perinatal asphyxia s.arulkumaran professor & head division of obstetrics & gynaecology...

Perinatal AsphyxiaPerinatal 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

pH is a log scale of H+

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

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

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

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

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.

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

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

There are difficulties in IP monitoring - detection of hypoxia

HIGH LIGHTED BY RESULTS OF 4’TH CESDI REPORT

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%

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

TO HELP DECISION MAKING – STRENGHTS & WEAKNESS OF

INTRAPARTUM SURVEILLANCE BY CTG SHOULD BE KNOWN

Can we detect hypoxia in time?

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

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.

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

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

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

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

Hypoxaemia > Hypoxia > Asphyxia

No need to have otherParameters like pH, SaO2ECG

Long standing hypoxic pattern

• No accelerations

• Markedly reduced baseline variability

• Shallow decelerations <15 beats

• May have a normal baseline rate

Hypoxaemia>HypoxiaNormal, NNU, HIE,?CP

Role of SaO2, pH, lactate, ECG ?

Hypoxia

Asphyxia> HIE > CP

?pH, lactate, SaO2,ECG

Intrauterine death

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

NormoxaemiapH, lactate, ECG, SaO2?

Hypoxaemia??pH, lactate, SaO2, ECG

Hypoxia?pH, lactate, SaO2, ECG

Asphyxia***

Depressed at birth, assistedVentilation, NNICU

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

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

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

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

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

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

Conversion pattern of CTGPoor outcome

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)

Figure 7

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