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Monitoring the fetus (normal and abnormal) “In Utero” |
updated 13 May 1999 |
Keywords
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The concept of fetal welfare. Normal growth Normal fetal growth and development is an integral part of successful pregnancy. During pregnancy fetal well being is assumed to be present if growth is normal and there is no evidence of altered fetal activity or behaviour. The factors responsible for normal fetal growth include both the genetic or biological potential of that individual and a number of modulating or regulating influences. However growth failure or constraint is rarely due to an absence of these influences. Far more commonly it is the result of failure of oxygen and nutrient supply as a result of vascular disease of the placenta or uteroplacental bed. The concept of fetal well being is to be distinguished from fetal normality. The latter implies biochemical metabolic or structural abnormality. The abnormal fetus may fail to grow normally. Most commonly this is the result of interference with the biological potential rather than vascular disease developing as the pregnancy progresses. Loss of Fetal Welfare. Fetal Compromise. Intrauterine Growth Restriction. Some neonates are small because they are born prematurely but others are small because of growth failure. Fetal growth failure (intrauterine growth restriction {IUGR}) may be associated with stillbirth and asphyxia. The term small for gestational age (SGA) identifies this phenomena when birthweight is in the lowest tenth centile for gestational age. Sustained fetal growth depends upon an adequate supply of oxygen and nutrients. IUGR develops when the needs of the fetus exceed the capacity of the placenta to supply. Whilst growth failure may be associated with fetal morbidity it can be regarded as an adaptive response to conserve vital nutrients and oxygen for essential metabolic processes The adverse factors restricting growth vary in severity. The most complete or severe restriction may result in fetal demise almost before there is time to recognise growth failure. It is important to recognise the fetus in whom growth is diminished, not simply because it may be born small but because of the other risks associated with oxygen and nutrient deprivation. A spectrum of perinatal morbidity is observed depending upon the duration and severity of the nutrient restriction. Manifestations may be seen in the antenatal period, in labour, in the early neonatal period, and later in childhood. Intrauterine fetal death may occur; studies of unexplained stillbirths reveal a large proportion to be small for dates. In labour, fetal distress and perinatal asphyxia are common. In the neonatal nursery the problems of hypoglycaemia, renal failure, and necrotising enterocolitis may all be seen, in addition to hypoxic ischaemic encephalopathy secondary to asphyxia. Polycythemia, thrombocytopenia, and hypocalcaemia are observed with increased frequency in IUGR infants. Long term development assessment in childhood indicates that the possibility of neurodevelopmental deficit is especially great in the premature infant that is also small for gestational age. Follow-up studies have shown that the risk of neurologic deficit is greater, the earlier the onset of growth retardation and the greater the immaturity at birth. The small infant born at term appears to have little risk of poor neurologic outcome in the absence of hypoxemia. Catch-up growth in the first year of life also correlates with good outcome. Clinical recognition of Fetal Growth Restriction Since the fetus in whom growth is restricted experiences increased rates of complications recognition is important. Information from the clinical history and physical examination is used to identify the fetus at risk. The clinical situations associated with a high risk are identified in the history. They are tabulated. Clinical Situations Associated with High Risk of IUGR
On physical examination measurement of the symphysis fundal height aids identification of the potentially small fetus. Tests of Fetal Welfare Doppler umbilical flow studies. This most recent addition to the cupboard of fetal welfare tests performs best as a screen for potential fetal compromise. Recording flow velocity waveforms from the umbilical artery is relatively simple. Analysis using indices such as the systolic/diastolic ratio allows recognition of the flow waveform pattern associated with an increase in flow resistance downstream (i.e. the umbilical placental circulation). A vascular lesion in the placenta is present in such patients and this may be described as umbilical placental insufficiency. It is believe that this placental lesion precedes the fetal effect - loss of fetal welfare. Abnormality in this study occurs before disturbance in ultrasound growth or FHR monitoring. Ultrasound imaging and measurement. Femur length, biparietal diameter, and abdominal circumference are commonly measured to assess fetal growth. The measures of abdominal circumference provide the best index to fetal weight. Various formulae have been derived to estimate fetal weight although there is no evidence that such estimates are superior to the plotting of individual values. Serial studies are necessary for the use of ultrasound to assess growth. An interval of two weeks between successive studies is necessary to look for growth. A single study should not be over-interpreted. Important additional ultrasound information is available. Fetal anomaly needs to be excluded. Assessment of amniotic fluid volume is most valuable. The placenta may be examined for evidence of infarction. Biophysical profile. This is a simple scoring system which combines a number of parameters of fetal welfare. An assessment of fetal tone, limb movements and breathing movements is combined with amniotic fluid volume and FHR reactivity in this index. More recent examination of this index has indicated that if the first four parameters are normal, then FHR monitoring results add no further discrimination. Poor fetal condition at birth correlates with a low score. This system or combination of some of these indices is widely used as the secondary screen of fetal welfare once a clinical risk has been detected. Fetal heart rate monitoring. This is the continuous beat by beat recording of the actual fetal heart rate. A normal fetal heart rate (FHR) tracing varies between 120 and 160 b.p.m. It shows variability due to the moment to moment adjustments in rate by the various CNS controllers of heart rate. It shows reactions or accelerations in heart rate with fetal movement. A normal reactive trace indicates fetal health. It may certainly be seen in association with a fetus subsequently delivered small for gestational age (in one study 80 percent of fetuses subsequently born SGA had normal FHR tracings). In such fetuses, failure of growth may be seen as an adaptation by the intact fetus to a restriction on supply of oxygen or nutrients. A fundamental difficulty with FHR monitoring interpretation is the distinction of the sleeping fetus from the flat tracing seen in situations of fetal hypoxaemia. Reduced variability may indicate rest activity cycles dominated by phases of inactivity. Pharmacological depression of FHR variability may also occur. Monitoring for prolonged periods may be necessary to clarify this. The most severe grade of FHR abnormality is the terminal tracing in which absent FHR variability is combined with decelerations in the actual FHR in association with uterine contractions. Such tracings indicate that fetal hypoxaemia and acidaemia is likely and fetal demise is possible. Recommended and Optional Readings and ResourcesSee reading list |
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Author/s: Prof Brian Trudinger, Dept of Obstetrics & Gynaecology, Westmead Hospital |