INTRODUCTION

The ability to anticipate, recognize, and manage PPH is a cornerstone of inpatient obstetric practice. It is not only critical that the obstetrician be well versed in its management but that facilities have the personnel, supplies, and equipment readily available to manage this obstetric emergency.

PPH continues to be one of the top causes of maternal mortality worldwide, responsible for up to a third of pregnancy-related deaths. In the developed world, hemorrhage is the most common reason for maternal admission to the intensive care unit (ICU), while in low-resource settings, obstetric hemorrhage is responsible for up to half of the postpartum deaths that occur.^1,2 The incidence of PPH is dependent upon the definition used, but it is generally estimated to be 1% to 5% of deliveries.^3,4 An analysis of temporal trends and risk factors for severe PPH reviewed 8.5 million deliveries in the United States A nationwide inpatient sample from 1999 to 2008 showed a rate of 2.8% for PPH, while 0.3% were complicated by severe PPH.⁴

Perhaps the most relevant fact is that obstetric hemorrhage is the most preventable cause of maternal mortality.⁵ Factors that contribute to mortality from hemorrhage are lack of obstetrical and anesthesia services and the availability of blood products. Recently, there have been state and national efforts to implement comprehensive hemorrhage protocols and patient safety bundles on obstetric hemorrhage. The common theme reiterated in contemporary hemorrhage management plans is the avoidance of “delay and denial”, as well as the active aggressive treatment of hemorrhage in earlier stages. Implementation of quality initiatives aimed at reducing morbidity and mortality from PPH has shown significant reductions in morbidity and has been proven successful in decreasing the rates of transfusion and hysterectomy.^6,7

DEFINITIONS

The definition of PPH is not standard in the literature, which makes it difficult to determine its true incidence. Historically, PPH has been defined by the volume of blood loss, either from estimated blood loss or through quantitative measurement. Typically, >500 mL of blood loss in a vaginal delivery and >1000 mL blood loss in a cesarean delivery is considered a PPH.^8,9 The problem with these definitions is that they are the same as the average estimated blood loss for vaginal and cesarean deliveries, respectively. The World Health Organization (WHO) defines primary PPH as 500 mL or more blood loss in the 24 hours after delivery.¹⁰ Recently, the American College of Obstetricians and Gynecologists (ACOG) standardized the definition of primary PPH as “cumulative blood loss of greater than 1000 mL, or blood loss accompanied by signs and symptoms of hypovolemia within 24 hours of the birth process,” and the organization continues to say that “cumulative blood loss of 500 to 999 mL alone should trigger increased supervision and potential interventions as clinically indicated.”¹¹ Finally, a PPH is either considered primary, occurring within the first 24 hours after delivery, or secondary, occurring from 24 hours to 2 weeks after delivery. Secondary hemorrhage is also referred to as late PPH or delayed PPH.

PATHOPHYSIOLOGY

There are multiple hemodynamic changes during pregnancy that are protective against obstetric hemorrhage, such as an increase in plasma volume of up to 50%, and an accompanying increase in red blood cell mass of up to 30%. These changes begin in the first trimester and are greatest in the second trimester, with total blood volume increasing by 40% to 45% by the 32nd week of pregnancy. Maternal cardiac output rises, resulting from an increase in stroke volume and heart rate. Around 15% of cardiac output goes to the uterus during pregnancy, which is equivalent to 500 to 700 mL/minute of blood flow through the uterine arteries at term. There is also an overall decrease in systemic vascular resistance, and pro-clotting factors such as Factors II, VII, VIII, IX, and X and fibrinogen are increased.¹²

In addition to the physiologic changes of pregnancy, there are other hemostatic mechanisms that occur at the time of delivery. Upon placental separation, vasospasm and clot formation are the first mechanisms to promote hemostasis. Systemic coagulation factors such as platelets and clotting factors as well as local decidual factors, promote clotting. In addition, the contraction of the myometrium provides hemostasis through mechanical compression of the maternal vessels in the placental bed. Both of these mechanisms are subject to dysregulation at the time of delivery. Depletion or dysfunction of clotting factors and platelets can lead to coagulopathy, and failure of the myometrium to contract properly results in uterine atony. The end result of both is PPH.

DIAGNOSIS

PPH occurs as the result of an underlying cause (Table 41-1). Determination of the etiology of hemorrhage is the key to identifying effective interventions. Physical examination and identification of risk factors can help guide the clinician to the underlying diagnosis. Active vaginal bleeding following delivery is generally due to uterine atony or retained fragments of placenta or membranes. This is easily assessed through uterine exploration and bimanual massage. If the uterine fundus is firm and there is still brisk vaginal bleeding, suspicion of a cervical laceration or a vaginal laceration should increase. In women who have a retroperitoneal, vulvar, or vaginal hematoma, the diagnosis can be obscured; it may not be recognized until signs of hemodynamic instability are present.

CAUSES OF POSTPARTUM HEMORRHAGE

Atony

The most common cause of PPH is uterine atony, accounting for about 80% of PPHs and occurring in approximately 1 in 20 deliveries.¹³ Atony occurs when the myometrium fails to contract following delivery and there is no mechanical compression of the spiral arteries. It is important to recognize that there are other causes of massive PPH, however, and treatment for uterine atony is unlikely to help if the hemorrhage results from another cause.

Retained Placental Fragments

Remnants of the placenta or membranes left in the uterus following delivery can bring about PPH through uterine atony, although they are more likely to cause a delayed PPH. It is important to examine the placenta after delivery and ensure that there are no missing fragments or lobes. If pieces are missing or if there is suspicion for retained products, manual exploration should both reveal them and allow for their removal. If manual exploration proves ineffective at removal, then uterine curettage becomes necessary.

Trauma

Cervical and Vaginal Lacerations

Genital tract lacerations are another cause of PPH. Firm uterine tone in the presence of persistent vaginal bleeding should heighten suspicion for lower genital tract lacerations. Risk factors for genital tract lacerations include delivery prior to complete dilation, macrosomic infants, precipitous delivery, episiotomy, or instrumental delivery. Significant and rapid PPH is likely to result from a cervical laceration and requires prompt attention upon recognition. Lacerations to the cervix and vaginal fornices can be challenging to repair and require good exposure, adequate lighting and appropriate anesthesia. For these reasons, it is recommended to move to the operating room to repair them.

Uterine Rupture

Uterine rupture is a complete separation of the uterine wall through all layers, including the serosa. It is more common in women with a previous uterine scar, but it does occur in women with unscarred uteri as well. Uterine rupture occurs at an overall rate of 1 in 2000, while in women with a uterine scar, the rate is between 0.3% and 1.0%.¹⁴ Risk factors associated with uterine rupture during trial of labor after cesarean (TOLAC) include multiple cesarean deliveries, single-layer closure of the hysterotomy, multiple gestations, induced or augmented labor, and a short intergestational interval.¹⁵ If there is active postpartum bleeding and suspicion for uterine rupture, manual exploration may confirm the diagnosis. Regardless, a laparotomy for confirmation and treatment is appropriate.

Hematomas

Vulvar hematomas result from trauma and bleeding in the superficial fascia of the anterior or posterior pelvic triangles. Because of the fascial investment, they extend to the skin and are noted by swelling and discoloration on the vulva. Treatment is usually surgical drainage and closure of the dead space in layers. In the case of vaginal or retroperitoneal hematomas, pain and hemodynamic instability may be the heralding signs of a massive occult hemorrhage. Vaginal hematomas are the result of soft tissue damage and vessel laceration at the time of delivery. Expectant management may be appropriate for vaginal hematomas that are small and nonexpanding. Larger and expanding hematomas will require surgical drainage. The vaginal hematoma bed does not require closure; rather, a tamponade packing is recommended.¹⁶

Retroperitoneal hematomas can be insidious and life-threatening because they often go unrecognized until hemodynamic instability is obvious. These hematomas occur from lacerations of the branches of the anterior division of the internal iliac artery. Laparotomy, hematoma evacuation, and ligation of the offending vessel constitute the standard treatment for retroperitoneal hematomas. Arterial embolization may be considered as well. It is important to note that blood loss from hematomas may be unrecognized or underestimated and may result in coagulopathy.

Abnormal Placentation

Problems with abnormal placentation, such as placenta accreta, increta, percreta, placental abruption, and placenta previa, are all associated with massive hemorrhage. Hemorrhage from these causes may occur in the antepartum, intrapartum, or postpartum period. If invasive placentation is known or suspected, arrangements for delivery at a center that specializes in these disorders should be considered. Blood products must be readily available to manage these diagnoses. A full discussion of placentation disorders can be found in Chapter 43.

Coagulopathy

Coagulopathy can be both a cause and a result of PPH (Table 41-1). In general, coagulopathy at the time of delivery is likely due to a consumptive coagulopathy. Coagulopathy is a clinical diagnosis that can be supported with laboratory testing. In patients with suspected coagulopathy a clot observation test can be performed prior to receiving lab results. 5 mL of blood in a red top tube should clot within 8 to 10 minutes. Absence of clot formation or rapid dissolution of clot is an indicator of coagulopathy. The key to the treatment of coagulopathy is correction of the underlying etiology. Rapid administration of blood components and clotting factors should ensue as soon as coagulopathy is suspected. The treatment of coagulopathy and blood product replacement is discussed in detail in Chapter 21.

Puerperal Uterine Inversion:

A rare and challenging cause of PPH.

Background

Uterine inversion occurs after delivery when the uterine fundus prolapses into the endometrial cavity, sometimes completely through the cervix, turning the uterus completely inside out. Although it is a rare occurrence, uterine inversion can occur following a vaginal delivery or a cesarean delivery. Uterine inversion is a life-threatening obstetric emergency because it can lead to massive PPH, hypovolemic shock, and death if not recognized and treated promptly. Uterine inversions are classified by the degree of the inversion and the time of occurrence (Table 41-2). If acute uterine inversion goes unrecognized and is not appropriately managed, it results in severe hemorrhage and shock, leading to maternal death. Mortality from uterine inversion has been reported to be as high as 15%.¹⁷

Pathogenesis

It is not always clear why uterine inversion occurs. Abnormal placentation, uterine anomalies, retained placenta, shortened umbilical cords, use of uterine relaxants, rapid labor and delivery, and fetal macrosomia are risk factors associated with uterine inversion, but they are present in <50% of cases.¹⁸ Uterine inversion also may occur with excessive umbilical cord traction and fundal pressure, especially with an atonic uterus. There is not sufficient evidence to draw a correlation between active management of the third stage of labor and uterine inversion.

Diagnosis

The diagnosis of uterine inversion is made based on clinical findings. The most common heralding symptom of uterine inversion is massive PPH, although the amount of bleeding can vary depending on the degree of inversion. Upon examination, the uterine fundus is notably absent from the abdomen, and often a smooth round mass in the vagina is present, which is sometimes confused with a myoma. If there is a question about the diagnosis, it can be confirmed with ultrasound.

Management

Much of the initial management of uterine inversion is identical to the management of PPH. One major difference is that upon recognition of uterine inversion, all uterotonics should be stopped immediately. There should be efforts to establish secure venous access with large-bore intravenous (IV) needles. Fluid boluses should be initiated and blood products ordered. Other personnel involved in the care of the patient, such as anesthesiologists, nursing staff, operating room personnel, and additional obstetric staff, need to be alerted of the situation where appropriate.

To stop the hemorrhage, the normal anatomy of the uterus must be restored. This should ideally occur in the operating room, where there is access to proper anesthesia and the ability to give uterine relaxants. It is reasonable to attempt replacement of the inverted uterus immediately because the longer the wait, the more likely that the cervix has contracted to form a constricting ring around the uterine fundus. If this has happened already, you should initiate uterine relaxants before further attempts at replacement. Do not attempt to remove the placenta before replacement. The placenta is unlikely to interfere with replacement and detachment will increase the already brisk rate of hemorrhage. An algorithm for the management of puerperal uterine inversion is shown in Figure 41-1.

Uterine Relaxants

Nitroglycerin is an excellent first-line choice of uterine relaxant to manage uterine inversion. A dose of 50 mcg IV is given initially, and up to four additional doses may be given to achieve relaxation necessary to replace the uterus. Inhaled anesthetics such as sevoflurane, desflurane, and isoflurane also function as uterine relaxants. Terbutaline 0.25 mg subcutaneous (SC) or IV also may be used, but it may not have as strong a relaxation effect as do nitroglycerin or inhaled anesthetics.

Replacement of the Inverted Uterus

To replace the inverted uterus to its normal anatomic position, a maneuver called the Johnson technique is used. One hand is placed inside the vagina, and the fingers are placed around the prolapsed fundus. After that, the fingers apply gentle upward pressure to the part of the fundus closest to the cervix, pushing up toward the umbilicus.¹⁹ This can be immediately attempted upon recognition of an inversion, and if unsuccessful, can be reattempted after uterine relaxants are given. If manual replacement fails despite the use of uterine relaxants, surgical correction is necessary.

The patient should be taken to the operating room if not already there, and laparotomy performed to relieve the inversion. Upon abdominal entry, the surgeon will note the marked absence of the normal postpartum uterus. Instead, there appears to be a constricting ring with an indentation in the center. Often, the round ligaments and adnexa appear to dive into the indentation.

The Huntington procedure should be attempted first, as it is less invasive. This is performed by using clamps such as Babcock clamps to grasp the round ligaments and pull the fundus out of its inverted state. This procedure is repeated until the uterus is restored to normal. If the round ligaments are not identifiable, then atraumatic clamps can be used on the myometrium. If available, an assistant my help with a hand from below to apply upward pressure on the fundus.²⁰ If the Huntington procedure is unsuccessful, the Haultain procedure can be attempted, which involves making an incision through the constricting ring and increasing the space that the fundus can be elevated through.²¹ Once the constricting ring has been incised, the Huntington procedure can be employed to return the uterus from its inverted state to its normal anatomical position, followed by repair of the incision. Once the uterus has been replaced, the placenta should be removed, and uterotonic agents should be administered to assist with uterine tone and involution. A hand should be used to keep the fundus in position until the provider is sure that there is firm tone. Alternatively, uterine packing or a uterine tamponade balloon can be placed to hold the uterus in place and as a treatment for hemorrhage.²² If hemorrhage and atony persist after replacement of the uterus, then other interventions, including hysterectomy, may be necessary.

EVALUATION

It is imperative that patients who have persistent vaginal bleeding following delivery be evaluated by a provider at the bedside. Assessment should include a review of the blood pressure, heart rate, respirations, oxygen saturations, and urine output, as they can be signs of acute blood loss. There should be some type of objective, quantitative measurement of blood loss, such as calibrated drapes under the buttocks and the weight of blood-soaked sponges. Patients who are unstable or who have had >1500 mL blood loss should go to the operating room, where there is proper lighting, access to anesthesia, and the ability to intervene surgically.

A trend of lowering blood pressure and increasing heart rate following delivery should be assumed to be from blood loss until proven otherwise, even if the source is not immediately obvious. The source of bleeding should be thoroughly assessed through bimanual exploration and external examination. When there is obvious vaginal bleeding, initial assessment should include evaluation of the uterine tone and exploration of the uterine cavity to remove any retained placental fragments or clots. Assessment should also include a systematic inspection of the entire reproductive tract. The uterus should be explored manually to assess tone, remove any remaining products of conception, and assess for any myometrial defects, especially in patients with a prior cesarean delivery. There should be a thorough visual evaluation of the cervix to identify any lacerations as well as visual inspection of the vaginal vault to identify bleeding from deep vaginal lacerations.

It is important to keep in mind that hemorrhage can be concealed if it occurs in the retroperitoneal space or in a vaginal or vulvar hematoma. These causes should be high on the differential when tachycardia and hypotension present immediately postpartum without obvious vaginal bleeding. Laboratory evaluation should include a complete blood count and coagulation studies (i.e. fibrinogen, prothrombin time, partial thromboplastin time).

TREATMENT

Treatment of PPH is guided by identification of the underlying etiology. Some causes of PPH have a surgical solution, such as cervical lacerations, vaginal lacerations, retained placental fragments, invasive placentation, uterine rupture, and uterine inversion. All of these require prompt operative intervention. If hemorrhage is caused by coagulopathy, the solution is correction of the underlying coagulopathy, replacement of blood products, and supportive care. Most PPHs, however, are due to uterine atony, and the treatment requires a variety of approaches, including supportive, medical, and surgical interventions. Regardless of the cause, a standardized multidisciplinary approach has been shown to reduce morbidity and mortality from PPH significantly.

The National Partnership for Maternal Safety: Consensus Bundle on Obstetric Hemorrhage⁷ delineates a set of evidence-based recommendations in a form that aids implementation and consistency of practice, known as a bundle. The bundle is organized into four action domains of Readiness, Recognition, Response, and Reporting, and further subdivided into specific key elements that can be implemented in individual centers. While implementation of all the elements are unlikely to be feasible in all settings, certain critical elements, such as prenatal assessment of hemorrhage risk, development of hemorrhage carts and medication kits, active management of the third stage of labor, and establishment of obstetric hemorrhage emergency management plans, are simple interventions that can be implemented most anywhere. Figure 41-2 shows an example of an obstetric hemorrhage emergency management plan. The typical contents of a PPH cart are listed in Table 41-3, and PPH medication kits are shown in Figures 41-3 and 41-4.

Active Management of the Third Stage of Labor

Active management of the third stage of labor has been widely accepted as an effective method of decreasing blood loss at the time of delivery.²³ This includes administration of oxytocin immediately following delivery of the infant, usually given as an infusion of 30 units in 500 mL of crystalloid titrated to uterine tone. In the absence of IV access, 10 units of oxytocin intramuscularly (IM) can be given. Other components of the active management of the third stage of labor include immediate delivery of the placenta with gentle cord traction, draining the bladder, and bimanual uterine massage.

Some attempt at quantification of blood loss is recommended as well. Persistent bleeding at this juncture should initiate a thorough evaluation and establishment of an etiology. If there is good uterine tone, causes other than atony must be identified and resolved.

Blood Loss up to 1000 mL

Active bleeding with cumulative blood loss >500 mL after a vaginal delivery, or >1000 mL at the time of cesarean delivery, should prompt an increase in interventions. Upon recognition that a hemorrhage is escalating, it is necessary to establish IV access with 16- to 18-gauge IVs to give fluids, medications, and blood replacement products. The bladder should be drained if necessary. Assessment of vital signs and oxygen saturations should increase in frequency to every 5 minutes. Initiate a fluid bolus and administer oxygen to maintain saturation levels above 95%. In cases where massive hemorrhage seems inevitable, it is prudent to establish central venous access as soon as possible.

In cases of uterine atony, uterotonic medications should be given as soon as excessive bleeding is identified. Oxytocin should be used in active management of the third stage of labor as prophylaxis for uterine atony. In cesarean deliveries, an additional 10 units of oxytocin can be administered directly into the myometrium to improve uterine tone. When there is >500 mL blood loss at vaginal delivery or 1000 mL at cesarean delivery, a second uterotonic medication should be administered if the cause is uterine atony.²³

Blood Loss 1000 to 1500 mL

When hemorrhage has progressed to over 1 L of blood loss and there continues to be active bleeding, preparations should be made for a blood transfusion. At least two units of packed red blood cells should be requested and transfused upon arrival. Anesthesia should be notified, if not already present, and additional nursing help should be requested. Additional uterotonic medications should be administered in the setting of persistent uterine atony, and consider also giving 1 g IV of tranexamic acid to help decrease fibrinolysis. Previously mentioned measures, such as documenting the cumulative blood loss, frequent assessment of vital signs, keeping the patient warm, and administering oxygen, should be performed as well. There should be consideration of other procedures that may be helpful in the management, such as dilation and curettage (D&C), uterine artery selective embolization, and using an intrauterine tamponade balloon. If bleeding is persistent or worsening, preparations should be made to proceed to the operating room.

Blood Loss Greater than 1500 ml

When postpartum blood loss has reached 1500 mL, or when a patient’s vital signs have become unstable, treatment should occur in the operating room with an established team leader and assigned roles. A coordinated effort and closed-loop communication between the obstetrician, the anesthesiologist, and nursing staff is necessary for the processes to run smoothly and efficiently. Obtaining laboratory values such as complete blood count (CBC), comprehensive metabolic panel (CMP), coagulation studies, and arterial blood gas (ABG) will help to guide treatment and should be obtained at least hourly.

Central hemodynamic monitoring and arterial lines also should be considered at this point as well as the need for vasopressor support and intubation. A laparotomy for either uterine artery ligation or a definitive hysterectomy should be considered at this time. Activation of a massive transfusion protocol should occur in facilities that have them. In those that do not have this resource available, notify the blood bank that there is a massive hemorrhage occurring and that it should keep ahead of orders for blood products. If necessary, trauma blood should be ordered. Replacement of blood products and surgical management of PPH will be covered elsewhere in this text (Chapters 21 and 69, respectively).

Uterotonic Medications

The choice of uterotonic medications and the order in which they are given depend upon patient contraindications to the drugs, availability of agents, and the clinical situation. Uterotonic medications, with their side effects and contraindications, are listed in Table 41-4.