Postpartum Hemorrhage

Background
Postpartum hemorrhage (PPH) is the leading cause of
maternal mortality. All women who carry a pregnancy
beyond 20 weeks gestation are at risk for PPH and its
sequelae. Although maternal mortality rates have declined
greatly in the developed world, PPH remains a leading cause
of maternal mortality elsewhere.

woman who has preexisting anemia, an underlying cardiac

condition, or a volume-contracted condition secondary to
dehydration or preeclampsia. For these reasons, various
authors have suggested that PPH should be diagnosed with
any amount of blood loss that threatens the hemodynamic
stability of the woman.
The diagnosis of PPH is usually reserved for pregnancies
that have progressed beyond 20 weeks gestation.
Deliveries at less than 20 weeks gestational age are
spontaneous abortions. Bleeding related to spontaneous
abortion may have etiologies and management in common
with those for PPH.
Epidemiology
Frequency

Postpartum
hemorrhage. Maternal morbidity by subregion, 1995.
The direct pregnancy-related maternal mortality rate in
the United States is approximately 7-10 women per
100,000 live births. National statistics suggest that
approximately 8% of these deaths are caused by PPH. [1] In
industrialized countries, PPH usually ranks in the top 3
causes of maternal mortality, along with embolism and
hypertension. In the developing world, several countries
have maternal mortality rates in excess of 1000 women per
100,000 live births, and World Health Organization
statistics suggest that 25% of maternal deaths are due to
PPH, accounting for more than 100,000 maternal deaths per
year.[2] The most recent Practice Bulletin from the
American College of Obstetricians and Gynecologists places
the estimate at 140,000 maternal deaths per year or 1
woman every 4 minutes.[3]
The rate of PPH increased from 1.5% in 1999 to 4.1% in
2009, and the rate of atonic PPH rose from 1% in 1999 to
3.4% in 2009. The risk of total PPH with a morbidly
adherent placenta was markedly higher.[4]
Problem
The definition of PPH is somewhat arbitrary and
problematic. PPH is defined as blood loss of more than 500
mL following vaginal delivery or more than 1000 mL
following cesarean delivery.[5] A loss of these amounts
within 24 hours of delivery is termed early or primary PPH,
whereas such losses are termed late or secondary PPH if
they occur 24 hours after delivery. This article focuses on
early PPH.
Estimates of blood loss at delivery are subjective and
generally inaccurate. Studies have suggested that
caregivers consistently underestimate actual blood loss.
Another proposal suggests using a 10% fall in hematocrit
value to define PPH, but this change is dependent on the
timing of the test and the amount of fluid resuscitation
given.[6] More importantly, the diagnosis would be
retrospective, perhaps useful for research but not so in
the clinical setting.
Another consideration is the differing capacities of
individual patients to cope with blood loss. A healthy woman
has a 30-50% increase in blood volume in a normal singleton
pregnancy and is much more tolerant of blood loss than a

United States and industrialized countries

The frequency of PPH is related to the management of the
third stage of labor. This is the period from the completed
delivery of the baby until the completed delivery of the
placenta. Data from several sources, including several large
randomized trials performed in industrialized countries,
indicate that the prevalence rate of PPH of more than 500
mL is approximately 5% when active management is used
versus 13% when expectant management is used. The
prevalence rate of PPH of more than 1000 mL is
approximately 1% when active management is used versus
3% when expectant management is used.[7, 8] See Medscape
Reference article Management of the Third Stage of
Labor.
Developing countries
The increased frequency of PPH in the developing world is
more likely reflected by the rates given above for
expectant management because of the lack of widespread
availability of medications used in the active management
of the third stage.[2] A number of factors also contribute to
much less favorable outcomes of PPH in developing
countries. The first is a lack of experienced caregivers who
might be able to successfully manage PPH if it occurred.
Additionally, the same drugs used for prophylaxis against
PPH in active management of the third stage are also the
primary agents in the treatment of PPH. Lack of blood
transfusion services, anesthetic services, and operating
capabilities also plays a role. Finally, the previously
mentioned comorbidities are more commonly observed in
developing countries and combine to decrease a woman's
tolerance of blood loss.
Etiology
PPH has many potential causes, but the most common, by a
wide margin, is uterine atony, ie, failure of the uterus to
contract and retract following delivery of the baby. PPH in
a previous pregnancy is a major risk factor and every
effort should be made to determine its severity and cause.
In a recent randomized trial in the United States,
birthweight,
labor
induction
and
augmentation,
chorioamnionitis, magnesium sulfate use, and previous PPH
were all positively associated with increased risk of PPH. [9]
In a large, population-based study, significant risk factors,
identified using multivariable analysis, were as follows:

Retained placenta (OR 3.5, 95% CI 2.1-5.8)

Failure to progress during the second stage of
labor (OR 3.4, 95% CI 2.4-4.7)
Placenta accreta (OR 3.3, 95% CI 1.7-6.4)
Lacerations (OR 2.4, 95% CI 2.0-2.8)
Instrumental delivery (OR 2.3, 95% CI 1.6-3.4)
Large-for-gestational-age (LGA) newborn (OR 1.9,
95% CI 1.6-2.4)
Hypertensive disorders (OR 1.7, 95%CI 1.2-2.1)
Induction of labor (OR 1.4, 95%CI 1.1-1.7)
Augmentation of labor with oxytocin (OR 1.4, 95%
CI 1.2-1.7). [10]
PPH is also associated with obesity. In a study by Blomberg,
the risk of atonic uterine hemorrhage rapidly increased
with increasing BMI; in women with a BMI over 40, the risk
was 5.2% with normal delivery and 13.6% with instrumental
delivery.[11]
As a way of remembering the causes of PPH, several
sources have suggested using the 4 T s as a mnemonic:
tone, tissue, trauma, and thrombosis.[12]
Tone
Uterine atony and failure of contraction and retraction of
myometrial muscle fibers can lead to rapid and severe
hemorrhage and hypovolemic shock. Overdistension of the
uterus, either absolute or relative, is a major risk factor
for atony. Overdistension of the uterus can be caused by
multifetal gestation, fetal macrosomia, polyhydramnios, or
fetal abnormality (eg, severe hydrocephalus); a uterine
structural abnormality; or a failure to deliver the placenta
or distension with blood before or after placental delivery.
Poor myometrial contraction can result from fatigue due to
prolonged labor or rapid forceful labor, especially if
stimulated. It can also result from the inhibition of
contractions by drugs such as halogenated anesthetic
agents, nitrates, nonsteroidal anti-inflammatory drugs,
magnesium sulfate, beta-sympathomimetics, and nifedipine.
Other causes include placental implantation site in the
lower
uterine
segment,
bacterial
toxins
(eg,
chorioamnionitis, endomyometritis, septicemia), hypoxia due
to hypoperfusion or Couvelaire uterus in abruptio placentae,
and hypothermia due to massive resuscitation or prolonged
uterine exteriorization. Recent data suggest that grand
multiparity is not an independent risk factor for PPH.
Tissue
Uterine contraction and retraction leads to detachment
and expulsion of the placenta. Complete detachment and
expulsion of the placenta permits continued retraction and
optimal occlusion of blood vessels.
Retention of a portion of the placenta is more common if
the placenta has developed with a succenturiate or
accessory lobe. Following delivery of the placenta and when
minimal bleeding is present, the placenta should be
inspected for evidence of fetal vessels coursing to the
placental edge and abruptly ending at a tear in the
membranes. Such a finding suggests a retained
succenturiate lobe.

The placenta is more likely to be retained at extreme

preterm gestations (especially < 24 wk), and significant
bleeding can occur. This should be a consideration in all
deliveries at very early gestations, whether they are
spontaneous or induced. Recent trials suggest that the use
of misoprostol for second trimester termination of
pregnancy leads to a marked reduction in the rate of
retained placenta when compared to techniques using the
intrauterine instillation of prostaglandin or hypertonic
saline.[13] One such trial reported rates of retained placenta
requiring D&C of 3.4% with oral misoprostol compared to
22.4% using intra-amniotic prostaglandin (p=0.002). [14]
Failure of complete separation of the placenta occurs in
placenta accreta and its variants. In this condition, the
placenta has invaded beyond the normal cleavage plane and
is abnormally adherent. Significant bleeding from the area
where normal attachment (and now detachment) has
occurred may mark partial accreta. Complete accreta in
which the entire surface of the placenta is abnormally
attached, or more severe invasion (placenta increta or
percreta), may not initially cause severe bleeding, but it
may develop as more aggressive efforts are made to
remove the placenta. This condition should be considered
possible whenever the placenta is implanted over a previous
uterine scar, especially if associated with placenta previa.
All patients with placenta previa should be informed of the
risk of severe PPH, including the possible need for
transfusion and hysterectomy.
Finally, retained blood may cause uterine distension and
prevent effective contraction.
Trauma
Damage to the genital tract may occur spontaneously or
through manipulations used to deliver the baby. Cesarean
delivery results in twice the average blood loss of vaginal
delivery. Incisions in the poorly contractile lower segment
heal well but are more reliant on suturing, vasospasm, and
clotting for hemostasis.
Uterine rupture is most common in patients with previous
cesarean delivery scars. Routine transvaginal palpation of
such scars is no longer recommended. Any uterus that has
undergone a procedure resulting in a total or thick partial
disruption of the uterine wall should be considered at risk
for rupture in a future pregnancy. This admonition includes
fibroidectomy; uteroplasty for congenital abnormality;
cornual or cervical ectopic resection; and perforation of
the
uterus
during
dilatation,
curettage,
biopsy,
hysteroscopy, laparoscopy, or intrauterine contraceptive
device placement.
Trauma may occur following very prolonged or vigorous
labor, especially if the patient has relative or absolute
cephalopelvic disproportion and the uterus has been
stimulated with oxytocin or prostaglandins. Using
intrauterine pressure monitoring may lessen this risk.
Trauma also may occur following extrauterine or
intrauterine manipulation of the fetus. The highest risk is
probably associated with internal version and extraction of
a second twin; however, uterine rupture may also occur

secondary to external version. Finally, trauma may result

secondary to attempts to remove a retained placenta
manually or with instrumentation. The uterus should always
be controlled with a hand on the abdomen during any such
procedure. An intraumbilical vein saline/oxytocin or
saline/misoprostol injection may reduce the need for more
invasive removal techniques.[7]
Cervical laceration is most commonly associated with
forceps delivery, and the cervix should be inspected
following all such deliveries. Assisted vaginal delivery
(forceps or vacuum) should never be attempted without the
cervix being fully dilated. Cervical laceration may occur
spontaneously. In these cases, mothers have often been
unable to resist bearing down before full cervical
dilatation. Rarely, manual exploration or instrumentation of
the uterus may result in cervical damage. Very rarely, the
cervix is purposefully incised at the 2- and/or 10-oclock
positions to facilitate delivery of an entrapped fetal head
during a breech delivery (Dhrssen incision).
Vaginal sidewall laceration is also most commonly associated
with operative vaginal delivery, but it may occur
spontaneously, especially if a fetal hand presents with the
head. Lacerations may occur during manipulations to resolve
shoulder dystocia. Lacerations often occur in the region
overlying the ischial spines. The frequency of sidewall and
cervical lacerations has probably decreased in recent years
because of the reduction in the use of midpelvic forceps
and, especially, midpelvic rotational procedures.
Lower vaginal trauma occurs either spontaneously or
because of episiotomy. Spontaneous lacerations usually
involve the posterior fourchette; however, trauma to the
periurethral and clitoral region may occur and can be
problematic.
Thrombosis
In the immediate postpartum period, disorders of the
coagulation system and platelets do not usually result in
excessive bleeding; this emphasizes the efficiency of
uterine contraction and retraction for preventing
hemorrhage.[5] Fibrin deposition over the placental site and
clots within supplying vessels play a significant role in the
hours and days following delivery, and abnormalities in
these areas can lead to late PPH or exacerbate bleeding
from other causes, most notably, trauma.
Abnormalities
may
be
preexistent
or
acquired.
Thrombocytopenia may be related to preexisting disease,
such as idiopathic thrombocytopenic purpura, or acquired
secondary to HELLP syndrome (hemolysis, elevated liver
enzymes, and low platelet count), abruptio placentae,
disseminated intravascular coagulation (DIC), or sepsis.
Rarely, functional abnormalities of platelets may also occur.
Most of these are preexisting, although sometimes
previously undiagnosed.
Preexisting abnormalities of the clotting system, such as
familial hypofibrinogenemia and von Willebrand disease,
may occur and should be considered. An expert panel
recently issued guidelines to aid in the diagnosis and
management of women with such conditions.[15] An underlying

bleeding disorder should be considered in a woman with any

of the following: menorrhagia since menarche, family
history of bleeding disorders, personal history of notable
bruising without known injury, bleeding from the oral cavity
or GI tract without obvious lesion, or epistaxis of longer
than 10 minutes duration (possibly requiring packing or
cautery). If a bleeding disorder is suspected, consultation
is suggested.
Acquired abnormalities are more commonly problematic.
DIC related to abruptio placentae, HELLP syndrome,
intrauterine fetal demise, amniotic fluid embolism, and
sepsis may occur. Fibrinogen levels are markedly elevated
during pregnancy, and a fibrinogen level that would be in
the reference range in the nonpregnant state should be
viewed with suspicion in the aforementioned clinical
scenarios.
Finally, dilutional coagulopathy may occur following massive
PPH and resuscitation with crystalloid and packed red blood
cells (PRBCs).
Risk factors and associated conditions for PPH are listed
above; however, a large number of women experiencing PPH
have no risk factors. Different etiologies may have common
risk factors, and this is especially true of uterine atony and
trauma of the lower genital tract. PPH usually has a single
cause, but more than one cause is also possible, most likely
following a prolonged labor that ultimately ends in an
operative vaginal birth.
Prevention
High-quality evidence suggests that active management of
the third stage of labor reduces the incidence and severity
of PPH.[8] Active management is the combination of (1)
uterotonic
administration
(preferably
oxytocin)
immediately upon delivery of the baby, (2) early cord
clamping and cutting, and (3) gentle cord traction with
uterine countertraction when the uterus is well contracted
(ie, Brandt-Andrews maneuver).
The value of active management in the prevention of PPH
cannot be overstated (see Management of the Third Stage
of Labor). The use of active versus expectant management
in the third stage was the subject of 5 randomized
controlled trials (RCTs) and a Cochrane meta-analysis. [16, 7,
8]
These trials included more than 6000 women, and the
findings are summarized in Table 1.
Table 1. Benefits of Active Management Versus Expectant
Management (Open Table in a new window)
Outcome

PPH
mL

of

Control Relative
Rate, % Risk
500 14

PPH of 1000 2.6

mL

95%
CI*

NNT 95%
CI

0.38

0.320.46

12

10-14

0.33

0.210.51

55

4291

Hemoglobin
9 g/dL

< 6.1

Blood
transfusion
Therapeutic
uterotonics
*CI:

0.4

0.290.55

27

2040

2.3

0.44

0.220.53

67

48111

17

0.2

0.170.25

6-8

Confidence

NNT:

Number

needed

interval

to

treat

The findings show a conclusive benefit for active

management, with an approximate 60% reduction in the
occurrence of PPH greater than or equal to 500 mL and
1000 mL, hemoglobin concentration of less than 9 g/dL at
24-48 hours after delivery, and the need for blood
transfusion. An 80% reduction in the need for therapeutic
uterotonic agents was noted. These results were all highly
significant as indicated by the 95% confidence interval
figures. The results indicate that for every 12 patients
receiving active rather than physiological management, one
PPH would be prevented. For every 67 patients so treated,
one patient would avoid transfusion with blood products.
One concern regarding active management is that retained
placenta may occur more frequently. This concern is not
supported by the trials. This is especially true if oxytocin
is used as the uterotonic.[17, 18] The US RCTs mentioned
above compared the use of active management protocols in
which the oxytocin was administered either immediately
after delivery of the baby or immediately after delivery of
the placenta. The authors stated that no statistically
significant difference was noted in the PPH rate and that
delaying administration until after placental delivery was
justified.
Noteworthy is the finding that early administration of
oxytocin (before placental delivery) did not increase the
rate of retained placenta. Additionally, the trial showed
trends toward a benefit for early administration of
oxytocin, including a 25% reduction in PPH and a 50%
reduction in the need for transfusion.[9] These findings are
clearly consistent with the previous RCTs and the early
administration of oxytocin with delivery of the baby is
strongly recommended.
They also stated that administration with delivery of the
baby did not increase the rate of retained placenta, but
they did not point out that this finding clearly supports
early administration. Additionally, the trial showed trends
toward a benefit for early administration of oxytocin,
including a 25% reduction in PPH and a 50% reduction in
the need for transfusion.[9] These differences may be due
to chance, but, given the results of the previous RCTs, the
administration of oxytocin with delivery of the baby would
seem to be strongly warranted.

Following delivery, administering a uterotonic drug that

lasts at least 2-3 hours is reasonable. [3] This could be 10 U
of oxytocin in 500 mL of intravenous fluid by continuous
drip, 200-250 mcg of ergonovine intramuscularly, or 250
mcg of 15-methyl prostaglandin F2-alpha (carboprost
[Hemabate]) intramuscularly. The use of misoprostol and a
long-acting oxytocin analogue (carbetocin) is being studied
for this use.[19] It has been suggested that distribution of
misoprostol ahead of childbirth in communities where home
birth is unavoidable can be an effective approach. However,
there is insufficient evidence to support this and there are
concerns that the drug might be used for starting labor or
terminating pregnancy.[20]
The presence of significant antepartum or intrapartum risk
factors warrants delivery in maternity units that have
readily available resources to deal with massive obstetric
hemorrhage. All medical facilities should have protocols for
dealing with PPH and obstetric hemorrhage.
Pathophysiology
Over the course of a pregnancy, maternal blood volume
increases by approximately 50% (from 4 L to 6 L). The
plasma volume increases somewhat more than the total RBC
volume, leading to a fall in the hemoglobin concentration
and hematocrit value. The increase in blood volume serves
to fulfill the perfusion demands of the low-resistance
uteroplacental unit and to provide a reserve for the blood
loss that occurs at delivery.[6]
At term, the estimated blood flow to the uterus is 500800 mL/min, which constitutes 10-15% of cardiac output.
Most of this flow traverses the low-resistance placental
bed. The uterine blood vessels that supply the placental
site traverse a weave of myometrial fibers. As these fibers
contract following delivery, myometrial retraction occurs.
Retraction is the unique characteristic of the uterine
muscle to maintain its shortened length following each
successive contraction. The blood vessels are compressed
and kinked by this crisscross latticework, and, normally,
blood flow is quickly occluded. This arrangement of muscle
bundles has been referred to as the "living ligatures" or
"physiologic sutures" of the uterus.[5]
Uterine atony is a failure of the uterine myometrial fibers
to contract and retract. This is the most important cause
of PPH and usually occurs immediately following delivery of
the baby, up to 4 hours after the delivery. Trauma to the
genital tract (ie, uterus, uterine cervix, vagina, labia,
clitoris) in pregnancy results in significantly more bleeding
than would occur in the nonpregnant state because of
increased blood supply to these tissues. The trauma
specifically related to the delivery of the baby, either
vaginally in a spontaneous or assisted manner or by
cesarean delivery, can also be substantial and can lead to
significant disruption of soft tissue and tearing of blood
vessels.
Presentation
Although the presentation of PPH is most often dramatic,
bleeding may be slower and seemingly less noteworthy but
may still ultimately result in critical loss and shock. This is
more likely to be true of bleeding secondary to retained

tissue or trauma. Nursing practices for routine care in the

postpartum period should include close observation and
documentation of maternal vital signs and condition, vaginal
blood loss, and uterine tone and size. The uterus should be
periodically massaged to express any clots that have
accumulated in the uterus or vagina.[21]
The usual presentation of PPH is one of heavy vaginal
bleeding that can quickly lead to signs and symptoms of
hypovolemic shock. This rapid blood loss reflects the
combination of high uterine blood flow and the most
common cause of PPH, ie, uterine atony. Blood loss is usually
visible at the introitus, and this is especially true if the
placenta has delivered. If the placenta remains in situ, then
a significant amount of blood can be retained in the uterus
behind a partially separated placenta, the membranes, or
both.
Even after placental delivery, blood may collect in an atonic
uterus. For this reason, the uterine size and tone should be
monitored throughout the third stage and in the so-called
fourth stage, following delivery of the placenta. This is
accomplished by gently palpating the uterine fundus. If the
cause of bleeding is not uterine atony, then blood loss may
be slower and clinical signs and symptoms of hypovolemia
may develop over a longer time frame. Bleeding from
trauma may be concealed in the form of hematomas of the
retroperitoneum, broad ligament or lower genital tract, or
abdominal cavity. The clinical findings in hypovolemia are
listed in Table 2.
Table 2. Clinical Findings in Obstetric Hemorrhage[22] (Open
Table in a new window)
Blood
Volume
Loss

Blood
Pressure
(systolic)

500-1000 Normal
mL
(1015%)

Symptoms
Signs

and Degree
Shock

Palpitations,
tachycardia,
dizziness

of

Compensated

1000Slight
fall Weakness,
1500 mL (80-100 mm tachycardia,
(15-25%) Hg)
sweating

Mild

1500Moderate
Restlessness,
2000 mL fall (70-80 pallor, oliguria
(25-35%) mm Hg)

Moderate

2000Marked fall Collapse,

air Severe
3000 mL (50-70 mm hunger, anuria
(35-50%) Hg)
Two important facts are worth bearing in mind. The first is
that caregivers consistently underestimate visible blood
loss by as much as 50%. The volume of any clotted blood
represents half of the blood volume required to form the
clots. The second is that most women giving birth are
healthy and compensate for blood loss very well. This,
combined with the fact that the most common birthing
position is some variant of semirecumbent with the legs

elevated, means that symptoms of hypovolemia may not

develop until a large volume of blood has been lost.[23]
Rapid recognition and diagnosis of PPH is essential to
successful management. Resuscitative measures and the
diagnosis and treatment of the underlying cause must occur
quickly before sequelae of severe hypovolemia develop. The
major factor in the adverse outcomes associated with
severe hemorrhage is a delay in initiating appropriate
management.
Contraindications
Other than nonconsent, absence of surgical expertise or
allergy to specific agents, the techniques used in the
management of PPH have no absolute contraindications. The
vast majority of cases (>99%) are handled without what
would traditionally be considered surgical intervention. In
most cases, surgical intervention is a last resort. An
exception is those cases in which uterine rupture or genital
tract trauma has occurred and surgical repair is clearly
indicated.
Transfusion of packed RBC and other blood products may
be necessary in the management of severe PPH. Some
women may refuse such an intervention on personal or
religious grounds. The most widely known group that does
not accept blood transfusion are Jehovahs Witnesses. The
wishes of the patient must be respected in this matter.
Significant increased risk of maternal mortality due to
obstetric hemorrhage has been noted in the Jehovahs
Witness population. The increased risk of death was found
to be 6-fold in a recent national review of 23 years
experience in the Netherlands and 44-fold in a much
smaller study of 391 deliveries in a US tertiary level
center.[24, 25] Discussion regarding the implications of such
prohibitions should be undertaken early in the pregnancy
whenever possible and subsequently reviewed.
In almost all cases in which surgical management is chosen
after medical management has failed, not attempting
surgery would lead to maternal death. Even an unstable
condition cannot be considered a true contraindication. One
type of surgery may be chosen over another, but when
medical management has failed, surgery is most likely the
only life-saving option
Laboratory Studies
In the antenatal period, a CBC is performed. Findings alert
caregivers to women with anemia and indicate interventions
to attempt to improve the hemoglobin level. Hemoglobin
levels below 10-10.5 g/dL have been associated with
adverse pregnancy outcome, and the rare patient with
thrombocytopenia will be identified.[26] Women admitted to
labor and delivery units should have a CBC performed if one
has not been performed recently. All women experiencing
antepartum bleeding should have a CBC.
Blood typing and antibody screening tests may also have
been performed in the antenatal period. If the results are
known and no blood group antibodies were present, then the
test may not need to be repeated upon admission. However,
many facilities routinely repeat this test (or at least draw a
sample to be held in the blood bank) in case blood is

urgently needed. The time frame between a request for

blood products of various types and their availability should
be known. In a patient at high risk of PPH, crossmatching
of 2-6 U of blood before delivery is prudent. Examples
include previous severe PPH, placenta previa, possible
placenta accreta, multiple previous cesarean deliveries,
known coagulation disorders, or severe thrombocytopenia.
The American Association of Blood Banks currently
recommends retesting women at high risk every 72 hours
for the development of antibodies.

to visualize other sites. For this reason, and because of the

rapidity of blood loss secondary to atony, management and
control of atony is paramount.
If the placenta has been delivered, inspection findings
suggest whether portions of it have been retained. If it is
undelivered or if retained clots or placental fragments are
distending the uterus and bleeding is persisting despite
appropriate ongoing treatment, manual exploration and
removal should be undertaken. This is simultaneously
therapeutic by emptying the uterus and permitting
contraction while also aiding in the diagnosis of placenta
accreta and uterine rupture. Cervical and vaginal
lacerations may also be palpated at this time.

Coagulation studies are no longer routinely performed in

pregnant women, including those about to undergo cesarean
delivery. Instead, history is relied on to uncover previous
episodes suggesting preexisting disorders of hemostasis.

If uterine atony has been controlled and bleeding from the

uterus is minimal, careful inspection of the lower genital
tract reveals bleeding sites in this area. Palpation and
inspection may also reveal hematomas that require
treatment. The cervix and vagina should be completely
visualized following all operative vaginal deliveries.

Once the diagnosis of PPH has been made, a CBC

and baseline coagulation studies should be performed.

Initially, the hemoglobin value does not reflect the

amount of blood loss.

A crossmatch for 4-6 U of PRBCs should be

requested and consideration given to notifying the blood
bank of the possible need for additional blood products in
short order.

Initial coagulation study findings are usually within

reference ranges; however, abnormalities may be noted.
This is most common when PPH is preceded by abruptio
placenta, HELLP syndrome, fatty liver of pregnancy,
intrauterine fetal demise, embolic events, or septicemia.
If the international normalized ratio and/or activated
partial thromboplastin time are elevated, the use of
fibrinogen, a thrombin time measurement, D-dimers, and a
blood film should be considered. In late pregnancy,
fibrinogen levels are 2-3 times the upper reference range
limit in the nonpregnant state, and a level within the
nonpregnant reference range should be viewed with caution
if the clinical picture suggests coagulopathy.

The onset of PPH is generally rapid. With proper diagnosis

and treatment, resolution usually occurs before further
laboratory work or imaging can be undertaken. In
experienced hands, bedside ultrasound may help reveal
clots or retained products; however, the treatment of PPH
includes manual exploration if bleeding persists. This
renders ultrasound redundant in the acute setting at a time
when treatment must not be delayed. Antenatal ultrasound
is indispensable for detecting high-risk patients with
predisposing factors for PPH, such as placenta previa, and
is becoming increasingly sensitive and specific in the
diagnosis of placenta accreta and its variants. Pelvic vessel
angiography is discussed in Treatment.
PPH usually manifests with such rapidity that diagnostic
procedures are almost entirely limited to a physical
examination of the involved structures.
Assessment of uterine tone and size is accomplished using a
hand resting on the fundus and palpating the anterior wall
of the uterus. The presence of a boggy uterus with either
heavy vaginal bleeding or increasing uterine size establishes
the diagnosis of uterine atony. The presence of uterine
atony and resulting hemorrhage usually prevents the
diagnosis of PPH from other causes because of an inability

Imaging Studies
The onset of PPH is generally rapid. With proper diagnosis
and treatment, resolution usually occurs before further
laboratory work or imaging can be undertaken. In
experienced hands, bedside ultrasound may help reveal
clots or retained products; however, the treatment of PPH
includes manual exploration if bleeding persists. This
renders ultrasound redundant in the acute setting at a time
when treatment must not be delayed. Antenatal ultrasound
is indispensable for detecting high-risk patients with
predisposing factors for PPH, such as placenta previa, and
is becoming increasingly sensitive and specific in the
diagnosis of placenta accreta and its variants. Pelvic vessel
angiography is discussed in Treatment.
Diagnostic Procedures
PPH usually manifests with such rapidity that diagnostic
procedures are almost entirely limited to a physical
examination of the involved structures.

Assessment of uterine tone and size is

accomplished using a hand resting on the fundus and
palpating the anterior wall of the uterus. The presence of
a boggy uterus with either heavy vaginal bleeding or
increasing uterine size establishes the diagnosis of
uterine atony. The presence of uterine atony and
resulting hemorrhage usually prevents the diagnosis of
PPH from other causes because of an inability to visualize
other sites. For this reason, and because of the rapidity
of blood loss secondary to atony, management and control
of atony is paramount.
If the placenta has been delivered, inspection
findings suggest whether portions of it have been
retained. If it is undelivered or if retained clots or
placental fragments are distending the uterus and
bleeding is persisting despite appropriate ongoing
treatment, manual exploration and removal should be
undertaken. This is simultaneously therapeutic by
emptying the uterus and permitting contraction while also
aiding in the diagnosis of placenta accreta and uterine

rupture. Cervical and vaginal lacerations may also be

palpated at this time.

If uterine atony has been controlled and bleeding

from the uterus is minimal, careful inspection of the
lower genital tract reveals bleeding sites in this area.
Palpation and inspection may also reveal hematomas that
require treatment. The cervix and vagina should be
completely visualized following all operative vaginal
deliveries.
Medical Therapy
The treatment of patients with PPH has 2 major
components: (1) resuscitation and management of obstetric
hemorrhage and, possibly, hypovolemic shock and (2)
identification and management of the underlying cause(s)
of the hemorrhage. For the purpose of discussion, these
components are discussed separately; however, remember
that successful management of PPH requires that both
components
be
simultaneously
and
systematically
addressed.
Management of obstetric hemorrhage
Patients with PPH require aggressive measures to restore
and maintain the circulating blood volume (and thereby
perfusion pressure) to vital structures. All medical units
involved in the care of pregnant women must have a
protocol for the management of severe obstetric
hemorrhage.[27] Management
of
massive
obstetric
hemorrhage outlines such a protocol for a pregnant woman
in either the antepartum or postpartum period.
[28]
Implement the protocol in a manner similar to a cardiac
arrest protocol, with the same attention to detail and
documentation. Just as with other advanced life support
protocols, conduct periodic reviews and practice drills.
The diagnosis of PPH is established by observing the
amount of bleeding and the patients clinical status. The
amount of blood lost and the patients level of
consciousness and vital signs are continually assessed. Once
the diagnosis is made, immediately notify appropriate staff
members. The magnitude and underlying cause of the
bleeding to some degree dictate which specialized
personnel are called, but a minimum of 1 obstetrician and 1
anesthetist is necessary. Skilled midwives or nurses can be
indispensable. Notifying blood transfusion services is
essential because the timely availability of blood products
is likely to be critical. As in a cardiac arrest, designate an
experienced person to document critical information and
times. Ensure the availability of an operating room. The
speed with which PPH occurs, becomes life-threatening,
and can be successfully managed with relatively simple
interventions sometimes makes it difficult to decide when
to institute the full protocol.
Fluid resuscitation
Fluid resuscitation of women experiencing obstetric
hemorrhage is sometimes overly conservative. Possible
reasons for this include (1) blood loss being generally
underestimated both in volume and rapidity, (2) women
initially compensating well for losses because of their good
health and the hypervolemia of pregnancy, (3) concerns
that overresuscitation leads to pulmonary edema, and (4)

failure to appreciate the dynamics of fluid shifts in the

body.
Immediately commence resuscitation. Raising the legs
improves venous return and is consistent with the
positioning used to diagnose and treat the underlying
causes of bleeding. Administer oxygen and obtain
intravenous access. All intravenous lines started on the
labor ward for other reasons must be placed with cannulas
of sufficient gauge if PPH develops. Twice as much fluid
can be infused through a 14-gauge intravenous line
compared with an 18-gauge intravenous line over the same
time period.[29] During labor, place at least 1 intravenous line
in women at risk for PPH; consider a second line in patients
at very high risk.
Perform the initial resuscitation with large volumes of
crystalloid solution, either normal saline (NS) or Lactated
Ringers solution (LRS), through peripheral intravenous
sites. Central venous access is not required for the vast
majority of patients with PPH, but do not delay establishing
such access if necessary. Draw blood for baseline
measurements at this time. NS is a reasonable solution in
the labor ward setting because of its low cost and
compatibility with most drugs and blood transfusions. The
risk of hyperchloremic acidosis is very low in the setting of
PPH. If large amounts (>10 L) of crystalloid are being
infused, a change to LRS can be considered.
Dextrose-containing solutions, such as 5% dextrose in
water or diluted NS in 5% dextrose in water, have no role
in the management of PPH. Remember that the loss of 1 L
of blood requires replacement with 4-5 L of crystalloid
because most of the infused fluid is not retained in the
intravascular space but instead shifts to the interstitial
space. This shift, along with oxytocin use, may result in
peripheral edema in the days following PPH. Healthy
kidneys easily excrete this excess fluid. Use wide-open
initial infusion rates, with the goal of infusing the required
replacement volume over minutes rather than hours. PPH of
up to 1500 mL in a healthy pregnant woman can usually be
managed by crystalloid infusion alone if the cause of
bleeding is arrested. Blood loss in excess of this usually
requires the addition of a PRBC transfusion.
Because a large portion of crystalloid fluid volume is lost to
the interstitial space, the use of colloids in resuscitation
has been examined. These solutions are largely retained
within the intravascular space and include albumin, dextran,
hydroxyethyl starch, and modified fluid gelatin. A metaanalysis in the Cochrane Library comparing resuscitation
with colloid solutions versus crystalloid favored the use of
crystalloids with respect to mortality.[30, 31]
For albumin or plasma protein fraction compared with NS,
18 trials reported data on mortality in 641 patients. The
pooled relative risk from these trials was 1.52 (95%
confidence interval, 1.08-2.13). The NS groups had a 1%
mortality rate, versus an 11% mortality rate in the colloid
group.
For dextran compared to NS, 8 trials compared reported
data on mortality in 668 patients. The pooled relative risk
was 1.24 (95% confidence interval, 0.94-1.65). Two other

recent meta-analyses on the same topic reached the same

conclusions.

ongoing. Hypocalcemia due to citrate intoxication is also

seldom observed.[32]

Large volumes of colloid solutions (>1000-1500 mL/d) can

have an adverse effect on hemostasis. No colloid solution
has been demonstrated to be superior to NS, and, because
of the expense and the risk of adverse effects with
colloids, crystalloid is recommended. Given these findings,
the authors recommend against the use of colloid solutions
in resuscitation outside the setting of an RCT.

Patients may refuse a transfusion of blood products based

on religious or other grounds. A patient's refusal of blood
products must be respected and must not be equated with
a desire for no intervention or be seen as an excuse for
suboptimal care. Several options, including the use of
autotransfusion, can be considered for the management of
these patients. Ensure that a care plan is in place
(seeTransfusion and Autotransfusion). An article by
Hughes et al reviewed the issues and management options
in patients who refuse transfusion. Clinicians should bear in
mind that the refusal may not extend to all related
products. Products that use recombinant technologies such
as human erythropoietin and activated factor VIIa are
usually acceptable.[33]

Blood transfusion
Order blood transfusions if blood loss is ongoing and
thought to be in excess of 2000 mL or if the patients
clinical status reflects developing shock despite aggressive
resuscitation. Data from various sources suggest that 1 in
16-40 women experiencing PPH requires a blood transfusion
if active third-stage management is used, whereas
approximately 1 in 9 requires a transfusion if expectant
management is used. Newer studies tend to have lower
transfusion rates than older studies.[8]
Whole blood is no longer available in most settings, and, for
many reasons, PRBCs are initially used with other blood
components and given only if indicated. Most medical units
have access to uncrossmatched O-type Rh-negative PRBCs
for catastrophic bleeding. In PPH, uncrossmatched ABOand Rh-compatible blood is usually available because a blood
group and antibody screen has already been performed.
Have full crossmatched blood available for transfusion
within 30 minutes. Clinicians must be aware of the
capabilities of their blood bank regarding timing, type, and
amount of blood products available in emergencies. Good
communication with the blood transfusion service is
essential, and the nature of the emergency and the
potential amount of blood products required must be
stressed.
The goal is to rapidly transfuse 2-4 U of PRBCs to replace
lost oxygen-carrying capacity and to restore circulating
volume. Administer the blood transfusion through a set
with an integrated filter, and use a blood warmer if the
infusion rate (>100 mL/min) or the total volume infused is
high. A rapid infusion set with an integrated warmer or a
pressure cuff may be used to increase the infusion rate.
PRBCs are very viscous, reducing the infusion rate. This
problem may be overcome by adding 100 mL of NS to each
unit. Do not use LRS for this purpose because the calcium
contained in the solution may cause clotting.
The risks of transfusion are well known and are covered
elsewhere (eg, seeTransfusion Reactions or Transfusion
and Autotransfusion), but they include infection,
transfusion reaction, and development of atypical
antibodies. Several other complications may be noted in
large-volume transfusions. The risk of hypothermia is
minimized by the use of blood warmers. Dilutional
coagulopathy may be observed and is discussed below.
Hyperkalemia and acidosis related to the use of stored
blood are theoretical risks but are seldom clinically
important if perfusion of vital organs is maintained.
Monitor electrolyte and acid-base status if the situation is

Coagulopathy
Women experiencing PPH do not usually have a preexisting
disorder of hemostasis; however, initial blood work includes
a coagulation screen and platelet count. In previously
healthy women, dilutional coagulopathy is not usually
observed until approximately 80% of the original blood
volume has been replaced. Regularly monitor hemostatic
test results in all women who require a massive transfusion.
If findings are abnormal in conjunction with ongoing
bleeding or oozing from puncture sites, mucous surfaces, or
wounds, additional blood products are required. Infuse
fresh frozen plasma (FFP), beginning with 4 U and following
with additional units to normalize the coagulation test
findings. Many authorities recommend the addition of 1 U
of FFP for every 5 U of PRBCs for patients who require
continued transfusion.
Thrombocytopenia is likely after 1.5-2 times the blood
volume has been replaced. Keep the platelet count more
than 50 X 109/L by using platelet transfusion. Each unit of
platelets increases the platelet count by approximately 10
X 109/L. (Platelets are usually given in packs of 5-6 U.) If
bleeding is continuing and the platelet count is less than 50
X 109/L, administer 10-12 U initially. If surgical
intervention is necessary, maintain the platelet count at
more than 80-100 X 109/L. Platelet preparations contain
some RBCs, and the administration of anti-D immunoglobulin
(RhoGAM, WinRho) is recommended for Rh-negative women
after the crisis has passed.[34]
If coagulation test results are abnormal from the onset of
PPH, strongly consider an underlying cause (eg, abruptio
placenta, HELLP syndrome, fatty liver of pregnancy,
intrauterine fetal demise, amniotic fluid embolus,
septicemia, preexisting disorder). Take specific steps to
treat the underlying cause and the hemostatic abnormality.
DIC may also develop if shock has led to marked
hypoperfusion of tissues, causing damage and release of
tissue thromboplastins. In such cases, laboratory test
results reveal that the D-dimer levels are elevated and
fibrinogen levels are very low, with a prolonged thrombin
time. The management of DIC is identical to that for a
patient with dilutional coagulopathy. Restoration and

maintenance of circulating volume along with blood product

replacement is essential.

1.
2.

Cryoprecipitate may be useful along with FFP because of

the markedly depressed fibrinogen levels. Cryoprecipitate
provides a more concentrated form of fibrinogen and other
clotting factors (VIII, XIII, von Willebrand factor) and is
faster to prepare in the blood bank. It is commonly given in
6- to 12-U doses and may also be helpful immediately
before any surgical intervention in patients with abnormal
coagulation test results. The use of heparin and
antifibrinolytic therapy is not recommended in women with
DIC of obstetric origin.

3.

Interest in and experience with recombinant activated

factor VIIa (RFVIIa) in massive hemorrhage situations is
growing. This experience has extended to severe
postpartum hemorrhage and results have been encouraging.
[35]
RFVIIa has been used when conventional medical
management has been unsuccessful and also when varying
degrees of surgical management, up to and including
hysterectomy have failed. Therapy is very expensive and
some suggest that use in less severe cases may be
potentially harmful.[36] RFVIIa may also be useful in cases
of severe PPH complicated by DIC.[37] Further study is
required before recombinant activated factor VII is put
into widespread use.
Seek the advice of a hematologist in cases of massive
transfusion or coagulopathy.
Response to resuscitation
Pay close attention to the patients level of consciousness,
pulse, blood pressure, and urine output during the course of
the management of massive hemorrhage. A urine output of
30 mL/h or more likely indicates adequate renal perfusion.
Closely monitor the CBC count, coagulation, and blood gas
values in addition to acid-base status. Pulse oximetry is
useful for evaluating tissue perfusion and oxygen
saturation. Frequent auscultation of the lung fields helps
detect pulmonary edema or the development of adult
respiratory distress syndrome. For patients in critical
condition with ongoing bleeding, the placement of a central
venous line may be helpful for resuscitation. Arterial line
placement also may aid in monitoring blood pressure and
allowing easy access for blood work. Few patients
experiencing PPH require such invasive monitoring; however,
consultation with appropriate specialists and placement in
an intensive care setting are preferred for those who do.
Management of massive obstetric hemorrhage
The following is a plan for managing massive obstetric
hemorrhage, adapted from Bonner.[28] The word order is a
useful mnemonic for remembering the basic outline.

Organization
Call
experienced
staff
(including
obstetrician and anesthetist).
2.
Alert the blood bank and hematologist.
3.
Designate a nurse to record vital signs,
urine output, and fluids and drugs administered.
4.
Place operating theater on standby.
Resuscitation
1.

lines.

Administer oxygen by mask.

Place 2 large-bore (14-gauge) intravenous

Take blood for crossmatch of 6 U PRBCs,

and obtain a CBC count, coagulation screen, urea
level, creatinine value, and electrolyte status.
4.
Begin immediate rapid fluid replacement
with NS or Ringer lactate solution.
5.
Transfuse with PRBCs as available and
appropriate.

Defective blood coagulation

1.
Order coagulation screen (International
Normalized
Ratio,
activated
partial
thromboplastin time) if fibrinogen, thrombin
time, blood film, and D-dimer results are
abnormal.
2.
Give FFP if coagulation test results are
abnormal and sites are oozing.
3.
Give
cryoprecipitate
if
abnormal
coagulation test results are not corrected with
FFP and bleeding continues.
4.
Give platelet concentrates if the platelet
count is less than 50 X 109/L and bleeding
continues.
5.
Use
cryoprecipitate
and
platelet
concentrates before surgical intervention.

Evaluation of response
1.
Monitor pulse, blood pressure, blood gas
status, and acid-base status, and consider
monitoring central venous pressure.
2.
Measure urine output using an indwelling
catheter.
3.
Order regular CBC counts and coagulation
tests to guide blood component therapy.

Remedy the cause of bleeding

1.
If antepartum, deliver the fetus and
placenta.
2.
If
postpartum,
use
oxytocin,
prostaglandin, or ergonovine.
3.
Explore and empty the uterine cavity, and
consider uterine packing.
4.
Examine the cervix and vagina, ligate any
bleeding vessels, and repair trauma.
5.
Ligate the uterine blood supply (ie,
uterine, ovarian, and/or internal iliac arteries).
6.
Consider arterial embolization.
7.
Consider hysterectomy.
Management of the underlying cause of PPH
Initial assessment
The patients risk factors and the events leading to the
diagnosis of PPH may suggest an underlying etiology, but
knowledge that most cases are caused by uterine atony and
the need to be systematic argues for a planned, stepwise
approach to assessment and management. The status of the
patient, the severity of the bleeding, and the response to
initial management steps determine if and when the
protocol for massive obstetric hemorrhage is instituted.
Uterine atony

Two well-designed trials indicate that oxytocin should be

the drug of choice for both prophylaxis and treatment of
post partum hemorrhage caused by uterine atony. [38]
Assess uterine size and tone by placing a hand on the
uterine fundus and massaging the uterus, which serves to
express any clots that have accumulated in the uterus or
vagina. If the uterus is found to be boggy and not well
contracted, commence vigorous massage and therapeutic
oxytocin. Oxytocin can be administered as a 5-U
intravenous bolus, as 20 U in 1 L of NS intravenously run as
fast as possible, or as 10 U intramyometrially with a spinal
needle if no immediate intravenous access is available.
Emptying the bladder may aid in ongoing assessment and
facilitate uterine contraction and subsequent therapeutic
maneuvers. Wearing a waterproof gown, elbow-length
gloves, and eye protection is prudent during the
management of PPH. Sterile technique is used.
If the uterus remains atonic, commence bimanual massage.
A hand is placed on the fundus, and the second hand is
placed anterior to the cervix in the vagina. Prepare the
perineum and vagina. The vaginal hand may be covered in
povidone-iodine solution (Proviodine) or a lubricant to allow
it to enter the vagina with less difficulty. Take care to
minimize the chance of causing or worsening trauma in the
lower genital tract. Trauma to the vaginal sidewalls and
cervix may be palpated as the hand is gently introduced
into the vagina, and blood clots may be evacuated from the
vagina, cervix, and lower uterine segment.
The vaginal hand is placed in the anterior fornix, and the
abdominal hand is placed on the posterior aspect of the
fundus. The uterus is raised from the pelvis, pivoted
anteriorly, and compressed between the two hands. The
compression expels clots and decreases bleeding. Massaging
the uterus between the hands aids in promoting and
sustaining contraction. Bimanual massage results in a
decrease in bleeding, even if the uterus remains relatively
atonic, thus allowing resuscitation a chance to begin to
catch up with blood loss.
Use other uterotonic agents if the uterus remains atonic
despite oxytocin administration and bimanual massage. The
traditional second-line agent for uterine atony has been
ergonovine (or ergotrate) given as an initial dose of 100 or
125 mcg intravenously or intramyometrially or 200 or 250
mcg intramuscularly. The maximum total dose is 1.25 mg.
Hypertension is a relative contraindication. In some
regions, the availability of ergot preparations has become
problematic. Every effort should be made to secure
supplies of this inexpensive and useful agent.
Many authorities now recommend the use of intramuscular
carboprost as the second-line agent when it is available.
The recommended dose is 250 mcg intramuscularly or
intramyometrially, not to exceed 2 mg (8 doses). Asthma is
a relative contraindication. Carboprost has been shown to
be 80-90% effective in stopping PPH in cases refractory to
oxytocin and ergonovine. Intramuscular administration of
these agents is not recommended if the patient
demonstrates evidence of shock because absorption would
be compromised.

Misoprostol may also become a valuable agent in the

treatment of PPH. One small case series reported that a
dose of 1000 mcg given rectally was effective in causing
sustained uterine contraction in 14 cases refractory to
oxytocin, ergonovine, or both.[39, 40] Recent trials are
examining
whether
the
more
rapid
onset
of
sublingual/buccal misoprostol will improve its efficacy in
the setting of acute PPH. [41] At this time, however,
misoprostol remains a third-line agent in the management
of PPH.[42] The low cost of the drug and its heat stability
(does not require refrigeration) makes it especially
appealing for use in the developing world. More trials are
pending.
Winikoff et al examined sublingual (SL) misoprostol for
PPH when oxytocin is not feasible to administer. Oxytocin
is considered the standard of care for treating postpartum
hemorrhage, but because of refrigeration requirements and
the need for intravenous administration, it is not always
clinically viable, particularly in primitive clinical settings.
Active bleeding was controlled within 20 min for 440 (90%)
women administered misoprostol 800 mcg SL (n=488) and
468 (96%) administered oxytocin 40 units IV (n=490)
(relative risk [RR], 0.94; 95% confidence interval [CI],
0.91-0.98). Additional blood loss of 300 mL or greater
after treatment occurred for 147 (30%) of women
receiving misoprostol and 83 (17%) receiving oxytocin (RR,
1.78; 95% CI, 1.40-2.26). The authors concluded that in
circumstances where it is not feasible to use oxytocin for
postpartum hemorrhage, misoprostol is a suitable
alternative.[43]
The investigational agent carbetocin has been compared
with oxytocin for prevention of postpartum hemorrhage.
Attilakos et al compared the effectiveness of carbetocin
and oxytocin when given for postpartum hemorrhage after
cesarean delivery in a double-blind, randomized trial. The
primary outcome measure was women who required
additional pharmacologic oxytocic interventions. Results
showed that significantly more women required additional
oxytocics in the oxytocin group compared with the
carbetocin group.[44]
Retained tissue
If the uterus continues to contract poorly or to relax when
bimanual compression and massage are stopped despite the
administration of uterotonics, perform manual exploration.
Some authorities advocate earlier exploration; however,
this is difficult without general anesthesia unless the
patient is in severe shock or an epidural is already in place.
Nitrous oxide (Entonox) may be useful in facilitating manual
exploration if general anesthesia is not available.
Ensure that resuscitation is well underway by this time,
and, if not already started, institute the massive
hemorrhage protocol. If possible, keep the vaginal hand in
situ throughout because it minimizes patient discomfort,
the risk of iatrogenic trauma, and, possibly, the risk of
subsequent infection. If the placenta was not delivered
before the onset of PPH, an attempt is now made to deliver
it with cord traction and uterine countertraction. Care
must be taken because the risk of uterine inversion is
greater if the uterus remains poorly contracted. Perform

manual removal if the placenta is not easily delivered or the

cord is avulsed.
Perform manual removal with a level of analgesia that
matches the clinical urgency of the situation. The hand is
passed through the cervix and into the lower segment. Care
is taken to minimize the profile of the hand as it enters,
keeping the thumb and fingers together in the shape of a
cone in order to avoid damage. Control of the uterine
fundus with the other hand is essential. If the placenta is
encountered in the lower segment, it is removed. If the
placenta is not encountered, the placental edge is sought.
Once found, the fingers gently develop the space between
the placenta and uterus and shear off the placenta. The
placenta is pushed to the palmar aspect of the hand and
wrist, and, once it is entirely separated, the hand is
withdrawn. Do not stop uterotonics while the manual
removal is being performed. Restart bimanual massage, and
have an assistant examine the placenta for completeness.
If the placenta has been previously delivered, then
exploration of the uterus is still indicated at this time. The
hand is introduced in the same manner, with control of the
uterine fundus with the other hand. Any clots are removed.
The cavity is gently explored with attention to any defects
suggestive of uterine rupture. Rupture in the absence of a
previous scar is uncommon. Rupture or dehiscence of a
previous lower segment scar does not usually bleed heavily.
The presence of a uterine rupture dictates that a
laparotomy be performed.
A partial uterine inversion can be detected as the hand is
introduced, just as a complete uterine inversion would have
been detected as the hand was placed in the vagina. If the
condition is encountered, return the uterus to its normal
position by pressure on the inverted fundus from within the
uterus. If retained placental tissue is encountered, it is
sheared off the uterine wall and delivered. Adherent
placental fragments may be left in situ or removed by
gentle curettage. The risks of curettage include uterine
perforation and increased bleeding caused by laceration of
uterine vessels. This may be somewhat minimized by the
use of a large, dull curette. Fragments left in situ may be
removed by curettage sometime after the crisis has
passed, although an increased risk of infection probably
ensues.
The administration of short-term, broad-spectrum
antibiotics following manual removal, manual exploration, or
instrumentation of the uterus in this context is commonly
advocated. Evidence is very limited, but a single small,
randomized trial supports the practice.[45]
Immediately resume bimanual massage and compression
following exploration and evacuation of the uterus. Continue
infusion of oxytocin, and administer repeat doses of other
uterotonics if the uterus fails to contract and maximal
doses have not already been given. The uterus may contract
well, and bleeding abates with massage, followed by uterine
relaxation and increased bleeding when compression and
massage are stopped. Prolonged massage at this point may
allow the uterus to contract and retract if it can be kept
empty of clots and if perfusion can be improved with

adequate resuscitation. Any period of decreased bleeding

allows fluid and blood component replacement to exceed
blood loss and help improve the patients status.
Surgical management is necessary if the uterus does not
remain contracted and bleeding persists despite all efforts.
Packing of the uterus may be an option until the operating
room is ready or if surgery is not an immediately available
option. Uterine packing fell into disfavor during the 1960s
as being nonphysiological, concealing ongoing blood loss, and
increasing the risk of infection; however, reports since
then have been favorable in very select circumstances when
all previously mentioned maneuvers have failed. [46] The
uterus and vagina must be tightly packed with continuous,
layered, 2- or 4-inch gauze under direct visualization using
a speculum and/or retractors or a purpose-built uterine
packer.[47] At times, packing may serve as a definitive
treatment. In these cases, the packing is usually removed in
24-48 hours in a setting where recurrent bleeding can be
managed if it occurs.
Intrauterine catheters for tamponade of bleeding have
also been used. In the past, large bulb Foley catheters or
Sengstaken-Blakemore tubes have been used. [48]More
recently, experience has been gained using catheters
specifically designed for postpartum hemorrhage. One such
device is the SOS Bakri tamponade balloon (Bakri, 2001). In
low resource settings, condoms and surgical gloves have
been used successfully to control bleeding. [49] Anti-shock
garments are also being evaluated in low resource settings
for both the definitive treatment of uterine atony as well
as a method to allow time to bring other treatments to
bear[50]
Manual examination helps to exclude a cervical or vaginal
laceration, but direct visualization confirms that bleeding is
coming from the uterus and excludes the possibility of
missing trauma to the lower genital tract. If packing is
meant to be definitive treatment, then ongoing assessment
of uterine size, blood loss, and patient status must be
maintained. Continue uterotonics and commence broadspectrum antibiotics. Remove the pack in 24-36 hours in a
setting that allows for appropriate management if bleeding
recurs. Packing may also be used as a temporizing measure
before arterial embolization (see Selective arterial
embolization). Isolated reports of successful uterine
tamponade with balloon devices have also been published. [51]
Genital tract trauma
Genital tract trauma is the most likely cause if bleeding
persists or is present despite a well-contracted uterus. Use
appropriate analgesia along with good lighting and
positioning, which facilitates excellent exposure. If not
already initiated, moving the patient to an operating room is
reasonable at this time. Experienced assistants and an
excellent circulating nurse are essential.
Directly visualize and inspect the cervix with the aid of
ring forceps. The anterior lip is grasped, and the cervix is
inspected by using a second ring forceps placed at the 2oclock position, followed by progressively "leap-frogging"
the forceps ahead of one another until the entire
circumference has been inspected. Small, nonbleeding

lacerations of the cervix do not need to be sutured. Suture

any laceration that is bleeding significantly or appears to
have the potential to bleed significantly. Each side of the
laceration can be grasped with a ring forceps back from
the torn edge, and gentle traction can be used to aid
exposure.
Use an absorbable, continuous interlocking stitch, and use
tapered (rather than cutting) needles for all repairs except
for the perineal skin. Ensure that the stitch begins above
the apex of the tear, as with vaginal lacerations and
episiotomies. If the apex cannot be visualized, place the
stitch as high as possible and then use it to apply gentle
traction to bring the apex into view. Polyglycolic sutures
have largely replaced catgut; however, the latter may be
somewhat less likely to tear the friable tissues of the
cervix and vaginal vault and may thus be useful in repairing
lacerations in these areas. The laceration must be observed
for bleeding after the torn edges of the cervix are
approximated. The ring forceps can be replaced and left on
for some time if oozing persists.
Lacerations of the vaginal vault must be well visualized and
their full extent realized prior to repair. Lacerations high
in the vaginal vault and those extending up from the cervix
may involve the uterus or lead to broad ligament or
retroperitoneal hematomas. The proximity of the ureters
to the lateral vaginal fornices, and the base of the bladder
to the anterior fornix, must be kept in mind when repair is
undertaken in these areas. Poorly placed stitches can lead
to genitourinary fistulas. An absorbable, continuous
interlocking stitch is used. The stitch must start and finish
beyond the apices of the laceration. Great care must be
taken because the tissue is usually very friable. Take a
good amount of tissue, and ensure that the needle reaches
the full depth of the tear. Ongoing bleeding and hematoma
formation are possible if small bites are taken.
Again, the laceration must be observed for bleeding after
the repair is complete. Pressure or packing over the repair
may achieve hemostasis or allow for better placement of
further hemostatic stitches. Cervical and vaginal vault
lacerations that continue to ooze or those that are
associated with hematomas may be amenable to selective
arterial embolization (see Selective arterial embolization).
Traumatic hematomas are rare and may be related to
lacerations or may occur in isolation. They include vulvar
and paravaginal hematomas in the lower genital tract and
broad ligament and retroperitoneal hematomas adjacent to
the uterus. Patients with lower genital tract hematomas
usually present with intense pain and localized, tender
swelling. Broad ligament hematomas may be palpated as
masses adjacent to the uterus. All may result in significant
blood loss that mandates resuscitation.
Lower genital tract hematomas are usually managed by
incision and drainage, although expectant management is
acceptable if the lesion is not enlarging.[52] Any bleeding
vessels are tied off, and oozing areas may be oversewn.
Place a Foley catheter because urinary retention can occur
because of pain and tissue distortion. Vaginal packing may
be useful following drainage and repair of a paravaginal

hematoma. Remove the pack in 24-36 hours. Embolization

may be used in both vaginal and vulvar hematomas that are
unresponsive to surgical management.
Broad ligament and retroperitoneal hematomas are initially
managed expectantly if the patient is stable and the lesions
are not expanding.[53] Ultrasound, CT scanning, and MRI all
may be used to assess the size and progress of these
hematomas. Selective arterial embolization may be the
treatment of choice if intervention is required in these
patients. Use surgical procedures to evacuate the
hematoma, and attempt to tie off any bleeding vessels.
Consider involving a surgeon with extensive experience
operating in the retroperitoneal space.
Coagulopathy
If manual exploration has excluded uterine rupture or
retained placental fragments, bleeding from a wellcontracted uterus is most commonly due to a defect in
hemostasis. A review of the history and risk factors along
with coagulation test results clarifies this diagnosis.
Proceed with blood product replacement as previously
described in order to correct abnormalities of hemostasis.
If the coagulation status is normal and bleeding is ongoing
despite a well-contracted uterus, then the possibilities of
uterine rupture or an inadequately repaired uterine incision
(if the patient had a cesarean delivery) must be considered.
Revisit any repair to the cervix or vagina before proceeding
to surgical management.
Surgical Therapy
Ongoing bleeding secondary to an unresponsive and atonic
uterus, a ruptured uterus, or a large cervical laceration
extending into the uterus requires surgical intervention.
Laparotomy for PPH following a vaginal delivery is rare. In a
review of emergency peripartum hysterectomies over a 5year period in Los Angeles, Calif, the rate was 1 in 1000
deliveries, but most of these cases began as cesarean
deliveries, usually for placenta previa.[54] A study from
Boston, Mass, found a rate of 1.5 in 1000 deliveries with
similar risk factors.[55] Canadian and Irish studies put the
rate at 0.4 and 0.3 per 1000 deliveries, respectively.
Adequately resuscitate the patient before surgery. This
includes optimizing hemoglobin and coagulation status as
previously described. Fully inform anesthetic and operating
room staff as to the nature of the case. Schedule for a
second surgeon to be in attendance, if possible. As
mentioned previously, sustained bimanual compression and
massage and uterine packing may be used to gain time to
mount a surgical response. Military antishock trousers
provide the equivalent of an approximately 500- to 1000mL autotransfusion and potentially gain time during a
resuscitation. Only the leg portion of the trousers are
inflated in the setting of PPH. Direct compression of the
aorta may be performed for a short period while the
operating room is prepared.
A recent systematic review examined various techniques
used when medical management is unsuccessful. These
included arterial embolization, balloon tamponade, uterine
compression sutures, and iliac artery ligation or uterine
devascularization. At present, no evidence suggests that

any one method is more effective for the management of

severe PPH. Randomized controlled trials of the various
treatment options may be difficult to perform. Balloon
tamponade is the least invasive and most rapid approach
and may thus be the logical first step.[56]
Laparotomy
The choice between a subumbilical vertical incision and a
Pfannenstiel incision for entry into the abdomen is left to
the individual surgeon. Both entries have support, and no
strong evidence indicates that either is superior in this
setting.[57] If concern exists regarding pathology in the
upper abdomen or if exposure is thought to be a concern,
the vertical incision is recommended. Broad-spectrum
antibiotic coverage is advised.
Upon entry, remove any free blood and inspect the uterus
and surrounding tissues for evidence of rupture or
hematoma. If uterine rupture is found, a rapid decision
must be made concerning the viability of repair versus
hysterectomy. Bleeding may be reduced in either instance
by grasping bleeding points on the torn edges with clamps.
The number of layers used for any repair is dictated by the
thickness of the tissue and the hemostatic response to
suturing. Principles are similar to those of cesarean
delivery incision repair. Ensure that bleeding is stopped and
not merely internalized because this would result in ongoing
vaginal bleeding or hematoma formation. Any repair must
be carefully observed for hemostasis before abdominal
closure is performed. Uterine exteriorization may improve
exposure and decrease operating time, but great care must
be taken to not worsen uterine trauma and to keep the
uterus warm and well perfused to avoid worsening atony.
Hemostasis must be reassessed after the uterus is
returned to the abdominal cavity. Consider placement of a
suction drain.
If the uterus is intact upon entry and the bleeding has
been caused by atony, then direct bimanual massage and
compression may be performed while systemic uterotonics
are continued. Direct injection of oxytocin, carboprost,
and/or ergonovine may be successful in overcoming atony.
Uterine artery ligation
Uterine artery ligation is a relatively simple procedure and
can be highly effective in controlling bleeding from uterine
sources. These arteries provide approximately 90% of
uterine blood flow. The uterus is grasped and tilted to
expose the vessels coursing through the broad ligament
immediately adjacent to the uterus. Ideally, place the
stitch 2 cm below the level of a transverse lower uterine
incision site. A large atraumatic (round) needle is used with
a heavy absorbable suture. Include almost the full
thickness of the myometrium to anchor the stitch and to
ensure that the uterine artery and veins are completely
included. The needle is then passed through an avascular
portion of the broad ligament and tied anteriorly. Opening
the broad ligament is unnecessary. Perform bilateral
uterine artery ligation. While the uterus may remain atonic,
blanching is usually noted and blood flow is greatly
diminished or arrested.

Local oozing may be controlled with direct injection or

compression with warm saline packs. In a series of 265
cases, a 95% success rate was reported using this
procedure in PPH unresponsive to uterotonics in patients
who had cesarean births.[58] Another series of 103 cases
had a 100% success rate if a stepwise approach was taken.
[59]
After initial uterine artery ligation, subsequent stitches
were placed 2-3 cm below the initial stitches following
bladder mobilization, and, finally, ovary artery ligation was
performed if required. Menstrual flow and fertility were
not adversely affected.
Ovarian artery ligation
The ovarian artery arises directly from the aorta and
ultimately anastomoses with the uterine artery in the
region of the uterine aspect of the uteroovarian ligament.
Ligation is performed just inferior to this point in a manner
similar to that of uterine artery ligation. The amount of
uterine blood flow supplied by these vessels may increase
following uterine artery ligation. The procedure is easy to
perform; however, the potential benefit must be weighed
against the time required to perform the ligations.
Internal iliac (hypogastric) artery ligation
Internal iliac artery ligation can be effective to reduce
bleeding from all sources within the genital tract by
reducing the pulse pressure in the pelvic arterial
circulation. One study indicated that pulse pressure was
reduced by 77% with unilateral ligation and by 85% with
bilateral ligation.[60] Hypogastric artery ligation is much
more difficult to perform, more commonly associated with
damage to nearby structures, and less likely to succeed
than uterine artery ligation. One study reported a success
rate of 42%. In patients who undergo hypogastric artery
ligation, uterine artery ligation has usually already failed.
Prerequisites for the procedure include a stable patient, an
operator experienced in the procedure, and a desire to
maintain reproductive potential. The retroperitoneal space
is entered by incising the peritoneum between the fallopian
tube and the round ligament. The ureter must be identified
and reflected medially with the attached peritoneum. The
external iliac artery is identified on the pelvic sidewall and
followed proximally to the bifurcation of the common iliac
artery. The ureter passes over the bifurcation. The
internal iliac artery is identified and followed distally
approximately 3-4 cm from its point of origin. The loose
areolar tissue is carefully cleared from the artery. A rightangle clamp is passed beneath the artery at this point, with
great care to avoid damage to the underlying internal iliac
vein.
A recommendation is to pass the clamp from lateral to
medial in order to minimize the chance of damage to the
adjacent external iliac vessels. Gentle elevation of the
artery with a Babcock clamp facilitates this maneuver.
Ligate the artery with heavy absorbable suture, but do not
divide it. Palpate the femoral and distal pulses before and
after the ligation to ensure that the external or common
iliac artery was not inadvertently ligated. If possible, place
the ligation distal to the posterior division of the artery

because this decreases the risk of subsequent ischemic

buttock pain. Identification of the posterior division may
be difficult, and ligation 3 cm from the internal iliac artery
origin usually ensures that it is not included.
Hysterectomy is required if internal iliac artery ligation is
unsuccessful. Patients in whom internal iliac artery ligation
has failed have greater morbidity than those in whom the
procedure has not been attempted. The likelihood of
benefit from the procedure must be balanced against the
potential risks. The advent of more effective uterotonic
agents, the fact that most cases of intractable
hemorrhage are now related to abnormalities of
placentation that are diagnosed or suggested before
delivery, and the option of embolization have lessened the
use of hypogastric artery ligation. The number of surgeons
comfortable using this procedure and the opportunities to
teach it are rapidly declining.
Hysterectomy
Hysterectomy is curative for bleeding arising from the
uterine, cervical, and vaginal fornices. The procedure of
peripartum hysterectomy is well described in several texts
and articles (eg, Hysterectomy), and the technique differs
little from that in nonpregnant patients. [61, 57] While the
organ is more vascular, the tissue planes are often more
easily developed. Total hysterectomy is preferred to
subtotal hysterectomy, although the latter may be
performed faster and be effective for bleeding due to
uterine atony. Subtotal hysterectomy may not be effective
for controlling bleeding from the lower segment, cervix, or
vaginal fornices. Take every opportunity to become involved
when peripartum hysterectomies are performed.
Selective arterial embolization
Angiographic embolization in the management of PPH was
first described more than 30 years ago. [62] As with all of
the surgical and most of the medical treatments of PPH, no
RCTs regarding its effectiveness have been conducted.
This is likely to remain the case for some time given the
relative rarity of intractable PPH. Several case series
suggest that selective arterial embolization may be useful
in situations in which preservation of fertility is desired,
when surgical options have been exhausted, and in managing
hematomas.[63] Follow-up of women undergoing successful
embolization for severe intractable PPH reports that
women almost invariably have a return to normal menses
and fertility.[64]
The major drawbacks of the procedure are the
requirement for 24-hour availability of radiological
expertise and the time required to complete the procedure.
Patients must be stable to be candidates for this
procedure. Complications include local hematoma formation
at the insertion site; infection; ischemic phenomena,
including uterine necrosis in rare instances; and contrastrelated adverse effects. Currently, most PPH cases
requiring hysterectomy are related to placenta previa.
These patients are commonly diagnosed before delivery and
are usually delivered by elective cesarean birth. This
planning may allow increased use of invasive radiological
services in the management of such cases.

A retrospective study by Park et al indicated that

transcatheter arterial embolization (TAE) is safe and
effective for secondary PPH. In the study, the procedure
was clinically successful in 47 of 52 patients (90.4%) being
treated for secondary PPH (caused in 23 cases by retained
placenta). Gelatin sponge particles were used in 48
patients, either alone or in combination with permanent
embolic materials (eg, microcoils, N-butyl cyanoacrylate);
embolization was performed with permanent materials
alone in the remaining four patients. Regular menstruation
returned in the 44 patients who were followed up (for a
mean 12.6-month period), and five patients were known to
become pregnant.[65]
B-Lynch and Cho sutures
Recent case series and case reports advocate the use of
transmural uterine compression sutures to rapidly control
bleeding. The initial reports described the B-Lynch
technique, which involves opening the lower segment and
passing a suture through the posterior uterine wall and
then over the fundus to be tied anteriorly. [66, 67] A similar
technique has been described without opening the uterus. A
long, straight needle is passed anterior to posterior
through the lower uterine segment; the suture is passed
over the fundus and then tied anteriorly.[68] Both techniques
use bilateral stitches. The most recent variant uses
multiple stitches passed transmurally and tied anteriorly at
various points over the uterine body. This technique may be
focused in the area of the placental bed in cases of
abnormal
placentation.[69] All
of
these
procedures
effectively produce tamponade by compressing together
the anterior and posterior walls.
Follow-up reports suggest a normal return to menses and
fertility, but the number of cases is small. The techniques
have the advantage of being very simple to perform and
may be a rapidly effective alternative to hysterectomy. [66]
Bleeding at cesarean delivery
In the past, most cases of intractable PPH followed vaginal
delivery and were due to uterine atony; however, more
recent case series and national databases show that more
cases are now associated with cesarean delivery. Cesarean
delivery for placenta previa carries a relative risk of 100
for peripartum hysterectomy, with many patients having a
diagnosis of placenta accreta.[70] High-resolution ultrasound
with color Doppler may allow antenatal diagnosis of placenta
accreta.
Whenever possible, delivery of the placenta at cesarean
delivery should be performed in an assisted fashion
following the administration of a uterotonic agent,
preferably oxytocin. This practice leads to less blood loss
and less infectious morbidity.[71, 72]
Uterine rupture has also become a more common cause of
severe PPH necessitating hysterectomy. The vast majority
of these cases occur in patients with a previous cesarean
birth. Counsel all women with placenta previa, and especially
those with a previous low segment uterine scar, in the
antenatal period regarding the risk of severe PPH and the
possible need for transfusion and even hysterectomy.

Ensure that these patients are cared for in facilities with

the resources to manage them successfully if complications
arise.[73]

recommendations for future pregnancies may be discussed

during the postoperative stay and reinforced at the
postdischarge visit.

The management of bleeding at cesarean delivery or

following uterine rupture is not greatly different from that
following vaginal delivery. Aggressive resuscitation is
performed with attention to restoration of circulating
volume and oxygen-carrying capacity and correction of
hemostatic defects. Direct bimanual compression may be
used in the case of atony. Retained tissue may be removed
under direct visualization. Abnormally adherent tissue is a
concern; leave it in situ if it cannot be easily removed.

Summary

Direct intramyometrial injection of uterotonics may be

undertaken. Vasopressin (0.2 U in 1 mL of NS) may also be
injected into the myometrium, with great care taken to
avoid intravascular injection. Individual vessels in the
placental bed may be ligated. Simple or box stitches may be
placed where continuous oozing is present. [69] In cases of
placenta previa, the lower uterine segment may be
temporarily packed; leaving a pack in the uterus is also an
option. The end of the pack is fed through the cervix and
into the vagina and is removed 24-36 hours later. Uterine
rupture or extension of a uterine incision requires excellent
visualization and careful repair with attention to adjacent
structures.
The stepwise surgical approach described above may be
used if these measures are unsuccessful and preservation
of fertility is desired. Strongly consider immediate
hysterectomy if further reproduction is not an issue or if
bleeding or damage to the uterus appears severe.
Embolization may be considered in this setting. Its
successful use has been described both intraoperatively to
preserve the uterus and after hysterectomy for continued
bleeding. Embolization may also be used for continued
postoperative vaginal bleeding.[74]
Persistent bleeding following hysterectomy may also be
managed by packing with gauze brought out through the
vagina or by a pelvic pressure pack composed of gauze in a
sterile plastic bag brought out through the vagina and
placed under tension. This pack is also known as a
parachute, mushroom, or umbrella pack. Place a Foley
catheter to monitor urine output and prevent urinary
retention. The placement of a suction drain may be useful
to monitor losses in cases of ongoing oozing. Always
consider coagulopathy in patients with continued slow blood
loss.
Postoperative Details
Continue resuscitation, and repeat laboratory tests.
Monitor vital signs, urine output, and any ongoing losses.
Care in an intensive care setting is advantageous, as is close
follow-up by the obstetric service. The patient must be
monitored for complications (see Complications).
Follow-up
Full documentation of the case is imperative, and a careful
explanation of events and interventions must be given to
the patient and family. Caregivers must be available and
approachable
for
questions.
Implications
and

PPH is a common complication of childbirth and a leading

cause of maternal morbidity and mortality. Clinicians should
identify risk factors before and during labor so that care
may be optimized for high-risk women. However, significant
life-threatening bleeding can occur in the absence of risk
factors and without warning. All caregivers and facilities
involved in maternity care must have a clear plan for the
prevention and management of PPH. This includes sound
resuscitation skills and familiarity with all medical and
surgical therapies available.
Complications
Most patients with PPH are quickly identified and
successfully treated before major complications develop.
The most common problem is anemia and loss of iron stores,
which results in fatigue in the postpartum period. Clinicians
and patients are more tolerant of low hemoglobin levels,
mild postural lightheadedness, and fatigue because of
current concerns over blood transfusion. The risks of
transfusion with blood products are well known and have
been previously described.
Not surprisingly, many of the complications of severe PPH
are related to massive blood loss and hypovolemic shock.
Damage to all major organs is possible; respiratory (adult
respiratory distress syndrome) and renal (acute tubular
necrosis) damage are the most common but are rare. These
conditions are best managed by specialists. Renal failure is
usually self-limited, and renal function recovers fully.
Temporary dialysis is seldom required. Pulmonary edema is
uncommon in this previously healthy group; however, it may
develop acutely or during the recovery phase because of
fluid overload or myocardial dysfunction. Response to
standard therapy is usually prompt.
Pregnant women are at increased risk of venous thrombosis
and embolic events. Many of the risk factors for PPH are
also risk factors for venous thrombosis and embolic events,
including operative vaginal delivery, cesarean delivery, and
pelvic surgery. Venous stasis due to shock and immobility
also contribute, and caregivers should maintain a high index
of clinical awareness.
Hypopituitarism following severe PPH (Sheehan syndrome)
is due to critical ischemia of the hypertrophied pituitary.
This condition should be considered if a failure to lactate
occurs. Isolated deficiencies of pituitary tropins and
hyperprolactinemia have also been reported.
Evidence suggests that prophylaxis against gastrointestinal
ulceration is useful in critically ill patients, especially those
requiring ventilation. The recommended agents are
sucralfate and histamine 2 blockers. Both are effective at
reducing the risk of ulcers. Sucralfate may be associated
with a lower incidence of pneumonia.[75]
Several of the complications related to surgical
interventions have been described. Complications include

sterility, uterine perforation, uterine synechiae (Asherman

syndrome), urinary tract injury and genitourinary fistula,
bowel injury and genitointestinal fistula, vascular injury,
pelvic hematoma, and sepsis. Consider ultrasound of the
kidneys following complicated emergency pelvic surgery in
order to exclude ureteric obstruction. Patients undergoing
uterine exploration, instrumentation, or laparotomy in this

context probably benefit from antibiotic coverage at the

time of the intervention. Good evidence suggests that all
patients having cesarean births should receive prophylactic
antibiotics.[76] The duration of antibiotic coverage following
surgery in these circumstance is unknown.