Ageing

Tests for serum vitamin B12 and red cell folate levels are commonly requested in elderly inpatients to rule out reversible causes of cognitive impairment (eg, delirium). This imposes some cost on the community. The evidence for the association of cognitive impairment and vitamin B12 deficiency is inconclusive. It is also unclear whether other markers, such as elevated mean corpuscular volume (MCV) and ...

Celia S M Ting · John C Oldroyd · Michele R Levinson

Objectives: To investigate the acceptability and feasibility of using end-of-life (EOL) care pathways in residential aged care facilities (RACFs).Design, setting and participants: Multistage action research approach involving interviews, surveys and prospective audits of deaths and EOL care pathway use among residents and staff of RACFs and associated general practitioners from 14 RACFs in Victoria and South Australia between April 2009 and July 2010.Intervention: ...

Dell E Horey BAppSc, MMedSc(ClinEpi), PhD · Annette F Street BEd(Hons), PhD · Alison F Sands MB BS(Hons), FRACGP

To the Editor: We congratulate Green and Maiorana1 on their recent article highlighting the value of exercise in obesity management. The urgent need for action to prevent further weight gain in adults and to reduce the proportion of the population that is obese was recognised 25 years ago. However, despite massive public health efforts to reduce obesity ...

Rosemary A McGinnes · Judy A Lowthian

Objectives: To explore the burden of illness associated with infectious syndromes and to measure the associated use of antimicrobials in residential aged care facilities (RACFs).Design, setting and subjects: Retrospective analysis of data for January 2006 to December 2010 from an infection surveillance system covering residents of four co-located RACFs, with a total of 150 residential care beds, in Melbourne, Victoria.Main outcome measures: Number of episodes and incidence of health care-associated infection (HCAI); rate of antimicrobial use; prescribing concordance with McGeer criteria for infection; frequency of clinical specimen collection.Results: There were 1114 episodes of an infectious syndrome over 267 684 occupied bed-days (OBD), affording an average HCAI rate of 4.16 episodes/1000 OBD annually over 5 years (95% CI, 3.92–4.41). The mean rate of antimicrobial use was 7.07 courses/1000 OBD (range, 6.71–7.84). Around 40% of antimicrobial prescribing was for episodes that did not fulfil the McGeer criteria for clinical infection; this included about half of suspected urinary tract and upper respiratory tract infections (URTI), and about one-third of suspected lower respiratory tract and skin infections. Antimicrobials were routinely prescribed for URTI and bronchitis. Of all episodes treated with antimicrobials, 36% had documentation that a clinical specimen was obtained.Conclusions: The HCAI rate remained relatively stable over time. Routine surveillance and feedback of infection rates to the facilities did not result in a noticeable decrease of infection burden over time. It is of immediate concern that antimicrobials were being prescribed for a large proportion of suspected infections that did not meet criteria for clinical infection. Opportunities exist to further improve the use of antimicrobials in the RACF setting.

Ching Jou Lim BPharm(Hons) · Susan C McLellan RN, GradCert InfectControl, GradDipNSInfectControl · Allen C Cheng FRACP, MPH, PhD · Joanne M Culton RN, GradCert InfectControl · Sneha N Parikh BA · Anton Y Peleg* MB BS, PhD, FRACP · David C M Kong* BPharm, MPharm, PhD

Time to find a systems-level model for a serious, undermanaged, but preventable problem For over 20 years, we have known that osteoporotic fractures predispose to further fractures and significant morbidity.1,2 We also understand that first and subsequent fragility fractures are associated with premature death.2-4 However, surprisingly little has happened over the past two decades to translate this knowledge into good clinical practice for our patients. Of course, anyone presenting with a low-trauma fracture to an Australian hospital will get it fixed in due time. But little happens after that. Nobody seems to ask why that person had a low-trauma fracture (or a second or third one) to begin with. Indeed, 75%–80% of patients who have had an osteoporotic fracture are neither being investigated nor treated for their underlying condition — osteoporosis.5,6 This systematic failure is all the more shocking as we have available to us not only one of the world’s best medical systems, but also subsidised pharmacotherapies with proven efficacy to reduce the risk of (re)fracture.7 Recent data from New South Wales reveal that 35% of patients admitted to hospital with an osteoporotic fracture were readmitted with another fragility fracture, often within 1–2 years of the initial event. This accounted for 16 225 essentially unnecessary admissions with a startling average length of stay of 22 days. Of those with refractures, 17% died during the period studied.8 These numbers represent a medical nightmare and a health care systems failure of huge and growing dimensions. Because the Australian population is ageing, the prevalence of osteoporosis has been steadily rising over the past few decades. Currently, 2.2 million Australians live with osteoporosis, and this number is projected to increase to 3 million by 2021.9 While 67 000 osteoporotic fractures were recorded in Australia in 2001, this figure had risen to more than 87 000 in 2007.9 In 2001, the annual total cost of osteoporosis to the Australian health system was estimated at $7.4 billion,10 and it does not require much imagination to anticipate that we will soon spend an even larger amount of our nation’s income on a medical problem that can be treated and, more importantly, effectively prevented. The reasons for such management failures are complex, and include inadequate awareness among doctors and patients of the health hazards related to osteoporosis, and the almost complete lack of effective medical postfracture care.6 While the fundamental need to improve osteoporosis recognition and management has been acknowledged worldwide, attempts to tackle this issue through simple educational campaigns have clearly not translated into improvements in treatment rates.11 In contrast, there is now high-quality evidence that the implementation of system-level models of care reduces refracture rates, morbidity and mortality, hospital bed days and other health system use. The most effective of these interventions are “fracture liaison services” that include targeted case-finding, systematic assessment, appropriate treatment and follow-up, and access to self-management education programs and support systems.12-15 While such programs have been developed by individual clinicians in Australia, most health services seem reluctant to meet the financial and logistical requirements for secondary fracture prevention services. Are we asking for too much? Would public funding for such services be justified? Let us look at the evidence. We recently reported on the clinical effectiveness of a fracture liaison service established in 2005 at Concord Repatriation General Hospital in Sydney.12 This outpatient service is available to all patients with osteoporotic fractures and, over 4 years, reduced the risk of refracture by 80% compared with standard care. Obviously, the service involves human resources and more use of bone densitometry, laboratory testing and medications. The question therefore was whether the benefits provided by the service would be cost-effective. A health-economic analysis published in the latest issue of Osteoporosis International shows that even though the service is comprehensive, it is also highly cost-effective.16 The economic model used for the analysis accounted for all major osteoporotic fractures (ie. hip, forearm, and humerus), their associated direct costs, changes in health utility and, in the case of hip fractures, increases in mortality. Fracture probabilities were calculated from the clinical data, and medical costs for the service and the control arm were derived from reported health resource consumption data. The (very conservative) analysis showed that reducing subsequent fractures through a fracture liaison service led to significant improvements in quality-adjusted life-years (QALYs). Despite higher treatment costs, the total cost of the intervention was only $1300 per patient over a 10-year period, that is, $130 per patient per year. The incremental cost-effectiveness ratio for the service (versus no intervention) was $20 210 per QALY gained, which means that the intervention represents excellent value for money. Indeed, when lower medication costs were introduced (as would be expected over time), the service was cost-saving; that is, the money saved by preventing fractures would be more than the cost of the service.16 The Concord fracture liaison service is one of various possible models, but conceptually can be implemented in any Australian health service. Its proven clinical and cost-effectiveness leave no excuses for not attempting to close the appalling gap in the postfracture care of patients at high risk of fracture.

Markus J Seibel MD, FRACP, PhD

The growing infection control challenges facing an ageing population In this issue of the Journal, a study of multiresistant bacterial intestinal carriage by Stuart and colleagues adds important detail to the emerging picture of multiple antibiotic resistance in non-hospital settings.1 The higher colonisation rate they found for Escherichia coli than for vancomycin-resistant enterococci (VRE) or Clostridium difficile in residential aged care facilities is a timely reminder that our surveillance and infection control resources should not be exclusively targeted at VRE or C. difficile. The simultaneous presence of these potential pathogens in the same aged care population raises the ugly spectre of carriage of two or more resistant organisms. The risk of contemporaneous multiresistant E. coli, C. difficile-associated diarrhoea and faecal incontinence might be considered the perfect infection control storm. As Stuart and colleagues rightly point out, data are lacking on the prevalence of community-acquired multiresistant gram-negative bacteria in Australia. By extrapolation from northern hemisphere studies, it appears that nursing homes and other long-term care facilities can function as potent reservoirs of multiresistant E. coli.2 Measuring the duration of enteric carriage after initial colonisation by a multiresistant strain may help determine the potential window for onward transmission, but we can anticipate variable and possibly strain-dependent transmissibility. The relatively small size of Stuart et al’s study, the presence of a single-strain case cluster and other specific features make it difficult to generalise from their results. However, observation of a dominant genotype of multiresistant E. coli in one aged care facility concords with a previous observation of single genotype clusters in long-term care facilities.3 The observed dominance of CTX-M (cefotaxime-hydrolysing) β-lactamase-mediated resistance is also consistent with the wider international trend, as noted in a recent nationwide study from Belgium.4 The mechanism of antibiotic resistance designated CTX-M-15 has been particularly successful on a global scale — the result of carriage of resistance-determining genes on multireplicon plasmids, combined with international travel.5 CTX-M-15 has become a prominent multiresistance determinant detected in the faeces of international travellers, particularly those returning from the Indian subcontinent or Africa.6 The route followed by multiresistant gram-negative bacteria brought to Australia by healthy, young international travellers to reach the residents of aged care facilities is unclear. But once aged care residents are colonised, Stuart et al’s data suggest spread of resistance among them, possibly assisted by transmissible bacterial genetic elements.1,3 In a survey of resistant E. coli in western Sydney, where CTX-M-15 predominates, 11 different conjugative plasmids were found, most of which had multiresistance regions.7 The challenges of aged care are many and will continue to grow as the number of people in need of residential care expands. There are many potential contributors to the emergence of multiresistant bacteria in residents of aged care facilities: multiple hospital admissions, excessive use of antibiotics (in terms of courses, duration and antimicrobial spectrum), incontinence, dementia, venous stasis ulcers, and difficulty implementing infection control practices in institutions where residents are free to move outside their rooms and mingle with others. Well established multiresistant bacteria such as community-acquired methicillin-resistant Staphylococcus aureus (MRSA) pose a significant problem in some aged care facilities and other long-term care units. Our failure to hold the MRSA threat at bay, even with the most stringent measures, should make us wary of trying to apply failed control strategies to a group of bacteria with a substantially different ecology. The “search-and-destroy” approach to infection control, with its heavy reliance on screening swabs and decolonisation, risks interfering with movement of aged care facility residents to and from hospital (when admission or discharge depends on documented screening status or completion of decolonisation) for little, if any, demonstrable benefit. The value of alternative approaches is also uncertain. To date, attempts to control intestinal carriage of multiresistant E. coli in long-term care residents using probiotic E. coli have been unsuccessful.8 This indicates the durability of multiresistant E. coli as a gastrointestinal coloniser. A control method for multiresistant bacteria that relies on surveillance and targeted infection control measures may seem appealing, but in reality is likely to be costly, impractical and ineffective. An alternative strategy9 is to use multiple measures targeting improvements in the skilled nursing care of those at identifiably higher risk of multiresistant bacterial infection, without prior surveillance culture. We recognise that this proposal will not sit comfortably with those who have long advocated a post-hoc, species-specific, search-and-destroy approach to organisms of interest. But with an estimated multimillion dollar annual cost of multiresistant bacteria control measures, and a residential aged care sector facing many challenges, we will be forced to explore all options. This should include considering a more public health-based approach, as long-term care facilities lie outside the remit of conventional hospital infection control. These options cannot be properly debated without additional, nationally representative data addressing the key questions raised by Stuart and colleagues, particularly the duration of gastrointestinal colonisation, the relationship between colonisation and subsequent infection, and the consistency of epidemiological data across a wider range of residential aged care facilities. Their timely study highlights a need for informed discussion of new measures to control multiresistant gram-negative bacteria in long-term residential care facilities. This could include a gamut of aged care measures aimed at reducing transmission, such as decreasing long-term care facility–hospital transfers through the use of advance care planning10 and hospital-in-the-home treatment.

Timothy J J Inglis DM, PhD, FRCPA · Christopher D Beer MB BS, PhD, FRACP

Objective: To assess the frequency of, and risk factors for, colonisation with vancomycin-resistant enterococci (VRE), Clostridium difficile and extended-spectrum β-lactamase (ESBL)-producing organisms in residential aged care facilities (RACFs).Design, setting and participants: We conducted a point prevalence survey in October – November 2010 in three RACFs associated with our health service. A single faecal sample was collected from each participating resident and screened for the presence of VRE, C. difficile and ESBL-producing organisms. Presence of risk factors for antibiotic-resistant organisms was identified using a questionnaire.Main outcome measures: Prevalence of colonisation with VRE, C. difficile and ESBL-producing organisms; molecular typing of ESBL-producing organisms; prevalence of risk factors including presence of a urinary catheter, recent inpatient stay in an acute care setting and recent antibiotic consumption.Results: Of 164 residents in the three facilities, 119 (73%) were screened. Mean age of screened residents was 79.2 years, and 61% were women; 74% had resided in the RACF for > 12 months, 21% had been given antibiotics within the past month and 12% had been in an acute care centre within the past 3 months. Overall rates of VRE (2%) and C. difficile (1%) colonisation were low, but ESBL-producing Escherichia coli was detected in 14 residents (12%) overall, with half of these residing in one wing of an RACF (27% of wing residents tested). Ten of the 14 ESBL-producing isolates had identical molecular typing patterns and belonged to genotye CTX-M-9. Eight of 13 residents had persistent colonisation on repeat testing 3 months later.Conclusion: We found a high prevalence of multiresistant ESBL-producing E. coli in RACF residents. A clonal relatedness of isolates suggests possible transmission within the facility. RACFs should have programs emphasising processes that will limit spread of these organisms, namely good hand hygiene compliance, enhanced environmental cleaning and dedicated antimicrobial stewardship programs.

Rhonda L Stuart MB BS, FRACP, PhD · Despina Kotsanas BSc(Hons), MClinEpi · Brooke Webb BAppSc(Lab Med) · Susan Vandergraaf BN · Elizabeth E Gillespie BN, MPubHlth · Geoffrey G Hogg MB BS, FRACP, FRCPA · Tony M Korman MB BS, FRACP, FRCPA

Objective: To determine perceptions of barriers to admission to subacute care from acute hospital care, and barriers to subsequent discharge from subacute care.Design, participants and setting: Web-based survey of key stakeholders using Likert scales and closed questions. Prompts were emailed repeatedly to potential participants in Australia between 15 May and 24 July 2009. Participants were physicians working in inpatient rehabilitation medicine and aged care units, as well as senior hospital managers with responsibility for patient flow.Main outcome measures: Perceived admission and discharge barriers in subacute care.Results: Half of the 101 respondents reported barriers to admission to subacute hospitals as moderate, severe or extreme, and 81% reported a similar grading of severity for barriers to discharge. There was no relationship between these perceptions and whether respondents worked only in the public hospital system (barriers to access: χ2 = 0.02 [df = 1; P = 1.0]; and barriers to discharge: χ2 = 0.0 [df = 1; P = 1.0]). The most commonly reported barriers to admission were: availability of beds (61% of respondents); physical, environmental and equipment inadequacies (62% of respondents); and allied health or nursing staff issues (55% of respondents). The most commonly reported barriers to discharge included: waiting for a more appropriate setting of care (76% of respondents) and funding for home modifications, equipment or carers (55% of respondents). There was no relationship between respondents’ position and their reporting of various admission (χ2 = 6.2; df = 8; P = 0.6) or discharge barriers (χ2 = 13.8; df = 12; P = 0.3).Conclusion: There is a strong perception among key stakeholders in subacute care that there are major barriers to patient admission and discharge. Redistributing proposed funding for inpatient subacute beds to measures for overcoming these barriers is likely to improve patient flow though the whole hospital system.

Peter W New MB BS, MClinEpi, FAFRM(RACP) · Peter A Cameron MB BS, MD, FACEM · John H Olver MB BS, MD, FAFRM(RACP) · Johannes U Stoelwinder MB BS, MD, FRACMA

To the Editor: Although Indigenous males are twice as likely and Indigenous females are half as likely to report being diagnosed with osteoporosis compared with their non-Indigenous counterparts,1 data on the interracial differences in osteoporotic risk factors are limited. Our study of 276 patients attending a tertiary hip fracture unit in Western Australia over a 5-year period is the first to report differences in common risk factors for hip fracture between Indigenous and non-Indigenous patients. Our data showed a lower likelihood of vitamin D deficiency and polypharmacy but higher likelihood of diabetes mellitus, renal disease and alcohol use among Indigenous patients with hip fracture compared with non-Indigenous patients. Using the local orthogeriatric database, we identified 46 Indigenous and 230 randomly selected non-Indigenous patients aged ≥ 45 years who were transferred to a hip fracture unit following surgery for a minimal-trauma fracture at Royal Perth Hospital from July 2005 to June 2010. High alcohol use was defined as alcohol intake exceeding guideline recommendations,2 and polypharmacy as the use of more than five medications. We used a laboratory cut-off of 25-hydroxyvitamin D (25-OHD) < 50 nmol/L to indicate a low vitamin D level. Indigenous status was self-reported during admission. We compared data for Indigenous and non-Indigenous patients using the Mann–Whitney U and Pearson χ2 tests. We used logistic regression (SPSS version 17; SPSS Inc, Chicago, Ill, USA) to examine the association between Indigenous status and the predictor variables. Our study was exempted as a quality assurance activity from formal ethics review by the Royal Perth Hospital Ethics Review Committee and the Western Australian Aboriginal Health Information and Ethics Committee. Risk factors among the two groups are shown in the Box. The most common risk factors among Indigenous patients were antihypertensive use, high alcohol use and diabetes. In the final multivariate model, Indigenous patients with hip fracture were significantly more likely to have diabetes and renal disease and to report high alcohol use, but significantly less likely to have a low vitamin D level and polypharmacy, after adjustment for age, sex and rural residency. These well described risk factors contribute to fracture risk through two mechanisms: falls and secondary osteoporosis. Diabetes-related complications such as visual impairment, stroke and peripheral neuropathy can increase fracture risk.3 In renal dysfunction, osteoporosis is related to cortical thinning and uraemic osteodystrophy.4 Excessive alcohol intake at a young age among Indigenous people may affect peak bone mass.5 The effect of alcohol on liver cirrhosis, cognition, falls due to intoxication and peripheral neuropathy may contribute to fracture risk. Risk stratification will be more robust if these results can be cross-validated in other institutions. Associations between hip fracture and risk factors in Indigenous patients compared with non-Indigenous patients at Royal Perth hospital, July 2005 – June 2010 Variable Indigenous (n = 46) Non-Indigenous (n = 230) P* Crude OR Adjusted† OR (95% CI) Continuous (mean [SD]) Age at hip fracture‡ (years) 81.4 (9.1) 82.3 (9.4) 0.58 0.99 1.03 (0.96–1.10) 25-OHD level (nmol/L) 59.9 (30.2) 40.9 (18.6) < 0.001 – – Categorical (no. [%]) Women 29 (63%) 161 (70%) 0.35 1.11 2.52 (0.51–12.31) Non-metropolitan 42 (93.3%) 38 (16.6%) < 0.001 70.37 70.32 (14.43–342.59) Low vitamin D level§ 15 (38.5%) 142 (69.6%) < 0.001 0.27 0.26 (0.07–0.91) Prior fracture 9 (19.6%) 52 (22.6%) 0.65 0.83 0.42 (0.09–1.90) High alcohol use¶ 19 (41.3%) 10 (4.3%) < 0.001 15.5 13.25 (1.89–92.92) Diabetes mellitus 21 (45.7%) 41 (17.8%) < 0.001 3.87 8.19 (2.02–33.18) Renal disease 16 (34.8%) 21 (9.1%) < 0.001 5.31 6.12 (1.29–29.05) Polypharmacy** 18 (39.1%) 137 (59.6%) 0.01 0.44 0.17 (0.04–0.72) Antihypertensive use 26 (56.5%) 118 (51.3%) 0.52 1.23 2.75 (0.70–10.76) 25-OHD = 25-hydroxyvitamin D. OR = odds ratio. * Mann-Whitney U or Pearson χ2 test. Level of significance: P < 0.05. † Multivariate logistic regression. ‡ Minimal-trauma fracture. § 25-OHD level < 50 nmol/L. ¶ Alcohol intake exceeding guideline recommendations.2 ** > 5 drugs.

Michelle M Y Lai · Nicholas G Waldron

To the Editor: In their editorial, Terpening, Hodges and Cordato argue for routine screening for dementia in Australia.1 Most of the editorial is devoted to discussing which test should be used, and the authors contend that the most-used test — the mini-mental state examination — has such poor test characteristics that it would be a very poor basis for routine screening. However, the discussion about which test to use ignores the elephant in the room — should we screen for dementia in the first place? In their 1968 World Health Organization public health paper on screening for disease, Wilson and Jungner stipulate that “There should be an accepted treatment for patients with recognized disease”.2 There is no evidence whatsoever that this is the case with dementia. Terpening and colleagues cite an article in their editorial in support of their assertion that “development of effective dementia treatments depends on earlier and more accurate identification of disease”.3 However, that article only states that early intervention might help to slow some forms of cognitive decline or progression to dementia. This is a very slim evidence base for routine mass screening. The development of effective treatments can never be a justification for routine population-wide screening. Even in a study environment, screening the study population with a view to developing treatments rather than testing them, would struggle to find ethics approval. The evidence is clear — there is no basis for screening for dementia. It would produce many false positives and false negatives, and would cause much anxiety without any benefit from early treatment. As long as no effective treatments are available, the case for screening for dementia is void.

Jan J Barendregt

To the Editor: Two studies in nursing homes in Sydney, New South Wales, in the 1990s1,2 showed inappropriately high use of psychotropic medications. A similar study was conducted in 2003.3 Over time, revision of management guidelines, warnings about potentially lethal side effects, and introduction of new drugs have contributed to changes in the pattern of use of psychotropic medications in aged care facilities. Following the same procedure as the earlier studies, in 2009, we examined medication use in nursing homes in half the catchment area of Sydney South West Area Health Service (SSWAHS). We obtained details of drugs prescribed for residents from medication record cards in 44 of the area’s 48 nursing homes and checked whether medications had been given as prescribed. If given regularly on at least 25 of the previous 28 days, use was recorded as regular. We noted whether medication prescribed “as required” had been taken. The SSWAHS ethics review committee approved the study. Medication cards of all 2465 residents (895 men, 1570 women; mean age, 78.7 and 84.2 years, respectively) were reviewed. The mean number of all medications charted per resident was 8.7. Data obtained from all four surveys on patients taking psychotropic medication regularly are shown in the Box. The catchment area expanded between the 1998 and 2003 surveys. However, half the nursing homes open in 1993 closed before 2009. Use of antipsychotic agents fell between 1993 and 1998. By 2003 there had been a change from conventional antipsychotics to a two-to-one preference for atypical antipsychotic medication. Since 2003, regular use of antipsychotic medication has increased by about 19%, although at a lower mean dosage than previously. The rise is mainly attributable to increased prescription of risperidone and needs continuing review to monitor for morbidity. The proportion of residents taking antipsychotic medication only as required has remained almost the same in each survey (range, 1.2%–1.4%). Regular use of anxiolytic and hypnotic medication has decreased, and of antidepressants has increased, since the 1990s. Only 3.5% of residents were regularly taking a tricyclic antidepressant in 2009. The proportions of residents prescribed anxiolytic or hypnotic medication only as required have also fallen (to 3.8% and 2.3%, respectively, in the 28 days preceding our audit). Our findings cannot be generalised. Recent evidence from Tasmania4 showed that 42% of residents were taking benzodiazepines regularly. Nevertheless, changes in medication use should provoke discussion. Number (%*) of Sydney nursing home residents taking psychotropic medication regularly Medication 19931 (n = 2414) 19982 (n = 1975) 20033 (n = 3093) 2009 (n = 2465) Any psychotropic† 1422 (58.9%) 957 (48.5%) 1461 (47.2%) 1170 (47.5%) Antipsychotics‡ 662 (27.4%) 447 (22.6%) 730 (23.6%) 690 (28.0%) Conventional‡ 662 (27.4%) 401 (20.3%) 251 (8.1%) 182 (7.4%) Haloperidol 190 (7.9%) 159 (8.1%) 167 (5.4%) 121 (4.9%) Thioridazine 354 (14.7%) 193 (9.8%) 17 (0.5%) — Chlorpromazine 53 (2.2%) 24 (1.2%) 25 (0.8%) 20 (0.8%) Trifluoperazine 57 (2.4%) 30 (1.5%) 16 (0.5%) 8 (0.3%) Pericyazine 15 (0.6%) 3 (0.2%) 10 (0.3%) 13 (0.5%) Fluphenazine 44 (1.8%) 23 (1.2%) 10 (0.3%) 11 (0.4%) Flupenthixol — 2 (0.1%) 9 (0.3%) 7 (0.3%) Zuclopenthixol — — — 9 (0.4%) Atypical‡ 48 (2.4%) 506 (16.4%) 537 (21.8%) Olanzapine — 8 (0.4%) 225 (7.3%) 180 (7.3%) Risperidone — 40 (2.0%) 219 (7.1%) 286 (11.6%) Quetiapine — — 18 (0.6%) 63 (2.6%) Amisulpride — — 4 (0.1%) 7 (0.3%) Clozapine — — 3 (0.1%) 7 (0.3%) Aripiprazole — — — 4 (0.2%) Hypnotics‡ 641 (26.6%) 335 (17.0%) 350 (11.3%) 274 (11.1%) Temazepam 530 (22.0%) 313 (15.8%) 307 (9.9%) 255 (10.3%) Nitrazepam 105 (4.3%) 17 (0.9%) 35 (1.1%) 17 (0.7%) Anxiolytics‡ 207 (8.6%) 123 (6.2%) 127 (4.1%) 117 (4.7%) Diazepam 113 (4.7%) 77 (3.9%) 92 (3.0%) 71 (2.9%) Oxazepam 72 (3.0%) 40 (2.0%) 32 (1.0%) 26 (1.1%) Antidepressants‡ 377 (15.6%) 316 (16.0%) 635 (20.5%) 630 (25.6%) Tricyclics 249 (10.3%) 120 (6.1%) 110 (3.6%) 86 (3.5%) Mianserin 87 (3.6%) 37 (1.9%) 22 (0.7%) 8 (0.3%) Moclobemide 21 (0.9%) 40 (2.0%) 20 (0.6%) 9 (0.4%) SSRIs 18 (0.7%) 103 (5.2%) 354 (11.4%) 338 (13.7%) Venlafaxine — — 81 (2.6%) 61 (2.5%) Mirtazapine — — 51 (1.6%) 126 (5.1%) Lithium 11 (0.5%) 8 (0.4%) 24 (0.8%) 17 (0.7%) — = Drug not approved for use or not prescribed in year of survey. SSRI = selective serotonin reuptake inhibitor. * All percentages are proportion of total number of residents. † Clonazepam and other anticonvulsants (apart from diazepam) were not included as psychotropic drugs. ‡ Numbers do not add to totals as some patients were prescribed more than one drug and some little-used psychotropic drugs are not listed.

John Snowdon · Daniel Galanos · Divya Vaswani

In recent years, a phenomenon of “late effects of the Holocaust” has emerged, with impacts on the psychological and physical health of ageing Holocaust survivors. As Holocaust survivors age, they may experience heightened anxiety around normal processes of ageing, worsened post-traumatic stress disorder with cognitive decline, and fear of the medical system. Holocaust survivors are at increased risk of osteoporosis, cardiometabolic disease due to hypothalamic–pituitary–adrenal axis dysfunction, cancer, and sequelae of Nazi medical experiments. From existing medical literature on this topic, practical principles of management are derived to create a framework for sensitive medical management of Holocaust survivors in Australia. The issues discussed are also relevant to the wider geriatric refugee or prisoner-of-war experience.

Elizabeth D Paratz · Benny Katz MB BS, FRACP, FFPMANZCA

In the absence of evidence of infection with the hepatitis C virus (HCV), detecting the immunological disorder of mixed cryoglobulinaemia is a challenge. Only after extensive investigation did we suspect that our patient’s recurrent acute dyspnoea, lower limb paraesthesia and renal impairment with active urinary sediment were attributable to the rare phenomenon of non-HCV-related mixed essential cryoglobulinaemia — our suspicion was confirmed by significant serum levels of cryoglobulins. (MJA 2010; 194: 142-144) Clinical recordIn October 2008, an 84-year-old man with increasing dyspnoea on exertion for 1 week was referred for hospital admission by his general practitioner. His medical history included rheumatic heart disease leading to aortic valve replacement (AVR) in 1973. In 2001, he underwent a redo AVR, a mitral valve replacement (non-mechanical) and coronary artery bypass grafting. He then required implantation of a permanent cardiac pacemaker for complete heart block. He had chronic kidney disease (Stage 3) of unknown cause and mild, well controlled asthma. He was a lifelong non-smoker and occasionally drank alcohol. At presentation, he was afebrile and haemodynamically stable, with a respiratory rate of 20 breaths per minute and oximetry of 95 per cent on room air. There were no signs of fluid overload or peripheral stigmata of infective endocarditis. Chest auscultation revealed bibasal crackles, and loud first and second heart sounds in keeping with previous valve surgery. Mild stasis eczema was the only notable skin lesion. He reported experiencing, for the past few months, lower limb paraesthesia and sicca-like symptoms. His daily medications included perindopril 2.5 mg, digoxin 125 μg, frusemide 40 mg and warfarin at varying doses. For asthma, he was prescribed a daily inhalation of fluticasone 250 μg, with salmeterol 25 μg, and inhalations of salbutamol 100 μg as needed. Results of blood, urine and sputum tests done at presentation are shown in Box 1; results showed an inflammatory response and renal impairment with active urinary sediment (repeat urinary analysis a week after presentation also revealed active urinary sediment). An electrocardiogram showed no arrhythmias. Chest x-ray at presentation showed air bronchograms at the right lower zone (Box 2). Our patient was admitted and treated for right lower lobe pneumonia with intravenous antibiotics. He was also prescribed high-dose oral steroids, with gradual tapering of doses. A computed tomography scan showed probable right lower chest infection. During the early weeks of his hospitalisation, the patient had further episodes of acute dyspnoea, and repeat chest x-rays showed bilateral migratory opacities (Box 3). Acute episodes of dyspnoea were treated with high-dose oral steroids and intravenous antibiotics; a regular regimen of low-dose steroids was maintained between episodes. During each acute episode, his biochemistry results showed an inflammatory response, with varying elevated serum levels of C-reactive protein (CRP): 243 mg/L; 332 mg/L; 73 mg/L; 16 mg/L; 148 mg/L; and 90 mg/L (reference range [RR], < 5.0 mg/L). With treatment, the CRP level fell to 5.3 mg/L. Repeated blood and urine cultures produced no growth. A transthoracic echocardiogram revealed a normal left ventricular ejection fraction and no regurgitation from the prosthetic valves, and a transoesophageal echocardiogram showed no valvular vegetations. The serum level of B-type natriuretic peptide was 246 ng/L (RR, < 100 ng/L), making acute left ventricle failure unlikely in view of the patient’s renal impairment. No respiratory viruses were detected in nasopharyngeal aspirate. The patient’s serological tests were negative for hepatitis B virus, hepatitis C virus (HCV), HIV, cytomegalovirus, mycoplasma, Chlamydia, Legionella pneumophila, Legionella longbeachae, Brucella, Histoplasma, and Toxoplasma. The result of the QuantiFERON-TB Gold assay (Celeste) was indeterminate. Serum electrophoresis was negative and no Bence–Jones protein was detected in urine. Liver ultrasound showed no evidence of chronic liver disease. Screening for autoimmune discrepancies was significant but inconclusive — test results for serum levels of rheumatoid factor (RF) and antinuclear antibody were positive but other antibody test results were negative or within reference ranges (Box 4). On further investigation (5 weeks after admission), the patient’s serum levels of complement components C3 and C4 were 0.77 g/L (RR, 0.70–1.60 g/L) and < 0.02 g/L (RR, 0.10–0.30 g/L), respectively; repeated test results were C3, 0.74 g/L and C4, < 0.02 g/L. Such a result — low C4 with normal C3 levels — may be due to cryoglobulinaema, C4 null alleles, hereditary angioedema or activation of the classical complement pathway. Types and levels of cryoglobulins found in the patient’s serum were: monoclonal IgM/kappa, 0.4 g/L and polyclonal IgG, 0.1 g/L. HCV RNA was not detected. On the basis of the presence of cryoglobulins in serum and supported by evidence of lung and inflammatory involvement, a diagnosis of mixed essential cryoglobulinaemia (Type II cryoglobulinaemia) was made. The patient was reviewed by an immunologist, who agreed with the diagnosis. To exclude lymphoma, particularly B-cell lymphoma which is the most frequent malignant complication of mixed cryoglobulinaemia, a bone marrow biopsy was done; no significant population of B-cell biomarkers (CD19+/CD20+ cells) was found, nor any other suggestion of lymphoma. Despite the investigative effort, we did not identify a cause for our patient’s cryoglobulinaemia. He gave informed consent for all investigations. DiscussionCryoglobulins are single or mixed immunoglobulins that, in serum and other body fluids, undergo reversible precipitation at low temperatures (below 37°C in serum). According to the Brouet classification, cryoglobulinaemia is grouped into three types based on the composition of the detected cryoglobulins. Type I cryoglobulinaemia, or simple cryoglobulinaemia, is the result of a monoclonal immunoglobulin, which rarely has RF activity and is not known to activate complement in vitro. The cryoglobulins of Types II and III cryoglobulinaemia (mixed cryoglobulinaemia) contain RF, which forms complexes with the “fragment crystallisable” (Fc) portion of polyclonal IgG. The actual RF may be monoclonal immunoglobulin (in Type II cryoglobulinaemia) or polyclonal immunoglobulin (in Type III cryoglobulinaemia). Types II and III cryoglobulinaemia represent 80% of all occurrences of the disease. HCV is associated with most cases of mixed cryoglobulinaemia, with the prevalence of anti-HCV antibodies or HCV RNA ranging from 70% to almost 100%.1 The clinical manifestations of cryoglobulinaemia are generally caused by the inflammatory effects of circulating immune complexes on multiple organs. The criteria for diagnosing mixed cryoglobulinaemia are: detection in serum of mixed cryoglobulins, along with purpura and leukocytoclastic vasculitis; or detection in serum of mixed cryoglobulins, along with peripheral neuropathy, membranoproliferative glomerulonephritis, chronic hepatitis or skin rashes.1 Signs and symptoms that our patient showed fulfilled the latter set of criteria. Although our patient had no skin lesion typical of the disease (and suitable for biopsy), nor evidence of liver disease, he had lower limb paraesthesia and tested positive for renal impairment and active urinary sediment. The success of steroid treatment indicated an inflammatory component to the problem. Furthermore, lung involvement is reported to be quite frequent in mixed essential cryoglobulinaemia,2 and migratory lung lesions have been associated with the disease.3 What is notable about this case is the lack of evidence of HCV infection. To the extent that we are able to establish (two PubMed searches of English-language articles were undertaken), it is the first reported case of mixed essential cryoglobulinaemia with migratory lung lesions and unrelated to HCV infection. 1 Results of patient’s blood, urine and sputum investigations at presentation Test Result Blood Haemoglobin 110 g/dL (RR, 135–180 g/dL) White cell count 9.2 x 109 cells/L (RR, 4.0–11.0 x 109 cells/L) Neutrophils 6.5 x 109 cells/L (RR, 2.0–8.0 x 109 cells/L) Platelets 174 x 109 cells/L (RR, 140–400 x 109 cells/L) C-reactive protein 243 mg/L (RR, < 5.0 mg/L) Sodium 138 mmol/L (RR, 135–145 mmol/L) Potassium 4.8 mmol/L (RR, 3.5–5.1 mmol/L) Urea 13.3 mmol/L (RR, 2.9–8.2 mmol/L) Creatinine 160 μmol/L (RR, 64–108 μmol/L) Cultures (three sets) No growth after 1 week incubation Urine Microscopic analysis Active sediment* Dipstick Moderate blood, 2 + leukocytes, trace protein Culture No growth after 1 week incubation Sputum Culture Normal respiratory flora RR = reference range. * Active urinary sediment is sediment found in a centrifuged urine sample and showing red cells, red cell casts and at times white cells and white cell casts; it indicates active kidney inflammatory disease such as glomerulonephritis, interstitial nephritis or vasculitis. 2 Patient’s chest x-ray at presentation showing air bronchograms at right lower zone (2 October 2008) 3 Patient’s chest x-rays several weeks after presentation showing bilateral migratory opacities (A, 16 November 2008; B, 24 November 2008) 4 Results of patient’s autoimmunity screening tests at presentation and 4 weeks after presentation Test Initial result Result at 4 weeks Rheumatoid factor (RR, < 20 IU/mL) 51 IU/mL < 20 IU/mL Anticyclic citrullinated peptide antibody (anti-CCP) < 6 U/mL — Antinuclear antibody (ANA) (RR, < 40 titre) > 2560 titre 640 (homogenous) titre Anti-double-stranded DNA antibodies negative — Anti-Sjögren’s syndrome A / anti-Sjögren’s syndrome B antibodies (anti SSA/SSB antibodies) negative — Direct Coombs test negative — Antithyroid peroxidise antibodies (RR, < 50 IU/mL) 1 IU/mL — Antithyroglobulin antibodies (RR, < 100 IU/mL) 7 IU/mL — Antitissue transglutaminase antibody (anti-TTG [IgA]) (RR, < 5 U/mL) 0 U/mL — RR = reference range

Muhammad Kashif Nadeem MB BS, MRCP · Mohammed A Khateeb MB BS, FRACP

Effective dementia care depends on early and accurate diagnosis It is predicted that over the next 40 years there will be a fourfold increase in the prevalence of dementia in Australia, as well as considerably more people with milder forms of cognitive impairment.1 To date, despite extensive research, no effective treatment for established dementia is available. As a result, taskforce policymakers conclude that there is insufficient evidence at present to warrant routine screening for dementia syndromes.2,3 However, emerging evidence shows that early non-pharmacological intervention can improve cognitive outcomes for patients with milder forms of cognitive impairment and those at risk of cognitive decline.4 Early diagnosis also enables patients to plan, with their caregivers, for the future, and deal with matters such as enduring power of attorney authorisation, before they lose the capacity to do so. Over two-thirds of people who notice symptoms of cognitive decline consult a physician for evaluation.5 However, up to 90% of mild cases are missed at the initial primary care assessment.6,7 So how can we improve early detection of cognitive impairment, and what evidence base do we have for dementia screening in Australia? A diagnosis of dementia relies on a full mental status assessment, with comprehensive history taking and physical examination. Presently, detailed neuropsychological testing is the gold-standard tool for objectively evaluating the magnitude and pattern of cognitive decline. However, neuropsychological evaluation is costly, time-consuming and not generally available as only specialist psychologists can do it. Consequently, general practitioners and specialist physicians, who evaluate most patients presenting with cognitive complaints, administer brief screening instruments such as the mini-mental state examination (MMSE) to assess cognition. In Australia, the use of such instruments has been propagated by guidelines for prescribing acetylcholinesterase inhibitors. The MMSE has many documented and widely appreciated shortcomings. It lacks diagnostic specificity and is insensitive to patient variables such as extreme levels of education, premorbid ability and poor command of English.8 It has also been criticised for its unsystematic and atheoretical construction, and its poor ability to detect milder forms of cognitive impairment.8,9 The idea that any brief screening tool would have sufficient sensitivity and specificity to diagnose dementia is unrealistic. However, when used as an adjunct to a good clinical history, a more accurate instrument, particularly one that can be serially administered, would potentially increase the reliability of diagnosis. A recent review of screening instruments available for mild cognitive impairment concluded that there are more useful screening tools than the MMSE.10 Some are in use in Australia, including the Addenbrooke’s Cognitive Examination – Revised (ACE-R); the Alzheimer’s Disease Assessment Scale — cognitive subscale (ADAS-cog); and the Montreal Cognitive Assessment battery. In addition, there are other screening instruments specifically validated for use in Australia, such as the General Practitioner assessment of Cognition (GPCog) and Rowland Universal Dementia Assessment Scale (RUDAS). Recently, the ACE-R was validated for use in an Australian population.11 The ACE-R, which incorporates the MMSE, has been shown to have more diagnostic sophistication, with improved sensitivity and specificity values, than the MMSE alone. This is not to say that the ACE-R is without limitations. For instance, it cannot fully assess some aspects of cognitive function (eg, non-verbal skills). Furthermore, the ACE-R takes on average 16 minutes to administer and is therefore unlikely to see much uptake by busy GPs; however, it could be used by nurses working in general practices. As with all screening tools, clinicians using the ACE-R in the primary care setting need to be trained to correctly score and interpret patients’ ACE-R performances. Development of effective dementia treatments depends on earlier and more accurate identification of disease. Cognitive screening tests will continue to evolve, and may in time be replaced with screening for disease-related biomarkers. However, such diagnostic biomarkers have yet to be discovered. With the number of people with dementia growing each year, the lack of adequately validated diagnostic tools is a serious concern. Empirical investigations to further evaluate and validate screening instruments for cognitive impairment are necessary as we strive to develop effective treatments for all forms of this debilitating disorder.

Zoe Terpening BPsych(Hons), MSc, DClinNeuropsych · John R Hodges MD, FRCP, FMedSci · Nicholas J Cordato MB BS, PhD, FRACP

Incorrect author details: Incorrect author details: In “A multilevel analysis of three randomised controlled trials of the Australian Medical Sheepskin in the prevention of sacral pressure ulcers” in the 6/20 December 2010 issue of the Journal (Med J Aust 2010; 193: 638-641), Damien Jolley’s qualifications and affiliation were incorrectly given. His qualifications should be shown as MSc(Epidemiol), MSc, AStat and his affiliation as the School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC. The html and pdf versions of this article were corrected on 10 January, 2011.

Patriek J Mistiaen · Damien J Jolley · Sunita McGowan · Mark B Hickey · Peter Spreeuwenberg · Anneke L Francke

Objective: To assess the effectiveness of the Australian Medical Sheepskin in preventing sacral pressure ulcers (PUs), based on combined data from existing published trials.Design and setting: Data from two randomised controlled trials (RCTs) among Australian hospital patients and one RCT among Dutch nursing home patients were pooled, comprising a total population of 1281 patients from 45 nursing wards in 11 institutions. These data were analysed in two ways: with conventional meta-analysis based on the published effect sizes; and with multilevel binary logistic regression based on the combined individual patient data. In the multilevel analysis, patient, nursing ward and institution were used as levels and we controlled for sex, age, PU risk and number of days of observation.Main outcome measure: Incidence of sacral PUs.Results: Overall, the incidence of sacral PUs was 12.2% in the control group versus 5.4% in the intervention group with an Australian Medical Sheepskin. Conventional meta-analysis showed significantly reduced odds of developing a PU while using the sheepskin (odds ratio [OR], 0.37 [95% CI, 0.17–0.77]). Multilevel analysis gave an OR of 0.35 and narrowed the confidence interval by almost 50% (95% CI, 0.23–0.55).Conclusions: These analyses of pooled data confirm that the Australian Medical Sheepskin is effective in preventing sacral PUs. Multilevel analysis of individual patient data gives a more precise effect estimate than conventional meta-analysis.

Patriek J Mistiaen RN, PhD · Damien J Jolley MSc(Epidemiol), MSc, AStat · Sunita McGowan RN, MSc · Mark B Hickey BAppSc(Hons) · Peter Spreeuwenberg MSc · Anneke L Francke RN, PhD

Clinical record A 78-year-old woman who was previously very active and in good health presented to hospital feeling unwell and with an extensive rash, involving both upper limbs (C3–T1 dermatomes), consistent with herpes zoster. Three weeks later, extensive diffuse left upper limb neuropathic pain developed over her C5–C7 dermatomes. The following week, her condition worsened to include progressive severe paresis of the left upper limb; weakness in the right hand; bilateral lower limb weakness; patchy areas of paraesthesia affecting many areas of the upper limbs, trunk and proximal lower limbs; severe constipation; and urinary retention, which required insertion of an indwelling catheter. She was bedbound and needed assistance with all self-care activities. About 10 days after the onset of weakness, a neurologist diagnosed a cervical myelopathy and recommended magnetic resonance imaging of the spine. This revealed an area of inflammation at C2–C4 involving the full thickness of the spinal cord at that level, consistent with transverse myelitis (Figure). She was diagnosed with herpes zoster myelitis. Sagittal T2-weighted magnetic resonance image with gadolinium enhancement showing an ovoid hyperintense lesion in the upper cervical spinal cord (arrow). About 6 weeks after her initial presentation, the patient was transferred to another acute hospital for further assessment. Detailed examination revealed asymmetric tetraparesis; upper limbs (left greater than right) were affected more than the lower limbs. On manual muscle testing she had muscle strength in her limbs as follows: 0/5 in the proximal and 1/5 in the distal left upper extremity, 4/5 in the right upper extremity and 2/5 in both lower limbs, with partial loss of sensation from her C4 to L3 dermatomes. Laboratory findings for full blood cell count, urea and electrolytes were unremarkable except for mild hyponatraemia and mild derangement of liver enzymes. Because of the severity of the herpes zoster infection, the patient was tested for underlying immunocompromise. She was found to have a κ monoclonal gammopathy of undetermined significance (12.0 g/L IgG; reference range [RR], 7.0–16.0 g/L) and borderline low values of immunoglobulins IgA (0.40 g/L; RR, 0.7–4.0 g/L) and IgM (0.31 g/L; RR, 0.4–3.0 g/L). It was thought that all of these immune abnormalities were of questionable significance. Treatment was initiated with intravenous methylprednisolone (1 g/day for 6 days) and intravenous (300 mg three times a day for 6 days) then oral (800 mg five times a day for 2 weeks) aciclovir. During the course of this treatment, gradual improvement in power of all four limbs became evident. She was subsequently admitted to a spinal rehabilitation unit and discharged 8 weeks later with evidence of ongoing neurological and functional improvement. Her hospital stay was complicated by severe postherpetic neuralgia, which was eventually controlled with gabapentin (400 mg three times a day). She recovered bladder function but needed aperients to achieve controlled faecal continence. At discharge, neurological examination revealed persisting asymmetric tetraparesis. She had 4/5 upper extremity muscle strength in C7–T1 myotomes on the left, 4/5 in L2 and L3 myotomes in both lower limbs and her remaining myotomes were of normal power. She was able to walk with a four-wheel frame or a single-point stick for 10–20 m and was independent for many activities of daily living. At follow-up 9 months after her initial presentation, her condition was still improving gradually. She had weaned off the gabapentin with no residual postherpetic neuralgia. She was able to walk short distances unaided and had regained full independence with most of her self-care using aids. Herpes zoster is associated with several neurological complications, including postherpetic neuralgia, aseptic meningitis, meningoencephalitis, transverse myelitis, peripheral nerve palsies, cranial nerve palsies and granulomatous cerebral angiitis.1 These complications are particularly prevalent among older people and patients with immunodeficiency. A causative relationship with herpes zoster in many of these syndromes is probably more common than suspected owing to difficulties in diagnosis and lack of awareness among clinicians. However, to our knowledge, there are no published reports of any known association between the neurological complications of herpes zoster, including myelitis, and postherpetic neuralgia. Transverse myelitis is a focal inflammatory disorder of the spinal cord. It results in sensory, motor and autonomic dysfunction 2 Onset may be acute, developing over a few hours or several days, or subacute, developing over 1 to 2 weeks. The critical factor is an abnormal immune response to infection, rather than the direct effect of an infectious agent.3 Transverse myelitis may be an isolated entity or may occur with a background of viral diseases, vaccinations, systemic lupus erythematosus, vasculitis, multiple sclerosis, heroin misuse or trauma.3 About 25%–40% of cases of transverse myelitis are caused by viral infections with herpes viruses or poliovirus.2 A recent publication provides useful additional information about transverse myelitis.4 Lessons from practice Herpes zoster myelitis is rare in the context of normal immunity; it is more common among patients with immunocompromise. Clinicians should be aware of the close temporal relationship between skin rash and the onset of myelitis so that appropriate investigations and treatment can be instigated. Magnetic resonance imaging of the spine should be performed to aid diagnosis. Although early treatment of herpes zoster myelitis is preferable, delayed treatment may also be worthwhile. Transverse myelitis following herpes zoster or herpes zoster myelitis (HZM) is rare, and typically occurs in hosts who are immunocompromised. Its onset is usually acute, occurring shortly after the appearance of the rash, with the development of sensory, motor and autonomic dysfunction.5 No diagnostic test is completely accurate, as the virus cannot usually be isolated from blood or cerebrospinal fluid in HZM.5 In most cases, diagnosis of HZM is clinical and based on detection of typical vesicular lesions in dermatomal distribution in association with clinical features of transverse myelitis. Suggested treatment involves high doses of corticosteroids and aciclovir.5 The prognosis ranges from spontaneous recovery to ascending neurological progression and death.6 The frequency of transverse myelitis during or after varicella infection is reported to be 0.3%.7 Devinsky and colleagues analysed their findings in 13 immunocompromised patients with HZM.8 The pathogenesis of HZM is unclear, but it may be due to direct viral invasion, which was demonstrated in one autopsy case.9 Diagnosing HZM can be challenging. The importance of a careful clinical assessment to establish the likelihood of this diagnosis and the level of the spinal cord damage, in combination with confirmatory magnetic resonance imaging (MRI)7cannot be overstated. MRI not only provides information about the site but also the extent of spinal cord involvement, and excludes other possible diagnoses. In our patient, HZM was diagnosed based on the temporal relationship of myelopathy to the rash and MRI findings. Although the area of the spinal cord that was involved on the MRI scan was less extensive than that affected by the herpetic rash, we do not see this as clinically inconsistent. There are no proven treatment regimens for HZM, but there is anecdotal evidence for treatment of HZM with high doses of aciclovir and corticosteroids.5,10 It appears that antiviral treatment was not provided early to our patient because it was not initially recognised that the rash was due to herpes zoster. Once HZM was diagnosed, this treatment was provided. Despite the delay of 3 weeks following the onset of rash, improvement appeared consistent with a clinical response to this therapy. Although early treatment of herpes zoster with antivirals is crucial to prevent the development of postherpetic neuralgia, there is little evidence that such treatment reduces the risk of HZM. To date, no evidence has emerged regarding the protective efficacy of the new live, attenuated herpes zoster vaccine (Zostavax) against HZM. Trials assessing the impact of antivirals or the herpes zoster vaccine on risk of HZM would require very large numbers of participants, given the rarity of this complication. Nevertheless, the vaccine has proven to be efficacious in reducing the incidence of and morbidity associated with herpes zoster and postherpetic neuralgia in older adults.11 It has been noted in a previous case report that, following the diagnosis of HZM, even delayed treatment with oral antivirals may prevent neurological progression.12 Our case provides support for this assertion.

Olivia L W Ong MB BS, BMedSci · Andrew C Churchyard PhD, MB BS, FRACP · Peter W New MB BS, MClinEpi, FAFRM(RACP)

CorrectionAcknowledgements omitted: In “A multimodal intervention to improve fragility fracture management in patients presenting to emergency departments” in the 2 August 2010 issue of the Journal (Med J Aust 2010; 193: 149-153), the acknowledgements were omitted. The following text should be inserted before “Competing interests”: Acknowledgements: We wish to thank the following for their contribution to our project: the National Health and Medical Research Council’s National Institute of Clinical Studies and Australian Department of Veterans’ Affairs Fellowship Program; the North Metropolitan Area Health Service, Perth (Sir Charles Gairdner Hospital, Osborne Park Hospital and area rehabilitation and aged care staff); and physicians and general practitioners involved in developing the consensus guidelines. The html and pdf versions of this article have been corrected.

Charles A Inderjeeth · Denise A Glennon · Kate E Poland · Katherine V Ingram · Richard L Prince · Victoria R Van · C D’Arcy J Holman

Objective: To implement and evaluate a multimodal intervention to improve osteoporosis treatment in patients with a fragility fracture.Design, setting and participants: Strategies to improve the management of patients discharged from an emergency department after presentation with fragility fracture were implemented prospectively in a large tertiary public hospital. Patients were surveyed by post to assess their awareness of osteoporosis and of the need for treatment. General practitioners and hospital clinicians completed an online questionnaire about their attitudes to osteoporosis and its management. A simplified consensus guideline was developed for local use. Our study was conducted between 1 October 2007 and 31 October 2008.Main outcome measures: Rates of referral of patients for osteoporosis review; rates of investigation and treatment.Results: Although most GPs (259/306 [85%]) accepted that it was their responsibility to assess and treat their patients and inform them of their osteoporosis risk, only 35/87 patients (40%) indicated awareness of their risk. After implementation of our project, the rate of bone mineral densitometry investigations improved from 6/200 (3%) to 39/87 (45%) (P < 0.05). The number of patients receiving calcium and vitamin D supplementation increased from 24/200 (12%) (for both supplements) to 29/87 (33%) and 32/87 (37%), respectively (P < 0.05). Initiation of specific treatments increased from 12/200 (6%) to 26/87 (30%) (P < 0.05). Referral of eligible patients to the Fragile Bone Clinic for osteoporosis review improved from 20/500 (4%) to 51/194 (26%). After being contacted by a fracture liaison nurse, 84% of these patients presented for osteoporosis review in the clinic.Conclusions: A major key to improving osteoporosis management is to actively identify all patients at risk and proactively engage and encourage them to seek assessment and management. A multimodal strategy involving a dedicated fracture liaison nurse may offer the greatest potential for improving education and patient follow-up and treatment.

Charles A Inderjeeth MB ChB, MPH, FRACP · Denise A Glennon MB BS, FRACP · Kate E Poland MB BS · Katherine V Ingram MB BS, FRACP · Richard L Prince MB BS, MD, FRACP · Victoria R Van BHSc · C D’Arcy J Holman MB BS, MPH, PhD