20 Intrauterine Resuscitation. Handbook CTG

Intrauterine Resuscitation

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Abigail Spring and Edwin Chandraharan

Handbook of CTG Interpretation: From Patterns to Physiology, ed. Edwin Chandraharan.

Published by Cambridge University Press. © Cambridge University Press 2017.

Key Facts

Intrauterine resuscitation is easy to perform and can result in a significant

improvement in the in-utero fetal condition.

The reversal of fetal hypoxia and acidosis may allow labour to continue safely

or optimize the fetal condition/well-being until urgent delivery is accomplished.

If not corrected, it may result in fetal decompensation leading to hypoxic injury.

Oxygen delivery to the fetus is dependent on:

Uterine oxygen delivery: maternal haemoglobin, oxygen saturation and

perfusion pressure, maternal position.

Utero-placental circulation: uterine activity (frequency, duration and

strength of contractions), size of ‘placental pools’.

Transfer of oxygen to the fetus: cord compression, cord prolapse.

Fetal circulation: high fetal haemoglobin concentration, fetal cardiac output

highly dependent on fetal heart rate (FHR).Key Features on the CTG Trace

Key Pathophysiology behind Patterns Seen on

the CTG Trace

‘Fetal distress’ is a nonspecific term used to describe concerns on the CTG

trace, and therefore, clinicians should instead use the term ‘suspected fetal

compromise’.

Decelerations – these may be early, variable, late or prolonged (>3 minutes).

Fetal bradycardia (<110 bpm persisting for >10 minutes).

Uterine hyperstimulation (increased frequency, strength or duration of

contractions associated with CTG changes).

Loss of baseline variability with preceding decelerations and rise in baseline

FHR.

Variable decelerations – repeated umbilical cord compression with each

contraction resulting in fetal systemic hypertension mediated through

baroreceptors.

Late decelerations – ongoing utero-placental insufficiency mediated through

chemoreceptors that respond to acidosis and increased carbon dioxide

concentration.

Prolonged declarations – maternal hypotension, uterine hyperstimulation

(hypertonus) often in response to oxytocin (Figure 20.1), sustained umbilical

cord compression or cord prolapse.Figure 20.1 Uterine hypertonus after the administration of oxytocin, which is relieved after

stopping oxytocin infusion and administration of terbutaline.

Recommended Management

Oxygen: High-flow oxygen administration via a non-rebreathe mask will

increase maternal oxygen saturation and partial pressure, thus increasing fetal

oxygenation. However, this is only recommended in patients with reduced

maternal oxygen saturation level (e.g. maternal cardiac arrest or maternal

hypovolumia secondary to massive placental abruption) as routine

administration of oxygen may be even harmful due to vasoconstriction of the

placental bed secondary to increased oxygen tension, especially in a growthrestricted fetus.

Fluid: One litre rapid intravenous infusion (unless fluid

restricted/contraindicated, i.e. preeclampsia), even if the woman is not

hypovolemic, will improve venous return and cardiac output and, therefore,

uterine blood flow. Fluid infusion may also help dilute oxytocin in cases of

uterine hyperstimulation.

Maternal repositioning: A change in maternal position, for example, left lateral,

may relieve aortocaval compression and cardiac output.

Stop oxytocics (i.e. syntocinon) and consider administration of tocolytics (e.g.

terbutaline 0.25 mg subcutaneously) if there is evidence of hyperstimulation –Key Tips to Optimize Outcome

Pitfalls

this will improve utero-placental perfusion and reduce cord compression

through uterine relaxation. Similarly, if prostaglandins are administered to

induce labour, this must be removed immediately and tocolytics should be

administered if there is no further improvement in the CTG trace.

Vasopressors (e.g. adrenaline) if maternal hypotension occurs secondary to

maternal collapse – this may be considered to restore cardiac output and

maternal BP.

A combination of interventions may be of a greater benefit.

Ensure continuous reassessment – after each intervention, it is important to

observe for subsequent improvement in the CTG trace including a reduction in

decelerations, a fall in baseline heart rate and improvement in baseline

variability or, in cases of prolonged deceleration, recovery to normal baseline

heart rate.

Assess progress of labour and the ‘wider clinical picture’ after improvement in

the CTG trace to determine whether continuation of labour is appropriate.

In chronic hypoxia or umbilical cord prolapse, if a delay in delivery is

anticipated (e.g. operating theatre being busy), tocolysis may help reduce

hypoxic stress by abolishing uterine contractions until urgent delivery is

accomplished.

If atonic postpartum haemorrhage (PPH) is not responding to standard oxytocics

after administration of terbutaline to relax the myometrium, propranolol 1 mg

intravenously should be considered to reverse the effects of terbutaline after

delivery in cases of refractory PPH not responding to standard oxytocic drugs.Consequences of Mismanagement

Exercise

1. A 29-year-old primigravida presented with spontaneous early labour at 39 + 4 weeks

of gestation. She was commenced on oxytocin at 5 cm dilation for failure to progress.

One hour later, her CTG trace (Figure 20.2) shows the following features.

Figure 20.2

Change in maternal position can, in some cases, result in worsening of cord

compression; thus, further positions should be tried including the right lateral or

knee-elbow position.

Use of tocolysis to reduce uterine activity and to improve fetal condition may

induce maternal tachycardia and hypotension (glyceryl trinitrate is not licenced

as an acute tocolytic agent).

A tocolytic may additionally predispose to atonic PPH during caesarean section

if immediate delivery is accomplished.

Worsening intrapartum hypoxic stress leading to hypoxic-ischaemic

encephalopathy and perinatal death.

Unnecessary operative interventions due to ‘CTG abnormalities’ secondary to

uterine hyperstimulation, which is a correctable cause.a. What is your diagnosis?

Two hours later, the CTG trace shows the following features (Figure 20.3).

Figure 20.3

b. What is your diagnosis?

c. What action will you take?

ObGyncases (Healthcare Touch)

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