Several unique and fascinating complications arise in multifetal pregnancies. These have been best described in twins but can be found in higher-order multifetal gestations. Most fetal complications due to the twinning process itself are seen with monozygotic twins. Their pathogenesis is best understood after reviewing the possibilities shown in Figure 45-1.
Only about 1 percent of all monozygotic twins will share an amnionic sac (Hall, 2003). Said another way, approximately 1 in 20 monochorionic twins are monoamnionic (Lewi, 2013). This configuration is associated with a high fetal death rate from cord entanglement, congenital anomalies, preterm birth, or twin-twin-transfusion syndrome, which is described subsequently. In a comprehensive review, Allen and associates (2001) reported that monoamnionic twins diagnosed antenatally and alive at 20 weeks have approximately a 10-percent risk of subsequent fetal demise. In a Dutch report of 98 monoamnionic twin pregnancies, the perinatal mortality rate was 17 percent (Hack, 2009). Umbilical cord entanglement, a frequent cause of death, is estimated to complicate at least half of cases (Fig. 45-12). Diamnionic twins can become monoamnionic if the dividing membrane ruptures and therefore have similar associated morbidity and mortality rates.
Monozygotic twins in a single amnionic sac. The smaller fetus apparently died first, and the second subsequently succumbed when umbilical cords entwined.
Unfortunately, there are no management methods that guarantee good outcomes for either or both twins. This is because of the unpredictability of fetal death from cord entanglement and the lack of an effective means of monitoring for it. Quinn and colleagues (2011) retrospectively evaluated the feasibility of inpatient continuous fetal heart monitoring in 17 sets of monoamnionic twins. After review of more than 10,000 hours of fetal tracing, these investigators concluded that this was possible in only 50 percent of cases. Importantly, an abnormal fetal heart rate tracing prompted delivery in only six cases. Morbid cord entanglement appears to occur early, and monoamnionic pregnancies that have successfully reached 30 to 32 weeks are at reduced risk. In the Dutch series described above, the incidence of intrauterine demise dropped from 15 percent after 20 weeks to 4 percent when gestational age exceeded 32 weeks (Hack, 2009).
Although umbilical cords frequently entangle, factors that lead to pathological umbilical vessel constriction are unknown. Color-flow Doppler sonography can be used to diagnose entanglement (Fig. 45-13). However, once identified, evidence to guide management is observational, retrospective, and subject to biased reporting. One proposed management scheme is based on a study by Heyborne and coworkers (2005), who reported no stillbirths in 43 twin pregnancies of women admitted at 26 to 27 weeks’ gestation for daily fetal surveillance. Conversely, there were 13 stillbirths in 44 women who were managed as outpatients and admitted only for an obstetrical indication. Because of this report, women with monoamnionic twins are recommended to undergo 1 hour of daily fetal heart rate monitoring, either as outpatients or as inpatients, beginning at 26 to 28 weeks. With initial testing, a course of betamethasone is given to promote pulmonary maturation (Chap. 42, Corticosteroids for Fetal Lung Maturation). If fetal testing remains reassuring, cesarean delivery is performed at 34 weeks and after a second course of betamethasone. This management scheme is used at Parkland Hospital and resulted in the successful 34-week delivery of the twins depicted in Figure 45-13.
Monochorionic monoamnionic cord entanglement. A. Despite marked knotting of the cords, vigorous twins were delivered by cesarean. B. Preoperative sonogram of this pregnancy shows entwined cords. C. This finding is accentuated with application of color Doppler. (Photographs contributed by Dr. Julie Lo.)
Aberrant Twinning Mechanisms
Several aberrations in the twinning process result in a spectrum of fetal malformations. These are traditionally ascribed to incomplete splitting of an embryo into two separate twins. However, it is possible that they may result from early secondary fusion of two separate embryos. These separated embryos are either symmetrical or asymmetrical, and the spectrum of anomalies is shown in Figure 45-14.
Possible outcomes of monozygotic twinning. The asymmetrical category contains twinning types in which one twin complement is substantially smaller and incompletely formed.
In the United States, united or conjoined twins have been referred to as Siamese twins–after Chang and Eng Bunker of Siam (Thailand), who were displayed worldwide by P. T. Barnum. Joining of the twins may begin at either pole and may produce characteristic forms depending on which body parts are joined or shared (Fig. 45-15). Of these, thoracopagus is the most common (Mutchinick, 2011). The frequency of conjoined twins is not well established. At Kandang Kerbau Hospital in Singapore, Tan and coworkers (1971) identified seven cases of conjoined twins among more than 400,000 deliveries–an incidence of 1 in 60,000.
As reviewed by McHugh and associates (2006), conjoined twins can frequently be identified using sonography at midpregnancy. This provides an opportunity for parents to decide whether to continue the pregnancy. As shown in Figure 45-16, identification of cases during the first trimester is also possible. A targeted examination, including a careful evaluation of the connection and the organs involved, is necessary before counseling can be provided. As shown in Figure 45-17, MR imaging can play an important adjunctive role in clarifying shared organs. Compared with sonography, MR imaging may provide superior views, especially in later pregnancy when amnionic fluid is diminished and fetal crowding is increased (Hibbeln, 2012).
Sonogram of a conjoined twin pregnancy at 13 weeks’ gestation. These thoracoomphalopagus twins have two heads but a shared chest and abdomen.
Magnetic resonance imaging of conjoined twins. This T2-weighted HASTE sagittal image demonstrates fusion from the level of the xiphoid process to just below the level of the umbilicus, that is, omphalopagus twins. Below the fused liver (L), there is a midline cystic mass (arrow) within the tissue connecting the twins. An omphalomesenteric cyst was favored given the location within the shared tissue. (Image contributed by Dr. April Bailey.)
Surgical separation of an almost completely joined twin pair may be successful if essential organs are not shared (Spitz, 2003; Tannuri, 2013). Consultation with a pediatric surgeon often assists parental decision making. Conjoined twins may have discordant structural anomalies that further complicate decisions about whether to continue the pregnancy.
Viable conjoined twins should be delivered by cesarean. For the purpose of pregnancy termination, however, vaginal delivery is possible because the union is most often pliable (Fig. 45-18). Still, dystocia is common, and if the fetuses are mature, vaginal delivery may be traumatic to the uterus or cervix.
Conjoined twins aborted at 17 weeks’ gestation. (Photograph contributed by Dr. Jonathan Willms.)
This is a grossly defective fetus or merely fetal parts, attached externally to a relatively normal twin. A parasitic twin usually consists of externally attached supernumerary limbs, often with some viscera. Classically, however, a functional heart or brain is absent. Attachment mirrors those sites described earlier for conjoined twins (see Fig. 45-14). Parasites are believed to result from demise of the defective twin, with its surviving tissues attached to and vascularized by its normal twin (Spencer, 2001). In a worldwide collaborative epidemiological study, parasitic twins were found to account for 3.9 percent of all conjoined twins and to occur more frequently in male fetuses (Mutchinick, 2011).
Early in development, one embryo may be enfolded within its twin. Normal development of this rare parasitic twin usually arrests in the first trimester. As a result, normal spatial arrangement of and presence of many organs is lost. Classically, vertebral or axial bones are found in these fetiform masses, whereas heart and brain are lacking. These masses are typically supported by their host by a few large parasitic vessels (Spencer, 2000). Malignant degeneration is rare (Kaufman, 2007).
Monochorionic Twins and Vascular Anastomoses
Another group of fascinating fetal syndromes can arise when monozygotic twinning results in two amnionic sacs and a common surrounding chorion. This leads to anatomical sharing of the two fetal circulations through anastomoses of placental arteries and veins. All monochorionic placentas likely share some anastomotic connections. However, there are marked variations in the number, size, and direction of these seemingly haphazard connections (Fig. 45-19). In their analyses of more than 200 monochorionic placentas, Zhao and colleagues (2013) found the median number of anastomoses to be 8 with an interquartile range of 4 to 14. With rare exceptions, anastomoses between twins are unique to monochorionic twin placentas.
Shared placenta from pregnancy complicated by twin-twin transfusion syndrome. The following color code was applied for injection. Left twin: yellow = artery, blue = vein; right twin: red = artery, green = vein. A. Part of the arterial network of the right twin is filled with yellow dye, due to the presence of a small artery-to-artery anastomosis (arrow). B. Close-up of the lower portion of the placenta displays the yellow dye-filled anastomosis. (From De Paepe, 2005, with permission.)
Artery-to-artery anastomoses are most common and are identified on the chorionic surface of the placenta in up to 75 percent of monochorionic twin placentas. Vein-to-vein and artery-to-vein communications are each found in approximately half. One vessel may have several connections, sometimes to both arteries and veins. In contrast to these superficial vascular connections on the surface of the chorion, deep artery-to-vein communications can extend through the capillary bed of a given villus (Fig. 45-20). These deep arteriovenous anastomoses create a common villous compartment or third circulation that has been identified in approximately half of monochorionic twin placentas.
Anastomoses between twins may be artery-to-vein (AV), artery-to-artery (AA), or vein-to-vein (VV). Schematic representation of an AV anastomosis in twin-twin transfusion syndrome that forms a “common villous district” or “third circulation” deep within the villous tissue. Blood from a donor twin may be transferred to a recipient twin through this shared circulation. This transfer leads to a growth-restricted discordant donor twin with markedly reduced amnionic fluid, causing it to be “stuck.”
Whether these anastomoses are dangerous to either twin depends on the degree to which they are hemodynamically balanced. In those with significant pressure or flow gradients, a shunt will develop between fetuses. This chronic fetofetal transfusion may result in several clinical syndromes that include twin-twin transfusion syndrome (TTTS), twin anemia polycythemia sequence (TAPS), and acardiac twinning.
Twin-Twin Transfusion Syndrome (TTTS)
The prevalence of this condition is approximately 1 to 3 per 10,000 births (Simpson, 2013). In this syndrome, blood is transfused from a donor twin to its recipient sibling such that the donor may eventually become anemic and its growth may be restricted. In contrast, the recipient becomes polycythemic and may develop circulatory overload manifest as hydrops. The donor twin is pale, and its recipient sibling is plethoric (Fig. 45-21). Similarly, one portion of the placenta often appears pale compared with the remainder.
Twin-twin transfusion syndrome at 23 weeks. A. Pale donor twin (690 g) also had oligohydramnios. B. The plethoric recipient twin (730 g) had hydramnios. (From Mahone, 1993, with permission.)
The recipient neonate may have circulatory overload from heart failure and severe hypervolemia and hyperviscosity. Occlusive thrombosis is another concern. Finally, polycythemia in the recipient twin may lead to severe hyperbilirubinemia and kernicterus (Chap. 33, Hyperbilirubinemia).
Any of the different types of vascular anastomoses discussed before may be found with monochorionic placentas. Classically, chronic TTTS results from unidirectional flow through arteriovenous anastomoses. Deoxygenated blood from a donor placental artery is pumped into a cotyledon shared by the recipient (see Fig. 45-20). Once oxygen exchange is completed in the chorionic villus, the oxygenated blood leaves the cotyledon via a placental vein of the recipient twin. Unless compensated—typically through arterioarterial anastomoses—this unidirectional flow leads to an imbalance in blood volumes (Lewi, 2013).
Clinically important twin-twin transfusion syndrome frequently is chronic and results from significant vascular volume differences between the twins. Even so, the pathogenesis is more complex than a net transfer of red blood cells from one twin to another. Indeed, in most monochorionic twin pregnancies complicated by the syndrome, there is no difference in hemoglobin concentrations between the donor and recipient twin (Lewi, 2013).
The syndrome typically presents in midpregnancy when the donor fetus becomes oliguric from decreased renal perfusion (Simpson, 2013). This fetus develops oligohydramnios, and the recipient fetus develops severe hydramnios, presumably due to increased urine production. Virtual absence of amnionic fluid in the donor sac prevents fetal motion, giving rise to the descriptive term stuck twin or polyhydramnios-oligohydramnios–syndrome—“poly-oli.” This amnionic fluid imbalance is associated with growth restriction, contractures, and pulmonary hypoplasia in the donor twin, and premature rupture of the membranes and heart failure in the recipient.
Cerebral palsy, microcephaly, porencephaly, and multicystic encephalomalacia are serious complications associated with placental vascular anastomoses in multifetal gestation. The exact pathogenesis of neurological damage is not fully understood but is likely caused by ischemic necrosis leading to cavitary brain lesions (Fig. 45-22). In the donor twin, ischemia results from hypotension, anemia, or both. In the recipient, ischemia develops from blood pressure instability and episodes of severe hypotension (Lopriore, 2011). Cerebral lesions may also be due to postnatal injury associated with preterm delivery. Quarello and associates (2007) reviewed data from 315 liveborn fetuses from pregnancies with twin-twin-transfusion syndrome and reported cerebral abnormalities in 8 percent.
Cranial magnetic resonance imaging study of a diamnionic–monochorionic twin performed on day 2 of life. The subarachnoid space and lateral ventricles are markedly enlarged. There are large cavitary lesions in the white matter adjacent to the ventricles. The bright signals (arrowheads) in the periphery of the cavitary lesions most probably correspond to gliosis. (From Bejar, 1990, with permission.)
If one twin of an affected pregnancy dies, cerebral pathology in the survivor probably results from acute hypotension. A less likely cause is emboli of thromboplastic material originating from the dead fetus. Fusi and coworkers (1990, 1991) observed that with the death of one twin, acute twin-twin anastomotic transfusion from the high-pressure vessels of the living twin to the low-resistance vessels of the dead twin leads rapidly to hypovolemia and ischemic antenatal brain damage in the survivor. In their systematic review of 343 twin pregnancies complicated by single fetal demise, Hillman and colleagues (2011) calculated a 26-percent risk of neurodevelopmental morbidity in monochorionic twins compared with 2 percent in dichorionic twins. They also found that this morbidity was related to gestational age at the death of the cotwin. If the death occurred between 28 and 33 weeks’ gestation, monochorionic twins had an almost eightfold risk of neurodevelopmental morbidity compared with dichorionic twins of the same gestational age. With fetal death after 34 weeks, the likelihood dramatically decreased—odds ratio 1.48.
The acuity of hypotension following the death of one twin with twin-twin-transfusion syndrome makes successful intervention for the survivor nearly impossible. 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 (Langer, 1997; Wada, 1998).
There have been dramatic changes in the criteria used to diagnose and classify varying severities of twin-twin transfusion syndrome. Previously, weight discordancy and hemoglobin differences in monochorionic twins were calculated. However, it was soon appreciated that in many cases these were late-onset findings. According to the Society for Maternal-Fetal Medicine (2013), TTTS is diagnosed based on two criteria: (1) presence of a monochorionic diamnionic pregnancy, and (2) hydramnios defined if the largest vertical pocket is > 8 cm in one twin and oligohydramnios defined if the largest vertical pocket is < 2 cm in the other twin. Only 15 percent of pregnancies complicated by lesser degrees of fluid imbalance progress to TTTS (Huber, 2006).
Once identified, TTTS is typically staged by the Quintero (1999) staging system:
Stage I—discordant amnionic fluid volumes as described above, but urine is still visible sonographically within the bladder of the donor twin.
Stage II—criteria of stage I, but urine is not visible within the donor bladder.
Stage III—criteria of stage II and abnormal Doppler studies of the umbilical artery, ductus venosus, or umbilical vein.
Stage IV—ascites or frank hydrops in either twin.
Stage V—demise of either fetus.
In addition to these criteria, there is evidence that cardiac function of the recipient twin correlates with fetal outcome (Crombleholme, 2007). Although fetal echocardiographic findings are not part of the staging system above, many centers routinely perform fetal echocardiography for TTTS. It has been theorized that early diagnosis of cardiomyopathy in the recipient twin may identify pregnancies that would benefit from early intervention. One system for evaluating cardiac function—the myocardial performance index (MPI) or Tei index—is a Doppler index of ventricular function calculated for each ventricle (Michelfelder, 2007). Although scoring systems that include assessment of cardiac function have been developed, their usefulness in prediction of outcomes remains controversial (Simpson, 2013).
At Parkland Memorial Hospital, evaluation before and during treatment includes anatomical and neurological fetal assessment using echocardiography, MPI calculation, Doppler velocimetry, and MR imaging; genetic counseling and amniocentesis; and placental mapping.
The prognosis for multifetal gestations complicated by TTTS is related to Quintero stage and gestational age at presentation. More than three fourths of stage I cases remain stable or regress without intervention. Conversely, outcomes in those identified at stage III or higher are much worse, and the perinatal loss rate is 70 to 100 percent without intervention (Simpson, 2013). Several therapies are currently used for TTTS, including amnioreduction, laser ablation of vascular anastomoses, selective feticide, and septostomy (intentional creation of a communication in the dividing amnionic membrane). Comparative data from randomized trials for some of these techniques are discussed below.
The Eurofetus trial included 142 women with severe TTTS diagnosed before 26 weeks. Participants were randomly assigned to laser ablation of vascular anastomoses or to serial amnioreduction (Senat, 2004). These investigators reported an increased survival rate to age 6 months for at least one twin with laser ablation compared with serial amnioreduction–76 versus 51 percent, respectively. Moreover, analyses of randomized studies confirm better neonatal outcomes with laser therapy compared with selective amnioreduction (Roberts, 2008; Rossi, 2008, 2009). In contrast, Crombleholme and associates (2007), in a randomized trial of 42 women, found equivalent rates of 30-day survival of one or both twins treated with either amnioreduction or selective fetoscopic laser ablation–75 versus 65 percent, respectively. Furthermore, evaluation of twins from the Eurofetus trial through 6 years of age did not demonstrate any additional survival benefit beyond 6 months or improved neurological outcomes in those treated with laser (Salomon, 2010).
At this time, laser ablation of anastomoses is preferred for severe TTTS (stages II-IV), although optimal therapy for stage I disease is controversial. After laser therapy, close ongoing surveillance is necessary. Robyr and colleagues (2006) reported that a fourth of 101 pregnancies treated with laser required additional invasive therapy because of either recurrent TTTS, or middle cerebral artery Doppler evidence of anemia or polycythemia. Recently, in a comparison of selective laser ablation of individual anastomoses versus ablation of the entire surface of chorionic plate along the vascular equator, Baschat and coworkers (2013) found that equatorial photocoagulation reduced the likelihood of recurrence.
Moise and associates (2005) compared amnioreduction and septostomy in a multicentered randomized trial of 73 women. Repeated procedures were performed for symptoms or if the greatest vertical pocket of amnionic fluid met the original inclusion criteria of 8 to 12 cm, depending on gestational age. Perinatal outcomes were the same in each group, with at least one survivor in 80 percent of pregnancies. The average number of additional procedures was two in each group. Much of this is moot, however, because intentional septostomy has largely been abandoned as treatment (Simpson, 2013).
Selective reduction has generally been considered if severe amnionic fluid and growth disturbances develop before 20 weeks. In such cases, both fetuses typically will die without intervention. Selection of which twin is to be terminated is based on evidence of damage to either fetus and comparison of their prognoses. Any substance injected into one twin may affect the other twin because of shared circulations. Therefore, feticidal techniques include methods to occlude the circulation of the chosen fetal umbilical vein or by umbilical cord occlusion using radiofrequency ablation, fetoscopic ligation, or coagulation with laser, monopolar, or bipolar cauterization (Challis, 1999; Chang, 2009; Donner, 1997). Even after these procedures, however, the risks to the remaining fetus are still appreciable (Rossi, 2009).
Twin Anemia Polycythemia Sequence (TAPS)
This form of chronic fetofetal transfusion is characterized by significant hemoglobin differences between donor and recipient twins without the discrepancies in amnionic fluid volumes typical of twin-twin-transfusion syndrome (Slaghekke, 2010). It is 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 (Simpson, 2013). The spontaneous form reportedly complicates 3 to 5 percent of monochorionic pregnancies, and it occurs in up to 13 percent of pregnancies after laser photocoagulation. Spontaneous TAPS usually occurs after 26 weeks and iatrogenic TAPS develops within 5 weeks of a procedure (Lewi, 2013). Although a staging system has been proposed by Slaghekke and colleagues (2010), further studies are necessary to better understand the natural history of TAPS and its management.
Twin-Reversed Arterial Perfusion (TRAP) Sequence
Also known as an acardiac twin, this is a rare—1 in 35,000 births—but serious complication of monochorionic multifetal gestation. In the TRAP sequence, there is usually a normally formed donor twin that has features of heart failure and a recipient twin that lacks a heart (acardius) and other structures. It has been hypothesized that the TRAP sequence is caused by a large artery-to-artery placental shunt, often also accompanied by a vein-to-vein shunt (Fig. 45-23). Within the single, shared placenta, arterial perfusion pressure of the donor twin exceeds that in the recipient twin, who thus receives reverse blood flow of deoxygenated arterial blood from its cotwin (Lewi, 2013). This “used” arterial blood reaches the recipient twin through its umbilical arteries and preferentially goes to its iliac vessels. Thus, only the lower body is perfused, and disrupted growth and development of the upper body results. Failure of head growth is called acardius acephalus; a partially developed head with identifiable limbs is called acardius myelacephalus; and failure of any recognizable structure to form is acardius amorphous, which is shown in Figure 45-24 (Faye-Petersen, 2006). Because of this vascular connection, the normal donor twin must not only support its own circulation but also pump its blood through the underdeveloped acardiac recipient. This may lead to cardiomegaly and high-output heart failure in the normal twin (Fox, 2007).
Twin reversed-arterial-perfusion sequence. In the TRAP sequence, there is usually a normally formed donor twin that has features of heart failure, and a recipient twin that lacks a heart. It has been hypothesized that the TRAP sequence is caused by a large artery-to-artery placental shunt, often also accompanied by a vein-to-vein shunt. Within the single, shared placenta, perfusion pressure of the donor twin overpowers that in the recipient twin, who thus receives reverse blood flow from its twin sibling. The “used” arterial blood (colored blue) that reaches the recipient twin preferentially goes to its iliac vessels and thus perfuses only the lower body. This disrupts growth and development of the upper body.
Photograph of an acardiac twin weighing 475 grams. The underdeveloped head is indicated by the black arrow, and its details are shown in the inset. A yellow clamp is seen on its umbilical cord. Its viable donor cotwin was delivered vaginally at 36 weeks and weighed 2325 grams. (Photograph contributed by Dr. Michael D. Hnat.)
Lewi and coworkers (2010) reviewed 26 cases of TRAP sequence identified in the first trimester. In one third, the pump twin died before planned intervention at 16 to 18 weeks. In more than half of all the cases, there was spontaneous cessation of flow to the acardiac twin, and such flow arrest was associated with subsequent death or neurological injury in 85 percent of the normal twins. Quintero and associates (1994, 2006) have reviewed methods of in utero treatment of acardiac twinning in which the goal is interruption of aberrant vascular communication between the twins. Of these methods, Lee (2007), Lewi (2010), Livingston (2007), and their colleagues found an approximate 90-percent survival rate following second-trimester radiofrequency ablation. This method cauterizes umbilical vessels in the malformed recipient twin to terminate blood flow from the donor. In a review of 118 complicated monochorionic twin gestations that underwent bipolar cord coagulation, Lanna and associates (2012) reported a fetal loss rate in those treated before 19 weeks of 45 percent compared with 3 percent in those treated after 19 weeks. Prompted by the high mortality rate of TRAP sequence in the first trimester, small case series of early intervention have been reported (O’Donoghue, 2008; Scheier, 2012). Importantly, efficacy and safety of intervention before fusion of the amnion and chorion has not been demonstrated convincingly (Lewi, 2013).
Complete Hydatidiform Mole with Coexisting Normal Fetus
Also termed a twin molar pregnancy, this is due to a complete diploid molar pregnancy comprising one conceptus, whereas the cotwin is a normal fetus. Reported prevalence rates range from 1 in 22,000 to 1 in 100,000 pregnancies (Dolapcioglu, 2009). It must be differentiated from a partial molar pregnancy in which an anomalous singleton fetus—usually triploid—is accompanied by molar tissue (Chap. 20, Clinical Findings).
Optimal management is not known for this twin gestation. Diagnosis is usually made in the first half of pregnancy, and termination at that time would remove the mole but also the normal fetus. However, pregnancy progression exposes the woman to the later postpartum dangers of persistent trophoblastic disease that requires chemotherapy and may be fatal. Despite this, pregnancy continuation is increasingly being recommended in cases with a karyotypically normal and nonanomalous twin, no early preeclampsia, and declining hCG levels (Sebire, 2002).
If observation and pregnancy progression is chosen, preterm delivery is frequently required because of persistent and heavy bleeding or severe preeclampsia. Dolapcioglu and coworkers (2009) reviewed 159 reported cases and reported a live birth in 35 percent. Preeclampsia and preterm birth each developed in a third. Niemann and colleagues (2007) reported that persistent trophoblastic disease rates following such a twin gestation were not increased compared with those after a singleton complete mole.