FIGO 2015 FIGO CONSENSUS GUIDELINES ON INTRAPARTUM FETAL MONITORING Safe Motherhood and Newborn Health Committee Co-ordinator for guideline development:

FIGO 2015

FIGO CONSENSUS GUIDELINES ONINTRAPARTUM FETAL MONITORING

Safe Motherhood and Newborn Health Committee Co-ordinator for guideline development: Diogo Ayres-de-Campos

FIGO CONSENSUS GUIDELINES ON INTRAPARTUM FETAL MONITORING

1960’s• Hon, Caldeyro-Barcia,

Hammacher• 3 different classifications

1970’s - 1980’s • Myer-Menk/Fischer, Cardiff, Birmingham,

Krebs• 21 different CTG classifications 1974-1984

Devoe LD et al. AJOG 1985;152:1047-53

FIGO1987

FIGO. IJOG 1987;25:159-67

FIGO 2015


Safe Motherhood and Newborn Health Committee Co-ordinator for guideline development: Diogo Ayres-de-Campos

FIGO CONSENSUS GUIDELINES ON INTRAPARTUM FETAL MONITORING


• Wide consensus• Include all currently available methods of

intrapartum fetal monitoring• Language accessible to all professionals• Simple and objective

• RCOG contacted to appoint person for writing of CTG chapter (Dec 2012). Nominated (Feb 2013)

• ACOG contacted to appoint person for writing of CTG chapter (Dec 2012). Nominated (Jan 2013)

• All FIGO member societies contacted to appoint one subject matter expert (Feb 2013)• Wide knowledge of the fetal monitoring scientific literature.• Good written English• Available to provide written feedback in less than 15

days



• 34 experts nominated by FIGO scientific societies (Feb 2013 to May 2013)

• 13 experts invited by FIGO based on literature search (May 2013 – Jul 2013)

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).

• ICM invited to write the chapter on intermittent auscultation (Jul 2013). Nominated (Oct 2013)



• 3 round email consensus process (3 weeks to reply)• Final agreement for name to be included in the panel• 1st and 2nd chapters (2 Oct 2013 – 10 Feb 2014)• 4th chapter (5 Mar 2014 – 31 Aug 2014)• 3rd chapter (20 Aug 2014 – 2 Jan 2015)• 5th chapter (5 Jan 2015 – 15 Mar 2015)


• No internal or external funding• 10 months to prepare• 18 months for the consensus process• 2029 emails exchanged






FIGO 2015


Diogo Ayres-de-Campos, Sabaratnan Arulkumaranfor the FIGO intrapartum fetal monitoring consensus panel

PHYSIOLOGY OF FETAL OXYGENATION AND THE MAIN GOALS

OF INTRAPARTUM FETAL MONITORING


Avoid adverse fetal outcome related to intrapartum hypoxia/acidosisAvoid unnecessary intervention, associated with increased maternal and fetal risks

Aims of intrapartum fetal monitoring


Blood gas or lactate analysis• in the umbilical cord, or in the newborn circulation during the first minutes of life, is the only objective way of quantifying hypoxia/acidosis occurring just prior to birth


Cord blood sampling• Unnecessary to clamp the cord• As soon as possible after birth (< 15 min)

• Artery and vein• Analysis within 30 min


Metabolic acidosisArterial pH < 7.00 and BD >12 mmol/l• already associated with adverse outcome when pH

< 7.05 and BDecf > 10 mmol/l

Arterial lactate > 10 mmol/l is an alternative, but 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 calculated by blood gas

analysers, slightly higher, can also be used


1-minute Apgar• important to decide newborn

resuscitation• low association with intrapartum

hypoxia/acidosis5-minute Apgar• stronger association with short- and long-

term neurological outcome and neonatal death


Unaffected by minor degrees of hypoxia/acidosisSubject to interobserver disagreementAffected by 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


Metabolic acidosis and low Apgars• vast majority recover quickly and have no

short- or long-term complications• few cases are of sufficient intensity and

duration to cause death or long-term morbidity


Hypoxic-ischemic encephalopathy (HIE)• Short-term neurological dysfunction caused

by hypoxia/acidosis• Metabolic acidosis, low Apgars, early imaging

of cerebral edema, changes in muscle tone, sucking difficulties, seizures or coma in first 48 h of life

• May be accompanied by other system dysfunctions


• other non-hypoxic causes • need to document metabolic acidosis in

umbilical artery or in newborn circulation during the first minutes of life for HIE

Neonatal encephalopathy


InfectionCongenital diseasesMetabolic diseasesCoagulation disordersAntepartum and post-natal hypoxiaBirth trauma

• Manifests at 1-4 years• Long-term neurological complication more

commonly associated with term intrapartum hypoxia/acidosis

• Only 10-20% cases are caused by hypoxia/acidosis

Cerebral palsy (spastic quadriplegic , dyskinetic )


• Metabolic acidosis• Low 1 and 5-minute Apgar scores• Grade 2 or 3 HIE• Early imaging of acute non-focal cerebral

anomaly• Spastic quadriplegic or dyskinetic type• Exclude other identifiable etiologies

Intrapartum hypoxia/acidosis as the cause of cerebal palsy in term infants


should indicate intervention at an early stage of hypoxia/acidosis in order to prevent rather than to predict adverse newborn outcomes

Intrapartum fetal monitoring

FIGO 2015


CARDIOTOCOGRAPHY

Diogo Ayres-de-Campos, Catherine Y. Spong, Edwin Chandraharanfor the FIGO intrapartum fetal monitoring consensus panel


Cardiotocography(kardia=heart, tokos=labour)

…is the term that best describes the continuous monitoring of the FHR and uterine contractions


1 cm/min

2 cm/min

3 cm/min

Paperspeed


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

Baseline

Basic CTG features


Normal 110-160 bpm

Tachycardia

> 160 bpm for more than 10 min (pyrexia, epidural, early stages of non-acute hypoxemia, βagonist 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 > 50 min in baseline or > 3 min in decelerations

• CNS hypoxia/acidosis, 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 s

>15 bpm>15 bpm


Abrupt decreases in FHR above baseline, > 15 bpm amplitude, > 15 secs

Decelerations

150

130

140

120

>15 s>15 s

>15 bpm>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 (umbilical 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• Tracings with variability and no accelerations, amplitude > 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.


Bodymovements

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


Tracing classification

*Decelerations are repetitive when associated with > 80% contractions. Absence of accelerations during labour is of uncertain significance.

Baseline

Variability

Decelerations

Interpretation

Clinical Management

Normal110-160 bpm

5-25 bpm

No repetitive* decelerations

Suspicious

Lacking at least one characteristic of

normality, but with no pathological

features

Pathological< 100 bpm

Reduced variabilityIncreased variability, or sinusoidal

pattern

Repetitive* late or prolonged decelerations > 30 min or > 20

min if variability is reduced. Prolonged deceleration > 5 min

No hypoxia/acidosis

No intervention necessary

Low probability of hypoxia/acidosis

Action to correct reversible causes,

close monitoring, or adjunct technologies

High probability of hypoxia/acidosis

Immediate action to correct reversible causes, adjunct

technologies or if not possible expedite delivery.

In acute situations, immediate delivery must be accomplished.


Reversible hypoxia/acidosis

TachyssystoleIatrogenic/spontaneous excessive contraction frequency

Maternal supine position(aorto-caval compression by pregnant uterus)

Sudden maternal hypotension(following epidural or spinal analgesia)Maternal respiratory complicationsAcute asma, etc.


Excessive uterine activity should be avoided, irrespective of FHR

changes, reversed by ocytocin or acute tocolysis

• Salbutamol• Terbutaline• Ritodrine• Atosiban• Nitroglycerine


Intravenous salbutamol started


Irreversible

Major placental abruption

Fetal hemorrhage

Uterine rupture


Mechanical complications of labour

Cord prolapse

Shoulder dystocia

Retention of aftercoming

head

FIGO 2015


INTERMITTENT AUSCULTATION

Debrah Lewis, Soo Downefor the FIGO intrapartum fetal monitoring consensus panel


The evidence for the benefits of continuous CTG

monitoring, as compared to IA, in both low and high risk

labours is scientifically inconclusive

Alfirevic Z et al. Cochrane 2013 May 31;5:CD006066Vintzileos AM et al. Obstet Gynecol 1995;85:149-55


Intermittent auscultation (IA)

• Recommended in all labours where there is no access to CTG

• Where CTG is available, may be used in low-risk cases

• ≈ ½ panel members believe that CTG should be preferred during the 2nd stage

MHR

contractions

FHR

Features to evaluate What to register

FHR

Duration: ≥ 60 secs(for 3 UC if abormal)

Number of bpmAccelerations and 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 Number of bpm



Baseline < 110 bpm or > 160 bpm

Decelerations

Presence of repetitive or prolonged (>3 mins) decelerations

Contractions More than 5 contractions in 10 mins

Abnormal findings


IJGO supplement to be distributed at the FIGO congress in Vancouver, Oct 2015

PowerpointpresentationCourses


• Common terminology• Shared knowledge• Basis for research and progress• Widespread clinical use

Documents

FIGO 2015 FIGO CONSENSUS GUIDELINES ON INTRAPARTUM FETAL MONITORING Safe Motherhood and Newborn Health Committee Co-ordinator for guideline development: