Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s...

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Perinatal Asphyxia Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London

Transcript of Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s...

Page 1: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Perinatal AsphyxiaPerinatal Asphyxia

S.Arulkumaran Professor & Head

Division of Obstetrics & Gynaecology St.George’s Hospital Medical School

University of London

Page 2: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Fetal Hypoxaemia > Hypoxia > Asphyxia

Respiratory & metabolic acidosis

Page 3: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

pH is a log scale of H+

Page 4: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Fetal response to hypoxemia

Time

Oxygen

satu

rati

on

Days and weeks Hours Minutes

Hypoxemia

Hypoxia

Asphyxia

more effective uptake of oxygenmore effective uptake of oxygen

Reduced activityReduced activity

decrease in growth rate decrease in growth rate

maintained energy balancemaintained energy balance

Page 5: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

The fetal response to hypoxia

Time

Oxygen

satu

rati

on

Days and weeks

Days > Hours

Minutes

Hypoxemia

Hypoxia

Asphyxia

surge of stress hormonessurge of stress hormones

redistribution of blood flowredistribution of blood flow

anaerobic metabolism in the anaerobic metabolism in the peripheral tissues peripheral tissues

maintained energy maintained energy balancebalance

Page 6: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Fetal response to asphyxia

Time

Oxygen

satu

rati

on

Days and weeks Hours Hours>Minutes

Hypoxemia

Hypoxia

Asphyxia

Alarm reactionAlarm reaction

anaerobic metabolism inanaerobic metabolism in peripheral tissues peripheral tissues

brain and heart organ brain and heart organ failurefailure

Page 7: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Umbilical artery A/B

Sequential Changes in Tests of Fetal well being

Growth

Fetal sizeless than5th centile

Aortic Aortic blood blood flowflow

Cerebral blood flow

AbnormalAbnormalvenousvenousflowflow

AbnormalFHRTrace

AFI Oligohydramnios

ModerateModerateseveresevereredistribnredistribn

Page 8: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

To prevent intrapartum hypoxia we have

to identify the fetus likely to be affected

• The fetus not troubled by the events of labour.

• Troubled but able to compensate and is in no immediate danger.

• Troubled and utilising key resources in an attempt to compensate or unable to fully compensate.

Page 9: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Screening for fetal hyoxiaCases at risk

• Obstetric H/O – IUGR, APH, Post term, reduced FM, multiple pregnancy, breech

• Meconium stained fluid – reduced quantity

• Intrauterine infection

• Iatrogenic – use of oxytocin, PG

Page 10: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Screening & Diagnosis of fetal hypoxia in labour

• Admission EFM

• Intermittent EFM

• Continuous EFM

• Fetal acoustic stimulation test (FAST)

• Fetal scalp blood sampling for pH, BD, lactate

• Fetal pulse oximetry

• Fetal ECG

Page 11: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

There are difficulties in IP monitoring - detection of hypoxia

HIGH LIGHTED BY RESULTS OF 4’TH CESDI REPORT

Page 12: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

CESDI – IP deaths Can be reduced by 50%

• IP deaths in ’94-’95 – 873 cases

• 1 in 1599 births – constituted 4.5% of all losses reported to CESDI

• Normally formed fetuses > 1500gGrades of Sub Optimal Care

Based on number of casesGrade III – 52%Grade II - 25%Grade I - 11%

Page 13: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

EFM – Difficulties in IP EFM & decision making

• LACK OF KNOWLEDGE TO INTERPRET TRACES

• FAILURE TO INCORPORATE CLINICAL PICTURE

• DELAY IN INTERVENTION

• COMMUNICATION / COMMON SENSE ISSUES

Page 14: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

TO HELP DECISION MAKING – STRENGHTS & WEAKNESS OF

INTRAPARTUM SURVEILLANCE BY CTG SHOULD BE KNOWN

Can we detect hypoxia in time?

Page 15: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Strengths

• If CTG is reactive and shows cycling the fetus is unlikely to be acidotic or to have previous insult

• If prolonged bradycardia of <80 bpm for > 15 – 20 mins – more chances that the fetus may be born acidotic

Page 16: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.
Page 17: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.
Page 18: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.
Page 19: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.
Page 20: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Most CTG abnormalities do not result in fetal acidosis

R. W. Beard, et al. The significance of the changes in the continuous foetal heart rate in the first stage of labour. J Obstet Gynaecol Br Commonw 78:865-881, 1971.

Page 21: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Fetal behavioural state - Cycling• Cycling with a reactive followed by a sleep pattern

suggests that the baby is likely to be neurologically normal

• Absence of cycling may be due to drugs, infection, cerebral haemorrhage, chromosomal or congenital malformation, previous brain damage

• Previously brain damaged baby may or may not show cycling but cord pH may be normal; may not show evidence of HIE but may exhibit signs of neurological damage – often manifesting later

Page 22: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.
Page 23: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Weakness• Patterns in between a reactive cycling and prolonged

bradycardia has good sensitivity but poor specificity

• With a given pattern the rate of development of hypoxia and acidosis is determined by the clinical situation – which can differ in severity (‘Feto-placental reserve’)

• Patterns can be suspicious or abnormal due to factors other than hypoxia – e.g. medication, chromosomal/ congenital malformation, infection, intracranial bleed

Page 24: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Review of CTG patterns from cases with CP or IP - SB

• Acute hypoxia – Prolonged bradycardia• Sub-acute hypoxia – Prolonged decelerations

The above two present with acute clinical events or in late 1’st or 2’nd stage. At times cause unknown

• Gradually developing hypoxia• Long standing hypoxia – reduced variability

+/- shallow decelerations

Page 25: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

ACUTE HYPOXIA

• MAY DEVELOP WITH PROLONGED BRADYCARDIA

• ABRUPTION, CORD PROLAPSE, SCAR RUPTURE

• UTERINE HYPERSTIMULATION / TOCOLYSIS

• Important considerations - CTG PRIOR TO BRADYCARDIA & CLINICAL PICTURE- TMS, IUGR, infection, APH etc

Page 26: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Hypoxaemia > Hypoxia > Asphyxia

No need to have otherParameters like pH, SaO2ECG

Page 27: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Long standing hypoxic pattern

• No accelerations

• Markedly reduced baseline variability

• Shallow decelerations <15 beats

• May have a normal baseline rate

Page 28: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Hypoxaemia>HypoxiaNormal, NNU, HIE,?CP

Role of SaO2, pH, lactate, ECG ?

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Page 31: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Hypoxia

Page 32: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Asphyxia> HIE > CP

?pH, lactate, SaO2,ECG

Page 33: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Intrauterine death

Page 34: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Subacute hyoxia

• Prolonged decelerations – More time below the baseline rate (e.g.>90 secs) and shorter duration at the baseline rate (<30 secs)

• Less than optimal circulation through the placenta

Page 35: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

NormoxaemiapH, lactate, ECG, SaO2?

Page 36: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Hypoxaemia??pH, lactate, SaO2, ECG

Page 37: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Hypoxia?pH, lactate, SaO2, ECG

Page 38: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Asphyxia***

Page 39: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Depressed at birth, assistedVentilation, NNICU

Page 40: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

GRADUALLY DEVELOPING HYPOXIA

• Accelerations do not appear

• BASELINE RATE increases and VARIABILITY reduces

• CONSIDER THE CLINICAL PICTURE (parity, cervical dilatation, rate of progress, high risk factors)

• IF REQUIRED PERFORM FBS X 2

Page 41: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.
Page 42: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.
Page 43: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Reactive – NormoxaemicNo stress – No need for pH, lactate, pSaO2, ECG

Page 44: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.
Page 45: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Decelerations ?? Contractions Stress –yes; distress??Hypoxaemia ?? BLR 140 bpm

Page 46: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.
Page 47: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Stress to distress – rise in baseline rateProbably getting hypoxic ?? BLR 165 bpm

Page 48: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.
Page 49: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Distressed? Tachycardia 165 bpm + reduced baseline variability < 5 bpmProbably hypoxia >asphyxia – Need FBS, lactate, ECG, SaO2

Page 50: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

?Asphyxia, Hypoxia + Metabolic acidosis?Needs another test or delivery

Page 51: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Conversion pattern of CTGPoor outcome

Page 52: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Lack of specificity• CTG is sensitive in identifying stress/distress to the

fetus

• May not indicate the precise time of injury or asphyxia prospectively – Conversion pattern (may be perfusion injury) and the sentinel event may give the clue to timing of injury retrospectively

• Onset of asphyxia is related to the feto-placental reserve & the duration CTG was abnormal (Systemic asphyxia Vs local ischaemia)

Page 53: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Figure 7

Page 54: Perinatal Asphyxia S.Arulkumaran Professor & Head Division of Obstetrics & Gynaecology St.George’s Hospital Medical School University of London.

Consider Clinical picture re-physiological reserve (IUGR,APH,PT, meconium etc.)Rate of progress of labour – parity, contractions, oxytocin, partogramDiagnosis of hypoxia > Asphyxia – additional methods pH, lactateResuscitative measures> no improvement > delivery

In utero diagnosis of fetal hypoxia?Hypoxaemia -> Hypoxia-> Asphyxia