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

2. Fetal Hypoxaemia > Hypoxia > Asphyxia
Respiratory & metabolic acidosis

3. pH is a log scale of H+

4. Fetal response to hypoxemia
more effective uptake of oxygen
Reduced activity
decrease in growth rate
maintained energy balance
Oxygen saturation
Hypoxemia
Hypoxia
Asphyxia
Days and weeks
Hours
Minutes
Time

5. The fetal response to hypoxia
surge of stress hormones
redistribution of blood flow
anaerobic metabolism in the peripheral tissues
maintained energy balance
Oxygen saturation
Hypoxemia
Hypoxia
Days > Hours
Asphyxia
Days and weeks
Minutes
Time

6. Fetal response to asphyxia
Alarm reaction
anaerobic metabolism in peripheral tissues
brain and heart organ
failure
Oxygen saturation
Hypoxemia
Hypoxia
Asphyxia
Days and weeks
Hours>
Minutes
Hours
Time

7. Sequential Changes in Tests of Fetal well being
Growth
Aortic
blood
flow
Moderate
severe
redistribn
Abnormal
FHR
Trace
Cerebral
blood
flow
Fetal size
less than
5th centile
Abnormal
venous
flow
Umbilical artery A/B
AFI
Oligohydramnios

8. The fetus not troubled by the events of labour.
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.

9. Screening for fetal hyoxia Cases 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

10. 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

11. There are difficulties in IP monitoring - detection of hypoxia
HIGH LIGHTED BY RESULTS OF 4’TH CESDI REPORT

12. 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 > 1500g
Grades of Sub Optimal Care
Based on number of cases
Grade III – 52%
Grade II %
Grade I %

13. 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

14. TO HELP DECISION MAKING – STRENGHTS & WEAKNESS OF INTRAPARTUM SURVEILLANCE BY CTG SHOULD BE KNOWN Can we detect hypoxia in time?

15. 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

20. 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: , 1971.

21. 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

23. 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

24. 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

25. 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

26. No need to have other
Parameters like pH, SaO2
ECG
Hypoxaemia > Hypoxia >
Asphyxia

27. Long standing hypoxic pattern
No accelerations
Markedly reduced baseline variability
Shallow decelerations <15 beats
May have a normal baseline rate

28. Hypoxaemia>Hypoxia
Normal, NNU, HIE,?CP
Role of SaO2, pH, lactate, ECG ?

31. Hypoxia

32. ?pH, lactate, SaO2,ECG
Asphyxia> HIE > CP

33. Intrauterine
death

34. 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

35. Normoxaemia
pH, lactate, ECG, SaO2?

36. Hypoxaemia??
pH, lactate, SaO2, ECG

37. Hypoxia?
pH, lactate, SaO2, ECG

38. Asphyxia***

39. Depressed at birth, assisted
Ventilation, NNICU

40. 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

43. Reactive – Normoxaemic
No stress – No need for pH, lactate, pSaO2, ECG

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

47. Stress to distress – rise in baseline rate
Probably getting hypoxic ?? BLR 165 bpm

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

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

51. Conversion pattern of CTG
Poor outcome

52. 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)

53. Figure 7

54. In utero diagnosis of fetal hypoxia?
Hypoxaemia -> Hypoxia-> Asphyxia
Consider
Clinical picture re-physiological reserve (IUGR,APH,PT, meconium etc.)
Rate of progress of labour – parity, contractions, oxytocin, partogram
Diagnosis of hypoxia > Asphyxia – additional methods pH, lactate
Resuscitative measures> no improvement > delivery