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.

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, 6] 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. [7] 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
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

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. [8, 9] 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. [10]
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). [11]
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. [12]
A study by Hanley et al reported that serotonin-norepinephrine reuptake
inhibitor exposure in late pregnancy was associated with a 1.6- to 1.9-fold
increased risk of postpartum hemorrhage. [13, 14]
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. [15]
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. [16] 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). [17]
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. [8]
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-o’clock positions to facilitate delivery of an entrapped fetal
head during a breech delivery (Dührssen 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. [18] 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. [9] 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. [19, 8, 9]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)
Control Relative 95% 95%
Outcome NNT †
Rate, % Risk CI* CI

0.32- 10-
PPH of 500 mL 14 0.38 12
0.46 14

PPH of 1000 0.21- 42-

2.6 0.33 55
mL 0.51 91

Hemoglobin < 0.29- 20-

6.1 0.4 27
9 g/dL 0.55 40

Blood 0.22- 48-

2.3 0.44 67
transfusion 0.53 111

Therapeutic 0.17-
17 0.2 7 6-8
uterotonics 0.25

*CI: Confidence interval

† NNT: Number needed 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. [20, 21] 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. [10] 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. [10] 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. [22] 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. [23]
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. [7]
At term, the estimated blood flow to the uterus is 500-800 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. [24]
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 [25] (Open Table in a new
window)
Blood Blood
Symptoms and Degree of
Volume Pressure
Signs Shock
Loss (systolic)

500-1000 Palpitations,
mL (10- Normal tachycardia, Compensated
15%) dizziness

1000-1500 Weakness,
Slight fall (80-
mL (15- tachycardia, Mild
100 mm Hg)
25%) sweating
1500-2000 Moderate fall
Restlessness,
mL (25- (70-80 mm Moderate
pallor, oliguria
35%) Hg)

2000-3000 Marked fall

Collapse, air
mL (35- (50-70 mm Severe
hunger, anuria
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. [26]
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.