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Articles » Multiple gestations » Twin to twin transfusion syndrome

1999-06-04-18 Twin-to-twin transfusion syndrome (Stuck twin) © Silva www.thefetus.net/

 

Twin-to-twin transfusion syndrome (Stuck twin)

Sandra Rejane Silva, MD2, Luís Flávio de Andrade Gonçalves, MD1 hilippe Jeanty, MD, PhD3

[1] Florianopolis, SC Brazil lufla@netco.com.br , [2] Sao Paulo – SP docsilva@apm.org.br [3] Nashville, TN jeanty@pov.net

Adapted and reproduced with permission from TKI Medcon Inc. http:/www.tki.com/

Definition

A condition whereby a donor twin bleeds into the circulation of a recipient twin. The donor twin become anemic, hypovolemic and looses amniotic fluid. The close apposition of the intertwin membrane fixes the donor fetus in a position thus the moniker of "stuck twin"

Sonographic features

The diagnosis of twin-twin transfusion syndrome is made by finding the following features:

  • Monochorionic placentation, with visualization of a separating membrane
  • Fetuses of the same sex
  • Mid-trimester polyhydramnios-oligohydramnios sequence (polyhydramnios at the recipient’s sac and oligohydramnios at the donor’s sac), in the absence of other causes of abnormal amniotic fluid volume.
  • Discordance in size, with the larger twin in the polyhydramniotic sac and the smaller stuck against the uterine wall.
  • Some other findings that might be observed are:
  • Weight discordance equal or over 20%.
  • Non-visualization of the donor’s bladder with enlarged recipient’s bladder.
  • Abnormal Doppler S/D ratio at the umbilical cord. The absent end diastolic flow in the donor’s umbilical artery accompanied by venous pulsation in the recipient’s umbilical vein are usually associated with a poor prognosis.
  • Hydrops or evidence of congestive heart failure of either twin. These signs are found more commonly at the recipient twin.

In the most severe forms, the diagnosis should not be difficult: a single placenta assive polyhydramnios in the sac of the recipient twin, a stuck donor twin attached t he uterine wall with poor mobility and obvious growth discordance. Milder forms of th isease are more difficult to diagnose due to the lack of uniform criteria, however, on hould suspect twin to twin transfusion in the presence of amniotic fluid discrepanc etween the cavities, regardless of the amount of weight discordance between the twins. A ntertwin hemoglobin difference >2.4 gm/dl in fetal blood obtained by cordocentesis ha een shown to be consistent with stuck twin syndrome.

A twin getting stuck… The amniotic cavity on the left is smaller and the fluid i ore echogenic. Conversely the fetus on the right (not visible) is developin olyhydramnios.

The folding membrane stage. Note the little white line on the left of the membran about at 9:00 on the image. This is the membrane folding onto itself as it becomes t arge to encompass the cavity of the donor twin.

The classical image of the "stuck twin". One twin is plastered at the to in fact, front) of the uterus. By gravity that twin should fall "down". By thi ime the membrane is difficult to identify since it is closely apposed against the dono win, much like a sheet of plastic on a vacuum-sealed object. Changing the patient’ osition will demonstrate that the stuck twin remains in the same position.

Very typically (even with amniodrainage) early severe twin-to-twin transfusion syndrom ill result in the demise of the donor twin, often followed rapidly by the demise of th ecipient twin. Note the difference in size between the recipient (left) and donor (right win.

 

Another "stuck" twin. Notice the pale aspect of its placenta compared to th emorrhagic appearance of the recipient’s placenta.

Injection of the umbilical circulation of the recipient twin with faint passage of contrast visible towards the donor side.

Prevalence

Twin to twin transfusion complicates about 15% of monochorial twin gestations and i esponsible for 17% of the perinatal mortality in multiple pregnancies.

Pathogenesis

If embryonic splitting occurs before day three after fertilization, two independen etuses with separate placentas will result. A single placenta with two amniotic cavitie ccurs if splitting takes place between days four and seven. If division of th mbryoblast occurs after about eight days, the twins share a single placenta and amnioti avity (monochorionic-monoamniotic twins). Division beyond day 12 results in conjoin wins.

When two fetuses share the same placenta, vascular anastomoses develop between thei irculations. These anastomoses can be of three types: vein-to-vein, artery-to-artery an rtery-to-vein. Even when there are multiple vascular c ctions within a singl lacenta, no transfusion should occur provided the anastomoses are balanced. Placenta rom pregnancies with twin to twin transfusion syndrome have fewer anastomoses, which ar ore likely to be solitary and of deep arteriovenous type than those without twin to twi ransfusion syndrome. Provided transfusion occurs, the donor or "pump" twi ecomes hypovolemic due to blood loss. Hypoxia develops because of placenta nsufficiency, which is also responsible for intrauterine growth retardation. Poor rena erfusion leads to oligohydramnios. This latter feature, when severe, is responsible fo he classical appearance of the stuck twin: the amniotic sac becomes too small, th mniotic membrane comes in close contact with the body of the "pump" twin an he fetus appears trapped to the uterine wall. Hypervolemia with increased renal perfusio eads to polyhydramnios in the sac of the recipient twin. Since there is no loss o rotein or cellular components from its circulation, colloid osmotic pressure draws wate rom the maternal compartment across the placenta, establishing a vicious cycle o ypervolemia, polyuria and hyperosmolarity leading to high output cardiac failure, hydrop nd polyhydramnios.


Some of the donor"s blood crosses circulation by goind through a rtery to vein c ction and is transferred to the recipient.

As the donor hemorrhages in the recipient, it becomes hypovolemic, oliguric (thu he decrease in amniotic fluid since swallowing of fluid is not changed). The recipien win has too much fluid and develops polyhydramnios. The combination displaces th embrane towards the donor twin and progressively corner the donor in a fixed position.

Prognosis

When the disease manifests during the second trimester there is a high risk o erinatal morbidity and mortality. Intrauterine hypoxia, preterm delivery and death of on etus (usually the donor) with subsequent death or hypoxic-ischemic sequelae (see twi mbolization syndrome) in the surviving twin are the most common complications to watc or in these pregnancies.

Management

Treatment includes aggressive amniocentesis to drain polyhydramnios in the sac of th ecipient twin and, more recently, ablation of communicating vessels on the placenta urface by neodimium:YAG laser guided by fetoscopy.

Differential diagnosis

Differential diagnosis should be mainly concerned with twins of discordant size withou ransfusion as the underlying pathophysiologic mechanism for the problem.

Some authors have proposed a new entity called twin oligohydramnios-polyhydramnio equence, in which twin-twin transfusion is included. Histopathological studies of th lacenta are required to differentiate twin-twin transfusion from the other condition ncluded in twin oligohydramnios-polyhydramnios sequence.

Isolated intra-uterine growth restriction can be considered if the growth discrepanc s less than 15% and the other features of the syndrome are not present.

Dichorionic twin pregnancy with fused placentas and growth restriction of one of th etuses is another condition that can leads to misdiagnosis. This can be excluded if th wins have different sexes or after birth, by histopathological analysis of the placenta.

Associated syndromes

The over-distension of the uterus caused by the polyhydramnios can causes preter abor, amniorrhexis, abruptio placentae, respiratory and abdominal discomfort.

The death of one twin can cause embolic phenomena (twin embolisation syndrome) an oagulation problems in the remaining twin, and sequelae such as neurological, cardiac an enal diseases are common among survivors.

 

References

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  • Howarth GR, et al. Management of early onset severe twin-twin transfusion syndrome in the absence of fetoscopic equipment by exteriorisation, ligation and replacement of the umbilical cord of the sacrificed twin. S Afr Med J. 1998 Mar; 88(3): 286.
  • van Gemert MJ, et al. Placental anatomy, fetal demise and therapeutic intervention in monochorionic twins and the transfusion syndrome: new hypotheses. Eur J Obstet Gynecol Reprod Biol. 1998 May; 78(1): 53-62.
  • Feldman DM, et al. Iatrogenic monoamniotic twins as a complication of therapeutic amniocentesis. Obstet Gynecol. 1998 May; 91(5 Pt 2): 815-816.
  • van Gemert MJ, et al. Haemodynamic model of twin-twin transfusion syndrome in monochorionic twin pregnancies. Placenta. 1998 Mar; 19(2-3): 195-208.
  • Denbow ML, et al. Neonatal cranial ultrasonographic findings in preterm twins complicated by severe fetofetal transfusion syndrome. Am J Obstet Gynecol. 1998 Mar; 178(3): 479-483.
  • Duncan KR, et al. The aetiology and management of twin-twin transfusion syndrome. Prenat Diagn. 1997 Dec; 17(13): 1227-1236.
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  • Cincotta RB, Fisk NM Current thoughts on twin-twin transfusion syndrome. Clin Obstet Gynecol 1997 Jun;40(2):290-302
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