Multiple pregnancy by dr. poly.

2. DR POLY BEGUM
MBBS; FCPS (OBST & GYNAE)
ASSISTANT PROFESSOR
DEPARTMENT OF OBSTETRICS & GYNAECOLOGY
DIABETIC ASSOCIATION MEDICAL COLLEGE

3. When more than one fetus simultaneously develops in
the uterus it is called Multiple Pregnancy.
Twin pregnancy represents 2 to 3% of all pregnancies.

4. Induction of ovulation, 10% with clomideand
30% with gonadotrophins.
Increase maternal age ? Due to increase
gonadotrophinsproduction.
Increases with parity.
Heredity usually on maternal side.
Race; Nigeria 1:20, North America 1:90, India
1:80.

5. Most common represents 2/3 of cases.
Fertilization of more than one egg by more
than one sperm.
Non identical ,may be of different sex.
Two chorion and two amnion.
Placenta may be separate or fused.

6. Constant incidence of 1:250 births.
Not affected by heredity.
Not related to induction of ovulation.
Constitutes 1/3 of twins.

7. Results from division of
fertilized egg:
0-72 H. Diamnioticdichorionic.
4-8 days Diamnioticmonochor.
9-12 days Monoamnio.monochor.
>12 days Conjoined twins.

8. 70% are diamniotic monochorionic.
30% are diamniotic dichorionic.

9. Very important as most of the complications
occur in monochorionicmonozygotic twins.

10. Very accurate in the first trimester, two sacs,
presence of thick chorion between amniotic
memb.
Less accurate in the second trimester the
chorion become thin and fuse with the
amniotic memb.

12. Different sex indicates dizygotictwins.
Separate placentas indicates dizygotictwins

14. By examination of the MEMBRANE,
PLACENTA,SEX , BLOOD group .
Examination of the newborn DNA and HLA
may be needed in few cases.

15. Anemia
Hydramnios
Preeclampsia
Preterm labour
Postpartum
hemorrhage
Cesarean delivery
Malpresentation
Placenta previa
Abruptio placentae
Premature rupture of
the membranes
Prematurity
Umbilical cord prolapse
Intrauterine growth
restriction
Congenital anomalies
Maternal Fetal

16. TWIN-TWIN transfusion.
Results from vascular anastemosisbetween
twins vessels at the placenta.
Usually arterio(donor) venous (recipient).
Occurs in 10% of monochorionictwins.

17. TWIN-TWIN transfusion
Chronic shunt occurs ,the donor bleeds into the
recipient so one is pale with oligohydraminose
while the other is polycythemicwith
hydraminose.
If not treated death occurs in 80-100% of cases.

18. Possible methods of treatment:
Repeated amniocentesis from recipient.
Indomethacin.
Fetoscopy and laser ablation of communicating
vessels.

19. Other Complications in MonochorionicTwins:
Congenital malformation. Twice that of singleton.
Umbilical cord anomalies. In 3 –4 %.
Conjoined twins. Rare 1:70000 deli varies. The
majority arethoracopagus.
PNMR of monochorionicis 5 times that of dichorionic
twins(120 VS 24/ 1000 births)

20. Increase blood volume and cardiac output.
Increase demand for iron and folic acid.
Maternal respiratory difficulty.
Excess fluid retention and edema.
Increase attacks of supine hypotension.

21. +ve family history mainly on maternal side.
+ve history of ovulation induction.
Exaggerated symptoms of pregnancy.
Marked edema of lower limb.
Discrepancy between date and uterine size.
Palpation of many fetal parts.

22. Auscultation of two fetal heart beats at two
different sites with a difference of 10 beats
USG
Two sacs by 5 weeks by TV USS.
Two embryos by 7 weeks by TV USS.

23. AIM
Prolongation of gestation age, increase fetal
weight.
Improve PNM and morbidity.
Decrease incidence of maternal complications.

24. Follow Up
Every two weeks.
Iron and folic acid to avoid anemia.
Assess cervical length and competency.

25. Fetal Surveillance
Monthly USS.from24 weeks to assess fetal
growth and weight.
A discordinateweight difference of >25% is
abnormal (IUGR).
Weekly CTG from 36 weeks.

27. Vertex-Vertex (50%)
Vaginal delivery, interval between twins not to
exceed 20 minutes.
Vertex-Breech (20%)
Vaginal delivery by senior obstetrician

28. Breech-Vertex( 20%)
Safer to deliver by CS to avoid the rare
interlocking twins( 1:1000 twins ).
Breech-Breech( 10%)
Usually by LUCS.

29. PNMRis 5 times that of singleton (30-50/1000
births).
RDSaccounts for 50% 0f PNMR.2
nd
twin is more
affected.
Birth trauma . 2
ND
twin is 4 times affected than
1
st
.
Incidence of SBis twice that of singleton.

30. Congenital anomalies is responsible for 15% of
PNMR.
Cerebral haemorrhageand birth asphyxiaare
responsible for 10% of PNMR.
Cerebral palsy is 4 times that of singleton .
50% of twins babies are borne with low
birth(<2500 gms.) from prematurity & IUGR.

31. Early in pregnancy usually no risk.
In 2
nd
or 3
rd
trimester:
Increase risk of DIC .
Increase risk of thrombosis in the a live one
The risk is much higher in monochorionicthan
in dichorionictwins

33. A] MATERNAL:
1.Anemia due to increase demand.
2.Increase incidence of PET(5 times).
3.Polyhydramniose in monochorionic
monozygotic twins.
4.Increase incidence of premature labour.

34. 5.Increase incidence of CS. And operative
delivary.
6.Increase incidence of placenta previa and
abruptio placenta.
7.Increase incidence of atonic postpartum
hemorrhage.

35. B] FETAL :
1.Increase perinatal morbidity and mortality.
2.Prematurity with or without rupture of
membrane.
3.Increase incidence of malpresentation.

36. 4.Increase incidence of cord prolapse.
5.Higher incidence of IUGR.
6.Increase incidence of congenital anomalies.