Title: Consultation
1Consultation Fetal Distress in Labour
- Max Brinsmead PhD FRANZCOG
- March 2010
2You are the obstetrician on call for labour ward
when this CTG arrives by fax.
3A CTG arrives from labour ward
- Analyse and classify this CTG
- What is the degree of urgency that requires your
further evaluation of this patient - What further information do you require
- About this patient?
- About the resources available to you
4A 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 gt20sec beyond the
contractions and lasting up to 2 minutes - Tocographic evidence of excessive uterine
activity - This is a pathological CTG (RCOG 2007
classification)
5Further 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
6Further 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
7List 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
8List and discuss the causes of fetal heart rate
decelerations
- 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
9List 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
10List and discuss the causes of fetal heart rate
decelerations
- Uterine hypercontractility
- Occurs in up to 40 of labours stimulated with
oxytocin gt12 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
11List 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
12List and discuss the causes of fetal heart rate
decelerations
- 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
13List 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
14List and discuss the causes of fetal heart rate
decelerations
- 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
15You 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
16You 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?
- 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
17You 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?
18You 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
19No 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 lt5 bpm
- What is the positive predictive value of this CTG
for fetal acidosis - What would be the optimal management of this
patient
20No 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 lt5 bpm
- What is the positive predictive value of this CTG
for fetal hypoxia - What would be the optimal management of this
patient
- With the exception of a pre terminal CTG this
test has no better than 50 PPV for fetal
hypoxia and acidosis - 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
21There 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
22There 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
23There 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
24There 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.
- 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