FSEP Flashcards
What bloods are taken in first trimster screening
Rubella antibody
HIV
syphilis
Hep B
Rhesus status/blood group
Rhesus antibodies
Iron level
Hba1c
OFFER: MSS1 if <14 weeks, MSS2 if >14 weeks + scan
MSS1 is papp-a and hcg - both elevated in DS typically
FGR.
What are the predictors of mortality for babies <30 weeks or >30 weeks?
What is the survival rate at >26 weeks in severe FGR?
Most common cause of FGR?
From 26-30 weeks babies less than 525g
>30 weeks babies less than 750g
The ‘viability’ cut off is therefore different in a non-FGR baby.
Survival at 26 weeks only just exceeds 50%
Causes:
INTRINSIC - fetal infections, chromosomal abnormalities
EXTRINSIC - placental insufficiency (most common)
Uterine artery pulsatile index - what is this telling us about?
This is telling us about the adequacy of placentation. It provides information from the maternal side of the placenta. Crap spiral arteries would give you a higher resistance.
What is the main diterminant of EFW?
What is the main determinant of this measurement?
Abdo circumfrance.
Liver size - indicates glycogen storage
When looking at the doppler of the ductus venosus - what does a diminished A wave tell us?
Reduction of cardiac myocontractility
What does the umbilical artery pulsatile index tell us?
What are the levels of dysfunction?
Increased resistance - increased resistance from placenta
Increased resitance –> absent end diastolic flow –> reversed end diastolic flow
The worse this gets the larger the area of the placenta which is dysfunctional
MCA doppler - what does this tell us?
What is normal?
What is abrnomal CPR?
Normal is high resistance.
When the fetus is organ sparing the resistance becomes low because the fetus is trying to get more blood to the brain. This can happen in a hypoxic state.
Ratio between the MCA doppler and the umbilical artery doppler. Means that they both might be ‘normal’ but the ratio is indicating that things are going south.
What levels of intrapartum pH and lactate would indicate delivery?
what levels would indicate repeat sampling and when?
What levels are ‘normal’ after birth?
When are dual cord lactates indicated?
pH <7.20
lactate >4.8
REPEAT in 30 minutes OR if CTG worsens if lactate 4.1-4.7 or pH 7.20-7.24
As the birthing process can be acid generating the arterial lactate can be up to 7.5, and the venous lactate should be at least 0.6 lower than this
Indications:
- when there has been an intrapartum FBS done
- when the apgar is <4 at 1 minute
- when the apgar is <7 at 5 minutes
- when there has been intervention for suspected fetal compromise
With baseline fetal heart rate what is the premature vs post -dates fetus likely to be like?
What is the main determinant of the difference in saying an antenatal vs intrapartum CTG is ‘normal’?
Immature baby = immature parasympathetic system. They are primarily sympathetic and therefore have higher BFHR
Post-dates = mature para, therefore lower BFHR
ANTENATAL NORMAL = reactive = 2 accellerations within 20 minutes
INTRAPARTUM NORMAL = 2 accelerations within the hour. Doesnt need to be ‘reactive’ because baby might just be moving less because it is working harder in labour
What are the indications for tocolysis?
What can be used?
Hyperstimulation - tachysystole or uterine hypertonis WITH ctg abnormalities
OR if you have an unhappy baby and you need to do CS and stop contractions in the meantime.
Terbutaline - 250mcg SC
Salbutamol - 100mcg IV
GTN - 400mcg spray SL
What are some drugs that can cause reduced variability?
Opiates, mag sulphate, calcium channel blockers
BB do not reduce the variability
What is acute bradycardia and what can the causes be?
bradycardia >5 minutes
Causes: maternal hypotension, cord compression, rapid decent, uterine hyperstimulation
What are the causes of fetal tachycardia
Maternal hypoxia
Infection - chorioamnionitis
Drugs - salbutamol, terbutaline - act on sympathetic system
Extreme prematurity (be more sympathetic to these babies
Cummulative or mild hypoxia - compensation
fetal tachyarrythmias e.g. SVT
Describe the pattern of early decellerations
What about the result of the CTG?
Occur with the contraction
Typically occur within the sleep cycle
Repetitive
Uniform in shape
Often occur within the range of 4-8cm
Cause: unlikely solely due to head compresison. Often occurs during sleep because the CNS is not as active and does not compensate for the increased pressure during a contraction
As the baby may be asleep it can be accompanied by no accelerations and reduced variability but does not reflect a hypoxic baby
Describe the typical pattern of variable decellerations
What are they due to?
Descripe the physiology of a variable decelleration
What does the depth of the variable decel tell you? The duration?
Vary in:
- depth
- shape
- duration
They typically have a rapid decent and recovery
Cause: CORD COMPRESSION EVENT
Physiology = acute cord compression causes acute hypoxia. This is picked up by the chemoreceptors in the baby which triggers acute bradycardia to compensate for a hypoxia. This happens by triggering the parasympathetic NS via the vagus nerve which inhibits the SAN
The depth or duration in isolation does not tell you much about the fetal condition. It just reflects how logn the cord is compressed for and how strong the vagal response it. However, a fetus with persistently broad, deep decels will run out of reserves quicker.
ABNORMAL CTGs:
Sinusoidal - what does this mean?
Sinusoidal usually refelects anaemia (severe), No variaility, complete loss of autonomic control
