TWIN PREGNANCY

Presenter: Dr Poonam Lama

MD Resident, 2nd year
OBG/GYN, NAMS

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INCIDENCE

Hellin’s rule:
• Twins 1 in 80 pregnancies

• Triplets 1 in 802

• Quadruplets 1 in 803 and so on

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RISK FACTORS

1. Race

2. Hereditary
3. Advancing age of mother

4. Parity

5. Maternal weight

6. ART

7. OCPs
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VARIETIES OF TWINS

1. Dizygotic twins (80%)

2. Monozygotic twins (20%)

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OUTCOME OF MONOZYGOTIC TWINNING

• 30%

66%

3%

<1%

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CONJOINED TWINS

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DETERMINATION OF ZYGOSITY
Dizygotic twins Monozygotic twins
A. Placenta and membranes
1. Number 2 placenta, separated or 1 placenta
most commonly fused at
margin appearing to be
one
2. Communicating vessels Absent Present
3. Chorionicity DADC DAMC, occasionally
DADC or MAMC
4. Intervening membranes 4 layers 2 layers
(2 amnions, 2 chorions) (2 amnions)
B. Sex Different or same Same
C. Genetic features (blood Differ Same
grouping, DNA
fingerprinting)
D. Reciprocal skin grafting No acceptance Acceptance

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SONOGRAPHIC DETERMINATION OF CHORIONICITY
AND AMNIONICITY

Accuracy best before 14 wks of pregnancy

Dichorionic pregnancy Monochorionic pregnancy

Twin peak sign or lamba sign T sign
Thick dividing membrane Thin dividing membrane
>_2mm < 2mm

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SUPERFECUNDATION

• Fertilization of 2 different ova released in the same cycle,

by separate acts of coitus within a short period of time.
• E.g. mother was sexually assaulted on the 10 th day of her
menstrual cycle and had intercourse 1 wk later with her
husband. She delivered black and white baby.

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SUPERFETATION

• Fertilization of 2 ova released in different menstrual

cycles.
• The nidation and development of one fetus over another
fetus is theoretically possible until the decidual space is
obliterated by 12 wks of pregnancy.

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LIE AND PRESENTATION

• Commonest lie: longitudinal (90%)

• Presentation:

1. Both vertex: 50%

2. First vertex and second breech: 30%

3. First breech and second vertex: 10%

4. Both breech: 10%

5. Rarest, both transverse: rule out conjoined twins

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MATERNAL PHYSIOLOGICAL CHANGES

1. Red cell mass: no increase

2. Plasma volume: by addition of 500 ml

so, exaggerated hemodilution and anemia

3. Increase in wt gain and cardiac output
4. Abdominal viscera and lungs compressed/displaced by
expanding uterus increased tidal volume and GFR

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DIAGNOSIS

HISTORY:
1. H/O ovulation inducing drugs specially gonadotrophins,
for infertility or use of ART???
2. F/h/o twinning (maternal side)???

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 SYMPTOMS

1. Increased nausea and vomiting

2. Cardio-respiratory embarrassment

3. Tendency of swelling of the legs, varicose veins

4. Unusual rate of abdominal enlargement and excessive
fetal movements

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 SIGNS

General examination
• Anemia more than in singleton pregnancy
• Unexplained wt gain, not explained by PE or obesity
• Common association- PE (25%)

Abdominal examination

A. Inspection
• Unduly enlarged
• Barrel shaped uterus
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 B. Palpation

• Height of uterus>>period of amenorrhea

• Palpation of too many fetal parts

• Girth of abdomen at the level of umbilicus>> normal

average at term (100 cm)

C. Auscultation: 2 distinct FHR at separate spots;

difference in FHR at least 10 bpm

 
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INVESTIGATIONS

1. USG

2. Biochemical tests: serum and urine levels of B hCG and

maternal serum AFP (MSAFP) higher compared to
singletons

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DIFFERENTIAL DIAGNOSIS

1. Hydramnios
2. Big baby
3. Pregnancy with fibroid or ovarian tumor
4. Pregnancy with ascites

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COMPLICATIONS
A. Maternal complications
During pregnancy During labor During puerperium

1. Nausea and vomiting 1. Early ROM and 1. Subinvolution

2. Anemia cord prolapse 2. Infection
3. Mechanical distress 2. Prolonged labor 3. Lactation failure
4. Pre-eclampsia (25%) 3. Increased
5. Hydramnios (10%) operative
6. Malpresentation interference
7. Preterm labor 4. Intrapartum hge
8. APH 5. PPH

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B. Fetal complications
1. Increased miscarriage rate esp in monozygotic twins
2. Prematurity (80%)
3. Congenital malformations: rate almost twice in
monochorionic twins than in dichorionic twins
4. Discordant twin growth (20%)
5. IUD of one fetus
6. Asphyxia and stillbirth
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UNIQUE FETAL COMPLICATIONS
A. Monoamnionic twins: cord entanglement
B. Aberrant twinning mechanisms of monozygotic twins:
a) Conjoined twins
b) External parasitic twins
c) Acardiac twin/TRAP sequence
d) Fetus in fetu
C. Monochorionic twins and vascular anastomoses:
a) Twin-twin transfusion syndrome (TTTS)
b) TRAP sequence
c) Twin anemia polycythemia sequence (TAPS)
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A. MONOAMNIONIC TWINS

• Umbilical Cord Entanglement: complicate approx 50% of

cases
• Pregnancies that have successfully reached 30-32 wks
are at reduced risk
• Recommendations:
a) After 26-28 wks 1 hr of daily FHR monitoring
b) With initial testing, 1st course of steroids
c) If fetal testing reassuring, 2nd course of steroids and
cesarean delivery at 34 wks

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B. ABERRANT TWINNING MECHANISMS

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External parasitic twins

• Consists of externally attached supernumerary limbs,

often with some viscera
• Functional heart or brain -nt
• Results from demise of
defective twin its surviving
tissues is attached to and
vascularized by its normal
twin

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Fetus in fetu

• Early in development, 1 embryo enfolded within its twin

• Its development arrested in 1st trimester

• Vertebral or axial bones found in these fetiform masses,

heart and brain lacking

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Monochorionic twins and vascular anastomosis

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Types of anastomosis

• 3 types of anastomoses: AA, VV and AV

• AA or VV anastomoses: superficial and bidirectional blood

flow; net flow between twins balanced, no TTTS

• VV anastomoses may be a/w decreased perinatal survival;

sudden changes in venous return fetal demise. However,

this association has not been confirmed by other series.

• AV anastomoses: deep, unidirectional

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TWIN-TWIN TRANSFUSION SYNDROME/TTTS

• Clinicopathological state where one twin appears to

bleed into the other through some kind of placental
vascular anastomoses.
• 5-17%
• Typically presents in midpregnancy

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Pathophysiology

• Results from unidirectional flow through A-V

anastomoses
• Deoxygenated blood from donor umbilical artery
pumped into a cotyledon shared by the
recipientoxygen exchange completed in chorionic
villus oxygenated blood leaves the cotyledon via a
umbilical vein of the recipient twin

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Results
Donor twin Recipient twin

1. Pale, anemic 1. Plethoric, polycythemic,

2. Restricted growth hyper-biliribunemia,
3. Hypotensive 2. Hypervolaemic, hypertensive
4. Hypovolemic 3. Hyperviscosity
5. Oligohydramnios 4. Polyhydramnios
5. Circulatory overloadheart
failure hydrops

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Diagnosis

• Previously, HB differences (>_5 g%) and wt discordancy

(>20%); late onset findings
• TTTS diagnosed based on 2 criteria:

1. Presence of DAMC pregnancy

2. Discordant AFV/ poly-oli sequence

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Staging: Quintero’s (1999) staging system

Stage I  Discordant AFV as described above

 Urine is still visible within the donor bladder
Stage II  Criteria of stage I, but
 Urine isn’t visible within the donor bladder
Stage III  Criteria of stage II
 Abnormal Doppler studies of the UA, UV, or ductus
venosus
Stage IV Ascites or frank hydrops in one or both twins
Stage V Demise of one or both twin

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Management and prognosis

• Prognosis for TTTS is related to Quintero stage and

gestational age at presentation
• Stage I: >3/4th cases remain stable or regress without
intervention
• >_Stage II: much worse, perinatal loss rate is 70-100%

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Therapies

1. Repeated amnioreduction

2. Laser ablation of vascular anastomoses: preferred for

severe TTTS (Stage II-IV)

3. Septostomy (creation of communication in the dividing

amniotic membrane)

4. Selective feticide

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• Solomon technique: modified laser technique;
coagulation done along entire vascular equator, not
selectively coagulating visible anastomosis one by one.
• Reduces recurrent TTTS and TAPS

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Fig. Fetoscopic laser ablation technique

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TWIN ANEMIA POLYCYTHEMIA SEQUENCE/TAPS

• Chronic fetofetal transfusion characterized by significant

differences in hemoglobin between donor and recipient
twins without the discrepancies in AFV typical of TTTS.

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• 2 forms:

1. Iatrogenic TAPS: upto 13% of pregnancies after laser

photocoagulation, within 5 wks of a procedure

2. Spontaneous TAPS: 3-5% of monochorionic

pregnancies, usually after 26 wks
• Dx: MCA PSV: in donor twin: >1.5 MoM
in recipient twin: <1.0 MoM

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Treatment

1. Fetal blood transfusion

2. Fetoscopic laser photocoagulation

3. Conservative management
4. Preterm delivery

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TWIN REVERSED ARTERIAL PERFUSION (TRAP)
SEQUENCE (ACARDIAC TWIN)
• 1 in 35,000 births

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• One twin: no cardiac structures

• Receive blood supply from the healthy twin by means of

A-A anastomoses and usually returns via VV anastomosis
back to the pump twin.
• Thus, the arterial system of the acardiac twin is perfused
in reverse with deoxygenated blood from the normal
twin (twin reversed arterial perfusion)

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• Normal twin: high output cardiac failure.
• Mortality of normal twin: approx 50%.
• 4 types of acardiac twins:

1. Acardiac acephalus
2. Acardiac acormus
3. Acardiac myelacephalus

4. Acardiac amorphus

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Management

• Interruption of A-A anastomoses by

- Endoscopic laser photocoagulation when pregnancy is

<24 weeks or

- Endoscopic or ultrasound guided ligature of the umb cord

of the acardiac twin when GA is more advanced.

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Discordant growth of twin fetuses

• Inequality in size of twin fetuses, calculated using larger

twin as index.
• Earlier discordancy, higher risk of fetal demise in smaller
twin

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Diagnosis

• USG
 Using EFW for each twin
Percent discordancy= wt of larger twin – wt of smaller twin
wt of larger twin
Discordance significant if EFW difference >_20%
 Also, AC value used; discordance significant if
AC difference >20 mm

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IUD OF ONE FETUS
• After 1st trimester , risk increases

• When one twin dies acute and massive blood

transfusion from the survivor to the dead twin severe

anemia in survivor systemic morbidities and DIC

• Risk to the surviving twin of death or neurological

abnormality in monochorionic pregnancy: 15% and 26%,

respectively. (RCOG, 2016)

• Most serious maternal complication: DIC 52

Management

• Depends on GA, cause of death and risk to surviving

fetus
• 1st trimester loss: no risk

• Dichorionic pregnancy: no affect on survivor

• Monochorionic pregnancy

If death occurs after 1st trimester but before viability,

termination of pregnancy considered
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• Delivery generally occurs within 3 wks of dx of fetal
demise –corticosteroids should be given
• Timing of elective delivery after conservative mx of a late
2nd or early 3rd trimester single fetal death is matter of
debate

 Dichorionic: delivered at term

 Monochorionic: 34-37 wog

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MANAGEMENT OF TWINS PREGNANCY

Antenatal management

• Aims:

1. Prevention of preterm birth

2. Evaluation of fetal growth

3. Assessment of fetal well being

4. Determination of time and best mode of deliver y

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 Diet: 40-45 kcal/kg/d
• Carbohydrate 40%
• Fat 40%

• Protein 20%
 Bed rest
 Prophylactic tocolysis: controversial

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 Progesterone: not useful

 Cervical circlage: not recommended

• Cervical length: at 24 wks

• <_25 mm: best predictor of preterm delivery before
32 wks
• >_35 mm: low risk for preterm delivery before 34 wks

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• Fetal growth evaluation
– Monochorionic twins: routine detailed ultrasound
scan between 18 and 20+6 wog
– USG assessment: uncomplicated monochorionic
pregnancies- every 2 wks from 16 weeks onwards
until delivery
– USG: 6 wkly in dichorionic twins

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Timing of delivery

• Perinatal mortality increased significantly in

 Singletons:after 42 wog
 Twins: after 38 wog

 Triplets: after 35 wog

Dichorionic pregnancy
• Uncomplicated: around 38 wog
• In case of prematurity and discordant fetal growth: based
on parameters of healthy twin
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 Monochorionic pregnancy
• Uncomplicated: around 37 wog
• In case of anomaly or discordant growth: timing based
on condition of compromised fetus

Monoamniotic twin: at 34-36 wog

Triplet pregnancy: at 35 wog

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Labor and delivery

A. Evaluation upon admission

• Fetal presentation

• Confirm fetal position and presentation sonographically

• If active labor confirmed during initital evaluation, decide

mode of delivery
• Cephalic presentation of first twin may be considered for
expectant mx
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B. Labor induction or stimulation
• Nulliparas and multiparas with twins: slower progression
of active labor
• Additional 1-3 hrs to complete first stage of labor
• Oxytocin alone or in combination with cervical ripening
can be safely used

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C. Delivery route
• If first twin is cephalic: vaginal delivery

• If 1st twin non cephalic: cesarean delivery

• Neonatal outcome: 2nd twin worse outcome regardless of

delivery method

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Procedure

• 1 experienced obstetrician, anesthetist, pediatrician, and

neonatal nurse
• IV line with ringer’s solution

• Blood cross matched and readily available

• Careful fetal monitoring is to be done

• Internal examination after ROM to exclude cord prolapse

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• Delivery of first twin: as for singleton pregnancy

- After the birth of the first twin, the oxytocin infusion is

immediately stopped if in use

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Vaginal delivery of 2nd twin

• Assess 2nd twin by abdominal and vaginal examinations:

presenting part, size and relationship to the birth canal
• If fetal head or breech is fixed in the birth canal
• Moderate fundal pressure applied
• ARM
• Digital examination of cx to exclude cord prolapse
• Labor is allowed to resume
• If contractions donot begin within approx 10 min
• Oxytocin to stimulate contractions

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• In the past, safest interval between delivery of 1 st and 2nd
twins: 30 minutes.
• As long as the quality of the fetal heart rate record is
good and no signs of impending intrauterine asphyxia: no
absolute time limit

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If transverse lie:
• 1st: ECV, if fails—IPV under epidural anesthesia

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Internal podalic version

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Locked twins

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• Mx:

a. Cesarean delivery

b. If 1st twin is already dead, decapitation, pushing up the

decapitated head, followed by delivery of the 2nd twin
and lastly delivery of decapitated head, at least saves
one baby

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INDICATIONS OF CESAREAN SECTION

1. 1st twin non cephalic presentation

2. Monoamniotic twins
3. Monochorionic twins with TTTS
4. Twins with complications: IUGR, conjoint twins
5. Collision of both heads at brim preventing engagement
of either head
6. Other obstetric indications
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References

• Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe

JS, Hoffman BL, et al. Fetal anomaly. Williams Obstetrics.
24th ed. USA: McGraw Hill Education; 2014.
• Practical guide to high risk pregnancy and delivery.
Arias.4th edition
• Management of monochorionic twin pregnancy. RCOG,
2016

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