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
What is TOPS?
Twin oligohydramnios / polyhydramnios sequence
‘Classical’ TTTS
What is TAPS?
Twin anaemia / polycythaemia sequence
Affects 3-5% of MC twins
Affects 10% of twins that undergo laser therapy for TOPS
Results in very slow transfusion from donor to recipient from miniscule artery vein anastomoses
Significant discordant MCA PSV without significant oligohydramnios / polyhydramnios
More common in later pregnancy
Treatment:
- Laser ablation
- Intra uterine RBC transfusion for donor twin
- If not treated, risk of neuro deficit for donor twin
Management of TTTS
Untreated stage 3-4 TTTS survival rate ~20%
Tertiary centre / MFM
Stage 1 observe, weekly USS and cervical length
Give steroids once viability attained
OPTIONS Laser ablation - 16-26/40 - Laser ablation does not appear to change (increase or decrease) the risk of overall death when compared to amnioreduction, but does result in more children being alive without neurological abnormality (Cochrane, 2014) - Recurrent TTTS in up to 14%
Serial amnioreduction
- Rationale: normalising fluid levels reduces maternal discomfort and improves uteroplacental perfusion
- Consider if laser ablation not possible, e.g. late gestation
- 25% of survivors have cerebral abnormalities
Septostomy
- Creates MCMA
- no longer done
Selective feticide
TOP
Selective IUGR in MC twins
15% of MC twins in the absence of TTTS
EFW <10th centile and / or discordance of >25%
Associated with:
- Unequal placental sharing and velamentous cord insertion
- Inter-fetal placental anastomoses
- Abnormal fetoplacental blood flow
The placental anastomoses may paradoxically benefit the smaller twin as transfusion from the larger twin may compensate for placental insufficiency - can sometimes push further than DCDA discrepancy
Types of sGR
I - growth discordance but positive diastolic velocities (forward flow) in both fetal UA PI
II - growth discordance with constant AREDV in one or both fetuses
III - growth discordance with cyclical / intermittent UA diastolic waveforms (positive followed by absent then REDF in a cyclical pattern over several minutes)
What is TRAP?
TWIN REVERSED ARTERIAL PERFUSION (TRAP) SEQUENCE
~1% of MC twins
Acardiac twin (with usually no cardiac tissue) being perfused by the anatomically ‘normal’ pump twin through a large A-A anastomosis
High perinatal mortality of the normal / pump twin (>50%) due to high output congestive heart failure and hydrops
Treatment:
- Refer to MFM
- Ideally Rx <16/40 - Cord occlusion therapy, especially if pump twin has signs of heart failure
- Amnio for genetic abnormalities
- Weekly USS
- AN steroids at viability
DEATH OF ONE TWIN / ACUTE FETO-FETAL TRANSFUSION SYNDROME
more common in MC and has global effects on the co-twin
Death (15%) or neurological disability (25%) in the survivor
- Occurs around the time of fetal death
- due to agonal hypotension –> blood volume of the survivor is dumped precipitously into the body of the co-twin through shared vascular communications - acute feto-fetal transfusion syndrome
Delivery of the survivor at a preterm gestation will not prevent further damage unless there is evidence of CTG abnormalities or significant fetal anaemia
MRI should be done 6 weeks after co-twin demise
MCA surveillance
Complications specific to MC vaginal delivery
Intrapartum acute feto-fetal transfusion
- Rare, affecting second twin after delivery of first twin
- Discordant Hb at birth (differentiate from TAPS by normal reticulocyte count, because acute transfusion)
MCMA twins
1% of MC twins
Very high risk pregnancy
Perinatal mortality 10-40%
- In part due to high rates of congenital anomalies (~20%)
Almost always have cord entanglement
Fortnightly scans from 16/40, increase once reach viability
Deliver by CS at 32-34 weeks after corticosteroids
Higher order multiple pregnancies
Selective reduction should be considered in all higher order pregnancies, including triplets
TRIPLETS
Aneuploidy screening
- Calculate from NT and maternal age only
Delivery by CS at 35/40 if uncomplicated
Fetal reduction to twins lowers PTB rate, but risk of miscarriage
Prenatal diagnostic testing with twins
Requires accurate mapping and reporting of fetal position, placental site and cord insertions
Amniocentesis
- Procedure-related losses after amniocentesis are approx equal to those of singletons, but the background miscarriage rates are greater in twins
- If MCDA twins, both sacs should be sampled during amnio unless MC confirmed <14/40 and the fetuses appear concordant for growth on anomaly scan
Selective TOP
Method depends on chorionicity
DC twins - intracardiac potassium or lignocaine
MC twins - cord occlusion
- Otherwise surviving twin is at risk of neurological sequalae
Miscarriage risk to the normal twin
<16/40 - 5%
>16/40 10-15%
Mode of delivery for twins
First twin breech
- Inter-twin locking - rare, ~1%
If leading twin cephalic, equivalent outcomes for SVB or CS - Higher risk of adverse perinatal outcomes for second twin but CS did not reduce this risk
- 45% CS rate even in planned vaginal delivery group
- Vaginally delivered second twins have a 4-fold increased risk of death
Neonatal morbidity after vaginal delivery was similar for non-vertex presenting and vertex second twin, particularly at lower gestational ages
5% CS rate for second twin
Internal podalic version and breech extraction for second twin
During vaginal delivery, the presentation of the second twin will change in up to 20% of cases
~30 mins is considered a reasonable time, after which delivery should be expedited
- Based on study that found deterioration in cord gases when interval is beyond 30 minutes
Preferred primary procedure for the second twin not presenting cephalic or breech
Higher success rates than ECV, with no increase in neonatal morbidity
If back up, grasp anterior foot
If back down, grasp posterior foot
Ideally perform with membranes intact
Incidence of PTB
PTB rate in Australia 7%
PTB rate in Australia higher for Indigenous mothers (14% vs. 8%)
Babies of Maori, Pacific and Indian women, and women <20y are more likely to be born at extremely preterm gestations
Poor countries and regions with more social disadvantage have higher preterm birth rates
- Teenage pregnancy more common
- BMI and poor nutrition status
- Infections
- Chronic disease
- Smoking
PTB - WHO definitions
Preterm birth = babies born alive before 37 completed weeks of pregnancy (7.5% of babies)
Moderate to late preterm 32-37 weeks - 6.3%
Very preterm 28-32 weeks - 1.2%
Extremely preterm <28 weeks - 0.5%
Prognosis and PTB
Two major determinants for morbidity and mortality:
- Gestation at delivery - Birthweight
Other factors associated with survival:
- Female gender
- Use of AN steroids
- Singleton birth
Survival:
- 8% at 23/40
- 74% at 28/40
Equates to improvement of 3% per day
Effect is lost >32/40 where no significant improvement in survival is demonstrated, however there is reduction in morbidity, particularly associated with RDS
Short term complications of PTB
Prolonged NICU stay RDS NEC Retinopathy of prematurity Sepsis Intraventricular haemorrhage Feeding difficulties
Childhood complications of PTB
Recurrent hospitalisation Long-term cognitive and sensory impairment Motor deficits Cerebral palsy Behavioural and psychological problems Developmental delay Chronic kidney disease Growth impairment Chronic lung disease
adulthood complications of PTB
Insulin resistance HTN Ischaemic heart disease Obesity Decreased reproduction Neurodevelopmental and social disabilities Early adult mortality
Aetiology of PTB
2/3 spontaneous, 1/3 “indicated preterm births”
Iatrogenic or medially indicated
Spontaneous labour / PPROM - multifactorial
- Cervical congenital anomaly, surgery, trauma
- Infection - ascending, intrauterine, systemic
- Multiple pregnancy, polyhydramnios
- Haemorrhage and placentation
- Endocrine - GDM, PCOS
- SE factors - smoking, drug use, deprivation, access to care
Labour is an inflammatory process
Anything that could trigger inflammation early –> PTL
Final pathway involves inflammatory reaction with upregulation of prostaglandins, cytokines and other inflammatory mediators within the cervix, myometrium and fetal membranes
