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Multifetal Pregnancy

 May result from two or more fertilization events


 From a single fertilization followed by an erroneous splitting of the zygote
 Or combination of both

Incidence and Epidemiology

 1-3%
 10% of perinatal mortality, morbidity and neurodevelopmental problems

Frequency of Multifetal Pregnancy

 Dizygotic twins- more common


 Monozygotic twins- 1 in every 250 pregnancies
o Greater incidence of abortion
 Vanishing twins
o Incidence of twins in the first trimester is much greater than the incidence of
twins at birth (10-40%)

Frequency of Preterm Labor in Multifetal Pregnancy

 Twins- 60%
 Triplets- 90%
 Quadruplets- 100%
<2500grams- very low birth weight related to fetal gestation
Increased risk is for each fetus and is not simply because there are more fetuses per
pregnancy
Adverse Outcomes Associated with Multifetal Pregnancies
 Congenital malformations
 Pre-eclampsia
 Post-partum hemorrhage
 Maternal Deaths
 Peripartum Hysterectomy
 Depression for the Mother

Twin Fetus

o Usually results from fertilization of


 two or separate ova – dizygotic or fraternal twin
 monozygotic or identical twins

Mechanisms of Multifetal Gestations


 Dizygotic twins
o Results from the maturation and fertilization of two ova during a single
ovulatory cycle
o Genes same with the other siblings
 Monozygotic twins
o Identical twins
o Same genetic heritage but not identical
o May be discordant for genetic mutations because of a post-zygotic
mutation
o Or same genetic disease but with marked variabilityin expression
o Monozygotic twinning
 A sense of a teratogenic event and increased incidence may be
associated with malformations
 Dizygotic of the same sex may appear more nearly identical at birth than the monozygotic.
 Division of one fertilized zygote into two does not necessarily results in equal sharing of
protoplasmic material.
Genesis of Monozygotic Twins
 Minor trauma to the blastocyst during assisted reproductive technology (ART)
 Outcomes depend on when division occurs
o Within 1st 72 hours after fertilization
 2 embryos, 2 amnions, 2 horions
 Diamonionic,dicrorionic twin pregnancies may also occur
 2 distinct placentas or a single, fused placenta may develop
o Between 4th and 8th day
 Diamnionic, monochorionic twin
o 8 days after fertilization
 Chorion and amnion have already differentiated, and division results in two
embryos withina common amnionic sac, a monoamnionic, monochorionic twin
pregnancies
o Conjoined twins result if twinning is initiated.

Superfetation

o Ovulation and fertilization during pregnancy

Superfecundation

o Fertilization of two ova within the same menstrual cycle but not at the same coitus nor
necessarily by sperm from the same male.

Pituitary Gonadotropin

 FSH level
o Common factor linking race, age, weight and fertility to multifetal gestation
 Increased fecundility and higher rate of dizygotic twinning have been reported in
women who conceive within 1 month after stopping OCPs, but not during subsequent
months
o May be due to sudden release of pituitary gonadotropin in amounts greater than
usual during the 1st spontaneous cycle after stopping hormonal contraception
 Declining fertility but increasing twinning with advancing maternal age
o Exaggerated pituitary release of FSH in response to decreased negative feedback
from impending ovarian failure

Risks for Twin-Specific Complications

 Relation in zygosity
 Increased rates of perinatal mortality and neurological injury in monochorionic
diamnionic twins compared with dichorionic pairs
 Fetal demise in one or both monochorionic twins was twice that in dichorionic multifetal
gestations

Biochemical Tests

 No biochemical test that reliably identifies multiple fetuses


 Serum and urine levels in beta-hCG and maternal serum alpha-fetoprotien (MSAFP) are
generally higher with twin compared with singletons

COMPLICATIONS OF MULTIFETAL PREGNANCIES

1. Spontaneous abortions- monochorial placentations


2. Congenital Malformations
 Monochorionic malformations almost twice as common with dichorionic
 Attributed to the high incidence of structural defects in monozygotic twins
3. Low Birthweights
 Restricted fetal growth and preterm deliveries
 Degree of growth restrictions in monozygotic twins is likely greater than that in
dizygotic pairs
 With monochorionic embryos, allocation of blastomeres may not be equal,
vascular anastomoses within the placenta may cause unequal distribution of
nutrients and oxygen, and discordant structural anomalies resulting from the
twinning event
4. Hypertension- 20%
 Prepregnancy BMI (>/= 30kg/m2) and egg donation
 Fetal number and placental mass are involved in preeclampia and pathogenesis
5. Preterm Birth
 Duration of gestation decreases with increasing fetal number

Prolonged Pregnancy
 Twin gestations have empirically been considered to be prolonged at 40 weeks
AOG

Long-Term Infant Development

 The cerebral palsy, risk is higher among twins and higher-order multiples
 Related to an icreased risk of fetal growth restriction, congenital anomalies,
twin-twin transfusion syndrome and fetal demise of a cotwin

Unique Fetal Complications

 Monoamnionic Twins
o High fetal death rate from cord enlargement, congenital anomalies, preterm
birth or TTTS

Aberrant Twinning Mechanisms

 A spectrum of fetal malformations


o Incomplete splitting of an embryo into two separate twins
o Early secondary fusion of two separate embryos: either symmetrical or
asymmetrical and the spectrum of anomalies
 Conjoined Twins
 Siamese twins
o Joining of the twins may be at either pole and may produce characteristic
forms depending on which body parts are joined or shared
o Viable conjoined twins should be delivered by Caesarean section
o For the purpose of pregnancy termination, however vaginal delivery is
possible because of the union is most pliable
 External Parasitic Twins
 Grossly defective fetus merely fetal parts, attached externally to a relatively
normal twin
 Parasitic twin
o Externally attached supernumerary limbs, often with some viscera
o A functional heart or brain is absent
 Results from demise of the defective twin, with its surviving tissues attached to
and vascularized by its normal twin
 3-9% of all conjoined twins and to occur more frequently
 Fetus-in-Fetu
 Early in development, one embryo may be enfolded within its twin
 Vertebral or axial bones are found in these fetiform masses
 Heart and brain are lacking
 Rare malignant degeneration
Monochorionic Twins and Vascular Anastomoses

 Monozygotic twinning results in two amnionic sacs and a common surrounding chorion
o This leads to anatomical sharing of the two fetal circulations through
anastomoses of placental arteries and veins
 Artery-to-artery anastomoses
 Most common
 Those with significant pressure or flow gradients, a shont will
develp between fetuses
 Clinical Syndromes associated with Chronic Fetofetal Transfusion
1. Twin-twin Transfusion Syndrome (TTTS)
 1-3 per 10, 000 births
 Blood is transfused from a donor twin to its recipient sibling such that
 Donor may eventually become anemic and its growth may be
restricted
o pale
 Recipient become polycythemic and may develop circulatory
overload manifested as hydrops
o Plethoric
o May die due to heart failure and severe hypervolemia and
hyperviscosity
o Polycythemia may also lead to severe hyperbilirubinemia
and kernicterus
 One portion of the placenta often appears pale compared with the
remainder
 Occlusive thrombosis is another concern
 Pathophysiology
o Unidirectional flow through arteriovenous anastomoses
o Deoxygenated blood from a donor placental artery is promted
into a cotyledon shared by the typically through arterioarterial
anastomoses leads to an imbalance to blood volume
o Syndrome typically presents in midpregnancy
 When the donor becomes oliguric from decreased
renal perfusion and develops oligohydramnios
 Recipient develops severe hydramnios, presumably
due to increased urine production
o Virtual absence of amnionic fluid in the donor sace prevents
fetal motion, giving rise to  Stuck twin or Polyhydramnios-
Oligohydramnios-Syndrome  Poly-Oh
o Amnionic Fluid Imbalance Associated with the following:
o Growth restriction, contractures and pulmonary
hypoplasia in the donor twin and premature rupture of
the membranes and heart failure in the recipient
TTTS Two Criteria
o Presence of a monchorionic diamnionic pregnancy
o Hydramnios- if the largest-vertical pocket s >8cm in one twin;
Oligohydramnios- if the largest vertical pocket is <2cm in the other
twin
 Only 15% of pregnancies complicated by lesser degrees of
fluid imbalance progress to TTTS
Staging System
o Stage 1
 Discordant amnionic fluid volumes as described above, but
urine is still visible
 Sonographically within the bladder of the donor twin
o Stage 2
 Criteria of stage 1, but urine is not visible within the donor of
the bladder
o Stage 3
 Criteria of stage 2, and abnormal Doppler studies of the
umbilical artery, ductus venosus, or umbilical vein
o Stage 4
 Ascites or frank hydrops in either twin
o Stage 5
 Demise of either fetus
 Cardiac Function of the Recipient Twin
o Myocardial Performance Index (MPI) or Tei Index
o Parland Memorial Hospital
 ECG, MPI calculation, Doppler velocimetry and MRI, genetic
counseling and amniocentesis and placental mapping
Management and Prognosis
o Prognosis of Multifetal Gestations is complicated by:
 TTTS related to Quintero Stage and Gestational age at
presentation
o More than ¾ of stage 1 remains stable or regress without
intervention
o Stage 3 or higher are much worse and the perinatal loss rate is 70-
100%
o Amnioreduction
o Laser Ablation of vascular anastomosis- for severe TTTS (stage 3 and
4)
o Selective feticide
o Selective reduction has generally been considered if severe
amnionic fluid and growth disturbance develop before 20
weeks
o Septostomy
o Intentional creation of a communication in the dividing
amnionic membrane
2. Twin anemia Polycythemia Sequence (TAPS)

 Significant hemoglobin differences between donor ad recipient twins


without the discrepancies in amnionic fluid volumes typical of twin-twin-
transfusion syndrome
 Diagnosed antenatally by middle cerebral artery (MCA) peak systolic
velocity (PSV) >1.5 multiples of the median (MoM) in the donor and <1.0
MoM in the recipient twin
3. Twin Reversed Arterial Perfusion (TRAP)
 Acardiac twin
 1 in 35,000 births
 Serious complication of monochromic multifetal gestation
 Normally formed donor twin that has features of heart failure and a
recipient twin that lacks a heart (acardius) and other structures
 Caused by a large artery-to-artery placental shunt, often also
accompanied by a vein-to-vein shunt
 Single shared placenta, arterial perfusion pressure of the donor twin
exceeds that in the recipient twin, who thus receive reverse blood flow of
deoxygenated arterial blood from its cotwin
 This used arterial blood reaches the recipient twin through its umbilical
arteries and preferentially goes to the iliac vessels
 Thus, only the lower body is perfused, and disrupted growth and
development of the upper body results
 Failure of the head growth is
o Acardius acephalus
 A partially developed head with identifiable limbs called
acardius myelocephalus
 Failure of any recognizable structure to form is called
acardius amorphous

Fetal Brain Damage

o Cerebral palsy, microcephaly and porencephaly and multicystic encephalomalacia


o Acuity of hypotension following the death of one twin with TTTS makes successful
intervention for the survivor nealy impossible
o Even with delivery immediately after a cotwin demise is recognized, the hypotension
that occurs at the moment of death has likely already caused irreversible brain damage

Complete Hydatidiform Mole with Coexisting Normal Fetus

 Twin molar pregnancy


 Due to a complete diploid molar pregnancy comprising one conceptus, whereas the
cotwin is a normal fetus
 Postpartum dangers of persistent trophoblastic disease that requires chemotherapy and
may be fatal

Etiopathogenesis

 Disconcordancy in monochorionic twins is usually attributed to placental vascular


anastomoses that cause hemodynamic imbalance between the twins
 Reduced pressure perfusion of the donor twin can cause diminished placental and fetal
growth
 Disconcordancy in dichorionic twins
o Different genetic growth potential, especially if they are oof opposite genders
o Because the placentas are separate and require more implantation space, one
placenta might have a suboptimal implantation site
o In uterocrowding is a factor in fetal-growth restriction

Diagnosis

 Fetal Biometry
o % disconcordancy = weight of larger twin – weight of smaller twin

Weight of the larger twin

o Abdominal circumference reflects fetal nutrition, some differe more than 20mm
or if the estimated fetal weight difference is 20% or more
o Weight disconcordancy > 25-30% most accurately predicts an adverse perinatal
outcome

Management

o Sonographic monitoring of growth within a twin pair and calculating disconcordancy has
become a mainstay in management
o Every 2 weeks in monochorionic twins
o Dichorionic twins are evaluated every 6 weeks
o Nonstress testing, biophysical profile scores and umbilical artery Doppler assessment

When to Deliver?

o 37 weeks AOG- monochorionic twins


o 38 weeks AOG- dichorionic twins

Fetal Demise

o Death of one fetus


o Vanishing twin: early
o Fetal compressus
o Fetus Papyraceus- Flattened remarkably through dessication
o Cotwin demise- 5x higher in monochorionic twins
o Neurological prognosis for a surviving cotwin depends almost exclusively on-chorionicity
o Management
o Based of gestational age, cause of the death and the risk to the surviving
twin/fetus
o If the loss occurs early in the 1st trimester
 Vanishing twin is considered harmless to the survivor
o If the loss occurs after the 1st trimester
 The risk of the death or damage to the survivor is largely limited to
monochorionic twin gestation
o Morbidity in the monochorionic twin survivor is almost always due to vascular
anastomoses, which often cause the demise of one twin followed by the sudden
hypotension of the other
o Monochorionic twin gestation dies after the 1st trimester but before viability,
pregnancy termination can be considered
o Death of one but not all fetuses results from a maternal complication such as
diabetic ketoacidosis or severe preeclampsia with abruption
o Management is based on the diagnosis and the status of both the mother and
surviving fetus
o Antenatal corticosterois for survivor is for lung maturity

Surveillance of Fetal Growth and Health

o Umbilical artery Doppler velocimetry led to a reduced perinatal mortality rate


o Smallest, most stressed twin fetus is typically more mature

Preterm Birth

o Bed rest—especially thwough hospoitalization, prophylactic administration of beta-


mimetic drugs or progestins, prophylactic cervical cerclage and pessary placement
o Predilection of Preterm birth
o Cervical length
 Fetal fibronectin concentration in the cervical canal
 At 24 weeks,
 a cervical length </=25mm was the best predictor of birth weight
before32 weeks
 At 28 weeks,
 an elevated fetal fibronectin level was the best predictor
o Treatment
 Tocolytic therapy ?
 Glucocortcoids for lung maturation
Internal Podalic Version

o Fetus in turned to a breech presentation using the hand placed into the uterus
o Obstetrician grasps the fetal feet to then effect delivery by breech extraction
 Strict protocol for second twin management
o Abdominal manipulation
o Intrapartum external version of a noncephalic second twin

Vaginal Delivery of the Second Twin

 Following Delivery of the First Twin


o Presenting part of the 2nd twin, its size and its relationship to the birth canal
 Should quickly and carefully ascertained by combined abdominal, vaginal
and at times intrauterine examination
o If fetal head or the breech is fixed in the birth canal
 Moderate fundal pressure and membranes are ruptured
o Immediately afterward, digital exam of the cervix is repeated to exclude cord
prolapse
 Labor is allowed to resume
o If contractions do not begin within approximately 10 minutes
 Dilute oxytocin may be used to stimulate contractions
 Safest interval between delivery of the 1st and 2nd twins were frequently cited as less
than 3 minutes

Mode of Delivery: Caesarean Section

1. Twin A- non-vertex
 Caesarean Section
2. Twin A- vertex; twin B- vertex
 Vaginally
o If the first twin presents cephalic, delivery can usually be accomplished
spontaneously or with forcep
 If not engaged 2nd twin
o Options are conversion to breech and deliver by breech extraction or CS
if felt the safest
3. Twin A- vertex; twin B- non-vertex
 Caesarean section
 Vaginal for both twin or breech extraction of twin B

Locked Twin

 First must present as breech and the second as cephalic


Theory
1. Fission- traditional
 Fertilized egg splits partially and delayed separation after day 12
2. Fusion
 Fertilized egg completely separates but stem cells find like-stem cells on
the other
 NOTE: Abnormal C inactivation: more females

Intrapartum Management

 Labor
o Establish the presentation and EFW by UTZ
o Oxytocin induction or augmentation
 Anesthesia
o Regional

Labor Induction or Stimulation

 Consortium of Safe Labor


o Nulliparas and multiparas with twins had slower progression of active labor
o Women with twins required between 1 and 3 additional hours to complete first
stage labor

Labor and Delivery

 Uterine contractile dysfunction, abnormal fetal presentation, umbilical cord prolapse,


placenta previa, placental abruption, emergent operative delivery, and postpartum
hemorrhage from uterine atony

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