twin–twin transfusion syndrome

Clin Perinatol 30 (2003) 591–600

Twin–twin transfusion syndrome

Ruben A. Quintero, MDFlorida Institute for Fetal Diagnosis and Therapy, St. Joseph’s Women’s Hospital,

13601 Bruce B. Downs Boulevard, Suite 250, Tampa, FL 33613, USA

Definition

Twin–twin transfusion syndrome (TTTS), a complication of monochorionic

multiple pregnancies, is defined sonographically as the combined presence of

polyhydramnios in one sac and oligohydramnios in the other sac in a mono-

chorionic–diamniotic twin gestation. Polyhydramnios is defined as a maximum

vertical pocket (MVP) greater than 8 cm and oligohydramnios is defined as an

MVP less than 2 cm (poly8-oligo2). Monochorionicity is established by the

presence of a single placenta, absence of a twin peak sign, thin dividing mem-

brane, and same gender.

Variations in the definition

Although TTTS affects mostly twin pregnancies, it can also occur in triplet or

higher order multiple gestations provided that at least two fetuses are mono-

chorionic. In monoamniotic twins, the lack of a dividing membrane precludes the

combined presence of polyhydramnios and oligohydramnios. In these patients,

the syndrome can be suspected by the presence of polyhydramnios and differ-

ences in bladder filling of the two fetuses. In monochorionic triplet pregnancies,

two or all three fetuses can be involved.

Definitions no longer used

Until a few years ago, TTTS was diagnosed postnatally if an intertwin

hemoglobin difference greater than 5 gm/dL [1] and a birth weight difference

greater than 20% [2] existed; however, in a study by Danskin and Neilson [3] in

178 twin pairs, only four pairs had a hemoglobin difference greater than 5g/dL

and a weight difference greater than 20%, and none of these pregnancies showed

evidence of polyhydramnios or oligohydramnios. Similarly, percutaneous umbil-

ical blood sampling in six TTTS patients failed to show hemoglobin differences

0095-5108/03/$ – see front matter D 2003 Elsevier Inc. All rights reserved.

doi:10.1016/S0095-5108(03)00051-4

E-mail address: [email protected]

R.A. Quintero / Clin Perinatol 30 (2003) 591–600592

greater than 5 g/dL, except in one pregnancy [4]. A difference of only 1.7 g/dL

was found in four patients by Saunders and colleagues [5], so the previous

pediatric criteria are no longer applicable.

Older sonographic criteria are also no longer applicable. Wittmann et al

suggested that the diagnosis be based on a discrepancy greater than 10 mm of the

biparietal diameter or the transverse diameter of the trunk between the twins and

on the hydramnios surrounding the larger twin [6]. Brennan et al suggested that

the presence of same sex, disparity in size or in the number of vessels in the

umbilical cords, a single placenta with different echogenicity of the cotyledons

supplying the two cords, and evidence of hydrops in either twin or congestive

heart failure in the recipient should be added to the criteria [7]. The definition

used today of poly8-oligo2 simplifies and standardizes the diagnosis of TTTS.

Incidence

TTTS occurs in approximately 5.5% to 17.5% [2,7–10] of all monochorionic

pregnancies. Variations in the reported incidences might reflect variations in the

definitions used because standard sonographic criteria did not exist at the time.

Etiology

TTTS appears to result from a net unbalanced flow of blood between two

monochorionic fetuses through placental vascular communications, which results

in a donor twin and a recipient twin. Although actual documentation of the

unbalanced blood flow remains elusive, it is apparent from our endoscopic

observations [11].

The first description of TTTS was given by Schatz in 1882, who noted that

certain placental cotyledons could be perfused by an artery from one twin and a

vein of the other twin [12]. Placental injection studies showed that anastomoses are

almost universally present in monochorionic placentas [10]. Two general types of

anastomoses, superficial and deep, can be present. Superficial anastomoses include

arterio–arterial and veno–venous anastomoses. Deep anastomoses correspond

to shared cotyledons perfused by an artery and a vein from each twin [13]. Deep

and superficial communications can be single or multiple and result in a net transfer

of blood from one twin to the other. An average of 3.1 anastomoses per placenta

are present in each twin pair. In addition to vascular anastomoses, monochorionic

placentas have individually perfused cotyledons, within which exchange of

blood between the fetuses does not take place. The mechanisms responsible for

the particular vascular design of monochorionic placentas are unknown.

Vascular anastomoses might be responsible for the development of TTTS if

the vascular design is such that it forces a net flow from donor to recipient [11].

Alternatively, vascular anastomoses might play a passive role in the development

of the syndrome but nonetheless allow its development. This is the case in

R.A. Quintero / Clin Perinatol 30 (2003) 591–600 593

monochorionic twins who are discordant for congenital heart disease, cardiomyo-

pathies, cord anomalies, or other conditions associated with uneven hemody-

namic competence.

Diagnosis

The diagnosis of TTTS is made with ultrasound by noting the presence of

combined polyhydramnios and oligohydramnios in a monochorionic–diamniotic

twin pregnancy. Polyhydramnios is defined as an MVP of greater than 8 cm, and

oligohydramnios is defined as an MVP of less than 2 cm. Differences in

estimated fetal weight are no longer used to define the syndrome. Adherence

to these criteria is important to distinguish TTTS from other entities. The use of

Doppler to define the syndrome is also unwarranted as evidenced by conflicting

reports from several authors [9,14–17]

Differential diagnosis

Simple amniotic fluid volume discordance

Differences in amniotic fluid volume not meeting the aforementioned cri-

teria can be present in up to 26% of all monochorionic twins (Nicolaides, per-

sonal communication).

Isolated polyhydramnios

Discordance can include an MVP greater than 8 cm in one sac but an MVP

greater than 2 cm in the other (ie, isolated polyhydramnios). Occasionally,

isolated polyhydramnios might be significant enough to warrant therapy (MVP

> 10 cm). We have treated one such case with a single therapeutic amniocentesis

without recurrence of the polyhydramnios and delivery of two healthy fetuses at

35 weeks.

Isolated oligohydramnios

Alternatively, the MVP in one sac might be less than 2 cm but the MVP in the

other sac might be less than 8 cm (ie, isolated oligohydramnios). Isolated

oligohydramnios can occur in cases of bilateral renal agenesis or other urinary

tract abnormalities of one fetus, undiagnosed premature rupture of membranes, or

in selective intrauterine growth restriction.

Staging of twin–twin transfusion syndrome

Aside from the common standard sonographic criteria of polyhydramnios

greater than 8 cm and oligohydramnios less than 2 cm, the sonographic

presentation of TTTS is not homogeneous. In this sense, and based on

observational data, we believe that the disease might follow a certain time course


characterized by progressive development of renal failure in the donor twin,

abnormal Doppler studies, congestive heart failure with hydrops, and fetal

demise. To this extent, we have proposed a staging system as follows [18]:

Stage I: The bladder of the donor twin is still visible.

Stage II: The bladder of the donor twin is no longer visible (in >60 min of

observation). This fetus is in renal failure.

Stage III: Critically abnormal Doppler studies characterized by absent or

reverse end-diastolic velocity in the umbilical artery, or pulsatile umbilical

venous flow, or reverse flow in the ductus venosus in either twin.

Stage IV: Hydrops of one or both fetuses.

Stage V: Demise of one or both fetuses.

Expectant management of patients might show no progression from one stage

to the next or sequential or nonsequential progressive disease. Regardless of

whether or not the disease follows an orderly pattern, the proposed staging system

has prognostic value. The value of this staging system is discussed in this article.

Treatment

Undoubtedly, the most controversial aspect of TTTS is treatment. Interpreta-

tion of published therapeutic results must be done with caution because not all

investigators have adhered to standard diagnostic sonographic criteria. Expectant

management of TTTS has been associated with almost 100% perinatal mortality

[19]. In a collective series reported by Nicolaides et al, only five of 106 preg-

nancies had a successful outcome [20]. Medical treatment with digoxin [21] or

indomethacin [22] has no role in treatment; however, it is possible to follow Stage

I patients expectantly as long as the degree of polyhydramnios is not large (MVP

8–9 cm) and the cervical length is adequate (>2.5 cm), particularly if the disease

is diagnosed after 22 to 24 weeks of gestation. Such pregnancies might remain

stable and not require invasive therapy. Invasive therapeutic alternatives include

serial amniocentesis, laser therapy, and umbilical cord occlusion. Other options

that have been proposed include purposeful disruption of the dividing membrane

(so-called ‘‘septostomy’’) and purposeful injection of fluid in the sac of the donor,

neither of which can be recommended today.

Serial amniocentesis

The goal of serial amniocentesis therapy is to decrease the likelihood of mis-

carriage or preterm labor by reducing the amniotic fluid volume in the sac of the

recipient twin [7,23–38]. The procedure is repeated as often as necessary

depending on the rate of reaccumulation of fluid in the sac of the recipient twin.

Occasionally, no further reaccumulation of fluid occurs and a single procedure

is all that is necessary. Although therapy can be started at any level of poly-


hydramnios, we do not normally start treatment until an MVP of 9 to 10 cm is

reached. Serial amniocentesis is associated with an overall success rate of 66%

(likelihood of at least one twin surviving) with an average risk of cerebral palsy

of 15%.

Technique of serial amniocentesis

There is no standard technique for performing serial amniocentesis. How

much fluid should be removed, at what rate, what needle, or what type of

anesthesia should be used are among the issues that could benefit from

standardization. Our technique involves the use of an 18-gauge Echotip needle

(Cook Ob/Gyn, Spencer, Indiana) under local anesthesia. The needle is inserted

in a placenta-free area taking care not to disrupt the dividing membrane.

Extension tubing is attached to the needle with a luer-lock adaptor connected

to wall suction (maximum vacuum pressure 200 mmHg). The patient is sedated

before this procedure with 5 to 10 mg of intravenous morphine sulfate and 5 to

10 mg of orally administered diazepam. This premedication, aside from the

sedation of the mother, results in decreased fetal movements of the recipient twin,

which facilitates the procedure. Fluid is removed until an MVP of approximately

6 to 7 cm is reached. No attempt to reach a particular level of MVP is made, but

the amount of fluid extracted by the amount of space surrounding the donor twin

is limited. If too much fluid is removed, the donor twin might become com-

promised because of cord compression and die because it is unable to change its

position within the uterine cavity.

Laser therapy

The goal of laser therapy is to eliminate blood exchange between the fetuses

[39–47], which halts the disease process altogether, allowing each fetus to

continue the pregnancy on its own. For many years, endoscopic identification of

the communicating vessels remained an unresolved issue. The original technique,

while fundamentally correct, did not specify how the vessels could be identified

[39,40]. The next step in the evolution of the technique involved targeting all

vessels that crossed the dividing membrane [41–43,45]. Although this technique

effectively interrupted vascular communications between the twins, it could also

target incorrectly many noncommunicating vessels because of the lack of

correlation between the vascular equator and the location of the dividing

membrane. In 1998, we described an anatomical, reproducible technique capable

of discerning communicating vessels from normal individually perfused areas of

the placenta called selective laser photocoagulation of communicating vessels

(SLPCV) [44]. Essentially, each placental artery is followed to its terminal end in

the placenta (arteries cross over veins). A returning vein from that cotyledon

should normally drain back to the same twin. If blood is drained to the other twin,

a deep arterio–venous anastomosis (AV) is present. Arterio–arterial or veno–

venous anastomoses are identified easily by noting lack of a terminal end for an

artery or a vein, respectively. Reliable techniques to treat patients who had


anterior placentas were also developed [48]. SLPCV is associated with an 85%

success rate (likelihood that at least one fetus survives) and a 3% to 5% risk of

cerebral palsy. SLPCV compares favorably with the previous nonselective

technique, resulting in a lower rate of dual fetal demise (5.6% versus 22%,

respectively) [47].

Umbilical cord occlusion

The goal of the umbilical cord occlusion technique is to stop blood exchange

between the fetuses at the level of the umbilical cord of one of the twins, which

can be accomplished by ligating the umbilical cord endoscopically, under

ultrasound guidance [49,50], or by using bipolar electrocautery under ultrasound

guidance [51]. The procedure is reserved for severe cases in which spontaneous

fetal death of one of the twins is likely to happen, particularly with the presence

of hydrops. Our rate of cord occlusion dropped from approximately 20% in 1997

to less than 5% in 2001 with a 76% successful pregnancy rate with no quotable

risk of cerebral palsy in patients treated with umbilical cord ligation.

Iatrogenic disruption of the dividing membrane (septostomy)

The goal of iatrogenic disruption of the dividing membrane (septostomy) is to

equilibrate the pressures between the two amniotic cavities [52]. Under ultra-

sound guidance, the dividing membrane is pierced repeatedly with a needle,

allowing fluid from the recipient twin’s sac to enter the donor twin’s sac.

Proponents of this technique have not shown that different amniotic fluid

pressures exist between the two cavities. We have shown that the amniotic fluid

pressures are similar despite large differences in amniotic fluid volumes [53].

Iatrogenic membrane disruption can result in a pseudomonoamniotic twin

pregnancy with cord entanglement and fetal demise [54]. In addition, the

resulting artificial improvement in the amniotic fluid volume of the donor twin’s

sac no longer reflects the urinary function of this fetus (which also applies to

cases in which purposeful amnioinfusion of the donor twin is performed), which

precludes adequate monitoring of the disease status of this twin. Lastly,

disruption of the dividing membrane significantly hampers the performance of

laser therapy (should this option be subsequently considered) or subsequent

amniocentesis because the floating dividing membrane interferes with these

procedures. Because septostomy is ill based, does not result in improvement of

the disease, and might actually harm the pregnancy, we strongly disagree with its

use and discourage its practice.

Amniocentesis versus laser

The controversy regarding the optimal treatment of TTTS has centered on the

use of amniocentesis or laser. Several factors led to almost irreconcilable

positions between the proponents of each approach: (1) lack of standard sono-

graphic criteria, (2) different inclusion criteria for gestational age, (3) dogmatic


views about the merits of each technique, and (4) the shortcomings of a surgical

technique in development. Risk factors for a poor pregnancy outcome with serial

amniocentesis have been identified. They include gestational age at diagnosis less

than 22 weeks, absent or reverse end diastolic velocity in the umbilical artery,

removal of greater than 1100 cc of amniotic fluid per week, or fetal hydrops [55].

Despite limitations, two prospective, nonrandomized clinical studies have shown

that laser therapy is superior to amniocentesis [41,46]. A randomized clinical trial

is underway in Europe to address these concerns.

Outcome analysis in patients treated with either amniocentesis or laser has not

been stratified by severity of the disease at presentation. Unfortunately, sub-

analysis of trials by risk factors might yield insufficient power to find statistical

differences. Our preliminary data comparing 78 patients treated with serial

amniocentesis and 95 patients treated with SLPCV show an inverse relationship

between fetal survival rates and Stage in the amniocentesis group (P < 0.001) but

not in the laser group. A direct relationship between fetal neurological morbidity

and Stage was also seen in the amniocentesis group but not in the laser group

[56]. These findings suggest that the optimal treatment of TTTS might be tailored

by Stage: Stage I and possibly Stage II patients (>22 weeks) could fare well with

serial amniocentesis, whereas Stage III and IV patients are probably best treated

with SLPCV. A prospective clinical trial to address this hypothesis is in prepa-

ration by our research groups.

Single intrauterine fetal demise

Death of one of the twins is a frequent phenomenon in the management of

twin–twin transfusion patients. This complication has been associated with death

or significant morbidity of the co-twin. Morbidity includes the development of

porencephalic cysts and other major neurological complications [57–60]. These

complications were originally thought to result from the release of thromboplastic

substances from the dead twin into the surviving twin. More recently, however,

an alternative mechanism has been proposed. Fetal blood sampling in one of the

twins before and after the demise of its co-twin has shown the development of

acute anemia in the surviving twin within a few hours, which suggests that

postmortem feto–fetal hemorrhage might be responsible for the development of

acute hypotension and thus might be responsible for the observed complications

[61,62]. Because this complication can only occur if the vascular communica-

tions between the twins are patent, this event can be avoided only through

occlusion of these vessels.

Summary

The understanding and management of twin–twin transfusion syndrome has

evolved significantly over the past few years. Improved and standardized sono-


graphic diagnostic criteria, understanding of the heterogeneic nature of the

syndrome, development of an anatomical and reproducible surgical technique

for the identification of vascular anastomoses, and technological advances and

developments now allow clinicians to view the disease as a more readily

understandable and treatable condition. Many tasks remain, including education

of peers, better screening and diagnosis, and further development of surgical

instruments. Generalization of treatment outcomes should no longer apply given

the varied results with disease stage. Confirmation of our tailored approach to

management of the disease according to stage should soon be corroborated with

an appropriate clinical trial.

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