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Postpartum Hemorrhage Overview

Background

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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
[1]
approximately 8% of these deaths are caused by PPH. 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
[2]
100,000 maternal deaths per year. The most recent Practice Bulletin from the
American College of Obstetricians and Gynecologists places the estimate at 140,000
[3]
maternal deaths per year or 1 woman every 4 minutes.
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
[4]
placenta was markedly higher.

Problem

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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
[5]
cesarean delivery. 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
[6]
dependent on the timing of the test and the amount of fluid resuscitation given. 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

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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
[7, 8]
See eMedicine article Management of the Third Stage of
management is used.
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
[2]
availability of medications used in the active management of the third stage. 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

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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
[9]
use, and previous PPH were all positively associated with increased risk of PPH.
A recently published, large population based study supported these findings with
significant risk factors, identified using a multivariable analysis, being: 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) and augmentation of labor with oxytocin (OR
[10]
1.4, 95% CI 1.2-1.7).
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
[11]
risk was 5.2% with normal delivery and 13.6% with instrumental delivery.
As a way of remembering the causes of PPH, several sources have suggested using the
[12]
4 T s as a mnemonic: tone, tissue, trauma, and thrombosis.

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
[13]
techniques using the intrauterine instillation of prostaglandin or hypertonic saline.
One such trial reported rates of retained placenta requiring D&C of 3.4% with oral
[14]
misoprostol compared to 22.4% using intra-amniotic prostaglandin (p=0.002).
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
[7]
invasive removal techniques.
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
[5]
contraction and retraction for preventing hemorrhage. 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
[15]
An underlying bleeding disorder should be considered in a woman with
conditions.
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

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High-quality evidence suggests that active management of the third stage of labor
[8]
reduces the incidence and severity of PPH. 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)
[16, 7, 8]
These trials included more than 6000 women,
and a Cochrane meta-analysis.
and the findings are summarized in Table 1.
Table 1. Benefits of Active Management Versus Expectant Management (Open Table in
a new window)
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
[17, 18]
The US RCTs mentioned above compared the use of
is used as the uterotonic.
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
[9]
in PPH and a 50% reduction in the need for transfusion. 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
[9]
the need for transfusion. 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
[3]
reasonable. 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
[19]
It has been suggested that distribution of misoprostol ahead of childbirth in
use.
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
[20]
might be used for starting labor or terminating pregnancy.
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

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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
[6]
uteroplacental unit and to provide a reserve for the blood loss that occurs at delivery.
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
[5]
"physiologic sutures" of the uterus.
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

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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
[21]
that have accumulated in the uterus or vagina.

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)

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
[23]
develop until a large volume of blood has been lost.
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

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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
[24, 25]
Discussion regarding the implications of such prohibitions should be
center.
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.
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