Review Note
Last Update: 03/02/2025 07:52 PM
Current Deck: ACG Part 2::Obstetrics
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Commit #293137
SS_OB 1.21 Describe the clinical methods used for foetal monitoring in labour
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Commit #293137Monitoring to assess for foetal hypoxia.
Methods for foetal monitoring in labour include:
- Midwife assessment by serial vaginal examinations, palpation of uterus, assessment of liquor and maternal pain and vitals – e.g. passage of meconium = foetal distress,
- CTG – cardiotocography – continuous recording of foetal HR obtained via an ultrasound transducer placed on mother’s abdomen – widely used method of assessing foetal well-being in pregnancies with increased risk of complications
- Cochrane review of 6 RCTs comparing CTG to no CTG showed no significant difference in perinatal mortality (2.3% vs 1.1%, RR 2.05, 95% CI 0.95-4.42) or preventable deaths or incidence of LUSCS, note they were poor studies and they only enrolled women at increased risk of complication
- Scalp electrode monitor of CTG
- Scalp foetal lactate measures
During normal labour hypoxemia occurs transiently with uterine contractions, which is tolerated well however there are 4 causes of asphyxia to baby in intra-partum period:
- Inadequate perfusion of maternal side of placenta (severe hypotension, aortocaval compression)
- Interruption of gas exchange across placenta (e.g. placental abruption)
- Interruption of umbilical blood flow (cord compression)
- Inability to withstand transient, intermittent hypoxia that occurs with contractions of normal labour in the compromised foetus (anemic or growth retarded foetus)
With hypoxia the baby will divert blood flow preferentially to brain, heart and adrenals and can reduce overall oxygen consumption to 50%, maintained for up to 45mins, after which there is an accumulation of lactate and gradual metabolic acidosis
Changes in foetal heart rate characteristics:
- Resting FHR usually between 110-160
- Persistent tachycardia – associated with hypoxia, fever, chorio, anemia, or drugs (sympathomimentcs or anticholinergics)
- Persistent bradycardia – hypoxia, congenital heart block and beta blocking drugs
- Baseline variability = difference between successive beats, normally more than 6, normal variability indicates normal interaction between SNS and PSNS and absence of cerebral hypoxia, acute hypoxia may initially increase variability, persistent hypoxia will cause loss of variability
- Early decelerations – occur with uterine contractions, usually <20 below baseline, onset & offset coincides with contraction, not bad – thought to be a result of vagal tone from mild hypoxia
- Late decelerations – begin 10-30s after beginning of contraction and end 10-30s after end of contraction, represent hypoxia and when combined with loss of variability is ominous sign of foetal distress
- Variable decelerations – vary in depth, shape and/or duration – suggest umbilical cord occlusion
- Reactivity – acceleration in response to foetal movement = sign of healthy baby
CTG tracing is accurate at predicting a healthy baby (99%) but it lacks specificity in that it has a poor positive predictive value for abnormal outcome – with a 35-50% false positive rate at predicting foetal compromise – thus if CTG suggests foetal compromise, foetal scalp blood pH is used to confirm or exclude acidosis, in general pH <7.2 is considered abnormal and delivery expedited
- Note that since the use of CTG the prevalence of cerebral palsy has not reduced – so the proportion of cerebral palsy caused by birth asphyxia is relatively small
- Note than foetal asphyxia = non-reassuring status based on CTG / monitors whereas foetal anoxia = complete cord occlusion, sustained bradycardia, tetanic uterus, uterine rupture etc and is time critical (lethal to baby within 10mins)
Gold coast notes : Update in anaesthesia – foetal compromise; Fetal assessment for anesthesiologists, 2013