Women's health

Objectives: To describe the management of early-pregnancy bleeding and miscarriage reported by general practitioners in Victoria.Design, setting, and participants: Self-administered, mailed survey of a stratified random sample of GPs in Victoria. Responses weighted by strata to reflect GP population.Main outcome measures: Reported management in referral; investigation (especially ultrasound); expectant versus interventional management; and prevention of rhesus iso-immunisationResults: 382 of 621 eligible GPs responded (response rate, 62%). GPs' reported referral was more likely if the patient had painful bleeding (55%) or if the pregnancy was not viable (77%). Ultrasound strongly influenced the assessment of bleeding. Two-thirds of doctors (262/369; 66%) would routinely order ultrasound for painless bleeding, and 328/369 (84%) for painful bleeding. Expectant management was recommended by 15/353 (4%) for incomplete miscarriage with light bleeding and by 6/351 (2%) when bleeding was heavy. Some GPs are uncertain of the indications for anti-D prophylaxis, including instrumentation of the uterus, for which 261/337 (77%) said they would routinely offer anti-D. There was less agreement about anti-D after threatened miscarriage, for which 213/353 (57%) said they offered the injection.Conclusions: GPs need a working knowledge of the management of early-pregnancy bleeding, and can probably encourage more rational management. There are significant areas where GPs are uncertain, often reflecting uncertainty elsewhere, and some areas where a minority of GPs are not aware of essential requirements.

Bruce McLaren DRANZCOG, FRACGP, MPH · Julia M Shelley MPH, PhD

Medicine and the Community For editoral comment, see Mason and Diamond; see also Nozza and Rodda Abstract - Methods - Subjects - Assay - Risk assessment - Results - Discussion - Acknowledgements - Reference - Authors' details - - - More articles on Obstetrics & gynaecology and women's health Abstract Objectives: To determine the vitamin D status of veiled or dark-skinned pregnant women, because of their known increased risk of vitamin D deficiency. Design: An audit of vitamin D status. Setting: An antenatal clinic in a major metropolitan teaching hospital, Melbourne, Victoria. Participants: Pregnant women attending the clinic who agreed to be screened. Main outcome measures: Serum 25-hydroxyvitamin D3 (25OHD3) level at first visit to the antenatal clinic. Results: Of 94 women, 82 were screened. Sixty-six women (80%) had 25OHD3 values below the test reference range (22.5-93.8 nmol/L). Conclusions: Our findings are a cause for concern, because vitamin D deficient women are at risk of bone disease and their children at risk of neonatal hypocalcaemia and rickets. Most of our vitamin D comes from the action of ultraviolet light on skin.1 People with a darker skin produce less vitamin D for a given sunlight exposure,1,2 and veiled women, regardless of the climate, are at a high risk of vitamin D deficiency because of their reduced skin exposure to sunlight.3-6 In pregnant women there is the added risk of vitamin D deficiency in the baby. We screened veiled or dark-skinned pregnant women attending an antenatal clinic at a major metropolitan teaching hospital in Melbourne, Victoria, to determine their vitamin D status. Methods Subjects Veiled and/or dark-skinned women attending the antenatal clinic at the Royal Women's Hospital, Melbourne, were advised that they were at increased risk of vitamin D deficiency, putting them at risk of osteomalacia and their children at risk of vitamin D deficiency related problems. Over a 10-month period (July 1999 - April 2000), all such women were asked to provide a blood sample so that their serum level of 25-hydroxyvitamin D3 (25OHD3) could be measured. Those who consented were given a pathology request form for a blood sample to be taken. Assay Serum samples were stored at - 20ºC, and the 25OHD3 assays were performed in batches in the complex chemistry laboratory at the Royal Children's Hospital, Melbourne, using the Incstar radioimmunoassay kit (Dade Behring, Melbourne). The reference range for this test was 22.5-93.8 nmol/L. The coefficient of variation between successive assays at a mean concentration of 43.9 nmol/L was 11.7%. The assay fulfilled the acceptability criteria of the Royal College of Pathologists of Australasia endocrinology quality assurance program. Risk assessment We recorded the date the blood sample was taken (summer was defined as November to April, and winter as May to October); the patient's facial skin colour (fair, intermediate or very dark skinned); and the degree and consistency of skin covering (women who covered their arms and wore a veil or scarf over their hair and neck at all times when outdoors were coded as "consistently covered"; those who uncovered in a private, outdoor environment as "inconsistently covered"; and those who did not generally cover their arms, hair and neck when outdoors as "uncovered"). Results Of 94 veiled or dark-skinned women attending the clinic during the study period, 82 had a blood sample taken. Two did not agree to be tested, and the remaining women did not go to have a blood sample taken. Serum levels of 25OHD3 are shown in Box 1. The median value was 14 nmol/L (range, 3-77 nmol/L). In 66 women (80%) the vitamin D level was below the reference level (< 22.5 nmol/L). Of the women with values below 22.5 nmol/L, 66% (21/32) had blood samples collected in summer and 90% (45/50) in winter (95% CI for difference, 6%-43%; P < 0.01 by χ2 test). Information on skin colour and covering was complete for 70 of the 82 women. The proportion of women with serum 25OHD3 values below 22.5 nmol/L, according to skin colour and covering, is shown in Box 2. Although numbers in some subgroups were extremely small, it did not appear that this additional information was helpful for clinical management. Among the 12 women with missing information, 11 (92%) had vitamin D levels under 22.5 nmol/L, and nine were tested in winter. Discussion Of the dark-skinned and/or veiled pregnant women we tested, 80% were at high risk of vitamin D deficiency, with serum 25OHD3 values below the reference range. The number of veiled and/or dark-skinned pregnant women attending the Royal Women's Hospital each year is not recorded, but, if they were evenly distributed among the five weekly clinics (as appears likely), we estimate that around 560 such women would attend each year. Inadequate sunlight exposure can occur even in Australia, especially among women with a modest dress code or those who limit sunlight exposure for other reasons (eg, valid concerns about the risk of skin cancer). However, vitamin D deficiency can be prevented or treated with dietary supplements. Dark-skinned or veiled women should be screened for vitamin D deficiency and those who are deficient should be given vitamin D supplements, whether or not they are pregnant, because of their high risk of bone disease. Their children are also at risk of vitamin D deficiency and their infants, if breast fed, should be given suitable infant vitamin D supplements (Penta-vite, Roche). We did not measure maternal parathyroid hormone (PTH) levels during the period of this audit, but now do so routinely. PTH is an important marker of bone health in the mother, and there is some evidence that fetal growth is inversely related to maternal PTH level and positively related to maternal calcium level at delivery.7 Research is needed to determine the optimal vitamin D level in pregnant women, in terms of outcome for themselves and their offspring, and to determine whether other groups of women are also vitamin D deficient. Data from Queensland (Associate Professor John McGrath, Director, Department of Psychiatry, University of Queensland, Brisbane, personal communication8) and from the Geelong Osteoporosis Study (Dr Julie Pasco, Study Coordinator, personal communication) suggest that vitamin D deficiency in women of reproductive age is not limited to specific ethnic or cultural groups. Acknowledgements We thank Peter Vervaart and Rhonda Greaves for undertaking the laboratory assays and staff in the Monday clinic at the Royal Women's Hospital for their help. Ruth Morley is supported by the Victorian Health Promotion Foundation (VicHealth). References Norman AW. Sunlight, season, skin pigmentation, vitamin D, and 25-hydroxyvitamin D: integral components of the vitamin D endocrine system. Am J Clin Nutr 1998; 67: 1108-1110. Feleke Y, Abdulkadir J, Mshana R, et al. Low levels of serum calcidiol in an African population compared with a North European population. Eur J Endocrinol 1999; 141: 358-360. el-Sonbaty MR, Abdul-Ghaffar NU. Vitamin D deficiency in veiled Kuwaiti women. Eur J Clin Nutr 1996; 50: 315-318. Ghannam NN, Hammami MM, Bakheet SM, Khan BA. Bone mineral density of the spine and femur in healthy Saudi females: relation to vitamin D status, pregnancy, and lactation. Calcif Tissue Int 1999; 65: 23-28. Taha SA, Dost SM, Sedrani SH. 25-Hydroxyvitamin D and total calcium: extraordinarily low plasma concentrations in Saudi mothers and their neonates. Pediatr Res 1984; 18: 739-741. Gannage-Yared MH, Chemali R, Yaacoub N, Halaby G. Hypovitaminosis D in a sunny country: relation to lifestyle and bone markers. J Bone Miner Res 2000; 15: 1856-1862. Brunvand L, Quigstad E, Urdal P, Haug E. Vitamin D deficiency and fetal growth. Early Hum Dev 1996; 45: 27-33. McGrath JJ, Kimlin MG, Saha S, et al. Vitamin D insufficiency in south-east Queensland [letter]. Med J Aust. 2001; 174: 150-151. (Received 14 Aug 2000, accepted 2 May 2001) Authors' details Royal Women's Hospital, Melbourne, VIC. Sonia R Grover, MD, FRACOG, Obstetrician. Clinical Epidemiology and Biostatistics Unit, Murdoch Children's Research Institute, and University of Melbourne Department of Paediatrics, Royal Children's Hospital, Melbourne, VIC. Ruth Morley, MB BChir, FRCPCH, Senior Research Fellow. Reprints will not be available from the authors. Correspondence: Dr Ruth Morley, Clinical Epidemiology and Biostatistics Unit, Murdoch Children's Research Institute, and University of Melbourne Department of Paediatrics, Royal Children's Hospital, Flemington Road, Parkville, VIC 3052. morleyrATcryptic.rch.unimelb.edu.au Make a comment 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/> Back to text 2: Proportion of women with serum vitamin D (25-hydroxyvitamin D3) levels under 22.5nmol/L, according to skin covering and skin colour Skin colour Skin covering* Very dark Intermediate Light Total Consistently covered 6/6 (100%) 1/2 (50%) 23/25 (92%) 30/33 (91%) Inconsistently covered 3/5 (60%) 1/3 (33%) 18/24 (75%) 22/32 (69%) Uncovered 2/2 (100%) 2/3 (67%) 0 (0) 4/5 (80%) Total 11/13 (85%) 4/8 (50%) 41/49 (84%) 56/70 (80%) *Consistently covered - women always covered up, including arms, hair and neck, when outdoors; inconsistently covered - women did not usually cover fully in their own garden; and uncovered - women did not generally cover their arms, hair and neck when outdoors. Back to text

Sonia R Grover · Ruth Morley

Position Statement Anticoagulation in pregnancy and the puerperium A Working Group on behalf of the Obstetric Medicine Group of Australasia MJA 2001; 175: 258-263 Abstract - Management and prophylaxis of venous thromboembolism in pregnancy and the puerperium - Acute venous thromboembolism - Prophylaxis of venous thromboembolism - General - Previous thromboembolism - Previous single VTE and no recognised thrombophilia - Previous recurrent VTE or idiopathic VTE - Familial thrombophilia - Hyperhomocysteinaemia - Antiphospholipid syndrome and VTE - Management and prophylaxis of obstetric problems associated with uteroplacental thrombosis - References - Authors' details - - More articles on Obstetrics & gynaecology and women's health Abstract For the management of acute thrombotic events in pregnancy therapeutic doses of low molecular weight heparins (LMWH) may be used, unless the shorter half-life of intravenous unfractionated heparin (UH) and predictable reversibility by protamine are important. Treatment should be continued up until delivery and into the puerperium. Pregnant women who have had an acute thrombotic event should be delivered by a specialist team. In the case of recent thrombosis, delivery should be planned and the time during which anticoagulation therapy is ceased around the time of delivery should be minimised. Therapeutic doses of LMWH contraindicate the use of regional anaesthesia, and a switch to intravenous UH before delivery may allow greater flexibility in this regard. Prophylactic doses of LMWH can be used to reduce the risk of recurrent thromboembolic events in pregnancy. The regimen used will depend on the previous history, the family history and the presence of risk factors, including the genetic and acquired causes of thrombophilia. Women with mechanical heart valves are at high risk during pregnancy and require therapeutic anticoagulation throughout pregnancy under the direction of experienced specialists. Low-dose aspirin can reduce the risk of recurrent pre-eclampsia by about 15%, but the role of UH and LMWH in the prevention of recurrent miscarriage or obstetric complications associated with uteroplacental insufficiency is still uncertain. Low molecular weight heparins (LMWH) are being used increasingly as standard treatment for venous thrombosis, replacing unfractionated heparin (UH) for both therapeutic and prophylactic anticoagulation. Compared with UH, LMWH have increased bioavailability and a longer half-life. They also have the benefits of ease of administration, often as a single daily dose, have reduced requirements for monitoring, and are associated with less heparin-induced thrombocytopenia, reduced bleeding complications and improved patient acceptability.1Heparins do not cross the placenta, whereas warfarin does.2,3 By contrast, warfarin is teratogenic between six and 12 weeks' gestation, and may cause fetal and neonatal bleeding if used during the second or third trimester. Except perhaps in women with mechanical heart valves, there is general agreement that UH or LMWH should be substituted for warfarin as soon as pregnancy is diagnosed. Long-term treatment with UH carries risks of maternal osteoporosis4-6 and heparin-induced thrombocytopenia. Consistent, long term therapeutic anticoagulation can be hard to achieve with subcutaneous UH, because of low bioavailability and the changing anticoagulant response to UH as pregnancy progresses, often requiring close laboratory monitoring. LMWH require much less monitoring and appear to carry a smaller risk of heparin-induced thrombocytopenia, bleeding, and probably osteoporosis.7-9 Data on the effectiveness and safety of LMWH in pregnancy are limited but systematic reviews are becoming available.10 Given the convenience of LMWH and doctors' increasing familiarity with their use, there is growing opinion that LMWH have a role in pregnancy in preference to UH. In this position paper we summarise current views and make consensus recommendations for anticoagulation in pregnancy and the puerperium. The consensus process followed for this article is summarised in Box 1. Management and prophylaxis of venous thromboembolism in pregnancy and the puerperium Acute venous thromboembolism Antenatal management: Clinical trials in non-pregnant patients show that LMWH are at least as effective and safe as UH in the initial management of acute proximal or calf deep venous thrombosis (DVT).1 Recurrence of thromboembolism is reduced by ongoing warfarin therapy and, in the case of proximal DVT, treatment should be continued for at least six months (C1). The standard initial treatment for pulmonary embolism, whether during pregnancy or not, remains intravenous UH (C2). For an antenatal DVT, treatment should start with a LMWH at the therapeutic dose recommended by the manufacturers9(Box 2) (C1). Intravenous UH may be preferred in situations where its short half-life and predictable reversibility by protamine sulfate are important (eg, when delivery or surgery may be imminent). Calf DVT should be treated in the same way as proximal DVT in pregnancy because of ongoing hypercoagulability during pregnancy (C2). If intravenous UH is used for the initial treatment of pulmonary embolism, therapeutic doses of LMWH may be commenced once the patient is haemodynamically stable (C1). Anticoagulation therapy should then be maintained until delivery (C1). It is generally recommended that therapeutic doses of UH or LMWH be continued throughout pregnancy.9,11,12 In practice, some clinicians change to a prophylactic dose of LMWH after 12 weeks of therapy if the woman is still pregnant, and continue with this dose until labour (Box 2) (C3). The rationale for this approach includes a declining risk of recurrence with time after acute venous thromboembolism (VTE),13 a desire to reduce osteoporosis associated with LMWH, and the suggestion from small trials in non-pregnant patients that lower prophylactic or intermediate doses of LMWH may be as effective as warfarin in preventing secondary recurrence of VTE.14-16 The safety of such a reduction of LMWH dose before 12 weeks after acute VTE in pregnancy needs to be established in clinical trials. Monitoring: There is no need to use an anti-factor Xa assay to monitor either therapeutic or prophylactic doses of LMWH (C2). Therapy with UH can be monitored and managed according to the activated partial thromboplastin time (APTT). Management of labour and delivery: Women requiring therapeutic anticoagulation should be counselled before delivery, which should be planned under the care of a specialist team (C1). Elective delivery allows for dose adjustment to minimise the opposing risks of bleeding at delivery and of further thrombosis.13 Vaginal delivery is preferable, as there is less risk of haemorrhage than with caesarean section. Delivery by caesarean section should be determined on the basis of obstetric indications (C1). The use of regional anaesthesia requires special consideration, and is outlined in Box 3. The intensity of anticoagulation therapy required during delivery depends on how recently the VTE occurred. If within the last month, each day without anticoagulation therapy is associated with a 1% absolute increase in the risk of recurrence.13 It is therefore important to minimise the time off anticoagulation. Intravenous UH should be substituted for LMWH 24-36 hours before obstetric intervention, aiming to maintain the APTT at 1.5-2 times baseline. After induction, UH therapy is ceased once labour is established, allowing the APTT to return to normal, usually within 4-6 hours. Women requiring elective caesarean section should cease UH therapy six hours before surgery to allow for the full range of obstetric and anaesthetic options (C1). If the VTE occurred between one and three months previously, therapeutic LMWH can be reduced to a prophylactic dose for 24-48 hours and labour can then be induced. The last dose of LMWH is given the night before induction. In women whose cervical assessment suggests that labour is likely to be established within a few hours of induction, the last dose of LMWH before induction may be withheld (C2). Women who have had a VTE more than three months previously and who are still receiving a therapeutic dose of LMWH can be switched to a prophylactic dose at 38 weeks' gestation, allowing spontaneous labour to occur. Again, LMWH are withheld at the onset of labour (C2). Alternatively, if a woman wishes to be assured of access to epidural anaesthesia, induction of labour can be offered, with the last dose of LMWH on the day before the day of induction (C2). Anti-embolism stockings, compression devices and electrical calf stimulators may be used and continued postpartum, especially if caesarean delivery is undertaken (C1). In all women in whom anticoagulants have been used, the third stage of labour should be managed actively with oxytocic therapy and controlled cord traction to minimise the risk of postpartum haemorrhage (C1). Postpartum management: Postpartum, anticoagulation therapy is usually recommenced at the same intensity as that used antenatally. Prophylactic doses can be recommenced within 2-6 hours of both vaginal and caesarean deliveries (C1). This may be prophylactic doses of LMWH or low-dose (12 000 U/24 h) UH infusion, if rapid reversal of anticoagulation may be required. Therapeutic doses of UH or LMWH may be reintroduced 24 hours after vaginal delivery (C2). Caution should be exercised in recommencing therapeutic doses of LMWH earlier than 24 hours after operative delivery because of the risk of surgical bleeding, but most women can be receiving therapeutic doses by 36-48 hours after caesarean section (C1). Warfarin therapy can then be initiated and, once therapeutic levels have been achieved, continued in place of LMWH to complete the six months of therapy and for at least six weeks postpartum. Neither medication contraindicates breastfeeding (C1). Prophylaxis of venous thromboembolism General VTE remains a major cause of maternal mortality in Australia, the United Kingdom and in the United States, occurring at a rate of approximately one death per 100 000 maternities.11,12,18 The rate is much higher in older women; in the UK, women aged over 39 years had a mortality rate of 1 per 3300 pregnancies.19 VTE can occur at any time during pregnancy; its prevalence is approximately equally distributed between the three trimesters.20 Although two-thirds of events occur antenatally, the day-by-day risk is greatest in the first weeks after delivery.20Major known risk factors for VTE in pregnancy and postpartum include caesarean section (particularly in labour), obesity, prolonged bed rest and immobility, pre-eclampsia, nephrotic syndrome, current infection and other recent surgery, in addition to previous VTE and thrombophilia. These risk factors often coexist and reinforce each other. A risk-assessment profile may be constructed, as suggested in the consensus report from the Royal College of Obstetricians and Gynaecologists,21 which recommends that: all "at risk" women should be monitored for symptoms and signs of VTE during the first week postpartum; hydration should be maintained and early mobilisation encouraged; graduated compression stockings with or without calf stimulation should be used during and after caesarean section in women at moderate risk (one or two risk factors); in women at high risk (three or more risk factors), LMWH or UH prophylaxis should be used and continued for at least five days. The efficacy or benefit of these interventions is unknown, as no high grade evidence is available. Previous thromboembolism In women who have had previous VTE, the risk of recurrence will be influenced by a number of factors, including whether the index event was spontaneous or provoked, the presence or absence of a family history of VTE, the presence of a known thrombophilia, or whether there has been more than one episode of VTE. The decision as to whether VTE prophylaxis is required throughout pregnancy or only postpartum may be based on this information (Box 4).22Women requiring prophylaxis during pregnancy can be managed with low-dose LMWH (Box 2). They can then be allowed to come into spontaneous labour (C2). LMWH are withheld at the onset of labour (C2). Alternatively, if such a woman wishes to be assured of access to regional anaesthesia, induction of labour can be offered, with the last dose of LMWH on the day before the day of induction (Box 3) (C2). Previous single VTE and no recognised thrombophilia Both earlier and more recent cohort data suggest that most pregnant women with a past history of a single precipitated thrombotic event in or out of pregnancy, or associated with the combined oral contraceptive pill, and who have no underlying thrombophilia, can be safely managed by careful observation before delivery and postpartum thromboprophylaxis for six weeks23 (C2). Previous recurrent VTE or idiopathic VTE Women who have either recurrent VTE, previous idiopathic VTE, or a previous VTE and a strong family history of VTE but with no demonstrated cause for thrombophilia, may be given thromboprophylaxis throughout pregnancy and for six weeks postpartum23,24 (C1). Familial thrombophilia Thromboembolism is a multifactorial disease, in many cases developing as a result of a thrombotic tendency (a thrombophilia) interacting with other factors, such as pregnancy.25,26 Situations in which such a thrombophilia may require consideration during pregnancy are: previous personal thromboembolic disease and known thrombophilia; no previous VTE, but a strong family history (ie, one or more first-degree relatives affected) and known thrombophilia; no previous VTE, strong family history, no previous investigations; no previous VTE, weak family history (ie, incidental finding of thrombophilia in a family member); and no personal or family history of VTE, but known thrombophilia detected after screening (eg, after obstetric complications or before starting to take the combined oral contraceptive pill). The known causes of familial thromboembolism differ in their risk of associated thrombosis.27 The prevalence of such thrombophilic disorders varies between populations.28 A combination of any two or more inherited factors substantially increases the risk of thromboembolism. Box 4 summarises the risk profiles of the various genetic thrombophilias and offers guidelines for therapy. Box 5 describes management during pregnancy of medical problems requiring anticoagulation outside pregnancy. Hyperhomocysteinaemia In women with a previous history of VTE and hyperhomocysteinaemia, it may be prudent to reduce plasma homocysteine concentrations by folate supplementation throughout pregnancy, in addition to other thromboprophylaxis (C2). Antiphospholipid syndrome and VTE The presence of a lupus anticoagulant or of moderately to strongly positive titres of anticardiolipin antibody (ACA) is a strong risk factor for recurrent VTE, especially in pregnancy. Suggestions for treatment are shown in Box 4. Unless there is an associated history of poor obstetric outcome (see below), low-dose aspirin therapy need not be added (C2). On the other hand, it is contentious whether women with a positive lupus anticoagulant with or without ACA with no previous history of VTE (eg, women with systemic lupus erythematosus) require any prophylactic treatment at all during pregnancy. Low-dose aspirin may be a reasonable option for such women (C1). Management and prophylaxis of obstetric problems associated with uteroplacental thrombosis A common pathophysiological link between various poor pregnancy outcomes, including recurrent miscarriage, stillbirth, placental abruption, fetal growth restriction and pre-eclampsia, is thrombosis in the uteroplacental circulation. Antiplatelet agents (especially low-dose aspirin) have been trialled, particularly for preventing pre-eclampsia. A recent systematic review has shown a 15% reduction in the incidence of recurrent pre-eclampsia when low-dose aspirin is used, less benefit for the prevention of preterm birth and no benefit for the prevention of fetal growth restriction.35 Whether LMWH or UH can be used safely and more effectively than just aspirin in placental vasculopathy, with or without thrombophilia, is currently under investigation. Only in the case of recurrent miscarriage associated with the antiphospholipid syndrome has the addition of UH to aspirin been shown to be beneficial.36 A number of small cohort studies in women with previous obstetric complications who were treated with LMWH showed a good outcome, but whether the outcome was related to the use of LMWH is uncertain.37,38While awaiting the results of further studies, and given the small numbers of affected women, no specific treatment recommendations can be made. We encourage clinicians to refer such patients to centres where randomised controlled trials are being carried out or where cohort studies are under way. Competing interests: The authors are grateful to Pharmacia Upjohn for an unrestricted financial grant towards the costs involved in the preparation of this article, although the company did not contribute in any way either to the analysis or to the recommendations. There are no other known conflicts of interest. Future research questions The working party identified further areas for research. These include: Comparison of LMWH versus intravenous UH in acute DVT and pulmonary embolism in pregnancy. High-dose versus low-dose LMWH therapy for secondary prophylaxis after acute DVT in pregnancy. The value of prospective blinded anti-Xa levels in the use of therapeutic LMWH in pregnancy. The timing, benefits and risks of any dose adjustment of LMWH/UH, particularly peripartum. Controlled longitudinal studies of bone density and fracture rates in women using long-term LMWH. Prevention of pregnancy-associated VTE: the risks and benefits of LMWH thromboprophylaxis during pregnancy and postpartum for specific groups. Prevention of adverse pregnancy complications related to placental insufficiency. Randomised studies to determine the efficacy of LMWH in improving subsequent pregnancy outcome in women with specific pregnancy complications and an underlying thrombophilia. A register of women being treated with anticoagulants during pregnancy. A register to determine the clinical significance of thrombophilias in particular patient groups. References Weitz J. Drug therapy: low molecular weight heparins. N Engl J Med 1997; 337: 688-698. Flessa H, Kapstrom AB, Glueck HI, Will JJ. Placental transport of heparin. Am J Obstet Gynecol 1965; 934: 570-573. Forestier F, Sole Y, Aiach M, et al. Absence of transplacental passage of fragmin (Kabi) during the second and the third trimesters of pregnancy. Thromb Haemostas 1992; 67: 180-181. Dahlman TC, Sjoberg HE, Ringertz H. Bone mineral density during long-term prophylaxis with heparin in pregnancy. Am J Obstet Gynecol 1994; 170: 1315-1320. Douketis JD, Ginsberg JS, Burrows RF, et al. The effects of long-term heparin therapy during pregnancy on bone density — a prospective matched cohort study. Thromb Haemost 1996; 75: 254-257. Barbour LA, Kick SD, Steiner JF, et al. A prospective study of heparin-induced osteoporosis in pregnancy using bone densitometry. Am J Obstet Gynecol 1994; 170: 862-869. Nelson-Piercy C. Heparin-induced osteoporosis in pregnancy. Lupus 1997; 6: 500-504. Farquharson RG. Heparin, osteoporosis and pregnancy. Br J Hosp Med 1997; 58: 205-207. Ginsberg J, Greer I, Hirsh J. Use of antithrombotic agents during pregnancy. Chest 2001; 199: 122S-131S. Sanson BJ, Lensing AW, Prins MH, et al. Safety of low molecular weight heparin in pregnancy: a systematic review. Thromb Haemost 1999; 81: 668-672. Greer IA. Thrombosis in pregnancy: maternal and fetal issues. Lancet 1999; 353: 1258-1265. Toglia M, Weg J. Current concepts: venous thromboembolism during pregnancy. N Engl J Med 1996; 335: 108-114. Kearon C, Hirsh J. Management of anticoagulation before and after elective surgery. N Engl J Med 1997; 336: 1506-1511. Pini M, Aiello S, Manotti C, et al. Low molecular weight heparin versus warfarin in the prevention of recurrences after deep vein thrombosis. Thromb Haemost 1994; 72: 191-197. Gonzalez-Fajardo J, Arreba E, Castrodeza J, Perez J, et al. Venographic comparison of subcutaneous low-molecular weight heparin with oral anticoagulant therapy in the long-term treatment of deep venous thrombosis. J Vasc Surg 1999; 30: 283-292. Das S, Cohen A, Edmonson R, et al. Low molecular weight heparin versus warfarin for prevention of recurrent venous thromboembolism: a randomized trial. World J Surg 1996; 20: 521-527. Tryba M. European practice guidelines: thromboembolism prophylaxis and regional anesthesia. Regional Anesthes Pain Med 1998; 23 (6 Suppl 2): 178-182. Maternal mortality committee. Maternal deaths in Australia 1991-1993. Canberra: NHMRC, 1998. Department of Health. Why mothers die. Report on confidential enquiries into maternal deaths in the United Kingdom 1994-1996. London: The Stationery Office; 1998. Ray JG, Chan WS. Deep vein thrombosis during pregnancy and the puerperium: a meta-analysis of the period of risk and the leg of presentation. Obstet Gynecol Surv 1999; 54: 265-271. Royal College of Obstetricians and Gynaecologists. Report of the RCOG Working Party on prophylaxis against thromboembolism in gynaecology and obstetrics. London: RCOG, 1995. McColl MD, Walker ID, Greer IA. The role of inherited thrombophilia in venous thromboembolism associated with pregnancy. Br J Obstet Gynaecol 1999; 106: 756-766. Brill-Edwards P, Ginsberg J, Gent M, et al. Safety of withholding antepartum heparin in women with a previous episode of venous thromboembolism. N Engl J Med 2000; 343: 1439-1444. Letsky EA. Peripartum prophylaxis of thrombo-embolism. Baillieres Clin Obstet Gynaecol 1997; 11: 523-543. Rosendaal FR. Venous thrombosis: a multicausal disease. Lancet 1999; 353: 1167-1173. Preston FE, Rosendaal FR, Walker ID, et al. Increased fetal loss in women with heritable thrombophilia. Lancet 1996; 348: 913-916. Gerhardt A, Scharf RE, Beckmann MW, et al. Prothrombin and factor V mutations in women with a history of thrombosis during pregnancy and the puerperium. N Engl J Med 2000; 342: 374-380. Seligsohn U, Lubetsky A. Genetic susceptibility to venous thrombosis. N Engl J Med 2001; 344: 1222-1231. Chan WS, Anand S, Ginsberg JS. Anticoagulation of pregnant women with mechanical heart valves — a systematic review of the literature. Arch Intern Med 2000; 160: 191-196. Arnaout M, Kazma H, Khalil A, et al. Is there a safe anticoagulation protocol for pregnant women with prosthetic valves? Clin Exp Obstet Gynecol 1998; 25: 101-104. Elkayam U. Pregnancy through a prosthetic heart valve. J Am Coll Cardiol 1999; 33: 1642-1645. Lee LH, Liauw PCY, Ng ASH. Low molecular weight heparin for thromboprophylaxis during pregnancy in 2 patients with mechanical mitral valve replacement. Thromb Haemost 1996; 76: 628-630. Sadler L, McCowan L, White H, et al. Pregnancy outcomes and cardiac complications in women with mechanical, bioprosthetic and homograft valves. Br J Obstet Gynaecol 2000; 107: 245-253. Rowan J, McCowan L, Raudkivi P, North R. Enoxaparin treatment in women with mechanical heart valves during pregnancy. Am J Obstet Gynecol. In press. Knight M, Duley L, Henderson Smart DJ, King JF. Antiplatelet agents for preventing and treating pre-eclampsia. Cochrane Database Syst Rev 2000; 2. Rai R, Cohen H, Dave M, Regan L. Randomised controlled trial of aspirin and aspirin plus heparin in pregnant women with recurrent miscarriage associated with phospholipid antibodies (or antiphospholipid antibodies). BMJ 1997; 314: 253-257. Brenner B, Hoffman R, Blumenfeld Z, et al. Gestational outcome in thrombophilic women with recurrent pregnancy loss treated by enoxaparin. Thromb Haemost 2000; 83: 693-697. Riyazi N, Leeda M, de Vries J, et al . Low-molecular-weight heparin combined with aspirin in pregnant women with thrombophilia and a history of preeclampsia or fetal growth restriction: a preliminary study. Eur J Obstet Gynecol Reprod Biol 1998; 80: 49-54. The authors of the Position Statement are listed below Authors' details Department of Obstetrics, University of Adelaide, Women's and Children's Hospital, North Adelaide, SA. William M Hague, FRCP, FRCOG, Senior Physician in Obstetric Medicine and Clinical Senior Lecturer. National Women's Hospital, Auckland, New Zealand Robyn A North, PhD, FRACP, Associate Professor in Obstetric Medicine. Flinders Medical Centre, Bedford Park, SA. Alexander S Gallus, FRCPA, FRACP, Haematologist and Professor. King Edward Memorial Hospital, Subiaco, WA. Barry N J Walters, MB BS, FRACP, Physician in Obstetric Medicine and Clinical Associate Professor, Department of Obstetrics and Gynaecology, University of Western Australia. Christopher Orlikowski, MB BS, FANZCA, Anaesthetist. Monash University, Monash Medical Centre, Melbourne, VIC. Robert F Burrows, FACOG, FRANZCOG, Professor of Maternal-Fetal Medicine. Mater Mothers' Hospital, South Brisbane, QLD Robert B Cincotta, FRANZCOG, CMFM, Specialist in Maternal-Fetal Medicine. North Western Adelaide Health Service, Adelaide, SA. Gustaaf A Dekker, PhD, FRANZCOG, Professor of Obstetrics and Gynaecology. Mercy Hospital for Women, East Melbourne, VIC. John R Higgins, MD, FRANZCOG, Senior Lecturer in Obstetrics and Gynaecology (currently, Professor of Obstetrics and Gynaecology, University College, Cork, Ireland). Royal Hospital for Women, Sydney, NSW. Sandra A Lowe, MD, FRACP, Physician in Obstetric Medicine. Royal North Shore Hospital, Sydney, NSW. Jonathan M Morris, MD, FRANZCOG, Senior Lecturer in Obstetrics and Gynaecology. Nepean Hospital, Sydney, NSW. Michael J Peek, PhD, FRANZCOG, Professor of Obstetrics and Gynaecology. Reprints will not be available from the authors. Correspondence: Dr W M Hague, Department of Obstetrics, Women's and Children's Hospital, North Adelaide, SA 5006. bill.hagueATadelaide.edu.au Make a comment 1: Consensus process The authors of this position statement are members of the Obstetric Medicine Group of Australasia (OMGA), with a particular clinical and research interest in managing pregnant women with thromboembolic problems. The authors were all members of the working party, and include six obstetricians, four obstetric physicians, an obstetric anaesthetist and a clinical haematologist. We met collectively in October 1999 to discuss the broad issues of the use of low molecular weight heparins in pregnancy before producing a draft document; this was subsequently modified by written comments and refined at teleconferences in May, June and September 2000. The position statement is a consensus statement inasmuch as there is little high-grade evidence from either randomised trials or other cohort studies on which to make recommendations, especially for management. Our recommendations have been annotated to reflect the degree of agreement among us as follows: C1 Complete consensus; C2 Near-complete consensus (nine or more of the 12 authors); and C3 No consensus. Back to text 2: Doses of low molecular weight heparins Low molecular weight heparin Therapeutic dose Prophylactic dose Dalteparin (Fragmin) 100U/kg twice daily 5000U daily Enoxaparin (Clexane) 1 mg/kg twice daily 40mg daily or 1.5mg/kg daily Back to text 3: Suggested guidelines for regional anaesthesia and levels of consensus (Box 1) Regional anaesthesia (epidural or spinal block) is contraindicated during anticoagulation therapy because of the increased (although unquantified) risks of spinal haematoma17 (C1). If a regional anaesthetic is desired in women who require anticoagulation therapy, an elective delivery will allow for a planned reduction in dose or a change to intravenous unfractionated heparin (UH) (C1). Therapeutic subcutaneous injections of low molecular weight heparins (LMWH) or UH should be ceased at least 24 hours, and preferably 36 hours, before regional anaesthesia (epidural or spinal block) (C1). Intravenous UH (used to permit a rapid return of the APTT to normal after cessation of the infusion) should be discontinued at least six hours, and preferably 12 hours, before regional anaesthesia (C1). In women receiving prophylactic LMWH, an interval of more than 20 hours from the last dose should allow the placement of a regional block with minimal risk of complications (C2). A normal activated partial thromboplastin time (APTT) does not ensure minimal anticoagulant effect of LMWH, and the platelet count should be determined to exclude heparin-induced thrombocytopenia (C2). If caesarean section is being undertaken, further doses of LMWH should be delayed for at least four hours after placement of an uncomplicated regional block, and longer if the regional block has been complicated (C1). Low-dose LMWH therapy can be continued after delivery if there have been no complications in the siting of the regional block.17 An epidural catheter can be removed 12-20 hours after a prophylactic dose of LMWH, and the next injection should be delayed by at least four hours after removal (C1). Women should be closely monitored postpartum for any symptoms or signs of spinal haematoma, in particular for numbness and weakness in the lower limbs, severe back pain, and bladder or bowel incontinence (C1). Back to text Box 4 consists of 4a, 4b, 4c, 4d. 4a: Suggested management guidelines and levels of consensus (see Box 1) Thromboprophylaxis against recurrent venous thromboembolism (VTE) in pregnant women with previous VTE and no identified thrombophilia, according to estimated pregnancy-related risk of thrombosis Single episode of VTE Thrombosis history Recurrent VTE Spontaneous Probable cause* Family history of VTE in one or more 1st degree relatives PrA (option ThA) (C2) PrA (C2) Negot (C2) No family history of VTE PrA (C1) Negot (C2) Nil (C2) *Risk factors present such as surgery, combined oral contraceptive pill. Back to text 4b: Anticoagulation to prevent venous thromboembolism (VTE) in pregnant women testing positive for lupus anticoagulant or anticardiolipin antibodies (ACA), according to estimated pregnancy-related risk of thrombosis Lupus anticoagulant and/or ACA IgG ACA IgG weak moderate-strong positive,* ACA Thrombosis history positive* IgM positive Recurrent VTE in pregnancy despite prophylaxis ThA (C1) ThA (C1) Recurrent VTE outside pregnancy ThA (C2) ThA (C2) Previous VTE PrA (C1) Negot (C1) No previous VTE Nil (C1) Nil (C1) *Based on the highest-ever titre measured in the individual patient. Back to text 4c: Preventing venous thromboembolism (VTE) in pregnant women with established thrombophilias, according to estimated pregnancy-related risk of thrombosis Thrombosis history Antithrombin deficiency (Very rare) Protein C deficiency (Rare) Protein S deficiency (Rare) FVL* or PGM† homozygous (Uncommon) FVL* or PGM† heterozygous (Common) Personal history of VTE independent of family history ThA (C2) PrA (C1) PrA (C1) PrA (C1) Negot (C1) Family history of VTE in one or more 1st degree relatives ThA/PrA (C3) PrA (C1) PrA (C1) PrA (C1) Negot (C1) Family history of VTE in a distant relative ThA/PrA (C3) PrA (C1) Negot (C1) Negot (C1) Nil (C1) No personal or family history of VTE ThA/PrA (C3) PrA (C1) Nil (C1) Nil (C1) Nil (C1) *G1691A mutation in the factor V gene [Factor V Leiden] causing activated protein C resistance; †G20210A mutation in the prothrombin (factor II) gene. Back to text 4d: Key to management recommendations ThA Therapeutic anticoagulation necessary throughout pregnancy and postpartum - very high risk (>20%). PrA Prophylaxis necessary throughout pregnancy and puerperium - high risk (10%-20%). Negot Need for prophylaxis negotiable on a case-by-case basis until further data become available - moderate risk (3%-10%). Nil Postpartum prophylaxis or no prophylaxis - low risk (3%). Back to text 5: Management during pregnancy of medical problems requiring anticoagulation therapy outside pregnancy (consensus levels are described in Box 1) Women with mechanical heart valves require therapeutic doses of anticoagulant medication throughout pregnancy to prevent valve thrombosis or maternal thromboembolic events9 (C1). Women with mechanical heart valves should be managed under joint subspecialty care (C1). The maternal benefits of warfarin (prevention of valve occlusion and systemic embolism) must be balanced against hazards to the fetus (congenital anomalies, intracranial haemorrhage and fetal loss).29 Unfractionated heparin (UH) and low molecular weight heparins (LMWH) are safe for the fetus, but there is still debate as to their therapeutic efficacy in the mother compared with that of warfarin.29-33 UH is associated with higher rates of maternal thromboembolic complications, including fatal events.29,33 There are limited data on the efficacy of LMWH in mechanical valves during pregnancy, but valve thrombosis may occur.34 High rates of maternal valve thrombosis occur if subtherapeutic doses of UH or LMWH are used.9,30 Women should participate in the choice of anticoagulation therapy (C2). In women with other diseases (eg, dilated cardiomyopathy) who require anticoagulation therapy to prevent thromboembolic complications, the use of therapeutic or prophylactic doses of LMWH will depend on the perceived risk of thromboembolism (C1). Back to text

Medicine and the Community The physical, sexual and emotional violence history of middle-aged women: a community-based prevalence study Danielle Mazza, Lorraine Dennerstein, Corrine V Garamszegi and Emma C Dudley MJA 2001; 175: 199-201 Abstract - Methods - Questionnaire - Study participants - Statistical analysis - Results - Domestic violence - Unwanted sexual experiences with someone other than a husband or partner - Childhood abuse - Discussion - Acknowledgement - Reference - Authors' details - - More articles on Obstetrics & gynaecology and women's health - More articles on Social issues Abstract Objectives: To determine current and lifetime rates of the experience of partner abuse and sexual violence in a community-based sample of middle-aged women and compare these to figures obtained in a general practice setting. Design and methods: This research was part of the Melbourne Women's Midlife Health Project (MWMHP), an observational, longitudinal, population-based study of 438 Australian-born women conducted over nine years. In 1996, during the sixth year of the study, we asked the MWMHP participants to complete a self-administered "violence questionnaire", incorporating a modified Conflict Tactics Scale and questions on sexual abuse experienced during childhood and adult life. Results: Of the 395 women remaining in the sixth year of follow-up of the MWMHP, 362 (92%) completed the questionnaire. Overall, 28.5% (n = 101) of the women had experienced some form of domestic violence (physical, sexual or emotional) during their lifetime; 5.5% (n = 15) of women had experienced severe physical abuse in the past year at the hands of a partner; and 11.8% (n = 42) of the women had experienced rape or attempted rape between the age of 16 and the time of our survey. Regarding abuse in childhood, 8.9% (n = 32) of women had experienced physical abuse, 42.3% (n = 152) had experienced non-contact sexual abuse, and 35.7% (n = 128) contact sexual abuse. Compared with the general-practice-based study, rates of childhood physical abuse and penetrative sexual abuse were similar, but rates of less intrusive child sexual abuse were significantly higher in our study. Conclusions: Doctors in all areas of medicine who are dealing with middle-aged women need to be aware of the levels of violence sustained by women throughout their lives. Such experiences may have a substantial impact on women's physical and mental wellbeing. Over the past 20 years, the high prevalence of violence against women has been exposed by rigorous research. Women's Safety Australia,1 a large community-based survey of 6300 women undertaken by the Australian Bureau of Statistics, found that 2.6% of women who currently had partners had experienced an incident of physical violence in the previous 12-month period; 8.0% reported an incident of physical violence at some time during their current relationship; and 1.9% of women had experienced an incident of sexual violence during the 12 months prior to the survey. Mazza and colleagues2 examined the prevalence of physical, sexual and emotional violence experienced by women attending general practitioners in metropolitan Melbourne. Their study found that, of women aged 18 years and over who were in relationships, more than a quarter had been victims of physical or emotional abuse by a partner in the previous year, with one in 10 experiencing severe physical violence. In two Australian studies undertaken in hospital emergency departments,3,4 about 19% of female attendees disclosed histories of domestic violence. It is now recognised that domestic violence has an important influence on the morbidity and mortality of women. Increased utilisation of healthcare facilities,5 chronic pain (particularly pelvic pain),6,7 functional gastrointestinal disorders,8 drug and alcohol dependence or misuse,9-11 attempted suicide11 and psychopathology12-14 are all strongly associated with the experience of violence. The aims of our study were to determine current and lifetime rates of the experience of partner abuse and sexual violence in a community-based sample of middle-aged women and to compare these to figures obtained in a general practice setting in a previous study.2 Methods Questionnaire The "violence questionnaire" that was handed to participants for self-completion was the same as that used in a prevalence study of domestic violence experienced by women attending general practices in Melbourne,2 with which we wanted to compare our study data. The questionnaire incorporated the Conflict Tactics Scale,15 with the modification that respondents were asked whether the tactic had occurred never, once or more than once in the past year, and with the addition of questions on emotional abuse. Physical violence was classified as minor or severe.2 Questions about sexual abuse were derived from the studies of Wyatt16 and Russell,17 both of which used multiple screening questions to allow time for the respondent to become accustomed to the nature of the questions. Childhood sexual abuse was classified as "contact" abuse (involving physical contact) or "non-contact" abuse. (For the purposes of our study, a "child" was defined as a person under 16 years of age.) Study participants The subjects of our study were participants in the sixth year of the Melbourne Women's Midlife Health Project (MWMHP),18 a longitudinal study of a community-based cohort of Australian-born women aged 45-55 years at the beginning of the study. An initial cross-sectional study undertaken in 1991 of a randomly selected community-based sample of 2001 women gathered baseline information regarding women's health experiences and variables related to these experiences.19 The MWMHP study was approved by the Human Research Ethics Committee of the University of Melbourne. Eligibility for the longitudinal phase of the study included women who at baseline were premenopausal, were not taking the oral contraceptive pill or hormone therapy, and had an intact uterus. Of the 779 women eligible to enter the longitudinal study, 56% (n=438) chose to do so. Volunteers for the longitudinal study were more likely than non-participants to report better self-rated health, paid employment, more than 12 years of education, having ever had a Pap smear, exercising at least once a week, and having undergone dilatation and curettage.19 In the MWMHP study, women were interviewed annually face-to-face in their own homes by trained interviewers. Information was collected on a range of variables, including sociodemographic factors, health status, lifestyle behaviours, menopausal status and hormone therapy use. By 1996, when our study was conducted, the retention rate of MWMHP participants was 90% (n = 395). Of these women, 23 who had experienced surgical menopause were not given the violence questionnaire, and a further 10 women refused to complete the questionnaire, leaving 362 women who took part in our study. Statistical analysis The Statistical Package for the Social Sciences (SPSS)20 was used to analyse the sample and determine the prevalence of different forms of violence reported by the women. A statistical comparison was made between the results of our study and the data (previously unpublished) for the subset of women aged 50-69 years (n = 411) from an earlier, general-practice-based study of violence2(Box 1). Ninety-five per cent approximate confidence intervals were used. Results Of the 362 questionnaires available, there were missing data for eight women who did not answer questions on adult violence, four who did not complete the adult sexual abuse questions, and four who did not answer either one or more questions on childhood violence. At the time of completing the violence questionnaire the women were between 51 and 62 years of age (mean, 54.6; SD, 2.42). Sixty-six per cent (238/362) were in paid employment and 77% (277/362) were married or living with a partner. The median parity was 3 (range, 0-9), and 35% of the women had had more than 12 years' education. Domestic violence Overall, 28.5% (101/354) of the women in our study had experienced some form of physical or emotional violence over their lifetime (Box 2). A comparison between our sample and the general-practice-based sample with regard to prevalence of violence experienced in the past year is shown in Box 1. Unwanted sexual experiences with someone other than a husband or partner Overall, 40.8% (146/358) of respondents had, between the age of 16 years and the present, experienced either unwanted sexual advances or been in a situation in which the threat of sexual assault was associated with violence or threat of violence. This included one or more of the following: experiencing rape or attempted rape; encountering sexual advances from someone in authority; or narrowly missing being sexually assaulted. A comparison between the responses in our study and the general practice study is shown in Box 1. Childhood abuse Childhood physical abuse had been experienced by 8.9% (32/358) of the women in our study, and more than one in three women had experienced some form of childhood sexual abuse. Our study showed similar levels of physical abuse and penetrative sexual abuse in childhood, but significantly higher levels of less intrusive child sexual abuse, compared with the general practice sample (Box 1). Discussion Using a longitudinal cohort study such as the MWMHP provides many benefits in a prevalence study. Principal among these is that the women surveyed have been interacting with the research staff for over six years and have therefore built up a degree of trust and comfort with these people. This may facilitate disclosure of sensitive issues such as domestic violence and sexual abuse. A limitation of the study is that in order to obtain some comparative value with other work the questions were delivered by self-administered questionnaire, allowing no opportunity for clarification or exploration of the issues being recorded. Also, the additional questions about emotional abuse had not previously been validated. Of interest is the fact that, despite the participants being a self-selected group of relatively well-educated and health-conscious women, there is a considerable lifetime prevalence of domestic violence among them. The fact that our community-based survey results were similar to those of the general-practice-based survey2 confirms that violence affects the lives of all kinds of women and that it may be a very important contributor to concurrent morbidity occurring at the menopause. In the area of child abuse, our data show similar levels of physical abuse and penetrative abuse but significantly greater levels of less intrusive sexual abuse than those found in the general practice sample. This is surprising given that prevalence rates of most forms of abuse are usually lower in community-based settings than in general practice.2 The greater levels in our sample may reflect a cohort effect or may be owing to the long-term relationship developed over six years of follow-up that may have led to more disclosures. Many studies have demonstrated a relationship between experience of violence and long-term morbidity. Our findings of a high prevalence of violence experienced by women over their lifetime suggest that doctors practising in all areas of medicine need to recognise and explore violence issues when considering middle-aged women's reasons for presenting with ill health. Acknowledgement This study was funded by the National Health and Medical Research Council, the Victorian Health Promotion Foundation, and the Australasian Menopause Society. References Australian Bureau of Statistics. Women's Safety Australia 1996, Canberra: ABS, 1996. (Catalogue No. 4128.0.) Mazza D, Dennerstein L, Ryan V. Physical, sexual and emotional violence against women: a general practice-based prevalence study. Med J Aust 1996; 164: 14-17. de Vries Robbe M, March L, Vinen J, et al. Prevalence of domestic violence among patients attending a hospital emergency department. Aust N Z J Public Health 1996; 20(4): 364-368. Roberts GL, O'Toole BI, Lawrence JM, Raphael B. Domestic violence victims in a hospital emergency department. Med J Aust 1993; 159: 307-310. Stark E, Flitcraft A, Zuckerman D, et al. Wife abuse in the medical setting: an introduction for health personnel. Monograph No. 7. Rockville, Maryland: National Clearinghouse on Domestic Violence, 1981. Schei B. Psycho-social factors in pelvic pain. A controlled study of women living in physically abusive relationships. Acta Obstet Gynecol Scand 1990; 69(1): 67-71. Walling MK, Recter RC, O'Hara MW, et al. Abuse history and chronic pain in women: I. Prevalences of sexual abuse and physical abuse. Obstet Gynecol 1994; 84(2): 193-199. Drossman DA, Leserman J, Nachman G, et al. Sexual and physical abuse in women with functional or organic gastrointestinal disorders. Ann Intern Med 1990; 113(11): 828-833. Burnam MA, Stein JA, Golding JM, et al. Sexual assault and mental disorders in a community population. J Consult Clin Psychol 1988; 56: 843-850. Winfield I, George LK, Swartz M, Blazer DG. Sexual assault and psychiatric disorders among a community sample of women. Am J Psychol 1990; 147: 335-341. McCauley J, Kern DE, Kolodner K, et al. The "battering syndrome": prevalence and clinical characteristics of domestic violence in primary care internal medicine practices. Ann Intern Med 1995; 123(10): 737-746. Gleason WJ. Mental disorders in battered women: an empirical study. Violence Vict 1993; 8(1): 53-68. Mullen PE, Romans-Clarkson SE, Walton VA, Herbison GP. Impact of sexual and physical abuse on women's mental health. Lancet 1988; 1: 841-845. Beitchman JH, Zucker KJ, Hood JE, et al. A review of the long-term effects of child sexual abuse. Child Abuse Negl 1992; 16: 101-118. Straus MA. Measuring intrafamily conflict and violence: the conflict tactics (CT) scales. J Marriage Fam 1979; 41(1): 75-88. Wyatt GE. The sexual abuse of Afro-American and white-American women in childhood. Child Abuse Negl 1985; 9: 507-519. Russell DEH. The incidence and prevalence of intrafamilial and extrafamilial sexual abuse of female children. Child Abuse Negl 1983; 7: 133-146. Dennerstein L, Smith A, Morse C, et al. Menopausal symptoms in Australian women. Med J Aust 1993; 159: 232-236. Burger HG, Dudley EC, Hopper JL, et al. The endocrinology of the menopausal transition: a cross-sectional study of a population-based sample. J Clin Endocrinol Metab 1995; 80(12): 3537-3545. SPSS for Windows. Statistical package for social sciences. Version 9.0. Chicago, Ill: SPSS Inc, 1999. (Received 2 Mar 2000, accepted 29 Mar 2001) Authors' details Office for Gender and Health, Department of Psychiatry, University of Melbourne, VIC. Danielle Mazza, MD, FRACGP, Research Fellow; Lorraine Dennerstein, AO, PhD, FRANZCP, Director; Corrine V Garamszegi, MWH, SRN, Research Assistant; Emma C Dudley, BSc(Hons), GradDip Epidemiol, Research Fellow. Reprints will not be available from the authors. Correspondence: Professor L Dennerstein, Office for Gender and Health, Department of Psychiatry, University of Melbourne, Royal Melbourne Hospital, Charles Connibere Building, Parkville, VIC 3050. ldennATunimelb.edu.au Make a comment 1: Number of women experiencing various types of violence among MWMHP* participants compared with the number of women aged 50-69 years reporting these experiences in a general practice setting† Type of abuse MWMHP study (%) General practice study (%) Difference in prevalence between the 2 studies (95% CI) P Adult experience of violence Overall physical and/or emotional abuse by partner in the past year 57 (20.9%) 80 (29.6%) -8.7% (-16.0%, -1.4%) Minor physical abuse by partner in the past year 46 (16.9%) 61 (22.8%) -5.9% (-12.6%, +0.8%) 0.088 Severe physical abuse by partner in the past year 15 (5.5%) 18 (6.7%) -1.2% (-5.2%, +2.8%) 0.550 Emotional abuse by partner in the past year 31 (11.3%) 54 (20.0%) -8.7% (-14.8%, -2.6%) All forms of sexual assault between 16 years of age and the present 146 (40.8%) 135 (33.3%) +7.5% (+0.6%, +14.4%) Unwanted sexual experience between 16 years of age and the present 85 (23.7%) 79 (19.8%) +3.9% (-2.0%, +9.8%) 0.189 Rape or attempted rape between 16 years of age and the present 42 (11.8%) 43 (10.7%) +1.1% (-3.4%, +5.6%) 0.640 Childhood experience of violence Physical abuse 32 (8.9%) 34 (8.6%) +0.3% (-3.7%, +4.3%) 0.856 Non-contact sexual abuse 152 (42.3%) 103 (25.5%) +16.8% (+10.2%, +23.4%) Contact sexual abuse 128 (35.7%) 110 (27.2%) +8.5% (+1.9%, +15.1%) Penetrative sexual abuse 24 (6.7%) 17 (4.2%) +2.5% (-0.8%, +5.8%) 0.129 * MWMHP = Melbourne Women's Midlife Health Project (our study was based on the cohort of women participating in the MWMHP study18 in its sixth year). † The group of women aged 50-69 years was a subset (previously unpublished data, n=411) of the 2181 women aged over 18 years who took part in a general-practice-based study of violence against women.2 ‡ Missing data from incomplete questionnaires were excluded when calculating prevalences. Back to text 2: Lifetime prevalence of domestic violence among middle-aged women (MWMHP* participants) Type of abuse Number of women Prevalence† (95% CI) Overall physical 101 28.5% and/or emotional (23.8%-33.2%) abuse Minor physical 79 22.4% abuse (18.4%-26.2%) Severe physical 31 8.8% abuse (5.9%-11.8%) Emotional abuse 60 17.0% (13.1%-20.9%) * MWMHP = Melbourne Women's Midlife Health Project (our study was based on the cohort of women participating in the MWMHP study18 in its sixth year). † Missing data from incomplete questionnaires were excluded when calculating prevalences. Back to text

Danielle Mazza · Lorraine Dennerstein

The continuing rise in the mean age for childbearing has a widespread impact on the practice of obstetrics. It has been accompanied by an escalation in the rate of caesarean section to around 25% in many tertiary centres and into the 35%–45% range in private practice. The reasons are complex, but advancing maternal age, patient request and obstetric litigation are all factors. Increasing maternal age has brought with it increased exposure to and awareness of the risks of fetal abnormalities. As a "screening test", maternal age alone performs poorly. At best, its sensitivity for detection of Down syndrome is only 30%, with a false positive rate of 5%–14%. Invasive procedures (chorionic villus sampling and amniocentesis) carry a risk to the pregnancy that is often unacceptable, especially for women who have used assisted reproductive techniques. There has been a rapid evolution of non-invasive screening methods. Biochemical screening of maternal serum in the second trimester (involving alpha-fetoprotein, unconjugated oestriol, and human chorionic gonadotropin [hCG]; the triple test), coupled with maternal age, has been shown to increase the sensitivity to 60% while maintaining the false positive rate at 5%. Technical advances have increased the application of ultrasonography. It can be used to examine the nuchal fold, which has been found to increase the risk of Down syndrome 10-fold when thickened to more than 6 mm in the second trimester. Large studies at 11–14 weeks' gestation have shown that "nuchal translucency" measurements, in combination with maternal age, increase sensitivity to 75%–80%.1 Combining this with first-trimester biochemical markers (free b subunit of hCG in serum, and pregnancy-associated plasma protein, PAPP-A) may increase the sensitivity to 90%. The latest report of the absence of nasal bone in the first trimester in fetuses with Down syndrome indicates that combination screening could improve the sensitivity to beyond 95% while maintaining a false positive rate of 5%.2 If these projections are substantiated in larger studies, Down syndrome screening will shift to the first trimester, with obvious benefit for the mother. The past decade has seen a veritable explosion in our understanding of fetal physiology and pathology. The concomitant development of ultrasound technology has enabled identification of a higher proportion of fetuses with structural abnormalities. Such diagnoses have made possible early correction of the developmental abnormalities. The most successful fetal therapy is the treatment of severe anaemia from Rhesus isoimmunisation by intrauterine fetal transfusions. Survival rates of over 90% have been achieved. With routine administration of anti-D immunoglobulin, and the consequent fall in the incidence of alloimmunisation, training and maintenance of skill and expertise will be a major challenge. Maternal drug therapies are widely used. They include folate for preventing neural tube defects; digoxin, with or without flecainide, for fetal tachyarrhythmias; corticosteroids for both fetal lung maturation and congenital adrenal hyperplasia; and immunoglobulin for fetal alloimmune thrombocytopenia. Direct invasive fetal procedures have also been tried over the last decade. Shunts have been inserted in fetuses with bladder-outlet obstruction, idiopathic pleural effusion, and congenital cystic adenomatous malformation of the lung. Open fetal surgery, such as for congenital fetal diaphragmatic hernia and fetal sacrococcygeal teratoma, is rapidly giving way to less invasive endoscopic approaches. With increasing maternal age and the widespread use of assisted reproductive technology comes a rise in multiple pregnancies, with the associated impact of prematurity and the specific complication of twin-to-twin transfusion syndrome, which affects 10%–15% of monochorionic twins. In severe cases, mortality is over 90%. Aggressive amnioreduction can result in survivals of about 60%, but up to 20% of the survivors have long term handicaps. Fetoscopic laser coagulation of the communicating vessels has improved the survival rate to 75%–80%, and reduced the long-term handicap rate to 5%.3,4 The principal changes in gynaecological therapy have come from the introduction of effective alternatives to major invasive surgery. The place of endoscopic surgery for treating ectopic pregnancy, investigation of pelvic disorders and removal of benign adnexal masses is established, but the true costs versus benefits of advanced laparascopic procedures, such as for hysterectomy, require further evaluation. The development of improved medical alternatives for treating menstrual disorders, including both oral and direct intrauterine delivery systems, have markedly reduced the number of major operations. Similarly, non-surgical therapies in other spheres of gynaecology, such as urogynaecology, are being developed and evaluated.5 Complementing these changes has been the active participation in the Cochrane Collaboration by women's health professionals, so that the specialty is no longer the holder of Archie Cochrane's "wooden spoon".

Fung Yee Chan · Jeremy J N Oats DM, FRANZCOG

Editorial The health of Australia's mothers and babies Improvements in the collection of perinatal statistics are needed to fill the gaps MJA 1996; 164: 198-199 Childbirth in Australia is relatively safe, as measured by the traditional outcomes of maternal and perinatal mortality. About 1 in 8000 mothers die from all direct, indirect and incidental causes associated with pregnancy and childbirth.1 The perinatal death rate, which includes fetal deaths and neonatal deaths up to 28 days of infants weighing at least 500 g, declined to 8.2 per 1000 births in 1993,2 the lowest level yet achieved. During the last two decades, all States and Territories have developed perinatal data systems that provide valuable information on maternal risk factors and complications and the outcomes of mothers and infants. This information, collected by midwives and medical practitioners, is increasingly being used for research and policy development and discussion about issues relating to pregnancy and childbirth. The 1992 report on Australian mothers and babies drew attention to births to teenage mothers, mothers born overseas and Australian Aboriginals and Torres Strait Islanders, and to factors associated with caesarean births.3 Teenage births. Births to teenage mothers in Australia, of just over 20 per 1000 in the early 1990s, were well below the peak of 55.5 per 1000 in 1971.4 However, these figures give an incomplete picture of teenage pregnancy because only South Australia and the Northern Territory have population-based data about induced abortions. Analysing trends in birthrates fails to indicate the total extent of teenage pregnancy. In 1992, 14 396 teenage mothers gave birth in Australia: 4115 were aged under 18 years (2503 were aged 17; 1133 were aged 16; 357 were aged 15; and 122 were under 15 years). The South Australian data showed that for every 100 births to teenage mothers, there were 82 induced abortions.5 Extrapolating from these data, the estimate of teenage pregnancies nationally in 1992 was in excess of 26 000. Based on these annual figures, about one in five teenagers will become pregnant at some stage between the ages of 15 and 19 years, and one in 10 will give birth. Women born overseas. Of all the women who gave birth in Australia in 1992, more than one in five (22.7%) were born overseas, and 6.3% of all mothers were born in Asia. Of those born in Asia, 3605 women (1.4% of all births) were from Vietnam, 2660 (1%) from the Philippines, 1881 (0.7%) from China, 1365 (0.5%) from Malaysia, 1164 (0.5%) from India and 1046 (0.4%) from Hong Kong. Perinatal outcome did not seem to differ greatly from that of infants of Australian-born mothers,6 but further research is needed to determine the effects of maternal risk factors on outcomes such as birthweight and perinatal mortality. The recent substantial increase in births to Asian-born mothers, notably Vietnamese and Chinese women, places extra demands on health services to ensure that their special needs are met, particularly in Sydney and Melbourne, where disproportionate numbers of people from non-English-speaking backgrounds live. These women often have vastly different cultural beliefs and practices associated with pregnancy and childbirth. Bicultural health workers are increasingly being recognised as having an important role in establishing support networks for these women, familiarising them with the Australian health system, and assisting them in overcoming language and attitudinal barriers. Australian Aboriginals and Torres Strait Islanders. Many aspects of caring for overseas-born women are also pertinent to health services for Australian Aboriginals and Torres Strait Islanders. In 1991, 7027 Aboriginal and Torres Strait Islander women gave birth, and 7257 did so in 1992, accounting for 2.9% of all mothers in both years. Many of these women travel long distances from remote communities to hospitals in larger centres, and thus frequently give birth in an unfamiliar environment. In 1992, one in four births in this group were to teenage mothers and almost one in three of these teenagers had had at least one other child. The average birthweight (3150 g) of babies born to Aboriginal Australians and Torres Strait Islanders was 206 g less than that of all Australian babies, and the proportion of babies that were of low birthweight (< 2500 g) was 12.9%, more than double the rate of 6.3% for all births. Caesarean births. The seemingly inexorable rise in deliveries by caesarean section in Australia continues unabated, with a peak at 18.3% of total deliveries in 1992. South Australia (22.1%) and Queensland (20.9%) consistently have the highest caesarean rates and Tasmania (16.1%) usually the lowest. The caesarean rate of 22.4% for women with private health insurance was more than 40% higher than the rate of 15.8% for women without insurance (partly attributable to more older women in the insured group). Caesarean rates for women with insurance having their first baby increased with maternal age, from 21.9% at 25-29 years to 28.1% at 30-34 years, 37.4% at 35-39 years, and 47.4% at 40-44 years. High caesarean rates were also associated with multiple births (39.2% for twins and 85.3% for triplets, compared with 18% for singleton births), with breech presentation in singleton births (73.8%), and with very low birthweight babies (53.8% for singleton babies weighing 1000-1499 g). Relatively simple measures, such as more detailed recording of the indications for caesarean section and obtaining an opinion from another obstetrician about whether operative intervention is indicated, have proved effective in reducing caesarean rates.7The Royal Australian College of Obstetricians and Gynaecologists should address the issue of high caesarean rates in Australia by requiring regular audits of hospitals and medical practitioners. The quality and usefulness of information about perinatal health can be enhanced in several ways. Firstly, it should be recognised that analysis of trends in teenage pregnancy and the formulation of preventive strategies require data about induced abortions as well as data about births. Secondly, by linking registrations of perinatal and infant deaths to information for all births from the perinatal data systems in every State and Territory, the association between maternal risk factors and outcomes can be better evaluated.8,9 Thirdly, while the patterns of risk factors, type of care and outcomes are remarkably consistent from year to year, shortening the interval between the year of birth and the publication of State and national reports is an important goal. Paul A L Lancaster Director, Australian Institute of Health and Welfare National Perinatal Statistics Unit, University of Sydney, NSW National Health and Medical Research Council. Report on maternal deaths in Australia 1988-90. Canberra: AGPS, 1993. Australian Bureau of Statistics. Perinatal deaths, Australia 1993. Canberra: ABS, 1994. (Catalogue No. 3304.0.) Lancaster P, Huang J, Pedisich E. Australia's mothers and babies 1992. Sydney: AIHW National Perinatal Statistics Unit, 1995. Australian Bureau of Statistics. Births, Australia 1993. Canberra: ABS, 1994. (Catalogue No. 3301.0.) Chan A, Scott J, McCaul K, Keane R. Pregnancy outcome in South Australia 1992. Adelaide: South Australian Health Commission, 1993. Guevara V, Taylor L. The health of mothers born in non-English-speaking countries and their babies, NSW 1990-1993. New South Wales Public Health Bull 1995; 6 Suppl S2: 1-52. Myers SA, Gleicher N. A successful program to lower cesarean section rates. N Engl J Med 1988; 319: 1511-1516. Perinatal Data Collection Unit. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Births in Victoria 1983-1992. Melbourne: Department of Health and Community Services, 1994. Gee V. Perinatal statistics in Western Australia. Tenth annual report of the Western Australian Midwives Notification System, 1992. Perth: Health Department of Western Australia, 1993.

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