Postpartum Hemorrhage 

Updated: Jun 27, 2018
Author: John R Smith, MD, FACOG, FRCSC; Chief Editor: Ronald M Ramus, MD 

Overview

Background

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

The pregnancy-related mortality ratio in the United States was 17.3 deaths per 100,000 live births in 2013. National statistics suggest that approximately 11.4% of these deaths are caused by PPH.[1] In industrialized countries, PPH usually ranks in the top 3 causes of maternal mortality, along with embolism and hypertension. In the developing world, several countries have maternal mortality rates in excess of 1000 women per 100,000 live births, and World Health Organization statistics suggest that 60% of maternal deaths in developing countries are due to PPH, accounting for more than 100,000 maternal deaths per year.[2]  A Practice Bulletin from the American College of Obstetricians and Gynecologists places the estimate at 140,000 maternal deaths per year or 1 woman every 4 minutes.[3]

The rate of PPH increased from 1.5% in 1999 to 4.1% in 2009, and the rate of atonic PPH rose from 1% in 1999 to 3.4% in 2009. The risk of PPH with a morbidly adherent placenta is markedly higher.[4]

Problem

The definition of PPH is somewhat arbitrary and problematic. PPH is defined as blood loss of more than 500 mL following vaginal delivery or more than 1000 mL following cesarean delivery.[5, 6] A loss of these amounts within 24 hours of delivery is termed early or primary PPH, whereas such losses are termed late or secondary PPH if they occur 24 hours after delivery. This article focuses on early PPH.

Estimates of blood loss at delivery are subjective and generally inaccurate. Studies have suggested that caregivers consistently underestimate actual blood loss. Another proposal suggests using a 10% fall in hematocrit value to define PPH, but this change is dependent on the timing of the test and the amount of fluid resuscitation given.[7] More importantly, the diagnosis would be retrospective, perhaps useful for research but not so in the clinical setting.

Another consideration is the differing capacities of individual patients to cope with blood loss. A healthy woman has a 30-50% increase in blood volume in a normal singleton pregnancy and is much more tolerant of blood loss than a woman who has preexisting anemia, an underlying cardiac condition, or a volume-contracted condition secondary to dehydration or preeclampsia. For these reasons, various authors have suggested that PPH should be diagnosed with any amount of blood loss that threatens the hemodynamic stability of the woman.

The diagnosis of PPH is usually reserved for pregnancies that have progressed beyond 20 weeks’ gestation. Deliveries at less than 20 weeks’ gestational age are spontaneous abortions. Bleeding related to spontaneous abortion may have etiologies and management in common with those for PPH.

Epidemiology

Frequency

United States and industrialized countries

The frequency of PPH is related to the management of the third stage of labor. This is the period from the completed delivery of the baby until the completed delivery of the placenta. Data from several sources, including several large randomized trials performed in industrialized countries, indicate that the prevalence rate of PPH of more than 500 mL is approximately 5% when active management is used versus 13% when expectant management is used. The prevalence rate of PPH of more than 1000 mL is approximately 1% when active management is used versus 3% when expectant management is used.[8, 9] See Medscape Reference article Management of the Third Stage of Labor.

Developing countries

The increased frequency of PPH in the developing world is more likely reflected by the rates given above for expectant management because of the lack of widespread availability of medications used in the active management of the third stage.[2] A number of factors also contribute to much less favorable outcomes of PPH in developing countries. The first is a lack of experienced caregivers who might be able to successfully manage PPH if it occurred. Additionally, the same drugs used for prophylaxis against PPH in active management of the third stage are also the primary agents in the treatment of PPH. Lack of blood transfusion services, anesthetic services, and operating capabilities also plays a role. Finally, the previously mentioned comorbidities are more commonly observed in developing countries and combine to decrease a woman's tolerance of blood loss.

Etiology

PPH has many potential causes, but the most common, by a wide margin, is uterine atony, ie, failure of the uterus to contract and retract following delivery of the baby. PPH in a previous pregnancy is a major risk factor and every effort should be made to determine its severity and cause. In a recent randomized trial in the United States, birthweight, labor induction and augmentation, chorioamnionitis, magnesium sulfate use, and previous PPH were all positively associated with increased risk of PPH.[10]

In a large, population-based study, significant risk factors, identified using multivariable analysis, were as follows:

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

  • Failure to progress during the second stage of labor (OR 3.4, 95% CI 2.4-4.7)

  • Placenta accreta (OR 3.3, 95% CI 1.7-6.4)

  • Lacerations (OR 2.4, 95% CI 2.0-2.8)

  • Instrumental delivery (OR 2.3, 95% CI 1.6-3.4)

  • Large-for-gestational-age (LGA) newborn (OR 1.9, 95% CI 1.6-2.4)

  • Hypertensive disorders (OR 1.7, 95%CI 1.2-2.1)

  • Induction of labor (OR 1.4, 95%CI 1.1-1.7)

  • Augmentation of labor with oxytocin (OR 1.4, 95% CI 1.2-1.7).[11]

PPH is also associated with obesity. In a study by Blomberg, the risk of atonic uterine hemorrhage rapidly increased with increasing BMI; in women with a BMI over 40, the risk was 5.2% with normal delivery and 13.6% with instrumental delivery.[12]

A study by Hanley et al reported that serotonin-norepinephrine reuptake inhibitor exposure in late pregnancy was associated with a 1.6- to 1.9-fold increased risk of postpartum hemorrhage.[13, 14]

As a way of remembering the causes of PPH, several sources have suggested using the “4 T’ s” as a mnemonic: tone, tissue, trauma, and thrombosis.[15]

Tone

Uterine atony and failure of contraction and retraction of myometrial muscle fibers can lead to rapid and severe hemorrhage and hypovolemic shock. Overdistension of the uterus, either absolute or relative, is a major risk factor for atony. Overdistension of the uterus can be caused by multifetal gestation, fetal macrosomia, polyhydramnios, or fetal abnormality (eg, severe hydrocephalus); a uterine structural abnormality; or a failure to deliver the placenta or distension with blood before or after placental delivery.

Poor myometrial contraction can result from fatigue due to prolonged labor or rapid forceful labor, especially if stimulated. It can also result from the inhibition of contractions by drugs such as halogenated anesthetic agents, nitrates, nonsteroidal anti-inflammatory drugs, magnesium sulfate, beta-sympathomimetics, and nifedipine. Other causes include placental implantation site in the lower uterine segment, bacterial toxins (eg, chorioamnionitis, endomyometritis, septicemia), hypoxia due to hypoperfusion or Couvelaire uterus in abruptio placentae, and hypothermia due to massive resuscitation or prolonged uterine exteriorization. Recent data suggest that grand multiparity is not an independent risk factor for PPH.

Tissue

Uterine contraction and retraction leads to detachment and expulsion of the placenta. Complete detachment and expulsion of the placenta permits continued retraction and optimal occlusion of blood vessels.

Retention of a portion of the placenta is more common if the placenta has developed with a succenturiate or accessory lobe. Following delivery of the placenta and when minimal bleeding is present, the placenta should be inspected for evidence of fetal vessels coursing to the placental edge and abruptly ending at a tear in the membranes. Such a finding suggests a retained succenturiate lobe.

The placenta is more likely to be retained at extreme preterm gestations (especially < 24 wk), and significant bleeding can occur. This should be a consideration in all deliveries at very early gestations, whether they are spontaneous or induced. Recent trials suggest that the use of misoprostol for second trimester termination of pregnancy leads to a marked reduction in the rate of retained placenta when compared to techniques using the intrauterine instillation of prostaglandin or hypertonic saline.[16] One such trial reported rates of retained placenta requiring D&C of 3.4% with oral misoprostol compared to 22.4% using intra-amniotic prostaglandin (p=0.002).[17]

Failure of complete separation of the placenta occurs in placenta accreta and its variants. In this condition, the placenta has invaded beyond the normal cleavage plane and is abnormally adherent. Significant bleeding from the area where normal attachment (and now detachment) has occurred may mark partial accreta. Complete accreta in which the entire surface of the placenta is abnormally attached, or more severe invasion (placenta increta or percreta), may not initially cause severe bleeding, but it may develop as more aggressive efforts are made to remove the placenta. This condition should be considered possible whenever the placenta is implanted over a previous uterine scar, especially if associated with placenta previa.

All patients with placenta previa should be informed of the risk of severe PPH, including the possible need for transfusion and hysterectomy.

Finally, retained blood may cause uterine distension and prevent effective contraction.

Trauma

Damage to the genital tract may occur spontaneously or through manipulations used to deliver the baby. Cesarean delivery results in twice the average blood loss of vaginal delivery. Incisions in the poorly contractile lower segment heal well but are more reliant on suturing, vasospasm, and clotting for hemostasis.

Uterine rupture is most common in patients with previous cesarean delivery scars. Routine transvaginal palpation of such scars is no longer recommended. Any uterus that has undergone a procedure resulting in a total or thick partial disruption of the uterine wall should be considered at risk for rupture in a future pregnancy. This admonition includes myomectomy; uteroplasty for congenital abnormality; cornual or cervical ectopic resection; and perforation of the uterus during dilatation, curettage, biopsy, hysteroscopy, laparoscopy, or intrauterine contraceptive device placement.

Trauma may occur following very prolonged or vigorous labor, especially if the patient has relative or absolute cephalopelvic disproportion and the uterus has been stimulated with oxytocin or prostaglandins. Using intrauterine pressure monitoring may lessen this risk. Trauma also may occur following extrauterine or intrauterine manipulation of the fetus. The highest risk is probably associated with internal version and extraction of a second twin; however, uterine rupture may also occur secondary to external version. Finally, trauma may result secondary to attempts to remove a retained placenta manually or with instrumentation. The uterus should always be controlled with a hand on the abdomen during any such procedure. An intraumbilical vein saline/oxytocin or saline/misoprostol injection may reduce the need for more invasive removal techniques.[8]

Cervical laceration is most commonly associated with forceps delivery, and the cervix should be inspected following all such deliveries. Assisted vaginal delivery (forceps or vacuum) should never be attempted without the cervix being fully dilated. Cervical laceration may occur spontaneously. In these cases, mothers have often been unable to resist bearing down before full cervical dilatation. Rarely, manual exploration or instrumentation of the uterus may result in cervical damage. Very rarely, the cervix is purposefully incised at the 2- and/or 10-o’clock positions to facilitate delivery of an entrapped fetal head during a breech delivery (Dührssen incision).

Vaginal sidewall laceration is also most commonly associated with operative vaginal delivery, but it may occur spontaneously, especially if a fetal hand presents with the head (compound presentation). Lacerations may occur during manipulations to resolve shoulder dystocia. Lacerations often occur in the region overlying the ischial spines. The frequency of sidewall and cervical lacerations has probably decreased in recent years because of the reduction in the use of midpelvic forceps and, especially, midpelvic rotational procedures.

Lower vaginal trauma occurs either spontaneously or because of episiotomy. Spontaneous lacerations usually involve the posterior fourchette; however, trauma to the periurethral and clitoral region may occur and can be problematic.

Thrombosis

In the immediate postpartum period, disorders of the coagulation system and platelets do not usually result in excessive bleeding; this emphasizes the efficiency of uterine contraction and retraction for preventing hemorrhage.[5] Fibrin deposition over the placental site and clots within supplying vessels play a significant role in the hours and days following delivery, and abnormalities in these areas can lead to late PPH or exacerbate bleeding from other causes, most notably, trauma.

Abnormalities may be preexistent or acquired. Thrombocytopenia may be related to preexisting disease, such as idiopathic thrombocytopenic purpura, or acquired secondary to HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count), abruptio placentae, disseminated intravascular coagulation (DIC), or sepsis. Rarely, functional abnormalities of platelets may also occur. Most of these are preexisting, although sometimes previously undiagnosed.

Preexisting abnormalities of the clotting system, such as familial hypofibrinogenemia and von Willebrand disease, may occur and should be considered. An expert panel recently issued guidelines to aid in the diagnosis and management of women with such conditions.[18] An underlying bleeding disorder should be considered in a woman with any of the following: menorrhagia since menarche, family history of bleeding disorders, personal history of notable bruising without known injury, bleeding from the oral cavity or GI tract without obvious lesion, or epistaxis of longer than 10 minutes duration (possibly requiring packing or cautery). If a bleeding disorder is suspected, consultation is suggested.

Acquired abnormalities are more commonly problematic. DIC related to abruptio placentae, HELLP syndrome, intrauterine fetal demise, amniotic fluid embolism, and sepsis may occur. Fibrinogen levels are markedly elevated during pregnancy, and a fibrinogen level that would be in the reference range in the nonpregnant state should be viewed with suspicion in the aforementioned clinical scenarios.

Finally, dilutional coagulopathy may occur following massive PPH and resuscitation with crystalloid and packed red blood cells (PRBCs).

Risk factors and associated conditions for PPH are listed above; however, a large number of women experiencing PPH have no risk factors. Different etiologies may have common risk factors, and this is especially true of uterine atony and trauma of the lower genital tract. PPH usually has a single cause, but more than one cause is also possible, most likely following a prolonged labor that ultimately ends in an operative vaginal birth.

Prevention

High-quality evidence suggests that active management of the third stage of labor reduces the incidence and severity of PPH.[9] Active management is the combination of (1) uterotonic administration (preferably oxytocin) immediately upon delivery of the baby, (2) early cord clamping and cutting, and (3) gentle cord traction with uterine countertraction when the uterus is well contracted (ie, Brandt-Andrews maneuver).

The value of active management in the prevention of PPH cannot be overstated (see Management of the Third Stage of Labor). The use of active versus expectant management in the third stage was the subject of 5 randomized controlled trials (RCTs) and a Cochrane meta-analysis.[19, 8, 9] These trials included more than 6000 women, and the findings are summarized in Table 1.

Table 1. Benefits of Active Management Versus Expectant Management (Open Table in a new window)

Outcome

Control Rate, %

Relative Risk

95% CI*

NNT †

95% CI

PPH of 500 mL

14

0.38

0.32-0.46

12

10-14

PPH of 1000 mL

2.6

0.33

0.21-0.51

55

42-91

Hemoglobin < 9 g/dL

6.1

0.4

0.29-0.55

27

20-40

Blood transfusion

2.3

0.44

0.22-0.53

67

48-111

Therapeutic uterotonics

17

0.2

0.17-0.25

7

6-8

*CI: Confidence interval

† NNT: Number needed to treat

 

The findings show a conclusive benefit for active management, with an approximate 60% reduction in the occurrence of PPH greater than or equal to 500 mL and 1000 mL, hemoglobin concentration of less than 9 g/dL at 24-48 hours after delivery, and the need for blood transfusion. An 80% reduction in the need for therapeutic uterotonic agents was noted. These results were all highly significant as indicated by the 95% confidence interval figures. The results indicate that for every 12 patients receiving active rather than physiological management, one PPH would be prevented. For every 67 patients so treated, one patient would avoid transfusion with blood products.

One concern regarding active management is that retained placenta may occur more frequently. This concern is not supported by the trials. This is especially true if oxytocin is used as the uterotonic.[20, 21] The US RCTs mentioned above compared the use of active management protocols in which the oxytocin was administered either immediately after delivery of the baby or immediately after delivery of the placenta. The authors stated that no statistically significant difference was noted in the PPH rate and that delaying administration until after placental delivery was justified.

Noteworthy is the finding that early administration of oxytocin (before placental delivery) did not increase the rate of retained placenta. Additionally, the trial showed trends toward a benefit for early administration of oxytocin, including a 25% reduction in PPH and a 50% reduction in the need for transfusion.[10] These findings are clearly consistent with the previous RCTs and the early administration of oxytocin with delivery of the baby is strongly recommended.

They also stated that administration with delivery of the baby did not increase the rate of retained placenta, but they did not point out that this finding clearly supports early administration. Additionally, the trial showed trends toward a benefit for early administration of oxytocin, including a 25% reduction in PPH and a 50% reduction in the need for transfusion.[10] These differences may be due to chance, but, given the results of the previous RCTs, the administration of oxytocin with delivery of the baby would seem to be warranted.

Following delivery, administering a uterotonic drug that lasts at least 2-3 hours is reasonable.[3] This could be 10 U of oxytocin in 500 mL of intravenous fluid by continuous drip, 200-250 mcg of ergonovine intramuscularly, or 250 mcg of 15-methyl prostaglandin F2-alpha (carboprost [Hemabate]) intramuscularly. The use of misoprostol and a long-acting oxytocin analogue (carbetocin) is being studied for this use.[22] It has been suggested that distribution of misoprostol ahead of childbirth in communities where home birth is unavoidable can be an effective approach. However, there is insufficient evidence to support this and there are concerns that the drug might be used for starting labor or terminating pregnancy.[23]

The presence of significant antepartum or intrapartum risk factors warrants delivery in maternity units that have readily available resources to deal with massive obstetric hemorrhage. All medical facilities should have protocols for dealing with PPH and obstetric hemorrhage.

Pathophysiology

Over the course of a pregnancy, maternal blood volume increases by approximately 50% (from 4 L to 6 L). The plasma volume increases somewhat more than the total RBC volume, leading to a fall in the hemoglobin concentration and hematocrit value. The increase in blood volume serves to fulfill the perfusion demands of the low-resistance uteroplacental unit and to provide a reserve for the blood loss that occurs at delivery.[7]

At term, the estimated blood flow to the uterus is 500-800 mL/min, which constitutes 10-15% of cardiac output. Most of this flow traverses the low-resistance placental bed. The uterine blood vessels that supply the placental site traverse a weave of myometrial fibers. As these fibers contract following delivery, myometrial retraction occurs. Retraction is the unique characteristic of the uterine muscle to maintain its shortened length following each successive contraction. The blood vessels are compressed and kinked by this crisscross latticework, and, normally, blood flow is quickly occluded. This arrangement of muscle bundles has been referred to as the "living ligatures" or "physiologic sutures" of the uterus.[5]

Uterine atony is a failure of the uterine myometrial fibers to contract and retract. This is the most important cause of PPH and usually occurs immediately following delivery of the baby, up to 4 hours after the delivery. Trauma to the genital tract (ie, uterus, uterine cervix, vagina, labia, clitoris) in pregnancy results in significantly more bleeding than would occur in the nonpregnant state because of increased blood supply to these tissues. The trauma specifically related to the delivery of the baby, either vaginally in a spontaneous or assisted manner or by cesarean delivery, can also be substantial and can lead to significant disruption of soft tissue and tearing of blood vessels.

Presentation

Although the presentation of PPH is most often dramatic, bleeding may be slower and seemingly less noteworthy but may still ultimately result in critical loss and shock. This is more likely to be true of bleeding secondary to retained tissue or trauma. Nursing practices for routine care in the postpartum period should include close observation and documentation of maternal vital signs and condition, vaginal blood loss, and uterine tone and size. The uterus should be periodically massaged to express any clots that have accumulated in the uterus or vagina.[24]

The usual presentation of PPH is one of heavy vaginal bleeding that can quickly lead to signs and symptoms of hypovolemic shock. This rapid blood loss reflects the combination of high uterine blood flow and the most common cause of PPH, ie, uterine atony. Blood loss is usually visible at the introitus, and this is especially true if the placenta has delivered. If the placenta remains in situ, then a significant amount of blood can be retained in the uterus behind a partially separated placenta, the membranes, or both.

Even after placental delivery, blood may collect in an atonic uterus. For this reason, the uterine size and tone should be monitored throughout the third stage and in the so-called fourth stage, following delivery of the placenta. This is accomplished by gently palpating the uterine fundus. If the cause of bleeding is not uterine atony, then blood loss may be slower and clinical signs and symptoms of hypovolemia may develop over a longer time frame. Bleeding from trauma may be concealed in the form of hematomas of the retroperitoneum, broad ligament or lower genital tract, or abdominal cavity. The clinical findings in hypovolemia are listed in Table 2.

Table 2. Clinical Findings in Obstetric Hemorrhage [25] (Open Table in a new window)

Blood Volume Loss

Blood Pressure (systolic)

Symptoms and Signs

Degree of Shock

500-1000 mL (10-15%)

Normal

Palpitations, tachycardia, dizziness

Compensated

1000-1500 mL (15-25%)

Slight fall (80-100 mm Hg)

Weakness, tachycardia, sweating

Mild

1500-2000 mL (25-35%)

Moderate fall (70-80 mm Hg)

Restlessness, pallor, oliguria

Moderate

2000-3000 mL (35-50%)

Marked fall (50-70 mm Hg)

Collapse, air hunger, anuria

Severe

 

Two important facts are worth bearing in mind. The first is that caregivers consistently underestimate visible blood loss by as much as 50%. The volume of any clotted blood represents half of the blood volume required to form the clots. The second is that most women giving birth are healthy and compensate for blood loss very well. This, combined with the fact that the most common birthing position is some variant of semirecumbent with the legs elevated, means that symptoms of hypovolemia may not develop until a large volume of blood has been lost.[26]

Rapid recognition and diagnosis of PPH is essential to successful management. Resuscitative measures and the diagnosis and treatment of the underlying cause must occur quickly before sequelae of severe hypovolemia develop. The major factor in the adverse outcomes associated with severe hemorrhage is a delay in initiating appropriate management.

Contraindications

Other than nonconsent, absence of surgical expertise or allergy to specific agents, the techniques used in the management of PPH have no absolute contraindications. The vast majority of cases (>99%) are handled without what would traditionally be considered surgical intervention. In most cases, surgical intervention is a last resort. An exception is those cases in which uterine rupture or genital tract trauma has occurred and surgical repair is clearly indicated.

Transfusion of packed RBC and other blood products may be necessary in the management of severe PPH. Some women may refuse such an intervention on personal or religious grounds. The most widely known group that does not accept blood transfusion are Jehovah’s 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 Jehovah’s Witness population. The increased risk of death was found to be 6-fold in a recent national review of 23 years experience in the Netherlands and 44-fold in a much smaller study of 391 deliveries in a US tertiary level center.[27, 28] Discussion regarding the implications of such prohibitions should be undertaken early in the pregnancy whenever possible and subsequently reviewed.

In almost all cases in which surgical management is chosen after medical management has failed, not attempting surgery would lead to maternal death. Even an unstable condition cannot be considered a true contraindication. One type of surgery may be chosen over another, but when medical management has failed, surgery is most likely the only life-saving option.

 

Workup

Laboratory Studies

In the antenatal period, a CBC is performed. Findings alert caregivers to women with anemia and indicate interventions to attempt to improve the hemoglobin level. Hemoglobin levels below 10-10.5 g/dL have been associated with adverse pregnancy outcome, and the rare patient with thrombocytopenia will be identified.[29] Women admitted to labor and delivery units should have a CBC performed if one has not been performed recently. All women experiencing antepartum bleeding should have a CBC.

Blood typing and antibody screening tests may also have been performed in the antenatal period. If the results are known and no blood group antibodies were present, then the test may not need to be repeated upon admission. However, many facilities routinely repeat this test (or at least draw a sample to be held in the blood bank) in case blood is urgently needed. The time frame between a request for blood products of various types and their availability should be known. In a patient at high risk of PPH, crossmatching of 2-6 U of blood before delivery is prudent. Examples include previous severe PPH, placenta previa, possible placenta accreta, multiple previous cesarean deliveries, known coagulation disorders, or severe thrombocytopenia. The American Association of Blood Banks currently recommends retesting women at high risk every 72 hours for the development of antibodies.

Coagulation studies are no longer routinely performed in pregnant women, including those about to undergo cesarean delivery. Instead, history is relied on to uncover previous episodes suggesting preexisting disorders of hemostasis.

  • Once the diagnosis of PPH has been made, a CBC and baseline coagulation studies should be performed.

  • Initially, the hemoglobin value does not reflect the amount of blood loss.

  • A crossmatch for 4-6 U of PRBCs should be requested and consideration given to notifying the blood bank of the possible need for additional blood products in short order.

  • Initial coagulation study findings are usually within reference ranges; however, abnormalities may be noted. This is most common when PPH is preceded by abruptio placenta, HELLP syndrome, fatty liver of pregnancy, intrauterine fetal demise, embolic events, or septicemia.

If the international normalized ratio and/or activated partial thromboplastin time are elevated, the use of fibrinogen, a thrombin time measurement, D-dimers, and a blood film should be considered. In late pregnancy, fibrinogen levels are 2-3 times the upper reference range limit in the nonpregnant state, and a level within the nonpregnant reference range should be viewed with caution if the clinical picture suggests coagulopathy.

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

PPH usually manifests with such rapidity that diagnostic procedures are almost entirely limited to a physical examination of the involved structures.

Assessment of uterine tone and size is accomplished using a hand resting on the fundus and palpating the anterior wall of the uterus. The presence of a boggy uterus with either heavy vaginal bleeding or increasing uterine size establishes the diagnosis of uterine atony. The presence of uterine atony and resulting hemorrhage usually prevents the diagnosis of PPH from other causes because of an inability to visualize other sites. For this reason, and because of the rapidity of blood loss secondary to atony, management and control of atony is paramount.

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

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

Imaging Studies

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

Diagnostic Procedures

PPH usually manifests with such rapidity that diagnostic procedures are almost entirely limited to a physical examination of the involved structures.

  • Assessment of uterine tone and size is accomplished using a hand resting on the fundus and palpating the anterior wall of the uterus. The presence of a boggy uterus with either heavy vaginal bleeding or increasing uterine size establishes the diagnosis of uterine atony. The presence of uterine atony and resulting hemorrhage usually prevents the diagnosis of PPH from other causes because of an inability to visualize other sites. For this reason, and because of the rapidity of blood loss secondary to atony, management and control of atony is paramount.

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

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

 

Treatment

Medical Therapy

The treatment of patients with PPH has 2 major components: (1) resuscitation and management of obstetric hemorrhage and, possibly, hypovolemic shock and (2) identification and management of the underlying cause(s) of the hemorrhage. For the purpose of discussion, these components are discussed separately; however, remember that successful management of PPH requires that both components be simultaneously and systematically addressed.

Management of obstetric hemorrhage

Patients with PPH require aggressive measures to restore and maintain the circulating blood volume (and thereby perfusion pressure) to vital structures. All medical units involved in the care of pregnant women must have a protocol for the management of severe obstetric hemorrhage.[30] Management of massive obstetric hemorrhage outlines such a protocol for a pregnant woman in either the antepartum or postpartum period.[31] Implement the protocol in a manner similar to a cardiac arrest protocol, with the same attention to detail and documentation. Just as with other advanced life support protocols, conduct periodic reviews and practice drills.

The diagnosis of PPH is established by observing the amount of bleeding and the patient’s clinical status. The amount of blood lost and the patient’s level of consciousness and vital signs are continually assessed. Once the diagnosis is made, immediately notify appropriate staff members. The magnitude and underlying cause of the bleeding to some degree dictate which specialized personnel are called, but a minimum of 1 obstetrician and 1 anesthetist is necessary. Skilled midwives or nurses can be indispensable. Notifying blood transfusion services is essential because the timely availability of blood products is likely to be critical. As in a cardiac arrest, designate an experienced person to document critical information and times. Ensure the availability of an operating room. The speed with which PPH occurs, becomes life-threatening, and can be successfully managed with relatively simple interventions sometimes makes it difficult to decide when to institute the full protocol.

A randomized double-blind, placebo-controlled trial by the WOMAN Trial Collaborators reported that tranexamic acid significantly reduced death due to bleeding in women with postpartum hemorrhage when compared to the placebo group (155 [1.5%] of 10,036 patients vs 191 [1.9%] of 9985 patients in the placebo group). The study also found that the effects of tranexamic acid was greater when given within 3 hours of giving birth (89 [1·2%] vs 127 [1·7%] in the placebo group. Adverse events did not differ significantly in the two groups.[32]

Fluid resuscitation

Fluid resuscitation of women experiencing obstetric hemorrhage is sometimes overly conservative. Possible reasons for this include (1) blood loss being generally underestimated both in volume and rapidity, (2) women initially compensating well for losses because of their good health and the hypervolemia of pregnancy, (3) concerns that overresuscitation leads to pulmonary edema, and (4) failure to appreciate the dynamics of fluid shifts in the body.

Immediately commence resuscitation. Raising the legs improves venous return and is consistent with the positioning used to diagnose and treat the underlying causes of bleeding. Administer oxygen and obtain intravenous access. All intravenous lines started on the labor ward for other reasons must be placed with cannulas of sufficient gauge if PPH develops. Twice as much fluid can be infused through a 14-gauge intravenous line compared with an 18-gauge intravenous line over the same time period.[33] During labor, place at least 1 intravenous line in women at risk for PPH; consider a second line in patients at very high risk.

Perform the initial resuscitation with large volumes of crystalloid solution, either normal saline (NS) or Lactated Ringer’s solution (LRS), through peripheral intravenous sites. Central venous access is not required for the vast majority of patients with PPH, but do not delay establishing such access if necessary. Draw blood for baseline measurements at this time. NS is a reasonable solution in the labor ward setting because of its low cost and compatibility with most drugs and blood transfusions. The risk of hyperchloremic acidosis is very low in the setting of PPH. If large amounts (>10 L) of crystalloid are being infused, a change to LRS can be considered.

Dextrose-containing solutions, such as 5% dextrose in water or diluted NS in 5% dextrose in water, have no role in the management of PPH. Remember that the loss of 1 L of blood requires replacement with 4-5 L of crystalloid because most of the infused fluid is not retained in the intravascular space but instead shifts to the interstitial space. This shift, along with oxytocin use, may result in peripheral edema in the days following PPH. Healthy kidneys easily excrete this excess fluid. Use wide-open initial infusion rates, with the goal of infusing the required replacement volume over minutes rather than hours. PPH of up to 1500 mL in a healthy pregnant woman can usually be managed by crystalloid infusion alone if the cause of bleeding is arrested. Blood loss in excess of this usually requires the addition of a PRBC transfusion.

Because a large portion of crystalloid fluid volume is lost to the interstitial space, the use of colloids in resuscitation has been examined. These solutions are largely retained within the intravascular space and include albumin, dextran, hydroxyethyl starch, and modified fluid gelatin. A meta-analysis in the Cochrane Library comparing resuscitation with colloid solutions versus crystalloid favored the use of crystalloids with respect to mortality.[34, 35]

For albumin or plasma protein fraction compared with NS, 18 trials reported data on mortality in 641 patients. The pooled relative risk from these trials was 1.52 (95% confidence interval, 1.08-2.13). The NS groups had a 1% mortality rate, versus an 11% mortality rate in the colloid group.

For dextran compared to NS, 8 trials compared reported data on mortality in 668 patients. The pooled relative risk was 1.24 (95% confidence interval, 0.94-1.65). Two other recent meta-analyses on the same topic reached the same conclusions.

Large volumes of colloid solutions (>1000-1500 mL/d) can have an adverse effect on hemostasis. No colloid solution has been demonstrated to be superior to NS, and, because of the expense and the risk of adverse effects with colloids, crystalloid is recommended. Given these findings, the authors recommend against the use of colloid solutions in resuscitation outside the setting of an RCT.

Blood transfusion

Order blood transfusions if blood loss is ongoing and thought to be in excess of 2000 mL or if the patient’s clinical status reflects developing shock despite aggressive resuscitation. Data from various sources suggest that 1 in 16-40 women experiencing PPH requires a blood transfusion if active third-stage management is used, whereas approximately 1 in 9 requires a transfusion if expectant management is used. Newer studies tend to have lower transfusion rates than older studies.[9]

Whole blood is no longer available in most settings, and, for many reasons, PRBCs are initially used with other blood components and given only if indicated. Most medical units have access to uncrossmatched O-type Rh-negative PRBCs for catastrophic bleeding. In PPH, uncrossmatched ABO- and Rh-compatible blood is usually available because a blood group and antibody screen has already been performed. Have full crossmatched blood available for transfusion within 30 minutes. Clinicians must be aware of the capabilities of their blood bank regarding timing, type, and amount of blood products available in emergencies. Good communication with the blood transfusion service is essential, and the nature of the emergency and the potential amount of blood products required must be stressed.

The goal is to rapidly transfuse 2-4 U of PRBCs to replace lost oxygen-carrying capacity and to restore circulating volume. Administer the blood transfusion through a set with an integrated filter, and use a blood warmer if the infusion rate (>100 mL/min) or the total volume infused is high. A rapid infusion set with an integrated warmer or a pressure cuff may be used to increase the infusion rate. PRBCs are very viscous, reducing the infusion rate. This problem may be overcome by adding 100 mL of NS to each unit. Do not use LRS for this purpose because the calcium contained in the solution may cause clotting.

The risks of transfusion are well known and are covered elsewhere (eg, see Transfusion Reactions or Transfusion and Autotransfusion), but they include infection, transfusion reaction, and development of atypical antibodies. Several other complications may be noted in large-volume transfusions. The risk of hypothermia is minimized by the use of blood warmers. Dilutional coagulopathy may be observed and is discussed below. Hyperkalemia and acidosis related to the use of stored blood are theoretical risks but are seldom clinically important if perfusion of vital organs is maintained. Monitor electrolyte and acid-base status if the situation is ongoing. Hypocalcemia due to citrate intoxication is also seldom observed.[36]

Patients may refuse a transfusion of blood products based on religious or other grounds. A patient's refusal of blood products must be respected and must not be equated with a desire for no intervention or be seen as an excuse for suboptimal care. Several options, including the use of autotransfusion, can be considered for the management of these patients. Ensure that a care plan is in place (see Transfusion and Autotransfusion). An article by Hughes et al reviewed the issues and management options in patients who refuse transfusion. Clinicians should bear in mind that the refusal may not extend to all related products. Products that use recombinant technologies such as human erythropoietin and activated factor VIIa are usually acceptable.[37]

Coagulopathy

Women experiencing PPH do not usually have a preexisting disorder of hemostasis; however, initial blood work includes a coagulation screen and platelet count. In previously healthy women, dilutional coagulopathy is not usually observed until approximately 80% of the original blood volume has been replaced. Regularly monitor hemostatic test results in all women who require a massive transfusion. If findings are abnormal in conjunction with ongoing bleeding or oozing from puncture sites, mucous surfaces, or wounds, additional blood products are required. Infuse fresh frozen plasma (FFP), beginning with 4 U and following with additional units to normalize the coagulation test findings. Many authorities recommend the addition of 1 U of FFP for every 5 U of PRBCs for patients who require continued transfusion.

Thrombocytopenia is likely after 1.5-2 times the blood volume has been replaced. Keep the platelet count more than 50 X 109/L by using platelet transfusion. Each unit of platelets increases the platelet count by approximately 10 X 109/L. (Platelets are usually given in packs of 5-6 U.) If bleeding is continuing and the platelet count is less than 50 X 109/L, administer 10-12 U initially. If surgical intervention is necessary, maintain the platelet count at more than 80-100 X 109/L. Platelet preparations contain some RBCs, and the administration of anti-D immunoglobulin (RhoGAM, WinRho) is recommended for Rh-negative women after the crisis has passed.[38]

If coagulation test results are abnormal from the onset of PPH, strongly consider an underlying cause (eg, abruptio placenta, HELLP syndrome, fatty liver of pregnancy, intrauterine fetal demise, amniotic fluid embolus, septicemia, preexisting disorder). Take specific steps to treat the underlying cause and the hemostatic abnormality.

DIC may also develop if shock has led to marked hypoperfusion of tissues, causing damage and release of tissue thromboplastins. In such cases, laboratory test results reveal that the D-dimer levels are elevated and fibrinogen levels are very low, with a prolonged thrombin time. The management of DIC is identical to that for a patient with dilutional coagulopathy. Restoration and maintenance of circulating volume along with blood product replacement is essential.

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

Interest in and experience with recombinant activated factor VIIa (RFVIIa) in massive hemorrhage situations is growing. This experience has extended to severe postpartum hemorrhage and results have been encouraging.[39] RFVIIa has been used when conventional medical management has been unsuccessful and also when varying degrees of surgical management, up to and including hysterectomy have failed. Therapy is very expensive and some suggest that use in less severe cases may be potentially harmful.[40] RFVIIa may also be useful in cases of severe PPH complicated by DIC.[41] Further study is required before recombinant activated factor VII is put into widespread use.

Seek the advice of a hematologist in cases of massive transfusion or coagulopathy.

Response to resuscitation

Pay close attention to the patient’s level of consciousness, pulse, blood pressure, and urine output during the course of the management of massive hemorrhage. A urine output of 30 mL/h or more likely indicates adequate renal perfusion. Closely monitor the CBC count, coagulation, and blood gas values in addition to acid-base status. Pulse oximetry is useful for evaluating tissue perfusion and oxygen saturation. Frequent auscultation of the lung fields helps detect pulmonary edema or the development of adult respiratory distress syndrome. For patients in critical condition with ongoing bleeding, the placement of a central venous line may be helpful for resuscitation. Arterial line placement also may aid in monitoring blood pressure and allowing easy access for blood work. Few patients experiencing PPH require such invasive monitoring; however, consultation with appropriate specialists and placement in an intensive care setting are preferred for those who do.

Management of massive obstetric hemorrhage

The following is a plan for managing massive obstetric hemorrhage, adapted from Bonner.[31] The word order is a useful mnemonic for remembering the basic outline.

  • Organization

    1. Call experienced staff (including obstetrician and anesthetist).

    2. Alert the blood bank and hematologist.

    3. Designate a nurse to record vital signs, urine output, and fluids and drugs administered.

    4. Place operating theater on standby.

  • Resuscitation

    1. Administer oxygen by mask.

    2. Place 2 large-bore (14-gauge) intravenous lines.

    3. Take blood for crossmatch of 6 U PRBCs, and obtain a CBC count, coagulation screen, urea level, creatinine value, and electrolyte status.

    4. Begin immediate rapid fluid replacement with NS or Ringer lactate solution.

    5. Transfuse with PRBCs as available and appropriate.

  • Defective blood coagulation

    1. Order coagulation screen (International Normalized Ratio, activated partial thromboplastin time) if fibrinogen, thrombin time, blood film, and D-dimer results are abnormal.

    2. Give FFP if coagulation test results are abnormal and sites are oozing.

    3. Give cryoprecipitate if abnormal coagulation test results are not corrected with FFP and bleeding continues.

    4. Give platelet concentrates if the platelet count is less than 50 X 109/L and bleeding continues.

    5. Use cryoprecipitate and platelet concentrates before surgical intervention.

  • Evaluation of response

    1. Monitor pulse, blood pressure, blood gas status, and acid-base status, and consider monitoring central venous pressure.

    2. Measure urine output using an indwelling catheter.

    3. Order regular CBC counts and coagulation tests to guide blood component therapy.

  • Remedy the cause of bleeding

    1. If antepartum, deliver the fetus and placenta.

    2. If postpartum, use oxytocin, prostaglandin, or ergonovine.

    3. Explore and empty the uterine cavity, and consider uterine packing.

    4. Examine the cervix and vagina, ligate any bleeding vessels, and repair trauma.

    5. Ligate the uterine blood supply (ie, uterine, ovarian, and/or internal iliac arteries).

    6. Consider arterial embolization.

    7. Consider hysterectomy.

Management of the underlying cause of PPH

Initial assessment

The patient’s risk factors and the events leading to the diagnosis of PPH may suggest an underlying etiology, but knowledge that most cases are caused by uterine atony and the need to be systematic argues for a planned, stepwise approach to assessment and management. The status of the patient, the severity of the bleeding, and the response to initial management steps determine if and when the protocol for massive obstetric hemorrhage is instituted.

Uterine atony

Two well-designed trials indicate that oxytocin should be the drug of choice for both prophylaxis and treatment of post partum hemorrhage caused by uterine atony.[42]

Assess uterine size and tone by placing a hand on the uterine fundus and massaging the uterus, which serves to express any clots that have accumulated in the uterus or vagina. If the uterus is found to be boggy and not well contracted, commence vigorous massage and therapeutic oxytocin. Oxytocin can be administered as a 5-U intravenous bolus, as 20 U in 1 L of NS intravenously run as fast as possible, or as 10 U intramyometrially with a spinal needle if no immediate intravenous access is available.[6]

Emptying the bladder may aid in ongoing assessment and facilitate uterine contraction and subsequent therapeutic maneuvers. Wearing a waterproof gown, elbow-length gloves, and eye protection is prudent during the management of PPH. Sterile technique is used.

If the uterus remains atonic, commence bimanual massage. A hand is placed on the fundus, and the second hand is placed anterior to the cervix in the vagina. Prepare the perineum and vagina. The vaginal hand may be covered in povidone-iodine solution (Proviodine) or a lubricant to allow it to enter the vagina with less difficulty. Take care to minimize the chance of causing or worsening trauma in the lower genital tract. Trauma to the vaginal sidewalls and cervix may be palpated as the hand is gently introduced into the vagina, and blood clots may be evacuated from the vagina, cervix, and lower uterine segment.

The vaginal hand is placed in the anterior fornix, and the abdominal hand is placed on the posterior aspect of the fundus. The uterus is raised from the pelvis, pivoted anteriorly, and compressed between the two hands. The compression expels clots and decreases bleeding. Massaging the uterus between the hands aids in promoting and sustaining contraction. Bimanual massage results in a decrease in bleeding, even if the uterus remains relatively atonic, thus allowing resuscitation a chance to begin to catch up with blood loss.

Use other uterotonic agents if the uterus remains atonic despite oxytocin administration and bimanual massage. The traditional second-line agent for uterine atony has been ergonovine (or ergotrate) given as an initial dose of 100 or 125 mcg intravenously or intramyometrially or 200 or 250 mcg intramuscularly. The maximum total dose is 1.25 mg. Hypertension is a relative contraindication. In some regions, the availability of ergot preparations has become problematic. Every effort should be made to secure supplies of this inexpensive and useful agent.

Many authorities now recommend the use of intramuscular carboprost as the second-line agent when it is available. The recommended dose is 250 mcg intramuscularly or intramyometrially, not to exceed 2 mg (8 doses). Asthma is a relative contraindication. Carboprost has been shown to be 80-90% effective in stopping PPH in cases refractory to oxytocin and ergonovine. Intramuscular administration of these agents is not recommended if the patient demonstrates evidence of shock because absorption would be compromised.

Misoprostol may also become a valuable agent in the treatment of PPH. One small case series reported that a dose of 1000 mcg given rectally was effective in causing sustained uterine contraction in 14 cases refractory to oxytocin, ergonovine, or both.[43, 44] Recent trials are examining whether the more rapid onset of sublingual/buccal misoprostol will improve its efficacy in the setting of acute PPH.[45] At this time, however, misoprostol remains a third-line agent in the management of PPH.[46] The low cost of the drug and its heat stability (does not require refrigeration) makes it especially appealing for use in the developing world. More trials are pending.

A meta-analysis that included data from 88,947 women reported that compared to oxytocin alone; ergometrine plus oxytocin, carbetocin monotherapy, or misoprostol plus oxytocin were all associated with a reduced risk for postpartum hemorrhage. In the oxytocin group, 10.5% had a postpartum hemorrhage of ≥ 500 mL compared with 7.2% in the ergometrine plus oxytocin group, 7.6% in the carbetocin group, and 7.7% in the misoprostol plus oxytocin group.[83]

Winikoff et al examined sublingual (SL) misoprostol for PPH when oxytocin is not feasible to administer. Oxytocin is considered the standard of care for treating postpartum hemorrhage, but because of refrigeration requirements and the need for intravenous administration, it is not always clinically viable, particularly in primitive clinical settings. Active bleeding was controlled within 20 min for 440 (90%) women administered misoprostol 800 mcg SL (n=488) and 468 (96%) administered oxytocin 40 units IV (n=490) (relative risk [RR], 0.94; 95% confidence interval [CI], 0.91-0.98). Additional blood loss of 300 mL or greater after treatment occurred for 147 (30%) of women receiving misoprostol and 83 (17%) receiving oxytocin (RR, 1.78; 95% CI, 1.40-2.26). The authors concluded that in circumstances where it is not feasible to use oxytocin for postpartum hemorrhage, misoprostol is a suitable alternative.[47]

A study by Quibel et al found that adding misoprostol with prophylactic routine oxytocin did not have an effect on the rate of postpartum hemorrhage risk and increased the rate of adverse events. The study reported that the rate of postpartum hemorrhage was 8.4% (68/806) in the misoprostol and 8.3% (66/797) in the placebo group (P=.98). In the misoprostol group there was a significant increase in adverse events with fever being the highest occurrence (30.4% in the misoprostol group vs 6.3% in the placebo group). The study was stopped after early results showed that misoprostol was associated with adverse events.[48]

A study by Diop et al that compared the efficacy of misoprostol and oxytocin when delivered by auxiliary midwives at maternity huts in Senegal via Uniject concluded that misoprostol could be more appropriate for community-level prophylaxis of postpartum hemorrhage.[49]

The investigational agent carbetocin has been compared with oxytocin for prevention of postpartum hemorrhage. Attilakos et al compared the effectiveness of carbetocin and oxytocin when given for postpartum hemorrhage after cesarean delivery in a double-blind, randomized trial. The primary outcome measure was women who required additional pharmacologic oxytocic interventions. Results showed that significantly more women required additional oxytocics in the oxytocin group compared with the carbetocin group.[50]

A double-blind study that compared heat-stable carbetocin with oxytocin after vaginal birth for postpartum hemorrhage prevention in 29,645 women reported that the frequency of blood loss of at least 500 ml or the use of additional uterotonic agents was 14.5% in the carbetocin group and 14.4% in the oxytocin group (consistent with noninferiority) and that the frequency of blood loss of at least 1000 ml was 1.51% in the carbetocin group and 1.45% in the oxytocin group (crossing the margin of noninferiority).[84]

Retained tissue

If the uterus continues to contract poorly or to relax when bimanual compression and massage are stopped despite the administration of uterotonics, perform manual exploration. Some authorities advocate earlier exploration; however, this is difficult without general anesthesia unless the patient is in severe shock or an epidural is already in place. Nitrous oxide (Entonox) may be useful in facilitating manual exploration if general anesthesia is not available.

Ensure that resuscitation is well underway by this time, and, if not already started, institute the massive hemorrhage protocol. If possible, keep the vaginal hand in situ throughout because it minimizes patient discomfort, the risk of iatrogenic trauma, and, possibly, the risk of subsequent infection. If the placenta was not delivered before the onset of PPH, an attempt is now made to deliver it with cord traction and uterine countertraction. Care must be taken because the risk of uterine inversion is greater if the uterus remains poorly contracted. Perform manual removal if the placenta is not easily delivered or the cord is avulsed.

Perform manual removal with a level of analgesia that matches the clinical urgency of the situation. The hand is passed through the cervix and into the lower segment. Care is taken to minimize the profile of the hand as it enters, keeping the thumb and fingers together in the shape of a cone in order to avoid damage. Control of the uterine fundus with the other hand is essential. If the placenta is encountered in the lower segment, it is removed. If the placenta is not encountered, the placental edge is sought. Once found, the fingers gently develop the space between the placenta and uterus and shear off the placenta. The placenta is pushed to the palmar aspect of the hand and wrist, and, once it is entirely separated, the hand is withdrawn. Do not stop uterotonics while the manual removal is being performed. Restart bimanual massage, and have an assistant examine the placenta for completeness.

If the placenta has been previously delivered, then exploration of the uterus is still indicated at this time. The hand is introduced in the same manner, with control of the uterine fundus with the other hand. Any clots are removed. The cavity is gently explored with attention to any defects suggestive of uterine rupture. Rupture in the absence of a previous scar is uncommon. Rupture or dehiscence of a previous lower segment scar does not usually bleed heavily. The presence of a uterine rupture dictates that a laparotomy be performed.

A partial uterine inversion can be detected as the hand is introduced, just as a complete uterine inversion would have been detected as the hand was placed in the vagina. If the condition is encountered, return the uterus to its normal position by pressure on the inverted fundus from within the uterus. If retained placental tissue is encountered, it is sheared off the uterine wall and delivered. Adherent placental fragments may be left in situ or removed by gentle curettage. The risks of curettage include uterine perforation and increased bleeding caused by laceration of uterine vessels. This may be somewhat minimized by the use of a large, dull curette. Fragments left in situ may be removed by curettage sometime after the crisis has passed, although an increased risk of infection probably ensues.

The administration of short-term, broad-spectrum antibiotics following manual removal, manual exploration, or instrumentation of the uterus in this context is commonly advocated. Evidence is very limited, but a single small, randomized trial supports the practice.[51]

Immediately resume bimanual massage and compression following exploration and evacuation of the uterus. Continue infusion of oxytocin, and administer repeat doses of other uterotonics if the uterus fails to contract and maximal doses have not already been given. The uterus may contract well, and bleeding abates with massage, followed by uterine relaxation and increased bleeding when compression and massage are stopped. Prolonged massage at this point may allow the uterus to contract and retract if it can be kept empty of clots and if perfusion can be improved with adequate resuscitation. Any period of decreased bleeding allows fluid and blood component replacement to exceed blood loss and help improve the patient’s status.

Surgical management is necessary if the uterus does not remain contracted and bleeding persists despite all efforts. Packing of the uterus may be an option until the operating room is ready or if surgery is not an immediately available option. Uterine packing fell into disfavor during the 1960s as being nonphysiological, concealing ongoing blood loss, and increasing the risk of infection; however, reports since then have been favorable in very select circumstances when all previously mentioned maneuvers have failed.[52] The uterus and vagina must be tightly packed with continuous, layered, 2- or 4-inch gauze under direct visualization using a speculum and/or retractors or a purpose-built uterine packer.[53] At times, packing may serve as a definitive treatment. In these cases, the packing is usually removed in 24-48 hours in a setting where recurrent bleeding can be managed if it occurs.

Intrauterine catheters for tamponade of bleeding have also been used. In the past, large bulb Foley catheters or Sengstaken-Blakemore tubes have been used.[54] More recently, experience has been gained using catheters specifically designed for postpartum hemorrhage. One such device is the SOS Bakri tamponade balloon (Bakri, 2001). In low resource settings, condoms and surgical gloves have been used successfully to control bleeding.[55] Anti-shock garments are also being evaluated in low resource settings for both the definitive treatment of uterine atony as well as a method to allow time to bring other treatments to bear[56]

Manual examination helps to exclude a cervical or vaginal laceration, but direct visualization confirms that bleeding is coming from the uterus and excludes the possibility of missing trauma to the lower genital tract. If packing is meant to be definitive treatment, then ongoing assessment of uterine size, blood loss, and patient status must be maintained. Continue uterotonics and commence broad-spectrum antibiotics. Remove the pack in 24-36 hours in a setting that allows for appropriate management if bleeding recurs. Packing may also be used as a temporizing measure before arterial embolization (see Selective arterial embolization). Isolated reports of successful uterine tamponade with balloon devices have also been published.[57]

Genital tract trauma

Genital tract trauma is the most likely cause if bleeding persists or is present despite a well-contracted uterus. Use appropriate analgesia along with good lighting and positioning, which facilitates excellent exposure. If not already initiated, moving the patient to an operating room is reasonable at this time. Experienced assistants and an excellent circulating nurse are essential.

Directly visualize and inspect the cervix with the aid of ring forceps. The anterior lip is grasped, and the cervix is inspected by using a second ring forceps placed at the 2-o’clock position, followed by progressively "leap-frogging" the forceps ahead of one another until the entire circumference has been inspected. Small, nonbleeding lacerations of the cervix do not need to be sutured. Suture any laceration that is bleeding significantly or appears to have the potential to bleed significantly. Each side of the laceration can be grasped with a ring forceps back from the torn edge, and gentle traction can be used to aid exposure.

Use an absorbable, continuous interlocking stitch, and use tapered (rather than cutting) needles for all repairs except for the perineal skin. Ensure that the stitch begins above the apex of the tear, as with vaginal lacerations and episiotomies. If the apex cannot be visualized, place the stitch as high as possible and then use it to apply gentle traction to bring the apex into view. Polyglycolic sutures have largely replaced catgut; however, the latter may be somewhat less likely to tear the friable tissues of the cervix and vaginal vault and may thus be useful in repairing lacerations in these areas. The laceration must be observed for bleeding after the torn edges of the cervix are approximated. The ring forceps can be replaced and left on for some time if oozing persists.

Lacerations of the vaginal vault must be well visualized and their full extent realized prior to repair. Lacerations high in the vaginal vault and those extending up from the cervix may involve the uterus or lead to broad ligament or retroperitoneal hematomas. The proximity of the ureters to the lateral vaginal fornices, and the base of the bladder to the anterior fornix, must be kept in mind when repair is undertaken in these areas. Poorly placed stitches can lead to genitourinary fistulas. An absorbable, continuous interlocking stitch is used. The stitch must start and finish beyond the apices of the laceration. Great care must be taken because the tissue is usually very friable. Take a good amount of tissue, and ensure that the needle reaches the full depth of the tear. Ongoing bleeding and hematoma formation are possible if small bites are taken.

Again, the laceration must be observed for bleeding after the repair is complete. Pressure or packing over the repair may achieve hemostasis or allow for better placement of further hemostatic stitches. Cervical and vaginal vault lacerations that continue to ooze or those that are associated with hematomas may be amenable to selective arterial embolization (see Selective arterial embolization).

Traumatic hematomas are rare and may be related to lacerations or may occur in isolation. They include vulvar and paravaginal hematomas in the lower genital tract and broad ligament and retroperitoneal hematomas adjacent to the uterus. Patients with lower genital tract hematomas usually present with intense pain and localized, tender swelling. Broad ligament hematomas may be palpated as masses adjacent to the uterus. All may result in significant blood loss that mandates resuscitation.

Lower genital tract hematomas are usually managed by incision and drainage, although expectant management is acceptable if the lesion is not enlarging.[58] Any bleeding vessels are tied off, and oozing areas may be oversewn. Place a Foley catheter because urinary retention can occur because of pain and tissue distortion. Vaginal packing may be useful following drainage and repair of a paravaginal hematoma. Remove the pack in 24-36 hours. Embolization may be used in both vaginal and vulvar hematomas that are unresponsive to surgical management.

Broad ligament and retroperitoneal hematomas are initially managed expectantly if the patient is stable and the lesions are not expanding.[59] Ultrasound, CT scanning, and MRI all may be used to assess the size and progress of these hematomas. Selective arterial embolization may be the treatment of choice if intervention is required in these patients. Use surgical procedures to evacuate the hematoma, and attempt to tie off any bleeding vessels. Consider involving a surgeon with extensive experience operating in the retroperitoneal space.

Coagulopathy

If manual exploration has excluded uterine rupture or retained placental fragments, bleeding from a well-contracted uterus is most commonly due to a defect in hemostasis. A review of the history and risk factors along with coagulation test results clarifies this diagnosis. Proceed with blood product replacement as previously described in order to correct abnormalities of hemostasis. If the coagulation status is normal and bleeding is ongoing despite a well-contracted uterus, then the possibilities of uterine rupture or an inadequately repaired uterine incision (if the patient had a cesarean delivery) must be considered. Revisit any repair to the cervix or vagina before proceeding to surgical management.

Surgical Therapy

Ongoing bleeding secondary to an unresponsive and atonic uterus, a ruptured uterus, or a large cervical laceration extending into the uterus requires surgical intervention. Laparotomy for PPH following a vaginal delivery is rare. In a review of emergency peripartum hysterectomies over a 5-year period in Los Angeles, Calif, the rate was 1 in 1000 deliveries, but most of these cases began as cesarean deliveries, usually for placenta previa.[60] A study from Boston, Mass, found a rate of 1.5 in 1000 deliveries with similar risk factors.[61] Canadian and Irish studies put the rate at 0.4 and 0.3 per 1000 deliveries, respectively.

Adequately resuscitate the patient before surgery. This includes optimizing hemoglobin and coagulation status as previously described. Fully inform anesthetic and operating room staff as to the nature of the case. Schedule for a second surgeon to be in attendance, if possible. As mentioned previously, sustained bimanual compression and massage and uterine packing may be used to gain time to mount a surgical response. Military antishock trousers provide the equivalent of an approximately 500- to 1000-mL autotransfusion and potentially gain time during a resuscitation. Only the leg portion of the trousers are inflated in the setting of PPH. Direct compression of the aorta may be performed for a short period while the operating room is prepared.

A recent systematic review examined various techniques used when medical management is unsuccessful. These included arterial embolization, balloon tamponade, uterine compression sutures, and iliac artery ligation or uterine devascularization. At present, no evidence suggests that any one method is more effective for the management of severe PPH. Randomized controlled trials of the various treatment options may be difficult to perform. Balloon tamponade is the least invasive and most rapid approach and may thus be the logical first step.[62]

Laparotomy

The choice between a subumbilical vertical incision and a Pfannenstiel incision for entry into the abdomen is left to the individual surgeon. Both entries have support, and no strong evidence indicates that either is superior in this setting.[63] If concern exists regarding pathology in the upper abdomen or if exposure is thought to be a concern, the vertical incision is recommended. Broad-spectrum antibiotic coverage is advised.

Upon entry, remove any free blood and inspect the uterus and surrounding tissues for evidence of rupture or hematoma. If uterine rupture is found, a rapid decision must be made concerning the viability of repair versus hysterectomy. Bleeding may be reduced in either instance by grasping bleeding points on the torn edges with clamps. The number of layers used for any repair is dictated by the thickness of the tissue and the hemostatic response to suturing. Principles are similar to those of cesarean delivery incision repair. Ensure that bleeding is stopped and not merely internalized because this would result in ongoing vaginal bleeding or hematoma formation. Any repair must be carefully observed for hemostasis before abdominal closure is performed. Uterine exteriorization may improve exposure and decrease operating time, but great care must be taken to not worsen uterine trauma and to keep the uterus warm and well perfused to avoid worsening atony.

Hemostasis must be reassessed after the uterus is returned to the abdominal cavity. Consider placement of a suction drain.

If the uterus is intact upon entry and the bleeding has been caused by atony, then direct bimanual massage and compression may be performed while systemic uterotonics are continued. Direct injection of oxytocin, carboprost, and/or ergonovine may be successful in overcoming atony.

Uterine artery ligation

Uterine artery ligation is a relatively simple procedure and can be highly effective in controlling bleeding from uterine sources. These arteries provide approximately 90% of uterine blood flow. The uterus is grasped and tilted to expose the vessels coursing through the broad ligament immediately adjacent to the uterus. Ideally, place the stitch 2 cm below the level of a transverse lower uterine incision site. A large atraumatic (round) needle is used with a heavy absorbable suture. Include almost the full thickness of the myometrium to anchor the stitch and to ensure that the uterine artery and veins are completely included. The needle is then passed through an avascular portion of the broad ligament and tied anteriorly. Opening the broad ligament is unnecessary. Perform bilateral uterine artery ligation. While the uterus may remain atonic, blanching is usually noted and blood flow is greatly diminished or arrested.

Local oozing may be controlled with direct injection or compression with warm saline packs. In a series of 265 cases, a 95% success rate was reported using this procedure in PPH unresponsive to uterotonics in patients who had cesarean births.[64] Another series of 103 cases had a 100% success rate if a stepwise approach was taken.[65] After initial uterine artery ligation, subsequent stitches were placed 2-3 cm below the initial stitches following bladder mobilization, and, finally, ovary artery ligation was performed if required. Menstrual flow and fertility were not adversely affected.

Ovarian artery ligation

The ovarian artery arises directly from the aorta and ultimately anastomoses with the uterine artery in the region of the uterine aspect of the uteroovarian ligament. Ligation is performed just inferior to this point in a manner similar to that of uterine artery ligation. The amount of uterine blood flow supplied by these vessels may increase following uterine artery ligation. The procedure is easy to perform; however, the potential benefit must be weighed against the time required to perform the ligations.

Internal iliac (hypogastric) artery ligation

Internal iliac artery ligation can be effective to reduce bleeding from all sources within the genital tract by reducing the pulse pressure in the pelvic arterial circulation. One study indicated that pulse pressure was reduced by 77% with unilateral ligation and by 85% with bilateral ligation.[66] Hypogastric artery ligation is much more difficult to perform, more commonly associated with damage to nearby structures, and less likely to succeed than uterine artery ligation. One study reported a success rate of 42%. In patients who undergo hypogastric artery ligation, uterine artery ligation has usually already failed.

Prerequisites for the procedure include a stable patient, an operator experienced in the procedure, and a desire to maintain reproductive potential. The retroperitoneal space is entered by incising the peritoneum between the fallopian tube and the round ligament. The ureter must be identified and reflected medially with the attached peritoneum. The external iliac artery is identified on the pelvic sidewall and followed proximally to the bifurcation of the common iliac artery. The ureter passes over the bifurcation. The internal iliac artery is identified and followed distally approximately 3-4 cm from its point of origin. The loose areolar tissue is carefully cleared from the artery. A right-angle clamp is passed beneath the artery at this point, with great care to avoid damage to the underlying internal iliac vein.

A recommendation is to pass the clamp from lateral to medial in order to minimize the chance of damage to the adjacent external iliac vessels. Gentle elevation of the artery with a Babcock clamp facilitates this maneuver.

Ligate the artery with heavy absorbable suture, but do not divide it. Palpate the femoral and distal pulses before and after the ligation to ensure that the external or common iliac artery was not inadvertently ligated. If possible, place the ligation distal to the posterior division of the artery because this decreases the risk of subsequent ischemic buttock pain. Identification of the posterior division may be difficult, and ligation 3 cm from the internal iliac artery origin usually ensures that it is not included.

Hysterectomy is required if internal iliac artery ligation is unsuccessful. Patients in whom internal iliac artery ligation has failed have greater morbidity than those in whom the procedure has not been attempted. The likelihood of benefit from the procedure must be balanced against the potential risks. The advent of more effective uterotonic agents, the fact that most cases of intractable hemorrhage are now related to abnormalities of placentation that are diagnosed or suggested before delivery, and the option of embolization have lessened the use of hypogastric artery ligation. The number of surgeons comfortable using this procedure and the opportunities to teach it are rapidly declining.

Hysterectomy

Hysterectomy is curative for bleeding arising from the uterine, cervical, and vaginal fornices. The procedure of peripartum hysterectomy is well described in several texts and articles (eg, Hysterectomy), and the technique differs little from that in nonpregnant patients.[67, 63] While the organ is more vascular, the tissue planes are often more easily developed. Total hysterectomy is preferred to subtotal hysterectomy, although the latter may be performed faster and be effective for bleeding due to uterine atony. Subtotal hysterectomy may not be effective for controlling bleeding from the lower segment, cervix, or vaginal fornices. Take every opportunity to become involved when peripartum hysterectomies are performed.

Selective arterial embolization

Angiographic embolization in the management of PPH was first described more than 30 years ago.[68] As with all of the surgical and most of the medical treatments of PPH, no RCTs regarding its effectiveness have been conducted. This is likely to remain the case for some time given the relative rarity of intractable PPH. Several case series suggest that selective arterial embolization may be useful in situations in which preservation of fertility is desired, when surgical options have been exhausted, and in managing hematomas.[69] Follow-up of women undergoing successful embolization for severe intractable PPH reports that women almost invariably have a return to normal menses and fertility.[70]

The major drawbacks of the procedure are the requirement for 24-hour availability of radiological expertise and the time required to complete the procedure. Patients must be stable to be candidates for this procedure. Complications include local hematoma formation at the insertion site; infection; ischemic phenomena, including uterine necrosis in rare instances; and contrast-related adverse effects. Currently, most PPH cases requiring hysterectomy are related to placenta previa. These patients are commonly diagnosed before delivery and are usually delivered by elective cesarean birth. This planning may allow increased use of invasive radiological services in the management of such cases.

A retrospective study by Park et al indicated that transcatheter arterial embolization (TAE) is safe and effective for secondary PPH. In the study, the procedure was clinically successful in 47 of 52 patients (90.4%) being treated for secondary PPH (caused in 23 cases by retained placenta). Gelatin sponge particles were used in 48 patients, either alone or in combination with permanent embolic materials (eg, microcoils, N-butyl cyanoacrylate); embolization was performed with permanent materials alone in the remaining four patients. Regular menstruation returned in the 44 patients who were followed up (for a mean 12.6-month period), and five patients were known to become pregnant.[71]

B-Lynch and Cho sutures

Recent case series and case reports advocate the use of transmural uterine compression sutures to rapidly control bleeding. The initial reports described the B-Lynch technique, which involves opening the lower segment and passing a suture through the posterior uterine wall and then over the fundus to be tied anteriorly.[72, 73] A similar technique has been described without opening the uterus. A long, straight needle is passed anterior to posterior through the lower uterine segment; the suture is passed over the fundus and then tied anteriorly.[74] Both techniques use bilateral stitches. The most recent variant uses multiple stitches passed transmurally and tied anteriorly at various points over the uterine body. This technique may be focused in the area of the placental bed in cases of abnormal placentation.[75] All of these procedures effectively produce tamponade by compressing together the anterior and posterior walls.

Follow-up reports suggest a normal return to menses and fertility, but the number of cases is small. The techniques have the advantage of being very simple to perform and may be a rapidly effective alternative to hysterectomy.[72]

Bleeding at cesarean delivery

In the past, most cases of intractable PPH followed vaginal delivery and were due to uterine atony; however, more recent case series and national databases show that more cases are now associated with cesarean delivery. Cesarean delivery for placenta previa carries a relative risk of 100 for peripartum hysterectomy, with many patients having a diagnosis of placenta accreta.[76] High-resolution ultrasound with color Doppler may allow antenatal diagnosis of placenta accreta.

Whenever possible, delivery of the placenta at cesarean delivery should be performed in an assisted fashion following the administration of a uterotonic agent, preferably oxytocin. This practice leads to less blood loss and less infectious morbidity.[77]

Uterine rupture has also become a more common cause of severe PPH necessitating hysterectomy. The vast majority of these cases occur in patients with a previous cesarean birth. Counsel all women with placenta previa, and especially those with a previous low segment uterine scar, in the antenatal period regarding the risk of severe PPH and the possible need for transfusion and even hysterectomy. Ensure that these patients are cared for in facilities with the resources to manage them successfully if complications arise.[78]

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

Direct intramyometrial injection of uterotonics may be undertaken. Vasopressin (0.2 U in 1 mL of NS) may also be injected into the myometrium, with great care taken to avoid intravascular injection. Individual vessels in the placental bed may be ligated. Simple or box stitches may be placed where continuous oozing is present.[75] In cases of placenta previa, the lower uterine segment may be temporarily packed; leaving a pack in the uterus is also an option. The end of the pack is fed through the cervix and into the vagina and is removed 24-36 hours later. Uterine rupture or extension of a uterine incision requires excellent visualization and careful repair with attention to adjacent structures.

The stepwise surgical approach described above may be used if these measures are unsuccessful and preservation of fertility is desired. Strongly consider immediate hysterectomy if further reproduction is not an issue or if bleeding or damage to the uterus appears severe. Embolization may be considered in this setting. Its successful use has been described both intraoperatively to preserve the uterus and after hysterectomy for continued bleeding. Embolization may also be used for continued postoperative vaginal bleeding.[79]

Persistent bleeding following hysterectomy may also be managed by packing with gauze brought out through the vagina or by a pelvic pressure pack composed of gauze in a sterile plastic bag brought out through the vagina and placed under tension. This pack is also known as a parachute, mushroom, or umbrella pack. Place a Foley catheter to monitor urine output and prevent urinary retention. The placement of a suction drain may be useful to monitor losses in cases of ongoing oozing. Always consider coagulopathy in patients with continued slow blood loss.

Postoperative Details

Continue resuscitation, and repeat laboratory tests. Monitor vital signs, urine output, and any ongoing losses. Care in an intensive care setting is advantageous, as is close follow-up by the obstetric service. The patient must be monitored for complications (see Complications).

Follow-up

Full documentation of the case is imperative, and a careful explanation of events and interventions must be given to the patient and family. Caregivers must be available and approachable for questions. Implications and recommendations for future pregnancies may be discussed during the postoperative stay and reinforced at the postdischarge visit.

Summary

PPH is a common complication of childbirth and a leading cause of maternal morbidity and mortality. Clinicians should identify risk factors before and during labor so that care may be optimized for high-risk women. However, significant life-threatening bleeding can occur in the absence of risk factors and without warning. All caregivers and facilities involved in maternity care must have a clear plan for the prevention and management of PPH. This includes sound resuscitation skills and familiarity with all medical and surgical therapies available.

Complications

Most patients with PPH are quickly identified and successfully treated before major complications develop. The most common problem is anemia and loss of iron stores, which results in fatigue in the postpartum period. Clinicians and patients are more tolerant of low hemoglobin levels, mild postural lightheadedness, and fatigue because of current concerns over blood transfusion. The risks of transfusion with blood products are well known and have been previously described.

Not surprisingly, many of the complications of severe PPH are related to massive blood loss and hypovolemic shock. Damage to all major organs is possible; respiratory (adult respiratory distress syndrome) and renal (acute tubular necrosis) damage are the most common but are rare. These conditions are best managed by specialists. Renal failure is usually self-limited, and renal function recovers fully. Temporary dialysis is seldom required. Pulmonary edema is uncommon in this previously healthy group; however, it may develop acutely or during the recovery phase because of fluid overload or myocardial dysfunction. Response to standard therapy is usually prompt.

Pregnant women are at increased risk of venous thrombosis and embolic events. Many of the risk factors for PPH are also risk factors for venous thrombosis and embolic events, including operative vaginal delivery, cesarean delivery, and pelvic surgery. Venous stasis due to shock and immobility also contribute, and caregivers should maintain a high index of clinical awareness.

Hypopituitarism following severe PPH (Sheehan syndrome) is due to critical ischemia of the hypertrophied pituitary. This condition should be considered if a failure to lactate occurs. Isolated deficiencies of pituitary tropins and hyperprolactinemia have also been reported.

Evidence suggests that prophylaxis against gastrointestinal ulceration is useful in critically ill patients, especially those requiring ventilation. The recommended agents are sucralfate and histamine 2 blockers. Both are effective at reducing the risk of ulcers. Sucralfate may be associated with a lower incidence of pneumonia.[80]

Several of the complications related to surgical interventions have been described. Complications include sterility, uterine perforation, uterine synechiae (Asherman syndrome), urinary tract injury and genitourinary fistula, bowel injury and genitointestinal fistula, vascular injury, pelvic hematoma, and sepsis. Consider ultrasound of the kidneys following complicated emergency pelvic surgery in order to exclude ureteric obstruction. Patients undergoing uterine exploration, instrumentation, or laparotomy in this context probably benefit from antibiotic coverage at the time of the intervention. Good evidence suggests that all patients having cesarean births should receive prophylactic antibiotics.[81] The duration of antibiotic coverage following surgery in these circumstance is unknown.

 

Questions & Answers

Overview

What is the mortality and morbidity associated with postpartum hemorrhage (PPH)?

How is postpartum hemorrhage (PPH) defined?

What is the prevalence of postpartum hemorrhage (PPH) in the US?

What is the global prevalence of postpartum hemorrhage (PPH)?

What causes postpartum hemorrhage (PPH)?

What are risk factors for postpartum hemorrhage (PPH)?

What are the 4T&#39;s causing postpartum hemorrhage (PPH)?

What is the role of tone in the etiology of postpartum hemorrhage (PPH)?

What is the role of tissue in the etiology of postpartum hemorrhage (PPH)?

What is the role of trauma in the etiology of postpartum hemorrhage (PPH)?

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How is postpartum hemorrhage prevented?

What is the pathophysiology of postpartum hemorrhage (PPH)?

What are the signs and symptoms of postpartum hemorrhage (PPH)?

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Workup

What is the role of lab tests in the workup of postpartum hemorrhage (PPH)?

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How is postpartum hemorrhage (PPH) diagnosed?

Treatment

How is postpartum hemorrhage (PPH) treated?

How is a protocol for management of postpartum hemorrhage (PPH) implemented?

What is the role of tranexamic acid in the treatment of postpartum hemorrhage (PPH)?

What is the role of fluid resuscitation in the treatment of postpartum hemorrhage (PPH)?

What is the role of blood transfusion in the treatment of postpartum hemorrhage (PPH)?

How is coagulopathy diagnosed in postpartum hemorrhage (PPH)?

What is included in fluid resuscitation monitoring during the treatment of postpartum hemorrhage (PPH)?

What are the steps in the "ORDER" plan for managing postpartum hemorrhage (PPH)?

What is included in the initial assessment of postpartum hemorrhage (PPH)?

How is uterine atony-related postpartum hemorrhage (PPH) treated?

How is postpartum hemorrhage (PPH) caused by tissue retention treated?

How is trauma-related postpartum hemorrhage (PPH) treated?

How is coagulopathy-related postpartum hemorrhage (PPH) treated?

What is the role of surgery in the treatment of postpartum hemorrhage (PPH)?

What is the role of laparotomy in the treatment of postpartum hemorrhage (PPH)?

What is the role of uterine artery ligation in the treatment of postpartum hemorrhage (PPH)?

What is the role of ovarian artery ligation in the treatment of postpartum hemorrhage (PPH)?

What is the role of internal iliac artery ligation in the treatment of postpartum hemorrhage (PPH)?

What is the role of hysterectomy in the treatment of postpartum hemorrhage (PPH)?

What is the role of angiographic embolization in the treatment of postpartum hemorrhage (PPH)?

What is the role of transmural uterine compression sutures in the treatment of postpartum hemorrhage (PPH)?

How is postpartum hemorrhage (PPH) following a cesarean delivery treated?

What is included in postoperative care following surgery for postpartum hemorrhage (PPH)?

What should be discussed with the patient treated for postpartum hemorrhage (PPH) prior to discharge?

What are the possible complications of postpartum hemorrhage (PPH)?