Multiple pregnancy Flashcards
Discuss twin pregnancies
-Incidence in spontaneously conceived twins (3)
-Overall incidence of twins (1)
-Number of twin pregnancies due to fertility treatment (1)
-Rate of rise of multiple pregnancies (2)
-Reasons why multiple pregnancies are more common (2)
- Incidence in spontaneous pregnancy
-1:90 for twins 1%
-1:10 000 triplets 0.01%
-1: 600 000 quads 0.001% - Overall incidence of twins
-1.3% in NZ - Number of with pregnancies due to fertility treatment
-14% - Rise in multiple pregnancies
-70% increase over last 30 years
-Spontaneous twins account for a third of overall rise - Reasons for multiple pregnancies
-Older age of mothers
-ART
Discuss multiple pregnancies
-What does zygosity mean
-What does chronicity mean
- Zygosity: Number of fertilised eggs that pregnancy develops from
- Chronicity: Number of chorionic membranes / number of placenta
Discuss dizygotic twins
-Incidence (1)
-Development (1)
-USS findings (4)
- Incidence - 70%
- Development
-Develop from two eggs and two sperm (non-identical) - USS findings
-Scan between 10-14 weeks
-Lambda sign
-2 separate placental masses
-Thick septal edge
-Different sexes
Discuss monozygotic twins
-Incidence of DCDA, MCDA, MCMA (3)
-Development of different types (4)
-USS findings (3)
- Incidence
-DCDA - 30%
-MCDA - 70%
-MCMA - 1%
-Conjoined - Development
DCDA - single egg and sperm - Splits day 1-3
MCDA - single egg and sperm splits day 4-8
MCMA - single egg and sperm Splits day 8-13
Conjoined - single egg and sperm splits day 13-15 - USS findings
-Single placental mass
-Thin septum <1.8mm
-A-A anastomoses
-T sign
Discuss maternal complications of multiple pregnancies (14)
-Miscarriage
-Hyperemesis
-Anaemia
-GDM 2 x risk
-Preterm birth - iatrogenic and spontaneous
-Hypertensive disease 4 x risk
-VTE
-APH - increased placental bed
-Polyhydramnios - TTTS
-Operative delivery
-PPH - larger placental bed, over distension
-PND
-Maternal mortality 2.5 x risk
-Obstetric cholestasis
Discuss fetal complications of multiple pregnancies (8 groups)
Increased mortality. Increases with increased number
-5:1000 singleton, 12/1000 twins, 31/1000 triplets
-Increased with monochronicity esp. 20-30 weeks
Chromosomal abnormalities
-DC - 2 x overall risk each fetus same risk as singleton
-MC - same risk as singleton but both twins affected
Structural abnormalities
-DC same risk as singleton so 2 x risk
-MC 2-3 times risk due to uneven distribution of inner cell mass
Fetal growth restriction 2-3 x risk. More common in MC
PPROM
PTB - 60% of twins born before 37/40. 9% before 32/40
Long term disability - 4-8 x increased risk of CP
Infant feeding difficulties
What are the monochorionic specific fetal risks (4)
-Cord entanglement
-Selective IUGR
-TTTS
-TAPS
-TRAP
Discuss aneuploidy screening in multiple pregnancies
-Which screening tools can be used for twins
-Which screening tools can be used for triplets
- Twin pregnancy can use MSS1, MSS2, NIPT
- Triplets can use MSS1 only
Discuss MSS1 in multiple pregnancies
-When should MSS1 be done
-Which multiple pregnancies is it validated for
-How are results given for DC and MZ
-What is the sensitivity and why is it impacted
- MSS1 do 11-13+6
- MSS1 can be used in all twin and triplet pregnancies
- Results
DC - gives a chance score for each twin
MC - gives an overall chance score for the pregnancy
For MC twins use average of NT as it can differ - Sensitivity
-Same as for singleton pregnancies.
-Sensitivity is reduced secondary to maternal serum biomarkers
Discuss NIPT for multiple pregnancies
-When should NIPT be done
-Which multiple pregnancies is it validated for
-Discuss sensitivity and specificity for MZ and DZ twins
-Discuss reasons for higher failure rate (4)
- When should NIPT be done - After 10 weeks
- Which multiple pregnancies is it validated for - twins only
- Sensitivity and specificity
-99% for both for MZ twins
-Slightly less sensitive in DZ twins - Reasons for higher failure rates in twins
-Failure rate in singletons 2% failure in twins 6%
-Low fetal fraction
-Maternal obesity
-Suboptimal sample collection
Discuss prenatal diagnosis
-What form of prenatal diagnosis should be used for DC twins and why
-What form of prenatal diagnostic test should be used for MZ twins and why
-What are the considerations for prenatal diagnostic testing
- What form of prenatal diagnosis for DC twins
-CVS (11+2 - 13+6)
-Can do KCL selective reduction and this is done better at early gestations - What form of prenatal diagnosis for MC twins
-Amniocentesis (15+)
-Can’t do KCL for selective reduction. Must do cord occlusion. Better done later - Considerations
-Puts whole pregnancy at risk even if only one twin affected
-KCL risk of loss of remaining twin = 15%
-Cord occlusion risk of loss of remaining twin 13%
Discuss the implications of death of one twin
-Impact in MCDA (5)
-Impact if DCDA (6)
- Impact to MCDA twins
-Risk of death of remaining twin - 40%
-PTB 70%
-Abnormal antenatal cranial imaging - 30%
-Abnormal postnatal cranial imaging - 40%
-Neurodevelopmental impairment - 30% - Impact to DCDA twins
-Risk of death of remaining twin - 15% (5-10%)
-PTB - 50%
-Abnormal antenatal cranial imaging - 15%
-Abnormal postnatal cranial imaging - 20%
-Neurodevelopmental impairment - 10%
-Increased risk of CP
Discuss management of DC twins where one has died
-Causes (6)
-Monitoring (5)
-Reasons for delivery (2)
-Postnatal management (2)
- Causes
-FGR - increased risk with discordance >30%
-PET
-Abruption, infection, anomalies, cord accidents - Monitoring
-Anti-D if RH negative
-Weekly CTG
-Fortnightly growth scans - Reasons for delivery
-Death of a DC twin is not a reason for delivery
-Deliver if there is a condition affecting pregnancy as a whole - PET/DIC/ chorio
-Delay delivery if possible till >34/40
-Give steroids and MGSO4 as necessary - Postnatal management
-4-6 week postnatal MRI
-Long term neurodevelopmental FU
Discuss management when one MC twin dies in utero
-Incidence
-Causes
-Impact to surviving twin
-Management
- Incidence
-Spontaneous demise in 1% of MC twins - Causes
-TTTS (50%), Selective FGR, Fetal anomalies, TRAP, cord entanglement - Impact to surviving twin
-Result in acute haemorrhage and anaemia in live twin
-Can result in fetal heart failure
-Can cause severe brain damage >25%
-If occurs before 24/40 then high risk of second twin demise but less risk of brain damage
-If occurs after 24/40 then less risk of second twin demise but increased risk of brain damage - Management
-Offer TOP if peri-viable
-MRI 4-6/52 post fetal demise to assess fetal brain injury +/- feticide if intracranial pathology
-Weekly USS with MCA-PSV
-Weekly CTG
-Aim delivery at 37/40
-No point delivering early as damage already done unless acute concern for live twin
Discuss management of DCDA twins
-Antenatal (8)
- Antenatal management
-Determine chronicity approx 14 weeks and do NT if desired
-Consider LDA if additional risk factors for PET/IUGR
-Aneuploidy screening MSS1/NIPT
-OGTT for GDM
-Monthly scans from 20/40
-Check FBC at 20 - 24 weeks and 28 weeks
-Manage FGR same as in singletons
-Fe and folic acid supplementation for maternal anaemia
-Educate around PTD and consider Cx length but no evidence for progresterone or Cerclage
Discuss management of monochorionic twins
-Antenatally
-Delivery mode
-Timing of delivery
- Antenatal management
-Confirm chronicity before 14 weeks by USS
-Consider Fe and folic acid supplement for maternal anaemia
-Consider LDA if other risk factors
-Offer screening MSS1/NIPT for aneuploidy. Discrepancy of NT and discordant CRL can be an early sign of TTTS
-Monitor for PET with weekly BP and urinalysis
-USS fortnightly from 16 weeks to evaluate for TTTS - look at fluid volume, bladder volume
-Commenced UAPI and MCA PSV from 20 weeks or earlier if clinically indicated. Continue fortnightly until delivered
-Detailed anatomy scan at 20 weeks. Increased anomaly rate
-Advise women to report sudden increase in abdo girth or SOB. May be TTTS
-Refer to MFM if concern for TTTS, TRAP, TAPS, sFGR - Mode of delivery
-Aim vaginal delivery if leading twin cephalic and no other complications in pregnancy - Timing of delivery
-36-37 weeks if no complications
Discuss twin to twin transfusion syndrome
-Incidence (4)
-Pathophysiology (4)
-Contributing factors (3)
-Timing (2)
-Presentation (5)
- Incidence
-15% of MCDA twins. Less in MCMA twins
-Causes 17% of all perinatal deaths in twins
-Causes 50% of deaths in MC twins - Pathophysiology
-TTTS includes TOPS (Classic TTTS) and TAPS
-Deep placental AV / VA anastomoses of large vessels.
-Results in large volume transfusion from one twin to another
-Donor fetus is hypovolemic and hypo-perfused leading to oligouria and oligohydramnios
-Recipient fetus is hypervolemic and hyperperfused leading to polyuria, polyhydramnios and cardiac failure and hydrops - Contributing factors
-Cord insertion
-Relative share of placenta
-Fetal growth discordance - Timing of TTTS
-Onset usually 20-30 weeks. Can be anytime even intrapartum - Presentation
-SOB, increased abdominal girth of mother
-May see discordant CRL or NT at 14/40 but not predictive
-Discordant DV and NT RR 21 for TTTS
-Oligo and poly on USS
-Discordant bladder volumes (suggests severe TTTS)
-Cardiac dysfunction, hydrops in severe cases of TTTS
Discuss twin to twin transfusion
-Staging (5)
- Staging - used Quintero staging. Based on USS finginds
Stage I - DVP <2cm in donor sac, DVP >8cm in recipient sac (DVP >10cm after 20/40)
Stage II - Fetal bladder in donor twin not visualised over 60mins of observation
Stage III - Absent or reversed UAPI or reversed DV
Stage IV - Fetal hydrops in one or both twins
Stage V - Fetal demise of one or both twins
NB: Growth discordance is not a feature in TTTS or staging
Discuss management for TTTS
-General points (2)
-Management options (4)
-RANZCOG recommendations (5)
- General points (From RANZCOG guideline)
-Manage in a tertiary setting
-Offer referral to center with facilities for laser surgery - Management options
Expectant management
-In mild or late onset (>26/40) TTTS can do expectant management.
Intentional septostomy created monoamniotic - not used in practice as no benefit over amnioreduction
Amnioreduction
-Short term solution. Doesn’t fix underlying problem
-May reduce risk of PTB and complications of polyhydramnios but increased risk of SROM, abruption, infection and can make laser more difficult.
Laser photocoagulation
-From 16-26 weeks
-Interrupts anastomoses and functionally divides placenta into 2 regions.
-Solomon technique reduces rates of TTTS and TAPS - RANZCOG recommendations
-Laser ablation is recommended for early onset severe TTTS
-Early referral to appropriate centre is recommended when optimal treatment can be given before severe disease or short cx
-Ongoing surveillance for TAPS post laser
-Consider cord occlusion of one twin esp. if fetal anomalies
-Can consider expectant management or amnioreduction in mild or late onset >26/40 TTTS
Discuss outcomes for TTTS
-Without treatment (2)
-Rate of mortality in those treated at each stage
-Rate of neurological impairment in those treated
- Outcomes without treatment
-90% mortality
-50% neurological impairment in survivors - With treatment - chance of one twin surviving
Stage I - 91%
Stage 2 - 88%
Stage 3 - 67%
Stage 4 - 50% - Rate of neurological impairment - 12%
Discuss TAPS - Twin anaemia polycythaemia sequence
-Pathophysiology (4)
-Incidence (2)
-Timing (1)
-Presentation (2)
-Management
- Pathophysiology
-AV anastomoses of small vessels <1mm that are superficial in the placenta
-Results in smaller volume transfusions
-Can result from laser therapy for TTTS (10%)
-Results in polycythemia for recipient and anaemia for donor - Incidence
-3-5% MC twins
-10% after laser therapy for TTTS - Timing
-Usually occurs late in third trimester - Presentation
-Screen for anaemia with MCA PSV dopplers - >1.5MoM in donor and < 0.8 in recipient.
-Screen in high risk groups - post laser therapy, sFGR, AbN UAPI, unexplained isolated polyhydramnios - Management
-Individualised management
Discuss acute feto-fetal transfusion syndrome
-Pathophysiology (3)
-Outcomes (3)
-Management (3)
- Pathophysiology
-Results from drop in heart rate or blood pressure in one twin leading to a sudden massive loss of blood from the acute donor twin
-Similar to when one twin dies in MC twins
-Recipient twin doesn’t necessarily demise - Outcomes
-Risk of death to donor twin 50%
-Risk of death to recipient twin 15%
-Risk of brain injury to recipient twin 20-30% - Management
-Delivery of surviving twin not indicated as damage done
-MRI 4-6 weeks post event
-Refer MFM
Discuss selective growth restriction
-Definition (2)
-Incidence (2)
-Timing (1)
-Causes (3)
- Definition
One twin has EFW <10th centile and there is >25% discordance between twins
Categorised further based on diastolic flow - important for prognosis - Incidence
-10-15% of monochorionic twins
-50% of those with TTTS - Causes
-Uneven sharing of placental territory
-Varying cord insertions
-Inter fetal anastamoses
Discuss Classification of selective fetal growth restriction in twins.
-Classification types
-Delivery timing for each type
-Clinical features for each type
-RANZCOG recommendations on delivery timing (1)
GRATACOS classification - based on diastolic flow
Type I - Positive EDF in both twins
-Deliver >34/40
-90% survival
Type II - Persistent absent or reversed EDF
-High risk deterioration and IUD of FGR twin
-Deliver 29/40
Type III - Intermittent absent or reversed EDF
-Low risk hypoxia to FGR twin
-10-15% risk of unexpected IUD of FGR
-Aim delivery 32/40
2. RANZCOG recommendations
-Management strategies poorly defined and get expert advice +/- transfer to tertiary service
Discuss twin reversed arterial perfusion (TRAP)
-Definition
-Incidence
-Cause
-Prognosis
- Definition
-Acardiac twin perfused due to placental anastomoses with other twin acting as a pump - Incidence
-1% of monochorionic twins - Causes
-Death of one twin early in pregnancy
-Reversed flow through cord to acardiac twin by pump twin via large AA anastomoses
-Perfuses lower body of acardiac twin - Prognosis
-Untreated mortality 50%
-Fetal cardiac failure from high output, hydrops, IUFD
Discuss management of TRAP
-Diagnosis (1)
-Management (3)
- Diagnosis
-Dopplers - Management
-Ref MFM
-Treatment not required is no evidence of compromise to pump twin
-Could consider cord occlusion or laser treatment
Discuss monochorionic monoamnionic twins
-Incidence (1)
-Survival rate (1)
-Risks in pregnancy (2)
-Delivery mode and timing (1)
- Incidence
1% of all twin pregnancies - Survival rate
60% - Risks in pregnancy
-Same risk but worse in MCMA twins + cord entanglement - Delivery timing and mode
-CS at 32-34 weeks
Discuss timing of delivery for uncomplicated twins
-DCDA
-MCDA
-MCMA
-Triplets
- DCDA - 37 - 38/40
- MCDA - 36-37/40
- MCMA - 32/40
- Triplets 35-36/40
Discuss risk of still birth
-Beyond 39/40 in DCDA
-Beyond 32/40 in MCDA
-How should pregnancies be managed if women decline planned delivery
1.IUD in DCDA twins >39/40 = 1:70
2.IUD in MCDA twins >32/40 = 1:23
3. If declining delivery should undergo:
-Weekly LV and dopplers and CTG
-Fortnightly growth
Discuss mode of delivery of twins
-Factors for vaginal delivery (6)
-Factors for CS (6)
- Factors for VB in twins
-Diamniotic twins
-Leading twin cephalic
-Forward flow of UAPI
-More than 32/40
-No obstetric contraindication to labour
-Second twin is not >25% larger than leading twin - Factors for CS in twins
-Monoamniotic
-Conjoined twins
-Absent or reversed EDF
-Leading twin breech
-Higher multiples
-Any other obstetric complication
Discuss intrapartum care for twin delivery
1. General points (4)
2. Monitoring (3)
3. Analgesia (4)
- General points
-IV access
-Experienced obstetrician, anaesthetics, paeds, MW
-Access to CS OT
-Cross matched blood - Monitoring
-Continuous CTG. Can use FSC for first twin
-Confirm presentation on arrival
-If Twin 2 has CTG concerns before twin 1 born then offer section if VB not achievable in 20 mins - Analgesia
-Recommend epidural
-Improves chance of vaginal birth
-Enables quick recourse to CS
-Enables IPV
Discuss management of the second stage of twin delivery (6 points)
- Following delivery of first twin USS for presentation of second
- If second twin not cephalic: ECV if oblique, IPV to breech is transverse (IPV more successful 95% vs 40%)
- Consider oxytocin following delivery of first twin. Better outcomes with active managment
- Only ARM if required once PP in pelvis and engaged
- Delay cord clamping unless TAPS
- Active management of third stage
- Aim interval delivery of 30-60 mins. No hard fast rule but decrease in pH with increased duration of intertwin birth interval
Discuss complications of twin delivery
-Retained second twin
-CS of second twin
-Locked twins
- Retained second twin - delivery >30mins post first twin
-Results in second twin compromise as uteroplacental unit disrupted - CS for second twin
- occurs 5% of the time
-Due to fetal distress, malposition, cord prolapse - Locked twins
-1:1000 twin deliveries
-Head of leading breech locks with head of second twin which is cephalic
Discuss the ELCS vs VB for twins RCT
-Aim (1)
-Study design (3)
-Primary outcomes (1)
-Secondary outcomes
- Aim:
-To determine whether planned ELCS results in less adverse perinatal outcomes for twin delivery cf VB - Study design
-RCT in 25 countries
-Women with twin pregnancies with leading first twin cephalic
-Excluded MCMA twins, twins with contraindication to VB, twins with fetal anomaly, where twin B was substantially bigger than twin A - Primary outcome
-Composite measure of fetal and neonatal (d28) death or serious neonatal morbidity - Secondary outcomes
-Composite measure of maternal mortality and morbidity
Discuss the ELCS vs VB for twins RCT
-Number included in the study (2)
-Results of primary outcome (3)
-Results of the secondary outcome (1)
- Number included in the study
~2800 women and 5600 fetuses - Results of primary outcome
-90% CS in ELCS group 43% in VB group
-No difference in composite outcome between groups
-No difference in subgroup analysis and composite measure so CS is not better in any subgroup e.g. very preterm, MCDA twins etc
-Planned CS did not reduce the risk of worse outcomes for the second twin - Results of the secondary outcome
-No difference in the maternal composite outcome
