Umbilical cord prolapse is defined as descent of
the umbilical cord into the lower uterine segment, where it may lie adjacent to
the presenting part (occult cord prolapse) or below the presenting part (overt
cord prolapse) . In occult prolapse, the umbilical cord cannot be palpated
during pelvic examination, whereas in funic presentation, which is
characterized by prolapse of the umbilical cord below the level of the
presenting part before the rupture of membranes occurs, the cord often can be
easily palpated through the membranes. Overt cord prolapse is associated with
rupture of the membranes and displacement of the umbilical cord into the
vagina, often through the introitus.
Prolapse of the umbilical cord to a level at or below the
presenting part exposes the cord to intermittent compression between the
presenting part and the pelvic inlet, cervix, or vaginal canal. Compression of
the umbilical cord compromises fetal circulation and, depending on the duration
and intensity of compression, may lead to fetal hypoxia, brain damage, and
death. In overt cord prolapse, exposure of the umbilical cord to air causes
irritation and cooling of the cord, resulting in further vasospasm of the cord
vessels.
The incidence of overt umbilical cord
prolapse in cephalic presentations is 0.5%, frank breech 0.5%, complete breech
5%, footling breech 15%, and transverse lie 20%. The incidence of occult
prolapse is unknown because it can be detected only by fetal heart rate changes
characteristic of umbilical cord compression. However, some degree of occult
prolapse appears to be common, given that as many as 50% of monitored labors
demonstrate fetal heart rate changes compatible with umbilical cord
compression. In most cases, the compression is transient and can be rectified
simply by changing the patient's position.
Whether occult or overt, umbilical
cord prolapse is associated with significant rates of perinatal morbidity and
mortality because of intermittent compression of blood flow and resultant fetal
hypoxia. The perinatal mortality rate associated with all cases of overt
umbilical cord prolapse approaches 20%. Prematurity, itself a contributor to
the incidence of umbilical cord prolapse, accounts for a considerable portion
of this perinatal loss.
Causes
Any obstetric condition that predisposes
to poor application of the fetal presenting part to the cervix can result in
prolapse of the umbilical cord. Cord prolapse is associated with prematurity
(< 34 weeks' gestation), abnormal presentations (breech, brow, compound,
face, transverse), occiput posterior positions of the head, pelvic tumors,
multiparity, placenta previa, low-lying placenta, and cephalopelvic
disproportion. In addition, cord prolapse is possible with hydramnios, multiple
gestation, or premature rupture of the membranes occurring before engagement of
the presenting part. A recent study revealed that obstetric intervention
contributes to nearly half of cases of umbilical cord prolapse. Examples cited
include amniotomy, scalp electrode application, intrauterine pressure catheter
insertion, attempted external cephalic version, and expectant management of
preterm premature rupture of membranes.
Overt cord prolapse can be diagnosed
simply by visualizing the cord protruding from the introitus or by palpating
loops of cord in the vaginal canal.
The diagnosis of funic presentation is
made by pelvic examination if loops of cord are palpated through the membranes.
Antepartum detection of funic presentation is discussed below.
Occult prolapse is rarely palpated
during pelvic examination. This condition can be inferred only if fetal heart
rate changes (variable decelerations, bradycardia, or both) associated with
intermittent compression of the umbilical cord are detected during monitoring.
The fetus in good condition whose
well-being is jeopardized by umbilical cord compression may exhibit violent
activity readily apparent to the patient and the obstetrician. Variable fetal
heart rate decelerations will occur during uterine contractions, with prompt
return of the heart rate to normal as each contraction subsides. If cord
compression is complete and prolonged, fetal bradycardia occurs. Persistent,
severe, variable decelerations and bradycardia lead to development of hypoxia,
metabolic acidosis, and eventual damage or death. As the fetal status
deteriorates, activity lessens and eventually ceases. Meconium staining of the
amniotic fluid may be noted at the time of membrane rupture.
Cesarean section is a major operative
procedure with known anesthetic, hemorrhagic, and operative complications.
These risks must be weighed against the real risk to the fetus of continued
hypoxia if labor were to continue.
Maternal risks encountered at vaginal
delivery include laceration of the cervix, vagina, or perineum resulting from a
hastily performed delivery.
The neonate at delivery may be
hypoxic, acidotic, or moribund. A pediatric team should be present to effect
immediate resuscitation of the newborn.
Patients at risk for umbilical cord
prolapse should be treated as high-risk patients. Patients with
malpresentations or poorly applied cephalic presentations should be considered
for ultrasonographic examination at the onset of labor to determine fetal lie
and cord position within the uterine cavity. Because most prolapses occur
during labor as the cervix dilates, patients at risk for cord prolapse should
be continuously monitored to detect abnormalities of the fetal heart rate.
Artificial rupture of membranes should be avoided until the presenting part is
well applied to the cervix. At the time of spontaneous membrane rupture, a
prompt, careful pelvic examination should be performed to rule out cord
prolapse. Should amniotomy be required and the presenting part remains
unengaged, careful needling of the membranes and slow release of the amniotic
fluid can be performed until the presenting part settles against the cervix.
The diagnosis of overt cord prolapse
demands immediate action to preserve the life of the fetus. An immediate pelvic
examination should be performed to determine cervical effacement and
dilatation, station of the presenting part, and strength and frequency of
pulsations within the cord vessels. If the fetus is viable, the patient should
be placed in the knee–chest position, and the examiner should apply continuous
upward pressure against the presenting part to lift and maintain the fetus away
from the prolapsed cord until preparations for cesarean delivery are complete.
Alternatively, 400–700 mL of saline can be instilled into the bladder in order
to elevate the presenting part. Oxygen should be given to the mother until the
anesthesiologist is prepared to administer a rapid-acting inhalation anesthetic
for delivery. Successful reduction of the prolapsed umbilical cord has been
described, but such an attempt may worsen fetal heart rate changes and should
not delay preparation for cesarean delivery. Abdominal delivery should be
accomplished as rapidly as possible through a generous midline abdominal
incision, and a pediatric team should be on standby in the event immediate
resuscitation of the newborn is necessary.
If cord compression patterns (variable
decelerations) of the fetal heart rate are recognized during labor, an
immediate pelvic examination should be performed to rule out overt cord
prolapse. If occult cord prolapse is suspected, the patient should be placed in
the lateral Sims or Trendelenburg position in an attempt to alleviate cord
compression. If the fetal heart rate returns to normal, labor can be allowed to
continue, provided no further fetal insult occurs. Oxygen should be
administered to the mother, and the fetal heart rate should be continuously
monitored electronically. Amnioinfusion can be performed via an intrauterine
pressure catheter in order to instill fluid within the uterine cavity and
possibly decrease the incidence of variable decelerations. If the cord
compression pattern persists or recurs to the point of fetal jeopardy (moderate
to severe variable decelerations or bradycardia), a rapid cesarean section
should be accomplished.
The patient at term with funic
presentation should be delivered by cesarean section prior to membrane rupture.
However, there is no consensus on management if the fetus is premature. The
most conservative approach is to hospitalize the patient on bed rest in the
Sims or Trendelenburg position in an attempt to reposition the cord within the
uterine cavity. Serial ultrasonographic examinations should be performed to
ascertain cord position, presentation, and gestational age.
Vaginal delivery can be successfully
accomplished in cases of overt or occult cord prolapse if, at the time of
prolapse, the cervix is fully dilated, cephalopelvic disproportion is not
anticipated, and an experienced physician determines that delivery is imminent.
Internal podalic version, midforceps rotation, or any other operative technique
is generally more hazardous to mother and fetus in this situation than is a
judiciously performed cesarean delivery. Cesarean delivery is the preferred
route of delivery in most cases. Vaginal delivery is the route of choice for
the previable or dead fetus.
Maternal complications include those
related to anesthesia, blood loss, and infection following cesarean section or
operative vaginal delivery. Maternal recovery is generally complete.
Although the prognosis for intrapartum
cord prolapse is greatly improved, fetal mortality and morbidity rates still
can be high, depending on the degree and duration of umbilical cord compression
occurring before the diagnosis is made and neonatal resuscitation is started.
If the diagnosis is made early and the duration of complete cord occlusion is
less than 5 minutes, the prognosis is good. Gestational age and trauma at
delivery also affect the final neonatal outcome. If complete cord occlusion has
occurred for longer than 5 minutes or if intermittent partial cord occlusion
has occurred over a prolonged period of time, fetal damage or death may occur.
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