Issues
Volume 174 Issue 6
Editorials Economy class syndrome Alex S Gallus, Ross I Baker (MJA 2001; 174: 264-265)Helping older people to remain in their own homes R Arthur Criddle, Leon Flicker (MJA 2001; 174: 266-267)Clinicians and guidelines: leading a horse to water... Claire L Jackson, Inge C de Jong (MJA 2001; 174: 267-268)Advancing the field of clinical ethics: particularity and practicality Bernadette Tobin (MJA 2001; 174: 269-270) Healthcare Incidence of nursing home placement in a defined community Jie Jin Wang, Paul Mitchell, Wayne Smith, Robert G Cumming, Stephen R Leeder (MJA 2001; 174: 271-275)Compliance with guidelines for continuity of care in therapeutics from hospital to community Andrea Mant, Wendy C Rotem, Linda Kehoe, Karen I Kaye (MJA 2001; 174: 277-280) Public health Mortality and life-years lost due to alcohol: a comparison of acute and chronic causes Tanya N Chikritzhs, Helen A Jonas, Tim R Stockwell, Penny F Heale, Paul M Dietze (MJA 2001; 174: 281-284) Medicine and the community Operative photography in gynaecological endosurgery Geoffrey D Reid, Adelyn Leong (MJA 2001; 174: 285-287) Position statement The management of varicella-zoster virus exposure and infection in pregnancy and the newborn period Anne-Marie Heuchan, David Isaacs, on behalf of the Australasian Subgroup in Paediatric Infectious Diseases of the Australasian Society for Infectious Diseases (MJA 2001; 174: 288-292) Evidence-based medicine Evidence-based medicine: how good is the evidence? David S Celermajer (MJA 2001; 174: 293-295) Clinical ethics Confidentiality Lynn Gillam, J Miles Little (MJA 2001; 174: 296-297) For debate Screening for colorectal cancer: what is the most cost-effective approach? Terry D Bolin, Helen M Lapsley, Melvyn G Korman (MJA 2001; 174: 298-301) Viewpoint SIDS: more facts and controversies Paul N Goldwater (MJA 2001; 174: 302-304) EBM in action Is isopropyl alcohol swabbing before injection really necessary? Christopher B Del Mar, Paul P Glasziou, Anneliese B Spinks, Sharon L Sanders (MJA 2001; 174: 306)
Editorials
Economy class syndrome
Editorial Economy class syndrome A misnomer for a syndrome for which the evidence is, as yet, missing MJA 2001; 174: 264-265 Two unexpected and widely reported deaths from pulmonary embolism (PE) after flights between Australia and the United Kingdom — one of a 28-year-old woman arriving in London, the other a 68-year-old man after landing in Melbourne — have provoked four months of worldwide media interest in air-travel-related PE and deep-vein thrombosis (DVT). News headlines and editorials have reported on its supposed incidence, causes and prevention. Now the Federal Government has launched an enquiry into the risks of long-haul flying. And there is inevitable talk of litigation. Air travellers are rightly concerned to know the level of risk, who is likely to be affected, and what precautions they should take. Answers are, however, constrained by a serious lack of definitive information, as the evidence is limited to case series of DVT or PE discovered during or soon after air travel, and a few case-control studies with limited power and contradictory results. Air travellers are rightly concerned to know the level of risk, who is likely to be affected, and what precautions they should take. Venous thromboembolism (VTE) during or soon after prolonged flight or travel by motor car has been recorded since 19541 and was labelled "economy class syndrome" in 1988 (two of the six cases were authors of that report, and paradoxically, one of the authors with DVT had travelled in business class).2 Case series have come from the Paris airports (Orly and Roissy, where the airport emergency medical service diagnosed PE in 70 incoming passengers during the 24 years to 19983), Heathrow Airport (where 11 of 61 inflight deaths reported to the coroner between 1979 and 1982 were caused by PE4), the island of Martinique (40 cases of flight-related VTE in six years5) and Réunion island (six cases in one year6). Lastly, in the Hawaiian Islands, 17%-25% of patients with VTE admitted to two Honolulu hospitals had a recent history of air travel.7,8 Others have extended this association to prolonged travel by bus, car, truck or train.9 Prolonged travel in a seated position can cause venous stasis, so that an association of VTE with travel would be consistent with Virchow's classic postulate that venous stasis contributes to VTE. However, the present evidence regarding air travel as a cause of VTE is circumstantial and could be misleading. VTE is a common disorder with an annual incidence of about one per 1000 population for DVT and 0.5 per 1000 for PE.10 Its incidence is age-dependent and rises to nearly 1% per annum in the elderly.11 Given the high community prevalence of VTE and exponential growth in worldwide air travel by all age groups, the reports of flight-related VTE from isolated islands and at busy airports could therefore be mere coincidence. Clinical suspicion of VTE is notoriously misleading, so that retrospective reports might be contaminated by diagnostic bias, and recall bias could influence surveys of predisposing air travel. Prospective case-control studies seek to minimise bias and estimate risk by obtaining a history of travel from patients with VTE and also from contemporary age-matched and sex-matched controls. Two recent studies from cities with busy international airports have given opposing results. In Nice, 39 of 160 patients with VTE (24.4%) had travelled during the previous four weeks (nine by plane, 28 by motorcar and two by train), compared with 7.5% of 160 age-matched but not sex-matched controls visiting a cardiology outpatient clinic. In this study, recent travel raised the odds ratio (OR) for VTE to 4.0 (95% confidence interval, 1.9-8.4; P < 0.0001).12 By contrast, when 788 patients with a clinically suspected DVT were interviewed in Amsterdam before diagnostic testing, recent travel was no more prevalent in the 186 patients who had DVT than in the 602 where tests excluded DVT (the OR for DVT after any recent travel, prolonged travel, or air travel was 1.0; 95% CI, 0.3-1.4).13 These case-control studies do not decide the issue, as the control groups were suboptimal12,13 or the study was too small to exclude an important effect of prolonged air travel.13 In the absence of good evidence to the contrary, it is prudent to assume that air travel can provoke VTE, although the absolute risk remains uncertain and is probably quite small in most people. This conclusion derives from the Paris airports emergency medical service report.3 By relating the number of people with PE detected during or immediately after a flight to the total number of arrivals, the report derived an overall incidence of about one PE per 3 000 000 arriving travellers3 ("true" risk is likely to be somewhat higher, as about two-thirds of travel-related VTE presents after patients leave the airport14). The Paris airports report also observed an obviously greater incidence when travel times were longer than 12 hours.3 As 10 of the 11 inflight deaths from PE recorded in the Heathrow report occurred during prolonged flights,4 it is likely that travel duration will prove to be important. It is essential that this still-isolated information is verified and extended with further studies. Advice on prevention is based on assumptions about pathogenesis. In addition to the presumption of venous stasis, there are studies of aircrew or volunteers during prolonged real or simulated flights that suggest dehydration,15,16 stress and climatic change,15 and early activation of the blood-clotting system17 might also contribute. Business and first class passengers are not immune, so more generous seating space is unlikely to be the answer (and "economy class syndrome" is most likely a misnomer). The following general advice has no direct supporting evidence but is common sense, harmless, inexpensive, and likely to be appropriate, particularly for flights longer than 6-8 hours.18,19 These general precautions are directed at preventing venous stasis and include regular foot exercises to activate the plantar and calf muscle pumps, a generous fluid intake, avoiding excessive alcohol (especially when combined with the use of hypnotics), and wearing loose clothing while travelling. Prolonged movement about the cabin during flight is discouraged because this may bring other hazards, including from unexpected clear air turbulence. Travellers with an above-average risk of thrombosis should seek specific medical advice on additional preventive measures before travelling. Case series suggest that people with previous VTE, chronic venous insufficiency, recent surgery, chronic heart and lung disease, cancer, old age and those who are overweight are all at greater than average risk. Oral contraceptives, hormone replacement and inherited thrombophilia (including factor V Leiden) may predispose, but there is no good published evidence for this. Screening for factor V Leiden (activated protein C resistance) is not recommended in this or any other context if there is no personal or family history of VTE, as about 5% of people of European descent have this polymorphism, and most will never develop thrombosis.11 As a generalisation, it usually takes two or three risk factors acting together to provoke VTE,11 and, as this is likely to apply also in travellers, it is people with several concurrent risk factors who are most likely to require specific prophylaxis. Aspirin alone is not likely to be appropriate, as the evidence that aspirin prevents DVT or PE is highly controversial and the plausible level of risk reduction is small.20,21 Prescribing aspirin for all travellers may also cause sufficient excess bleeding to negate any benefit. Graded pressure support stockings to be worn during flight must be carefully fitted: too tight and they become a tourniquet, too loose and they are ineffective. And they are contraindicated in some people with advanced peripheral vascular disease. People at highest risk (including those with previous VTE) should consider self-injecting a low molecular weight heparin before and perhaps for some days after travel. Few people die of PE without some warning from unexpected breathlessness, chest pain, or leg symptoms. Information kits about DVT and PE, predisposing factors and various clinical presentations should therefore be widely distributed to travellers before they leave home. People should know that, although symptoms of VTE may arise during flight, they are more often first noticed some time after landing. More importantly, we need better evidence. If the present media crisis and federal inquiry brings a greater awareness that VTE may develop during or soon after prolonged travel, and if it triggers a productive collaboration of airlines with investigators to measure the real risk and evaluate preventive measures, then it will have served a useful purpose. Alex S Gallus Professor of Haematology and Director of Pathology Services Flinders Medical Centre and Repatriation General Hospital Adelaide, SA Ross I Baker Director, Thrombosis and Haemophilia Service, Royal Perth Hospital and Clinical Senior Lecturer in Medicine, University of Western Australia Perth, WA Homans J. Thrombosis of the deep leg veins due to prolonged sitting. N Engl J Med 1954; 250: 148-149. Cruikshank JM, Gorlin J, Jennett B. Air travel and thrombotic episodes: the economy class syndrome. Lancet 1988; 2: 497-498. Clerel M, Caillard G. Thromboembolic syndrome from prolonged sitting and flights of long duration: experience of the Emergency Medical Service of the Paris Airports. Bull Acad Natl Med 1999; 183: 985-997. Sarvesvaran R. Sudden natural deaths associated with commercial air travel. Med Sci Law 1986; 26: 35-38. Ribier G, Zizka V, Cysique J, et al. Venous thromboembolic complications following air travel. Retrospective study of 40 cases recorded in Martinique. Rev Med Interne 1997; 18: 601-604. Paganin F, Laurent Y, Gaüzere BA, et al. Pulmonary embolism on non-stop flights between France and Reunion Island [letter]. Lancet 1996; 347: 1195-1196. Eklof B, Kistner RL, Masuda EM, et al. Venous thromboembolism in association with prolonged air travel. Dermatol Surg 1996; 22: 637-641. Mercer A, Brown JD. Venous thromboembolism associated with air travel. Aviat Space Environ Med 1998; 69: 154-157. Tardy B, Page Y, Zeni F, et al. Phlebitis following travel. Presse Medicale 1993; 22: 811-814. Van Beek ER, Bller HR, ten Cate JW. Epidemiology of venous thromboembolism. In: Tooke JE, Lowe GDO, editors. A textbook of vascular medicine. London: Arnold, 1996: 471-488. Rosendaal FR. Venous thrombosis: a multicausal disease. Lancet 1999; 353: 1167-1173. Ferrari E, Chevallier T, Chapelier A, Baudouy M. Travel as a risk factor for venous thromboembolic disease: a case-control study. Chest 1999; 115: 440-444. Kraaijenhagen RA, Haverkamp D, Koopman MMW, et al. Travel and risk of venous thrombosis. Lancet 2000; 356: 1492-1493. Bounameaux H. Thromboembolism and air travel [letter]. Lancet 1988; 2: 797. Carruthers M, Arguelles AE, Mosovich A. Man in transit: biochemical and physiological changes during intercontinental flights. Lancet 1976; 1: 977-981. Simons R, Krol R. Jet lag, pulmonary embolism, and hypoxia. Lancet 1996; 348: 416. Bendz B, Rostrup M, Sevre K, et al. Association between acute hypobaric hypoxia and activation of coagulation in human beings. Lancet 2000; 356: 1657-1658. Kesteven PL. Traveller's thrombosis. Thorax 2000; 55 (Suppl 1): S32-S36. Ferriman A. Travellers should be warned of thrombosis risk. BMJ 2000; 321: 1310. Sors H, Meyer G. Place of aspirin in prophylaxis of venous thromboembolism. Lancet 2000; 355: 1288-1289. Cohen A, Quinlan D. PEP trial [letter]. Lancet 2000; 356: 247. Make a comment
Alex S Gallus · Ross I Baker
Helping older people to remain in their own homes
Editorial Helping older people to remain in their own homes Community assistance should emphasise preventing and ameliorating disabilty rather than simply compensating for it MJA 2001; 174: 266-267 Australia is ageing rapidly. It is projected that between 1996 and 2016 the general population will increase by 21% or 3.1 million, the number of people over the age of 65 years will increase by 59% or 1.3 million, and those over the age of 80 years will increase by 76% or 368 000.1It is this last statistic which best represents the growing need for services for older people, as people aged over 80 years are disproportionate consumers of the major support systems — 68% of people in nursing homes are aged over 80 years.1 Despite the use of federal targets for residential care based on population ratios and increased funding for home support services, there is pressure on all parts of the aged care system, including residential care.2 What measures can the Australian community initiate to both increase the quality of life for older Australians and decrease the expenditure requirement for the more costly items of care? Over the past 15 years the policy of the State and Federal governments has been to provide services to allow individuals to remain in their own homes for as long as possible. This policy of support for home care has intrinsic appeal and there have been substantial real increases in funding. Federal expenditure on Home and Community Care (HACC) has increased in inflation-adjusted terms from 561 million dollars in 1991-92 to 799 million dollars in 1997-98.1 In addition, the Federal Government spent $2.8 billion dollars, or approximately 0.5% of GDP, on residential care in 1997-98.1 So, if expenditure has grown, why do we have increasing numbers of older people in acute hospital beds awaiting residential care placement, and long waiting times for community care?2 Answers to these questions lie in the interplay of the total health and welfare systems. Over the past 15 years there has been a relative decrease in the number of beds in the nursing home sector and a small increase in hostel beds, which is almost entirely consumed by people who have been assessed as requiring high-level care.2 Also, because the provision of residential care is based on the number of people aged over 70 years, and an increasing proportion of these will be aged over 80 years, there is an expected decrease in the number of beds relative to the number of people who need them the most. More insidiously, State governments have effectively capped their expenditure on assessment and rehabilitation services, as well as opting out of the residential care sector (the public nursing home sector frequently supplied special-needs residential care as well as slow-stream rehabilitation beds). Thus, the availability of assessment, rehabilitation and specialised residential care beds has decreased at a time when it is needed most. It has been suggested that there should be more emphasis on home-based rehabilitation, as a broad range of rehabilitation services in the home can be streamlined and individualised, based on the individual's abilities and condition, and using the family to supplement care.3,4 Rehabilitation attempts to help individuals regain freedom of movement and functional independence, and to reintegrate as fully as possible into community life. Although different settings for individuals will be appropriate at certain stages, the development of community-based rehabilitation by multidisciplinary teams can be effective in promoting the independence of patients and reducing their demand for other community services.5 Home rehabilitation programs can emphasise a task-and-context-oriented approach, educate patients, and apply information in practical situations to solve problems in the home. These programs are usually short-term, providing interventions to individuals who are experiencing or at risk of some degree of functional decline. In this issue of the Journal, Wang and colleagues identify factors that are associated with an increased risk for needing nursing home care in the future.6 With each five-year increase in age there is a doubling of the likelihood of admission to nursing home care. This risk reaches a peak of 35% in the group aged 85 and over. The doubling of risk every five years is similar to the changes in incidence of a number of important conditions known to produce high rates of disability, such as dementia and hip fracture. Although dementia is the commonest condition found in people in residential care,7 cognition was not measured at baseline in the study of Wang et al. However, other disabilities, such as special sensory impairment, arthritis and walking difficulty, were strongly associated with subsequent nursing home admission. As Wang et al point out, these factors are often modifiable, and older people may benefit from community-based rehabilitation programs to improve mobility and independence. Falls may contribute to the need for nursing home admissions, and research has suggested that most are potentially preventable,8 although the effects of intervention are not as dramatic as might be expected.9 Falls-prevention programs with a multi-intervention approach, either clinic-based or through home visits, are effective in meeting the needs of a large number of older people at risk of falls.9 Specific other problems associated with nursing home placement, such as undernutrition and incontinence, are also potentially remediable. Directing further funds to a plethora of HACC agencies providing untargeted maintenance services for some of the personal-care needs of frail older people is unlikely to markedly decrease the need for residential care. Revolutionary changes in either information technology10 or biotechnology11 may produce dramatic benefits, although this can only be speculative at this stage. For now, a focus on targeted assessment and rehabilitation strategies may both give older people a better quality of life and reduce the demand for residential care. An example of this would be providing home-based physiotherapy to an older person who was experiencing decreased mobility and falls, rather than just delivering meals and providing home help. Community rehabilitation teams that work with the acute care sector, HACC services and primary care offer some prospect of improvement in services for older people. R Arthur Criddle Physician, Department of Geriatric Services Sir Charles Gairdner Hospital, Nedlands, WA Leon Flicker Professor, Department of Medicine — Geriatric Medicine University of Western Australia, Royal Perth Hospital, Perth, WA Acknowledgements: The authors would like to thank Caroline Reberger for helpful comments and criticism. Gibson D, Benham C, Racic L, editors. Older Australia at a glance. Canberra: Australian Institute of Health and Welfare, 1999 (Catalogue no. AGE 12). Flicker L. Health care for older people in residential care — who cares? Med J Aust 2000; 173: 77-79. Brocklehurst JC, Morris P, Andrews K, et al. Social effects of stroke. Soc Sci Med 1981; 15: 35-39. Young J. Rehabilitation and older people. BMJ 1996; 313: 677-681. Evans RL, Connis RT, Hendricks RD, Haselkorn JK. Multidisciplinary rehabilitation versus medical care: a meta-analysis. Soc Sci Med 1995; 40: 1699-1706. Wang JJ, Mitchell P, Smith W, et al. Incidence of nursing home placement in a defined community. Med J Aust 2001; 174: 271-275. Rosewarne R, Opie J, Bruce A, et al. Care needs of people with dementia and challenging behaviour living in residential facilities. Canberra: AGPS, 1997. Clemson L, Cumming RG, Roland M. Case-control study of hazards in the home and risk of falls and hip fractures. Age Ageing 1996; 25: 97-101. Gillespie LD, Gillespie WJ, Cumming R, et al. Interventions for preventing falls in the elderly (Cochrane Review). In: The Cochrane Library, Issue 4. Oxford: Update Software, 2000. Celler BG, Lovell NH, Chan DKY. The potential impact of home telecare on clinical practice. Med J Aust 1999; 171: 518-521. Schenk D, Barbour R, Dunn W, et al. Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse. Nature 1999; 400: 173-177. Make a comment
Leon Flicker
Healthcare
Incidence of nursing home placement in a defined community
Healthcare Incidence of nursing home placement in a defined community Jie Jin Wang, Paul Mitchell, Wayne Smith, Robert G Cumming and Stephen R Leeder MJA 2001; 174: 271-275 For editorial comment, see Criddle & Flicker Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Genetics Abstract Objective: To assess cumulative incidence and non-cognitive factors predicting nursing home placement in a defined older population. Design and setting: Six-year follow-up of a population-based cohort living west of Sydney. Participants: 3654 non-institutionalised residents aged 49 years or older (82.4% of those eligible) participated in baseline examinations during 1992 to 1994. Main outcome measures: Permanent nursing home admission for long-term institutionalised aged care in New South Wales, confirmed by records of approvals by the regional Aged Care Assessment Team and subsidy payments by government. Results: After excluding 384 participants who moved from the area or were lost to follow-up, 162 participants (5.0%) had been admitted to nursing homes on a permanent basis by October 1999. Of participants who died since baseline, 20% had been admitted to a nursing home before death. Of those alive, 1.6% were current nursing home residents. Six-year cumulative incidence rates for nursing home placement were 0.7%, 1.1%, 2.4%, 3.9%, 9.0%, 18.3% and 34.9% for people aged 55-59, 60-64, 65-69, 70-74, 75-79, 80-84 and 85 years or older, respectively. Non-cognitive factors at baseline predicting subsequent nursing home admission included each additional year of age (risk ratio [RR], 1.14), fair or poor compared with excellent self-rated health (RR, 2.9, 3.6), walking difficulty (RR, 3.6) and current smoking (RR, 1.9). People owning their homes had a decreased likelihood of nursing home placement (RR, 0.6). Conclusions: Incidence rates of institutional aged care doubled for each five-year interval from the age of 60 years. A range of non-cognitive factors predict nursing home placement. Although there is a rich literature describing risk factors for nursing home placement,1-5 few studies have reported its incidence in a defined older general population.2,5-9 Most cohort studies of nursing home placement have been conducted in samples of at-risk older persons, and mostly in the United States.1-3,5-7,10,11In Australian communities, the Dubbo Study reported a 1.7% cumulative incidence of nursing home admission during a 4.2-year follow-up of 1237 men and 1568 women aged 60 years and over.8,12 A population-based cohort study of hip fracture and risk of institutionalisation in western Sydney9 reported a 5% incidence of nursing home placement among 160 control patients (without hip fracture) aged 65 years and over during 14 months. Although the Australian Institute of Health and Welfare has estimated the lifetime probability of nursing home use by age and sex,13 no Australian reports have provided age-specific and sex-specific incidence or predictors of nursing home placement from a defined general older population. As the proportion of frail older people living in the community increases,14 studies of the incidence of and predictions of nursing home placement could assist in making accurate projections of future demands for nursing homes. The purpose of this report is to describe age-specific and sex-specific six-year cumulative incidence of nursing home placement in a defined, representative older Australian urban population. We also aimed to assess baseline non-cognitive factors associated with placement. Methods Participants We used participants in the Blue Mountains Eye Study, a population-based cohort study of vision and health parameters among non-institutionalised residents, initially aged 49 years and over, living in a defined area west of Sydney. The study area includes two postcode areas (2780, 2782), which comprise the suburbs Katoomba, Leura, Medlow Bath and Wentworth Falls. The baseline study population was fairly representative of Australia's ethnic mix, but was older and had slightly higher socioeconomic status than the State population for this age.15This project was approved by the Western Sydney Area Human Research Ethics Committee and written, informed consent was obtained from all 3654 participants. Baseline examinations were performed from 14 January 1992 to 10 January 1994, with a participation rate of 82.4% overall. Baseline non-participants had a slightly higher proportion of persons aged 80 years and over (10% in participants v. 16.8% in non-participants).16 All participants were invited to attend five-year follow-up examinations from 29 May 1997 to 2 December 1999. Deaths were identified by cross-matching study participants with Australian National Death Index data. Assessing nursing home admissions Australians requiring institutional aged care need prior assessment and approval from a regional hospital Aged Care Assessment Team (ACAT) to determine whether they need respite or permanent care, and low-level or high-level care. People who need low-level care receive approval for hostel admission and those needing high-level care receive approval for nursing home admission. In assessing cumulative incidence of nursing home admission, we included participants who had been given permanent placement in nursing homes in NSW only; those admitted to hostels were excluded. We identified participants living in nursing homes during the follow-up period from information provided by family members, relatives or neighbours. Records of participants who had died since baseline or with whom we lost contact were cross-checked with ACAT records at the Blue Mountains District Hospital. This allowed us to identify people for whom permanent nursing home placement had been approved since their baseline examination to December 1999. This list was further cross-checked against records of subsidy payments by staff in the Aged Care and Planning Branch at the New South Wales State Office of the Commonwealth Department of Health and Aged Care (people admitted to nursing homes receive government subsidy payments that are paid directly to the nursing home). Assessing non-cognitive factors Baseline characteristics were collected during face-to-face interviews with all participants using a standardised questionnaire. Participants were asked whether they regularly used community support services, including Meals-on-Wheels, Home Care or community nurse visits. They were asked whether they owned their home, or were renting or living in a relative's home, and whether they lived alone, with a spouse or with others. Occupational prestige was assessed using the Daniel Occupational Prestige Scale.17 A detailed medical history was taken, including history of angina, heart attack, stroke, hypertension, diabetes, arthritis or gout. There were questions about smoking, alcohol consumption, falls, regular exercise and self-reported hearing loss. Participants in whom the examiner noted difficulty in walking or use of a cane, walker or wheelchair were categorised as having a "walking disability". Global self-rated health was assessed by asking, "For someone of your age, how would you rate your overall health? Would you say it is excellent, good, fair, or poor?" Visual acuity was measured while participants wore their current glasses, by means of a LogMAR chart, and was followed by a standardised subjective refraction.16 Visual acuity in each eye was recorded as the number of letters read correctly (from 0 [< 6/60] to 70 [6/3], after refraction). Statistical analysis Age-standardised incidence rates for nursing home placement in the study population were calculated by direct standardisation to the 2001 Australian projected population (series II);18 95% confidence intervals of the standardised rates were calculated using the Breslow method.19 We excluded the 49-year-old participants to compute incidence rates for persons aged 50 years or older. For those who had died since being admitted, the duration (in days) of nursing home residence was calculated from the date of admission to date of death. χ2 Statistics were used to compare the characteristics of participants who were followed (ie, those who attended follow-up interviews, those who had died, and those admitted to nursing homes) with those who had moved. Cox proportional hazard regression analyses were performed with SAS.20 Our model was based on the conceptual framework for studies of determinants of medical care use described by Andersen and Newman.3,21 This includes three study factor types: predisposing factors (eg, age, education, living status [eg, living alone]), enabling factors (eg, financial status or paying resource for use of services), and need factors (eg, disabilities, impairments, health status). We also assessed health-risk behaviours (eg, smoking, alcohol consumption) in relation to nursing home placement. Nursing home placement was the hazard event, and time to event was calculated as days since baseline examination to nursing home admission. Age was included in the model as a continuous variable. Sociodemographic measures and presence of diseases or impairments were defined dichotomously. Each study factor was assessed initially by age-adjusted Cox regression. Final multivariate models were constructed to assess the risk ratio of each factor at baseline to subsequent nursing home placement, while adjusting for other covariables, including a multivariate Cox regression model without the vision variable (Model 1) and a Cox model with the vision variable (Model 2). Interactions between each study variable and time to event were checked, with no significant interaction found. Risk ratios (RR) and 95% confidence intervals (95% CI) are presented. Results The study population comprised 3654 participants aged 49-97 years. By the time of the follow-up examinations in 1997-1999, 384 of the 3654 baseline participants (10.5%) had moved away from the study area and were excluded from this study. Comparison of baseline characteristics for the remaining 3270 participants and the 384 who moved away showed that those who had moved out of the area were younger (40% were aged < 60 years, compared with 26% in the remaining participants), slightly less likely to own their home (81% v. 89%), to have had cancer (5.7% v. 8.8%), and were more likely to report diabetes (9.9% v. 6.6%). The two people admitted to hostels (rather than nursing homes) were also excluded, leaving 3268 participants. These comprised 1846 women (56.5%) and 1422 men (43.5%). By October 1999, 162 participants (5.0%) were confirmed to have been admitted for permanent nursing home care in NSW, including 104 women (5.6%) and 58 men (4.1%). Of the 604 participants who died since the baseline examination, 120 (19.9%) were admitted to a nursing home before death. Among the remaining 2664 study participants still alive, 42 (1.6%) were current nursing home residents in December 1999. An additional 26 people (0.8%) had received local ACAT approval for nursing home admission, but, as we could not confirm that they had ever received subsidy payments, these people were included in our analyses as not having been admitted to a nursing home. Incidence of nursing home placement To compute incidence rates for nursing home admission for people aged 50 years or older, 17 people aged 49 years were excluded. Box 1 shows six-year cumulative crude age-specific and sex-specific incidence of nursing home placement in five-year age groups. From age 60 years, incidence rates for increasing five-year age intervals doubled. The age-standardised six-year incidence rate was 4.55% (95% CI, 3.83%-5.26%) for people aged 50 years or older, 5.77% (95% CI, 4.63%-6.91%) for women and 3.25% (95% CI, 2.40%-4.10%) for men. The median duration of nursing home residence until death among 120 nursing home residents who died was 145 days, ranging from one day to 5.4 years (lower quartile, 35 days; upper quartile, 1.4 years). Non-cognitive factors predicting nursing home placement Baseline non-cognitive predisposing factors for nursing home placement (age, marital status, living status), enabling factors (home ownership, job prestige), need factors (disabilities, diseases, impairments), and health-risk behaviours (smoking, alcohol consumption, exercise) were all significantly associated with subsequent nursing home admission, after adjusting for age (Box 2). Some significant findings could have arisen by chance as a result of the multiple comparisons made. In the multivariate Cox regression model, age, lack of home ownership, reduced (fair or poor) self-rated health, presence of a walking disability and current smoking at the baseline interview were significantly associated with an increased risk of subsequent nursing home placement (Box 3, Model 1). People who regularly consumed alcohol at baseline had a reduced risk of subsequent nursing home placement. For each one-line reduction in best-corrected visual acuity at baseline, there was a borderline association with subsequent nursing home placement (Box 3, Model 2). Discussion Blue Mountains Eye Study participants were drawn from a defined suburban area with well established community support services. We were able to identify baseline study participants who received ACAT approval for admission to a nursing home and could also confirm their placement in permanent nursing home care, as well as its duration since admission. Our study has a number of limitations. Firstly, we could have underestimated or overestimated the number of people placed in nursing homes if those who had moved out of the area were more or less likely to be admitted. As this group had a slightly younger mean age, we may have slightly overestimated the incidence of nursing home placement. A potential underestimate could also have arisen as (i) participants were slightly less likely to be aged 80 or more years than non-participants,16 and (ii) 26 participants given approval for nursing home admission, but for whom admission was not confirmed, were excluded. Secondly, although cognitive impairment is the most frequent disability leading to nursing home placement, we did not assess cognitive status at baseline, so could not include this among factors predicting admission. The result of measuring cognitive status and incorporating these data into the predictive model might have either (i) caused the effect of non-cognitive factors to disappear or be reduced in magnitude, or (ii) continued to show associations between non-cognitive factors and admission. At baseline, the study population included non-institutionalised residents aged 49-97 years, and virtually all participants (98%) had visual acuity from both eyes measured reliably, so we feel it is unlikely that many participants had significant dementia or cognitive impairment at that time. The US Long-Term Care Channeling Demonstration found that effects on the use of aged-care facilities of self-rated health, home ownership and physical impairment were independent of cognitive impairment.3 Further, as some non-cognitive factors are modifiable, it is important to recognise their effects on outcomes if these effects are independent of cognitive impairment. Although we did not specifically assess activities of daily living (ADL), we did assess whether participants had difficulty in walking, which may be a marker for ADL limitation. Despite these reservations, to our knowledge this is the first population-based study to provide age-specific and sex-specific incidence for nursing home admission in an Australian community. Our six-year crude incidence of nursing home placement (5.0% among people aged 50 or more years) was substantially higher than the overall rate reported from the Dubbo Study (1.7% over 4.2 years among people aged 60 or more years),8,12 but lower than for a group of normal control subjects (5% over 1.2 years).9 The Dubbo Study reported higher nursing home admission rates in women than in men.8 Although we found no overall difference between the sexes, a substantially higher incidence was found for women aged 80 years or older. This finding is in keeping with an Australian Institute of Health and Welfare report, which provided age-sex profiles of 73 552 nursing home residents in 1994.22 This report shows similar proportions for women and men up to age 75, but three times as many female as male Australian nursing home residents above this age. The Dubbo Study also reported that age and disability were significant factors in a multivariate model predicting nursing home admission.8 The likelihood of nursing home admission in the Dubbo Study increased by 13% for each year of age; this is identical to the age effect in our multivariate Cox regression model (13%-14% per year). Among relatively old and frail US Medicare beneficiaries, those who owned their homes were reported to have 30% fewer nursing home admissions;3 this finding was attributed to the strong sense of attachment and place associated with home ownership. In our population, people owning their home at baseline were 60% less likely to have subsequent nursing home admission. We classified lack of home ownership as an enabling factor, as people in this group are more likely to be dependent on pensions. Nursing home admission for these people may not result in additional costs over and above their pension, while means testing may require home owners to pay a substantial sum up-front for nursing home placement. Home owners might be able or may prefer to "buy in" support services to assist them in staying at home longer. They may also have a stronger emotional attachment to a house they have lived in for decades. The multivariate model derived from our data contained five significant predictive factors and one protective factor. These five factors represent all three categories in Andersen and Newman's conceptual framework for determinants of use of medical care,21 and so may be applicable in describing determinants of institutional aged-care use in Australia as well as in the US. As shown in previous reports,23,24 our findings also suggested that reduced vision might be a marker or an independent predictor of nursing home admission. Our study showed that there was a substantially higher prevalence of visual impairment among nursing home residents than people of similar age living in the community.25 This finding highlights the need for older persons being assessed for nursing home placement to have their vision and hearing tested for treatable causes of sensory impairment. Acknowledgements We greatly appreciate assistance from ACAT staff at the Blue Mountains District Hospital, Wentworth Area Health Service and from staff in the Aged Care and Planning Branch, New South Wales State Office, Commonwealth Department of Health and Aged Care, for their help in confirming nursing home placement. This study was supported by the Australian Department of Health and Family Services and the Save Sight Institute, University of Sydney. Dr Wang held a National Health and Medical Research Council Public Health Postgraduate Research Scholarship (No. 987445) when this study was conducted. References Kane RA, Kane RL. Evidence about the need for care. Long-term care: Principles, programs and policies. New York: Springer, 1987: 25-32. Jette AM, Branch LG, Sleeper LA, et al. High-risk profiles for nursing home admission. Gerontologist 1992; 32: 634-640. Greene VL, Ondrich JI. Risk factors for nursing home admissions and exits: a discrete-time hazard function approach. J Gerontol 1990; 45 (6 Suppl): S250-S258. Murtaugh CM, Kemper P, Spillman BC. The risk of nursing home use in later life. Med Care 1990; 28: 952-962. Wolinsky FD, Callahan CM, Fitzgerald JF, Johnson RJ. The risk of nursing home placement and subsequent death among older adults. J Gerontol 1992; 47 (4 Suppl): S173-S182. Dwyer JW, Barton AJ, Vogel WB. Area of residence and the risk of institutionalization. J Gerontol 1994; 49 (2 Suppl): S75-S84. Tinetti ME, Williams CS. Falls, injuries due to falls, and the risk of admission to a nursing home. N Engl J Med 1997; 337: 1279-1284. McCallum J, Simons L, Simons J, Wilson J. Best Practice Paper 6. Hospital and home: a longitudinal study of hospital, residential and community service use by older people living in Dubbo, NSW. Sydney, NSW Office on Ageing, Social Policy Directorate, 1994: 1-35. 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. Cohen MA, Tell EJ, Wallack SS. The risk factors of nursing home entry among residents of six continuing care retirement communities. J Gerontol 1988; 43 (1 Suppl): S15-S21. Lord SR. Predictors of nursing home placement and mortality of residents in intermediate care. Age Ageing 1994; 23(6): 499-504. McCallum J, Simons L, Simons J, et al. The continuum of care for older people. Aust Health Rev 1995; 18: 40-55. Liu Z. The probability of nursing home use over a lifetime. Canberra: Australian Institute of Health and Welfare, 1998: 1-21. (Welfare Division Working Paper No. 16.) Australian Institute of Health and Welfare. Aged and respite care in Australia: extracts from recent publications. Canberra: AIHW, 1997: 1-102. Wang JJ, Mitchell P, Smith W, Leeder SR. Factors associated with use of community support services in an older Australian population. Aust N Z J Public Health 1999; 23: 147-153. Attebo K, Mitchell P, Smith W. Visual acuity and the causes of visual loss in Australia. The Blue Mountains Eye Study. Ophthalmology 1996; 103: 357-364. Congalton AA. Status and prestige in Australia. Melbourne: F W Cheshire, 1969: 1-160. McLennan WAS. Population projections: 1997 to 2051. Canberra: Australian Bureau of Statistics, 1998: 1-130. Breslow NE. Rates and rate standardisation. Statistical methods in cancer research. Vol. II. Lyon: International Agency for Research on Cancer, 1987: 48-79. SAS [computer program]. Version 6.12. Cary, NC: SAS Institute Inc, 1995. Andersen R, Newman JF. Societal and individual determinants of medical care utilization in the United States. Milbank Mem Fund Q Health Soc 1973; 51: 95-124. Jenkins A. Client profiles for aged care services in Australia: Canberra, Australian Institute of Health and Welfare, 1996: 1-58. (Welfare Division Working Paper No. 11.) Peterson R, Kirchner C. Prevalence of blindness and visual impairment among institutional residents. Statistical brief No. 11. J Vis Impairm Blindness October 1980: 323-326. Tielsch JM, Javitt JC, Coleman A, et al. The prevalence of blindness and visual impairment among nursing home residents in Baltimore. N Engl J Med 1995; 332: 1205-1209. Mitchell P, Hayes P, Wang JJ. Visual impairment in nursing home residents: the Blue Mountains Eye Study. Med J Aust 1997; 166: 73-76. (Received 19 Jun, accepted 5 Oct, 2000) Authors' details University of Sydney, NSW. Jie Jin Wang, MB BS, MMed(Clin Epi), Epidemiologist, Department of Ophthalmology, Save Sight Institute; Paul Mitchell, MD, PhD, Associate Professor, Department of Ophthalmology, Save Sight Institute; Robert G Cumming, MB BS, PhD, Associate Professor, Department of Public Health; Stephen R Leeder, MB BS, PhD, Professor and Dean, Faculty of Medicine. National Centre for Epidemiology and Population Health, Australian National University, Canberra, ACT. Wayne Smith, BMed, PhD, Senior Fellow. Reprints will not be available from the authors. Correspondence: Associate Professor Paul Mitchell, Department of Ophthalmology, University of Sydney, Eye Clinic, Westmead Hospital, Hawkesbury Road, Westmead, NSW, Australia, 2145. paulmiATwestgate.wh.usyd.edu.au Make a comment 1: Six-year cumulative crude incidence rates (95% CI) for nursing home placement among participants aged 50 years or older, by five-year age group and sex Age at baseline (years) Women (n=1838) Men (n=1415) Total (n=3253) 50-54 0.0 0.0 0.0 55-59 0.8 (0.01-1.8) 0.5 (0.01-1.5) 0.7 (0.01-1.4) 60-64 1.3 (0.03-2.5) 0.8 (0.01-1.9) 1.1 (0.2-1.9) 65-69 3.0 (1.2-4.8) 1.8 (0.2-3.4) 2.4 (1.2-3.7) 70-74 3.9 (1.6-6.1) 4.0 (1.3-6.7) 3.9 (2.2-5.6) 75-79 8.6 (4.9-12.3) 9.5 (5.0-13.9) 9.0 (6.1-11.8) 80-84 21.0 (13.7-28.4) 14.9 (7.7-22.1) 18.3 (13.1-23.5) 85+ 38.4 (28.0-48.7) 27.9 (14.3-41.5) 34.9 (26.6-43.1) Back to text 2: Baseline characteristics associated with nursing home placement in the following six years (age-adjusted Cox regression model) Status at the baseline examination Nursing home placement (n=162) No nursing home placement (n=3106) Age-adjusted risk ratios (95% CI) Predisposing factors Age (per year) 1.17 (1.15-1.19) Female 104 (64.2%) 1742 (56.1%) 1.1 (0.8-1.5) Not currently married 101 (63.1%) 1110 (35.8%) 1.5 (1.1-2.1) Living alone 77 (48.7%) 821 (26.6%) 1.3 (0.9-1.8) Enabling factors Not owning home 36 (23.4%) 300 (9.9%) 1.9 (1.3-2.8) Low job prestige 84 (54.9%) 1152 (37.7%) 1.5 (1.1-2.0) Need factors Self-ranked health Excellent 15 (9.7%) 619 (20.3%) 1 Good 64 (40.8%) 1695 (55.5%) 1.4 (0.8-2.5) Fair 61 (39.4%) 629 (20.6%) 3.5 (2.0-6.2) Poor 15 (9.7%) 109 (3.6%) 5.0 (2.4-10.3) Walking disability 67 (41.4%) 176 (5.7%) 4.3 (3.0-6.1) Reported fall(s) in past year 75 (51.4%) 695 (24.5%) 1.9 (1.3-2.6) Regular use of community services 38 (26.0%) 136 (4.6%) 2.3 (1.5-3.4) History of: Stroke 23 (14.5%) 155 (5.0%) 1.8 (1.1-2.7) Gout 31 (22.5%) 327 (11.4%) 1.7 (1.2-2.6) Diabetes 17 (10.5%) 198 (6.4%) 1.9 (1.1-3.1) Heart disease 44 (27.9%) 486 (15.7%) 1.4 (1.0-2.0) Cancer 22 (13.9%) 266 (8.6%) 1.3 (0.8-2.0) Arthritis 105 (67.3%) 1493 (48.4%) 1.4 (0.99-1.9) Diabetic retinopathy 7 (4.6%) 67 (2.2%) 2.7 (1.3-5.7) Visual impairment 36 (22.6%) 113 (3.6%) 1.6 (1.1-2.5) Per-line reduction in visual acuity 1.09 (1.04-1.15) Moderate to severe hearing loss 48 (39.0%) 383 (16.8%) 1.3 (0.9-1.9) Health-risk behaviours Smoking Never 97 (59.9%) 1580 (50.9%) 1 Past 45 (27.8%) 1079 (34.8%) 0.8 (0.5-1.1) Current 20 (12.4%) 444 (14.3%) 1.6 (0.96-2.6) Alcohol consumption (any regular) 68 (42.0%) 2020 (65.0%) 0.5 (0.4-0.7) Regular walking exercise 60 (42.9%) 1871 (62.9%) 0.6 (0.4-0.8) Body mass index (kg/m2) Underweight (<20) 21 (14.9%) 169 (5.6%) 1.9 (1.2-3.2) Normal weight (20-25) 59 (41.8%) 1130 (37.4%) 1 Overweight (26-29) 41 (29.1%) 1208 (40.0%) 0.9 (0.6-1.3) Obese (>30) 20 (14.2%) 515 (17.0%) 1.1 (0.7-1.9) Denominators vary slightly because of missing data. Back to text 3: Baseline characteristics predicting nursing home placement in the following six years (multivariate Cox regression model) Multivariate-adjusted risk ratios (95% CI) Status at baseline Model 1 Model 2 Predisposing factors Age (per year) 1.14 (1.12-1.16) 1.13 (1.11-1.16) Enabling factors Not owning home 1.7 (1.1-2.5) 1.7 (1.2-2.5) Need factors Self-ranked health Excellent 1.0 1.0 Good 1.4 (0.8-2.5) 1.3 (0.7-2.4) Fair 2.9 (1.6-5.2) 2.8 (1.5-5.0) Poor 3.6 (1.7-7.6) 3.3 (1.6-7.1) Walking disability 3.6 (2.5-5.3) 3.4 (2.3-5.0) Smoking Never 1.0 1.0 Past 0.8 (0.6-1.2) 0.8 (0.5-1.1) Current 1.9 (1.1-3.2) 1.8 (1.1-3.1) Alcohol consumption (any regular) 0.7 (0.5-0.9) 0.7 (0.5-0.9) Per-line decrease in best-corrected visual acuity 1.04 (0.99-1.10) Back to text
Paul Mitchell · Wayne Smith · Robert G Cumming · Stephen R Leeder
Medicine and the community
Operative photography in gynaecological endosurgery
Medicine and the community Operative photography in gynaecological endosurgery Geoffrey D Reid and Adelyn Leong MJA 2001; 174: 285-287 Abstract - Methods - Results - Discussion - References - Authors' details - - More articles on Surgery Abstract Objectives: To define the attitude of patients, doctors and nurses to operative photographs captured at gynaecological endosurgery, and to determine the value of these photographs in patient education. Design and setting: Postal questionnaire survey of specialists, general practitioners, nurses and patients at a tertiary referral hospital in south-west Sydney. Participants: All patients who underwent endoscopic gynaecological surgery between 1 February and 1 May 1998, and for whom good quality operative photographs were available, and medical and nursing staff randomly selected from lists of practitioners within the Southwest Sydney Area Health Service. Main outcome measures: Opinions on whether operative photodocumentation assists patients in understanding their condition; the value to patients of these records; whether operative photographs assist referring doctors in subsequent management of patients; the use of operative photographs in medical records or as personal records for patients; whether photographs may lead to anxiety or be used in medicolegal action. Results: All patients believed operative images were valuable in helping them understand their condition. 19 of 20 specialists (95%), 85 of 123 general practitioners (69%) and 23 of 28 nursing staff (82%) also believed that operative images assist patients in understanding their disease. Nearly all patients denied that operative images would create anxiety, and specialists, general practitioners and nurses also felt that the photographs would not cause anxiety. 78% of general practitioners expressed a desire to receive operative images. Conclusions: Photographic records of operative procedures are regarded as valuable by both referring doctors and their patients. Patients find photographs useful in understanding their disease. Intraoperative photography is now widely available, but is underused by referring practitioners and consulting specialists. The essential value of intraoperative photography is that it provides accurate records of clinical findings (examples are shown in Box 1). However, its role may extend to providing documentation for personal records, to communication with referring practitioners and to complementing operative or legal reports. Images may be particularly useful in situations where multiple treatment options exist (eg, where infertility caused by tubal disease can be managed by tubal surgery or assisted reproductive technologies). Photographic records may enable more appropriate decisions to be be made after reflection or consultation. Documentation is ideal for comparison before and after surgery, or for monitoring the progress of certain diseases. In gynaecological practice, the documentation of normal findings is particularly useful, especially when investigating pelvic pain. Image capture is useful for validating the operative procedure. When images are shown at the postoperative visit, the patient has no doubt that the planned procedure has been performed, that all areas under suspicion have been thoroughly inspected and that the appropriate findings have been recorded. Apart from some historical reports,1-7 the usefulness and acceptability of intraoperative photography have not been addressed in the current medical literature. We aimed to assess the views of patients, doctors and nurses about intraoperative photographic documentation. Methods We invited all 28 patients who underwent endoscopic surgery between 1 February and 1 May 1998 for whom good quality operative photographs were available to participate in the study. Medical and nursing staff were randomly selected from lists of practitioners within the Southwest Sydney Area Health Service. We approached 40 specialists (20 gynaecologists and 20 anaesthetists), 200 general practitioners and 40 nurses. Medical and nursing staff were surveyed by postal questionnaire. Patients were shown their photographs at a postoperative visit and then sent a postal questionnaire one week later. The questionnaire included the questions shown in Box 2, and participants were invited to provide free-text commentary on any related issues. Informed consent was obtained from all patients for their opinions to be published. Results Response rates were 50% (20 of 40) for specialists (12 gynaecologists and eight anaesthetists), 61.5% (123 of 200) for general practitioners, 70% (28 of 40) for nurses and 100% (all 28) for patients. Our results are summarised in Box 2. All patients surveyed believed operative images were valuable in helping them understand their disease, or their normal findings, and most specialists, GPs and nurses also believed that operative images assist patients in understanding their condition. Importantly, nearly all patients denied that operative images would create anxiety, and specialists, general practitioners and nurses also felt that they would not cause such a problem. Free-text responses from patients highlighted the option of seeking a second opinion when the initial surgical procedure was well documented photographically. Our survey showed that all groups surveyed had a positive attitude towards having operative images included in the medical record. Seventy-eight per cent of general practitioners expressed a desire to receive operative images. It was apparent that GPs found the photographs useful for patient counselling; a considerable number of free-text responses suggested: operative imaging is useful as proof of operation and proof of communication; operative imaging may be useful in a medicolegal setting; and operative imaging is good, but the most important requirement is for comprehensive and timely written communication about a patient's admission. However, almost half of the nursing staff surveyed thought that general practitioners should not receive photographic images. There was considerable variation in attitudes towards patients' being given the images to keep in their possession. Almost 90% of patients wanted them, while nearly 70% of general practitioners believed they should not have them. There was some concern among the health professionals about the potential for operative images to lead to medicolegal problems for the surgeon. A number of respondents expressed the belief that operative images would be supportive rather than detrimental in a medicolegal setting. Discussion Our findings show that patients value operative images highly and are not made anxious by photographs of their "insides". The vast majority of participating patients appreciated open communication of surgical findings. However, our questions were directed, and whether these responses represent true appreciation of disease pathology (or its absence) or a perceived increased level of care is not clear. The fact that many of the nursing staff surveyed thought that general practitioners should not receive photographic images may reflect a poor understanding of the relationship between general practitioners and specialists. We agree with the comment of a number of GPs that the most important requirement is for comprehensive and timely written communication about a patient's admission, and believe that operative imaging should always be regarded as an adjunct to conventional communication. Photographic recording of operative procedures is useful as part of routine documentation, and is regarded as valuable by both referring doctors and their patients. Patients, in particular, find photographs useful in the understanding of their disease. References Estes JW. To become pregnant. In: Carmichael AG, Ratzan RM, editors. Medicine in literature and art. Köln: Könemann Verlagsgesellschaft GmbH, 1991: 31-33. Estes JW. Surgical problems and solutions. The medical skills of ancient Egypt. Canton, MA: Science History Publications, 1989. McFall K. A notable anniversary in the history of medical illustration. J Audiov Media Med 1997; 20: 5-10. Burns SB. The nude in medical photography: a historical perspective, with modern legal ramifications. J Biol Photogr 1996; 64: 15-26. Nordentoeft S. Uber Endoskopie Geschlossener Cavitaten mittels eines Trokar-Endoskops. Verh Dtsch Ges Chir 1912; 41: 412. Cohen MR, Guterman HS. A pelvic photoscope. Obstet Gynecol 1953; 1: 544. Clyman MJ. A new panduldoscope -- diagnostic, photographic, operative aspects. Obstet Gynecol 1963; 21: 343. (Received 10 Jul 2000, accepted 19 Jan 2001) Authors' details Liverpool Hospital, Liverpool, NSW. Geoffrey D Reid, MRCOG, FRACOG, Director of Gynaecological Endoscopy; Adelyn Leong, MB BS, MRACOG, Clinical Fellow. Reprints will not be available from the authors. Correspondence: Dr G D Reid, Division of Women's and Child Health, Locked Bag 7103, Liverpool BC, NSW 1871. rejoyceATbigpond.com Make a comment 1: Eamples of interoperative images Severe pelvic destruction from endometriosis. A 6cm left ovarian chocolate cyst. Pelvic sidewall endometriosis. Caecal endometriosis. Back to text 2: Attitudes of participating specialists, general practitioners, nurses and patients to operative images Questions Specialists (n=20) General practitioners (n=123) Nursing staff (n=28) Patients (n=28) Do operative images help in the understanding of the patient's disease? No/Slightly 1 (5%) 38 (29%) 5 (18%) 0 Mostly/Yes 19 (95%) 85 (69%) 23 (82%) 28 (100%) Do operative images create anxiety for patients? No/Slightly 19 (95%) 114 (93%) 27 (96%) 28 (100%) Mostly/Yes 1 (5%) 9 (7%) 1 (4%) 0 Should operative images be included in the patient's medical record? No 0 19 (15%) 2 (7%) 1 (4%) Yes 20 (100%) 104 (85%) 26 (93%) 27 (96%) Should operative images be sent to the referring general practitioner? No 3 (15%) 27 (22%) 12 (43%) 5 (18%) Yes 17 (85%) 96 (78%) 16 (57%) 23 (82%) Should operative images be given to patients? No 8 (40%) 81 (66%) 17 (61%) 3 (11%) Yes 12 (60%) 42 (34%) 11 (39%) 25 (89%) Will operative images lead to medicolegal problems? No 6 (30%) 46 (37%) 10 (36%) n/a Perhaps 11 (55%) 67 (54%) 15 (54%) n/a Yes 3 (15%) 10 (8%) 3 (11%) n/a n/a=not applicable. Back to text
Geoffrey D Reid · Adelyn Leong
Position statement
The management of varicella-zoster virus exposure and infection in pregnancy and the newborn period
MJA 2001; 174: 288-292 Abstract - Recommendations 1A - Recommendations 1B - Recommendations 2 - Recommendations 3 - Recommendations 4 - References - Authors' details - - More articles on Obstetrics & gynaecology and women's health Abstract Zoster immunoglobulin (ZIG) should be offered to pregnant, varicella-seronegative women with significant exposure to varicella-zoster virus (VZV) (chickenpox) infection. Oral aciclovir prophylaxis should be considered for susceptible pregnant women exposed to VZV who did not receive ZIG or have risk factors for severe disease. Intravenous aciclovir should be given to pregnant women who develop complicated varicella at any stage of pregnancy. Counselling on the risk of congenital varicella syndrome is recommended for pregnant women who develop chickenpox. ZIG should be given to a baby whose mother develops chickenpox up to 7 days before delivery or up to 28 days after delivery. Intravenous aciclovir should be given to babies presenting unwell with chickenpox, whether or not they received ZIG. Breastfeeding of babies infected with or exposed to VZV is encouraged. A mother with chickenpox or zoster does not need to be isolated from her own baby. If siblings at home have chickenpox, a newborn baby should be given ZIG if its mother is seronegative. The newborn baby does not need to be isolated from its siblings with chickenpox, whether or not the baby was given ZIG. After significant nursery exposure to VZV, ZIG should be given to seronegative babies and to all babies born before 28 weeks' gestation. Varicella-zoster virus (VZV) (chickenpox) infection can cause severe morbidity in the pregnant woman, the fetus, and the newborn baby. 1. Management of VZV infection in pregnancy The implications of primary VZV infection in pregnancy for the mother and for the fetus vary with the period of gestation. For the mother, the risk of adverse effects is greatest in the third trimester, whereas for the fetus the risk is greatest in the first and second trimesters. A. Maternal risk In normal adults, the mortality and morbidity of primary VZV infection is greater than in children. Only about 2% of all cases occur in adulthood, but they account for 25% of all VZV-related deaths.1 Pneumonitis is 25 times more common in adults.1,2A 1995 Australian study assessed VZV seronegativity in women presenting to antenatal clinics and found 22% of women aged 14-19 years, 14% of those aged 20-24 years, 5% of those aged 25-29 years and 2% of those aged 30 years and over had not had previous exposure and were therefore susceptible to VZV infection.3 Anecdotally, chickenpox infection in pregnancy is more severe than in non-pregnant adults, but there is scant supporting evidence.4 A survey of 164 000 pregnancies in the United Kingdom described 98 women with chickenpox, of whom seven developed severe illness and two died.5 The UK confidential inquiry into maternal deaths from 1985 to 1997 reported only seven deaths associated with VZV in pregnancy, all of which occurred in the second half of pregnancy. Other reports have also suggested increased severity of illness in the second half of pregnancy.6 Zoster immunoglobulin (ZIG), given prophylactically at the time of exposure, is known to prevent or reduce the severity of chickenpox.7-9 Aciclovir, an antiviral agent, shortens the duration of illness in young adults if administered during the incubation period or within 24 hours of the onset of the rash.10,11 When administered prophylactically (7 to 9 days after family exposure) it may be up to 84% protective against infection and able to modify the illness in the remaining family members.12 Although aciclovir is not licensed for use in pregnancy (because of concerns about adverse fetal effects), there have been no reports of adverse effects among hundreds of cases over several years of monitoring.13 Management algorithms (Boxes 1 and 2) have been devised for varicella exposure in pregnancy. Recommendations 1A Zoster immunoglobulin (ZIG) (Box 3) All pregnant women who have significant exposure to VZV infection (defined as "living in the same household as a person with active chickenpox or herpes zoster or face-to-face contact with a person with chickenpox or uncovered zoster for at least 5 minutes"), who have no history of chickenpox and who are seronegative (or serological testing is not readily available), should be offered ZIG.4-6 (E3) ZIG should be administered within 72 hours of exposure for maximal effect, although it may provide some benefit up to 96 hours after exposure for immunocompromised subjects.14 (E3) ZIG is ineffective, and should not be given, once clinical illness is established.15 (E4) Aciclovir (Box 3) There is no high level evidence on the use of aciclovir in pregnancy. Based on consensus view, we recommend: Consideration should be given to using oral aciclovir prophylaxis for susceptible pregnant women with significant exposure (defined above) who have not received ZIG, or who have any underlying risk factors, such as chronic lung disease, cigarette smoking,16 systemic corticosteroid treatment,17 impaired immunity,18 or are in the second half of pregnancy (Box 3). (E4) Intravenous aciclovir should be given for varicella pneumonitis or other complications at any stage of pregnancy.4,6,19 These complications include respiratory symptoms, neurological symptoms, haemorrhagic rash and/or continued fever or appearance of new lesions after 6 days.4 (E4) Extrapolation from data in children suggests that patients receiving systemic corticosteroid therapy or those with underlying immunodeficiency should be treated with intravenous aciclovir at the earliest sign of chickenpox.18,20,21 (E4) Management of delivery of the baby There is no evidence that ending the pregnancy speeds maternal recovery. Expedited delivery should only be considered for fetal compromise or if the gravid uterus is thought to be critically impairing maternal ventilation. B. Fetal risk Chickenpox in pregnancy may result in fetal varicella which is usually benign and self-limiting.1 Occasionally, it produces a characteristic pattern of abnormalities known as "congenital varicella syndrome" (CVS).22,23 CVS very occasionally follows maternal zoster infection.5 The risk of CVS after first-trimester maternal chickenpox was estimated from prospective studies as 2.2% (range, 0-9%; 95% CI, 0-4.6%).24-26 In a large prospective European study, the incidence of CVS was 0.4% after maternal chickenpox in the first 12 weeks of pregnancy, rising to 2% between weeks 13 and 20.24 After 20 weeks the risk is far lower, although isolated cases have been reported.3 The incidence of CVS in Australia is 1 in 107 000 pregnancies.27 The congenital defects are usually severe, causing cicatricial skin lesions, limb hypoplasia or paresis, microcephaly and ophthalmic lesions.22,24,28 It is hypothesised that these lesions result from virus reactivation in utero or disseminated zoster infection.2,29 Herpes zoster (shingles) occurs in early childhood in about 1% of otherwise asymptomatic infants exposed to maternal varicella during the second or third trimester.24At present, there is no reliable marker of in-utero virus reactivation or the predicted development of CVS. Serological tests are an insensitive marker of fetal VZV infection and subsequent fetal damage.24 The polymerase chain reaction (PCR) has been used to detect VZV in amniotic fluid: a negative PCR is associated with a favourable outcome, but a positive PCR correlates poorly with the development of CVS.26 As amniocentesis carries a risk of fetal loss, amniotic fluid PCR has a limited role. While ZIG may prevent or modify the course of chickenpox in pregnancy, it may not abolish the risk of fetal infection. Therefore, close ultrasound monitoring for the development of fetal abnormalities after maternal chickenpox or administration of ZIG in pregnancy is recommended. Recommendation 1B Counselling on the risk of congenital varicella syndrome is recommended for women who develop chickenpox during pregnancy. (E4) 2. Management of babies of mothers with perinatal chickenpox Maternal chickenpox in the peripartum period poses a risk of severe neonatal varicella, with a mortality rate up to 30%.30,31 The increased peripartum severity is attributed to a large transplacental inoculum of virus in the absence of protective maternal antibody. The timing of maternal infection in relation to delivery determines the risk to the infant.31 Infection with onset more than seven days before delivery ensures adequate transplacental passage of specific anti-VZV antibody to protect the infant.32 Infection with onset 7 days or less before delivery puts the infant at risk of severe neonatal varicella. Passive immunisation of the baby by giving ZIG immediately after delivery prevents or attenuates neonatal varicella and is essential.7,33 Maternal varicella starting 1-2 days after delivery is also associated with an increased risk of severe neonatal varicella from transplacental spread of the virus.30 However, babies of seronegative mothers exposed postnatally to varicella in the first 28 days after delivery apparently have increased risk of severe illness compared with older infants.33 If the mother develops chickenpox postnatally, her baby is evidently seronegative. Therefore, ZIG is recommended for seronegative babies up to 28 days old exposed to varicella.34,35 Recommendations 2 ZIG is indicated for the baby if maternal varicella develops up to 7 days before delivery or if the mother develops chickenpox up to 28 days after delivery.7,15,31-33 (E3) ZIG should be given to the baby as early as possible after delivery or exposure, but must be within 72 hours.31,32 (E4) Maternal herpes zoster is not an indication for ZIG administration to the baby. (E4) Clinical follow-up of infants receiving ZIG is essential and they should be admitted to hospital if any rash develops, because severe varicella can still occur despite passive immunisation.35,36 (E4) Intravenous aciclovir should be administered (a) to babies presenting with chickenpox who are unwell (eg, poor feeding, tachypnoea), whether or not they received ZIG; (b) to any high risk neonate who develops chickenpox and who inadvertently did not receive ZIG prophylaxis or for whom it was delayed beyond 24 hours; and (c) to immunocompromised neonates who develop chickenpox, including those who are premature or being treated with corticosteroids.18,21 (E4) Routine aciclovir prophylaxis in conjunction with ZIG is not currently recommended in the neonatal population, due to lack of evidence. (E4) Breastfeeding of infected or exposed babies is encouraged. (E4) A mother and/or her baby with active vesicles should be isolated from other mothers and babies, but an infected mother does not need to be isolated from her own baby. (E4) 3. Management of neonates exposed to VZV infection on the postnatal wards or at home The commonest neonatal exposure to VZV is when one or more siblings develops chickenpox in the weeks after delivery. The risk of the newborn developing severe disease from postnatal exposure is considerably less than from transplacentally acquired varicella, but some babies with postnatal exposure will develop severe disease.34 The risk to the newborn baby is determined primarily by the presence or absence of transplacentally acquired maternal IgG antibody. If the mother has had chickenpox, the risk from siblings is negligible. If not, the baby should be given ZIG, which will minimise the risk.34,35 Recommendations 3 ZIG should be administered to a baby up to 28 days old exposed to VZV if the mother is seronegative, her serostatus can not be determined, or if the infant was born at or before 28 weeks' gestation.15,37 (E3) A newborn baby does not need to be isolated from its siblings with chickenpox, whether or not the baby was given ZIG. (E4) Parents should be advised that medical attention should be sought if any signs of chickenpox develop. (E4) Admit to hospital for aciclovir treatment if baby becomes unwell (eg, poor feeding, tachypnoea). (E4) The role of prophylactic aciclovir is unproven. 4. Management of VZV exposure within the neonatal unit VZV poses a particular threat in this setting, because babies born prematurely are relatively deprived of the usual third-trimester transfer of transplacental antibodies.37-39 Spread of VZV is primarily by the respiratory route, so isolation in a separate room is desirable for babies with pneumonitis, and essential if they require artificial ventilation. Staff handwashing is important in reducing spread of the virus. VZV vaccines are now available in Australia, and immunisation of susceptible staff is strongly recommended.35 A significant exposure in the neonatal unit or on the postnatal ward is defined as:10,15 patient sharing the same open ward as a person with chickenpox or zoster; face-to-face contact with a person with chickenpox or zoster for at least 5 minutes; and contact for one hour or more with person (staff or patient) with chickenpox lesions or who developed lesions up to 48 hours later. All staff who have had significant exposure to an index case (see above) and who do not have a history of previous chickenpox infection or of VZV vaccination should have serological tests. If they are VZV antibody negative, they should be removed from clinical duties from days 7-21 after exposure (days 7-28 if they receive ZIG). Recommendations 4 Infants born after 28 weeks' gestation15 should only be given ZIG if they have had significant exposure (defined above) and serological tests show the mother to be seronegative. (E4) All infants born at or before 28 weeks' gestation or born weighing under 1000 g11,37,38 with significant exposure should be given ZIG regardless of the results of serological testing of the mother. (E4) Quarantine of cases should continue until all lesions have crusted.15 (E3) Quarantine of contacts should be from days 7-21 after exposure, and from days 7-28 after exposure if they received ZIG.15 (E3) Although quarantine of cases and those considered to have significant contact is recommended, this should not compromise medical and nursing care of a sick infant. (E4) Infants with pneumonitis requiring ventilation must be isolated. Where isolation facilities are unavailable, cases should be transferred to a unit with isolation facilities. (E4) Aim to discharge all patients requiring quarantine from hospital as soon as possible. (E4) Background and evidence basis of recommendations This position statement was circulated to all members of the Australasian Subgroup in Paediatric Infectious Diseases (ASPID) for comments. The comments were analysed by the authors, discussed with colleagues, and subsequent versions incorporating the comments were re-circulated to all ASPID members. The recommendations of ASPID on the management of VZV exposure and infection in pregnancy and the neonatal period are endorsed by the Royal Australian and New Zealand College of Obstetricians and Gynaecologists. The recommendations are based on the following levels of evidence (simplified from the NHMRC's "Quality of evidence ratings")40 E1 Level I Systematic review or meta-analysis of all relevant randomised controlled trials (RCTs) E2 Level II Well-designed RCTs E3 Level III Well-designed cohort or case-control studies E4 Level IV Consensus opinion of ASPID members References Joseph CA, Noah ND. Epidemiology of chickenpox in England and Wales, 1967-85. BMJ 1988; 296: 673-676. Centers for Disease Control. Varicella-zoster immune globulin for the prevention of chickenpox. MMWR Morb Mortal Wkly Rep 1984; 33: 84-90. Chant KG, Sullivan EA, Burgess MA, et al. Varicella-zoster virus infection in Australia. Aust N Z J Public Health 1998; 22: 413-418. Gilbert GL. Chickenpox during pregnancy. BMJ 1993; 306: 1079-1080. Nathwani D, Maclean A, Conway S, Carrington D. Varicella infections in pregnancy and the newborn. A review prepared for the UK Advisory Group on Chickenpox on behalf of the British Society for the Study of Infection. J Infect 1998; 36 Suppl 1: 59-71. Smego RA Jr, Asperilla MO. Use of acyclovir for varicella pneumonia during pregnancy. Obstet Gynecol 1991; 78: 1112-1116. Brunell PA, Ross A, Miller LH, Kuo B. Prevention of varicella by zoster immune globulin. N Engl J Med 1996; 280: 1191-1194. Gershon AA. Prevention and treatment of varicella zoster virus infection. Pediatr Infect Dis J 1984; 3 (Suppl): 34-36. Bose B, Kerr M, Brookes E. Varicella zoster immunoglobulin to prevent neonatal chickenpox. Lancet 1986; 1: 449-450. Lin TY, Huang YC, Ning HC, Hsueh C. Oral acyclovir prophylaxis after intimate contact. Pediatr Infect Disease J 1997; 16: 1162-1165. Balfour HH Jr, Rotbart HA, Feldman S, et al. Aciclovir treatment of varicella in otherwise healthy adolescents. The Collaborative Aciclovir Varicella Study Group. J Pediatr 1992; 120: 627-633. Azano Y, Yoshikawa T, Suga S, et al. Postexposure prophylaxis of varicella in family contact by oral acyclovir. Pediatrics 1993; 92: 219-222. Andrews EB, Yankasksas BC, Cordero JF, et al. Aciclovir in pregnancy registry: 6 years' experience. The Acyclovir in Pregnancy Registry Advisory Committee. Obstet Gynecol 1992; 79: 7-13. US Department of Health and Human Services. Prevention of Varicella: Recommendations of the Advisory Committee on Immunisation Practices. MMWR Morb Mortal Wkly Rep 1996; 45 (RR-11): i-36. American Academy of Pediatrics. Varicella-zoster infection. In: Peter G, editor. 2000 Red Book: Report of the Committee of Infectious Diseases, 25th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2000: 624-638. Grayson ML, Newton-John H. Smoking and varicella pneumonia. J Infect 1988; 16: 312. Rice P, Simmons K, Carr R, Banatvala J. Near fatal chickenpox during prednisolone treatment. BMJ 1994; 309: 1069-1070. Balfour HH. Intravenous acyclovir therapy for varicella in immunocompromised children. J Pediatr 1984; 104: 134. Haake DA, Zakowski PC, Haake DL, Bryson YJ. Early treatment with acyclovir for varicella pneumonia in otherwise healthy adults. Rev Infect Dis 1990; 12: 788-797. Feldman S, Hughes WT, Daniels CB. Varicella in children with cancer: 77 cases. Pediatrics 1975; 56: 388-397. Reiches NA, Jones JF. Steroids and varicella. Pediatrics 1993; 92: 288-289. La Foret, Lynch LL. Multiple congenital defects following maternal varicella. N Engl J Med 1947; 236: 534-537. Scharf A, Scerr O, Enders G, Helftenbein E. Virus detection in the fetal tissue of a premature delivery with congenital varicella syndrome. A case report. J Perinat Med 1990; 18: 317-322. Enders G, Miller E, Cradock-Watson J, et al. Consequences of varicella and herpes zoster in pregnancy: prospective study of 1739 cases. Lancet 1994; 343: 1548-1551. Pastuszak A, Levy M, Schick B, et al. Outcome after maternal varicella infection in the first 20 weeks of pregnancy. N Engl J Med 1994; 330: 901-905. Mouly F, Mirlesse V, Meritet J, et al. Prenatal diagnosis of fetal varicella zoster virus infection with polymerase chain reaction of amniotic fluid in 107 cases. Am J Obstet Gynecol 1997; 177: 894-898. Forrest JM, Mego S, Burgess MA. Congenital and neonatal varicella in Australia. J Paediatr Child Health 2000; 36: 108-113. Higa K, Dan K, Manabe H. Varicella-zoster virus infections during pregnancy: hypothesis concerning the mechanisms of congenital malformations. Obstet Gynecol 1987; 69: 214-222. Birthistle K, Carrington D. Fetal varicella syndrome -- a reappraisal of the literature. A review prepared for the UK Advisory Group on Chickenpox on behalf of the British Society for the Study of Infection. J Infect 1998; 36 Suppl 1: 25-29. De Nicola LK, Hanshaw JB. Congenital and neonatal varicella. J Pediatr 1979; 94: 175-176. Erlich RM, Turner JAP, Clarke M. Neonatal varicella. J Pediatr 1958; 53: 139-147. Miller E, Cradock-Watson JE, Ridehalgh MKS. Outcome of newborn babies given anti-varicella zoster immunoglobulin after perinatal maternal infection with varicella zoster virus. Lancet 1989; 2: 371-373. Hanngren K, Grandien M, Granstrom G. Effect of zoster immunoglobulin for varicella prophylaxis in the newborn. Scand J Infect Dis 1985; 17: 343-347. Rubin L. Disseminated varicella in the neonate and implications for immunoprophylaxis in neonates exposed to varicella. Pediatr Infect Dis J 1986; 56: 100-102. Australian Technical Advisory Group on Immunisation, Commonwealth Department of Health and Aged Care. The Australian immunisation handbook. 7th edition. Canberra: NHMRC/AGPS, 2000: 231-238. Reynolds L, Struik S, Nadel S. Neonatal varicella: varicella zoster immunoglobulin (VZIG) does not prevent disease. Arch Dis Child Fetal Neonatal Ed 1999; 81: F69-F70. Linder N, Waintraub I, Smetana Z, et al. Placental transfer and decay of varicella-zoster virus antibodies in preterm infants. J Pediatr 2000; 137: 85-89. Conway SP, Dear PRF, Smith I. Immunoglobulin profile of the preterm baby. Arch Dis Child 1985; 60: 208-212. Wang E, Prober C, Arvin A. Varicella zoster virus antibody titres before and after administration of zoster immune globulin to neonates in an intensive care nursery. J Pediatr 1985; 103: 113-114. National Health and Medical Research Council. How to use the evidence: assessment and application of scientific evidence. Table 1.3. <http://www.health.gov.au/nhmrc/publicat/pdf/cp69.pdf> (accessed February 2001). Authors' details King George V Hospital, Sydney, NSW. Anne-Marie Heuchan, MB, MRCP, Fellow in Neonatal Medicine. The Children's Hospital at Westmead, Sydney, NSW. David Isaacs, MD, FRACP, FRCPCH, Paediatric Infectious Diseases Physician; and Clinical Professor, University of Sydney. Reprints will not be available from the authors. Correspondence: Professor D Isaacs, Department of Immunology and Infectious Diseases, The Children's Hospital at Westmead, PO Box 4001, Westmead, NSW 2145. davidiATchw.edu.au Make a comment 1: Management of significant exposure* to varicella zoster virus (VZV) during pregnacy (Algorithm 1) *Significant exposure is defined as living in the same household as a person with active chickenpox or herpes zoster or face-to-face contact with a person with chickenpox or zoster for at least 5 minutes. Risk factors for severe maternal VZV infection are second half of pregnancy, underlying lung disease, immunocompromised, and smoker. See Box 3 for dosage of zoster immunoglobulin (ZIG) and aciclovir. Recommendations based on consensus view. Back to text 2: Management of chickenpox in pregnancy (Algorithm 2) *Complications: respiratory symptoms, haemorrhagic rash, persistent fever >6 days, and new lesions developing >6 days. At high risk are those women in the second half of pregnancy with underlying lung disease, who are immunocompromised, and who smoke. See Box 3 for doses of aciclovir. Recommendations based on consensus view. Back to text 3: Administration and dosage of zoster immunoglobulin (ZIG) and aciclovir Zoster immunoglobulin High-titre ZIG is available from the Red Cross Blood Transfusion Service in Australia on a restricted basis for the prevention of VZV infection in high-risk subjects. Each vial contains 2mL (16% solution of gammaglobulin fraction of human plasma from donors with high titre of varicella antibodies + thiomersal 0.01% w/v). The recommended dose is 2mL for children 0-5 years, 4mL for children 6-12 years and 6mL for adults.32 Administration is by intramuscular injection, with few adverse effects other than local discomfort reported. This can be lessened if the ZIG is at room temperature when administered. ZIG should never be given intravenously.36 Aciclovir Aciclovir appears to be a safe and relatively well tolerated drug, although it may impair renal function if given to patients who are not adequately hydrated.17 It is not licensed for use in pregnancy but appears to be safe12 and its use is indicated in the high-risk situations outlined. The recommended intravenous dose for treating VZV infection in adults and infants is 10-20mg/kg every 8 hours. The oral dose for adults is 800mg five times daily. The use of oral aciclovir in neonates is not recommended. Back to text
on behalf of the Australasian Subgroup in Paediatric Infectious Diseases of the Australasian Society for Infectious
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