Postpartum Hemorrhage

Understanding the underlying etiology of PPH is crucial in its prevention, treatment, and management. The underlying causes of PPH are often described using the “Four T’s”: tone, tissue, trauma, and thrombin. ^{[2, 4]}

Tone

Uterine atony refers to the failure of the myometrium to contract, preventing effective compression of uterine blood vessels and leading to continued blood loss. Multiple factors contribute to uterine atony. Some include but are not limited to prolonged labor or rapid labor, overdistended uterus from multiple gestation pregnancy, polyhydramnios, macrosomia, prolonged oxytocin use during labor, and uterine infections.  

Tissue  

Incomplete removal of the placenta or the presence of retained amniotic membranes can lead to PPH. The retained tissue prevents effective uterine contractions and leads to continued bleeding. Additionally, abnormal placentation resulting in placenta accreta spectrum can lead to failure of the placenta to detach properly from the uterine wall, thus increasing the patient’s risk for hemorrhage.  

Trauma 

Trauma to the genital tract can cause PPH. If the patient undergoes a vaginal delivery, lacerations of the cervix, vagina, and perineum may lead to significant hemorrhage. Operative vaginal deliveries utilizing forceps or vacuum, use of episiotomy, and occurrence of uterine inversion can increase the patient’s risk of trauma-related PPH. Cesarean deliveries can also contribute to trauma if injuries to vasculature or organs in the abdomen and pelvis occur. Additionally, cesarean deliveries that are complicated by dense adhesive disease or active phase or second stage arrest, or that are performed in emergent fashion, are at higher risk for trauma.  

Thrombin

Coagulopathies can be preexisting to pregnancy or acquired. Preexisting causes that could contribute to PPH include von Willebrand disease or idiopathic thrombocytopenic purpura. Acquired coagulopathies during pregnancy and labor include disseminated intravascular coagulation (DIC) that is secondary to other obstetric emergencies, such as placental abruption, preeclampsia, amniotic fluid embolism, or sepsis.

ACOG defines primary PPH as a cumulative blood loss of at least 1 liter or any bleeding with signs of hypovolemia within 24 hours after delivery, although worldwide definitions may vary. Historically, clinicians have visually underestimated blood loss when volumes are high, resulting in delayed diagnosis and treatment of hemorrhage.

To reduce morbidity and mortality, protocols have been developed to facilitate expeditious diagnosis, and quantitative blood loss measurement has been suggested. ^{[5, 6]}  This involves weighing blood-soaked materials and subtracting the dry weight to determine the exact amount of blood lost. Blood should also be collected in calibrated containers such as suction canisters and calibrated under-buttocks drapes. The use of these methods increases the likelihood of having an accurate assessment of the volume of blood lost.

Additionally, hemorrhage tool kits have been created to delineate severity classifications. ^[3]  Each class is defined by volume of blood loss, vital signs of the patient, and a stepwise protocol for intervention.

Vital signs of the birthing patient are crucial in the diagnosis of PPH. If the patient develops hypotension and tachycardia, this could signify the development of PPH.

Laboratory testing, including a complete blood cell count, fibrinogen, and other coagulation studies, aids in the diagnosis of PPH. Some concerning findings include anemia, thrombocytopenia, and normal or low fibrinogen when fibrinogen levels in pregnancy are usually elevated; thus normal or low fibrinogen levels should raise suspicion for the development of DIC. Ultrasonography also aids in the diagnosis of PPH by helping to detect whether blood is accumulating in the uterus and whether there is concern for a retained placenta.

Furthermore, it is important to note that many birthing people are young and healthy and can compensate well despite a high blood loss. Therefore, significant changes in vital signs could indicate a late diagnosis of PPH or signify that the amount of blood loss is catastrophic. Utilization of clinical knowledge and acumen assists in prompt diagnosis of PPH.

Effective prevention of PPH begins with the identification of risk factors and the implementation of standardized protocols during the intrapartum and postpartum periods. Proactive interventions reduce the likelihood of excessive bleeding and improve outcomes of the birthing patient.

Active management of the third stage of labor is recommended. ^{[2, 7]}  This includes the routine use of oxytocin, controlled umbilical cord traction, and uterine massage after delivery of the placenta. Oxytocin, the preferred first-line uterotonic, is typically administered intramuscularly (IM) or intravenously (IV) immediately following delivery to promote uterine contraction and minimize bleeding. There is no significant difference in hemorrhage risk based on the timing of initiating postpartum oxytocin (following the delivery of the anterior shoulder of the baby, after delayed cord clamping, or after placental delivery). ^[8]  Controlled cord traction helps reduce the risk of retained placenta, whereas gentle fundal massage following placental expulsion encourages further uterine contraction and expulsion of clots. See the Medscape article Management of the Third Stage of Labor. 

Risk assessment is another key strategy in the identification and management of risk factors. High-risk factors may include characteristics such as a history of PPH, known coagulopathy, and placenta accreta spectrum. Other factors are multiple prior births, prior uterine surgeries, uterine infections, fibroids, and multiple gestations. ^{[9, 10]}  Moreover, the prenatal period is also a key time to optimize treatment of anemia prior to delivery. If a patient has evidence of iron deficiency anemia, oral or IV iron supplementation should be considered.

When hemorrhage is suspected or diagnosed, management should be initiated quickly based on the suspected etiology. A stepwise approach can aid in identification of the cause and lead to resolution before the onset of morbidity. As uterine atony is the most common cause of PPH, a fundal massage should be performed to assess the uterine tone. If the uterus is found to be boggy, fundal or bimanual massage should be continued and the bladder should be emptied to promote uterine contractions. Adequate fluid resuscitation with IV crystalloid and blood product transfusion in a 1:1:1 ratio of packed red blood cells, platelets, and fresh frozen plasma should be administered when necessary. Additional details regarding blood component transfusions can be found at Transfusion and Autotransfusion.

Uterotonic medications are the cornerstone of medical management of PPH secondary to uterine atony. Oxytocin is the first-line agent and acts rapidly. It can be given IV, IM, or intrauterine. If bleeding persists, methylergonovine can be used unless contraindicated by hypertension. Carboprost, a prostaglandin, is effective but should be avoided in patients with asthma. Misoprostol, administered orally or rectally, is an additional medication that can be given to manage PPH medically. Standard dosing and frequency have been previously outlined. ^{[2, 3, 11]}

Tranexamic acid (TXA) is an antifibrinolytic agent that should be used as adjunct medication in hemorrhage. The World Maternal Antifibrinolytic (WOMAN) trial demonstrated that TXA reduces maternal death due to bleeding when used soon after delivery and has since been implemented in many obstetric hemorrhage management protocols. When 1 g of IV TXA is given within 3 hours of diagnosis of PPH, death due to bleeding is reduced by nearly one third. ^[12]  TXA can be given a second time 30 minutes after the initial administration.

Nonpharmacologic techniques such as uterine tamponade should also be considered in cases of uterine atony. Intrauterine tamponade can be achieved with devices such as the Jada suction system or Bakri balloon or by manual uterine packing.

Although most postpartum hemorrhages can be controlled by medical management, a surgical approach can be lifesaving when pharmacologic and other nonsurgical strategies fail. The initial procedure of choice is often dictated by the cause of PPH, the route of delivery, and the timing of PPH. To reduce the risk of severe morbidity and mortality, the decision to move to a surgical method should be made swiftly when more conservative measures are unsuccessful. Here we will discuss surgical options from the least to the most invasive.

Minimally invasive techniques are as follows:

• Laceration repair

• Uterine evacuation

• Vascular embolization and occlusion

Techniques at the time of laparotomy are as follows:

• Uterine compression

• Vascular ligation

• Hysterectomy

Minimally invasive techniques 

Laceration repair 

Genital tract trauma is the most likely cause if bleeding is persistent or is present despite a well-contracted uterus. Genital tract laceration leading to hemorrhage primarily requires procedural management for resolution. The vulva, vagina, and cervix are the most common anatomic sites of laceration that necessitates transvaginal repair.

Multiple strategies for suture repair can be effective. A running, locked technique is often employed using an absorbable suture such as polyglycolic acid. Incorporation of the laceration apex is imperative. Expeditious repair can be aided with adequate exposure to the laceration including optimal lighting, positioning, and utilization of vaginal retractors. Adequate anesthesia is also necessary, and repair in the operating room should be considered. Additionally, consideration can be made for 24 hours of vaginal packing following laceration repair if continued venous oozing is identified.

Extensive genital tract injury involving adjacent structures, such as the uterus, bladder, rectum, and retroperitoneum, leading to hemorrhage is rare. Lacerations high in the vaginal vault and those extending up from the cervix may involve the uterus or lead to broad ligament or retroperitoneal hematomas. The proximity of the ureters to the lateral vaginal fornices, and the base of the bladder to the anterior fornix, must be kept in mind when repair is undertaken in these areas. Poorly placed stitches can lead to genitourinary fistulas. Additional techniques may be required in these circumstances, and a laparotomy may be necessary.  

Expanding lower genital tract hematomas may be managed by incision and drainage when interventional vascular specialists are unavailable or interventional approaches are otherwise contraindicated. Surgically, any bleeding vessels are ligated, oozing areas may be oversewn, and the surgical bed is packed. It is recommended to place a Foley catheter to avoid urinary retention secondary to pain and tissue distortion. 

Uterine evacuation 

Uterine evacuation is effective at managing hemorrhage associated with uterine atony and retained products of conception such as the placenta. The usual approach is via a suction curettage, although manual removal and sharp curettage may also be utilized.  

For suction curettage, an electric suction or manual vacuum aspirator can be used transvaginally. These devices create a negative pressure system to aid in clearing the uterine contents. The size of the cannula is chosen based on an estimated volume of uterine contents to be evacuated and dilation of the cervix. Efficient evacuation lessens additional hemorrhage. See the Medscape article Dilation and Curettage With Suction for more details. 

Manual removal of products of conception or clot burden can also be utilized. These strategies may be used transvaginally or intraoperatively during a cesarean delivery. When manual removal of the placenta is required, care should be taken to identify a distinct plane along the uteroplacental margin. A high index of suspicion should be maintained for the possibility of a morbidly adherent placenta, which would necessitate more extensive treatment.  

Each evacuation technique requires adequate anesthesia, and antiseptic techniques are recommended. The routine use of a single dose of antibiotics is advised. Some clinicians utilize ultrasound guidance, although ultrasonography has not been shown to consistently reduce complication rates in this setting. 

Vascular embolization and occlusion 

Pelvic vascular embolization is a highly successful, minimally invasive approach to control postpartum hemorrhage. 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. The procedure utilizes diagnostic angiography followed by introduction of an agent to occlude the selected arteries. The preferred agents are dissolvable and temporary, although permanent substances are also available.

The success rate of uterine artery embolization following PPH has been reported as higher than 90%. ^{[3, 13]}  Access to this technique may be limited by the availability of personnel and equipment; thus, early communication with an interventional specialist is warranted. Although not an absolute contraindication, patients are preferably hemodynamically stable and noncoagulopathic prior to embolization. Active monitoring of the patient’s clinical status should continue throughout the procedure.

Vascular occlusion balloons can also be placed by an interventional vascular specialist. These balloons can be placed within the hypogastric and common iliac arteries, and even the aorta. They are then later inflated to temporarily occlude the pelvic vasculature, minimizing hemorrhage. This technique is most frequently used prophylactically in surgical cases of high suspicion for massive hemorrhage.

Techniques requiring laparotomy

The choice between a vertical midline incision and a Pfannenstiel incision for entry into the abdomen is left to the individual surgeon. If concern exists regarding pathology in the upper abdomen or if exposure is thought to be a concern, the vertical incision is recommended. A self-retaining retractor can aid with visualization and exposure. Routine antibiotic prophylaxis is advised. 

Upon entry, remove any free blood and inspect the uterus and surrounding tissues for evidence of rupture or hematoma. When free blood is encountered without an obvious source of bleeding, upper abdominal structures should be explored, such as the liver, spleen, and visceral arteries. Consider placing a suction drain at the completion of the case. With a pelvic source of bleeding, viability of tissue should be evaluated, and the choice of uterine compression, vascular ligation, or hysterectomy made promptly.

Initial temporizing techniques may be needed in cases of concern for imminent exsanguination or when time for product repletion and transfusion would be of benefit. Following laparotomy, manual compression of the aorta is a quick and effective strategy to reduce vascular flow to the pelvis. Direct pressure is applied to the aorta above the sacral promontory to compress against the vertebrae. If a uterine source is suspected, a tourniquet can also be secured. Any flexible catheter or drain may be placed near the lower uterine segment and cinched to mechanically occlude the vascular supply to the uterus. Once hemodynamic stability is achieved, compression of the aorta and the uterine tourniquet may be released, and the intended surgery completed.

Uterine compression

Multiple uterine compression strategies have been described to manage PPH related to uterine atony. The most common technique is the B-Lynch suture, which has been shown to be safe and preserves the potential for future pregnancy. ^{[14, 15, 16]}

In this technique, an absorbable suture on a large needle is used. Traditionally, a #1 or #2 chromic gut suture is suggested for its rapid absorption, to prevent bowel herniation through the suture loop during uterine involution. To complete this procedure, first the suture is placed vertically, inferior to superior, within the lower uterine segment on the lateral aspect of the anterior uterus. The suture is then looped over the fundus and re-enters the lower uterine segment in the posterior wall in a transverse fashion. The suture is looped back over the top of the fundus to the anterior uterus. The final suture is secured vertically, superior to inferior, within the lateral lower uterine segment, opposite to the initial stitch. The uterus is then manually compressed while the suture is tied down securely.

Additional techniques such as Hayman, Pereira, and Cho have been described, representing modifications of the B-Lynch suture. Each has the goal of compressing the uterus in an anterior-posterior orientation and/or a superior-inferior orientation.

Vascular ligation

Vascular ligation can range from a simple procedure to a complex and precarious surgical endeavor depending on the targeted vasculature. Uterine artery ligation, for example, is straightforward and highly effective in controlling bleeding from uterine sources. These arteries provide approximately 90% of uterine blood flow.

To perform this procedure, an absorbable suture is passed through an avascular portion of the broad ligament and anchored to a full thickness of myometrium to completely encompass the uterine artery and vein. Ideally, this is placed at the uterocervical junction and performed bilaterally.  Although the uterus may remain atonic, blanching is usually noted, and blood flow is greatly diminished or arrested.

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. 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. 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.

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

Hysterectomy is curative for bleeding arising from the uterine, cervical, and vaginal fornices regardless of the etiology of the hemorrhage. In the WOMAN trial, 3.5% of patients with PPH underwent hysterectomy. ^[12]

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. Although the organ is more vascular, the tissue planes are often more easily developed. Total hysterectomy is preferred to subtotal hysterectomy; however, the latter may be performed more quickly and is effective for bleeding due to uterine atony. Supracervical hysterectomy may not be effective for controlling bleeding from the lower segment, cervix, or vaginal fornices or when placenta accreta spectrum with placenta previa is suspected.

Most patients with PPH are rapidly identified and successfully treated before major complications develop. Those patients with morbidity may have short-term and/or long-term effects.

Short-term complications

The most common short-term problem is anemia and loss of iron stores. Increased intake of dietary iron, oral supplementation, or IV iron can be considered. Blood transfusion is also a major component of the management of PPH and symptomatic anemia. Blood transfusion reactions are uncommon but can include infection, electrolyte abnormalities, allergic reactions, alloimmunization, volume overload, and thromboembolic events.

Major morbidity is often associated with massive blood loss and hypovolemic shock. Damage to all major organs is possible; respiratory damage (adult respiratory distress syndrome) and renal damage (acute tubular necrosis) are the most common but are rare and likely require intensive management from specialists. Pulmonary edema is uncommon in previously healthy patients; however, it may develop acutely or during the recovery phase because of fluid overload or myocardial dysfunction. Response to standard therapy is usually prompt. Abdominal compartment syndrome from large intra-abdominal bleeding can occur and should be considered in the differential diagnosis of known bleeding with acute distension.

Pregnant persons are at increased risk for 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, pelvic surgery, and peripartum infection. Venous stasis due to shock and immobility also contributes, and caregivers should maintain a high index of clinical awareness.

Long-term complications

Long-term morbidity may also occur. 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.

Complications related to surgical interventions include sterility, uterine perforation, uterine synechiae (Asherman syndrome), urinary tract injury, bowel injury, fistula, vascular injury, pelvic hematoma, and sepsis. It has been suggested that internal iliac artery ligation may reduce ovarian reserve in the short term. ^[17]

Patients who are undergoing laparotomy or uterine exploration or instrumentation should receive preoperative antibiotics. Consider additional evaluation following emergency pelvic surgery to exclude ureteral obstruction.

Mortality

PPH is a leading cause of maternal mortality. ^{[1, 2]}  The maternal mortality rate due to PPH varies greatly by the health of the pregnant population and the resources available for treatment. Mortality associated with PPH worldwide has been reported to range from 0.01% to 20%. Most maternal deaths due to obstetric hemorrhage may be preventable.