Perinatal Asphyxia

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

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

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

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

8. 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 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

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 - 25% Grade I - 11%

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 KNOWNCan 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 78:865-881, 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