Antenatal assessment of fetal wellbeing
This includes tests which could be applied during the antenatal period to identify fetuses at risk of intrauterine hypoxia and death. Tests for biochemical assessment of placental function (measuring plasma HPL and oestriol) have been abandoned from clinical use, as they are poor predictors of fetal outcome.Measurements of fetal growth:
The most reliable indication of fetal well-being is normal growth.
Assessment of fetal size by abdominal palpation (is not to be undervalued, especially if the observations are made by one observer and carefully recorded).
The fundus-symphysis pubis height (is often measured, in centimeters, with a tape measure).
Repeated ultrasound examination of the biparietal diameter of the fetal head, the abdominal circumference and femur length.
Investigation of circulatory and other fetal responses:
Asking the mother to keep records of the fetal movements or kick counts.
Recording the fetal heart rate over a period of 20 minutes with a cardiotocograph (CTG). A normal fetus has periods of inactivity during which the heart rate shows little variation, and episodes of active movement, during which the heart rate shows increased beat-to-beat variation and accelerations. Uterine contractions of pregnancy may cause temporary slowing of the rate. A fetus that shows none of the normal variations in heart rate, or one that shows prolonged slowing of the heart rate with a uterine contraction, may be at risk of hypoxia. Antenatal CTG will continue to play an important part in the evaluation of fetal wellbeing.
Cardiotocography:
Antenatal CTG uses external (indirect) methods of monitoring the fetal heart rate. The interval between successive beats is measured allowing a continuous assessment of fetal heart rate.
The woman should be comfortable and in a left lateral or semi-recumbent position (avoiding compression of the maternal vena cava). An external ultrasound transducer for monitoring the fetal heart and a tocodynometer (stretch gauge) for recording uterine activity are secured overlying the uterus. Recordings are then made for at least 30 minutes, and the output from the CTG machine is conventionally an ink tracing of fetal heart rate and a second tracing of uterine activity.
Fetal cardiac physiology:
Fetal cardiac behaviour is regulated through sympathetic and parasympathetic signals and by vasomotor, chemoreceptor and baroreceptor mechanisms. Pathological events such as fetal hypoxia modify these signals and also fetal cardiac response.Fetal heart rate variability: under normal physiological conditions the interval between successive heart beats (beat-to-beat) varies. This is called "short-term variability" and increases with increasing gestational age. In addition to these beat-to-beat variations in heart rate, there are longer-term fluctuations in heart rate occuring between two to six times per minute. Normal baseline variability (10-25 bpm) reflects a normal fetal autonomic nervous system. As well as gestational age, baseline variability is modified by fetal sleep states and activity, and also by hypoxia, fetal infection, and drugs suppressing the fetal CNS, such as opioids, and hypnotics, all of which reduce baseline variability. Baseline variability is considered abnormal when it is less than 10 beats per minute.
Baseline fetal heart rate: fetal heart rate falls with advancing gestational age as a result of maturing fetal parasympathetic (vagal) tone. It is best determined over a period of 5-10 minutes. The normal FHR at term is 110-150 beats per minute (bpm), whilst prior to term 160 bpm is taken as the upper limit of normal. A rate lower than 110 bpm is termed a fetal bradycardia. Fetal bradycardia (<110bpm) can arise with any acute reduction in fetal oxygenation such as:
Cord compression. 2. Abruption. 3. Uterine hyperstimulation.
Fetal tachycardia (> 180bpm) can be due to:
Congenital tachycardia.
Maternal infection, maternal pyrexia (esp. secondary to chorioamnionitis).
Maternal tachycardia in thyrotoxicosis, or in response to pain.
Fetal infection.
Acute fetal hypoxia.
Fetal anaemia.
Drugs such as adrenoceptor agonist (ritodrine).
Fetal heart rate accelerations: these are increases in the baseline fetal heart rate of at least 15 bpm, lasting for at least 15 seconds. The presence of two or more accelerations on a 20-30 minute CTG defines a reactive trace. Normally they are a good sign of fetal health.
Fetal heart rate decelerations: these are transient reductions in fetal heart rate of 15 bpm or more, lasting for more than 15 seconds. Decelerations that occur in the presence of other abnormal features, such as reduced variability or baseline tachycardia, are more likely to reflect fetal hypoxia.
i.e. normal fetal heart : baseline rate 110-150 bpm, variability 10-25 bpm, two accelerations in 20 min., no decelerations.
3. Stress and non-stress Cardiotocography: performing an antenatal CTG with the mother positioned comfortably is called a non-stress test. Fetuses that demonstrate suboptimal non-stress CTG tracings may be subjected to contraction stress tests. These tests are carried out in the same way as non-stress tests except that an oxytocin infusion is administered intravenously to induce uterine contractions. A positive test result is fetal cardiac decelerations in response to uterine contractions, and is abnormal.
4. Biophysical profile:
Biophysical variable
normal (score 2)(in 30min)abnormal (score 0)(1n 30min)
Fetal breathing movements
>1 episode for 30sec
absent/ <30sec.
Gross body movements
>3body/limb movements
<3 movements
Fetal tone
>1 episode body/limb
extension followed by return
to flexion.
Slow, or absent extension-flexion
of body or limb
Reactive fetal heart rate
>2 accelerations with fetal movements
<2 accelerations, or 1+ decelaration
Qualitative amniotic fluid
>1 pool of fluid,
at least 1cm x 1cm.
Either no measurable pool,
or a pool <1cm x 1cm.
Doppler U/S: essentially, Doppler ultrasound is mainly employed to predict and monitor pregnancies at risk of pre-eclampsia and intrauterine growth restriction. It can involve simple assessment of the umbilical artery pulsatility index, which measures placental resistance to blood flow, or detailed assessment of arterial and venous blood flow within the fetus. Fetal Doppler studies provide the most accurate information on fetal oxygenation and cardiac function. The umbilical artery has been the most extensively studied vessel probably because signals can be obtained with inexpensive continuous wave Doppler equipment. Only by studying fetal vessels with the more expensive colour Doppler machines can important information on the fetal response to hypoxia be made. Waveforms from the umbilical artery provide information on feto-placental blood flow and should be performed on high-risk mothers (like mothers with hypertension, or where there is an SGA fetus). Normally diastolic flow in the umbilical artery increases (i.e. resistance falls) throughout gestation. Absent or reversed diastolic flow in the umbilical artery is a particularly serious development with a strong correlation with fetal distress and intrauterine death.
Falling oxygen levels in the fetus result in a redistribution of blood flow to protect the brain, heart, adrenals and spleen, and vasoconstriction in all other vessels. The middle cerebral artery will show increasing diastolic flow (falling PI) as hypoxia increases, while a rising resistance in the fetal aorta reflects compensatory vasoconstriction in the fetal body. When diastolic flow is absent in the fetal aorta, this implies fetal acidaemia.
When late diastolic flow is absent in the ductus venosus, then delivery should be considered, as fetal death is imminent.
Assay of hormones and enzymes to assess feto-placental function:
Measuring human placental lactogen and oestriol are now rarely performed.