High risk obs Flashcards
What are the implications of SGA?
Increased risk of AN and intrapartum stillbirth
- 3-4x increased perinatal mortality
- compromise 40% of stillbirths in NZ (<10th)
Increased risk of neonatal mortality and morbidity
Increased risk of childhood handicap and impaired school performance
Increased risk of adult morbidity and mortality
- Barker hypothesis = developmental origins of adult disease hypothesis
- Proposes that CVD and T2DM in adult life originate through adaptations of the fetus where it is undernourished in utero
Small for gestational age (SGA)
Fetal growth restriction
Infant (newborn) with birthweight <10th centile, or
Fetus with an EFW or an AC on a customised growth chart <10th centile for gestation
FGR is a fetus that has failed to reach its growth potential
- Not all FGR infants are SGA
SUBOPTIMAL GROWTH IS SUSPECTED WHEN: Discrepancy between HC and AC AC >5th but is crossing centiles by >30th centile Change in AC of <5mm over 14 days EFW crossing centiles by >30
Risk factors for SGA
History of previous SGA or stillbirth (3-fold increase)
Maternal age >40y
Maternal or paternal history of being SGA at birth
Smoking >10 cigarettes/day (if smoke-free by 15/40, no increase in risk)
Cocaine use
Some maternal diseases
Heavy early pregnancy bleeding
Low PAPP-A <5th centile at time of NT scan
DEVELOPED RISK FACTORS Fetal echogenic bowel Current PET Severe gestational HTN Unexplained APH or abruption Low gestational weight gain
Symphyseal fundal height - tell me about it
Serial SFH recommended from 24/40
- If <10th on customised chart, or crosses centiles, refer for USS
- Routine USS for low risk women does not improve outcomes
Serial ultrasound if SFH measurement inaccurate
- BMI >35
- Large fibroids
- Hydramnios
Sensitivity for detecting SGA approx 30%
Significant intra and inter-observer variation
Discuss aetiology of placental insufficiency
Non-pregnant - Low flow, High pressure circulation
Normal pregnancy
- trophoblasts from the placenta invade the spiral arteries –> decidual layer
Result- High flow, low pressure circulation
Allows a dramatic increase in blood flow from ~50ml/min in the first trimester to 500ml/min at term
Pregnancy with FGR
- Trophoblast invasion is often inadequate
- Reduced perfusion on the intervillous space
Antenatal management of SGA
Early onset <32/40
- refer MFM
- consider karyotype
- detailed anatomy scan
- TORCH screen (organisms most a/w FGR - CMV, rubella, HSV, varicella)
Give advice on FM
Sleeping on side, PET symptoms
Regular BP and urine
Optimal interval for serial screening is >2 weeks with fewer false positive diagnoses of SGA if 3 week interval
Monitoring (AFI/Dopplers, CTG) up to twice weekly for SGA fetus
Why and when do uterine artery dopplers
In those at high risk of severe or early SGA
at 20-24 weeks
may help identify the subgroup at highest risk
Failure of trophoblast invasion of the myometrial spiral arteries in the early stages of pregnancy may lead to persistent high resistance vessels or notching and abnormal flow after the 1st trimester
Very abnormal uterine artery Doppler –> ~60% risk of SGA or PET requiring delivery <34/40
Dopplers to stratify risk in SGA
Normal UAPI
- Plan delivery by 40+0
Subgroups a/w higher risk of morbidity - deliver by 38/40:
- Abn MCA Doppler
- Abnormal CPR
- Abnormal uterine artery Doppler studies at SGA diagnosis
- EFW <3rd
* if can’t measure MCA/CPR, deliver by 38/40
Abn UAPI, but + EDF
- Twice-weekly fetal and maternal surveillance as outpatient
- Deliver 37 - 37+6
Absent or reversed EDF
- refer same day for IP monitoring
- AEDV - deliver from 34/40
- REDF - deliver from 32/40
Key points of
Disproportionate Intrauterine Growth Intervention Study at Term (DIGITAT)
Optimum time for delivery in SGA pregnancies is ~38/40
- Lowest risk of severe FGR and perinatal morbidity
- Cost effective
No increased risk of CS
Expectant management associated with increase in severe IUGR and PET
Expectant management was twice-weekly CTGs and daily fetal movement monitoring
- No good evidence to support this surveillance, but in DIGITAT there were no perinatal deaths in >600 SGA pregnancies
Intrapartum monitoring for SGA
Unit with NICU
cEFM
Present early in labour to monitor
Consider balloon induction or ARM (to reduce hyper stimulation)
Mode of delivery
- Increased risk of CS, especially with abn UA PI and MCA, or AC <5th
Neonatal monitoring for SGA
Infants confirmed to be SGA at birth require monitoring for hypoglycaemia, hypothermia and jaundice
BSL 1.2 –> NICU
Jaundice more common b/c of polycythaemia
Consider Ix
- Placenta for histo
- Karyotype
- infections
SGA post-natal care and counselling
20% recurrence risk
Review history to identify modifiable factors and/or treat maternal disease
Avoiding a short or long interpregnancy interval
In future pregnancies:
- Accurate dating by early USS
- Serial USS
- Low dose aspirin may be effective when FGR is secondary to PET
Delivery indications before 32/40
Maternal indications for delivery
Absent A wave in ductus venous - indicates fetal cardiac demonpensation
Reduced STV (<3) Or recurrent decels on CTG
Between 26 and 29 weeks of gestation, each day in utero has been estimated to improve survival by 1-2%
Truffle notes
- safety net trigger delivery overall rate 38%
- up to 52% in late DV changes group being delivered for other indications
- only 10% actually delivered for absent a wave
What is zygosity?
What proportion are MZ and DZ?
Refers to the genetic makeup of the twins / number of fertilised zygotes
Monozygotic = same genetic material
- 1/3
Dizygotic = simultaneous fertilisation of two eggs by two sperm = different genetic material
- 2/3 of twins
- Always DCDA
What stages of splitting result in different types of twins
Monozygotic
- Cleavage occurs by day 3 –> DCDA
- Cleavage within day 4-8 –> MCDA, most common (70% of MZ twins)
- Cleavage day 9-12 –> MCMA 1-2%
- Cleavage after 13 days then conjoined twins with incomplete division of the embryo - “unlucky number 13”
Epidemiology of twins
70% dichorionic, 30% monochorionic
- 1% of MC twins are MCMA
MZ twinning rates are constant throughout the world
3-5 per 1,000 births
DZ twinning rates affected by:
- Maternal age (increasing)
- Race
- Nutrition
- Geographical location
- ART - Increases DC and MC twinning
Combined first trimester screening
Sensitivity: 72-80%
Use of nasal bone assessment can improve sensitivity to 89% for a fixed 5% false positive rate
Nuchal translucency:
MC:
- Uses mean NT for both
-Higher FPR, NT can reflect early manifestation of other complications such as TTTS
DC:
- Uses individual NT for each
- Can calculate fetal specific risk or pregnancy specific (sum of both)
Triplet - USS markers alone, serum unreliable
NIPT for twins?
Meta-analysis found 99% sensitivity for trisomy 21, 85% for trisomy 18 in twins
Note limited number of MZ twin pregnancies in this meta-analysis, but sensitivity probably similar to singleton
Higher failure rate with first sample (2% singletons, 6% twins) due to lower fetal fraction of the two fetuses used to avoid false negatives in discordant DZ twins
Fetal implications of twins
Increased structural abnormalities
- DZ - 2x singleton b/c 2 babies
- higher in MZ (3-fold) due to uneven distribution of the inner cell mass when it splits - Abnormalities are often midline, particularly cardiac
Increased chromosomal abnormalities
Preterm birth
- 60% twins born <37/40. 5x DCDA, 10x MCDA
- Cochrane review - No indication bedrest, tocolytics, progesterone, cervical cerclage to prevent spontaneous PTB in twins
FGR (in 25%)
APH - larger placental surface, increased praevia and abruption
Larger placental surface, increased praevia and abruption
Stillbirth - higher for MC (5x higher)
Increased risk of cerebral palsy - 4-8x greater in twins, even when adjusted for gestational age and birthweight, 47x greater in triplets
Feeding difficulties
Maternal risks of twins
Hyperemesis PET / hypertensive disease (4x) Anaemia GDM (2x increased risk) PPH Adverse puerperal mood change (PND) Operative delivery Maternal mortality (2.5x increased risk)
What are specific risks of MC twins
Higher fetal loss rates than DC twins, mainly due to second trimester loss
May have a higher risk of associated neurodevelopmental morbidity
MC specific complications:
- TTTS
- Selective IUGR
- Death of one twin
- TRAP
Pathophysiology for MC twin complications
95% of MC twins have a shared placenta with vascular anastomoses between the two circulations
Anastomoses are bidirectional in 80% which rarely leads to issues, but means direct vascular connection in case of fetal death.
10-15% suffer an adverse outcome because of these connections
Three types:
- Artery to artery
- Vein to vein
- Artery to vein
Superficial are a-a and v-v = protective
Deep are a-v –> unidirectional flow = TTTS –> donor and recipient twin
Scanning in MCDA twins
USS signs such as discordant NT or CRL in the first trimester increase the likelihood of later diagnosis of TTTS or IUGR
2 weekly USS from 16/40
- Shown to reduce the incidence of ‘late stage’ TTTS
SDP for each twin
Review bladder and stomach
Biometry
UAPI
MCA PSV from 20/40
Quintero staging and associated survival ( of at least 1 with Rx) with TTTS
The course of TTTS is unpredictable and may involve improvement or rapid deterioration with a short time span
I: 90%
D - oligo, bladder visible, normal doppler
R - poly (>8cm <20/40, >10cm after 20/40)
II: 88%
D - no bladder
III: 67%
Critically abnormal doppler in either twin
IV: 50%
hydrops in either twin
V:
1 or both babies have died