Multiples Flashcards
What are the risks of death of one twin
+ the rates of each
Co twin demise
6X higher in MC (12% vs 4%)
Premature delivery
MC before 34/40 70%
DC 60%
Neurological impairment
thromboplasin theory
ischemic theory
present 6 days to 6 weeks
How often does death of one twin occur?
in T1 vs T2/3
In MC vs DC
T1 - vanishing twin
25% twins at 6/40 will not be there at 12/40
T2/3
MC losses 4-11%
DC losses 1-5%
What is the etiology of 1 twin death in
DCDA
MCDA
MCMA
DCDA
FGR (esp in discordance 30%)
PET (can help)
Other normal things abruption, GDM, abnormalities
MCDA TTTS 50% Unexpected 1-6% sIUGR Fetal abnormalities TRAP (rare) Iatrogenic
MCMA 50% cord entanglement Fetal abnormalities 25% (usually discordant) TTTS less common
What are the signs a surviving twin has neurological damage
Present 6/7 to 6/52
Periventricular leukomalacia Multicystic encephalomalacia Porencephaly Hydrancephaly Microcephaly
Management
What is the general management for 1Twin demine
Steroids
MgSO4
Paediatric consult
If the live twin is normally grown, cephalic and leading then vaginal delivery can be considered
If the dead twin in leading or malpresentation then caesarean is recommended
Risk of DIC if more then 4 weeks is very low but can consider weekly fibrinogen / platelet / PT
Full coags before regional anesthetic or delivery
Psychological support
Timing of delivery + specific management with 1 twin demised
DCDA
MCDA
MCMA
Steroids
MgSO4
Paediatric consult
DIC monitoring
DCDA
delay until 34 weeks
Serial USS growth doppler CTG
MCDA Likely neurological injury already occurred Weekly USS MRI 3/52 after death If abnormal talk to paeds / TOP Anaemia with abn PSV poor prognosis
MCMA
Delivery by 28 weeks
Rare, usually both demise
What is the risk of twin pregnancies of: CP Congenital abnormalities infant death Spont PTB IUGR
CP is 4-8 X higher 1.5/1000 singleton 7:1000 Twins 30:1000 triplets Congenital abnormalities 12X increased risk congential heart defects 70% twin not effected Major abnormalities in 5% Spont PTB 50% IUGR 25% MC pregnancies
What are the maternal risks of a twin pregnancy ?
Hyperemesis Anaemia Gestational diabetes PET Operative delivery LSCS Social emotional impact of having twins PTB PPROM
Post natal depression
Divorce
How to dx twins on early USS
Early ultrasound scanning
Dx by 11-14 weeks
DCDA – Twin peak sign
MCDA – T sign
MOD for twins
The twin birth study – Toronto
If T1 is cephalic, and after 32 weeks then planned VB is best practice (level 1 evidence)
If experienced operator is in attendance
40% EMLSCS rate
Increase resp disease in ELLSCS
At delivery what is the risk to T2
Mortality
LSCS risk
outcomes
EMLSCS for T2 4-10%
Delivery related death of T2 is 1:300
Overall poorer outcomes T2
What timing of splitting causes what types of twins ?
Depends on timing of splitting
D0-3
DCDA twins as 2 embryos amnions and chorions develop
2 placentas or a single fused placenta may develop
D4-8
MCDA
D8+
MCMA
D13+
Conjoined
Are all monozygous twins monochorionic?
Monozygous twins
Can be MCMA
Most are MCDA 1/400 pregnancies
1/9 are DCDA = in same sex DCDA twins zygosity cannot be determined without DNA sampling as could be early splitting
Why is the number of twins going up?
Rate of multiple pregnancy is affected by
Maternal age, ethnicity, parity
Use of ART
Monozygotic twinning is pretty stable
2% of all births are multiples
Reduction in ART associated multiple pregnancies
20% of multiples are related to ART
What % of twins are monoamniotic
1%
What is the rate of cord entanglement
Most common cause of fetal death
Risk of death increases by 2% every week from 15 weeks
30% by 30 weeks
Delivery planned by 32 weeks (RCOG says delivered by 32-34 weeks by LSCS)
Prediction based on USS or CTG has been suggested but no good evidence and risk of false positive and PTB
What is the diagnosis of TTTS
Diagnoses
one twin SDP less then 2, and recipient SDP over 8
Can have abnormal dopplers
Assess for hydrops including cardiomegaly, ascites, oedema, abnormal ductus venosus
so occur in monoc
What are the 2 types of TTTS
TOPS
Twin oligohydramnios / polyhydramnios Sequence
10% of MC twins
Seen midtrimester
‘classical’ TTTS
this is usually 10-15% unbalanced transfusion
TAPS Twin Anaemia/ Polycythemia Sequence 5% of MC twins 10% of twins post lazer treatment Slow transfusion 5-15 ml / 24 hours from donor to recipient
MCA above 1.5 MoM in one and below 0.8 In the other
Large Hb discordance without amniotic fluid discordance
Risks of TTTS
SRM + PTB from Poly Cardiac failure Hydrops Death of one twin - 50% co twin survival - 50% deficit - loss of the co twin (25%) or significant long term neurological deficit (25)
Prematurity
Neurological damage - can assess for ventriculomegaly
IUGR
20% but fetal size is not part of the diagnostic criteria or staging criteria
Stages TTTS
Stage 1: donor bladder visible, EDF positive in both vessels in both fetuses.
Stage 2: donor bladder not visible, EDF positive in both vessels in both fetuses.
Stage 3: EDF absent or reversed in either vessel in either fetus.
Stage 4: presence of ascites or hydrops in either fetus; usually the recipient.
Stage 5: fetal Death
Management TTTS
Conservative
Poor outcome unless stage 1
40% of stage one can stabilise and resolve
USS weekly
Amnioreduction not as successful as laser and can make later laser more difficult - may have a role in late onset
Laser 16-28 weeks Median age 21 weeks Deliver by 34-36+6 Weekly USS
What are the risks with laser for TTTS
Risks:
PPROM
PTL 10-15% within 2 weeks of the procedure
Loss of one or both twins – overall survival 75%, survival of both twins 66%
Neurological damage – close MRI surveillance
Monitor for IUGR + TAPS as still unequal sharing of the placenta
Solomon technique is lazering the placenta to dichorionise it – this reduces but doesn’t remove the TAPS risk
Selective termination
How do you do it
Especially if one twin have a major anomaly / neurological damage
Selective feticide by intravascular injection of an abortifacient is not an option in monochorionic pregnancies because of the presence of placental anastomoses. The potential risks of intrafetal/umbilical cord ablative procedures should be discussed prospectively, including the risk of co‐twin loss and neurological morbidity.
Monitoring for disseminated intravascular coagulopathy is not indicated in monochorionic twin pregnancies undergoing selective reduction.
Long term sequalae of PTB
RDS Ventilatory assistance Chronic lung disease Hypotension needing inotropes Oliguric renal failure Neurodevelopmental disability Serial amnioreduction – disability 20% Laser – 4-13% overall impairment up to 18% Severity at diagnosis relates to long term outcomes Long term paeds follow up