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
Risk factors for PTB
Hx of preterm birth - 15% if 1 previously, 40% if 2 and 67% if 3 prior - Only 10% of pre-term births occur in those with Hx of spontaneous PTB Hx of mid-tri loss Short cervix in mid tri 2+ LLETZ / 20mm LLETZ / cone Prev D&C / STOP Prev CS at fully Congenital uterine anomalies Multiple pregnancy Polyhydramnios Low BMI Smoking, cocaine Low SES Vaginal bleeding Increased maternal age Ethnicity Use of ovulation induction drugs ART Short inter-pregnancy interval Maternal medical issues Infection Poor antenatal care
Interventions with no effect on rate of PTB
Self-palpation of UA
Home monitoring using uterine contraction monitor
Routine digital assessment of cervical length
Use of antioxidants (Vitamin C and E)
Abstinence
There is an association with stress, physical work and PTL, however little evidence that behavioural modification reduces PTB rate
Western Australia Preterm Birth Prevention Initiative
Whole 9 months study
Reduced PTB rate by 7.6% in 1 year
- No pregnancy to be ended prior to 38+ weeks unless clear medical or obstetric justification
- Measurement of cervix length to be included in all mid-pregnancy scans, conducted routinely at 18-20 weeks
- PV progesterone 200mg nocte if cervix <25mm between 16 and 24/40
- If cervix <10mm, management can include, cerclage, vaginal progesterone, or both
- PV progesterone 200mg nocte in those with prior Hx of spontaneous PTB between 20 and 34/40
- Offer smoking cessation
- Dedicated PTB prevention clinic established at teritary centres
Cervical screening recommendations
Consider assessment of cervical length at 18-24 weeks in women at low risk of PTB
TVS more accurate
Median cervical length at 20 weeks = 42mm 25mm is 3rd centile for population 15mm - 4% chance of preterm birth <33/40 <15mm - risk increases dramatically 5mm --> 78%
Funnelling = effacement of the internal aspect of the cervix
Much less reliable as a predictor because it is subject to inter- and intra-observer variation and artefact
Indications for cervical screening
Screening in high risk women - a long cervix (>25-30mm) is reassuring
- Screening has a high sensitivity and PPV (both >60%) in women with a prior PTB and a singleton pregnancy, therefore intervention most effective in this population
High NPV if symptomatic but long cervix
Routine screening (Cochrane, 2013) - Knowledge of TVS cervical length was associated with a non-significant decrease in PTB <37/40 and <34/40 –> insufficient evidence for routine screening
Prevention of PTB
Screen ALL and treat at first visit with MSU for asymptomatic bacteriuria
Cochrane 2015
- Treatment of bacteriuria results in reduced incidence of:
○ Bacteriuria
○ Pyelonephritis
○ Low birthweight
PTB
Screen and treat ALL pregnancy women for chlamydia
- 5% of women positive, 15% in Maori
- 5-fold increased risk in PTB
- Treating chlamydia may not reduce the risk of PTL, but other obvious benefits
BV -
- a/w 2-5x increased risk, but no evidence treatment helps
Smoking cessation
Marijuana - increased risk of PTB
Contraception and pregnancy planning
Fish oil - Cochrane review, 11% reduced risk
What is FFN and how is it useful?
Glycoprotein found in high concentrations in the cervicovaginal secretions, before fusion of the membranes occurs at around 21/40
Disruption of the choriodecidual interface >21/40 –> secretion of FFN into the cervix and vagina
High NPV >99% (of not delivering within 1 week)
Use quantitative fFN reduces admissions and costs without impacting adverse outcomes
Mode of delivery for preterm
BREECH
Extremely preterm <28/40
- CS a/w significantly reduced IVH
- NNT to prevent neonatal death = 8
After 28/40, not enough evidence to guide (Cochrane)
- individualise
CEPHALIC
- Lack of strong evidence to suggest benefits of one mode of delivery over another
- Ventouse CI <34
Forceps - relative CI <34
PPROM incidence
3% of pregnancies between 22+0 and 36+6
Majority deliver within 1/52 of PPROM
Diagnosis of SROM
Pooling of fluid
If pooling not seen, can test vaginal fluid
- Placental alpha-microglobulin-1 test (PAM-1) = Amnisure
PAMG-1 concentrations are >1000 times higher in amniotic fluid than is found in unexposed vaginal secretions
High sensitivity 99.0% and specificity 100% when used correctly
Management of PPROM
400mg QID if erythromycin ethylsuccinate for 10 days
Expectant management should be favoured
RCTs comparing immediately delivery and expectant management between 34+0 and 36+6
PPROMT - Similar risks of neonatal sepsis (2% vs. 3%), IOL increased the risk of respiratory morbidity
Steroids - Reduces risk of RDS, intraventricular haemorrhage, NEC
Tocolysis
- Not show to prolong delivery interval or reduce neonatal morbidity
- Consider to allow steroids or transfer
Indications for PV progesterone
Vaginal progesterone is recommended for asymptomatic women with a short cervix (<25mm) on TV cervical length assessment in the midtrimester
Vaginal progesterone therapy should be considered for women with a singleton pregnancy with a history of previous spontaneous preterm singleton birth
- And offer TV cervical length
If multiple pregnancy is the only risk factor, progesterone alone does not make a difference
Singleton pregnancy (EPPPIC) - PV progesterone reduces PTB <37/40 and <34/40, non-significant <28/40
Better in women with short cervix, rather than history indicated
Biological plausibility for progesterone and its effects which facilitate uterine quiescence during pregnancy
Reduces myometrial sensitivity to oxytocin
Blocks adrenergic receptors and prostaglandin synthesis
Cervical cerclage - Hx indicated
RCOG:
- Recommends history-indicated cerclage should be offered if 3 or more previous PTB and/or second trimester losses
- Should not be routinely offered if 2 or fewer - offer these women monitoring with TVS
Data suggests that monofilament suture a/w less perinatal death and PTB - Mersilene tape a/w increased pro-inflammatory cytokines
Evidence from various meta analyses suggests that cervical cerclage likely to reduce incidence of PTB in women consider to be at ‘very high risk’ of a second trimester miscarriage due to a cervical factor
- Likely those whose with >3 prior PTB or second trimester losses
Some studies suggest if fewer PTB/misc then cerclage a/w worse outcomes
Cervical - USS indicated
USS indicated cerclage benefits women with pre-existing PTB risk factors
- Reduce unnecessary cerclage
- Birth <35/40 and CL <25mm
Rescue cerclage
Acute presentation of dilated cervix
- Cervical dilatation with no contractions or PPROM
- Miscarriage ‘ almost inevitable’
<24/40
Time gained is vital but outcome will depend on GA at insertion
Counselling should include information about care at birth at peri-viable gestational age
RCT (small numbers) 50% reduction in PTB <34/40 when compared to bed rest
Timing of steroids
Betamethasone 11.4mg IM 24h apart
<34+6
PTB is expected within the next 7 days
Repeat dose:
<32+6
>7 days following a single course of steroids
PTB is expected within the next 7 days
- single dose 11.4mg betamethasone max of 3
Betamethasone > dexamethasone
- Less neonatal cystic periventricular leukomalacia
- Larger reduction in RDS
Risks and benefits for steroids
MATERNAL
- No maternal health benefits
- No serious health harms
- GI upset, Glucose intolerance, Insomnia, Pain/brusing at injection site , Weight gain, Cushing syndrome
INFANT Benefits: - Perinatal death - Neonatal death - RDS (NNT 13) - IVH - NEC - Systemic infection within 48h - Need for NICU and duration of respiratory support Single dose - no differences for birthweight, APGAR
Compared to no repeat, reduced risk of:
- RDS
- Serious neonatal composite outcome
- PDA
- Use of mechanical ventilation, oxygen supplementation, surfactant and inotropes
Reduced mean body size - by hospital discharge, no difference
Borderline reduction in birthweight and HC
Tocolysis
No improvement in perinatal mortality or morbidity has been shown with use of tocolytic drugs
- Studies often underpowered
Consider if the few days gained would be put to good use
- Completing corticosteroids
- In utero transfer
Cochrane meta-analysis comparing nifedipine to other tocolytics
Less RDS, NEC and intraventricular haemorrhage
MgSO4 for preterm birth
Meta-analyses of RCTs have found that MgSO4 administered to women is established PTL or having a planned PTB in the following 24h reduces cerebral palsy (RR 0.68) and motor dysfunction in the offspring
The benefit is greatest before 30+0
NNT 46 to prevent 1 CP in <30/40
Timing: Minimum of four hours before birth
Suspected mechanisms for MgSO4 in neuroprotection
MgSO4 may block NMDA receptors on oligodendrocytes
Also implicated in tissue protection against free radial activity
Acts as a vasodilator
Reduces vascular instability
Prevents hypoxic damage
Maternal side effects of MgSO4
Common (50% experience some side effects):
- Flushing
- Nausea and vomiting
- Headaches
- Sweating
- Injection site issues
More unusually:
- Hypotension
- Tachycardia
- Toxicity
Rarely in those with neuromuscular disorders:
- Muscle weakness
- Paralysis
MgSO4 toxicity treatment
Calcium gluconate
- IV 1g (10ml of 10% solution) slowly over 10 mins
Management of macrosomia
USS estimation of fetal size for suspected LGA unborn babies should not be undertaken in a low-risk population
Cochrane review 2016 - management of suspected fetal macrosomia (birthweight >4000g)
IOL shortly before term in non-diabetic women:
1. Reduces mean neonatal birthweight
2. Reduces the chance of neonatal fracture (NNT to prevent one fracture = 60)
3. Reduces the chance of shoulder dystocia
4. Does not increase the rate of CS or instrumental delivery
5. May increase the chance of third and fourth degree tears (paucity of evidence)
Incidence and associations of polyhydramnios
Incidence ranges from 1-2% Associated with: - PTB - Abruption - Fetal anomalies
Most common mechanisms:
- Decreased fetal swallowing
- Increased urination
Causes of polyhydramnios
Fetal anomalies and neoplasms (1/3 of cases)
Congenital mesoblastic nephroma
Aneuploidy
- Trisomy 18 (especially if poly + FGR)
- Trisomy 21 can be a/w poly, likely related to duodenal atresia
High fetal cardiac output states / anaemia TTTS Maternal diabetes Fetal infection (parvovirus) Fetal Bartter syndrome
Maternal drug use, including lithium
Maternal hypercalcaemia
Idiopathic - 40% of cases
Evaluation of polyhydramnios
Medical history
- Heritable diseases
- Consider infection - in the absence of maternal signs and symptoms or fetal findings (other than poly), congenital infection is an unlikely cause of isolated polyhydramnios
Anatomy scan
Assess fetal growth
Re-screen for diabetes
Evaluate for fetal hydrops, fetal anomalies
Measure MCA PSV
Offer genetic counselling and fetal genetic studies if
- Congenital anomaly is detected
- Severe polyhydramnios, even if appear isolated
Consider Bartter syndrome
If severe polyhydramnios and symptomatic (SOB, abdo discomfort), can do decompression amniocentesis to normalise fetal volume
Outcomes / risks of poly
Many idiopathic cases resolve spontaneously Maternal respiratory compromise PROM PTL and PTB Fetal malposition Macrosomia Umbilical cord prolapse Placental abruption upon SROM Longer second stage Postpartum atony - Increased risk of PPH
SGA with poly have poorest outcomes
2-5x increased perinatal mortality
Risks of oligo
Adequate volume of amniotic fluid is critical to normal fetal movement and lung development, and for cushioning the fetus and umbilical cord from uterine compression Risk of: - Fetal deformation - Pulmonary hypoplasia - Umbilical cord compression - Risk for fetal or neonatal death
Causes of oligo
MATERNAL Medical or obstetric complications associated with uteroplacental insufficiency PET Chronic HTN Collagen vascular disease Nephropathy Thrombophilia Medications (e.g ACE-I)
FETAL Chromosomal abnormalities Congenital abnormalities Growth restriction Demise Post-term Rupture membranes Infection
PLACENTAL
Abruption
Twin to twin transfusion
Placental thrombosis or infarction
Recurrent APH and Rhesus negative
If recurrent bleeding after 20+0, give at minimum of 6 weekly intervals
NZ blood bank - up to 2 weekly intervals
When to give other blood products in bleeding
Fresh frozen plasma
- 4 units of FFP (12-15 ml/kg or total 1L) for every 6 units of red cells, or if PTT and/or APTT are >1.5x mean control
Platelets concentrates
- If plasma count <50 x 109/L
Cryoprecipitate
- If fibrinogen <1 g/l
Aetiology of placental abruption
3-6 per 1000 pregnancies
70% in low risk pregnancies
Bleeding often concealed
Perinatal mortality rate as high as 48%
Two potential mechanisms:
- Acute inflammation
- Chronic vascular dysfunction
What is a couvelaire uterus
If large pressure generated in the uterus, the blood can extend into the myometrium –> becomes weakened and can rupture with increased intrauterine pressure during contractions
Uterus appears severely bruised and is infiltrated with blood
Risk factors for placental abruption
Abruption in a previous pregnancy (10% recurrence) PET/HTN FGR Non-vertex presentation Polyhydramnios Advanced maternal age Multiparity Low BMI Pregnancy following ART Intrauterine infection Premature rupture of membranes Multiple pregnancy Abdominal trauma Smoking (90% increase in the risk of abruption) Cocaine and amphetamines First trimester bleeding increases the risk of abruption in later pregnancy Maternal thrombophilias
Definitions of placenta praaevia
and incidence
1 in 200 pregnancies at term 5-28% at 20/40 - 3% of those remain at term Migration is less likely if: - Placenta is posterior - Previous CS
Placenta praevia
- When the placenta lies directly over the internal os
Low lying placenta
-Placental edge is <20mm from the internal os on TA or TV scanning in pregnancies >16/40
Risk factors for placenta praevia
Previous placenta praevia Previous Caesarean section (RR 2.6) Previous TOP Multiparity Advanced maternal age (>40y) Multiple pregnancy Smoking Deficient endometrium due to presence or history of: - Uterine scar - Endometritis - MROP - Curettage - Submucosal fibroid Assisted conception
Antenatal management of LLP
Rescan at 32/40 +/- 36/40
Optimise Hb and iron
Hospitalise in 3rd trimester dependent of woman - Cochrane review - no difference between home and hospital but increasing risk of em LSCS and transfusion after 2x APH. Shortened cervix at 34/40 increases risk of emergency delivery and massive haemorrhage
If IP - valid G&H, consider VTE prophylaxis
Steroids
- RCOG: Single course is recommended between 34+0 and 35+6, or earlier if increased risk of PTB
Timing of delivery
Late preterm (34+0 to 36+6) - if Hx of vaginal bleeding or other risk factors for preterm delivery Uncomplicated praevia, consider delivery between 36+0 and 37+0
Risk of emergent bleed:
- 4.7% by 35/40
- 30% by 37/40
Definition of accreta
Abnormal adherence of the placenta in whole or in parts to the underlying uterine wall in the partial or complete absence of decidua
Histopathological term
Accreta - Chorionic villi adheres superficially to the myometrium without interposing decidua
Increta - Villi penetrate deeply into the uterine myometrium down to the serosa, but do not extend to the outermost layers of the uterus
Percreta - Villous tissue perforates through the entire uterine wall and may invade the surrounding pelvic organs
The neo-vascularisation caused by the growing placenta percreta may soften the tissues of the adjacent organs and stimulate invasion
Pathophysiology of accreta
It is believed that the decidua basalis, a layer than prevents invasion of the trophoblast cells deeper into the myometrium, can be damaged due to previous surgery
Risk factors for accreta
Previous accreta Other uterine surgery AMA ART Previous CS (incidence if praevia vs. no praevia) - 0 - 3% vs. 0.2% - 1 - 11% vs. 0.3% - 2 - 40% vs. 0.5% - 3 - 61% vs. 2% - 4 - 67% vs. 2.3%
Diagnosis of accreta
USS imaging is highly accurate when performed by a skilled operator with experience in diagnosing placenta accreta spectrum
- Sensitivity 90%
- Specificity - 96%
USS findings:
- Abnormality of bladder / uterus interface
- loss of the clear zone (plan in myometrium under placental bed)
- Abnormal placental lacunae
- Myometrial thinning
- Focal exophytic mass
Doppler:
- abnormal vascularity between bladder wall and below placenta
MRI may be used to complement USS to assess the depth of invasion and lateral extension of myometrial invasion
Antenatal management of placenta accreta
Elective admission from 34/40 advised with steroid cover
Treat anaemia / iron deficiency
Emergency contingency plan is strongly recommended
Recommend patient remains close to the hospital for the duration of the third trimester
If suspected, manage on the assumption that accreta is present
Surgical management options of placenta accerta
Planned delivery at 35+0 to 36+5
Interventional radiology - balloons to iliac arteries, needs further evaluation
- Potential complications: iliac artery thrombosis or rupture, ischaemic nerve injury
Ureteric stents - consider if bladder involvement
Deliver baby and attempt delivery of the placenta
- high likelihood of hysterectomy
- can increase blood loss, not first line
Delivery baby via a uterine incision distant from the placenta, quick repair of uterus and en bloc hysterectomy
- preferable option
Deliver baby via uterine incision distant from the placenta, trim cord close to insertion site, full repair of uterus, and then conservative management
- 1/3 will still require hysterectomy because of uncontrollable bleeding
- risks of infection, use of resources
- good fertility rates after, but risk of recurrence
- no evidence for MTX
Incidence and pathophysiology of vasa praevia
Prevalence: 1 in 2500
Survival 97% when diagnosed antenatally
44% survival when diagnosis made during delivery
Fetal vessels crossing the internal os through the free placental membranes
Unprotected by placental tissue or Wharton’s jelly of the umbilical cord
Types of vasa praevia
Type 1 - occurs secondary to a velamentous cord insertion (90%)
Type 2 - occurs when fetal vessels connect lobes of a placenta, e.g. succenturiate lobe (10%)
Risk factors for vasa praevia
IVF - Increases the risk of type 1 vasa praevia to ~1 in 250
Placenta praevia
Bilobed placenta
Succenturiate placental lobes
A history of LLP in the second trimester
Multiple pregnancy
Velamentous cord insertion
- Occurs in ~1% of all pregnancies
- Vasa praevia occurs in 2% of velamentous placental cord insertions
Diagnosis of vasa praevia
TV USS sensitivity 100% and specificity 99% when performed with colour Doppler
There is insufficient evidence to support universal screening in routine FAS
The presence of velamentous cord insertion, succenturiate lobe, placenta praevia, IVF pregnancy or other risk factors at the FAS should prompt further evaluation by TV USS performed by appropriately trained personnel
Management of vasa praevia
Vasa praevia diagnosed in the second trimester resolves in ~20% prior to delivery
- Therefore repeat USS at 32/40
Given the speed at which fetal exsanguination can occur, recommend hospital admission from 30-32 weeks
- Especially in cases of multiple pregnancies, APH, TPTL
- Evidence for hospitalisation is weak
Outpatient management of select asymptomatic singleton cases with a long, closed cervix on serial TVS and a negative FFN
Elective CS at 34-36 weeks with steroids from 32/40 - in asymptomatic
If vasa praevia, and develop PROM or labour at viable gestational, CS should be performed immediately
Total fetal blood volume at term is ~80-100ml/kg
- Neonatal resuscitation +/- immediately transfusion with O Rh negative blood
Placental pathological exam should be performed to confirm diagnosis
Uterine rupture definition
Full thickness loss of integrity of the uterine wall and visceral peritoneum
Uterine rupture is rare with an unscarred uterus
- 0.5-2 per 10,000
5% risk of recurrence
Uterine scar dehiscence = does not involve the visceral peritoneum
FGM definition
Female genital mutation.
all procedures involving partial or total removal of the external female genitalia or other injury to the female genital organs whether for cultural or other non-therapeutic reasons
RANZCOG’s statement on FGM
RANZCOG “ condemns the practice of any form of FGM as a violation of the human rights of girls and women”
- FGM is prohibited by specific legislation in all States and Territories of Australia, and in NZ
- Legislation also prohibits providing any assistance with procuring or facilitating the performance of FGM whether within Au/NZ or overseas where the female is an Au/NZ citizen
Type 1 FGM
Clitoroidectomy
Partial or total removal of the clitoris and/or the prepuce
Type 2 FGM
Partial or total removal of the clitoris and the labia minora +/- excision of the labia majora
Type 3 FGM
Infibulation
Narrowing of the vaginal orifice with creation of a covering seal by cutting and appositioning the labia minora and/or the labia majora +/- excision of the clitoris
Type 4 FGM
All other harmful procedures to the female genitalia for non-medical purposes
Women at risk of FGM
Africa especially North East
- Somalia (98%), Sudan, Egypt (91%), Ethiopia, Sierra Leone, Guinea, Djibouti, Mali
Also few populations in Middle East and Asia
In Sudan and Somalia, more than 80% of women have undergone FGM (mostly type 3)
Communities of all religions practice FGM
- Highest prevalence among Muslin girls and women
- FGM is not condoned by any religion
Protective factors for reducing FGM
Education
Wealth
Long term consequences of FGM
Impaired sexual function - Infertility Recurrent UTI, prolonged voiding, urethral damage --> stricture, dysuria, chronic urinary obstruction Increased risk BV Local scar complications (e.g. keloid, epidermoid inclusion cysts) Local pain - chronic neuropathic pain Menstrual problems - haematocolpos Difficulty with minor gynae procedures PTSD, anxiety, depression
Antenatal management of FGM
Explain law in NZ/Au
Consider SW / psych referral
if required, offer antenatal deinfibulation (second trimester, otherwise can be done in labour)
Offer STI, HBV, HCV, HIV screening
Recommend labour in hospital
Refer to obstetrician with special interest in FGM
Carefully document exam findings to avoid repeat exams
Potential issues with FGM in pregnancy
Difficulty with VE, intrapartum procedures (ARM, FSE placement), IDC
Increased likelihood of severe perineal trauma and vaginal laceration, episiotomy, risk of CS, prolonged labour and PPH
Fear of childbirth
Increased need for neonatal resuscitation, risk of stillbirth and early neonatal death
Deinfibulation indications
Issues with sexual function, normal voiding, menstruation
To facilitate VE, speculums and intrapartum care
Brief description of deinfibulation
Surgical procedure to restore the vaginal introitus in a women who has previously undergone type 3 FGM
Minor procedure
Extend incision anteriorly to allow visualisation of the external urethral meatus
- but not far enough to injure the buried clitoris or clitoral stump (risk of heavy bleeding)
Approximate skin edges with fine, absorbable suture
Maternal health benefits of deinfibulation
Improve urine flow and perineal hygiene
Facilitate gynaecology exams / procedures (e.g. Speculums and smears - for cervical cancer prevention)
Reduced risk of perineal trauma and lessen the severity of such trauma - allows more space for the delivery of the fetus
Secondary to this, decreases the risk of PPH and its subsequent risks
Intrapartum care of FGM
Recommend labour at hospital, with immediate access to emergency obstetric care
- IV line + FBC and G&H in labour
Anterior episiotomy may be required at the time of delivery
No an indication for CS
Routine episiotomy not necessary
- But will frequently be required because of increased scarring and lack of normal skin elasticity
Re-infibulation for non-medical purposes related solely to cultural, religious or other social customs is against the law
Follow up appointment at 6/52
Timing of delivery for twins
ARCH study - better outcomes for policy of routine delivery at 37/40 for DCDA
DCDA
Between 37+0 and 38+0
MCDA
Between 36+0 and 37+0 (if otherwise uncomplicated)
Increased risk of antepartum stillbirth after 37/40
MCMA
Between 32+0 and 34+0
High risk of fetal death
TCTA or DCTA triplet
Between 35+0 and 36+0 (if otherwise uncomplicated
Risks of CS for placenta praevia
- Blood loss >1000ml 20%
- Blood transfusion 12%
- Peripartum hysterectomy 5%
- Preterm delivery <37 weeks 44%
- Admission to intensive care approximately 1%
- Mortality <1%
- Ureteric injury 0.4%
Cochrane 2018 – non-clinical interventions for reducing unnecessary caesarean section
- Childbirth training workshops for mothers and couples
- Nurse and midwifery led relaxation techniques
- Psychosocial couple based prevention programs
- Implementing clinical practice guideline combined with mandatory second opinion for caesarean section for maternal request
- Collaborative midwifery -laborist 1:1 care with 24h available obstetrician
