CLINICAL OBSTETRICS AND GYNECOLOGY
Volume 66, Number 2, 344–356
Postpartum
Hemorrhage—
Epidemiology, Risk
Factors, and Causes
KARA PATEK, MD, and PERRY FRIEDMAN, MD
Corewell Health William Beaumont University Hospital, Royal
Oak, Michigan
Abstract: The incidence of postpartum hemorrhage
(PPH) is increasing worldwide and in the United
States. Coinciding, is the increased rate of severe
maternal morbidity with blood transfusion in the
United States over the past 2 decades. Consequences
of PPH can be life-threatening and carry significant
cost burden to the health care system. This review will
discuss the current trends, distribution, and risk
factors for PPH. Causes of PPH will be explored in
detail.
Key words: postpartum hemorrhage, epidemiology,
risk factors, causes, atony, uterine atony
Epidemiology
INTRODUCTION
Hemorrhage is the leading cause of ma-
ternal death worldwide, with two-thirds
of these occurring in the postpartum
period.1 In the United States, postpartum
hemorrhage (PPH) is the fifth leading
Correspondence: Kara Patek, MD, Beaumont Hospital,
Royal Oak, MI. E-mail: kara.patek@corewellhealth.
org
The authors declare that they have nothing to disclose.
CLINICAL OBSTETRICS AND GYNECOLOGY
344 | www.clinicalobgyn.com
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Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.
cause of maternal mortality, accounting
for 11% to 12% of maternal deaths.2 PPH
also accounts for a significant amount of
severe maternal morbidity, defined by the
American College of Obstetrics and Gy-
necology and the Society for Maternal
Fetal Medicine as an unintended outcome
in the birthing process that may have
significant short-term and long-term
consequences to an individual’s health.
As such, it is imperative that obstetricians
have a thorough understanding of the
topic to predict which patients are at
increased risk of postpartum hemorrhage,
as well as identify the cause of the hem-
orrhage when it occurs so that it may be
promptly treated.
One of the biggest limitations when
considering the epidemiology of PPH is
that there is no universally accepted defi-
nition. In 2014, the American College of
Obstetrics and Gynecology developed the
reVITALize program, which defines post-
partum hemorrhage as a blood loss equal to
or greater than 1000 mL or blood loss
accompanied by signs and symptoms of
/ VOLUME 66 / NUMBER 2 / JUNE 2023

hypovolemia within 24 hours of delivery.3
However, older studies or studies published
in other countries may have used lower
blood loss thresholds, which limits inter-
pretability when compared with newer
data. The definition of severe PPH is also
highly variable in the literature, with thresh-
olds of > / = 1000 mL, > / = 1500 mL, and
2000 mL of blood loss, or the inclusion of
blood transfusion or the need for surgi-
cal procedures being included in some
definitions.4–6
In addition, much of the published data
comes from retrospective review of elec-
tronic health records, which are subject to
inaccurate or incomplete charting and
rely primarily on estimates of blood loss
while ignoring complementary informa-
tion such as changes in hematocrit, ad-
ministration of uterotonic medications or
blood products, and the need for addi-
tional surgical procedures, which may be
useful in making the diagnosis. To high-
light the implications of this, a recently
published digital phenotyping algorithm
used any of the following: EBL or QBL
exceeding 1000 mL, critically low hema-
tocrit ( ≤ 21), or a greater than 12-point
drop from baseline resulting in a mini-
mum ≤ 25 within 48 hours of delivery, 1
of 30 diagnostic codes selected as indica-
tors of PPH, the administration of any
uterotonic medication except oxytocin,
and deliveries where Bakri balloon place-
ment or surgical intervention was re-
quired to identify cases of PPH. They
reported that this digital phenotype iden-
tified cases of PPH from non-PPH with a
sensitivity of 96%, specificity of 77%, PPV
of 88%, NPV of 91%, and accuracy of
89%, which allowed them to identify 3
times as many deliveries complicated by
PPH than would have been identified
based on blood loss alone.7
INCIDENCE
The incidence of PPH is increasing
worldwide and in the United States.8–10
The incidence of severe PPH alone has
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Epidemiology, Risk Factors 345
increased by almost 9% per year between
1999 and 2008.10 In a large National
Inpatient Sample (NIS)-based analysis of
data from 2012 to 2013, PPH occurred in
3% of deliveries (41,210/1,352,691).11
Retrospective data from a large Califor-
nian hospital system of 261,964 pregnant
patients between 2010 and 2017 found a
slightly higher rate of PPH, of ~5% of
hospitalizations, with 0.3% experiencing
severe PPH based on transfusion, labora-
tory, and blood loss data.12
Similarly, the rate of severe maternal
morbidity with blood transfusions has
increased in the United States over the
past 2 decades (Fig. 1). A cross-sectional
study using the NIS database found that
the rate of PPH requiring blood trans-
fusions increased from 1.6 per 1000 deliv-
ery hospitalizations in 2001-2002 to 3.8 in
2011-2012 (P < 0.001). In addition, the
overall rate of PPH with a procedure
other than a blood transfusion ie, hyster-
ectomy, repair of obstetric laceration, and
uterine artery ligation/embolization) also
rose from 0.9 to 1.9 per 1000 delivery
hospitalizations when comparing these
same timeframes (P < 0.001). The trends
were similar for vaginal and cesarean
birth.13
The incidence of PPH due to uterine
atony specifically appears to be increasing
in developed countries.8,14 Several studies
have reported an increase in PPH secon-
dary to uterine atony. A cross-sectional
study of the NIS database noted a 14.1%
increase from 2001-2002 to 2011-2012 in
induced vaginal deliveries but, in con-
trast, an 18.3% drop in PPH secondary
to uterine atony in vaginal deliveries that
were spontaneous and an over 60% in-
crease in PPH due to uterine atony in
cesarean deliveries.13,15
Sade and colleagues sought to assess
the trends of change in risk factors over
time for PPH from 1988 to 2014. They
reported that perineal and vaginal tears
exhibited a rising trend while the delivery
of a large for gestational age neonate
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346 Patek and Friedman
FIGURE 1. CDC Severe Maternal Morbidity in the United States. Cdc.gov/reproductivehealth/
maternalinfanthealth/severematernalmorbidity.html#rates. Accessed 9/10/2022.
(defined as birthweight at or above the
90th percentile for gestational age) de-
creased. Authors suggest that rising rates
of perineal and vaginal lacerations may
be explained by increased awareness and
improved diagnosis over the study period.
Both perineal and vaginal tears, as well as
delivery of an large for gestational age
neonate, were independent risk factors for
PPH. Although pre-eclampsia, vacuum-
assisted delivery, and retained placenta
were also independently associated with
PPH, the trends of change for these risk
factors over time were not statistically
significant.16 Although the etiology of
the increasing incidence of PPH is not
well understood, delays in the provision
of appropriate care, even in patients
already in the hospital, have been
postulated to account for a proportion
of preventable maternal morbidity.17
COST OF ILLNESS
Consequences of PPH can include blood
transfusion, thromboembolism, hyster-
ectomy, pituitary necrosis (Sheehan’s
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syndrome), prolonged hospital stay,
ICU admission, and maternal death.
Compared with individuals without se-
vere PPH, those with severe PPH had
116 times, 87 times, and 5.3 times the
risk of hysterectomy, acute renal failure,
and sepsis, respectively.18 Severity of
bleeding and patient outcomes may re-
late to the etiology of the hemorrhage.
For example, PPH attributed to nona-
tonic etiologies are associated with lon-
ger length of stay (3.67 vs. 2.98 [atonic]
and 2.63 [non-PPH], P < 0.001) and
higher inpatient mortality rates (104 per
100,000 vs. 19 [atonic] and 3 [non-PPH],
P < 0.001) compared with individuals
who experienced atonic hemorrhage or
no postpartum hemorrhage.11
Maternal hemorrhage carries a signif-
icant cost burden as well. Medi-Cal,
California’s Medicaid health care pro-
gram, which paid for 47.3% of births
complicated by maternal hemorrhage in
the state of California in 2011, incurred
an estimated incremental cost of mater-
nal hemorrhage deliveries (including

antepartum, intrapartum, and postpar-
tum hemorrhage) of $105,956,000. In
the study year, in cases without ante-
partum hemorrhage, immediate and de-
layed PPH conferred an incremental
cost of $9,206,000, $648,000, and
$18,623,000 for delivery by scheduled
cesarean, vaginal birth after cesarean,
and vaginal birth, respectively.19
DISTRIBUTION
Severe maternal morbidity (SMM) dispro-
portionately affects minority individuals
in the United States.20–22 Using NIS data
from 2012 to 2014, over 360,000 individ-
uals with a diagnosis of PPH (~3.2% of
deliveries) were included in an analysis
looking at self-reported maternal race and
ethnicity and SMM, as defined by the
CDC. Authors found that the risk for
severe morbidity, including transfusion,
was significantly higher among non-
Hispanic black individuals than non-His-
panic white, Hispanic, Asian, or Pacific
Islander individuals and remained signifi-
cantly higher even when the transfusion
was excluded. Furthermore, they reported
that non-Hispanic black individuals were
also at higher risk for disseminated intra-
vascular coagulation and hysterectomy
compared with non-Hispanic white
individuals.23 Similar findings were re-
ported by Tangel and colleagues, where
black individuals were 53% more likely
than non-Hispanic white individuals to
receive a blood transfusion and 36% more
likely to undergo hysterectomy.24 Minor-
ity individuals who experience SMM due
to PPH have a 5-fold increased risk for
mortality when compared with non-His-
panic white individuals.23,25
Importantly, the increased risk of
SMM for black individuals has been
shown to persist despite the comorbidity
index score, a scoring system that eval-
uates patients underlying risk for morbid-
ity and mortality based on maternal
comorbidities.23 Furthermore, these dis-
parities persist in the highest income
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Epidemiology, Risk Factors 347
brackets and educational groups and
remain even after adjusting for rural
locations and delivery sites.24,26–29
Reasons for racial disparity in obstet-
ric outcomes are incompletely under-
stood. More traditional explanations
for maternal health disparities focused
on the contribution of an individual’s
comorbidities, such as obesity and
chronic hypertension; however, attention
has increasingly shifted to systems-level
factors as well as social factors.22 Break-
down in patient-provider communica-
tion, lower health literacy, lack of
shared decision-making and cultural tai-
loring of counseling, as well as under-
representation of minority populations
in medicine have been suggested as
contributing factors.30 The quality of
obstetric care and the lack of clear
quality standards have also been high-
lighted as a potential source of inequit-
able provision of care, which could lead
to poorer outcomes for specific patient
populations.31 Proposed obstetric care
bundles aimed at reducing peripartum
racial and ethnic disparities have focused
on obtaining reliable data on patient
identity, including race and ethnicity, for
accurate data measurement, addressing
implicit bias among health care providers,
addressing institutional bias, and improv-
ing patient-centered communication.32
Implementation of a safety bundle aimed
at reducing perinatal racial/ethnic dispar-
ities has been published; however, there is
a lack of outcome data at this time, so it
remains unknown whether this interven-
tion results in a reduction of disparate
outcomes for minority patients.33
Risk Factors
Although there are many well-described
risk factors for PPH, many cases occur in
individuals without identifiable risk
factors.34,35 Hence, vigilant clinical as-
sessment is important in the management
of all patients in labor and delivery units.
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348 Patek and Friedman

FIGURE 2. Risk factors and protective factors for PPH.

Risk factors for PPH are typically classi-
fied into 1 of 3 categories: maternal
factors, pregnancy-related factors, and
fetal factors. In addition, aspects of early
management when PPH occurs have been
shown to relate to the risk of severe
hemorrhage in patients with PPH, and
as such, it seems appropriate to consider
a fourth category of hospital/provider
factors. (Fig. 2).
MATERNAL FACTORS
There are many well-described maternal
factors associated with an increased
risk of PPH, including parity, maternal
age, BMI, ethnicity/race, hypertensive

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disorders, diabetes mellitus, and uterine
leiomyomata.
Several large cohort studies found
an association between primiparity and
an increased risk of PPH and severe
PPH when compared with individuals
having a subsequent baby.35,36 Simi-
larly, one of the large retrospective
cohort studies mentioned above also
reported an association between individ-
uals aged 35 years or older (advanced
maternal age) and severe PPH compared
with those aged 20 to 34 years (aOR 1.15,
95% CI 1.1–1.2).35 Similarly, a Dutch
population-based cohort study reported
that increasing maternal age was associ-
ated with PPH, with individuals 40 years
of age or above having an RR of 1.14
(95% CI 1.09–1.19) and those between 35
and 39 years having an RR of 1.08 (95%
CI 1.06–1.09). Importantly, PPH was the
highest contributing factor to composite
adverse maternal outcomes in individuals
with advanced maternal age.37
An association between BMI and the
risk of PPH is less well defined with mixed
results. The Australian study referenced
above found that overweight (defined as
BMI 25 to <30) and obese (defined as
BMI 30 or greater) individuals were more
likely to experience a severe PPH than
those with a normal BMI (defined as BMI
18.5 to <25) (aOR 1.18, 95% CI 1.1–1.3,
and aOR 1.40, 95% CI 1.3–1.5, for over-
weight and obese individuals, respec-
tively).35 In contrast, a systematic review
of 27 studies examining risk factors for
atonic PPH showed that obesity (not
defined) was not associated with an in-
creased risk for atonic PPH specifically.38
A secondary analysis of a large random-
ized controlled trial looking at different
oxytocin regimens to prevent uterine atony
found that Hispanic and non-Hispanic
white ethnicity is an independent risk factor
for treated uterine atony following a vag-
inal birth with OR of 2.1 (95% CI 1.3–3.4)
and 1.6 (95% CI 1.0–2.5), respectively.39
Similarly, a systematic review of 27 studies
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Epidemiology, Risk Factors 349
found that Hispanic ethnicity and Asian
race were associated with atonic postpar-
tum hemorrhage when compared with
non-Hispanic whites (OR 1.23, 95% CI
1.20–1.25 and OR 1.39, 95% CI 1.33–1.46,
respectively).38 Although this association
has been identified, authors of this study
caution the reader when interpreting this
data, as causation has not been established,
and it is unclear whether this relationship is
a biological or social one or a byproduct of
disparities or systemic racism. Further-
more, the incorporation of race or ethnicity
into risk-prediction algorithms may further
perpetuate health care disparities.40,41
Pre-eclampsia and pregestational diabe-
tes mellitus have been identified as
independent risk factors for abnormal
postpartum uterine bleeding from uterine
atony.38,39 A systematic review of 27
studies looking specifically at risk factors
for atonic PPH found that hypertensive
disorders of pregnancy were associated
with an OR of 1.84 (95% CI 1.45–2.33)
for PPH secondary to uterine atony. Of
particular note, magnesium exposure was
not associated with atonic PPH in this
review, a factor which is included in some
risk assessment tools. A study looking at
magnesium sulfate’s effect on spontaneous
and oxytocin-induced contractions in
in vitro myometrium demonstrated a re-
laxant effect in a dose-dependent and time-
dependent manner, which does support a
plausible physiological link with the risk of
hemorrhage.42 A 2016 meta-analysis of 5
trials looking at blood loss at cesarean
birth in individuals on magnesium sulfate
for pre-eclampsia found no difference in
intrapartum or postpartum blood loss in
individuals with pre-eclampsia who re-
ceived magnesium sulfate compared with
those who did not.43 Similarly, a recent
retrospective cohort study looking at 124
patients with pre-eclampsia with severe
features or eclampsia found that calcu-
lated blood loss at cesarean birth was not
different between individuals who received
magnesium sulfate during the delivery and
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350 Patek and Friedman
those who did not.44 A retrospective cross-
sectional study of hospitalizations for de-
livery in the State of New York from 1998
to 2007 found that individuals with hem-
orrhage requiring massive blood transfu-
sion (defined as 10 units or more of blood)
were significantly more likely to have
severe pre-eclampsia, and, using multivari-
able regression modeling, severe pre-
eclampsia conferred an aOR of 10.4
(95% CI 7.7–14.2) for requiring massive
transfusion for obstetric hemorrhage.45
Additional maternal factors associ-
ated with PPH include the use of
ART, prepregnancy anemia, and ute-
rine leiomyomas.5,46
PREGNANCY-RELATED FACTORS
Placental abnormalities carry one of the
highest risks for PPH and severe PPH.46
Severe PPH is more likely in individuals
with pregnancies complicated by placenta
previa, placenta accreta spectrum, and
with placental abruption.35,45,46 In a ret-
rospective cross-sectional study of deliv-
ery hospitalizations using the Health care
Cost and Utilization Project State Inpa-
tient Data set for New York between 1998
and 2007, abnormal placentation ac-
counted for 26.6% of cases of massive
blood transfusion (defined as 10 or more
units of blood), with another 16.7% due to
placental abruption.45
Previous PPH is associated with the
recurrence of PPH and has been associ-
ated with the severity of a subsequent
hemorrhage.5,36,46 Importantly, this may
be an underestimate as coded data extrac-
tion found an incidence of recurrent PPH
of 19.1% compared with 27.4% when
medical record data was audited.47
Additional pregnancy-related risk fac-
tors for PPH which have been identified
include induction of labor, chorioamnio-
nitis, duration of the second and third
stages of labor, episiotomy, obstetric anal
sphincter injuries, high vaginal or cervical
lacerations, cesarean birth, and manual
placental removal at cesarean birth.
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Labor induction and augmentation
with pitocin have been shown to be an
independent risk factor for PPH secon-
dary to uterine atony and severe PPH in
individuals with PPH.35,39 Furthermore,
induced cervical ripening has been identi-
fied as a risk factor for severe hemorrhage
in patients experiencing PPH.36 Patients
with labor abnormalities are 50% more
likely to have a PPH after cesarean birth
and 80% more likely to have PPH after
vaginal birth.48 There is an association
between suspected clinical chorioamnio-
nitis and a clinically significant deterio-
ration in uterine contractility. Given that
increased atony may be a result of re-
duced uterine contractility, it is not sur-
prising that clinical chorioamnionitis has
also been found to be an independent risk
factor for treated uterine atony.39,49,50
A prolonged second stage of labor,
defined as > 1 hour from complete
dilation to birth of the neonate for multi-
parous patients and > 2 hours for nulli-
parous patients, was found to be an
independent risk factor for treated uterine
atony following vaginal birth.39 However,
this was not supported in a recent system-
atic review of 27 studies that specifically
assessed risk factors for atonic PPH, and
data remains conflicted on whether pro-
longed labor is associated with severe
PPH38 Duration of the third stage of
labor appears to be longer in patients
who experience PPH than in those who
do not, with individuals with PPH having
~10 minute longer duration of the third
stage of labor than those without.15
Lacerations have also been associated
with an increased risk for PPH. Episiot-
omy, for both spontaneous and instru-
mental vaginal deliveries, third or fourth
degree lacerations, and high vaginal and
cervical lacerations have all been associ-
ated with PPH and severe hemorrhage in
individuals experiencing PPH compared
with those without PPH.35,36,38
Delivery by cesarean birth and a his-
tory of prior cesarean birth is associated

with the risk of severe PPH.12,36,46 In a
retrospective cohort study from a large
Californian hospital system including
over 260,000 delivery admissions between
2010 and 2017, hospitalizations where a
severe PPH did occur had a 62.9% cesar-
ean birth rate versus 26.4% cesarean birth
rate in hospitalizations without severe
PPH.12 Importantly, a large retrospective
cohort study found individuals who expe-
rienced cesarean birth in labor, whether
planned or unplanned, were more likely
to experience a severe PPH than those
who experienced unassisted vaginal birth.
Prelabor cesarean birth, whether planned
or unplanned, was associated with re-
duced odds of severe PPH.35 Moreover,
manual removal of placenta at the time of
cesarean birth was found to be signifi-
cantly associated with hemorrhage com-
pared with spontaneous delivery of the
placenta; however, neither blood trans-
fusion requirements nor operating times
differed between these 2 groups.51
Several protective factors for PPH have
also been identified in the literature. The
use of amnioinfusion has been identified
as protective against uterine atony requir-
ing treatment following a vaginal birth.39
In a large French cohort study of 4550
individuals with PPH secondary to uterine
atony after vaginal birth, epidural anes-
thesia was found to be a protective factor
against severe blood loss in individuals
with PPH.36 Interestingly, a smaller co-
hort study reported that individuals who
did not perform skin-to-skin and ab-
stained from breastfeeding were almost
twice as likely to have a PPH ( > 500 mL)
when compared with individuals who had
both (P < 0.001). This finding held true for
individuals both at ‘lower’ risk (defined as
individuals who had a normal vaginal
birth, and excluding antepartum hemor-
rhage, placental previa, polyhydramnios,
and induction or augmentation of labor)
and ‘higher’ risk (defined as individuals
who had any of the following: coagulation
defects, placental anomalies, including
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Epidemiology, Risk Factors 351
antepartum hemorrhage, polyhydram-
nios, induction or augmentation of labor,
and operative birth including cesarean
birth) of hemorrhage.52 In contrast, how-
ever, in a secondary analysis of a 3-arm
double-blind, randomized clinical trial for
different doses of oxytocin looking at the
primary outcome of uterine atony or
hemorrhage, breastfeeding was associated
with an increased risk of PPH compared
with individuals who did not breastfeed.39
Assessment of commonly prescribed
medications in pregnancy and the risk of
PPH has also been published. Unsurpris-
ingly, peripartum anticoagulation use has
been found to be a risk factor for PPH,
particularly severe PPH, while the receipt
of 17-hydroxyprogesterone caproate
within 7 days of delivery and late preg-
nancy calcium-channel blocker use for
hypertension management have not been
associated with PPH risk.5,53,54
FETAL FACTORS
Fetal factors, which are consistently asso-
ciated with increased risk for PPH, include
intrauterine fetal demise, macrosomia,
and multifetal gestation. Intrauterine fetal
demise has been associated with severe
PPH and hemorrhage requiring massive
blood transfusion when compared with
the delivery of a liveborn neonate.35,45,46
Fetal macrosomia, defined as a birth-
weight of 4000 grams or more, has been
associated with severe PPH and appears to
be a risk for atonic PPH specifically.35,38,46
Twin gestation was found to be an inde-
pendent risk factor for treated uterine
atony and for severe PPH compared with
those delivering a singleton.35,38,39
HOSPITAL/PROVIDER FACTORS
In a French cohort study of 4550 individ-
uals with PPH secondary to uterine atony
after vaginal birth, several aspects of PPH
management were associated with the
severity of hemorrhage: administration of
oxytocin more than 10 minutes after PPH
diagnosis with risk increasing even further
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352 Patek and Friedman
at more than 20 minutes after diagnosis,
manual examination of the uterine cavity
more than 20 minutes after diagnosis, and
calling for additional assistance from a
senior obstetrician and anesthesiologist
more than 10 minutes after diagnosis of
PPH. These findings remained significant
after controlling for the characteristics of
the individuals, their labor, and deliveries
before the PPH occurred. Authors found
that delivery in a public nonteaching
hospital was a risk factor for severe hem-
orrhage in individuals experiencing PPH.
In this study, the number of annual deliv-
eries and the presence of a 24-hour obste-
trician were not associated with the
severity of PPH.36 Studies in the United
States have found conflicting results re-
garding obstetric outcomes and hospital
volume and location.55,56
A Dutch study looked at whether
restrictive versus liberal fluid administra-
tion was more likely to result in progres-
sion to more than 1000 mL blood loss in
individuals identified as having 500 mL of
bleeding with ongoing loss in the third
stage of labor. Restrictive fluid adminis-
tration was defined as clear fluids at 0.75
to 1.0 times the volume of blood lost, and
liberal fluid administration was clear flu-
ids at 1.5 to 2.0 times the volume lost. The
authors found that there was no statistical
difference between progression to blood
loss greater than 1000 mL, need for blood
transfusion, alteration in coagulation
parameters, or adverse events between
the 2 groups.57
Risk-Assessment Tools
Despite the identification of multiple risk
factors for PPH, a reliable and high-
performing prediction tool using combina-
tions of multiple risk factors does not yet
exist. A recent (2020) publication reviewed
14 published PPH prediction models and
found that none were ready for clinical use
due to the high risk of bias and the need for
robust external validation. Furthermore,
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none were applicable to the general ob-
stetric population.58
The following year, the California Ma-
ternal Quality Care Collaborative PPH
risk-assessment tool was evaluated in a
retrospective cohort study from a large
Californian hospital system, including over
260,000 delivery admissions between 2010
and 2017, classifying patients into low-risk,
medium-risk, and high-risk groups. The
rate of PPH using the standard definition
of blood loss of 1000 mL or more was 3.2%
in the low-risk group, 10.5% in the
medium-risk group, and 10.2% in the
high-risk group. The rate of severe PPH
(defined as any of the following: (1) trans-
fusion of 4 or more units of packed red
blood cells; (2) transfusion of 1–3 units of
packed red blood cells with a hematocrit of
<18%; or (3) blood loss of 1500 mL with a
hematocrit of <18%) was 0.2% in the low-
risk group, 0.5% in the medium-risk group
and 1.3% in the high-risk group. Notably,
42.7% of hemorrhages occurred in hospi-
talizations that were classified as low
risk.12 In another retrospective study pub-
lished in 2021, the implementation of the
Association of Women’s Health, Obstetric
and Neonatal Nurses hemorrhage risk
assessment tool showed a sensitivity of
85%, specificity of 51%, PPV of 10%, and
NPV of 98% for high- versus low-risk
individuals for predicting PPH. When
comparing outcomes pre-implementation
and post-implementation of the hemor-
rhage risk assessment tool, rates of any
blood transfusion were slightly decreased,
and deliveries with EBL > / = 1,000 mL
also fell significantly (6.3% to 5.9%,
P = 0.014). Findings suggest that the tool
performs moderately well to identify pa-
tients at high risk for hemorrhage, and
awareness of a patient’s risk assessment
score might impact patient outcomes.59
Causes
Keeping in mind that the source of bleed-
ing at the time of delivery may be uterine,

cervical, vaginal, periurethral, periclitor-
al, perineal, perianal, or rectal, one must
have a broad differential diagnosis when
assessing a patient who is experiencing
PPH or signs and symptoms of hypovo-
lemia. There are 4 broad categories de-
scribed when considering the etiology of a
PPH; these are denoted as the ‘4 T’s’:
Tone, Tissue, Trauma, and Thrombin.34
Uterine atony results from an abnor-
mality in uterine contractility following a
vaginal or cesarean birth. Because a term
uterus receives ~600 mL of blood per
minute and control of bleeding in the
immediate postpartum period is primarily
reliant on the contraction of the myome-
trium to constrict uterine blood vessels,
abnormalities in this process place a
patient at risk for significant blood loss
in a short amount of time. Failure of the
myometrium to contract may be the result
of prolonged oxytocin use, high parity,
chorioamnionitis, uterine over-distention,
multiple or large uterine leiomyomata, or
the administration of medications such as
general anesthesia. In addition, uterine
inversion as a cause of PPH may also be
considered in the category of ‘tone’, as an
inverted uterus is unable to contract
normally and is highly associated with
PPH as well as signs and symptoms of
hypovolemic shock. Risk factors for ute-
rine inversion are placenta accreta spec-
trum, short umbilical cord, congenital
weakness of the uterine wall or cervix,
fundal placenta insertion site, uterine
tumors, fetal macrosomia, manual re-
moval of the placenta, inappropriate
fundal pressure and excessive cord trac-
tion, as well as the use of uterotonic
agents before placenta removal.60 Despite
the recognition of many risk factors for
uterine atony, PPH commonly occurs in
individuals without risk factors.39
Most studies report that uterine atony
(‘tone’) accounts for 70% to 80% of cases
of PPH, although there may be overlap
between causes or cases where bleeding is
Copyright r 2023 Wolters Kluwer Health, Inc. All rights reserved.
Epidemiology, Risk Factors 353
multifactorial, which could account for
variation in published data.61 For exam-
ple, in 1 study, uterine atony accounted
for only 38.9% of cases of severe PPH;
however, atony due to retained placental
tissues was categorized into the group of
placental-related causes of hemorrhage
and thus excluded from the atony
group.46 In addition, the use of hospital
data (ie, ‘coded’) has been associated
with overestimating the contribution of
uterine atony as a cause of postpartum
hemorrhage.47 Genital tract laceration
(‘trauma’), retained placenta (‘tissue’),
and abnormalities of coagulation
(‘thrombin’) make up the remainder of
cases of PPH. While genital tract lacer-
ations are reported to make up about 20%
of cases of PPH, ‘trauma’ accounted for
only 2.82% of severe PPH at a referral
hospital for critical pregnant individuals
in China.34,46 Retained placental tissue
accounts for ~10% of cases but was
responsible for a majority of severe PPH
cases, 55.8%, in that same referral
hospital.46 The prevalence of coagulop-
athy is typically around 1% of cases of
PPH but accounts for a significant per-
centage (15%) of cases requiring massive
blood transfusion.34,45
Secondary PPH, hemorrhage occur-
ring beyond 24 hours following delivery,
accounts for only 1% to 2% of PPH cases.
Causes of secondary PPH extend to in-
clude uterine subinvolution, retained
products of conception, endomyometritis,
uterine arteriovenous malformation, and
inherited coagulopathies such as von
Willebrand’s disease.34
Ultimately, a thorough understanding
of the epidemiology, risk factors, and
causes of PPH will allow for anticipation
and thorough and prompt patient assess-
ment and management in cases of PPH.
This information is also useful for the
development of prevention protocols,
which may help to reduce the burden of
disease.
www.clinicalobgyn.com
354 Patek and Friedman
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