Umbilical Cord Compression

Umbilical cord compression is squeezing of the cord between the fetus and the uterine wall, the pelvis or the cord itself, which cuts blood flow and oxygen to the fetus. Causes include oligohydramnios, nuchal cord, true knot, short cord, cord presentation, cord prolapse and strong contractions. It is the commonest cause of variable decelerations in labour. It matters because brief compression is harmless, while prolonged or repeated compression causes fetal hypoxia and acidosis.

• Risk factors: oligohydramnios, membrane rupture, long cord, malpresentation, multiple pregnancy, oxytocin hyperstimulation.
• The cord vein is compressed first, causing a rise in fetal heart rate, then the arteries, causing the deceleration.
• Most compression resolves with a change of position.

Women have no symptoms in labour, and the sign is on the fetal heart tracing. Late in pregnancy, reduced fetal movements may be the only warning.

• Heart rate falls abruptly with contractions and recovers quickly in mild cases.
• Meconium stained liquor with decelerations suggests hypoxia.
• Differential diagnosis: head compression, placental insufficiency, uterine hyperstimulation, abruption, uterine rupture, maternal hypotension, cord prolapse.
• Complications: fetal hypoxia, acidosis, low Apgar score, hypoxic ischaemic encephalopathy, emergency caesarean section, stillbirth, neonatal death.

The approach is to recognise the pattern on cardiotocography and to find the cause.

• Variable decelerations: abrupt fall of 15 beats per minute or more, lasting 15 seconds to 2 minutes, with changing shape and timing.
• Atypical features: slow return to baseline, loss of the early rise, overshoot, rising baseline, reduced variability, which suggest hypoxia.
• Vaginal examination for cord prolapse or presentation; ultrasound for amniotic fluid index and cord position; fetal scalp lactate where available (above 4.8 mmol/L is abnormal).
• Where cardiotocography is unavailable, listen to the fetal heart for 1 minute after every contraction in labour with a Pinard or hand-held Doppler.

The principle is to relieve pressure on the cord, correct reversible causes and deliver quickly if the tracing is pathological.

• Supportive: change maternal position to left or right lateral, or knee chest if the cord is prolapsed; stop oxytocin; oxygen 10 L/minute by mask while preparing for delivery; two cannulae; empty the bladder; continuous monitoring.
• Pharmacological: Ringer's lactate 500 to 1000 mL IV over 15 to 30 minutes; terbutaline 0.25 mg subcutaneous once for hyperstimulation; ephedrine 5 to 10 mg IV for hypotension after epidural; cefazolin 2 g IV before caesarean section; oxytocin 10 IU IM at birth.
• Procedures: amnioinfusion with sodium chloride 0.9 percent 500 mL intrauterine over 30 minutes then 3 mL per minute for repeated variable decelerations with oligohydramnios; assisted vaginal delivery when fully dilated; caesarean section aiming for birth within 30 minutes of the decision for persisting pathological tracing, and within 15 minutes for bradycardia or cord prolapse.
• Red flags: bradycardia below 100 beats per minute for 3 minutes, absent variability, cord felt in the vagina, thick meconium, maternal collapse.
• Follow-up: umbilical cord blood gas at birth; newborn Apgar score and neurological examination; observation for 24 hours, or 72 hours if depressed at birth.