Fetal Distress

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. Gestational and antepartum factors can modify the fetal response to them.¹

Reduced liquor volume, maternal hypovolaemia and fetal growth restriction are known associations.

The overall risk of fetal distress (defined as need for prompt Caesarean delivery) was shown to be 3.1% in an unselected population.²
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.

Risk factors

Women with a history of:

• Stillbirth
• Intrauterine growth retardation
• Oligohydramnios or polyhydramnios
• Multiple pregnancy
• 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.^3,4

• Intrauterine growth retardation
• Raised vascular resistance (measured in umbilical artery by 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 mother's abdomen:
  • Normal range at term is 110-160 bpm.
  • Fetal bradychardia (<110 bpm) or tachycardia (>160 bpm) 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 urgent delivery required.⁵

Delivery within 30 minutes has become the standard for audit purposes, but it is rarely achieved and its clinical significance has been called to question.^6,7

See also Intrapartum Fetal Monitoring record.

• Signs of fetal distress require monitoring with a view to induction of labour.
• Continuing fetal distress during labour may indicate need for Caesarean section.⁸
• 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 section:⁹
  • This is an initial infusion of a 250-500 ml 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. It is not, however recommended by NICE.⁵
  • The potential adverse effects include umbilical cord prolapse, uterine scar rupture and amniotic fluid embolism.
  • It has also been used in pregnancies complicated by oligohydramnios, with similar positive outcomes.¹⁰