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Postpartum Hemorrhage Nursing CE Course for APRNs

2.5 ANCC Contact Hours

0.5 ANCC Pharmacology Hours

About this course:

This learning activity aims to provide a comprehensive overview of postpartum hemorrhage (PPH), outlining the prevalence, risk factors, clinical features, causes, diagnostic criteria, and evidence-based treatment modalities.

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Postpartum Hemorrhage 

Disclosure Statement

This learning activity aims to provide a comprehensive overview of postpartum hemorrhage (PPH), outlining the prevalence, risk factors, clinical features, causes, diagnostic criteria, and evidence-based treatment modalities.

Upon completion of this module, learners will be able to:

  • analyze the risk factors and common causes of PPH
  • describe the clinical features of and diagnostic criteria for PPH
  • use the components of a PPH risk-assessment tool to determine the level of individual risk
  • explain the complications of PPH in the pregnant individual
  • summarize the benefits, risks, adverse effects, and monitoring parameters for drugs used for the treatment of PPH


Postpartum hemorrhage (PPH) is the leading preventable cause of death among postpartum individuals. PPH is a global problem; when it occurs, it is considered a medical emergency requiring immediate intervention. According to the World Health Organization (WHO), PPH is a complication in 14 million or 5% of all deliveries and is responsible for over 25% of maternal deaths worldwide. Every 4 minutes, an individual dies due to PPH. Unfortunately, there is underreporting of the incidence of PPH, and some cases may be attributed to another cause of death. In low-income countries, PPH outcomes are poor compared to higher-income countries, and PPH is the primary cause of maternal mortality in low-income countries. In the United Kingdom (UK), the rate of maternal death from PPH is 0.01% or 1 in 100,000 births compared to 20% or 1 in 1,000 births in low-income African areas. This variation is attributed to a lack of resources, poor nutrition, limited maternal care, and the prevalence of diseases such as malaria, which affects the placenta (WHO, 2020).

PPH is also one of the most common causes of maternal mortality in the US. Between 2016 and 2018, 11.1% of all maternal deaths were attributed to PPH. PPH occurs in an estimated 1% to 6% of all deliveries. Maternal mortality rates due to PPH vary based on race and ethnicity. PPH is the leading cause of death among American Indian and Alaska Natives (AIANs), accounting for 19.7% of all maternal deaths, followed closely by Asian Pacific Islanders (APIs) at 19.5% and 15.8% of all Hispanic maternal deaths. PPH is responsible for 9.7% of non-Hispanic Black and 9.1% of non-Hispanic White maternal deaths. AIANs and APIs are twice as likely to die from PPH than non-Hispanic Black or non-Hispanic White individuals. These variations in mortality rates due to PPH can be attributed to the limited resources for high-quality prenatal care and qualified healthcare providers (HCPs) who are knowledgeable and equipped to care for patients at high risk for PPH in specific communities (Centers for Disease Control and Prevention [CDC], 2022; Declercq & Zephyrin, 2020; Wormer et al., 2022).

In addition to maternal mortality, severe PPH (blood loss > 1,000 mL) is the most common cause of maternal morbidity. As a result of PPH, an individual may experience respiratory distress syndrome, acute renal failure, shock, myocardial ischemia, and reproductive loss due to hysterectomy. PPH can also lead to chronic anemia, which is considered a severe life-threatening illness in low-income countries where treatment is unavailable. PPH causes acute and long-term complications in 20 million individuals globally, equating to 4.5 to 6.7 for every 1,000 deliveries (Rath, 2011).


Various terms are associated with PPH, including early or late and primary or secondary. Early or primary PPH occurs during delivery or within the first 24 hours post-delivery. Late or secondary PPH occurs 24 hours post-delivery up to 12 weeks postpartum. The risk of maternal mortality due to PPH decreases as the postpartum period progresses. In the US between 2007 and 2016, PPH caused 20% of maternal deaths during pregnancy or delivery, 12% of deaths within 42 days of delivery, and 3% of deaths between 43 days and 1-year post-delivery (Belfort, 2022a; Declercq & Zephyrin, 2020).

Risk Factors and Causes

Many factors increase an individual's risk of PPH. Some of these are easily identifiable before delivery, and the care team can be prepared in advance. Based on risk, delivery options and birth plans can be adjusted for the maximum safety of the pregnant individual and their fetus. Risk factors can be divided based on the cause, such as maternal history, surgical history, fetal factors, and placental or uterine issues or abnormalities (Watkins & Stem, 2020). Risk factors for PPH include:

  • Medical or surgical risks
    • personal history of PPH during a previous pregnancy
    • maternal family history of PPH, including mother or sister
    • leiomyomata (uterine fibroids)
    • previous cesarean delivery or uterine surgery
  • Fetal-induced risks
    • large-for-gestational-age fetus
    • multifetal gestation
    • polyhydramnios
    • fetal macrosomia (birthweight ≥ 4,000 g)
  • Maternal risks
    • hypertensive disorders of pregnancy, including preeclampsia and eclampsia
    • anemia
    • inherited coagulopathies (e.g., von Willebrand disease [vWD])
    • acquired coagulopathies (e.g., hemolysis, elevated liver enzyme levels, and low platelet levels (HELLP) syndrome)
    • attempting a vaginal birth after cesarean (VBAC)
    • prolonged labor
    • oxytocin (Pitocin)-induced labor
    • failure to progress during the second stage of labor
    • the use of assistive devices during delivery (e.g., forceps)
    • race/ethnicity
    • obesity
    • precipitous labor
    • pregnancy via assisted reproductive technology
    • post-term pregnancy
    • magnesium sulfate administration during labor
    • the use of an antithrombotic or antidepressant during pregnancy, especially selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors (SNRIs)
  • Placenta/uterine issues
    • placental accreta (slight penetration of myometrium), increta (deep penetration of myometrium), or percreta (placenta perforates the uterine wall and can attach to nearby organs)
    • placenta previa
    • placental abruption
    • retained placenta
    • chorioamnionitis (inflammation of the chorion of the placenta)
    • uterine inversion
    • uterine overdistention
    • uteroplacental apoplexy (a severe form of placental abruption; Belfort, 2022a; Lowdermilk et al., 2016; Watkins & Stem, 2020)

There are risk-assessment tools that can assist HCPs in identifying individuals at an increased risk of developing PPH. One such tool was developed by the Association of Women's Health, Obstetric and Neonatal Nurses (AWHONN). Table 1 outlines the risk assessment developed by AWHONN. When used appropriately, risk assessment tools have accurately identified 60% to 85% of patients who will experience PPH; however, approximately 1% of individuals identified as low risk based on risk factors ended up experiencing PPH (American College of Obstetricians and Gynecologists [ACOG], 2017; Colalillo et al., 2021).

Table 1

AWHONN PPH Risk Assessment 

Low Risk

Moderate Risk

High Risk



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single-fetus pregnancy

multiple-gestation pregnancy

hematocrit (HCT) < 30%

no personal or maternal history of PPH

presence of large uterine fibroids

personal or maternal history of PPH

uterus without scarring

history of any procedure leading to uterine scarring, including cesarean delivery

presence of placental previa, accreta, increta, or percreta

history of ≤ 4 deliveries

history of > 4 deliveries

identified coagulation deficiencies


vaginal bleeding upon presentation to the provider or care facility

use of magnesium sulfate during labor or delivery

vital sign changes (i.e., tachycardia, hypotension, or tachypnea)

administration of oxytocin (Pitocin) over an extended period

  • (ACOG, 2017; Colalillo et al., 2021)

There are four primary causes of PPH. These causes are identified by the mnemonic the 4 Ts (ACOG, 2017; Belfort, 2022a):

  • Tone - uterine atony
  • Tissue - retained placenta
  • Trauma - lacerations, forceps-assisted birth, vacuum-assisted birth, cesarean delivery
  • Thrombin - coagulation (Belfort, 2022a)


Uterine atony is the most common cause of PPH. Uterine atony occurs in 1 in 40 births in the US, and 70% to 80% of all PPH cases are caused by uterine atony. An individual's vascular system is exposed when the placenta detaches from the uterine wall. To close these vessels and prevent bleeding, the uterus contracts. Uterine atony occurs when the uterus cannot contract effectively following delivery of the placenta or does not contract when palpated by the HCP, preventing proper clotting. There are two types of uterine atony: diffuse and focal. When diffuse atony occurs, most of the hemorrhaged blood is contained within the uterus, limiting accurate estimations of the total blood volume lost. When focal atony occurs, there is only localized atony. Upon assessment, one area of the uterus (e.g., the fundal region) is contracting as expected, while another area (e.g., the lower segment) remains dilated and soft or boggy. Focal atony can be challenging to assess with palpation alone (Belfort, 2022a; Lowdermilk et al., 2016).

The most common risk factors for the development of uterine atony include a personal history of PPH in a previous pregnancy and prolonged labor. Other risk factors for uterine atony include a large-for-gestational-age fetus; the presence of multiple fetuses; polyhydramnios; the use of halogenated anesthesia drugs such as halothane (Fluothane), enflurane (Ethrane), isoflurane (Forane), sevoflurane (Ultane), or desflurane (Suprane) during delivery; the use of magnesium sulfate; chorioamnionitis; and uterine inversion. Although uterine atony is the leading cause of PPH, it is highly responsive to treatment with uterotonic medications such as oxytocin (Pitocin), misoprostol (Cytotec), ergometrine (Ergotrate), or methylergometrine (Methergine). Therefore, PPH caused by uterine atony does not usually require blood products. Due to the prevalence of uterine atony, the administration of uterotonic medications prophylactically has become standard practice. The prophylactic administration of oxytocin (Pitocin) is described below (Belfort, 2022a; Lowdermilk et al., 2016).


Retained tissue following delivery also inhibits uterine contractions. The placenta is considered retained when it is not expelled or delivered within 30 minutes of fetal delivery despite interventions. Slight traction can be applied to the umbilical cord coupled with a gentle external massage of the uterus to promote placental delivery. Retained placental fragments cause excessive bleeding. Upon assessment, the uterus feels boggy due to the uterine atony that results from an inability to contract normally. An ultrasound can be performed to assess for placental fragments, or the HCP may choose to complete a manual exam. If retained tissue is present, the initial intervention is manually removing the tissue to promote natural contraction. HCPs may also utilize uterine curettage to assist in the removal of placental fragments. These procedures can be uncomfortable for patients. Supplemental medication is not usually required if an epidural or another kind of regional anesthesia is administered for delivery. If the patient has not received anesthesia, it is recommended that nitrous oxide or halogenated anesthetics be administered via inhalation, or other analgesic medications should be administered intravenously (IV). Nitroglycerin (Nitrostat) or an alternative tocolytic medication is also administered IV to promote uterine relaxation to facilitate the removal of the retained tissue. Even after the removal of the retained tissue, the patient continues to be at an increased risk for PPH (Lowdermilk et al., 2016).

In some instances, retained placenta or placental fragments are due to abnormal placental development and adherence to the uterine wall. This abnormal adherence can be partial or complete and is labeled based on the degree of adhesion: placenta accreta, placenta increta, and placenta percreta. Placenta accreta is the most common abnormal placental adherence and is growing in incidence due to the increase in cesarean deliveries performed. In these cases, attempts to separate the placenta from the uterine lining manually can result in further damage, including laceration or perforation of the uterus, increasing the risk of PPH. Other risk factors for retained tissue are the presence of placenta previa, a history of uterine surgery (including cesarean delivery), endometrium abnormalities, fibroids, parity, and maternal age. Although these placental abnormalities can be discovered during an ultrasound, they are often not diagnosed until after delivery, when excessive bleeding occurs after removing the retained tissue. Often, the administration of blood products is needed to replace the blood volume lost. In some cases, a hysterectomy is necessary to prevent maternal mortality due to PPH (Lowdermilk et al., 2016).


Due to multiple variables, birth can cause physical trauma to a pregnant individual. Locations that commonly experience trauma are the cervix, vagina, and perineum. Lacerations to these areas can lead to PPH. A laceration should be suspected if bleeding following delivery continues despite the uterine contracting as expected upon assessment. Bleeding from a laceration can be described as oozing, a trickle, or frank blood loss. Factors that increase the risk of trauma during delivery consist of delivery via cesarean section, precipitous labor, anatomical anomalies of the pregnant individual, abnormal fetal presentation, a fetus that is large for their gestational age, presence of scarring from a previous injury or surgical procedure, vaginal birth facilitated with the use of instruments such as forceps, or having a midline episiotomy. Two specific risk factors for PPH after a cesarian section are undergoing a cesarean section after reaching complete dilation and the incision made to deliver the fetus. An incision that is too low in the uterine segment, is too straight and not curved enough, or is not initially large enough for the fetus to be easily delivered increases the risk for PPH. PPH can also be caused by uterine rupture (Belfort, 2022a; Lowdermilk et al., 2016).

When there is evidence that bleeding originates from a cervical laceration, a high vaginal laceration, or is complicated by arterial blood loss, intervention and repair of the damaged area are necessary. If significant blood loss originates from a distal vaginal, perineal, vulvar, or periclitoral laceration without clotting, repair of these areas is indicated. If it is suspected that PPH is caused by trauma to the uterine artery, a transfer to the operating room or interventional radiology for further assessment and treatment is indicated. If vital signs become unstable following precipitous labor, the patient should be assessed for genital tract hematomas. These hematomas can be labial, vaginal, broad ligament, or retroperitoneal. Often, treatment is conservative; however, vital sign changes can indicate that the hematoma is rapidly enlarging and progressing in severity. If this occurs, an incision and drainage (I&D) procedure is required to treat the hematoma. Due to the additional care required and the risk of infection following an I&D, many providers prefer utilizing arterial embolization to manage enlarged hematomas. Vital sign changes without a visible cause strongly indicate that the individual may be bleeding into the intraperitoneal or retroperitoneal spaces. This type of PPH is considered a medical emergency, and resuscitative equipment should be located near the patient. At the same time, diagnostic imaging and transportation to interventional radiology or the operating room for treatment should occur (ACOG, 2017).

Any lacerations that occur are often quickly recognized and sutured to prevent bleeding. Once suturing occurs, the patient should receive the same care as an individual that underwent an episiotomy. The patient may require analgesics to reduce pain and the application of cold or hot compresses as needed. Lacerations in the perineum often cause patients anxiety about their first bowel movement post-delivery. Patients should be encouraged to increase their daily fiber and fluid intake to prevent constipation, especially when using opioid analgesics for pain control. Without adequate fluid intake, increasing dietary fiber intake may exacerbate constipation. Stool softeners can help promote bowel activity and prevent further injury at the incision site by decreasing the need for straining (Lowdermilk et al., 2016).


Coagulation disorders complicate 1 in 500 births in the US and cause 7% of all PPH cases. Coagulation disorders can be inherited or acquired. The most common inherited coagulation disorders causing PPH are vWD and idiopathic thrombocytopenic purpura (ITP). Acquired coagulation abnormalities are more common in patients with intrauterine fetal demise, placental abruption, HELLP syndrome, amniotic fluid embolism, or sepsis which can lead to disseminated intravascular coagulopathy (DIC; Belfort, 2022a; Watkins & Stem, 2020; Wormer et al., 2022).

ITP is an autoimmune disorder that involves platelets. In this condition, antiplatelet antibodies target the platelets, decreasing their lifespan. ITP increases the risk of PPH following cesarean delivery or when lacerations occur following vaginal delivery. If the condition is diagnosed during the antenatal period, administering corticosteroids or IV immunoglobulin can prevent PPH from ITP. When bleeding occurs despite prophylactic treatment, platelets can be administered IV to promote clotting. When bleeding persists despite medical management, a splenectomy may be performed. vWD is an inherited form of hemophilia. Although considered a rare disorder, vWD is the most common clotting disorder in women of reproductive age. It is caused by a deficiency in the blood clotting protein von Willebrand factor (vWF). Symptoms present in patients with vWD that can be identified prior to pregnancy include frequent nosebleeds, bruising easily, prolonged bleeding time, and factor VIII deficiency. Individuals with vWD are at an increased risk of hemorrhage up to 4 weeks post-delivery. Treatment includes the administration of desmopressin (DDAVP) since it promotes the release of vWF. Other treatment options include administering plasma products containing factor VIII and vWF or concentrated antihemophilic factors (Lowdermilk et al., 2016).

The most common causes of acquired coagulation disorders leading to PPH are amniotic fluid embolism and placental abruption. Experiencing an amniotic fluid embolism is rare, but when it occurs, it is considered an obstetric emergency. Due to the inability to prevent this type of embolism and its unpredictable trajectory, outcomes are often poor. Patients with an amniotic fluid embolism present with a triad of symptoms, including rapid respiratory decline, hemodynamic changes, and DIC. Due to coagulation changes, an amniotic fluid embolism almost always leads to PPH. Treatment includes fluid volume expansion and initiation of a massive transfusion protocol. Placental abruption also requires the initiation of massive transfusion protocols, accounting for 17% of all protocol use cases. Visual hemorrhage may not be present following placental abruption due to intrauterine bleeding; however, patients may report pelvic pain. Uterine tachycardia is evident if the patient is being monitored using a tocodynamometer. Contractions on the monitor appear as high-frequency and low-amplitude (ACOG, 2017; Belfort, 2022a; Watkins & Stem, 2020; Wormer et al., 2022).

Uterine Anomalies 

In addition to the 4 Ts, PPH can be caused by uterine anomalies such as inversion or subinvolution of the uterus (ACOG, 2017).

Inversion of the Uterus 

Inversion of the uterus occurs when the uterus inverts or turns inside out following delivery. Inversion of the uterus is rare, with an incidence of only 1 in 3,700 to 1 in 20,000 vaginal births and 1 in 1,860 cesarean deliveries. If a patient has a history of inversion of the uterus, their risk in subsequent pregnancies increases to 1 in 26 births. When uterine inversion occurs, it is considered a medical emergency. The inversion of the uterus can be incomplete, complete, or prolapsed. Incomplete inversion cannot be visualized. Assessment findings include a mass that can be palpated through the cervix while dilated. Complete inversion is noted when the lining of the fundus crosses through the cervical os and can be felt within the vagina. A prolapsed inversion is the most apparent form of uterine inversion. When prolapse occurs, a large, red, round mass protrudes approximately 20 to 30 cm outside the vaginal opening. Risk factors for the development of an inverted uterus include implantation of the placenta in the fundus, application of forceful fundal pressure, application of excessive traction on the umbilical cord when attempting to dislodge the placenta, fetal macrosomia, a short umbilical cord, tocolysis, uterine atony, prolonged labor, nulliparity, and placental tissue that is adhered to the uterine wall abnormally. Initial signs and symptoms include pain, shock, and hemorrhage with an inability to palpate the uterus abdominally (ACOG, 2017; Lowdermilk et al., 2016; Wormer et al., 2022).

The umbilical cord should not be pulled unless there are clear indications that the placenta has been separated from the uterine wall to prevent inversion of the uterus. Uterine inversion is a medical emergency requiring immediate intervention, including fluid resuscitation and returning the uterus to its proper position within the abdominal cavity. The provider does this by placing their fist or palm against the fundus and applying upward pressure to return the uterus to its proper position. Before attempting to reposition the uterus, HCPs may administer tocolytics or halogenated anesthetics to relax the uterus. Terbutaline (Bricanyl, Marex), magnesium sulfate, halogenated general anesthetics, and nitroglycerin (Nitrostat) can be used for this purpose. There is no evidence that one drug is superior to any other. After the uterus is properly placed, oxytocic medications are administered to maintain uterine positioning, and prophylactic broad-spectrum antibiotics are initiated to prevent infection. Supportive treatment can be used to prevent a recurrence following successful uterus replacement and corrected inversion. Intrauterine tamponade balloons or uterine compression sutures can be placed in the uterus to prevent inversion and maintain proper uterine placement (ACOG, 2017; Lowdermilk et al., 2016; Wormer et al., 2022).

Subinvolution of the Uterus 

Late PPH, occurring more than 24 hours after delivery, can be caused by subinvolution of the uterus. This occurs when there is a delay in the uterus returning to its pre-pregnancy size. Possible causes of subinvolution of the uterus include retained tissue or infection of the pelvis. Signs and symptoms include prolonged lochial discharge and irregular and excessive bleeding enough to be categorized as hemorrhage. Upon physical exam, the uterus presents as boggy and larger than expected for the time after delivery. The cause of the subinvolution dictates the treatment. If placental fragments are retained, treatment includes performing a D&C to remove the tissue. If an infection is identified, treatment involves initiating antibiotic therapy. In addition to these treatment options, ergonovine (Ergotrate) or methylergonovine (Methergine) is often given at 0.2 mg every 3 to 4 hours for 24 to 48 hours (Lowdermilk et al., 2016).


A diagnosis of PPH is based on clinical assessment. Different diagnostic tools can be used to determine if PPH is present. There are also various classification or staging systems for the severity of PPH. The ACOG defines PPH as blood loss of at least 1000 mL or any amount of blood loss combined with symptoms of hypovolemia within 24 hours of delivery, independent of the status of the fetus or mode of delivery. This definition differs from more traditional definitions outlined by other organizations. Despite these guidelines, the ACOG notes that an estimated blood loss greater than 500 mL following a vaginal delivery is abnormal and requires close monitoring and possible intervention. The guidelines proposed by the ACOG aim to reduce the number of patients incorrectly treated for PPH (ACOG, 2017).

The California Maternal Quality Care Collaborative (CMQCC) has also created a staging system to determine the severity of PPH. This system has four stages from 0 to 3 (Belfort, 2022a):

  • Stage 0: this stage includes every individual in labor or actively delivering.
  • Stage 1: this stage is characterized by an estimated blood loss following vaginal. Delivery of ≥ 500 mL or following cesarean delivery of ≥ 1000 mL with continued hemorrhaging that is not controlled; signs of a concealed hemorrhage such as tachycardia (≥ 100 bpm), hypotension (≤ 85/45 mmHg), and hypoxia (SpO2 ≤ 95%); or the presence of mental status changes.
  • Stage 2: the estimated blood loss for either type of delivery is ≥ 1500 mL with continued hemorrhaging or further deterioration and instability of vital signs.
  • Stage 3: this stage is characterized by the presence of continued hemorrhaging despite treatment with an estimated blood loss of > 1500 mL, or the patient has received more than 2 units of packed red blood cells (PRBCs), or their vitals further deteriorate or remain unstable, or there is the potential that the patient is experiencing DIC.

Another classification system used for PPH is the Advanced Trauma Life Support classification. This system uses four classes to demonstrate the progression of PPH based on signs and symptoms (Belfort, 2022a):

  • Class I: the patient has lost 15% of their total blood volume, and their heart rate is normal to slightly elevated above baseline with no changes to other vital signs.
  • Class II: between 15% and 30% of total blood volume has been lost, and there are signs of hypovolemia, including tachycardia (100 to 120 bpm), tachypnea (20 to 24 breaths/min), decreased pulse pressure, prolonged capillary refill, and skin that is cool and clammy to the touch. Even if bleeding is light or minimal, PPH protocols should be initiated when tachycardia and tachypnea are present, even if the patient is normotensive, as this can be an indicator of compensated hypovolemic shock.
  • Class III: the loss of 30% to 40% of a patient's total blood volume leading to profound hypotension with systolic blood pressure (SBP) < 90 mmHg or a decrease in blood pressure by 20% to 30% compared to baseline and mental status changes; these changes may be attributed to the decrease in pain and anxiety that occurs following delivery but should be treated as PPH until proven otherwise due to the risk of maternal mortality associated with PPH. Other signs and symptoms that may be present include tachycardia (≥ 120 bpm) with a thready pulse, tachypnea, decreased urine output, and sluggish capillary refill.
  • Class IV: a loss of ≥ 40% of total blood volume resulting in hypotension with an SBP ≥ 90 mmHg, tachycardia with a heart rate ≥ 120 bpm, mental status changes, oliguria or anuria, sluggish capillary refill, and skin that is cool and moist to the touch.

When PPH is suspected, laboratory studies should be performed to provide further information about the patient's vascular status and give the HCP more information to direct treatment. Treatment must not be delayed by waiting for laboratory testing results. It should also be considered that the patient's status may have further deteriorated or improved by the time laboratory results are available. Examples of laboratory testing that should be performed include a complete blood count (CBC), coagulation studies, and type and screen or crossmatch. A CBC is used to monitor hemoglobin, hematocrit, and platelet counts. A type and screen or crossmatch are completed in preparation for the patient needing a blood transfusion to replace blood volume. Coagulation studies and fibrinogen levels are monitored to determine if the patient is experiencing DIC or if an underlying coagulation issue needs to be addressed (ACOG, 2017; Wormer et al., 2022).

Estimating Blood Loss 

In the past, blood loss volume was based on changes in HCT. PPH was suspected when the HCT decreased by 10%; however, obtaining these results is not immediate. This delay makes it difficult to determine changes in blood volume in real time and may delay treatment leading to poor maternal outcomes. Historically, blood loss was also estimated by weighing linens or pads saturated in fluid and HCP visual estimation. According to the ACOG, estimating blood loss via visual assessment is inaccurate. Often, HCPs underestimate the amount of blood lost when relying on visual estimation. To decrease the morbidity and mortality rates from PPH, the Alliance for Innovation on Maternal Health developed patient safety bundles that are being implemented in hospitals and birthing centers across the US. One component of these safety bundles is accurately quantifying cumulative blood loss. The quantification of blood loss (QBL) is recommended based on standardized methods utilized for every birth (ACOG, 2019; Befort, 2022; Watkins & Stem, 2020):

  • Volumetric measurement requires that blood be collected and measured in a graduated container, which may include suction canisters or drapes that have calibrated pockets.
  • Gravimetry requires a known dry weight of supplies; after delivery, the weight of the saturated supplies is determined. The difference between dry and wet weights in grams equates to a volume in mL.
  • Colorimetry uses an application on a smart device with a camera that can calculate blood loss. The application works by filtering out non-blood contents from blood in a specific photograph; it then approximates the hemoglobin mass present, which is then subtracted from the pre-procedure hemoglobin level.
  • Visual aids are posters or other visual representatives demonstrating how to estimate blood loss based on the color and appearance of the blood on commonly used supplies, including a pad, bed sheet, or surgical sponge.

When visually estimating blood loss, HCPs must consider other sources of fluid that can appear mixed in with the blood, such as urine, amniotic fluid, or irrigation fluid (Belfort, 2022a).


Treatment of PPH focuses on stabilizing and resuscitating the patient while simultaneously completing diagnostics to determine the cause of the PPH. Once the cause is known, specific treatment can be initiated. For example, lacerations causing excessive blood loss should be repaired. Any retained placental tissue should be removed. The goal of treatment is to address the underlying cause of the PPH and prevent further blood loss, maintain adequate perfusion to limit effects on vital organs, and stabilize the patient. Available treatment modalities consist of pharmacologic management, non-surgical treatments, and surgical interventions (Wormer et al., 2022).

Pharmaceutical Interventions 

Pharmaceutical interventions include administering uterotonic agents such as oxytocin (Pitocin), ergot alkaloids, and prostaglandins (Wormer et al., 2022). The most common medications used to treat PPH are:

  • oxytocin (Pitocin)
  • carboprost (Hemabate)
  • methylergonovine maleate (Methergine)
  • misoprostol (Cytotec)
  • tranexamic acid (TXA, Cyklokapron; ACOG, 2017; Wormer et al., 2022)

Oxytocin (Pitocin) 

Oxytocin (Pitocin) is the first-line treatment and prevention option for PPH. Oxytocin (Pitocin) is a synthetically produced version of the natural form produced and released from the posterior pituitary gland. It stimulates myometrium contraction, constricting uterine blood vessels and decreasing blood flow. When used prophylactically, it can be administered as a continuous IV infusion, IV bolus, or intramuscularly (IM) when IV access is not available. Unfortunately, there are no standard recommendations for infusion rates when administered as a continuous infusion. However, the infusion should be at a rate sufficient to maintain uterine contraction (ACOG, 2017; Evensen et al., 2017; Lagrew, 2022). Prophylactic initial dosing based on the route of administration is as follows:

  • infusion: 10 units to 30 units diluted in 500 mL 0.9% normal saline solution or 20 units to 60 units diluted in 1000 mL 0.9% normal saline solution at a standard rate
  • bolus: initial administration of 1 unit to 3 units to promote an increase in uterine tone; follow bolus dose with a continuous infusion to maintain the uterine tone
  • IM: 10 units can be administered once following delivery of the placenta, but this route is not ideal (ACOG, 2017; Lagrew, 2022)

When administered as treatment, the initial dosing is 10 units to 40 units diluted in 500 to 1000 mL of 0.9% normal saline solution. A bolus dose can be given over 10 to 15 minutes before starting the maintenance dose. Oxytocin (Pitocin) infusion should not exceed 30 to 40 units/hour (ACOG, 2017; Lagrew et al., 2022).

Oxytocin (Pitocin) should not be administered by multiple routes simultaneously. Adverse effects include nausea, vomiting, seizures, uterine rupture, impaired uterine perfusion, and hyponatremia. Prolonged use can also cause water intoxication due to antidiuretic effects. The rapid administration of concentrated oxytocin (Pitocin) should be done cautiously due to the risk of tachycardia and hypotension. This is especially true for patients with uterine atony. When administering higher doses of oxytocin (Pitocin), HCPs should monitor pulse oximetry, blood pressure, heart rate, and cardiac rhythm continuously. Oxytocin (Pitocin) is contraindicated in instances of fetal distress when delivery is not imminent. It should be used cautiously when cervical cancer is present, or the patient has a history of uterine surgery (Evensen et al., 2017; Woods, 2023).

Carboprost (Hemabate)

This is one of the second-line drugs to treat PPH due to uterine atony. Carboprost (Hemabate) works by increasing the number of available oxytocin receptors, thereby improving uterine contractility. It also causes vasoconstriction, leading to decreased blood flow. Carboprost (Hemabate) is administered IM or directly into the myometrium layer of the uterus. Dosing is 250 mcg repeated every 15 to 90 minutes as needed up to a maximum dose of 2 mg or eight doses. Adverse effects include nausea, vomiting, diarrhea, flushing, fever, bronchospasm, and hypertension. This medication should not be used in patients with a history of asthma, other pulmonary diseases, renal or hepatic failure, or cardiac disease (ACOG, 2017; Evensen et al., 2017; Woods, 2023).

Methylergonovine Maleate (Methergine) 

Along with carboprost (Hemabate), Methylergonovine maleate (Methergine) is used as a second-line drug to treat PPH. Methylergonovine maleate (Methergine) is an ergot alkaloid that decreases hemorrhage by promoting uterine contraction and vascular constriction. Dosing is 0.2 mg administered either via IM injection or orally. Dosing is repeated every 2 to 4 hours as needed when given IM and every 6 to 8 hours when given orally. Oral dosing can continue for 1 week to prevent the recurrence of PPH. Adverse effects include nausea, vomiting, diarrhea, and hypertension. Symptoms of toxicity consist of hallucinations, chest pain, or myocardial infarction. Methylergonovine maleate (Methergine) should not be administered to individuals with cardiovascular disease, hypertension, or preeclampsia. It must be used cautiously in patients diagnosed with human immunodeficiency virus (HIV) who are being treated with protease inhibitors (ACOG, 2017; Evensen et al., 2017; Lagrew et al., 2022).

Misoprostol (Cytotec) 

Misoprostol (Cytotec) is a prostaglandin E1 analog approved by the US Food and Drug Administration (FDA) for treating and preventing stomach ulcers. It has been used off-label in obstetric patients for labor induction, abortion, and control of PPH. Due to adverse effects and inconsistent results, treatment with misoprostol (Cytotec) is only recommended for patients with asthma or hypertension who are unable to tolerate treatment with carboprost (Hemabate) and methylergonovine (Methergine). Misoprostol (Cytotec) can be administered orally or sublingually. In the past, the drug could be administered rectally; however, due to an extended onset of action, that route is no longer recommended. The dosing of misoprostol (Cytotec) is 600 mcg orally or 800 mcg sublingually. Adverse effects include nausea, vomiting, diarrhea, pyrexia, headaches, and shivering. Misoprostol (Cytotec) must be used cautiously in patients with a history of cardiovascular disease (Evensen et al., 2017; Lagrew et al., 2022).

Tranexamic Acid (Cyklokapron) 

Using TXA (Cyklokapron) has been shown to decrease PPH maternal mortality when initiated within 3 hours of identifying the presence of PPH. TXA (Cyklokapron) is a lysine analog and antifibrinolytic and works by inhibiting the natural breakdown of fibrin and fibrinogen by plasma. TXA (Cyklokapron) is an adjuvant treatment for all causes of PPH. The recommended dosing is 1 gram IV administered over 10 minutes. Dosing can be repeated after 30 minutes if bleeding continues or stops and then restarts within 24 hours after the initial dose. Adverse effects include nausea, vomiting, diarrhea, hypotension, dermatitis, seizures, visual disturbances, or dizziness. Treatment is contraindicated in patients with subarachnoid hemorrhage or intravascular clotting. Due to its high renal clearance, TXA (Cyklokapron) is contraindicated in patients with renal failure (Evensen et al., 2017; Lagrew et al., 2022).

Blood Transfusion 

There are instances where a blood transfusion is needed post-delivery. Administration of PRBCs is used to maintain an HCT of 21% to 24%. It is estimated that in the US, a blood transfusion is needed in 0.5% to 1.4% of all deliveries. Although blood transfusions are not uncommon, the need for a mass transfusion is rare, only occurring in 2.3 to 9.1 per 10,000 deliveries. Different standards used to define a mass transfusion range from the administration of 4 units of PRBCs in 1 hour to 10+ units administered in 24 hours. In order to improve maternal outcomes, facilities should have a protocol in place with system-wide and regional collaboration to ensure that sufficient volumes of blood products are readily available when needed. Two pathways exist for obtaining blood products in an emergent situation. The first is the emergent release of PRBCs. In this case, the blood bank immediately releases 2 units of PRBCs to be available at the patient's bedside. If a type and crossmatch has already been completed, crossmatched blood should be used; however, if a crossmatch has not occurred, transfusion should not be delayed, and O-negative blood should be used as a substitute. A mass transfusion protocol (MTP) must be initiated if bleeding continues. When an MTP is activated, 4 units to 6 units of PRBCs, 4 units of fresh frozen plasma (FFP), and 1 unit of platelets are made available for administration to the patient. The ACOG recommends an initial transfusion ratio of PRBCs to FFP to plasma of 1:1:1, mimicking the ratio found in whole blood. A survey of hospitals across the nation found that 80% follow a 1:1 PRBC-to-plasma ratio. Previously promoted protocols followed ratios of 4:4:1 or 6:4:1 of PRBC to FFP to plasma. FFP should be infused to maintain an INR below 1.5 to 1.7, and platelets should be infused to maintain a platelet count above 50,000/uL. Because of the influence of PPH on maternal mortality rates, the Joint Commission now requires facilities that provide labor and delivery care to have an MTP in place (ACOG, 2017; Lagrew et al., 2022).

Although transfusions often improve maternal outcomes and prevent mortality, there are adverse effects of administering blood products. When following an MTP, there is a risk of hyperkalemia due to the volume of PRBCs administered. There is also the risk of citrate toxicity due to the citrate used to preserve blood products. Citrate toxicity can cause or exacerbate hypocalcemia. Other transfusion-related adverse reactions include febrile nonhemolytic transfusion reactions (FNTRs) and acute hemolytic transfusion reactions (AHTRs). FNTRs are characterized by a temperature of above 38 ˚C (100.4 ˚F) or an increase in temperature by 1 ˚C (1.8 ˚F) with the presence of chills and rigors within 4 hours of the blood transfusion. AHTRs occur due to ABO incompatibility and are characterized by a fever, chills, nausea, vomiting, dyspnea, oliguria, hemoglobinuria, and chest, abdominal, and flank pain. Aggressive fluid resuscitation can lead to serum dilution affecting coagulation abilities. This extra fluid can also lead to pulmonary edema and respiratory complications (ACOG, 2017; Goldman, 2020).

Uterine Tamponade 

If the administration of uterotonic medications, TXA (Cyklokapron), and bimanual uterine massage do not control PPH, the HCP may use uterine tamponade. Uterine tamponade involves using a simple intrauterine balloon catheter, uterine pack, or vacuum-assisted suction to decrease bleeding until other interventions, including surgery, can be initiated if necessary (Belfort, 2022b; Moldenhauer, 2022).

Many institutions utilize a uterine tamponade kit due to its ease and speed of use. These kits include a catheter, a condom, sterile string, a 60 mL syringe, IV tubing, and a 500 mL bag of IV fluid (e.g., 0.9% normal saline solution). To make the uterine tamponade, the condom is placed over the catheter and tied at the opening to secure it to the catheter. The condom-covered catheter is then inserted through the cervix into the uterus. Once properly placed, 300 mL to 500 mL (or until the condom is visualized at the level of the cervix) of the IV solution is instilled through the catheter into the condom. This process expands the condom until it presses against the uterine wall, providing pressure to stop the bleeding. A similar device is known as the Bakri balloon. This is a silicone balloon inflated with 500 mL of solution after insertion into the uterus. Surgical intervention is indicated if bleeding does not stop within 15 minutes after insertion. The individual should be monitored; if bleeding does not return after 6 hours to 24 hours, the instilled solution can be removed at a rate of 200 mL per hour. If bleeding resumes, the condom should be re-inflated (ACOG, 2017; Belfort, 2022b; Moldenhauer, 2022).

Another form of uterine tamponade involves packing the uterus with gauze or kerlix until firm pressure is applied. A hemostatic agent such as 5,000 units of thrombin can be applied to the packing material to promote clotting. Multiple pieces of gauze are often tied together, and strict counts are performed to ensure they are all removed and to prevent the retention of a single gauze. A newer technique to treat intrauterine bleeding is a vacuum-induced uterine tamponade. This device provides low vacuum pressure at 70 mmHg to 90 mmHg. The vacuum can remove clots and excess blood from the uterus and promote contraction. Once bleeding is controlled, and the uterus starts to contract for at least 30 minutes, the vacuum can be removed (ACOG, 2017; Belfort, 2022b; Moldenhauer, 2022).

Regardless of the technique used, patients must be monitored closely to determine whether further intervention is needed. In addition to uterine tamponade, the patient should be given 20 units of oxytocin (Pitocin) diluted in 1000 mL of solution and at least one dose of prophylactic antibiotics. Common antibiotics used include ampicillin (Ampi) 2 g IV or cefazolin (Ancef) 1 g IV (Moldenhauer, 2022).

Uterine Artery Embolization 

This procedure is reserved for medically stable individuals with persistent bleeding. Fluoroscopy is used to identify the source of the bleeding. Once the damaged vessel is identified, the area is occluded. This procedure is completed in interventional radiology. The benefits of this procedure include saving the patient's reproductive organs, which can preserve future fertility and the chance for subsequent pregnancies (ACOG, 2017; Wormer et al., 2022).

Surgical Treatment 

More aggressive surgical management via exploratory laparotomy is indicated when less-invasive interventions or medical management do not control or stop bleeding. When delivery occurs via cesarean section, the same surgical site may be used. In the case of a vaginal delivery, a vertical midline incision is created to increase visualization of the abdominal cavity (ACOG, 2017).

Vascular Ligation

Vascular ligation aims to decrease blood flow to the uterus and decrease hemorrhage. The first-line approach is ligating the bilateral uterine arteries, which is known as an O'Leary stitch. Sutures can also be placed in the vessels located within the utero-ovarian ligaments (ACOG, 2017).

Uterine Compression Sutures 

Uterine compression sutures are an effective alternative when less-invasive treatments have been ineffective in slowing or stopping PPH from uterine atony. Compression sutures are placed to compress the blood vessels, decreasing blood flow and increasing the likelihood that coagulation will occur. Uterine compression sutures can preserve the uterus, leading to preserved fertility. The success of uterine compression sutures for managing uterine atony that is not responsive to medical management is approximately 60% to 75%. Various uterine compression suture techniques are used to treat PPH, the most common being the B-Lynch technique named for Christopher Balogun-Lynch. When using the B-Lynch technique, compression is achieved by placing sutures from the cervix to the fundus, enveloping the uterus and providing a similar effect as manual compression. Another suturing technique, the Cho suture technique, involves suturing the area of bleeding using multiple squares and rectangles. The needle is passed through the site of bleeding to compress the cavity by passing the suture through the anterior to the posterior wall and then back through from the posterior wall to the anterior wall, repeating the same procedure 2 to 3 cm upward and laterally. One complication of uterine compression sutures is uterine necrosis; however, this complication is rare, and the exact cause is unknown (ACOG, 2017; Kim et al., 2020).


When all other interventions to control bleeding have failed, a hysterectomy can be performed. The ACOG considers a hysterectomy to be a definitive treatment, as sources of bleeding are removed, and vessels supplying the uterus are closed. A hysterectomy results in permanent sterility and increases the risk of postoperative complications such as bladder injury and infection. No matter the cause of PPH, when symptoms progress to include hypovolemia, hypoxia, hypothermia, acidosis, and electrolyte imbalances, performing a hysterectomy can prevent maternal mortality. A hysterectomy should be performed early when a patient experiences uterine rupture or placenta accreta. When a hysterectomy is delayed in favor of fertility-saving measures, the likelihood of maternal mortality increases (ACOG, 2017; Belfort, 2022b).


Per the ACOG (2019), an estimated 54% to 93% of maternal deaths due to PPH are preventable. To prevent poor outcomes from PPH and improve early identification and initiation of treatment, the Joint Commission set recommendations that hospitals that care for pregnant individuals, including those in labor, must establish protocols and early warning triggers to initiate treatment. The protocols set should be utilized by HCPs. Simulations should be completed to ensure that, in the case of PPH, each individual knows what to do and who is responsible for specific tasks. Problems arising during the simulations should be addressed and fixed so they do not occur in a real-life patient scenario. The Council on Patient Safety in Women's Health also outlined recommendations and steps that should be followed when PPH occurs to decrease the severity and prevent progression to mortality. These recommendations included using hemorrhage carts, staff huddles, rapid response teams, massive transfusion protocols, and Advanced Life Support in Obstetrics (ALSO) training to improve patient outcomes (Evensen et al., 2017).

Although HCPs cannot predict which individuals will experience PPH, a proactive approach during the antenatal period can prevent poor maternal outcomes. If the patient has uterine fibroids, polyhydramnios, or a history of bleeding disorders, these conditions should be addressed and corrected if possible. If it is identified that the patient has a rare blood type or specific antibodies, the institution where delivery is to occur should ensure that compatible blood is available for transfusion if necessary. Utilizing oxytocin (Pitocin) 10 units via IM injection or as a continuous infusion at 10 units or 20 units diluted in 1000 mL of IV solution administered at 125 to 200 mL/hr for 1 to 2 hours can promote uterine contraction, which helps close exposed blood vessels after placental separation and prevent PPH (Moldenhauer, 2022).

Care Considerations

Some problems in managing PPH that lead to increased maternal morbidity and mortality include misdiagnosis or delay in diagnosis, failure in treatment or delayed treatment, and system failures. A misdiagnosis or delayed diagnosis is often attributed to discrepancies in HCPs’ understandings of the definition of PPH, how much blood loss requires intervention, and an underestimation of the amount of blood lost. Visual estimations of blood loss are inaccurate, which can lead to delayed treatment. There is also a lack of HCP education and training on recognizing PPH and few protocols outlining what assessment criteria need to be met to diagnose and treat an individual for PPH. System failures include a lack of necessary equipment to treat individuals experiencing PPH, a lack of protocols outlining the responsibilities of team members, and inadequate interdisciplinary communication. The problems of misdiagnosis and system failure lead to treatment failure. Treatment failures that can arise include the inadequate or inappropriate use of oxytocics. This can also be due to a lack of access to the proper medications to treat PPH. Treatment with PRBC or other coagulation factors can be delayed due to misdiagnosis or a lack of access or availability. Failure to recognize clinical indications of PPH or ignoring the clinical signs is also considered a treatment failure (ACOG, 2019; Rath, 2011).


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