frequently than men (χ2 test; P < 0.001): 64% (63/98) of femoral-neck fractures and 73% (125/171) of all other fractures (95% CI, 66%-80%). Interestingly, in women, the proportion of fractured neck of femur to all fractures was 33.5% (63/188) (95% CI, 27%-40%), whereas in men it was 43% (35/81) (95% CI, 32%-54%). Fracture rate overall was not found to be related to advancing age in either sex. Admission: The total number of patients admitted to hospital was 419, or 57.2% of all older patients with falls (representing 38% of all older patients admitted during the study period). Sixty-three per cent of those 85 years or older were admitted, compared with 60% of the 75-84 year olds and 50% of the 65-74 year olds (χ2 test; P = 0.009). Of the 269 patients with fractures, 200 (74%) were admitted. There was no statistically significant difference in the fracture admission rate across the age groups (χ2 test; P = 0.53). Of the 200 patients admitted, in 49% the cause of the fracture was intrinsic. Patients admitted to hospital after a fall had a mean length of stay of 10.4 days (95% CI, 10.2-10.6) and a median stay of 6 days (range, 1-129 days). Hospitalisation for more than 10 days was necessary in 35% (146/419) of patients. Deaths: Thirty-two patients died in hospital, representing 4.4% of all patients presenting to the ED after a fall: half of those who died were over 85 years of age and half were from nursing homes. In those who died, the cause of the fall was intrinsic rather than extrinsic (27/32), and the most common injury was a fracture of the neck of the femur (10/32). Data analysis: Multivariate analysis of place of residence or mobility and extrinsic cause, recurrent falls, fracture/no fracture and admission showed no significant interaction. Discussion We found that older patients presenting to the ED after a fall had a high injury rate (71%), high admission rates (57%) and often prolonged hospitalisation (> 10 days in about a third of those admitted). Our study complements others performed in Australia and elsewhere on older patients who fall, particularly those who present to an ED.11,12Some studies have found that women in the community fall more frequently than men,17 and others, as we did, found no difference.18 Institutionalised patients have been reported to have higher fall rates than patients living at home,17,19 but most of our patients lived at home and walked unaided. Falls may be caused by an environmental hazard alone or a simple syncopal event, or there may be a complex interaction of environment, physical illness, and type of activity. Changes in vision, vestibular function and proprioception affect physical stability, and musculoskeletal changes affect gait. Postural hypotension from dehydration, drug effects or autonomic dysfunction may be involved. Additionally, acute illness such as respiratory tract infection, arrhythmias, carotid sinus hypersensitivity,20 cardiac failure and neurological problems (eg, Parkinson's disease) may increase the risk of falling. All these intrinsic factors may be compounded by environmental hazards.5,6,17 We found gait disturbance, syncope, central nervous system lesion, postural hypotension and dizziness to be the most common intrinsic causes, and these were statistically more likely to be the underlying reason for a fall as age increased. The proportion of patients with falls in association with alcohol misuse contrasts with the findings of Adams et al.21 They surveyed older patients over an eight-week period for alcohol use, and found a negative relationship between alcohol use and falls. A high proportion of our patients with alcohol misuse lived at home, with perhaps easy access to alcohol. These patients had a greater risk of extrinsic and recurrent falls, a potential relationship that warrants further study. A UK study found that most falls in the community do not result in serious injury.17 We found that patients presenting to the ED after a fall have a high rate of injuries, consistent with previous reports,17,22 but the rate was significantly higher than that found by Tinetti et al.23 We found women to be statistically more likely to suffer a fracture than men. Grisso et al,10 in an older inner-city population in the United States, found that women generally had higher rates of fall injury than men. In addition, they found that injury rates increased with advancing age, a finding that we could not confirm. There were fewer hip fractures in older men than older women in our study, confirming previous findings.24 This is probably related to the higher prevalence of osteoporosis in women. Previous reports have shown that older men with hip fracture have higher mortality rates than age-matched women.23 The high admission rate in our study, which increased in older patients, is only slightly higher than that found by Richardson,11 but this was in patients over 75 years, in whom a higher admission rate is expected. A UK study found admission was needed in only 34% of patients.22 Admission rates for patients with a fracture did not vary significantly across our three age groups, nor were they different according to place of residence or prefall mobility. Length of hospital stay similarly did not depend on place of residence or prefall mobility, differing from the Richardson study, in which a significant relationship was found between accommodation status and outcome at 90 days.11 US studies report that 75% of deaths after a fall occur in patients over 65 years.6 We found that the single most important factor associated with death was hip fracture, a finding similar to that in previous studies.7,11 Modification of the environment and dealing with intrinsic problems such as drug side effects and gait dysfunction can reduce falls,25-27 prevent hospitalisation26 and shorten length of stay.15 If 95% of problems can be identified from the history and physical examination alone, as suggested by Rubenstein et al,15 the emergency physician is well able to identify those patients at risk of further falls. Intrinsic causes can be treated and the patient's general practitioner or specific falls prevention programs can then proceed to modify the risk of recurrence. References Australian Bureau of Statistics. Australia in brief (Census data, 1996). Canberra: ABS, 1998. <www.abs.gov.au> Davis JA. Older Australia: a positive view of ageing. Sydney: Harcourt Brace, 1994. Smith RD, Widiatmoko D. The cost-effectiveness of home assessment and modification to reduce falls in the elderly. Aust N Z J Public Health 1998; 22: 436-440. Spaite DW, Criss EA, Valenzuela TD, et al. Geriatric injury: an analysis of prehospital demographics, mechanisms and patterns. Ann Emerg Med 1990; 19: 1418-1421. Tinetti ME, Speechley M. Prevention of falls among the elderly. N Engl J Med 1989; 320: 1055-1059. Nelson RC, Murlidhar AA. Falls in the elderly. Emerg Med Clin North Am 1990; 8: 309-324. Rubenstein LZ, Josephson KR, Robbins AS. Falls in the nursing home. Ann Intern Med 1994; 121: 442-451. Nevitt MC, Cummings SR, Kidd S, Black D. Risk factors for recurrent nonsyncopal falls: a prospective study. JAMA 1989; 261: 2663-2668. Gostynski M, Ajdacic-Gross V, Gutzwiler F, Michel JP. Epidemiological analysis of accidental falls by the elderly in Zurich and Geneva. Schweiz Med Wochenschr 1999; 129: 270-275. Grisso JA, Schwarz DF, Wishner AR, et al. Injuries in an elderly inner city population. J Am Geriatr Soc 1990; 38: 1326-1331. Richardson DB. Elderly patients in the emergency department: a prospective study of characteristics and outcome. Med J Aust 1992; 157: 234-239. Stathers GM, Delpech V, Raftos JR. Factors influencing the presentation and care of elderly people in the Emergency Department. Med J Aust 1992; 156: 197-200. Baker SP, O'Neill B, Haddon W. The Injury Severity Score. J Trauma 1974; 14: 187. Needs Assessment and Health Outcomes Unit. A demographic profile of the Central Sydney Area Health Service from the 1996 Census. Sydney: Central Sydney Area Health Service, March 1998. Rubenstein LZ, Robbins AS, Josephson KR, Schulman BL. The value of assessing falls in an elderly population: a randomised clinical trial. Ann Intern Med 1990, 113: 308-316. Minitab Statistical Software [computer program], version 12. State College, Pa: Minitab Inc, 1998. Blake AJ. Falls in the elderly. Br J Hosp Med 1992; 47: 268-272. Campbell AJ, Borrie MJ, Spears GF, et al. Circumstances and consequences of falls experienced by a community population 70 years and over in a prospective trial. Age Ageing 1990; 19: 136-141. Cummings SR, Nevitt MC. Falls [editorial]. N Engl J Med 1993; 331: 872-873. Ward CR, McIntosh S, Kenny RA. Carotid sinus hyersensitivity -- a modifiable risk factor for fractured neck of femur. Age Ageing 1999; 28: 127-133. Adams WL, Magruder-Habib K, Trued S, Broome HL. Alcohol abuse in elderly Emergency Department patients. J Am Geriatr Soc 1992; 40: 1236-1240. Davies AJ, Kenny RA. Falls presenting to the Accident and Emergency Department: types of presentation and risk factor profile. Age Ageing 1996; 25: 362-366. Tinetti ME, Speechley M, Ginter SF. Risk factors for falls among elderly persons living in the community. N Engl J Med 1988; 319: 1701-1707. Diamond TH, Thornley SW, Sekel R, Smerdely P. Hip fracture in elderly men: prognostic factors and outcomes. Med J Aust 1997; 167: 412-414. Province MA, Hadley EC, Hornbrook MC, Lipsitz LA. The effects of exercise on falls in elderly patients: a preplanned meta-analysis of the FICSIT trials. JAMA 1995; 273: 1341-1347. Close J, Ellis M, Hooper R, Glucksman E. Prevention of falls in the elderly trial (PROFET): a randomised controlled trial. Lancet 1999; 353: 93-97. Tinetti ME, Baker DI, McAvay G, Claus EB. A multifactorial intervention to reduce the risk of falling among elderly people living in the community. N Engl J Med 1994; 331: 821-827. (Received 10 Aug 1999, accepted 29 May 2000) Authors' details Department of Emergency Medicine, Royal Prince Alfred Hospital, Sydney, NSW. Anthony J Bell, MB BS, Emergency Medicine Registrar. Janet K Talbot-Stern, MD, FACEM, FACEP, Director, Emergency Department; and Clinical Senior Lecturer, Department of Surgery, University of Sydney. Department of Medicine, University of Sydney, Sydney, NSW. Annemarie Hennessy, MB BS, PhD, Senior Lecturer. Reprints will not be available from the authors. Correspondence: Dr A J Bell, Department of Emergency Medicine, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW 2050. Make a comment 1: Patients presenting to the emergency department, by age group, June - November, 1997 65-74 years (n=2060) 75-84 years (n=1672) ≥85 years (n=757) Total (n=4489) Presentation after a fall Other presentations 295 (14.3%) 1765 317 (19.0%) 1355 191 (25.2%) 566 803 (17.9%) 3686 χ2 test for age trend (P<0.001). Back to text 2: Age and sex distribution of patients presenting to the emergency department after a fall compared with the catchment population 65-74 years 75-84 years ≥85 years Men Presentation after a fall Proportion of catchment population 124/263 (47%) 15415/32185 (47.9%) 107/279 (38%) 7251/18448 (39.3%) 52/191 (27%) 1650/6038 (27.3%) Women Presentation after a fall Proportion of catchment population 139/263 (53%) 15770/32185 (49.0%) 172/279 (62%) 11187/18448 (60.6%) 139/191 (73%) 4388/6038 (72.7%) Back to text Back to text 4: Multivariate analysis (logistic regression) of alcohol misuse and selected variables in older patients presenting to the emergency department after a fall Variable Alcohol misuse odds ratio (95% CI) Age at presentation 5.5 (2.8-10.6) Extrinsic cause of fall 1.72 (1.05-2.83) Recurrent falls 2.24 (1.35-3.72) Back to text 5: Fractures in older patients presenting to the emergency department after a fall, by age group (years) Fracture 65-74 (n=263) 74-85 (n=279) >85 (n=191) Total (n=733) Neck of femur 28 (11%) 37 (13%) 33 (17%) 98 (13.4%) Other 74 (28%) 59 (21%) 38 (20%) 171 (23.3%) No fracture 161 (61%) 183 (66%) 120 (63%) 464 (63.3%) Back to text

Anthony J Bell · Janet K Talbot-Stern · Annemarie Hennessy

Editorial Alcohol and cardiovascular disease: still a research priority? MJA 2000; 173: 116-117 More precision in measuring drinking levels and patterns will give a firmer basis for advice about drinking The evidence amassed to date on the link between moderate alcohol intake and reduced risk of dying of cardiovascular disease might be thought already sufficient to bracket sceptics of alcohol's protective effect with doubters of manned lunar missions and members of the Flat Earth Society. Published studies demonstrating this link can now be counted in the hundreds, and no fewer than six plausible underlying biological mechanisms have been identified.1 In this issue of the Journal yet another study reports this link: Simons and colleagues show moderate alcohol intake to be associated with increased survival in elderly people.2 Their study is an elegant example of the genre and drawn from a highly respected prospective study of risk factors for death and illness in the population of Dubbo, New South Wales. The two fields of epidemiology and alcohol studies have much to learn from each other Alternative explanations for the protective effect of moderate alcohol intake, relying on ever more tenuous confounding effects, have been discredited one by one. The apparently protective effect of moderate alcohol consumption has so far survived the use of controls for sociodemographic status,3 for the "sick quitter hypothesis"4 (ie, the suggestion that many abstainers have stopped drinking because of serious illness), for the amount of cholesterol in the diet,5 and even for the degree of social isolation.6 As evidenced in the study by Simons et al,2 the protective effect is fairly specific to cardiovascular disease and does not operate for other major causes of death in older people such as cancer. While a handful of recent studies have failed to find a protective effect for moderate drinking,7,8 these are still heavily outnumbered by those with positive findings.1 In fact, the range of different countries and cultures in which the phenomenon has been documented is also testimony to its robustness, even if different levels of consumption appear to provide the benefit in different drinking cultures.1 So, does medical science need further research on this topic? My contention is that, while the basic protective properties of moderate alcohol consumption appear to have been identified, the precision of the measurement of drinking levels and patterns in these studies needs to be sharpened if we are to have a firmer basis for advising people how to drink to avoid ill-health. The recent major systematic review commissioned by the National Health and Medical Research Council to underpin revisions to Australia's national guidelines on low risk drinking found that nearly all epidemiological studies in this area only attempt to measure one of the important dimensions of alcohol consumption: total volume of drinking, usually expressed as average intake per day.1 Despite recent evidence that pattern of drinking plays a role independent of volume,9 large-scale epidemiological studies rarely include simple items in their questionnaires tapping this dimension, such as frequency of drinking five or more drinks in one day, or maximum amount consumed on one day. Simons et al make a rare contribution to our knowledge by providing an analysis of mortality risk, based not only on average volume of alcohol across all days, but also on usual amount consumed on a drinking day. Clearly, these can be very different measures (eg, seven drinks in a day once a week versus one drink every day of the week).2 While the power of the analyses in Simons et al is limited by sample size, usual consumption of five or more drinks for men and of three or four drinks in a day for women was not associated with a significantly reduced risk of death.2 It should be noted, however, that questions regarding "usual" consumption tend to suffer from a bias towards low-consumption occasions and against less frequent occasions of high intake.10 Forthcoming World Health Organization guidelines on measurement of alcohol consumption advise that a superior method is the "graduated quantity frequency", in which respondents are asked how often they drink at each of different levels of consumption, starting with the highest (eg, "How often do you drink 20 drinks on one day?").10 The same guidelines identify another problem bedevilling attempts to convert the results of alcohol studies into precise advice for drinkers: assumptions about the alcohol content of drinks reported vary between studies and are usually not empirically based. A number of studies from different countries have attempted to document usual-serve sizes employed by random samples of drinkers and found these to vary significantly from those usually assumed by researchers.11,12 One study found that the bias created towards under-reporting of consumption was massive in one particular population subgroup: Afro-American women.13 One striking consequence of a failure to measure pattern of alcohol consumption adequately can be the false identification of special benefits from one type of alcoholic beverage over another. Wine is often reported as being most associated with benefits, but being a wine drinker as opposed to a beer and spirits drinker is a marker for many other things, including a tendency towards a more consistent pattern of daily drinking rather than occasional "bingeing".14 A well known Danish study,3 often cited as evidence for a greater benefit of wine over other drinks, measured alcohol consumption by only asking about how much people usually drank if they drank every day. Because this is a less frequent pattern for heavy drinkers of beer and spirits, many of the latter will have been falsely categorised as light or moderate drinkers, thus significantly biasing against finding protective effects for these beverages. The two fields of epidemiology and alcohol studies have much to learn from each other. If epidemiological studies of risk factors for heart disease do not improve their measurement of patterns and levels of alcohol use, it will remain very hard to give precise advice to drinkers who wish to minimise harms and maximise benefits of alcohol consumption. In reality, despite hundreds of studies into the protective effects of alcohol in relation to heart disease, research into this area has only just begun. Timothy R Stockwell Director National Centre for Research into the Prevention of Drug Abuse Curtin University of Technology, Perth, WA Single E, Ashley MJ, Bondy S, et al. Evidence regarding the level of alcohol consumption considered to be low-risk for men and women. Final report. Canberra: National Health and Medical Research Council, 2000. URL: <http://www.nhmrc.health.gov.au/advice/alc-comp.htm> (accessed 29 June 2000). Simons LA, McCallumJ, Friedlander Y, et al. Moderate alcohol intake is associated with survival in the elderly: the Dubbo Study. Med J Aust 2000; 173: 121-124. Gronbaek M, Deis A, Sorensen TIA, et al. Mortality associated with moderate intakes of wine, beer or spirits. BMJ 1995; 310: 1165-1169. Rehm J, Sempos CT. Alcohol consumption and all-cause mortality: questions about causality, confounding and methodology. Addiction 1995; 90: 493-498. Rehm J, Sempos CT. Alcohol consumption and all-cause mortality. Addiction 1995; 90: 471-480. Murray RP, Rehm J, Shaten J, Connett JE. Does social integration confound the relation between alcohol consumption and mortality in the Multiple Risk Factor Intervention Trial (MRFIT)? J Stud Alcohol 1999; 60: 740-745. Leino EV, Romelsjo A, Shoemaker C, et al. Alcohol consumption and mortality. II. Studies of male populations. Addiction 1998; 93: 205-218. Hart CL, Smith GD, Hole DJ, Hawthorne VM. Alcohol consumption and mortality from all causes, coronary heart disease, and stroke: results from a prospective cohort study of Scottish men with 21 years follow up. BMJ 1999; 318: 1725-1729. Rehm J, Ashley KJ, Room R, et al. On the emerging paradigm of drinking patterns and their social and health consequences. Addiction 1996; 91: 1615-1621. World Health Organization (Substance Abuse Department). International guidelines for monitoring alcohol consumption and harm. Geneva: WHO. In press. Stockwell T. Information provided in Australia about the size of "standard drinks". Med J Aust 1992; 156, 295. Lemmens P. The alcohol content of self-report "standard drinks". Addiction 1994; 89: 593-602. Kaskutas L, Graves K. An alternative to standard drinks as a measure of alcohol consumption. Paper presented at International Conference on the Measurement of Drinking Patterns, Alcohol Problems and the Connection; 2000 April 2-7; University of Stockholm, Sweden. In press. Doll R. One for the heart. BMJ 1997; 315: 1664-1668. Make a comment

Timothy R Stockwell

Caring For Older People Healthcare for older people in residential care -- who cares? Leon Flicker MJA 2000; 173: 77-79 Increasing needs should be met with improved organisation of services Recently in Melbourne, several older people in a high-level-care residential facility (nursing home) were reportedly found to have an infestation with the mite Sarcoptes scabiei. They were supposedly treated with a dilute topical application of a mixture of volatile hydrocarbons, commonly known as kerosene. Quite rightly, this practice was widely condemned,1 as it does not conform to accepted evidence-based guidelines, which recommend the topical application of compounds such as permethrin, which are safer and more effective.2 This incident has raised questions as to whether the standard of healthcare is adequate throughout the residential care industry. The residential care system has undergone major changes over the past 15 years. It is a system that has traditionally been divided into two tiers: high-level care (nursing home care) and low-level care (hostel care). This situation has been somewhat muddled by legislative changes enacted in October 1997 allowing residential care facilities to house residents of any degree of dependency, and in fact 18% of residents in hostels are classified as requiring "high-level" care (Commonwealth Department of Health and Aged Care, WA Branch, personal communication), a situation that should mean that nursing attention is available 24 hours a day.3 However, statistics analysed and reported by the Federal Government over the period 1985-1997 demonstrate a consistent trend towards fewer nursing home beds and slightly more hostel beds,3 a trend which has probably continued over the past three years. Despite a rapidly ageing population, there has been virtually no growth in the number of nursing home places. In Australia there were 71 503 nursing home beds in 1985 and 74 233 in 1997 -- a reduction in the ratio of beds per 1000 persons aged 70 years and over from 66.5 to 47.6. Over the same period, there has been real growth in the number of hostel places from 34 885 to 64 825 places, or an increase in the ratio from 32.5 to 41.6 beds per 1000 persons aged 70 years and over. These changes have produced predictable results, with a notable and sustained increase in levels of dependency of residents in nursing homes and hostels. In 1987, 30% of permanent nursing home residents were categorised as "high dependency" (Residential Classification Scale Index 1 or 2); in 1997, this proportion was 56%. In 1992, only 54% of hostel residents required assistance with personal care, whereas in 1997, 80% of residents required such assistance.3 Older people in residential care are the sickest and frailest subsection of an age group that manifests the highest rates of disability in the Australian population. For example, in 1998, only 5.2% of people aged 65-69 years required assistance with self-care activities (eg, bathing, dressing, grooming), while in the age group 80 years and over 31.4% of people required such assistance.3 As people age, they are not only more likely to have a severe or profound disability but are also more likely to be cared for in residential care. Approximately 15% of Australians aged over 65 years living in the community have a severe or profound disability, whereas 93% of people in residential care have such a disability. While one-third of older Australians aged 65 years and over with severe or profound disability live in non-private dwellings, the rates rise from only 13% of the 65-69-year-old group to over 50% of women over the age of 80 years. This increase is almost certainly due to two main factors: the decreased availability of informal carers for the oldest age group, and the increasing level of disability. What are the medical conditions underlying these dependency statistics? Unfortunately, although the Federal Government is responsible for both medical and residential care, few data are available on the common medical conditions of elderly people in residential care. Probably the commonest condition seen in these people is some form of dementia. In 1996, there were an estimated 134 809 people with dementia in Australia (this estimate does not include all people with mild disease).4 Approximately half of these individuals were housed in residential care.3 Estimates of the prevalence of dementia in people in hostels and nursing homes were 28% and 60%, respectively, although rates of cognitive impairment were even more alarming, at 54% and 90%, respectively.5 The main disabling conditions of the 707 600 people aged 65 years and over with a profound, severe or moderate disability (less than 20% of whom were housed in residential care) were arthritis, other musculoskeletal conditions, dementia, eye disease and stroke.3 It would appear that much of the disability suffered by people in residential care is related to chronic degenerative conditions. The pressure of caring for people with increasingly complex and disabling conditions within the residential care system may place other parts of the healthcare system under stress -- for example, the readmission of nursing home patients to the acute hospital system with acute complications of chronic medical problems. Such admissions (eg, the referral to an acute hospital of a nursing home resident with severe Alzheimer's disease complicated by hypostatic pneumonia) may be precipitated by avoidance of ethically difficult management decisions. Another part of the health and welfare system that may come under pressure is community care, despite substantial real increases in Commonwealth expenditure on Home and Community Care (HACC). This expenditure has increased, in inflation-adjusted terms, from $561 million in the financial year 1991-92 to $799 million in 1997-98.3 The pressure exerted by reduced availability of residential care has led to a waiting time of several weeks for community care in many parts of Australia, despite the necessity of providing care to patients discharged from a crowded acute hospital system. How should the provision of healthcare for people in nursing homes and hostels be organised? This issue has essentially not been addressed to date, and improvement in this area will require more than increased funding. Over the past 15 years, the focus of aged care services has been to prevent or delay the need for residential care by comprehensively assessing patients to identify those who might benefit from multidisciplinary rehabilitation and community services. The rationale for this approach is sound and clearly evidence based,6 and the policy has been very successful. While cynics may claim that the Federal Government has promoted the policy to halt the previous exponential growth in nursing home care, there is no doubt that older people themselves eschew the residential care option to remain in their own homes, if at all possible.7 However, the healthcare of people who go into residential care seems to be far less coordinated. Recent developments (part of the Enhanced Primary Health Care Initiative) that support medical practitioners in screening the over-75-years group and in care planning, exclude people in nursing homes. Furthermore, the organisation and proposed evaluation of this initiative do not appear ideal.8The very high prevalence of cognitive impairment among people in residential care limits the usefulness of surveying residents about their perceived needs and decreases their ability to be effective advocates for their own care. I believe several steps need to be taken to improve healthcare for people in residential facilities: We need to recognise that most older people do not choose residential care for "social" reasons. They do so because of chronic medical conditions resulting in permanent disability. Healthcare professionals need professional development involving training, peer review and transparency of operations, something that is apparent from the experience of acute care hospitals. (While accreditation of facilities may be a useful and long overdue stage in the development of residential care facilities, it is unlikely to improve the quality of healthcare provided.) Educational institutions, expert groups and professional organisations need to form strategic partnerships to establish what is currently accepted best practice in residential care and where investment should be made in targeted research. Health professionals working in the residential care environment should be trained in dealing with people who have major disabilities. This particularly applies to general practitioners, who should be encouraged to acquire specific qualifications and rewarded by increased remuneration. We need to develop a multidisciplinary team approach to healthcare delivery in residential facilities. Appropriate agencies, such as governments and private health insurers, need to provide sufficient funding to support the level of professional care required. Medical practitioners and some other health professionals may be able to get expert support from regional aged care teams; however, these services are currently under considerable stress because their funding has not kept pace with the increasing number of older people requiring care.3 A wider role for geriatricians and psychogeriatricians in supporting these developments is crucial.9 There is no need for the widespread nihilism that has pervaded the issue of healthcare in residential facilities -- indeed, it has been shown that legislative changes10 and educational initiatives11 can decrease the rate of inappropriate psychotropic drug use in nursing home residents. Healthcare for people in residential care is provided not only by medical practitioners, but also by other professionals. The largest group of professional carers are nurses, for whom professional and best practice guidelines are similarly underdeveloped. For example, there are no guidelines specifying which of the available care strategies for people with dementia (such as validation therapy,12 reality orientation13 or reminiscence therapy14) works best, and for whom. Similarly, other healthcare workers, such as dentists, pharmacists and allied health practitioners, all need to pay special attention to this vulnerable section of the population. A recent survey of Adelaide dentists15 revealed that their interest in and provision of services to people in residential care were low and that dentists provided little educational assistance for staff of nursing homes. A concurrent survey of the needs of the residents found a high level of standard dental treatment needs, with the severely cognitively impaired residents having the highest incidence of oral disease.15 Clearly, a diverse range of best practice guidelines for the care of residents of nursing homes and hostels is needed, together with appropriate resources to implement them. It is sometimes argued that these residents have "reached the end of the road" and that further attention to their needs is unjustified. This argument is usually rejected by the very many Australians whose relatives and friends are housed in residential care. Perhaps more telling is the realisation that entry into residential care is a common occurrence in our society, and in fact any individual who lives to the age of 65 years has a 33% chance of requiring a nursing home bed during their remaining life and a 20% chance of requiring a hostel bed.3 It is in the interests of all members of society to provide more adequate healthcare in this challenging environment. Disclosure statement: No conflict of interest. References Kerin J. Care for aged: a kerosene dip. The Australian Feb 25, 2000: 5. Walker GJA, Johnstone PW. Interventions for treating scabies. The Cochrane Library. Issue 1. Oxford: Update Software, 2000. Updated quarterly. Gibson D, Benham C, Racic L, editors. Older Australia at a glance. Canberra: Australian Institute of Health and Welfare, 1999. (Catalogue No. AGE 12.) Henderson AS, Jorm AF. Dementia in Australia. Canberra: AGPS, 1998. Rosewarne R, Opie J, Bruce A, et al. Care needs of people with dementia and challenging behaviour living in residential facilities. Canberra: AGPS, 1997. Stuck AE, Siu AL, Wieland GD, et al. Comprehensive geriatric assessment: a meta-analysis of controlled trials. Lancet 1993; 342: 1032-1036. McAllister NL, Hollander MJ. Seniors' perceptions of and attitudes towards the British Columbia continuing care system. Health Rep 1993; 5: 409-418. Byles JE. A thorough going over: evidence for health assessments for older persons. Aust N Z J Public Health 2000; 24: 117-123. Draper BM. Medical care in aged-care facilities: new directions. Med J Aust 1999; 171: 94-96. Hughes CM, Lapane KL, Mor V. Impact of legislation on nursing home care in the United States: lessons for the United Kingdom. BMJ 1999; 319: 1060-1063. Snowdon J. Follow-up survey of psychotropic drug use in Sydney nursing homes. Med J Aust 1999; 170: 299-301. Neal M, Briggs M. Validation therapy for dementia. The Cochrane Library. Issue 1. Oxford: Update Software, 2000. Updated quarterly. Spector A, Orrell M, Davies S, Woods B. Reality orientation for dementia. The Cochrane Library. Issue 1. Oxford: Update Software, 2000. Updated quarterly. Spector A, Orrell M, Davies S, Woods RT. Reminiscence therapy for dementia. The Cochrane Library. Issue 1. Oxford: Update Software, 2000. Updated quarterly. Australian Institute of Health and Welfare Dental Statistics and Research Unit. The Adelaide dental study of nursing homes. Research report. [Adelaide]: AIHW, October 1999. (Catalogue No. DEN 50.) Make a comment

Leon Flicker

Fitness And Health Healthy ageing: what role can physical activity play? Adrian E Bauman and Ben J Smith MJA 2000; 173: 88-90 Moderate activity is clearly beneficial for elderly people and should be actively promoted by general practitioners Epidemiological evidence - Strength, flexibility and prevention of falls in the elderly - Special needs of the frail elderly - Implications for practice - References - Authors' details - - More articles on General practice and primary care In an ageing Australia, important approaches to spiralling healthcare costs are primary and secondary prevention. The second most important area for risk factor reduction, after tobacco use, is physical inactivity, in terms of its contribution to the overall burden of disease for Australia.1 This applies equally to older patients and to the general community. Recent evidence, summarised in the 1996 United States Surgeon General's Report and elsewhere, has identified consistent epidemiological evidence for health benefits of physical activity at least as great as treating hypertension or cholesterol reduction.2,3Nonetheless, physical activity remains a poor relation in population disease prevention. In contrast to exponential increases in the volume of research in exercise science or broader disease prevention, research into physical activity in the elderly has remained quite static over recent decades.4 Our purpose was to review the available evidence for health benefits of physical activity among older adults. A summary of our key points is given in the Box. Epidemiological evidence The benefits of regular moderate physical activity are now acknowledged internationally.2,3 Health benefits for older adults are mostly similar to those for the general community: there is evidence of reduced risk of all-cause mortality and reduced rates of coronary heart disease among moderately active elderly men and women.2Population studies in diverse cohorts (such as 40 000 Iowan postmenopausal women and 472 elderly Dutch men) report similar findings -- a graded dose-response relationship between activity and all-cause mortality and coronary heart disease deaths.5,6 A South Australian study identified a mortality risk 74% greater in elderly people who were completely sedentary, compared with the (mostly moderately) active.7 Further, even those aged over 60 years who change from being sedentary to engaging in at least moderate levels of activity accrue a clear health benefit.8 New findings repeatedly confirm that aerobic or vigorous activities are not essential for these cardiovascular benefits. For those who are sedentary, accumulating half an hour of moderate activity on most days of the week seems sufficient. This finding is replicated across studies which adjust for other risk factors and for clinical comorbidity, and which measure physical activity in diverse ways. This notion is particularly important for older adults, where adherence to physical activity will be much more likely if they perceive they are capable of performing the activity, such as moderate walking.9 There is good evidence that regular moderate activity protects against the development of diabetes in populations quite independent of body weight.2,3,10 Up to half of people with diabetes are completely sedentary,11 presenting a further clinical opportunity for secondary prevention, as physical activity is part of optimal management. Moderate physical activity may also reduce the risk of ischaemic stroke in the elderly,12 and there is clear evidence, pooled across almost 30 studies, that physical activity reduces colon cancer risk, and may have a role in reducing breast cancer incidence in postmenopausal women.2,3 In addition, physical activity is recognised as being associated with improved mental health, and is a clinical approach to mild anxiety and depression.2 Cohort studies in the elderly show that more active people have a reduced risk of developing depression, and are more likely to maintain wellbeing.13 Clinical data suggest that moderate exercise regimens are anxiolytic, but that vigorous activity may have less effect, or even be counterproductive, among older adults. Finally, the quality and duration of sleep may be improved by activity, both for those living in the community14 and for nursing home residents.15 One important idea raised by the epidemiological literature is the notion of "compression of morbidity". Population studies suggest that the "disability-free years" can be increased in people who remain active,16 and that overall healthy lifestyles could postpone disability by up to five years.17 This has ramifications for improved functional status and quality of life. The concept of risks versus benefits of activity is worth exploring. The transient increases in the risk of acute cardiac events and sudden death following bouts of vigorous activity are not found for moderate activity, and overall, even for vigorous activity, the benefits outweigh the risks. This provides further support for encouraging moderate activity in middle-aged and older adults. Strength, flexibility and prevention of falls in the elderly Physical activity is commonly seen as a means of maintaining strength and vigour, and staving off the functional declines of ageing. Muscle strength is closely related to functional capacity, and has consistently been found to improve as a result of progressive resistance training.18 Resistance training techniques include using gymnasium equipment and elastic tubing, home-based exercise and even walking. Strength-building programs have additional benefits, such as improving mobility and balance and aiding in weight maintenance. Physical activity can help improve balance. This in turn helps older people by improving mobility and functional capacity, and reducing the risk of falls and injuries. Regular, gentle exercise classes, involving aerobic, strength, balance and coordination activities, improve balance when undertaken twice weekly over 12 months.19 Even a supervised program of gentle exercise such as tai chi may help to maintain balance.20 Flexibility is another domain of physical performance that is necessary for daily activities such as climbing stairs, rising from a chair or bed, or walking. The evidence is less clear here, but some studies have shown yoga and flexibility training, supervised aerobics classes and walking and upper-body training can benefit flexibility.21 Two key public health issues related to these areas of physical functioning are osteoporosis, and falls and injuries. Some studies indicate that older people who have stayed active have significantly lower losses of bone mineral density than their sedentary counterparts. However, as bone mineralisation is completed by late adolescence, strategies later in life may have less of a role in preventing osteoporosis. The American College of Sports Medicine concluded that functional loading through physical activity exerts a positive influence on bone mass, but that the types of program that may be most effective in producing beneficial results are still uncertain.21 Physical activity is a beneficial component of falls prevention, because of its effects on muscle strengthening and balance, and possibly on bone density. In the meta-analysis of the seven Frailty and Injuries Cooperative Studies Intervention Trials (FICSIT), participation in an exercise program was found to reduce the risk of falling, although some programs were supplemented by education and other interventions.22 The Cochrane review also found that activity had a beneficial role, particularly when supplemented by additional measures such as medications review and home modification among elderly people identified as at risk of falling.23 Many of these studies used supervised rather than at-home exercise interventions. Special needs of the frail elderly Initiating activity programs is more problematic in the frail elderly or in those with multiple comorbidities. This group may require medical screening and assessment before they begin. The frail elderly have typical problems that may make physical activity more difficult. Many may benefit from more moderate or even light activities; many of these can be carried out in residential settings and community centres. Apart from walking programs, other locally based interventions to improve mobility, increase strength and improve balance can be implemented and achieve improvements in this age group.15,21 In addition to strength training, working to reduce polypharmacy, and making residential environments more physical activity friendly are also important. A recent controlled trial has identified positive outcomes of intensive exercise and resistance training among 100 hostel residents with a mean age of 87 years -- even in this frail elderly group physical activity, gait velocity and muscle strength improved.24 Implications for practice There are two quite distinct forms of recommendation for physical activity. One is the opportunistic recommendation for regular walking and moderate activity for all adults to prevent chronic disease; the other focuses on strength, mobility and balance, and has quality-of-life and falls prevention benefits among older age groups, but may require more intensive program attendance. Recommending physical activity to people over 65 is cost effective,25 and a worthwhile part of many patient encounters in general practice. The counselling objectives are to identify achievable, moderate activities, increase confidence among patients that they can perform the activity, and highlight the importance of these activities in delaying disability. It is useful to know about local programs for referring patients to, and to encourage people to exercise with someone else. A New Zealand study identified general practice-based advice as being more effective if focused on written "exercise prescriptions" rather than verbal advice alone.26 However, it is not easy to train doctors to promote physical activity to the elderly,27 and other strategies may support this process. Given the time constraints of practice, allied health professionals may provide specialised counselling in this area. Another New Zealand study ascertained lower rates of falls among women aged over 80 years who were referred to a physiotherapist for an exercise intervention delivered through general practice.28 These improvements were maintained even at two years of follow-up. In a Victorian controlled trial, education of practitioners, extensive GP advice and home follow-up increased physical activity time per week among patients aged at least 65 years.29 Further, in this issue of the Journal, Halbert and colleagues show that having a qualified exercise scientist in the GP's surgery to provide detailed advice and exercise plans provided a sustained increase in self-reported physical activity.30 Thus, adjunctive methods like these may enhance the range of health outcomes, and achieve more than GP advice alone. It appears that many of the benefits of activity are reasonably acute, and it may be recent physical activity which confers many of the chronic disease and musculoskeletal benefits.21,31 Hence the advice "use it or lose it" should be as prevalent as antismoking messages. Given the credibility with which doctors' advice about exercise in older adults is perceived in the general community,32 each consultation presents an important -- and possibly overdue -- opportunity for promoting health to older adults. References Mathers C, Vos T, Stevenson C. The burden of disease and injury in Australia. AIHW publication PHE 17. Canberra: Australian Institute of Health and Welfare, 1999. US Surgeon General's Report. Physical activity and health. Atlanta, Ga: US Department of Health and Human Services, Centers for Disease Control, 1996. Bauman A, Owen N. Physical activity of adult Australians: epidemiological evidence and potential strategies for health gain. J Sci Med Sport 1999; 2: 30-41. Lidor R, Miller U, Rotstein A. Is research on aging and physical activity really increasing? A bibliometric analysis. J Aging Physical Activity 1999; 7: 182-195. Bijnen FCH, Feskens EJM, Caspersen CJ, et al. Baseline and previous physical activity in relation to mortality in elderly men -- The Zutphen Elderly Study. Am J Epidemiol 1999; 150: 1289-1296. Kushi LH, Fee RM, Folsom AR, et al. Physical activity and mortality in post-menopausal women. JAMA 1997; 277: 1287-1292. Finucane P, Giles LC, Withers RT, et al. Exercise profile and subsequent mortality in an elderly Australian population. Aust N Z J Public Health 1997; 21: 155-158. Blair SN, Kohl HW, Barlow CE, et al. Changes in physical fitness and all cause mortality: a prospective study of healthy and unhealthy men. JAMA 1995; 273: 1093-1098. Kriska A. Physical activity and the prevention of type 2 diabetes mellitus. How much for how long? Sports Med 2000; 29: 147-151. Hu FB, Sigal RJ, Rich-Edwards JW, et al. Walking compared with vigorous physical activity and risk of type 2 diabetes in women. A prospective study. JAMA 1999; 282: 1433-1439. Hays LM, Clark DO. Correlates of physical activity in a sample of older adults with type 2 diabetes. Diabetes Care 1999; 22: 706-712. Wannamethee SG, Shaper AG. Physical activity and the prevention of stroke. J Cardiovasc Risk 1999; 6: 213-216. Morgan K, Bath PA. Customary physical activity and psychological wellbeing: a longitudinal study. Age Ageing 1998; 27 Suppl 3: S35-S40. King AC, Oman RF, Brassington GS, et al. Moderate intensity exercise and self rated quality of sleep in older adults. A randomised controlled trial. JAMA 1997; 277: 32-37. Alessi CA, Yoon EJ, Schnelle JF, et al. A randomized trial of a combined physical activity and environmental intervention in nursing home residents: do sleep and agitation improve? J Am Geriatr Soc 1999; 47: 784-791. Leveille SG, Guralnik JM, Ferrucci L, Langlois JA. Aging successfully until death in old age: opportunities for increasing active life expectancy. Am J Epidemiol 1999; 149: 654-664. Vita PJ, Terry RB, Hubert HB, Fries JF. Aging, health risks, and cumulative disability. N Engl J Med 1998; 338: 1035-1041. Healthy ageing and physical activity. State Health Publication No. (HP) 980195. Sydney: New South Wales Health Department,1999. Lord S, Ward J, Williams P, Strudwick M. The effect of a 12-month exercise trial on balance, strength, and falls in older women: a randomised controlled trial. J Am Geriatr Soc 1995; 43: 1198-1206. Wolfson L, Whipple R, Derby C, et al. Balance and strength training in older adults: intervention gains and Tai Chi maintenance. J Am Geriatr Soc 1996; 44: 498-506. American College of Sports Medicine. Position stand on exercise and physical activity for older adults. Med Sci Sports Exercise 1998; 30: 992-1008. Province M, Hadley E, Hornbrook M, Lipsitz L. The effects of exercise on falls in elderly patients: a preplanned meta-analysis of the FICSIT trials. JAMA 1995; 273: 13411-1347. Gillespie L, Gillespie W, Cumming R, et al. Interventions to reduce the incidence of falling in the elderly. Cochrane Database Systematic Reviews 1998; 3. Fiatarone MA, O'Neill EF, Ryan ND, et al. Exercise training and nutritional supplementation for physical frailty in very elderly people. N Engl J Med 1994; 330: 1769-1775. Munro J, Brazier J, Davey R, Nicholl J. Physical activity for the over 65s: could it be a cost effective exercise for the NHS? J Public Health Medicine 1997; 19: 397-402. Swinburn B, Walter LG, Aroll B, et al. The green prescription study: a randomised controlled trial of written exercise advice provided by general practitioners. Am J Public Health 1997; 88: 288-291. Eckstrom E, Hickam DH, Lessler DS, Buchner DM. Changing physician practice of physical activity counselling. J Gen Intern Med 1999; 14: 376-278. Campbell AJ, Robertson CM, Gardner MM, et al. Falls prevention over two years: a randomised controlled trial in women aged over 80 years. Age Ageing 1999; 28: 513-518. Kerse NM, Flicker L, Jolley D, et al. Improving the health behaviours of elderly people: randomised controlled trial of a general practice education programme. BMJ 1999; 319: 683-687. Halbert JA, Silagy CA, Finucane PM, et al. Physical activity and cardiovascular risk factors: effects of advice from an exercise specialist in Australian general practice. Med J Aust 2000; 173; 85-87. Sherman SE, D'Agostino RB, Silbershatz H, Kannel WB. Comparison of past versus recent physical activity in the prevention of premature death and coronary artery disease. Am Heart J 1999; 138: 900-907. Booth M, Bauman A, Owen N, Gore C. Physical activity preferences and sources of assistance, and perceived barriers to increase activity among physically inactive Australians. Preventive Med 1997; 26: 131-137. Authors' details School of Community Medicine, University of New South Wales, Sydney, NSW. Adrian E Bauman, FAFPHM, PhD, Professor of Public Health and Epidemiology, School of Community Medicine, University of New South Wales. National Centre for Health Promotion, University of Sydney, NSW. Ben J Smith, MPH, Research Assistant. Reprints will not be available from the authors. Correspondence: Professor A E Bauman, Epidemiology Unit, Locked Bag 7017 Liverpool BC, NSW 1871. Make a comment Evidence for physical activity and exercise promotion in the elderly Evidence for: Level of evidence Comments Decreased incidence of and mortality from cardiovascular disease and diabetes with moderate activity Level III Replicated across many well designed population-based cohort studies Decreased incidence of falls in the elderly who engage in regular physical activity Level I and II Some systematic review data, several individual randomised controlled trials; needs resistance training, as well as training for balance and gait Improved functional status and quality of life in the elderly who engage in regular physical activity Level II and III Some randomised controlled trials for functional status; mostly observational (cohort) studies for quality of life Benefit of counselling and advice for moderate physical activity from general practitioners Level II Several randomised controlled trials but effects are modest; may be better if written advice is given, and if allied health professionals are involved Back to text

Adrian E Bauman · Ben J Smith

Editorial Clinical pathways and fractured neck of femur The generalisability and cost effectiveness of clinical pathways need further research MJA 2000; 172: 415-416 The proportion of Australians aged 65 and over is projected to continue increasing for the next 50 years.1 Fractures of the neck of femur are common in this age group and are associated with increased risk of morbidity and mortality, long-term institutionalisation and costly management. Their impact on a public healthcare system funded by an ever-diminishing number of tax-paying workers is a major concern. Increasing attention is being given to improving management of these fractures and rehabilitation of patients.2-5 Morbidity and mortality rates have been reduced through increased surveillance for and treatment of complications, such as wound and other infections, pressure sores and deep venous thrombosis. Early involvement of multidisciplinary teams in patient rehabilitation and early mobilisation have been used in large hospitals to reduce delays and optimise treatment for previously ambulatory patients. These programs result in fewer perioperative complications and enable patients to return home and resume functional independence earlier, reducing the number who need long term residential aged care.2,3 However, these improvements come at a cost -- direct costs, such as salaries of additional staff for multidisciplinary teams,6 and indirect costs, such as when patients are sent home early, and postdischarge care is assumed by family and community.7 Pressure on hospital administrations to contain or reduce costs may result in outcomes of little, if any, benefit to the patient, but which may have a substantial impact on others living with or looking after the patient. Little is known about the nature and extent of this potential impact. Implementation of these efforts needs to be both preceded and accompanied by careful evaluation and assessment. Among strategies that attempt to achieve savings is the development and use of clinical pathways, as outlined by Choong and colleagues8 in this issue of the Journal. A clinical pathway is a type of management plan formulated for a specified condition, which defines expected daily activities, identifies lines of responsibility for those activities, and indicates goals for the patient to achieve along the way.9 These pathways are based on a multidisciplinary perspective and collaboration. Introduction of a clinical pathway requires considerable commitment and investment of time from many departments within the hospital, as well as substantial changes to the medical record. It also raises concerns about the medicolegal implications of non-compliance with the pathway in the event of an adverse outcome. All these issues require further study.10,11 Clinical pathways have been successfully implemented for a variety of conditions and settings, overseas and in Australia. However, patient groups have been relatively homogeneous, such as those having elective hip, knee or other surgery. In contrast, hip-fracture patients are very heterogeneous, ranging from the fit, active (albeit osteoporotic) "young" elderly, to the very frail, bedridden 90-years-plus residents of nursing homes. A clinical pathway developed from evidence-based practices may be the most efficient way to restore the mobility of elderly patients and ensure their discharge back to their pre-admission residence. However, because of the high level of comorbidities in these patients, the potential for variation from the pathway is high.2 Choong and colleagues describe a controlled trial of a clinical pathway for patients with proximal femoral fracture in a major teaching hospital.8 Modest benefits were found for the hospital budget, and clinical outcomes for patients on the pathway appeared no worse than for patients who received standard hospital treatment. Use of the pathway seemed to have little real effect on shortening stay in comparison with the control group; the major difference in stay was found for patients who required review by the Aged Care Assessment Team and were therefore likely to be frailer. The frail elderly have not usually been seen as a target group for clinical pathways, but future studies of this group may show that they benefit from this approach without adverse outcomes on complications or discharge destinations. This study illustrates the problems of assessing the usefulness of clinical pathways, which should be addressed in the design of future studies. The clinical relevance of short reductions in length of hospital stay (1.4 days in this instance) is open to question. Economic aspects need to be documented as part of study design to allow analysis of cost effectiveness. The real effectiveness of the pathway for the community, rather than just the hospital, remains unclear, and future studies need to include strategies to assess that effect. The overall economic benefit to the community should take into account the increased use of community services, use of interim or permanent residential care, and extra costs and stress for families who provide a large proportion of the care after discharge from hospital.3 Clinical pathways have developed primarily in large metropolitan hospitals with resources to research and implement the process, while proximal femoral fractures are treated in a wide range of hospitals with varying levels of funding and allied health support. These pathways may have the potential to improve clinical outcomes and costs in hospitals where the number of femoral fracture patients is too small to warrant an orthogeriatric unit or where there is no access to a designated rehabilitation unit. Ultimately, the generalisability of this approach will become evident as more research in this area is reported. Recent reports in the Journal highlight the difficulties in transforming evidence into practice.12,13 Despite these difficulties, compliance with evidence-based best practice in the management of fractured neck of femur, together with preventive measures such as early management of osteoporosis and falls prevention programs, should help lessen the current and future economic and personal burden of hip fracture in Australia. Cheryl E Swanson Research Scientist, Division of Orthopaedic Surgery Catherine E Yelland Director, Geriatric Assessment and Rehabilitation Unit Gregory A Day Senior Lecturer, Division of Orthopaedic Surgery University of Queensland and Royal Brisbane Hospital Brisbane, QLD Cooper C, Campion G, Melton IJ III. Hip fractures in the elderly: a world-wide projection. Osteoporosis Int 1992; 2: 285-289. March LM, Chamberlain AC, Cameron ID, et al. How best to fix a broken hip. Med J Aust 1999; 170: 489-494. Swanson CE, Day GA, Yelland CE, et al. The management of elderly patients with femoral fractures. A randomized controlled trial of early intervention versus standard care. Med J Aust 1998; 169: 515-518. Dowsey M, Kilgour M, Santamaria N, Choong PFM. A prospective study of clinical pathways in hip and knee arthroplasty. Med J Aust 1999; 170: 59-62. Sanders KM, Nicholson GC, Ugoni AM, et al. Health burden of hip and other fractures in Australia beyond 2000. Med J Aust 1999; 170: 467-470. Farnsworth MG, Kenny P, Shiell A. The costs and effects of early discharge in the management of fractured hip. Age Aging 1994; 23: 190-194. Caplan G, Board N, Paten A, et al. Decreasing lengths of stay: the cost to the community. Aust N Z J Surg 1998; 68: 433-437. Choong PFM, Langford AK, Dowsey MM, Santamaria NM. Clinical pathway for fractured neck of femur: a prospective controlled study. Med J Aust 2000; 172: 423-427. Tallis G, Balla JI. Critical path analysis for the management of fractured neck of femur. Aust J Pub Heath 1995; 19: 155-159. Kitchiner DJ, Bundred PE. Clinical pathways: a practical tool for specifying, evaluating and improving the quality of clinical practice. Med J Aust 1999; 170: 54-55. Dwyer P. Legal implications of clinical practice guidelines. Med J Aust 1998; 169: 292-293. Doust JA, Silagy CA. Applying the results of a systematic review in general practice. Med J Aust 2000; 172: 153-156. Rubin GL, Frommer MS, Vincent NC, et al. Getting new evidence into medicine. Med J Aust 2000; 172: 180-183. Make a comment Choong

Cheryl E Swanson · Catherine E Yelland · Gregory A Day

Healthcare Clinical pathway for fractured neck of femur: a prospective, controlled study Peter F M Choong, Anna K Langford, Michelle M Dowsey and Nick M Santamaria MJA 2000 172: 423-426 For editorial comment, see Swanson et al Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Orthopaedic surgery Abstract Objective: To assess outcomes of using a clinical pathway for managing patients with fractured neck of femur. Design: Prospective, pseudorandomised, controlled trial. Setting: St Vincent's Hospital, Melbourne, Victoria (a tertiary referral, university teaching hospital), 1 October 1997 to 30 November 1998. Participants: 111 patients (80 women and 31 men; mean age, 81 years) admitted via the emergency department with a primary diagnosis of fractured neck of femur. Interventions: Management guided by a clinical pathway (55 patients) or established standard of care (control group, 56 patients). Main outcome measures: Timing of referrals and discharge planning; total length of stay; and complication and readmission rates within 28 days of discharge. Results: Patients managed according to the clinical pathway had a shorter total stay (6.6 versus 8.0 days; P = 0.03), even if assessment for placement by the Aged Care Assessment Service was required (9.5 versus 13.6 days; P = 0.03). There were no significant differences in complication and readmission rates between pathway and control patients (complication rates, 24% versus 36%; P = 0.40; readmission rates, 4% versus 11%; P = 0.28). Conclusion: Coordinated multidisciplinary care of patients with fractured neck of femur reduces length of stay without increasing complications. By 2050, a quarter of Australia's population will be aged over 65 years, and the incidence of hip fractures is consequently expected to increase fourfold.1 The logistic challenge posed by this increasing incidence and the fourfold greater resources needed by patients over 65 years compared with the average patient2 will be compounded by the expected continuing decline in bed availability. Improving the efficiency of health service delivery to patients with hip fractures may help improve overall availability of acute hospital beds for other elective surgery. Clinical pathways are proposed as a means of providing high quality care in a timely and cost-effective manner. These pathways consist of treatment protocols that aim to streamline and standardise management with multidisciplinary input from medical, nursing, paramedical and administrative staff. They have been used successfully to improve outcomes after elective hip and knee joint replacement.3 This led us to examine the impact of such a coordinated approach on acute and unpredictable admissions such as in patients with femoral-neck fractures. However, surgery for acute hip fracture differs significantly from hip joint replacement as it is non-elective and patient needs and clinical course are more variable. We conducted a prospective, controlled study to assess the effectiveness of clinical pathways for improving outcomes of patients undergoing surgery for acute fracture of the neck of femur. Specifically, we examined time to mobilisation, length of hospital stay, and complication and readmission rates as indices of outcome. Methods We used a pseudorandomised, controlled study design to compare the outcomes of patients whose management was guided by a clinical pathway with those who received the established standard of care in our orthopaedic unit. As the preparation and implementation of the clinical pathway was a quality improvement initiative, ethics committee approval was deemed unnecessary. Setting and participants The study was conducted at St Vincent's Hospital, Melbourne, Victoria (a tertiary referral hospital affiliated with the University of Melbourne). Participants were all patients who underwent standard surgical treatment for acute fracture of the neck of femur (by internal fixation using compression hip screw and plate or hemiarthroplasty) at the hospital between 1 October 1997 and 30 November 1998. In this period, 126 patients were admitted with a diagnosis of fractured neck of femur. Fifteen were excluded from the study, five because they were transferred to another institution for treatment, eight because of associated medical conditions that precluded surgical intervention, and two because of a decision to undertake non-standard surgery. One hundred and eleven patients were allocated to one of two groups (control or clinical pathway) by an administrative clerk, who was independent of the study and unaware of the study hypothesis. Patients were allocated on the basis of their unit record number -- even numbers to the control group (56 patients), and odd numbers to the clinical pathway group (55 patients). A retrospective analysis of a historical treatment group (n = 118) showed a mean length of stay of 11.8 days (range, 2.6-40.0 days; SD, 7.3). To detect a reduction in length of stay of a third at a significance level of 0.05 with a power of 0.8 would require two groups, each with a minimum of 55 participants. Management regimens Management regimens for the clinical pathway and control groups are compared in Box 1. Options for discharge destinations for all patients comprised rehabilitation in an in-patient rehabilitation facility attached to the hospital or in another hospital, patients' own home (with or without domiciliary care services), hostel or nursing home. Patients were deemed suitable for fast-stream rehabilitation in the on-site rehabilitation facility if they had the potential to regain or improve on their prefracture status, were able to achieve this outcome in less than a month, and had a high probability of returning to their previous living environment. Patients who were not expected to regain their prefracture functional level, were not expected to achieve this level in less than two months or were expected to need a higher level of care than before the fracture were referred to the Aged-Care Assessment Service (ACAS) for placement in slow-stream rehabilitation, nursing home, hostel or special accommodation, depending on patient medical conditions and limitations. This service was mediated by a social worker who, together with a medical registrar, prepared the patient for thrice-weekly assessment by a consultant geriatrician which could take place on three occasions per week. Outcome measures Duration of stay: Times in the various stages of the admission were recorded prospectively. Definitions of times were: To surgery: time between admission and theatre; To mobilisation: time between surgery and the patient first walking with the use of aids; To ACAS assessment: time between submission of the referral to ACAS and first assessment by the geriatrician; and Total length of stay: time from admission to discharge from hospital. Inpatient complications: Patients were assessed daily for confusion (disorientation in time, place or person). Wound infection was defined as all wound erythema lasting longer than 24 hours. Deep vein thrombosis was diagnosed clinically and confirmed by ultrasonography, and urinary tract infection was confirmed microbiologically. Postdischarge complications and readmissions: All patients' medical records were examined 28 days after discharge to identify postdischarge complications or readmissions related to the fracture. This time was chosen as we expected the patient to have recovered significantly from their surgery by then. Statistical analyses Results were analysed using SPSS version 8.0.4 Continuous and normally distributed data were compared with t tests for independent groups. Data that were not normally distributed, such as length of stay, were transformed logarithmically before this analysis; consequently, geometric means are reported for these data. Multiple linear regression with a general linear model was used to test for interactions between groups and the variables age, sex, referral to ACAS and premorbid status. Proportions were compared between groups using the z test. P values < 0.05 were regarded as significant. Results The 111 patients comprised 80 women and 31 men, with mean age 81 years. Control and pathway patients did not differ significantly in median age (82 versus 84 years; P = 0.1), number with premorbid conditions (19 versus 18; P = 0.94), number who did not speak English (16 versus 13; P = 0.6) or were confused on admission (24 versus 22; P = 0.98). Outcomes Durations of stay Durations at various stages of the admission for pathway and control patients are compared in Box 2. No significant differences were found between the groups in mean time in the emergency department or mean time from admission to surgery. Pathway patients walked significantly earlier than control patients, but the difference (1.6 versus 2.0 days) was not clinically important. However, the pathway group had a significantly shorter total length of stay than the control group (mean, 6.6 versus 8.0 days; P = 0.03). This meant that control patients stayed 21% longer than pathway patients. After adjusting the log-transformed length-of-stay values for the possible confounding variables of age, sex, aged-care assessment and premorbid status with multiple linear regression, we found that none of these variables produced significant between-group interactions. Group (pathway versus control) remained the most significant factor influencing total length of stay. Referral for aged-care assessment Fifteen of the 55 pathway patients and 18 of the 56 control patients were referred for ACAS assessment. This referral was preoperative for three pathway and two control patients. Time from referral to first assessment by a geriatrician differed only slightly between pathway and control patients: mean times were 2.5 days for pathway patients (range, 1-8 days) and 2.8 days for control patients (range, 0-8 days). Patients who were referred to ACAS had significantly longer total stays than those who were not referred (11.7 versus 6.5 days; P < 0.001; difference, 5.2 days; 95% CI, 3.0-7.5 days). This difference remained significant when the control and pathway groups were analysed separately. However, mean length of stay was significantly shorter for pathway patients referred to ACAS than for control patients referred to ACAS (9.5 versus 13.6 days; Box 2). We explored the possibility of confounding variables for patients referred to ACAS and found that there were none, suggesting that group membership (pathway or control) was the most influential factor affecting length of stay. Postdischarge destinations were similar in pathway and control groups referred to ACAS: 12/15 pathway patients and 16/18 control patients proceeded to slow-stream rehabilitation. Discharge destinations Discharge destinations are shown in Box 2. Patients in each group were most often discharged into fast-stream rehabilitation, followed in frequency by slow-stream rehabilitation or nursing homes. Complications and readmissions There were no significant differences between pathway and control patients in numbers who were confused postoperatively (23/55 versus 31/56) and in rates of other inpatient complications (10/55 versus 14/56 patients), postdischarge complications (3/55 versus 6/56), or readmission rates (2/55 versus 6/56). Discussion We found that use of a clinical pathway for management of fractured neck of femur reduced mean length of hospital stay from 8.0 to 6.6 days, suggesting that a proactive, multidisciplinary approach can reduce hospital stay for this condition. To date, only a few studies5-7 have reported results of a coordinated, multidisciplinary approach to management of fractured neck of femur in Australia. They found, similarly to our study, that these early-intervention programs reduced the length of stay of elderly patients with this condition compared with standard care.5-7 However, actual length of stay varied greatly between studies (from 11.38 days to 32.55 days). This variation highlights the limitations in management inherent in individual institutions because of variation in local factors such as availability of ACAS and support services and patient characteristics. Length of stay in the pathway group at our hospital, which was two to four times shorter than at other hospitals,5-7 may have benefited from our on-site rehabilitation unit. Although we found that use of a clinical pathway reduced total length of stay, the change (1.4 days) was not dramatic. This may be because the strong culture of continued refinement of care in our orthopaedic department had already reduced length of stay for many classes of orthopaedic conditions, including fractured neck of femur. Nevertheless, the reduction of 1.4 days in the clinical pathway group was encouraging. Unlike a previous study,5 our study included patients with language and cognitive difficulties. This choice was made to minimise any selection bias, as patients susceptible to osteoporotic fractures are in an age group which commonly has cognitive difficulties and as our patient population includes a large proportion of non-English-speaking people. We believed that their inclusion would test the efficacy of clinical pathways in the delivery of multidisciplinary care. We observed no difficulties applying the pathway to patients who had cognitive difficulties or did not speak English. Importantly, while use of clinical pathways reduced total length of stay, we found no significant clinical difference in time to mobilisation or complication or readmission rates between the two groups. This contrasted with our earlier findings on the effect of clinical pathways in elective joint replacement surgery.3 Possible explanations for the difference include the frequent existence of unstable and often untreated premorbid conditions in patients with fractured neck of femur, which require attention during their acute admission. In contrast, patients undergoing elective joint replacement have the benefit of preadmission assessment clinics which may resolve expected medical, allied health or discharge issues before admission. Up to a third of our patients with fractured neck of femur were referred for ACAS assessment for placement. Patients who required this assessment stayed significantly longer than patients who did not, possibly reflecting their respective comorbidities and the shortage of aged-care beds in the community. While the time between ACAS referral and consultation was similar for pathway and control patients, total length of stay was four days shorter for pathway than for control patients. It is likely that the daily review of patients' health status promoted by the clinical pathway optimised their readiness for discharge and prompted more regular reviews of discharge plans by the ACAS team. Interestingly, time between ACAS referral and consultation ranged up to eight days in both pathway and control groups. Reasons for this large range were not recorded and warrant further investigation. Some authors have identified that acute care, convalescence, rehabilitation and surgery accounted for more than 90% of total costs for fractured neck of femur, and that the main factors explaining cost variation were the number of days spent in acute care and convalescence or rehabilitation.9,10 However, our study was not designed to evaluate cost-effectiveness of clinical pathways, and, although use of the clinical pathway reduced length of stay by 1.4 days, we did not quantify costs involved in administering the pathway compared with control care. The net cost-effectiveness of our pathway is therefore unknown. Despite the weakness of a limited study, we showed that a multidisciplinary approach using clinical pathways for fractured neck of femur can reduce length of stay without increasing patient morbidity. Acknowledgements We wish to acknowledge the assistance of a special grant from the Victorian Centre for Ambulatory Care Innovation and Michael Bailey, statistical consultant, Alfred Hospital, Melbourne, Victoria. References Sanders KM, Nicholson GC, Ugoni AM, et al. Health burden of hip and other fractures in Australia beyond 2000. Med J Aust 1999; 170: 467-470. Day RO, Henry DA, Muirden KD, et al. Non-steroidal anti-inflammatory drug induced upper gastrointestinal haemorrhage and bleeding. Med J Aust 1992; 157: 810-812. Dowsey MM, Kilgour ML, Santamaria NM, Choong PF. Clinical pathways in hip and knee arthroplasty: a prospective, randomised controlled study. Med J Aust 1999; 170: 59-62. SPSS Inc. SPSS Base 8.0 for Windows. Chicago, (Ill): SPSS Inc, 1998. Swanson CE, Day GA, Yelland CE, et al. The management of elderly patients with femoral fractures. A randomised controlled trial of early intervention versus standard care. Med J Aust 1998; 169: 515-518. Tallis G, Balla JI. Critical path analysis for the management of fractured neck of femur. Aust J Public Health 1995; 19: 155-159. Cameron I, Lyle D, Quine S. Accelerated rehabilitation after proximal femoral fracture: a randomised controlled trial. Disabil Rehabil 1993; 15: 29-34. Lavernia CJ. Hemiarthroplasty in hip fracture care: effects of surgical volume on short-term outcome. J Arthroplasty 1998; 13: 774-778. French FH, Torgerson DJ, Porter RW. Cost analysis of fracture of the neck of femur. Age Ageing 1995; 24: 185-189. Hollingworth W, Todd C, Parker M, et al. Cost analysis of early discharge after hip fracture. BMJ 1993; 307: 903-906. (Received 2 Aug 1999, accepted 25 Jan 2000) Authors' details Department of Orthopaedics, St Vincent's Hospital, Melbourne, VIC. Peter F M Choong, MD, FRACS, Director of Orthopaedics, Professor of Orthopaedics; Anna K Langford, RN, BN, Clinical Nurse Specialist; Michelle M Dowsey, RN, BN, Clinical Nurse Specialist. University of Melbourne, Melbourne, VIC. Nick M Santamaria, MEdSt, PhD, Senior Research Fellow. Reprints: Professor P F M Choong, Department of Orthopaedics, St Vincent's Hospital, 41 Victoria Parade, Fitzroy, VIC 3065. PeterChoongATc031.aone.net.au Make a comment 1: Treatment regimens for control and clinical pathway patients with fractures of the femoral neck Control groupClinical pathway groupEmergency departmentAssessment X-rays Orthopaedic referral Orthopaedic consultation Transfer to wardAssessment Information checklist (prefracture placement, health status, carer) Preoperative investigations (including x-ray) Orthopaedic referral Transfer to wardWard (preoperative)Schedule surgery Preoperative tests ordered Anaesthetic assessmentOrthopaedic consultation Schedule surgery Anaesthetic assessmentWard (postoperative)Strict bedrest X-ray within 48 hours Physiotherapy referral after x-ray MobiliseX-ray within 24 hours Mobilise day after surgeryDocumentationAd hoc patient progress notesSpecific pathway documentation specifying responsibilities by discipline and time frame, to be signed on task completion Coded data collection sheetMedicationProphylactic antibiotics 24h Thromboprophylaxis until discharge (low molecular weight heparin, thigh length stockings)Prophylactic antibiotics 24h Thromboprophylaxis until discharge (low molecular weight heparin, thigh length stockings)Discharge planningBegun postoperatively Depends on patient progress Discharge phone call and summary to discharge destinationBegun on admission Depends on premorbid independence level Discharge package with information on wound care, expected milestones, contact details, simple exercises, equipment for staple removal. Back to text Back to text

Anna K Langford · Michelle M Dowsey · Nick M Santamaria

Editorial The Bone and Joint Decade: 2000-2010 The United Nations has endorsed a Decade to focus attention on worldwide epidemic of musculoskeletal diseases MJA 2000; 172: 307-308 In January this year, the Bone and Joint Decade was launched in Geneva by the World Health Organization. The Decade was initiated because of the epidemic of musculoskeletal disease that is occurring worldwide as the population ages.1 In late November 1999, the Secretary-General of the United Nations, Kofi Annan, signed the UN Declaration of Support for the Decade. The launch came after almost two years of negotiation by health professionals, led principally by orthopaedic surgeons and rheumatologists. These health professionals garnered support from other musculoskeletal medicine specialists and patient groups. It is hoped that orthodox and complementary practitioners and patient groups involved in musculoskeletal disease and trauma will become involved as the Decade develops. Following the official launch, some 80 delegates from around the world spent three days at the World Health Organization, evaluating the significant burden of musculoskeletal disease on both developed and developing societies. In the WHO/World Bank Global Burden of Disease Project, musculoskeletal conditions represent more than half of all chronic conditions2 and are the most common cause of severe long-term pain and physical disability.3 There is now...evidence that, for chronic rheumatic diseases, something can be done. In Australia, musculoskeletal diseases are the second most common cause of presentations to a general practitioner4 and the third leading cause of health system expenditure, with an estimated total cost of over $3 billion in 1993-19945 (Box). This compares with an estimated total cost of $3.5 billion for circulatory diseases, $2.5 billion for respiratory diseases and $1 billion for endocrine disorders.6Furthermore, in 1993-1994,1 musculoskeletal diseases accounted for nearly 300 000 hospital admissions, nearly 15 million medical services and over 13 million prescriptions.5 Significant disability due to musculoskeletal disease has been noted in more than half of people aged over 65 years,7 and is also commonly self-reported in population samples.8 Indeed, osteoarthritis (the most common form of arthritis) accounts for over 5% of years lost due to disability in Australia.9 What is the Bone and Joint Decade and what is its intended impact? One objective is to create national networks of professional and patient organisations which will establish their own national goals and agendas. The desire is to develop a patient "focus", with individuals living with rheumatic disease being significantly involved in the process. Some 80 countries have established national coordinators, and over 20, including Australia, have endorsed the Decade. The Decade has four major aims: To raise awareness of the growing burden of musculoskeletal disorders on society; To promote prevention of musculoskeletal disorders and empower patients through education campaigns; To advance research on prevention, diagnosis and treatment of musculoskeletal disorders; and To improve diagnosis and treatment of musculoskeletal disorders. Groups such as the Arthritis Foundation of Australia, the Australian Rheumatology Association and the Australian Orthopaedic Association are already actively pursuing some of these aims and will play major roles in developing activities for the Decade in Australia. Although one focus of the Decade may well be on the aged and diseases causing disability (eg, osteoporosis, osteoarthritis and back pain), the Decade will also address the increasing problem of musculoskeletal trauma. This is of particular relevance to young populations in both developed and developing countries. Much more information is needed on the epidemiology of trauma, risk factors, ways of minimising damage to tissues after trauma, and strategies to enhance rehabilitation. The recently advertised National Health and Medical Research Council Trauma Research Partnerships will be helpful in this regard. The past decade has seen enormously exciting advances in the management of osteoporosis and in our understanding of the basic mechanisms of inflammation, which produces so much pain and disability in diseases such as rheumatoid arthritis. These advances include an understanding of the role of genetic markers in osteoporosis, elucidation of risk factors for falls and subsequent fractures, and development of the bisphosphonates. More recently, exciting advances have occurred in the therapeutics of musculoskeletal diseases, previously little changed for decades. These include the development of monoclonal antibodies to substances such as tumour necrosis factor, new specific antirheumatic drugs, and the cyclooxygenase-2 (COX-2) specific inhibitors, which have the potential to reduce pain and inflammation without major gastrointestinal adverse reactions. Musculoskeletal surgery, particularly joint replacement, has revolutionised the lives of many elderly (and some younger) Australians. Hip and knee replacements are among the most cost-effective interventions in medicine, comparing favourably to coronary bypass surgery and renal dialysis,10 and very significantly improve the quality of life in patients with a variety of rheumatic diseases.11 In addition, data suggesting that osteoarthritis of the knee is related to obesity and can be alleviated to some extent by weight reduction present a cogent argument for primary prevention.12 Many musculoskeletal conditions produce chronic pain, which itself strongly contributes to disability and decreased quality of life. Strategies to address chronic musculoskeletal pain will also be a priority of the Decade. The hope is that the Bone and Joint Decade will focus attention on these important diseases, demonstrating to healthcare providers that a relatively modest investment can produce significant benefits. The Bone and Joint Decade will try to bring together these important strands of research, education and service to improve the lot of the millions of Australians who suffer each week from a rheumatic condition. A meeting of professional groups, patients and patient organisations and healthcare providers will shortly be convened to begin planning for the Decade in Australia. The 1990s were designated the Decade of the Brain, and spawned enormous interest around the world in the neurosciences, which is now starting to have significant spin-offs in treatment. It should be remembered that that Decade began with a significant financial investment from the United States Congress, while the Bone and Joint Decade has had no such funding as yet. This week is National Arthritis Week and professional and patient groups around Australia will focus attention on these important chronic and disabling diseases and their impact on society. They should proceed in the knowledge that there is now a considerable groundswell of energy worldwide and evidence that, for chronic rheumatic diseases, something can be done. Peter M Brooks Executive Dean, Health Sciences University of Queensland, Brisbane, QLD John A L Hart Clinical Associate Professor of Surgery Monash University, Melbourne, VIC and Australian Coordinator of the Bone and Joint Decade Hazes JM, Woolf AD. The bone and joint decade 2000-2010. J Rheumatol 2000; 27: 1-3. Dieppe P. Osteoarthritis. Acta Orthop Scand Suppl 1998; 281: 2-5. Murray JL, Lopez AD, editors. The global burden of disease: a comprehensive assessment of mortality and disability from diseases, injuries and risk factors in 1990 and projected to 2020. Cambridge, Mass: Harvard University Press, 1996. Britt H, Sayer GP, Miller GC, et al. General practice activity in Australia 1998-1999. Canberra, ACT: Australian Institute of Health and Welfare, 1999. AIHW Cat No. GEP 2. Mathers C, Penn R. Health system costs of injury, poisoning and musculo-skeletal disorders in Australia 1993-94. Canberra: Australian Institute of Health and Welfare, 1999. AIHW Cat No. HWE 12 (Health and Welfare Expenditure Series No. 6). Mathers C. Burden of disease and health system costs of heart disease, depression and back problems in Australia. Presented at the National Health and Medical Research Council National Forum. Canberra; 24 Mar 1998. March LM, Brnabic AJM, Skinner JC, et al. Musculoskeletal disability among elderly people in the community. Med J Aust 1998; 168: 439-442. Hill CL, Parsons J, Taylor A, Leach G. Health related quality of life in a population sample with arthritis. J Rheumatol 1999; 26: 2029-2035. Mathers C, Vos T, Stevenson C. The burden of disease and injury in Australia. Canberra: Australian Institute of Health and Welfare, 1999. AIHW cat. no. PHE 17. Liang MH, Cullen KE, Larson MG, et al. Cost effectiveness of total joint arthroplasty in osteoarthritis. Arthritis Rheum 1986; 29: 937-943. March LM, Cross MJ, Lapsley H, et al. Outcomes after hip or knee replacement surgery for osteoarthritis. A prospective cohort study comparing patients' quality of life before and after surgery with age-related population norms. Med J Aust 1999; 171: 235-238. Hart DJ, Spector TD. The relationship of obesity, fat distribution and osteoarthritis in women in the general population. The Chingford Study. J Rheumatol 1993; 20: 331-335. Make a comment Back to text

Peter M Brooks

Clinical Update Genetic testing for Alzheimer's disease Peter K Panegyres, Jack Goldblatt, Ian Walpole, Carmela Connor, Toni Liebeck and Karen Harrop MJA 2000; 172: 339-343 Abstract - Recommendations for gene testing in Alzheimer's disease - Conclusions - Acknowledgements - References - Authors' details - - More articles on Genetics Abstract Genetic factors are important in the development of Alzheimer's disease (AD). Familial AD can result from rare mutations in some genes. Other genes, such as the apolipoprotein E gene (APOE), operate as risk factors for late-onset sporadic AD. On a background of advances in the genetics of AD we suggest a way in which genetic information may be used in the diagnosis of AD. If there is a positive family history of early-onset dementia and the clinical features suggest AD, patients may be tested for presenilin and amyloid precursor protein gene mutations with appropriate pretest and post-test counselling. Predictive testing should be performed under guidelines developed by the World Federation of Neurology and the Human Genetics Society of Australasia. The usefulness of APOE genotyping as an adjunct to conventional diagnostic tests is unknown; data suggest it has low sensitivity and specificity and may have little predictive value in an individual patient. APOE genotyping should not be performed in asymptomatic individuals, except as part of an ethically approved research project; this recommendation is supported by a number of international consensus statements. APOE testing should not be used as a diagnostic test without adequate pretest and post-test counselling, education and support. APOE testing should not be used as a sole diagnostic test in the work-up of patients with AD. Genetic risk factors other than APOE require validation and should not be used routinely, except as part of an ethically approved research protocol. Alzheimer's disease (AD) is one of the major healthcare problems facing First World countries. In 1995, 130 000 Australians aged over 65 years had moderate to severe dementia, and by 2041 the number of people with dementia in Australia is expected to increase by 254%.1 In recent years there have been major advances in the elucidation of genetic factors in both familial and sporadic AD. Unfortunately, the accumulation of this genetic information has outpaced understanding among the medical and genetic communities of the most appropriate way it can be used clinically. This has led to diagnostic kits for DNA markers having to be withdrawn because of misuse in counselling individuals about future risks.2 Consumer-led demand for diagnostic tests and pressure from companies that make them raise major ethical considerations about the role of genetic testing in managing families at possible risk. These developments have encouraged us to develop evidence-based recommendations on the use of molecular genetic testing in Alzheimer's disease. Background information on the genetics of Alzheimer's disease is provided in Box 1. Recommendations for gene testing in Alzheimer's disease Diagnosis of dementia The diagnosis of AD requires assessment by a clinician skilled in diagnosing dementia, using the criteria established by the National Institute of Neurological and Communicative Disorders and Stroke - Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA),4 shown in Box 2. The diagnosis can sometimes be difficult, and expertise is required to distinguish AD clinically from other disorders such as frontotemporal atrophy and prion diseases, especially in younger patients. The diagnostic work-up of the patients is best performed in a facility with counselling and support staff to help patient and carer cope with the diagnosis of dementia. Collaboration with a neuropathology laboratory can enhance such a service by providing postmortem confirmation of the diagnosis. Education, counselling, support A multidisciplinary team, including a neurologist or specialist physician, neuropsychologists, social workers, allied health workers (occupational therapists, speech therapists), all working together with the patient's general practitioner, helps patients and their carers understand the diagnosis of AD and its implications. Contact with a caring, multidisciplinary team can support the patient, carer, and family in crises such as the development of intercurrent medical problems requiring hospitalisation and respite for patient or carer. Such a team can advise the patient, carer and family on the suitability and appropriateness of genetic testing. Genetic testing If genetic testing is considered then the staff of the multidisciplinary team must know the implications, risks and limitations of the proposed tests and counsel patients, carers and families accordingly. They must have the expertise to counsel patients, carers and families about psychosocial implications, confidentiality, and issues related to employment and insurability, of the genetic tests requested. Accredited laboratory and DNA result disclosure The laboratory that tests the DNA specimen must be accredited by the National Association of Testing Authorities, Australia, which advises on specimen handling, the maintenance of strict confidentiality, and good laboratory practice (Box 3). The DNA result should be given to the clinician who requested the test, who will disclose the result to the patients and carer in strictest confidence with the help of counsellors. As has been shown with Huntington's disease,34 follow-up by counsellors will help to decrease adverse reactions such as suicide, attempted suicide and psychiatric hospitalisation. Familial early-onset AD If there is a positive family history of early-onset dementia, and pedigree analysis suggests autosomal dominant AD, the patient and family should be referred to a clinician with an interest in familial dementia for confirmation of the diagnosis. The patient and family should then be managed by a multidisciplinary team of experts in genetic neurodegenerative disorders (such as Huntington's disease) and predictive gene testing. Genetic testing should only be offered in a comprehensive, structured, clinico-laboratory program where mutations in PS1, PS2 and APP would be sought in affected individuals. Gene testing is not recommended for sporadic cases of early-onset AD without a definite family history. Predictive testing in unaffected and asymptomatic individuals from families in which causative mutations have been discovered must follow guidelines as developed for Huntington's disease.5-8 Only about 6% of patients at risk of Huntington's disease request the gene test, probably because many at-risk people decide against the test once they receive full information of its implications.35 The likelihood of suicide, attempted suicide or psychiatric hospitalisation after predictive testing is no greater than in the general population with symptomatic Huntington's disease, and this is probably the result of good counselling and support.34 Similar considerations may apply to AD. Like Huntington's disease, AD is an incurable condition with devastating consequences, and there are ethical issues (such as patients not wanting to know, and implications for employment and insurability) relating to predictive gene testing in such situations. These ethical issues probably contribute to the low uptake of testing for Huntington's disease and will probably be relevant to AD also. Other dilemmas in predictive testing for AD relate to performing tests in individuals with 25% risk when an unaffected or undiagnosed parent does not request a gene test; a positive result in such individuals would result in an unwanted gene result for the parent. This represents a difficult situation for predictive gene testing programs. Similar problems arise in twins if only one wants to be tested. For ethical reasons, as in Hungtington's disease, children should not be tested for AD. DNA banking should be considered for individuals with a family history of AD who may not want a test at present, or who may not have any of the recognised mutations -- future testing could be carried out if other mutations are recognised. Sporadic AD In patients with the clinical diagnosis of sporadic AD, gene testing for APOE ε4 status or other genetic factors is not recommended. The clinical usefulness of these tests has not been established, and there is no evidence that they improve the sensitivity and specificity of the clinical diagnosis of AD sufficiently to alter the standard diagnostic work-up of these patients. The APOE ε4 genotype should never be used as a sole diagnostic test for the diagnosis of AD. Conclusions Our recommendations are summarised in Box 4. Acknowledgements A National Health and Medical Research Council fellowship awarded to Dr Panegyres supported this work. References Henderson AS, Jorm AF. Dementia in Australia. Aged and Community Care Service Development and Evaluation Report No. 35. Canberra: AGPS, 1998. Lehrman S. Genetic testing for Alzheimer's disease "not appropriate". Nature 1997; 389: 898. Tanzi RE, Kovacs DM, Kim T-W, et al. The gene defects responsible for familial Alzheimer's disease. Neurobiol Dis 1996; 3: 159-168. McKhann G, Drachman DD, Folstein M, et al. Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of the Department of Health and Human Services Task Force in Alzheimer's disease. Neurology 1984; 34: 939-944. World Federation of Neurology: Research Committee. Research Group on Huntington's Chorea. Ethical issues policy statement on Huntington's disease molecular genetics predictive test. J Neurol Sci 1989; 94: 327-332. Went L. Ethical issues policy statement on Huntington's disease molecular genetics predictive test. International Huntington Association. World Federation of Neurology. J Med Genet 1990; 27: 34-38. Guidelines for the molecular genetics predictive test in Huntington's disease. International Huntington Association (IHA) and the World Federation of Neurology (WFN) Research Group on Huntington's Chorea. Neurology 1994; 44: 1533-1536. Walpole I, Bankier A, Blackwell J, et al. Guidelines for DNA predictive testing. Bull Hum Genet Soc Austral 1998; 11: 10-14. Goate AM, Chartier-Harlin MC, Mullan MC, et al. Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease. Nature 1991; 349: 704-706. Blacker D, Tanzi RE. The genetics of Alzheimer disease. Arch Neurol 1998; 55: 294-296. Levy-Lehad E, Wasco W, Podrkaj P, et al. Candidate gene for the chromosome 1 familial Alzheimer disease locus. Science 1995; 269: 973-977. Saunders AM, Strittmatter WJ, Schmechel D, et al. Association of apolipoprotein E allele epsilon 4 with late-onset familial and sporadic Alzheimer's disease. Neurology 1993; 43: 1467-1472. Strittmatter WJ, Saunders AM, Schmechel D, et al. Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease. Proc Natl Acad Sci USA 1993; 90: 1977-1993. Gomez-Isla T, West HL, Rebeck GW, et al. Clinical and pathological correlates of apolipoprotein E ε4 in Alzheimer's disease. Ann Neurol 1996; 39: 62-70. Jonker C, Schmand B, Lindeboom J, et al. Association between apolipoprotein E ε4 and the rate of cognitive decline in community-dwelling elderly individuals with and without dementia. Arch Neurol 1998; 55: 1065-1069. Hyman BT, Gomez-Isla T, Briggs M, et al. Apolipoprotein E and cognitive change in an elderly population. Ann Neurol 1996; 40: 55-66. Mayeux R, Saunders AM, Shea S, et al. Utility of the apolipoprotein E genotype in the diagnosis of Alzheimer's disease. N Engl J Med 1998; 338: 506-511. McConnell LM, Sanders GD, Owens DK. Evaluation of genetic tests: APOE genotyping for the diagnosis of Alzheimer's disease. Genet Test 1999; 3: 47-53. American College of Medical Genetics and American Society of Human Genetics Working Group on APOE and Alzheimer Disease. Statement on use of apolipoprotein E testing for Alzheimer disease. JAMA 1995; 274: 1627-1629. McConnell LM, Koenig BA, Greely HT, Raffin TA, and Alzheimer Disease Working Group of the Stanford Programme in Genomics, Ethics and Society. Genetic testing and Alzheimer disease: Has the time come? Nature Medicine 1998; 4: 757-759. National Institute on Aging and Alzheimer's Association Working Group. Apolipoprotein E genotyping in Alzheimer's disease. Lancet 1996; 347: 1091-1095. Post SG, Whitehouse PJ, Binstock RH, et al. The clinical introduction of genetic testing for Alzheimer disease. JAMA 1997; 277: 832-836. Relkin NR, Kwon YJ, Tsai J, Gandy S. The National Institute on Aging/ Alzheimer's Association recommendations on the application of apolipoprotein E genotyping to Alzheimer's disease. Ann NY Acad Sci 1996; 802: 149-171. Jobst KA, Hindley NJ, King E, Smith AD. The diagnosis of Alzheimer's disease: a question of image? J Clin Psychiatry 1994; 55 Suppl: S22-S31. Spinnler H, Della Sala S. The role of clinical neuropsychology in the neurological diagnosis of Alzheimer's disease. J Neurol 1988; 235: 258-271. Zakzanis KK. Quantitative evidence for neuroanatomic and neuropsychological markers in dementia of the Alzheimer's type. J Clin Exp Neuropsychol 1998; 20: 259-269. Bullido MJ, Artiga MJ, Recuero M, et al. A polymorphism in the regulatory region of APOE associated with risk for Alzheimer's dementia. Nat Genet 1998; 18: 69-71. Blacker D, Wilcox MA, Laird NM, et al. Alpha-2 macroglobulin is genetically associated with Alzheimer disease. Nat Genet 1998; 19: 357-360. Kang DE, Saitoh T, Chen X, et al. Genetic association of the low density lipoprotein receptor-related protein gene (LRP), an apolipoprotein E receptor, with late-onset Alzheimer's disease. Neurology 1997; 49: 56-61. Montoya SE, Aston CE, Dekosky ST, et al. Bleomycin hydrolase is associated with risk of sporadic Alzheimer's disease. Nat Genet 1998; 18: 211-212. Lehmann DJ, Johnston C and Smith AD. Synergy between the genes for butyrylcholinesterase K variant and apolipoprotein E4 in late onset confirmed Alzheimer's disease. Hum Mol Genet 1997; 11: 1933-1936. Panegyres PK, Mamotte CDS, Vasikaran SD, et al. Butyrylcholinesterase K variant and Alzheimer's disease. J Neurol 1999; 246: 369-370. Payami H, Schellenberg GD, Zareparsi S, et al. Evidence for association of HLA-A2 allele with onset age of Alzheimer's disease. Neurology 1997; 49: 512-518. Almqvist EW, Bloch M, Brinkman R, et al. On behalf of an international Huntington disease collaborative group. A worldwide assessment of the frequency of suicide, suicide attempts, or psychiatric hospitalization after predictive testing for Huntington's disease. Am J Hum Genet 1999; 64: 1293-1304. Taylor SD. Demand for predictive genetic testing for Huntington's disease in Australia, 1987 to 1993. Med J Aust 1994; 161: 351-354. (Received 2 Aug 1999, accepted 14 Feb 2000) Authors' details Neurosciences Unit, Health Department of Western Australia, Perth, WA. Peter K Panegyres, PhD, FRACP, Neurologist, and NHMRC Fellow, Department of Neuropathology, Royal Perth Hospital. Carmela Connor, MPsychol, Senior Clinical Psychologist. Toni Liebeck, BSW, Senior Social Worker. Genetic Services of WA, King Edward Memorial Hospital for Women, Perth, WA. Jack Goldblatt, MD, FRACP, Director. Ian Walpole, MB BS, FRACP, Consultant Geneticist. Karen Harrop, BSc, Genetic Counsellor. Reprints: Dr P K Panegyres, Department of Neuropathology, Royal Perth Hospital, Wellington Street, Perth, WA 6000. peter.panegyresATrph.health.wa.gov.au Make a comment 1: The genetics of Alzheimer's disease Familial early-onset Alzheimer's disease Studies of families in which Alzheimer's disease (AD) was inherited in an autosomal dominant pattern led to the discovery of three pathogenic loci that account for about 50% of all cases of early-onset AD3 (Table). As the condition is heterogeneous, every family with early-onset AD should be offered investigation as part of a coordinated DNA testing program for neurological disease. Mutations in the amyloid precursor protein gene (APP) were the first mutations related to early-onset AD,9 and account for 10%-20% of familial AD.10 Two presenilin genes, PS1 and PS2, are also associated with early-onset familial AD -- almost 50% of cases result from mutations in PS1,10 while mutations in PS2 are rare.11 As reproducibility in PS1 mutation testing has not been established in some laboratories, caution is warranted. Implications for genetic testing: Gene testing for early-onset AD is probably best performed in the context of well-designed, ethically approved research projects involving large families with clear documentation in multiple-affected members who inherited the condition in an autosomal dominant fashion. In some Australian centres, patients with early-onset AD are routinely tested outside of research protocols. As mutations in the presenilin and amyloid precursor protein genes do not account for all cases of early-onset AD, negative screening results for these mutations in an affected individual would not exclude a genetic cause of the disease. Sporadic late-onset Alzheimer's disease APOE: Over 90% of patients with AD have no family history of the condition. One of the more important discoveries in the understanding of these sporadic late-onset cases was that a polymorphism of the apolipoprotein E gene (APOE) was a risk factor (Table).12,13 APOE has three alleles, designated ε2, ε3 and ε4. The ε4 allele is associated with AD in 20%-30% of the general population and in 45%-60% of patients with AD.14 The homozygous genotype, APOE ε4/ε4, is found in 12%-15% of patients with AD, but in only 2%-3% of the general population.14 While not everyone homozygous for APOE ε4 develops dementia, having this genotype might increase the chance of AD developing at an earlier age.15 Approximately 30% of people homozygous for APOE ε4 develop AD.16 The odds ratio for this, based on analysis of 1899 patients aged over 65 years, is 1.37 (versus 0.53 for the APOE ε2 allele).16 In this same study, the age-adjusted odds ratio for incident dementia in individuals homozygous for the ε4 allele was 1.89, and 25% of cognitively normal subjects had at least one ε4 allele. Further, absence of an ε4 allele does not prevent the development of dementia and AD, and 85% of elderly people with the APOE ε4/ε4 genotype did not have evidence of cognitive decline.16 In a pathologically proven series, a single APOE ε4 allele had a sensitivity of 65% and a specificity of 68% for the diagnosis of AD.17 When used with conventional clinical criteria, APOE ε4 testing might increase the diagnostic sensitivity and specificity by 5%-10%; therefore, its role requires further validation.15,17 Implications for genetic testing: APOE ε4 genotyping should not be used in the routine assessment of patients with suspected dementia, as it does not add significant information to other diagnostic investigations such as computed tomography (CT) and neuropsychological assessment.18 If the DNA test is performed it should not be done without adequate pretest counselling as to its limitations and implications, or without adequate post-test psychosocial support. The results need to be stored confidentially in view of the implications for other, unrelated conditions (eg, APOE allele status was used to predict risk in cardiovascular disease long before its significance in AD was known), insurability, employment and psychosocial coping for affected individuals and at-risk families. Thus, APOE genotyping should only be performed as part of a well-structured, ethically approved research study investigating issues about the role of APOE in the pathogenesis of AD. The evidence does not support using APOE e4 genotyping as a predictive test for the development of AD, as the exact significance of an APOE ε4 allele in asymptomatic individuals has not been confirmed.19-23 APOE ε4 genotyping should not be used as a sole diagnostic test for AD. Diagnosis requires specialist referral for investigations, such as a CT scan (which has a 94% positive predictive value24) and neuropsychological tests (85%-90% positive predictive value for the diagnosis of dementia, with less than 5% overlap of neuropsychology scores between patients and controls25,26). A positive APOE ε4 test is not diagnostic of Alzheimer's disease, as a single APOE ε4 allele has a positive predictive value of 65% and a negative predictive value of 68%. The presence of the APOE ε4 allele does not exclude other causes of dementia. For example, a 1998 study showed that about 5% of patients with clinical criteria for the diagnosis of AD were homozygous for APOE ε4, but did not have pathological features of AD.17APOE ε4 diagnostic kits should not be used in the clinical assessment of dementia. (Although such kits were previously available in the United States, they had to be withdrawn because of misuse.2) Other genetic factors: A number of genetic factors in addition to APOE ε4 have been associated with sporadic AD (Table). These include APOE A/T polymorphism in the promoter region,27α2 macroglobulin 5' splice site deletion on exon 18,28 low-density lipoprotein-receptor-related protein,29 the G/G homozygous state of the bleomycin hydrolase gene,30 butyrylcholinesterase K variant,31,32 and the major histocompatibility A2 antigen.33 The contribution of these factors to the diagnosis of AD requires more research, as they have not been sufficiently validated to be used routinely. Implications for genetic testing: These genetic factors need confirmation and further analysis as to their role in the diagnosis of AD and should not be used as diagnostic or predictive tests outside of research programs. Clinical application of genetic factors in Alzheimer's diseaseChromosomeDiagnostic testing*Predictive testing†Pathogenic loci Presenilin 1 (PS1)14++ Presenilin 2 (PS2)1++ Amyloid precursor protein (APP)21+ + Risk loci Apolipoprotein E (APOE ε4)19± - Apolipoprotein E -491AA19- - α2 Macroglobulin12-- Low-density receptor-related protein12- - Bleomycin hydrolase17-- Butyrylcholinesterase K variant3-- *In symptomatic individuals with clinical evidence of autosomal dominant familial or sporadic Alzheimer's disease, using NINCDS-ADRDA criteria for the diagnosis of Alzheimer's disease.4 †In asymptomatic individuals using guidelines as developed for Huntington's disease.5-8 -491AA=A/A polymorphism at position -491 in the transcription regulation region of APOE. Back to text 2: National Institute of Neurological and Communicative Disorders and Stroke - Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA) criteria for the clinical diagnosis of Alzheimer's disease4 I. The criteria for the clinical diagnosis of probable Alzheimer's disease include: Dementia established by clinical examination and documented by the Mini-Mental Test, Blessed Dementia Scale, or some similar examination, and confirmed by neuropsychological tests; Deficits in two or more areas of cognition; Progressive worsening of memory and other cognitive functions; No disturbance of consciousness; Onset between ages 40 and 90, most often after age 65; and Absence of systemic disorders or other brain diseases that could account for the progressive deficits in memory and cognition. II. The diagnosis of probable Alzheimer's disease is supported by: Progressive deterioration of specific cognitive functions such as language (aphasia), motor skills (apraxia), and perception (agnosia); Impaired activities of daily living and altered patterns of behaviour; Family history of similar disorders, particularly if confirmed neuropathologically, and laboratory results showing: normal lumbar puncture as evaluated by standard techniques, normal pattern or non-specific changes in an electroencephalogram, such as increased slow-wave activity, and evidence of cerebral atrophy on computed tomography, with progression documented by serial observation. III. Criteria for diagnosis of definite Alzheimer's disease are: The clinical criteria for probable Alzheimer's disease, and Histopathological evidence from a biopsy or autopsy. Back to text 3: Australasian centres where genetic testing for presenilin, APP mutations and APOE genotyping and counselling is available Applied Molecular Biology Unit Biochemistry State Health Laboratory Brisbane, QLD Department of Pathology Royal Brisbane Hospital, Brisbane, QLD Molecular Pathology Laboratory Sullivan Nicolaides Pathology Taringa, QLD Laboratory and Community Genetics Kolling Institute of Medical Research Royal North Shore Hospital St Leonards, NSW Institute of Medical and Veterinary Science [IMVS] Adelaide, SA The Neurosciences Unit, Health Department of Western Australia, and Department of Neuropathology, Royal Perth Hospital, Perth, WA Hollywood Private Hospital Perth, WA Molecular Pathology Laboratory Canterbury Health Laboratories Christchurch, New Zealand Back to text 4: Recommendations for genetic testing in Alzheimer's disease Mutation testing for abnormalities in PS1, PS2 and APP should only be considered where the family history is appropriate and by referral to appropriate comprehensive, predictive testing programs. The absence of known mutations does not protect against the development of other types of dementia. The use of APOE ε4 genotyping as an adjunct to conventional diagnostic measures is unknown and the data suggest that it has low sensitivity and specificity and is of little diagnostic value in an individual patient. It has low predictive value in asymptomatic individuals and its use in this situation should be discouraged, except in well-defined research protocols with appropriate institutional ethics approval. APOE ε4 genotyping should not be used as the sole diagnostic test in patients in whom AD is suspected on clinical grounds. APOE ε4 genotype testing should not be offered without adequate pre-test and post-test counselling, education and support in patients in whom AD is suspected on clinical grounds. Genetic testing should follow carer or patient consent. APOE ε4 genotype analysis should not be performed in asymptomatic individuals. This position is supported by a number of overseas consensus statements.19-23 Other DNA-based genetic risk factors should not be used in the routine assessment of patients, except as part of an ethically approved research protocol. Back to text

Peter K Panegyres · Jack Goldblatt · Ian Walpole · Carmela Connor · Toni Liebeck · Karen Harrop

Editorial The hip fracture threat Fighting back with a cheap, safe and neglected weapon -- vitamin D with calcium MJA 1999; 170: 459-460 In Australia (as in other developed countries), fractures of the proximal femur are one of the major hazards of old age, particularly in women, in whom the incidence reaches about 3% per annum in the ninth decade.1 Hip fracture, with its associated significant mortality and high rate of residual disability,2 is widely regarded as the ultimate expression of osteoporosis. In fact, this fracture is as much due to more frequent falls in the elderly as to reduced bone density.2,3 As hip fracture is so clearly a function of ageing, its prevalence is bound to increase with increasing longevity, but the scale of this increase is not widely appreciated. In this issue of the Journal, two reports, one by Sanders et al 4 and the other by Pocock et al 5, predict an alarming virtual doubling in hip fracture incidence in Australia (from about 15 000 to 30 000 per annum) in the next 20 years, assuming age-specific rates remain constant. The scenario presented by these authors is made even more disturbing by Pocock and colleagues' assessment of the scope for a preventive screening program.5 Applying optimistic assumptions of 60% of the target population screened, 60% complying with therapy, and the therapy being 50% effective, they found that the number of hip fractures would still increase by over 50% in the next 20 years. This is not surprising in view of the diversity of risk factors involved in both bone fragility and falls in the elderly. Bone fragility is a function not only of bone density (in which there is a major genetic component6), but also of bone turnover7 and bone architecture.8 Falls are subject to even more risk factors, including impaired vision, muscle weakness, postural hypotension (including the use of diuretics, because of their hypotensive action) and long-acting sedatives. Other risk factors for low bone density or frequent falls include smoking, physical inactivity, low body weight and inadequate exposure to sunlight.9 Most preventive measures for hip fractures in the elderly have been directed at the bone itself, and oestrogens,10 bisphosphonates11 and calcitriol12 have all been shown to reduce fracture rates. However, even if increasing use of these potent and relatively expensive agents could reverse fracture risk in selected individuals, this would have only a limited impact at the population level.9 In this rather bleak scenario, there is one relatively simple approach that should perhaps be pursued more actively than it is at present, namely the greater use of vitamin D and calcium in the elderly, particularly in those who are housebound or in institutions. It is 30 years since histological evidence of vitamin D deficiency in hip fracture patients was first reported in England,13 and over 20 years since this histological evidence was confirmed by demonstrating low serum levels of 25-hydroxyvitamin D in these patients.14 After confirmation of these findings in many other countries, vitamin D insufficiency (ie, a low serum level of 25-hydroxyvitamin D without overt evidence of rickets/osteomalacia) was uncovered in women with hip fractures and in nursing home residents in sunny South Australia.15 Subsequent studies confirmed the poor vitamin D status of nursing home residents in New South Wales16 and Victoria,17 and it is now generally accepted that vitamin D insufficiency, and associated secondary hyperparathyroidism16 with high bone turnover,18 are as common among elderly citizens in Australia as elsewhere, both because physical infirmity reduces exposure to sunlight and because age-related thinning of the skin reduces its capacity to synthesise cholecalciferol.19 Although there is some disagreement about the threshold level of 25-hydroxyvitamin D in plasma that triggers secondary hyperparathyroidism (we find the threshold to be at about 40-50 nmol/L, but thresholds as high as 100 nmol/L have been suggested20), there is consensus that quite mild vitamin D insufficiency stimulates parathyroid hormone secretion. These observations might be regarded as academic were it not for a French trial in which 800 units of vitamin D and 1200 mg of calcium daily for 18 months normalised serum 25-hydroxyvitamin D and parathyroid hormone levels and reduced the hip fracture incidence by 43% in 877 female nursing home residents (compared with 888 controls).21 Although the rapidity of this therapeutic effect could hardly have been due to a change in bone density, it might be explained by a reduction in bone turnover from reduced parathyroid activity, combined with improved muscle strength and a consequent reduction in falls from the action of vitamin D on muscle.22 A subsequent Dutch study, showing that 400 units of vitamin D without calcium given daily for three years had no effect on hip fracture rate in subjects not in institutions,23 does not vitiate the French trial, which used more vitamin D, combined it with calcium and targeted a vitamin D-insufficient population. We do not wish to imply that vitamin D (with calcium) is the be-all and end-all of hip fracture prevention, or to deny that aged-care services need to be strengthened to cope with an ageing population. We do suggest, however, that vitamin D (with calcium) -- a preventive measure that is not only cheap and safe but simultaneously targets both bone and muscle -- is an attractive but neglected weapon in the campaign against hip fractures. Perhaps the time has come to set up task forces at Federal and/or State levels to consider this and other options. Howard A Morris Chief Medical Scientist Allan G Need Divisional Head, and Senior Visiting Physician, Division of Clinical Biochemistry Institute of Medical and Veterinary Science, and Department of Medicine, University of Adelaide, SA B E Christopher Nordin Senior Specialist and Visiting Professor Division of Clinical Biochemistry, Institute of Medical and Veterinary Science, and Department of Pathology, University of Adelaide, SA March L, Chamberlain A, Cameron I, et al. Prevention, treatment and rehabilitation of fractured neck of femur. Health Outcomes Project 1996. Sydney: Public Health Unit, Northern Sydney Area Health Service, 1996. (ISBN 07310 9633 9). Also on the internet <http://www.mja.com.au/public/issues/iprs2/march/fnof.pdf> Brockelhurst JC, Exton-Smith AN, Lempert Barber SM, et al. Fracture of the femur in old age: a two-centre study of associated clinical factors and the cause of the fall. Age Ageing 1978; 7: 7-15. Dargent-Molina P, Favier F, Grandjean H, et al. Fall-related factors and risk of hip racture: the EPIDOS prospective study. Lancet 1996; 348: 145-149. Sanders KM, Nicholson GC, Ugoni AM, et al. Health burden of hip and other fractures in Australia beyond 2000. Projections based on the Geeong Osteoporosis Study. Med J Aust 1999; 170: 467-470. Pocock NA, Culton NL, Harris ND. The potential effect on hip fracture incidence of mass screening for osteoporosis. Med J Aust 1999; 170: 486-488. Slemenda CW, Christian JC, Williams CJ, et al. Genetic determinants of bone mass in adult women: a reevaluation of the twin model and the potential inportance of gene interaction on heritability estimates. J Bone Miner Res 1991; 6: 561-567. Melton LJ, Khosla S, Atkinson EJ, et al. Relationship of bone turnover to bone density and fractures. J Bone Miner Res 1997; 12: 1083-1091. Faulkner KG, Cummings SR, Black D, et al. Simple measurement of femoral geometry predicts hip fracture: the study of osteoporotic fractures. J Bone Miner Res 1993; 8: 1211-1217. Cummings SR. Prevention of hip fractures in older women: a population-based perspective. Osteoporos Int 8 (Suppl 1): S8-S12. Weiss NS, Ure CI, Ballard JH, et al. Decreased risk of fractures of the hip and lower forearm with postmenopausal use of oestrogen. N Engl J Med 1980; 303: 1195-1198. Liberman UA, Weiss SR, Broll J, et al. Effect of oral alendronate on bone mineral density and the incidence of fractures in postmenopausal osteoporosis. N Engl J Med 1995; 333: 1437-1443. Tilyard M, Spears GFS, Thomson J, Dovey S. Treatment of postmenopausal osteoporosis with calcitriol or calcium. N Engl J Med 1992; 326: 357-362. Aaron JE, Gallagher JC, Anderson J, et al. Frequency of osteomalacia and osteoporosis in fractures of the proximal femur. Lancet 1974; 2: 229-233. Baker MR, McDonnell H, Peacock M, Nordin BEC. Plasma 25-hydroxyvitamin D concentrations in patients with fractures of the femoral neck. BMJ 1979; 1: 589. Morris HA, Morrison GW, Burr M, et al. Vitamin D and femoral neck fractures in elderly South Australian women. Med J Aust 1984; 140: 519-521. Brock K, Reid J, Fraser D. Effect of type of accommodation on the vitamin D status of the elderly in Sydney, Australia. In: Norman AW, Bouillon R, Thomasset M, editors. Vitamin D: chemistry, biology and clinical applications of the steroid hormone. Riverside, Calif: University of California, 1997: 885-886. Stein MS, Scherer SC, Walton SL, et al. Risk factors for secondary hyperparathyroidism in a nursing home population. Clin Endocrinol 1996; 44: 375-383. Gallagher JC, Kinyamu HK, Fowler SE, et al. Calciotropic hormones and bone markers in the elderly. J Bone Miner Res 1998; 13: 475-482. Need AG, Morris HA, Horowitz M, Nordin BEC. Effects of skin thickness, age, body fat, and sunlight on serum 25-hydroxyvitamin D. Am J Clin Nutr 1993; 58: 882-885. McKenna MJ, Freaney R. Secondary hyperparathyroidism in the elderly: means to defining hypovitaminosis D. Osteoporos Int 1998; Suppl 8: S3-S6. Chapuy MC, Arlot ME, Duboeuf F, et al. Vitamin D3 and calcium to prevent hip fractures in elderly women. N Engl J Med 1992; 327: 1637-1642. Boland R. Role of vitamin D in skeletal muscle function. Endocrine Rev 1986; 7: 434-448. Lips P, Graafmans WC, Ooms ME, et al. Vitamin D supplementation and fracture incidence in elderly persons. Ann Intern Med 1996; 124: 400-406. 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/> We appreciate your comments.

Howard A Morris · Allan G Need

For Debate The potential effect on hip fracture incidence of mass screening for osteoporosis Nicholas A Pocock, Nicole L Culton and Neil D Harris MJA 1999; 170: 486-488 For editorial comment, see Morris et al; see also Sanders et al. With ageing of the Australian population, treatment of osteoporosis-related hip fractures will impose an increasing burden on the healthcare system. Based on current age-adjusted hip fracture incidence and population projections for New South Wales, we estimated a 90% increase in hip fractures by the year 2021. Contributing significantly to this increase will be the number of men reaching the high risk age group for osteoporotic hip fractures. A suggested solution -- screening and appropriate therapy for individuals at high risk of osteoporosis -- may have only a modest impact. Our calculations show that, even with optimistic screening and therapy compliance rates, hip fractures could still increase by over 50%. Other approaches need to be further explored. Introduction - Discussion - References - Authors' details - - More articles on Public and environmental health Introduction Osteoporosis-related hip fractures are a high-cost item in the Australian healthcare budget, and place considerable demands upon the limited resources of the public health system. This burden will increase in the first quarter of the next century as the projected Australian population over 65 years of age increases from the current level of 2.25 million to between 4.02 and 4.05 million by 2021.1 To avoid this impending healthcare crisis, several reports have suggested a screening program to identify individuals at high risk of osteoporosis, followed by appropriate intervention to reduce the number of hip fractures.2-6The possible introduction of a mass-screening program for osteoporosis raises a number of issues. Cost effectiveness is of major importance, and there are reports to indicate that screening for osteoporosis may well be cost effective.3,5,6 However, few data exist on the impact of a screening program on the healthcare system, and, in particular, on the demand for acute-care hospital beds, which has important implications for healthcare planning. To assess the impact of screening on the demand for hospital beds for hip fracture treatment, we have used available population projections for New South Wales (NSW) to calculate the likely number of hip fractures in people aged 65 years or older by the year 2021. We then assessed the potential of a screening program, coupled with effective therapy, to reduce hip fracture incidence using available data on population capture rates of current large screening programs, and data on therapy compliance and drug-efficacy rates. Our methods and the results we obtained are shown in the Box. Discussion Current costs of osteoporotic hip fractures in Australia exceed $400 million annually,15 and hip fracture treatment is making great demands on an already overstretched hospital infrastructure.2,7,16,17In 1994-95, there were 52017 admissions to NSW hospitals of patients over 65 years of age with major hip fractures. Without further intervention, our calculations show that, even with a low population growth model, this figure may rise by the year 2021 to 9800 hip fracture admissions annually in this age group, an increase of about 89%. A major cause will be the increase in the number of men reaching the high risk age group for osteoporotic hip fractures. In 1997, the population of men in NSW over 80 years of age numbered about 60 300.1 This is projected to increase to about 123 900 by 2021,1 an increase of 106%. A 65% increase in the number of women over 80 years of age is expected in the same interval. Our calculations show the limited preventive effect on increasing hip fracture incidence of an active interventional screening and therapy program for osteoporosis. Even with a relatively optimistic 60% screening and therapy compliance rate, hip fractures may still increase by about 55% compared with 1994-95. In view of the age of the target population (the average age of hip fracture patients in NSW is 82 years7), 40% capture and therapy compliance rates may be more realistic, suggesting that hip fractures may increase by 74% compared with 1994-95. It is also possible that capture and therapy compliance rates in the target population might not even achieve these levels. We also used the lowest of a number of population growth models.1 If faster population growth occurs, the increase in hip fractures will exceed our predictions, with correspondingly more serious implications for the healthcare system. We assumed the screening technique would identify all patients at increased risk of hip fracture and all would be offered therapy. This optimistic assumption is almost certainly incorrect and thus our calculations overestimate the benefits of a screening program. On the other hand, compared with current drug regimens, advances in therapy may decrease fracture risk. Moreover, therapies with minimal toxicity and which have demonstrated benefit, such as vitamin D and calcium, could be applied widely to high risk patients in nursing homes and other institutions.2,13 However, the potential benefit of such an approach is limited, as, at present, only 29% of hip fracture patients are admitted from nursing homes and an additional 9% from hostels.7 Our analysis does not address the cost efficacy of a screening program for osteoporosis. Nor does it address the possible role of population education in preventing osteoporosis. Recent raised community awareness of osteoporosis may translate in the future into consumer-driven demand for preventive action from healthcare providers and more self- initiated prevention. The recent increased demand for acute-care hospital beds in NSW has been partly met by reducing the average length of stay in hospital and increasing the number of day-only procedures. However, there is a limit to how much of the demand for hospital services can be met by these means. The average length of stay for hip fracture treatment in NSW has already been reduced from 31.5 days in 198018 to 11 days in 1995,7 and there is likely to be only limited additional gain from future efforts to reduce hospital stay for these patients.7 The increased number of hip fractures by 2021 will require considerable additional hospital resources, and, in view of the seasonal variation in hip fracture incidence,18 may impose an extreme burden on hospital services at certain times of the year. To cope with this, health service providers need to address the issue of future hospital bed availability for hip fractures. Failure to plan adequately may result in delay in treating other, less urgent, patients. In conclusion, Australia, like other Western countries, must cope with the health problems of an ageing population in the early part of the next century, with osteoporotic hip fractures likely to be a major component of the expected increased demand for acute-care hospital services. A preventive program based on mass screening for osteoporosis and treatment of high risk individuals may have only a limited impact. While potentially of benefit, this approach would be insufficient by itself, and additional or alternative approaches to this problem, such as education of the community, need to be further explored. References Australian Bureau of Statistics. Population projections for New South Wales 1997 to 2051. Canberra: ABS, 1998. (Catalogue No. 3222.0.) Wark JD. Osteoporosis: the emerging epidemic. Med J Aust 1996; 164: 327-328. Garton MJ, Cooper C, Reid D. Perimenopausal bone density screening -- will it help prevent osteoporosis? Maturitas 1997; 26: 35-43. Kanis JA. Assessment of fracture risk and its application to screening for postmenopausal osteoporosis: synopsis of a WHO report. Osteoporos Int 1994; 4: 368-381. Tosteson AN, Rosenthal DI, Melton LJ, Weinstein MC. Cost effectiveness of screening perimenopausal white women for osteoporosis: bone densitometry and hormone replacement therapy. Ann Intern Med 1990; 113: 594-603. Black DM. Why elderly women should be screened and treated to prevent osteoporosis [review]. Am J Med 1995; 98 Suppl 2A: 67S-75S. March L, Chamberlain A, Cameron I, et al. Prevention, treatment and rehabilitation of fractured neck of femur. Health Outcomes Project 1996. Sydney: Public Health Unit, Northern Sydney Area Health Service, 1996 (ISBN 07310 9633 9). Updated information provided by personal communication. Also on the internet <http://www.mja.com.au/public/issues/iprs2/march/fnof.pdf> Barratt AL, Cockburn J, Redman S, et al. Mammographic screening: results from the 1996 National Breast Health Survey. Med J Aust 1997; 167: 521-524. Salzman C. Medication compliance in the elderly. J Clin Psychol 1995; 56 Suppl 1: 18-22. McElnay JC, McCallion CR, al-Deagi F, Scott M. Self-reported medication non-compliance in the elderly. Eur J Clin Pharmacol 1997; 53: 171-178. Wren BG, Brown L. Compliance with hormonal replacement therapy. Maturitas 1991; 13: 17-21. Rozenberg S, Vandromme J, Kroll M, et al. Compliance to hormone replacement therapy [review]. Int J Fertil Menopausal Stud 1995; 40 Suppl 1: 23-32. Black DM, Cummings SR, Karpf DB, et al. Randomised trial of alendronate on risk of fracture in women with existing vertebral fractures. Lancet 1996; 348: 1535-1541. Seeman E. Osteoporosis: trials and tribulations [review]. Am J Med 1997; 103 Suppl 2A: 74S-87S. Randell A, Sambrook PN, Nguyen TV, et al. Direct clinical and welfare costs of osteoporotic fractures in elderly men and women. Osteoporos Int 1995; 5: 427-432. Lord SR. Femoral neck fractures: admissions, bed use, outcomes and projections. Med J Aust 1996; 145: 493-496. Lord SR. Hip fractures: changing patterns in hospital bed use in NSW between 1979 and 1990. Aust N Z J Surg 1993; 63: 352-355. Lau EM, Gillespie BG, Valenti L, O'Connell D. The seasonality of hip fracture and its relationship with weather conditions in New South Wales. Aust J Public Health 1995; 19: 76-80. (Received 13 Nov 1998, accepted 13 Mar 1999) Authors' details Department of Nuclear Medicine and Bone Densitometry, St Vincent's Hospital, Sydney, NSW. Nicholas A Pocock, MD, FRACP, Senior Staff Specialist. Nicole L Culton, BAppSc, Research Officer. Neil D Harris, BA(Comm), RN, Research Officer. Reprints will not be available from the authors. Correspondence: Associate Professor N A Pocock, Department of Nuclear Medicine and Bone Densitometry, St Vincent's Hospital, Sydney, NSW 2010. Email: n.pocockATunsw.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/> How many hip fractures can we prevent in New South Wales Methods To determine the predicted NSW population of those aged 65 years and over in 2021, we used the most recent Australian Bureau of Statistics population projections (low population growth model).1 To calculate the likely absolute numbers of hip fractures in 2021, we assumed similar age-adjusted hip fracture rates to those currently found in NSW.7 In women, the annual incidence of hip fractures in NSW (based on figures for 1995-96) ranges from 1.77/1000 in the 65 to 69 years age group, to 33.21/1000 in the over-85 group.7 In men, the respective rates are 1.01/1000 and 18.45/1000.7 These hip fracture incidences were applied to the NSW population predictions to derive the expected number of hip fractures in 2021 for the low population growth model. It is difficult to estimate the likely capture rate of an osteoporosis screening program (ie, the proportion of the target population using the service), as the population at risk of osteoporotic fractures is generally older than those targeted by current screening programs (eg, mammographic screening for breast cancer). In addition, an osteoporosis screening program would need to include men, and no comparable screening programs for men currently exist in Australia. In the absence of a more suitable model, a recent study of the data from the 1996 National Breast Health Survey reported that about 50% of the target population have participated in the Program within the past two years.8 For our analysis we have made projections using 10%, 20%, 40%, 60% and 80% population capture rates. There is no current consensus on the best osteoporosis screening program. For our study, however, we assumed a hypothetical best-case scenario in which the screening technique would identify all patients at increased risk of fracture, and therapy would be offered to all at-risk subjects. Reported compliance rates for long term medical therapy vary widely.9 While figures of up to 80% have been reported,10 particularly with medications which have few side effects, lower compliance rates are more common for medications with adverse or unpleasant side effects (eg, hormone replacement therapy).11,12 There are few data available on long term compliance with therapy for osteoporosis, such as bisphosphonates, calcitriol or the latest generation of selective oestrogen receptor modulators. The possible efficacy of a screening and treatment program was calculated separately for compliance rates of 20%, 40%, 60% and 80%. The efficacy of a treatment program targeted at high risk individuals depends not only on compliance with therapy, but also on drug efficacy. Available data suggest that current therapies for osteoporosis may have about 50% efficacy in reducing fractures.13,14 While it is possible that more effective therapeutic regimens will become available in the future, we used a value of 50% drug efficacy. Results In 2021, the projected age-specific NSW population for men and women over the age of 65 years (low population growth model) is shown in Table 1.1 Based on these population figures, and on recent data on age-specific admission rates for hip fractures,7 by 2021 we predict there will be about 9800 hip fracture admissions annually in NSW in subjects aged 65 years and older (Table 2). This is an increase of about 89% above current levels and compares with an expected 14% to 22% increase in the entire NSW population during the same period.1 In Table 3 the impact of an osteoporosis screening program and effective therapy in 2021 is shown for NSW men and women over 65 years at different capture rates and therapy compliance levels. The potential efficacy of a screening program would vary widely depending on population capture rates and therapy compliance. With an optimistic 60% population capture rate and 60% long term therapy compliance, with the low population growth model, a screening program might potentially prevent 1767 admissions for hip fractures. In this situation, hip fracture admissions in NSW in 2021 would still be 55% higher than in 1994-95. Back to text

Nicholas A Pocock · Nicole L Culton · Neil D Harris

Lynette M March, Anne C Chamberlain, Ian D Cameron, Robert G Cumming, Alan J M Brnabic, Terrence P Finnegan, Susan E Kurrle, Jennifer M Schwarz, Sydney M L Nade, Tom K F Taylor, and members of the Fractured Neck of Femur Health Outcomes Project Team* MJA 1999; 170: 489-494 Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details This article was first published in an unedited form after internet peer review. Click here to read the unedited version and the transcript of the review process. - - More articles on Orthopaedic surgery Abstract Objectives: To develop evidence-based guidelines for the treatment of proximal femoral fractures to optimise functional outcome while minimising length of stay in hospital. Data sources: Systematic literature search of MEDLINE and CINAHL computer databases, bibliographies, and current contents of key journals for 1966-1995. Study selection: English-language randomised controlled trials of all aspects of acute-care hospital treatment of proximal femoral fracture among subjects aged 50 years and over with proximal femoral fractures not due to metastatic disease. Data extraction: Two independent reviewers, blinded to authors, institution and study results, followed a standard Cochrane Collaboration protocol and assessed study quality and treatment conclusions. When necessary, a third review was performed to reach consensus. Results: Of the 120 articles published between 1966 and December 1995, 97 met the inclusion criteria. Fifteen clinical interventions were reviewed. Five were supported by National Health and Medical Research Council (NHMRC) level I evidence (prophylactic anticoagulants, prophylactic antibiotics, regional anaesthesia, pressure-relieving mattresses, and internal surgical fixation), two had no supporting randomised controlled trial evidence (time to surgery, time to mobilisation after surgery) and the remainder were classified as having Level II evidence. A review of current practice (1993-94) identified wide variability in these interventions across five acute-care hospitals in the Northern Sydney Area Health Service. Conclusions: Randomised controlled trial evidence (NHMRC Levels I and II) exists for many, but not all, aspects of hip fracture treatment. There is a need for changes to be made to some aspects of practice in accordance with evidence-based guidelines. Introduction Each year, fractures of the proximal femur (hip fracture) affect 4% of women and 2% of men aged 85 years or more. In 1995, this led to about 15 000 hospital admissions across Australia. Given current age-specific hip fracture rates1 and the expected ageing of the population,2 we calculated that by the year 2021 admissions for hip fracture will more than double. Conservative estimates of the current costs of acute inpatient care for these patients are $7.8 million in the Northern Sydney Area Health Service and $46.3 million for the whole of New South Wales (NSW).1 This does not include other costs, such as rehabilitation, support services, residential care, family assistance and changes in quality of life. The death rate in the 12 months after hip fracture is about 25%, four times greater than for community-living age-matched controls.3 Most survivors do not return to their prefracture level of independence and physical abilities.4The main objective of this study was to answer two questions about treatment of proximal femoral fractures: "What is the right thing to do?" and "Are we doing the right thing?", and then to develop evidence-based clinical guidelines for hip-fracture treatment. A systematic approach was taken, with a focus on health outcomes;5 we aimed to make recommendations that would optimise functional outcome while minimising length of stay in hospital. Methods What is the right thing to do? We performed a systematic review of randomised controlled trials (RCTs) and meta-analyses that included patients over 50 years with proximal femoral fractures. In the absence of an RCT (there were none published for "time to surgery" and "time to mobilisation after surgery"), we searched for observational studies. The main literature source was English language articles identified from MEDLINE and CINAHL from 1966 to December 1995. Search words used were "hip fractures", "proximal femoral fractures", "fractured neck of femur", together with specific interventions and clinical indicators (Box 1). The searches were limited to English language, RCTs, meta-analyses, age 50 years or over, and proximal femoral fractures not due to metastatic disease. In addition, manual searches were conducted of current issues of key specialty and general journals, our personal literature, libraries, bibliographies of the published articles and personal contact with those working in areas relevant to hip fracture, including the Cochrane Collaboration Musculoskeletal Injuries Group. Articles were distributed randomly to the assessors by the use of a random numbers table. The assessors, who were all experienced in the critical appraisal of scientific literature, were blinded to the authors, institutions and journal of publication of the articles. Articles were read independently by two assessors. Disagreements were resolved by a third assessment and a consensus meeting. Results and data on study quality were recorded according to Cochrane Collaboration guidelines for the assessment of study quality.6 Guidelines for ranking the level of evidence were those devised by the National Health and Medical Research Council (NHMRC).7 Are we doing the right thing? The study population for the medical audit came from the five acute-care Northern Sydney Area Health Service public hospitals during the 1993-94 financial year. All admissions for proximal femoral fracture in the 12 months were included. Patients with multiple injuries or fractures due to metastatic cancer were excluded. Data were extracted by trained medical record reviewers. A second audit, conducted by an independent reviewer in a 10% random subsample, showed more than 90% agreement. Patients were identified by ICD-9 code 820 (fracture of neck of femur) and by the following procedural codes: 79.15 Closed reduction of fracture with internal fixation -- femur 79.35 Open reduction of fracture with internal fixation -- femur 81.51 Total hip replacement 81.52 Partial hip replacement 81.53 Revision of hip replacement Development of evidence-based guidelines The key steps in the process of care for the acute management of hip fracture were identified by discussion with clinical staff and review of medical records (Box 1) and a specific clinical question was asked for each (eg, "Do low pressure mattresses reduce the number and severity of pressure sores?"). All supporting trial evidence was summarised in table format with author, year, interventions tested, number of subjects, ranking of bias (low, moderate, high), adequate concealment of allocation to groups (yes/no), summary of results of the individual articles with odds ratios and 95% confidence limits and, where possible, a calculation of the number needed to treat.6 Data were in a suitable format for meta-analysis for "prophylactic antibiotics" and "type of anaesthesia", but summary statistics were not generated for the other treatment modalities. Full details of all articles and these summaries are available from the authors and are on the Internet.1 From these tables, a one-page summary was generated for each clinical intervention, together with recommendations for clinical practice and suggestions for future study. These were circulated among the review team and the orthopaedic clinical groups. The results of the medical literature review and medical record audit were presented to medical and nursing staff in each hospital in oral and written form. Local practice was compared with practice in the other hospitals and to evidence-based best practice. After all these steps, a single page of draft guidelines was developed with NHMRC levels of evidence listed for each clinical recommendation. These were circulated and presented for further discussion before being adopted. Results The right thing to do Of the 120 articles published between 1966 and December 1995, 97 met the inclusion criteria. Articles were excluded if they did not report randomised trials, if they had insufficient numbers of patients with hip fracture, or if they were judged to be of poor quality by two independent assessors.1 Our conclusions from the literature review addressed 15 issues, and what we found, on the basis of available evidence, is given in Box 1. Box 2 presents the evidence-based clinical guidelines and average practice (1993-94) for each of the clinical interventions (as well as for acute-care-hospital length of stay) among the five acute-care hospitals audited. Average practice is given as unweighted averages across all five hospitals of the frequency of adherence to evidence-based best practice, plus the range from lowest to highest frequency. The guidelines can be applied to most, but not all, patients who sustain a proximal femoral fracture. Individual circumstances and comorbidities will always influence decision-making. These guidelines should be updated as new evidence becomes available. What we are doing In all, 729 consecutive admissions were audited and will be the subject of a more detailed report evaluating the implementation of the guidelines. No significant variation was shown among the five acute-care hospitals with respect to the patients' age (mean, 82.4 years; 18% were 90 years or older), sex (81% female), admissions from nursing homes (28.7%) and fracture type (51% intracapsular, 43% extracapsular, 6% unknown). All patients had at least one comorbidity, 71.7% had two or more and almost a third had five or more. Mortality at 12 months was 18%1 for non-nursing-home patients and 38% for nursing-home patients. At the four-month follow-up, 16% of patients required a new nursing-home admission. There was considerable variation in the clinical interventions (Box 2), particularly evident for "time to surgery", "preoperative traction", "pressure gradient stockings", "type of anaesthesia" (spinal) and "urinary catheterisation". Prophylactic antibiotics (intravenous) were used in the majority of patients in all five hospitals, but most continued their use longer than evidence and basic principles require. Giving additional oral antibiotics, for which there is no supporting evidence, was also common practice (lowest hospital rate, 32%; highest hospital rate, 83%). Surgical wound drains were used almost universally, with most remaining in place beyond 24 hours. Delay in mobilisation after surgery was associated with an increased length of stay. The hospital with the longest time to mobilisation also had the longest acute-care stay (median, 13 days v. overall median, 9 days). Three-quarters of patients who were admitted from their own home were discharged to a rehabilitation facility. Acute-care stay for these patients (median, 11 days) was considerably longer than for those returning to a nursing home (median, 6 days). The day of the week on which a patient was admitted was also found to be associated with length of stay, and this effect occurred both between and within the five hospitals. Patients admitted on a Thursday were likely to spend an extra two days in the acute-care facility (median, 11 days) compared with those admitted on other days (median, 9 days). Discussion Our study reports the completion of a project which followed a structured approach to health-outcomes research, as advocated by the NSW Health Department.5 We developed evidence-based guidelines for the management of proximal femoral fractures. The method we used adhered closely to the guidelines for the development of guidelines published by the NHMRC.7 To our knowledge, this is the first time evidence-based guideline development has been performed within the context of clinical practice, ensuring that the recommendations for best-practice interventions are realistic. The levels of evidence for each recommendation were made explicit, with all the supporting evidence available for discussion. Clinical staff were involved throughout the process, and each step was systematically developed and evaluated. Thus, the support for our conclusions is robust. Current practice, identified by medical record audit, was compared with evidence-based best practice and areas of care requiring modification were identified. A number of steps in patient treatment were supported by high level evidence, but wide variability in the routine use of these treatments was seen among the five participating hospitals. There was little or no supporting evidence for some common practices, including preoperative traction and the extended use of wound drains. Although not measured systematically, we observed great variability in clinicians' response to this information, ranging from relief to frank disbelief, and many showed considerable reluctance to drop a "time-honoured practice". Prevention strategies involving medical therapies, such as prophylactic anticoagulants and antibiotics, were in widespread use and compared favourably with other audits.105,106 However, non-pharmaceutical prevention strategies, including pressure-decreasing mattresses, oxygen saturation monitoring and nutritional supplements, were not in routine use in any hospital. Despite high level evidence for the use of prophylactic anticoagulants, the exact timing of initial administration of anticoagulation remained in doubt, with surgical and anaesthetic staff expressing concern about its use in combination with regional anaesthesia. There is an extremely small, but nevertheless serious, risk of spinal haematoma with this combination. On the balance of available evidence, the benefits appear to outweigh the risk of harm, but it remains a controversial area, suggesting that further trials on types and timing of anticoagulants are required. The evidence that regional anaesthesia was associated with reduced mortality and morbidity compared with general anaesthesia also met with a mixed response, with anaesthetists being completely polarised in their views. The published meta-analysis on this topic41 did have flaws (duplication of patients, not all RCTs), but our review team reassessed the original articles according to the Cochrane Collaboration protocol and performed a repeat analysis, excluding studies which appeared to be duplicated, and reached the same conclusion, albeit with a more conservative estimate of benefit (summary odds ratio for mortality, 0.68; 95% CL, 0.49, 0.96). The optimum time from admission to surgical operation has long been a vexed question. Only observational studies,8-12 with their inherent biases and conflicting results, were available to guide recommendations. Longer time to surgery is likely to increase the risk of complications and the total length of stay, and early surgery on patients who are medically stable has not been shown to cause any harm. We found considerable variability in time to surgery, with up to 20% of patients waiting longer than 72 hours. This may reflect the lack of availability of out-of-hours surgical facilities and, to a lesser extent, the achievement of medical stability, but these patients continue to be "poor surgical relations" and are not given the priority they deserve. Earlier mobilisation also has resource implications and is dependent, in part, on the availability of physiotherapy staff, but also on a patient's general condition. While there are no randomised controlled trials to indicate the optimal time for mobilisation, a review of all trials of surgical treatment showed that ambulation on the first or second day after surgery had no adverse effects,56-88,98 and a cohort study has now reached the same conclusions.107 The day of admission appeared to influence both delay to surgery and overall acute length of stay, suggesting that the practice of adding these patients to a routine list, rather than making special arrangements for them, may be a factor in prolonging length of stay. Patients requiring transfer to rehabilitation facilities generally stayed several days longer in the acute-care ward compared with those discharged to nursing-home care. This suggests a need to address difficulties with the process of assessment for rehabilitation and/or the availability of rehabilitation beds. Costs could be reduced by earlier transfer to rehabilitation from the more expensive acute-care ward, but whether this would mean longer-term cost savings remains to be determined. Our study identified considerable variation in current management of patients who have sustained hip fractures. It has some limitations, being restricted to English language articles and to evidence published up to January 1996. As a result, a few relevant references may have been missed. However, we recommend that these guidelines be applied to most elderly patients admitted with hip fracture, as we have shown that sufficient information now exists to challenge treatments based solely on tradition or individual perceptions. The current "epidemic" of proximal femoral fractures108 makes it essential that the best possible use is made of scarce resources to achieve optimal outcomes. Acknowledgements We acknowledge the support and assistance of the NSW Health Department's Health Outcomes Program Grants Scheme, the Cochrane Musculoskeletal Injuries Group, the staff and administration of the five acute-care public hospitals, the Northern Sydney Public Health and Health Service Development Units and the Swedish Hip Fracture Group. This study would not have been possible without the help of the other members of the Project team: Dr Don Holt, Mr Wayne Salvage, Mr John Skinner, Dr Krishna Hort, Mr Peter Whitecross, Mrs Barbara Carfrae, Ms Bronwyn Christiansen, Ms Loray Dudley, Ms Catherine Ferry, Ms Jill Makaroff, Ms Sarah Michael, Ms Melanie Saunders, Ms Katherine Scott, Ms Julia Sweeney, Ms Lorraine Heaslett, Mrs Carolyn Cole, Mr Terry Black. References March L, Chamberlain A, Cameron I, et al. Prevention, treatment and rehabilitation of fractured neck of femur. Report from the Northern Sydney Area Health Service Fractured Neck of Femur Health Outcomes Project, 1996. (ISBN 07310 9633 9.) Also on the internet: <http://www.mja.com.au/public/issues/iprs2/march/fnof.pdf> Australian Bureau of Statistics. Projections of the populations of Australia, States and Territories, 1984-2021 (Catalogue No. 3222.0) ISSN: 0816-3391. Katelaris AG, Cumming RG. Health status before and mortality after hip fracture. Am J Public Health 1996; 86: 557-560. Cumming RG, Klineberg R, Katelaris A. Cohort study of risk of institutionalisation after hip fracture. Aust N Z J Public Health 1996; 20: 579-582. Irwig L. An approach to evaluating health outcomes. NSW Public Health Bulletin 4 (12). Sydney: NSW Department of Health, 1993. The Cochrane Collaboration Reviewers' Handbook 1994. Section VI: Preparing and maintaining systematic reviews. Cochrane Collaboration, 1994: 1-75. (Version 3.0.2 Sept 1997 on the internet <http://wwwsom.fmc.flinders.edu.au/fusa/cochrane/ cochrane/hbook.htm>) National Health and Medical Research Council Quality of Care and Health Outcomes Committee. Guidelines for the development and implementation of clinical practice guidelines. Canberra: NHMRC/AGPS, 1995. (ISBN 0644 356766.) Bredahl C, Nyholm B, Hindsholm KB, et al. Mortality after hip fracture: results of operation within 12 hours of admission. Injury 1992; 23: 83-86. Dolk T. Operation in hip fracture patients -- analysis of the time factor. Injury 1990; 21: 369-372. Hoerer D, Volpin G, Stein H. Results of early and delayed surgical fixation of hip fractures in the elderly: a comparative, retrospective study. Bull Hosp Jt Dis 1993; 53: 29-33. Parker MJ, Pryor GA. The timing of surgery for proximal femoral fractures. J Bone Joint Surg Br 1992; 74: 203-205. Villar RN, Allen SM, Barnes SJ. Hip fractures in healthy patients: operative delay versus prognosis. BMJ 1986; 293: 1203-1204. Anderson GH, Harper WM, Connolly CD, et al. Preoperative skin traction for fractures of the proximal femur: a randomised, prospective trial. J Bone Joint Surg Br 1993; 75: 794-796. Finsen V, Borset M, Buvik GE, Hauke I. Pre-operative traction in patients with hip fracture. Injury 1992; 23: 242-244. Needoff M, Radford P, Langstaff R. Pre-operative traction for hip fractures in the elderly: a clinical trial. Injury 1993; 24: 317-318. Hofman A, Geelkerken RH, Wille J, et al. Pressure sores and pressure-decreasing mattresses: controlled clinical trial. Lancet 1994; 343: 568-571. Nuffield Institute of Health, University of Leeds and the NHS Centre for Reviews and Dissemination. How effective are pressure-relieving interventions for the prevention and treatment of pressure sores? Effective Health Care Bulletin 1995; 2(1). York: University of York, 1995. Brown AG, Visram AR, Jones RD, et al. Pre-operative and post-operative oxygen saturation in the elderly following spinal or general anaesthesia -- an audit of current practice. Anaesth Intensive Care 1994; 22: 150-154. Fugere F, Owen H, Ilsley A, et al. Changes in oxygen saturation in the 72 hours after hip surgery: the effect of oxygen therapy. Anaesth Intensive Care 1994; 22: 724-728. Agnelli G, Cosmi B, Di Fillipo P, et al. A randomised, double blind placebo controlled trial of dermatan sulphate for prevention of DVT in hip fracture. Thromb Haemost 1992; 67: 203-208. Antiplatelet Trialists' Collaboration. Collaborative overview of randomised trials of antiplatelet therapy III: Reduction in venous thrombosis and pulmonary embolism by antiplatelet prophylaxis among surgical and medical patients. BMJ 1994; 308: 235-296. Barsotti J, Gruel Y, Rosset P, et al. Comparative, double-blind study of two dosage regimens of low-molecular-weight heparin in elderly patients with a fracture of the neck of the femur. J Orthop Trauma 1990; 4: 371-375. Bergqvist D, Efsing HO, Hallbook T, Hedlund T. Thrombo-embolism after elective and post-traumatic hip surgery: a controlled, prophylactic trial with dextran 70 and low-dose heparin. Acta Chir Scand 1979; 145: 213-218. Bergqvist D. Orgaran in hip fracture surgery. Haemostasis 1992; 22: 104-108. Collins R, Scrimgeour A, Yusuf S, Peto R. Reduction in fatal pulmonary embolism and venous thrombosis by peri-operative administration of subcutaneous heparin: overview of results of randomized trials in general, orthopedic and urologic surgery. N Engl J Med 1988; 318: 1162-1173. Gerhart TN, Yett HS, Robertson LK, et al. Low-molecular weight heparinoid compared with warfarin for prophylaxis of deep vein thrombosis in patients who are operated on for fracture of the hip. J Bone Joint Surg Am 1991; 73: 494-502. Imperiale TF, Speroff T. A meta-analysis of methods to prevent venous thrombo-embolism following total hip replacement. JAMA 1994; 271: 1780-1785. Consensus Statement. Prevention of venous thrombo-embolism (Chairman, Nicolaides AN). Int Angiol 1997; 16: 3-38.. Lahnborg G. Effect of low dose heparin and dihydroergotamine on frequency of post-operative deep vein thrombosis in patients undergoing post-traumatic hip surgery. Acta Chir Scand 1980; 146: 319-322. Lassen MR, Borris LC, Christiansen HM, et al. Clinical trials with low-molecular weight heparins in the prevention of post-operative thrombo-embolic complications: a meta-analysis. Semin Thromb Hemost 1991; 17(Suppl 3): 284-290. Morris GK, Mitchell JR. Warfarin sodium in the prevention of deep venous thrombosis and pulmonary embolism in patients with fractured neck of femur. Lancet 1976; 2: 869-872. Morris GK, Mitchell JR. Preventing venous thrombo-embolism in elderly patients with hip fractures: studies of low-dose heparin, dipyridamole, aspirin and flurbiprofen. BMJ 1977; 1: 535-537. Nurmohamed MT, Rosendaal FR, Buller HR, et al. Low molecular weight heparin versus standard heparin in general and orthopaedic surgery: a meta-analysis. Lancet 1992; 340: 152-156. Oertli D, Hess P, Durig M, et al. Prevention of deep vein thrombosis in patients with hip fractures: low-molecular weight heparin versus dextran. World J Surg 1992; 16: 980-984. Pini M, Spadini E, Carluccio L, et al. Dextran/aspirin versus heparin/dihydro-ergotamine in preventing thrombosis after hip fractures. J Bone Joint Surg Br 1985; 67: 305-309. Powers PJ, Gent M, Jay RM, et al. A randomised trial of less intense post-operative warfarin or aspirin therapy in the prevention of venous thrombo-embolism after surgery for fractured hip. Arch Intern Med 1989; 149: 771-774. Rogers PH, Walsh PN, Marder VJ, et al. Controlled trial of low-dose heparin and sulfinpyrazone to prevent venous thrombo-embolism after operation on the hip. J Bone Joint Surg Am 1978; 60: 758-762. Stranks GJ, McKenzie NA, Grover ML, et al . The A-V Impulse System reduces deep-vein thrombosis and swelling after hemiarthroplasty for hip fracture. J Bone Joint Surg Br 1992; 74: 775-778. Williams JW, Eikman EA, Greenberg SH, et al. Failure of low-dose heparin to prevent pulmonary embolism after hip surgery or above the knee amputation. Ann Surg 1978; 188: 468-474. Fisher CG, Blachut PA, Salvian AJ, et al. Effectiveness of pneumatic leg compression devices for the prevention of thromboembolic disease in orthopaedic trauma patients: a prospective, randomised study of compression alone versus no prophylaxis. J Orthop Trauma 1995; 9: 1-7. Sorenson RM, Pace NL. Anesthetic techniques during surgical repair of femoral neck fractures: a meta-analysis. Anesthesiology 1992; 77: 1095-1104. Coad NR. Post-operative analgesia following femoral neck surgery: a comparison between 3-in-1 femoral nerve block and lateral cutaneous nerve block. Eur J Anaesthesiol 1991; 8: 287-290. Hood G. Post-operative analgesia after triple nerve block for fractured neck of femur. Anaesthesia 1991; 46: 138-140. Bodoky A, Neff U, Heberer M, Harder F. Antibiotic prophylaxis with two doses of cephalosporin in patients managed with internal fixation for a fracture of the hip. J Bone Joint Surg Am 1993; 75: 61-65. Boyd RJ, Burke JF, Colton T. A double-blind, clinical trial of prophylactic antibiotics in hip fractures. J Bone Joint Surg Am 1973; 55: 1251-1258. Buckley R, Hughes GN, Snodgrass T, Huchcroft SA. Perioperative cefazolin prophylaxis in hip fracture surgery. Can J Surg 1990; 33: 122-127. Ericson C, Lindgren L, Lindberg L. Cloxacillin in the prophylaxis of post-operative infections of the hip. J Bone Joint Surg Am 1973; 55: 808-813, 843. Garcia S, Lozano ML, Gatell JM, et al. Prophylaxis against infection: single dose cefonicid compared with multiple dose cefamandole. J Bone Joint Surg Am 1991; 73: 1044-1048. Gatell JM, Garcia S, Lozano L, et al. Perioperative cefamandole prophylaxis against infections. J Bone Joint Surg Am 1987; 69: 1189-1193. Hedstrom SA, Lidgren L, Sernbo I, et al. Cefuroxime prophylaxis in trochanteric hip fracture operations. Acta Orthop Scand 1987; 58: 361-364. Hjortrup A, Sorensen C, Mejdahl S, et al. Antibiotic prophylaxis in surgery for hip fractures. Acta Orthop Scand 1990; 61: 152-153. Karachalios T, Lyritis GP, Hatzopoulos E. Antibiotic prophylaxis in the surgical treatment of peri-trochanteric fractures: a comparative trial between two cephalosporins. Chemotherapy 1990; 36: 448-453. McQueen MM, Littlejohn MA, Miles RS, Hughes SP. Antibiotic prophylaxis in proximal femoral fracture. Injury 1990; 21: 104-116. Nungu KS, Larsson S, Wallinder L, Holm S. Bone and wound fluid concentrations of cephalosporins: oral cefadroxil and parenteral cefuroxime compared in 52 patients with a trochanteric fracture. Acta Orthop Scand 1995; 66: 161-165. Tengve B, Kjellander J. Antibiotic prophylaxis in operations on trochanteric femoral fractures. J Bone Joint Surg Am 1978; 60: 97-99. Aune AK, Ekeland A, Odegaard B, et al. Gamma nail vs compression screw for trochanteric femoral fractures. Acta Orthop Scand 1994; 65: 127-130. Bannister GC, Gibson AG, Ackroyd CE, et al. The fixation and prognosis of trochanteric fractures: a randomised, controlled trial. Clin Orthop 1990; 254: 242-246. Bridle SH. Fixation of intertrochanteric fractures of the femur: a randomised, prospective comparison of the gamma nail and the dynamic hip screw. J Bone Joint Surg Br 1991; 73: 330-334. Chapman MW, Bowman WE, Csongradi JJ, et al. The use of Ender's pins in extra-capsular fractures of the hip. J Bone Joint Surg Am 1981; 63: 14-28. Dalen N, Jacobsson B, Eriksson PA. A comparison of nail-plate fixation and Ender's nailing in pertrochanteric fractures. J Trauma 1988; 28: 405-406. Davis TR, Sher JL, Checketts RG, Porter BB. Inter-trochanteric fractures of the femur: a prospective study comparing the use of the Kuntscher-Y nail and a sliding hip screw. Injury 1988; 19: 421-426. Desjardins AL, Roy A, Paiement G, et al. Unstable inter-trochanteric fracture of the femur: a prospective, randomised study comparing anatomical reduction and medial displacement osteotomy. J Bone Joint Surg Br 1993; 75: 445-447. Esser MP, Kassab JY, Jones DH. Trochanteric fractures of the femur: a randomised, prospective trial comparing the Jewett nail-plate with the dynamic hip screw. J Bone Joint Surg Br 1986; 68: 557-560. Gargan MF, Gundle R, Simpson AH. How effective are osteotomies for unstable intertrochanteric fractures? J Bone Joint Surg 1994; 76: 789-792. Goldhagen PR, O'Connor DR, Schwarze D, Schwartz E. A prospective, comparative study of the compression hip screw and the gamma nail. J Orthop Trauma 1994; 8: 367-372. Hogh J, Lund B, Lucht U. Trochanteric and subtrochanteric fractures: the operative results in a prospective, comparative study of Ender nailing and McLaughlin osteosynthesis. Acta Orthop Scand 1981; 52: 639-643. Hornby R, Evans JG, Vardon V. Operative or conservative treatment for trochanteric fractures of the femur: a randomised, epidemiological trial in elderly patients. J Bone Joint Surg Br 1989; 71: 619-623. Leung KS, So WS, Shen WY, Hui PW. Gamma nails and dynamic hip screws for peri-trochanteric fractures: a randomised, prospective study in elderly patients. J Bone and Joint Surg Br 1992; 74: 345-351. Lund B, Hogh J, Lucht U. Trochanteric and sub-trochanteric fractures. One year follow-up of a prospective study of Ender and McLaughlin osteosynthesis. Acta Orthop Scand 1981; 52: 645-648. Nungu S, Olerud C, Rehnberg L. Treatment of intertrochanteric fractures: comparison of Ender nails and sliding screw plates. J Orthop Trauma 1991; 5: 452-457. Pitsaer E, Samuel AW. Functional outcome after intertrochanteric fractures of the femur: does the implant matter? A prospective study of 100 consecutive cases. Injury 1993; 24: 35-36. Sernbo I, Johnell O, Gardsell A. Locking and compression of the lag screw in trochanteric fractures is not beneficial. A prospective, randomised study of 153 cases. Acta Orthop Scand 1994; 65: 24-26. Sernbo I, Johnell O, Gentz CF, Nilsson JA. Unstable inter-trochanteric fractures of the hip: treatment with Ender pins compared with a compression hip-screw. J Bone Joint Surg Am 1988; 70: 1297-1303. Stark A, Brostrom LA, Barrios C, et al. A prospective, randomised study of the use of sliding hip screws and Ender nails for trochanteric fractures of the femur. Int Orthop 1992; 16: 359-362. Emery RJ, Broughton NS, Desai K, et al. Bipolar hemiarthroplasty for sub-capital fracture of the femoral neck: a prospective, randomised trial of cemented Thompson and uncemented Moore stems. J Bone Joint Surg Br 1991; 73: 322-324. Elmerson S, Andersson GB, Irstam L, Zetterberg C. Internal fixation of femoral neck fracture: no difference between the Rydell four-flanged nail and Gouffon's pins. Acta Orthop Scand 1988; 59: 372-376. Lu-Yao GL, Keller RB, Litternberg B, Wenberg JE. Outcomes after displaced fractures of the femoral neck: a meta-analysis of one hundred and six published reports. J Bone Joint Surg Am 1994; 76: 15-25. Madsen F, Linde F, Andersen E, et al. Fixation of displaced femoral neck fractures: a comparison between sliding screw plate and four cancellous bone screws. Acta Orthop Scand 1987; 58: 212-216. Kuokkanen H, Korkala O, Antii-Poika I, et al. Three cancellous bone screws versus a screw angle plate in the treatment of Garden I and II fractures of the femoral neck. Acta Orthop Belg 1991; 57: 3-57. Olerud C, Rehnberg L, Hellquist E. Internal fixation of femoral neck fractures: two methods compared. J Bone Joint Surg Br 1991; 73: 16-19. Radford PJ, Needoff M, Webb JK. A prospective, randomised comparison of the dynamic hip screw and the gamma locking nail. J Bone Joint Surg Br 1993; 7: 789-793. Rehnberg L, Olerud C. Fixation of femoral neck fractures: comparison of the Uppsala and von Bahr screws. Acta Orthop Scand 1989; 60: 579-584. Sernbo I, Johnell O, Baath L, Nilsson JA. Internal fixation of 410 cervical hip fractures: a randomised comparison of a single nail versus two hook-pins. Acta Orthop Scand 1990; 61: 411-414. Sikorski JM, Barrington R. Internal fixation versus hemiarthroplasty for the displaced subcapital fracture of the femur: a prospective, randomised study. J Bone Joint Surg Br 1981; 63: 357-361. Skinner P, Riley D, Ellery J, et al. Displaced subcapital fractures of the femur: a prospective, randomized comparison of internal fixation, hemiarthroplasty and total hip replacement. Injury 1989; 20: 291-293. Sorensen JL, Varmarken JE, Bomler J. Internal fixation of femoral neck fractures. Dynamic Hip and Gouffon screws compared in 73 patients. Acta Orthop Scand 1992; 63: 288-292. Svenningsen S, Benum P, Nesse O, Furset OI. Internal fixation of femoral neck fractures: compression screw compared with nail plate fixation. Acta Orthop Scand 1984; 55: 423-429. van Vugt AB, Oosterwijk WM, Goris RJ. Osteosynthesis versus endoprosthesis in the treatment of unstable intra-capsular hip fractures in the elderly: a randomised, clinical trial. Arch Orthop Trauma Surg 1993; 113: 39-45. Cobb JP. Why use drains? J Bone Joint Surg Br 1990; 72: 993-995. Varley GW, Milner SA, Turner GM, et al. Ultrasound assessment of the efficacy of wound drains. J R Coll Surg Edinb 1994; 39: 97-99. Varley GW, Milner SA. Wound drains in proximal femoral fracture surgery: a randomised, prospective trial of 177 patients. J R Coll Surg Edinb 1995; 40: 416-418. Skelly JM, Guyatt GH, Kalbfleisch R, et al. Management of urinary retention after surgical repair of hip fracture. Can Med Assoc J 1992; 146: 1185-1189. Bastow MD, Rawlings J, Allison SP. Benefits of supplementary tube feeding after fractured neck of femur: a randomised controlled trial. BMJ 1983; 287: 1589-1591. Delmi M, Rapin CH, Bengoa JM, et al. Dietary supplementation in elderly patients with fractured neck of femur. Lancet 1990; 335: 1013-1016. Sloan JP, Wing P, Dian L, Meneilly GS. A pilot study of anabolic steroids in elderly patients with hip fractures. J Am Geriatr Soc 1992; 40: 1105-1111. Tkatch L, Rapin CH, Rizzoli R, et al. Benefits of oral protein supplementation in elderly patients with fracture of the proximal femur. J Am Coll Nutr 1992; 11: 519-525. Zauber NP, Zauber AG, Gordon FJ, et al. Iron supplementation after femoral head replacement for patients with normal iron stores. JAMA 1992; 267: 525-527. Brostrom LA, Barrios C, Kronberg M, et al. Clinical features and walking ability treatment of trochanteric hip fractures in the early post-operative period after hip fracture. Ann Chir Gynaecol 1992; 81: 66-71. Cameron ID, Lyle DM, Quine S. Accelerated rehabilitation after proximal femoral fracture. Disabil Rehabil 1993; 15: 29-34. 100. Fordham R, Thompson R, Holmes J, et al. A cost-benefit study of geriatric-orthopaedic management of patients with fractured neck of femur. Discussion paper. York: Centre for Health Economics, University of York, 1986. Gilchrist WJ, Newman RJ, Hamblen DL, Williams BO. Prospective randomised study of an orthopaedic-geriatric inpatient service. BMJ 1988; 297: 1116-1118. Kennie DC, Reid J, Richardson IR, et al. Effectiveness of geriatric rehabilitative care after fractures of the proximal femur in elderly women: a randomised clinical trial. BMJ 1988; 297: 1083-1086. Oyewole MF, Moloney A. A randomised, controlled trial of a high-support hospital discharge team for elderly people. Age Ageing 1994; 23: 228-234. Reid J, Kennie DC. Geriatric rehabilitative care after fractures of the proximal femur: one year follow-up of a randomised, clinical trial. BMJ 1989; 299: 25-26. Todd CJ, Freeman DJ, Camilleri C, et al. Differences in mortality after hip fracture: The East Anglia audit. BMJ; 1995; 310: 904-908. Tallis G, Balla JJ. Critical path analysis for the management of fractured neck of femur. Aust J Public Health 1995; 19: 155-159. Koval KJ, Friend KD, Aharonoff GB, et al. Weightbearing after hip fracture: a prospective series of 596 geriatric hip fracture patients. J Orthop Trauma 1996; 10: 526-530. Cooper C, Campion G, Melton LJ. Hip fracture in the elderly: a word-wide projection. Osteoporos Int 1992; 2: 285-289. (Received 28 Jul 1998, accepted 19 Mar 1999) Authors' details Northern Sydney Area Health Service Public Health Unit, Hornsby Ku-ring-gai Hospital, Sydney, NSW. Lynette M March, Associate Professor; and Senior Staff Specialist in Clinical Epidemiology. Alan J M Brnabic, Statistician. Fractured Neck of Femur Health Outcomes Project, Health Services Development, Royal North Shore Hospital, Sydney, NSW. Anne C Chamberlain, Project Officer; Jennifer M Schwarz, Research Assistant. University of Sydney Rehabilitation Studies Unit, Royal Rehabilitation Centre, NSW. Ian D Cameron, Associate Professor; and Director. Department of Public Health and Community Medicine, University of Sydney, NSW. Robert G Cumming, Associate Professor. Department of Aged Care and Rehabilitation, Royal North Shore Hospital, Sydney, NSW. Terrence P Finnegan, Senior Staff Specialist. Rehabilitation and Aged Care Services, Hornsby Ku-ring-gai Hospital, Sydney, NSW. Susan E Kurrle, Staff Specialist. Department of Surgery, University of Sydney, NSW. Sydney M L Nade, Emeritus Clinical Professor of Orthopaedics. Department of Orthopaedics and Traumatic Surgery, University of Sydney, Royal North Shore Hospital, Sydney, NSW. Tom K F Taylor, Professor; and Head. Reprints: Associate Professor L M March, Department of Rheumatology, The Royal North Shore Hospital, St Leonards, NSW 2065. Email: lmarcATdoh.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: Systematic literature review of 15 aspects of treatment of proximal femoral fracture--conclusions and evidence level1. Time to surgery (Level III)8-12 No randomised-trial evidence is available and observational studies give a range of conclusions. Early surgery (within 24-36 hours) is recommended for most patients once medical assessment has been made and the patient's condition stabilised appropriately. Undue delay to surgery inevitably increases length of stay and may lead to more complications, including more pressure sores, pneumonia and confusion. 2. Preoperative traction (Level II)13-15 Routine use of preoperative skin and tibial pin traction should be abandoned. Pain should be adequately controlled with narcotic analgesia and/or nerve block. 3. Prevention of pressure sores (Level I)16,17 Patients should be nursed on one of a range of foam-based low pressure mattresses rather than standard hospital mattresses. Patients at very high risk of pressure sores should ideally be nursed on a large-cell, alternating-pressure air mattress or similar pressure-decreasing bed. 4. Oxygen therapy (Level II)18,19 Some evidence supports its routine use for the first 72 hours after surgery. All patients should have oximetry assessment from the time of emergency admission to 48 hours after surgery and oxygen administered as necessary. 5. Prophylactic anticoagulants (Level I)20-39 Unless there is a specific contraindication, patients should receive unfractionated low dose heparin (LDH) or low molecular weight heparin (LMWH), with a preference for the latter. This should commence as soon as possible after admission. 6. Pressure gradient stockings (Level II)40 Patients should be wearing these as soon as possible after admission. 7. Type of anaesthesia (Level I)41 Regional anaesthesia (spinal or epidural) appears to be associated with reduced short-term mortality and morbidity (confusion and thromboembolism) when compared with general anaesthesia and is recommended for most patients. 8. Type of analgesia (Level II)42,43 Pain should be adequately controlled with narcotic analgesia before and immediately after surgery. Femoral nerve blocks are useful in selected cases. 9. Prophylactic antibiotics (Level I)44-55 Prophylactic intravenous antibiotics should be given at induction of anaesthesia. Prolonged antibiotic use is of no proven benefit for prophylaxis of wound infection. 10. Type of surgery Extracapsular (trochanteric) fractures (Level I)56-74 should be treated surgically. A compression hip screw and plate has less chance of failure, leading to reoperation, compared with a fixed device and may prove to be more cost-effective in the long term. Undisplaced intracapsular fractures (Level I)75-88 should have internal fixation with a widely used method that is familiar to the surgeon (cancellous screws or compression screw and plate). Displaced intracapsular fractures (Level II)75-88 have no clearly superior surgical treatment. The options for surgical treatment of this fracture are internal fixation or arthroplasty. Internal fixation is associated with a higher risk of implant failure than hemiarthroplasty (femoral head replacement). At present the choice of treatment is best determined by patient factors (including age, presence of arthritis, availability and cost of the different types of treatment, surgeon experience and preference). 11. Surgical wound drains (Level II)89-91 May not be required as often as currently used and early removal is advised (around 24 hours after insertion). 12. Urinary catheterisation (Level II)92 Avoid indwelling catheters (where possible). Intermittent catheterisation is preferable and has been shown not to increase the incidence of urinary tract infections. 13. Nutritional status (Level II)93-97 All patients should have a nutritional assessment so that protein supplementation can be given as indicated. 14. Mobilisation (Level III)56-88,98 No randomised controlled trial evidence was available. A review of studies related to types of surgery1 concluded that almost all patients should be mobilised on the first or second day, taking as much weight on the fractured leg as the patient can tolerate. 15. Rehabilitation (Level II)99-104 Early assessment by a specialist team (within three days of admission) and active rehabilitation as soon as patient is mobile on a support frame is recommended for those who were independent before their fracture. Back to text 2: Evidence-based guidelines for acute management of proximal femoral fractureAverageRecommendation1993-94 practiceClinical intervention(level of evidence)(min-max)*1. Time to surgery8-12Within 24 hours of admission (Level III-3)15% (6%-24%)2. Preoperative traction13-15Not necessary -- adequate analgesiashould be given (Level II)57% (41%-64%)3. Prevention of pressure sores16,17Pressure care mattress to be used assoon as possible after admission (Level I) Not routine4. Oxygen therapy18,19O2 saturation monitored from timeof admission (Level II)Not routineO2 administered for 48 hours after surgery and if O2 saturation < 95% (Level II)Not routine5. Prophylactic anticoagulants20-39To commence as soon as possibleafter admission (Level I)87% (82%-98%)6. Pressure-gradient stockings40To be worn as soon as possible afteradmission (Level II)40% (16%-70%)7. Type of anaesthesia41Regional anaesthesia recommendedfor most patients (Level I)54% (14%-75%)8. Type of analgesia42,43Femoral nerve block in selected cases(Level II)Not routine9. Prophylactic IV antibiotics44-55At induction of anaesthesia (Level I)95% (86%-98%)10. Type of surgeryExtracapsular and undisplacedintracapsular fractures: compression screw device (Level I)56-7494% (83%-100%)Displaced intracapsular fractures:hemiarthroplasty (Level II)75-8861% (52%-67%)11. Surgical wound drains89-91Remove as soon as possible -- consider from 24 hours (Level II) Not recorded12. Urinary catheterisation92If possible, avoid indwelling catheters(Level II)66% (40%-90%)13. Nutritional status93-97Routine assessment -- provision of protein supplements as needed (Level II) Not routine14. Mobilisation56-88,98Early assisted ambulation -- by 48 hoursMedian Day 3after surgery (Level III)(Days 2-5)15. Rehabilitation99-104Early assessment by specialist team(Level II)Not routine16. Acute hospital length of stayEarly discharge to nursing home (Day 5)Median Day 6(Level IV)(Days 5-9)Early transfer to rehabilitation unit (Day 7)Median Day 11(Level II)(Days 8-16)Level of evidence -- National Health and Medical Research Council (Australia) 7I:Evidence obtained from a systematic review of all relevant randomised controlled trials (RCTs). II:Evidence obtained from at least one properly designed RCT. III - 1:Evidence obtained from well-designed controlled trials without randomisation. III - 2:Evidence obtained from well-designed cohort or case-control analytic studies, preferably from more than one centre or research group. III - 3:Evidence obtained from multiple time series with or without the intervention. Dramatic results in uncontrolled experiments could also be regarded as this type of evidence. IV:Opinions of respected authorities, based on clinical experience, descriptive studies, or reports of expert committees.* Unweighted average across all five acute-care hospitals of the frequency of adherence to evidence-based best practice in 1993-94. (min-max) = range of values from lowest rate (min) to highest rate (max). Back to text

Lynette M March · Anne C Chamberlain · Ian D Cameron · Robert G Cumming · Terrence P Finnegan · Susan E Kurrle · Jennifer M Schwarz

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 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

Editorial Hospital in the home: take the evidence and run The time for apathy and cynicism towards home-based care is over MJA 1999; 170: 148-149 Australians are credited with making global contributions in biomedical research,1 and the same can now be said for their contribution to developing acute home-based care. Hospital in the home (HIH) units have been established for more than four years in Australia (mainly in Victoria), yet in this short time important work of international standard has shown that HIH is a safe, effective, acceptable and efficient alternative to acute hospitalisation for certain patients and conditions.2-5 Now, in this issue of the Journal, Caplan and colleagues,6 from New South Wales (a virtual HIH desert), report a randomised controlled trial (RCT) of home versus hospital care, something that has hitherto seldom been reported in the medical literature (the only other similar RCT is an Australian study in patients with cystic fibrosis7). Caplan et al found that frail elderly patients requiring intravenous therapy or low molecular weight heparin deserve active consideration for HIH care: there were fewer geriatric complications and greater patient and carer satisfaction in the HIH group. Although no differences in the rates of adverse events and death were found, the small numbers of patients involved meant that the study's power to draw these conclusions was limited. HIH care around the world has varied widely, and so too have the studies it has generated. Thus, for the Cochrane review of HIH care,8 a meta-analysis was not possible, and for good reason. In HIH studies so far there have been: Variations in intervention models; Non-uniformity of conditions, patients and therapies; and Relatively small patient numbers, allowing only for large effects to be detected. Other factors impeding meta-analysis have included: The impact of dedicated and motivated staff self-selected to care for the intervention groups; The refusal of some patients to consent to remain in hospital when HIH treatment was offered as an option; The need for units to be well established before any trial; and The reluctance of established HIH programs to reduce their throughput. Landmark RCTs of HIH care of patients with deep venous thrombosis have taken four years to complete,9 and RCTs of home-based care in the United Kingdom have really examined postdischarge coordination.10 Americans are educated by their constitution to hold some truths to be self-evident, and the appropriateness of HIH appears to be one of them. They have demonstrated this with an expenditure of 2 billion dollars per annum on HIH programs in the absence of RCT evidence.11,12 If HIH were, for example, an imaging technology, it would have crossed the threshold from the novel and experimental. But hospitals are insecure -- they have difficulty letting go even when the evidence is there. So, let us assume that this issue of the Journal is a defining moment for HIH in Australia, and NSW in particular. Let us assume that hospital administrators will conclude that the time is now right for a concerted move to HIH care, and that to deny appropriate patients this intervention is no longer sustainable and may even be unethical. Let us even fantasise that private insurers will look favourably at the benefits of HIH care now that they will receive an injection of 1.5 billion dollars of public funds (Private Health Insurance Incentives Bill 1998 (Cwlth)). How could these interested groups move on with the development of HIH? They might be forgiven for concluding that models for HIH are somewhat ill-defined. In fairness, HIH units have been influenced by the manner in which they were funded, and the background of the staff who volunteered to take on the task. The studies have concentrated on comparisons with inhospital care rather than between HIH models. A more analytical approach is now required, but some principles have emerged. Firstly, let us get the definition clear. The substitution of acute hospital stay is at the heart of HIH.13 Thus, HIH is the delivery of care and services which, without HIH, can only be provided by admission to hospital. At present, the healthcare interventions suited to HIH are intravenous therapy of all types (including antibiotics, antifungals and antivirals, some chemotherapeutic agents, corticosteroids, inotropes, and blood products), and acute anticoagulation. Acute rehabilitation, insulin initiation and some complex wound care are also included in some HIH programs. Although new applications will be found, it is important that HIH should adhere to the demonstrable substitution of hospital inpatient care and not establish intermediate care programs or duplicate current community services. HIH is probably best established through a stand-alone unit within the hospital, with its own budget and staff. It has its own technologies, such as computerised pumps and peripherally inserted central catheters, and is skilled in the use of pharmaceuticals at home. It has its own body of research. It is expert at assessing people for acute home-based care, with involvement in the actual delivery of that care continually updating its expertise. It accepts patients from all other hospital units, services and disciplines. It is therefore generalist in its approach -- a dangerous attribute in a modern hospital environment -- yet is rapidly accumulating its own core of specialist knowledge. It is able to embrace specialist requirements through direct staffing of nurses with appropriate experience, or through the education of current staff. It is developing specific standards that will allow improvement in quality and benchmarking. Australian Council on Healthcare Standards (ACHS) clinical indicators for HIH care are expected this year.14 HIH units should offer nurse-administered and medically supervised and attended care. The ability to establish venous access and detect, treat or transfer patients with complications of illness or therapy is required. Twenty-four-hour nursing and medical telephone support, with the ability to visit after hours, is mandatory. There should be clear lines of clinical responsibility and continuity within HIH, and between it and the hospital, with a clear link to the hospital (in Victoria patients retain their inpatient status while in HIH). Community-based healthcare service providers may then be able to deliver HIH services. When patients understand and consent to the service level offered, their acceptance is high, as is their subsequent satisfaction.5 Patients who have had nosocomial infections or have chronic or relapsing illnesses best understand the advantages of HIH. There is also a level of community altruism, whereby people understand that, as long as they are cared for appropriately, traditional hospital space should go to those who need it more. To keep this faith, Australian HIHs should reject the notion of these programs being built entirely around self-administration of therapy. Even with all of these inputs, HIH will still offer care equivalent to traditional hospital care at a lower cost.11,15 Future studies of hospital and HIH patients examining costs and quality-of-life measures will acknowledge the additional advantages of HIH care. To date, Australian costing studies of HIH have suffered from the problems described earlier for the conduct of trials, together with inconsistent cost-accounting across different hospitals.16 But, even if HIH offered no cost advantage in direct care, in the context of waiting lists and emergency department backlogs HIH offers capital expansion of the hospital's work at a fraction of the usual cost. Until recently, hospitals have only seen their future as involving exponential growth. The view that the hospital is an Aladdin's cave, where the rich rewards of medical and nursing skill and biotechnology are gathered and bestowed on those who surrender themselves, might be usefully reassessed.17 But the real danger is that any such reassessment will merely result in briefer glimpses of the skills and technology where they are genuinely required. This appears to be the current direction of public hospital reform. Hospitals have been accustomed to taking responsibility for only those within their walls. While understandable, this limits the effective use of the technologies and skills held tight within those walls. HIH urges hospitals to adapt their infrastructure to take responsibility for the delivery of appropriate, high quality acute care in and for their community. State and federal health authorities could assist with genuine, targeted medium to long term incentives. Caplan et al offer the best evidence yet that the time for apathy and cynicism towards HIH should be over. We are at the end of a century of unparalleled advances in medical science and hospital care. Any pause in the speed of advance, or any rationing of access due to the burgeoning costs of acute-care delivery, can allow Western healthcare systems to take stock.18 In their review, the return to home-based care, so prevalent before the early 20th century, should be seen as maximising the quality use of technology to fulfil the wishes of the patients and their families, reasserting their pre-eminent position within the acute-care system into the 21st century. Michael Montalto Director, Frankston Hospital in the Home Executive Member, Australian Home and Outpatient Intravenous Therapy Association, Frankston Hospital, Frankston, VIC Bourke PF, Butler L. Mapping Australia's basic research in the medical and health sciences. Med J Aust 1997; 167: 610-613. Grayson L, Silvers J, Turnidge J. Home intravenous antibiotic therapy: a safe and effective alternative to inpatient care. Med J Aust 1995; 162: 249-252. Lowenthal R, Piaszczyk A, Arthur G, O'Malley S. Home chemotherapy for cancer patients: cost analysis and safety. Med J Aust 1996; 165: 184-187. Montalto M. How safe is hospital in the home? Med J Aust 1998; 168: 277-280. Montalto M. Patient and carer satisfaction with hospital in the home care. Int J Qual Healthcare 1996; 8: 243-251. Caplan G, Ward J, Brennan N, et al. Hospital in the home: a randomised controlled trial. Med J Aust 1999; 170: 156-160. Wolter JM, Bowler S, Nolan P, McCormack J. Home intravenous therapy in cystic fibrosis: a prospective randomized trial examining clinical, quality of life and costs. Eur Respir J 1997; 10: 896-900. Sheppard S, Illife S. Effectiveness of hospital at home compared with inhospital care. Cochrane Review in: The Cochrane Library, Issue 3, 1998. Oxford: Update Software, 1998. Koopman M, Prandoni P, Piovalli F, et al. Treatment of venous thrombosis with intravenous unfractionated heparin administered in the hospital as compared with subcutaneous low molecular weight heparin administered at home. N Engl J Med 1996; 334: 682-687. Richards S, Coast J, Gunnell D, et al. Randomised controlled trial comparing effectiveness and acceptability of an early discharge hospital at home scheme with acute hospital care. BMJ 1998; 316: 1796-1801. Balinsky W. Home care -- current problems and future solutions. San Francisco: Jossey-Bass Publishing, 1994. Tice A, Marsh P, Craven P. Response to a call for a randomised controlled trial. Am J Med 1993; 94: 115. Grayson L. Hospital in the home -- is it worth the hassle? Med J Aust 1998; 168: 262. Clinical indicators for hospital in the home -- Final Report to the Victorian Department of Human Services. Melbourne: ACHS Care Evaluation Program. October 1998. Montalto M, Watts J. Considering the cost of hospital in the home care. Report to the Victorian Department of Human Services. Melbourne: Centre for Health Program Evaluation, 1998. KPMG Consulting Services. KPMG hospital in the home evaluation. Melbourne: Victorian Government Department of Human Services, 1997. Stoeckle J. The citadel cannot hold: technologies go outside the hospital, patients and doctors too. Milbank Q 1995; 73: 3-17. Komesaroff P, Clunie G, Duckett S. What is the future of the hospital system? Med J Aust 1997; 166: 17-22. 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/>

Michael Montalto

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

Hip fractures and osteoporosis in men Drug therapies for men must be based on studies in men MJA 1997; 167: 404-405 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/>". - ©MJA1997 In 1990, 30% of the 1.7 million hip fractures worldwide occurred in men.1 The absolute number of hip fractures will increase with the growing number of elderly people, and with the increasing age-specific incidence of hip fractures.2 The predicted number of hip fractures worldwide for the year 2025 is 1.2 million in men and 2.8 million in women.1 In this issue of the Journal, Diamond et al.3 report a 20% mortality within six months of hip fracture among elderly men. While fracture-related complications in the men were comparable with those of randomly selected age-matched women with hip fracture, 14% of men died during admission, compared with only 6% of women. This difference was not statistically significant, and women were not followed after discharge, so further comparison of mortality was not possible. Interestingly, 32% of men and 28% of women were admitted from institutions where protein malnutrition, vitamin D deficiency, illness, falls and hip fractures are more common than in the community;4 50% of men and 42% of women were discharged to institutions. Despite important limitations of this study -- its small sample size (only 51 men, with 10 lost to follow-up) and the absence of control groups -- it does highlight the high morbidity and mortality associated with hip fractures in elderly Australians, and suggests that mortality may be higher in men than in women. In this, it concurs with the findings of Poor et al., who reported a mortality of 20.7% in men and 7.5% in women with hip fractures.5,6 Among the 131 men they studied, hospital mortality was 11.5% and 30-day mortality was 16%, while 79% of the survivors resided in nursing homes at one year. The problem of osteoporosis and fractures in men is likely to increase Fifty-eight per cent of these 131 men, compared with 94% of the age-matched community-residing male controls, were alive at one year, and the risk of death increased with higher levels of coexisting illness, age and with activity status at the time of fracture.6 Immediately after fracture, overall survival was similar for both patients and controls who had no pre-existing comorbid conditions. Survival was reduced for both groups with increasing numbers of coexisting illnesses, and was lower in the cases than controls at each level of comorbidity (see Box). Dementia, cerebrovascular disease, chronic lung disease, congestive heart failure and myocardial infarction significantly influenced survival. As neither fracture alone nor illness alone accounted for the excess mortality, it seems an interaction between fracture and its consequences with the coexisting illnesses may be responsible. Bone strength is determined by bone size, mass and architecture. Men with fractures have smaller bones than controls: those with femoral neck fractures have reduced femoral neck width, and those with spinal fractures have reduced vertebral body width. Bones may be smaller because of reduced peak bone size and reduced periosteal appositional growth. Smaller bones have lower bone density because they have attained a lower peak bone mass or because bone has been lost. Osteoporosis in old age is the result of genetic and environmental factors during growth and ageing, and both periods need to be studied. Hypogonadism during growth and delayed puberty may result in reduced peak bone size and bone density. Later in life, age-related hypogonadism and the resultant decline in testosterone levels may contribute to bone loss. Hypogonadism is present in around 20% of elderly men in the community (own unpublished data), and in around 50% of men with spine or hip fractures.7 Osteoporosis can also result from vitamin D deficiency, which is common among institutionalised elderly men, and may cause osteomalacia, secondary hyperparathyroidism, increased bone turnover and bone loss. Bone loss accelerates (rather than ceases) in elderly men or women with secondary hyperparathyroidism, partly because this condition causes increased intracortical porosity and cortical thinning which predispose to hip fractures. Excessive alcohol consumption (also noted by Diamond et al.), is an important attributable risk factor for osteoporosis in men. There is no proven treatment for osteoporosis in men because there have been no appropriate randomised controlled trials. Calcium supplements are safe and may slow bone loss, at least in women.8 Vitamin D deficiency should be suspected in housebound or institutionalised elderly men and should be treated (after excluding malabsorption) with daily vitamin D supplements. The purported efficacy of 1 a ,25-dihydroxyvitamin D3 for osteoporosis in women has led to it being approved in Australia for treating osteoporosis in men. Hypogonadism should be treated with testo sterone (which may increase bone mineral density [BMD] in eugonadal men, but only short term trials have been done). The possible increased risk of prostatic cancer associated with testosterone therapy needs to be considered in any cost-benefit analysis. Several small short term trials in men with idiopathic or secondary osteoporosis suggest that bisphosphonates increase BMD and reduce bone turnover. Studies in women with primary osteoporosis, and in animals suggest that drugs such as alendronate and etidronate appear to be the best options at this time. However, as long term safety data are limited, these drugs must be given cautiously. The bisphosphonates may remain in bone indefinitely, alendronate can cause gastric irritation or oesophageal ulceration, and etidronate can cause focal osteomalacia when given for prolonged periods. Sodium fluoride increases BMD but not bone strength and should not be used in osteoporosis in men or women. There is no evidence for a favourable effect of anabolic steroids in men. The problem of osteoporosis and fractures in men is likely to increase. To use drugs in men based on evidence from studies in women is not an appropriate long term solution. Drug therapy for men must be based on studies of efficacy, safety and quality of life in men. As with all measures in preventive medicine, potential drug therapy must be safe because most people who are treated derive no benefit. For example, if the incidence of fracture is two per 100 men per year, and a drug has a 50% antifracture efficacy, in any year 98 men will not have had a fracture with or without treatment, one will have a fracture anyway, and, in one, fracture will be prevented -- 99 will derive no benefit. Clearly, treatments must be safe. Age-specific hip fracture incidence rates in men with low BMD must be determined prospectively to enable us to establish drug efficacy. For example, if the incidence of fracture is two per 100 men per year, 1260 men with hip fracture and 1260 controls will be needed to detect a 50% risk reduction by a drug in a three-year study. Smaller sample sizes may be adequate if high risk groups with low baseline BMD and fractures are recruited. Studies with endpoints such as BMD, histomorphometry, biochemical measurements of bone turnover and biomechanical testing of bone biopsy specimens may provide at least some clarification of appropriate drugs for use in men. Ego Seeman Associate Professor of Medicine, Austin & Repatriation Medical Centre, University of Melbourne, VIC Cooper C, Campion G, Melton LJ. Hip fractures in the elderly: a world-wide projection. Osteoporosis Int 1992; 2: 285-289. Seeman E. Osteoporosis in men. Aust Fam Physician 1997; 26: 135-143. Diamond TH, Thornley SW, Sekel R, Smerdley P. Hip fracture in elderly men: prognostic factors and outcomes. Med J Aust 1997; 167: 412-415. Rudman IW, Rudman D. High rates of fracture for men in nursing homes. Am J Physical Med 1989; 68: 2-5. Poor G, Atkinson EJ, Lewallen DG, et al. Age-related hip fractures in men: clinical spectrum and short-term outcomes. Osteoporosis Int 1995; 5: 419-426. Poor G, Atkinson EJ, OOFallon WM, Melton LJ III. Determinants of reduced survival following hip fractures in men. Clin Orthop 1995; 319: 260-265. Stanley HL, Schmitt BP, Poses RM, Diess WP. Does hypogonadism contribute to the occurrence of a minimal trauma hip fracture in elderly men. J Am Geriatr Soc 1991; 39: 766-771. Reid IR, Ames RW, Evans MC, et al. Long term effects of calcium supplementation on bone loss and fractures in post menopausal women -- a randomized controlled trial. Am J Med 1995; 98: 331-335. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Ego Seeman

Driving and dementia: balancing personal independence and public safety Drivers with dementia require standardised on-road assessment of their driving safety MJA 1997; 167: 406-407 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/>". - ©MJA1997 In this issue of the Journal, Lipski addresses the important topic of driving by people with dementia.1 Although older drivers drive fewer kilometres than younger drivers, and are less likely to drive at night or in heavy traffic, their crash rate per kilometre driven may be the highest of any age group, and they are more likely to be killed when involved in a crash.2 Several retrospective studies have found that people with dementia are involved in more accidents than age-matched control subjects, and that many drivers with dementia continue to drive despite having had crashes.3-5 Notably, these studies do not agree on issues such as whether the duration of the dementia is an accurate predictor of driving ability, and many rely on reports by caregivers of driving history and crashes, the reliability of which are uncertain. Recent neuropathological findings in 98 older drivers killed in traffic accidents showed that 33% had neuritic plaque scores indicating certain Alzheimer's disease (AD) and, in a further 20%, findings were suggestive of AD.6 This raises the possibility that more accidents are attributable to AD than previously thought. In contrast, another study of Michigan State records showed that road crash and violation rates among AD patients did not differ significantly from those of matched controls;7 this study did not control for mileage driven, and reduced driving exposure of AD patients may have kept their crash rate equal to that of control subjects. Drachman and Swearer investigated crash rates for patients with AD over a 10-year period.8 They also did not control for mileage driven, but found that, although the AD patients had fewer reported crashes than 16-24 year old drivers, they had more than twice as many in the years after the onset of their AD, than matched control subjects. Doctors cannot reliably predict driving competence or increased crash risk in drivers with AD on the basis of a clinical examination There are few reports on actual driving performance of people with dementia. Fitten and colleagues examined the performance of patients with mild AD and patients with mild vascular dementia.9 Compared with control groups, the groups with AD and vascular dementia had lower mean scores on the driving test and made more errors in the complex stages of the course. In addition, a retrospective analysis of crashes and driving violations for these patients was consistent with road test results. However, Hunt and colleagues found that, while 40% of drivers with mild dementia of the Alzheimer type (DAT) were unsafe, some others may drive safely. The driving competency of individuals with DAT could not be determined reliably from self report.10 Fox and colleagues found that 63% of licensed drivers diagnosed with probable AD failed a standardised on-road evaluation.11 Conversely, 37% passed this evaluation, suggesting that a diagnosis of AD alone may be insufficient justification for stopping people from driving. These studies of on-road driving behaviour of patients with dementia indicate that older drivers with a range of cognitive abilities can be safely and reliably evaluated by a road test, with validity equal to that of driver licence tests. As noted by Lipski,1 while data increasingly show risks to individuals and the community associated with driving by people with dementia, there are few guidelines for helping doctors determine who can or cannot drive. This assessment may be further complicated if any of the new drugs currently undergoing clinical trial for AD are found to enhance performance on cognitive or driving tasks. Doctors cannot reliably predict driving competence or increased crash risk in drivers with AD on the basis of a clinical examination.10 There is also a lack of consensus about the predictive validity of neuropsychological assessment for driving competence among patients with dementia, partly because of the different neuropsychological tests employed in different studies. While the Mini Mental State Examination has been proved to significantly predict driving competence in studies of patients with dementia, its specificity and sensitivity were not sufficient for efficient prediction of driving safety.11 In the light of recent empirical data, we recommend that if a doctor learns that an older patient gets lost while driving or has been involved in a crash, the possibility of a progress ive dementing illness as a cause of their driving difficulties should be investigated. In many cases, licence cancellation may be indicated without on-road assessment. If licence cancellation threatens a general practitioner's long term relationship with a patient and his or her family, referral to an appropriate specialist may be preferable. In cases of disagreement, an on-road driving test may help the family, and possibly the patient, accept that the patient is incompetent to drive. In patients for whom unsafe driving behaviours have not been reported, an on-road assessment is currently the most valid means of determining driver competence and safety. The driving test should be standardised, designed for neurologically impaired people, include some complex traffic situations, and, ideally, should be available in both urban and rural areas. It has been suggested that patients with dementia who drive with the assistance of a passenger or "copilot" should be assessed with, and subsequently permitted to drive with, the "copilot".12 However, several logistic and legal problems (surrounding such questions as: Who is licensed to drive? How can the presence of the "copilot" be ensured? Can the cognitive status of the "copilot" be monitored?) render this proposal impractical. For patients whose driving tests indicate safe and competent driving, driving performance must be reviewed regu larly (e.g., six-monthly), or after a noticeable increase in dementia severity. Criteria for driving competence and licence cancellation should be discussed with the patient and family. If assessment indicates that the patient should stop driving, the patient and family should be involved in discussion of transport alternatives which may be available from family or friends, or through community transport options. Counselling of the patient and family about lifestyle changes and future planning of transportation may be critical to compliance as well as to psychological wellbeing, as driving cessation may be associated with depressive symptoms. As a society, we need to devote more planning and resources to provision of safe, convenient and affordable transportation alternatives for those unable to drive. Gillian K Fox Clinical Neuropsychologist, Rehabilitation Studies Unit, University of Sydney, NSW. Guy M Bashford Staff Specialist, Department of Rehabilitation and Geriatrics, Illawarra Area Health Service, Warrawong, NSW Lipski PS. Driving and dementia: a cause for concern. Med J Aust 1997; 167: 453-454. Waller PF. Renewal licensing of older drivers. Transportation in an aging society. Vol. 2. Washington, D. C.: Transportation Research Board, 1988: 72-100. Friedland RP, Koss E, Kumar A, et al. Motor vehicle crashes in dementia of the Alzheimer type. Ann Neurol 1988; 24: 782-786. Lucas-Blaustein MJ, Filipp L, Dungan C, Tune L. Driving in patients with dementia. J Am Geriatr Soc 1988; 36: 1087-1091. Gilley DW, Wilson RS, Bennett DA, et al. Cessation of driving and unsafe motor vehicle operation by dementia patients. Arch Intern Med 1991; 151: 941-946. Johansson K, Bogdanovic H, Kalimo H, et al. Alzheimer's disease and apolipo- protein E e 4 allele in older drivers who died in automobile accidents. Lancet 1997; 349: 1143-1144. Trobe JD, Waller PF, Cook-Flanagan CA, et al. Crashes and violations among drivers with Alzheimer disease. Arch Neurol 1996; 53: 411-416. Drachman DA, Swearer JM. Driving and Alzheimer's disease: the risk of crashes. Neurology 1993; 43: 2448-2456. Fitten LJ, Perryman KM, Wilkinson CJ, et al. Alzheimer and vascular dementias and driving. JAMA 1995; 272: 1360-1365. Hunt L, Morris JC, Edwards D, Wilson BS. Driving performance in persons with mild senile dementia of the Alzheimer type. J Am Geriatr Soc 1993; 41: 747-53. Fox GK, Bowden SC, Bashford GM, Smith DS. Alzheimer's disease and driving: prediction and assessment of driving performance. J Am Geriatr Soc 1997; 45: 949-953. Shua-Haim JR, Gross JS. The "co-pilot" driver syndrome. J Am Geriatr Soc 1996; 44: 815-817. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Gillian K Fox · Guy M Bashford

Hip fracture in elderly men: prognostic factors and outcomes Terrence H Diamond, Stephen W Thornley, Ronald Sekel and Peter Smerdely For editorial comment, see Seeman 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/>". Abstract - Introduction - Methods - Statistical analysis - Results - Discussion - References - Authors' details - ©MJA1997 Abstract Objective: To examine prognostic factors and outcomes after hip fracture in men aged 60 years and older. Design and setting: Cohort study of all men presenting to St George Hospital (a 650-bed tertiary care centre) with hip fractures in 1995, recruited retrospectively from medical records and evaluated prospectively at six and 12 months after fracture. Patients: 51 men aged 60 years or more (and, for comparison, 51 age-matched women) who presented with hip fracture not caused by high impact injuries or local bone disease. Main outcome measures: Prognostic factors (such as pre-existing illness and osteoporotic risk factors) and outcome data (such as fracture-related complications, mortality, and level of function as measured by the Barthel index of activities of daily living at six and 12 months postfracture). Results: Median age of the 51 men was 80 years (interquartile range, 74-86 years); four were aged under 70 years. Outcome assessment was possible for 41 men (80%). Similar proportions of men and women came from institutions (32% v. 28%), and similar additional proportions required institutionalisation after discharge (18% v. 14%). Fracture-related complications affected similar proportions of men and women (30% v. 32%), and mean length of hospital stay was similar. Fourteen per cent of men died in hospital compared with only 6% of women (P = 0.06). Men had more risk factors for osteoporosis (P < 0.01). Physical functioning (measured by the Barthel index) deteriorated significantly in men from 14.9 at baseline to 13.4 at six months (P < 0.05) and 12.4 at 12 months (P < 0.05) after fracture. Conclusion: Compared with women, elderly men presenting with hip fracture have higher mortality and have more risk factors for osteoporosis. Like women with hip fracture, men are usually fragile, with pre-existing medical illness and fracture-related complications contributing to their overall poor outcomes. MJA 1997; 167: 412-415 Introduction The incidence of hip fracture in elderly men is approximately one-third of that reported in elderly women.1-5 In a recent Australian study, the incidence of hip fracture in men was calculated as 19.4 per 1000 population per year, with the highest incidence in those aged 80 years and older.3 The economic and social implications of hip fracture in the Australian community are enormous, with the overall cost approximating $420 million annually.6 Previous studies have shown an increased morbidity and mortality associated with hip fracture in elderly women, in whom outcomes are usually poor and partly related to age and medical conditions.7-12 Until recently, there have been comparatively few data on hip fracture in elderly men.12-19 Given the importance of hip fracture, we analysed the mortality and functional outcome of hip fracture in elderly men (aged 60 years and over) who presented to our hospital. Methods St George Hospital is a 650-bed tertiary care referral centre serving a population of 195 000 in the southern metropolitan area of Sydney. Patients admitted to this hospital with hip fractures are usually treated with internal fixation of the fractured hip within 24-48 hours of admission. We retrospectively audited the medical records of all men and women with hip fractures presenting to St George Hospital between 1 January and 31 December 1995. Men were eligible for the study if they were aged 60 years or over, and if their hip fracture was not the result of high impact injuries or local bone disease. The prognostic factors and outcomes following hip fracture of eligible men were compared with those of an equal number of age-matched women who presented with hip fractures during the same 12-month period. Ethical approval for this study was granted by the St George Hospital Ethics Committee. From the hospital medical records, we recorded: Patient's age; Prognostic factors, such as pre-existing illness, osteoporotic risk factors14,17-19 and type of fracture; and Outcome data, such as fracture-related complications, length of hospital stay, mortality, and level of function (as measured by the Barthel index of activities).20 These data are routinely recorded by the orthopaedic intern or registrar, appropriate consultative services, occupational therapist, and/or aged care and rehabilitative services. The Barthel index consists of a questionnaire containing 10 questions pertaining to activities of daily living, such as mobility, bathing, dressing, and toilet use, and is scored out of a total of 20 points -- the lower the score, the worse the disability. Any additional data that were required were obtained by telephone interviews with the patients and/or their family members. Subsequently, patients were followed up prospectively six and 12 months after hip fracture by telephone interview. We obtained data pertaining to whether they were living at home or in an institution, and then used the original 10 questions on the Barthel index questionnaire again to assess activities of daily living, self-care ability and mobility. Statistical analysis Results were analysed with StatCalc21 statistics package. Data for men and women were compared by Student's t test or analysis of variance, where applicable. The main predictors of death and institutionalisation were determined by stepwise regression analysis; the variables entered into the equation included the patient's age, smoking history, alcohol intake, pre-existing medical illness, prefracture Barthel score, length of hospital stay, and fracture-related complications. Results One hundred and eighty-nine people had presented with hip fracture during 1995, comprising 57 men (30%) and 132 women (70%). Six of the men were excluded because their fractures were related to high impact injuries or local bone disease. Hence, we compared the prognostic factors and outcomes following hip fracture of the remaining 51 men with those of 51 age-matched women of the 132 who presented with hip fractures during the same period. Forty-one men (80%) were contactable for assessment of outcomes at six and 12 months. We were unable to contact 10 men, either by a mailed questionnaire or through the telephone directory services. Their names had not been recorded in the death registry of the New South Wales Bureau of Births, Deaths and Marriages. They were considered lost to follow-up. Box 1 (below) compares the clinical data of the men and women with hip fracture. The median age of the 51 eligible men was 80 years; four were aged less than 70 years. Their mean length of hospital stay was 13 days (range, 3-55 days). Sixteen men (32%) came from hostels or nursing homes before admission. Thirty men (58%) were classified radiologically as having trochanteric fractures and 21 (42%) as having cervical fractures; they did not differ with respect to clinical presentation or postfracture outcomes (data not shown). Compared with women, men had a higher prevalence of excessive alcohol consumption (chi-squared = 13.95; P = 0.004) and current smoking (chi-squared = 14.96; P = 0.0004). Forty-eight men (95%) had at least one medical problem before admission; the mean number of medical problems per patient was three (range, 0-4). Forty-seven women (92%) had at least one medical problem, with a mean number of medical problems per patient of two (range, 0-4) (Box 2). Forty men (78%) had at least one risk factor for osteoporosis; the mean number of risk factors per patient was one (range, 0-3). Similarly, 36 women (72%) had at least one risk factor for osteoporosis (not including menopausal status), with a mean number per patient of one (range, 0-4) (Box 2). Ten men (20%) with hip fractures died: seven during hospital admission and another three during the first six months after fracture. More men than women with hip fractures died during their acute hospital admission, but this difference was not significant (P = 0.06). Fifteen men (30%) developed fracture-related complications, five of whom died in hospital. Those who had complications developed an average of two complications each (range, 0-4). This was similar for women; 16 (32%) developed fracture-related complications, three of whom died in hospital, and the average number of complications was one (range, 1-4). The occurrence of individual fracture-related complications did not differ significantly between men and women with hip fracture. Fracture-related complications were the single most important predictor of death in men (odds ratio [OR], 13.5; 95% CI, 1.74-132; P = 0.06). By contrast, the most important predictor in women was the prefracture Barthel index score. In men, age, smoking history, alcohol intake, pre-existing medical illness, prefracture Barthel index score, and length of hospital stay did not contribute significantly to the fracture-related mortality. The Barthel index score (mean, 14.9 at baseline) deteriorated significantly by six months (mean, 13.4; P < 0.05) and 12 months (mean, 12.4; P < 0.05). The baseline Barthel score did not differ significantly between men and women. After fracture, an additional nine men required hostel or nursing home accommodation. This correlated significantly with both the patient's age and the per cent decline in the Barthel index score (r = 0.41; P = 0.0002). Discussion Our findings support the limited published data on hip fracture in men.12-19 As in other studies,3-5 we found that men represented 30% of all hip fractures, and that men who sustained hip fractures were elderly, had pre-existing medical conditions5,13-16 and at least one risk factor for osteoporosis.14,18,19 Compared with the men in our study, women with hip fractures had fewer risk factors for osteoporosis (P < 0.01). Although our study has the major limitation of small sample size, it is the first Australian study to show a significant decline in physical functioning in men after hip fracture. A decline in physical functioning has been noted in both men and women after hip fracture, with many survivors requiring institutionalisation. Almost one-third (32%) of our men originated from institutionalised care, and an additional 18% were subsequently discharged to institutionalised care. Age and percent decline in Barthel index score were the most important criteria leading to their institutionalisation. While the use of the Barthel index may potentially identify individuals who will need long term institutionalisation, this is only a gross assessment of activities of daily living. Thirty per cent of the men in our study returned home to their previous level of function as measured by the Barthel index, but anecdotally many reported a decline in more subtle activities not measured by this index. In a study by Marotolli et al., 29% of all hip fracture patients were institutionalised at six months postfracture.13 Another study reported that 79% of the patients surviving at one year were residing in nursing homes or intermediate care facilities, while those who returned home had significant functional decline, with almost 60% limping or requiring a cane or walker.15 Reported rates of mortality and morbidity in men with hip fracture vary from 13%-44%,1,4,5,9,10,11,16,22 with the likelihood of a man dying after hip fracture increased by 83% and the likelihood of subsequent hospital admission after hip fracture increased by 231%.5 In our study, 20% of men with hip fractures died, either during the initial hospital admission or within the first six months after fracture. Although not statistically significant, we found that, compared with women, twice as many men with hip fractures died during the acute hospital admission (P = 0.06). These data are consistent with those of many other studies which have shown higher postfracture mortality rates in men.1,10,22 For example, Holt et al. recorded 17% mortality in men compared with 11.5% in women,22 while Jacobsen et al. reported mortality rates per 1000 person-months postfracture of 33.7 in white men compared with 17.2 in white women.10 In our study, death occurred predominantly within the first two months postfracture, and fracture-related complications was the strongest predictor of death. In a longitudinal study of ageing, Wolinsky and colleagues found a one-year postfracture mortality among 7527 members of approximately 24%, with the greatest risk of dying in the first six months after hip fracture (hazard-risk ratio, 57.4; 95% CI, 43.7-75.3); survival rates estimated at six months postfracture returned to a trend similar to that of control subjects.5 Despite the limitations of small sample size and a lack of control subjects who had not had hip fracture, this study shows men who present with hip fracture are usually elderly and fragile and have numerous risk factors for osteoporosis, pre-existing medical illnesses and fracture-related complications. In men, this results in higher postfracture mortality compared with age-matched women, as well as in significant functional decline. This study highlights the need to identify men with osteoporosis in the community, and the need to find effective strategies for preventing hip fracture. References Cummings SE, Kelsey JL, Nevitt MC, O'Dowd KJ. Epidemiology of osteoporosis and osteoporotic hip fractures. Epidemiol Rev 1985; 7: 178-208. Lord SR. Hip fractures: changing patterns in hospital bed use in NSW between 1979 and 1990. Aust N Z J Surg 1993; 63: 352-355. Jones G, Nguyen T, Sambrook PN, et al. Symptomatic fracture incidence in elderly men and women: the Dubbo Osteoporosis Epidemiology Study (DOES). Osteoporosis Int 1994; 4: 277-282. Cumming RG, Klineberg RJ. Case-control study of risk factors for hip fractures in the elderly. Am J Epidemiol 1994; 139: 493-503. Wolinsky FD, Fitzgerald JF, Stump TE. The effect of hip fracture on mortality, hospitalization and functional status: a prospective study. Am J Public Health 1997; 87: 398-403. Wark JD. Osteoporosis: the emerging epidemic. Med J Aust 1996; 164: 327-328. Aitken JM. Relevance of osteoporosis in women with fracture of the femoral neck. BMJ 1984; 288: 597-601. Pettiti DB, Sidney S. Hip fracture in women. Clin Orthop 1989; 246: 150-155. Myers AM, Robinson EG, Van Natta ML, et al. Hip fractures among the elderly: factors associated with in-hospital mortality. Am J Epidemiol 1991; 134: 1128-1137. Jacobsen SJ, Goldberg J, Miles TP, et al. Race and sex differences in mortality following fracture of the hip. Am J Public Health 1992; 82: 1147-1150. Cooper C, Atkinson EJ, Jacobsen SJ, et al. Population-based study of survival after osteoporotic fractures. Am J Epidemiol 1993; 137: 1001-1005. Marotolli RA, Berkman LF, Cooney LM. Decline in physical function following hip fracture. J Am Geriatr Soc 1992; 40: 861-866. Marotolli RA, Berkman LF, Leo-Summers L, Cooney LM. Predictors of mortality and institutionalisation after hip fracture: The New Haven EPESE Cohort. Am J Public Health 1994; 84: 1807-1812. Seeman E. Osteoporosis in men: epidemiology, pathophysiology and treatment possibilities. Am J Med 1993; 95 (Suppl 5A): 23S-28S. Poor G, Atkinson EJ, Lewallen DJ, et al. Age-related hip fractures in men: clinical spectrum and short-term outcomes. Osteoporosis Int 1995; 5: 419-426. Poor G, Atkinson EJ, O'Fallon WM, Melton LJ. Determinants of reduced survival following hip fractures in men. Clin Orthop 1995; 319: 260-265. Ringe JD. Hip fractures in men. Osteoporosis Int 1996; 6 (Suppl 3): 48-51. Looker AC, Mussolino ME, Madans JH, Orwoll ES. Risk factors for hip fractures in white men: The NHANES I Epidemiologic Follow up Study [abstract]. J Bone Miner Res 1996; 11: 233. Smerdely P, Thornley S, Sekel R, Diamond T. Subclinical vitamin D deficiency is the major biochemical risk factor associated with hip fracture in elderly men [abstract]. J Bone Miner Res 1996; 11: 233. Mahoney F, Barthel D. The Barthel index. Maryland State Med J 1965; 14: 61-65. StatCalc (Epi Info) [computer program]. Version 6.046. Geneva: WHO, 1997. Holt EM, Evans RA, Hindley CJ, Metcalfe JW. 1000 femoral neck fractures: the effect of pre-injury mobility and surgical experience on outcome. Injury 1994; 25: 91-95. (Received 25 Mar, accepted 10 Jul, 1997) Authors' details St George Hospital, Sydney, NSW. Terrence H Diamond, FRACP, Senior Endocrinologist, Department of Endocrinology; Stephen W Thornley, FRACP, Endocrine Registrar, Department of Endocrinology; Ronald Sekel, FRCS, Senior Orthopaedic Surgeon, Department of Orthopaedic Surgery; Peter Smerdely, PhD, FRACP, Endocrinologist, Department of Aged Care. Reprints: Dr T Diamond, Department of Endocrinology, St George Hospital, 32 Belgrave Street, Kogarah, NSW 2217. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Terrence H Diamond · Stephen W Thornley · Ronald Sekel · Peter Smerdely

Use of inpatient hospital services by people aged 90-99 years Josephine H Harris, Paul M Finucane, Denise C Healy and Anthony C Bakarich 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/>". Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - ©MJA1997 Abstract Objective: To examine the use of inpatient hospital services by people aged 90-99 years. Design: Retrospective case note review. Setting: Flinders Medical Centre, a 516-bed university teaching hospital in Adelaide, South Australia. Patients: All patients aged 90-99 years on the separation register for 1995. Main outcome measures: Patient demographic characteristics, principal diagnosis, length of hospital stay and outcome, including destination at discharge. Results: In 1995, 317 separations involved 214 patients aged 90-99 years; 148 patients (69%) were admitted to hospital once, 43 (20%) twice and 23 (11%) three times or more. In 54% of separations, patients came from the community, and these were less likely to be emergency admissions (72%) than were admissions from hostels (87%) and nursing homes (93%). Patients had a wide range of acute medical and surgical problems and a median of five documented comorbidities. Patients survived to leave hospital in 290 separations (91%) and returned directly to their previous living circumstances in 212 (67%). Median hospital stay was 5.0 days, and in 25% of separations stay was one day or less. Patients admitted under the care of geriatricians had more emergency admissions (98%) and longer mean hospital stays (8.9 days) than those admitted under surgeons (69%; 5.9 days) or other physicians (66%; 5.0 days). Conclusion: Despite the acute nature of their illnesses and their multiple medical problems, most hospitalised nonagenarians in this study returned directly to their previous living circumstances after short hospital stays. MJA 1997; 167: 417-420 Introduction Australia's rapidly ageing population and changing patterns of health care delivery are combining to increase the number of old people using acute hospital services.1 The greatest proportional population increase is among the very old; between 1990 and 1995 the estimated number of people aged 85 years and over in Adelaide grew by 27.3%, while the general population grew by only 3%.2 The impact on hospital services is substantial. For example, inpatient separations for people aged 90 years and over at Flinders Medical Centre, Adelaide, increased by 66% between the 1989-90 and 1994-95 financial years, from 274 to 454 separations annually (unpublished data). Little is known about the characteristics of hospitalised nonagenarians. Existing studies either have few subjects3 or include only medical4 or only surgical patients.5-7 To our knowledge, no study has focused on hospitalised nonagenarians in Australia. Our lack of knowledge about this group may hinder development of appropriate clinical services to meet their needs and allow prejudices and unfounded negative stereotypes to proliferate. For example, it has been implied that some patients present to hospital with acute social rather than medical crises,8 and that elderly patients become "bed blockers" who are difficult to discharge from hospital.9 Elderly patients are satirised and derided in fiction,10 while their right to access expensive medical technology is debated in scientific publications.11 To learn more about the use of acute hospital services by very elderly people, we reviewed the case notes of all people aged 90 years and over who were admitted to our hospital in 1995. In particular, we focused on the demographic characteristics of this group, the problems for which they were hospitalised and the outcomes of hospitalisation. Methods Setting and subjects We examined retrospectively the case notes of all people aged 90-99 years on the separation register for Flinders Medical Centre during 1995. The Centre, with 516 beds, is the largest hospital in the southern metropolitan region of Adelaide and the principal teaching hospital of Flinders University. Relative to other Australian public hospitals of a similar size, a large proportion of its caseload is non-elective (Dr C Baggoley, Director of Emergency Department, Flinders Medical Centre, personal communication). The emphasis is on acute care; hospitalised patients needing rehabilitation are generally transferred to other public and private facilities in the region. Some acute surgical specialties (e.g., urology and vascular surgery) are largely provided at a sister institution. Flinders Medical Centre has an age-related admission policy whereby elderly patients with complex medical problems are admitted under the care of a geriatrician, while those with more specific problems are admitted under the appropriate specialist physician or surgeon. The study group was identified from a computerised age and sex register of all separations. This included day-only patients (length of stay, 0-1 days), but excluded those attending the emergency department who were subsequently not admitted. Data collection and analysis The principal diagnosis for each separ ation was obtained from the hospital's Australian national diagnosis-related group (AN-DRG) coding system and verified by review of all case notes. The diagnosis was further classified according to the major body system affected. Comorbidities and cognitive impairment were identified from the discharge letter. Data were analysed with the Statview statistical package.12 Other data were derived from the case notes. Differences between patient groups were assessed by chi-squared tests for all characteristics except length of hospital stay, which was assessed by the Kruskal-Wallis one-way analysis of variance by ranks, a non-parametric test. The association between patients' living circumstances before and after hospitalisation was determined by Cohen's k test.13 The study received ethical approval from Flinders Medical Centre's Committee on Clinical Invest igation. Results During 1995, 317 of the hospital's 27 833 inpatient separations (1.1%) involved 214 patients aged 90-99 years. Patient characteristics Of the 214 patients, 157 (73%) were women and 57 (27%) were men, with median age, 92 years. Age distribution was 57%, 90-93 years; 27%, 94-95; and 16%, over 95. Before initial hospitalisation, 111 subjects (52%) lived in the community, 58 (27%) in hostels and 45 (21%) in nursing homes. Most subjects (148; 69%) were admitted to hospital once during 1995, 43 (20%) twice and 23 (11%) three times or more. The maximum number of separations per patient in the year was six. Separation characteristics The major reason for each hospitalisation (identified as the principal diagnosis at separation) is shown in Box 1. Orthopaedic problems (especially fractured neck of femur) and cardiovascular disorders (especially myocardial ischaemic syndromes and congestive cardiac failure) were most common. Most separations (80%) had been classed as emergency admissions. Median number of comorbidities was five (range, 0-14), with fewer than four comorbidities recorded for 31% of separations, and eight or more for 14%. Cognitive impairment, either acute or chronic was documented for 94 separ ations (30%). Length of hospital stay is shown in Figure 1 (below). Median stay was 5.0 days (range, 1-74 days) and the mean was 6.9 days (SD, 8.3 days), compared with 3.7 days for the total inpatient population. Seventy-eight separations (25%) were day-only; in 10% of cases this was because of early death. Outcomes Destinations at separation are shown in Figure 2. Overall, patients returned directly to their previous living circumstances in 212 separations (67%), were transferred to other hospitals for continuing rehabilitation or "step down" care in 56 (18%) or to a more supportive residential environment in 22 (7%), and died in 27 (9%). The percentage who returned directly to their previous living circumstances rose to 91% when deaths and hospital transfers were excluded, and the trend for this return was statistically significant (Cohen's k = 0.85, P < 0.001). Hospital stay was shorter for patients who returned directly to their previous living circumstances (mean [SD], 5.2 [5.7] days) than for those who did not (mean [SD], 10.5 [11.2] days). Comparison of patients from the community and from residential care Characteristics of patients admitted from different living circumstances are compared in Box 2. Women predomin ated in all categories, but the proportion of women was higher among those admitted from residential care, especially nursing homes, than among those from the community. Patients from residential care were more likely to have emergency admissions and be under the care of surgeons than those from the community, but less likely to be under the care of physicians (other than a geriatrician). The proportions under the care of geriatricians were similar in each category. Hospital stay did not differ significantly between patients from different living circumstances (mean in days [SD]: community, 7.4 [10.0]; hostels, 6.9 [6.1]; and nursing homes, 5.6 [5.4]; Kruskal-Wallis test statistic, T = 3.46; P = 0.18). However, mortality rose progressively in patients from the community (6%), hostels (9%) and nursing homes (16%), in that order. Comparison of surgical and medical patients Patients admitted under the care of different specialists are compared in Box 3. Most patients were admitted under the care of surgeons (133, 42%), while 126 (40%) were admitted under the care of geriatricians and 58 (18%) under the care of other physicians. Patients admitted under the care of physicians other than geriatricians were most likely to have day-only separations, to be living in the community and to return directly to the community. In contrast, admissions under geriatricians were almost all emergencies and were least likely to be day-only. Hospital stay was significantly longer for these patients (mean in days [SD]: geriatricians, 8.9 [9.6]; surgeons, 5.9 [6.6]; other physicians 5.0 [8.2]; Kruskal-Wallis T = 28.98; P < 0.001). However, when day-only separations were excluded, the difference lost significance (mean in days: geriatricians, 10.0; surgeons, 7.9; other physicians, 8.3; Kruskal-Wallis T = 5.74; P = 0.06). Mortality was highest for patients admitted under geriatricians (12%) and lowest for those admitted under surgeons (5%), but this difference was not statistically significant. Discussion This study challenges some negative stereotypes about use of acute hospital services by very elderly people. We found that people aged 90-99 years accounted for 1.1% of all separations, with most (54%) coming from the community. Over 90% survived to leave hospital and most returned to their previous living circumstances after a median hospital stay of just under a week. They presented with a wide range of acute problems, predominantly orthopaedic and cardiovascular problems. Only a small proportion were frequent users of inpatient beds. The limitations of this study need to be recognised. Its retrospective nature and reliance on case notes mean that some information, particularly about comorbidities and presence of cognitive impairment, may be inaccurate and may underestimate their true extent. However, validity was enhanced by the use of defined objective measures, not subject to observer bias. The extent to which our results may be generalised is uncertain. Although Flinders Medical Centre is mostly typical of large university teaching hospitals, it has a higher proportion of non-elective cases. Differences in its clientele, range of services and service delivery are also possible. There are no data on nonagenarians admitted to other Australian hospitals for comparison. Nor can we readily compare our study results with those from other countries, as these have excluded particular patient groups, such as medical6,7,14 or surgical4 patients or those living in residential care.3 Nevertheless, others have found similarly that hospitalised nonagenarians present with a wide range of medical and surgical problems. The longer mean hospital stays in other studies may reflect different patient profiles or management practices. We found that more nonagenarians were admitted under the care of surgeons than under geriatricians or other physicians. Those admitted under surgeons had the lowest mortality, with 95% surviving to leave hospital, even though almost 70% were admitted as emergencies. It is recognised that surgical patients in general have lower mortality rates than medical patients,15 and our study suggests that this holds true for the very old. We did not determine the number who actually underwent a surgical procedure, so cannot estimate perioperative mortality. Others have estimated it to be 10%-30%,5-7,14 with a higher mortality rate for emergency compared with elective procedures.15 However, recent advances in anaesthetic and surgical techniques17 have probably improved survival prospects for very elderly surgical patients. Our finding that nonagenarians admitted under the care of geriatricians were most likely to be admitted as emergencies, to have documented cognitive impairment and to come from residential care, probably reflects the hospital's policy of assigning this type of specialist to very elderly patients with complex medical conditions. This may also explain why patients admitted under geriatricians were less likely to return directly to the community and had longer hospital stays. Alternatively, the longer hospital stays after admission under geriatricians can be explained by casemix factors as, for example, the difference was not statistically significant when day-only patients were excluded. It was notable that 25% of all separ ations were day only, suggesting that strategies to minimise hospital stay with day surgery and other day procedures are being applied successfully to the very old as well as to younger age groups. Further, hospital stay was twice as long in people who needed transfer to a rehabilitation facility or more supportive level of residential care. While it is widely recognised that inability to readily access rehabilitation and residential care facilities prolongs stay in acute hospitals, our study provides quantitative evidence for this. We believe that many people can be reassured by this study. Firstly, hospital administrators and health planners can be reassured that very elderly people seem to make appropriate use of acute hospital services. Secondly, health professionals can take a positive approach to treating acute illness in their elderly patients. Finally, and perhaps most importantly, very elderly people needing acute hospitalisation can be optimistic in the knowledge that most will survive and return home after a short hospital stay. Acknowledgements We gratefully acknowledge Dr Michael Clark (Department of Rehabilitation and Aged Care) for his assistance with statistical analyses. This survey was supported by a research grant from Flinders 2000, a research foundation based at Flinders Medical Centre. References Lipski P. Optimum care of the elderly in an acute general hospital. Med J Aust 1996; 164: 5-6. Australian Bureau of Statistics. Estimated resident population by age and sex in statistical local areas of South Australia. Canberra: ABS, 1991 and 1996. (Catalogue no. 3204.4). Patterson C, Crescenzi C, Steel K. Hospital use by the extremely elderly (nonagenarians): a two-year study. J Am Geriatr Soc 1984; 32: 350-352. Saint Jean O, Thibert JB, Holstein J, et al. Hospitalisation en medecine interne des nonagenaires. Etude de 150 sejours. Rev Med Interne 1993; 14: 825-831. Ackermann RJ, Vogel RL, Johnson LA, et al. Surgery in nonagenarians: morbidity, mortality and functional outcome. J Fam Pract 1995; 40: 129-135. Hosking MP, Warner MA, Lobdell CM, et al. Outcomes of surgery in patients 90 years of age and older. JAMA 1989; 261: 1909-1915. Cohen JR, Johnson H, Eaton S, et al. Surgical procedures in patients during the tenth decade of life. Surgery 1988; 104: 646-651. Hobbs R. Rising emergency admissions. BMJ 1995; 310: 207-209. Lewis H, Purdie G. The blocked bed: a prospective study. N Z Med J 1988; 101: 575-577. Shem S. The house of God. London: Bodley Head, 1978. Callahan D. Controlling the costs of health care for the elderly -- fair means and foul. N Engl J Med 1996; 335: 744-746. Apple Macintosh statview statistical package. Version 512+. Calabasas, Cal: Brain Power Inc, 1986. Cohen JA. A coefficient of agreement of nominal scales. Educ Psychol Meas 1960; 20: 37-46. Denney JL, Denson JS. Risk of surgery in patients over 90. Geriatrics 1972; 27: 115-118. Green J, Passman LJ, Wintfeld N. Analysing hospital mortality: the consequences of diversity in patient mix. JAMA 1991; 265: 1849-1853. Adkins RB, Scott HW. Surgical procedures in patients aged 90 years and older. South Med J 1984; 77: 1357-1364. Finucane P, Phillips G. Preoperative assessment and postoperative management of the elderly surgical patient. Med J Aust 1995; 163: 328-330. (Received 2 Jun, accepted 27 Aug 1997) Authors' details Department of Rehabilitation and Aged Care, Flinders University of South Australia, Adelaide, SA. Josephine H Harris, BM BS(Hons), Medical Registrar; Paul M Finucane, FRACP, FRCPI, Professor; Denise C Healy, RN, RM, Research Assistant. Flinders Medical Centre, Adelaide, SA. Anthony C Bakarich, RN, BN, Assistant Director of Nursing. Reprints will not be available from the authors. Correspondence: Dr J H Harris, Flinders Medical Centre, Bedford Park, SA 5042. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Josephine H Harris · Paul M Finucane · Denise C Healy · Anthony C Bakarich

Urinary symptoms as men age: the reassurance of an evidence-based approach Medical intervention is not usually necessary for men with uncomplicated lower urinary tract symptoms if quality of life is not affected MJA 1997; 167: 62-63 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/>". Make a comment - - ©MJA1997 A high prevalence of uncomplicated lower urinary tract symptoms (LUTS) in an Australian community-based population is reported in this issue of the Journal, although the authors, Pinnock and Marshall, note that despite these symptoms many men and women do not experience substantive dissatisfaction with their quality of life.1 This study is timely, as it follows the recently launched National Health and Medical Research Council (NHMRC) evidence-based Clinical practice guidelines for the management of uncomplicated lower urinary tract symptoms in men.2 Developed by a multidisciplinary working party, the NHMRC Guidelines and two derivative documents, ". . . is it my prostate Doc?" A guide for general practitioners3 and " To pee . . . or not to pee". A guide for men about their urinary symptoms,4 emphasise the need to assess not only the presence of symptoms but also their nature and the "bother" they cause. The distinction between symptoms alone and their impact on quality of life is an important one. There is strong evidence that uncomplicated urinary symptoms in a man are very unlikely to represent any serious threat to his health. For example, the incidence of unsuspected and clinically significant upper-tract obstruction secondary to lower-tract abnormality in these men is very low (0.8%-2.5%).2 Accordingly, the outcome of interest for men (as typified by Pinnock and Marshall's study) is an improvement in their quality of life as related to urinary symptoms, not avoidance of a serious threat to life itself. Thus, measurement of quality of life becomes the key. Only men themselves can assess how bothered they are by their uncomplicated urinary tract symptoms and how much they subsequently improve. How do we encourage men whose quality of life is severely compromised by their urinary symptoms to consult their medical practitioners? Pinnock and Marshall provide another important finding -- that the prevalence of LUTS is similar in men and women aged 55 or more. The factors responsible for LUTS remain to be fully determined -- while urine outflow obstruction in men and pelvic floor dysfunction in women are possible causes, it is probable that many of the changes are simply age related.2 Unfortunately, the use of terms such as "benign prostatic hyperplasia or hypertrophy" (BPH) and "prostatism" inadvertently imply that enlargement of the prostate is the definitive cause of the symptoms. However, the severity of urinary symptoms does not correlate with the presence of BPH or the degree of prostatic enlargement.2 Accordingly, the acronym "LUTS" is preferable to other terminology,5 as it permits a pragmatic definition of the symptom complex without necessarily implying a full understanding of its underlying pathology.2 When is intervention warranted for uncomplicated LUTS? The strongest predictor of the outcome of intervention for uncomplicated LUTS in men is the degree of "bother" the symptoms cause.6 If a man is not particularly bothered by his symptoms, he can be reassured they are unlikely to represent a health threat and that intervention is unlikely to improve his outcome. If he is moderately or significantly bothered, then medical and surgical interventions are more likely to improve his quality of life. While it has been argued that urodynamic parameters or residual urine volume can predict clinically significant differences in the outcome of surgical treatment, this assertion has not been validated in the literature.2 Pinnock and Marshall found that men with high levels of dissatisfaction with the symptoms did not necessarily complain or seek help. Conversely, a smaller, but still substantial, proportion of men who were "not dissatisfied" with their symptoms did visit their doctor because of these symptoms. These findings present a dual challenge. How do we encourage men whose quality of life is severely compromised by their urinary symptoms to consult their medical practitioners? And, because there is little need for or benefit from treatment of symptoms causing minimal bother, how do doctors reassure most men that medical care is unnecessary? We argue that the most effective means of achieving this balance will be via the dissemination and implementation of the NHMRC Guidelines for consumers and their practitioners.7 Of increasing concern to us is the insistence of detractors of the NHMRC Guidelines that early prostate cancer must be excluded as a cause of LUTS and, accordingly, that men must be fully investigated for this malignancy.8,9 Men with uncomplicated LUTS are at no greater risk of early prostate cancer than are their asymptomatic counterparts.2,10 As the evidence to date for prostate cancer screening does not yet meet rigorous public health criteria,11 we believe that the testing of men with LUTS for early prostate cancer is equally unjustified and has the potential to undermine an evidence-based approach to health care. In our view, prostate-specific antigen testing is ethical only when a man has been fully informed of the facts, uncertainties and consequences.12 The NHMRC Guidelines provide eight specific recommendations for further research to clarify those issues poorly supported by empirical evidence. Two priorities were larger randomised trials of the newer urological interventions (such as prostatic heating) against conventional surgical treatments, and methodological research to develop more robust outcome measures. The need for better research is self-evident, especially as the Guidelines are scheduled for review in two years. In the interim, it is our view that, in the absence of strong evidence supporting particular investigations or specific treatments, responsible guidelines should err on the side of conservatism; they should not support a more interventionist position in anticipation of some as yet unidentified future benefit. Men's health will not improve with an unquestioning acceptance of intervention for its own sake. We need to pursue an evidence-based approach with both confidence and compassion, finding new ways to accelerate rigorous, yet relevant, clinical research in areas of need. Concurrently, we need to share the empirical uncertainties of everyday clinical practice more widely with our patients, their partners, our fellow practitioners, and politicians. Geoffrey H L Hirst Urologist, Mater Hospitals, Brisbane, QLD Jeanette E Ward Associate Professor; Director, Needs Assessment and Health Outcomes Unit Central Sydney Area Health Service, Sydney, NSW Pinnock CB, Marshall VR. Troublesome lower urinary tract symptoms in the community: a prevalence study. Med J Aust 1997; 167: 72-75. National Health and Medical Research Council clinical practice guidelines. The management of uncomplicated lower urinary tract symptoms in men. Canberra: AGPS, 1996. National Health and Medical Research Council ". . . is it my prostate Doc?". A guide for general practitioners. Canberra: AGPS, 1996. National Health and Medical Research Council "To pee . . . or not to pee". A guide for men about their urinary symptoms. Canberra: AGPS, 1996. Abrams P. New words for old: lower urinary tract symptoms for "prostatism" [editorial]. BMJ 1994; 308: 929-930. Wasson JH, Reda DJ, Bruskewitz RC, et al. A comparison of transurethral surgery with watchful waiting for moderate symptoms of benign prostatic hyperplasia. The Veterans Affairs Cooperative Study Group on Transurethral Resection of the Prostate. N Engl J Med 1995; 332: 75-79. Thomson R, Lavender M, Madok R. How to ensure that guidelines are effective. BMJ 1995; 311: 237-242. Royal Australasian College of Surgeons media release: Urological Society of Australasia. Men shouldn't ignore urinary symptoms: urologists. April 9, 1997. Royal Australasian College of Surgeons media release: Urological Society of Australasia. Prostate screening, a personal choice: surgeons. August 27, 1996. Rietbergen JB, Kranse R, Boeken Kruger AE, et al. Additional value of the AUA7 symptom score in prostate cancer (PC) detection. J Urol 1997; 157: 467. Commonwealth Department of Health and Family Services prostate cancer screening. Australian Health Technology Advisory Committee (a standing committee of NHMRC). Canberra: AGPS, 1996. Hirst GH, Ward JE, Del Mar CB. Screening for prostate cancer: the case against. MJA 1996; 164: 285-288. To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia. We appreciate your comments.

Jeanette E Ward

Troublesome lower urinary tract symptoms in the community: a prevalence study Carole B Pinnock and Villis R Marshall For editorial comment see Hirst & Ward 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/>". Abstract - Introduction - Method - Population surveyed - Survey questionnaire - Results - Discussion - Key points of study - References - Authors' details - ©MJA1997 Abstract Objective: To determine the prevalence of troublesome lower urinary tract symptoms (LUTS) in men and women in the community. Design: Interview-based prevalence survey. Setting: Metropolitan and rural communities in South Australia, September, 1995. Subjects: Probability sample of 1204 men and 1686 women (aged over 18 years) weighted to reflect the age and sex distribution of the South Australian population. Data collected: Presence of storage (irritative) and voiding (obstructive) symptoms, based on the International Prostate Symptom Score questionnaire; satisfaction with urinary condition (quality-of-life measure); and visits to a doctor for urinary symptoms in the preceding 12 months. Results: The prevalence of one or more troublesome LUTS was 26% (318/1204) for men and 39% (662/1686) for women (all ages) and 48% (314/649) for men and women over 65. The most common troublesome symptoms in men and women were nocturia and frequency. Symptoms were significantly age-related in men, but less so in women, in whom symptom prevalence exceeded 30% for all age groups. Ten per cent of men (123/1204) and 15% of women (249/1686) had visited a doctor for a urinary problem in the previous 12 months. Nine per cent of men (104/1204) and 16% of women (274/1686) were substantially dissatisfied with their urinary condition. Symptom prevalence and dissatisfaction with urinary condition were significantly associated with visiting the doctor ( P < 0.0001), but only 28% (88/318) of men and 27% (179/662) of women with troublesome LUTS saw a doctor, and 63% (65/104) of men and 59% (162/274) of women dissatisfied with their urinary condition did not seek medical help. Conclusions: Although the prevalence of troublesome LUTS in the community is high, the number of people whose quality of life is substantially affected is much lower. The impact of these symptoms upon quality of life is a major reason for patients to see a doctor, yet many who are "bothered" by the symptoms do not do so. MJA 1997; 167: 72-75 Introduction As the community ages, conditions affecting the quality of life and activity of older people become of increasing concern. Lower urinary tract symptoms (LUTS) caused by benign prostatic hyperplasia (BPH) have been termed "prostatism" and may greatly affect the quality of life of older men;1-3 the consequent cost of treatment to the community is high.4 The prevalence of clinically demonstrated BPH is 20% in men aged 40-49 years and 40%-50% in those over 65 years.1,5,6 To document the prevalence of symptoms related to BPH, the International Prostate Symptom Score (IPSS)7 grades the presence of seven LUTS (nocturia, intermittency, urgency, weak stream, incomplete emptying, hesitancy, frequency) on a severity scale of 0-5. It also includes a disease-specific quality-of-life question. However, LUTS measured with the IPSS and related symptom scores may have a range of aetiologies. Urinary symptoms such as urgency and urge incontinence may be caused by idiopathic detrusor instability, changes in muscle contractility, and other non-obstructive causes related to ageing.8,9 The IPSS is thus a non-specific measure of LUTS possibly caused by BPH, and this is reflected by studies that have shown high symptom scores in men with other lower urinary tract conditions,10 and in women.11-13 In an Australian general practice survey, urological problems were given as 1.7% of reasons for encounter with a doctor (all ages, both sexes),14 while in older men 7%-14% of encounters were for urinary problems.15 But the number of people significantly "bothered" by LUTS appears to be very much greater than the number seeking medical help for the problem.5,6,15 Symptom prevalence varies between countries, but there is evidence that similar levels of symptoms have a similar impact on daily activities of living in different countries.16,17 The prevalence of LUTS has been measured with the IPSS or related indices in the Netherlands,18 Canada,19 the United Kingdom,5 France,20 Japan,21 Spain,22 New Zealand,23 Scotland and the United States;17 no community-based surveys of symptom prevalence have been undertaken in Australia. Because of this, we undertook a community survey to determine the prevalence of troublesome LUTS in men and women in South Australia. The symptoms surveyed are described as uncomplicated by the National Health and Medical Research Council.8 Our objective was not to derive a severity score, but to determine the presence or absence of troublesome symptoms, their impact on quality of life, and the proportion of individuals seeking medical help for such a problem. Method Population surveyed The Omnibus survey, a multiple-user household interview survey undertaken for health organisations in South Australia (SA), was used for the study. The methodology and results of its use in other studies have been reported.24-26 The sampling method provides a probability sample of the SA population: in the metropolitan sample, 10 dwellings are chosen from each of 320 census collection districts (1991 census) using a random starting point and selection is then based on every fourth household. One person aged over 15 years (the person whose birthday was last) is chosen per household. In the country sample, all cities/towns with a population of 10 000 or more are chosen, and the balance of the sample is chosen from centres with a population of 1000 or more, with weighting proportional to size. The sampling method was the same as for metropolitan dwellings. Sixty interviewers conducted 3016 interviews from the 4200 households selected. Data are weighted by the inverse of the individual's probability of selection, then reweighted to benchmarks derived from estimated resident population at 30 June 1993 by age, sex and local government area from the Australian Bureau of Statistics. The data analysed and presented have thus been weighted to represent the age and sex structure of the SA population. Survey questionnaire The questions were derived from the American Urological Association-7 BPH questionnaire,27 adopted by the World Health Organization (WHO) as the IPSS,7 and have been validated for test/retest reliability, validity and clarity. Respondents were asked if, in the previous 12 months, any of the following urinary symptoms were troublesome: a strong need to urinate (pass water) with little or no warning; needing to go again less than two hours after finishing urination; needing to get up twice or more at night to urinate; having a weak urinary stream; stopping and starting several times when urinating; wetting underclothes;20 and whether there were other troublesome urinary symptoms. Respondents were asked about the presence or absence of "troublesome symptoms" -- they were not asked to grade symptom severity. They were also asked about quality-of-life7 (level of satisfaction with their urinary condition, in seven categories: delighted, pleased, mostly satisfied, mixed, mostly dissatisfied, unhappy, terrible), and whether they had seen a doctor about any urinary problem in the past 12 months. Questions were piloted for ease of understanding, internal consistency and sensitivity in a group of 18 men, and subsequently in 50 further interviews with men and women. To ensure completeness and accuracy of recording, five per cent of each interviewer's work was selected at random and the respondent re-interviewed with selected questions. After data checking, any missing responses were followed up by telephone. Statistical analysis was done with SPSS for Windows version 6.1 (SPSS, Chicago, Ill, USA). Statistical significance was calculated with Pearson chi-squared tests, unless otherwise indicated. Results The initial sample drawn was 4200 houses, of which 4067 were occupied and defined as "households". Of these, 3016 households participated, a response rate of 74.2%. Of the 3016 people interviewed, 1734 were women (57.5%) and 1281, men (42.5%). The major reasons for non-response were refusal (601; too busy, not interested) and contact not established after six visits (293); 75.6% of interviews were in the metropolitan area and 24.4% in the country. Respondents were evenly spread across all age groups. Only adults aged over 18 years are included in the analysis reported here (1204 men, 1686 women). Twenty-six per cent of men (318/1204) and 39% of women (662/1686) reported one or more troublesome urinary symptoms, with no differences between rural and metropolitan respondents (men or women) (Box 1). The most common symptoms in both men and women were frequency and nocturia (Box 2). In men, nocturia increased significantly with age (from 4% in 18- to 24-year-olds to 33% in those over 65 years; P < 0.00001). Weak stream also increased, from 2% in 18- to 24-year-olds to 12% in men over 65 (P < 0.00001). Urgency, frequency and mild incontinence were reported more frequently by women than by men (all, P < 0.001), and, as stated above, the overall prevalence of troublesome urinary symptoms (i.e, prevalence of more than one symptom) was also higher in women (P < 0.00001). The prevalence of one or more storage (irritative) symptoms (i.e., urgency, frequency or nocturia) was 23% in men and 33% in women (P < 0.0001), with the prevalence of one or more voiding (obstructive) symptoms (i.e., weak stream and intermittency) being 6.7% and 6.4%, respectively (difference not significant). Under the category "other", the most common symptom was stress incontinence (n= 17/44; 38%) in women and medication side-effects in men (n= 4/16; 25%). Age-specific symptom prevalence varied between men and women. For men, there was a clear age dependence, with symptom prevalence exceeding 20% only after age 45. In women, the age-related increase was weaker, and symptom prevalence exceeded 30% in all age groups. For men and women over 65, symptom prevalence was 48% (314/649). While the percentage of respondents reporting troublesome urinary symptoms was high (Box 1), only 28% of men (88/318) and 27% of women (179/662) with troublesome LUTS had visited a doctor about a urinary problem during the preceding 12 months. Satisfaction with urinary condition seems to be a better predictor of visits to the doctor than symptom prevalence (one or more symptoms) -- only 6% (23/397) who were "pleased" with their urinary condition had visited a doctor for urinary symptoms, compared with 60% (39/65) who were "unhappy" with their urinary condition (P < 0.00001). Discussion This first study of LUTS in the Australian community shows a high prevalence of troublesome LUTS, which occurred across all ages, but particularly in older age groups (48% of men and women over 65 reported one or more symptoms). Other reports also show a high prevalence of urinary symptoms for older men, ranging from 35% in a United States study28 to more than 90% of men in a Canadian study.19 Specific symptom prevalence can also be high (e.g., 61% for urgency,6 and 51% for hesitancy5 ). Most studies show that the prevalence of mild symptoms is high, and that symptoms which substantially affect quality of life or trigger a visit to the doctor have a lower prevalence.3 The prevalence of severe or bothersome symptoms is often as low as 25% to 30% of the total symptom prevalence,5,29 suggesting that adaptation to mild symptoms may occur. A review of moderate to severe symptoms in four community-based studies reported prevalence rates of 14%-33% for men over 40 years,16 and agrees with the 37% (220/593) of men over age 45 reporting one or more troublesome urinary symptoms in our study. In our study the most common troublesome symptoms for men were nocturia and frequency. This agrees with studies in France,20 the Netherlands,29 and the United Kingdom,5 but not Scottish studies1,6 or a French study.3 Methodological differences, such as the wording of questions and framing of population sampling methods, may account for these differences. In our study, the prevalence of urinary symptoms associated with "prostatism" in men was the same for men and women aged 55 and over (Box 2). Other studies in clinical or selected populations have also reported high symptom scores in women.11-13 However, we found the prevalence of LUTS in women did not show the same age-specific trend as for men, and storage symptoms (urgency, frequency and nocturia) were more prevalent in women (33% [563/1686] for one or more symptoms) than men (23% [274/1204]), while voiding symptoms were similar in both groups. In a study of women with voiding symptoms undergoing urodynamic evaluation, relatively few women had outflow obstruction.11 While the overall prevalence of LUTS, particularly in those aged 55 and over, was similar in men and women in our study, the symptom profile (age-specific trend and individual symptom prevalences) differed, reflecting their potentially different aetiologies. For both men and women, impact on quality of life (measured by satisfaction with urinary condition) was strongly correlated with visits to the doctor, with this correlation being similar in men and women. This argues against some reports of men's "stoicism" in the face of urinary symptoms.1 However, the finding also suggests that men and women may be equally reluctant to seek medical assistance for LUTS. Sixty-three per cent (65/104) of men and 59% (162/274) of women substantially dissatisfied with their urinary condition were not visiting a doctor for the condition, which agrees with the substantial numbers not seeking help reported in other studies.1,5 Conversely, the small proportion of our participants who had seen a doctor despite being "delighted" with their urinary condition may represent preventive activity, such as checkups, or concern, for example, about prostate cancer. Other studies report a substantial impact of moderate to severe LUTS on quality of life. Activities of daily living were affected in 51% of men with clinically defined BPH,1 and working-age men reported symptoms as more bothersome than retirement-age men, despite experiencing them less frequently.6 People may be reluctant to seek help for LUTS because these symptoms are considered a normal part of ageing, because of the perceived stigma of the symptoms or fear of possible treatments,1 or (in men) because of stoicism.30 These possibilities need to be addressed in future studies, as does the possibility that rural men who were dissatisfied with their urinary condition were less likely than urban men to seek medical help (P = 0.057). The main reason patients visit doctors about their urinary condition may be to reduce its effect on their daily activities, and this is therefore an objective of treatment. Conservative measures such as bladder training, pelvic muscle exercises, diet and fluid-intake management as well as attention to functional factors may be helpful in achieving this when symptoms are mild. Key points of study High prevalence of troublesome lower urinary tract symptoms (LUTS) in Australian men (26%) and women (39%). Far fewer men and women are substantially dissatisfied with their urinary condition (9% men, 16% women) and seeking treatment (10% men, 15% women). But fewer than half of those who are substantially dissatisfied with their urinary condition seek medical help (38% men, 41% women). LUTS in men and women has different aetiologies and symptom profiles, although the prevalence of one or more symptoms in people over the age of 65 years is the same (48%). The impact on quality of life is the major reason for people to seek medical help. Conservative management strategies may reduce this impact when surgical or medical treatment is not indicated. References Garraway WM, McKelvie GB, Russell EBA, et al. Impact of previously unrecognised benign prostatic hyperplasia on the daily activities of middle-aged and elderly men. Br J Gen Pract 1993; 43: 318-321. Abramson ZH, Gofin J, Abramson JH. Obstructive prostatic symptoms: a community survey in Jerusalem. Int J Epidemiol 1994; 23: 797-804. Sagnier P, MacFarlane G, Teillac P, et al. Impact of symptoms of prostatism on level of bother and quality of life of men in the French community. J Urol 1995; 153: 669-673. Ahlstrand C, Carlsson P, Jonsson B. Estimated total costs of treating benign prostatic hyperplasia in Sweden. Scand J Urol Nephrol 1995; 29: 57-63. Jolleys JV, Donovan JL, Nanchahal K, et al. Urinary symptoms in the community: how bothersome are they? Br J Urol 1994; 74: 551-555. Tsang KK, Garraway WM. Prostatism and the burden of benign prostatic hyperplasia on elderly men. Age Ageing 1994; 23: 360-364. Mebust W, Bosch R, Donovan J, et al. Symptom evaluation, quality of life and sexuality. In: Second international consultation on benign prostatic hyperplasia. Paris: World Health Organisation, 1993: 131-143. National Health and Medical Research Council. Clinical practice guidelines. The managment of uncomplicated lower urinary tract symptoms in men. Canberra: AGPS, 1996. Yalla SV. Correlation of American Urological Association Symptom Index with obstructive and non-obstructive prostatism. J Urol 1995; 153: 674-680. Stoevelaar H, van de Beek C, Nijs H, et al. The symptom questionnaire for benign prostatic hyperplasia: an ambiguous indicator for an ambiguous disease. Br J Urol 1996; 77: 181-185. Chancellor MB, Rivas DA. American Urological Association symptom index for women with voiding symptoms: lack of index specificity for benign prostate hyperplasia. J Urol 1993; 150: 1706-1709. Chai TC, Belville WD, McGuire EJ, Nyquist L. Specificity of the American Urological Association voiding symptom index: comparison of unselected and selected samples of both sexes. J Urol 1993; 150: 1710-1713. Lepor H, Machi G. Comparison of AUA symptom index in unselected males and females between 55 and 79 years of age. Urology 1993; 42: 36-40. Bridges-Webb C, Britt H, Miles D, et al. Morbidity and treatment in general practice in Australia 1990-1991. Med J Aust 1992; 157: Suppl Oct 19: S1-S57. Ward J, Sladden M. Urinary symptoms in older men, their investigation and management: is there an epidemic of undetected morbidity in the waiting room? Fam Pract 1994; 11: 251-259. Bosch R. Use of the International Prostate Symptom Score (IPSS) in epidemiological studies and clinical practice -- a review. In: Third International Consultation on Benign Prostatic Hyperplasia. Monaco: World Health Organisation, 1995. Guess HA, Chute CG, Garraway WM, et al. Similar levels of urological symptoms have similar impact on Scottish and American men -- although Scots report less symptoms. J Urol 1993; 150: 1701-1705. Bosch JL, Niemer AQ, Kirkels WJ, Schroder FH. Signs and symptoms of benign prostatic hyperplasia in men screened for prostatic carcinoma. Prog Clin Biol Res 1994; 386: 97-107. Norman RW, Nickel JC, Fish D, Pickett SN. 'Prostate-related symptoms' in Canadian men 50 years of age or older: prevalence and relationships among symptoms. Br J Urol 1994; 74: 542-550. Sagnier PP, MacFarlane G, Richard F, et al. Results of an epidemiological survey using a modified American Urological Association symptom index for benign prostatic hyperplasia in France. J Urol 1994; 151: 1266-1270. Tsukamoto T, Kumamoto Y, Masumori N, et al. Prevalence of prostatism in Japanese men in a community-based study with comparison to a similar American study. J Urol 1995; 154: 391-395. Hunter D, Berra-Unamuno A, Martin-Gordo A. Prevalence of urinary symptoms and other urological conditions in Spanish men 50 years old or older. J Urol 1996; 155: 1965-1970. Nacey J, Morum P, Delahunt B. Analysis of the prevalence of voiding symptoms in Maori, Pacific Island and Caucasian New Zealand men. Urology 1995; 46: 506-511. Wilson D, Wakefield M, Taylor A. The South Australian Health Omnibus Survey. Health Prom J Aust 1992; 2: 47-49. MacLennan A, Wilson D, Taylor A. Prevalence and cost of alternative medicine in Australia. Lancet 1996; 347: 569-573. MacLennan A, Taylor A, Wilson D. Changes in the use of hormone replacement therapy in South Australia. Med J Aust 1995; 162: 420-422. Barry MJ, Fowler F, O'Leary M, et al. The American Urological Association Symptom index for benign prostate hyperplasia. J Urol 1992; 148: 1549-1557. Diokno AC, Brown MB, Goldstein N, Herzog AR. Epidemiology of bladder emptying symptoms in elderly men. J Urol 1992; 148: 1817-1821. Bosch JL, Hop WC, Kirkels WJ, Schroder FH. The International Prostate Symptom Score in a community-based sample of men between 55 and 74 years of age: prevalence and correlation of symptoms with age, prostate volume, flow rate and residual urine volume. Br J Urol 1995; 75: 622-630. McCallum J. Older Men's Health: Stoicism versus successful ageing. Proceedings of the National Men's Health Conference. Melbourne: AGPS, 1995. (Received 24 June 1996, accepted 17 Feb 1997) Authors' details Repatriation General Hospital Daw Park, South Australia Carole Pinnock, PhD, Principal Research Scientist, Division of Surgery; Villis R Marshall, MD, FRACS, Professor and Head, Department of Surgery, Flinders Medical Centre, and Division of Surgery, Repatriation General Hospital Daw Park. Reprints: Dr CB Pinnock, Division of Surgery, Repatriation General Hospital Daw Park, Daws Road, Daw Park, SA 5041. E-mail: spinncb AT rgh.sa.gov.au ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Carole B Pinnock · Villis R Marshall