MONITOREO FETAL INTRAPARTO CONSENSO FIGO 2015.pptx

2015 FIGO CONSENSUS GUIDELINES ON
INTRAPARTUM FETAL MONITORING
Safe Motherhood and Newborn Health Committee - FIGO
Coordination + texts: Diogo Ayres-de-Campos
Illustrations: Dimitri Santos
FIGO INTRAPARTUM FETAL
MONITORING COURSE

INTRODUCTION

FIGO
1985
IJOG 1987;25:159-67

• Wide consensus
• Common terminology, accessible
language
• Simple, objective, easy to remember
• Including management options
• Basis for research and progress
• Widespread clinical use
2015 FIGO
guidelines

• FIGO societies contacted to appoint
one subject matter expert
• RCOG and ACOG contacted to appoint
one co-author each for CTG chapter
• ICM invited to write the chapter on
intermittent auscultation

34 experts appointed by national societies
Daniel Surbek (Switzerland), Gabriela Caracostea (Romania), Yves
Jacquemyn (Belgium), Susana Santo (Portugal), Lennart Nordström
(Sweden), Vladas Gintautas (Lithuania), Tullia Todros (Italy), Branka Yli
(Norway), George Farmakidis (Greece), Sandor Valent (Hungary), Bruno
Carbonne (France), Kati Ojala (Finland), José Luis Bartha (Spain), Joscha
Reinhard (Germany), Anneke Kwee (Netherlands), Romano Byaruhanga
(Uganda), Ehigha Enabudoso (Nigeria), John Anthony (South Africa), Fadi
Mirza (Lebanon), Tak Yeung Leung (Hong Kong), Ramon Reyles
(Philipines), Park in Yang (South Korea), Henry Murray (Australia and
New Zealand), Yuen Tannirandorn (Thailand), Krishna Kumar (Malaysia),
Taghreed Alhaidari (Iraq), Tomoaki Ikeda (Japan), Ferdousi Begum
(Bangladesh), Jorge Carvajal (Chile), José Teppa (Venezuela), Renato Sá
(Brasil).

16 experts invited based on literature
search
Lawrence Devoe (USA), Gerard Visser (Netherlands), Richard Paul (USA),
Barry Schifrin (USA), Julian Parer (USA), Philip Steer (UK), Vincenzo
Berghella (USA), Isis Amer-Wahlin (Sweden), Susanna Timonen (Finland),
Austin Ugwumadu (UK), João Bernardes (Portugal), Justo Alonso
(Uruguay), Ingemar Ingemarson (Sweden), Sabaratnam Arulkumaran
(UK), Catherine Spong (USA), Edwin Chandraharan (UK).

• 3-round email consensus
• Agreement to be included in
panel
• No internal or external funding
• 10 months to prepare
• 18 months for the consensus

• Launched at the XXI FIGO World Congress
of Gynecology and Obstetrics in Vancouver
(Oct 2015)
• Published open access in the IJGO
(Oct 2015)
http://www.ijgo.org/issue/S0020-7292(15)X0017-8

Endorsed/supported by:

PHYSIOLOGY OF FETAL OXYGENATION
AND THE MAIN GOALS OF

Energy – aerobic metabolism
• glucose and O2
• CO2
• Maternal respiration
• Maternal circulation
• Placental perfusion
• Placental gas exchange
• Umbilical and fetal circulation

Reduced O2 concentration in arterial blood
Hypoxemia
Reduced O2 concentration in tissues
Hypoxia

Anaerobic metabolism
• limited time
• 19× less energy
• lactic acid

Metabolic acidosis (or acidemia)
 arterial pH due to intracellular
acids
• H+ of lactic acid is
transferred slowly across the
placenta

Circulating bases
buffer intracellular acids (H+)
• Bicarbonate
• Hemoglobin
• Plasma proteins
Metabolic acidosis can be
quantified by pH and base
deficit (depletion of buffers)

Metabolic acidosis
Arterial pH < 7.00 and BD >12
mmol/l
Arterial lactate > 10 mmol/l is an alternative
(reference values may vary according to device)

BDecf believed by some experts to be the
best representative of H+ concentration of
metabolic origin in the different fetal
compartments
BDblood slightly higher, can also be used

Carbonic acid
Reduction in arterial pH due to diminished
placental CO2 elimination and H+ accumulation
Respiratory acidemia
CO2 + H2O H2CO3 HCO3
- + H+
quickly reversible with re-establishment
of placental gas exchange → no injury
Bicarbonate

Metabolic acidosis (hypoxia)
Respiratory acidemia (↓ gas exchange)
Mixed acidosis
Metabolic component has the
greatest potential for harm, as it
indicates  cell oxygen and
energy

Umbilical cord blood gas analysis
Only objective way of quantifying
hypoxia/acidosis occurring just prior to birth
(or newborn circulation in first min of life)

• innocuous to the newborn
• relatively inexpensive
• enhances experience with monitoring
• important medical-legal value
Local guidelines and resources
Recommended in suspected fetal hypoxia/acidosis and/or
Apgars
Umbilical blood sampling

SAMPLING TECHNIQUE
• Unnecessary to clamp the cord
• Sampling as soon as possible after birth (< 15 min)
• 1-2 ml from artery and vein, heparinised syringes
• Remove air bubbles, cap syringes, roll with fingers
• Analysis within 30 min

Arterial blood reflects
fetal acid-base status
better than venous
important to obtain blood from
both artery and vein
vein
arteries

• Sampling of wrong vessel
• Mixed sampling
vein
arteries

Difference in pH < 0.02
Difference in pCO2 < 5 mm Hg (0.7 kPa)
Same vessel or mixed sampling
Arterial pH < vein pH
pCO2 < 22 mm Hg (2.9 kPa)
Contamination from vein or from air

Median art. pH = 7.25 (p5=7.06, p95=7.37)
Median art. BDecf = 2.8 (p5=-1.8, p95=10.0)
Median art. BDblood = 5.6 (p5=-0.28, p95=11.48)
TERM BIRTHS

When placental gas exchange is
preserved there is slow H+ transfer
Hyperventilation  fetal pH
Acidemia  fetal pH

Compromised
cell function
↓ pH + ↓ energy
production
Cell death
Organ damage
Death

depressed when hypoxia/acidosis is sufficiently
intense and prolonged to affect these systems
Apgar scores
Pulmonary, cardiovascular, neurological functions

Unaffected by minor
hypoxia/acidosis
Non-hypoxic causes::
• prematurity
• birth trauma
• infection
• meconium aspiration
• congenital anomalies
• pre-existing neurological lesions
• medication administered to the mother
• early endotracheal aspiration
Apgar scores

1-minute Apgar
• important to decide newborn resuscitation
• low association with intrapartum hypoxia
5-minute Apgar
• stronger association with short- and long-
term neurological outcome and neonatal
death

Metabolic acidosis and low Apgars
• Vast majority recover quickly
• Few are of sufficient intensity and duration to
cause death or long-term morbidity

Hypotonia: majority recover
Seizures: 20-30% have
sequelae
Coma: majority with sequelae
Hypoxic-ischemic encephalopathy
(HIE)
• Neurological changes in first 48 h
• Metabolic acidosis
• Other system dysfunctions may occur

Infection
Congenital diseases
Metabolic, coagulation disorders
Antepartum and post-natal hypoxia
Birth trauma
• 1-4 years
• Neurological complication more commonly
associated with term intrapartum hypoxia
• 80-90% NOT caused by intrapartum hypoxia
Cerebral palsy (spastic quadriplegic, dyskinetic )

Progressive
Hypoxemia
Progressive
Grade 1
Grade 2
Grade 3 CP
Transitory
Reversible
Normal oxygenation
Hypoxia
HIE
Fetal death

INTRAPARTUM EVENTS LEADING
TO FETAL HYPOXIA/ACIDOSIS

Reversible causes

Contractions compress myometrial vessels,
 placental perfusion and may compress the cord
The interval between contractions is
crucial to re-establish fetal oxygenation

•  oxytocin, removing PGs
• Acute tocolysis (salbutamol,
terbutaline, ritodrine, atosiban,
nitroglycerine)
• Push on alternate contractions
• Turn mother on her side
Excessive uterine activity
Maternal pushing aggravates the effect

Cord compression
Low-lying cord, cord knot, nuchal
cord
Oxygenation may
still recover
between
contractions

Maternal supine position
Aorto-caval compression by uterus
Turn mother on her side

Sudden maternal hypotension
Following epidural or spinal analgesia
Rapid fluid administration
Efedrine IV bolus

Irreversible causes

Major placental abruption
Blood loss,  gas exchange
Uterine rupture
Blood loss,  gas exchange
Umbilical cord prolapse
Cord compression

Fetal hemorrhage
Ruptured vasa praevia,
fetal-maternal hemorrhage
Expedite delivery

Maternal causes

Maternal cardio-respiratory
disfunction
Severe asthma, cardiorespiratory arrest,
thromboembolism, etc
Reversible nature?
Speed of recovery?

Mechanical complications

Shoulder dystocia, retention of the
head
Specific management

Avoid adverse fetal outcome related to
intrapartum hypoxia/acidosis
Avoid unnecessary intervention, associated
with increased maternal and fetal risks
Aims of intrapartum fetal monitoring

Fetal monitoring should
indicate intervention at an
early stage of
hypoxia/acidosis in order to
prevent adverse newborn
outcomes

In order to avoid adverse outcome,
fetal surveillance requires timely
clinical response, and the ready
availability of adequate equipment and
trained staff

1st BREAK

CARDIOTOCOGRAPHY

Cardiotocography (CTG)
(kardia=heart, tokos=labour)
…is the term that best
describes the continuous
monitoring of FHR and
uterine contractions

Supine recumbent position
Half-sitting, upright
Lateral recumbent
Prolonged monitoring in this
position should be avoided
(aorto-caval compression)
Tracing acquisition

(wireless)
Allows mother to move freely
Should be preferred when available
Telemetry

1cm/min
1, 2 or 3 cm/min
20 or 30
bpm/cm
Paper scales

Some experts feel that 1 cm/min provides
sufficient detail for clinical analysis, and
has the advantage of reducing tracing
length
Other experts feel that the small details are
better evaluated using higher papers speeds

The paper scale should be the one with which
healthcare professionals are most familiar
Inadvertent use of paper scales to which staff are
unaccustomed may lead to erroneous
interpretations
1 cm/min 3 cm/min

External FHR monitoring (Doppler US)

Spike removal

Signal
modulation

t
Autocorrelation

Provides an approximation to true FHR,
but sufficiently accurate for analysis
May not record arrhythmias

MHR monitoring
Double-counting
Half-counting
Artefacts (particularly during 2nd stage)

Internal FHR monitoring (ECG)
t

CONTRA-INDICATIONS
Active genital herpes
Seropositive hepatitis B, C, D and
E
Seropositive HIV
Suspected fetal blood disorders
If artificial ROM is inappropriate
Uncertainty about presenting part
Membranes ruptured
Clear identification of presenting part
Avoid delicate fetal structures
Preferably avoided < 32 weeks (unless there is no alternative)

External FHR is recommended for routine
monitoring, if quality is acceptable
Careful repositioning of probe in 2nd stage
In all atypical tracings exclude MHR
(auscultation, US, internal FHR)

Indications for internal FHR
Acceptable record not possible with external FHR
Suspected fetal cardiac arrythmia
… and no contra-indications

GUARD
RING
PRESSURE
SENSOR
increased myometrial tension measured through abdominal wall
External UC monitoring (Tocodynamometer)

• incorrect toco placement or displacement
• reduced tension on elastic band
• abdominal adiposity
… may lead to failed registration

Frequency of contractions
Intensity and duration
Basal intra-uterine pressure
YES
NO

Quantitative information on intensity and
duration of contractions and basal uterine tone
Internal UC monitoring (IUP)

Disposable catheter (expensive)
Requires ruptured membranes
Contra-indications: haemorrhage, low lying placenta
Small risk of fetal injury, placental haemorrhage, infection
Not recommended for routine clinical use

• Preferably with dual channel monitors
• Duplicate monitoring of same twin may occur (alarms)
• Some experts believe that the presenting twin should
preferably be monitored internally (signal quality)
Monitoring of twins

↑ 20
bpm

Should be considered,
if available and not causing discomfort
(especially in the 2nd stage when accelerations coincide
with contractions and/or the MHR is elevated)
Simultaneous MHR monitoring

Identification
Name, place
Paper speed, date and time of start and end
Part of patient record
Digital CTG archives
Secure file backup system
Tracings readily available for review
Tracing storage

• Basic CTG features
• Tracing classification
Tracing analysis

Mean level of the most horizontal and less oscillatory
FHR segments. Estimated in 10-min periods, expressed
in bpm
Baseline

Normal 110-160 bpm
Tachycardia
> 160 bpm for more than 10 min (pyrexia,
epidural, early stages of non-acute hypoxemia,
β agonist or parasympathetic drugs, arrhythmias)
Bradycardia < 110 bpm for more than 10 min
(hypothermia, beta-blockers and fetal arrhythmias)

Average bandwidth amplitude in 1-min
segments
Variability
1 min
120
125
115
Subjectivity in visual evaluation

Reduced
variability
< 5 bpm for more than 50 min in baseline
or more than 3 min in decelerations
• Hypoxia/acidosis of CNS, previous cerebral injury, infection, CNS
depressants or parasympathetic blockers

Increased
variability
(saltatory)
Bandwidth > 25 bpm for more than 30 min
• Incompletely understood
• Hypoxia/acidosis of rapid evolution

Abrupt increases in FHR above baseline, > 15 bpm
amplitude, > 15 secs
Accelerations
• Most coincide with fetal movements
• Reactive fetus without hypoxia/acidosis
150
130
140
120
>15 s
>15 bpm

Abrupt decreases in FHR below baseline, > 15 bpm
amplitude, > 15 secs
Decelerations
150
130
140
120
>15 s
>15 bpm

Early
decelerations
Shallow, short-lasting, with normal
variability and coincident with contractions
• Believed to be caused by fetal head compression
• Do not indicate fetal hypoxia/acidosis

Variable
decelerations
Rapid drop (onset-nadir in < 30 sec), rapid
recovery, good variability. Varying size,
shape and relation to uterine contractions
• Baroreceptor-mediated response to ↑ BP (cord compression)
• Seldom associated with important hypoxia/acidosis
• Majority of decelerations

Late
decelerations
Gradual onset and/or gradual return to
baseline, and/or reduced variability.
Onset > 20 sec after start of contraction, nadir
after acme and return to baseline after end
• Chemoreceptor-mediated response to hypoxemia
• With  variability and no accelerations, amplitude only > 10 bpm

Prolonged
deceleration
> 3 min
• Likely to include a chemoreceptor-mediated component
• If > 5 min,  variability, and FHR < 80 bpm  emergency intervention

• Severe anemia, acute hypoxia/acidosis, infection, cardiac
malformations, hydrocephalus, gastroschisis
Sinusoidal
pattern
Regular, smooth, undulating, resembling
sine wave. Amplitude 5-15 bpm, frequency
3-5 cycles/min, > 30 min, no accelerations

Pseudo-sinusoidal pattern
• Analgesic administration, fetal sucking and other mouth movements
Pseudo-
sinusoidal
pattern
Jagged “saw-tooth” appearance. Duration
seldom exceeds 30 min. Normal patterns
before and after

Tachysystole
> 5 contractions in 10 min in two successive
10-min periods, or averaged over 30 min.

Body
movements
Eye
movements
+ +
Active sleep
-
-
CTG
Deep sleep
+++ +
Active awakeness
• Cycling represents the hallmark of neurological responsiveness
• Transitions become clearer > 32-34 weeks
• Deep sleep may last 50 min
Behavioural states

Deep sleep Active sleep

Active awakeness (difficulty in baseline estimation)

Tracing classification
*Decelerations are repetitive when associated with > 50% contractions.
Absence of accelerations in labour is of uncertain significance.
Baseline
Variability
Decelerations
Interpretation
Clinical
Management
Normal
110-160 bpm
5-25 bpm
No repetitive*
decelerations
Suspicious
Lacking at least one
characteristic of
normality, but with
no pathological
features
Pathological
< 100 bpm
Reduced variability.
Increased variability.
Sinusoidal pattern.
Repetitive* late or prolonged
decelerations for > 30 min (or > 20
min if reduced variability).
Deceleration > 5 min
No
hypoxia/acidosis
No intervention
necessary to
improve fetal
oxygenation state
Low probability of
hypoxia/acidosis
Action to correct
reversible causes if
identified, close
monitoring, or
adjunctive methods
High probability of
hypoxia/acidosis
Immediate action to correct
reversible causes, adjunctive
methods or if this is not possible
expedite delivery.
In acute situations, immediate
delivery should be accomplished.

Clinical decision
• gestational age
• medication administered to the mother
• integrated with clinical information

Baseline 130 bpm
Accelerations
Non-repetitive decelerations
Normal variability
Case 1
Normal

Baseline 154 bpm
No accelerations
Non-repetitive decelerations
Normal variability
Normal
Case 2

Baseline 180 bpm
No accelerations
Repetitive late decelerations (> 30 min)
Reduced variability (> 50 min)
Pathological
Case 3

Baseline 140 bpm
No accelerations
Repetitive variable decels. (1 late+ prol)
Normal variability
Suspicious
Case 4

Baseline 148 bpm
Accelerations
Repetitive decelerations, one > 5 min
Reduced variability at the end
Case 5
Pathological

Baseline 130 bpm
Accelerations
Repetitive decels (not late/prolonged)
Normal variability
Case 6
Suspicious

Baseline 132 bpm
Acceleration
Deceleration > 5 min
Reduced variability in deceleration
Case 7
Pathological

Baseline 146 bpm
No accelerations
Repetitive variable decels (1 prolonged)
Normal variability
Case 8
Suspicious

Reversible causes
Excessive uterine activity ( oxytocics,
tocolysis)
Supine position (change maternal positions)
Sudden hypotension (fluids, ephedrine)
Irreversible causes
Uterine rupture
Major placental abruption
Umbilical cord prolapse
Maternal or mechanical complications
Fetal haemorrhage

Intravenous
salbutamol started

Limitations of CTG

Signal loss

MHR monitoring

CTG analysis is subject to considerable
intra- and interobserver disagreement
(decelerations, variability, suspicious-pathological)

High predictive
value for NO
hypoxia/acidosis
Low predictive
value for
hypoxia/acidosis
Limited predictive value of abnormal CTGs
BJOG 1993;100(suppl 9):4-7

Cochrane Database Syst Rev. 2013 May 31;5:CD006066
12 trials (circa 37,000 women)
↓ neonatal seizures (RR=0.50, 95%CI 0.31-0.80)
↑ c-sections (RR=1.66, 95%CI 1.30-2.13)
↑ instrumental deliveries (RR=1.16, 95%CI 1.01-1.32)
= perinatal mortality (RR=0.85, 95%CI 0.59-1.23)
= cerebral palsy (RR=1.20, 95%CI 0.52-2.79)
RCTs comparing CTG with IA

• Trials carried out > 25 years ago
• Different CTG monitor technologies
• Different interpretation guidelines
• Different experience with CTG
• Different use of adjunctive methods

The evidence for the benefits of CTG
when compared to IA is inconclusive
Difficult to establish how these RCTs
relate to current clinical practice

CTG monitoring should not be
regarded as a substitute for good
clinical observation and judgement,
or as an excuse for leaving the
mother unattended

2nd BREAK

INTERMITTENT AUSCULTATION

The technique of listening to the fetal
heart rate for short periods of time
without a display of the resulting
pattern

Pinard stethoscope
DeLee
stethoscope

Handheld Doppler
Power independent
with self-winding
power source
www.pet.org.za

• Recommended in all labours where
there is no access to CTG
• Where CTG is available, it may be
used in low-risk cases

Antepartum Intrapartum
• No serious health conditions
• No diabetes or pre-eclampsia
• No vaginal hemorrhage
• Normal fetal growth,
amniotic fluid and Doppler
• Normal antenatal CTGs
• No previous uterine scar
• Normal fetal movements
• No ROM> 24 hours
• Singleton, term, cephalic
• Normal UC frequency
• No induction/augmentation
• No epidural
• No abnormal hemorrhage
• No fresh or thick meconium
• No temp > 38ºC
• Active 1st stage < 12 h
• 2nd stage < 1 hour
• Clearly audible normal FHR
Required conditions

Advantages
• Promotes increased contact and support
• Facilitates assessment of other parameters
• Can be acquired in different
positions/locations
• Favours maternal mobility
• Easier availability and sustainability
• Variability is not adequately evaluated
• No independent confirmation/record
• More labour intensive
Disadvantages

Stethoscope Doppler
• Inexpensive
• Readily available
• No consumables needed
• Slow learning curve
• Difficult to identify
accelerations/decelerations
• Variability not evaluated
• May be difficult to use
in certain maternal positions
• More confortable for woman
• FHR audible to all present
• More confortable in certain
maternal positions
• Calculates and displays FHR
• Low variability suspected
• Costly to buy and maintain
• Sensor prone to damage
• May pick up the MHR

Technique
Identify fetal position by palpation
Simultaneous evaluation of
FHR (fetal back, “galloping sound”)
MHR (maternal pulse)
UC + fetal movements (hand in fundus)

MHR
UC + fetal
movements
FHR

Features to evaluate What to register
FHR
Duration: ≥ 60 secs
(for 3 UC if abormal)
FHR in bpm
Accelerations/decelerations
(presence or absence)
Timing: during and ≥ 30
secs after UC
Interval: Every 15 min in
active phase. Every 5 min
in 2nd stage
Uterine
contractions
Before and during IA (in
order to detect ≥ 2 UCs)
Frequency (in 10 min)
Fetal
movements
At the same time as UCs Presence or absence
MHR At the time as IA MHR in bpm

Baseline < 110 bpm or > 160 bpm
Decelerations
Presence of repetitive or prolonged
(>3 min) decelerations
Contractions More than 5 contractions in 10 mins
Abnormal findings
 Extend evaluation over 3 UC to confirm
 If CTG available  continuous CTG

FHR < 110 bpm for > 5 min  delivery
FHR >160 bpm for 3 UCs – assess for
possible causes of tachycardia
When CTG is not available
Repetitive decelerations – assess reversible
causes of hypoxia, if no effect  delivery

ADJUCTIVE TECHNOLOGIES

Adjunctive technologies are aimed at
reducing false-positives with CTG and
the resulting unnecessary
intervention

• Fetal blood sampling (FBS)
• Fetal stimulation (FS)
• Fetal electrocardiography (CTG+ST)
• Computer analysis of CTGs (cCTG)
• Continuous pH and lactate (discontinued)
• Pulse oximetry (discontinued)
Adjunctive
technologies

FBS for pH and
lactate
• Good correlation with carotid
and umbilical blood
• Capillary blood may be
affected by redistribution of
circulation
Introduced in 1962

Technique
•Vaginal exam - presenting part, ROM, ≥ 3 cm.
• Amnioscope with light held tightly in place.
• Presenting part dried with small swabs.
• Thin layer of paraffin to form blood drop.
• 1-2 mm incision in fetal skin.
• Collection in heparin-coated capillary.
• Inpection of incision, and pressure if
bleeding.
(disposable or re-usable set)

• Suspicious or pathological CTGs
• NOT advised in severe and acute events
(causes further delay)
Indications

Same contra-indications as
internal FHR monitoring
• Failed FBS with pH – 10%
Blood clotting, insufficient blood,
air bubbles, blood gas measurer.
• Failed FBS with lactate – 1.5%
5 mcl vs. 50 mcl
Point-of-care measurement

pH
Lactate
Attitude
Normal
> 7.25
< 4.2
Intermediate
7.20-7.25
4.2-4.8
Abnormal
< 7.20
> 4.8
No further action
usually required, but
if CTG remains
grossly abnormal,
repeat FBS 60 min.
Measures to improve
fetal oxygenation, and
if CTG pattern persists
or worsens, repeat
FBS 20-30 min
Actions towards
normalization of the CTG
pattern or rapid delivery
Lactate values need to consider the apparatus used for measurement
After 3 normal results, consideration of further testing is rarely needed
Interpretation

• May  operative deliveries (moderate level of evidence)
• No evidence that fetal outcomes are improved
• Mainly used in central and northern Europe
• Not patient- or user-friendly.
• Time-consuming (~18 minutes pH, ~2 min lactate)
• Information quickly becomes outdated
• Difficult to perform in early labour
• Small risk of infection and bleeding
Benefits and limitations

Fetal stimulation (FS)
• Rubbing with fingers
• most widely used
• easiest to perform
• less invasive
• similar results to others
• Forceps to clasp skin
• Vibro-acoustic stimulation (maternal abdomen)

• Reduced variability - deep sleep vs.
hypoxia/acidosis
• Accelerations and normal CTG
 very predictive of absent hypoxia/acidosis
• No accelerations, no change in pattern
 limited predictive value
Indications

• FS may reduce FBS use by 
50%
• Not evaluated in RCTs

Fetal electrocardiography (CTG+ST)
• Fetal electrode
• Average ECG (30 cycles)
• T-wave amplitude, ST shape
• ST events (relevant ST changes)
Commercialised in 2000
P
Q
R
S
T

Increased T-wave
amplitude
Miocardial glycogenolysis
and anaerobic metabolism
P
Q
R
S
T
Depressor effect of hypoxia
on myocardium
(infection, malformations,
prematurity)
Type 2 and 3
byphasic STs
P
Q
R
S
T
P
Q
R
S
T

CTG
ST
T-wave amplitude
Byphasic STs

Episodic T-wave elevation
ST events
Basal T-wave elevation
Relevant byphasic STs

• Suspicious or pathological CTGs
• If ↓variability and no accelerations at
start, ST information may be
unreliable.
• FBS
• Measures to improve CTG
Indications

Same contra-indications to
internal FHR monitoring
• Not extensively studied < 36 weeks
• Continuous information

• Unique CTG classification system
• Normal
• Intermediate
• Abnormal
• Preterminal
• Intervention according to ST
event

ST events in
normal CTGs
No measure
necessary

• Rare cases of CTG evolving from
normal to abnormal CTGs without ST
events
• Abnormal CTG > 60 min or quickly
deteriorating  reassessment by senior
• When CTG indicates a severe and/or
acute event  immediate action

ST signal loss may
hide ST events

RCTs comparing CTG with CTG+ST
• Plymouth (2434 women) AJOG 1993;169:1151-60
• Swedish (4966 women) Lancet 2001;358:534-8
• Finnish (1483 women) BJOG 2006;113:419-23
• French (799 women) AJOG 2007;197:299
• Dutch (5681 women) AJOG 2010;115: 1173-
80
• American (11108 women) NEJM 2015;373:632-41

• Differences in RCT methodology
• Several systematic reviews:
• Lower need for FBS
• Modest reduction in operative deliveries
• Conflicting results for perinatal mortality
P
Q
R
S
T

•  metabolic acidosis over time published
by a few centres
• Importance of training
• ST events in ≈ 50% well-oxigenated
fetuses
P
Q
R
S
T

• Reproducible
• Objective evaluation of parameters that
are difficult to assess visually (variability)
Computer analysis of CTGs
(cCTG)

• All incorporated in central monitoring
stations
• Real-time visual and sound alerts
• Raise attention, prompt evaluation and action

• CTG or CTG+ST analysis
• Similar colour-coding of alerts
• No management recommendations
• Different mathematical algorithms

• Satisfactory comparison with experts
• Good prediction of newborn acidemia
• Two RCTs concluded (not published)
Evaluation

• Reproducible and quantifiable approach
• Promising technology
• Continued optimisation
• Further studies to compare systems and
evaluate effect on outcomes and
interventions
Conclusions

Further research and development is
needed, to remove the uncertainty that
surrounds them, and to provide more
robust evidence on how they affect
adverse outcome and intervention rates
Adjunctive technologies

CASE DISCUSSION

MONITOREO FETAL INTRAPARTO CONSENSO FIGO 2015.pptx

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