MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or

circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express
prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law.
Subscriber Agreement

Obstetrics and Gynecology Clinics

Volume 26 Number 3 September 1999
Copyright 1999 W. B. Saunders Company

419

EMERGENT CARE
UTERINE EMERGENCIES
Atony, Inversion, and Rupture

Daylene L. Ripley MD
Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, University of
Florida College of Medicine, Gainesville, Florida
Address reprint requests to
Daylene L. Ripley, MD
Division of Gynecologic Oncology
Department of Obstetrics and Gynecology
University of Florida College of Medicine
1600 SW Archer Avenue
Gainesville, FL 32610

Postpartum hemorrhage is the most common cause of morbidity and

mortality in pregnancy. Uterine atony, rupture, and inversion are three
potentially fatal causes of hemorrhage that may occur before, during, or after
delivery. These obstetric emergencies require immediate attention. Although
they occur uncommonly, the obstetric team must be aware of these potential
complications to be prepared for rapid and appropriate intervention. A delay
in treatment leads to a high rate of both maternal and fetal mortality.

UTERINE ATONY
Uterine atony is the most common cause of postpartum hemorrhage, accounting
for more than 90% of cases. The definition of postpartum hemorrhage has
traditionally been described as immediate postpartum bleeding in excess of 500
mL. In fact, the average blood loss at the time of delivery is approximately 500
mL for a vaginal delivery and 1000 mL for a cesarean delivery. Nevertheless,
clinicians significantly underestimate blood loss, and it is reasonable to use the
clinical impression of 500 mL of blood loss as a critical point to prepare for the
management of postpartum hemorrhage.
[13]

Following delivery of the placenta, myometrial contraction causing

420

vasoconstriction is the primary mechanism by which hemostasis is achieved.

Usually, the uterus contracts spontaneously or responds to manual massage. The
uterus should be firm and the fundus palpated at or just below the umbilicus
immediately after delivery of the placenta. The uterus may contract but then relax,
with recurrent bleeding from the open vessels at the site of placental separation.
Uterine atony is most likely immediately following delivery.
Etiology
Although several factors are known to increase the risk for uterine atony, some
patients in whom uterine atony develops have no identifiable risk factor.
Recognition of the known risk factors will allow the obstetric team to anticipate
and prepare for appropriate management in most patients.
Because the overdistended uterus is prone to atony, women with multiple
gestations, macrosomic infants, or hydramnios must be considered at risk. General
anesthesia, especially with the use of halogenated hydrocarbons that relax the
uterus, prolonged labor, and precipitous labor increase blood loss. Inductions or
augmentations with oxytocin and the administration of magnesium sulfate have
also been noted to increase postpartum bleeding from atony. In addition, high
parity, previous episodes of uterine atony, and chorioamnionitis have been shown
in some studies to lead to a higher incidence of uterine atony.
Diagnosis

Uterine atony may lead to heavy visible bleeding, but relying on this sign alone
is insufficient. Blood may collect in the cavity of the uterus and distend it,
concealing as much as 1000 mL of blood. Frequent palpation to assess the
location of the uterine fundus is necessary to recognize an enlarging uterus.
Uterine atony may also lead to bleeding that is moderate over a prolonged period
and may result in massive blood loss in a few hours. Surprisingly, most deaths
occur not from gross hemorrhage but because of ineffective management of slow
steady bleeding. Because of the pregnancy-induced expansion of blood volume,
these cases of postpartum hemorrhage may remain unrecognized until a large
volume loss has occurred. Close observation, uterine palpation, and an assessment
of vaginal bleeding and sequential vital signs are mandatory for at least the first
hour after delivery. The observation period should be extended if there is any
concern.

421

Management
The identification of patients at risk for atony allows for improved management
simply by being prepared for this complication. Antepartum correction of anemia
can be achieved if time permits, and antenatal banking of autologous blood can be
considered. High-risk patients should be typed and cross-matched upon arrival at
the labor and delivery unit.
The first step in the management of uterine atony is uterine massage to stimulate
myometrial contraction. Simultaneously, intravenous access is secured, preferably
with two large-bore peripheral lines. Obtaining adequate intravenous access
should not be delayed because peripheral access may become more difficult with
progressive blood loss. Oxytocin (Pitocin, Syntocinon) infusion routinely follows
delivery of the placenta, but rapid infusion of oxytocin, 20 to 40 U/L in saline
solution, must be ensured. The oxytocin must be suspended in crystalloid prior to
infusion because an undiluted intravenous bolus of oxytocin can cause cardiac
arrest or aggravate hypotension.
The uterine cavity is carefully explored for defects or retained products. The
vagina and cervix are inspected for lacerations. If the cavity is empty and the
uterus remains atonic and unresponsive to massage, methylergonovine
(Methergine) or ergonovine (Ergotrate), 0.2 mg, may be given intramuscularly. If
needed, the 0.2-mg dose can be repeated every 2 to 4 hours. Because these ergot
derivatives have a pressor effect and may cause hypertension, the patient's blood
pressure must be checked prior to their administration.
If the patient's blood pressure is high or if the ergot derivatives fail to improve
uterine tone, 250 mug of the 15-methyl derivative of prostaglandin F2alpha ,

carboprost (Hemabate), may be given intramuscularly or injected directly into the

myometrium every 15 to 90 minutes to a maximum of eight doses. Side effects of
15-methyl prostaglandin F2alpha include diarrhea, hypertension, vomiting, fever,
flushing, and tachycardia. Prostaglandin F2alpha is contraindicated in patients with
active cardiac, renal, pulmonary, or hepatic disease. Both ergot derivatives and
prostaglandin F2alpha are contraindicated in asthmatics.
[21]

Kupferminc and co-workers performed intrauterine irrigation with

prostaglandin F2alpha in 18 patients with uterine atony for the management of
severe postpartum hemorrhage. The patients had failed to respond to oxytocin,
methylergonovine, and uterine massage. A Foley catheter was placed into the
uterine cavity, the balloon inflated with 5 mL of sterile saline, and the cavity
infused with 500 mL of saline solution containing 20 mg of prostaglandin F2alpha .
The solution was infused at a rate of 3 to 4 mL/minute for the first 10 minutes and
then reduced to 1 mL/minute for a period of 12 to 24 hours. Of the 18 patients, 17
responded within
[16]

422

minutes, as evidenced by a firm contracted uterus with cessation of uterine

bleeding. The one patient not responding was found to have placenta increta at the
time of hysterectomy. No side effects were reported. The results suggest that
intrauterine infusion of prostaglandin F2alpha may serve as a simple, safe, and
effective method of treating uterine atony.
During the administration of uterotonic agents, bimanual compression may
control hemorrhage. The physician places his or her fist in the vagina and presses
on the anterior surface of the uterus while an abdominal hand placed above the
fundus presses on the posterior wall. Blood for transfusion should be made
available. Fortunately, the blood type and results of the Coombs' test are known in
almost all pregnant patients. If the patient has not been cross-matched previously,
this should be requested.
In the past, if uterine atony did not respond to the measures described previously,
uterine packing was commonly performed in an attempt to tamponade uterine
bleeding. This maneuver is no longer advocated because it keeps the uterine
cavity dilated, which, in turn, may lead to increased bleeding and a delay in
appropriate treatment. If bleeding persists, the vagina and cervix should be
reinspected for lacerations, the uterine cavity reexplored, and preoperative
preparations begun.
Sequential vital sign documentation and studies to obtain the hematocrit and
coagulation profile should be performed to guide in treatment decisions. It is

paramount to be aware of the patient's desire for future reproduction before

proceeding to surgery.
At exploratory laparotomy, a surgical assistant should gently compress the aorta to
decrease blood flow to the pelvic vessels in an effort to diminish blood loss.
Stepwise uterine devascularization with ovarian, hypogastric, or uterine artery
ligation will typically control bleeding. If the patient no longer desires fertility and
is otherwise stable, the procedure of choice is hysterectomy.
Zorlu and co-workers reviewed the indications for emergent peripartum
hysterectomies in Turkey. They analyzed two time periods, 1985 to 1989 and
1990 to 1994. In the earlier time period, uterine atony was the most common
indication for hysterectomy. During the later time period, placenta accreta became
the most common indication, correlating with an increased rate of cesarean
section. At the same time, the management of atony improved with the use of
medical management and more frequent performance of hypogastric artery
ligation. Zorlu and colleagues documented the efficacy of hypogastric artery
ligation in obstetric hemorrhage. Among the various causes of postpartum
hemorrhage in their study group, uterine atony had the lowest failure rate at 18%.
Placenta accreta and uterine rupture had higher failure rates of
[41]

[41]

423

40% and 60%, respectively. This study demonstrated that medical management is
effective and can decrease the need for surgical intervention. If surgical
intervention becomes necessary, the physician should be encouraged to attempt
hypogastric artery ligation, especially in cases of uterine atony, in an attempt to
avoid hysterectomy in patients desiring future fertility.
Selective artery embolization may be an alternative to open surgery. Morbidly
obese patients may be candidates for this approach if embolization may be more
quickly and safely accomplished than a surgical procedure.

UTERINE INVERSION
When the placenta is removed by placing traction on the umbilical cord, the uterus
may be turned inside out. Uterine inversion is rare and occurs in approximately 1
in 6400 to 1 in 2100 deliveries. Complete inversion is easily recognized,
whereas incomplete inversion may be more difficult to identify. Puerperal
inversion has been described as first-degree, in which the fundus has inverted but
has not passed through the cervix; second-degree, in which the inverted fundus
has passed through the cervix into the vagina; and third-degree, in which the
[33]

[27]

inverted fundus is outside the vulva. Inversion has also been classified as acute
when it occurs without contraction of the cervix, subacute when the cervix has
contracted, and chronic when greater than 4 weeks have elapsed.
[15]

[38]

Etiology
If strong traction is placed on an umbilical cord that is firmly attached to the
fundus of the uterus, the consequence may be complete inversion of the uterus.
The placenta may not have undergone separation at Nitabuch's layer or may be
firmly adherent to the myometrium as in placenta accreta, resulting in uterine
inversion when the umbilical cord is pulled upon. Uterine atony and the use of
fundal pressure may further contribute to easy inversion. The practice of allowing
for spontaneous placental separation will avoid uterine inversion in patients with
fundal implantation, placenta accreta, and a hypotonic uterus, hence avoiding the
majority of these complications.
Diagnosis
Complete inversion is easily diagnosed, but incomplete inversion may be less
apparent. Incomplete inversion may be palpated as a depression

424

or defect of the uterine fundus on abdominal examination. Transvaginally, the

fundus can be palpated protruding to, or through, the cervix. If the placenta
remains attached to the uterine wall after inversion, placenta accreta must be
suspected.
Management
Because uterine inversion may be rapidly fatal owing to associated hemorrhage, it
must be resolved immediately. The longer the uterus remains inverted, the more
difficult it becomes to return it back into the normal pelvic position owing to
edematous changes of the uterus and the development of a constriction ring at the
cervix. Because complete inversion is typically easy to recognize, treatment can
be instituted within seconds. As the obstetrician begins manipulation of the uterus,
the anesthesiologist simultaneously institutes pharmacologic uterine relaxation.
The uterus is manually reinserted by pushing the fundus with a fisted hand along
the axis of the vagina through the cervix and back into the pelvis. An alternative
method is to place one palm on the underside and the other palm on the topside of
the uterus, compressing the uterus and then progressively pushing the uterus back
through the cervix.

In most cases, the placenta will have separated. In the event the placenta remains
attached, it must be carefully inspected for accreta while intravenous access,
anesthesia assistance, and uterine relaxation are effected. Once conditions are
optimal, the placenta can be removed immediately prior to replacing the uterus or
manually removed after the uterus has been successfully repositioned. The
placenta must not be removed prematurely because massive hemorrhage may
occur. In the patient with accreta, the placenta may be inseparable, requiring
abdominal surgery.
Precise communication with nursing and anesthesia staff is crucial. The
obstetrician should ensure that the routine administration of oxytocin is withheld
until the uterus is replaced. Once the uterus is in the normal position, oxytocin can
be administered and any uterine relaxants discontinued. The hand of the
obstetrician should be held in place until the uterus initiates contraction to avoid
recurrent inversion.
Hydrostatic methods have been reported for the correction of partial inversion.
An occluding cup is placed in the vagina and saline infused above the cup. This
maneuver creates hydrostatic pressure and pushes the fundus past the ring and into
normal position. The benefit of this method is that it avoids the vasovagal
response that sometimes occurs with manual manipulation.
[20]

[34]

In the rare event that the uterus cannot be replaced by manual

425

manipulation, surgical intervention is necessary. Following laparotomy, the fundus

can be pushed from below and pulled from above by the placement of a suture
through the myometrium. In the Huntington technique, Allis clamps are placed
2 cm below the level of the constricting ring. Gentle retraction upward is exerted
on the clamps, and new clamps are serially placed 2 cm below the previous
clamps and traction applied until the uterus has been completely replaced. If the
uterus is resistant to replacement, the limiting factor is the presence of a
constriction ring through which the fundus cannot pass. In this situation, it
becomes imperative that the constriction ring is incised at the posterior aspect of
the uterus with a vertical incision as described in the Haultian procedure. Once the
ring is released, the fundus can then pass through, and the defect is repaired.
[33]

[33]

If placenta accreta prevents removal of the placenta, the uterus should be replaced
with the placenta intact and hysterectomy performed.
Pharmacologic uterine relaxation has traditionally been achieved by initiating
general anesthesia with a halogenated agent. An alternative to general anesthesia
is the administration of intravenous nitroglycerine, which is a vascular smooth

muscle relaxant. Peng and co-workers first reported the administration of 500
mug of nitroglycerine intravenously in 15 patients to induce uterine relaxation for
removal of a retained placenta. Uterine relaxation occurred in approximately 90
seconds and persisted for 1 minute. Unfortunately, this method was often
accompanied by hypotension, a potentially hazardous side effect in a
hemorrhaging patient. DeSimmone and co-workers used smaller doses of 50 to
100 mug with reduced side effects. Dayann and Schwalbe successfully used a
100-mug bolus of intravenous nitroglycerine to achieve uterine relaxation in a
patient with uterine inversion without causing hypotension. Alternative methods
of obtaining uterine relaxation include an intravenous push of terbutaline, 0.25
mg, or intravenous injection of magnesium sulfate, 2.0 g over 10 minutes.
Although effective in achieving uterine relaxation, the tachycardia associated with
terbutaline injection may be unacceptable and the effect of magnesium prolonged
and difficult to reverse.
[26]

[10]

[9]

UTERINE RUPTURE
Rupture of the uterus is described as complete or incomplete and should be
differentiated from dehiscence of a cesarean section scar. Complete rupture
describes a full-thickness defect of the uterine wall and serosa resulting in direct
communication between the uterine cavity and the peritoneal cavity. Incomplete
rupture describes a defect of the uterine wall that is contained by the visceral
peritoneum or broad

426

ligament. In patients with prior cesarean section, dehiscence describes partial

separation of the scar with minimal bleeding, with the peritoneum and fetal
membranes remaining intact.
Uterine rupture is responsible for 5% of maternal deaths in the United States each
year. Maternal deaths in cases of uterine rupture result from hemorrhagic shock,
sepsis, disseminated intravascular coagulation, pulmonary embolism, paralytic
ileus, and renal failure. Fetal mortality is high. In a review of 1381 cases of
uterine rupture, Suner and co-workers calculated a 61.5% fetal mortality rate. In
addition, morbidity, specifically neurologic damage in surviving infants, is high.
[36]

[36]

Uterine rupture may occur spontaneously prior to the onset of labor, during labor,
or at the time of delivery. Although rupture most commonly occurs in the third
trimester, it can occur even in early pregnancy. Rupture may occur in a completely
normal uterus or as a consequence of prior injury, anomaly, or uterine
manipulation.

The incidence of uterine rupture varies depending on the types of defects included
in the report. In general, the incidence has remained stable, but the predominant
etiology has changed with the increase of cesarean sections and the increased
acceptance of a trial of labor following cesarean delivery. The reported incidence
for all pregnancies is 0.05%, increasing to 0.8% after previous lower segment
cesarean section.
After classic cesarean section, the incidence is greater than
5%. In 1997, Miller and colleagues reviewed cases of intrapartum rupture in
patients with an unscarred uterus over a 12-year period and found only 1 case in
16,849 deliveries. This decreased incidence of rupture in the unscarred uterus is
most likely explained by improved antenatal diagnosis and labor and delivery
practices.
[11] [18]

[11]

[19]

Etiology
The clinical presentation of uterine rupture has changed considerably. In the past,
the most common predisposing factors were grandmultiparity and obstetric
trauma from prolonged or neglected labor, fetal macrosomia, malpresentation,
internal podalic version, breech extraction, manual cervical dilatation, and
instrumental vaginal deliveries. Today, fetal macrosomia and malpresentation are
detected with ultrasound, and prolonged and difficult vaginal deliveries have been
replaced for the most part by cesarean sections. As a result, obstetric trauma is less
common, and rupture of the unscarred uterus has become rare in the United
States.
Prior surgical procedures or manipulations resulting in uterine scaring are the
most common cause of uterine rupture. Cesarean section, myomectomy,
perforation, cornual resection, hysteroscopic procedures,

427

laparoscopic trocar injuries, and penetrating abdominal wounds are reported

insults preceding uterine rupture.
Scarred Uterus
Prior cesarean section is currently the most common risk factor for rupture. There
is wider acceptance of attempted vaginal birth after cesarean section, and this
trend is increasing. In addition, there is increased use of misoprostol and oxytocin
in these patients. Farmer and co-workers reported that two thirds of women with
a prior cesarean section underwent a trial of labor, with a 0.8% rate of rupture.
[11]

Women undergoing classic cesarean incisions, which enter the body of the uterus,
are at a greater risk for rupture and more frequently experience rupture prior to the
onset of labor. Rupture may occur weeks prior to term, making these cases

impossible to prevent. In contrast, incisions limited to the noncontractile portion

of the uterus rarely rupture prior to the onset of labor.
Some obstetricians have suggested that epidural anesthesia should be withheld in
women undergoing a trial of labor owing to the possibility that it may mask the
pain of uterine rupture; however, the classic "tearing" pain is rarely reported, even
in patients without anesthesia. In contrast, Ruddick and co-workers reported on
a woman in whom uterine rupture was accompanied by pain despite a functional
epidural. Therefore, it seems inappropriate to withhold epidurals routinely in all
candidates for a vaginal birth after cesarean section. The risk of epidural
anesthesia inhibiting maternal cardiovascular response to hemorrhage from
sympathetic blockade is not clearly demonstrated but may be of some concern.
[31]

Intrapartum amnioinfusion in women undergoing a trial of labor after previous

cesarean delivery was retrospectively reviewed by Ouzounain and co-workers.
A total of 122 women undergoing a trial of labor received amnioinfusions. One
uterine rupture occurred, demonstrating an incidence of 0.8%, the same rate
previously reported in all trials of patients undergoing labor. Therefore, patients
undergoing previous cesarean delivery seem to be amnioinfusion candidates. The
saline was administered by gravity flow in this study; forced infusion of saline in
any patient is potentially hazardous.
[22]

Patients with a history of uterine myomectomy are at risk for uterine rupture.
Operative reports describe the extent of myometrial incision and whether the
endometrial cavity was entered or not. When the endometrial cavity has been
entered previously, it has been recommended that a trial of labor not be attempted.
Nevertheless, several cases of rupture have been reported in which the
endometrium reportedly was not entered. Ozeren and co-workers described a
case of spontaneous
[23]

428

uterine rupture at 12 weeks' gestation in a patient who had undergone a

myomectomy 2.5 years earlier. Interestingly, the uterine cavity was not entered,
and a single capsulated myoma was removed measuring 8 7 5 cm. At
laparotomy, a 3-cm transverse fundal defect was found in the region of the
previous myomectomy.
Uterine rupture has occurred following laparoscopic myomectomies as well.
Pelosi and Pelosi reported a case of uterine rupture at 33 weeks' gestation
following a laparoscopic superficial subserous myomectomy. Despite the
superficial nature of the myoma and despite confirmation of an intact cavity by
intrauterine instillation of methylene blue, spontaneous rupture occurred at the
prior operative site. These reports indicate that all pregnancies following

[4] [25]

[25]

10

myomectomy may be complicated by uterine rupture. Unfortunately, rupture may

occur at any time prior to the onset of labor, even very early in pregnancy, making
it difficult to predict and prepare for intervention. Nevertheless, uterine rupture
following myomectomy is uncommon, estimated to occur in approximately 1 of
40 subsequent pregnancies.
[23]

Hysteroscopic procedures, including resection of uterine septa, myomectomy, or

lysis of synechiae, may predispose to uterine rupture. Accidental perforation of
the myometrium during hysteroscopic procedures may further increase this risk.

[14]

Arbab and co-workers reported five cases of early uterine rupture in patients
with a history of previous salpingectomy with cornual resection who subsequently
underwent in vitro fertilization (IVF) and embryo transfer. In all of these patients,
uterine rupture occurred during the first or second trimester at the site of prior
cornual resection. Cornual resection may lead to placenta accreta at the prior
resection site or weakening of the myometrium predisposing to rupture. Patients
undergoing IVF may be a subset of patients at higher risk for uterine rupture. As a
group, these patients have frequently undergone uterine manipulation. Arbab and
colleagues suggested that IVF candidates be observed closely with ultrasound to
locate the site of the gestational sac and placentation.
[3]

[3]

Certainly, the various modalities used at the time of uterine surgery may impact
on the extent of myometrial injury. Electrocautery used to obtain hemostasis at the
site of a small laceration or perforation may cause extensive thermal damage with
tissue necrosis. Electrocautery and laser surgery may cause significantly more
myometrial injury than sharp dissection, but there are no data available to
compare the risks associated with different surgical modalities.
Unscarred Uterus
Rarely, spontaneous rupture occurs in an unscarred unmanipulated uterus prior to
the onset of labor.
Typically, rupture of the unscarred uterus is iatrogenic.
[17] [37]

429

The unscarred uterus may rupture during operative deliveries, midforceps and
vacuum deliveries, and breech version and extraction. The application of external
force to the uterine wall during external cephalic version and vigorous fundal or
suprapubic pressure may lead to rupture. Excess fundal pressure should never be
applied in an attempt to effect delivery. Overdistention of the uterus from multiple
gestation, hydramnios, and forced intra-amniotic installation of saline may
increase the risk for rupture. Fetal anomalies such as hydrocephaly may also lead
to rupture.

11

Patients with congenital uterine anomalies, either corrected or uncorrected, should

be considered at high risk for rupture. Pregnancy in the rudimentary horn may
lead to rupture in the first or second trimester. Rupture usually occurs prior to 20
weeks' gestation when implantation occurs in the rudimentary horn. Basbug and
co-workers described a case of rupture of a rudimentary horn at 16 weeks'
gestation. They found that the conceptus that implanted in the rudimentary horn
lacked a decidual layer, consistent with placenta accreta. In review of the
literature, they identified eight cases involving rupture of the rudimentary horn in
association with placenta accreta. In these cases, rupture occurred in all three
trimesters. In patients who have undergone resection of a rudimentary horn,
uterine rupture may occur at the site of resection, as seen in patients with prior
myomectomies.
[29]

[5]

Unrecognized transverse lie in the laboring patient will eventually lead to uterine
rupture and maternal and fetal death. Inspection and palpation of the abdomen
combined with pelvic examination should lead to the diagnosis of transverse lie
and, in turn, to cesarean delivery if version into a stable vertical lie cannot be
achieved.
Grandmultiparity imparts many postpartum risks. Para seven or greater increases
the risk of rupture by 20-fold. Uterine stimulation in these patients should be
avoided or given sparingly and with caution.
[12]

Blunt trauma in the pregnant woman rarely leads to uterine rupture unless there is
direct impact of substantive force. Rupture of the gravid uterus complicates only
0.6% of traumatic events. Although the incidence of fetal demise following
traumatic uterine rupture approaches 100%, the maternal mortality rate is less than
10%, and most deaths are the result of concurrent injuries. Placental abruption is
a more common complication of trauma; the symptoms of rupture and abruption
may be difficult to distinguish on clinical examination. The inappropriate
placement of seat belts has caused devastating lacerations of the uterus and fetus.
The lower seat belt should be worn across the upper thigh, below the protuberant
abdomen, and the shoulder strap should cross between the breasts, allowing up to
3 inches of slack. Although the use of air bags has been controversial, they
should not be substituted for seat belt restraints.
[24]

[2]

430

Uterine Stimulation
Oxytocin is used daily in the practice of obstetrics. Physicians may become
complacent in its use when, in fact, it should be regarded as a powerful drug.
Intravenous oxytocin has resulted in uterine rupture and marked hypertonic
uterine contractions resulting in fetal injury. Appropriate use of oxytocin must

12

include continuous monitoring and the performance of a cesarean section when

failure to progress occurs despite adequate uterine contractions. Prolonged labor
in the presence of cephalopelvic disproportion may lead to development of a
retraction ring, which is palpated as a ridge extending across the uterus
somewhere between the symphysis and the umbilicus. If a retraction ring is
palpated, abdominal delivery should be performed immediately owing to the risk
of uterine rupture and fetal injury. In a patient with a contracted pelvis, the risk of
rupture increases with the use of oxytocin.
The use of prostaglandins has also resulted in uterine rupture. A randomized trial
of oxytocin versus misoprostol for cervical ripening and the induction of labor
was initiated by Wing and co-workers in 1998. Following uterine rupture in 2 of
17 women receiving misoprostol, the study was closed. The type of uterine
incision was undocumented in both cases of rupture, although one case seemed to
have a transverse defect on laparotomy. Sciscione and co-workers also reported
uterine rupture in a patient with two prior low transverse cesarean deliveries. The
patient received two doses of 50 mug of misoprostol intravaginally. At the time of
delivery, the fetus was noted to have been extruded through a large uterine
perforation at the site of prior scarring. Prior cesarean section is not required for
prostaglandins to result in uterine rupture as reported by Bennett. She
documented uterine rupture in a patient who had previously undergone dilation
and curettage after receiving two doses of 25 mug of misoprostol intravaginally.
In this case, the course of labor was complicated by tachysystole, which may have
had a role in the rupture.
[39]

[32]

[7]

Chapman and colleagues evaluated the risk of uterine rupture in midtrimester

pregnancy terminations. The incidence of rupture was significantly higher among
women with a prior cesarean delivery (3.8%) when compared with patients
without a prior cesarean (0.2%). There was an increased need for blood
transfusions in women with a prior cesarean delivery as well. The increased
cesarean rate and more widespread use of prenatal diagnosis in current practice
may increase the occurrence of rupture during midtrimester pregnancy
termination.
[8]

Diagnosis
Ultrasound has been used to examine the uterus in women who have undergone
previous cesarean sections in an attempt to assess the

431

risk for rupture in subsequent labor. Essentially, the risk of a defective scar is
directly related to the degree of thinning of the lower uterine segment at around 37
weeks of gestation. Although the positive predictive value is low, the high

13

negative predictive value may reassure obstetricians to allow a trial of labor in

patients with a thicker lower uterine segment.
[30]

The signs and symptoms of uterine rupture may be bizarre, and identifying the
cause may be difficult unless the possibility of rupture is kept in the differential
diagnosis. Rupture of the uterus during labor may lead to the classic description
by the patient that something is "ripping" or "tearing." If the patient ceases to have
uterine contractions and has new onset of vaginal hemorrhage coupled with the
development of fetal bradycardia, the diagnosis is clear. Unfortunately, this classic
presentation rarely occurs.
The placement of intrauterine pressure catheters has been advocated in high-risk
patients in the hope that a drop in the uterine pressure reading would coincide
with uterine rupture. Rodriguez and co-workers reported on 39 women who had
intrauterine pressure catheters in place at the time of uterine rupture. None of the
39 patients demonstrated loss of contractions or decreased intrauterine pressure.
Four patients, in fact, demonstrated an increased baseline uterine pressure, as did a
patient reported on by Beckmann and co-workers. Therefore, intrauterine
pressure may increase, decrease, or remain unchanged, making it an ineffective
method of identifying uterine rupture.
[28]

[6]

Loss of station of the fetal presenting part has been helpful in recognizing uterine
rupture. The presenting part may actually recede to a higher station when other
fetal parts are extruded through the rupture site. When this happens, fetal parts
may be palpated outside the uterus on abdominal examination. If the diagnosis is
suspected but is unclear, sonography may be helpful. Zisow reported a case of
shoulder dystocia as a severe consequence of uterine rupture. Following delivery
of the fetal head, the body could not be delivered. At laparotomy for abdominal
delivery, the fetal body was found anterior to an already contracted anteriorally
ruptured uterus. An abdominally assisted vaginal delivery was accomplished.
Presumably, the rupture and expulsion of the fetus into the abdominal cavity
occurred during pushing at full dilatation, marked by the patient's complaint of
abdominal pain and decreased fetal heart rate.
[40]

Maternal vital signs are late indicators of severe hemorrhage owing to the
increased blood volume and heart rate in the term gravid patient. Most reports of
uterine rupture describe patients with normal blood pressure or even elevated
blood pressures without tachycardia.
Fetal distress is the most consistent finding in uterine rupture. The physician
should be aware of risk factors for rupture because signs and

432

14

symptoms may not be clear, with rupture diagnosed early only if the obstetric
team remains suspicious.
Management
Mortality rates for both mother and fetus are high. Prompt diagnosis and
immediate treatment are the keys to improving the prognosis in uterine rupture.
The identification or suspicion of uterine rupture must be followed by an
immediate and simultaneous response from the obstetric team. Large-bore
intravenous access and rapid infusion of crystalloid must be accomplished. Typespecific whole blood should be obtained as soon as possible and the anesthesia,
surgical, and neonatal teams assembled for immediate laparotomy and delivery.
Surgery should not be delayed owing to hypovolemic shock because it may not be
easily reversible until the hemorrhage is controlled. Upon entering the abdomen,
aortic compression can be applied to decrease bleeding. Oxytocin should be
administered to effect uterine contraction to assist in vessel constriction and to
decrease bleeding. Hemostasis can then be achieved by ligation of the hypogastric
artery, uterine artery, or ovarian arteries. This maneuver decreases arterial
bleeding and allows better visualization of the defect and may be safer than
initially repairing the rupture site. Because successful pregnancy has been
accomplished following both ovarian and hypogastric artery ligation, this action
does not eliminate the choice of uterine repair.
At this point, a decision must be made to perform hysterectomy or to repair the
rupture site. The procedure that is performed is determined, in part, by the urgency
of the situation, the skill and experience of the surgeon, and the patient's desire for
future fertility. In most cases, hysterectomy should be performed. In selected
cases, repair of the rupture can be attempted. When rupture occurs in the body of
the uterus, hemorrhage may be easily controlled. When the rupture site is in the
anterior lower segment, bladder rupture must be ruled out by clearly mobilizing
and inspecting the bladder to ensure that it is intact. This avoids injury on repair of
the defect as well. A lower segment lateral rupture can cause transection of the
uterine vessels. The vessels can retract toward the pelvic side wall, and the site of
bleeding must be isolated before placing clamps to avoid injury to the ureter and
iliac vessels. Typically, longitudinal tears, especially those in a lateral position,
should be treated by hysterectomy, whereas low transverse tears may be repaired.
If a repair rather than hysterectomy is performed in a patient who does not desire
future fertility, a bilateral tubal ligation should be performed. Patients who have
uterine repairs should be counseled regarding

433

15

their risk for repeat rupture with subsequent pregnancies. Steth reported on 13
patients who had uterine rupture repair with 21 subsequent pregnancies. Four
patients experienced recurrent uterine rupture for a rate of 4.3%. This is in
contrast to the rate of 19% reported by Aguero and Kizer in the same year.
Clearly, the risk for rupture is high and most likely depends on the site and extent
of myometrial damage.
[35]

[1]

In instances of uterine rupture, an awareness of risk factors, a recognition of

clinical signs and symptoms, and prompt surgical intervention are the keys to
optimal maternal and perinatal outcomes.
References
1. Aguero

O, Kizer S: Obstetric prognosis of the repair of uterine rupture. Surg Gynecol Obstet
127:528-530, 1968 Citation
2. American

College of Obstetrics and Gynecologists: Automobile passenger restraints for children

and pregnant women. American College of Obstetrics and Gynecologists. Technical Bulletin No.
74, December 1983
3. Arbab

F, Boulieu D, Bied V, et al: Uterine rupture in first or second trimester of pregnancy after
in vitro fertilization and embryo transfer. Hum Reprod 11:1120-1122, 1996 Abstract
4. Arcangeli

S, Pasquarette MM: Gravid uterine rupture after myolysis. Obstet Gynecol 89(5 part
2):857, 1997 Citation
5. Basbug

M, Soyuer I, Aygen E: Placenta accreta associated with rupture of a rudimentary horn

pregnancy. Int J Gynecol Obstet 57:199-201, 1997
6. Beckmann

CRB, Byler M, Jackson K: Increasing baseline intrauterine pressure associated with

impending spontaneous uterine rupture. Int J Gynecol Obstet 58:239-240, 1997
7. Bennett

BB: Uterine rupture during induction of labor at term with intravaginal misoprostol.
Obstet Gynecol 89:832-833, 1997 Abstract
8. Chapman

SJ, Crispens M, Owen J, et al: Complications of midtrimester pregnancy termination:

The effect of prior cesarean delivery. Am J Obstet Gynecol 175:889-892, 1996 Full Text
9. Dayann

SS, Schwalbe SS: The use of small-dose intravenous nitroglycerine in a case of uterine
inversion. Anesth Analg 82:1091-1093, 1996 Citation
10. DeSimmone

CA, Norris MC, Leighton BL: Intravenous nitroglycerine aids manual extraction
of a retained placenta. Anesthesiology 73:787, 1990 Citation
11. Farmer

RM, Kirschbaum T, Potter D, et al: Uterine rupture during trial of labor after previous
cesarean section. Am J Obstet Gynecol 165:996-1001, 1991 Abstract

16

12. Fuchs

K, Peretz BA, Marcovici R, et al: The "grand multipara"--Is it a problem? A review of

5785 cases. Int J Gynaecol Obstet 23:321-326, 1985 Abstract
13. Gilstrap

LC, Ramin SM: Postpartum hemorrhage. Clin Obstet Gynecol 37:824-830, 1994

Citation
14. Gurgan

T, Yarali H, Urman B, et al: Uterine rupture following hysteroscopic lysis of synechiae

due to tuberculosis and uterine perforation. Hum Reprod 11:291-293, 1996 Abstract
15. Kitchin

J, Thiagaraja H, May H, et al: Puerperal inversion of the uterus. Am J Obstet Gynecol

123:51-58, 1975 Abstract
16. Kupferminc

MJ, Gull I, Bar-Am A, et al: Intrauterine irrigation with prostaglandin F 2 -alpha for
management of severe postpartum hemorrhage. Acta Obstet Gynecol Scand 77:548-550, 1998
Abstract
17. Langton

J, Fishwick K, Kumar B, et al: Spontaneous rupture of an unscarred gravid uterus at 32

weeks' gestation. Hum Reprod 12:2066-2067, 1997 Citation
18. Miller

DA, Diaz F, Paul RH: Vaginal birth after cesarean: A 10-year experience. Obstet Gynecol
84:255-258, 1994 Abstract
19.

434

Miller DA, Goodwin J, Gherman RB, et al: Intrapartum rupture of the unscarred uterus. Obstet
Gynecol 89:671-673, 1997 Abstract
20. Ogueh

O, Ayida G: Acute uterine inversion: A new technique of hydrostatic replacement. Br J

Obstet Gynaecol 104:951-952, 1997 Citation
21. Oleen

MA, Mariano JP: Controlling refractory atonic postpartum hemorrhage. Am J Obstet

Gynecol 162:205-208, 1990 Abstract
22. Ouzounian

JG, Miller DA, Paul RH: Amnioinfusion in women with previous cesarean births: A
preliminary report. Am J Obstet Gynecol 174:783-786, 1996 Full Text
23. Ozeren

M, Ulusoy M, Uyanik E: First-trimester spontaneous uterine rupture after traditional

myomectomy: Case report. Isr J Med Sci 33:752-753, 1997 Abstract
24. Pearlman

MD, Tintinalli JE, Lorenz RP: Blunt trauma during pregnancy. N Engl J Med
323:1609-1613, 1990 Citation
25. Pelosi

MA III, Pelosi MA: Spontaneous uterine rupture at thirty-three weeks subsequent to

previous superficial laparoscopic myomectomy. Am J Obstet Gynecol 177:1547-1549, 1997 Full
Text
26. Peng ATC,

Gorman RS, Shulman SM, et al: Intravenous nitroglycerine for uterine relaxation in

17

the postpartum patient with retained placenta. Anesthesiology 71:172-173, 1989 Citation
27. Platt

LD, Druzin ML: Acute puerperal inversion of the uterus. Am J Obstet Gynecol 141:187190, 1981 Citation
28. Rodriguez

MH, Masaki DI, Phelan JP, et al: Uterine rupture: Are intrauterine pressure catheters
useful in the diagnosis? Am J Obstet Gynecol 161:666-669, 1989 Abstract
29. Rolen

AC, Choquette AJ, Semmens JP: Rudimentary uterine horn: Obstetric and gynecologic
implications. Obstet Gynecol 27:806-813, 1966 Citation
30. Rozenberg

P, Goffinet F, Philippe HJ, et al: Ultrasonographic measurement of lower uterine

segment to assess risk of detects of scarred uterus. Lancet 347:281-284, 1996 Abstract
31. Ruddick

V, Niv D, Hetman-Peri M, et al: Epidural analgesia for planned vaginal delivery

following previous cesarean section. Obstet Gynecol 64:621-623, 1984 Abstract
32. Sciscione

AC, Jguyen L, Manley JS, et al: Uterine rupture during preinduction cervical ripening
with misoprostol in a patient with previous cesarean delivery. Aust N Z J Obstet Gynaecol 38:96,
1998 Abstract
33. Shah-Hosseini

R, Evrard JR: Puerperal uterine inversion. Obstet Gynecol 73:567-570, 1989

Abstract
34. Sher

G: Correction of postpartum utrine inversion by the application of intravaginal hydrostatic

pressure. Am J Obstet Gynecol 134:601-602, 1979 Citation
35. Steth

SS: Results of treatment of rupture of the uterus by suturing. J Obstet Gynaecol Br

Commonw 75:55-58, 1968 Citation
36. Suner

S, Jagminas L, Piepert JF, et al: Fatal spontaneous rupture of a gravid uterus: Case report
and literature review of uterine rupture. J Emerg Med 14:181-185, 1996 Abstract
37. Sweeten

KM, Graves WK, Athanassiou A: Spontaneous rupture of the unscarred uterus. Am J

Obstet Gynecol 172:1851-1856, 1995 Full Text
38. Watson

P, Besch N, Watson A: Management of acute and subacute puerperal inversion of the

uterus. Obstet Gynecol 55:12-16, 1980 Abstract
39. Wing

DA, Lovett K, Paul RH: Disruption of prior uterine incision following misoprostol for
labor induction in women with previous cesarean delivery. Obstet Gynecol 91:828-830, 1998
Abstract
40. Zisow

DL: Uterine rupture as a cause of shoulder dystocia. Obstet Gynecol 87:818-819, 1996

Abstract
41. Zorlu

CG, Turan C, Isik AZ, et al: Emergency hysterectomy in modern obstetric practice. Acta
Obstet Gynecol Scand 77:186-190, 1998 Abstract

18

MD Consult L.L.C. http://www.mdconsult.com

Bookmark URL: /das/journal/view/21285679/N/10889036?ja=149741&PAGE=1.html&ANCHOR=top&source=MI

19