Fetal Distress

The main cause of antepartum fetal distress is uteroplacental insufficiency.
Factors within labour are complex but processes such as uteroplacental vascular disease, reduced uterine perfusion, fetal sepsis, reduced fetal reserves, and cord compression can be involved alone or in combination, and gestational and antepartum factors can modify the fetal response¹. Reduced liquor volume, maternal hypovolaemia and fetal growth restriction are known associations.

Women with a history of:

• Stillbirth
• Intrauterine growth retardation
• Oligohydramnios or polyhydramnios
• Multiple pregnancies
• Rhesus sensitisation
• Hypertension
• Diabetes and other chronic diseases
• Decreased fetal movements
• Post-term pregnancy.

There is some evidence that maternal age over 35 years is an independent risk factor for uteroplacental insufficiency and fetal distress.^2,3

The overall risk of prompt Caesarean delivery for fetal distress was 3.1% in a recent paper⁴.
The risk exceeded 20% in patients with severe pre-eclampsia, post-term or fetal growth restricted fetuses with abnormal Doppler studies, moderate/severe asthma and severe hypothyroidism.

• Intrauterine growth retardation.
• Raised vascular resistance measured in umbilical artery on ultrasound.
• Fetal hypoxia or acidosis on fetal blood sampling during labour.

Antenatal

• Non-stress test - monitors fetal heart rate acceleration following fetal movement. Non-reactive result suggests fetal distress requiring further assessment.
• Contraction stress test - measures response of fetal heart rate to spontaneous or nipple /oxytocin -stimulated contraction. Late decelerations suggest fetal distress.
• Biophysical profile - measures fetal breathing and gross body movements, fetal tone and heart rate acceleration and amniotic fluid volume to develop a score.

During labour

• Continuous fetal heart rate monitoring - uses electrode attached to fetal scalp or detector on mothers abdomen:
  • Normal range at term is 110-160 bpm.
  • Fetal bradychardia (<110bpm) or tachycardia (> 160bpm) may be associated with hypoxia but several other factors can cause tachycardia, e.g. maternal pyrexia or dehydration.
  • Late decelerations, defined as uniform,repeated, periodic slowing of the fetal heart rate, whose onset is from mid to end of the contraction, with its nadir more than 20 seconds after the peak intensity of the contraction, suggest fetal hypoxia.
  • Fetal scalp blood monitoring:
    pH >7.25 repeat if CTG continues to deteriorate.
    pH 7.21-7.24 repeat in 30 mins.
    pH <7.20 aim for delivery within 30 minutes⁵.

Delivery within 30 minutes has become the standard for audit purposes, but it is rarely achieved⁶ and it's clinical significance has been called to question⁷.
See also Fetal Monitoring.

• Signs of fetal distress require monitoring with a view to induction of labour.
• Continuing fetal distress during labour may indicate need for Caesarean section⁸.
• Term or post-mature fetuses may produce meconium stained liquor. This can be detrimental to the fetal lungs by producing a chemical pneumonitis if inhaled.
• Amnio-infusion has been shown to be beneficial in this situation, with a reduced risk of Caesarean section⁹. This an initial infusion of a 250-500ml bolus of warmed normal saline, through a double lumen intrauterine pressure catheter. (Uterine pressure and fetal heart rate ( via scalp electrode) are monitored constantly.) It is thought to dilute meconium and reduce the risk of meconium aspiration. The potential adverse effects include umbilical cord prolapse, uterine scar rupture and amniotic fluid embolism.However it is not recommended by NICE¹⁰.
• It has also been used in pregnancies complicated by oligohydramnios, with similar positive outcomes¹¹.