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Presentation Transcript

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 <80 bpm for > 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 < 5 bpm Probably hypoxia >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