Twinning Problems

Placentas from twins provide the pathologist with the unique opportunity to compare different placental features with neonatal outcome. Thus, the fetus accompanied by a velamentous insertion of the umbilical cord is usually more growth-restricted than one with a normal cord and is thus uniquely exposed also to the prenatal hazards of anomalous cord insertion. Multiple births also have not only a much higher incidence of prematurity but they also suffer a manifold increased frequency of cerebral palsy compared with singletons. Studies have suggested that some of these cerebral lesions may have a prenatal onset because cystic areas of former white matter necrosis can be evident at birth (Bejar et al., 1990). Larroche (1986) described a case that also demonstrated these prenatal lesions; she found other cases of prenatal encephalopathies with trauma and other prenatal events. Central nervous system damage of prenatal onset appears to be commoner in monozygotic, monochorionic twins than in dizygotic multiples. It is therefore imperative that the membrane relation of all twins be firmly established at the time of delivery or during placental study, if one wants to understand the origin of the lesions. This point is particularly important when one twin has died prenatally. Coagulative, destructive events in the survivor are then especially common and these are usually confined to monochorionic twins. They generally have a prenatal onset, as sonographic studies have clearly shown (Patten et al., 1989), and commence soon after the death of one fetus (Liu et al., 1992; Benirschke, 1993). A particularly illustrative case with which we have had personal connection demonstrates clearly how such problems may be inaccurately adjudicated. It was superbly summarized in a book by Werth (1998).

As stated earlier, monochorionic twins not only have a higher rate of prematurity but they suffer perinatal mortality more frequently (Baldwin, 1994). The highest mortality attends monoamnionic twins. Monoamnionic/ monochorionic (MoMo) twins entangle their cords frequently and this may cause restrictions to venous return from the placenta. This complication often kills one or both fetuses; in others one can infer venous return problems from existing thrombi. Further, vascular anastomoses between twins may allow rapid shifts of blood from one twin to the other, which may lead to acute anemia and hypotension in utero. Neonatal anemia seen in one of twins, where the other had recently died in utero has been difficult to interpret prior to detailed placental studies. It goes without saying that the umbilical cords of twins must be labeled at delivery, so that it becomes possible to assign specific placental lesions to individual infants. It is also necessary to identify and record the presence of a fetus papyraceus, as it may have great relevance in affecting the development of the surviving twin through interplacental vascular anastomoses. Perhaps the cause of the death of one twin was sublethal to the other.

Inflammatory processes also have an important impact on fetal well-being and they are frequently correlated with cerebral palsy. As was discussed in some detail in the consideration of infections (Chapter 20), in twins, chorio-amnionitis much more often affects twin A, that is to say the twin closest to the cervical os. When one has knowledge of the location of twins in utero, this may lead to a better appreciation of possible aspiration pneumonia and other fetal effects.

Twins have a high frequency of velamentous and marginal insertion of their umbilical cords, and these inser-tional abnormalities are often correlated with single umbilical artery. The membranous vessels may have ruptured during delivery and have caused acute anemia, or they may be thrombosed, which often produces dire fetal sequelae. Cords with a single umbilical artery are more common in twins, and not only when the cords are marginally inserted. When twins are delivered by cesarean section, the twin located in the lower uterine segment may actually be delivered as the second twin. Therefore, recording the distance of membrane rupture from the edge of the placenta aids in assigning the correct position of twins in utero when labeling of cords is inadequate. This point has particular relevance with respect to inflammation and to the possible rupture of velamentous vessels.

Twins with velamentous insertion of the umbilical cord are usually smaller than those with more normal cord position. Such discrepancy in size does not automatically affirm the diagnosis of the transfusion syndrome, as is all too readily done; that diagnosis requires the demonstration of the responsible arteriovenous (AV) shunts in the monochorionic twin placenta. The twin-to-twin transfusion syndrome (TTTS) is a most important aspect of monozygotic twinning. It is largely responsible for the frequent occurrence of hydramnios in twin pregnancy that leads to the high frequency of premature delivery of monochorionic twins. Although anemia and plethora of the neonatal twins may be obvious, this finding alone does not accurately attest to the underlying cause, the presence of an AV fistula in the placenta. Plethora can occur in one twin when for instance the first-born twin has been allowed to drain blood into the second, while this one was still in utero. This is sometimes referred to as acute rather than chronic twin-to-twin transfusion. A surviving twin also may partially and acutely exsanguinate into a stillborn twin while in utero, with resulting acute hypotension. Knowledge of the time when clamping of the cords was done may also be important when interpreting discordant hemoglobin values of twins. When one twin is small for gestational age, possibly because it had a velamentous insertion of the cord, large surface anastomoses may drain blood from the larger twin into the smaller member while still in situ, an apparent paradox to the findings of the transfusion syndrome. But this is not the equivalent of the classical transfusion syndrome. For all these reasons, it is important that the nature of interfetal placental blood vessel anastomoses be ascertained, possibly by injection of the placental vasculature. The findings are best recorded by making a drawing of these connections; they cannot otherwise be readily reconstructed.

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