Consultation – Fetal Consultation – Fetal Distress in LabourDistress in Labour

Max Brinsmead PhD FRANZCOGMax Brinsmead PhD FRANZCOGMay 2015May 2015

You are the obstetrician on call for labour You are the obstetrician on call for labour ward when this CTG arrives by fax. ward when this CTG arrives by fax.

A CTG arrives from labour wardAnalyse and classify this CTGWhat is the degree of urgency that

requires your further evaluation of this patient

What further information do you requireAbout this patient?About the resources available to you

A CTG arrives from labour ward Baseline FHR

Possibly 140 bpm at the beginning and probably 150 at the end of this recording

Short term variability ≈ 5 bpm Within normal limits but not totally reassuring

There are no accelerations present Atypical variable decelerations

With most contractions, to a depth of 100 bpm with onset, nadir and recovery >20sec beyond the contractions and lasting up to 2 minutes

Tocographic evidence of excessive uterine activity

This is a pathological CTG (RCOG 2007 classification)

Further information required… Are there any risk factors

for fetal hypoxaemia Any other signs of fetal

distress The stage of labour The experience of the

person caring for this patient

Access to scalp sampling Access to theatre Paediatric resources

Further information required… Are there any risk factors

for fetal hypoxaemia Any other signs of fetal

distress The stage of labour The experience of the

person caring for this patient

Access to scalp sampling Access to theatre Paediatric resources

Nullipara at 41.5w undergoing induction of labour after a normal pregnancy

No liquor with attempted amniotomy. Oxytocin 12 mU/min

“3 cm dilated and 50% effaced”

In the care of a midwife No scalp sampling

available “Theatre doing an

orthopaedic case” Specialist paediatrician

on call. Level 2 nursery

List and discuss the causes of fetal heart rate decelerations Maternal hypotension Cord prolapse and

compression Uterine

hypercontractility Uteroplacental

insufficiency Maternal drugs Acute events Second stage labour

List and discuss the causes of fetal heart rate decelerations Maternal hypotension Can be caused by supine

position, epidural anaesthesia or drugs that lower BP

Correct by rolling the patient on her side and provide IV fluids by rapid infusion

Adrenergic agents are sometimes used by anaesthetists to correct spinal hypotension

List and discuss the causes of fetal heart rate decelerations Cord prolapse and

compression Cord prolapse occurs

with prematurity, high presenting part or malpresenation

Cord compression occurs with oligohydramnios +/- IUGR

May be recognised in its early stages by an acceleration deceleration-type CTG or variable decelerations

Immediate VE to exclude obvious cord presentation or prolapse is desirable

List and discuss the causes of fetal heart rate decelerations

Uterine hypercontractility Occurs in up to 40% of labours stimulated with oxytocin >12 mU/min

May be due to a high baseline tone, frequent or prolonged contractions

Is difficult to diagnose using external tocography

Takes up to 45 minutes to recover after cessation of oxytocin

Can also occur after vaginal or oral prostaglandins and spontaneously in a few multigravida

List and discuss the causes of fetal heart rate decelerations Uteroplacental insufficiency Usually associated with a

pregnancy at risk e.g. hypertension, small for dates, smoking, recurrent APH etc.

Classically causes late decelerations

May be compounded by cord compression with oligohydramnios

So severe variable decelerations or other CTG signs of fetal acidosis such as tachycardia or reduced short term variability may occur

List and discuss the causes of fetal heart rate decelerations Maternal drugs Sedative drugs and

narcotics cause reduced short term variability rather than decelerations

But a bolus of local anaesthetic reaching the fetal myocardium can cause bradycardia

And this can occur with paracervical block and sometimes epidural anaesthesia

List and discuss the causes of fetal heart rate decelerations Acute events e.g.

Placental abruption Uterine rupture Fetal haemorrhage Maternal collapse from

eclampsia, embolism, high spinal etc.

Usually associated with profound and prolonged bradycardia

Abruption usually associated with PV bleeding

Dark bleeding from vasa previa can be tested for fetal haemoglobin

Uterine rupture practically never occurs in a nulliparous patient

Maternal collapse usually self evident when priority should be given to maternal resuscitation

List and discuss the causes of fetal heart rate decelerations Second stage labour Decelerations are

common in the second stage of labour

Due to head compression +/- any contribution from cord entanglement & compression

The depth and width of decelerations, recovery after dips and nature of any interval CTG is helpful in assessment

Plus the clinical background – more likely to be significant in the fetus at risk

You assess this patient 12 min later. Oxytocin infusion has ceased. There is no improvement in the CTG. The midwife reports fresh meconium. What do you do next? Why?

Reassure the patient Quickly evaluate any

antenatal record that is available

Perform abdominal and vaginal examination

Attach a scalp clip Reassure the patient

You assess this patient 12 min later. Oxytocin infusion has ceased. There is no improvement in the CTG. The midwife reports fresh meconium. What do you do next? Why?

Reassure the patient Maternal anxiety reduces uterine perfusion

It is desirable to quickly establish rapport and cooperation with the patient

It is also desirable to strengthen team performance by “taking charge”

You assess this patient 12 min later. Oxytocin infusion has ceased. There is no improvement in the CTG. The midwife reports fresh meconium. What do you do next? Why?

Quickly evaluate the AN record (if possible)

• If all the information is readily available in a format familiar to you then you can quickly look for risk factors for fetal hypoxia

• Assists is interpreting the CTG and assessing fetal reserve

• Provides cues that may assist in patient communication or cooperation e.g. first name, age, status, history of sexual abuse etc.

• Any contraindication to scalp clip such as HIV?

You assess this patient 12 min later. Oxytocin infusion has ceased. There is no improvement in the CTG. The midwife reports fresh meconium. What do you do next? Why?

Perform abdominal and vaginal examination

Attach a scalp clip

• Requires removal of abdominal straps

• Exclude abruption, assess fetal size, position and how much head is palpable in the hope that immediate assisted delivery may be possible

• Exclude cord prolapse and presentation, assess stage of labour and how fast the process is going

• A scalp clip is the best method of FHR assessment

• And an acceleratory response to this trauma would be reassuring

No antenatal records available. Mother anxious but cooperative. Uterus NAD & relaxing. EFW average. Head 2/5 palpable, back to the left. Cx 4 cm & effaced. Head at spines -1, LOT. No FH response to scalp clip attachment. CTG deteriorating – wider deeper decelerations & variability <5 bpm

• What is the positive predictive value of this CTG for fetal acidosis

• What would be the optimal management of this patient

No antenatal records available. Mother anxious but cooperative. Uterus NAD & relaxing. EFW average. Head 2/5 palpable, back to the left. Cx 4 cm & effaced. Head at spines -1, LOT. No FH response to scalp clip attachment. CTG deteriorating – wider deeper decelerations & variability <5 bpm

• What is the positive predictive value of this CTG for fetal hypoxia

• What would be the optimal management of this patient

o With the exception of a pre terminal CTG this test has no better than ≈ 50% PPV for fetal hypoxia and acidosis

o Fetal scalp sampling for pH or lactate. Lactate requires a smaller blood sample, cheaper & more robust equipment & is less prone to interference from exposure to air

There are no facilities for scalp sampling. You cannot access a theatre for Caesarean for 45 – 60 minutes. List and discuss the pros and cons of the various options for intrauterine resuscitation that you may consider in the interim.

• Maternal oxygen administration

• Uterine tocolysis• IV Fluids• Betamimetic drugs• Nitroglycerin or Nifedipine

• Amnioinfusion

There are no facilities for scalp sampling. You cannot access a theatre for Caesarean for 45 – 60 minutes. List and discuss the pros and cons of the various options for intrauterine resuscitation that you may consider in the interim.

• Maternal oxygen administration

• Administration in short bursts (up to 10 min) has been shown by fetal oximetry to improve fetal oxygenation

• But animal studies suggest that it can be detrimental in the longer term because it causes uterine vasoconstriction

There are no facilities for scalp sampling. You cannot access a theatre for Caesarean for 45 – 60 minutes. List and discuss the pros and cons of the various options for intrauterine resuscitation that you may consider in the interim.

• Uterine tocolysis• IV Fluids• Betamimetic drugs• Nitroglycerin or Nifedipine

• The rapid IV infusion of 250 – 500 ml of crystalloid causes ≈ 20 min of uterine diastole. This can be useful esp. if maternal hypotension is contributing to reduced uterine perfusion

• RCTs of “intrauterine resuscitation” with betamimetics demonstrate improved neonatal outcomes without significant maternal risk

• Anecdotal reports suggest sublingual nitroglycerin and nifedepine can be similar

There are no facilities for scalp sampling. You cannot access a theatre for Caesarean for 45 – 60 minutes. List and discuss the pros and cons of the various options for intrauterine resuscitation that you may consider in the interim.

• Amnioinfusion • RCTs of amnioinfusion for meconium or suspected cord compression show improved CTGs, reduced rates of CS and improved neonatal outcomes

• But these are restricted to settings without standard peripartum surveillance

• No effect on overall perinatal mortality has been demonstrated

• And maternal risks remain incompletely explored

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