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

pH is a log scale of H+

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

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

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

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

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.

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

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 > 1500g Grades of Sub Optimal Care Based on number of cases Grade 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

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

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

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

Hypoxia

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

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

Normoxaemia pH, lactate, ECG, SaO2?

Hypoxaemia?? pH, lactate, SaO2, ECG

Hypoxia? pH, lactate, SaO2, ECG

Asphyxia***

Depressed at birth, assisted Ventilation, 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 – Normoxaemic No stress – No need for pH, lactate, pSaO2, ECG

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

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

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

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

Conversion pattern of CTG Poor 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

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