Although the blood volume is increased in multiple pregnancy, maternal anemia often develops because of greater demand for iron by the fetuses. However, prior anemia, poor diet, and malabsorption may precede or compound iron deficiency during multiple pregnancy. Respiratory tidal volume is increased, but the woman pregnant with twins often is “breathless” (possibly due to increased levels of progesterone).
Marked uterine distention and increased pressure on the adjacent viscera and pelvic vasculature are typical of multiple pregnancy. Lutein cysts and even ascites are the result of abnormally high levels of chorionic gonadotropin in occasional multiple pregnancies. Placenta previa develops more frequently because of the large size of the placenta or placentas.
The maternal cardiovascular, respiratory, gastrointestinal, renal, and musculoskeletal systems are especially subject to stress in multiple pregnancy, combined with greater maternal-fetal nutritional requirements. Multiple pregnancy is classified as high-risk because of the increased incidence of maternal anemia, urinary tract infection, preeclampsia-eclampsia, hemorrhage (before, during, and after delivery), and uterine inertia.
A. Placental and Cord
The placenta and membranes of monozygotic twins may vary considerably (
Fig 17-1), depending on the time of initial division of the embryonic disk. Variations are noted below.
(1) Division prior to the morula stage and differentiation of the trophoblast (third day) results in separate or fused placentas, 2 chorions, and 2 amnions. (This process grossly resembles dizygotic twinning and accounts for almost one-third of monozygotic twinning.)
(2) Division after differentiation of the trophoblast but before the formation of the amnion (fourth to eighth days) yields a single placenta, a common chorion, and 2 amnions. (This accounts for about two-thirds of monozygotic twinning.)
(3) Division after differentiation of the amnion (8th-13th days) results in a single placenta, 1 (common) chorion, and 1 (common) amnion. This is rare.
(4) Division later than day 15 may result in incomplete twinning. Just prior to that time (day 13-15), division may result in conjoined twins.
At delivery, the membranous T-shaped septum or dividing membrane of the placenta between the twins must be inspected and sectioned for evidence of the probable type of twinning (
Fig 17-2). Monozygotic twins most commonly have a transparent (< 2 mm) septum made up of 2 amniotic membranes only (no chorion and no decidua). Dizygotic twins almost always have an opaque (thick) septum made up of 2 chorions, 2 amnions, and intervening decidua.
A monochorionic placenta can be identified by stripping away the amnion or amnions to reveal a single chorion over a common placenta. In virtually every case of monochorionic placenta, vascular communications between the 2 parts of the placenta can be identified by careful dissection or injection. In contrast, dichorionic placentas (of dizygotic twinning) only rarely have an anastomosis between the fetal blood vessels.
Placental and membrane examination is a certain indicator of zygosity in twins with monochorionic placentas because these are always monozygotic. Overall, approximately 1% of twins are monoamniotic and these too are monozygotic. Determination of zygosity is clinically significant in case intertwin organ transplantation is needed later in life, as well as for assessing obstetrical risks. Monozygotic twins can rarely be discordant for phenotypic sex when one twin is phenotypically female due to Turner syndrome (45,XO) and its sibling is male, 46,XY.
Monochorionic placentation is associated with more disease processes as a result of placental vascular problems. Inequities of the placental circulation in one area (marginal insertion, partial infarction, or thinning) may lead to growth discordance between the twins. Due to vascular anastomoses in monochorionic placentation, multifetal reduction can only be performed with dichorionic placentation.
The most serious problem with monochorionic placentas is local shunting of blood - also called twin-to-twin transfusion syndrome. This occurs because of vascular anastomoses to each twin that are established early in embryonic life. The possible communications are artery to artery, vein to vein, and combinations of these. Artery-to-vein communication is by far the most serious; it is most likely to cause twin-to-twin transfusion. In uncompensated cases, the twins, although genetically identical, differ greatly in size and appearance. The recipient twin is plethoric, edematous, and hypertensive. Ascites and kernicterus are likely. The heart, liver, and kidneys are enlarged (glomerulotubal hypertrophy). Hydramnios follows fetal polyuria. Although ruddy and apparently healthy, the recipient twin with hypervolemia may die of heart failure during the first 24 hours after birth. The donor twin is small, pallid, and dehydrated (from growth restriction, malnutrition, and hypovolemia). Oligohydramnios may be present. Severe anemia, due to chronic blood loss to the other twin, may lead to hydrops and heart failure.
Both twins are threatened by prolapse of the cord. The second twin may be harmed by premature separation of the placenta, hypoxia, constriction ring dystocia, operative manipulation, or prolonged anesthesia.
Velamentous insertion of the cord occurs in about 7% of twins but in only 1% of singletons. There is a corresponding increase in the potentially catastrophic vasa previa. The incidence of 2-vessel cord (single umbilical artery) is 4-5 times higher in monozygotic twins than in singletons.
Monochorionic, monoamniotic twins (1:100 sets of twins) have less than a 50% likelihood of both surviving because of cord entanglement that compromises fetal-placental blood flow. Some authors advocate planned cesarean delivery at 32-34 weeks in an attempt to prevent in utero demise due to cord accidents.
Earlier and more precise sonography has revealed the incidence of multiple gestation to be 3.29-5.39% before 12 weeks. However, in over 20% of such cases one or more of the pregnancies spontaneously disappears. Although this event may be associated with vaginal bleeding, the prognosis remains good for the remaining twin. This loss has been termed the “vanishing twin.”
Major malformations are present in approximately 2% of twin infants, compared with 1% of singletons, while minor malformations are found in 4% of twins compared with about 2.5% in singletons. Monozygotic twins are at higher risk than dizygotic twins.
Conjoined or Siamese twins result from incomplete segmentation of a single fertilized ovum between the 13th and 14th days; if cleavage is further postponed, incomplete twinning (2 heads, 1 body) may occur. Lesser abnormalities are also noted, but these occur without regard to specific organ systems. Conjoined twins are described by site of union: pygopagus (at the sacrum); thoracopagus (at the chest); craniopagus (at the heads); and omphalopagus (at the abdominal wall). Curiously, conjoined twins usually are female. Numerous conjoined twins have survived separation.
Each twin and its placenta generally weigh less than the newborn and placenta of a singleton pregnancy after the 30th week, but near term the aggregate weight may approach twice that of a singleton. In general, the larger the number of fetuses, the greater the degree of growth restriction. Interestingly, multifetal reduction of triplets to twins before 12 weeks results in a growth pattern typical of twins rather than triplets, who are growth restricted compared with twins. Thus the number of fetuses residing in the uterus later in pregnancy, and not their embryonic potential, seems to govern growth. Normal-weight twins that differ considerably in birthweight commonly have diamnioticdichorionic placentas. This suggests independent intrauterine growth of co-twins. The converse is true of twins with fused diamniotic-dichorionic placentas. Low-birthweight monochorionic twins are the rule rather than the exception. Low birthweight in the various types of multiple pregnancy probably is evidence of growth restriction due to inadequate nutrition. This is at least partially responsible for the much higher early neonatal mortality rate of newborns from multiple births.
Monozygotic twins are smaller and succumb more often in utero than dizygotic twins. Prematurity is the major reason for the increased risk of neonatal death and morbidity in twins. Growth restriction, competition for nutrition, cord compression and entanglement, and operative delivery are also responsible for a significant part of the perinatal mortality rate in multiple pregnancy.
In growth-restricted human fetuses, the brain and heart seem to be relatively less affected than the liver or peripheral musculature. Because placental growth and function are limited, hormone alterations may develop to trigger early labor. Moreover, restricted fetal growth has a small but lasting effect on postnatal physical development.
In late pregnancy, the fetus is jeopardized by the frequency of premature delivery, abnormal presentation and position, and hydramnios.
A fetus acardiacus is a parasitic monozygotic fetus without a heart. It is thought to develop from reversed circulation, perfused by 1 arterial-arterial and 1 venous-venous anastomosis. This represents TRAP, the twin reversed arterial perfusion syndrome. The otherwise normal donor twin is at risk for cardiac hypertrophy and failure, and has a 35% mortality. Various methods of cord occlusion are being studied as in utero therapy.
Fetus papyraceous is a small, blighted, mummified fetus usually discovered at the delivery of a well-developed newborn. This occurs once in 17,000-20,000 pregnancies. The cause is thought to be death of one twin, amniotic fluid loss, or reabsorption and compression of the dead fetus by the surviving twin.
Figure 17-1. Placental variations in twinning. (After Potter. Reproduced, with permission, from Benson RC: Handbook of Obstetrics & Gynecology, 8th ed. Lange, 1983.)
Figure 17-2. Amniotic membranes of twins. (Reproduced, with permission, from Benson RC: Handbook of Obstetrics & Gynecology, 8th ed. Lange, 1983.)
Revision date: June 18, 2011
Last revised: by Andrew G. Epstein, M.D.