One umbilical cord prolapse occurs for every 300 artificial rupturing of
Abstract: Rupturing the amniotic sac (amniotomy) became a routine part of
obstetrical care with the introduction of active management, without evidence of
benefit. One risk of amniotomy is it can cause umbilical cord prolapse. In the 30
years since active management was introduced, the rates at which amniotomy
causes umbilical cord prolapse have not been directly studied. Two case
controlled studies from Turkey from 2002 and 2006 are the only published
studies that provide enough data to show the rate of cord prolapse caused by
amniotomy. They show that for every 300 amniotomies performed, a 1 cord
prolapse occurs immediately after rupturing the membranes.
Amniotomy & Cord Prolapse
0% 10%20% 30%40%50% 60% 70%80%90% 100%
Rate of Artificial Rupture of Membranes
Cord Prolapse per 1000 births
Rate of cord prolapse directly increases with increasing rates of artificial rupture
of membranes. Where artificial rupture of membranes is never practiced, no cord
prolapse is reported. Rates of 3-4/1000 cord prolapses were reported with 26%-
89% rates of AROM (Dilbaz 2006, Uygur 2002). In a study of inductions which
usually includes AROM, a 7/1000 rate of UCP was reported.
The incidence of cord prolapse ranges from 0.1% to 0.6% (Lin 2006). About
10% of full term births, excluding inductions, start with spontaneous rupture of
membranes (Dilbaz et.al 2006, Zlatnik 1992). Amniotomy is routinely performed
at most hospital births during the first stage of labor where the sac did not break
spontaneously. Practitioners practicing in environments where vaginal exams
are routine generally think that membranes rupture spontaneously during the first
stage of labor. This may be because the sac often ‘spontaneously’ ruptures
directly following and likely as a result of a vaginal exam. Practitioners who
practice no routine vaginal exams and 0.4% rates of amniotomy report either the
sac breaks at the start of labor or the sac does not break until the woman pushes
or does not break until after the fetal head emerges in an intact sac. (Cohain
In 1984 Dublin’s active management was introduced (O'Driscoll 1984) including
amniotomy as a part of the protocol to prevent cesareans for dystocia. Parts of
this protocol such as amniotomy were widely adopted in the absence of strong
evidence that selective parts of the protocol were independently advantageous.
A 2007 Cochrane review updated to 2011(Smyth, Alldred, Markham 2007) of 15
trials (5,583 women) investigated the risks and benefits of routine amniotomy vs.
intention to leave membranes intact. Cochrane found no statistically significant
difference in length of labor between the amniotomy and control groups.
However, it should be noted that in no case was the research carried out as
designed. Instead 30%-60% of the women in the control groups that were not
supposed to undergo amniotomy received an amniotomy before 5 cm dilation.
There are no RCT studies comparing amniotomy to groups where amniotomy
was not or rarely performed.
One excuse given for amniotomy is to determine if there is meconium. However,
knowing there is meconium present before the birth has the potential to increase
anxiety of the staff and/or the mother and does not improve outcomes.
Drawbacks of amniotomy
Amniotomy is known to increase the risk of putting more pressure on the cord
than intact membranes, resulting in fetal distress (Smyth, Alldred, Markham
Umbilical cord prolapse (UCP): Ruptured membranes are one of the two
prerequisites for cord prolapse. The largest review found 10% of cord prolapses
to be “associated with” amniotomy. (Lin 2006) A recent review of 33,519
intended vaginal births (Gabbay-Benziv et. al. 2013) documented 26 cases of
cord prolapse immediately following amniotomy (1/1289 births) but does not say
what the rate of amniotomy was so we cannot calculate the rate at which
amniotomy caused cord prolapse. Cord prolapse immediately following
amniotomy is detailed in a case study. (Richardson 2009) At a planned attended
homebirth, amniotomy was performed because the woman had been in labor for
5-6 hours and having contractions every 10 minutes. Cord prolapse immediately
followed amniotomy. “The midwife continued to put pressure on the baby’s head to prevent
occlusion of the cord...warm swabs were placed around the cord and the midwife remained with her fingers
applying pressure to the baby’s head to prevent occlusion of the cord....Once in the cold air, the cord
collapsed, fetal heart fell to 40 beats per minute.” Although the death was a direct result of
the unnecessary amniotomy, the conclusion of the article did not blame
amniotomy, but rather concluded that women who live on the fourth floor should
be denied homebirths because of the difficulty of transfer. This denial of harm of
amniotomy is typical of cord prolapse research. A systematic search on Medline
for the keywords ‘Risk factors Cord prolapse’ found 34 studies whose purpose
was to identify risks of cord prolapse but only 7 evaluated amniotomy as a
possible risk factor while 27 only looked at the mother and baby, but not at the
birth practitioner as the cause.
3.3 Early onset GBS disease of the newborn (EOGBS)
The rate of EOGBS at vaginal birth in the absence of amniotomy has neither
been studied nor published. Although research is lacking showing decreased
infections when amniotomy is not practiced, we do know that newborn infections
are associated with longer intervals between ruptured membranes and delivery
(Seaward et.al. 1998), 3 or more digital vaginal exams (Heath et.al. 2009), and
scalp electrodes (Keski-Nisula et. al. 1997). Scalp electrodes double the rate of
GBS colonization in amniotic fluid (Keski-Nisula et. al. 1997). Seaward et al
(1998) found that an induction with oxytocin in women that were GBS(+) with
PROM reduced the colonization rate from 8% in non-induced patients and
patients induced with prostaglandin to 2% in the induced patients. The most likely
explanation for this difference was shortening the time period when the uterine
cavity had no barrier from the vagina.
In Texas 3,546 elective cesareans delivering 3,590 infants without antibiotic
prophylaxis with intact membranes (Ramus, McIntire, Wendel 1999), where 15%
of women were presumed to be GBS carriers, found no cases of EOGBS
disease. In vitro study has not been able to demonstrate GBS crossing
membranes, even at concentrations of 1,000,000,000 CFU (Kjaergaard et al
1999). Further investigation into how GBS could cross intact membranes
demonstrated that GBS failed to invade amnion cells under a variety of assay
conditions (Winram etal 1999) and fetal membranes demonstrated an inhibitory
effect on GBS (Kjaergaard et al 2001). The evidence supports the assertion that
GBS cannot cross intact amniotic membranes.
Keeping the membranes intact reduces the time GBS has to ascend and results
in 5% of full term births being born in a caul (Cohain 2010) never exposed to
3.4 Increased pain
Increased labor pain following amniotomy has been reported. (Robinson 2000)
3.5 Vasa previa
The 1999 American College of Obstetricians and Gynecologists Committee on
Practice Bulletins on Induction of labor. mentions that if the amnihook
accidentally ruptures a placental artery or vein during amniotomy, the baby could
lose significant blood volume.
Despite the known risks and poor scientific evidence of benefit, amniotomy is
routine. A medical advantage of amniotomy is not supported by the Cochrane
data base. A simple causal relationship between amniotomy and cord prolapse,
occasionally resulting in fetal death, has been published. The sac and amniotic
fluid are anti-bacterial, protecting the fetus from infection and pressures on the
cord. A potentially catastrophic event such as cord prolapse may serve to
remind us of the virtue of avoiding unnecessary interventions.
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