| | Antenatal screening and predicting hypertension in pregnancy for midwivesReceived 26 June 2009; received in revised form 7 September 2009; accepted 16 September 2009. Summary BackgroundThe cause of hypertension in pregnancy remains unknown and results in increased risk of complications for mother and baby. Symptoms of developing pre-eclampsia, such as an elevated blood pressure, can be vague and singular. The purpose of this literature review is to evaluate research investigating antenatal screening practices for hypertension which fall within the midwives scope of practice. MethodInclusion criteria for this literature review were English language, peer reviewed primary research journal articles, published in the previous 20 years where the population under study was pregnant with reported outcomes of prevention, screening or prediction of hypertension in pregnancy. A large number of papers (n = 201) were identified and these were screened and subsequently excluded if they addressed diagnostic testing, screening and interpretation that depended solely on a medical practitioner. ResultsThere was no single predictive factor found, however the relevant papers included in this review (n = 33) found evidence of modifiable, non-modifiable and clinical assessment factors for inclusion in a midwifery screening model. ConclusionsFurther research should be focused on the factors observed by midwives during history taking and the antenatal course in the second and third trimesters and whether or not these can be synthesised in to a hypertension-specific diagnostic tool for use in midwifery practice. Introduction  The cause of hypertension in pregnancy remains unknown and results in an increased risk of complications for mother and baby.1 The Society of Obstetric Medicine of Australia and New Zealand (SOMANZ) classify hypertension in pregnancy as pre-eclampsia (PE), eclampsia, gestational hypertension (GH), and chronic hypertension. Defined as a disorder that combines hypertension with or without proteinuria, PE involves one or more organ system whereas GH is the onset of hypertension after 20 weeks gestation without organ involvement and returns to normal within 3 months of delivery.2 Although much is known of predisposing factors for hypertension in pregnancy, screening is limited to measurement of blood pressure (BP) reading with further investigations undertaken if PE or GH is suspected. Symptoms of developing PE, such as an elevated BP, can be vague and singular. A number of systematic reviews published on the screening and prevention of PE identify a core group of factors that can be used to predict and subsequently help prevent this disease. However, these reviews have largely addressed medical practice. As midwifery-based antenatal care becomes an increasingly prevalent choice for healthy low-risk women,3 prediction and the early diagnoses of PE becomes more important, particularly in remote areas or in clinics without access to medical staff. The purpose of this literature review is to evaluate research investigating antenatal screening practices which fall within the midwife's scope of practice as defined by the Australian Nursing and Midwifery Council's National Competency Standards and the Australian College of Midwives’,4 National Midwifery Guidelines for Consultation and Referral.5 Literature search strategy and databases searched  An electronic database search was performed using Medline, Pub Med, CINAHL, Ebscohost, and Scopus and the Boolean strategy. Keywords used singularly and in combination included: pre-eclampsia; screening; trimester (1st and 2nd); pregnancy; blood pressure; tests; induced hypertension; pregnancy-induced hypertension; toxaemia; risks; antenatal; and midwives/midwife. The search strategy involved a three-phase approach. Initially, criteria for inclusion were primary research, published in English language, in peer reviewed journals within the previous 20 years where the population under study was pregnant, with reported outcomes of prevention, screening or prediction of hypertension in pregnancy. A large number of papers (n = 201) were identified under the initial search terms. A preliminary review of these studies revealed that many focused on risk factors, published guidelines and policies, and populations of high-risk women or women with already diagnosed PE (n = 42) and these were subsequently excluded. The remaining papers underwent secondary screening, and analysis. Although midwives can refer and implement screening tests, the diagnoses and interpretation of specific results including Doppler ultrasonography, and complex haematological changes remains outside the midwives current scope of practice. Those papers involving research outcomes based on the use of Ultrasonography, predictors based on pathology testing and results, and physical assessment and testing determined by a medical practitioner were subsequently excluded (n = 146). Table 2 summarises studies excluded in this second phase. Thirty-three papers which reflected the scope of midwifery care practice remained and have been included in this third phase of review (Table 1). Factors which increase the risk of GH and PE have been identified from existing literature and are recognised by SOMANZ (2008). They can be used by midwives in practice. These include: nulliparity; age greater than (>) 40 years; family history of PE in a mother or sister; previous PE; Body Mass Index (BMI) > 25; multiple pregnancies; pre-existing diabetes; and diastolic BP measurement greater than 80 mmHg at the initial antenatal visit. The analysis indicated evidence of modifiable, non-modifiable and clinical assessment factors which may be included in a midwifery model that predicts PE. | | |  | Included study | Study design | Sample size | Title |  |
|---|
 | Modifiable factors |  |  | Duckitt (2005) | Systematic review | 52 studies | Risk factors for preeclampsia at antenatal booking |  |  | Meher (2006) | Systematic review | 1 study | Garlic for preventing pre-eclampsia and its complications |  |  | Hofmeyer (2007) | Systematic review | 12 studies | Dietary Calcium supplementation for prevention of pre-eclampsia and related problems |  |  | Cnossen (2007) | Bivariate meta analysis | 36 studies | Accuracy of body mass index in predicting pre-eclampsia |  |  | Olsen (2000) | RCT | 1,647 patients from 19 hospitals in Europe | Randomised clinical trials of fish oil supplementation in high risk pregnancies |  |  | Kumar (2009) | RCT | 524 participants from India | Calcium supplementation for prevention of pre-eclampsia |  |  | Rumbold (2006) | RCT | 1,877 participants in multicentre Australian trial | Vitamins C and E and risks of preeclampsia and perinatal complications |  |  | Poston (2006) | RCT | 2,410 participants from 25 hospitals | Vitamin C and Vitamin E in pregnant women at risk for pre-eclampsia |  |  | Mamun (2005) | Cohort study | 2,934 participants (children) | Family and early life factors associated with changes in overweight status between ages 5 and 14 years |  |  | Belogolovkin (2007) | Cohort study | 29,268 participants from a multicentre study | The effect of low body mass index on the development of gestational hypertension and preeclampsia |  |  | Oken (2007) | Cohort study | 1,718 participants form USA | Diet during pregnancy and risk of preeclampsia or gestational hypertension |  |  | Triche (2008) | Cohort study | 2,291 participants in USA | Chocolate consumption in pregnancy and reduced likelihood of preeclampsia |  |  | Theroux (2007) | Cohort study | 1,835 participants in USA | Preventing pre-eclampsia, do vitamins work? |  |  | Osterdal (2009) | Cohort study | 85,139 participants in Denmark | Does leisure time physical activity in early pregnancy protect against pre-eclampsia? |  |  | Ruma (2008) | Cohort study | 775 participants in USA | Maternal periodontal disease, systemic inflammation, and risk for preeclampsia |  |  | Pick (2005) | Cohort study | 101 participants from USA | Assessment of diet quality in pregnant women using the healthy eating index |  |  |
|  |  | Non-modifiable factors |  |  | Trogstad (2008) | Cohort study | 20,846 participants in Norway | Previous abortions and risk of pre-eclampsia |  |  | Trogstad (2009) | Cohort study | 20,846 participants in Norway | The effect of recurrent miscarriage and infertility on the risk of pre-eclampsia |  |  | Mostello (2008) | Cohort study | 103,860 participants from birth certificate | Recurrence of pre-eclampsia: effects of gestational age at delivery of the first pregnancy, BMI, paternity, and interval between births |  |  | Caughey (2005) | Retrospective cohort study | 127,544 participants from linked data in USA | Maternal ethnicity, paternal ethnicity, and paternal ethnic discordance |  |  | Carr (2005) | Case–control study | 10,723 participants using linked data in USA | A sister's risk: family history as a predictor of preeclampsia |  |  | Silva (2008) | Cohort study | 3,547 women in the Netherlands | Low socioeconomic status is a risk factor for preeclampsia: the generation R study |  |  | Carvalho (2006) | Cohort study | 29 participants in Brazil | Predictive factors for pregnancy hypertension in primiparous adolescents |  |  |
|  |  | Clinical assessment |  |  | Conde-Agudelo (2004) | Systematic review | 87 studies | Screening |  |  | Cnossen (2008) | Systematic review | 34 studies | MAP |  |  | Miller (2007) | Cohort study | 1,655 participants for Sweden and USA | First trimester mean arterial pressure and risk of preeclampsia |  |  | The HAPO Study Cooperative Research Group (2008) | Observational cohort | 23,316 participants from 16 international multicentres | Hyperglycaemia and adverse pregnancy outcomes |  |  | Tomoda (1994) | Cohort study | 125 participants form Japan | Prediction of pregnancy-induced hypertension by isometric exercise |  |  | Baker (1994) | Cohort study | 200 participants from UK | The use of the hand grip test for predicting pregnancy induced hypertension |  |  | Watson (1995) (Meher and Duley, 2006) | Cohort study | 97 participants from USA | Pressor response to cycle ergometry in the midtrimester of pregnancy: can it predict preeclampsia? |  | | | |
| | |  | Excluded studies | Study design | Sample size | Title |  |
|---|
 | Ultrasonography |  |  | Arduini (1987) | Experimental trial | 3,359 pregnancies | Utero-placental blood flow velocity waveforms as predictors of pregnancy-induced hypertension |  |  | Atkinson (1994) | Prospective screening study | 3,107 pregnancies | The predictive value of umbilical artery Doppler studies for preeclampsia or fetal growth retardation in a preeclampsia prevention trial |  |  | Audibert (2005) | Cohort, observational | 3,058 pregnancies | Prediction of preeclampsia or intrauterine growth restriction by second trimester serum screening and uterine Doppler velocimetry |  |  | Bower (1994) | Prospective screening study | 210 pregnancies | Doppler ultrasound screening as part of routine antenatal scanning: prediction of pre-eclampsia and intrauterine growth retardation |  |  | Cobellis (2006) | Intervention cohort | 4,293 pregnancies | Mid-trimester fetal-placental velocimetry response to nifedipine may predict early the onset of pre-eclampsia. 1 |  |  | Dept of Obstetric and Gynaecology, Akita | Intervention cohort | 93 pregnancies | A study for predicting toxaemia of pregnancy by the diastolic notch in pulsed Doppler flow velocity waveforms of the uterine arteries—quantitative analysis of the diastolic notch as uterine arterial index (UTAI)] |  |  | Deurioo (2007) | Prospective screening study | 433 pregnancies | Colour Doppler ultrasound of spiral artery blood flow for prediction of hypertensive disorders and intra uterine growth restriction: a longitudinal study |  |  | De Paco (2008) | Experimental trial | 60 pregnancies | Maternal cardiac output between 11 and 13 weeks of gestation in the prediction of preeclampsia and small for gestational age |  |  | Espinoza (2007) | Prospective cohort | 534 women | Identification of patients at risk for early onset and/or severe preeclampsia with the use of uterine artery Doppler velocimetry and placental growth factor. 1 |  |  | Florio (2005) | Prospective screening study | 166 women | Factor II: C activity and uterine artery Doppler evaluation to improve the early prediction of pre-eclampsia on women with gestational hypertension |  |  | Gudnasson (2004) | Prospective screening study | 878 women | Preeclampsia—abnormal uterine artery Doppler is related to recurrence of symptoms during the next pregnancy |  |  | Jacobson (1990) | Intervention cohort | 93 participants from UK | The value of Doppler assessment of the uteroplacental circulation in predicting preeclampsia or intrauterine growth retardation |  |  | Khalil (2009) | Cohort, observational | 3,348 women | Pulse wave analysis: a preliminary study of a novel technique for the prediction of pre-eclampsia |  |  | Khaw (2008) | Prospective observational cohort | 534 participants from UK | Maternal cardiac function and uterine artery Doppler at 11–14 weeks in the prediction of pre-eclampsia in nulliparous women |  |  | Melchiorre (2008) | Intervention cohort | 93 pregnancies | First-trimester uterine artery Doppler indices in term and preterm pre-eclampsia |  |  | Mirpuri (2001) | Prospective screening study | 108 women | High-frequency ultrasound imaging of the skin during normal and hypertensive pregnancies |  |  | Nicolaides (2006) | Nested case control study | 124 women | A novel approach to first-trimester screening for early pre-eclampsia combining serum PP-13 and Doppler ultrasound |  |  | Onwudiwe (2008) | Cohort, observational | 65 women | Prediction of pre-eclampsia by a combination of maternal history, uterine artery Doppler and mean arterial pressure |  |  | Parra (2005) | Experimental trial | 570 women | Screening test for preeclampsia through assessment of uteroplacental blood flow and biochemical markers of oxidative stress and endothelial dysfunction |  |  | Phupong (2003) | Cohort, observational | 540 women | Predicting the risk of preeclampsia and small for gestational age infants by uterine artery Doppler in low-risk women |  |  | Pilalis (2007) | Prospective cohort | 565 women | Screening for pre-eclampsia and fetal growth restriction by uterine artery Doppler and PAPP-A at 11–14 weeks gestation |  |  | Plasencia (2008) | Intervention cohort | 2,430 women | Uterine artery Doppler at 11 + 0 to 13 + 6 weeks and 21 + 0 to 24 + 6 weeks in the prediction of pre-eclampsia |  |  | Riskin-Mashiah (2002) | Prospective screening study | 93 pregnancies | Transcranial Doppler measurement of cerebral velocity indices as a predictor of preeclampsia |  |  | Torricelli (2006) | Intervention cohort | 20 pregnancies | Low-molecular-weight heparin improves the performance of uterine artery Doppler velocimetry to predict preeclampsia and small-for-gestational age infant in women with gestational hypertension |  |  | Tranquilli (2007) | Prospective screening study | 433 pregnancies | The relative weight of Doppler of the uterine artery and 24-h ambulatory blood pressure monitoring in predicting hypertension in pregnancy and preeclampsia |  |  | Yu (2005) | Prospective screening study | 2,615 pregnancies | An integrated model for the prediction of preeclampsia using maternal factors and uterine artery Doppler velocimetry in unselected low-risk women |  |  |
|  |  | Pathology |  |  | Bahado-Singh (2002) | Intervention cohort | 568 participants from USA | The role of hyperglycosylated hCG in trophoblast invasion and the prediction of subsequent pre-eclampsia |  |  | Baker (1992) | Cohort, observational | 34 participants from UK | Comparative study of platelet angiotensin II binding and the angiotensin II sensitivity test as predictors of pregnancy-induced hypertension |  |  | Baumann (2008) | Cohort, observational | 148 participants from Switzerland | First-trimester serum levels of soluble endoglin and soluble fms-like tyrosine kinase-1 as first-trimester markers for late-onset preeclampsia |  |  | Buhimschi (2008) | Prospective screening study | 284 participants from USA | Proteomic profiling of urine identifies specific fragments of SERPINA1 and albumin as biomarkers of preeclampsia |  |  | Chafetz (2007) | Prospective screening study | 425 participants from Israel | First-trimester placental protein 13 screening for preeclampsia and intrauterine growth restriction |  |  | D’Anna (2008) | Prospective screening study | 144 participants from Italy | Second trimester neutrophil gelatinase-associated lipocalin as a potential prediagnostic marker of preeclampsia |  |  | Davidson (2003) | Retrospective cohort | 225 participants from Scotland | Maternal serum activin, inhibin, human chorionic gonadotrophin and alpha-fetoprotein as second trimester predictors of pre-eclampsia |  |  | De Vivo (2008) | Cohort, observational | 104 participants from Italy | Endoglin, PlGF and sFlt-1 as markers for predicting pre-eclampsia |  |  | Dreyfus | Intervention cohort | | The prediction of preeclampsia: reassessment of clinical value of increased plasma levels of fibronectin |  |  | Florio (2004) | Prospective screening study | 58 participants from Italy | The measurement of maternal plasma corticotropin-releasing factor (CRF) and CRF-binding protein improves the early prediction of preeclampsia |  |  | Ghorashi (2008) | Nested case control study | 40 participants from Iran | The relationship between serum concentration of free testosterone and pre-eclampsia |  |  | Gonen (2008) | Intervention cohort | 1,366 women from Israel | Placental protein 13 as an early marker for pre-eclampsia: a prospective longitudinal study |  |  | Gredmark (1999) | Intervention cohort | 657 participants from Sweden | Total fibronectin in maternal plasma as a predictor for preeclampsia |  |  | Ho (1992) | Intervention cohort | 66 participants from Taiwan | The predictive value of the homeostasis parameters in the development of preeclampsia |  |  | Hogg (2000) | RCT | 437 participants from UK | Second-trimester plasma homocysteine levels and pregnancy-induced hypertension, preeclampsia, and intrauterine growth restriction |  |  | Jones (1996) | Cohort, observational | 238 participants from Australia | Fibronectin as a predictor of preeclampsia: a pilot study |  |  | Konijnenberg (1997) | Prospective screening study | 244 participants from The Netherlands | Can flow cytometric detection of platelet activation early in pregnancy predict the occurrence of preeclampsia? A prospective study |  |  | Kyle (1995) | RCT | 495 participants from UK | The angiotensin sensitivity test and low-dose aspirin are ineffective methods to predict and prevent hypertensive disorders in nulliparous pregnancy |  |  | Lambert-Messerlain (2000) | Retrospective cohort | 360 participants from USA | Second-trimester levels of maternal serum human chorionic gonadotropin and inhibin a as predictors of preeclampsia in the third trimester of pregnancy |  |  | Leal (2009) | Prospective screening study | 697 participants from UK | First-trimester maternal serum tumour necrosis factor receptor-1 and pre-eclampsia |  |  | Levine (2005) | Nested case control study | 240 participants from USA | Urinary placental growth factor and risk of preeclampsia |  |  | Levy (2007) | Intervention cohort | 103 participants from West Indies | Booking blood pressures and plasma nitrite in Jamaican women with pre-eclampsia |  |  | Livingstone (2001) | Nested case control study | 880 participants from USA | Placenta growth factor is not an early marker for the development of severe preeclampsia |  |  | Lynch (2008) | Observational cohort | 701 participants from USA | Alternative complement pathway activation fragment Bb in early pregnancy as a predictor of preeclampsia |  |  | Madazli (2005) | Prospective screening study | 122 participants fro Turkey | Prediction of preeclampsia with maternal mid-trimester placental growth factor, activin A, fibronectin and uterine artery Doppler velocimetry |  |  | Margarit (2005) | Prospective observational cohort | 96 women from Greece | Second trimester amniotic fluid endothelin concentration. A possible predictor for pre-eclampsia |  |  | Mello (2002) | Longitudinal study | 187 participants from Italy | Individual longitudinal patterns in biochemical and haematological markers for the early prediction of pre-eclampsia |  |  | Meyers (2007) | Case control | 74 participants from USA | Evidence for multiple circulating factors in preeclampsia |  |  | Moore Simas (2007) | Prospective screening study | 94 participants from USA | Angiogenic factors for the prediction of preeclampsia in high-risk women |  |  | Muller (1996) | Cohort, observational | 5,776 participants from North America | Maternal serum human chorionic gonadotropin level at fifteen weeks is a predictor for preeclampsia |  |  | O’Brien (1999) | Prospective cohort | 325 participants from UK | Failure of platelet angiotensin II binding to predict pregnancy-induced hypertension |  |  | Ong (2001) | Prospective screening study | 668 participants from UK | First-trimester maternal serum levels of placenta growth factor as predictor of preeclampsia and fetal growth restriction |  |  | Osmanagaoglu (2005) | Intervention cohort | 85 participants from Turkey | Coagulation inhibitors in preeclamptic pregnant women. |  |  | Parretti (2006) | Intervention cohort | 829 participants from Italy | Preeclampsia in lean normotensive normotolerant pregnant women can be predicted by simple insulin sensitivity indexes |  |  | Poon (2008) | Prospective cross-sectional observational study | 2,679 participants from UK | Urine albumin concentration and albumin-to-creatinine ratio at 11(+0) to 13(+6) weeks in the prediction of pre-eclampsia |  |  | Poon (2009) | Prospective screening study | 8,141 participants from UK | First-trimester maternal serum pregnancy-associated plasma protein-A and pre-eclampsia |  |  | Poston (2006) | RCT | 2,410 participants from 25 hospitals | Vitamin C and vitamin E in pregnant women at risk for pre-eclampsia (VIP trial): randomised placebo-controlled trial |  |  | Pouta (1998) | Prospective screening study | 1,037 participants from Finland | Midtrimester N-terminal proatrial natriuretic peptide, free beta hCG, and alpha-fetoprotein in predicting preeclampsia |  |  | Purwosunu (2009) | Intervention cohort | 372 participants from Japan | Prediction of preeclampsia by analysis of cell-free messenger RNA in maternal plasma |  |  | Raty (1999) | Prospective screening study | 4,356 participants from Finland | Prediction of pre-eclampsia with maternal mid-trimester total renin, inhibin A, AFP and free beta-hCG levels. 1 |  |  | Rodgers (2006) | Prospective observational cohort | 381 participants from Hong Kong | Oxidative stress in midpregnancy as a predictor of gestational hypertension and pre-eclampsia |  |  | Roiz-Hernandez (2006) | Prospective cohort | 784 participants from Mexico | Human chorionic gonadotropin levels between 16 and 21 weeks of pregnancy and prediction of pre-eclampsia |  |  | Romero (2008) | Case control | 350 participants from USA | First-trimester maternal serum PP13 in the risk assessment for preeclampsia |  |  | Rudra | Nested case control study | 733 participants from Sweden | A prospective study of early-pregnancy plasma malondialdehyde concentration and risk of preeclampsia |  |  | Salako (2003) | Prospective screening study | 100 participants fro Nigeria | Microalbuminuria in pregnancy as a predictor of preeclampsia and eclampsia |  |  | Shaarawy (2000) | Prospective screening study | 80 participants from Egypt | Plasma endothelin-1 and mean arterial pressure in the prediction of pre-eclampsia |  |  | Shaarawy (2001) | Intervention cohort | 155 participants from Egypt | The clinical value of microtransferrinuria and micro albuminuria in the prediction of pre-eclampsia |  |  | Song (2004) | Intervention cohort | 132 pregnancies from China | Predicting pregnancy-induced hypertension with dynamic hemodynamics |  |  | Stepan (2008) | Prospective observational cohort | 77 participants from Germany | Circulatory soluble endoglin and its predictive value for preeclampsia in second-trimester pregnancies with abnormal uterine perfusion |  |  | Thornton (1989) | Cohort, observational | 400 participants from UK | A prospective study of haemostatic tests at 28 weeks gestation as predictors of pre-eclampsia and growth retardation |  |  | Vaillant (1996) | Prospective screening study | 434 participants from France | Validity in nullipara's of increased beta-human chorionic gonadotrophin at mid-term for predicting pregnancy-induced hypertension complicated with proteinuria and intrauterine growth retardation |  |  | Vattern (2007) | Nested case control study | 746 participants from Norway | Changes in circulating level of angiogenic factors from the first to second trimester as predictors of preeclampsia |  |  | Vattern (2008) | Case control | 29,948 participants from Norway | Changes in circulating level of IGF-I and IGF-binding protein-1 from the first to second trimester as predictors of preeclampsia |  |  | Wald (2006) | Nested case control study | 480 participants in UK | Screening in early pregnancy for pre-eclampsia using Down syndrome quadruple test markers |  |  | Waller (1996) | Retrospective cohort | 51,008 participants via medical records in USA | The association between maternal serum alpha-fetoprotein and preterm birth, small for gestational age infants, preeclampsia, and placental complications |  |  | Woolcock (2008) | Cohort, observational | 39 from NSW | Soluble Flt-1 as a diagnostic marker of pre-eclampsia |  |  | Yie (2005) | Intervention cohort | 24 participants from Canada | Low plasma HLA-G protein concentrations in early gestation indicate the development of preeclampsia later in pregnancy |  |  |
|  |  | Physical assessment |  |  | Brown (2001) | Intervention cohort | 122 participants from Australia | Twenty-four-hour automated blood pressure monitoring as a predictor of preeclampsia |  |  | Easterling (1999) | RCT | 56 participants from USA | Prevention of preeclampsia: a randomized trial of atenolol in hyperdynamic patients before onset of hypertension |  |  | Eneroth-Grimfors (2008) | Experimental trial | 40 participants from Sweden | Evaluation of three simple physiologic tests as predictors of pregnancy-induced hypertension. A pilot study |  |  | Hermida (1998) | Prospective screening study | 152 participants from Spain | Blood pressure excess for the early identification of gestational hypertension and preeclampsia |  |  | Hermida (2001) | Prospective screening study | 328 participants from Spain | Evaluation of the blood pressure load in the diagnosis of hypertension in pregnancy |  |  | Higgins (1997) | Intervention cohort | 1,102 participants from Ireland | Can 24-hour ambulatory blood pressure measurement predict the development of hypertension in primigravidae? |  |  | Innes (1999) | Retrospective cohort | 4,440 participants from USA | A woman's own birth weight and gestational age predict her later risk of developing preeclampsia, a precursor of chronic disease |  |  | Kazerooni (2006) | Prospective screening study | 102 participants in Iran | Second trimester cardiac output and its predictive value for preeclampsia |  |  | Martin (1999) | Retrospective cohort | 970 participants from USA | Early risk assessment of severe preeclampsia: admission battery of symptoms and laboratory tests to predict likelihood of subsequent significant maternal morbidity |  |  | Mikolajczk (2008) | Retrospective cohort | 533 participants from USA birth records | Effects of interpregnancy interval on blood pressure in consecutive pregnancies |  |  | Moretti (2004) | Intervention cohort | 124 participants from USA | Increased breath markers of oxidative stress in normal pregnancy and in preeclampsia |  |  | Ohkuchia (2006) | Cohort, observational | 1,518 participants from Japan | Normal and high-normal blood pressures, but not body mass index, are risk factors for the subsequent occurrence of both preeclampsia and gestational hypertension: a retrospective cohort study |  |  | Ramon (2000) | Experimental trial | 202 participants from Spain | Blood pressure patterns in normal pregnancy, gest hypertension + preeclampsia |  |  | Romero-Gutierrez (2004) | Prospective screening study | 160 participants from Mexico | Homeostatic model assessment and risk for hypertension during pregnancy: a longitudinal prospective study |  |  | Spinapolice (1998) | Experimental trial | 32 participants from USA | Effective prevention of Gestational hypertension in Nulliparous women at high risk as identified by the rollover test |  |  | Stamillio (2000) | Retrospective cohort | 1,998 participants from USA medical records | Can antenatal clinical and biochemical markers predict the development of severe preeclampsia? |  |  | Takase (2003) | Prospective screening study | 43 participants from Japan | Flow-mediated dilation in brachial artery in the second half of pregnancy and prediction of pre-eclampsia. 1 |  |  | Urdzik (2007) | Retrospective cohort | 578 participants from Czech Republic | Prediction of preeclampsia using the integrated test markers |  |  | Verwoerd (2002) | Case control | 110 participants from South Africa | Primipaternity and duration of exposure to sperm antigens as risk factors for pre-eclampsia |  |  | Watson (1995) | Intervention cohort | 97 participants from USA | Pressor response to cycle ergometry in the midtrimester of pregnancy: can it predict preeclampsia? |  |  | Yamamoto (2001) | Cohort, Observational | 224 participants from Japan | Waist to hip circumference ratio as a significant predictor of preeclampsia, irrespective of overall adiposity |  | | | |
Modifiable factors  A modifiable risk factor is one that can be altered with intervention thereby decreasing the risk of the complication it causes. Midwives are at the forefront of information gathering and using thorough history taking and accurate assessment can identify potential risk factors. The accuracy of this information is vital to allow the clinician to formulate and provide optimal individualised care for mother and baby. High BMI and its association with PE has been documented in a systematic review of the risk factors for PE identified during antenatal booking with a BMI > 35 kg/m2 found to double the risk of developing PE.6 Cnossen et al. performed a bivariate meta-analysis to determine the ability of BMI to predict PE.7 BMI (calculated from both self-reported or first booking height and weight) although helpful, was not useful as a single predictive factor. While reporting bias may be a consideration in this approach, the work of Mamun et al. demonstrates a strong correlation between the accuracy of self-reported and booking BMI,8 suggesting the clinician is able to accept either measurement. A longitudinal study evaluated the relationship between low BMI in first trimester and the incidence of PE and GH compared with normal and high BMI.9 Women with a BMI < 19.8 kg/m2 had less incidence of GH and PE. However, the cohort of low BMI women were found to be younger therefore less likely to have underlying conditions that predispose to PE. The author offers that this may be due to the absence of metabolic disorders which can manifest with increasing BMI and the association of other complications such as increased incidence of intrauterine growth retardation. Women often seek advice from midwives regarding diet, vitamins and exercise during pregnancy in order to establish and maintain a healthy lifestyle for themselves and their babies. To offer the best advice, midwives must practice from an evidence-based perspective by being aware of all current literature relating to this facet of antenatal care. Studies which examine diet vary in their methodological approaches and quality. A systematic review on the use of garlic for prevention of PE and its complications10 did not provide an adequate evidence base to be able to recommend increased garlic intake during pregnancy. The premise that garlic may lower blood pressure therefore preventing uterine constriction associated with PE is an area requiring further study. A prospective cohort study (n = 1718) examined the association of a number of vitamins, fatty acids and calcium with the development of PE using a food frequency questionnaire in the first trimester.11 No significant association for any particular diet component was reported however, a potential benefit of a regular intake of oily fish (n − 3 fatty acids) was identified. This was in contrast to a large randomised trial which concluded that fish oil had no effect on hypertension in pregnancy.12 A further study involving food in pregnancy examined chocolate consumption in early pregnancy and its effect on PE incidence.13 The authors acknowledge that their results may suggest chocolate consumption decreases the risk of PE however; the evidence is not strong enough make public health recommendations due in part to the possibility of under and over-reporting of chocolate consumption by the participants through self-reported questionnaires. Midwives are often asked for advice during the course of antenatal care regarding vitamins and mineral use in pregnancy. The role of calcium in reducing the incidence of PE has been reported in a number of research studies detailed in a Cochrane review.14 It was concluded that adequate dietary calcium in early pregnancy should be encouraged and that supplementation appears to reduce the risk of PE. One study concluded calcium supplements reduced the incidence of PE where dietary intake of calcium was below recommended levels.15 This is relevant to midwifery practice when an observational study has shown that pregnant women may not be receiving the recommended intake of calcium through diet alone.16 Two randomised controlled trials proposed that Vitamins C and E reduced the risk of PE17, 18 although neither proved this to be the case. One study reported Vitamin C and E increased the rate of low birth weight babies18 while Theroux sought to assess the association between PE pre-conception multivitamin use finding further research was required as the results were inconclusive.19 Advice regarding exercise and general well-being has long been a part of midwifery care to promote positive maternal and baby outcomes. One study examined physical activity and another oral health; both being aspects of health care that midwives can address with their clients. Osterdal et al. investigated whether physical activity in early pregnancy decreases the risk of PE reporting there was no protective effect observed. Their data demonstrated physical activity in excess of 270 min/week could increase the risk of developing PE.20 Oral hygiene was researched to investigate if it could be classed as a risk factor for PE with results showing that periodontal disease with systemic inflammation, measured as C-reactive protein, is associated with increased incidence of PE.21 These modifiable risk factors have the ability to be altered before and during a pregnancy by the women following advice, education and support from the midwife providing antenatal care. Non-modifiable factors  Non-modifiable risk factors cannot be altered as they are reliant on external factors such as family history, previous pregnancies, age and ethnicity. Midwives are able to identify these factors during the compilation of the patient's history, providing an opportunity to form an accurate assessment of their patient. Trogstad et al. aimed to estimate the risk of PE in primiparous women with history of spontaneous and induced abortions.22 This observational research surveyed 20,846 women participating in the Norwegian Mothers and Child study. After adjusting for confounders, results showed that two or more induced abortions provide similar protection from PE to that of one previous pregnancy without PE. Concurrent research on the same cohort further investigated if recurrent miscarriage and infertility contributed to PE.23 Information regarding PE was compared with that of the Norwegian Birth registry and concluded that, when combined, the risk factors for infertility and recurrent miscarriages may contribute to the development of PE. The exposure data for these studies was based on self-reported questionnaires. However, this method of data collection is prone to under and over-reporting of conditions. Some of the criticisms of this method are confusion in participant's responses due to understanding of data required and reluctance of participants to disclose sensitive information. Mostello et al. aimed to research the incidence of PE recurrence by examining the gestational age at delivery of the first pregnancy, BMI, paternity (defined as paternal status unknown or different from previous pregnancy) and birth interval in a large population-based cohort study (n = 103,860). Linked by maternal name and date of birth, data from birth and fetal death certificates24 were studied. Increasing BMI and early delivery of previous pregnancies complicated by PE both contributed to its risk of recurrence however, there was no increased risk identified with change in paternal status. The limitations in the methodology of the study include the possible lack of consistency in data input. The death certificates could not include severity of pre-eclampsia and the possibility of under-reporting of underlying medical conditions which could contribute to PE were recognised by the researchers.24 During initial antenatal interview with the midwife, information is collected relating to the women's ethnicity. This information was examined using parental ethnicity and discordance to determine the association between these factors and PE.25 The retrospective cohort study (n = 127,544) showed a decrease in the rate of PE in populations with Asian paternity. In Australia in 2006–2007, over 25% of immigrants were from Asian countries, making parental ethnicity an important component of the antenatal history.2 Family history is another integral part of the interview. A systematic review examined whether a medical history of PE in mothers and sisters led to a predisposition to PE.6 Inclusion of familial history questions was supported by a large population-based case–control study (n = 10,723),26 which reported women who developed PE were 2.3 times more likely to have a sister who also developed PE. However, this association may be confounded by behavioural factors such as obesity and smoking that might cluster in families.27 Another smaller study (n = 368) discovered that in primigravida, a family history of PE is associated with a four-fold risk of severe PE.39 Economic status is an area not necessarily assessed by midwives unless it is an issue evident for the women they care for. A cohort study examined whether low socioeconomic status as a risk factor for PE. Using educational level as an indicator of socioeconomic status,28 results showed that women in the lower socioeconomic group were more likely to develop PE. However, this finding should be interpreted cautiously. Although the response rate was 68%, lower educated women were less likely to respond. Additionally, the use of a self-reported questionnaire may have contributed to differing interpretations of educational status by participants. The conclusions demonstrated a correlation between low socioeconomic status and PE however, these phenomena were largely unexplained, so further exploration of any association is needed. Carvallo et al. performed a small study (n = 29) to examine predictive factors in adolescents (16–19 years) and the development of PE.29 Results showed the best predictors of this condition were family history and diastolic blood pressure measurements at differing periods of the day, however further research with a larger cohort is needed to verify these results. These factors are unable to be altered during pregnancy; however reinforcement of their importance during the antenatal period can be stressed by midwives. This information, in combination with both modifiable and clinical assessment factors can be used to help identify patients at higher risk of developing PE. Clinical assessment  In 2004, the World Health Organisation conducted a systematic review assessing all tests used to prediction PE, and found that there is no definitive, low-cost, predictive test available.30 Another extensive systematic review highlighted numerous risk factors for hypertension in pregnancy however; many screening strategies such as the presence of antiphospholipid antibodies and interpreting Doppler-based measurements are beyond the current scope of practice of the midwife. Most recognised risk factors which contribute to PE would result in the pregnancy being categorised as “high-risk”—which, according to National Midwifery Guidelines for Consultation and Referral, would require obstetric-led antenatal care. Hence, this is beyond the scope of practice of the midwife.6 Blood pressure measurement remains one of the most definitive predictors of PE and is a key component of antenatal assessment at each visit.31 Duckitt reviewed four studies, all examining BP readings, and concluded that a systolic blood pressure of >130 doubled the risk of PE. Additionally, this review also showed that initial or booking BP was a vital component to give insight to prediction of PE.6 The gold standard of measurement of blood pressure is the mercury sphygmomanometers2, 38; however standardised practice should be employed by practitioners to avoid possible inaccurate readings. “The woman should be seated comfortably with her legs resting on a flat surface. The systolic blood pressure is accepted as the first sound heard and the diastolic blood pressure the disappearance of sounds completely. Correct cuff size is important for accurate blood pressure recording, with a larger cuff used if the upper arm circumference is greater than 33 cm” [2, p. 4]. If automated devises are used then it is vital that they are checked and calibrated at least monthly to maintain accuracy and used according to manufacturer's specifications. A large international research project which was reliant on BP measurement by automatic machines in sixteen centres alleviated the potential for inconsistency by providing each centre with an identical machine, with monthly checking by the research team with mercury sphygmomanometers to detect any discrepancies in values.31 A retrospective cohort study examined if the combination of BMI and high-normal BP can be used as a predictor.32 The results showed that being overweight or obese may not be an independent risk factor for development of PE compared with just having high-normal BP; however, this study noted that further research is necessary before conclusions can be made. A systematic review and meta-analysis was completed on the accuracy of mean arterial pressure (MAP) and BP measurements and their predictive qualities, and found that the MAP was a better predictor than BP alone.33 MAP could therefore be used by midwives during their routine antenatal care. Miller et al. used a prospective cohort (n = 1655) and found that although first trimester MAP is strongly associated with increased risk of developing PE, it will not predict with accuracy those women who will develop PE.34 Cnossen et al. in their systematic review of 34 studies (n = 60,599) explored the accuracy of using systolic/diastolic BP, mean BP, and increasing BP to predict PE and found that MAP was in fact a better predictor. Further research is recommended to develop algorithms that combine all predictive factors in order to identify women who will develop PE.33 A large research study (n = 25,505) recently examined the effects of maternal glucose levels and adverse outcomes.31 They found that there was an association with glucose levels lower than the diagnostic level for diabetes and the incidence of PE in both fasting and 2 h results. Research by several authors relating to physical testing of hand grip and BP response to exercise has been conducted to attempt to predict PE using non-invasive interventions. Tomoda tested women by a use of a hand grip test by measurement of systolic pressure,35 Baker by hand grip alone,36 and Watson by aerobic exercise to increase heart beat up to 140 beats/min.37 Although these tests are able to be performed within the midwives’ scope of practice, the reliability of operator, the amount of time required and unpredictable nature of the test does not lend itself to introduction to routine testing. Accurate clinical assessment is essential to provide ongoing antenatal care in the second and third trimester. Midwives may be able to assess all facets of the antenatal course, including oral glucose tolerance tests, blood pressure readings, and reviewing previously documented history to identify women at risk with the use of tool designed to correlate this information. This is important as timely referral has been a key component in reducing maternal and neonatal morbidity.1 Treatment of hypertensive disorders once diagnosed remains outside the midwives scope of practice,5 but as elevated BP is often the first clinical indicator of PE, midwives are obligated to refer the woman for further investigations and treatment according to guidelines set by medical organisations such as SOMANZ2 and Australian College of Midwives.5 Discussion  This literature review aimed to identify predictors of hypertension in pregnancy that could be used by midwives in their scope of practice. The important role of obtaining an accurate medical, family and obstetric history is predominately that of the booking midwife. There are number of factors that can be assessed at this time that have shown to reflect the women's predisposition to development of PE. Physical baseline characteristics such as BMI, age and blood pressure measurement need to be documented accurately. These assessments can be complemented by information relating to paternity, and ethnicity. Family history has been reinforced as a risk factor, indicating the need to ask comprehensive questions regarding mothers and sisters history relating to PE which can alert the midwife to possible association to developing PE. The initial history appointment needs to be completed both comprehensively and thoroughly, so all relevant information is gathered and assessed, allowing the care giver to formulate an individual care pathway. Advice given to clients by midwives regarding health and well-being has always been a necessary part of antenatal care. The studies that have been reviewed here did not identify any singular factor that would decrease the risk of PE, however regular exercise, a healthy diet rich in calcium and omega 3 may not only be helpful for prevention of PE, but overall good health for mother and baby and therefore could be safely recommended by midwives. The need for early referral to medical staff from midwifery-based care of complicated pregnancies to help decrease the long term detrimental effects of hypertension in pregnancy has been well documented and midwives need to be vigilant during their client's antenatal course. Midwives within their scope of practice have the opportunity to both identify and predict PE and are in a position to identify risk factors and thereby provide the best possible care for their mothers and babies. Conclusion  Hypertension in pregnancy is a condition that concerns all maternity care providers. Midwives are in the unique position of gathering data from the initial presentation of the women for antenatal care and continuing through the antenatal course. This review found 33 papers that specifically addressed prevention, screening and prediction of PE within the scope of practice of the midwife. Reviewing research relating to modifiable factors, non-modifiable factors and clinical assessment provides a useful framework for gathering information that could predict PE such as family history, parity, previous pregnancy details and highlights the importance of accurate and timely assessment of BP, BMI, OGTT and fetal assessment which may prove vital for the early prediction of PE. This review focused on healthy low-risk women, women who would not automatically be referred for early testing or monitoring, but could screened for hypertension in pregnancy by midwives. Further research should focused on the factors assessed by midwives during history taking and the antenatal period and whether or not these can be synthesised in to a hypertension-specific diagnostic tool for use by midwives in practice. Acknowledgments  The author would like to acknowledge Mater Mothers’ Research Centre and Golden Casket Midwifery Research Scholarship for research and funding support. 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a The University of Queensland, The School of Nursing and Midwifery, Edith Cavell Building, Herston, Queensland, Australia b Mater Mothers’ Research Centre, Level 2, Quarters Building, Mater Health Services, Annerley Road, Woolloongabba, Brisbane, Queensland, Australia Corresponding author at: Mater Mothers’ Research Centre, Level 2, Quarters Building, Mater Health Services, Annerley Road, Woolloongabba, Brisbane, Queensland 4102, Australia. Tel.: +61 7 3163 1591.
PII: S1871-5192(09)00071-7 doi:10.1016/j.wombi.2009.09.002 © 2009 Australian College of Midwives. Published by Elsevier Inc. All rights reserved. | |
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