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Clinical guidelines

National guide to a preventive health assessment for Aboriginal and Torres Strait Islander people Second edition

Antenatal care

Author Dr Eileen Rafter
Expert reviewers Assosciate Professor Wendy Cavilla, Dr Vivienne Manessis

Overview

Aboriginal and Torres Strait Islander mothers and babies experience an increased risk of maternal, fetal and neonatal death, pre-term birth and low birthweight when compared with non-Indigenous mothers and babies.1 Poor health and social disadvantage contribute to these poorer perinatal outcomes. Aboriginal and Torres Strait Islander mothers have higher rates of chronic disease such as diabetes and kidney disease, higher rates of sexually transmissible infections and anaemia, higher rates of smoking and alcohol consumption in pregnancy, higher rates of adolescent pregnancies and limited access to affordable nutritious food and health services.2

As for all pregnant women, the antenatal care offered to Aboriginal and Torres Strait Islander women should be woman-centred.2 This means that the care focuses on the individual woman’s needs and preferences and that the woman is informed and involved in decision making. Other important factors in improving antenatal care are continuity of carer, allowing adequate time for communication and to establish trust and rapport, and health provider awareness of local community sociocultural factors and health needs.2,3

This chapter focuses on some key aspects of antenatal screening that are of particular relevance to Aboriginal and Torres Strait Islander women and is not a comprehensive guide to all antenatal screening. The first antenatal visit – which should take place in the first trimester – is particularly important. At this visit a comprehensive history, examination and discussion with the woman establishes the necessary schedule of tests and visits. The majority of screening tests are also carried out. Psychosocial assessment is also important at this stage; screening for issues such as domestic violence, financial stress, mental health disorders and substance use, including alcohol.

In addition to general recommendations for the first antenatal visit, specific recommendations have been made for the following priority areas: smoking cessation, alcohol consumption, genitourinary infection screening, mineral and vitamin deficiency, and diabetes.

Smoking cessation

Tobacco smoking is one of the most important preventable causes of adverse pregnancy outcomes. These adverse events include premature birth, placental abruption (double the risk for smokers who consume more than 20 cigarettes a day), spontaneous abortion, low birthweight,4 stillbirth5 and placenta praevia.6 Children exposed to tobacco smoke in-utero have a higher risk of SIDS, asthma and respiratory and ear infections. In addition there is some evidence that in-utero exposure is associated with psychological problems such as attention and hyperactivity problems, disruptive and negative behaviour3 and poorer educational performance.7 Although some studies show the harmful effect of smoking in pregnancy is dose related,8,9 this does not obviate the need to clearly and consistently recommend complete smoking cessation as the safest option.2 The risk of low birthweight is greater if the woman continues to smoke in the third trimester, with one study showing that if a woman is able to give up smoking by her fourth month of pregnancy, her risk of delivering a low birthweight baby decreases to nearly that of a non-smoker.10

Aboriginal and Torres Strait Islander women are three times more likely to smoke during pregnancy than non-Indigenous Australian women, with current smoking prevalence estimated at around 50–60%.11 Higher risk groups include teenagers and women who experience socioeconomic hardship.8,12,13 Maternal smoking contributes to a greater proportion of the risk of prematurity and low birthweight for Aboriginal and Torres Strait Islander babies when compared with non-Indigenous babies.13

A higher proportion of women stop smoking during pregnancy than at other times in their lives, leading to the hypothesis that pregnancy may be a ‘teachable moment’ for smoking cessation.9 However, some women who stopped smoking in pregnancy resume after birth and there is a lack of evidence on how to prevent this.14 Some women may also take up smoking again during pregnancy so it is important to continue enquiring about smoking and exposure to secondhand smoke throughout pregnancy.2

The US, UK and Australia have developed guidelines recommending all pregnant women receive brief interventions to promote smoking cessation in pregnancy.14,15 These guidelines are currently based on the ‘5As’ (see Chapter 1: Lifestyle, introduction). There have been many studies on smoking cessation strategies in pregnant women using a range of interventions including advice, counselling, hypnosis, telephone support, motivational interviewing, written and electronic resources, cognitive behavioural therapy, measurement of the byproducts of tobacco smoking, use of nicotine replacement therapy and assessment of readiness to quit.9 Such strategies have also been found to be beneficial in studies involving Aboriginal and Torres Strait Islander women.16 Overall smoking cessation strategies used in early pregnancy can reduce smoking in later pregnancy and lead to a reduction in low birthweight and premature birth.9 Trials using cognitive behavioural therapy have the strongest evidence and demonstrate statistically significant improvements in mean birthweight. There is no evidence for negative psychological impacts from behavioural interventions and indeed the psychological impact may be positive, with women feeling that ‘somebody cared’ about their health and wellbeing.9 This suggests a caring, empathic and non-judgemental approach is more likely to result in improved outcomes.

Addressing any underlying factors such as depression, low self esteem and personal, social or marital disharmony are important strategies to promoting smoking cessation. Qualitative research in Aboriginal and Torres Strait Islander women has identified the following factors that may affect motivation or ability to quit: smoking being perceived as reducing stress, smoothing social interactions, providing ‘time out’, relieving boredom, controlling weight and being part of the social norm.10,17 For some women smoking may be seen as a less immediate problem compared with other issues. In some areas of Australia it is important to enquire about levels of chewing tobacco as well as smoking. There is some evidence that women with partners who smoke find it harder to quit and are more likely to relapse if they do quit.18 However, there is a lack of evidence on the effectiveness and cost effectiveness of interventions aimed at encouraging partners and family members who smoke to quit and help pregnant women to stop smoking.14

There is mixed evidence on the effectiveness of nicotine replacement therapy (NRT) for promoting smoking cessation in pregnancy. A Cochrane review9 found that NRT did not have a significant benefit over other types of interventions but there have been no direct comparisons of NRT with any other strategy. The safety of NRT in terms of effect on fetal development and birth outcomes remains unclear. If NRT is used in pregnancy there are some recommendations that the dose of prescribed nicotine in pregnancy should be similar to a smoking dose and that intermittent forms of NRT are preferred to continuous use formulations as the total dose of nicotine will be less.19

Alcohol consumption

Alcohol consumption in pregnancy causes problems for both the mother and baby. For the baby, it is associated with increased risk of severe birth defects such as brain damage, facial deformities and growth problems, and more subtle changes such as learning and behavioural problems. This range of problems is known as fetal alcohol spectrum disorder. The risk to the baby is highest in the first trimester, including the first weeks following conception when the mother may not realise she is pregnant.3 Women who drink alcohol during pregnancy are also more likely to have problems such as miscarriage, bleeding during pregnancy, low birthweight babies, stillbirth, poor nutrition, anaemia and injuries.3 It is important to ask women about their use of alcohol and other substances at the first antenatal visit and, if appropriate, at subsequent visits, in a sensitive, non-judgemental way. A completely safe level of alcohol in pregnancy has not been determined.3 Not drinking alcohol in pregnancy, particularly in the first 3 months, is the safest option.2 If women choose to drink they should be advised to avoid getting drunk and drink no more than two standard drinks on any 1 day and less than seven standard drinks in a week.3

Genitourinary and bloodborne virus infection screening

Several genitourinary infections are associated with adverse outcomes in pregnancy and there is a higher prevalence of many of these infections in Aboriginal and Torres Strait Islander women when compared with non-Indigenous women.

Sexually transmissible infections

There is considerable state and regional variation in rates of chlamydia, gonorrhoea and trichomonas infection, with some rural and remote communities in the Northern Territory, Queensland and Western Australia having particularly high rates. Aboriginal and Torres Strait Islander people resident in major cities in South Australia, Victoria and Western Australia have three times the rate of chlamydia infection while those resident in remote and regional areas of Australia have up to seven times the rate of chlamydia infection, compared with the non-Indigenous population.20 One study in an urban setting showed an approximately 20% prevalence of STIs in pregnant Aboriginal and Torres Strait Islander women and 36% in women under 20 years of age. There was a prevalence of 14.4% chlamydia, 6.1% gonorrhoea and 7.2% trichomonas.21 STIs are higher in the population aged under 25 years in general (which is significant for Aboriginal and Torres Strait Islander pregnant women given the higher proportion of teenage pregnancies in this cohort) and in women with a recent change in sexual partner. Besides age, other predictors for STIs identified in this study include harmful alcohol use and unwanted pregnancy.

Some studies have found chlamydia is associated with early premature delivery22 and intrauterine growth restriction23 and if not treated it is associated with low birthweight and infant mortality.24 Babies born to mothers with chlamydia also have higher rates of ophthalmia neonatorum, lower respiratory tract infection and pneumonia.25,26 Similarly, case reports suggest an association between untreated gonorrhoea infection in pregnancy and pre-term delivery, premature rupture of membranes, low birthweight, postpartum endometritis and ophthalmia neonatorum.27 There is some evidence that infection with Trichomonas vaginalis in pregnancy is associated with pre-term birth and low birthweight28,29 but again, it is not clear whether this association is causal.

Studies have shown that treating chlamydia infection during pregnancy reduces the incidence of premature rupture of membranes, pre-term birth and low birthweight babies but there is no significant evidence to show that it leads to a decrease in the incidence of neonatal conjunctivitis or pneumonia.24,30–33 However, in the case of trichomonas, a Cochrane review looking at interventions in pregnancy found that treatment with metronidazole, while yielding parasitological cure rates of 90%, did not reduce pre-term birth and in one trial might even have increased it.34

Due to its high prevalence in the under 25 years population, screening and treatment of chlamydia is recommended in pregnant women in this age group.2,35 In addition, screening for chlamydia and gonorrhoea in populations with a high prevalence of STIs is recommended.2,3,35 While trichomonas infection can be highly prevalent in some Aboriginal and Torres Strait Islander communities there is no evidence that screening for it improves pregnancy outcomes, and treatment of asymptomatic trichomonas in pregnancy may cause harm.34,36 

Syphilis

Syphilis infection during pregnancy can cause miscarriage, stillbirth and congenital syphilis infection (causing permanent impairment, debilitation and disfigurement in affected babies). Syphilis is easily and safely treated in pregnancy with antibiotics, which can prevent these complications.37 

Syphilis infection is rare in Australia but more common in the Aboriginal and Torres Strait Islander population, particularly in more remote areas. For the period 2005–09 the diagnosis of syphilis infection was more than four times higher in the Aboriginal and Torres Strait Islander population than the rest of the Australian population, with women aged 29–40 years being diagnosed at 28 times the rate for non-Indigenous women in the same age group.38

Studies have shown that universal screening significantly increases the detection of pregnant women with syphilis compared with selective screening of women at risk39,40 and this is cost effective even in areas of low prevalence.37,41 For this reason, and for the benefits that treatment of syphilis in pregnancy provides to both mother and baby, universal screening for syphilis infection is recommended in most guidelines.2,42 For women who test positive for syphilis in early pregnancy, or for women from a population of high prevalence, a second screening test for syphilis is recommended early in the third trimester of pregnancy and at birth.2,3 

The initial test for syphilis is usually a blood test for serum antibodies of treponema (eg. enzyme immunoassay Treponema pallidum haemagglutination assay: EIA-TPHA). If this is positive, a non-treponemal test (eg. VDRL or RPR) will be performed by the laboratory to confirm diagnosis and enable a quantitative value of disease activity. Positive results should be interpreted with caution as past treated episodes of syphilis may still produce a low positive result and other trepanematoses (eg. yaws, pinta) may give a false positive for syphilis. Expert advice should be sought for positive results and consideration of testing for other STIs is advised.

HIV, hepatitis B and hepatitis C

Antenatal diagnosis of HIV and hepatitis B infection in the mother allows for the implementation of interventions during pregnancy or at the time of birth that can greatly reduce the risk of transmission of these infections to the child. In the case of HIV, one study found that between 2003 and 2006, the rate of mother-to-child transmission was 1% in women diagnosed antenatally who used at least two interventions (antiretrovirals during pregnancy and delivery by caesarean section) compared with a 50% rate of transmission where there was no antenatal diagnosis or no interventions used.43 The diagnosis of hepatitis B infection antenatally allows for the administration of vaccination and immunoglobulin to the baby on the day of delivery to prevent mother-to-child transmission.

Studies have shown that screening for HIV or hepatitis B based on risk factors alone would miss a large proportion of pregnant women infected with one or both of these viruses.44,45 For this reason, and to prevent transmission to the baby, universal screening for hepatitis B and HIV early in pregnancy is recommended in most guidelines.2,3,46 It is important that appropriate counselling and consent is provided prior to testing.

The benefits of hepatitis C screening during pregnancy are doubtful as there is no way of preventing mother-to-child transmission or of treating the virus during pregnancy. For this reason, guidelines do not recommend universal screening. However, some guidelines do suggest that screening of those at risk of hepatitis C infection may be appropriate, although there is little evidence for this.2,3 The risk factors for hepatitis C infection are a history of incarceration, blood transfusion or invasive procedure overseas (or before 1990 in Australia), injecting drug use, needlestick injury or tattooing (see Chapter 8: Sexual health and bloodborne viruses).

Asymptomatic bacteriuria

Asymptomatic bacteriuria in pregnancy increases the likelihood of pyelonephritis with an incidence of about 30% in affected women.47 There is some evidence that untreated asymptomatic bacteriuria may be associated with low birthweight and pre-term birth. However, other factors may be involved and there may only be an association if the bacteriuria progresses to pyelonephritis.48 Asymptomatic bacteriuria during pregnancy may be more common among Aboriginal and Torres Strait Islander women than non-Indigenous women.46,49,50

A Cochrane review found that antibiotic treatment of asymptomatic bacteriuria is effective in clearing the bacteriuria and can reduce the incidence of pyelonephritis by 75%.51 Other evidence shows that screening for asymptomatic bacteriuria reduces the incidence of pyelonephritis from 23.2 per 1000 women with no screening to 16.2 with dipstick testing and 11.2 with urine culture.52 Dipstick urinalysis has high specificity but low sensitivity53 and a midstream urine specimen for culture is recommended. There may be a role for dipstick testing in areas where access to pathology services is limited but infection should still be confirmed with culture.

There is no consensus in the literature about the best timing and frequency for testing of bacteriuria in pregnancy but current Australian guidelines recommend a single urine culture at the first antenatal visit.2

Asymptomatic bacterial vaginosis

Bacterial vaginosis is a decrease of lactobacilli and an increase in pathogenic bacteria (including Gardnerella vaginalis, mobiluncus, bacteroides, prevotella and mycoplasma) in the vagina, which may cause vaginal discharge and malodour or may be asymptomatic. Asymptomatic bacterial vaginosis in pregnancy is associated with an increased risk of pre-term birth,54 even if the bacterial vaginosis spontaneously resolves later in pregnancy.55 It is more common among women of low socioeconomic status and women who had low birthweight babies in previous pregnancies.56 Several large studies in the 1990s in the general population found the prevalence of bacterial vaginosis to be in the range of 9–23%,57–59 while a study in remote central Australia found a prevalence of 26–36% among non-pregnant women attending clinics for a woman’s health assessment.60

A Cochrane review found that treatment of bacterial vaginosis with antibiotics eradicates the infection but does not change the risk of pre-term birth, low birthweight or premature rupture of membranes in women at low risk of pre-term birth.61 However, two small studies in the review did show a decrease in the risk of pre-term rupture of membranes and low birthweight in women with previous pre-term birth who were treated for asymptomatic bacterial vaginosis. Screening for asymptomatic bacterial vaginosis in women at low risk of pre-term birth is not recommended.2,30,62 Women at increased risk for pre-term birth may be offered vaginal swab testing and treatment for asymptomatic bacterial vaginosis. Women with symptoms of bacterial vaginosis may also be offered testing and treatment for symptom resolution.3,62 Possible adverse effects from treatment need to be taken into account.

Mineral and vitamin deficiency screening and supplementation

Pregnancy increases nutritional demands on the body. This can exacerbate underlying nutritional deficiencies and lead to potentially adverse effects on the mother.63 A pregnant woman’s nutritional status influences the growth and development of the fetus and forms the foundation for the child’s later health.64 Women from socioeconomically disadvantaged groups and those with limited access to fresh foods may have nutritional deficiencies. Current guidelines suggest that pregnant women with risk factors for nutritional deficiencies may benefit from a multinutrient preparation.2 Although there are demonstrated benefits from iron and folic acid supplementation, there is limited evidence of improved pregnancy outcomes from multiple micronutrient supplements.63 Further, there is evidence that vitamin A, C or E supplements may in fact cause harm and so these are not recommended for use in pregnancy.2

The following describes the micronutrients that are particularly important in pregnancy.

Vitamin D

Ninety percent of vitamin D is obtained through synthesis in the skin from sun exposure and the vitamin D status of a newborn is determined by the vitamin D status of its mother. Risk factors for vitamin D deficiency include darker skin, season, and a BMI greater than 30.65,66 A history of limited sun exposure is also a risk factor but the association is weaker.65 Some studies have shown vitamin D deficiency in pregnancy to be associated with an increased risk of pre-eclampsia and gestational diabetes, although these studies are not consistent.67 Other population based studies have shown an association between maternal vitamin D deficiency and lower birthweights and small for gestational age babies.68 Lack of vitamin D may adversely affect fetal bone mineralisation and tooth enamel, increase the risk of hypocalcaemic fits in babies, cause rickets in children and osteomalacia in adults, although these consequences are rare.69 

There is mounting evidence of the prevalence of vitamin D deficiency in pregnant Australian women. A recent study showed a vitamin D deficiency (levels less than or equal to 25 nmol/L) or insufficiency (levels between 26 and 50 nmol/L) prevalence of 35% in Canberra and 25.7% in outer southwest Sydney.65 Other studies have found deficiency prevalence ranging from 5.2% in Victoria66 to 15% in Sydney.70 However, there have been few studies on the prevalence of vitamin D deficiency in the Aboriginal and Torres Strait Islander population of Australia. One small study in Adelaide did show some evidence of vitamin D deficiency in Aboriginal women.71 Another more recent study, also in South Australia (n=58), found vitamin D insufficiency to be highly prevalent among Aboriginal adults, with low mean values in all seasons other than summer.72

Vitamin D supplementation during pregnancy improves serum levels in both mothers and their babies and importantly no adverse effects have been reported.73 The question remains, however, whether routine supplementation improves pregnancy outcomes. Currently there is no evidence to suggest that routine supplementation improves pregnancy outcomes in healthy women without risk factors for vitamin D deficiency. There may be some benefit from supplementation in women at risk of deficiency but the evidence is limited.2,46 Further research is required to determine the optimal timing and dosing of vitamin D supplementation in pregnancy. Therefore decision making about whether to offer screening for vitamin D deficiency in pregnancy should take into consideration the individual’s risk factors, the season and climate.2 In women with proven vitamin D deficiency, supplementation should be initiated, depending on the level of severity and the clinical situation.

Iron

Pregnancy increases the body’s demand for iron due to the expanded red cell volume, the demands of the developing fetus and placenta and blood loss around the time of delivery. Iron deficiency is the most common cause of anaemia in pregnancy in Central Australia and the Top End of the Northern Territory.3 Depending on the level of severity, anaemia can cause tiredness in the mother, heart failure and increased chance of postpartum anaemia. Low iron stores in the mother can cause anaemia in the baby, which is associated with developmental delay. Risk factors for reduced iron stores early in pregnancy include poor diet, five or more previous pregnancies, adolescent pregnancy, multiple pregnancy and recent or current breastfeeding of another child.3 Universal screening for anaemia in pregnancy is advised in all pregnancy guidelines.2,3,46,74

Although routine oral iron supplementation in pregnancy has been demonstrated to reduce the incidence of anaemia there is a paucity of evidence assessing its outcome on other clinically relevant maternal and neonatal outcomes such as low birthweight, pre-term birth, delayed development and infection.75 Because oral iron supplementation can cause dose related gastrointestinal side effects and haemoconcentration75,76 routine supplementation of women with normal haemoglobin levels is not recommended during pregnancy.2,46 Iron supplementation should be considered in pregnant women who are anaemic, particularly if they are symptomatic or have other health concerns.2,3 In women with proven iron deficiency, iron supplementation should be initiated, depending on the level of severity and the clinical situation.

Folic acid

There is strong evidence that folic acid supplementation protects against neural tube defects in pregnancy.77–79 In Australia, although there has been a reduction in the incidence of babies born with neural tube defects in the general population, there has not been a reduction in incidence for Aboriginal babies.80 One study found the prevalence of neural tube defects in Aboriginal and Torres Strait Islander babies in Western Australia to be almost double that of the non-Indigenous population.81 This may, in part, be due to lower levels of folate intake through restricted food choices. There is also evidence that knowledge about the benefits of folic acid supplementation is at a lower level among Aboriginal and Torres Strait Islander women, particularly adolescents.81

Daily supplementation with folic acid (400–500 mcg) is recommended for all pregnant women, prior to conception and for the first 12 weeks of pregnancy.2,3,46 Specific attention needs to be given to promoting folic acid supplementation to Aboriginal and Torres Strait Islander women of childbearing age and providing information to individual women at the first antenatal visit.2 Higher doses of folic acid (5 mg) are recommended for women at increased risk of neural tube defects.3,74,82 These include women with a previous pregnancy with a neural tube defect, pre-pregnancy diabetes, multiple pregnancy, haemolytic anaemia and women on anticonvulsant medication.

Iodine

In Australia there is documented prevalence of mild to moderate iodine deficiency in school children, healthy adults, pregnant women and people with diabetes.83 Data are lacking on the prevalence of iodine deficiency among Aboriginal and Torres Strait Islander communities. Iodine requirements increase substantially in pregnancy and lactation to support the neuropsychological development of the fetus. Mandatory fortification of bread is estimated to increase population intakes by an average of 46 mcg per day. This will meet the needs of most of the population but an increased intake in pregnant and lactating women would be desirable. A recent National Health and Medical Research Council literature review concluded that there is good evidence for the safety and efficacy of iodine supplementation in pregnant and lactating women and the risks of iodine deficiency significantly outweigh any potential risks during the perinatal period.84 On this basis, iodine supplementation (up to 150 mcg per day) is recommended for pregnant women in Australia.

Diabetes

Diabetes in pregnancy can include pre-existing known type 1 or type 2 diabetes, undiagnosed pre-existing diabetes and gestational diabetes, which is defined as the onset of glucose intolerance in the second half of pregnancy. All forms of diabetes in pregnancy have increased risks for both the mother and baby, depending on the level of glycaemic control. Diabetes in pregnancy is associated with an increased risk of induced labour, pre-term birth, caesarean section and pre-eclampsia. Babies of mothers with diabetes in pregnancy have higher rates of stillbirth, fetal macrosomia, low APGAR scores, neonatal hypoglycaemia, and admission to special care baby units.85 Babies born to mothers with pre-existing diabetes have a higher risk of congenital malformations of the spine, heart and kidneys.86 In addition, there is evidence that an adverse intrauterine environment is a risk factor in later life for metabolic disturbances in the babies of diabetic mothers. Raised maternal glycaemic levels are associated with increased adiposity in childhood and other adverse metabolic factors that may increase the risks of cardiovascular disease and diabetes.87,88 Women with gestational diabetes also have an increased risk of developing type 2 diabetes later in life and an increased risk of gestational diabetes in subsequent pregnancies.

The number of women with undiagnosed pre-pregnancy type 2 diabetes and gestational diabetes mellitus in the general population is increasing.89 Aboriginal and Torres Strait Islander women are 10 times more likely to have pre-existing type 2 diabetes and 1.5 times more likely to develop gestational diabetes than non-Indigenous women.85 Therefore a large proportion of Aboriginal and Torres Strait Islander women will have known or undiagnosed diabetes mellitus at antenatal booking.

There is currently a lack of uniformity in the approach to diagnosing gestational diabetes.90 The International Association of Diabetes and Pregnancy recently published new recommendations for the diagnosis of diabetes in pregnancy, which should provide a more consistent approach to diagnosing both pre-existing diabetes in pregnancy and gestational diabetes.91,92 These recommendations are based on data showing that there appears to be a linear association between maternal plasma glucose concentration and adverse pregnancy outcomes, including at levels below the previous criteria for a diagnosis of gestational diabetes.91 It is likely that the International Association of Diabetes and Pregnancy recommendations will be adopted in forthcoming Australian guidelines (Table 9.1).

Although specific management recommendations are beyond the scope of this guide, studies have shown that even for mild gestational diabetes, treatment with diet and lifestyle modifications decreases the incidence of fetal macrosomia and pre-eclampsia.93,94 Strict glycaemic control is the foundation of diabetes management in pregnancy. Specific management guidelines are recommended for further guidance (see Resources).

Recommendations: General assessment at the first antenatal visit
Preventive intervention typeWho is at risk?What should be done?How often?Level/strength of evidence
Screening All pregnant women2,95 Discuss and plan the schedule of antenatal visits with the pregnant woman based on her individual needs
For an uncomplicated pregnancy review every 4 weeks until 28 weeks, then every 2 weeks thereafter
At first antenatal visit IB
Offer an ultrasound to determine gestational age and detect multiple pregnancies (best performed between 8 and 13 weeks + 6 days gestation) At first antenatal visit IIIB
Measure blood pressure, height and weight and calculate BMI
Repeated weighing during pregnancy should be confined to circumstances where clinical management is likely to be influenced
At first antenatal visit
Opportunistic
IIIB
GPP
Auscultate for heart murmurs, in areas with a high prevalence of rheumatic heart disease At first antenatal visit GPP
Advise women to have oral health checks and treatment if required (see Chapter 4: Dental health) At first antenatal visit IIB
Offer Pap test if due During first trimester GPP
Offer testing for rubella immunity At first antenatal visit IIB
Check blood group and antibodies At first antenatal visit and 28 week visit IB
Discuss the purpose and implications of testing for chromosomal abnormalities to promote an informed decision
In those wishing to proceed offer women first trimester combined screeningβ for chromosomal abnormalities between 11 and 13 weeks + 6 days gestation
Provide support to women in regional and remote areas to access this screening. If nuchal thickness ultrasound is unavailable, offer maternal serum screening† between 15 and 17 weeks gestation
At first antenatal visit IB
Offer ultrasound to assess for fetal morphology abnormalities At 18–20 weeks GPP46
Pregnant women at risk of pre-eclampsia‡ Offer proteinuria testing At first antenatal visit and each subsequent visit IIB2
Immunisation All pregnant women Review influenza immunisation status and offer where appropriate (see Chapter 11: Respiratory health) Opportunistic GPP96
β First trimester combined screening includes nuchal thickness ultrasound and plasma beta human chorionic gonadotropin (beta-HCG) and pregnancy associated plasma protein A (PAPP-A)
† Maternal serum screening includes plasma maternal serum alpha fetoprotein (AFP), unconjugated oestriol and total human chorionic gonadotropin (HCG)
‡ Risk factors for pre-eclampsia include age >40 years, first or multiple pregnancy, BMI >30, diabetes, vascular or kidney disease, personal or family history of pre-eclampsia, raised blood pressure at first visit, pregnancy interval >10 years
Recommendations: Smoking cessation
Preventive intervention typeWho is at risk?What should be done?How often?Level/strength of evidence
Screening All pregnant women Regularly assess smoking status and remind patients to limit/avoid exposure to cigarette smoke At first and subsequent antenatal visits IB2,3,9,14,15
Record in the handheld pregnancy record (if available) or otherwise use local protocols to record this information GPP14,15
Behavioural Pregnant women who smoke Offer interventions to assist smoking cessation ranging from brief advice to more intensive, multicomponent interventions (see Chapter 1: Lifestyle) At first and subsequent antenatal visits IB2,9
Chemoprophylaxis Pregnant women who smoke at least 10–15 cigarettes/day requesting additional assistance with smoking cessation Consider nicotine replacement therapy (NRT) with discretion, noting that the safety of NRT in terms of effect on fetal development and birth outcomes remains unclear
Discuss the risks and benefits taking into account overall clinical circumstances
If deemed necessary, intermittent forms of NRT are recommended rather than continuous use formulations to reduce the total dose of nicotine3,19
At each antenatal visit IB2,3,9,14,15
Recommendations: Genitourinary and bloodborne virus infections
Preventive intervention typeWho is at risk?What should be done?How often?Level/strength of evidence
Screening Pregnant women aged <25 years Offer chlamydia testing with a nucleic acid amplification test (NAAT), most commonly by PCR, using either a first void urine, self obtained low vaginal swab or endocervical swab At first antenatal visit IIC2,3,30
Pregnant women from communities with a high prevalence of STIs Offer testing for chlamydia as above and consider testing for gonorrhoea At first antenatal visit and consider repeat testing at 36 weeks gestation GPP2,3
All pregnant women
Pregnant women from communities with a high prevalence of STIs
Offer testing for syphilis, HIV and hepatitis B
Hepatitis C (HCV) testing is not routinely recommended. Screening may be discussed if there are identifiable risk factors for HCV infection (see Chapter 8: Sexual health, for risk factors)
Offer additional tests for syphilis infection
At first antenatal visit
At 28 weeks gestation and at birth
IA–IIB2,3,46
All pregnant women Offer testing for asymptomatic bacteriuria with a midstream urine microscopy and culture At first antenatal visit IA2,3,30,62
In areas with limited access to pathology testing, dipstick urine tests may be used to exclude asymptomatic bacteriuria but positive results must be confirmed by midstream urine culture GPP2
Women with previous pre-term birth Offer vaginal swab testing and treatment for asymptomatic bacterial vaginosis (eg. Gardnerella vaginalis, Bacteroides spp.) Before 20 weeks pregnancy GPP2
Environmental Women with positive results for an STI or bloodborne virus Ensure adequate recall systems are implemented for follow up
Recommend partner treatment and contact tracing
(See Chapter 8: Sexual health and bloodborne viruses)
N/A GPP2
Recommendations: Alcohol consumption
Preventive intervention typeWho is at risk?What should be done?How often?Level/strength of evidence
Screening All pregnant women Ask about alcohol consumption At first and subsequent antenatal visits GPP3
Behavioural All pregnant women and women planning a pregnancy Advise that not drinking alcohol is the safest option in pregnancy, particularly in the first 3 months At first and subsequent antenatal visits
(as appropriate)
GPP2
Pregnant women who drink alcohol Advise women to avoid getting drunk
Advise women to have no more than two standard drinks on any 1 day and fewer than seven standard drinks in 1 week
At first and subsequent antenatal visits GPP3,46
Recommendations: Nutritional assessment and supplementation
Preventive intervention typeWho is at risk?What should be done?How often?Level/strength of evidence
Screening All pregnant women Offer a full blood examination to assess for anaemia At first antenatal visit, and at 28 and 36 weeks gestation 1A2,3,46
Women at risk of vitamin D deficiency (limited sun exposure, dark skin, BMI >30) Consider testing for vitamin D levels, particularly in the non-summer months At first antenatal visit GPP2,46,65,74,82,97,98
Behavioural All pregnant women Provide information on the benefits of a healthy diet in pregnancy and give practical, tailored advice on healthy eating Early in pregnancy GPP3,46
Chemorophylaxis All pregnant women and those considering pregnancy Recommend 500 mcg of folic acid daily to reduce the risk of newborn neural tube defects At least 1 month prior to pregnancy and for the first 12 weeks of pregnancy IA2,3,46,74,82
Women with diabetes Recommend a higher dose of 5 mg of folic acid daily to reduce the risk of newborn neural tube defects At least 1 month prior to pregnancy and for the first 12 weeks of pregnancy IC46,74,97,98
Pregnant women with proven vitamin D deficiency Advise vitamin D supplementation – dose titrated according to clinical situation* (see Resources) At diagnosis IIB2,46,73,82
Pregnant women who are not iron deficient Routine iron supplementation is not recommended N/A IB2,46,76
Pregnant women with proven iron deficiency Offer iron supplementation – oral or intramuscular – dose titrated according to clinical situation At diagnosis  IB3,74,75
All pregnant women Offer iodine supplementation with 150 mcg/day (see Resources) At first antenatal visit IIA84
* Vitamin D supplementation is not subsidised under the Pharmaceutical Benefits Scheme
Recommendations: Diabetes
Preventive intervention typeWho is at risk?What should be done?How often?Level/strength of evidence
Screening Pregnant women at risk of undiagnosed diabetes mellitus (BMI >30 kg/m2, family history of diabetes, previous gestational diabetes) Measure fasting blood glucose
If not feasible, alternatives include random blood glucose or HbA1c (see Chapter 14: Type 2 diabetes prevention and early detection)
At first antenatal visit IA3,92
Pregnant women who do not have pre-existing diabetes Perform a 75 g 2 hour oral glucose tolerance test (OGTT) for diagnosis of gestational diabetes (see Table 9.1 and Table 9.2) Between 24 and 28 weeks gestation IA92
If a 2 hour OGTT is consistently difficult to achieve, consider alternative tests such as a random blood glucose or a 50 g, 1 hour glucose challenge. If either are abnormal then recommend a 75 g 2 hour oral OGTT GPP74
Women postpartum diagnosed with gestational diabetes Perform a 75 g fasting OGTT At 6 weeks postpartum GPP3,99
Behavioural Pregnant women with diabetes Offer advice and resources to promote good glycaemic control throughout pregnancy – encourage a healthy diet and exercise
Consider referral to specialist services, where available, and consult specific management guidelines for ongoing care (see Resources)
At diagnosis IA91,99
Non-pregnant women who have had gestational diabetes in the past Advise women of the future risk of developing diabetes and give advice about healthy diet, exercise and weight (see Chapter 1: Lifestyle)
Screen for diabetes with a fasting blood glucose (see Chapter 14: Type 2 diabetes prevention and early detection)
At postpartum checks and as part of an annual health assessment IIB3,99,100
Table 9.1. The International Association of Diabetes and Pregnancy Guidelines for diagnosing pre-existing diabetes and gestational diabetes in pregnancy*
Diagnostic criteria for pre-existing diabetes

One of the following measures of glycaemia is recommended for diagnosing
pre-existing diabetes. If random plasma glucose is used, the diagnosis should be confirmed with either a fasting plasma glucose or HbA1c

Measure of glycaemiaConsensus threshold
FPG (fasting plasma glucose) ≥7.0 mmo/L
Hb1c ≥6.5%
RPG (random plasma glucose) ≥11.1 mmol/L (confirmation with FPG/ HbA1c recommended)
Diagnostic criteria for gestational diabetes
Using a 75 g 2 hour oral glucose tolerance test, one or more of these values is diagnostic of gestational diabetes
Glucose measureGlucose concentration
FPG ≥5.1 mmol/L*
1 hour plasma glucose ≥10 mmol/L
2 hour plasma glucose ≥8.5 mmol/L*
* At the time of writing these criteria had not been published by the Australian Diabetes in Pregnancy Society. Current criteria for gestational diabetes are FPG ≥5.4 mmol/L and 2 hour plasma glucose ≥7.9 mmol/L
Source: Metzger BE, Gabbe SG, Persson B, et al 201092 
Table 9.2. Current interpretive criteria for 75 g OGTT in pregnancy in Australia
Glucose measureGlucose concentration
Fasting Above 5.4
2 hour Above 7.9

Resources

Guidelines for management of diabetes in pregnancy (Australasian Diabetes in Pregnancy Society)
www.ranzcog.edu.au/publications/ statements/coll-end-statements/ADIPS-gdm-management-guidelines

Screening guideline for gestational diabetes (Kimberley Aboriginal Medical Services Council)
http://resources.kamsc.org.au/ downloads/cd_dip.pdf

Guidelines for treatment of vitamin D deficiency (King Edward Memorial Hospital)
www.kemh.health.wa.gov.au/ development/manuals/O&G_guidelines/sectionb/1/b1.1.9.pdf
Dietary guidelines for Australian adults (NHMRC)
www.gofor2and5.com.au/ DataStore/files/pdf/n33.pdf

Iodine, public statement: iodine supplementation for pregnant and breastfeeding women (NHMRC)
www.nhmrc.gov.au/_files_nhmrc/ publications/attachments/new45_statement.pdf

Clinical practice guidelines on depression and related disorders in the perinatal period (beyond blue)
www.beyondblue.org.au/ index.aspx?link_id=6.1246

Australian guidelines to reduce health risks from drinking alcohol (NHMRC)
www.nhmrc.gov.au/_files_nhmrc/ publications/attachments/ds10-alcohol.pdf.

References

  1. Laws P, Li Z, Sullivan EA. Australia’s mothers and babies 2008. Perinatal statistics series no. 24. Canberra: Australian Institute of Health and Welfare, 2010.
  2. The Child Health and Wellbeing Subcommittee and the Maternity Services Inter-Jurisdictional Committee under the Australian Health Ministers’ Advisory Council. Clinical practice guidelines antenatal care: first trimester (draft). AHMAC, 2011.
  3. Congress Alukura and Nganampa Health Council Inc. Minymaku Kutji Tjukurpa: women’s business manual, 4th edn. Alice Springs: Central Australian Aboriginal Congress Alukura Branch and Nganampa Health Council Inc, 2008.
  4. Office of the Surgeon General. The health consequences of smoking: a report of the Surgeon General. Rockville: US Department of Health and Human Services, 2004.
  5. Raymond EG, Cnattingius S, Kiely JL. Effects of maternal age, parity, and smoking on the risk of stillbirth. Br J Obstet Gynaecol 1994;101(4):301–6.
  6. Castles A, Adams EK, Melvin CL, Kelsch C, Boulton ML. Effects of smoking during pregnancy. Five meta-analyses. Am J Prev Med 1999 Apr;16(3):208–15.
  7. Batstra L, Hadders-Algra M, Neeleman J. Effect of antenatal exposure to maternal smoking on behavioural problems and academic achievement in childhood: prospective evidence from a Dutch birth cohort. Early Hum Dev 2003;75(1–2):21–33.
  8. Chan DL, Sullivan EA. Teenage smoking in pregnancy and birthweight: a population study, 2001–2004. Med J Aust 2008;188(7):392–6.
  9. Lumley J, Chamberlain C, Dowswell T, Oliver S, Oakley L, Watson L. Interventions for promoting smoking cessation during pregnancy. Cochrane Database Syst Rev 2009;Oct 18;(3):CD001055.
  10. Heath DL, Panaretto K, Manessis V, et al. Factors to consider in smoking interventions for Indigenous women. Aust J Prim Health 2006;12(2):131–6.
  11. Laws PJ, Abeywardana S, Walker J, Sullivan EA. Australia’s mothers and babies 2005. Perinatal statistics series no 20. Sydney: Australian Institute of Health and Welfare, 2007.
  12. Titmuss AT, Harris E, Comino EJ. The roles of socioeconomic status and Aboriginality in birth outcomes at an urban hospital. Med J Aust 2008;189(9):495–8.
  13. Wills RA, Coory MD. Effect of smoking among Indigenous and non-Indigenous mothers on preterm birth and full-term low birthweight. Med J Aust 2008;189(9):490–4.
  14. National Institute for Health and Clinical Excellence. How to stop smoking in pregnancy and following childbirth. PH26. London: National Institute for Health and Clinical Excellence, 2004. Cited October 2011. Available at www.nice.org.uk/ nicemedia/live/13023/49345/49345.pdf.
  15. Flenady V, New K, MacPhail J. Clinical practice guideline for smoking cessation in pregnancy. Brisbane: The Centre for Clinical Studies, Mater Health Services, 2005. Cited October 2011. Available at www.stillbirthalliance.org.au/ doc/Guideline_for_Smoking_Cessation _in_Pregnancy.pdf.
  16. Power J, Grealy C, Rintoul D. Tobacco interventions for Indigenous Australians: a review of current evidence. Health Promot J Austr 2009;20(3):186–94.
  17. Gilligan C, Sanson-Fisher RW, D’Este C, Eades S, Wenitong M. Knowledge and attitudes regarding smoking during pregnancy among Aboriginal and Torres Strait Islander women. Med J Aust 2009;190(10):557–61.
  18. Fang WL, Goldstein AO, Butzen AY, et al. Smoking cessation in pregnancy: a review of postpartum relapse prevention strategies. J Am Board Fam Pract 2004;17(4):264–75.
  19. Dempsey DA, Benowitz NL. Risks and benefits of nicotine to aid smoking cessation in pregnancy. Drug Saf 2001;24(4):277–322.
  20. National Notifiable Diseases Surveillance System Annual Report Writing Group. Australia’s notifiable diseases status, 2008: annual report of the National Notifiable Diseases Surveillance System. Commun Dis Intell (serial on the internet), 2010;34(3). Cited October 2011. Available at www.health.gov.au/ internet/main/publishing.nsf/content/cda-cdi3403-pdf-cnt.htm/ $FILE/cdi3403a.pdf.
  21. Panaretto KS, Lee HM, Mitchell MR, et al. Prevalence of sexually transmissible infections in pregnant urban Aboriginal and Torres Strait Islander women in northern Australia. Aust N Z J Obstet Gynaecol 2006;46(3):217–24.
  22. Rours GI, Duijts L, Moll HA, et al. Chlamydia trachomatis infection during pregnancy associated with preterm delivery: a population-based prospective cohort study. Eur J Epidemiol 2011;26(6):493–502.
  23. The John Hopkins Study Investigators. Association of Chlamydia trachomatis and Mycoplasma hominis with intrauterine growth retardation and preterm delivery. The John Hopkins Study of Cervicitis and Adverse Pregnancy Outcome. Am J Epidemiol 1989;129(6):1247–57.
  24. Cohen I, Veille JC, Calkins BM. Improved pregnancy outcome following successful treatment of chlamydial infection. JAMA 1990;263(23):3160–3.
  25. Preece PM, Anderson JM, Thompson RG. Chlamydia trachomatis infection in infants: a prospective study. Arch Dis Child 1989;64(4):525–9.
  26. Schachter J, Grossman M, Sweet RL, Holt J, Jordan C, Bishop E. Prospective study of perinatal transmission of Chlamydia trachomatis. JAMA 1986;255(24):3374–7.
  27. Lacey CJ, Milne JD. Preterm labour in association with Neisseria gonorrhoeae: case reports. Br J Vener Dis 1984;60(2):123–4.
  28. Cotch MF, Pastorek JG, Nugent RP, et al. Trichomonas vaginalis associated with low birth weight and preterm delivery. The Vaginal Infections and Prematurity Study Group. Sex Transm Dis 1997 Jul;24(6):353–60.
  29. Saurina GR, McCormack WM. Trichomoniasis in pregnancy. Sex Transm Dis 1997 Jul;24(6):361–2.
  30. Ryan GM, Jr., Abdella TN, McNeeley SG, Baselski VS, Drummond DE. Chlamydia trachomatis infection in pregnancy and effect of treatment on outcome. Am J Obstet Gynecol 1990;162(1):34–9.
  31. Black-Payne C, Ahrabi MM, Bocchini Jr JA, Ridenour CR, Brouillette RM. Treatment of Chlamydia trachomatis identified with Chlamydiazyme during pregnancy. Impact on perinatal complications and infants. J Reprod Med 1990;35(4):362.
  32. Nugent RP, Rao AV, Klebanoff A, Lou Y, Regan JA, Kaslow A. Double-blind placebo-controlled treatment trial of Chlamydia trachomatis endocervical infections. Infect Dis Obstet Gynecol 1997;5:10–7.
  33. McMillan JA, Weiner L, Lamberson H, et al. Efficacy of maternal screening and therapy in the prevention of chlamydia infection of the newborn. Infection 1985;13(6):263–6.
  34. Gulmezoglu AM. Interventions for trichomoniasis in pregnancy. Cochrane Database Syst Rev 2002(3):CD000220.
  35. Meyers D, Wolff T, Gregory K, et al. USPSTF recommendations for STI screening. Am Fam Physician 2008;77(6):819–24.
  36. Okun N, Gronau KA, Hannah ME. Antibiotics for bacterial vaginosis or Trichomonas vaginalis in pregnancy: a systematic review. Obstet Gynecol 2005;105(4):857–68.
  37. Walker GJ. Antibiotics for syphilis diagnosed during pregnancy. Cochrane Database Syst Rev 2001(3):CD001143.
  38. National Centre in HIV Epidemiology and Clinical Research. Bloodborne viral and sexually transmissible infections in Aboriginal and Torres Strait Islander people: surveillance and evaluation report 2010. Sydney: National Centre in HIV Epidemiology and Clinical Research, University of New South Wales, 2010. Cited October 2011. Available at www.med.unsw.edu.au/ nchecrweb.nsf/resources/ATSIP-1/$file/ ATSIP2010_WEB201102.pdf.
  39. Cameron ST, Thong KJ, Young H, Liston WA. Routine antenatal screening for syphilis in Lothian: a study of the results 1988 to 1994. Br J Obstet Gynaecol 1997;104(6):734–7.
  40. Duthie SJ, King PA, Yung GL, Ma HK. Routine serological screening for syphilis during pregnancy – disposable anachronism or fundamental necessity? Aust N Z J Obstet Gynaecol 1990;30(1):29–31.
  41. Connor N, Roberts J, Nicoll A. Strategic options for antenatal screening for syphilis in the United Kingdom: a cost effectiveness analysis. J Med Screen 2000;7(1):7–13.
  42. World Health Organization. Guidelines for the management of sexually transmissible infections. Geneva: WHO, Department of Reproductive Health and Research, 2004. Cited October 2011. Available at http://whqlibdoc.who.int/ publications/2003/924154626 3.pdf.
  43. McDonald AM, Zurynski YA, Wand HC, et al. Perinatal exposure to HIV among children born in Australia, 1982–2006. Med J Aust 2009;190(8):416–20.
  44. Chou R, Smits AK, Huffman LH, Fu R, Korthuis PT. Prenatal screening for HIV: a review of the evidence for the US Preventive Services Task Force. Ann Intern Med 2005;143(1):38–54.
  45. Jensen L, Heilmann C, Smith E, et al. Efficacy of selective antenatal screening for hepatitis B among pregnant women in Denmark: is selective screening still an acceptable strategy in a low–endemicity country? Scand J Infect Dis 2003;35(6–7):378–82.
  46. National Institute for Health and Clinical Excellence. Antenatal care. Routine care for the healthy pregnant woman. CG62. London: National Institute for Health and Clinical Excellence, 2008. Cited October 2011. Available at www.nice.org.uk/ nicemedia/pdf/CG062NICE guideline.pdf.
  47. Whalley P. Bacteriuria of pregnancy. Am J Obstet Gynecol 1967;97(5):723–38.
  48. Meis PJ, Michielutte R, Peters TJ, et al. Factors associated with preterm birth in Cardiff, Wales. II. Indicated and spontaneous preterm birth. Am J Obstet Gynecol 1995;173(2):597–602.
  49. Bookallil M, Chalmers E, Andrew B. Challenges in preventing pyelonephritis in pregnant women in Indigenous communities. Rural Remote Health 2005 Jul–Sep;5(3):395.
  50. Hunt J. Pregnancy care and problems for women giving birth at Royal Darwin Hospital. Melbourne: Centre for the Study of Mothers’ and Children’s Health, La Trobe University, 2004.
  51. Smaill F, Vazquez JC. Antibiotics for asymptomatic bacteriuria in pregnancy. Cochrane Database Syst Rev 2007;Apr 18;(2):CD000490.
  52. Rouse DJ, Andrews WW, Goldenberg RL, Owen J. Screening and treatment of asymptomatic bacteriuria of pregnancy to prevent pyelonephritis: a cost-effectiveness and cost-benefit analysis. Obstet Gynecol 1995 Jul;86(1):119–23.
  53. Deville WL, Yzermans JC, van Duijn NP, Bezemer PD, van der Windt DA, Bouter LM. The urine dipstick test useful to rule out infections. A meta-analysis of the accuracy. BMC Urol 2004 Jun 2;4:4.
  54. Flynn CA, Helwig AL, Meurer LN. Bacterial vaginosis in pregnancy and the risk of prematurity: a meta-analysis. J Fam Pract 1999;48(11):885–92.
  55. Gratacos E, Figueras F, Barranco M, et al. Spontaneous recovery of bacterial vaginosis during pregnancy is not associated with an improved perinatal outcome. Acta Obstet Gynecol Scand 1998;77(1):37–40.
  56. French JI, McGregor JA, Parker R. Readily treatable reproductive tract infections and preterm birth among black women. Am J Obstet Gynecol 2006;194(6):1717–26.
  57. Goldenberg RL, Klebanoff MA, Nugent R, Krohn MA, Hillier S, Andrews WW. Bacterial colonization of the vagina during pregnancy in four ethnic groups. Vaginal Infections and Prematurity Study Group. Am J Obstet Gynecol 1996;174(5):1618–21.
  58. Hillier SL, Krohn MA, Nugent RP, Gibbs RS. Characteristics of three vaginal flora patterns assessed by gram stain among pregnant women. Vaginal Infections and Prematurity Study Group. Am J Obstet Gynecol 1992;166(3):938–44.
  59. Pastore LM, Royce RA, Jackson TP, Thorp JM, Jr, Savitz DA, Kreaden US. Association between bacterial vaginosis and fetal fibronectin at 24–29 weeks’ gestation. Obstet Gynecol 1999 Jan;93(1):117–23.
  60. Smith KS, Tabrizi SN, Fethers KA, Knox JB, Pearce C, Garland SM. Comparison of conventional testing to polymerase chain reaction in detection of Trichomonas vaginalis in indigenous women living in remote areas. Int J STD AIDS 2005;16(12):811–5.
  61. McDonald HM, Brocklehurst P, Gordon A. Antibiotics for treating bacterial vaginosis in pregnancy. Cochrane Database Syst Rev 2007;Jan 24;(1):CD000262.
  62. Yudin MH, Money DM. Screening and management of bacterial vaginosis in pregnancy. J Obstet Gynaecol Can 2008;30(8):702–16.
  63. Haider B, Bhutta Z. Multiple-micronutrient supplementation for women during pregnancy. Cochrane Database Syst Rev 2006;Oct 18;(4):CD004905.
  64. Gluckman PD, Hanson MA, Pinal C. The developmental origins of adult disease. Matern Child Nutr 2005 Jul;1(3):130–41.
  65. Perampalam S, Ganda K, Chow KA, et al. Vitamin D status and its predictive factors in pregnancy in 2 Australian populations. Aust N Z J Obstet Gynaecol 2011;51(4):353–9.
  66. Teale GR, Cunningham CE. Vitamin D deficiency is common among pregnant women in rural Victoria. Aust N Z J Obstet Gynaecol 2010;50(3):259–61.
  67. Ansary A, Palacios C, De Regil LM, Peña Rosas JP. Vitamin D supplementation for women during pregnancy. Cochrane Database Syst Rev 2010;Dec 08;(12):CD008873.
  68. Leffelaar ER, Vrijkotte TG, van Eijsden M. Maternal early pregnancy vitamin D status in relation to fetal and neonatal growth: results of the multi-ethnic Amsterdam born children and their development cohort. Br J Nutr 2010;104(1):108–17.
  69. National Institute for Health and Clinical Excellence. Improving the nutrition of pregnant and breastfeeding mothers and children in low income households. PH11. London: National Institute for Health and Clinical Excellence, 2008. Cited October 2011. Available at www.nice.org.uk/ nicemedia/live/11943/40097/ 40097.pdf.
  70. Bowyer L, Catling-Paull C, Diamond T, Homer C, Davis G, Craig ME. Vitamin D, PTH and calcium levels in pregnant women and their neonates. Clin Endocrinol (Oxf) 2009 Mar;70(3):372–7.
  71. Benson J, Wilson A, Stocks N, Moulding N. Muscle pain as an indicator of vitamin D deficiency in an urban Australian Aboriginal population. Med J Aust 2006;185(2):76–7.
  72. Vanlint SJ, Morris HA, Newbury JW, Crockett AJ. Vitamin D insufficiency in Aboriginal Australians. Med J Aust 2011;194(3):131–4.
  73. Yu CK, Sykes L, Sethi M, Teoh TG, Robinson S. Vitamin D deficiency and supplementation during pregnancy. Clin Endocrinol (Oxf) 2009 May;70(5):685–90.
  74. Women and Newborn Health Service. Antenatal shared care guidelines for general practitioner. 4th edn. Perth: King Edward Memorial Hospital, 2010. Cited October 2011. Available at www.kemh.health.wa.gov.au/ development/manuals/guidelines/ 2577.pdf.
  75. Reveiz L, Gyte GM, Cuervo LG. Treatments for iron-deficiency anaemia in pregnancy. Cochrane Database Syst Rev 2007;Apr 18;(2):CD003094.
  76. Peña-Rosas J, Viteri F. Effects and safety of preventive oral iron or iron + folic acid supplementation for women during pregnancy. Cochrane Database Syst Rev 2009;Oct 7;(4):CD004736.
  77. Czeizel AE, Dudas I. Prevention of the first occurrence of neural-tube defects by periconceptional vitamin supplementation. N Engl J Med 1992;327(26):1832–5.
  78. De-Regil LM, Fernández-Gaxiola AC, Dowswell T, Peña-Rosas JP. Effects and safety of periconceptional folate supplementation for preventing birth defects. Cochrane Database Syst Rev 2010 Oct 6;Oct 6;(10):CD007950.
  79. MRC Vitamin Study Research Group. Prevention of neural tube defects: results of the Medical Research Council Vitamin Study. Lancet 1991 Jul 20;338(8760):131–7.
  80. Bower C, D’Antoine H, Stanley FJ. Neural tube defects in Australia: trends in encephaloceles and other neural tube defects before and after promotion of folic acid supplementation and voluntary food fortification. Birth Defects Res A Clin Mol Teratol 2009;85(4):269–73.
  81. Bower C, Eades S, Payne J, D’Antoine H, Stanley F. Trends in neural tube defects in Western Australia in Indigenous and non-Indigenous populations. Paediatr Perinat Epidemiol 2004;18(4):277–80.
  82. The Royal Australian and New Zealand College of Obstetricians and Gynaecologists. Vitamin and mineral supplementation in pregnancy. RANZCOG College Statement: C-Obs 25. Melbourne: RANZCOG, 2008. Cited October 2011. Available at www.ranzcog.edu.au/the-ranzcog/policies-and-guidelines/college-statements/279-vitamins-and-minerals-supplementation-c-obs-25.html.
  83. Li M, Ma G, Guttikonda K, Boyages SC, Eastman CJ. Re-emergence of iodine deficiency in Australia. Asia Pac J Clin Nutr 2001;10(3):200–3.
  84. National Health and Medical Research Council. Iodine supplementation during pregnancy and lactation: a literature review. NHMRC, 2009. Cited January 2012. Available at www.nhmrc.gov.au/_files_nhmrc/ publications/attachments/ new45_literature_review.pdf.
  85. Australian Institute of Health and Welfare. Diabetes in pregnancy: its impact on Australian women and their babies. Diabetes series no. 14. Canberra: AIHW, 2010.
  86. Evers IM, de Valk HW, Visser GH. Risk of complications of pregnancy in women with type 1 diabetes: nationwide prospective study in the Netherlands. BMJ 2004;328(7445):915.
  87. Boney CM, Verma A, Tucker R, Vohr BR. Metabolic syndrome in childhood: association with birth weight, maternal obesity, and gestational diabetes mellitus. Pediatrics 2005 Mar;115(3):e290–6.
  88. Hillier TA, Pedula KL, Schmidt MM, Mullen JA, Charles MA, Pettitt DJ. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007 Sep;30(9):2287–92.
  89. Lawrence JM, Contreras R, Chen W, Sacks DA. Trends in the prevalence of preexisting diabetes and gestational diabetes mellitus among a racially/ethnically diverse population of pregnant women,1999–2005. Diabetes Care 2008 May;31(5):899–904.
  90. Metzger BE, Coustan DR. Summary and recommendations of the Fourth International Workshop-Conference on Gestational Diabetes Mellitus. The Organizing Committee. Diabetes Care 1998 Aug;21(Suppl 2):B161–7.
  91. Contreras M, Sacks DA, Bowling FG, et al. The Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study. Int J Gynaecol Obstet 2002;78(1):69–77.
  92. Metzger BE, Gabbe SG, Persson B, et al. International association of diabetes and pregnancy study groups recommendations on the diagnosis and classification of hyperglycemia in pregnancy. Diabetes Care 2010 Mar;33(3):676–82.
  93. Crowther CA, Hiller JE, Moss JR, McPhee AJ, Jeffries WS, Robinson JS. Effect of treatment of gestational diabetes mellitus on pregnancy outcomes. N Engl J Med 2005;352(24):2477–86.
  94. Landon MB, Spong CY, Thom E, et al. A multicenter, randomized trial of treatment for mild gestational diabetes. N Engl J Med 2009;361(14):1339–48.
  95. Three Centres Antenatal Care Consensus Guidelines. Routine weighing: literature review for three centres antenatal care consensus guidelines. Melbourne: Royal Women’s Hospital, 2005. Cited January 2012. Available at http://3centres.com.au/ library/public/file/guidelines/new_ guidelines/litreview_weighing.pdf.
  96. National Health and Medical Research Council. The Australian immunisation handbook, 9th edn. Canberra: Commonwealth of Australia, 2008. Cited October 2011. Available at www.health.gov.au/ internet/immunise/publishing.nsf/content/ handbook-home.
  97. The Royal Woman’s Hospital. Vitamin D: antenatal screening. Melbourne: The Royal Woman’s Hospital, 2006. Cited October 2011. Available at www.thewomens.org.au/ VitaminDAntenatalScreening.
  98. Southern Health. Vitamin D in pregnancy and the term newborn guideline. Melbourne: Southern Health, 2009. Cited October 2011. Available at www.southernhealth.org.au/ icms_docs/3569_Vitamin_D_in_pregnancy _and_breastfeeding_guideline.pdf.
  99. National Collaborating Centre for Women’s and Children’s Health. Diabetes in pregnancy. Management of diabetes and its complications from pre-conception to the postnatal period. NICE CG63. London: National Institute of Clinical Excellence, 2008. Cited October 2011. Available at www.nice.org.uk/ nicemedia/live/11946/41320/41320.pdf.
  100. Colagiuri S, Davies D, Girgis S, Colagiuri R. National evidence based guideline for case detection and diagnosis of type 2 diabetes. Canberra: NHMRC and Diabetes Australia, 2009. Cited October 2011. Available at www.nhmrc.gov.au /_files_nhmrc/publications/attachments/ di17-diabetes-detection-diagnosis.pdf
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