Antenatal Flashcards
What is the Pathogenesis of abnormal placentation in preeclampsia
Abnormal placentation and consequent ischaemia:
- the spiral arteries in the placental bed do not undergo normal vascular remodelling as trophoblast invasion is abnormal. The invading placenta is unable to optimise its blood supply from maternal uterine vessels. The spiral arteries fail to adapt to become high- capacitance and low- resistance vessels
- uteroplacental ischaemia either from poor implantation in underlying microvascular disease or underperfusion of a relatively large placenta (eg diabetes, twins, hydropic fetus)
What if the Pathogenesis of maternal response in preeclampsia
Normal pregnancy is associated with a systemic inflammatory response which is exacerbated in preeclampsia
- metabolic disturbance (high triglyceride) and exaggerated inflammatory response with higher levels of pro- inflammatory cytokines associated with endothelial dysfunction
- endothelial cell activation leads to increased capillary permeability, increased endothelial expression of cell adhesion molecules and pro- thrombotic factors, platelet activation and increased vascular tone. There is a decrease in prostacyclin synthesis and an increase in thromboxane A2 synthesis. This may contribute to platelet activation and vasoconstriction
- these factors cause widespread microvascular damage and dysfunction which lead to the clinical manifestations of the maternal syndrome such as hypertension, proteinuria and hepatic disturbance
What is the angiogenic pathophysiology of preeclampsia
Under physiologic conditions and normal pregnancy, vascular endothelial growth factor (VEGF) and transforming growth factor (TGF- beta1) maintain endothelial health by interacting with their endogenous endothelial receptors
- anti- angiogenic factors secreted by the placenta in excess produce systemic endothelial dysfunction by antagonising VEGF AND TGF- beta1 signalling in preeclampsia
So increased anti- angiogenic factors and decreased placental growth factor in the maternal circulation, weeks before the onset of preeclampsia
Delivery timing for abnormal placentation spectrum
Delivery by CS at:
34- 36 weeks for vasa previa
35- 36+6 for placenta accreta
36- 37 weeks for placenta previa if asymptomatic; 35- 36 weeks if previous APH
Recommended healthy weight gain in pregnancy as per WHO
Bmi < 18.5= 12.5- 18 kg
Bmi 18.5- 24.9 = 11.5- 16 kg
Bmi 25- 29.9 = 7- 11.5 kg
Bmi 30 and above = 5-9 kg
Evidence behind umbilical artery Doppler
Cochrane 2017:
Decreases perinatal mortality and leads to fewer obstetric interventions including IOL and CS (mod qual evidence)
MCA dopplers use and when to do
<34 weeks: only perform if abnormal UAPI
Limited predictive value in preterm babies so should not be used to time delivery
> 34 weeks: perform regardless of UAPI
Helps to time delivery in term infants as it is an early sigh of fetal hypoxia, reflecting brain sparing
Moderately predictive of acidosis at birth and CS for fetal distress for fetuses >34 weeks
RCT evidence lacking though
Ductus venosus use
Perform in preterm (<34 weeks) SGA infants with abnormal UAPI
Use to time delivery in preterm infants - moderate predictive value for acidaemia and adverse outcome in preterm infants
Quintero staging for TTTS
Stage 1:
< 20 weeks: twin 1 DVP <2cm, twin 2 DVP >8cm
> 20 weeks: twin 1 DVP <2cm, twin 2 DVP >10cm
Stage 2:
Absent bladder in oligo twin
Stage 3:
Critical dopplers (absent or reversed UAPI) in either twin
Stage 4:
Hydrops in either twin
Stage 5:
Fetal demise of one or both twins
Pathophysiology of TTTS
Caused by AV anastomoses of large vessels that are deeper in the placenta
Results in large volume transfusion
GRATACOS classification for selective fetal growth restriction monochorionic twins
Type 1
- positive EDF in both twins
- deliver 34- 35 weeks
Type 2:
- persistent absent or reversed EDF
- deliver at 30- 32 weeks
Type 3:
- intermittent absent or reversed EDF
- delivery from 32 weeks
