Intrapartum science Flashcards
Stages of labour
Stage 1
- effacement and dilatation of the cervix up to fully
i) latent phase up to 4cm
ii) active phase from 4cm onwards
Stage 2
- from fully dilated to delivery of baby
i) propulsive phase (until fetal head touches pelvic floor)
ii) expulsive phase - delay if >2h nulliparous or >1h multip
Stage 3
- delivery of placenta
Curve of Carus
Angulation of birth canal
J shape
Mechanism of labour
Engagement
- transverse or oblique diameter of fetal head enters pelvic brim
- asynclitism occurs prior
Descent to below ischial spines and flexion
Fetal head rotation to OA position, shoulders enter pelvis
Extension and delivery of head
Restitution
Delivery of shoulders and rest of body
Labour dystocia
Prolonged latent phase
- 3.5% in primip
- relates to delayed cervical ripening
- no benefit in augmentation with oxytocin
Primary dysfunctional labour
- cervical dilatation <1cm/hr during active phase of stage 1 (after 4cm)
- 26% in primip, 8% multip
Secondary arrest
- cessation of cervical dilation for 2 hours with a history of previously normal dilation
- 6% primip, 2% multip
- usually due to fetal malposition
Breech presentation
30% at 28weeks, 3% at term
Extended (frank) breech mostly, also flexed (complete) and footling
Fetal risks - intracranial haemorrhage, brachial plexus injury, limb fractures, spinal cord injury
Causes:
- pregnancy related - multiparity, multiple pregnancy, prematurity
- fetal structural - hydrocephalus, myelomeningocele
- fetal growth - FGR, oligo or polyhydramnios
- placental - praevia, short umbilical cord
- uterine - bicornuate
- pelvic - contracted
(baby is usually cephalic due to piriform shape of uterus, and calcified fetal skull denser)
Shoulder dystocia
When failure of shoulders to deliver with gentle downward traction on fetal head (usually anterior shoulder problem)
0.6% incidence, 15% recurrence rate
See turtle necking, or external rotation failure
Fetal distress due to reduction in O2, from fetal chest compression and uterine contraction
Complications:
- asphyxia
- brachial plexus injury - 10% of dystocias, 10% of those give permanent neurological injury
- fractures of clavicle (15%) and humerus (1%)
Risk factors - only predict 15% of cases
- fetal macrosomia
- maternal diabetes (even if normal growth)
- maternal obesity
- previous shoulder dystocia
- prolonged labour
- instrumental delivery
2300 CS needed to prevent 1 permanent neurological injury from shoulder D
Fetal physiology in labour
Maternal placental blood flow 500ml/min, stops when uterine contraction >30mmHg
Fetus needs 30-90s between contractions to regain normal blood gases
Umbilical cord circulation not affected by 1st stage of labour, but stops during active pushing stage
Cell metabolism
- fetal glycogen stores generated in third trimester (so more reserve if not preterm)
- in hypoxia, anaerobic metabolism so using blood glucose and stored glycogen to produce energy
- energy produced by anaerobic metabolism is 1/20th of that produced via aerobic
Fetal response to hypoxaemia
= decrease in O2 content of arterial blood with normal cell and organ function
Effective uptake of O2 -> reduced activity (reduced FMs and reduced fetal breathing) -> decreased growth rate
Fetal response to hypoxia
= O2 deficiency which affects peripheral tissues
Surge of stress hormones (increased sympathetic activity) -> reduction in peripheral blood flow -> redistribution of blood flow in favour of central organs -> peripheral tissue anaerobic metabolism
Fetal response to asphyxia
= when cellular energy production is no longer sufficient to meet fetal demands
Maximum activation of sympathetic nervous system -> anaerobic metabolism in central organs -> utilisation of glycogen reserves in liver and heart -> cardiovascular failure
Criteria for diagnosis of acute intrapartum hypoxia causing brain damage
Evidence of metabolic acidosis in umbilical arterial vessels - pH <7, base excess >12
Early onset of severe or moderate neonatal encephalopathy in term babies
Cerebral palsy of spastic quadriplegic or dyskinetic type
CTG records
Heart ultrasonic sensor - fetal heart rate based on R-R interval on ECG
Tocodynamometer - uterine contractions
1cm/min speed recording
Baseline HR - 110-160 at term. Need at least 10 mins, record between contractions
Variability on CTG
Normal 5-25
>25bpm = saltatory pattern
Sinusoidal - smooth undulating sine wave, very concerning for fetal anaemia or feto-maternal haemorrhage, 3-5 cycles/min
Reduced variability in sleep cycle or preterminal (>50mins)
Accelerations and decelerations on CTG
Acceleration - increase in HR of more than 15 for more than 15s
- should have 2 accelerations in 20 min period for sign of adequate oxygenation
Deceleration - drop in HR of more than 15 for more than 15s
- early = reflex generated drop occurring during contraction, lowest point at peak of contraction. Not related to hypoxia but due to mechanical forces acting on fetus.
- late = often signify hypoxia, may be associated with placental insufficiency
- variable = most, due to cord compression. Uncomplicated if <60s but risk of hypoxia increases if last >60s.
Classification of CTG features
Normal if all 4 features reassuring
Suspicious if 1 feature non-reassuring
Pathological if 1 feature abnormal or >2 features non-reassuring
REASSURING
- baseline 110-160
- variability 5-25
- no decels
- accelerations
NON-REASSURING
- baseline 100-109, or 161-180
- variability <5 for 30-50mins
- early decels
- variable decels with over 50% of contractions occurring for 90 mins
- single prolonged decel up to 3mins
ABNORMAL
- baseline <100 or >180
- sinusoidal for >10 mins
- variability <5 for 90 mins
- late or atypical decels with over 50% of contractions occurring for 30 mins
- single prolonged decel >3min
Patterns of hypoxic change on CTG
ACUTE - if sudden drop in baseline, fetal pH drops by 0.01/min
- causes unknown (50%), abruption, scar rupture, cord prolapse, uterine hyperstimulation, epidural top-up
SUBACUTE - if FH below baseline majority of the time or may see saltatory, fetal pH drops by 0.01/2-3mins
EVOLVING (decels -> loss of accelerations -> tachycardia -> loss of variability -> stepladder to death)
CHRONIC - higher baseline, shallow decels, reduced variability, absence of accelerations
Evolving hypoxia
Stress stage - decels without rise in baseline
Distress stage - tachy 20-30 above baseline, reduction in baseline variability
Collapse stage - sudden decline in FH in step-wise manner to terminal bradycardia
aka step-ladder to death
ST analysis
= STAN
as ST interval of fetal ECG reflects function of fetal myocardium during stress
Combines fetal HR with ST interval analysis
Analysis considers 30 ECG complexes at a time and calculates T/QRS ratio
Hypoxia causes fetal adrenaline surge, myocardial anaerobic metabolism
Adrenaline surge activates glycogenolysis
Increased glycogenolysis -> K release
K -> increased T wave amplitude
Rate of increase in T wave amplitude depends on amount of glycogen fetus needs to utilise to maintain myocardial energy balance
Types of STAN event
Biphasic ST
- seen in initial phase of hypoxia, when fetus not capable of responding to hypoxia
- in myocardial dysfunction, due to cardiac malformation or infections
- repeated grade 2 and 3 events are abnormal
Baseline rise in T/QRS ratio
- if rise lasting >10mins
- reflects fetal response to hypoxia with anaerobic metabolism
- significant if >0.05
Episodic rise in T/QRS ratio
- if returns to baseline in <10mins
- reflects fetal distress
- significant if >0.10
