29 Role of the Anaesthetist in the Management of Fetal Compromise during Labour. Handbook CTG

 29

Role of the Anaesthetist in the

Management of Fetal Compromise

during Labour

◈

Anuji Amarasekara and Anthony Addei

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

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

Fetal asphyxia leads to fetal compromise, which, if not corrected or circumvented, will

result in decompensation of physiologic responses (primarily redistribution of blood

flow to preserve oxygenation of vital organs) and cause permanent central nervous

system damage and other damage or death.

Key Facts

Anaesthetists participate directly and indirectly in the management of fetal

compromise during labour.

Fetal well-being can be assessed during high-risk labour by electronic FHR

monitoring using a CTG to monitor changes in FHR.

Decelerations and fetal bradycardia have been described after all types of

effective labour analgesia (epidural, spinal and combined spinal epidural, and

intravenous opioids).Key Pathophysiology

More dramatic hypoxia-inducing events include placental abruption, cord

prolapse and antepartum or intrapartum (fetal) haemorrhage.

All these may lead to fetal compromise and may necessitate emergency delivery.

Regardless of the aetiology of FHR abnormalities, it is important to manage

these changes correctly when they occur.

Obstetric cases account for 0.8 per cent of general anaesthetics in the Fifth

National Audit Project (NAP5) on Accidental Awareness during General

Anaesthesia (AAGA) Activity Survey. However, obstetric cases account for

approximately 10 per cent of reports of AAGA, making it the most markedly

overrepresented of all surgical specialties.

Reduction in oxygen delivery to the fetus is associated with fetal compromise.

Metabolic acidosis results from persistent hypoxia via anaerobic

metabolism and production of lactic acid.

Oxygen delivery to the fetus is dependent on maternal circulation, placental

transfer and fetal circulation.

Uterine oxygen delivery = uterine blood flow × arterial oxygen content. Uterine

blood flow is determined by perfusion pressure (arterial – venous pressure) and

resistance.

Aortocaval compression occurs when the pregnant uterus compresses the

inferior vena cava and descending aorta within the abdomen. This can result in

reduced blood flow to the utero-placental unit and maternal hypotension. The

effect is maximal in supine position.

In labour, intrauterine pressure increases during contractions. Initially the uterine

veins become compressed, and intervillous blood volume increases until

intrauterine pressure is sufficient to stop arterial flow.

Placental oxygen transport occurs along a gradient from maternal to fetal blood.The method of anaesthesia may affect neonatal outcome by transplacental drug

transfer and by influencing maternal haemodynamics and hence placental perfusion.

Intrauterine fetal resuscitation (IUFR) can result in significant improvements in the

condition of the fetus.

Recommended Management

Fetal haemoglobin (HbF) has a higher affinity for oxygen than adult

haemoglobin. The fetus also has higher haemoglobin, 16.5 g/dL (range, 15–18.6

g/dL), which helps to ensure adequate oxygen content.

Oxygen carriage to vital organs of the fetus is also dependent on fetal cardiac

output and adequate umbilical circulation. Fetal stroke volume is relatively

fixed, and FHR is the major determinant of cardiac output.

Occlusion of the umbilical cord will restrict delivery of oxygenated blood to the

fetus via the umbilical vein.

Rapid, coordinated, multidisciplinary approach is vital to minimizing fetal

compromise that can lead to permanent damage to the baby.

The anaesthetist has a role in assessing the mother quickly and initiating or

continuing resuscitation as required.

The goal of IUFR is to optimize the fetal condition in utero so that labour may

continue safely or to improve fetal well-being prior to emergency delivery.

IUFR consists of simple (SPOILT) steps:

Syntocinon: Stop syntocinon infusion to reduce the intensity and frequency

of uterine contractions, leading to improved placental perfusion.

Position: Left lateral position of the mother to relieve aortocaval

compression and improve venous return and placental perfusion.

Oxygen: High-flow oxygen with Hudson mask and reservoir bag to increase

maternal oxygen saturation (e.g. in cases of maternal collapse and maternal

hypoxia).Key Issues

Key Tips to Optimize Outcome

IV fluids: Rapid fluid infusion to restore maternal vascular volume. This

may also help to dilute oxytocin in blood in cases of uterine

hyperstimulation.

Low BP: Vasopressor (phenylephrine 50 μg – 100 μg increments; or

ephedrine 3 mg – 6 mg increments) if low maternal blood pressure.

Tocolytics should be used to provide uterine relaxation to improve

placental oxygenation if there is evidence of uterine hyperstimulation.

In cases of significant fetal compromise unresponsive to IUFR, or which show

only a transient response, early delivery of the fetus may be indicated. Delivery

by a ‘category 1’ caesarean section may be required.

The decision as to the method of anaesthesia is a balance between degree of

urgency and level of concern about maternal risks of general anaesthesia. In

cases of imminent fetal demise, delays may become clinically significant.

A controversial case series describing ‘rapid sequence spinal anaesthesia’ as an

alternative to general anaesthesia for urgent caesarean section has been

published.

Good communication helps to identify and prepare a plan for at-risk patients on

the labour ward who may become an emergency. This may make the difference

between the possibility of planned, timely regional anaesthesia and emergency

general anaesthetic.

Obstetric anaesthesia is regarded as a high-risk subspecialty for AAGA.

Undue haste in situations that are not true emergencies may cause maternal

and/or fetal harm due to anaesthesia and surgical complications.The use of IUFR is based on an understanding of maternal physiology, oxygen

transfer, effects of uterine contractions and evidence from numerous publications

in literature.

Variable decelerations may result from cord compression. Relief of such

compression may be achieved by trying several right or left lateral positions.

Avoid prolonged maternal oxygen administration, which should only be

administered in cases of maternal hypoxia and maternal collapse.

Care must be taken to avoid fluid overload in fluid-restricted patients (e.g.

preeclampsia, cardiac disease).

Avoid tocolytics in antepartum haemorrhage and abruption.

Be prepared for increased blood loss from a relaxed uterus.

Electronic fetal monitoring should be restarted in theatre and maintained as long

as possible.

Avoid maternal hypotension.

Uterine blood flow is not subject to autoregulation. Uterine perfusion is

therefore correlated with blood pressure. A maternal pressure fall >20 per

cent of baseline systolic figure will produce a substantial reduction in

uterine perfusion. This will aggravate any acute intrapartum fetal

compromise. Thorough evaluation, fluid preloading, patient positioning and

drugs can minimize the incidence and degree of hypotension after

sympathetic blockage from a spinal or epidural anaesthetic, but it may

occur even under the best circumstances. The anaesthetic management can

be challenging when acute intrapartum fetal compromise is superimposed

on chronic or preexisting fetal compromise. Underlying chronic fetal

compromise may be secondary to preeclampsia, hypertension, postmaturity

or diabetes. These disorders reduce fetal reserve and the ability to

successfully mount a compensatory response to intrapartum hypoxic stress.

It is important to avoid even mild hypotension in order to maintain uterine

blood flow and placental perfusion in such cases.Pitfalls

References

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2. Chandraharan E, Arulkumaran S. Prevention of birth asphyxia: responding appropriately to

cardiotocograph (CTG) traces. Best Pract Res Clin Obstet Gynaecol 2007;21(4):609–24.

3. Maharaj D. Intrapartum fetal resuscitation: a review. Int J Gynec Obstet 2007;9(2).

4. Weale NK, Kinsella SM. Intrauterine fetal resuscitation. Anaesth Intens Care Med

2007;8:282–5.

5. Kinsella SM, Girgirah K, Scrutton MJL. Rapid sequence spinal for category-1 urgency

caesarean section: a case series. Anaesthesia 2010;65:664–9.

6. Bogad D, Plaat F. Be wary of awareness – lessons from NAP5 for obstetric anaesthetists.

Int J Obstet Anesth 2015;24:1–4.

7. Simpson KR. Intrauterine resuscitation during labor: should maternal oxygen administration

Failure to change maternal position. (If fetal compromise persists, try right

lateral or knee-elbow position because umbilical cord compression rather than

aortocaval compression may be the cause).

Failure to restart FHR monitoring in theatre.

Routine oxygen administration to the mother.

Fetal oxygen saturation depends on placental perfusion rather than maternal

oxygen saturation. The promotion and restoration of adequate fetal oxygen

delivery should take the form of appropriate maternal positioning, reduction

of uterine activity and appropriate intravenous fluid and vasopressor

therapy to help ensure adequate uterine blood flow. Supplemental oxygen

should be used to improve maternal oxygen saturation as required.

Failure to communicate within a team may result in undue haste or delays.be a first-line measure? Semin Fetal Neonatal Med 2008;13(6):362–7.

8. Dyer RA, Schoeman LK. Fetal distress. In: Ginosar Y, Reynolds F, Halpern S, Weiner C,

editors. Anesthesia and the fetus. UK: Wiley Blackwell; 2013.

9. Fawole B, Hofmeyr GJ. Maternal oxygen administration for fetal distress. Cochrane

Database Syst Rev 2012;12:CD0000136.

10. Hamel MS, Anderson BL, Rouse DJ. Oxygen for intrauterine resuscitation: of unproved

benefit and potentially harmful. Am J Obstet Gynecol 2014; 211(2):124–7.