Perinatal Asphyxia: Perinatal Asphyxia S.Arulkumaran
Professor & Head
Division of Obstetrics & Gynaecology
St.George’s Hospital Medical School
University of London
Fetal Hypoxaemia > Hypoxia > Asphyxia: Fetal Hypoxaemia > Hypoxia > Asphyxia Respiratory & metabolic acidosis
Slide3: pH is a log scale of H+
Fetal response to hypoxemia: Fetal response to hypoxemia Time Oxygen saturation Days and weeks Hours Minutes Hypoxemia Hypoxia Asphyxia more effective uptake of oxygen
Reduced activity
decrease in growth rate
maintained energy balance
The fetal response to hypoxia: The fetal response to hypoxia Time Oxygen saturation Days and weeks Days > Hours Minutes Hypoxemia Hypoxia Asphyxia surge of stress hormones
redistribution of blood flow
anaerobic metabolism in the peripheral tissues
maintained energy balance
Fetal response to asphyxia: Fetal response to asphyxia Time Oxygen saturation Days and weeks Hours Hours>
Minutes Hypoxemia Hypoxia Asphyxia Alarm reaction
anaerobic metabolism in peripheral tissues
brain and heart organ
failure
Sequential Changes in Tests of Fetal well being: Sequential Changes in Tests of Fetal well being
To prevent intrapartum hypoxia we have to identify the fetus likely to be affected : 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: 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: 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 : 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%: 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: 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? : TO HELP DECISION MAKING – STRENGHTS & WEAKNESS OF INTRAPARTUM SURVEILLANCE BY CTG SHOULD BE KNOWN Can we detect hypoxia in time?
Strengths : Strengths If CTG is reactive and shows cycling the fetus is unlikely to be acidotic or to have previous insult
If prolonged bradycardia of 15 – 20 mins – more chances that the fetus may be born acidotic
Most CTG abnormalities do not result in fetal acidosis: 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: 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: 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: 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: 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
Slide26: Hypoxaemia > Hypoxia >
Asphyxia No need to have other
Parameters like pH, SaO2
ECG
Long standing hypoxic pattern: Long standing hypoxic pattern No accelerations
Markedly reduced baseline variability
Shallow decelerations <15 beats
May have a normal baseline rate
Slide28: Hypoxaemia>Hypoxia
Normal, NNU, HIE,?CP Role of SaO2, pH, lactate, ECG ?
Slide31: Hypoxia
Slide32: Asphyxia> HIE > CP ?pH, lactate, SaO2,ECG
Slide33: Intrauterine
death
Subacute hyoxia : 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
Slide35: Normoxaemia pH, lactate, ECG, SaO2?
Slide36: Hypoxaemia?? pH, lactate, SaO2, ECG
Slide37: Hypoxia? pH, lactate, SaO2, ECG
Slide38: Asphyxia***
Slide39: Depressed at birth, assisted
Ventilation, NNICU
GRADUALLY DEVELOPING HYPOXIA : 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
Slide43: Reactive – Normoxaemic
No stress – No need for pH, lactate, pSaO2, ECG
Slide45: Decelerations ?? Contractions
Stress –yes; distress??
Hypoxaemia ?? BLR 140 bpm
Slide47: Stress to distress – rise in baseline rate
Probably getting hypoxic ?? BLR 165 bpm
Slide49: Distressed? Tachycardia 165 bpm + reduced baseline variability asphyxia – Need FBS, lactate, ECG, SaO2
Slide50: ?Asphyxia, Hypoxia + Metabolic acidosis?
Needs another test or delivery
Slide51: Conversion pattern of CTG
Poor outcome
Lack of specificity: 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: Figure 7
Slide54: 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 In utero diagnosis of fetal hypoxia?
Hypoxaemia -> Hypoxia-> Asphyxia