|SILENT RISK - Issues about the Human Umbilical Cord|
|Jason H. Collins, M.D.
Charles L. Collins, M.D.
Candace C. Collins, M.D.
This Book is:
Umbilical Cord Accidents
Jason H Collins MD
when umbilical venous or umbilical arterial blood flow is compromised to a degree that it leads to fetal injury or death. The human umbilical cord is vulnerable to a variety of malformations, lesions, mechanical and iatrogenic events throughout pregnancy, labor and delivery. Medical and lay literature on UCA has accumulated since the Collaborative Perinatal Project (CPP). (1),(2),(3).The CPP data is used by the National Institutes of Health to study current obstetrical issues. Two reviews of UCA from the CPP study including; true knot, nuchal coils, and body loops suggests an association with extremes of umbilical cord length as a fetal risk factor for fetal malformation, injury and stillbirth.(4)(5) A review of stillbirths from the CPP suggests that UCA's (such as nuchal cord, true knot, and prolapse) have at least an incidence of 1.5 stillbirths/1000 births.(6) This review article summarizes the published medical literature on UCA since the CPP. The primary reference list in this review will provide the reader with ready access to secondary source publications before 1960. For each UCA issue such as single umbilical artery (SUA) , reviews were referenced where available (there may be >100 articles on SUA). Encountered during this review were innumerable photos, tables, and drawings which contribute to the understanding of UCA and which can be found within the quoted references.
Since 1960 and the CPP development of ultrasonography,
fetal monitoring, animal models of umbilical cord compression and
numerous case reports have provided a better understanding of how
UCA can affect the fetus. An assimilation of UCA studies and stillbirth
studies in humans and animals allows an initial insight into how
often UCA's are encountered. Pathologic examination of UCA's and
interpretation of fetal monitoring methods adds evidence to UCA
being a cause of fetal stress, injury and death. Research is needed
into the underlying mechanisms of umbilical cord accidents. The
human umbilical cord has been studied since recorded history. Although
UCA stillbirth is difficult to prove in humans, it is not uncommon
in mammals.(7) One of the first published accounts of an
UCA in western medical writings was by William Smellie in his Treatise
on Midwifery in 1750, London, England: a nuchal cord associated
stillbirth.One of the first published drawings of an UCA was by
Andrew Bell in the Encyclopedia Britanica 1st edition 1769 Edinburgh,
Scotland, depicting a fetal death with a combination of one nuchal
cord, a body loop and a true knot. There are over 25 separate types
of UCA's which have been well described and catalogued in current
pathology texts. (8),(9),(10),(11) Numerous published case
reports since the CPP have described observations associated with
witnessed UCA stillbirths. What is suggested by these reports is
the fetus may not be dying suddenly. The fetus may have changes
in blood supply due to cord compression that it adjusts to and compensates
for several hours or days until it no longer can. This suggests
there may be time to evaluate and deliver the fetus at risk of an
UCA associated stillbirth. Most stillbirths occur antepartum (8/1000)
or 60% after 34 wks and 25% occur between 36-40 weeks. UCA's stillbirths
tend to occur between 36-38wks, as for most stillbirths.(11),(12),(13),(14),(15),(16),(17),(18)
It may also be that a common time of fetal death is during maternal
sleep. This event could be related to diurnal rhythms influencing
maternal blood pressure (causing hypotension), uterine contractures
(reducing uterine blood flow>35%) and fetal cortisol reduction,
between 2-4 A.M.(19),(20),(21),(22),(23),(24)
What is the occurrence of UCA associated Stillbirth.
Another perspective is the spectrum of UCA stillbirth
over the course of pregnancy: 60% prior to 20 weeks, 5% from 20-36
weeks and @15% from 36- 40 weeks.(36),(37) In practical terms,
one out of every three to five deliveries will have an umbilical
cord finding. One out of 100 deliveries will be at risk of an UCA
stillbirth. Of the 2 UCA stillbirths /1,000 births, one will be
premature and one will be a term stillbirth. For comparison, a significant
shoulder dystocia with injury occurs in 1/1,000 births, a significant
case of preeclamsia occurs 2/1000 births.(38),(39)
Some reports have difficulty relating fetal death
to UCA. Pathologic evidence for UCA as the primary cause of death
is not always apparent and confounding factors can present difficulty
in determining a clear cause of death. A careful pathologic examination
is indicated in all UCA related deaths. (40),(41),(42),(43),(44),(45)
Two separate reviews of stillbirth studies looking at umbilical
cord etiologies disagreed with the previous diagnosis of cause of
fetal death. One review saw UCA as an etiology where there was none
originally, the other saw confounding factors where UCA were the
cause originally.(46),(47) There is evidence of UCA as a
cause of death in mammals, especially horses. The pathologic markers
for cord compression are well described in these veterinarian cases.(48),(49),(50),(51),(52)
Small case studies have demonstrated evidence for umbilical cord
involvement as the cause of fetal death in humans. In some reports
the cause of umbilical cord disruption was not seen at delivery
but shown by pathologic review. (53),(54) Also reported are
maternal (55)(56), fetal (57) and iatrogenic induced
injury to the umbilical cord with subsequent failure as the cause
of injury or death.(58),(59),(60),(61),(62),(63),(64),(65),(66),(67),(68),(69),
UCA can also repeat in the same patient. Reported
cases have described subsequent pregnancies with similar UCA (Constriction,
ELUC-excessively long umbilical cords) although not necessarily
stillbirth. (75), (76) Cases collected by us (on file) have
reported as many as 4 separate deliveries from the same mother,
each with a true knot. It is not unusual for a nuchal cord to be
repetitive in pregnancies from the same mother and family. It is
not unusual to see similar patterns of UCA repeat from case to case.
For instance, the pattern of most nuchal cords (>80%) are wrapped
right to left around the fetal neck. Most torsion is (>70%) counterclockwise
(sinestral, left-handed) away from the fetus. This suggests the
fetus maneuvers in the same direction most of the time when stimulated.
Is there an inherent reflex, similar to Moro's reflex which allows
for this? The fetus can develop entanglement and escape from it.
It is possible for a 20 week fetus with a triple nuchal cord to
free itself of the loops by 28 weeks.(77),(78) Did the loops
unwind or did they slip over the fetal body? Nuchal loops may slip
over the fetal body as the most common form of escape from entanglement.
Because in case reports these patterns are similar, it suggests
UCA stillbirths are not random but due to specific intrauterine
behavior of the fetus. These behaviors are limited in scope, just
as a newborn is limited in its' movements. Because there are purposeful
reasons for UCA, the same factors can lead to repeat events in the
same mother. UCA can no longer be dispelled as random. Overall,
stillbirth may be a statistically significant risk factor for subsequent
pregnancies. There are no studies looking specifically at UCA associated
stillbirth repetition.(15),(79),(80),(81) Table I
lists the incidence of common UCA's in humans.
What umbilical cord fundamental factors might contribute
Tensile strength: Several reports have measured the
breaking point of the human umbilical cord. Because of the differences
among cords in Wharton's jelly, collagen content, and muscle layer
structure there is a range of breakage points and sites.(87),(88)
The average load required to break the majority of human umbilical
cords is 10-14 lbs. The range being 4-24lbs (at term- 1.81-10.89
Kg). Cords ruptured 22.5% of the time at the placental end (without
description of the attachment).(89),(90),(91) Umbilical cord
traction forces of 8 lbs usually separated the placenta from the
uterus. Otherwise most cord ruptures were within 12 inches of the
fetus. The human umbilical cord is elastic and will stretch to 12.5%
of its length. The tensile strength may average 2.5% of fetal weight
. As a result some fetuses may tolerate more traction and loss of
slack during entanglement than others.(92),(93),(94),(95)
Diameter/Circumference: The human umbilical cord has
a reported average diameter of 1.5 cm and a separately reported
average circumference of 3.6 cm after birth. The umbilical vein
and artery have been measured before and after birth . The ultrasound
average vein diameter is 8mm with an average artery diameter of
4 mm at term . (96),(97),(98),(99)
Wharton's Jelly content: Umbilical cords can be large
(thick) and exceed an average of 4cm in circumference, especially
at the umbilicus. The average weight is 15 gms/ 10 cm at term and
dependent on male gender, prepregnancy maternal weight and birthweight
.(8) Umbilical cord swellings at the attachment to the fetus should
be examined before cutting and clamping the cord. The section may
contain urachal elements, bowel, embryonic remnants or a vascular
anomaly. Documentation of umbilical cord fetal end swellings should
be made at delivery and edema noted.(100),(101),(102),(103)
Umbilical cords can be lean (thin), < 1cm in circumference and
lack Wharton's jelly. Postdates fetuses and IUGR fetuses are associated
with lean cord appearances . This finding may suggest poor nutrition
and lack of glycogen in fetal tissues.(584),(585) Alteration
of umbilical cord water and molecular content may also play a role
as an independent risk factor for poor outcomes.(104),(105),(106),(107)
The average cross sectional area of the human umbilical cord is
14 sq/cm. Lean umbilical cords may be different in blood flow characteristics.
They may also be more vulnerable to compression which requires Doppler
studies of blood flow to determine whether or not there are compressed
segments. Amniotic fluid content must also be normal before assessment
of abnormal cords can be made. There are no studies comparing UCA
in thick vs lean cords.(108),(109),(110),(584,(585)
Length : The human umbilical cord can be totally absent
or reach a length of 300cm.(111),(112) Umbilical cord length
is the only factor associated and documented as a definite risk
factor for poor fetal outcome. There is an association of abnormal
cord length with neurological abnormalities and low IQ values. A
multivariate analysis of a small sample of pregnancies ( n 1087
births) reported an association with long cords and IUGR only. An
evaluation of all umbilical cords for extremes of length and development
should be considered at all deliveries at this time due to findings
in larger studies.(113),(114),(115),(116),(117),(118)
Absent or Short (< 35cm) umbilical cords (@ 3%
of cords) have been described and reported in cases of congenital
anomalies. A short cord may be due to reduced fetal activity (such
as with twinning; monoamniotic and conjoined), as a primary failure
of elongation (genetic ?), and in association with Sirenomelia (lack
of adequate fetal blood pressure), Shisis, Anencephaly (lack of
hypothalamic hormones?), Acardia (cardiac output?) and adhesions
(Early Amniotic Rupture Sequence -EARS). There may be additional
factors involved in cord lengthening which are not tension related.
Absolutely short cords can interfere with the mechanics of labor
and delivery while exhibiting changes in fetal heart rate patterns.
This restriction of decent (which is relative to the placental position
and insertion) leads to an increase in the incidence of cesarean
section ,forcep and vacuum extractions. Relatively short cords (lengths
compromised by fetal entanglement causing loss of slack) can interfere
with delivery as well.(119),(120),(121),(122),(123),(124),(125),(126),
Long umbilical cords (>70CM @ 4% of cords) are
documented to be directly associated with poor fetal outcome and
associated with UCA especially; fetal entanglement, true knots,
(sometimes multiple) and torsion. Placental changes are associated
with long cords suggesting blood flow disruption or increased resistance.(130)
Male cords are longer than female cords and term vertex fetuses
may have longer lengths than term Breech fetuses (with the duration
of presentation unknown). Multigravida cord length may be longer
than primagravida cord length (the first pregnancy having a shorter
length than the third , this may imply more room for movement-tension
or more blood supply/hormone production/fetal-maternal weight gain).
Twin gestations may have fetuses with discordant lengths and shorter
lengths than singletons. Single umbilical artery vessel structure
is increased in long cords. There are no studies considering maternal
smoking, alcohol, caffeine, or cocaine ingestion and umbilical cord
length in humans (animal studies report shorter cord lengths than
controls).(131) Umbilical cord function is not readily impaired
by longness and venous return from the placenta to the fetus is
maintained regardless of length.(132),(133) There are no
studies measuring the umbilical cord prenatally and evaluating the
risk factor of cord length for poor fetal outcomes.(458),(134),(135),(136),(137)
Umbilical Cord vessel number: Reports of five vessels
(153) ,four vessels, fused cords in twins and two vessel
cords have associated fetal conditions. (138),(139),(140),(141),(142),(143),(144),
Single Umbilical Artery (SUA) cases have been reported
with a variety of genetic, anomalous and stillbirth outcomes.(146),(147),(148),(149),(150),(151)
Umbilical Cord Attachments: There is specialized anatomy
for the umbilical cord attachment to the placenta and fetus.(182)
Failure of these attachments will cause fetal death.(183),(184)
The umbilical ring is designed to allow for fetal growth without
umbilical cord detachment until delivery. The umbilical ring is
innervated and these nerves have branches which connect to the vagus
trunks and phrenic nerves. There are connecting branches to the
right adrenal gland and maybe to the proximal umbilical cord . This
neuronal pattern may suggest an umbilical ring to ductous venosous
feedback system which partly regulates blood flow to the fetal cardiovascular
system.(185),(186), (187),(188),(189),(190),(191),(192), (193),(194),(195),(196),(197),(198)
Failure of proper umbilical cord development at the fetal attachment
can cause stillbirth. As stated previously, absent umbilical cord
syndrome is fatal. Other defects can be due to embryonic structures
and remnants at the proximal cord. Proximal umbilical cysts, urachal
anomalies and vitiline vessel anomalies have been well described
in pathology texts. (8),(9),(10,(11) Periumbilical skin length
may also have extremes of which long skin lengths have been noted
in dysmorphic children and UCA in horses. (49: pg 602),(199)
Constriction is the narrowing of the umbilical stump
attachment and is usually a cause of early stillbirth. Constriction
should not be confused with Torsion (an UCA that can occur associated
with constriction). Constriction may be caused by a variety of factors
which eventually impede blood flow. Case reports provide the majority
of insights into constriction which has not been prenatally diagnosed.
Constriction does repeat in the same mother suggesting a genetic
origin. From interviews, several verbal case histories have been
documented of constriction stillbirth where one mother experienced
four episodes in a row. (200),(201),(202),(203),(204) Placental
attachments can be malformed and result in fetal morbidity and mortality
(@ 10% of term placentas). IVF patients may be predisposed to placental
attachment malformation.(205),(206),(207),(208) Marginal
cord insertion (2.7%-15%), velamentous cord insertion including
vasa previa (33%-12wks to 26.5%-16wks to 1.7%-11% 38wks) and furcate(1%?)
insertion are susceptible to compression, torsion and rupture depending
on intrauterine location. Abnormal placental attachment can affect
fetal weight and may be detectable by 20 week ultrasound. Vasa Previa
is at high risk for fetal demise especially with rupture of membranes
(50% risk of death). The initial event of implantation of the fertilized
egg may dictate the potential for the placental insertion outcome.
Fetal heart rate screening may detect insertion compression by the
fetus causing both tachycardia and bradycardia unresolved by patient
repositioning. These observations at a prenatal visit might prompt
an ultrasound review of placental location and umbilical cord placental
insertion. A finding of a bilobed placenta or two vessel cord should
also be suspicious for a velamentous cord insertion (12.55% have
SUA).(209),(210), (211),(212),(213),(214),(216),(217) Studies
are needed differentiating umbilical cord-placental insertion, placental
location and fetal outcome.(218) The distribution of fundal
located insertions from lateral, cervical, anterior and posterior
are unknown. The occurrence of fetal compression risk based on cord
insertion location is unknown.(219),(220),(221),(222)
UCA'S that are common. Keeping the before mentioned
discussion in mind there are many variables which determine individual
UCA. There are over 25 different types of UCA described in published
medical literature. Since the CPP, information has accumulated which
suggests that these events collectively are common. UCA occurs throughout
gestation from conception to delivery with predispositions in each
trimester. Table (I) lists the common UCA of which one is likely
to be encountered every year by an obstetrical caregiver. Common
UCA include Nuchal cord, torsion, true knot, body/extremity loops,
velamentous insertion, marginal insertion, SUA, constriction, and
prolapsed cord. A review of published literature to date regarding
these UCA suggest they are important risk factors to be considered
in preventing fetal morbidity and mortality.(223) By comparison,
.1% of IUGR fetuses born at 38wks are at risk for stillbirth or
1 IUGR death/1000 births (224)
Torsion may be a common UCA. Stillbirth is associated
with torsion and usually the cause of death is identified by the
pathologist.(225),(226),(227) There is no definition of torsion
published. It is a common cause of death in horses and is readily
recognized by veterinarians as the cause of death (not a death artifact).(49),(228)
Torsioned umbilical cords can be untwisted .(48) This is
different from natural helixes which cannot be untwisted. In equine
studies, a nonhelical umbilical cord is normal. Long straight equine
umbilical cords tend to be twisted by the fourth month of gestation
with an average of 3 twists. The twists can be removed by rotating
the foal at birth. Intense twisting can cause urachal and vessel
obstruction.(229),(230) These twists can cause umbilical
blood flow obstruction if they exceed the ability of the cord to
absorb the torque. Torque is absorbed by buckling or snarling "Hockling"
as with a telephone receiver cord. (231),(235;Fig 6&7)
If tension is applied, kinking results blocking blood flow. The
incidence of torsion is unknown in liveborns. A prospective prenatal
study of UCA's estimated torsion to occur in 10% of deliveries depending
on a definition of 1 twist/ 9cm of cord length or less. The umbilical
cord was "untwisted" at birth to its fundamental 6-8 helixes
and twists compared to length.(19) A current study from China
reported the occurrence of torsion to be 6.14% with a fetal death
rate of 39.29%.(232),(233) This observation is not the same
as a hyperhelical umbilical cord which is made up of helices which
cannot be untwisted. The embryo develops 6-8 helices from @ 6-10
weeks when at that time it forms a physiologic umbilical hernia.
"The characteristic helical structure of umbilical cord appears
at an early stage of development and the basic pattern does not
alter as pregnancy proceeds" to term.(234) Helices grow
by increasing the "pitch" in between each vein/artery
turn. As the umbilical cord lengthens the helices get further apart.
Twisting brings the helices closer together (causing the pitch to
shorten). The average length cord has 6-8 helices and 3 twists (or
11 coils/spirals/turns/curls).(235) This fact allows a determination
of torsion in a liveborn. If the twists to cord length (without
the helices) exceed 1 twist/ 9cm or less, torsion exists. Obviously
this can not be determined until delivery, but it is an observation
which should be documented as will be discussed. Umbilical cord
torsion is associated with placental thrombosis, amniotic bands,
and umbilical ring constriction.(11),(231),(236,(237),(238),(239),(240)
Nuchal Cord is a common UCA. Nuchal cord (which occurs
@ 15% of deliveries) is separate from nuchal loops which by definition
does not encircle the fetal neck (which also occurs @ 15%). Nuchal
cord can be one encirclement to eight and has been reported in conjoined
There are two types of nuchal cord. Type A and Type
B.(246),(247) The risk of fetal injury or death due to a
nuchal cord is a difficult analysis when reviewing past literature.
There are no prospective prenatal studies to determine fetal effects.
One review of multiple nuchal loop cases could not detect an increase
in fetal mortality. A review of fetuses with nuchal cord identified
before 28wks could not detect an increase in poor outcomes. These
studies may be incomplete and require larger cohort groups. If the
fetal death rate due to nuchal cord alone is 1 death/2000 births,
then a larger study with a no risk cohort is needed to determine
risk factors of death. It may also be that multiple nuchal loops
is not a risk factor so much as the specific situation where there
is no slack. Umbilical cord compression occurs when there is loss
of slack and tension is created on the UCA ( regardless of loop
numbers ). Case reports of single and multiple loops of nuchal cord
have documented fetal compromise prenatally. Metabolic studies have
suggested fetal physiologic changes with nuchal cords. There are
no studies comparing umbilical cord placental insertion, placental
location, nuchal cord presence and fetal outcome. Without prenatal
assessment, it would be difficult to identify at delivery a tight
nuchal cord which was tight before labor. In an extensive study
on neurologic injury and its association with nuchal cord, tightness
was not identified prenatally.(248),(249),(250),(251),(252),(253),
Body loops and Extremity loops may be more common
than previously reported. Vaginal delivery mechanics undo these
points of cord compression probably before they can be observed.
Prenatal documentation of occult cord compression would be needed
to accurately determine how often the fetus is affected. The CPP
reported no ill effects from cord body part entanglement (BP- UCA)
in singletons. The issue may be that these fetuses are stillborn
before labor and are not accounted for as labor related UCA or stillbirths
with BP-UCA. These cases in some senarios are not recognized after
birth because the compressed cord loop or segment is undone by the
mechanics of birth. Four published studies were identified reporting
specifically on BP-UCA other than the CPP. One reported a Body Loop
incidence of @ <0.5% with a 10% stillbirth rate. A prospective
study using Doppler velocimetry, NST and imaging for body loops
reported an occurrence of BP-UCA of 23.23% with a fetal distress
rate of 85.29%.The cesarean section rate in this group was 88.28%.(266),(267),(268)
Umbilical cord prolapse and Funic presentation can
occur from .5% to 1% of pregnancies . Breech presentation, twins,
long umbilical cord and preterm birth are common associated risk
factors. One large study reviewed 56,283 births and documented 132
cases of prolapse. Outcomes included six stillbirths, six neonatal
deaths and one neurologic injury. This is similar to the CPP report
in that neurologic morbidity was low. The CPP also reported a higher
frequency of stillbirth. This may be due to the time to delivery
was usually within 30 minutes in the reported large study. Fetal
heart rate monitoring was "ominous" in 41% of cases and
questionable in 16% of cases. One report on time to delivery suggests
this may not be relevant. Funic presentation can be identified with
ultrasound and cord compression during labor can be evaluated with
Doppler velocimetry as an adjunct to fetal heart rate monitoring.
Recommendations for reducing complications due to funic presentation
and umbilical cord prolapse have been published.(285),(286),(287),(288),(289),(290),(291),(292),
Is there UCA morbidity ? In addition to mortality
from UCA, there is also an issue of morbidity from UCA. The CPP
noted UCA associated fetal effects such as; meconium, asphyxia,
fetal growth disruption, and low IQ values.(297),(298),(299),(300),(301),(302)
It is unknown to what extent the fetus is injured by umbilical cord
blood flow changes in utero.(303) Since the CPP only two
studies could be located addressing UCA morbidity directly.(304),(305)
UCA's were related to prolonged second stage of labor, failure of
decent of the presenting part ,postpartum bleeding, and fetal distress.
A case report on failure of decent due to a nuchal cord and reports
of consequences of tight nuchal cord illustrate the contribution
of UCA to fetal morbidity.(306),(581) In human case reports
UCA associated injuries documented are ; neurologic, cardiac, renal,
pulmonary, gastrointestinal, hepatic, vestibular and ophthalmic.
In one study, meconium and in another study, funisitis affected
umbilical cord vessels (causing spasm?) leading to fetal ischemia
and pulmonary injury.(246),(307),(308),(309),(310),(311),(312),(313),(314),(315),(316),(317),
Pathologic evidence of umbilical cord involvement
in fetal injury that has been reported consists of : pleural petechiae,
empty thymus, placental chorangiosis, placental vessel thrombi,
umbilical cord edema ,obvious knot cinching with umbilical venous
congestion, ruptured vessels due to velamentous formation, pulmonary
debris from gasping and torsion with and without constriction and
amniotic bands.(327),(328) There are published laboratory
findings associated with UCA cases. Fetuses with a UCA will experience
biochemical alterations in levels of ; ACTH/Cortisol, Erythropoiten,
Triglycerides, Endothelin, WBC shifts, NRBC shifts, and urine electrolytes.
(329) For asphyxia in general, organ damage may be more prevalent
than previously suspected and occur in a predetermined sequence.
(330),(331),(332),(333),(334) Animal study literature has
accumulated which simulates a variety of fetal organ effects due
to umbilical cord compression. As in humans , there are varying
presentations depending on the time and duration of the stimulus
along with the gestational age of the animal fetus. Prospective
studies are needed examining fetuses born live with UCA and the
potential associated morbidity.(334),(335),(336),(337),(338),(339),
What clinical signs may help to evaluate a fetus
at risk for UCA ?
Hyperactivity is a fetal response associated with cord length risk factors. This fetal behavior may be related to intrauterine seizure or blood flow disturbance which may stimulate the fetus to react reflexly and excessively. Studies of animal models (rats, sheep) have reproduced forms of hyperactivity with cord compression. Hyperactivity may be a prenatal behavior capable of repositioning the fetus . In the rat model umbilical cord compression triggered lateral trunk curls, head tosses, and foreleg extensions. These movement patterns are uncharacteristic of normal spontaneous movements. (personal communication with Laura Bennet ; Liggins Institute),(350),(351),(352) A specific study of "excessive fetal activity" in humans did not detect poor fetal outcome and did not report on UCA risk. The fetal movements recorded may have been normal fetal behavior. Time of observation (bedtime and 12mn-6am) may need to be included in any future study.(353),(354) Fetal jerking movements and fetal hiccups may also be related to fetal blood flow disturbances especially cord compression. These maternal observations should be taken seriously.(355),(356),(357) Decreased fetal movement should be investigated with the objective to rule out umbilical cord entanglement and UCA especially in no risk patients.(358),(359),(360) Fetal breathing movements may be an indication of fetal well-being with gasping or absence of fetal breathing suggesting developing asphyxia.(361),(362),(363) Fetal heart rate detection prenatally should include a recording to document changes in baseline and FHR patterns associated with umbilical cord compression. Umbilical cord compression has varying effects on fetal physiology depending on the degree of the stimulus and a duration of the interruption of blood flow. Gestational age of the fetus also determines the response to umbilical blood flow changes. These fetal responses have been clearly described in animal models and human case reports.(364),(365),(366),(367) In lamb fetuses, repetitive intermittent cord compression ellicits a pattern of fetal heart rate responses which are V shaped, U shaped and W shaped in the early period of compensation. These changes are simultaneous with cord stimulation and due to chemoreceptor and baroreceptor responses (which are for quick fetal compensation). As the repeated stimulus continues, the fetal heart rate patterns form the more obvious variable deceleration appearance and eventually the late deceleration appearance. These patterns form based on late fetal compensation due to acidosis, peripheral vasoconstriction, increases in catacholamines, cortisol and various biochemical defenses. A 50% reduction in umbilical blood flow is necessary to stimulate the formation of these patterns.(368),(369),(370),(371),(372),(373) Similar fetal heart rate patterns are present in human fetuses with cord entanglement. W waves, Lambda waves, Spikes and slow recovery of variable decelerations have been documented in case reports. There are no studies quantifying the number of cord compression patterns over time and fetal outcomes.(374),(375),(376),(377),(378),(379),(380),(381),(382),(383),(384)
Observations by ultrasonography of fetal umbilical
cord grasping provide another in vivo confirmation of fetal heart
rate response. These case reports demonstrate the degree of cord
compression needed to stimulate recognizable patterns similar to
those seen in fetal sheep.(385),(386),(387),(388)
Fetal Heart Rate Monitoring remains a controversial
means of evaluating fetal well-being. (389),(390),(391) A
review of Non Stress Test (NST) studies concluded that, "NST
is a relatively good predictor of adverse outcome when morbidities
and moralities are combined". This review did not specifically
analyze UCA related NST.(392) Fetal heart rate normalcy has
been reported which allows comparison of UCA influenced FHR patterns.
Umbilical cord compression patterns are described previously which
differ from normal.(393),(394),(395),(396) Studies specifically
evaluating UCA and screening by means of NST and or OCT have been
few.(397) A recent evaluation of NST to detect UCA's relied
on the classic variable deceleration pattern. In a double blind
study design, NST could not be demonstrated as a reliable screen
test in half of the 50 UCA cases. In a review of 2000 NSTs , 46%
had decelerations in response to fetal activity. Because 3 deaths
occurred due to abnormal cord position, it was concluded that this
FHR pattern be evaluated with ultrasound and OCT for cord compression.
A similar study of decelerations with fetal movement noted the additional
association with small for gestational age fetuses and the likelihood
of abnormal cord position. The SGA group with cord compression decelerations
had an increase risk of cesarean section.(398),(399),(400)
Another study reviewing a large cohort reported an accuracy of 76%
in predicting cord compression from a NST. One study which used
V wave,U wave and W wave as the key determinate reported NST could
be a useful test especially if done with an CST. (401),(402)
Cases of cord entanglement in humans, studied by observing the cardiac
electromechanical interval PEP (prolonged ejection period), noted
the PEP to be prolonged. In animal models (sheep,baboon), EKG analysis
noted T QRS changes and PR interval changes with cord compression.
Atrioventricular block with extrasystolies have been noted with
umbilical cord compression.(128),(403),(404),(405),(406),(407),(408),(409),(410),(411),(412)
These observations illustrate that there is an effect on the
fetal heart when umbilical blood flow is altered. At this time the
clinical relevance is that a tool is available to detect UCA .What
is needed is a means to gage the UCA impact on the fetus (413),(414)
Umbilical Cord Compression has been studied under
controlled laboratory conditions. There are numerous animal models
which suggest chronic , intermittent, and acute umbilical cord compression
cause specific fetal physiologic responses over time. Computer modeling
of the fetal placental circulation has aided our understanding of
this unique circulatory system.(415),(416),(417),(418),(419)
Interruption of umbilical blood flow greater than 50% is significant
for creating fetal hypoxia. Sustained and or repetitive compression
eventually leads to fetal compromise.(420) Occlusion of the
uterine artery has similar effects on the fetus with specific differences
on the fetal heart and brain. Combined umbilical cord occlusion
and uterine artery occlusion has effects on fetal organs and metabolism
.(421),(422),(423),(424),(425) The physiologic model for
prenatal umbilical cord compression is that the fetus once it has
developed a UCA is compromised. Cord compression; whether chronic,
intermittent or acute, ultimately stimulates the fetus to shunt
its blood flow, vasoconstrict its extremities and protect itself
through a centralized circulation (heart,adrenal,brain). The initial
sensor in detecting blood flow interruption is the umbilical ring
(as previously described). The next physiologic mechanism affected
by changes in umbilical vein blood flow is at the ductous venosus
(dv). The dv changes its shape to stream oxygenated blood to the
fetal heart. Because it is innervated, it may also send neurologic
responses to the brain.(426),(427) Baroreceptor and chemoreceptor
responses occur with release of catacholamines, cortisol, vasopressin
,angiotenson and other biochemical agents to initiate a fetal response
to developing hypoxia. Fetal metabolism of glucose and gluconeogenesis
are induced by cord compression. Arterial lactate elevations may
be a measurable result of umbilical cord compression.(428),(429)
These protective steps over time can give way to bradycardia,
vasodilation of the carcass, fetal hypotension, acidosis, depletion
of glycogen stores and blunting of the cortisol response. Eventually
fetal compensation will fail, peripheral vasodilation will occur
with heart failure, arrhythmias and fetal death. These insights
suggest that return of the fetal heart rate to a reassuring pattern
after intermittent decelerations, that the biochemistry of the fetus
is not restored immediately to normal or reassuring.(430)
Short term rapid biochemical defenses such as catacholamines, are
replaced by long-term endocrine and paracrine biochemistry . These
agents are metabolized at a slower rate eventually leading to devastating
fetal effects . In an intermittent cord compression sheep model
with term fetuses (1 complete occlusion every 5 min),fetal collapse
occurs in 45min to one hour . In a model of 5 min complete cord
compression repeated every 30 minutes the fetuses died after 3 or
4 occlusions.(431),(432),(433),(434),(435)- This process
is different from chronic asphyxia with placental insufficiency,
fetal anemia, or fetal infection. The question is, how does umbilical
cord compression happen in utero and when does cord compression
occur prenatally to the degree simulated in the animal models? (436),(437)
There are human case reports and studies which correlate with these
animal model observations. There are human case examples which are
well known for acute and chronic asphyxia due to cord compression
such as: prolapsed umbilical cord, vasa previa rupture, or monoamniotic
twin entanglement. Clinical signs which may be present given the
biochemical status of the fetus at risk of umbilical cord compression
compensation are; Hiccups, Hyperactivity, Decreased fetal movement
and Fetal heart rate changes. Normal physiologic hiccups last <
5-10 min (especially after 32 wks). Cord compression hiccups, stimulating
the ductous venosous, last > 10-15 min and occur > 4X / 24
hrs. Hyperactivity (especially during maternal sleep) may signify
uterine ischemia, Decreased movement >50% may imply a centralized
fetal circulation, Fetal heart rate baseline elevations > 150
bpm, Fetal heart rate bradycardia >100bpm may signal early fetal
acidosis. Umbilical cord compression patterns frequently repeating
on a NST ( such as W sign, Lambda sign , Spikes and possibly PAC's)
should be investigated. These patterns are due to cord compression
and are very distinct on NSTs. (438),(439),(440)
Numerous published reports have identified umbilical
cord morphology and abnormalities with ultrasound.(441),(442),(443),(444),(445),(446)
Real time black and white ultrasound is able to evaluate umbilical
cord structural abnormalities.(447),(448),(449),(450),(451),(452),(453),(454)
Individual case reports have accumulated which demonstrate the
ability of prenatal ultrasound to study the human umbilical cord
, see Table III . (455-517)
The placental umbilical cord insertion site can be
studied with black and white ultrasound.(518),(519) Umbilical
cord blood flow can be studied with Color Doppler velocimetry techniques.(520)
Doppler velocimetry has demonstrated alterations in blood flow with
nuchal cords, true knots, single umbilical arteries and in fetuses
with underdevelopment and cardiac failure .(521),(522) Because
of these advances, recent articles have recommended prenatal review
of the umbilical cord.(269),(523),(524),(525) One article
recommends a prospective observational study.(526)
Can UCA be managed once detected by fetal monitoring and or prenatal ultrasound? Can UCA management prevent stillbirth and what studies in humans validate this? To date case reports suggest UCA can be identified and managed.
For example, Monoamniotic twins (MAT) have a 70% or
more risk of cord entanglement. These cases have been prenatally
diagnosed with a variety of umbilical cord complications which can
have 10% mortality if managed, to a 70% mortality if unmanaged.
Several cases of monoamniotic triplets has been reported managed
for cord entanglement complications.(527),(528),(529),(530),(531)
This experience of fetal injury and loss has stimulated development
of monoamniotic twin case management for UCA. In a study comparing
managed MAT with published case histories of unmanaged MAT there
was an improvement in perinatal survival of 92%. Thirteen case sets
with a control group of seventy seven case sets (without prenatal
diagnosis) showed a 71% reduction in the relative risk of perinatal
mortality in the study group.(532),(533),(534),(535),(536),(537)
In one case report, cord entanglement was originally diagnosed
at 20 weeks. Amnioreduction was instituted to control fetal movements
and diminish the risk of complications. Another similar report achieved
diagnosis of MAT-UCA at 10 to 18 weeks and followed prenatally with
ultrasound and NST.(538),(539) Evaluation of MAT with Doppler
studies have detected cord compression and changes in umbilical
blood flow. An umbilical artery waveform notch was observed in one
report as an indicator of cord compression.(540),(541),(542),(543),(544),(545)
(546),(547), (548), (549), (550)
These MAT studies and case reports provide the best
evidence of fetal effects from UCA . It is possible to identify
UCA with ultrasound in the first trimester. It is possible to follow
umbilical cord blood flow with Doppler velocimetry. Its is feasible
to monitor fetal well-being with fetal movement awareness, NST,
and biophysical profile when UCA is present. Finally, there is evidence
that fetal morbidity and mortality can be reduced when UCA is managed
in MAT. What is needed is a prospective study in MATs and singletons.
Can the risk of UCA be predetermined and prevented.
The practical goal of 21st Century Obstetrics is not only to successfully deliver an infant but to do so without a poor outcome. This includes the best possible start in life mentally and physically.(441),(585) SADS ( sudden antenatal death syndrome, which accounts for @ 30,000 fetal deaths a year) is an important national health policy issue. UCA is a type of SADS which can be detected with ultrasound and can be managed with already established obstetrical practices. There may be UCA morbidity present in liveborns where previously unexpected. The interval from 36-38 weeks may require more scrutiny of the fetus, especially where a UCA is identified. Once more information is known about UCA, it may ultimately be recommended to consider delivery of the fetus at term and not manage the UCA associated fetus postdates. There may be a synergistic effect between maternal hypotension-uterine contracture-fetal cortisol-between 2-4 am and umbilical cord compression putting the fetus at risk for injury or unexplained stillbirth. A complete autopsy and placental-umbilical cord study should be considered when a UCA stillbirth is encountered. Evaluating all births with a placental-umbilical cord review may be cost prohibitive, but all stillbirths should be considered for pathologic review if the answers to unexplained stillbirth and direct cause of death are to be discovered.(586),(587),(588),(589) Research efforts should be encouraged into the study of stillbirth due to SADS and Umbilical Cord Accidents.(590) Well designed prospective studies are needed to evaluate the ability of ultrasound to consistently identify UCA. Management of prenatally diagnosed UCA and determination of fetal intervention, will create the ability to avoid stillbirth.(591),(592) Possible risk factors such as maternal hypotension need review. Finally the effects of UCA stillbirth on the family is significant. Care and support for the whole family is required and a suitable explanation of cause of death is needed .(593),(594),(595),(596) "Women want to be informed and have high expectations about the safety of their unborn child".(12)
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Table I. Umbilical Cord Accident
Table III. UCA Prenatally Diagnosed With Ultrasound
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