Vanishing Twin Syndrome: Pathogenesis, Symptoms, Diagnosis & Treatment
The vanishing twin, or fetal resorption, is a fetus from a multiple pregnancy which dies in the uterus in then partially or completely absorbed by the mother or brother. The appearance of this phenomenon is sometimes called vanishing twin syndrome.
Occasionally instead of complete absorption, the dead fetus may be compressed by the growing brother into a pergament structure, known as fetus papyraceus. If the fetus is absorbed completely, there aren`t any further complications besides the first trimester bleeding.
If the even appears during the second or third trimester, the severe complications may include:
- Premature labor.
- Infection by fetal elimination.
Even at the end of pregnancy, a fetus papyraceus can block the cervix and make necessary a C-section.
The vanishing twin can die due to:
- A placenta poorly implanted.
- An abnormality which may determine a major organ failure or their complete lack to the fetus.
- A chromosomal abnormality incompatible with life.
Frequently, the twin is an empty egg which never develops beyond the early stages of embryogenesis.
The frequency of the syndrome is of 1 to 8 pregnancies and may remain unknown in many cases. The phenomenon appears frequently in pregnancies created as a result of IVF. Ultrasound scans are performed early in these pregnancies, so if the multiple conception took place, it can be noticed more than one amniotic sac in the first few weeks and after a period of time the brothers will disappear.
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Abnormalities which cause the disappearance of a fetus rather seem to be present in the early stage of development than after an acute injury. The fetal or placental analysis frequently shows chromosomal abnormalities. These malformations which include diploidy, triploidy and the alternation of sexual chromosomes are highlighted at placental tests, skin biopsies and chorionic villi. The studies of the viable twin`s chromosomes are normal. That`s why is considered that the vanishing twin has presented a chromosomal abnormality.
Researchers have proposed that vanishing twin syndrome may determine spastic cerebral palsy at the viable brother. A possible mechanism is the transfusion of thromboplastin proteins from the death brother at the viable one, leading to disseminated intravascular coagulation (DIC). Supposedly, DIC results from reversing the blood flow from the death brother to the viable one, carrying the thromboplastin proteins in circulation. This high load with thromboplastin proteins is considered as leading to a status of DIC in viable fetus with damage in the central nervous system.
Another proposed theory is the effect of the high amount of blood lost by the viable fetus against the low vascular resistance system of the death fetus through the placental anastomoses. This transfusion may determine large fluctuations in the intravascular pressures leading to intravascular hemorrhage and cerebral palsy.
The developing mechanism of aplasia cutis is vascular, with a decreased perfusion in the affected area by the death of the brother.
Signs & Symptoms
This syndrome represents is the identification of a multifetal pregnancy with the secondary disappearance of one or more fetuses. The multifetal pregnancy rate at conception is higher than the noted incidence at birth. The syndrome has been identified more frequently from introducing ultrasounds in early pregnancy. The IVF techniques have improved the understanding of the syndrome because these pregnancies are closely monitored and the number of fertilized zygotes that are implanted is known.
In this syndrome may occur:
- Total fetal resorption.
- The formation of a papyraceus fetus (mummified or compressed fetus).
- The development of a subtle abnormality of the placenta such as cyst or amorphous material.
The First Trimester
Morbidity varies in the appearance of the phenomenon during the first trimester. It`s usually limited. The mother is prone to the development of vaginal bleeding and cramps. If the event occurs late, morbidity can be similar to the one from the second or third trimester.
The Second & Third Trimester
Maternal complications include:
- Premature labor.
- Infection through retained fetus.
- Severe puerperal hemorrhage.
- Consumptive coagulopathy and obstruction of birth canal by a fetus papyraceus, which cause dystocia and requires C-section.
Evolution of the Disease
Synchronization of this event affects the prognosis of the viable twin and maternal complications. If the event appears in the second half of pregnancy:
- The fetus may develop cerebral palsy or apalsia cutis.
- The mother may develop premature birth, infections, hemorrhage puerparel, consumptive coagulopathy or birth blocking.
- The recent phenomenon causes the increase of plasma protein A associated with the pregnancy and free beta-HCG.
- Alpha-fetoprotein is increased compared with a normal pregnancy.
- Human chorionic gonadotropin growth rate is lower than in a normal pregnancy.
Ultrasound is used to confirm the diagnosis of early twin pregnancy. Monitoring the placenta through ultrasound shows the loss of a fetus in the pregnancy evolution.
Amniocentesis after the diagnosis of a vanishing twin by ultrasound detects XY cells by FISH and PCR.
Chorionic villi sampling is useful if the placenta has a mosaic pattern, but at birth there`s only one result.
- Deciduous reaction on ultrasound.
- Amniotic cavity observed on ultrasound as a second fetus.
- Chorionic sac considered the second fetus.
- Extraembryonic coelom seen as the second fetus.
- Subchorionic bleeding or hydropic villi change of considered the second fetus.
If a papyraceus fetus is residual, the pregnancy needs to be monitored carefully by series of ultrasounds for evaluating the viable fetus. The risks are:
- Premature labor.
- Obstruction of birth canal.
- The death of the surviving fetus by chorioamnionitis or placental abruption.
This fetus is at risk of low birth weight and gestational age. Uncomplicated vanishing twin syndrome doesn`t require special medical therapy.
In addition, the loss of a twin brother, the fetus which survives shows an increased risk of cerebral palsy, especially if the syndrome occurs in the second half of pregnancy. Other forms of morbidity reported to the surviving fetus are aplasia cutis or areas of skin necrosis. At brothers connected by placental vascularization, transient hypotension at the viable fetus at the time of death leads to poor perfusion and skin necrosis.