MCDA Twin Pregnancy
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Transcript of MCDA Twin Pregnancy
MCDA
Supervisor: Dr Rafaie
Presenter: Tan Lee Na
19th September 2014
Are twins good?
Introduction
Both babies share one placenta
1/3 of twins in the UK have MC
placentas
Recent increase in multiple
pregnancies due to ART
Particular challenges: vascular
placenta anastomoses that are almost
universal and connect umbilical
circulation of both twins
Diagnosis: first trimester
Chorionicity and amnionicity: best accuracy in
1st trimester
MCDA
Diagnosis:
second trimester
A photographic record should be
retained
MCDA
Bidirectional arterio-arterial anastomosis
If unable to determine chorionicity,
treat as monochorionic until
proven otherwise
Dating
Use the largest baby to estimate gest
age to avoid risk of estimating it from a
baby with early growth pathology
Assign nomenclature: transverse (left
or right) or vertical (upper or lower)
Management: first trimester
First trimester screening for
aneuploidy
Anatomical survey
?prediction of MCDA complications
First trimester aneuploidy
screening:
Offer information:
- greater likelihood of T21 in multiple
pregnancies
- different options for screening (problem with
biochemical screening)
- false positive rates of screening tests are
higher in multiple pregnancies
- higher rate of complications of invasive tests
(threshold for invasive test is higher)
- implications relating to selective fetal
reduction
Aneuploidy screening
1st trimester screen: combined test (NT + bHCG + PAPP-A)
Calculate the risk per pregnancy for monochorionic twins (as opposed to risk per baby for dichorionic twins)
If unable to do, consider 2nd trim serum screening, however potential problems arise such as double invasive testing because risk of T21 cannot be calculated separately for each baby
Subsequent Management
Aim
◦ Timely detection of TTTS
◦ Detection of other complications such as
selective IUGR, TOPS, TRAPS, single fetal
demise
TTTS
Vascular Anastomoses 95% monochorionic placentas have
these but only 10-15% suffer adverse
outcomes
TTTS and TRAP are the most well
recognised complications
Suggested aetiology: deep
anastomoses within placental mass
are usually btwn arteries and veins
which allow unidirectional blood flow
Suggested aetiology: cont..
Endocrinal imbalance, donor twin has
hypovolaemia RAS activation
increased ADH vasoconstriction
oliguria and AF
Recipient twin: hypervolaemia atrial
natriuretic peptide polyuria and
AF, also BP leading to cardiac
failure and hydrops, eventually death
TTTS
Quintero Staging System
Stage I: The fetal bladder of the donor twin remains visible
sonographically. Discrepancy in AFV with MVP ≤2 cm in
one sac and MVP ≥8cm (<20 weeks) or ≥10 cm (>20
weeks) in the other sac
Stage II: The bladder of the donor twin is collapsed and not
visible by ultrasound.
Stage III: Critically abnormal fetal Doppler studies noted.
This may include absent or reversed end-diastolic velocity
in the umbilical artery, absent or reverse flow in the ductus
venosus, or pulsatile flow in the umbilical vein.
Stage IV: Fetal hydrops present.
Stage V: Demise of either twin.
TTTS: How to diagnose?
Can we predict TTTS in first trimester?
◦ CRL and NT discrepancy at 11-14 weeks: CRL
discrepancy marker for subsequent sFGR, NT
discrepancy not predictive
◦ NT: discordance >20% shows risk of severe
TTTS is > 30%, if <20% then risk of TTTS <
10%
◦ CRL: discordance >10% predictive of early
onset disease <20 weeks
ISUOG
6 Oct 2010: Intertwin CRL discrepancy in MC twins is an early feature of GR rather than TTTS
20 Apr 2007: Discordance in NT in the prediction of severe TTTS
31 Aug 2006: First trimester discordance in CRL predicts timing of development of TTTS
TTTS: Ultrasound Features
Discordant growth
Discordant liquor
◦ Donor MVP < 2cm
◦ Recipient MVP > 8cm
+/- discordant bladder size
+/- abnormal doppler in one or both twin.
+/- fetal hydrops or fetal demise
BUT………………
In severe early TTTS, the prominent
feature is discordant liquor
Growth may not be
significantly affected in
early pregnancy
Frequency of follow up
Booking by 10 weeks
At least 9 antenatal appointment
At least 2 appointments with specialist
obstetricians
Dating scan followed by scans at
16,18,20,22,24,28,32,34 weeks
Why do we need to detect early
TTTS?
If left untreated, fetal mortality can
reach 80%, survivors face significant
risk of long term cardiac, renal and
neurological sequelae
Timely intervention can save lives!!!
(one or both babies)
Management options of early
severe TTTS
Amnioreduction
Septostomy
Selective laser ablation of communicating vessels
Management cont..
Amnioreduction: survival rates 60-65%
Septostomy: decrease in need to rpt procedure and survival rate similar, however risk of inter-twin cord entanglement
Laser ablation: most logical therapeutic approach, placental vessels traced endoscopically from origins and ablate all anastomoses, survival rate 70-81%, consider in ALL stages of TTTS to improve perinatal outcome
TTTS occurs at later part of
pregnancy: management options
Expectant
Serial amnioreduction
Decide timing of
delivery!
Recommendation (RCOG)
Severe TTTS presenting < 26 weeks
should be treated by laser ablation
rather than amnioreduction or
septostomy
Little information about maternal
morbidity after laser
Suggestion: USG (brain imaging, fetal
measurement, doppler) at least
weekly, consideration to deliver at 34
weeks, usually by CS
Complications of laser
ablation Most common: PROM (9%)
Placental abruption 1%
Miscarriage 8%
NICE March 2006
Monochorionic placenta
Twin Anaemia Polychytemia
Sequence (TAPS)
Twin Anaemia
Polychytemia Sequence
(TAPS)
Monochorionic Twin (5%)
Spontaneous or after incomplete Laser
treatment for TTTS
Same pathology as TTTS (Milder form)
Large intertwin hemoglobin differences in
the absence of amniotic fluid discordances
Usually in 3rd trimester.
Presence of arterial-arterial anastomoses is protective
against TTTS
In TAPS: either less A-V anastomoses or more A-A
anastomoses
TAPS: Antenatal Diagnosis
No apparent growth and liquor
discordance
Main feature: discordance in MCA
blood flow
MCA Peak systolic velocity
measurement (PSV)
◦ Moderate to severe anaemia: PSV MoM >
1.5
◦ Polycythaemia: PSV MoM < 0.8Even in apparently uncomplicated MCDA, it is
advised to do MCA doppler in every patient after 24
weeks
TRAPS (Twin reversed arterial
perfusion sequence) Also called acardiac
twinning
High perinatal mortality of
the normal ‘pump’ twin due
to CCF and hydrops
Treatment:
◦ Expectant
◦ Cord occlusion of the acardiac
twin if show evidence of heart
failure in the pump-twin
Selective IUGR in MCDA
Differentiate from TTTS by absence of
polyhydramnios in one of the amniotic
sacs, although the small twin may
have oligohydramnios owing to
placental insufficiency
Scans after 24 weeks to detect fetal
growth restriction
Discordant Growth*
Abdominal Circumference difference > 20 mm
EFW difference > 20%** ( Larger twin as a reference)
BPD > 6 mm
FL > 6 mm
* Usually accompanied with abnormal UA doppler
** Latest evidence suggests that difference by 18% is significant
Why is MCDA different
compared to DCDA?
Death in one twin may lead to death of the other twin
Neurological sequelae in surviving twin
Importance of close monitoring and timely decision for
delivery!!!
• try to achieve good survival of both fetuses
• at least survival of one fetus with minimal neurological
sequelae
Single fetal demise
Risk to surviving twin of death or
neurological abnormality is 12% and 18%,
respectively
Risks are not restricted to MC pregnancies
with a prior diagnosis of TTTS
Caused by acute haemodynamic changes
around time of death, as survivor
haemorrhaging part of its circulating volume
into the circulation of the dying twin leading
to hypotension and low perfusion and
eventually ischaemic end organ damage
Subsequent management
Detailed counselling and record in case
notes
Rapid delivery is unwise unless there are
significant CTG abnormalities or evidence of
anaemia in the survivor (MCA doppler) or if
fetal death occurs late in pregnancy
Evidence of fetal compromise could
represent continuing damage to the brain
and other organs, therefore conservative
management is often appropriate
Management continued….
Plan for brain imaging by 4 weeks to
establish whether serious cerebral morbidity
has occurred as such manifestation on CNS
are variable and takes up to 4 weeks to
occur
Fetal MRI provides earlier and more detailed
information about brain lesions than USG
If pre-viable: TOP is an option
Timing of delivery: 34-36 weeks
? Intervention to prevent
concordant fetal demise or
neurological sequelae
If single fetal demise is diagnosed
early: intrauterine fetal blood
transfusion of the surviving twin may
be considered
Timing of delivery
Deliver at 36-37, does not appear to be a/wincreased risk of serious adverse outcomes
Appropriate to aim for vag birth unless there are accepted, specific clinical indications for CS eg twin one lying breech or previous CS
60% of twins: spontaneous birth before 37 weeks
Prolonging pregnancy beyond 38 weeks increases risk of fetal death
If elective birth declined, offer weekly appointment with specialist obstetrician, offer USG at each visit and perform biweekly biophysical profile assessments, fortnightly fetal growth scans
Take home
message!!
MCDA: its all about
discordance!!
TTTS Discordant liquor
Selective IUGR Discordant
growth
TAPSDiscordant MCA
PSV
TRAPS/discorda
nt fetal
anomalies
discordant fetal
anomalies
Reference
RCOG
ISUOG
NICE clinical guideline, Sept 2011,
Multiple pregnancy
StratOG