Umbilical cord insertion
Marginal or velamentous insertion
by placental migration or misalignment of the embryo and placenta at implantation, umbilical cords sometimes miss the placental
surface. Those cords with a marginal insertion are often referred to as Battledore, while those with visible vessels in the
membranes are referred to as velamentous (1% of insertions). There are two potential sets of complications. The best documented
is the risk of vessel rupture with vasa previa when velamentous vessels cross over the cervical os. Velamentous vessels may
also occur with a normal insertion of the umbilical cord and they occur between any placental lobes. The second set of complications
is that the vessels are exposed to injury or thrombosis, and possible decreased blood flow evidenced by lower birth weight.
It is not immediately obvious why they would be more vulnerable to injury than vessels on the surface of the placenta as long
as the membranes are attached to the wall of the uterus.
Velamentous insertions are much more common in twins, even
passing through the septum between the twins. The evidence that they are more common with fetal malformation is debatable
and requires further clarification.
Furcata or interposed insertion:
In these insertions the vessels leave Wharton’s jelly
before reaching the surface of the placenta and course through the amniotic cavity. In furcata the vessels appear naked with
a “fork like” appearance. Interposed vessels have a thin fold of membrane draped over the vessel forming a tent
anchored to the fetal surface. While I can’t formally explain the physics, twisting the umbilical cord twists and collapses
these free vessels. This type of insertion could lead to occlusion of fetal blood flow and fetal death or asphyxial injury.
The distance of uncovered vessels can vary from millimeters to centimeters, and the shorter instances may not be vulnerable
to twist. The longer free vessel examples are rare, and the published literature is anecdotal without a large population study.
Severed velamentous vessels
An infant can hemorrhage from torn velamentous vessels with varying amounts
and rapidity. Most such cases are associated with vasa previa. Whether such deaths might be preventable by testing vaginal
hemorrhage for fetal blood cells or by other interventions is controversial. Velamentous vessels are commonly severed during
Cesarean section or the third stage of labor, and are not significant. We inspect all velamentous vessels. If there is a torn
segment, this is sampled histologically to look for fibrin or acute inflammation which indicates longer duration. We also
correlate any pallor or loss of blood in the placental vessels and any increase in nucleated red cells.
Risks and associations other than vasa previa from non-central umbilical cord
A prospective study of 1000 placentas failed to demonstrate a significant association of the location of the umbilical
cord insertion with low birth weight, intrauterine fetal death, threatened abortion, premature delivery, fetal malformation
or intrauterine fetal hypoxia (not further defined)1. They lumped marginal and velamentous cords into a single
“peripheral insertion” category and did no analyze them separately. This category had 72 placentas, approximately
7%, while only 1% would have been expected to be velamentous.
A clinical study of velamentous insertion in 12,750 high risk patients found
216 cases, excluding twins and malformations or aneuploidy2. There was a significant but small increase in velamentous
insertions in primigravidas, and not surprisingly a decreased incidence with prior Cesarean sections. (A primigravida by definition
could not have had a prior Cesarean section, but this is not discussed in the paper). Of the pregnancy and delivery variables,
there were 7 abruptions in the velamentous insertions (3% versus .75% P <.001). There was also a statistical increase in
bloody amniotic fluid. The authors state that there were no cases of vasa previa. It strains credulity to believe that none
of those abruptions were misdiagnoses of cases with vasa previa and fetal hemorrhage. In a logistic regression that hopefully
compensated for the increases incidence of preeclampsia in primigravidas, there was a significant but small increase in infants
delivered before 37 weeks of gestation, and of those with a birth weight <2,500 g. Of more concern is an increase in 5
minute Apgar scores less than 7 (assuming prematurity is controlled for), and abnormal FHR patterns, and borderline significance
for venous pH less than 7.15. Were these cases of vasa previa with hemorrhage or compression of vessels that accounted for
the differences between groups. In 48 cases with fetal Doppler studies, all abnormalities were believed due to preeclampsia.
There was no direct evidence of flow abnormalities from the velamentous vessels per se. Only one velamentous cord insertion
of 80 cases was detected by routine ultrasound (done from 1989 to 1993).
A review of 15,865 singleton deliveries, using the clinical record of the obstetrician’s
observation of the delivered placenta, found 77 (0.5%) velamentous cord insertions3. There were 268 twins with
5 velamentous insertions (2%). Of 82 velamentous insertions, 3 were vasa previa (0.02% of deliveries). The mothers with velamentous
insertion were more likely to be older than 35 years, more likely to be primiparous, and less likely to have a prior Cesarean
section. (The last two variables are not independent!). Of the outcome variables, there was a significant increase in meconium
stained fluid, blood stained fluid, abruption placenta, variable decelerations, and intervention with forceps or vacuum extractor.
No prenatal ultrasound examinations including the cases with vasa previa had diagnosed velamentous cord insertion.
A study of 148 placentas measured by computer the distance of the insertion from the center of mass of the placenta
as well as the shortest distance to the margin and the longest4. The study tested whether the scatter of measurements
were consistent with an attempt by the body to target the center of the placenta, or consistent with relative migration of
the placenta after the insertion was centrally placed (trophotropism). The findings were more consistent with the former,
that is insertions were random about the center. The author expected that if the eccentricity of the insertion were due to
placental migration then the displacement of the cord insertion would have been along the long axis of the placenta. The study
does not disprove such migration from having some effect especially in twins or low implantations of the placenta. The mathematics
is difficult to follow and I can not independently confirm the conclusions, and the details of how the program was done are
not included in this 1968 study. The data fit very tightly an equation ½ (longest distance to margin from insertion) over
(the shortest distance from the insertion) equals the (distance between the insertion and the center of mass) over (the shortest
distance from the insertion to the margin) plus ½. This equation holds for circles
and some sets of convex surfaces. I suspect that this striking result is just a consequence of the procedure of determining
and measuring these distances, but I am not sure.
A retrospective study of 183 “products of conception,” 6 of 18
(33%) specimens from 9 to 12 weeks of gestation had a velamentous cord insertion, 9 of 34 (26%) specimens from 13 to 16 weeks of gestation and in 7 of 63 (11%) specimens from 17 to 38 weeks of gestation5.
“Of the 28 specimens with velamentous insertion of the cord, the placenta was distinctly formed in 10.” 7 of the 28 (25%) velamentous insertion specimens had malformation, compared to 12 of 155 (8%) with normal
insertion, which was a significant difference. Only one velamentous insertion was in a twin. The author distinguishes insertion
velamentosa from interposition velamentosa. The former has an arterial anastomosis before branching in the membranes; the
latter has unbranching arteries in the membranes that anastomose in the placenta. The author argues that the increased incidence
of velamentous insertion is evidence that the insertion is a detriment to survival. He gives a detailed discussion of possible
mechanisms of development of velamentous insertion. He postulates that the difficulty
of maintaining circulation may be the cause of the higher incidence of malformation. [He does not give credence to the possibility
that placental growth might center some early cases of apparent membranous insertion.]
A Finnish study comparing 355 patients with elevated serum screening human
chorionic gonadotropin to 4935 with normal values found a doubling of the incidence of velamentous cord insertion, as well
as approximately a doubling of the risk of preeclampsia6. The 95% confidence interval is 1.47 – 4.69. Another
Finnish study of 170 cases of placental abruption found a doubling of velamentous umbilical cord insertion7. A
third Finnish study found an increased incidence (7.5%) of velamentous cord insertion in women with placenta previa8.
There was no biological rationale offered for these associations.
Two cases of fetal death from vasa previa, one with a torn velamentous vein, and the other with intact velamentous
vessels associated with a bilobed placenta were presented with a review of the medical literature from 1801-19519.
The author suggests looking at the blood from vaginal bleeding for nucleated red cells in hemorrhage occurring before or at
the rupture of membranes and associated with fetal heart rate abnormalities. The fetal mortality was greater than 50% and
the lesion was seldom diagnosed prior to delivery of the placenta. Subsequent reviews have added very little new information.
Three cases of vasa previa presented in 1965 demonstrated fetal death following delivery from a ruptured vessel, fetal
survival without hemorrhage but with cord compression pattern of the fetal heart rate, and survival from hemorrhage that was
diagnosed as vasa previa by the Apt test prior to delivery10.
A comprehensive review of vasa previa was associated with a case report in 198011. Vasa previa is defined
as vessels unsupported by placenta or Wharton’s jelly that cross over the cervical os in front of the presenting part.
The author notes that Torrey defined two kinds of hemorrhage from velamentous vessels, those with bare vessels crossing the
cervical os, i.e. vasa previa, and those that rupture without crossing over the os. Once fetal hemorrhage has occurred the
fetal prognosis is poor with a mortality greater than 50%. Neither tests for fetal blood in vaginal blood, nor amnioscopy
were often cited in cases in which antepartum or intrapartum diagnosis was made. Palpation of the vessels was often cited.
There have been many associated finding with velamentous insertion and vasa previa including single umbilical artery and abnormal
form or location of the placenta.
A case report of vasa previa with deep variable decelerations leading to Cesarean
section demonstrated long, large, unbranched velamentous vessels that were seen over the cervical os at Cesarean section12.
A report of 4 cases of vasa previa emphasized that in 2 cases the vessel rupture
and hemorrhage can occur prior to rupture of membranes13. Two of the
cases were due to velamentous vessels between placental lobes.
Seven cases of vasa previa were reported from 35,000 deliveries14.
They estimated 1% velamentous placentas which resulted in a calculated 1 vasa previa for every 50 velamentous cord insertions.
Five of their cases were diagnosed prepartum, three did not have ruptured vessels. Two of the infants with hemorrhage and
antepartum diagnosis died, but one with prompt transfusion survived.
Velamentous cord insertions in twins
A study of 38 diamniotic, monochorionic twins demonstrated not only increased
velamentous cord insertions in comparison to singletons, but also statistically significantly increased, 7 of 11 (64%), in
twin to twin transfusion syndrome (defined as polyhydramnios/ oligohydramnios without other detectable cause) compared to
5 of 27 (18%) diamniotic monochorionc twins without transfusion, P <.0115. The cord from the smaller twin was
inserted in the septum in 3 of the transfusion cases. In another the smaller twin’s cord inserted into the marginal
membranes, and in 3 the site was undocumented. In the twins without transfusion syndrome the cord inserted in the marginal
membranes in 3, and the site was undocumented in two. The authors argue that pressure from the polyhydramnios on the velamentous
vessels was a factor in unbalancing the twin circulations and at least increased the effect of twin to twin transfusion. [I
do not understand why the increased pressure would not have the same effect on all placental surface vessels. Perhaps those
over the placenta respond differently because of their branches to the intervillous space? The hypotheses that the correlation
is accidental or that the mechanism is more indirect and complex have not been eliminated]
A retrospective study of 64 diamniotic, monochorionic twin placentas, there
was a 9 fold relative risk of velamentous umbilical cord insertion compared to having normal insertions on both disks in infants
with birth weight discordancy16. There was no increased risk for dichorionic twins with birth weight discordancy.
[This study is published only in abstract]
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