Women's health

Editorial Caesarean section: a matter of choice? Women need more information, whether or not it leads to a decrease in caesarean section rates MJA 1999; 170: 572-573 With 20% of all births in Australia being by caesarean section (CS), we have one of the highest rates among First World countries.1 There are, of course, variations from State to State and between the public and private sectors, but this high average rate is of ongoing concern to obstetricians, health administrators and consumer groups. Many reasons for these high rates have been advanced, including better survival prospects for very preterm infants; the threat of litigation leading to earlier intervention in labour; fewer operative vaginal deliveries; and routine abdominal delivery for breech presentation. The widespread use of electronic fetal monitoring and epidural analgesia, and the need for repeat CS, have also been cited. Despite much discussion, the appropriate CS rate for any population has yet to be defined; for instance, the target CS rate set by the US Department of Health and Human Services of 15% of births by the year 2000 is an arbitrary figure widely questioned by obstetricians in the United States.2,3In this issue of the Journal, Turnbull et al present the results of a cross-sectional survey of South Australian women who underwent CS.4 Their aim was to determine the extent of women's involvement in the decision to perform the operation. Although more than 80% of women having elective CS and 50% of those having emergency CS reported such involvement, 20%-50% of women overall were not completely satisfied either with the decision, their input into it, or the amount of information provided to them. Turnbull and colleagues concluded that giving women more information might contribute to a drop in CS rates. Certainly, it is desirable that all pregnant women receive adequate information about the possible course of labour and the reasons why emergency CS might be recommended. Elective CS should probably be regarded differently as far as the decision-making process is concerned -- there is always time to discuss the surgery with medical advisers, partners and friends. But when labour, in particular first labour, has a high chance of ending in CS, women should be better informed of this so that they regard it as a possible normal event, rather than a surprising and disappointing outcome of a planned vaginal birth.5 Several studies have documented an association between emergency CS and subsequent psychological problems, especially postnatal depression.6,7 In the presence of high caesarean rates, such an association would pose a significant health problem for mothers and babies. The psychological sequelae have been linked to a sense of failure on the part of women who anticipated and prepared for a normal vaginal delivery, suggesting that the incidence of attributable postnatal depression might decline if women were more prepared for CS as a possible mode of delivery. Turnbull's article also raises the question of whether, given adequate information, most women who have had a previous CS will opt for an attempt at vaginal delivery in a subsequent pregnancy. Several studies indicate that about 70% of these women will be able to deliver vaginally; this is usually a happy outcome for the woman concerned, and uses fewer health dollars than a repeat CS. However, the 30% of women who will not achieve a vaginal birth also need to be considered; among these will be some with resulting severe psychological problems, as well as those sustaining complications, such as uterine rupture requiring hysterectomy. Although uterine rupture is uncommon, it is more likely to occur with trial of labour than with a repeat CS.2,3,8,9 Women considering vaginal delivery after a CS birth need full, unbiased information about all alternatives if they are to make an informed choice. There is evidence that there are some women who feel quite positive about CS, even requesting the operation when medical indications are slight or non-existent.3,10 More than 25% of the women in Turnbull's study indicated that they had "insisted on", or were "keen to have", a caesarean delivery. Mould et al, in a study of 102 women undergoing CS in a London hospital, found that more than 10% felt the decision for surgery to be entirely their own, and that 50% would opt for CS in a further pregnancy.11 How these women who insist on a CS would respond to extra information is unknown. Al-Mufti and colleagues surveyed the personal responses of London obstetricians (a highly informed group) to various hypothetical pregnancy situations: 31% of female obstetricians, and 8% of male obstetricians, would choose elective CS, for themselves or their partners, for an uncomplicated singleton cephalic presentation at term; higher percentages favoured CS for relatively minor indications. Possible stress incontinence, anal sphincter damage and compromised sexual function following vaginal delivery were among the reasons given. Al-Mufti rather archly suggests that perhaps CS should be offered to all pregnant women, "an option apparently available to all obstetricians".12 Turnbull's study is to be commended as an attempt to quantify the reasons for the decision to have a CS, and as a step towards providing the most appropriate and accurate information for women. However, certain assumptions were made in assessing the degree of satisfaction of the women surveyed, and there was no comparison with women experiencing a spontaneous vaginal delivery. Furthermore, Turnbull's final recommendation -- a randomised controlled trial of an information "package" -- would pose considerable methodological problems, including accruing sufficient participants; blinding the intervention (with some participants getting an information package and some not); and ensuring that patients in the control arm did not independently obtain the same information elsewhere. Regrettably, not all questions in medicine, especially those concerned with counselling, are answerable by randomised controlled trials.13-15 For the moment, it is clear that we must continue to monitor and assess Australian CS rates, and that women must be as well informed as possible about CS, especially emergency CS, long before labour. Many women may opt for a vaginal birth after a previous caesarean delivery, others will not, and others still may request CS for relatively minor indications. We must remember that providing full, unbiased information about birth and CS is not merely to enable health administrators to reach arbitrary targets, but to allow women to make a considered choice (even though that choice may be deplored by other groups of consumers or healthcare providers). Caroline M de Costa Senior Lecturer in Obstetrics and Gynaecology North Queensland Clinical School, University of Queensland, Cairns, QLD Day R, Sullivan E, Lancaster P. Australia's mothers and babies 1996. Sydney: Australian Institute of Health and Welfare National Perinatal Statistics Unit, 1999. (Perinatal Statistics Series No. 7.) Sachs BP, Kobelin C, Castro MA, Frigoletto F. The risks of lowering the cesarean delivery rate. N Engl J Med 1999; 340: 54-57. What is the right number of caesarean sections? [editorial] Lancet, 1997; 349: 815. Turnbull D, Wilkinson CS, Yaser A, et al. Women's role and satisfaction in the decision to have a caesarean section. Med J Aust 1999; 170: 580-583. Hillan EM. Issues in the delivery of midwifery care. J Adv Nurs 1992; 17: 274-278. Boyce PM, Todd AL. Increased risk of postnatal depression after emergency caesarean section. Med J Aust 1992; 157: 172-174. Fisher J, Astbury J, Smith A. Adverse psychological impact of operative obstetric interventions: a prospective longitudinal study. Aust N Z J Psych 1997; 31: 728-738. McMahon M, Luther E, Bowes W, Olshan A. Comparison of a trial of labor with an elective second cesarean section. N Engl J Med 1996; 335: 689-695. Paul RH. Towards fewer cesarean sections -- the role of a trial of labour [editorial]. N Engl J Med 1996; 335: 735-736. Grant JM. Women are satisfied with caesarean section [editorial]. Br J Obstet Gynaecol 1996; 103: vii-viii. Mould TAJ, Chong S, Spencer JAD, Gallivan S. Women's involvement with the decision preceding their caesarean section and their degree of satisfaction. Br J Obstet Gynaecol 1996; 103: 1074-1077. AI-Mufti R, McCarthy A, Fisk NM. Obstetricians' personal choice and mode of delivery [letter]. Lancet 1996; 347: 544. Brewin CR, Bradley C. Patient preferences and randomised controlled trials. BMJ 1989; 229: 313-315. Knottnerus JA, Dinant GJ. Medicine based evidence, a prerequisite for evidence based medicine [editorial]. BMJ 1997; 315: 1109-1110. Solomon MJ, McLeod RS. Surgery and the randomised controlled trial: past, present and future. Med J Aust 1998; 169: 380-383. Photo courtesy Dr P Mason, Department of Obstetrics and Gynaecology, Cairns Base Hospital, QLD

Research Women's role and satisfaction in the decision to have a caesarean section Deborah A Turnbull, Chris Wilkinson, Anisa Yaser, Vanessa Carty, John M Svigos and Jeffrey S Robinson MJA 1999; 170: 580-583 For editorial comment, see "de Costa" Rapid reader response (with authors' reply) added 28/6/99: see Chung Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Obstetrics & gynaecology and women's health Abstract Objective: To examine women's role in the decision to perform caesarean section (CS). Design: Cross-sectional survey. Written questionnaires were completed seven weeks after giving birth by CS. Setting: An obstetric tertiary referral hospital (Women's and Children's Hospital, Adelaide, South Australia), July to December 1996. Participants: A consecutive sample of women who underwent CS over a six-month period. To be eligible, women had to be at least 18 years old, able to complete a questionnaire in English and well enough to consent to study participation. Main outcome measures: Women's involvement in decision making, stated preference for CS, and satisfaction with obstetric care. Results: 278 women (76.4%) returned questionnaires: 171 women (61.5%; 95% confidence interval [CI], 55.8%-67.2%) reported being involved in the decision to have a CS. Factors influencing their decision were physical duress and partner's reaction during labour (emergency CS), considerations about recovery, planning for the event and pain (elective CS), and information from the doctor (both groups). Half the women "strongly agreed" that they were satisfied with the decision to have a CS, but 40.9% only "agreed" and 4.7% were "not sure". About 20% reported they needed more information on other options, and only 28.8% "strongly agreed" that they had been given good information to prepare for the possibility of CS. 27.9% of women (95% CI, 22.5%-33.2%) "agreed" or "strongly agreed" that they had "insisted on a CS" and 21.3% (95% CI, 16.4%-26.2%) that they had told the staff they were "keen to have a CS". Given the option of a vaginal delivery, 37.8% of women (95% CI, 22.5%-55.2%) with a breech presentation, and 34% of women (95% CI, 21.2%-48.8%) who had had a previous CS, chose a CS. Conclusions: It is of concern that over a third of women felt they had not been involved in the decision to have a CS; others were very positive about CS, but an appreciable proportion may not have received sufficient information. A broad-based strategy of providing more information to women and their partners could be one way of ensuring appropriate CS rates and should be tested in a randomised controlled trial. Introduction Despite national policy documents calling for a reduction in medical interventions in birth,1 Australia now has one of the highest caesarean section (CS) rates among First World countries.2 At the same time, it is recognised that the "ideal" or "correct" rate is difficult to derive,3 given the varying risk profiles of women attending different institutions. A range of strategies aimed at obstetricians4,5 have had limited success in reducing CS rates. The assumption is often made that the decision to perform a CS is made on clinical grounds only.6 The role of maternal request in decision-making has been raised,7 but so far studies from the woman's perspective have tended to use small samples with unique characteristics.8,9Our study examines the role of women in the decision to have a CS in an effort to identify an alternative approach to lowering the rates. Methods Setting The study was conducted at the Women's and Children's Hospital in Adelaide, South Australia. In 1996, this State had the highest CS rate of any State in Australia (23.1% v. national average of 19.5%).10 The Women's and Children's Hospital is a major obstetric tertiary referral centre for South Australia and much of the Northern Territory. In 1996, 23% (811/3536) of the women giving birth at the hospital were considered to have very high risk pregnancies and the CS rate for high risk pregnancies at the Women's and Children's Hospital was 43.9% (356/811).11 During that year, the overall CS rate was 25.4% (898/3536). Sample Over a six-month period (July to December 1996) questionnaires were sent to consecutive women who underwent CS. To be eligible for our study, the women had to be at least 18 years old, able to complete a questionnaire in English, and well enough to give consent to participate in the study (as decided by the senior midwife on the postnatal ward). We aimed to receive responses from about 288 women having a CS. This would provide a true population proportion of 60% (to within 5%) of women stating they had a say in the decision. To obtain this sample, we allowed for a non-eligibility, non-response rate of about 25% and thus sampled from a consecutive population of 375 women. Questionnaire The questionnaire was developed on the basis of a review of published reports, a review of existing questionnaires, and interviews with women, obstetricians, midwives and perinatal epidemiologists. It consisted of a combination of questions with forced-choice responses (mainly presented as a complete statement with a five-point response scale ranging from "strongly agree" to "strongly disagree"), open-ended questions and questions on demographic characteristics. (The questionnaire is available from the authors.) Procedure Ethical approval was obtained from the Hospital Ethics Committee, and, with the Committee's permission, a member of the research team (A Y), not involved in providing care, approached women on the postnatal ward between the second and fourth day and sought written consent for participation in the study. Questionnaires were sent to the participating women's homes seven weeks after the birth, to give women time to recover and to minimise biases such as the "halo" effect and social desirability (ie, the effect on respondents of the intensity of labour; and their tendency soon after the event to be uncritical of healthcare providers, particularly if they think their comments can be attributed to them).12 Follow-up of non-respondents included the mailing of a second questionnaire and a telephone call. A summary of the results was sent to participating women at the conclusion of the study. Data analysis The data were analysed using SPSS for Windows13 and Epi Info 6.14 We assessed whether variables such as age, language spoken at home, age left school, type of care, and type of CS distinguished between those who reported involvement in the decision and those who reported no involvement. Categorical data were analysed by χ2 tests. Point estimates and odds ratios are presented with 95% confidence intervals (CI). Results Sample Our sample consisted of 375 women having a CS over a six-month period. Of these, 11 (2.9%) women were not eligible, and 16 (4.3%) were "missed" by the researcher (mainly because they were discharged before contact). Thus, there was a defined sample of 364 women (taking the conservative view that all of the 16 missed women were in fact eligible and thus could be included in the sample). Completed questionnaires were obtained from 278 women (76.4% of our defined sample). The sample included women from a range of sociodemographic backgrounds receiving a diversity of care, including private obstetric care, hospital clinic care and different models of publicly funded midwifery care. About a third of the sample had an elective CS. Women's involvement in decision to have a caesarean section 171 women (61.5% of the study group; 95% CI, 55.8%-67.2%) reported that they were involved in the decision to have a CS. 81.4% (70/86) of those having an elective CS reported involvement in the decision, compared with 53.2% (100/188) of those having an emergency CS (odds ratio [OR] = 3.85; 95% CI, 2.01-7.47). Women cared for by a private obstetrician were less likely to report involvement in the decision (51.9%; 40/77) compared with women receiving other models of care (67.0%; 120/179) (OR, 0.53; 95% CI, 0.30-0.95). Reasons for the decision to have a caesarean section The 171 women who reported involvement in the decision were asked an open-ended question: "What led you to make the decision to have a CS?". A content analysis of the 164 responses to this question indicated that women framed their responses in terms of medical risks and benefits and not in terms of non-clinical personal issues. The questions with forced-choice responses gave women the opportunity to reveal that other factors were also important (Table 1). All women were very likely to have been influenced in their decision by information from their doctor. Women who had an elective CS were influenced by factors such as their recovery and the ability to plan. In contrast, women who had an emergency CS were influenced by the physical stress of labour ("I just couldn't go on any longer"), as well their partner's reaction in the labour ward. Other issues which distinguished the two groups were considerations about pain and previous negative experiences of childbirth: and in each of these about twice as many women with an elective CS agreed or strongly agreed that these issues had influenced their decision. In addition, about four times as many women with an elective CS reported that they had been influenced by family and friends during their pregnancy. Rejecting alternative options to caesarean section We examined women's responses to: Vaginal delivery after previous CS (women who had had one previous CS) Fifty of 209 women (23.9%) for whom these data were available reported one previous CS; 17 of these women (34.0%; 95% CI, 21.2%-48.8%) reported that their doctor talked to them about the possibility of having a vaginal delivery, but they did not subsequently try to have the baby vaginally. Vaginal breech delivery Of the total sample, 62 women (22.3%) reported that they had a breech presentation, and were asked "Did the doctor suggest that it would be possible to have the baby vaginally even though it was positioned bottom first?". In 14 of 37 women (37.8%; 95% CI, 22.5%-55.2%) with whom the doctor had discussed this option, the women reported "I decided against it". External cephalic version The women with a breech presentation were also asked "Did the doctor talk to you about the possibility of turning your baby while it was still in the womb?". In 12 of 39 women (30.8%; 95% CI, 17.0%-47.6%) with whom the doctor had discussed this option, the woman reported "I decided against it". Reporting preference for caesarean section "I insisted on a CS" Women having an emergency CS were less likely to agree with this statement. Demographic factors did not affect the response. Agreement: 27.9% of 269 women (95% CI, 22.5%-33.2%) (including 13.8% who strongly agreed); 18.8% of 181 women having emergency CS v. 46.4% of 84 women having elective CS (OR, 0.27; 95% CI, 0.15-0.49). "I told the staff at the very start that I was keen to have a CS" Women having an emergency CS were less likely to agree with this statement, and the only demographic factor affecting the response was educational level, with women in an intermediate category for education being more likely to agree. Agreement: 21.3% of 268 women (95% CI, 16.4%-26.2%) (including 11.6% who strongly agreed); 13.3% of 181 women having an emergency CS v. 38.5% of 83 women having an elective CS (OR, 0.24; 95% CI, 0.13-0.47), and 29.2% of 106 women in an intermediate education category v. 16% of 159 women in lower and higher education categories (χ2 = 6.31, df = 2, P = 0.04). "At the beginning of my pregnancy, I really wanted to have this baby vaginally" Agreement was not affected by demographic factors, but fewer women attending a private obstetrician agreed (non-significant difference), and fewer women having an elective CS agreed. Agreement: 64.6% of 274 women (95% CI, 58.9%-70.3%) (agreed or strongly agreed); 57.3% of 75 women in private obstetric care v. 68.0% of 178 women in other care (OR, 0.63; 95% CI, 0.35-1.15), and 52.4% of 84 women having elective CS v. 71.0% of 186 women having emergency CS (OR, 0.45; 95% CI, 0.26-0.79). Satisfaction Interpretation of the results for satisfaction is based on the assumption that women who answered anything other than "strongly agree" to positively worded items were not entirely satisfied or may have experienced problems with their care. This approach has been recommended in previous research15 and has been applied to other Australian studies examining satisfaction in childbirth.16 An appreciable number of women were only able to "agree" to such items or were "not sure" about their care (Table 2). For example, while half the women were satisfied with the decision to have a CS (as judged by indicating "strongly agree"), a further 40.9% only "agreed" and 4.7% were "not sure". Similarly, about a third and a half of women, respectively, were unable to "strongly agree" that they were "confident in the final decision" and "believe that caesarean section was the only alternative". More than two-thirds of women were unable to "strongly agree" that they had been "given good information to prepare for the possibility of a CS". Using the related assumption that we should pay attention to any level of affirmative responses (ie, "strongly agree", "agree", or "not sure") to negatively worded items, it can be seen that about 20% of women reported that they "needed more information on other options". Similarly, between about one in 10 and one in four women expressed some degree of dissatisfaction with the decision-making process. Discussion Over a third of the women in our study felt that they were not involved in the decision to have a CS, and an appreciable proportion expressed some degree of dissatisfaction with the decision, or may not have been given sufficient information. The strengths of our study include the good response rate and the fact that we used a hospital-based sample of women, including those with private health insurance. This is an important consideration given that about one-third of childbearing women are privately insured.10 The study also avoided some of the pitfalls of recently published research which relied on women giving feedback to the clinicians involved in their care.17 A shortcoming of our study was that it was conducted in only one hospital and may not be representative of women attending other Australian centres. For example, the average age of women in our study was 30 years, compared with a mean age for childbearing women in Australia of 28.6 years.10 The broader implications of the findings need to be considered, and should be the subject of further research. Clearly, there would be public health benefits in increasing the proportion of women who feel that they have been involved in the decision to have a CS, to avoid the possibility of psychological sequelae.18 While this may not be possible for the 50% of women who felt uninvolved in the decision to have an emergency CS, there may be scope for addressing the one in five women who felt uninvolved in the decision to have an elective CS. There are, of course, some absolute indications for CS (eg, major placenta praevia, massive placental abruption where the baby is still alive, transverse lie with shoulder presentation, and cord prolapse before full dilatation), and alternatives in these instances would not be discussed. These defined reasons may comprise up to 5%-8% of all births,19 and may account for a proportion of those who felt uninvolved in the decision-making process. Our study findings suggest that an informational package would be worth testing in a randomised controlled trial. This package should be broad based, rather than targeted to specific sociodemographic groups. In addition, it should be aimed not only at women, but also their partners, and families and friends. The package, which would include videos, posters and pamphlets, should address issues such as recovery after a CS and the risks and benefits of alternatives to CS. Evaluation of outcomes could be stratified for type of CS (elective or emergency), as it is possible that education would have a more substantial impact on elective CS rates, which appear to be influenced by non-clinical issues outside the labour ward experience. Any such intervention should aim to provide women with balanced information for making a truly informed choice. It is imperative that health messages are not framed in a way that makes women feel inadequate, or that they have failed in some aspect of their pregnancy. To this end, any evaluation of interventions should include outcome data examining not only intervention rates and associated morbidity, but also looking at psychosocial outcomes, such as maternal well-being and satisfaction. The need for information is well recognised in countries such as Britain, where there has been a major drive to develop evidence-based information pamphlets for pregnant women on issues such as ultrasound scans.20 This is not to suggest that information alone will address the high rates of CS,21 which relate to a multiplicity of factors. However, this strategy may help to create a different clinical climate and would at least partially meet the needs of the almost one in five women who agreed that they needed (or were unsure whether they needed) more information on other options. Acknowledgements We wish to thank the women who participated in the study. We would also like to thank the obstetricians and the postnatal ward midwives of the Women's and Children's Hospital for their support. This study was funded by a grant from the Women's and Children's Hospital Foundation and was supported by the Department of Public Health, University of Adelaide. Dr Yaser's position was funded by the Commonwealth Government Jobskills Participation Scheme. References Commonwealth Department of Health, Housing and Community Services. Goals and targets for Australia's health in the year 2000 and beyond. Canberra: AGPS, 1993. National Health and Medical Research Council. Options for effective care in childbirth. Canberra: AGPS, 1996. What is the right number of caesarean sections [editorial]? Lancet 1997; 349: 815. Wilkinson C, McIlwaine G, Boulton-Jones C, Cole S. Is a rising caesarean section rate inevitable? Br J Obstet Gynaecol 1998; 105: 45-52. Molloy D, Richardson P. Caesarean section -- public versus private. Why the differential? A reply to "Obstetric intervention and the economic imperative". Br J Obstet Gynaecol 1993; 101: 88-90. Spurrett B, Cook CM. Why we choose caesarean section: a prospective study. Aust N Z J Obstet Gynaecol 1997; 37: 297-300. Controversies in management. Should doctors perform an elective caesarean on request? BMJ 1998; 317: 462-465. Shepherd McCC. Patent decision making: the case of delivery method after a previous caesarean section. Culture Med Soc 1987; 11: 495-508. Ryding EL. Investigation of 33 women who demand a caesarean section for personal reasons. Acta Obstet Gynaecol Scand 1993; 72: 280-285. Day P, Sullivan EA, Lancaster P. Australia's mothers and babies 1996. Sydney: Australian Institute of Health and Welfare National Perinatal Statistics Unit, 1999. (Perinatal Statistics Series No. 7.) Computerised Maternity Database. Adelaide: Women's and Children's Hospital, Clinical Information Services Database, 1998. Lumley J. Assessing satisfaction with childbirth. Birth 1985; 12 (3): 141-145. SPSS (Statistical package for the social sciences) [computer program], standard version. Chicago, Ill: SPSS Inc, 1997. Epi Info (Word processing, database and statistical program for public health) [computer program], version 6.03. Atlanta, Ga: Centers for Disease Control and Prevention, 1996. Carey RG, Posavac EJ. Using patient information to identify areas for service improvement. Health Care Manage Rev 1982; 7(2): 43-48. Brown S, Lumley J. Satisfaction with care in labour and birth. A survey of 790 Australian women. Birth 1994; 21(1): 4-13. Mould TA, Chong S, Spencer JAD, Gallivan S. Women's involvement with the decision preceding their caesarean section and their degree of satisfaction. Br J Obstet Gynaecol 1996; 103: 1074-1077. 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. Francome C, Savage W. Caesarean section in Britain and the United States -- 12% or 24%: is either the right rate? Soc Sci Med 1993; 37: 1199-218. Oliver S, Rajan L, Turner H, et al. Informed choice for users of health services: views of ultrasonography leaflets on women in early pregnancy, midwives, and ultrasonographers. BMJ 1996; 313: 1251-1253. Fraser W, Maunsell E, Hodnett E, Moutquin J. Randomised controlled trial of a prenatal vaginal birth after cesarean education and support programme. Am J Obstet Gynecol 1997; 176: 419-425. (Received 21 Sep 1998, accepted 30 Apr 1999) Authors' details University of Adelaide, Adelaide, SA. Deborah A Turnbull, MPsych(Clin), PhD, Senior Lecturer in Public Health (Epidemiology), Department of General Practice; Anisa Yaser, MB BS, Research Officer, Department of Public Health; Vanessa Carty, MPsych, Research Student, Department of Public Health; Jeffrey S Robinson, FRCOG, FRACOG, Professor, and Head, Department of Obstetrics and Gynaecology. Department of Perinatal Medicine, Women's and Children's Hospital, Adelaide, SA. Chris Wilkinson, MPH, FRACOG, Staff Specialist Obstetrician Gynaecologist. John M Svigos, FRCOG, FRACOG, Senior Visiting Medical Officer. Reprints will not be available from the authors. Correspondence: Dr D A Turnbull, Department of General Practice, University of Adelaide, SA 5005. Email: dturnbull@medicine.adelaide.edu.au 1: Reasons women give for deciding to have a caesarean section (CS)* Elective Emergency†OR (95% CI)Information from doctor 75.7% (53/70)77.4% (79/102)0.91 (0.42-1.98)Considerations about recovery60.0% (42/70)36.3% (37/102)2.64 (1.35-5.18)Partner's attitude in general44.3% (31/70)35.3% (36/102)1.46 (0.75-2.85)Couldn't go on any longer21.2% (14/66)44.5% (45/101)0.34 (0.15-0.72)Could plan what was going to happen38.6% (27/70)16.0% (16/100)3.30 (1.52-7.22)Considerations about pain30.4% (21/69)15.7% (16/102)2.35 (1.06-5.26)Previous pregnancy/labour awful26.5% (18/68) 12.0% (12/100)2.64 (1.10-6.41)Partner's reaction in the labour room8.8% (6/68)23.8% (24/101)0.31 (0.10-0.85)Influence of family/friends during pregnancy15.7% (11/70)3.9% (4/102)4.57 (1.27-20.39)Felt too old4.5% (3/67)2.0% (2/102)2.34 (0.26-28.63)Previous infertility4.3% (3/69)2.0% (2/101) 2.25 (0.25-27.48)Medical risks/benefits not that important21.4% (15/70)27.0% (27/100) 0.74 (0.34-1.61)*Missing data are excluded. †Some totals exceed 100 (= number of women with emergency CS who indicated that they were involved in the decision-making process), because two additional women answered some of these questions, but denied involvement in the decision. Back to text 2: Women's satisfaction with decision to have a caesarean section (CS)*StronglyNotStronglyItemagreeAgreesureDisagreedisagreeSatisfaction with the decision itselfSatisfied with the decision (n = 274)50.4%40.9%4.7%2.9%1.1%Confident in the final decision (n = 276)62.3%31.2%2.9%2.9%0.7%Believe that a CS was the only alternative (n = 276)53.3%26.8%12.3%5.4%2.2%Now feel a bit cheated (n = 274)5.1%10.9%9.1%28.5%46.4%Believe that CS may not have been necessary (n = 275)2.2%2.5%14.2%31.3%49.8%Satisfaction with information provisionGiven good information about why CS was necessary (n = 275)58.2%33.1%4.7%3.3%0.7%Needed more information on otheroptions (n = 272)2.9%4.4%11.8%48.5%32.4%Given good information to prepare for possibility of CS (n = 274)28.8%40.1%10.2%12.8%8.0%Satisfaction with decision-making processFelt pressured to try to have the baby vaginally (n = 272)4.0%7.4%5.1%34.9%48.5%Unhappy about the amount of say in the decision (n = 275)5.5%6.5%5.8%45.1%37.1%Took too long to make decision (n = 274)7.7%9.9%8.4%38.7%35.4%Felt pressured by staff to have a CS (n = 272)1.8%3.3%3.3%36.8%54.8%* Missing data are excluded. Back to text Reader response to: Women's role and satisfaction in the decision to have a caesarean section I commend the authors for this paper. However I wonder if the contention that unless the respondents "strongly agree" or "strongly disagree", the response is mixed is debatable. Patient satisfaction is multidimensional and to focus on patient's response to assess whether for example the information given has been adequate may be unnecessarily harsh on the care givers. Almost all major decisions are accompanied by a degree of regret and doubt by a proportion of people. To infer, unless the patient is entirely satisfied with something, that the care given was somehow less than satisfactory is to demand too much of a complex human relationship, that of a technically dependent patient and a care giver. I note that only 61.5% felt that they were involved in the decision to have a caesarean section, and only 81.4% in the elective cases where presumably there was ample time to ask for further information. I presume that they had in fact legally consented to the decision. What would have been interesting is a personality study on all the respondents. It may be that information are not the issue but the inherent psychological characteristics of the study subjects. Information packs may be useful but the decision to consent to a caesarean section rests with the woman alone. Packs aimed at her partner, family and friends may do more harm than good where there are conflicting opinions. One only has to look at the diverse response in this study itself to confidently predict that there will be such conflict amongst any group and an already potentially emotional decision may be further complicated. Tony Chung Associate Professor Department of Obstetrics & Gynaecology The Prince of Wales Hospital Shatin, NT Hong Kong SAR, China Submitted by email 24/6/99, posted online with author response 28/6/99. Reply by the authors We would like to thank Dr Chung for his thoughtful reply to our paper. The use of 'strongly agree' and 'strongly disagree' as markers of satisfaction has a precedence in the literature on satisfaction with hospital care.1 Importantly, it has been used in relation to maternity service provision.2 Although this approach may seem unnecessarily critical, it avoids over-simplistic interpretations, as demonstrated in a British report into this issue which concluded (after using disputed methodology) that attempts to reduce caeasrean section rates may be futile, because of women's preferences.3-5 Dr Chung's second point relates to the issue of legal consent. In contrast, our paper examines participation in decision making, for which the signing of informed consent is only one part of a broader process. The paper does not intend to infer that the requirements for informed consent for a procedure have been neglected. The point about measuring women's personalities is an interesting one. There is research which finds increased psychological morbidity in women demanding caesarean section in the absolute absence of clinical indications.6 In contrast to this somewhat rare individual,6 our study examines a cross-section representing about one quarter of the women at the study hospital. Dr Chung's point implies that the problem rests with these women. This seems an unreasonable assumption to make of such a large proportion of childbearing women. It is imperative that we avoid 'blaming' the women. Finally Dr Chung is concerned that the provision of information to the broader community may lead to conflict. Our research suggests that there is already an involvement of family and friends in the decision making process. It is for this very reason that we hypothesize that providing evidenced based information may lead to a more beneficial outcome. To this end any randomized controlled trial evaluating such a strategy should include not only clinical outcomes but also psychosocial variables such as anxiety, feelings of failure and reassurance. Deborah Turnbull Chris Wilkinson Submitted by email 28/6/99, posted online 28/6/99. 1. Carey RG, Posavac EJ. Using patient information to identify areas for service improvement. Health Care Manage Rev 1982; 7(2): 43-48. 2. Brown S, Lumley J. Satisfaction with care in labour and birth. A survey of 790 Australian women. Birth 1994; 21(1): 4-13. 3. Mould TA, Chong S, Spencer JAD, Gallivan S. Women's involvement with the decision preceding their caesarean section and their degree of involvement. Br J Obstet Gynaecol 1996; 103: 1074-1077. 4. Grant JM, Women are satisfied with caesarean section [editorial; comment]. Br J Obstet Gynaecol 1996; 103 (11): 7-8. 5. Hemminki E. Cesarean Sections: Women's choice at giving birth? Birth 1997; 24: 124-125. 6. Ryding EL. Investigation of 33 women who demanded a cesarean section for personal reasons. Acta Obstet Gynecol Scand 1993; 72: 280-285. Back to top of article Back to reader response

Deborah A Turnbull · Chris Wilkinson · Anisa Yaser · Vanessa Carty · John M Svigos · Jeffrey S Robinson

Safe motherhood: impossible dream or achievable reality? John O'Loughlin Empowerment of women is the only way to ensure safer motherhood MJA 1997; 167: 622-625 Introduction - Maternal mortality in Australia - Maternal mortality in developing countries - Maternal injury - Consequences of maternal death - Causes of unsafe motherhood - The solution - References - Authors' details - Pictures - - - ©MJA1997 Introduction In Australia and other developed countries, women embark on pregnancy with little or no fear for their own safety. Along with the other great strides that medical science has taken in this century, there have been huge reductions in maternal and perinatal mortality rates. In developed countries, maternal mortality rates are no longer used as measures of the quality of obstetric services. The emphasis has long since shifted to perinatal mortality and morbidity. But how safe is motherhood today in the developing countries of the world or among disadvantaged minority groups? Maternal mortality in Australia The World Health Organization (WHO) defines maternal death as "the death of a woman while pregnant, or within 42 days of the completion of the pregnancy, irrespective of the duration and the site of the pregnancy, from any cause related to or aggravated by the pregnancy or its management".1 In Australia each year there are about 260 000 confinements,2 and in 1990 there were 25 maternal deaths3 (i.e., nine per 100 000 live births). This is comparable with the lowest rates reported globally. However, these figures hide an unpalatable fact. Births to women of Australian Aboriginal or Torres Strait Islander descent represent about 3% of the total number of births per year, but account for about 30% of the overall maternal mortality.4 Accordingly, in 1990, the maternal mortality rate among Aboriginals and Torres Strait Islanders was about 40 per 100 000 live births, as opposed to 2-3 per 100 000 live births in non-Aboriginal women. Governments continue to spend very large amounts of money in an attempt to remove this discrepancy, but clearly have not been successful. Money alone cannot improve the socioeconomic status of this disadvantaged group. Maternal mortality in developing countries The difficulties experienced by Aboriginal women in Australia are reflected to a far greater degree among the peoples of the developing world. UNICEF and WHO estimates, based on a new approach to data collection, show that in 1990, 585 000 women died from causes related to pregnancy and childbirth.3 This is in excess of one death per minute. Over 140 000 died from haemorrhage; about 75 000 died from attempting to abort themselves; another 75 000 died from the brain and kidney damage of eclampsia; 100 000 died of sepsis; and about 40 000 died from obstructed labour.5 Eighty-seven per cent of births occur in developing nations, and these births account for 99% of maternal deaths (Box 1). Maternal injury For every woman who dies from a pregnancy-related condition, about 30 more (i.e., over 15 million women per year) sustain a severe and permanent injury, such as chronic pelvic inflammatory disease, vaginal, rectal and perineal tearing leading to urinary and faecal incontinence, or Sheehan's syndrome (excessive blood loss causing pituitary gland necrosis and thus ovarian, adrenal and thyroid insufficiency).5 "Obstetric fistula" is a vesicovaginal fistula resulting from pressure necrosis from the fetal head on vagina and bladder tissues during prolonged and obstructed labour. As a consequence, there is a constant and uncontrollable flow of urine from the vagina. The woman and her clothing smell, her vulva becomes excoriated and painful, and she is often banished from her home to live with the domestic animals. She must walk everywhere as she cannot use any form of transport; she loses her family, her friends and often in despair surrenders her own life. Approximately 80 000 women develop obstetric fistula each year.5 Female genital mutilation -- the cutting away of the external genitalia, often including the clitoris -- is performed on girls aged 4-12 years. Approximately two million girls are so mutilated every year, mainly in Egypt, Ethiopia, Kenya, Nigeria, Somalia and Sudan.5 It is designed to preserve virginity and ensure marriageability. Giving birth is extremely painful -- the scarred vaginal opening cannot stretch to allow passage of the fetal head -- and results in injury and extensive tearing, often causing permanent damage.5 In developing countries women not uncommonly have up to 10 pregnancies during their lifetime. Based on the probability that some will suffer more than one obstetric injury during their lifetime, the total number of women affected can be conservatively estimated at some 300 million, more than a quarter of the adult women now alive in the developing world.5 Consequences of maternal death The 585 000 women in the world who die in pregnancy each year leave behind them at least one million motherless children. The death of a mother is almost twice as dangerous for her surviving children as the death of a father, and her daughters are almost twice as likely to die as her sons. 6 Women in developing nations are the major producers of food. They are responsible for 60%-80% of all food production in Africa, and 40% in Latin America. 7 Furthermore, unpaid household labour by women is worth about four trillion (10 12 ) US dollars per year, or about a third of world economic production (1993 global figures). 8 Clearly, addressing maternal health in developing nations is also sound economics. Causes of unsafe motherhood To find solutions we need to know and understand the causes of maternal mortality and morbidity: Poverty; Poor access to health services; Pregnancies -- too many, too close, too early, too late; Poor nutrition and health; and Low social and economic status of women. All of these are interlinked; a positive change in one is likely to lead to positive changes in all of the others. 1. Poverty There has been no significant decline in poverty rates throughout most of the developing world over the past decade.9 In developing countries the individual family is likely to be impoverished, with no resources for emergencies. When daily survival of the family is at risk, mothers will use fewer resources for their own health. Moreover, most developing countries spend less on health and welfare than they do on servicing their debts.7 However, poverty does not necessarily mean poor maternal health. India, although a nation making economic progress, is still beset by the problems of the developing world -- a dense population and widespread poverty and illiteracy. Kerala State, in south-west India, however, has achieved a maternal mortality rate a third of the rate in the rest of India (Box 2). 2. Access to maternal health services In general, most women in the developing world, particularly in rural areas, have no access to adequate maternal health services. Only low cost strategies unlikely to make a major impact on overall maternal health have been introduced to combat this problem. These are: More antenatal care: Most major obstetric complications occur without warning and can kill within hours. Appreciable delay between the onset of the complication and the initiation of effective treatment can be fatal. Most women in the developing world who die in childbirth do so remote from a hospital. In most instances they would not have attended for antenatal care, and neither would their death have been prevented by it. A study in Zimbabwe in 1994 showed that a lack of antenatal care contributed to only 7% of all rural and 10% of all urban maternal deaths.12 Traditional birth attendants: It is claimed that 55% of women in the developing world are assisted in labour by trained birth attendants,13 and that there is a correlation between countries with high mortality rates and a low percentage of trained birth attendants.13 However, many birth attendants have had no formal medical training and their actions may be guided by cultural prejudice. Government training programs have often been inadequate or ineffectual, and many graduates can neither predict nor cope with serious complications.5 Screening: The screening of pregnant women to determine high and low risk groups, although useful, will not detect a no-risk group. Every pregnancy, irrespective of risk category, may develop a life-threatening complication and needs prompt access to skilled obstetric intervention. Recognition of the limitations of these low cost strategies has led to the concept of "essential obstetric care". Essential obstetric care: Essential obstetric care incorporates the provision of properly trained and skilled birth attendants able to recognise abnormality in labour, able to deal with unpredictable complications as they arise, and able to arrange transfer to a facility which can cope with obstetric emergencies. In India, about three-quarters of the 150 000 women who die each year in childbirth live within a few kilometres of a health unit or district hospital, but those in attendance often fail to recognise complications early enough or arrange for transport to a health facility. Such facilities, even if acces sible, are often inadequately staffed or equipped. Even in the United Kingdom, despite good standards of nutrition, health and hygiene, maternal mortality rates did not fall until the advent of skilled obstetric care, surgery and anaesthesia for the treatment of haemorrhage, obstructed labour and sepsis. Cultural barriers: Often cultural barriers exist that militate against the use of whatever obstetric services are in existence. Many women expect to deliver at home and many refuse to see a male doctor. Many husbands refuse to provide money for medical treatment, or won't allow their wives to be removed from the family compound. Ignorance of potential complications of labour is widespread: obstructed labour can be regarded as a consequence of a wife's infidelity.5 3. Pregnancies too early, too late, too many, too close Frequent pregnancies interspersed with long lactation periods deplete maternal energy, iron, and calcium stores. Women in Bangladesh and Pakistan spend more than half of their time between the ages of 15 and 45 either pregnant or breastfeeding.5 The greater the number of pregnancies, the greater the risk of complications. Teenage pregnancy and pregnancy in the 40s likewise increase maternal risk. Cultural determinants and inequality of the sexes mean that many women have no reproductive choice. If all women who did not want any more children were able to stop becoming pregnant, the birth rate would drop by 57% in Latin America, 23% in Africa and 43% in Asia.14 Of all maternal deaths, 58% could be prevented by a combined approach of general fertility reduction, abortion services, and family planning targeted at high risk groups.15 Almost 50% of couples in the developing world have little or no access to family planning;6 less than 2% of all government health spending and less than 2% of international aid goes to family planning.5 Contraceptive technology is well advanced, and research into distribution methods shows that even poor societies can afford good family planning programs.16 Furthermore, it is possible to supply contraception in ways that are acceptable to all countries and cultures.5 The most important ingredient is the will of governments (rather than resources) to provide these services (Box 3, below). 4. Poor nutrition and health Most women in developing countries suffer from malnutrition during pregnancy and lactation. Custom and tradition have ensured that women have a clearly defined provider role. They are the labourers in the field, and their toil provides the family with food, but men and boys are fed before women and girls.17 About a third of women in Sub-Saharan Africa have an inadequate daily calorie intake,18 while 60%-70% of pregnant women in developing countries are anaemic19,20 and therefore more likely to die from postpartum haemorrhage.21 Protein, mineral and vitamin deficiencies are also widespread, but these can be easily rectified by health authorities with relatively cheap intervention programs. R educing protein-energy malnutrition is more complex.7 5. The low socioeconomic status of women In developing countries, on average, women earn 50%-70% of the income earned by men for similar work, and in Asia the wage gap reaches 50%.22 Women often do the tasks which require considerable physical exertion, regularly working 15 hours a day.23,24 Strenuous physical activity contributes to poor pregnancy outcomes, but women's health is seen by women and by others as a low priority. This acceptance comes from a lack of knowledge and education. Knowledge is power, and they have little knowledge. Illiteracy rates may be almost 50% higher for women than for men,25 and women without formal education have a greater risk of maternal mortality than educated women.26,27 Although education and social welfare are not aimed at improving maternal health, increased spending in these areas leads to sustained reduction in maternal mortality and morbidity.10 The solution -- empowerment of women At the Safe Motherhood conference in Nairobi, Kenya, in 1987, the world set itself the target of reducing maternal morbidity by half by the year 2000. It was considered that almost all conditions that lead directly to maternal morbidity are either preventable or treatable, and that with access to better medical facilities a reduction of unnecessary loss of life of this order was achievable. In many areas of the developing world various initiatives and programs have been implemented and it is to be hoped that some progress will be made. However, with the publication of the 1990 maternal mortality estimates,3 derived by new and improved methods, it became apparent that the magnitude of the problem was even greater than previously realised, and that major intervention would be necessary if these targets were to be realised. Better access to family planning services, widespread provision of essential obstetric care and programs to deal with malnutrition in women can be provided by making a relatively small increase in the overall health budget or by changing health care priorities. Authorities such as the World Health Organization and the World Bank 7 have clearly demonstrated that increased expenditure in these areas will produce handsome economic returns. Why, then, is women's health not given greater priority? The reason is the male-dominated culture of much of the developing world. Control can only be exercised by power and this power resides in the hands of men. This describes the lot of women in much of the Third World. Without knowledge they are powerless, and will remain so. Just as we have found with Australian Aboriginal women, women in the developing world will never achieve satisfactory health outcomes until they themselves, through the acquisition of knowledge and learning, are able to compete, at all levels of society, for their fair and equitable share of power and influence. For these women, empowerment is the ultimate key, the way forward to safe motherhood. References National Health and Medical Research Council. Health Care Committee. Report on maternal deaths in Australia 1988-1990. Canberra: AGPS, 1993: 5. Day P, Lancaster P, Huang J. Australia's mothers and babies, 1992. Sydney: Australian Institute of Health and Welfare, National Perinatal Statistics Unit, 1997. World Health Organization/UNICEF. Revised 1990 estimates of maternal mortality. A new approach by WHO and UNICEF . Geneva: WHO/UNICEF, April 1996. O'Connor MC, Bush A. Pregnancy outcomes of Australian Aborginals and Torres Strait Islanders [editorial]. Med J Aust 1996; 164: 516-517. UNICEF. The progress of nations. Adamson P, editor. New York: UNICEF, 1996: 3-9. Pittrof R, Stanfield P. Raising awareness of safe motherhood. A collaborative project. Action for Safe Motherhood (UK) and Teaching Aids at Low Cost. St Albans, UK: TALC, October 1995. World Bank. World Development Report 1993. Investment in health. New York: Oxford University Press, 1993: 6, 9, 113. Freedman LP, Maine D. Women's mortality: a legacy of neglect. In: Koblinsky M, Timyan J, Gay J, editors. The health of women -- a global perspective. Boulder: Westview Press, 1993: 147-170. World Bank. World Development Report 1992. New York: Oxford University Press, 1992. Franke RW, Chasin BH. Kerala State, India: radical reform as development. Int J Health Services 1992; 22: 139-156. State of the World's Children. Oxford: Oxford University Press, 1996. Mbizvo MT, Fawcus S, Lindmark G, Nystr¿m L and the Maternal Mortality Study Group. A community based study of maternal mortality in Zimbabwe. Lund: Reprocentralen HSC, Uppsala University, 1994. World Health Organization: coverage of maternity care. A tabulation of available information, 3rd edition. Geneva: WHO: 1993 (WHO/FHE/MSM/93.7:12.) Eschen A, Whittaker M. Family planning. A base to build on for women's reproductive health. In: Koblinsky M, Timyan J, Gay J, editors. The health of women -- a global perspective. Boulder: Westview Press, 1993: 105-131. Winikoff B, Sullivan M. Assessing the role of family planning in reducing maternal mortality. Stud Fam Plan 1987; 18: 128-143. Potts M. Costs, finance and human resources. In: Senanayake P, Kleinman R, editors. Family planning, meeting challenges, promoting choices. Proceedings of the IPPF Congress, 1992. Cranforth UK: Parthenon Publishing Group, 1992: 709: 21. Government of Lesotho, Health Ministry. Lesotho country paper. Presented at the Conference on Safe Motherhood for the Southern African Development Coordinating Council (SADCC) countries. Harare, Zimbabwe: 1990. Mhloyi, M. Maternal mortality in the SADCC region. Background paper for the Conference on Safe Motherhood for the Southern African Development Coordinating Council (SADCC) countries. Harare, Zimbabwe: SADCC, 1990. DeMaeyer D, Adies-Tegman M. The prevalence of anaemia in the world. World Health Stat Q 1985; 38: 302-316. Jordan EA, Sloan LS. The prevalence of anaemia in developing countries 1979-89. An annotated bibliography. Arlington, Va: MotherCare 1991. (MotherCare Working Paper 7A.) United Nations Fund for Population Activities (UNFPA). State of the world population 1989. Investing in women: the focus of the nineties. New York: United Nations Population Fund, 1989. United Nations Department of International Economic and Social Affairs (UNDIESA). The world's women: trends and statistics 1970-1990. New York: United Nations, 1991. Bleiberg FM, Burn TA, G oihman S, Gouba E. Duration of activities and energy expenditure of female farmers in dry and rainy season in Upper Volta. Br J Nutrit 1980; 43: 71-82. Roberts SB, Paul AA, Cole TJ, Whitehead RG. Seasonal changes in activity, birth weight and lactation performance in rural Gambian women. Trans R Soc Trop Med Hyg 1982; 76: 668-678. United Nations Educational Scientific and Cultural Organization. Statistical yearbook 1992. Paris: UNESCO, 1992. Harrison KA. Approaches to reducing maternal and perinatal mortality in Africa. In: Philpott RH, editor. Maternity services in the developing world. What the community needs. London: Royal College of Obstetricians and Gynaecologists, 1980: 52-69. Briggs N. Illiteracy and maternal health: educate or die. Lancet 1993; 341: 1063-1064. This is an abridged version of the 57th Edward Stirling Memorial Lecture, given at the University of Adelaide on 21 August 1996. Authors' details 43 Walter Street, North Adelaide, SA. John O'Loughlin, FRACOG, FRCOG, Obstetrician and Gynaecologist; member of the Executive Board of the International Federation of Gynecology and Obstetrics. Reprints will not be available from the author. Correspondence: Dr J O'Loughlin, 43 Walter Street, North Adelaide, SA 5006. - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia. We appreciate your comments.

John O'Loughlin

Abstract Objectives: To estimate the number of pregnant women in New South Wales who had not been tested for gestational diabetes mellitus (GDM) during the period 1991-1994. Design: The number of women not tested for GDM was estimated from the recorded data available in the NSW Midwives Data Collection (MDC) annual reports and compared with three incidence surveys. Main outcome measure: The number of pregnant women not tested for GDM. Results: Over the four-year period, the average annual recorded MDC incidence of GDM was 2.2%. This percentage was adjusted up to 3.3% after review of the MDC validation study and an incidence study. However, the expected incidence of GDM from three incidence surveys was 6.6%. Thus, half of the pregnant women in NSW do not appear to have been tested for GDM. Conclusion: For the four-year period 1991-1994, an estimated 50% of women in NSW were probably not tested for GDM. MJA 1997; 167: 14-16 Introduction Gestational diabetes mellitus (GDM) is carbohydrate intolerance of variable severity with onset or first recognition during the current pregnancy.1 Undiagnosed, and therefore untreated, diabetes is a serious disorder of pregnancy with an increased perinatal mortality rate.2,3,4 Following the Australasian Diabetes in Pregnancy Society's (ADIPS) 1991 recommendation that all pregnant women should be tested for GDM in every pregnancy,5 the NSW Midwives Data Collection (MDC) recorded a gradual increase in the number of women with GDM from 1.5% in 1991 to 2.7% in 1994. In contrast, from surveys in other Australian centres since 1991, the incidence of GDM ranges from 5.5%-8.8%.4,6-8 The difference between these rates and those recorded by the MDC suggests that many women are still not being tested for GDM in NSW and are at risk of complications which could either be prevented or substantially reduced. The purpose of our study was to estimate the extent of undiagnosed GDM in NSW for the period 1991-1994 by estimating the number of pregnant women who had not been tested for GDM. Methods We obtained data from the NSW MDC annual reports for 1991-1994. It is a statutory requirement under the Public Health Act 1991 (NSW) that all births (including home births) are reported to the MDC, which records information on maternal medical and obstetric conditions, delivery and infant characteristics. Incidence of GDM recorded on the MDC was compared with the incidence of GDM found in three different Australian surveys. The sources of these data are shown in Box 1. The three surveys used the 75 g oral glucose tolerance test for the diagnosis of GDM based on the ADIPS criteria.5 According to these criteria, GDM is diagnosed if the fasting plasma glucose level is ≥ 5.5 mmol/L and/or the two-hour plasma glucose level is ≥ 8.0 mmol/L. By combining these data, we obtain an average incidence of GDM, which we refer to as the expected incidence. At the Mercy Hospital for Women in Melbourne, a 50 g glucose load is used and capillary blood samples taken for plasma glucose measurement; a diagnosis of GDM is made if the glucose level at one hour is ≥ 9.0 mmol/L and the glucose level at two hours is ≥ 7.0 mmol/L. The incidence of GDM during the period 1991-1994 was 8.8%.4 While the glucose load and diagnostic criteria are different, a comparison of the Mercy Hospital and ADIPS criteria found that they diagnosed similar women and in the same proportion.9 While the incidence of GDM will vary depending on the ethnic composition of the population being examined, these surveys all included a majority of people of European extraction. Validation of the NSW Midwives Data Collection A 1990 validation study of the MDC, using a 1% sample, found that the recording of data relating to GDM had a sensitivity of 66.7% and a specificity of 99.6%.10 That is, when a case of GDM was recorded it was accurate, but only two-thirds of the known cases were recorded. Therefore, by increasing the recorded MDC incidence by 50% (representing the underestimation of GDM according to the sensitivity data), we are likely to obtain the actual MDC incidence, which we refer to as the estimated incidence. A 1993 survey carried out in the Wollongong area to determine the incidence of GDM was compared with the recorded MDC incidence of GDM in the area.6 The MDC recorded a rate of 5.0%, while the survey found a rate of 7.2%. A 50% addition to the recorded MDC incidence (as indicated by the validation study) gave a figure of 7.5%, which is similar to the 7.2% found in the survey. Therefore, the addition of a 50% correction factor to the recorded MDC incidence of GDM is a reasonable approximation. Results The proportion of women with a diagnosis of GDM recorded by the MDC for each different Area Health Service in NSW between 1991 and 1994 is shown in Box 2. It was assumed that the accuracy of data recording in all Area Health Services was equal and had not changed over the four-year period. For the whole of NSW, the percentage of women diagnosed with GDM increased from 1.5% in 1991 to 1.9% in 1992 (P < 0.001) and from 1.9% in 1992 to 2.6% in 1993 (P < 0.001). There was no significant change between 1993 and 1994. For the four-year period, the overall recorded MDC incidence of GDM was 2.2%. In the Sydney metropolitan area, the incidence of GDM ranged from a high of 3.1% in the Central Sydney Area Health Service to a low of 1.5% in the Northern Sydney Area Health Service. The incidence of GDM in the main metropolitan areas of Sydney, Newcastle and Wollongong was 2.4%, which was significantly higher than the country areas (1.6%) (P < 0.001). Some country areas also showed marked changes over the four-year period. For example, the proportion of women diagnosed with GDM increased from 0.8% to 2.7% in the Mid West Area Health Service and declined from 3.4% to 0.8% in the Far West Area Health Service. By applying the 50% correction factor to the recorded MDC incidence of 2.2%, the estimated incidence of GDM is 3.3%. However, the expected incidence of GDM is 6.6% (Box 1). Therefore, half of the pregnant women in NSW during the period 1991-1994, or 173 534 women, were probably not tested for GDM. Discussion The expected incidence of GDM was derived from pooled incidence data from the three surveys where the diagnosis had been based on the ADIPS criteria. The lowest incidence was reported in the two surveys which used data gathered from prenatal clinics.7,8 A higher incidence was reported in the survey which included private patients in the data collection.6 The higher rate found in the survey which included private patients could be anticipated, as private patients are older than clinic patients and increasing age is a high risk factor for developing GDM.4 Thus, the expected incidence of GDM of 6.6% is likely to be conservative. The recorded MDC incidence of GDM for 1991-1994 was lower than the expected incidence. With the application of the 50% correction factor to the recorded MDC incidence (as suggested by the MDC validation study and by data collection in the Wollongong area6 ) and a conservative estimate for the expected incidence of GDM, it is possible that half of all the women who delivered in NSW between 1991 and 1994 were not tested for GDM. Some women may have decided not to be tested for GDM. Others may not have been able to tolerate the glucose solution. In most cases, however, the decision not to test would have undoubtedly been made by the clinician responsible. Box 2 shows that testing for GDM is not evenly distributed, with a recorded MDC incidence range of 0.7%-3.2%. Of particular concern is that lower than average rates of testing were found in areas where a higher than average rate of GDM could be anticipated. In metropolitan Sydney, the lowest number of recorded cases of GDM were from the Northern Sydney Area Health Service. The MDC has shown that this is also the Area Health Service with the highest proportion of women aged 35 years or over at the time of delivery, a risk factor for GDM. An incidence of GDM of at least 10%4 could be anticipated in this age group. Women with an Aboriginal background have a high incidence of GDM.8 The New England and Macquarie Area Health Service, with a high proportion of Aboriginal Australians, had a rate of GDM less than the non-metropolitan average. The Far West Area Health Service also has a high proportion of Aboriginal Australians, and the recorded incidence of GDM there fell over the four-year period from 3.4% to 0.8%. Observational studies of women with untreated GDM have found a higher perinatal mortality rate than that found in glucose-tolerant women.2,3 At the Mercy Hospital for Women in Melbourne, Beischer et al. showed that, despite a steady reduction in the overall perinatal mortality rate, women who were not tested for GDM (and therefore not treated) had a significantly higher perinatal mortality rate than women who were tested.4 An estimate can be made of the excess perinatal mortality rate for women in NSW who have not been tested for GDM ( Box 3). Although the recorded incidence of GDM has increased (particularly in the two years after the ADIPS recommendation for universal testing was made), our results confirmed our belief that not all pregnant women in NSW are being tested for GDM. This may have implications for perinatal mortality rates. References Metzger BE. Summary and recommendations of the Third International Workshop-Conference on Gestational Diabetes Mellitus; 1991 Dec. Diabetes 1991; 40 Suppl 2: 197-201. O'Sullivan JB, Charles D, Mahan CM, et al. Gestational diabetes and perinatal mortality rate. Am J Obstet Gynecol 1973; 116: 901-904. Pettitt DJ, Knowler WC, Baird R, et al. Gestational diabetes: infant and maternal complications of pregnancy in relation to third-trimester glucose tolerance in the Pima Indians. Diabetes Care 1980; 3: 458-464. Beischer NA, Wein P, Sheedy MT, et al. Identification and treatment of women with hyperglycaemia diagnosed during pregnancy can significantly reduce perinatal mortality rates. Aust N Z J Obstet Gynaecol 1996; 36: 239-247. Martin FIR. The diagnosis of gestational diabetes. Med J Aust 1991; 155: 112. Moses R, Griffiths R, McPherson S. The incidence of gestational diabetes in the Illawarra area of New South Wales. Aust N Z J Obstet Gynaecol 1994; 34: 425-427. Martin FIR, Ratnaike S, Wootton A, et al. The 75 g oral glucose tolerance in pregnancy. Diabetes Res Clin Pract 1995; 27: 147-151. Yue DK, Molyneaux LM, Ross GP, et al. Why does ethnicity affect prevalence of gestational diabetes? The underwater volcano theory. Diabet Med 1996; 13: 748-752. Henry OA, Shelley-Jones DC, Oats JN, et al. Comparison of the 50 g capillary plasma glucose tolerance test with the 75 g venous plasma glucose tolerance test in pregnancy. J Obstet Gynecol Res 1996; 22: 215-219. Epidemiology and Health Services Evaluation Branch, Public Health Division, NSW Health Department. Validation Study of the New South Wales Midwives Data Collection 1990. Public Health Bull 1993; 4 Suppl 8: S5. (Received 15 Jan, accepted 8 May, 1997) Authors' details Illawarra Area Health Service, NSW. Robert G Moses, FRACP, Clinical Director of Diabetes Services. Prince of Wales Hospital, Sydney, NSW. Stephen Colagiuri, FRACP, Director of Diabetes Services.

Robert G Moses · Stephen Colagiuri

Withdrawal of nifedipine capsules: jeopardising the treatment of acute severe hypertension in pregnancy? Mark A Brown, Lesley M E McCowan, Robyn A North, Barry N Walters (for the Council of the Australasian Society for the Study of Hypertension in Pregnancy) Short-acting oral nifedipine has been withdrawn from the Australian market because of reports of its adverse effects after long-term treatment in non-pregnant patients with heart disease. This will have a major impact on the treatment of acutely hypertensive pregnant women, in whom the drug has proven to be safe, effective and easy to administer. Should pregnant women be forced to use less suitable agents, thus threatening their own and their babies' health? (MJA 1997; 166: 640-643) Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Introduction - Antihypertensive medications in pregnancy - Adverse effects of nifedipine - Risk-benefit analysis of nifedipine in pregnancy - Withdrawal of nifedipine from the Australian market - Conclusions - Acknowledgement - References - Authors' details Make a comment - - ©MJA1997 Introduction Pre-eclampsia is the development of hypertension after 20 weeks' gestation in a woman with no known history of hypertension or renal disease, whose blood pressure was normal in the first half of the pregnancy and returns to normal after delivery.1 Despite advances in maternal and neonatal care, it remains an important cause of maternal morbidity (and sometimes mortality) and of fetal prematurity, growth retardation and perinatal death. The dangers of cerebral haemorrhage in pre-eclampsia and of convulsions (eclampsia) have led to the belief that severe hypertension (systolic blood pressure 170 mmHg and/or diastolic blood pressure 110 mmHg) should be treated promptly in pre-eclamptic women. However, the ability to treat acute hypertensive crises in pregnancy is about to be retarded considerably because of recommendations by the Australian Drug Evaluation Committee (ADEC) to withdraw short-acting nifedipine capsules,2 one of the most common drugs for treating acute severe hypertension in pregnancy, effective from 1 May 1997. Antihypertensive medications in pregnancy There are only a few options for the treatment of acute severe hypertension in pregnancy. Nifedipine (given orally or sublingually) and hydralazine (given intravenously or, sometimes, intramuscularly) are the most commonly used agents. They have both been endorsed for use for severe hypertension in pregnancy by the Australasian Society for the Study of Hypertension in Pregnancy (ASSHP) on the basis of clinical studies and extensive clinical experience by members of the ASSHP and other societies.1 Intravenous diazoxide was one of the earliest drugs to be used.3 It is effective but can cause sudden maternal hypotension, maternal hyperglycaemia and fetal hypoglycaemia, uterine atony and fetal distress. It is best given as incremental small-dose boluses to avoid a sudden drop in blood pressure. Intravenous labetalol has been used less widely but is at least as effective as intravenous diazoxide.3 Its safety in preterm infants has been questioned,4 with higher perinatal mortality than in subjects given hydralazine in one study. Intravenous glyceryl trinitrate is a potential candidate for treating severe hypertension in pregnancy.5 It has not yet been used widely and there is a risk that its predominant venodilator effect could reduce preload and compromise an already threatened cardiac output.6 Intravenous sodium nitroprusside is an excellent drug for acute severe hypertension, but its use in pregnancy is precluded by the risk of fetal cyanide toxicity.7 Adverse effects of nifedipine Unfortunately, some authors fail to discriminate between pregnant and non-pregnant subjects when providing recommendations about the continued use of nifedipine capsules. For example, Grossman et al. did a MEDLINE search of articles from 1966 to 1994 using the terms "side-effects" and "nifedipine" to document serious adverse effects with oral or sublingual nifedipine.8 They recommended that, given the seriousness of the reported adverse cardiac events and the lack of any clinical documentation attesting to a benefit, the use of nifedipine capsules for hypertensive emergencies and pseudoemergencies should be abandoned. Only one case of fetal distress was reported in this review9 (although we have noted three other cases), in a pregnant woman whose blood pressure fell from 150/115 mmHg to 90/55 mmHg, hardly a surprising event and one which could have occurred with any drug which lowered the blood pressure to this extent. A more disturbing report by Rehman et al. noted that 98% of hospitalised patients receiving nifedipine capsules failed to have a bedside evaluation and only half had had their blood pressure followed up within an hour of treatment.10 This is poor medical practice and a good reason to improve medical education, but not a reason to withdraw a drug from the market. Risk-benefit analysis of nifedipine in pregnancy Many small studies, comprising a total of about 150 pregnant women, have shown that nifedipine will acutely lower maternal blood pressure within 30 minutes of administration, without compromising the fetus.11-22 In studies involving approximately 200 pregnant women treated with nifedipine over a longer period, no adverse fetal effects were recorded.12,23-27 Three case reports (of four patients) have, at the same time, reported the potential risk of sudden hypotension following the use of nifedipine in severe pre-eclampsia, particularly when combined with magnesium sulfate (used parenterally as convulsion prophylaxis in pre-eclampsia).9,28,29 However, in a more recent prospective study, 10 women with severe pre-eclampsia already receiving intravenous magnesium sulfate were given between 10 mg and 40 mg nifedipine orally. Blood pressure was well controlled in each woman, none had significant hypotension and there was no fetal distress.30 Sudden hypotension has been reported with other antihypertensive drugs used to acutely lower blood pressure in pregnancy, including hydralazine.3,31 The risk of sudden hypotension with any form of acute antihypertensive therapy can be minimised by concomitant plasma volume expansion1,20,32 and avoidance of diuretics, as pre-eclampsia is a volume-contracted state compared with normal pregnancy.33 Several studies have found that nifedipine lowers maternal blood pressure without adversely affecting uteroplacental blood flow.13,14,17,23,34 Several studies have compared intravenous hydralazine with nifedipine in pre-eclampsia;12,19,20,35 all showed nifedipine to be of equal or greater efficacy and safety for both mother and fetus. Visser and Wallenburg observed similar maximum reductions in blood pressure during administration of each drug, but greater falls in pulmonary capillary wedge pressure as well as increased occurrence of fetal distress in women receiving hydralazine.20 In one randomised trial, there were fewer preterm infants and less acute fetal distress in the group of women given nifedipine than in the group of women given intravenous and then oral hydralazine.12 The most recent and largest studies showed that maternal and fetal outcomes were similar in pregnant women with severe hypertension (diastolic blood pressure > 120 mmHg) who received either sublingual nifedipine or intravenous hydralazine.36 The authors concluded that sublingual nifedipine may be advantageous "for use by midwives who work in rural areas where speed is essential in reducing acute hypertension . . ." Nifedipine also relaxes the myometrium, and therefore has a potentially important role in the treatment of preterm labour. In five separate randomised trials involving a total of 290 women, nifedipine was as effective as ritodrine for tocolysis and was associated with fewer serious maternal side effects.37-41 No adverse fetal effects were attributable to nifedipine in studies reporting on more than 350 women treated with the drug in preterm labour.42 Recent prospective data have provided further support for the safety of nifedipine, even when used in early pregnancy.43 Withdrawal of nifedipine from the Australian market The "position of comfort" -- that nifedipine can be used safely and easily in an emergency (before insertion of an intravenous cannula) -- has been lost. The plan to withdraw nifedipine capsules arose out of concern over the potential adverse effects (myocardial infarction, death) in non-pregnant patients with hypertension and ischaemic heart disease receiving long-term treatment with the drug.44-46 In New Zealand, the Ministry of Health has stated that nifedipine and some other calcium antagonists are contraindicated in pregnancy.47 There is no basis for this pronouncement in studies of nifedipine use in human pregnancy. As nifedipine was never officially listed in the Australian Register of Therapeutic Goods for use in pregnancy, clinicians cannot argue to retain the drug for the treatment of hypertension in pregnancy. The simple solution could be to accept defeat and rely on parenteral hydralazine. However, the most recent preparation of this drug is not marketed for intramuscular use (presumably because of its variable absorption), so that treatment must be delayed until an intravenous cannula is inserted. This delay adds to the dangers of severe hypertension for the pregnant woman. Moreover, it has been speculated that parenteral hydralazine will also be withdrawn shortly as it has been superseded by better drugs with fewer side-effects in non-pregnant patients. We now face the following situation: nifedipine capsules have been withdrawn from sale, and it is possible that intravenous hydralazine and diazoxide will also be withdrawn from the Australian market. Intravenous labetalol is not available in Australia, and magnesium sulfate, while known to have some blood pressure lowering effects, is not a sufficiently powerful antihypertensive agent for treatment of severe hypertension in pre-eclampsia. Therefore, intravenous sodium nitroprusside and glyceryl trinitrate will be the only agents left for the treatment of acute severe hypertension in pregnancy. The former can induce fetal cyanide toxicity, while the latter has been subject to far fewer studies in pregnancy than nifedipine, hydralazine or diazoxide -- and both drugs require highly skilled dose titration. Why do pregnant women now face the very real prospect that we will no longer be able to treat their severe hypertension as efficiently as before? In part, this relates to the bureaucratic nature of administering such matters -- if a drug has not been officially listed for an approved indication in the Australian Register of Therapeutic Goods (and nifedipine was never listed for use in pregnancy), then, despite widespread clinical use for that purpose, it can be withdrawn from the market by the pharmaceutical regulatory authorities. To be fair, this is probably the safest approach overall. At the same time, however, this situation highlights deficiencies in clinical and scientific interaction among clinicians, pharmaceutical companies and government agencies. The pharmaceutical company concerned has long known that nifedipine was being used for treating severe hypertension in pregnancy. They, of course, could not endorse such an action, but could have worked with clinicians to study the clinical outcomes in a proper manner, leading to an application for approval of a new indication. They chose not to do so. We clinicians are as much at fault here for not taking such an initiative when the company failed to do so. ADEC tried to balance these issues in its most recent consideration of the problem, but had no option other than to withdraw nifedipine capsules from sale. In New Zealand, nifedipine capsules are now available only in hospitals, which limits the access of rural practitioners to this drug. Perhaps this situation should force us to reconsider the speed at which we need to lower blood pressure in pre-eclampsia. Pregnancy outcomes are very good when severe hypertension is treated rapidly (over 20-30 minutes) and cerebral haemorrhage and eclampsia are now relatively rare. This does not mean there is necessarily a causal relationship between such treatment and the low rates of intracerebral haemorrhage and eclampsia. However, it would be difficult to prove a causal relationship because of the rarity of these complications as well as the ethical problems involved in randomising severly hypertensive pregnant women to a trial comparing rapid reductions in blood pressure (e.g., using nifedepine) with slower reductions (e.g., using oral clonidine or methyldopa). Conclusions The "best case" scenario is that withdrawal from sale of nifedipine capsules and intramuscular hydralazine will leave Australian clinicians with only intravenous diazoxide and intravenous hydralazine to fill an essential therapeutic niche (with intravenous labetalol still available in New Zealand). None of these drugs can be given urgently in hospitals without resident medical staff, and even in the larger tertiary hospitals resident medical staff can be delayed in other wards or operating theatres. Such delays could result in serious complications for the pregnant woman and her baby. The "worst case" scenario is that none of these drugs (nifedipine, labetalol, hydralazine or diazoxide) will be available for the treatment of acute severe hypertension in pregnancy. Pregnant women will then suffer from inadequate treatment or be exposed to the side effects of the remaining antihypertensive drugs, which are currently not recommended for use in pregnancy. Is all this enough to justify continued availability of short-acting nifedipine in pregnant women in Australia and New Zealand? Most clinicians would rapidly respond "yes" as they continue to practise medicine as both an art and a science. The "art" of using nifedipine successfully in pregnancy is well known to most of us, but, although the above review of the available literature shows that nifidepine capsules are as safe as any other drugs currently used to treat acute severe hypertension in pregnancy, we have failed to gather the science to a sufficient extent. We hope our patients will not suffer as a result of our combined shortfalls. Acknowledgement We thank Mrs Jodie Hendley for assistance in preparing this manuscript. References Brown MA, Buddle ML. Hypertension in pregnancy: maternal and fetal outcomes according to laboratory and clinical features. Med J Aust 1996; 165: 360-365. Australian Drug Evaluation Committee. Resolution No. 5857. Commonwealth of Australia Gazette No. GN 10, 25 October 1995. (See also Resolution No. 7129. 5-6 December 1996.) Michael CA. Intravenous labetalol and intravenous diazoxide in severe hypertension complicating pregnancy. Aust N Z J Obstet Gynaecol 1986; 26: 26-29. Visser W, Wallenburg HCS. Should labetalol be used in severe early onset preeclampsia patients? Protagonist and presentations. Proceedings of the 8th World Congress on Hypertension in Pregnancy; 1992 Nov 8-12; Buenos Aires, Argentina. Abstract 104: 290. Ramsay B, de Belder A, Campbell S, et al. A nitric oxide donor improves uterine artery diastolic blood flow in normal early pregnancy and in women at high risk of pre-eclampsia. Eur J Clin Invest 1994; 24: 76-78. Visser W, Wallenburg HCS. Central hemodynamic observations in untreated preeclamptic patients. Hypertension 1991; 17: 1072-1077. Baker A. Management of severe pregnancy induced hypertension, or gestosis, with sodium nitroprusside. Anaesth Intensive Care 1990; 18: 361-365. Grossman E, Messerli FH, Grodzicki T, Kowey P. Should a moratorium be placed on sublingual nifedipine capsules given for hypertensive emergencies and pseudo emergencies? JAMA 1996; 276: 1328-1331. Impey L. Severe hypotension and fetal distress following sublingual administration of nifedipine to a patient with severe pregnancy induced hypertension at 33 weeks. Br J Obstet Gynaecol 1993; 100: 959-961. Rehman F, Mansoor GA, White WB. Inappropriate physician habits in prescribing oral nifedipine capsules in hospitalised patients. Am J Hypertens 1996; 9: 1035-1039. Walters BNJ, Redman CWG. Treatment of severe pregnancy-associated hypertension with the calcium antagonist nifedipine. Br J Obstet Gynaecol 1984; 91: 330-336. Fenakel K, Fenakel G, Appelman Z, et al. Nifedipine in the treatment of severe preeclampsia. Obstet Gynecol 1991; 77: 331-337. Hanretty KP, Whittle MJ, Howie CA, Rubin PC. Effect of nifedipine on Doppler flow velocity waveforms in severe preeclampsia. BMJ 1989; 299: 1205-1206. Lindow SW, Davies N, Davey DA, Smith JA. The effect of sublingual nifedipine on uteroplacental blood flow in hypertensive pregnancy. Br J Obstet Gynaecol 1988; 95: 1276-1281. Duggan PM, McCowan LME, Stewart AW. Antihypertensive drug effects on placental flow velocity waveforms in pregnant women with severe hypertension. Aust N Z J Obstet Gynaecol 1992; 32: 335. Lurie S, Fenakel K, Friedman A. Effect of nifedipine on fetal heart rate in the treatment of severe pregnancy-induced hypertension. Am J Perinatal 1990; 7: 285-286. Pirhonen JP, Erkkola RU, Ekblad UU. Uterine and fetal flow velocity waveforms in hypertensive pregnancy: the effect of a single dose of nifedipine. Obstet Gynecol 1990; 76: 37-41. Puzey MS, Ackovic KL, Lindow SW, Gonin R. The effect of nifedipine on fetal umbilical artery Doppler waveforms in pregnancies complicated by hypertension. S Afr Med J 1991; 79: 192-194. Seabe SJ, Moodley J, Becker P. Nifedipine in acute hypertensive emergencies in pregnancy. S Afr Med J 1989; 76: 248-250. Visser W, Wallenburg HCS. A comparison between the haemodynamic effects of oral nifedipine and intravenous dihydralazine in patients with severe preeclampsia. J Hypertens 1995; 13: 791-795. Childress CH, Katz VL. Nifedipine and its indications in obstetrics and gynaecology. Obstet Gynecol 1994; 83: 616-624. Levin AC, Doering PL, Hatton RC. Use of nifedipine in the hypertensive diseases of pregnancy. Ann Pharmacother 1994; 28: 1371-1378. Moretti MM, Fairlie FM, Akl S, et al. The effect of nifedipine therapy on fetal and placental Doppler waveforms in pre-eclampsia remote from term. Am J Obstet Gynecol 1990; 163: 1844-1848. Constantine G, Beevers DG, Reynolds AL, Luesley DM. Nifedipine as a second line antihypertensive drug in pregnancy. Br J Obstet Gynaecol 1987; 94: 1136-1142. Greer IA, Walker JJ, Bjornsson S, Calder AA. Second line therapy with nifedipine in severe pregnancy induced hypertension. Clin Exp Hypertens Pregnancy 1989; B8: 277-292. Sibai BM, Barton JR, Akl S, et al. A randomized prospective comparison of nifedipine and bed rest versus bed rest alone in the management of preeclampsia remote from term. Am J Obstet Gynecol 1992; 167: 879-884. Jayawardana J, Lekamge N. A comparison of nifedipine with methyldopa in pregnancy induced hypertension. Ceylon Med J 1994; 39: 87-90. Hata T, Manabe A, Hata K, Kitao M. Changes in blood velocities of fetal circulation in association with fetal heart rate abnormalities: effect of sublingual administration of nifedipine. Am J Perinatal 1995; 12: 80-81. Waisman GD, Mayorga LM, Camera MI, et al. Magnesium plus nifedipine: potentiation of hypotensive effect in preeclampsia? Am J Obstet Gynecol 1988; 159: 308-309. Scardo JA, Vermillion ST, Hogg BB, Newman RB. Haemodynamic effects of oral nifedipine in pre-eclamptic hypertensive emergencies. Am J Obstet Gynecol 1996; 175: 336-340. Vink GJ, Moodley J, Philpott RH. Effect of dihydralazine on the fetus in the treatment of maternal hypertension. Obstet Gynecol 1980; 55: 519-522. Paterson-Brown S, Robson SC, Redfern N, et al. Hydralazine boluses for the treatment of severe hypertension in pre-eclampsia. Br J Obstet Gynaecol 1994; 101: 409-413. Brown MA, Gallery EDM. Volume homeostasis in normal pregnancy and pre-eclampsia. Baillieres Clin Obstet Gynaecol 1990; 8: 287-310. Hirose S, Yamada A, Kasugai M, et al. The effect of nifedipine and dipyridamole on the Doppler blood flow waveforms of umbilical and uterine arteries in hypertensive pregnant women. Asia-Oceania J Obstet Gynaecol 1992; 18: 187-193. Martins-Costa S, Ramos JG, Barros E, et al. Randomised, controlled trial of hydralazine versus nifedipine in pre-eclamptic women with acute hypertension. Clin Exp Hypertens Pregnancy 1992; B11: 25-44. Jegasothy R, Paranthaman S. Sublingual nifedipine compared with intravenous hydralazine in the acute treatment of severe hypertension in pregnancy: potential for use in rural practice. J Obstet Gynaecol Res 1996; 22: 21-24. Bracero LA, Leikin E, Kirshenbaum N, Tejani N. Comparison of nifedipine and ritodrine for the treatment of preterm labour. Am J Perinatol 1991; 8: 365-369. Meyer WR, Randall HW, Graves WL. Nifedipine versus ritodrine for suppressing preterm labor. J Reprod Med 1990; 35: 649-653. Ferguson JE, Dyson DC, Schutz T, Stevenson DK. A comparison of tocolysis with nifedipine or ritodrine: an analysis of efficacy and maternal, fetal and neonatal outcome. Am J Obstet Gynecol 1990; 163: 105-111. Kupferminc M, Lessing JB, Yaron Y, Peyser MR. Nifedipine versus ritodrine for suppression of preterm labor. Br J Obstet Gynaecol 1993; 100: 1090-1094. Read MD, Wellby DR. The use of a calcium antagonist (nifedipine) to suppress preterm labour. Br J Obstet Gynaecol 1986; 93: 933-937. Ray D, Dyson D. Calcium channel blockers. Clin Obstet Gynecol 1995; 38: 317-322. Magee LA, Schick B, Donnenfeld AE, et al. The safety of calcium channel blockers in human pregnancy: a prospective, multicenter cohort study. Am J Obstet Gynecol 1996; 174: 823-828. Psaty BM, Heckbert SR, Koepsell TD, et al. The risk of myocardial infarction associated with antihypertensive drug therapies. JAMA 1995; 275: 620-625. Buring JE, Glynn RJ, Hennekens CH. Calcium channel blockers and myocardial infarction. A hypothesis formulated but not yet tested. JAMA 1995; 274: 654-645. Horton R. Spinning the risks and benefits of calcium antagonists. Lancet 1995; 346: 586-587. New Zealand Ministry of Health. Managing high blood pressure in pregnancy. Prescriber Update 1994; 7: 2-10. (Received 26 Aug 1996, accepted 28 Jan 1997) Authors' details Departments of Medicine, Renal Medicine and Obstetrics, St George Hospital, Kogarah, NSW. Mark A Brown, FRACP, MD, Associate Professor of Medicine. Department of Obstetrics and Gynaecology, University of Auckland School of Medicine, National Women's Hospital, Auckland, NZ. Lesley M E McCowan, FRCOG, FRNZCOG, Senior Lecturer in Obstetrics and Gynaecology; Robyn A North, PhD, FRACP, Senior Lecturer in Obstetric Medicine. King Edward Memorial Hospital for Women, Perth, WA. Barry N Walters, FRACP, Physician in Obstetric Medicine. Council of the Australasian Society for the Study of Hypertension in Pregnancy, 145 Macquarie Street, Sydney, NSW 2000. No reprints will be available. Correspondence: Dr M A Brown, Departments of Medicine, Renal Medicine and Obstetrics, St George Hospital, Kogarah, NSW 2217. To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia. We appreciate your comments.

Mark A Brown · Robyn A North · Barry N Walters

Evaluation of sexual health services within Australia and New Zealand Caron Marks, Robin L Tideman and Adrian Mindel MJA 1997; 166: 348-352 For comment see Fairley Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - Figure 1 - Figure 2 - - ©MJA1997 Abstract Objective: To examine and compare specialised services for patients with sexually transmitted diseases (STDs) in Australia and New Zealand. Design: Postal questionnaire survey. Participants and Setting: All STD facilities in Australia and New Zealand in 1993. Main Outcome Measures: Patient numbers and demography; staffing levels; the role of nurses; diagnostic and treatment protocols; contact-tracing policies; and the availability of specialist medical services and community and education programs. Results: 83 of 100 clinics responded; 52 were urban, 21 rural, and nine remote. 95% were open to men and women. Staffing levels were similar in Australia and New Zealand and there was considerable consistency in diagnostic techniques and treatment among clinics. Australian clinics more often used ciprofloxacin or ceftriaxone as the treatment of first choice for gonorrhoea; New Zealand clinics were more likely to test for Chlamydia using direct immunofluorescence; and Australian clinics were more likely to test for hepatitis A and offer hepatitis B vaccination to a broader range of patients. 88% of clinics always traced contacts for gonorrhoea, 86% for syphilis and 77% for Chlamydia . 98% of clinics offered HIV test counselling, and 78% STD health education. Conclusions: The number of sexual health services has increased over the past decade. Other improvements include most clinics being open to both men and women, and consistency in the diagnosis, treatment and contact tracing of STDs. However, given the lack of adequate comparative data and the variable quality of national surveillance data, it is difficult to determine whether current facilities are meeting service needs. MJA 1997; 166: 348-352 Introduction The control of sexually transmitted diseases (STDs) depends on health promotion, education, the provision of adequate facilities for the diagnosis, treatment and contact tracing of STDs, and ongoing research.1 One of the more comprehensive national STD services (involving more than 200 standardised clinics) is in the United Kingdom.2,3 By contrast, Australia currently has a fragmented STD control system in which each State and Territory works independently and with different health policies. There are no nationally agreed guidelines for the diagnosis, treatment and tracing of contacts of patients with STDs,4 availability of different tests varies across the continent, and treatment protocols may vary according to antibiotic resistance patterns and financial constraints. A 1983 survey of public STD facilities throughout Australia found that almost all clinics were located in major cities, leaving large areas of rural Australia unserviced by public clinics.5 Other deficiencies identified included inadequate opening times, lack of facilities in some clinics for treating both men and women, insufficient staff, inadequate contact tracing, limited use of facilities for teaching purposes, and inadequate maintenance of their role as reference centres for other practitioners and agencies. This survey included all 20 public STD facilities Australia-wide, and concluded that these facilities were "inadequate to meet the needs of the population".5 Over the past decade there have been many changes to sexual health care, including more clinics and better training for staff. Consequently, we felt that it was timely to establish what STD services were available from public and private STD clinics and Family Planning Clinics (FPCs); whether STD clinical services were adequately staffed; to determine the range of diagnostic, treatment, and contact-tracing services; and whether clinics were providing the community with education, counselling and other specialist services. Finally, we compared services in Australia and New Zealand and noted geographic differences in the provision of services within Australia. Methods In 1993 we identified all STD treatment facilities in Australia and New Zealand. These included all known public and private sexual health clinics, and the main Family Planning Clinic (FPC) in each State. Most facilities were identified through the National Venereology Council of Australia and the Family Planning Association of New South Wales, with the remainder found when clinics identified centres in their area which had been overlooked. A questionnaire and prepaid addressed envelope were posted to the director (senior doctor or nurse) of each clinic. The 65-item questionnaire sought information about the geographic location and physical structure of clinics, as well as staffing, diagnosis, treatment and contact tracing for the various STDs, specialist medical services, and community and educational programs run by the facility. Non-respondents were sent a second questionnaire two months after the first. Statistical analysis The results were analysed using the Statistical Package for the Social Sciences (SPSS).6 Descriptive statistics, frequency distributions, χ2 and Fisher's exact test were used. There was no weighting of the data by size of clinic. Chi-square tests, when used to compare therapies for the various STDs, involve all treatments, ranging from "most commonly used" to those "never used". When reporting significant differences the χ2 takes into account all these modalities. However, the figures reported show only a description of where the differences lie. The rural/remote areas classification system was used to classify Australian facilities into rural and remote areas by means of postcodes,7 while the New Zealand Yearbook was used to classify those in New Zealand.8 Results We identified 101 STD facilities, one of which had closed down. From the remaining 100 clinics, 83 questionnaires were returned (72 on the first mailout and an additional 11 on the second). Geographic distribution and type of facility Fifty-six clinics were in Australia and 27 were in New Zealand. Sixty-three per cent were in inner-city and suburban areas, 26% in rural areas and 11% in remote areas (Box 1). Seventy-nine clinics (95%) were public and four (5%) were private. There were 71 STD clinics and five FPCs. One private facility identified itself as a specialist venereology practice, and three as general practices specialising in STDs and HIV. The remaining three clinics identified themselves as "other". Seventy-nine clinics (95%) were open to both men and women. Staffing Box 2 shows that the median number of patients seen per year decreased as the facilities became more remote. Clinics in Australia saw a greater median number of patients per year and had more doctors, nurses, laboratory and clerical staff than those in New Zealand. However, the only significant difference was for full-time equivalent clerical staff, with a median of 1 (range, 0-4.3) for Australia, compared with 0 (range, 0-2.4) for New Zealand (P = 0.002). The most common duties of nurses at STD facilities included history taking, clinical examination and testing for STDs. Only 26% of clinics allowed nurses to prescribe treatment; more nurses in rural and remote areas were allowed to prescribe treatment than those in urban areas (36% v. 16%), but this difference was not significant. Nurses took histories "sometimes" (options were "always", "sometimes" and "never") in over 80% of clinics in New South Wales, compared with 39% in Victoria (P = 0.02), and examined patients at 70% of NSW clinics, compared with 22% in Victoria (P = 0.02). There were no significant differences in nursing duties between New Zealand and NSW. However, comparing New Zealand with Victoria showed that New Zealand nurses were more likely to take histories (P = 0.003), examine patients (P = 0.005), and test patients for STDs (P = 0.002). Diagnosis and treatment Gonorrhoea: Eighty-one clinics (99%) used culture, and 77 (94%) used Gram stain to diagnose gonorrhoea. The three most common treatments for gonorrhoea were amoxycillin plus probenecid, ciprofloxacin, and ceftriaxone, used in 63%, 24% and 12% of clinics, respectively (Box 3). New Zealand clinics were more likely than Australian clinics to use amoxycillin plus probenecid as first-line therapy for gonorrhoea (93% v. 49%; P = 0.01). Urban clinics in both Australia and New Zealand were more likely to use ciprofloxacin than rural and remote clinics (51% v. 21%; P = 0.02). Syphilis: Forty-seven clinics (57%) used dark-ground microscopy for diagnosing primary syphilis. For screening, 61 (74%) used the rapid plasma reagin (RPR) test, 58 (71%) the Treponema pallidum haemagglutination antibody (TPHA) test, and 25 (31%) the Ven ereal Disease Research Laboratory (VDRL) test. Fifty Australian clinics (91%), compared with 11 New Zealand clinics (41%), used the RPR test for screening (P < 0.001). The fluorescent treponemal antibody test (FTA) was used by 61 (75%) clinics to confirm the diagnosis. Procaine and benzathine penicillins were the first-choice treatments in all facilities. Chlamydia and non-gonococcal urethritis: Chlamydia was most commonly diagnosed by direct immuno fluorescence (DIF), which was used by 44 clinics (54%), followed by: enzyme immunoassay (EIA) from swabs, 39 clinics (48%); culture from swabs, 35 clinics (43%); and EIA from urine, 10 clinics (12%). Australian clinics were more likely to use culture to diagnose chlamydial infection than New Zealand clinics (58% v. 11%; P < 0.001), while New Zealand clinics were more likely to use DIF than Australian clinics (74% v. 44%; P = 0.01). Urban centres were significantly more likely to use culture to diagnose Chlamydia than rural and remote centres (58% v. 17%; P < 0.001). Most clinics used doxycycline as first-line treatment for Chlamydia and non-gonococcal urethritis (92% and 91%, respectively). Genital herpes: Herpes simplex virus (HSV) was diagnosed by viral culture (79 clinics [96%]), EIA (16 clinics [20%]), and serological testing (10 clinics [12%]). Acyclovir was used to treat primary HSV infections by 79 clinics (98%), for long term suppression by 70 clinics (86%), and for recurrences of HSV infection by 58 clinics (72%). Human immunodeficiency virus (HIV): All the clinics surveyed routinely offered counselling and voluntary HIV testing to all persons considered to be at risk of HIV infection. Fifty-two clinics (64%) had facilities to manage HIV- positive patients. Forty-one clinics (51%) provided antiretroviral therapy and prophylaxis and treatment of opportunistic infections. Genital warts: Cryotherapy was the first-line treatment for human papillomavirus infection in 55 clinics (69%), and podophyllin was the second most common treatment option, used in 17 clinics (21%). Australian clinics were more likely to use podophyllin than New Zealand clinics (16/53 [30%] v. 3/27 [11%]; P = 0.03). Trichomoniasis and bacterial vaginosis: To diagnose trichomoniasis, wet-film microscopy was the most common technique, used in 67 clinics (83%), while culture was used by 39 clinics (48%). Gram staining was the most common diagnostic technique for identifying bacterial vaginosis (74 clinics [93%]). Alternative diagnostic techniques used included culture to identify Gardnerella vaginalis and other anaerobes (56 clinics [70%]), vaginal pH testing (44 clinics [55%]), and the potassium hydroxide test (which identifies volatile amines) (41 clinics [51%]). Most clinics used metronidazole to treat trichomoniasis (53/80 [66%]) and bacterial vaginosis (50/79 [63%]). Viral hepatitis: Forty-four clinics (55%) offered antibody testing for hepatitis A and 79 (98%) for hepatitis C. Australian clinics were significantly more likely to offer antibody testing for hepatitis A than New Zealand clinics (36/54 [67%] v. 8/26 [31%]; P = 0.003). When screening for hepatitis B infection, 65 clinics (81%) meas ured surface antigen (HBsAg), 57 (71%) measured core antibody (HBcAb), and 48 (60%) measured surface antibody (HBsAb). Figure 1 shows clinic policies for hepatitis B vaccination. Vaccination was recommended for health care workers by 52/53 (98%) Australian clinics, compared with 19/27 clinics (70%) in New Zealand (P < 0.001); for heterosexuals with multiple partners, these figures were 44/53 (83%) and 15/27 (56%), respectively (P = 0.01); and for intravenous drug users (IVDUs), 52/53 (98%) and 21/27 (78%), respectively (P = 0.002). Contact tracing Seventy-one clinics (87%) offered contact tracing for patients with STDs. Many centres employed multiple techniques. In 67 clinics (94%), staff negotiated with patients to advise their own contacts, 53 clinics (75%) used face-to-face discussions between contacts and clinic staff, 45 (63%) had staff visit contacts at home, and 38 (54%) traced contacts by phone. Twenty-one of the 71 clinics (30%) employed specially trained contact tracers. Doctors were involved in contact tracing in 22 clinics (28%), counsellors in 23 (32%), and nurses in 44 (62%). Patients were encouraged to inform their own contacts in 28 clinics (39%). All 21 clinics in NSW stated that they undertook contact tracing, compared with 9/13 (69%) clinics in Victoria (P = 0.01), and NSW clinics were significantly more likely to involve counsellors in contact tracing than Victorian clinics (62% v. 8%; P = 0.002). There were a number of differences in contact-tracing policies between Australia and New Zealand. Australian facilities were more likely than New Zealand clinics to involve doctors (22/55 [40%] v. 1/27 [4%]; P = 0.001), less likely to trace contacts by telephone (21/55 [38%] v. 18/27 [67%]; P = 0.02), and less likely to trace contacts by having staff visit them (22/55 [40%] v. 23/27 [85%]; P < 0.001). Box 4 summarises the contact-tracing practices for each STD. Most clinics always traced contacts of patients with gonorrhoea, syphilis, Chlamydia , HIV and trichomoniasis. Only one of the five FPCs (20%) provided contact tracing, compared with 65 of 66 (98%) sexual health clinics (Fisher's exact test, P < 0.0005). Additional services provided by STD clinics The facilities surveyed offered a range of additional services. Eighty-one facilities (98%) offered counselling before and after HIV testing, 78 (95%) functioned as a referral service for further specialist counselling, 68 (84%) offered family planning advice, and 48 (59%) offered relationship counselling. Other services are outlined in Figure 2. Sixty-eight (82%) of the responding clinics offered education programs to other health professionals, schools or youth groups, while 46 (55%) offered some form of higher education/university courses. Discussion Our findings show that the number of STD facilities in Australia increased considerably over the past decade, and that facilities in New Zealand and Australia were broadly comparable (although, in Australia, there was still a marked urban predominance of clinics). Other improvements were that most clinics were open to men and women, and offered a wide range of teaching and other special services. Relative to the 1983 survey of Australian STD services by Bradford and Philpot,5 we found an increase in the number of nurses and doctors, while the number of patients seen annually was similar. However, over the past decade clinics have become more involved in managing patients with complex medical problems, including HIV, hepatitis B and C, disseminated herpes simplex virus infection, and cervical intraepithelial neoplasia.4,9 Increased availability of services does not necessarily lead to improvement in the sexual health of the community. The best measure of improvement is a reduction in the incidence of sexually transmitted diseases. In Australia, disease patterns have been difficult to in terpret because the collection of epidemiological data for most STDs (with the exception of gonorrhoea) from the States and Territories is uneven.4 None the less, there is considerable evidence to suggest that there has been a dramatic reduction in reported cases of gonorrhoea, syphilis and chlamydial infections since 1981,10-12 with the most marked improvements in the large metropolitan centres. By contrast, the incidence of gonorrhoea, syphilis, Chlamydia and donovanosis remained extremely high in many rural Aboriginal communities, particularly in the Northern Territory, far north Queensland, and the Pilbara and Kimberley regions of Western Australia.13-15 These areas all have a limited number and quality of sexual health facilities, and improvements in clinical services and intervention programs are urgently needed. Our findings show considerable consistency in diagnosis and treatment of STDs throughout Australia and also between Australia and New Zealand, with most facilities following the diagnostic and treatment guidelines produced by the United States Centers for Disease Control (CDC)16 or those of the Venereology Society of Victoria.17 However, we did identify some differences between Australia and New Zealand in the treatment of first choice for gonorrhoea, the method of detecting chlamydial infection, and in the likelihood that hepatitis A tests would be requested. There were also differing policies on hepatitis B vaccination and on tracing contacts of patients with STDs. Varying patterns of antibiotic resistance in strains of the organism that causes gonorrhoea (penicillinase-producing Neisseria gonorrhoeae ) were more common in Australia, particularly along the east coast,18 than in New Zealand, and resistance to quinolones occurs in strains infecting a sizeable minority of travellers from the Philippines and neighbouring countries;19 this may explain the difference in antibiotic treatment. Other factors contributing to the differences in practice include local availability of diagnostic tests, variation in populations attending clinics (travellers,20,21 sex-industry workers22,23 and homosexual men24-26 ) and local variations in clinical practice. The differences in hepatitis A testing policy and hepatitis B vaccination policy are intriguing, and may include differing financial arrangements between the clinical services in the two countries, availability of testing and vaccination from other sources (in particular, the recommendation for universal HBV vaccination in New Zealand),27 and differing populations28,29 and perceptions of risk.30 Differences in contact-tracing policies probably reflect availability of staff, local working practices, or variation in the understanding of contact tracing. There are a few minor differences between urban clinics and those in rural and remote settings, with a greater proportion of urban clinics using ciprofloxacin to treat gonorrhoea, using culture to diagnose Chlamydia , and requesting hepatitis A testing. This also reflects differences in the population groups attending different clinics (urban centres attract a higher proportion of overseas travellers, sex workers and homosexual and bisexual men than rural and remote centres), antibiotic sensitivities and local availability of tests. Overall, the availability of contact-tracing services was excellent. However, it is of some concern that 4% of clinics never and 9% only sometimes traced contacts for gonorrhoea, 8% never traced contacts for syphilis and 2% never traced contacts for Chlamydia . Although we surveyed only five FPCs, our finding that only one of these five provided contact tracing is of concern, particularly with Chlamydia , which is often diagnosed within these facilities.31 Barriers to contact-tracing services within FPCs should be explored and solutions considered. One possible solution would be to encourage closer links between sexual health and family planning services. Our findings in this survey should be of assistance in future sexual health service planning. In addition, the remarkable consistency in the diagnosis, treatment and contact tracing of STDs in Australia and New Zealand should encourage the development of national guidelines. Acknowledgements We thank Professor G Berry and Associate Professor B Donovan for their assistance with this manuscript. References Adler MW. Sexually transmitted diseases. In: Holland WW, Detels R, Knox G, editors. Oxford textbook of public health. Vol. 21. 2nd Ed. Oxford: Oxford University Press, 1991: 345-357. Bingham JS. Genitourinary medicine should remain a separate specialty. Genitourin Med 1996; 27: 312. Adler MW, Belsey EM, O'Connor BH, et al. Facilities and diagnostic criteria in sexually transmitted disease clinics in England and Wales. Br J Vener Dis 1978; 54: 2-9. Mulhall BP, Hart G, Harcourt C. Sexually transmitted diseases in Australia: a decade in change. Epidemiology and surveillance. Ann Acad Med Singapore 1995; 24: 569-578. Bradford DL, Philpot CR. A survey of sexually transmitted disease centres in Australia. Br J Vener Dis 1983; 59: 330-334. SPSS: Statistical package for the social sciences [computer program], version 7.0. Chicago, Ill: SPSS Inc, 1995. Rural/remote areas classification. Canberra: Department of Human Services and Health, 1994. New Zealand Official Yearbook 1993. 96th Ed. Wellington: New Zealand Department of Statistics, 1993. Donovan B, Finlayson RJ, Mutimer K, et al. HIV infection in sexually transmissible disease practice in Sydney: the effects of legislation, public education and changing clinical spectrum. Int J STD AIDS 1990; 1: 21-27. The Australian gonococcal surveillance programme. The incidence of gonorrhoea and the antibiotic sensitivity of gonococci in Australia, 1981-1991. Genitourin Med 1993; 69: 364-369. Hart G. STD epidemiology in Australasia; Syphilis and gonorrhoea. Venereology 1992; 5: 115-120. Garland SM, Gertig DM, McInnes JA. Genital Chlamydia trachomatis infection in Australia. Med J Aust 1993; 159: 90-96. Annual report of the national notifiable diseases surveillance system, 1992 - part 2. Syphilis. Commun Dis Intell 1993; 17(22): 507-508. Bowden FJ. Surveillance of sexually transmitted diseases in the Northern Territory of Australia. Venereology , 1995; 8(1): 21-25. Main J, Patel A, Bowden FJ. Surveillance of donovanosis in the Northern Territory. Venereology 1995: 8: 16-19. sexually transmitted diseases treatment guidelines. Centers for Disease Control and Prevention. MMWR Morb Mortal Wkly Rep 1993; 42(RR-14): 1-102. Management guidelines for sexually transmissible diseases and genital infections. 4th ed. Melbourne: Venereology Society of Victoria, 1995. Anonymous. The incidence of gonorrhoea and the antibiotic sensitivity of gonococci in Australia, 1981-1991 . The Australian Gonococcal Surveillance Programme. Genitourin Med 1993; 69(5): 364-369. Tapsall JW, Schultz TR, Philip EA. Characteristics of Neisseria gonorrhoeae isolated in Australia showing decreased sensitivity to quinolone antibiotics. Pathology 1992; 24: 27-31. Mulhall BP, Hu M, Thompson M, et al. Planned sexual behaviour of young Australian visitors to Thailand. Med J Aust 1993; 158: 530-535. Mulhall BP. Sexually transmissible diseases and travel. Br Med Bull 1993; 49(2): 394-411. O'Connor CC, Berry G, Rohrsheim R, Donovan B. Sexual health and use of condoms among local and international sex workers in Sydney. Genitourin Med 1996; 72: 47-51. Philpot CR, Harcourt JM, Edwards JM. A survey of female prostitutes at risk of HIV infection and other sexually transmissible diseases. Genitourin Med 1991; 67: 384-388. Rowbottom JH, Tapsall JW, Plummer DC, et al. An outbreak of a penicillin-sensitive strain of gonorrhoea in Sydney men. Genitourin Med 1994; 70: 196-199. Forsyth JRL, Sherrard J, Traynor P. Resurgent gonorrhoea in homosexual men [letter]. Lancet 1990; 336: 878. McNulty A. Anorectal gonorrhoea revisited. Venereol 1993; 6(4): 109-111. Goldwater PN. History of hepatitis B vaccination in New Zealand: lessons for Australia? Aust J Pub Health 1993; 17: 221-225. Stewart T, Crofts N. An outbreak of hepatitis A among homosexual men in Melbourne. Med J Aust 1993; 158: 519-521. Stokes ML. Infectious diseases: hepatitis A survey results. NSW Public Health Bull 1992; 3: 7-12. Anderson B, Bodsworth NJ, Rohrsheim R, Donovan B. Hepatitis B virus infection and vaccination status of high risk people in Sydney: 1982 and 1991. Med J Aust 1994; 161: 368-371. Garland SM, Gertig DM, McInnes JA. Genital Chlamydia trachomatis infection in Australia. Med J Aust 1993, 159: 90-96. (Received 9 Apr, accepted 1 Nov, 1996) Authors' details Academic Unit of Sexual Health Medicine, Sydney Hospital, Sydney, NSW. Caron Marks, BSc, MA, Research Assistant; Robin L Tideman, MB BS, Clinical Research Coordinator; Adrian Mindel, FRACP, MD, Professor of Sexual Health Medicine. Reprints: Ms C Marks, Academic Unit in Sexual Health Medicine, Sydney Hospital, GPO Box 1614, Sydney, NSW 2001. E-mail: cmarks AT extro.ucc.su.oz.au - - To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Caron Marks · Robin L Tideman · Adrian Mindel

Oral retinoids and pregnancy Annabelle Chan, Marshall Hanna, Malcolm Abbott and Rosemary J Keane MJA1996; 165: 164-167 Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Introduction - Adverse reactions - Teratogenicity - Prescribing guidelines - Compliance - Pregnancy prevention programs - Recommendations - Conclusions - Acknowledgements - References - Authors' details Register to be notified of new articles by email - - ©MJA 1996 The oral retinoids isotretinoin and etretinate are uniquely effective in the treatment of severe cystic acne and keratinisation disorders. Because of their known teratogenicity, there are strict prescription guidelines, but exposure during pregnancy still occurs. A dedicated effort by women and their clinicians is required, involving patient selection, education and informed consent, detailed contraceptive counselling, and careful monitoring and management, including pregnancy testing before commencement of therapy. (MJA 1996; 165: 164-167) Introduction T he Australian Drug Evaluation Committee lists only five drugs in Medicines in pregnancy 1 as Category X -- drugs that have such a high risk of causing permanent damage to the fetus that they should not be used in pregnancy or when there is a possibility of pregnancy. The oral retinoids isotretinoin (Roaccutane, Roche) and etretinate (Tigason, Roche) are two of the five listed. The newly released acitretin (Neotigason, Roche) should also be included. These synthetic retinoids closely resemble naturally occurring vitamin A, essential for the maintenance of visual and reproductive function and for proliferation and differentiation of epithelial tissues. 2 They were released in the United States and Europe in 1982 and in Australia towards the end of 1985. Acitretin was released in Australia in late 1995 to replace etretinate, as it is more rapidly eliminated from the body. Isotretinoin is uniquely effective in severe cystic acne, and etretinate and acitretin in severe psoriasis and other keratinisation disorders which have proved recalcitrant to all other therapies. This accounts for their availability on prescription despite their teratogenicity . Adverse reactions The commonly reported adverse reactions (which are largely dose-related, of early onset and reversible on discontinuation) include dryness of the lips, mouth and eyes, hair loss and pruritus. 3 Less common but more severe, probably idiosyncratic, reactions (which may occur after weeks or months of therapy) include altered vision, headache, joint and muscle pain, abnormally raised serum transaminase levels, serum lipid changes, as well as increases in serum triglyceride and chol esterol levels and an increase in low density : high density lipoprotein ratio. Rare reactions include mental depression, severe hepatitis, diffuse hyperostosis of the spine and benign intracranial hypertension. Teratogenicity The most serious side effect, teratogenicity, was foreshadowed by animal studies, so that, at the time the drugs were released, strong warnings against exposure during pregnancy were given. The retinoids are believed to interfere with the activity and migration of cranial neural crest cells during development and thus cause craniofacial, thymic, conotrun cal heart and central nervous system malformations 4,5 (Box 1). Intellectual deficits in more than half the children exposed in utero have also been reported in follow-up studies to five years of age. 6 Isotretinoin Any fetal exposure during the first trimester within the therapeutic dose range of isotretinoin may be teratogenic. 7 Isotretinoin has a short elimination half-life of about 20 hours and the recommended contraception period after cessation of therapy is one month. Estimates from prospectively reported (i.e., before outcome was known) exposed pregnancies place the risk of teratogenicity for isotretinoin for first trimester exposure at around 28%, 7 reducing to around 4% for pregnancies occurring within one month of cessation of treatment 8 (Box 2). Etretinate Birth defects associated with etretinate include meningomyelocele, craniofacial and skeletal abnormalities and brain defects. 4,5 Etretinate is readily taken up into adipose tissue and slowly released from it. Thus, it has a long elimination half-life (120 days or more 2 ) and the recommended contraception period after therapy is two years. The best estimate from the literature of the risk of teratogenicity for exposure to etretinate during pregnancy is about 26%, 9 but the risk is likely to be less, as the pregnancies considered probably include retrospectively reported ones (in which there is a tendency to under-report normal outcomes). The risk for pregnancies occurring within two years of cessation of treatment appears to be considerably less, about 2%. All estimates are based on relatively few pregnancies (Box 2). Acitretin In spite of a shorter elimination half-life of 50 hours, a two-year contraception period after therapy has also been recommended for acitretin, as in some women there is conversion of acitretin to etretinate during therapy. 2,3,9 Up to 1994, there had been no exposures to acitretin during pregnancy reported prospectively to the manufacturer (Roche) with known outcomes; of three reported retrospectively, one aborted fetus had characteristic defects, one baby had high frequency hearing loss and a third was normal. None of the 32 prospectively reported pregnancies conceived in the two-year period after therapy has resulted in an infant with a birth defect (S Weber, Roche Products Medical Information Department, personal communication). Prescribing guidelines In Australia, authority to prescribe oral retinoids for specified conditions needs to be obtained under the Pharmaceutical Benefits Scheme, and they can only be prescribed by dermatologists (except in regions where there is no derm atologist available and a specialist physician may have authority to prescribe under State law). However, in the United States and Canada, 10 general practitioners and physicians may also prescribe these drugs. Roche recommends that: The possibility of pregnancy must be ruled out by a pregnancy test within two weeks before commencing treatment. Treatment should be commenced on the second or third day of the next normal menstrual period. An effective form of contraception should be used for at least one month before treatment, during treatment and for at least one month after cessation of treatment with isotretinoin, and for two years after treatment with etretinate and acitretin. Women should be effectively counselled about the risks to a fetus, and if pregnancy does occur they should immediately stop taking the drug and seek medical advice. To increase understanding of the implications of treatment, a specially designed consent form should be signed by the patient before commencing treatment. Breastfeeding should not occur while a woman is taking oral retinoids. The drugs should not be given to others, and should be kept out of reach of children. The manufacturer has also made available to dermatologists patient information pamphlets (also in several languages other than English), contraceptive guidelines and a special consent form for treatment. A warning that the product causes birth defects is carried on the drug package as well as the dispensed product. The Australasian College of Der matologists has provided comprehensive guidelines for prescription, focusing on signed informed consent for treatment, the performance of tests for pregnancy, liver function and lipid levels before treatment, and the importance of regular review. Compliance Despite these measures, exposure to the drugs during pregnancy has occurred both in Australia 11,12 and in other countries. While most women have been advised of the teratogenicity of the drugs, there has been less strict compliance with pregnancy tests and signed consent before initiation of treatment, with 4% of dermatologists in the Netherlands, 13 73% in the United States 14 and 80% in Australia 11 undertaking pregnancy tests, and 59% in the United States 14 obtaining signed consent for therapy. About a third of the women in the United States and Canada with exposure during pregnancy were already pregnant at the time therapy was commenced; 4,7 33% in one study 4 and 40% in the other 7 were not using contraception, while 26% were using less reliable methods and 65% of those taking oral contraception reported using contraception irregularly. 7 Women under 25 years showed the poorest compliance (50%) with contraceptive use. 7 Use of oral retinoids for other than the specified indications has been reported, 13,14 as well as prescription by unauthorised doctors, 12 and use of drugs left over from previous prescriptions or obtained from friends or relatives. 7 Pregnancy prevention programs Pregnancy prevention programs 15,16 instituted in 1988 by the manufacturer and the US Food and Drug Administration included additional features such as a check list of selection criteria for suitable patients, a self-evaluation test for patients, drug packages with drawings of associated birth defects and "avoid pregnancy" icons, a contraception referral program with reimbursement for the first visit by the manufacturer, a recommendation to use two forms of contraception simultaneously, 16 and periodic communications with prescribers and pharmacists. Encouraging outcomes were achieved among participants, such as a low pregnancy rate of 3.4 per 1000 courses of treatment with isotretinoin, 15 and a trend towards more appropriate use of contraception among women who were counselled with the entire program. 16 Even so, compliance with the guidelines, such as pregnancy testing (64% 15 ), waiting until the next menstrual period before commencing therapy (70% 15 ) and use of effective contraception, was still incomplete. Recommendations While the search continues for safer drugs, how can we reduce the risk of pregnancy in women taking oral retinoids while achieving maximum benefits from this unique group of drugs? (see Box 3). Conclusions A recent study 20 has provided further support for the teratogenicity of preformed vitamin A in dosages of 10 000 IU or more daily in the form of supplements. The recommended daily amount of vitamin A for women in Australia is 2500 IU and supplements exceeding this or heavy consumption of liver and liver products 2 should be avoided, particularly during therapy with oral retinoids, as well as during pregnancy. The successful implementation of a pregnancy prevention program during oral retinoid therapy could be viewed as a pregnancy rate no greater than the failure rate of the recommended contraceptive method. If this is taken as 0.3 per 100 woman-years for the combined oral contraceptive pill 18 (with the potential to be less with the simultaneous use of another method), then the pregnancy rate during therapy with isotretinoin, with an average contraception period of six months per woman per course (four months for treatment 11 and one month before and after therapy), ideally should not exceed 1.5 per 1000 courses of treatment. The estimated rates of 3.1 terminations per 1000 courses of treatment with isotretinoin 12 and 3.4 pregnancies per 1000 courses of treatment 15 recently reported are relatively low but can be reduced further. This requires the wholehearted commitment of women and their clinicians. Acknowledgements We are grateful to the staff of the South Australian Health Commission Library for helping us to obtain the references and many others not listed, and to Roche Products Medical Information Department for additional references and statistics on exposed pregnancies. References Australian Drug Evaluation Committee. Medicines in pregnancy. An Australian categorisation of risk of drug use in pregnancy. 2nd ed. Canberra: AGPS, 1992. Chalmers RJG. Retinoid therapy -- a real hazard for the developing embryo. Br J Obstet Gynaecol 1992; 99: 276-278. Saurat J-H. Side effects of systemic retinoids and their clinical management. J Am Acad Dermatol 1992; 27: S23-S28. Lammer EJ, Chen DT, Hoar RM, et al. Retinoic acid embryopathy. N Engl J Med 1985; 313: 837-841. Rosa FW, Wilk AL, Kelsey FO. Teratogen update: vitamin A congeners. Teratology 1986; 33: 355-364. Teratology Society: recommendations for isotretinoin use in women of childbearing potential. Teratology 1991; 44: 1-6. Dai WS, LaBraico JM, Stern RS. Epidemiology of isotretinoin exposure during pregnancy. J Am Acad Dermatol 1992; 26: 599-606. Dai WS, Hsu M-A, Itri LM. Safety of pregnancy after discontinuation of isotretinoin. Arch Dermatol 1989; 125: 362-365. Geiger J-M, Baudin M, Saurat J-H. Teratogenic risk with etretinate and acitretin treatment. Dermatology 1994; 189: 109-116. Hogan DJ, Strand LM, Lane PR. Isotretinoin therapy for acne: a population-based study. Can Med Assoc J 1988; 138: 47-50. Lee M, Cooper A. Survey of Australian isotretinoin prescribing. Australas J Dermatol 1991; 32: 13-16. Chan A, Keane RJ, Hanna M, Abbott M. Terminations of pregnancy for exposure to oral retinoids in South Australia, 1985-1993. Aust N Z J Obstet Gynaecol 1995; 35: 422-426. Eurocat. Surveillance of the retinoic acid embryopathy: a pharmacy based study. Eurocat Newsletter December 1992; 6(4). Doering PL, Araujo OE, Frohnapple DJ, et al. Patterns of prescribing isotretinoin: focus on women of childbearing potential. Am Pharmacother 1992; 26: 155-161. Mitchell AA, Van Bennekom CM, Louik C. A pregnancy-prevention program in women of childbearing age receiving isotretinoin. N Engl J Med 1995; 333: 101-106. Pastuszak A, Koren G, Rieder MJ. Use of the retinoid pregnancy prevention program in Canada: patterns of contraception use in women treated with isotretinoin and etretinate. Reprod Toxicol 1994; 8: 63-68. Kovacs G. Oral contraceptives -- can we make them more effective? Med J Aust 1993; 159: 224-225. Ceyrac DL, Serfaty D, Lefrancg H. Retinoids and contraception. Dermatology 1992; 184: 161-170. Sturkenboom MCJM, de Jong-van den Berg LTW, van Voorst-Vader PC, et al. Inability to detect plasma etretinate and acitretin is a poor predictor of the absence of these teratogens in tissue after stopping acitretin treatment. Br J Clin Pharmacol 1994; 38: 229-235. Rothman K, Moore LL, Singer MR, et al. Teratogenicity of high vitamin A intake. N Engl J Med 1995; 333: 1369-1373. Authors' details South Australian Health Commission, Public and Environmental Health Service, Adelaide, SA. Annabelle Chan, FAFPHM, Senior Medical Consultant, Pregnancy Outcome Unit; and South Australian Birth Defects Register, Women's and Children's Hospital, North Adelaide, SA. Malcolm Abbott, AUA, FSHP, Pharmacist, Therapeutic Goods Section; currently Rural Pharmacist, Territory Health Services, Katherine District, NT. Rosemary J Keane, RN, RM, Midwife, Pregnancy Outcome Unit. Flinders Medical Centre, Adelaide, SA. Marshall Hanna, FRACP, FACD, Senior Visiting Dermatologist, Department of Dermatology. Reprints and Correspondence: Dr A Chan, South Australian Health Commission, Public and Environmental Health Service, PO Box 6, Rundle Mall, Adelaide, SA 5000. To top of article ©MJA 1996 < URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Annabelle Chan · Marshall Hanna · Malcolm Abbott · Rosemary J Keane

For Debate Trauma in pregnancy and cerebral palsy: is there a link? The link between maternal trauma during pregnancy and cerebral palsy remains to be proven Marisa T Gilles, Eve Blair, Linda Watson, Nadia Badawi, Louisa Alessandri, Vivienne Dawes, Aileen J Plant and Fiona J Stanley MJA 1996; 164: 500-501 Introduction - Acknowledgements - References - Authors' details - - Articles on similar material Introduction Maternal trauma during pregnancy has been implicated in the aetiology of cerebral palsy in the surviving offspring.1,2 In 1991, a child with cerebral palsy received a settlement of three million dollars after it was alleged that the mother's negligent driving of a motor vehicle resulted in an accident which caused cerebral palsy in the child.1 The case rested on the testimony of an expert witness whose argument was based on a case series of six children with cerebral palsy born to mothers who had been involved in motor vehicle accidents. (Bergin AM, Stack JP, Stephenson JBP, King M. Cerebral palsy after motor accidents in pregnancy. Proceedings of the British Paediatric Neurology Association, Dublin, 1990 [unpublished data].) Possible mechanisms for the association between pregnancy trauma and cerebral palsy include reduced placental bloodflow, placental embolisation and placental abruption. To address the issue of trauma in pregnancy and subsequent cerebral palsy, we examined the Western Australian Cerebral Palsy Register3 (a subset of the Maternal and Child Health Research Database)4 which collects information on all children in the State who develop cerebral palsy (updated to the age of five years). We also examined the Hospital Morbidity Data System, which collects information on all acute hospital admissions. These two databases were selected in order to compare the rates of cerebral palsy in the offspring of women who, during their pregnancy, had trauma that required hospitalisation with the rates of cerebral palsy in the children of women who did not experience trauma. The Box outlines the methods and results of our study. Despite the fact that this was a population-based study over 11 years (1982-1992), the unadjusted relative risk of having a child with cerebral palsy after exposure to trauma was 1.4 (95% confidence interval, 0.34-5.77), which was not statistically significant. It was inappropriate to adjust for gestational age or low birth weight as they may have been factors in the aetiological pathway (e.g., trauma may induce a premature birth). Trauma occurs more commonly during the third trimester of pregnancy than at any other time in a woman's life.5 The incidence of trauma during pregnancy is reported to be about seven to eight per cent, but hospitalisation for trauma in pregnancy is rare. In the years of our study, only 0.3% of pregnant women were hospitalised. However, the severity of maternal trauma does not correlate well with the degree of fetal damage. Even minor trauma can cause fetal death and preterm labour,6-8 but few studies have considered the effect on long-term fetal outcome.2 Women who are not hospitalised (because of apparently minor trauma) may still have fetal compromise. In addition, women experiencing domestic violence may avoid medical attention, and hence such women may be under-represented in our study. Domestic violence during pregnancy, reported at rates between 8% and 17%, has been linked to fetal death, fetal distress and intrauterine growth retardation.9-11 The existence of one woman who was admitted to hospital for trauma at 28 weeks' gestation but had not been recorded as pregnant in the Hospital Morbidity Data System calls into question the validity of this data system in recording certain admission and discharge details relevant to our study. For example, in the presence of major trauma a pregnancy may be overlooked or not recorded, especially if the woman is in early pregnancy. This would lead to an underestimation of the number of women experiencing trauma during pregnancy who did not have a child with cerebral palsy, as only those women who were coded as being pregnant in the Hospital Morbidity Data System were included in the sample population. Our study has not resolved whether major trauma during pregnancy is associated with long term neurological problems in the child. In view of increasing litigation in this area, larger analytical studies into the outcomes following physical trauma during pregnancy are needed. This will best be achieved when better mechanisms for recording details of trauma during pregnancy, including domestic violence, are developed. Acknowledgements This study would not have been possible without the financial support of Healthway and PHRDC, who fund the Cerebral Palsy Register; data provided by the Health Department of WA; the expertise of Dr Richard Hockey, who carried out the linkage; and the editorial support generously supplied by Dr Ian Rouse and Dr Jennifer Kurinczuk. References Lynch v Lynch & Anor. Supreme Court of New South Wales (1991). Australian Tort Reports 81-117. Anquist KW, Parnes S, Cargill Y, Tawagi G. An unexpected fetal outcome following a severe maternal motor vehicle accident. Obstet Gynecol 1994; 84: 656-658. Stanley FJ, Watson L. Methodology of a cerebral palsy register. The Western Australian experience. Neuroepidemiology 1985; 4: 146-160. Stanley FJ, Croft ML, Gibbins J, Read AW. A population database for maternal and child health research in Western Australia using record linkage. Paediatr Perinat Epidemiol 1994; 8: 433-447. Patterson RM. Trauma in pregnancy. Clin Obstet Gynecol 1984; 27: 32-38. Williams JK, McClain L, Rosemurgy AS, Colorado NM. Evaluation of blunt abdominal trauma in the third trimester of pregnancy: Maternal and fetal considerations. Obstet Gynecol 1990; 75: 33-37. Farmer DL, Adzick S, Crombleholme WR, et al. Fetal trauma: relation to maternal injury. J Pediatr Surg 1990; 25: 711-714. Murdoch Eaton DG, Ahmed Y, Dubowitz LMS. Maternal trauma and cerebral lesions in preterm infants. Case reports. Br J Obstet Gynaecol 1991; 98: 1292-1294. Macfarlane J, Parker B, Soeken K, Bullock L. Assessing for abuse during pregnancy. Severity and frequency of injuries and associated entry into prenatal care. JAMA 1992; 267: 3176-3178. Dye TD, Tolliver NJ, Lee RV, Kenney CJ. Violence, pregnancy and birth outcome in Appalachia. Paediatr Perinat Epidemiol 1995; 9: 35-47. Webster J, Sweett S, Stolz TA. Domestic violence in pregnancy. A prevalence study. Med J Aust 1994; 161: 466-470. Stanley FJ, Watson L. Trends in perinatal mortality and cerebral palsy in Western Australia, 1967 to 1985. BMJ 1992; 304: 1658-1663. World Health Organization. International Classification of Diseases. 1975 revision, Vol 1. Geneva: Presses Centrales, 1977. Gee V. The 1991 Western Australian Birth Cohort. Statistical Series 34. Perth: Health Department of Western Australia, 1994: 5. Authors' details Health Statistics Branch, Health Department of Western Australia, Perth, WA. Marisa T Gilles, FAFPHM, Research Registrar; and Research Registrar, National Centre for Epidemiology and Population Health, Canberra. TVW Telethon Institute for Child Health Research, Perth, WA. Eve Blair, PhD, Senior Research Officer; Linda Watson, Research Assistant; Nadia Badawi, MSc, MRCPI, Paediatric Research Fellow; Louisa Alessandri, BSc(Hons), PhD, Research Officer; Fiona J Stanley, MD, FAFPHM, Professor of Paediatrics. Department of Public Health, The University of Western Australia, Perth, WA. Aileen J Plant, PhD, FAFPHM, Senior Lecturer. Women's Cancer Screening Service, Health Department of Western Australia, Perth, WA. Vivienne Dawes, FAFPHM, Medical Officer. No reprints will be available. Correspondence: Linda Watson, TVW Telethon Institute for Child Health Research, PO Box 855, West Perth, WA 6872. E-mail: Linda@ichr.uwa.edu.au Material trauma and cerebral palsy: a Western Australian population-based study, 1982-1992 Cerebral Palsy Register The study population was extracted from the Cerebral Palsy Register, a data subset of the Maternal and Child Health Research Database, and consisted of mothers of all children with cerebral palsy born between 1982 and 1992 inclusive, excluding those children who had a documented postnatal cause of cerebral palsy. A year-of-birth cohort of the Cerebral Palsy Register is only considered complete at the age of five years. Thus, by including the years 1990 to 1992 it is possible that as yet unregistered cases of cerebral palsy may have been misclassified as not having cerebral palsy. However, because cerebral palsy is rare (approximately 2 per 1000 live births),12 the effect of this error is very small. Hospital Morbidity Data System The sample population comprised all women between the ages of 14 to 50 with an ICD-9 external cause of injury (excluding poisons, drugs and medical misadventure)13 and the additional code for pregnancy in the Hospital Morbidity Data System. To validate the Hospital Morbidity Data System, a second method of identifying cases was used. The period of pregnancy was defined as the time between the second postmenstrual week and delivery, and the dates defining this period were identified for each pregnancy that resulted in a child with cerebral palsy. Database linkage Data from the Cerebral Palsy Register were linked with the births file, another subset of the Maternal and Child Health Research Database, to obtain identifying data for each mother in the study group, such as surname, maiden name, date of birth and address at the time of delivery. Using these identifying data, mothers were linked to the Hospital Morbidity Data System to determine exposure to trauma requiring hospitalisation during pregnancy. Statistical analysis Data were analysed using two-by-two contingency tables, and the relative risk was calculated with 95% confidence intervals. Results 529 children were born with cerebral palsy between 1982 and 1992, inclusive (extracted from the Cerebral Palsy Register). (See Box.) 770 pregnant women were hospitalised for trauma between 1982 and 1992 (extracted from the Hospital Morbidity Data System). The details of two of the mothers hospitalised for trauma during their pregnancy matched the details of two mothers of children with cerebral palsy. The incidence of cerebral palsy in children of women hospitalised for trauma during pregnancy was 2.6 per 1000 pregnant women. The incidence of cerebral palsy in children of women who did not experience trauma requiring hospitalisation during their pregnancy was 1.8 per 1000 pregnant women. A woman exposed to trauma requiring hospitalisation during pregnancy had 1.4 times the risk of having a child with cerebral palsy compared with a woman who had not had this experience (unadjusted relative risk, 1.4; 95% confidence interval, 0.34-5.77). The number of cases was small and this result was not statistically significant (Box). One mother who had a child with cerebral palsy and had been hospitalised for trauma during pregnancy was not recorded as being pregnant on the Hospital Morbidity Data System. Inclusion of this case in the two-by-two analysis increased the relative risk to 2.2 (95% confidence interval, 0.66-6.69), but only those women coded as being pregnant in the Hospital Morbidity Data System were included in the sample population (see text). Back to text

Marisa T Gilles · Eve Blair · Linda Watson · Nadia Badawi · Louisa Alessandri · Vivienne Dawes · Aileen J Plant · Fiona J Stanley