Postpartum Hemorrhage

Etiology

The primary causes of PPH are the 4 “T’s”: tone (uterine atony), trauma (lacerations or uterine rupture), tissue (retained placenta or clots), and thrombin (coagulation deficiency). Uterine atony is the most common cause of PPH, accounting for approximately 70% of cases. A vast array of risk factors are associated with PPH, including advanced maternal age, nulliparity, and grand multiparty. However, most risk factors are related to underlying causes.[6][7][8][9] 

Secondary PPH is associated with retained placentas, subinvolution of placental sites, inherited coagulopathies, and infectious etiologies. The following risk factors are associated with the 4 main etiologies:

• Uterine atony: Chorioamnionitis, magnesium sulfate therapy, prolonged labor or precipitous delivery, labor induction or augmentation, uterine fibroids, uterine inversion, or conditions resulting in uterine overdistention (eg, multiple gestation, fetal macrosomia, or polyhydramnios) 
• Trauma: Cesarean delivery, instrument-assisted vaginal birth, midline episiotomy, precipitous delivery, and persistent occiput posterior position 
• Tissue: Prior Cesarean birth, placenta accreta, placental abruption and associated hypertension, and uterine anomalies 
• Coagulopathy: Severe preeclampsia and eclampsia, HELLP (hemolysis, elevated liver-enzyme level, and low platelet count) syndrome, intrauterine fetal death, placental abruption, amniotic fluid embolism, or inherited coagulopathies (eg, von Willebrand disease) [4][5][10][11]

Epidemiology

PPH occurs in approximately 1% to 3% of all deliveries and is the leading cause of obstetric morbidity and mortality worldwide,[12]  accounting for approximately 8% of maternal deaths in developing countries and 20% of maternal deaths in developed countries. The United States has one of the highest maternal mortality rates at 11% and continues to rise, increasing from 8 to 40 cases per 10,000 deliveries.[5] In Europe, PPH occurs in approximately 13% of deliveries. Uterine atony, the primary cause of PPH, accounts for 70% to 80% of all hemorrhages.[13]

Pathophysiology

Physiologic changes during pregnancy, including an increase in uterine blood flow from approximately 100 mL/min in a nonpregnant uterus to 700 mL/min, coagulation changes resulting in a hypercoagulable state, and postpartum changes (eg, myometrial contraction and local decidual hemostatic factors) cause significant bleeding. Therefore, conditions that lead to a failure of these mechanisms can result in PPH. A loss of an approximate total blood volume of more than 1500 mL will typically cause clinical features of hypovolemia.[5]

History and Physical

Postpartum Hemorrhage Clinical Evaluation

An accurate clinical assessment of blood loss volume and evaluation of the underlying etiology is essential for promptly diagnosing PPH and initiating effective interventions. Initial patient evaluation should include a rapid clinical assessment and review of the patient's risk factors. Clinical features of significant blood loss, including tachycardia, tachypnea, and hypotension, may be masked initially, as pregnant women can have a blood loss of more than 1000 mL before signs of hypovolemia are apparent. Clinicians should remember that more than 25% of blood volume, or approximately 1500 mL or more, is likely lost when signs of hypovolemia are present. Prompt PPH recognition is difficult due to this delay in clinical features of hypovolemia. Continued assessment during delivery and postpartum is recommended, including visual estimation, weighing surgical sponges and drapes, and serial vital signs.[5][14] Serial vital signs should include heart rate, blood pressure recordings every 15 min, respiratory rate, and peripheral oxygen saturation. During PPH evaluation, clinicians should also be aware of cognitive biases affecting their ability to diagnose PPH quickly. These biases include implicit biases, which are unconscious stereotypes that affect a clinician's response to or treatment of certain patients (eg, unconscious discrimination). Normalcy bias can cause clinicians to dismiss signs and symptoms of hypovolemia as normal or temporary (eg, anxiety). Anchoring biases are when clinicians only consider the first suspected diagnosis.

Examining the patient during the hemorrhage can help identify the probable cause of bleeding focused on any specific risk factors. A rapid assessment of the entire lower genital tract, including vaginal walls, cervix, and labia, for lacerations, hematomas, or signs of uterine rupture (eg, regression of fetal presenting part and maternal abdominal tenderness), should be performed.[15][16] The placenta should be examined to determine if the tissue remains intact, and a manual examination with extraction should be performed for any retained placental tissue; a bedside ultrasound assessment may be a part of the evaluation.[17]

A soft, "boggy" or noncontracted uterus is the common finding with uterine atony. Uterine inversion presents as a round bulge or mass with palpation of the fundal wall in the cervix or lower uterine segment, resulting from excessive umbilical cord traction or abnormally adherent placenta. Widespread bleeding, including from venipuncture sites, is a sign of disseminated intravascular coagulation. Patients may also present with acute vaginal bleeding peri- or postpartum. The patient may also have an increased heart rate, respiratory rate, and dizziness. As the patient loses blood, they may feel cold, have decreased blood pressure, and syncopal episodes. Patients may also have signs and symptoms of shock (eg, confusion, blurry vision, clammy skin, and weakness).[4][5]

Blood Loss Quantification

Several studies have established that PPH blood loss totals are typically clinically underestimated, resulting in a misdiagnosis of excessive bleeding and, therefore, delayed interventions. Quantitative blood loss methods have been recommended for more accurate calculations, including graduated under-buttock drapes, laparotomy pads, sponge weighing, artificial intelligence-enabled technology, and irrigation canisters. These methods are more helpful than previous strategies involving awaiting hemoglobin changes and are meant to assist in the early recognition of PPH. However, clinical outcomes have not improved because clinicians may prioritize numeral parameters over the broad clinical picture. As such, waiting to begin PPH protocols until a specific blood loss threshold is met could lead to less favorable outcomes. Any amount of obstetric bleeding with clinical features of hypovolemia or a blood loss of more than 500 mL should precipitate PPH assessment and consideration of interventional protocols. Blood loss quantification should involve an interprofessional team of healthcare professionals, including physicians, nurses, and technicians, to ensure accurate estimations when active bleeding continues.[14][18]

Evaluation

Laboratory studies are included as part of PPH protocols to help assess the degree of blood loss and guide interventions. PPH laboratory panels typically include complete blood count with platelet count, partial thromboplastin time, plasma thromboplastin, fibrinogen, comprehensive metabolic panel, ionized calcium, pH, and blood gases in addition to the routine prenatal laboratory studies that are obtained on admission (eg, blood type and antibody screening).[19] However, some interventions should not be withheld pending the results of these studies. Complete blood count to assess hemoglobin, hematocrit, and platelets can be evaluated at intervals, although lab values lag behind the clinical presentation. Coagulation studies and fibrinogen are useful in patients with suspected disseminated intravascular coagulation, including patients with secondary PPH, placental abruption, or preeclampsia. An indwelling bladder catheter may monitor the patient's fluid status and assess urine output.[5][10]

Treatment / Management

General Postpartum Hemorrhage Management

The approach to treating PPH is focused on the patient's resuscitation when identifying and treating the underlying cause. Maintaining the patient's hemodynamic stability ensures continued perfusion to vital organs. As soon as PPH is identified, 2 large bore peripheral intravenous (IV) catheters (14- or 16G) should be placed, and maternal blood type and antibody screen should be confirmed in anticipation of aggressive corrective measures. Direct assessment of cumulative blood loss is essential, and a focus on early initiation of protocols for releasing blood products and massive transfusion protocols is necessary. Crystalloid and colloid IV fluids should be administered as indicated, and clinicians should also evaluate patients to identify the underlying cause and tailor treatments.[20](A1)

Uterine Atony Management

Uterine atony is the most common cause of PPH; therefore, clinicians should assess patients for this etiology. A soft uterus without physiologic contraction following delivery indicates uterine atony. Removal of clots and bimanual massage should be performed as the first step to mitigate excessive uterine bleeding. Medical management with uterotonic agents is typically the initial pharmacologic intervention if uterine atony is identified. While oxytocin is recommended routinely at delivery, additional uterotonic medications are necessary in up to 25% of patients with PPH. Furthermore, the use of multiple uterotonic agents can have a synergistic effect. 

Pharmacologic agents used in PPH management include:

• Oxytocin: The International Federation of Gynecology and Obstetrics recommends giving oxytocin 10 international units (IU) IV or intramuscularly (IM) first-line for uterine atony if not administered prophylactically. The oxytocin hormone is naturally produced by the posterior pituitary and works rapidly, with an onset of action within 1 to 6 minutes, to cause uterine contraction following IV administration. Oxytocin has minimal adverse events and may be given during bimanual massage in response to hemorrhage. 

  Methylergonovine: Ergot alkaloids (eg, ergometrine, ergonovine, and methylergonovine) are serotonergic receptor agonists and partial α-adrenergic receptor agonists that cause sustained uterine contractions. The onset of action is approximately 1 to 3 minutes. Methylergonovine 200 μg IM or IV is typically recommended but is relatively contraindicated in patients with hypertension.

• Carboprost: As a 15-methyl prostaglandin F2-α analog, carboprost acts on prostaglandin receptors to stimulate uterine contractions. The recommended dosage is 250 μg IM or intramyometrially every 15 to 90 minutes for a maximum of 8 doses, with peak serum concentrations reached in approximately 15 minutes. Carboprost is contraindicated in severe hepatic, renal, and cardiovascular disease and may cause bronchospasm in patients with asthma.

• Misoprostol: Misoprostol is a prostaglandin E1 analog with a more prolonged onset of action than other uterotonics, depending on the administration route, which includes oral, sublingual, rectal, or buccal routes. The analog should be avoided in patients with anticoagulant therapy or cardiovascular disease; adverse effects may include nausea, diarrhea, and fever.

• Tranexamic acid: Tranexamic acid (TXA) is not uterotonic but inhibits fibrinolysis and is frequently used with uterotonic medications. The recommended dosage is 1 g of tranexamic acid IV over 10 minutes within 3 hours of delivery after a PPH diagnosis. TXA's onset of action is typically 5 minutes and is contraindicated in patients with a history of hypercoagulopathy.[10]

If bimanual massage and uterotonic medications are insufficient to control hemorrhage, uterine tamponade may be considered. An intrauterine balloon tamponade system can be used, typically by filling an intrauterine balloon with 250 to 500 mL of normal saline. Uterine tamponade may be useful in those with lower uterine segment atony, where uterotonic agents may have a delayed onset of action. If an intrauterine balloon is not readily available, the uterus may be packed with gauze, or multiple large Foley catheters may be placed concurrently. An accurate count of what is placed in the uterus is critical to prevent retained foreign bodies. Compression sutures with a rapidly absorbing suture (eg, chromic) may also be considered, as they are effective in 90% of cases, according to current literature on protocols for PPH. Complications include uterine necrosis and intrauterine synechiae. Compression sutures may affect future pregnancies, though the incidence of successful pregnancy after uterine compression sutures ranges from 11% to 75%.[17][21]

Obstetrical Trauma 

Rapid identification of the cause of PPH and the initiation of treatment should be simultaneous, including identifying genital lacerations. If lacerations are identified as the source of bleeding, they should be repaired quickly and bleeding should be reassessed. Transfer to an operating suite with anesthesia assistance may be indicated if uterine artery laceration is suspected. Genital tract hematomas may be suggested by clinical deterioration in the absence of other findings or genital pressure. Management of rapidly expanding hematomas includes packing, arterial embolization, or suturing. Routine antibiotic prophylaxis is not recommended. See StatPearls' companion references, "Perineal Lacerations" and "Lower Genitourinary Trauma," for more information.

Uterine Inversion

Uterine inversion, when the uterus protrudes through the introitus following delivery, is characterized by hypotension disproportionate to the amount of bleeding. Uterine inversion typically appears as a blue-gray mass protruding from the vagina. Immediate manual replacement of the uterus with the placenta in place (if not already detached) should be performed by pushing the protruding fundus with a steady pressure back through the vagina into the pelvis. However, if the uterus cannot be replaced, tocolytic agents (eg, nitroglycerin, terbutaline, magnesium sulfate, or halothane) should be administered to relax the uterus and cervix. If the uterus is still unable to be replaced, a laparotomy is performed, and the uterus can be replaced by gentle upward traction; the cervical ring may have to be incised to allow uterine replacement. Following uterine replacement, uterotonics should be administered to facilitate uterine contraction and control bleeding.

Retained Placenta

In patients with placenta accreta, a planned Cesarean delivery, with or without hysterectomy, is typically performed between 34 and 37 weeks gestation. Due to the complexity of the procedure, Cesarean hysterectomy involves interprofessional collaboration. Additionally, the ureters may be stented before the procedure to avoid injury. In patients suspected to have retained products of conception, manual intrauterine exploration or uterine ultrasonography is typically sufficient to diagnose retained products of conception (eg, succenturiate lobe). An ultrasound finding of an echogenic mass within the endometrial cavity immediately after delivery is consistent with a retained placenta. For patients who have findings consistent with retained products of conception, manual removal or banjo curette, with or without ultrasound guidance, is performed. If the placenta is unable to be manually detached, the patient should be counseled on retained placenta complications and potential hysterectomy while being transferred to an operating room. See StatPearls' companion reference, "Placenta Accreta," for more information.

Coagulopathy

In patients with placental abruption or amniotic fluid embolus resulting in PPH, acute coagulopathy should be considered, as these conditions frequently cause a consumptive coagulopathy. Coagulopathies should also be considered in patients with secondary PPH. Blood transfusion and fluid replacement are required for most PPH caused by coagulopathies. Obstetrical transfusion protocols comprising packed red blood cells (RBCs), fresh-frozen plasma, and platelets in various ratios are utilized to correct coagulation deficits and maintain the hemoglobin level at more than 7 to 8 g/dL, the fibrinogen level greater than 2 g/L, and the platelet count at 50,000 to 75,000 µL.[10]

Additional Postpartum Hemorrhage Management Strategies

In patients with continued PPH due to any etiology unresponsive to initial interventions, other management options include hypogastric artery ligation, uterine artery embolization, and hysterectomy. Uterine artery embolization may be considered in a patient who is stable with persistent bleeding. Fluoroscopy is used to identify and occlude bleeding vessels. While those who are unstable are not a candidate for this modality, benefits include uterine conservation and preservation of fertility. However, studies have demonstrated that patients who have undergone uterine artery embolization have an increased risk of infertility, preterm delivery, and intrauterine growth restriction.

Exploratory laparotomy is typically indicated in the setting where less invasive measures for postpartum hemorrhage have failed or if the suspected reason for postpartum hemorrhage (eg, morbidly adherent placenta) is elucidated. A midline vertical abdominal incision should be considered to maximize exposure; however, the existing incision may be used if the patient had a Cesarean delivery. Vascular ligation sutures may be attempted to decrease pulse pressure in the uterus. Bilateral uterine artery ligation (O'Leary sutures) or bilateral utero-ovarian ligament ligation sutures may be placed. Hypogastric artery ligation can also be performed; however, as this procedure entails a retroperitoneal approach, the approach is rarely used. The definitive treatment for postpartum hemorrhage is a hysterectomy. A peripartum hysterectomy is associated not only with permanent sterility but also an increased surgical risk with a higher risk of bladder and ureteral injury. Supracervical hysterectomy may be performed alternately as a faster surgery with potentially fewer complicated risks.[5]

Hemodynamic Management

Implementing an effective blood transfusion protocol when the underlying etiology is being assessed and treated is critical to patient resuscitation and achieving hemodynamic stability. Severe hemorrhage leads to acidosis, hypothermia, and coagulopathy, which must be quickly corrected to avoid the risk of mortality. Therefore, other patient status indicators, including heart rate, respirations, peripheral oxygen saturation, temperature, and blood gases, should be monitored in addition to blood pressure. In patients with severe PPH, a massive transfusion protocol must frequently be initiated, which is standard in most institutions. Massive transfusion is defined as a transfusion of more than 10 units of packed RBCs within 24 hours or 4 RBC units in 1 hour with additional units anticipated. Most massive transfusion protocols recommend a combination of packed RBCs, fresh-frozen plasma, platelets, and cryoprecipitate in fixed ratios. The most common ratio utilized is 1:1:1 (1 unit of packed RBCs, 1 unit of fresh-frozen plasma, and 1 unit of platelets); other recommended protocols include 6:4:1 and 4:4:1.

Lactate and electrolyte levels must be monitored throughout the transfusion to determine adequate vascular perfusion and correct metabolic abnormalities. Hyperkalemia, hypocalcemia, and hypomagnesemia commonly occur secondary to massive transfusion, and lactic acidosis indicates persistent tissue hypoperfusion. Complications associated with massive transfusions include transfusion-related lung injury, pulmonary edema, transfusion-associated circulatory overload, and blood transfusion reactions. Other adjunct strategies that may be considered include cell salvage (ie, autologous blood transfusion), sometimes used in patients at high risk for PPH (eg, known placenta accreta), recombinant activated factor VII, and vasopressors (eg, phenylephrine or norepinephrine).[15] See StatPearls' companion reference, "Massive Transfusion," for more information. Clinicians should discuss the need for blood transfusion with all patients who are pregnant during their prenatal visits and upon hospital admission to guide hemodynamic management, particularly in patients refusing blood products (eg, Jehovah Witnesses). Following patient stabilization, decisions for additional transfusions should be based on clinical symptoms and laboratory studies.[10][22](B3)

Differential Diagnosis

The differential diagnosis for the causes of early PPH include:

• Uterine atony
• Lacerations
• Uterine inversion
• Retained placenta
• Uterine rupture
• Coagulopathy
• Endometritis
• Chorioamnionitis

Prognosis

Post-partum hemorrhage is a leading cause of maternal and fetal morbidity in the United States; however, correct and timely institution of treatment can vastly improve patient outcomes. Patients who had PPH in a previous delivery are at risk of having PPH in subsequent deliveries. Implementation of standardized PPH protocols and interprofessional simulation training has helped improve patient outcomes. Additionally, increased efforts to enhance coordination among healthcare team members in response to PPH have contributed to reduced maternal morbidity.[10]

Complications

Blood loss occurs in PPH, putting the patient at risk of hypovolemic shock. When patients lose 20% of blood, they develop tachycardia, tachypnea, narrowed pulse pressure, and delayed capillary refill. This may lead to ischemic injury to the liver, brain, heart, and kidneys. Sheehan syndrome, or postpartum hypopituitarism, is also a complication of excessive blood loss seen in postpartum hemorrhage.

Complications related to PPH management include the following:

• Transfusion-related acute lung injury
• Infection
• Pulmonary edema
• Hemolytic transfusion reactions
• Intrauterine synechiae
• Preterm delivery
• Infertility