MULTIPLE GESTATION
Supervisor:
Prof. Hanan BinGouth
Prepared by:
Mohsen Al-solaimani
Definition
 A multiple gestation occurs when >1 fetus is carried
during a pregnancy.
Incidence
 twin birth rate in 2019 was 32.1 per 1,000 live
births
 The rate of MZ twinning has remained relatively
constant (3.5 per 1,000 births).
 The rate of DZ twinning is approximately 1 in
100 births
 The birth rate of triplet and higher order
multiples peaked in 1998
at 194 per 100,000 live births and has declined
steadily to 87.7 per 100,000 live births in 2019.
Pathophysiology
 Classification.
1. Twin placentation is classified according to the
placental disk (single, fused,or separate), number of
chorions (monochorionic or dichorionic), and number of
amnions (monoamniotic or diamniotic)
2. Heterosexual (assuredly dizygotic) twins always have a
dichorionic placenta.
3. Monochorionic twins are always of the same sex. All
monochorionic twins are believed to be monozygotic. In 70%
of monozygotic twin pregnancies, the placentas are
monochorionic, and the possibility exists for commingling of
the fetal circulations. Less than 1% of twin pregnancies
are monoamniotic.
Pathophysiology
 B. Placental complications. Twin gestations are
associated with an increased frequency of anomalies of
the placenta and adnexa, for example, a single
umbilical artery or velamentous or marginal cord
insertion The cord is more susceptible to trauma from
twisting. The vessels near the insertion are often
unprotected by Wharton jelly and are especially prone to
thrombosis when compression or twisting occurs.
Intrapartum fetal distress from cord compression and
fetal hemorrhage from associated vasa previa are
potential problems with velamentous insertion of the
cord.
Multiple Gestation prepared and presented by Dr.Mohsen Al-solaimani.pptx
Pathophysiology
 Determination of zygosity. The most efficient way to identify
zygosity is as follows:
1. Gender examination. Male-female pairs are dizygotic.
The dichorionic placenta may be separate or fused.
2. Placental examination. Twins with a monochorionic
placenta (monoamniotic or diamniotic) are monozygotic. If
doubt exists on a gross inspection of the dividing
membranes, a transverse section should be studied. The
zygosity of twins of the same sex with dichorionic
membranes cannot be immediately
known. Genetic studies are needed (eg, blood typing, human
leukocyte antigen typing, DNA markers, and chromosome
marking) to determine zygosity.
Risk factors
 ART
 Family history of twins,
 Paternal age (peak at 35–39years),
 Previous twin gestation,
 Increasing parity, maternal height, fecundity, social class,
frequency of coitus,
 Exogenous gonadotropins, clomiphene, or in vitro
fertilization.
 The risk of twinning decreases with undernourishment. Ethnic
background (African Americans > Caucasians > Asians) is a
preconception risk factor for naturally conceived multiple
gestation births.
Clinical presentation
 Twins are more likely to have prematurity, fetal growth
restriction, congenital anomalies, and twin-twin transfusion.
A. Prematurity and uteroplacental insufficiency are the
major contributors to perinatal complications. In 2015, 1% of
singletons, 10% of twins, and 36% of triplets had birthweights
of <1500 g.
B. Fetal growth restriction. The incidence of low birthweight
in twins is approximately 50% to 60%, a 5 to 7 times higher
than the incidence of low birthweight in singletons. In general,
the more fetuses in a gestation, the smaller is their weight for
gestational age Twins tend to grow at normal rates up to
about 30 to 34 weeks’ gestation when they reach a combined
weight of 4 kg. Thereafter, they grow more slowly.
 Two-thirds of twins show some signs of growth restriction at
birth.
Clinical presentation
 Uteroplacental insufficiency. The incidence of acute
and chronic uteroplacental insufficiency is increased in
multiple gestations.
 Five-minute Apgar scores of 0 to 3 are reported for 5% to
10% of twin gestations.
 These low scores may relate to acute stresses of labor,
cord prolapse (1%–5%), or trauma during delivery
superimposed
on chronic uteroplacental insufficiency.
Congenital anomalies
 Birth defects are 2 to 3 times more common in
monozygotic twins than in singletons or dizygotic twins
 Three mechanisms deformations caused by intrauterine
space constraint, disruption of normal blood flow
secondary to placental vascular anastomoses, and defects
in morphogenesis. Such defects are usually discordant in
monozygotic twins; however, in purely genetic conditions
(eg, chromosomal abnormalities or single-gene defects),
concordance would be the rule.
 Twins conceived by IVF have twice the risk of major
congenital anomalies compared with twins conceived
Congenital anomalies
1. Anomalies unique to multiple pregnancies. Certain anomalies,
such as conjoined twins and acardia, are unique to multiple
pregnancies.
2. Deformations. Twins are more likely to suffer from intrauterine
crowding and restriction of movement, leading to synostosis,
torticollis, facial palsy, positional foot defects, and other defects.
3. Vascular disruptions. Disruptions related to monozygotic
vascular shunts may result in birth defects. Acardia occurs from
an artery-to-artery placental shunt, in which reverse flow leads to
the development of an amorphous recipient twin. In utero death of
a co-twin may result in a thromboembolic phenomenon, including
DIC, cutis aplasia, porencephaly, hydranencephaly, limb reduction
defects, intestinal atresias, gastroschisis.
Twin-twin transfusion syndrome
1. Vascular anastomoses. Almost all monochorionic
placentas demonstrate vascular anastomoses, whereas
dichorionic placentas rarely do. Vascular anastomoses may
be superficial direct communications easily visible on
inspection between arteries (most common) or veins
(uncommon), deep connections from arteries to veins via
villi, or combinations of superficial and deep connections.
Twin-twin transfusion syndrome
 2. Incidence. Despite the high frequency of vascular
anastomosis in monochorionic placentation, the twin-twin
transfusion syndrome is relatively uncommon (∼15% of
monochorionic gestations).
Twin-twin transfusion syndrome Clinical
manifestations
Clinically, the twin-twin transfusion syndrome is diagnosed when twins have a
hemoglobin difference of >5 g/dL and is due to artery-to-vein anastomoses.
a. The donor twin tends to be pale and have a low birthweight,
oligohydramnios, anemia, hypoglycemia, decreased organ mass,
hypovolemia, and amnion nodosum. Donor twins often require volume
expansion, red blood cell transfusion, or both.
b. The recipient twin is frequently plethoric and has a high birthweight,
polyhydramnios, polycythemia or hyperviscosity, increased organ mass,
hypervolemia, and hyperbilirubinemia. Recipient twins often require partial
exchange transfusion.
c. Infants born with twin-twin transfusion syndrome have an increased risk
of being diagnosed with antenatally acquired severe cerebral lesions and are
at an increased risk of neurodevelopmental sequelae, even when treatment is
initiated antenatally. Antenatal treatment with fetoscopic selective laser
coagulation may reduce the risk of death or long-term impairment.
Diagnosis
Multiple gestation is usually diagnosed prenatally by
ultrasound as early as 5 weeks (can see gestational sacs)
and by an increased AFP (in twin pregnancies, the average
AFP is double that found in a singleton pregnancy).
Management
A. Site of delivery. When a complicated twin gestation has been
identified, delivery should ideally be conducted at a high-risk perinatal
center with experienced pediatric delivery teams in attendance.
B. Physical examination. Infants should be examined for evidence of
fetal growth restriction, congenital anomalies, and twin-twin transfusion
syndrome. Central hematocrits should be obtained in both infants.
When 1 of the infants has a congenital anomaly, the other twin is at
increased risk for complications. In particular, death of 1 fetus puts the
others at risk for fetal disseminated intravascular coagulation.
C. Complications in newborn period. The 2nd-born twin is more
likely to develop RDS and bronchopulmonary dysplasia and to die.
D. Co-bedding of multiples. Although co-bedding multiples was once
common
practice, the safety or the benefit of this practice has not been
Management
 Risks beyond the neonatal period
1. Catch-up growth. In monozygotic twins, birthweight
differences may be as much as 20%, but the lighter twin
has a remarkable ability to make up intrauterine growth
deficits.
2. Social problems. Parents of multiple births may have
an increased level of stress and may respond differently
to their children compared with singletons. Counseling for
parents of twins may be invaluable.
Prognosis (Twins)
The perinatal death rate for twins may be higher in the second twin,
especially if the second twin is smaller. Delivery may be considered
at 37 weeks to minimize the risk of stillbirth in dichorionic twins.
1. Monoamniotic twins. have the highest mortality rate because of
cord entanglement.
2. Monozygotic twins. Monozygotic twins have a perinatal mortality
and morbidity rate 2 to 3 times that of dizygotic twins.
3. Fetal death in twins. When the cause of death is intrinsic to 1
dichorionic fetus and does not threaten the other fetus,
complications are rare. Hazardous intrauterine environments
threaten both twins, whether monochorionic or dichorionic.
With monochorionic placentas, the incidence of major complications
or death in the surviving twin is approximately 50%.
Prognosis (Triplets)
 The neonatal mortality rate for triplets is 18.8%, and the
perinatal mortality rate is 25.5%. The risk of death or
neurodevelopmental impairment has been shown to be
increased in extremely low birthweight triplets and other
higher order multiples compared to singletons .
Multiple Gestation prepared and presented by Dr.Mohsen Al-solaimani.pptx

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Multiple Gestation prepared and presented by Dr.Mohsen Al-solaimani.pptx

  • 1. MULTIPLE GESTATION Supervisor: Prof. Hanan BinGouth Prepared by: Mohsen Al-solaimani
  • 2. Definition  A multiple gestation occurs when >1 fetus is carried during a pregnancy.
  • 3. Incidence  twin birth rate in 2019 was 32.1 per 1,000 live births  The rate of MZ twinning has remained relatively constant (3.5 per 1,000 births).  The rate of DZ twinning is approximately 1 in 100 births  The birth rate of triplet and higher order multiples peaked in 1998 at 194 per 100,000 live births and has declined steadily to 87.7 per 100,000 live births in 2019.
  • 4. Pathophysiology  Classification. 1. Twin placentation is classified according to the placental disk (single, fused,or separate), number of chorions (monochorionic or dichorionic), and number of amnions (monoamniotic or diamniotic) 2. Heterosexual (assuredly dizygotic) twins always have a dichorionic placenta. 3. Monochorionic twins are always of the same sex. All monochorionic twins are believed to be monozygotic. In 70% of monozygotic twin pregnancies, the placentas are monochorionic, and the possibility exists for commingling of the fetal circulations. Less than 1% of twin pregnancies are monoamniotic.
  • 5. Pathophysiology  B. Placental complications. Twin gestations are associated with an increased frequency of anomalies of the placenta and adnexa, for example, a single umbilical artery or velamentous or marginal cord insertion The cord is more susceptible to trauma from twisting. The vessels near the insertion are often unprotected by Wharton jelly and are especially prone to thrombosis when compression or twisting occurs. Intrapartum fetal distress from cord compression and fetal hemorrhage from associated vasa previa are potential problems with velamentous insertion of the cord.
  • 7. Pathophysiology  Determination of zygosity. The most efficient way to identify zygosity is as follows: 1. Gender examination. Male-female pairs are dizygotic. The dichorionic placenta may be separate or fused. 2. Placental examination. Twins with a monochorionic placenta (monoamniotic or diamniotic) are monozygotic. If doubt exists on a gross inspection of the dividing membranes, a transverse section should be studied. The zygosity of twins of the same sex with dichorionic membranes cannot be immediately known. Genetic studies are needed (eg, blood typing, human leukocyte antigen typing, DNA markers, and chromosome marking) to determine zygosity.
  • 8. Risk factors  ART  Family history of twins,  Paternal age (peak at 35–39years),  Previous twin gestation,  Increasing parity, maternal height, fecundity, social class, frequency of coitus,  Exogenous gonadotropins, clomiphene, or in vitro fertilization.  The risk of twinning decreases with undernourishment. Ethnic background (African Americans > Caucasians > Asians) is a preconception risk factor for naturally conceived multiple gestation births.
  • 9. Clinical presentation  Twins are more likely to have prematurity, fetal growth restriction, congenital anomalies, and twin-twin transfusion. A. Prematurity and uteroplacental insufficiency are the major contributors to perinatal complications. In 2015, 1% of singletons, 10% of twins, and 36% of triplets had birthweights of <1500 g. B. Fetal growth restriction. The incidence of low birthweight in twins is approximately 50% to 60%, a 5 to 7 times higher than the incidence of low birthweight in singletons. In general, the more fetuses in a gestation, the smaller is their weight for gestational age Twins tend to grow at normal rates up to about 30 to 34 weeks’ gestation when they reach a combined weight of 4 kg. Thereafter, they grow more slowly.  Two-thirds of twins show some signs of growth restriction at birth.
  • 10. Clinical presentation  Uteroplacental insufficiency. The incidence of acute and chronic uteroplacental insufficiency is increased in multiple gestations.  Five-minute Apgar scores of 0 to 3 are reported for 5% to 10% of twin gestations.  These low scores may relate to acute stresses of labor, cord prolapse (1%–5%), or trauma during delivery superimposed on chronic uteroplacental insufficiency.
  • 11. Congenital anomalies  Birth defects are 2 to 3 times more common in monozygotic twins than in singletons or dizygotic twins  Three mechanisms deformations caused by intrauterine space constraint, disruption of normal blood flow secondary to placental vascular anastomoses, and defects in morphogenesis. Such defects are usually discordant in monozygotic twins; however, in purely genetic conditions (eg, chromosomal abnormalities or single-gene defects), concordance would be the rule.  Twins conceived by IVF have twice the risk of major congenital anomalies compared with twins conceived
  • 12. Congenital anomalies 1. Anomalies unique to multiple pregnancies. Certain anomalies, such as conjoined twins and acardia, are unique to multiple pregnancies. 2. Deformations. Twins are more likely to suffer from intrauterine crowding and restriction of movement, leading to synostosis, torticollis, facial palsy, positional foot defects, and other defects. 3. Vascular disruptions. Disruptions related to monozygotic vascular shunts may result in birth defects. Acardia occurs from an artery-to-artery placental shunt, in which reverse flow leads to the development of an amorphous recipient twin. In utero death of a co-twin may result in a thromboembolic phenomenon, including DIC, cutis aplasia, porencephaly, hydranencephaly, limb reduction defects, intestinal atresias, gastroschisis.
  • 13. Twin-twin transfusion syndrome 1. Vascular anastomoses. Almost all monochorionic placentas demonstrate vascular anastomoses, whereas dichorionic placentas rarely do. Vascular anastomoses may be superficial direct communications easily visible on inspection between arteries (most common) or veins (uncommon), deep connections from arteries to veins via villi, or combinations of superficial and deep connections.
  • 14. Twin-twin transfusion syndrome  2. Incidence. Despite the high frequency of vascular anastomosis in monochorionic placentation, the twin-twin transfusion syndrome is relatively uncommon (∼15% of monochorionic gestations).
  • 15. Twin-twin transfusion syndrome Clinical manifestations Clinically, the twin-twin transfusion syndrome is diagnosed when twins have a hemoglobin difference of >5 g/dL and is due to artery-to-vein anastomoses. a. The donor twin tends to be pale and have a low birthweight, oligohydramnios, anemia, hypoglycemia, decreased organ mass, hypovolemia, and amnion nodosum. Donor twins often require volume expansion, red blood cell transfusion, or both. b. The recipient twin is frequently plethoric and has a high birthweight, polyhydramnios, polycythemia or hyperviscosity, increased organ mass, hypervolemia, and hyperbilirubinemia. Recipient twins often require partial exchange transfusion. c. Infants born with twin-twin transfusion syndrome have an increased risk of being diagnosed with antenatally acquired severe cerebral lesions and are at an increased risk of neurodevelopmental sequelae, even when treatment is initiated antenatally. Antenatal treatment with fetoscopic selective laser coagulation may reduce the risk of death or long-term impairment.
  • 16. Diagnosis Multiple gestation is usually diagnosed prenatally by ultrasound as early as 5 weeks (can see gestational sacs) and by an increased AFP (in twin pregnancies, the average AFP is double that found in a singleton pregnancy).
  • 17. Management A. Site of delivery. When a complicated twin gestation has been identified, delivery should ideally be conducted at a high-risk perinatal center with experienced pediatric delivery teams in attendance. B. Physical examination. Infants should be examined for evidence of fetal growth restriction, congenital anomalies, and twin-twin transfusion syndrome. Central hematocrits should be obtained in both infants. When 1 of the infants has a congenital anomaly, the other twin is at increased risk for complications. In particular, death of 1 fetus puts the others at risk for fetal disseminated intravascular coagulation. C. Complications in newborn period. The 2nd-born twin is more likely to develop RDS and bronchopulmonary dysplasia and to die. D. Co-bedding of multiples. Although co-bedding multiples was once common practice, the safety or the benefit of this practice has not been
  • 18. Management  Risks beyond the neonatal period 1. Catch-up growth. In monozygotic twins, birthweight differences may be as much as 20%, but the lighter twin has a remarkable ability to make up intrauterine growth deficits. 2. Social problems. Parents of multiple births may have an increased level of stress and may respond differently to their children compared with singletons. Counseling for parents of twins may be invaluable.
  • 19. Prognosis (Twins) The perinatal death rate for twins may be higher in the second twin, especially if the second twin is smaller. Delivery may be considered at 37 weeks to minimize the risk of stillbirth in dichorionic twins. 1. Monoamniotic twins. have the highest mortality rate because of cord entanglement. 2. Monozygotic twins. Monozygotic twins have a perinatal mortality and morbidity rate 2 to 3 times that of dizygotic twins. 3. Fetal death in twins. When the cause of death is intrinsic to 1 dichorionic fetus and does not threaten the other fetus, complications are rare. Hazardous intrauterine environments threaten both twins, whether monochorionic or dichorionic. With monochorionic placentas, the incidence of major complications or death in the surviving twin is approximately 50%.
  • 20. Prognosis (Triplets)  The neonatal mortality rate for triplets is 18.8%, and the perinatal mortality rate is 25.5%. The risk of death or neurodevelopmental impairment has been shown to be increased in extremely low birthweight triplets and other higher order multiples compared to singletons .