Twins have 4X increased risk of
congenital anomalies
Dizigotic: May have placental fusion, but never has vascular anastomoses
1:20 Nigerians, 1:80
Caucasians, 1:150 Japanese
Monozygotic
(Incidence: 3.5/1000)
fused placenta always has some degree of arterial
anastomosis
have increased risk of congenital abnormalities
compared with dizygotes
1. Dichorionic-diamnionic (33%) with morula
splitting prior to day 4.
- 10% risk of mortality
- 25% of placentas fuse
- thick (1-2mm) membrane separating two sacs indicates
dichorionic twins in first trimester, and this with infiltrating
placenta gives the "twin chorionic
peak sign"
2. Monochorionic-diamniotic (66%) with polarizing
blastocyst at day 4-8 with division before amnion develops over
embryonic plate.
- 25% risk of mortality
- two yolk sacs, with thin
whispy amnions between them. Single chorion prevents
placenta from entering between amnions, with low signal at thin peak.
The amnion may not be seen until 2nd trimester. But can use gravity and
positioning to see if twin shifts into area.
- 75% have single placenta
3. Monochorionic-monoamniotic (<1%) blastocyst
polarizing at 8-13 days
- 50% mortality. C/S at 32 wks
- fuzed placenta with arterial anastomoses.
- single yolk sac
- If no definitive evidence of mono-mono with cord/limb
entanglement, must confirm lack of amnion by dye injection into amnion
with resulting concentration into gut (check by CT)
4. Conjoined twins. division of disk after day 13.
occurs 1//50k
degree of
fusion variable, rarely separable.
Twin Monitoring
GA is best assessed early in pregnancy using
composit of both. FL measurements are most reliable for determining GA
later in pregnancy.
1st and 2nd trimester follows same grwth charts as
singleton Then in 3rd trimester weight gein drops with resultant IUGR
due to 3000g uterine max carrying capacity
Biophysical
profile, sometimes performed up to 2x/wk with any signs of
abnormality
A difference of 20mm in AC or 15% in EFW is evidence
of significant growth discordance
Clubfoot and crowding is common in any type of twins
Twin-Twin
Transfusion/Perfusion Issues
- all monochorionic twins share some degree of placental vascular
communication. Therefore never selectively terminate either of the
monochorionic twins.
- amniotic fluid volume differences is the primary finding
Twin-Twin
Transfusion Syndrome
blood and nutrients are
progressively shunted between a donor and a recipient twin, with the
donor becoming anemic and growth restricted. Eventually the donor twin
loses all of its amniotic fluid resulting in "stuck twin" where
movement is restricted and the fetus is fixed in the nondependant
portion of the uterus, while the recipient floats in polyhydramnios.
recipient:
large and vigorous initially, then CHF, hydrops leading to death
donor:
umbilical artery doppler demonstrates severe high resistance
Tx: selective
amniocentesis of large twin can aid both with small twin regainign some
fluid and circulation pressure.
Acardiac
Parabiotic Syndrome ( Twin reversed arterial perfusion sequence)
pairing of arteries and
veins between twins results in preferential perfusion to the lower body
of an acardiac twin. (see normal
fetal
circulation ) Doppler shows reversal of blood
flow with the umbilical artery
(usually single) flow toward the acardiac twin by the "pump twin"
pump twin is usually
normal, and if high output cardiac failure/hydrops absent or treated
(by amniocentesis or ligation of acardiac twin) will survive normally.
Intrauterine demise
of one Twin
early in pregancy occurs
50% of time (both mono/dichorionic)
one twin will vanish, or
may become hyalinized as a fetal remnant (fetus papyraceous)
Monochorionic twins with
vascular anastomoses can get twin-twin embolization syndrome where
necrotic tissue is sent to healthy twin leading to DIC. Usually the
brain, small intestine, kidneys affected
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