This document summarizes the current management of single fetal demise (sIUFD) in twin pregnancies. It discusses that sIUFD occurs in 3.7-6.8% of twin pregnancies and increases risks for the surviving twin. The management approach depends on chorionicity, gestational age, and whether the demise occurred in the first, second, or third trimester. For monochorionic twins after the first trimester, the surviving twin has increased risks of death, neurological issues, and preterm birth due to shared blood flow between twins. Conservative monitoring is recommended when possible to allow further fetal development, though delivery may be considered if the in utero environment is deemed hostile.

1. October 2019 Management of
twin pregnancy
with single fetal
demise
Done By:
Kareem Fisal Alnakeeb
Supervised By:
Dr/ Mohamed Sayed Abdelhafez
Dr/ Hossam El Sonny

2. 1
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 considerably 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
management strategies.
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 survivor 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 anomalies, 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 subsequent IUFD. Similar to the
situation in singletons, the etiology of IUFD often remains elusive. Chorionicity
(related to the placental angioarchitecture of inter-twin circulations), rather than
zygosity, is an important determinant of the risk of intrauterine mortality and

3. 2
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).
Figure 1 Management of sIUFD in twin pregnancies
Fetal demise in dichorionic twins
The prevalence of sIUFD among dichorionic (DC) twins is lower than that reported
for MC twins. When maternal conditions 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
sIUFD
DC MC
Term/ near- term Preterm Preterm:
ongoing death
Delivery
Conservative
Conservative
Consider
intrauterine
blood
transfusion
Delivery
+
Hostile
environment

4. 3
follow 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
complications, 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 disseminated 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
coagulation 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 prophylaxis 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 transferred 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 monozygotic 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 co-twin is a well-known complication.

5. 4
A 2006 meta-analysis [19] assessed the risk of co-twin mortality, neurological
morbidity, 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 concordant 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 frequency 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 mortality of the surviving co-twin have been
proposed. These are known as the “twin embolization syndrome” and
“hemodynamic 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 surviving
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 cystic 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 outcome of the surviving fetus. It is hypothesized that sudden and significant

6. 5
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,
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 documented [17, 18, 27].
Nicolini et al. reported on eight pregnancies with sIUFD that underwent blood
sampling either 24 h before or after sIUFD. Four of the five pregnancies were not
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 cordocentesis 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 complicated 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 anastomosis
increases the incidence of intrauterine death, fetal anemia, 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.

7. 6
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 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

8. 7
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), microcephaly (cerebral atrophy), hydranencephaly,
porencephaly, hemorrhagic lesions of white matter, post-hemorrhagic hydrocephalus,
bilateral renal cortical necrosis, unilateral absence of a kidney, gastrointestinal tract
atresia, gastroschisis, hemifacial 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 termination 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

9. 8
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.
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 prematurity 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 intrauterine 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 sonographic findings of the brain and
underwent late termination, 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 chorionicity [19].

10. 9
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 better outcome [6, 22]. Kilby et al. [12], Prömpeler et al. [21], and others [4]
maintained that fetal outcome is mainly gestational age dependent and the goal
should be to prolong pregnancy. Once conservative management is chosen, close
surveillance of the survivor should be performed including non-stress testing and
sonographic biophysical profiles 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].
Timing of elective delivery after conservative management 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].

11. 10
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 delivery 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 outcomes 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 pregnancies 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 unexpected
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].

12. 11
The population-based data also suggested that as many as 30% of the stillbirths
could have been avoided with elective preterm births at 34 weeks without any
neonatal deaths among twins born at 34–35 weeks [31]. This latter observation
supports the idea that MC twins may benefit from elective preterm birth [5] or
suggests that, perhaps, a strict (and costly) protocol of very close surveillance could
make the difference 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
by increased neonatal morbidity due to iatrogenic prematurity. 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 variables 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 manage and
often are delivered between 34 and 37 weeks.
References

13. 12
[1 ] Bajoria R, Wee LY, Anwar S, Ward S. Outcome of twin pregnancies complicated by single intrauterine
death in relation to vascular anatomy of the monochorionic placenta. Hum Reprod.1999;14:2124 – 30.
[2 ] Barigye O, Pasquini L, Galea P, Chambers H, Chappell L, Fisk NM. High risk of unexpected late fetal
death in monochorionic twins despite intensive ultrasound surveillance: a cohort study. PLoS Med.
2005;2:e172.
[3 ] Carlson NJ, Towers CV. Multiple gestation complicated by the death of one fetus. Obstet Gynecol.
1989;73:685 – 9.
[4 ] Cattanach SA, Wedel M, White S, Young M. Single intrauterine fetal death in a suspected monozygotic
twin pregnancy. Aust N Z J Obstet Gynaecol. 1990;30:137 – 40.
[5 ] Cleary-Goldman J, D ’ Alton ME. Uncomplicated monochorionic diamniotic twins and the timing of
delivery. PLoS Med. 2005;2:e180.
[6 ] D ’ Alton ME, Newton ER, Cetrulo CL. Intrauterine fetal demise in multiple gestation. Acta Genet Med
Gemellol (Roma).1984;33:43 – 9.
[7 ] de Laveaucoupet J, Audibert F, Guis F, Rambaud C, Suarez B, Boithias-Gu é rot C, et al. Fetal magnetic
resonance imaging (MRI) of ischemic brain injury. Prenat Diagn. 2001;21:729 – 36.
[8 ] Enbom JA. Twin pregnancy with intrauterine death of one twin. Am J Obstet Gynecol. 1985;152:424 –
9.
[9 ] Evans MI, Lau TK. Making decisions when no good choices exist: delivery of the survivor after
intrauterine death of the co-twin in monochorionic twin pregnancies. Fetal Diagn Ther.2010;28:191 – 5.
[1 0 ] Hillman SC, Morris RK, Kilby MD. Co-twin prognosis after single fetal death: a systematic review and
meta-analysis. Obstet Gynecol. 2011;118:928 – 40.
[1 1 ] Karl WM. Intrauterine death in a twin: implications for the survivor. In: Ward RH, Whittle M, editors.
Multiple pregnancy. London: RCOG Press; 1995. pp. 218 – 30.
[1 2 ] Kilby MD, Govind A, O ’ Brien PM. Outcome of twin pregnancies complicated by a single intrauterine
death: a comparison with viable twin pregnancies. Obstet Gynecol. 1994;84:107 – 9.
[1 3 ] Lewi L, Gucciardo L, Van Mieghem T, de Koninck P, Beck V, Medek H, et al. Monochorionic
diamniotic twin pregnancies: natural history and risk stratifi cation. Fetal Diagn Ther. 2010;27:121 – 33.
[1 4 ] Lewi L, Jani J, Blickstein I, Huber A, Gucciardo L, Van Mieghem T, et al. The outcome of
monochorionic diamniotic twin gestations in the era of invasive fetal therapy: a prospective cohort study.
Am J Obstet Gynecol. 2008;199:514.e1 – 8.
[1 5 ] Mari G, Deter RL, Carpenter RL, Rahman F, Zimmerman R, Moise KJ Jr, et al. Noninvasive diagnosis
by Doppler ultrasonography of fetal anemia due to maternal red-cell alloimmunization. Collaborative
Group for Doppler Assessment of the Blood Velocity in Anemic Fetuses. N Engl J Med. 2000;342:9 –
14.
[1 6 ] Nakata M, Sumie M, Murata S, Miwa I, Kusaka E, Sugino N. A case of monochorionic twin pregnancy
complicated with intrauterine single fetal death with successful treatment of intrauterine blood
transfusion in the surviving fetus. Fetal Diagn Ther. 2007;22:7 – 9.
[1 7 ] Nicolini U, Pisoni MP, Cela E, Roberts A. Fetal blood sampling immediately before and within 24 hours
of death in monochorionic twin pregnancies complicated by single intrauterine death. Am J Obstet
Gynecol. 1998;179:800 – 3.
[1 8 ] Okamura K, Murotsuki J, Tanigawara S, Uehara S, Yajima A. Funipuncture for evaluation of
hematologic and coagulation indices in the surviving twin following co-twin ’ s death. Obstet Gynecol.
1994;83:975 – 8.
[1 9 ] Ong SS, Zamora J, Khan KS, Kilby MD. Prognosis for the co-twin following single-twin death: a
systematic review. Br J Obstet Gynaecol. 2006;113:992 – 8.

14. 13
[2 0 ] Patten RM, Mack LA, Nyberg DA, Filly RA. Twin embolization syndrome: prenatal sonographic
detection and signifi cance. Radiology. 1989;173:685 – 9.
[2 1 ] Pr ö mpeler HJ, Madjar H, Klosa W, du Bois A, Zahradnik HP, Schillinger H, et al. Twin pregnancies
with single fetal death. Acta Obstet Gynaecol Scand. 1994;73:205 – 8.
[2 2 ] Puckett JD. Fetal death of second twin in second trimester. Am J Obstet Gynecol. 1988;159:740 – 1.
[2 3 ] Quintero RA, Mart í nez JM, Berm ú dez C, L ó pez J, Becerra C. Fetoscopic demonstration of
perimortem feto-fetal hemorrhage in twin-twin transfusion syndrome. Ultrasound Obstet Gynecol.
2002;20:638 – 9.
[2 4 ] Robertson EG, Neer KJ. Placental injection studies in twin gestation. Am J Obstet Gynecol.
1983;147:170 – 4.
[2 5 ] Romero R, Duffy TP, Berkowitz RL, Chang E, Hobbins JC. Prolongation of a preterm pregnancy
complicated by death of a single twin in utero and disseminated intravascular coagulation. Effects of
treatment with heparin. N Engl J Med. 1984; 310:772 – 4.
[2 6 ] Santema JG, Swaak AM, Wallenburg HC. Expectant management of twin pregnancy with single fetal
death. Br J Obstet Gynaecol. 1995;102:26 – 30.
[2 7 ] Senat MV, Bernard JP, Loizeau S, Ville Y. Management of single fetal death in twin-to-twin transfusion
syndrome: a role for fetal blood sampling. Ultrasound Obstet Gynecol. 2002;20:360 – 3.
[2 8 ] Senat MV, Loizeau S, Couderc S, Bernard JP, Ville Y. The value of middle cerebral artery peak systolic
velocity in the diagnosis of fetal anemia after intrauterine death of one monochorionic twin. Am J Obstet
Gynecol. 2003;189:1320 – 4.
[2 9 ] Spellacy WN. Antepartum complications in twin pregnancies. Clin Perinatol. 1988;15:79 – 86.
[3 0 ] Tanawattanacharoen S, Taylor MJ, Letsky EA, Cox PM, Cowan FM, Fisk NM. Intrauterine rescue
transfusion in monochorionic multiple pregnancies with recent single intrauterine death. Prenat Diagn.
2001;21:274 – 8.
[3 1 ] Tul N, Verdenik I, Novak Z, Premru Sr š en T, Blickstein I. Prospective risk of stillbirth in
monochorionic-diamniotic twin gestations: a population based study. J Perinat Med. 2011;39:51 – 4.
[3 2 ] Woo HH, Sin SY, Tang LC. Single foetal death in twin pregnancies: review of the maternal and neonatal
outcomes and management. Hong Kong Med J. 2000;6:293 – 300.