eMedicine Specialties > Obstetrics and Gynecology > Obstetrical Complications

Postpartum Hemorrhage

John R Smith, MD, FRSCS, FACOG,, Maternal-Fetal Medicine, Departments of Obstetrics & Gynecology and Diagnostic Imaging, Credit Valley Hospital, Mississauga, Ontario
Barbara G Brennan, MD, PhD, FRCSC, FACOG,, Division of Maternal-Fetal Medicine, Associate Professor, Department of Obstetrics and Gynecology, McMaster University

Updated: Sep 24, 2009

Introduction

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 direct pregnancy-related maternal mortality rate in the United States is approximately 7-10 women per 100,000 live births. National statistics suggest that approximately 8% of these deaths are caused by PPH.¹ In industrialized countries, PPH usually ranks in the top 3 causes of maternal mortality, along with embolism and hypertension. In the developing world, several countries have maternal mortality rates in excess of 1000 women per 100,000 live births, and World Health Organization statistics suggest that 25% of maternal deaths are due to PPH, accounting for more than 100,000 maternal deaths per year.² The most recent Practice Bulletin from the American College of Obstetricians and Gynecologists places the estimate at 140,000 maternal deaths per year or 1 woman every 4 minutes.³

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.⁴ 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.⁵ 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.

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.^6,7 See eMedicine 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.⁸  
 
A recently published, large population based study supported these findings with significant risk factors, identified using a multivariable analysis, being: retained placenta (OR 3.5, 95% CI 2.1-5.8), failure to progress during the second stage of labor (OR 3.4, 95% CI 2.4-4.7), placenta accreta (OR 3.3, 95% CI 1.7-6.4), lacerations (OR 2.4, 95% CI 2.0-2.8), instrumental delivery (OR 2.3, 95% CI 1.6-3.4), large for gestational age (LGA) newborn (OR 1.9, 95% CI 1.6-2.4), hypertensive disorders (OR 1.7, 95%CI 1.2-2.1), induction of labor (OR 1.4, 95%CI 1.1-1.7) and augmentation of labor with oxytocin (OR 1.4, 95% CI 1.2-1.7).⁹
 
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.¹⁰
 
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.¹¹ 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).¹²  
 
Failure of complete separation of the placenta occurs in placenta accreta and its variants. In this condition, the placenta has invaded beyond the normal cleavage plane and is abnormally adherent. Significant bleeding from the area where normal attachment (and now detachment) has occurred may mark partial accreta. Complete accreta in which the entire surface of the placenta is abnormally attached, or more severe invasion (placenta increta or percreta), may not initially cause severe bleeding, but it may develop as more aggressive efforts are made to remove the placenta. This condition should be considered possible whenever the placenta is implanted over a previous uterine scar, especially if associated with placenta previa.
 
All patients with placenta previa should be informed of the risk of severe PPH, including the possible need for transfusion and hysterectomy.
 
Finally, retained blood may cause uterine distension and prevent effective contraction.
 
Trauma
 
Damage to the genital tract may occur spontaneously or through manipulations used to deliver the baby. Cesarean delivery results in twice the average blood loss of vaginal delivery. Incisions in the poorly contractile lower segment heal well but are more reliant on suturing, vasospasm, and clotting for hemostasis.
 
Uterine rupture is most common in patients with previous cesarean delivery scars. Routine transvaginal palpation of such scars is no longer recommended. Any uterus that has undergone a procedure resulting in a total or thick partial disruption of the uterine wall should be considered at risk for rupture in a future pregnancy. This admonition includes fibroidectomy; uteroplasty for congenital abnormality; cornual or cervical ectopic resection; and perforation of the uterus during dilatation, curettage, biopsy, hysteroscopy, laparoscopy, or intrauterine contraceptive device placement.
 
Trauma may occur following very prolonged or vigorous labor, especially if the patient has relative or absolute cephalopelvic disproportion and the uterus has been stimulated with oxytocin or prostaglandins. Using intrauterine pressure monitoring may lessen this risk. Trauma also may occur following extrauterine or intrauterine manipulation of the fetus. The highest risk is probably associated with internal version and extraction of a second twin; however, uterine rupture may also occur secondary to external version. Finally, trauma may result secondary to attempts to remove a retained placenta manually or with instrumentation. The uterus should always be controlled with a hand on the abdomen during any such procedure. An intraumbilical vein saline/oxytocin or saline/misoprostol injection may reduce the need for more invasive removal techniques.⁶
 
Cervical laceration is most commonly associated with forceps delivery, and the cervix should be inspected following all such deliveries. Assisted vaginal delivery (forceps or vacuum) should never be attempted without the cervix being fully dilated. Cervical laceration may occur spontaneously. In these cases, mothers have often been unable to resist bearing down before full cervical dilatation. Rarely, manual exploration or instrumentation of the uterus may result in cervical damage. Very rarely, the cervix is purposefully incised at the 2- and/or 10-o’clock positions to facilitate delivery of an entrapped fetal head during a breech delivery (Dührssen incision).
 
Vaginal sidewall laceration is also most commonly associated with operative vaginal delivery, but it may occur spontaneously, especially if a fetal hand presents with the head. Lacerations may occur during manipulations to resolve shoulder dystocia. Lacerations often occur in the region overlying the ischial spines. The frequency of sidewall and cervical lacerations has probably decreased in recent years because of the reduction in the use of midpelvic forceps and, especially, midpelvic rotational procedures.
 
Lower vaginal trauma occurs either spontaneously or because of episiotomy. Spontaneous lacerations usually involve the posterior fourchette; however, trauma to the periurethral and clitoral region may occur and can be problematic.
 
Thrombosis
 
In the immediate postpartum period, disorders of the coagulation system and platelets do not usually result in excessive bleeding; this emphasizes the efficiency of uterine contraction and retraction for preventing hemorrhage.⁴ 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.¹³ 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

Table 1. Benefits of Active Management Versus Expectant Management

*CI: Confidence interval
† NNT: Number needed to treat

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.⁵
 
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.⁴
 
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.¹⁸
 
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 Hemorrhage¹⁹

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.^21,22  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.²³ 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

Management of massive obstetric hemorrhage

• 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

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.⁴⁸ A study from Boston, Mass, found a rate of 1.5 in 1000 deliveries with similar risk factors.⁴⁹ 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.⁵⁰

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.⁵¹ 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.⁵² Another series of 103 cases had a 100% success rate if a stepwise approach was taken.⁵³ 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.⁵⁴ 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.^55,51 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.⁵⁶ 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.⁵⁷ Follow-up of women undergoing successful embolization for severe intractable PPH reports that women almost invariably have a return to normal menses and fertility.⁵⁸

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.

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.^59,60 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.⁶¹ 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.⁶² 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.⁵⁹

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.⁶³ 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.^64,65

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.⁶⁶

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.⁶² 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.⁶⁷

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.

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.⁶⁸
 
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.⁶⁹ The duration of antibiotic coverage following surgery in these circumstance is unknown.
 
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.

Future and Controversies

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.

Multimedia

Media file 1: Postpartum hemorrhage. Maternal morbidity by subregion, 1995.

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Keywords

postpartum hemorrhage, PPH, postpartum bleeding, obstetrical hemorrhage, obstetric hemorrhage, uterine atony, atonic uterus, uterine myometrial fibers, 4 T's, 4 Ts, tone, tissue, thrombosis, maternal mortality, labor, labour, cesarian delivery, cesarian section, C-section, C section, caesarian section, caesarian delivery, uterine rupture, cervical laceration, episiotomy, oxytocin, labor induction, pregnancy complications, problem pregnancy, high-risk pregnancy, maternal morbidity, third-stage management, third stage of labor, management of third stage of labor, 3rd stage of labor, placenta previa, placenta accreta, pregnancy, parturition, birthing, delivery, fatty liver of pregnancy, intrauterine fetal demise, IUFD, amniotic fluid embolus, amniotic fluid emboli, septicemia in pregnancy

Contributor Information and Disclosures

Author

John R Smith, MD, FRSCS, FACOG,, Maternal-Fetal Medicine, Departments of Obstetrics & Gynecology and Diagnostic Imaging, Credit Valley Hospital, Mississauga, Ontario
John R Smith, MD, FRSCS, FACOG, is a member of the following medical societies: American College of Obstetricians and Gynecologists, College of Physicians and Surgeons of Ontario, Royal College of Physicians and Surgeons of Canada, and Society of Obstetric Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Barbara G Brennan, MD, PhD, FRCSC, FACOG,, Division of Maternal-Fetal Medicine, Associate Professor, Department of Obstetrics and Gynecology, McMaster University
Barbara G Brennan, MD, PhD, FRCSC, FACOG, is a member of the following medical societies: American College of Obstetricians and Gynecologists, Canadian Medical Protective Association, College of Physicians and Surgeons of Ontario, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, and Society of Obstetric Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Michel E Rivlin, MD, Professor, Coordinator of Quality Assurance/Quality Improvement, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine
Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, and Royal College of Surgeons of Edinburgh
Disclosure: Nothing to disclose.

CME Editor

Frederick B Gaupp, MD, Consulting Staff, Department of Family Practice, Hancock Medical Center
Frederick B Gaupp, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.

Chief Editor

Michel E Rivlin, MD, Professor, Coordinator of Quality Assurance/Quality Improvement, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine
Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, and Royal College of Surgeons of Edinburgh
Disclosure: Nothing to disclose.

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