perinatal asphyxia s.arulkumaran professor & head division of obstetrics & gynaecology...
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Perinatal AsphyxiaPerinatal Asphyxia
S.Arulkumaran Professor & Head
Division of Obstetrics & Gynaecology St.George’s Hospital Medical School
University of London
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Fetal Hypoxaemia > Hypoxia > Asphyxia
Respiratory & metabolic acidosis
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pH is a log scale of H+
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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
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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
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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
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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
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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.
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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
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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
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There are difficulties in IP monitoring - detection of hypoxia
HIGH LIGHTED BY RESULTS OF 4’TH CESDI REPORT
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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%
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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
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TO HELP DECISION MAKING – STRENGHTS & WEAKNESS OF
INTRAPARTUM SURVEILLANCE BY CTG SHOULD BE KNOWN
Can we detect hypoxia in time?
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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
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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.
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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
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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
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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
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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
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Hypoxaemia > Hypoxia > Asphyxia
No need to have otherParameters like pH, SaO2ECG
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Long standing hypoxic pattern
• No accelerations
• Markedly reduced baseline variability
• Shallow decelerations <15 beats
• May have a normal baseline rate
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Hypoxaemia>HypoxiaNormal, NNU, HIE,?CP
Role of SaO2, pH, lactate, ECG ?
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Hypoxia
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Asphyxia> HIE > CP
?pH, lactate, SaO2,ECG
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Intrauterine death
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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
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NormoxaemiapH, lactate, ECG, SaO2?
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Hypoxaemia??pH, lactate, SaO2, ECG
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Hypoxia?pH, lactate, SaO2, ECG
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Asphyxia***
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Depressed at birth, assistedVentilation, NNICU
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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
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Reactive – NormoxaemicNo stress – No need for pH, lactate, pSaO2, ECG
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Decelerations ?? Contractions Stress –yes; distress??Hypoxaemia ?? BLR 140 bpm
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Stress to distress – rise in baseline rateProbably getting hypoxic ?? BLR 165 bpm
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Distressed? Tachycardia 165 bpm + reduced baseline variability < 5 bpmProbably hypoxia >asphyxia – Need FBS, lactate, ECG, SaO2
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?Asphyxia, Hypoxia + Metabolic acidosis?Needs another test or delivery
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Conversion pattern of CTGPoor outcome
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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)
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Figure 7
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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