Fetal Growth AssessmentBackground
Chapter One
BACKGROUND AND LITERATURE REVIEW
1.1Introduction
Fetal size is associated with pregnancy outcome. The growth-restricted fetus is at increased risk of pre term delivery, perinatal death and infant morbidity and mortality due to hypoxia, acidosis, hypoglycemia and hypocalcemia. The fetus with macrosomia (birth weight > 4000g) is at risk of stillbirth, perinatal asphyxia, meconium aspiration and birth injuries such as shoulder dystocia and fractures. Neonatal complications for these large babies include hypoglycemia, hypocalcemia and jaundice whilst the mother may suffer pre-eclampsia, postpartum haemorrhage and perineal trauma. Features that predispose to a large baby include gestational diabetes mellitus (GDM), a large maternal stature, increased maternal age, sedentary lifestyle or maternal obesity. Estimating fetal size/growth should be an important component of obstetric care, particularly in pregnancies complicated with gestational diabetes and fetal overgrowth that can lead to a macrosomic baby with its associated birth complications. The following literature review confirms that fetal size estimation can be difficult due to many contributing factors such as maternal body habitus, uterine distortions due to pathology, maternal ethnic variations as well as different techniques used to calculate the size of the fetus.
This thesis reviews the variability in assessing gestational age, fetal size, growth and weight and the variations seen in different racial groups. It then considers the diverse approach to obtaining accurate ultrasonic measurements for many parts of the fetal body and the mathematical modelling for fetal size/growth curve formatting. The thesis also examines fetal growth and ultrasonic estimation of fetal size, in the third trimester of pregnancy in both Caucasian and Chinese women living in Australia. The Chinese population was chosen due to the increasing number of immigrants settling within the Northern Sydney Health Area in New South Wales, Australia. The statistical variations seen in birth weight, interventions and complications between the Caucasian and Chinese at a local hospital during a routine audit prompted the question of ethnic differences influencing birth outcomes. This instigated the research that led to this thesis, which investigates pregnancies at risk of fetal macrosomia, both with and without gestational diabetes mellitus and the prevalence of birth intervention and complications, such as post partum haemorrhage in pregnancies thus affected. Finally the chapter summarises the works of the authors and lists the objectives of this study.
1.2Fetal Growth
Fetal growth is determined by a complex interaction of genetic, environmental and socio-economic factors (Vorherr 1982) with normal birth standards based on a combination of gestational age at birth, head size, length and birth weight (Varner 1987). Maternal risk factors strongly influence fetal size (Goldenberg 1993) and when these are combined with individual maternal profiles and population variances it could help explain the difference seen in fetal growth. The recommended maternal weight gain in Caucasian pregnancies, according to Taylor and Pernoll (1976) is between 10-12 kg with the average fetus accounting for approximately 3500 g of this gain. The remainder of the weight gain is from amniotic fluid (750g), placenta (1000g), blood volume (1500g), interstitial fluid (1500g), breasts (500g) and maternal fat upwards of 1500g. Taylor and Pernoll (1976) further described the various birth weight outcomes as follows. An immature infant is between 20 and 28 weeks gestation and weighs less than <1000grams whilst a premature infant is between 28 and 38 weeks gestation and weighs between 1000-2500 grams. A low birth weight infant is less than 2500g, a small for gestational age infant is less than two standard deviations below the mean weight for gestation, a mature infant weighs more than 2500g and is between 38-40 weeks gestation, a post-mature infant is more than 42 weeks gestation and finally the excessive size infant which weighs more than 4500 grams and termed macrosomic.
Normal fetal growth is not only reflected in birth weight but is defined according to population standards and percentiles (Brooke et al 1981, Dunn 1985, Gardosi et al 1992a, 1995b). Fetal measurement graphs and birth weight graphs are divided into standard deviations or percentiles where 50% of the measured population will be above the mean and 50% below the mean of the relevant graphs. The smallest 10% will be classed as less than the 10th percentile and therefore small for gestational age and the largest 10% greater than the 90th percentile will be large for gestational age (Deter 1981, Gallivan & Robson 1993, Jeanty 2001). Eight to ten percent of all Caucasian births are macrosomic, or have a birth weight above 4000 grams, which places them above the 90th percentile (Benson and Doubilet 1998) and 2% of these macrosomia births are greater than 4500 grams. Individual fetal growth curves are created by plotting gestational age and estimated fetal weight onto a weight graph displaying at least the 10th, 50th and 90th percentile limits (McCalum & Brinkley 1979, Hadlock 1990, Jeanty 2001). Brandt (1963) and Naey & Tafaril (1985) supported the theory that nutrition and lifestyle during pregnancy influenced birth weight. Taylor et al (1976) was of the opinion that any increase in mean birth weight over time may be due to better nutrition but there has been no corresponding change in female pelvic size. This fact alone can account for any increase in birth intervention and complications.
1.2.1The Small for Gestational Age Fetus
The small for gestational age (SGA) fetus as mentioned previously, is less than the 10th percentile below the population mean for the stage of gestation (Hughey 1984). SGA may be as a result of a combination of factors including obstetric background (Visser 1986), maternal stature, genetic disorders and maternal diseases such as hypertension, anemia, heart disease, renal disease, malabsorption and autoimmune disease (Varner 1987). Chesley (1978) termed the phrases “disease of theories” to describe pre-eclampsia with one of the theories being compromised placental perfusion. Unstable maternal pre-eclampsia can cause utero-placental insufficiency and placental abruption, which may result in intrapartum fetal distress or stillbirth (Fox 1987). Spirt and Gordon (2001) described placental insufficiency as being a “nonspecific clinical term with no known morphologic basis” and said that decreased uteroplacental blood flow may be due to anoxia secondary to maternal vascular problems. Sebire and Talbert (2001) analysed the placenta with a closer look at the pathophysiology of placental hemodynamics in uteroplacental compromise and concluded that the dynamic placenta allows local control of vascular smooth muscle tone, which in turn regulates the ventilation and perfusion differences. Up to 30% of placental attachment can be lost with no corresponding loss of function (Crawford 1962). Reduced placental function is the major cause of small for gestational age (Spirt & Gordon 1984a, 2001b) as a result of placenta previa, infarction and abruption (Varner 1987). Placental abruption occurs in up to 1 in 89 deliveries with fetal death occurring in 1 in 500 to 750 deliveries (Pernoll 1987) and can be diagnosed with ultrasound (Nyberg et al (1987). Mabie and Sibai (1987) cited the association of maternal pre-eclampsia with pre-term delivery and the complications arising from pre-maturity including hypothermia, meconium aspiration syndrome, hypoxia and acidosis, polycythemia and long term complications such as a lower IQ and learning disorders (Varner 1987). Nicolaides et al (1988) showed that an absence of end diastolic frequencies in the umbilical artery was a sign of fetal hypoxia and acidosis. Detection of the small fetus is critical for an improved obstetric outcome and a number of authors including Hadlock (1982), Seeds (1984), Hughey (1984) Deter (1992), Benson & Doubilet (1998) and Jeanty (2001) used ultrasonic fetal measurements to assess fetal size so that early clinical management could be implemented. Chang et al (1993) went further by comparing doppler waveform indices and serial ultrasound measurements of abdominal circumference and fetal weight to identify fetal growth retardation.
1.2.2The Large for Gestational Age Fetus
The large for gestational age (LGA) fetus is defined as being above the 90th percentile at any stage during pregnancy (Varner 1987). This is the same definition given for fetal macrosomia, or hypersomatism, by Golditch and Kirkman (1978), Hadlock (1989), Shah (1993), Benson (1998) and Jeanty (2001). Macrosomia is described in greater detail in section 1.4. Normal fetal growth in the third trimester may be assessed not only clinically but by ultrasonically measuring fetal parameters, such as head, abdomen and femur, then applying these measurements to either a graph or a fetal weight formula. Hadlock (1982) thought that a fetus can be defined as having normal growth if the head circumference (HC) / abdominal circumference (AC) ratio is 10 - 90%. Hadlock’s definition was confirmed by Deter (1982), Doubilet and Benson (1990) and Jeanty (2001) amongst others. A large fetus will have a head circumference (HC) to abdominal circumference (AC) ratio of greater than 90% whilst a fetus with macrosomia will show the AC > HC > 90% (Hadlock 1985). Schlater (1987) said that a difference between the head circumference and chest circumference of 1.6cms was an indicator of macrosomia but the clinical usefulness of this theory is questionable as the measurement has not been implemented into any routine ultrasound scanning protocols currently in use by Australian ultrasound centres. Fetal weight gain can be estimated by the difference in weight between two ultrasound examinations (Garrett & Robinson 1971, Ogata 1980, Gallivan 1993). Benson and Doubilet (1998) created fetal weight percentiles in the third trimester, with the resultant data showing mean fetal weight gain increases by approximately 240g per week until 37 weeks gestation, after which the rate of gain in a normally growing fetus gradually declines.
1.3Clinical Evaluation of Fetal Size and Growth
Physicians and midwives rely on physical examination of the pregnant woman to estimate fetal size by uterine palpation and measurement of the fundal height. This technique is made more difficult by large maternal body habitus and uterine fibroids or other pelvic masses, which can give a false indication of size, as well as amniotic fluid and the bulk of the placenta (Benson 1998). Multiple pregnancies are particularly difficult to evaluate (Benson 1987, MacGillivray 1978). Taylor and Pernoll (1976) described the fundal height, measured from the symphysis pubis, as one of the more reliable clinical examinations to assess fetal size with the height of the fundus in centimetres, being equivalent to the week of gestation from about 22 to 36 weeks. When estimating fetal size for mode of delivery one of the methods historically used for calculating fetal weight was Johnson’s formula, which could only be used if the fetus is in the vertex position:
Fetal weight (grams) = ( fundal height (cms) – n) x 155
If the head is above the ischial spines then n = 12 or, if head is below the ischial spines then n = 11. For patients over 90kg 1cm is subtracted from the fundal height prior to calculation. Although clinically irrelevant nowadays Pernoll (1987) claimed that this formula was accurate to within 375 grams in 75% of cases even though it did not make allowances for the fetus in breech or transverse lie.
Infant size can be related to maternal stature (Varner 1987, Hardy 1999) and Roher’s ponderal index (PI) is used to assess infant symmetry with a weight for length relationship at birth. The normal ponderal index is 1.8 at 28 weeks gestation, which increases by 0.05 per week to be 2.8 at 40 weeks gestation. An asymmetric infant will have a low PI if it is small for gestational age or a high PI if it is large for gestational age.
PI = birth weight x 100 / (crown-heel length)3
1.3.1Predictors and Consequences of Excessive Growth
Although the mean weight of Caucasian infants has remained relatively constant over the past ten years the rate of macrosomia births (greater than 4000g), according to Northern Sydney Health statistics (2003), is increasing with 10% of births with macrosomia in 1992, 14% in 2000 and over 15% in 2003. The Australian Bureau of Statistics Report (2003) shows this trend is reflected in other centers throughout Australia.
Catanzarite et al (1976) stressed the importance of antenatal fetal assessment, suggesting, like Taylor and Pernoll (1976) that fundal height measurements could give an indication of excessive growth. Catanzarite was in favour of fetal monitoring, where appropriate, with the aim of detecting those fetuses being compromised by the pregnant environment. Excessive fetal growth can often be associated with maternal profile with a high body mass index (>30), large stature, obesity, increased age, previous infant with macrosomia, postdatism and diagnosed diabetes or gestational diabetes being indicative of a pregnancy at risk of fetal overgrowth. Varner (1987) described some of these risk factors, giving rates of increased risk with maternal obesity for example having a 4 to 12 fold risk of an infant with macrosomia. Hardy (1999) assessed macrosomia predictors amongst a multiethnic group, concluding that the women’s non-pregnant body mass index followed by blood glucose levels could be used to identify the pregnancies at risk of macrosomia. Varner (1987) maintained that between 28% and 53% of fetal macrosoma can be identified by a thorough clinical history and physical examination of the mother and also suggested that birth weight correlated more closely with maternal stature rather than maternal weight. Schlater (1987) disagreed with this, believing that diagnosing fetal macrosomia by abdominal palpation to be “notoriously inaccurate”. If excessive fetal growth is identified then appropriate action can be taken to lessen the risks to both the mother and baby during birth. The consequences of excessive growth can be divided into maternal, fetal and neonatal risks.
1.3.2Maternal Risks
The risk to the mother with a large for gestation (LFG) infant include postpartum haemorrhage, reproductive tract injury, perineal injury with vaginal delivery and the risks of an emergency caesarean section and postpartum hysterectomy (Bhatia et al 1987). Failure to progress in labour is a precursor for fetal distress and emergency caesarean section (Varner 1987). Pre-eclampsia tends to occur in the second half of pregnancy and is a condition combining hypertension, edema and proteinuria which, according to Mabie and Sibai (1987), affects up to eight percent of all pregnancies and accounts for nearly 20% of maternal deaths (McDonald 1978). The risk of a subsequent large baby is up to four times greater (Varner 1987) and so it is important to check for latent gestational diabetes mellitus in the early second trimester (Crowther et al 2005). Post partum haemorrhage (PPH), defined by Kapernick (1987) and Novy (1982) as blood loss greater than 500ml following vaginal delivery, occurs in up to 8% of vaginal deliveries and is directly responsible for approximately 16% of maternal deaths. PPH may be caused by an atonic uterus due amongst other things, to over distension, lacerations or episiotomy from delivery of a large baby, coagulation problems or retained placental tissue. Episiotomies and lacerations account for 20% of PPH cases, the atonic uterus is responsible for 50% of PPH cases and retained placenta 5-10% (Kapernick 1987). PPH may occur up to six weeks post delivery and this influenced Lee et al (1981) to assess the postpartum uterus with ultrasound to detect any retained products of conception such as placental remnants. Placental abnormalities can increase the likelihood of PPH. One such abnormality is placenta accreta, which can be assessed with ultrasound, which is where the placenta adheres directly to the myometrium instead of being separated by a layer of deciduas (Tabsh 1982, Pasto 1983). Placenta accreta may be present in as many as 1 in 2000 births. In Australia PPH is responsible for amaternal mortality of 1:100,000 births (National Health Statistics 1998)and for significant morbidity, including the need for transfusion and/or postpartum hysterectomy with further associated risks.
1.3.3Fetal Complications
The higher the fetal weight the higher the incidence of birth complications (Jung 1997 & Hod 1998). Excessive fetal growth results in increased perinatal morbidity and mortality due to delayed progress in labour, traumatic vaginal deliveries, which are up to 23% of all macrosomia births, and emergency caesarean section (Dunsted et al 1985). The problems of difficult labour due to the large fetus may cause fetal complications including the risk of still-birth, increased incidence of birth injuries such as shoulder dystocia, fractures, facial palsy and birth asphyxia leading to cerebral palsy and mental retardation (Schlater 1987). Excessive uterine distension due to a large fetus can be a predisposing factor to placental abruption (Schlater 1987), which, as mentioned earlier, occurs in up to 1 in 89 of deliveries with fetal death occurring in 1 in 500 to 750 of deliveries (Pernoll 1987). Pulsed doppler assessment of the umbilical cord arteries can assist with identifying the macrosomic fetus that is continuing to grow (Trudinger (1991). The flow velocity waveforms from the umbilical cord arteries will display a high resistant pattern when the fetus ceases to grow. Golditch and Kirkman (1975) proposed that the large fetus could be managed by offering elective caesarean section. Gonik et al (1983) and Harris (1984) suggested maneuver techniques to assist with avoiding shoulder dystocia but even with the implementation of these ideas shoulder dystocia still occurs in up to 10% in cases of macrosomia. Varner (1987) surmises that males account for sixty percent of macrosomic births and that there is about 150 gram difference between the sexes for each week of gestation in late pregnancy.
1.3.4Neonatal Risks
Neonatal complications of excessive growth include low apgar score, birth injury, hypoglycemia, which increases the risk of neuro-behavioural problems (Bhatia and Sokol 1987), hypocalcaemia, polycythemia, jaundice, feeding difficulties and admission to neonatal intensive care unit.
1.4Macrosomia
The Oxford Medical Dictionary defines macrosomia as:
“ Macrosomia. n. abnormally large size. In fetal macrosomia a large baby is associated with poorly controlled maternal diabetes. The increased size is due to excessive production of fetal insulin and thence to increased deposition of glycogen in the fetus.”
Fetal macrosomia is a term used to describe fetuses that are greater than the 90th percentile on fetal growth charts, with babies that are born greater than 4000 grams in weight described as being macrosomic (Benson 1988, Hadlock 1989, Shah 1993). Macrosomia is a clinical problem that can lead to birth injury, intervention, postpartum haemorrhage and other adverse outcomes. Northern Sydney Area Health Statistics show that macrosomia births are increasing not only for Caucasians but for other ethnic groups. Although Rodrigues et al (2000) and Hadlock (1989) defined macrosomia as birth weight greater than the 90th percentile for gestational age, the actual weight at which macrosomia is called is debatable. Whilst some authors such as Modanlou, Dorchester et al (1980), Boyd and Usher (1983) and Varner (1987) defined macrosomia as birth weight greater than or equal to 4500 grams others such as Schlater (1987), Bhatia, Sokol, Pernoll (1987), Wollschlaeger et al (1999), Parry et al (2000), Chauhan et al (2000), Hadlock (1992) and Benson and Doubilet (1998) called it a weight of 4000 grams and above. Rouse and Owen (1999) used both a 4000 gram and 4500 gram cut off to study prophylactic caesarean delivery for fetal macrosomia determined by ultrasonic weight estimation. Neither weight cut off made a difference to the results due to the inaccuracy of the weight estimations. Hadlock (1988) and Jeanty (2001) claimed that the limitations of estimating fetal weight include the difficulty in obtaining ultrasonic images at the correct imaging plane for measuring the abdominal circumference. Benson and Doubilet (1998) agreed with Hadlock and went further by saying that in the diabetic pregnancy, weight formulas using a combination of head, abdomen and femur have a 95% confidence range of plus/minus 24%. More importantly, according to Hadlock (1984), fetal weight charts are usually based on fetuses with normal body proportions whilst fetuses with macrosomia have an increase in body fat and thus there is a tendency to over estimate weight by up to 4%. This was in agreement with Bernstein et al (1992), who concluded that fetal fat influenced the ultrasound estimation of fetal weight in diabetic mothers. What was not taken into account in all of these studies was ethnicity, maternal stature and genetics which can strongly influence fetal size and birth weight (Brooke 1981, Wan & Woo 1984,Wilcox et al 1993, Lai & Yeo 1995, de Jong 1998). Whilst a birth weight of 4000 grams may be called macrosomic in one population, the potential birth complications due to macrosomia may be present at a lower birth weight in a population with smaller maternal stature.