Issues

Volume 172 Issue 11

5 June 2000

Editorials Evaluating policy and practice: what are the effects of early hospital discharge after childbirth? Judith M Lumley (MJA 2000; 172: 524-525)Medical research in Australia: into the new millennium John W Funder (MJA 2000; 172: 525-526)ARDS: nothing new? Andrew D Bersten, Ian R Doyle (MJA 2000; 172: 527-528)Cancer in the family: risks and management Judy Kirk, Richard Kefford (MJA 2000; 172: 529-530) Research Early discharge and postnatal depression: a prospective cohort study Jane F Thompson, Christine L Roberts, Marian J Currie, David A Ellwood (MJA 2000; 172: 532-536)Management of gestational diabetes with a conservative insulin protocol Richard W Simpson, Shanne J Kast (MJA 2000; 172: 537-540) Public Health Making a difference to socioeconomic determinants of health in Australia: a research and development strategy Jane M Dixon, Robert M Douglas, Richard M Eckersley (MJA 2000; 172: 541-544) Medicine and the Law Determining the validity of advance directives Paul Biegler, Cameron Stewart, Julian Savulescu, Loane Skene (MJA 2000; 172: 545-548) Viewpoint Active and passive cigarette smoking and breast cancer: is a real risk emerging? Robert C Burton, Nabil Sulaiman (MJA 2000; 172: 550-552) Lessons From Practice Back pain in an elderly man -- more than just a fall Eric B K Wong (MJA 2000; 172: 554-555) MJA Practice Essentials -- Neurology Multiple sclerosis Michael P Pender (MJA 2000; 172: 556-562)

Editorials

Mental health 5 June 2000 Free

Evaluating policy and practice: what are the effects of early hospital discharge after childbirth?

Editorial Evaluating policy and practice: what are the effects of early hospital discharge after childbirth? Large, specific, randomised trials are the only way to answer this question MJA 2000; 172: 524-525 Two years ago the Journal published an article which described early hospital discharge after birth as a major risk factor for postnatal depression.1 There was also a strongly worded editorial supporting that conclusion.2 In this issue the message is reversed, with the finding by Thompson and colleagues that there is no evidence of increased risk.3 This is no trivial disagreement. A quarter of a million women give birth in Australia each year, virtually all of them spending less time in hospital than their mothers did, with close to 40% having an "early discharge" by the definition used in both articles (within 72 hours of birth).4Depression is a distressing and disabling condition for those directly affected, and particularly so in women with a new baby, who have just taken on a 24-hour-a-day, seven-day-a-week job. The effects of maternal depression may flow on to other vulnerable family members. Doctors and midwives, hospitals, policymakers and the general public need to know whether early discharge is safe or not. One problem in answering this question is the paucity of evidence from randomised trials on length of hospital stay after childbirth. Not only are there relatively few trials, but those that have been published have rarely measured maternal health outcomes such as depression, breastfeeding duration, confidence, or breastfeeding problems. The limited evidence from trials shows either no difference in depression between women discharged early and late, or a lower proportion of women becoming depressed after early discharge.5,6 The article by Thompson and colleagues3 is the third Australian population-based study which has shown no relationship between early discharge and depression after birth.7-10 All three of these studies were large enough to detect a twofold increase in the odds of becoming depressed after early discharge, as was found in the Nepean hospital-based study published in the Journal two years ago.1 All three, and the Nepean study, used the Edinburgh Postnatal Depression Scale (EPDS) with the same cut point of a score of more than 12 for probable depression, though the Victorian studies measured the point prevalence with a single score of more than 12 at six or eight months after birth, the ACT group measured the period prevalence from eight through 16 and 24 weeks, and the Nepean group required two or more scores over 12, from six, through 12, 18 and 24 weeks, confirmed by a structured clinical interview to measure the period prevalence of major depression. The difference in findings between the Nepean study and the other three studies is surprising. Thompson and colleagues suggest that an important contributing factor might be the routine provision of a postnatal visit from a midwife and more practical help at home in the ACT than at Nepean.3 However, this was not the case in the 1993/94 Victorian Survey of Recent Mothers, which found that only 66% of women who went home within 48 hours of birth, and only 27% of those going home on the third or fourth day, had a home visit from a midwife8 -- findings much closer to those of the Nepean study. It is also unlikely that temporal factors explain the discrepancy in findings, as the Victorian survey took place at a very similar time to the Nepean study. Public knowledge and expectations about postnatal stay would have been similar in both study populations. In interpreting non-experimental descriptive and observational studies, the key problem is selection bias -- in what ways do women who leave hospital early differ from those who stay longer, and are these differences in themselves factors which have a bearing on women's chances of becoming depressed in the following months? Predictable factors associated with shorter postnatal stays include maternal age less than 25 years, multiparity, unassisted birth, birth at term, low medical risk, birth centre care, and not having private health insurance. Psychological predictors of depression were measured in both the ACT and Nepean studies; they were not significantly associated with length of stay. The six vignettes in the Box describe some groups of women who will be over-represented (A, C, D, E) and under-represented (B, F) among new mothers going home early, despite having uncomplicated vaginal births at term. Young women are often over-represented in group D8 and women from diverse overseas backgrounds in group E.11 As all these women "chose" their length of stay, these vignettes draw attention to problems with the notion of "choice" as a key determinant. Some choices are constrained by factors outside the woman's control, especially social isolation and absence of a partner or other social support, which are common associations of depression at this life stage. We also know that women are not necessarily free to choose their length of stay, as almost a quarter of those discharged early in both the ACT study,3 and in Victoria,8,9 thought their stay had been too short. The vignettes also remind us that the relative proportions of women from groups A, C and E in study populations could easily contribute to, or even explain, the differing associations between length of stay and subsequent depression reported from different studies. Given the inevitability of such selection biases, which are impossible to adjust for, if we really want to know whether shortening postnatal stay is safe and cost-effective, or whether domiciliary midwifery or other postnatal support improves outcomes for mothers and babies, there is no alternative but to test these policies in randomised trials. Judith M Lumley Director Centre for the Study of Mothers' and Children's Health La Trobe University, Melbourne, VIC Hickey AR, Boyce PM, Ellwood D, Morris-Yates AD. Early discharge and risk of postnatal depression. Med J Aust 1997; 167: 244-247. Buist A. Counting the costs of early discharge after childbirth. Med J Aust 1997; 167: 236-237. Thompson JF, Roberts CL, Currie MJ, Ellwood DA. Early discharge and postnatal depression: a prospective cohort study. Med J Aust 2000; 172: 532-536. Day P, Sullivan EA, Ford J, Lancaster P. Australia's Mothers and Babies 1997. (Perinatal Statistical Series No. 9). Sydney: AIHW National Perinatal Statistics Unit, 1997. (AIHW Cat. No. PER 12.) Waldenström U. Early and late discharge after hospital birth: fatigue and emotional reactions in the postpartum period. J Psychosom Obstet Gynaecol 1988; 8: 127-135. Carty EM, Bradley CF. A randomized, controlled evaluation of early postpartum hospital discharge. Birth 1990; 17: 199-204. Small R, Lumley J, Brown S. To stay or not to stay: are fears about shorter lengths of stay justified? Midwifery 1992; 8: 170-177. Brown S, Lumley J, Small R. Reasons to stay, reasons to go. Victorian women talk about early discharge. Melbourne: Centre for the Study of Mothers' and Children's Health, 1995: 27-54. Brown S, Lumley J. Reasons to stay, reasons to go: results of an Australian population-based survey. Birth 1997; 24: 148-158. Brown S, Lumley J, Small R. Early obstetric discharge: does it make a difference to health outcomes? Paediatr Perinat Epidemiol 1998; 12: 49-71. Yelland J, Small R, Lumley J, et al. Support, sensitivity, satisfaction: Filipino, Turkish and Vietnamese women's experiences of postnatal hospital stay. Midwifery 1998; 14: 144-154. Make a comment Examples of scenarios in which women select different lengths of stay Group Description Length of stay Maternal health outcomes A Healthy mother, healthy baby, good or excellent family support Chooses to go home at 24-48 hours to be with her family in a restful atmosphere and establish breastfeeding Likely to be good B Healthy mother, healthy baby, good or excellent family support Chooses to stay in hospital for 5 or more days to establish breastfeeding, recover from the birth and have a good rest Likely to be good C Mother with major responsibilities at home and little or no family support Goes home as soon as she can ? D Mother who dislikes life in hospital Leaves as soon as she can, even despite strong advice to stay ? E Mother who does not find the hospital able to provide her with enough support and is unable to get enough rest there Leaves much earlier than she had planned to Possibly poor F Mother who has had a long, exhausting labour; baby who is difficult to feed; slow establishment of breastfeeding; mother loses self-confidence Stays much longer than she had planned to Possibly poor Back to text

Judith M Lumley

Genetics 5 June 2000 Free

Cancer in the family: risks and management

Editorial Cancer in the family: risks and management A recent NHMRC publication addresses the clinical implications of cancer genetics for Australian families MJA 2000; 172: 529-530 A family history of cancer is widely recognised as an important risk factor for common cancers, with 5%-10% of cancers considered attributable to genetic predisposition. A recent National Health and Medical Research Council (NHMRC) publication for health professionals, Familial aspects of cancer: a guide to clinical practice,1 addresses the clinical implications of cancer genetics. Why do we need such a guide, and what does it cover? Cancer genetics Knowledge of the genetic basis of cancer has increased dramatically in the past decade. It is now clear that cancers evolve in Darwinian fashion, exploiting mutations in genes that regulate cellular growth, death and differentiation. The cumulative acquisition of defects in a number of these genes facilitates the progressive selection of cells towards a highly malignant and uncontrolled state of cellular proliferation and immortality. In the majority of cancers, these mutations are acquired in particular cells over a lifetime (somatic mutations). There are, however, families displaying clear inherited predisposition to certain common cancers, including breast, ovarian, colorectal and prostate cancer and melanoma. The affected members of these families carry an inherited (germline) mutation in one of their "cellular fitness" genes. Germline mutations affect all body cells, but give certain tissues a genetic head start down the cascade of genetic errors that results in cancer. Genes prone to such inherited abnormalities are called "cancer susceptibility" genes. The individuals carrying mutations in these genes often carry a very high lifetime chance (> 50%) of developing cancer. Implications for clinical practice The improved ability to detect individuals at high risk of cancer through analysis of family history and/or genetic testing has fortunately been accompanied by major advances in screening, surveillance and prevention. The clinical usefulness of such advances is exemplified in the management of familial adenomatous polyposis (FAP), a condition caused by a dominantly inherited mutation in the adenomatous polyposis coli (APC) gene. Individuals with FAP develop hundreds of adenomatous polyps, of which one or more may, if untreated, become malignant, often at an early age. Until recently, all at-risk individuals required regular screening sigmoidoscopy from the early teenage years. Now, after being genetically tested, only those family members found to carry the mutation need to undergo intensive cancer screening and eventually prophylactic colectomy.2 Similarly, genetic testing for hereditary non-polyposis colorectal cancer has proved to be acceptable to families, and may reduce the cost of unnecessary screening colonoscopy in those family members found not to carry a mutation.3Familial cancer clinics have now been set up in response to the growing public and professional awareness of family history as a risk factor for cancer. These clinics provide pedigree analysis, risk assessment and advice to those at high risk of cancer, and may also carry out genetic testing (if appropriate) in association with genetic counselling. The NHMRC document1 stratifies risk categories for people with a family history of diseases such as breast and colorectal cancer. It identifies those who may benefit from referral to familial cancer clinics and the role of general practitioners and specialists in managing high risk families. In the context of a detailed ethical discussion, an attempt is made to designate those who may benefit from genetic testing (see Box). Why national guidelines? A coordinated national policy on cancer genetics has arisen in response to a number of factors: In recent years there has been heightened public awareness of the problem and increased demand for access to familial cancer services from those at perceived risk of cancer. (At the Familial Cancer Service at Westmead Hospital, for example, referrals, carefully screened for adherence to eligibility criteria, increased from 120 new families in 1996 to almost 300 in 1999); Health authorities have understandable concerns about the potential for proliferation of unregulated, unevaluated genetic testing facilities for cancer, as has occurred in the United States, and the need for public education and guidance in this area; Scientists face considerable challenges in assuring quality for complex, new and constantly evolving diagnostic tests, overcoming difficulties in resource management, and ensuring the timely and appropriate translation of relevant technologies from a research to a diagnostic environment. While similar documents have been produced by other international groups,4-7 these issues need to be addressed in a manner relevant to the Australian population. Guidelines based on US data for breast cancer, for example, may be quite inappropriate for Australia, and specific mutations in melanoma susceptibility genes may be more highly penetrant under the influence of Australian sunlight.8,9 In 1995 the Australian Cancer Network (ACN), in joint sponsorship with the NHMRC National Breast Cancer Centre (NBCC) and the Human Genetics Society of Australasia, convened the ACN Cancer Genetics Working Party to draft national guidelines for clinical practice. The current guidelines are the culmination of an extensive consultation and collaboration process. The future In such a rapidly changing field, future refinements of the guidelines will depend on the availability of high quality Australian data from national epidemiological studies. These studies will provide information on the frequency and penetrance of mutations in cancer susceptibility genes in the Australian population and the effect of local environmental factors on those mutations. A welcome spin-off of the endeavour to compile this guide has been the unification of diverse research interests throughout Australia in well organised, comprehensive consortia investigating the cancer genetics of breast cancer, melanoma and colorectal cancer.* In parallel with these exciting developments in research, we need to improve the accessibility of such information to general practitioners.10 The NBCC and the ACN have already moved toward the provision of more succinct information for GPs with their publications Current best advice about familial aspects of breast cancer11 (under current revision to incorporate familial ovarian cancer) and Advice about familial aspects of bowel cancer: a guide for general practitioners (ACN, in preparation). Consumer information has been developed to accompany these documents. The National Cancer Control Institute is also fostering a national approach to education and data management for families with a genetic predisposition to malignancy. The energy, goodwill and collaborative spirit associated with the preparation of these new guidelines provide a strong basis for the ongoing care of cancer families in Australia. Judy Kirk Senior Staff Specialist Familial Cancer Service and Westmead Institute for Cancer Research Westmead Hospital, Westmead, NSW Richard Kefford Professor of Medicine, Westmead Institute for Cancer Research Westmead Hospital, Westmead, NSW *Breast cancer: The Kathleen Cuningham Consortium for Research on Familial Breast Cancer (kConFab) research project (see <http://www.pmci.unimelb. edu.au/kconfab>), led by Joseph Sambrook, and the Australian Breast Cancer Family Study, led by John Hopper (j.hopperATgpph.unimelb.edu.au). Colorectal cancer: The Australasian Colorectal Cancer Study, led by Jeremy Jass (j.jassATmailbox.uq.edu.au). Melanoma: The Australian Melanoma Family Study, led by Graham Mann (gmannATmail.usyd.edu.au) National Health and Medical Research Council. Familial aspects of cancer: a guide to clinical practice. Endorsed Nov 1999. Available at: <http://www.nhmrc.health.gov.au/publicat/cp-home.htm>. Accessed 2 May 2000. (Catalogue No. 993839X.) Gardner M, St John J. Gene testing and genetic counselling in familial polyposis. Med J Aust 1995; 162: 457. Stanley AJ, Gaff CL, Attomaki AK, et al. Value of predictive genetic testing in management of hereditary non-polyposis colorectal cancer (HNPCC). Med J Aust 2000; 172: 313-316. Burke W, Daly M, Garber J, et al. Recommendations for follow-up care of individuals with an inherited predisposition to cancer. II. BRCA1 and BRCA2. Cancer Genetics Studies Consortium. JAMA 1997; 277: 997-1003. Burke W, Petersen G, Lynch P, et al. Recommendations for follow-up care of individuals with an inherited predisposition to cancer. I. Hereditary nonpolyposis colon cancer. Cancer Genetics Studies Consortium. JAMA 1997; 277: 915-919. Eisinger F, Alby N, Bremond A, et al. Recommendations for medical management of hereditary breast and ovarian cancer: the French National Ad Hoc Committee. Ann Oncol 1998; 9: 939-950. Kefford RF, Newton Bishop JA, Bergman W, Tucker MA. Counseling and DNA testing for individuals perceived to be genetically predisposed to melanoma: a consensus statement of the Melanoma Genetics Consortium. J Clin Oncol 1999; 17: 3245-3251. Cannon-Albright LA, Meyer LJ, Goldgar DE, et al. Penetrance and expressivity of the chromosome 9p melanoma susceptibility locus (MLM). Cancer Res 1994; 54: 6041-6044. Bishop JA, Wachsmuth RC, Harland M, et al. Genotype/phenotype and penetrance studies in melanoma families with germline CDKN2A mutations. J Invest Dermatol 2000; 114: 28-33. Gupta L, Ward JE, Hayward RS. Clinical practice guidelines in general practice: a national survey of recall, attitudes and impact. Med J Aust 1997; 166: 69-72. National Breast Cancer Centre. Current best advice about familial aspects of breast cancer. Sydney: NBCC, 1997. Available at: <http://www.nbcc.org.au/ pages/info/resource/nbccpubs/advice.htm>. Accessed 2 May 2000. Make a comment Familial aspects of cancer: a guide to clinical practice New NHMRC guidelines1 address the following key issues: Importance of an accurate, extended family history in assessing cancer risk Identification of rare families with a genetic predisposition to one of the common malignancies (eg, breast, ovarian, colorectal or prostate cancer, or melanoma) Role of familial cancer clinics in the management of families at risk Evolving role of genetic testing in risk assessment Requirement for genetic counselling in association with genetic testing Ethical issues relating to genetic counselling and testing for cancer predisposition Management, screening and cancer prevention for individuals found to be at high risk or potentially high risk of developing cancer Continued need for national collaborative research in this field Back to text

Judy Kirk · Richard Kefford

Research

Mental health 5 June 2000 Free

Early discharge and postnatal depression: a prospective cohort study

Research Early discharge and postnatal depression: a prospective cohort study Jane F Thompson, Christine L Roberts, Marian J Currie and David A Ellwood MJA 2000; 172: 532-536 For editorial comment see Lumley Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' Details - - More articles on Psychiatry Abstract Objectives: To determine whether women discharged from hospital ≤ 72 hours after childbirth (early discharge) were at greater risk of developing symptoms of postnatal depression during the following six months than those discharged later (late discharge), their reasons for early discharge and their level of postnatal support. Design and setting: Population-based, prospective cohort study with questionnaires at Day 4, and at 8, 16 and 24 weeks postpartum, conducted at all birth sites in the Australian Capital Territory (ACT). Participants: Women resident in the ACT giving birth to a live baby from March to October 1997. Main outcome measure: A score > 12 on the Edinburgh Postnatal Depression Scale (EPDS). Results: 1295 (70%) women consented to participate; 1193 (92%) were retained in the study to 24 weeks and, of these, 1182 returned all four questionnaires. Of the 1266 women for whom length-of-stay data were available, 467 (37%) were discharged early and 799 (63%) were discharged late. There were no significant differences between the proportion of women discharged early who ever scored > 12 on the EPDS during the six postpartum months and those discharged late (17% v. 20%), even after controlling for other risk factors (adjusted OR, 0.67; 95% CI, 0.44-1.01). Of women discharged early, 93% had at least one postnatal visit at home from a midwife and 81% were "very satisfied" with the care provided. Most women (96%) reported they had someone to help in practical ways. Conclusions: Women discharged early after childbirth do not have an increased risk of developing symptoms of postnatal depression during the following six months. In Australia, and internationally, the length of time spent in hospital following childbirth has been steadily decreasing since the early 1980s. This has prompted concern about the consequences of early discharge for both mothers and babies.1,2 Postnatal depression (PND) is a common disorder with long-term consequences for both mother and infant.3,4 It has been associated with psychosocial and obstetric factors3,5-7 and possibly dissatisfaction with length of stay.8,9 The association with early discharge is not clear. A small randomised controlled trial of early discharge from Sweden10 reported no difference in depression, while in a similar Canadian study women discharged early were less likely to be depressed.11 In observational studies, women discharged early have been reported to be either equally8,9,12,13 or less likely14,15 to be depressed. A recent Australian study reported an increased risk of PND in women discharged early.16 However, this study made no detailed assessment of support available to women, a factor that may be critical to emotional wellbeing of new mothers.17Here, we aimed to investigate whether early discharge following childbirth was associated with an increased risk of PND, why women elect early discharge, and to examine the social support available to women after discharge from hospital. Methods Participants This population-based, prospective cohort study included women resident in the ACT, planning to reside there for at least six months, aged ≥ 16 years, who gave birth to a live baby between March and October 1997 in any of the ACT's two public hospitals (one included a birth centre), two private hospitals, or at home. Women were excluded if their baby was admitted to the neonatal intensive care unit or adopted, if critically ill themselves, unable to give informed consent or complete the questionnaires for other reasons, or participating in another study. Participants were compared with all women who gave birth in the ACT during 1997 using data from the ACT Maternal and Perinatal Data Collection.18 Procedure The study was approved by the ACT Department of Health & Community Care Research Ethics Committee, and the ethics committees of participating hospitals. Postnatal ward or domiciliary midwives gave information sheets to women in the first few days after giving birth. Participants gave written informed consent when completing the first questionnaire as close to Day 4 as possible. They were then mailed questionnaires at eight, 16, and 24 weeks postpartum. Questionnaires The first questionnaire covered sociodemographic characteristics of mother and partner, a nine-item personality scale identifying "vulnerable" and "resilient" personality dimensions;16 a maternity "blues" questionnaire;19 a subset of four items from the Medical Outcomes Study Social Support Scale;20 questions about availability of and satisfaction with practical support, emotional support from partner, and a single summary question assessing global satisfaction with partner scored on a five-point Likert scale. Three questions asked about the nature of women's past relationship with their parents in relation to warmth/care, overprotection/controlling and independent decision making, with responses on a four-point scale. Questions were also included about the mother's history of depression (at any time as well as during or after a pregnancy) and whether the infant was breastfed. In the second questionnaire, women were asked to indicate whether any of a list of 30 possible reasons for their actual length of stay applied to them and whether they thought their length of stay was too long, about right or too short. The third questionnaire included questions about the number of and satisfaction with domiciliary visits. Satisfaction was measured by quality of care, accessibility and convenience,21 and a single summary question assessing overall satisfaction with care. Postnatal depression Postnatal depression was assessed at eight, 16 and 24 weeks using the 10-item Edinburgh Postnatal Depression Scale (EPDS), a self-report measure of depression developed for use in the postpartum period.22-24 Women scoring above 12 are likely to be suffering from a depressive illness. Length of stay For comparability with previous Australian research,16 and in keeping with ACT definitions, early discharge was defined as discharge up to 72 hours after giving birth, and late discharge as more than 72 hours after giving birth. Power of study A sample size of 944 is sufficient to detect with 95% confidence and 80% power an increase in prevalence of PND in the early discharge group at eight, 16 or 24 weeks from 7% to 14%,16 assuming 30% are discharged early and an overall attrition rate of 25%. To allow for variations in these assumptions, we set a target sample size of 1200 women. Statistical analyses The prevalences of EPDS scores greater than 12 were compared between women discharged early and late by means of contingency tables and unconditional logistic regression. We used logistic regression to assess the effect of previously identified risk factors on the association between early discharge and high EPDS scores. Six separate models were fitted for women ever scoring > 12 during the six postpartum months; for those who scored > 12 at eight weeks, 16 weeks or 24 weeks; and for women who scored > 12 on either two occasions or all three occasions. Results are expressed as crude and adjusted odds ratios (OR) with 95% confidence intervals. Results Study population Of 1961 ACT residents asked to participate in the study, 105 were ineligible and 1295 (70%) of the remainder agreed to participate. After 24 weeks, 1193 (92%) remained in the study. Of the 1295 who agreed to participate, 869 (67%) gave birth in a public hospital, 411 (32%) in a private hospital, and 15 (1%) at home, of whom six were transferred to hospital. Compared with all women who gave birth in 1997, participants were slightly older, more likely to be married or in a defacto relationship, to have given birth in a private hospital, and to have been discharged late (Box 1). The 102 (8%) who were lost to follow-up differed from those who remained in that they were significantly (P ≤ 0.001) more likely to be aged < 25 years (32% v. 12%), unmarried (14% v. 4%), born in a non-English-speaking country (19% v. 9%), and public patients (74% v. 56%). They were not significantly more likely to be in the early discharge group (46% v. 36%), but were significantly (P ≤ 0.001) less likely to be in paid employment in the previous 12 months (56% v. 74%), to have a paid position to resume after maternity leave (43% v. 63%) and to have been educated beyond Year 11 (60% v. 82%). They did not differ with respect to the following factors known to be associated with PND: vulnerable personality, level of social support, past history of depression, dissatisfaction with relationship with partner, or dissatisfaction with past relationship with mother. Length of stay After excluding the nine women who gave birth at home and were not transferred to hospital, and the 20 with missing data, there were length-of-stay data for 1266 (98%) women, 467 (37%) with early and 799 (63%) with late discharge. The early discharge group was significantly (P ≤ 0.001) more likely to be aged < 25 years (21% v. 10%), public patients (80% v. 44%) or to have delivered in a public hospital (94% v. 52%), multiparous (61% v. 54%), and to have given birth at > 39 weeks' gestation (85% v. 75%). Women discharged early were also significantly (P ≤ 0.001) more likely to have had a spontaneous onset of labour (74% v. 55%), an unassisted vaginal birth (90% v. 56%) and to formula-feed their infant from birth (10% v. 5%). They were significantly (P ≤ 0.001) less likely to have been in paid employment in the past 12 months (68% v. 76%), to have a paid position to resume (55% v. 66%) and to have been educated beyond Year 11 (74% v. 84%). They were significantly (P ≤ 0.001) less likely to rate their length of stay as "about right" than women discharged late (72% v. 82%), and more likely to rate their length of stay as "too short" (23% v. 8%). There were no statistically significant differences in vulnerable personality (17% v. 16%), level of social support (median score, 7 for both groups), past history of depression (29% v. 29%), maternity blues score (median score, 4 v. 5), dissatisfaction with partner (8% v. 6%), and past relationship with mother (not warm/caring, 6% v. 5%; overprotective/controlling, 52% v. 52%; did not encourage independent decision-making, 20% v. 21%). Postnatal depression Of the 1252 (97%) women with complete data at eight weeks postpartum, 129 (10%) scored > 12 on the EPDS. At 16 weeks, 91 of 1219 (8%) and at 24 weeks 90 of 1187 (8%) scored > 12. The cumulative incidence of an EPDS score > 12 over the six months of follow-up was 224/1295 (17%). Among women with complete data, 37/1172 (3%) had EPDS scores > 12 on two occasions and 23/1172 (2%) on all three occasions. Length of stay and postnatal depression Women discharged early were not more likely to ever score > 12 on the EPDS during the six months of follow-up than women discharged late: 72/429 (17%) compared with 150/751 (20%). The association between length of postnatal stay and PND symptoms remained statistically non-significant after adjusting for other risk factors (Box 2). This finding was robust for other outcome measures (Box 3). For all outcomes there was a consistent trend towards a reduced risk of PND symptoms for women discharged early. Reasons for choosing early discharge Reasons were given by 447 women (96%). The most common reason was a preference to be at home with their partner or family (74%). Other reasons were feeling confident with their baby and preferring to be at home (73%); so the father could be more involved in baby care (47%); being unhappy in hospital and unable to sleep or rest (41%); greater privacy (41%); to rest or recover after the birth (40%); not liking hospitals (34%); to establish breastfeeding (33%); and to have time to focus on the baby (32%). Of the women discharged early, 15% said they did not feel they had a choice about length of stay, and 14% felt under pressure from midwives to leave early. Women discharged early who felt they had no choice about length of stay were not significantly more likely to ever score > 12 on the EPDS (17% v. 17%), and neither were those who felt pressured to leave early (21% v. 16%; P = 0.4). Early discharge and postnatal support All women discharged within three days were eligible for home visits from midwives. Data were available on the number and nature of these visits for 432 women discharged early (93%). Of these, 404 (94%) had at least one visit, and 176 (41%) were visited up to Day 7. The maximum number of visits in the first seven days was 12, and 107 women (27%) were visited at least once after seven days. Eighty-eight per cent of the women thought the number of visits was "just right", while 8% thought it "not enough" and 4% "too many". Overall, 81% of these women said they were "very satisfied" with the care provided at home, 15% "satisfied in some ways but not in others" and 4% "very dissatisfied". Some women discharged after 72 hours were also eligible for and received home visits. The participating public hospitals' policy was for home visiting to be available up to Day 3, but sometimes this extended beyond 72 hours depending on the time of birth. Home visits were also available in cases of special need, and community-based maternal and child health nurses and midwives also offer some home visiting. Of the women discharged late, 364 (47%) received at least one visit at home from a midwife. In addition to support provided by health professionals, 96% of women discharged early reported that they had someone to help in practical ways in the first eight weeks postpartum. For 92% this was a partner, and for 47% their mother. Other family members (22%), friends (20%) and mothers-in-law (19%) were the next most common sources of help. The help received was satisfactory for 90% of the respondents; however, 23% said that they would like to know more people who could be asked for help. There were no statistically significant differences between women discharged early or late in availability of and satisfaction with practical help. Discussion The postnatal stay has become shorter without being properly evaluated in randomised controlled trials (RCTs). As shorter stays have become standard practice, the window of opportunity for conducting an appropriate RCT may have been lost.25 The best alternatives are prospective studies with heterogeneous samples of sufficient size to detect clinically significant effects of short postnatal stays. We found that women resident in the ACT electing short postnatal stays were not at increased risk for developing symptoms of PND. Our finding is consistent with those from two Victorian surveys,8,13 but differs from that of a study in Sydney which found a significantly increased risk of PND during the first six months in mothers discharged within three days.16 There are several possible explanations for the discrepant results between this study and our own, including differences in the outcome measures, population characteristics, postnatal support and reasons for early discharge. The same assessment tool to identify possible cases was used in the Victorian,8,13 Sydney16 and ACT studies, but in the Sydney study a psychiatric interview was added to confirm the diagnosis of PND. The use of a psychiatric examination is unlikely to explain differences in the results, as high scores on the EPDS coincide closely with diagnoses of PND. A validation study in Australian women found the EPDS to be highly sensitive (100%) and specific (96%), with a positive predictive value of 70%.22 Differences in the characteristics of women discharged early may also contribute to the different outcomes observed. In both the Sydney and the ACT studies, women discharged early were more likely to be multiparous, to have a lower level of education and to formula feed their infants in the first week than women discharged late. However, the women discharged early in the Sydney study16 were more likely than those in our study to report a poor relationship with parents and to have a history of depression; these associations were controlled for in the statistical analyses in the Sydney study and so cannot fully explain their different findings. Low levels of social support have been identified as a risk factor for PND,5 and another possible explanation for the differences in findings is that the two populations differed in the extent, nature of and satisfaction with postnatal support provided to women through early discharge programs and non-professional contacts. The authors of the Sydney study reported that only half of the women who elected early discharge participated in an early discharge program with domiciliary midwifery care.26 In our study, 94% of the women discharged early had had at least one visit from a midwife at home and the level of satisfaction with this care was high. Also, only 4% of women discharged early said they had no one to provide practical support at home. An overwhelming majority reported that their partners assisted them and most were satisfied with the level of help. Early discharge was introduced partly to offer more choices in care in a climate of increasing consumer participation in decisions. However, economic imperatives to increase patient throughput may lead to increasing pressure on women to leave hospital earlier than they would otherwise choose. The Sydney study26 did not report reasons for early discharge. Reasons given by women for leaving ACT hospitals early were generally positive, although 15% felt they did not have a choice and 14% felt pressured to leave (not mutually exclusive reasons). Several things should be considered when interpreting the results of our study. Firstly, as the Sydney study found double the rate of PND after early discharge,16 we formed our null hypothesis (that early discharge makes no difference) in the expectation that it would be disproved. Instead, we found no evidence of a significant difference in the rate of PND; in fact, early discharge tended to a protective effect (but this was not statistically significant). Our study does not prove that there is not an increased rate of PND for early discharge. However, in this population, it is unlikely that the true risk for early discharge was double that for late discharge. Secondly, although only 70% of women approached participated in the study, the characteristics of women who did participate were similar in important respects to those of the source population. However, our findings may not be generalisable to populations with differing PND risk factors or early discharge programs. Lastly, the women in our study selected their length of postnatal stay. Although we have controlled for known determinants, confounding by unknown determinants for PND cannot be excluded. We found that women who selected early discharge from hospital after childbirth and received midwifery support at home, and who were well supported by other family members, were not more likely to experience depressive symptoms in the first six months after childbirth. Very few women in this study were discharged early without home support, so it was not possible to determine whether early discharge without support was associated with an increased risk of PND symptoms. It may be important to ensure that all women discharged early after childbirth, in particular those lacking other sources of support, receive additional help from the healthcare system. What constitutes adequate postnatal support could be examined by RCTs comparing different patterns of home visiting. Acknowledgements This work was supported by a project grant from The Canberra Hospital Private Practice Fund. Additional funding was provided by The Canberra Hospital Auxiliary, the Nurses' Board of the ACT, and the ACT Department of Health & Community Care. The assistance of the midwives in recruiting women for this study is gratefully acknowledged. Robyn Attewell provided statistical advice. We are especially grateful to the women of the ACT who so generously gave their time to complete this study. References Buist AE. Counting the costs of early discharge after childbirth [editorial]. Med J Aust 1997; 167: 236-237. Braveman P, Egerter S, Pearl M, et al. Problems associated with early discharge of newborn infants. Early discharge of newborns and mothers: a critical review of the literature [review]. Pediatrics 1995; 96: 716-726. Boyce PM, Stubbs JM. The importance of postnatal depression. Med J Aust 1994; 161: 471-472. Murray L, Cooper P. Effects of postnatal depression on infant development. Arch Dis Childhood 1997; 77: 99-101. O'Hara MW, Swain AM. Rates and risk of postpartum depression -- a meta-analysis. Int Rev Psychiatry 1996; 8: 37-54. Boyce PM, Todd AL. Increased risk of postnatal depression after emergency caesarean section. Med J Aust 1992; 157: 172-174. Warner R, Appleby L, Whitton A, Faragher B. Demographic and obstetric risk factors for postnatal psychiatric morbidity. Br J Psychiatry 1996; 168: 607-611. Astbury J, Brown S, Lumley J, Small R. Birth events, birth experiences and social differences in postnatal depression. Aust J Public Health 1994; 18: 176-184. Dowswell T, Piercy J, Hirst J, et al. Short postnatal hospital stay: implications for women and service providers. J Public Health Med 1997; 19: 132-136. Waldenström U. Early and late discharge after hospital birth: fatigue and emotional reactions in the postpartum period. J Psychosomatic Obstet Gynaecol 1988; 8: 127-135. Carty EM, Bradley CF. A randomized, controlled evaluation of early postpartum hospital discharge. Birth 1990; 17: 199-204. Beck CT, Reynolds MA, Rutowski P. Maternity blues and postpartum depression. J Obstet Gynecol Neonatal Nurs 1992; 21: 287-293. Brown S, Lumley J, Small R. Early obstetric discharge: does it make a difference to health outcomes? Paediatr Perinat Epidemiol 1998; 12: 49-71. Burnell J, McCarthy M, Chamberlain GVP, et al. Patient preference and postnatal hospital stay. J Obstet Gynaecol 1982; 3: 43-47. James ML, Hudson CN, Gebski VJ, et al. An evaluation of planned early postnatal transfer home with nursing support. Med J Aust 1987; 147: 434-438. Hickey AR, Boyce PM, Ellwood D, Morris-Yates AD. Early discharge and risk for postnatal depression. Med J Aust 1997; 167: 244-247. Barclay KM, Chamberlain ME, Homer CS, Barclay LM. Early discharge and risk for postnatal depression [letter]. Med J Aust 1998; 168: 419-420. Bourne M. Maternal and perinatal status, ACT, 1997 tables. Canberra: Clinical Epidemiology and Health Outcomes Centre, ACT Department of Health & Community Care, 1999. Kennerley H, Gath D. Maternity blues. 1. Detection and measurement by questionnaire. Br J Psychiatry 1989; 155: 356-362. Sherbourne CD, Stewart AL. The MOS social support survey. Soc Sci Med 1991; 32: 705-714. Kenney P, Cameron S, King M, et al. Evaluation of obstetric early discharge: client satisfaction. Centre for Health Economics Research & Evaluation. Discussion Paper Series No 10. 1992. Boyce P, Stubbs J, Todd A. The Edinburgh postnatal depression scale: validation for an Australian sample. Aust N Z J Psychiatry 1993; 27: 472-476. Cox JL, Holden JM, Sagovsky R. Detection of postnatal depression: development of the 10-item Edinburgh Postnatal Depression Scale. Br J Psychiatry 1987; 150: 782-786. Murray L, Carothers AD. The validation of the Edinburgh Postnatal Depression Scale on a community sample. Br J Psychiatry 1990; 157: 288-290. Thompson JF, Roberts CL, Ellwood DA. Early discharge after childbirth: Too late for a randomised trial? Birth 1999; 26: 192-195. Hickey AR, Boyce PM, Morris-Yates AD, Ellwood DA. Early discharge and risk for postnatal depression [letter]. Med J Aust 1998; 168: 420. (Received 7 Oct 1999, accepted 3 Apr 2000) Authors' Details The Canberra Hospital, Garran, ACT. Jane F Thompson, MSc, PhD, Senior Research Officer, Women's & Children's Health. Marian J Currie, BapplSc, GDPH, Midwife, Maternity and Gynaecology Outpatients and Fetal Medicine Unit. David A Ellwood, FRANZCOG, Dphil, Professor of Obstetrics and Gynaecology, The Canberra Clinical School. New South Wales Centre for Perinatal Health Services Research, Departments of Obstetrics and Gynaecology and Public Health and Community Medicine, School of Population Health Services Research, University of Sydney, NSW. Christine L Roberts, MB BS, MHP, Senior Lecturer. Reprints: Dr J F Thompson, Women's and Childrens Health, The Canberra Hospital, PO Box 11, Woden, ACT 2606. jane.thompsonATact.gov.au ©MJA 2000

Jane F Thompson · Christine L Roberts · Marian J Currie · David A Ellwood

Medicine and the law

Ethics 5 June 2000 Free

Determining the validity of advance directives

Medicine And The Law Determining the validity of advance directives Paul Biegler, Cameron Stewart, Julian Savulescu and Loane Skene MJA 2000; 172: 545-548 Abstract - Ethics - Legislation - Common law - Duties of treating physicians in determining legal validity of advance directives - Conclusions - References - Authors' details - - More articles on Ethics Abstract We examine the ethical principles underpinning advance directives (ADs) and the legal duties of doctors in determining their validity. A physician attending an incompetent patient with an acute life-threatening illness, and an AD refusing treatment, should ensure that the AD is legally valid before making the treatment decision. Treatment against a patient's wishes, as expressed in a valid AD, compromises patient autonomy and may constitute battery. Conversely, withholding treatment in accordance with an AD that is not legally valid risks substantial harm to the patient and may constitute breach of the duty of care and negligence. Legally valid directives should be respected. If an AD is not legally valid, the patient should be treated in his or her best interests. If uncertain, the physician should treat according to the patient's best interests while seeking legal advice. An advance directive (AD) is a statement by a competent person expressing the intention to refuse medical treatment in the future, at a time when he or she may no longer be competent to make a treatment decision.1 ADs have arisen in the context of an increasing need to respect and promote patient autonomy.2 They have received widespread international support and, in the United States, ADs now have a statutory basis in all 50 States.3 Three Australian States (Victoria, South Australia and Queensland) and two Territories (the Northern Territory and the Australian Capital Territory) now have legislation which provides for ADs (Box 1). Although New South Wales, Tasmania and Western Australia do not have similar legislation, ADs may still be valid under common (judge-made) law in these States. Despite their prevalence in the United States, ADs have, in many instances, failed to guide clinical decision-making, and their utility has been questioned.4 Of particular concern is the dilemma facing clinicians when the AD rules out treatment which the doctor believes is in the patient's best interests.5 Treatment in the presence of a valid AD compromises patient autonomy and may constitute battery.6 However, withholding treatment in accordance with a legally invalid AD risks substantial harm to the patient and may constitute breach of the duty of care and negligence.7 We contend that being equipped with a clear process for determining the legal validity of an AD can reduce the uncertainty of physicians in such situations. Legally valid ADs should be respected. If the AD is not legally valid, or if the physician is uncertain, treatment decisions should be based on an assessment of the patient's best interests.8 We look at the ethical foundations and the Australian law pertaining to ADs and offer recommendations to medical practitioners seeking to ascertain the legal validity of ADs. Ethics "Autonomy" comes from the Greek autos-nomos, meaning "self-rule" or "self-determination". The concept of respect for autonomy was enunciated by John Stuart Mill, who said that the sole justification for interfering in another person's action is if that action will harm others -- "His own good, either physical or moral, is not a sufficient warrant".9 This principle, known as Mill's "harm principle", is the grounds for the moral right of a patient to refuse medical treatment, even if such treatment is life-saving, and for a doctor not to interfere in this action. Mill did have one caveat to his stance. He felt that it was acceptable to restrain a person from causing self-harm if that person's action was not fully informed. Take the example of a person crossing a burning bridge without knowing it is burning. Intervening here would be acceptable and this has been labelled "weak or soft paternalism". Intervening if the person was fully informed about the consequences of his or her actions has been labelled "strong or hard paternalism" and is unacceptable.10 Modern theorists have elaborated the notion of autonomy and concluded that an autonomous decision is one that is freely made, by a competent person, based on his or her most recent set of values. It should also be applicable to the circumstances in question, with a full understanding of the relevant facts.11,12 The relevance to ADs is that, unless a directive expresses an autonomous decision, acting upon it may in fact violate patient autonomy and result in serious harm. An example is a patient with HIV who signs a directive refusing resuscitation or admission to an intensive care unit. The patient has a life-threatening allergic reaction to a drug early in the course of the disease, when the prognosis suggests many good years of life. If the patient did not intend the AD to apply in this circumstance, then to allow this patient to die would be to fail to respect his or her autonomy. Treatment here would be weak paternalism (see also Box 3). The law provides a framework for safeguarding patient autonomy in such situations. Legislation The Australian legislation covering ADs is outlined in Box 1. Common law The validity of ADs at common law is yet to be tested in an Australian court. The case law from other jurisdictions suggests the following factors should be considered. The competence of the decision-maker The patient must have been competent to refuse treatment when the AD was drafted. The test for competence rests on the question of whether the patient understood the nature and purpose of the treatment when he or she made the decision to refuse it.13,14 The true scope and basis for the decision The AD must cover the circumstances that have arisen. The evidence must confirm the true scope and basis of the decision; that is, that the anticipatory decision was based on an informed opinion and was intended to apply to the circumstances which have arisen.6,15 Evidence of a decision which consists of remote, general, spontaneous or casual comments will not support the claim of anticipatory decision-making.16 However, evidence of cogent and serious decision-making which consists of written evidence or eye-witness accounts is usually strong enough to support the veracity of an anticipatory decision.17 Evidence of oral directions can, by itself, support the finding of a valid anticipatory decision.18-20 Undue influence The decision to refuse treatment must be free from the undue influence of others. Undue influence may impair the decision-making process and invalidate the directive. Enquiries must be made as to both the strength of will of the patient and the relationship of the patient with the persuader. If the patient was in pain or under the influence of drugs when the decision was made, or was persuaded by someone with close familial ties, the decision may not have been the result of the patient's free will. Such decisions are not legally binding on doctors.15 Duties of treating physicians in determining legal validity of advance directives In the case of directives completed under a statutory scheme, a physician treating an incompetent patient is not required to investigate whether the patient's decision was voluntary, reasonably informed or that the patient was 18 years or over when the directive was signed. The witnesses to the directive attest to those matters. In Victoria, South Australia and Queensland, the witnesses also attest to the patient's capacity to refuse treatment at the time of completing the AD. The obligations of the treating physician are more onerous in relation to common law directives and legal advice may be required in this setting. A schema for determining the validity of ADs from both the legislative and the common law perspective is outlined in Box 2, and an example is given in Box 3. Conclusions In order to respect patient autonomy, avoid harm to patients and reduce the risk to doctors of civil or criminal liability, physicians need to determine the legal validity of advance directives before making their treatment decision. In cases of uncertainty treatment decisions should be made in the patient's best interests while legal advice is sought as to the validity of the directive. References Robertson GS. Making an advance directive. BMJ 1995; 310: 236-238. Kerridge IH, McPhee J, Lowe M, Flynn B. Advance directives. In: Freckelton I, Petersen K, editors. Controversies in health law. Sydney: The Federation Press; 1999: 302. Tonelli MR. Pulling the plug on living wills. A critical analysis of advance directives. Chest 1996; 110: 816-822. Teno JM, Licks S, Lynn J, et al. Do advance directives provide instructions that direct care? SUPPORT Investigators. Study to understand prognoses and preferences for outcomes and risks of treatment. J Am Geriatr Soc 1997; 45: 508-512. Danis M, Southerland LI, Garrett JM, et al. A prospective study of advance directives for life-sustaining care. N Engl J Med 1991; 324: 882-888. Skene L. When can doctors treat patients who cannot or will not consent? Monash University Law Review 1997; 23 (1): 77. Dix A. Law for the medical profession in Australia. Melbourne: Butterworth-Heinemann, 1996: 563. Luttrell S. Making decisions about medical treatment for mentally incapable adults in the UK. Lancet 1997; 350: 950-953. Mill JS. Utilitarianism, on liberty and considerations on representative government. Everyman library. London: J M Dent and Sons, 1910. Ten CL. Paternalism and levels of knowledge: a comment on Rainbolt. Bioethics 1989; 3: 135-139. Dworkin G. The theory and practice of autonomy. Cambridge: Cambridge University Press, 1988. Savulescu J. Good reasons to die [doctoral dissertation]. Melbourne: Monash University, June 1994. Lord Brandon in Re F (Sterilisation Mental Patient) [1989] 2 Fam 376, 419-420. Gillick v West Norfolk and Wisbech AHA [1986] AC 112. Re T [1992] 2 Fam 458, 473 (Lord Donaldson). Matter of Jobes 529 A 2d 434, 443 (NJ, 1987). Matter of Peter 529 A 2d 419 (NJ, 1987). Re Chad Swan 569 A 2d 1202 (Me, 1990). Leach v Akron General Medical Center 426 NE 2d 809 (Ohio Comm Pl, 1980). Matter of Eichner 420 NE 2d 64 (NY, 1981). Authors' details Emergency Department, Monash Medical Centre, Melbourne, VIC. Paul Biegler, MB BS, FACEM, Staff Specialist. Department of Law and Justice, Division of Law, Macquarie University, Sydney, NSW. Cameron Stewart, BEc, LLB(Hons), GradDipJur, Associate Lecturer. The Murdoch Institute, Royal Children's Hospital, and Centre for the Study of Health and Society, University of Melbourne, Melbourne, VIC. Julian Savulescu, MB BS, PhD, Associate Professor, and Director, Ethics Program. Law School, University of Melbourne, Melbourne, VIC. Loane Skene, LLM (Mon), LLB (Hons), Associate Professor and Reader. Reprints will not be available from the authors. Correspondence: Dr P Biegler, Emergency Department, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168. pbieglerATnetlink.com.au Make a comment 1: Legislation in Australia providing for advance directives Victoria Act: Medical Treatment Act 1988 (Vic). Type of advance directive: Refusal of treatment certificate (RTC). Treatment refused must relate to a current condition ("current condition" is not defined by the Act but presumably refers to a condition that the person has at the time of completing the RTC). The document must be in the form prescribed by the Act ("in the form" is also not defined, but presumably means in language consistent with that used in the Act). Legally valid if completed voluntarily by a person of sound mind over 18 years who is informed about their condition. Must be signed by a registered medical practitioner and another person who attest to these matters. The patient does not need to sign. Revoked by patient clearly indicating this wish to another person. Palliative care: The RTC does not cover refusal of palliative care, which is defined as "the provision of reasonable medical procedures for the relief of pain, suffering and discomfort; or the reasonable provision of food and water". Physicians’ liability: Under the Act, a doctor who treats a patient despite a valid certificate may commit the statutory offence of medical trespass. This offence would arise in addition to common law claims of battery. Doctors who comply with an RTC are granted immunity from civil claims, criminal charges or professional misconduct proceedings, provided the doctor acts in good faith and with reasonable care. South Australia Act: Consent to Medical Treatment and Palliative Care Act 1995 (SA). Type of advance directive: An "anticipatory grant" refusing consent to medical treatment. The directive is only effective for patients in the terminal stages of a terminal illness or in a persistent vegetative state, who are not competent to make treatment decisions. "Terminal illness" is defined as "an illness or condition that is likely to result in death" and terminal stage as "the phase of the illness reached when there is no real prospect of recovery or remission of symptoms". Legally valid if made by a patient of sound mind over the age of 18 years. Must be in the prescribed form, signed by the patient and witnessed by one person, who need not be a medical practitioner. Revoked by patient orally or in writing (not stipulated in the Act). Physicians’ liability: Physicians honouring directives under the Act are granted immunity from civil and criminal liability if they act in good faith, without negligence and in accordance with proper standards of professional practice. Australian Capital Territory Act: Medical Treatment Act 1994 (ACT), based on the Medical Treatment Act 1988 (Vic). Type of advance directive: "Direction" refusing treatment generally or treatment of a particular kind. Treatment does not have to relate to a current condition, as it does in Victoria. Legally valid if patients are of sound mind over 18 years. Direction must be in the prescribed form and witnessed by two people, neither of whom needs to be a medical practitioner. It can be signed by the patient or by another person at the patient’s direction, but it does not have to be signed to be valid. Revoked by patient clearly indicating his or her wish to another person. Palliative care: Does not cover refusal of palliative care. Physicians’ liability: A physician honouring a certificate in good faith is protected from civil and criminal liability, as well as claims of professional misconduct. Queensland Act: Powers of Attorney Act 1998 (Qld) Type of advance directive: "Advance health directives." Directions to withhold or withdraw life-sustaining measures cannot operate unless: the patient has a terminal illness or an incurable condition and is not expected to live more than a year, or is in a persistent vegetative state, or is permanently unconscious, or has a severe illness with no reasonable prospect of being able to live without the continued application of life-sustaining measures; and (if the direction concerns artificial hydration or nutrition) the life-sustaining measure would be contrary to good medical practice; and the patient has no reasonable prospect of regaining capacity for health matters. Legally valid if the directive is in the prescribed form, signed by the patient or another person at the patient’s direction and witnessed by two people, one of whom must be a medical practitioner. The witnesses must certify that the patient had the capacity to make the treatment decision at the time of completing the directive. Revoked by patient indicating his or her wish in writing. Physicians’ liability: Physicians are protected from criminal and civil liability if they honour the directive in good faith. Northern Territory Act: Natural Death Act 1988 (NT). Type of advance directive: "Directives" refusing treatment are only effective in the case of terminal illness, which is defined as "Such an illness, injury or degeneration of mental or physical faculties that death would, if extraordinary measures were not undertaken, be imminent; and from which there is no reasonable prospect of a temporary or permanent recovery, even if extraordinary measures were undertaken". Extraordinary measures are defined in the Act as "medical or surgical measures that prolong life, or are intended to prolong life, by supplanting or maintaining the operation of bodily functions that are temporarily or permanently incapable of independent operation". Legally valid if made by patients of sound mind who are over 18 years. Must be in the prescribed form, signed by the patient and witnessed by two people, who need not be medical practitioners. The treating doctor cannot be a witness. Revoked by patient orally or in writing (not stipulated by the Act). Palliative care: Does not cover refusal of palliative care. Physicians’ liability: Physicians complying with directives in good faith are protected from criminal and civil liability. Back to text 2: Schema of obligations of treating physicians Incompetent patient presents with acute life-threatening illness and an advance directive (AD) refusing treatment Step 1: Physician determines whether the AD conforms with State legislative requirements The form of the AD is correct The AD has the required signatures There is no evidence that the AD has been revoked (check with relatives, friends and the patient's GP) Victoria - the presenting condition for which treatment is now required is the same as, or has been caused by, the "current condition" as specified on the refusal of treatment certificate (RTC); Australian Capital Territory - treatment generally or treatment of a particular kind has been refused. There is no evidence that the patient was incompetent at the time of making the directive (witnesses are not required to attest to competence); South Australia - the patient is in the terminal phase of a terminal illness or in a persistent vegetative state; Northern Territory - the patient has a terminal illness. There is no evidence that the patient was incompetent at the time of making the directive (witnesses are not required to attest to competence); Queensland - the patient is suffering from one of the conditions outlined in Box 1, and the directive is not uncertain or contrary to good medical practice (section 106 of the Powers of Attorney Act 1998). If ALL of the criteria for Step 1 are satisfied Step 2: Comply with the AD (if uncertain proceed to Step 6). If ANY of the criteria for Step 1 are not satisfied Step 3: Determine common law validity of the AD. No evidence that the person was incompetent when they made the AD. AD covers the proposed treatment and the circumstances that have arisen. (i) It should not be ambiguous about the nature of the treatment being refused; and (ii) It should have been expressed to refuse treatment in the circumstances that have arisen. No evidence that the AD was procured by undue influence. If ALL of the criteria for Step 3 are satisfied Step 4: Comply with the AD (the difficulty of a physician's rapidly ascertaining these data in the acute setting is acknowledged) (if uncertain proceed to Step 6). If ANY of the criteria for Step 3 are not satisfied Step 5: Set aside the AD and treat according to the patient's best interests. Step 6: Legal advice should be sought if uncertainty exists about Steps 2-5. Faced with a delay in determining the validity of the AD, the physician should commence and continue any treatment deemed to be in the patient's best interests until such time as the AD is determined to be legally valid. Back to text 3: Example of an advance directive (AD) and physicians' decision-making A patient with HIV signs an AD refusing resuscitation or admission to an intensive care unit. The patient has an anaphylactic reaction to a drug early in the disease. Ethics If the AD was not intended to apply in this circumstance, withholding treatment would be to fail to respect this person's autonomy and would constitute a serious harm. Legislation Victoria The directive would be invalid because the presenting condition of anaphylaxis differs from the current condition of HIV as specified on the certificate. South Australia, Northern Territory, Queensland The directive would be invalid because the patient is not in the terminal phase of a terminal illness (SA, NT, QLD); in a persistent vegetative state (SA, QLD); and is not permanently unconscious with no reasonable prospect of regaining capacity for health matters (QLD). Australian Capital Territory The situation in the ACT is more complex. It seems that if the patient's AD was executed under the Medical Treatment Act 1994 (ACT) it may, in fact, be legally valid. However, we have argued that it would be ethically wrong to allow this person to die, and the directive would not be valid under other States' legislation or common law (see below). What should the doctor do? The uncertainty raised by the ACT situation should lead the doctor to act in the patient's best interests, which, in this case, probably favour resuscitation, while seeking legal advice. If in doubt, the patient's best interests must be the foremost consideration. Common Law The directive is unlikely to be valid at common law because the scope of the decision does not cover the circumstances that have arisen. Treatment decisions in these jurisdictions should thus be based on an assessment of the patient's best interests, which, in this case, as mentioned, probably favours treatment. Back to text

Paul Biegler · Cameron Stewart · Julian Savulescu · Loane Skene

Viewpoint

Cancer 5 June 2000 Free

Active and passive cigarette smoking and breast cancer: is a real risk emerging?

Viewpoint Active and passive cigarette smoking and breast cancer: is a real risk emerging? Recent studies may explain the apparent inconsistencies between earlier results Robert C Burton and Nabil Sulaiman MJA 2000; 172: 550-552 Conflicting results on smoking and breast cancer - Postulated mechanisms - Resolving the conflicts - Where to from here? - References - Authors' details - - More articles on Public and environmental health Cigarette smoking has been suggested as a cause of breast cancer, but many studies addressing the relationship have yielded inconsistent results. A possible explanation is that many of these studies have overlooked the potential effects of passive exposure to cigarette smoke when assessing the effects of active smoking. A further source of confusion is the hypothesised existence of a window of vulnerability to tobacco smoke carcinogens during childhood and adolescence.1 We summarise the epidemiological evidence for a causal association between smoking and breast cancer and consider recent studies on the effects of active and passive exposure to cigarette smoke in the context of this hypothesised window of vulnerability. Conflicting results on smoking and breast cancer A review of publications on the relationship between smoking and breast cancer to 1984 found more evidence for a protective than for a harmful effect of cigarette smoking.2 In contrast, a 1990 review reported that the summary odds ratio (OR) for breast cancer in smokers compared with non-smokers was 1.12 for case-control studies (95% CI, 1.06-1.19) and 1.14 for cohort studies (95% CI, 1.02-1.27).3 A large case-control study of about 7000 case and 9000 control participants, published in 1996, found no relationship between cigarette smoking and breast cancer.4Conflicting results have also emerged from large, well designed cohort studies. A 1989 analysis of the United States Nurses' Cohort Study (about 120 000 women) found no relationship between cigarette smoking and breast cancer.5 In contrast, the American Cancer Society Cohort Study (about 600 000 women) reported in 1994 that women who were current smokers at the time of death had a higher breast cancer mortality than non-smokers (relative risk [RR], 1.26; 95% CI, 1.05-1.50).6 Furthermore, mortality tended to increase with the amount and duration of smoking; for example, RR was 1.74 (95% CI, 1.15-2.62) for women who smoked 40 or more cigarettes per day. Postulated mechanisms A range of biological and epidemiological explanations have been proposed for these varying results. On the one hand, cigarette smoking may have a protective effect, as women who smoke have an earlier menopause, with fewer total years of menstruation,7,8 and weigh less than non-smokers,7,9 and also cigarette smoking alters oestrogen metabolism.10,11 That is, the negative effect of cigarette smoking on oestrogen production may reduce the risk of oestrogen-dependent diseases.2On the other hand, cigarette smokers may have increased risk of breast cancer, as carcinogens from tobacco smoke absorbed into the bloodstream may produce carcinogenesis of breast ductal epithelium.12 Several polycyclic aromatic hydrocarbons are produced by tobacco combustion, including the carcinogens benzo[a]pyrene, which is mutagenic for the p53 tumour suppressor gene in humans,13 and 7,12-dimethylbenz[a]anthracene, which is used to induce mammary tumours in animals.14 Data reported recently from the Carolina breast cancer study showed that archival breast cancer tissue from current cigarette smokers had a higher prevalence of p53 mutations than breast cancer tissue from never smokers: 40.4% versus 24.8%.15 Of particular interest was the finding that p53 mutations of the type found in lung cancers from smokers were detected in breast cancer tissues from 21% of current smokers but only 5% of never smokers. In addition, Palmer and colleagues hypothesised that women's risk of breast cancer is increased by exposure to cigarette smoke during childhood and adolescence, as these are times of rapid breast growth.1 They reported two case-control studies of breast cancer risk among women who smoked 25 or more cigarettes per day compared with never active smokers. These studies found that ORs for smokers who began smoking before the age of 14 years, compared with never active smokers, were 2.6 (95% CI, 1.0-6.8) and 1.9 (95% CI, 0.9-4.1), respectively. In contrast, ORs were lower for those who began smoking later, at ages 18-21 years, compared with never active smokers: 1.1 (95% CI, 0.7-1.7) and 1.2 (95% CI, 0.7-1.8), respectively.15 Resolving the conflicts The explanation for much of the discrepancy between the above results on active smoking and breast cancer may be that the studies did not consider passive exposure to tobacco smoke.16 This issue has been addressed by three recent case-control studies which compared smokers with women who had no exposure to tobacco smoke, either active or passive.12,17,18 They found ORs ≥ 2.0 for the overall risk of breast cancer in ever smokers (two studies12,18) or ever smokers with premenopausal breast cancer (one study17) compared with women with no active or passive exposure to tobacco smoke. Selected data from these three studies are shown in the Box. These three studies also examined the association between breast cancer and passive exposure to cigarette smoke, as did two other case-control studies19,20 and two cohort studies.16,21 Data from the Hirayama cohort, reported in 1998 (91 540 women), showed that spouses who were passively exposed had an RR of 1.32 (95% CI, 0.83-2.09).16 A recent Korean cohort study on spouses' passive exposure to smoke and lung cancer (160 130 women) also found an increased risk of breast cancer (RR, 1.7; 95% CI, 1.0-2.8).21 Selected data from the five case-control studies on the effects of passive exposure to cigarette smoke, including effects of age of exposure, are shown in the Box. Two studies found a significant exposure-response effect in terms of the number of smokers and smoker-years to which women were passively exposed. The age of passive exposure also appeared important, as Palmer et al observed for active exposure in two previous case-control studies.1 Smith et al found childhood exposure to be almost as important as adult exposure,19 and Lash and Aschengrau found that the risk of breast cancer in females passively exposed to cigarette smoke was highest when exposure occurred before the age of 12 years, less when it occurred at 12-20 years, and least when it occurred after the age of 20.18 Furthermore, they found an OR of 7.5 (95% CI, 1.6-36) for the occurrence of breast cancer in girls exposed to passive smoking who were also active smokers before the age of 12 years. It should be noted that, as there were few case and control participants, 95% confidence intervals were wide, and the estimates should be viewed with caution. The ORs shown in the Box suggest a causal association between active and passive exposure to cigarette smoke and breast cancer (ORs > 2.0 are considered to indicate a strong association22). Interestingly, a recent review of established and possible aetiological factors in breast cancer found that only age, strong family history, mutations in BRCA-1 or BRCA-2 genes, country of birth and atypical cells in nipple aspirates were associated with ORs over 4.0.23 Lash and Aschengrau based their study on a model of susceptibility of breast tissue to tobacco smoke which was derived from new knowledge on breast tissue development and susceptibility to chemical carcinogens.18 The physiological development of the mammary gland involves four different lobule types, representing sequential developmental stages.24 During sexual maturation (puberty), breast tissues evolve from lobule type 1 (highest doubling rate and greatest susceptibility to carcinogens) to type 2 (intermediate doubling rate and susceptibility to carcinogens). During pregnancy, or gradually with premenopausal ageing, breast tissues evolve to type 3 (low doubling rate and susceptibility to carcinogens). Type 4 lobules (maximal expression of development and differentiation) develop during lactation. Therefore, the window of maximum vulnerability of girls to tobacco-smoke-induced breast cancer should be from birth through puberty. Where to from here? Clearly, further studies are needed to investigate and better measure the effects of active and passive exposure to cigarette smoke in various phases of childhood, adolescence and adult life. Furthermore, the recent studies reviewed here involved women in Europe and the United States who presented with breast cancer in the 1980s and 1990s. Their exposure to cigarette smoke during the hypothesised window of vulnerability would have occurred mainly in the 1930s to 1950s, and would reflect the smoking habits of teenage and young women and their parents at that time. Therefore, Australian data are urgently needed, as exposures may have differed in this country. Finally, if active and passive exposure to cigarette smoke in childhood and adolescence proves to cause breast cancer, then the current smoking habits of Australian teenage girls are of even greater concern. The 1996 survey on use of tobacco and alcohol among Australian secondary students revealed that 14%-20% of girls aged 12-15 years were current smokers in the period 1984-1996, and that they smoked an average of 18.7-21.2 cigarettes per week.25 By the age of 12 years, 32% of girls had experimented with cigarette smoking.25 A proportion of Australia's future burden of breast cancer may already have been initiated. References Palmer JR, Rosenberg L, Clarke EA, et al. Breast cancer and cigarette smoking: a hypothesis. Am J Epidemiol 1991; 134: 1-13. Baron JA. Smoking and estrogen-related disease. Am J Epidemiol 1984; 119: 9-22. MacMahon B. Cigarette smoking and cancer of the breast. In: Wald N, Baron J, editors. Smoking and hormone-related disorders. Oxford: Oxford University Press, 1990: 154-166. Baron JA, Newcomb PA, Longnecker MP, et al. Cigarette smoking and breast cancer. Cancer Epidemiol Biomarkers Prev 1996; 5: 399-403. London SJ, Colditz GA, Stampfer MJ, et al. Prospective study of smoking and the risk of breast cancer. J Natl Cancer Inst 1989; 81: 1625-1631. Calle EE, Miracle-McMahill HL, Thun MJ, et al. Cigarette smoking and risk of fatal breast cancer. Am J Epidemiol 1994; 139: 1001-1007. Willett WC, Stampfer MJ, Brian C, et al. Cigarette smoking, relative weight and menopause. Am J Epidemiol 1983; 117: 651-658. Kaufman DW, Slone D, Rosenberg L, et al. Cigarette smoking and age at natural menopause. Am J Public Health 1980; 70: 420-422. Istvan JA, Cunningham TW, Garfinkel L. Cigarette smoking and body weight in the cancer prevention study I. Int J Epidemiol 1992; 21: 849-853. MacMahon B, Trichpoulos D, Cole P, et al. Cigarette smoking and urinary estrogens. N Engl J Med 1982; 307: 1062-1065. Michnovicz JJ, Hershcope RJ, Naganuma H, et al. Increased 2-hydroxylation of estradiol as a possible mechanism for the anti-estrogenic effect of cigarette smoking. N Engl J Med 1986; 315: 1305-1309. Morabia A, Bernstein M, HŽritier S, et al. Relation of breast cancer with passive and active exposure to tobacco smoke. Am J Epidemiol 1996; 143: 918-928. Denissenko MF, Pao A, Tang M, Pfeifer GP. Preferential formation of benzo[a]pyrene adducts at lung cancer mutational hot spots in P53. Science 1996; 274: 430-432. Huggins CB. Selective induction of hormone-dependent mammary adenocarcinoma in the rat. J Lab Clin Med 1987; 109: 262-266. Conway K, Edmiston SN, Cui L, et al. The prevalence and spectrum of p53 mutations in the Carolina breast cancer study suggests a role for cigarette smoking in breast cancer development. Proc Amer Assoc Cancer Res 2000; 41: 222. Wells AJ. Breast cancer, cigarette smoking and passive smoking. Am J Epidemiol 1998; 147: 991-992. Johnson KC, Hu J, Mao Y, et al. Passive and active smoking and breast cancer risk in Canada, 1994-1997. Canadian Cancer Registries Epidemiology Research Group. Cancer Causes Control 2000; II: 211-221. Lash TJ, Aschengrau A. Active and passive cigarette smoking and the occurrence of breast cancer. Am J Epidemiol 1999; 149: 5-12. Smith SJ, Deacon JM, Chilvers CE. Alcohol, smoking, passive smoking and caffeine in relation to breast cancer risk in young women. UK National Case-Control Study Group. Br J Cancer 1994; 70: 112-119. Sandler DP, Wilcox AJ, Evesan RB. Cumulative effects of lifetime passive smoking on cancer risk. Lancet 1985; 1: 312-315. Jee SH, Ohrr H, Kin IS. Effect of husbands smoking on the incidence of lung cancer in Korean women. Int J Epidemiol 1999; 28: 824-828. Beaglehole R, Bonita R, Kjellstršm T. Basic epidemiology. Geneva: World Health Organization, 1993. Kelsey JL, Bernstein L. Epidemiology and prevention of breast cancer. Annu Rev Public Health 1996; 17: 47-67. Russo J, Russo I. Toward a physiological approach to breast cancer prevention. Cancer Epidemiol Biomarkers Prev 1994; 3: 353-364. Hill D, White V, Letcher W. Tobacco use among Australian secondary students in 1996. Aust N Z J Public Health 1999; 23: 252-259. Authors' details Anti-Cancer Council of Victoria, Melbourne, VIC. Robert C Burton, MD, PhD, Director; Nabil Sulaiman, MD, PhD, Epidemiologist. Reprints will not be available from the authors. Correspondence: Dr R C Burton, Anti-Cancer Council of Victoria, 1 Rathdowne Street, Carlton, VIC 3053. directorATaccv.org.au Make a comment &copy 2000 Medical Journal of Australia. Smoking and risk of breast cancer in case-control studies that controlled for, or investigated the effects of, passive exposure to tobacco smoke* Smoking exposure Adjusted odds ratio for breast cancer† (95% CI) Reference Active smoking (Referent group never exposed, actively or passively) 1.0 Current smoker, cigarettes per day 1-9 10-19 ≥20 1.5 (0.9-3.9) 2.1 (0.9-4.8) 5.1 (2.1-12.6) Morabia et al12 Ever smoker, average lifetime cigarettes per day 1-9 10-19 ≥20 2.2 (1.0-4.4) 2.7 (1.4-5.4) 4.6 (2.2-9.7) Morabia et al12 Ever smoker, cigarettes per day while active smoker 1-9 10-19 ≥20 2.5 (1.2-5.2) 2.3 (1.1-4.6) 2.0 (1.0-4.0) Johnson et al17 Smoking relative to first full-term pregnancy Only before Only after Before and after 5.6 (1.5-21) 2.1 (1.1-4.0) 1.1 (0.6-2.0) Lash and Aschengrau18 Passive exposure (Referent group never exposed, actively or passively, unless shown otherwise) 1.0 Duration of exposure 1-50 hours/day-years‡ >50 hours/day-years 3.1 (1.5-6.2) 3.2 (1.6-6.3) Morabia et al12 Total smoker-years (residential plus occupational) 1-13 14-32 33-70 >70 1.5 (0.5-4.4) 2.0 (0.9-4.5) 2.9 (1.3-6.6) 3.0 (1.3-6.6) Johnson et al17 Timing of passive exposure Before age 12 years Age 12-20 years After age 20 years 4.5 (1.2-16) 3.8 (1.1-13) 2.4 (0.9-6.1) Lash and Aschengrau18 Never§ Childhood only Adulthood only Both 1.00 1.98 (0.35-11.36) 2.65 (0.80-8.83) 3.13 (1.05-9.38) Smith et al19 Number of household smokers§ 0 1 2 3 or more 1.0 2.0 2.4 3.3 Sandler et al20 *Selected data are shown, with 95% CIs when given in the cited article. †Adjusted for multiple risk factors, including alcohol intake, except in Sandler et al.20 ‡Hours/day-years=hours/day x duration for all episodes of passive exposure. For example, 50 hours/day-years could represent 1 hour per day for 50 years, 2 hours per day for 25 years, or 12.5 hours per day for 4 years, and so on. § Some members of both referent and exposed groups were active smokers. Back to text

Robert C Burton · Nabil Sulaiman

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19 June 2000 Free

Investigating Australia's burden of disease

Alan D Lopez

Public health 19 June 2000 Free

The Australian Burden of Disease Study: measuring the loss of health from diseases, injuries and risk factors

Colin D Mathers · Chris E Stevenson · Stephen J Begg

Notable cases 19 June 2000 Free

Australian bat lyssavirus infection: a second human case, with a long incubation period

Jeffrey N Hanna · Ian K Carney · Greg A Smith · Joseph E Deverill · John A Botha · Ina L Serafin · Bruce J Harrower · Peter F Fitzpatrick · Jeffrey W Searle

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Reconciliation, social equity and Indigenous health

Sandra J Eades

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Schizophrenia today

David L Copolov · Bruce S Singh

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Illness or disease? The case of chronic fatigue syndrome

Andrew R Lloyd · Ian B Hickie · Robert H Loblay

Indigenous health research 15 May 2000 Free

Reducing premature death and renal failure in Australian Aboriginals

Wendy E Hoy · Philip R Baker · Angela M Kelly · Zhiqiang Wang

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