J. Perinat. Med. 41 (2013) 65–69 • Copyright © by Walter de Gruyter • Berlin • Boston. DOI 10.
1515/jpm-2012-0019
Single fetal death in twin gestations
Isaac Blickstein* and Sharon Perlman
Department of Obstetrics and Gynecology,
Kaplan Medical Center, Rehovot, Israel, affiliated with
the Hadassah-Hebrew University School of Medicine,
Jerusalem, Israel
Abstract
Twin pregnancies are at higher risk for fetal mortality when
compared with singleton pregnancies. Single fetal demise
occurs in 3.7–6.8% of all twin pregnancies and consider-
ably increases the complication rate in the co-twin including
fetal loss, premature delivery, and end-organ damage. In this
review, we summarize the current information on the etiology
of single twin demise, the pathophysiology of injury to the
surviving twin, and the preventive and secondary manage-
ment strategies.
Keywords: End-organ damage; fetal death; premature
delivery; twin gestation.
Introduction
Single intrauterine fetal demise (sIUFD) occurs in roughly
3.7–6.8% of twin pregnancies [8, 12, 32]. Death may occur
anytime and increases mortality and morbidity of the survi-
vor twin secondary to the cause of death of the co-twin, to
preterm labor, or both. sIUFD in twin pregnancy thus further
complicates an already complicated case and has different
consequences in terms of fetofetal effects and fetomaternal
problems compared with a singleton pregnancy.
The etiology of sIUFD in twin pregnancy could be either
similar to that in singletons or unique to the twinning process.
sIUFD might be caused by genetic and anatomical anoma-
lies, abruption, placental insufficiency, absolute or relative
(discordant) growth restriction, cord abnormalities, infection,
and maternal disease, including diabetes and hypertension. In
monochorionic (MC) pregnancies, sIUFD may result from
the twin-twin transfusion syndrome (TTTS). Monoamniotic
twins are at increased risk of cord entanglement and subse-
quent IUFD. Similar to the situation in singletons, the etiol-
ogy of IUFD often remains elusive. Chorionicity (related to
*Corresponding author:
Isaac Blickstein
Department of Obstetrics and Gynecology
Kaplan Medical Center
76100 Rehovot
Israel
E-mail: blick@netvision.net.il
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the placental angioarchitecture of inter-twin circulations),
rather than zygosity, is an important determinant of the risk
of intrauterine mortality and morbidity, thus the sequelae of
sIUFD in a twin pregnancy mainly depends on chorionicity
and, evidently, on the gestational age at diagnosis. This paper
reviews the current management of sIUFD (Figure 1).
Fetal demise in dichorionic twins
The prevalence of sIUFD among dichorionic (DC) twins is
lower than that reported for MC twins. When maternal con-
ditions that are potentially associated with fetal death are
excluded, and the well-being of the survivor is established,
no immediate intervention should be taken as sIUFD in DC
twins is not associated with fetofetal effects, and the risk for
the survivor is negligible. It is, however, recommended to fol-
low such cases with weekly assessments of the biophysical
profile along with growth assessment of the survivor.
The risk of preterm delivery before 34 weeks’ gestation is
increased in DC pregnancies complicated by sIUFD and is
reported to be as high as 57% [19]. However, in the absence
of spontaneous preterm delivery or other obstetric complica-
tions, elective preterm delivery of the survivor is not indicated.
For similar reasons, sIUFD in DC twins is not an indication
for abdominal delivery.
Unlike the case of IUFD in singletons, maternal dissemi-
nated intravascular coagulation (DIC, the so-called dead fetus
syndrome) is, for an unclear reason, extremely rare or never
exists in multiples [25]. Hence, except for a baseline coagu-
lation profile including fibrinogen level, there is no need to
follow these (DC as well as MC) pregnancies with serial
coagulation studies. Also, in D-negative women, anti-D pro-
phylaxis should be considered when transfer of D-positive
blood might be anticipated. Kleihauer-Betke test in maternal
blood may measure the amount of fetal erythrocytes trans-
ferred to the maternal circulation and help in establishing the
amount of anti-D that should be given to the mother.
Fetal demise in MC twins
Assisted reproduction technology (ART) has markedly
increased the number of multiple pregnancies with the vast
majority (roughly 95%) being DC. However, ART also increases
fivefold the frequency of monozygotic twinning. Monozygotic
gestations might be DC or MC, but the MC subset of monozy-
gotic twins notoriously carries an exceptionally increased risk
of pregnancy loss, congenital abnormalities, TTTS, selective
intrauterine growth restriction, and intrauterine death.
The prevalence of MC twinning among cases of sIUFD
in twins is 50–70% [26]. Poor prognosis of the surviving
66 Blickstein and Perlman, Single fetal death in twin gestations
sIUFD
DC MC
Preterm:
Hostile Term/near- Preterm
environment term ongoing death
+
- before or after sIUFD. Four of the five pregnancies were not
Delivery Delivery
Conservative
Conservative
Consider
intrauterine
blood
transfusion
Figure 1 Management of sIUFD in twin pregnancies.
co-twin is a well-known complication. A 2006 meta-analysis
[19] assessed the risk of co-twin mortality, neurological mor-
bidity, and preterm labor of the surviving co-twins following
sIUFD after 14 weeks’ gestation. The risk of MC and DC co-
twin death was 12% and 4%, respectively. The odds of MC
twin death following sIUFD after 20 weeks of gestation was
six times higher compared with that in DC twins. The risk of
neurological abnormality in the surviving MC and DC co-
twin was 18% and 1%, respectively. These data are concor-
dant with those reported in a recently published meta-analysis
by Hillman et al. [10].
The observed disadvantaged survival difference between
DC and MC twins has been attributed to placental vascular
anastomoses, which are invariably present in MC placentas
and (almost) never seen in DC placentas. The reported fre-
quency of vascular connections in MC placentas approaches
98% in placental injection studies [24, 29].
Based on the unique MC vascular architecture, two main
theories to explain the increased risk of morbidity and mortal-
ity of the surviving co-twin have been proposed. These are
known as the “twin embolization syndrome” and “hemody-
namic imbalance.”
Historically, poor prognosis had been related to some form
of DIC caused by an influx of thromboplastin-like substance
from the dead twin to its co-twin via the placental vascular
anastomoses. Thromboembolic material may be seen in sur-
viving co-twins, but there is still some doubt as to whether the
thrombi have arisen from the circulation within the dead twin
or as a result of hemodynamic changes within the survivor.
The resulting DIC was postulated to cause infarcts and cys-
tic changes in the survivor ’s renal, pulmonary, hepatic, splenic,
and neurological systems [1]. However, fetal blood sampling
did not reveal abnormal coagulation status in the surviving fetus
[18]. Moreover, intracranial sonographic anomalies appeared
too early to support this mechanism. Thus, the embolization
theory has been discarded. Currently, it is held that fetofetal
hemorrhage is the main mechanism leading to the adverse out-
come of the surviving fetus. It is hypothesized that sudden and
significant fall in vascular resistance around the time of death
of one twin causes shunting of blood from the surviving fetus
to the dead fetus. This leads to hypoperfusion, hypotension,
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and fetal anemia in the survivor and, in turn, results in tissue
hypoxia, acidosis, and tissue damage particularly within the
central nervous system. This theory was based on the finding
that although fetal blood sampling of the surviving fetus did not
show coagulation derangements, fetal anemia was clearly doc-
umented [17, 18, 27]. Nicolini et al. reported on eight pregnan-
cies with sIUFD that underwent blood sampling either < 24 h
anemic before the sIUFD (hematocrit: 33–40%) and neither
were their co-twins, but all survivors sampled within 24 h after
the death of their co-twin were anemic.
Similarly, Okamura et al. [18] obtained fetal blood from
five MC twin survivors after sIUFD and found that all five
were anemic, particularly when the twin death occurred
within 24 h of sampling. Perimortem fetoscopic observation
further supports this theory [23].
Of note is the fact that diagnosis of fetal anemia via cor-
docentesis has been replaced by the reliable and noninvasive
sonographic measurement of the middle cerebral artery peak
systolic velocity to detect fetal anemia [15, 16, 28]. Bajoria
et al. [1] determined outcomes of twin pregnancies compli-
cated by sIUFD in relation to vascular anatomy of the MC
placenta. They established that in the absence of TTTS, the
presence of superficial arterio-arterial or veno-venous anasto-
mosis increases the incidence of intrauterine death, fetal ane-
mia, and neurological handicap. It is hypothesized that these
large bidirectional anastomoses are of low resistance and
allow a pretty rapid blood shunting from the live fetus to the
dead fetus, in contrast to the relatively steady hemodynamic
state achieved along the high-resistance arteriovenous/veno-
arterial channels with blood shunt in the opposite direction.
This observation also refutes the thromboembolic theory, as
the gradient is such that thromboembolic material could not
flow from the dead fetus to the circulation of the survivor.
Regardless of the mechanism, no dispute exists about the
poor prognosis for the surviving co-twin. The major dilemma
in cases of sIUFD is how soon to deliver the survivor. The
risks of leaving the surviving twin in a potentially hostile
intrauterine environment that may have caused the death of
the co-twin must be balanced against the risks of preterm
delivery. Hillman et al. [10] recently meta-analyzed the effect
of gestational age at the time of demise of one twin on the
subsequent odds of death of its co-twin. The odds ratio if
death occurred at 13–27 or at 28–34 weeks’ gestation had no
effect on the risk of death of the co-twin. This report further
justified decision-making based on gestational age.
First trimester loss (the vanishing twin
syndrome)
The vanishing twin syndrome (or embryonic loss in a multiple
pregnancy) is a well-known phenomenon since the early days
of ultrasonography. Over the years, it became clear that many
more twins are formed than born. This means that many are
lost during the first trimester. The reason of embryonic loss, as
well as the magnitude of the phenomenon, is unknown. What
is known is that embryonic loss in polychorionic multiples
 Blickstein and Perlman, Single fetal death in twin gestations
is probably harmless to the survivor. In fact, some scholars
believe that many singletons actually had a co-twin during the
first trimester. In MC twins, however, the prognosis for the
survivor is unknown because it is unknown if the very early
MC placenta has anastomoses, and if present, it is unknown if
these anastomoses are functional. Because signs of TTTS are
not seen before the second trimester, and because presumable
signs, such discordant nuchal translucency, may be seen not
earlier than at 10 weeks’ gestation, it is, at present, prudent
to deduce that embryonic loss in MC pregnancies before that
age is also probably harmless to the survivor. There are some
unsupported hypotheses that loss of an MC twin may lead
to the so-called twin reversed arterial perfusion sequence.
Because this deduction is no more than an educated guess,
follow-up of the survivor with ultrasound and possibly with
third-trimester magnetic resonance imaging (MRI) to exclude
brain and kidney abnormalities is advocated.
Fetal demise between the first trimester
and viability
The risk of damage to the survivor is significant in this period.
Ultrasound scan may provide information concerning end-
organ damage of the survivor; however, detection of cerebral
injury depends on the time interval from the insult to the scan.
Unlike hemorrhagic lesions, ischemic lesions in the early
phase may be difficult to visualize.
Patten et al. [20] have demonstrated that a normal initial
scan cannot rule out damage and that sonographic evidence of
intracranial abnormalities in the surviving twin may manifest
as early as 7 days after the death of its co-twin. Structural
abnormalities observed in survivors include neural tube
defects, optic nerve hypoplasia, hypoxic ischemic lesions
of the white matter (multicystic encephalomalacia), micro-
cephaly (cerebral atrophy), hydranencephaly, porencephaly,
hemorrhagic lesions of white matter, post-hemorrhagic hydro-
cephalus, bilateral renal cortical necrosis, unilateral absence
of a kidney, gastrointestinal tract atresia, gastroschisis, hemi-
facial microsomia, and aplasia cutis of the scalp, trunk, or
limbs [11]. Sonographic scan might be complemented with
MRI [7]. If time permits, the best timing for MRI is at 32
weeks or later, when white matter is developed and minor
(yet clinically important) lesions in the white matter can be
visualized. Considering risks and timing, the option of ter-
mination of the entire pregnancy should be discussed with
the parents. The patient should be informed, however, that
despite the ominous prognosis, the chance of a favorable out-
come is greater than that of an adverse outcome.
Fetal demise at the late second and early third
trimester
This scenario presents clinicians with most difficult choices
and the potential dilemma of either delivery of a premature
twin or conservative management with the risk of morbidity
and mortality to the survivor as pregnancy advances.
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67
Because premature fetuses are more susceptible to insults
leading to neurological and other long-term complications
and given that the surviving fetus seems to be intact, most
clinicians will not intervene, as the synergic effects of prema-
turity and low birth weight superimpose upon the potential
damage to the co-twin.
Intrauterine transfusion (before or after viability) may save
the survivor by replacing the blood lost from the survivor to
the dead fetus. Such treatment would be effective, obviously,
only if performed at the reversible phase of the hypovolemic
insult to the survivor. Clearly, the window for a potentially
effective treatment is very narrow.
Senat et al. [27] transfused in utero 6 of 12 surviving
albeit anemic fetuses within 24 h after demise of the co-
twin. Four of the six had normal neurological development
at 1 year of age. A less optimistic observation was reported
by Tanawattanacharoen et al. [30] who performed intra-
uterine rescue transfusion in seven anemic fetuses within
24 h after death of a co-twin due to TTTS. Two severely
acidemic fetuses at blood sampling died in utero within 24
h of the procedure, two surviving twins had abnormal sono-
graphic findings of the brain and underwent late termina-
tion, two cases continued to an uneventful delivery with
good neonatal outcome, and one case was delivered a week
after the procedure, at 28 weeks, but died within the first
day of life.
Once choosing a conservative management, one should
be aware, however, to the natural history of approximately
90% deliveries within 3 weeks from the time of diagnosis of
sIUFD [6]. Preterm delivery is therefore common and steroid
prophylaxis for lung maturity enhancement should be given.
Interestingly, the risk for preterm labor is not affected by cho-
rionicity [19].
Prompt delivery vs. close surveillance
When the intrauterine environment is judged to be hostile
and potentially responsible to the death of one of the twins,
delivery becomes a more realistic option at this period of
gestation. D’Alton et al. [6] delivered by cesarean section
14 out of 15 fetuses upon confirmation of sIUFD provided
that the second twin was not severely immature. Such an
aggressive approach, however, did not prove to have a bet-
ter outcome [6, 22]. Kilby et al. [12], Prömpeler et al. [21],
and others [4] maintained that fetal outcome is mainly ges-
tational age dependent and the goal should be to prolong
pregnancy. Once conservative management is chosen, close
surveillance of the survivor should be performed includ-
ing non-stress testing and sonographic biophysical pro-
files along with growth assessment. As mentioned earlier,
sonography, with or without MRI, is used to detect end-
organ damage. Unfortunately, normal fetal surveillance is
not a guarantee for a good outcome. Neurological damage
may occur in the surviving co-twin with normal antenatal
ultrasound findings, reactive cardiotocography tracings,
and an intact brainstem as detected by postnatal computed
tomography [6].
68 Blickstein and Perlman, Single fetal death in twin gestations
Timing of elective delivery after conservative manage-
ment for late second trimester sIUFD is a matter of debate
in the literature. Cattanach et al. [4] favor conservative man-
agement until 37 weeks’ gestation as long as surveillance
tests are normal. Santema et al. [26] suggested intravenous
tocolytics treatment for impending preterm labor before 34
weeks’ gestation. Others advocate delivery at 32 weeks after
documentation of lung maturity, even when the fetus is in no
apparent distress [3, 9].
Fetal demise at term
In many of these circumstances, especially when the etiology
of fetal demise is unknown, the clinician may opt for delivery
instead of continued close monitoring of the pregnancy.
The mode of delivery should be tailored to the patient’s
condition and to the fetal size and presentation. Vaginal deli-
very is not contraindicated in cases of single fetal demise;
however, an obstructed labor can occur if the dead twin is
presenting.
Prophylaxis
Preterm birth is the common denominator of most adverse
outcomes related to twinning in general and to MC twins in
particular. Therefore, the source of many of the adverse out-
comes associated with MC twins might, in fact, be a result
of preterm birth. Although the inherent pathology associated
with MC twins leads to increased prevalence and a wide range
of fetal and placental malformations, not all MC twin preg-
nancies are a priori complicated [13, 14]. However, even this
subset of apparently “uncomplicated” MC twins was found
to be at a considerable excess risk (about 4% per pregnancy)
of IUFD [2]. In their discussion of the unexpected IUFD rate
among these MC twins, Cleary-Goldman and D’Alton [5]
suggested that elective preterm delivery (at 34–35 weeks)
might be a reasonable policy to avoid unexpected IUFD.
Several other hospital-based studies found a much lower risk,
but had an important disadvantage of coming from tertiary
centers, some with special interest in MC twinning, which
do not represent the population at large. A recent population-
based study, however, confirmed the excessive risk of unex-
pected IUFD in apparently uncomplicated MC twins, with a
prospective risk of 6.2% (95% CI, 4.2–9.1%) stillbirths per
pregnancy after 33 weeks of gestation [31].
The population-based data also suggested that as many
as 30% of the stillbirths could have been avoided with elec-
tive preterm births at 34 weeks without any neonatal deaths
among twins born at 34–35 weeks [31]. This latter observa-
tion supports the idea that MC twins may benefit from elec-
tive preterm birth [5] or suggests that, perhaps, a strict (and
costly) protocol of very close surveillance could make the dif-
ference for these high-risk twin gestations. In the absence of
randomized studies, as well of corroborative or contradicting
data from other populations, one has to acknowledge that the
potential benefit from decreased IUFD rates might be offset
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by increased neonatal morbidity due to iatrogenic prematu-
rity. Hence, although elective preterm delivery of apparently
uncomplicated gestations seems to be a new hidden cost of
MC twins, this issue is still very controversial.
Summary
Single fetal demise poses real risks for the surviving co-twin,
especially for MC twins, when morbidity in the survivor is
caused by hemodynamic instability. The most important vari-
ables in counseling are gestational age and chorionicity. It is
clear that all twin pregnancies with a single dead fetus should
be managed in a tertiary referral center. In the absence of
other obstetrical problems, DC pregnancies can be delivered
at term, whereas MC pregnancies are more difficult to man-
age and often are delivered between 34 and 37 weeks.
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The authors stated that there are no conflicts of interest regarding the
publication of this article.
Received January 30, 2012. Revised March 23, 2012. Accepted
March 29, 2012. Previously published online June 30, 2012.