Management of postpartum hemorrhage

Author: Tommy C. Norris
Date: Feb 1, 1997

Postpartum hemorrhage represents a serious obstetric emergency and is a significant cause of maternal morbidity and mortality. In the United States, ongoing bleeding following delivery is responsible for up to 4 percent of maternal deaths, exclusive of abortive outcomes.[1] Higher mortality rates have been reported in undeveloped countries and in some rural areas of America.[2]

Postpartum hemorrhage occurs in 4 to 8 percent of vaginal deliveries.[3,4] Since hemorrhage is sometimes difficult to detect, the true incidence of this postpartum complication may be even higher than the reported percentages. Furthermore, the discrepancies in the incidence reported for postpartum hemorrhage may also be related to the imprecise definition of this complication.


The traditional definition of postpartum hemorrhage is a blood loss of more than 500 mL following delivery.[4] However, based on careful quantitation, the average blood loss in a vaginal delivery is actually greater than 500 mL, and the average blood loss in a cesarean delivery exceeds 1,000 mL. Thus, the clinical determination of blood loss consistently underestimates the actual blood loss.[5] According to some investigators, postpartum hemorrhage should be defined as a decrease in the hematocrit of 10 points or more between the time of admission and a time after delivery or as the need for fluid transfusion following delivery.[3] This definition is more objective and more reliable than the traditional definition of postpartum hemorrhage.

Regardless of the definition, postpartum hemorrhage can be difficult to recognize for several reasons. As noted, physicians frequently underestimate the amount of blood that is lost in a delivery. In addition, physicians often fail to recognize the significance of slow, steady blood loss.[6] Most deaths related to postpartum hemorrhage do not occur because of gross hemorrhage but because of continuous blood loss over several hours.[6] Furthermore, postpartum hemorrhage can occur without external bleeding. The hemorrhaging may occur intra-abdominally, into the broad ligament or into hematomas arising from uterine rupture or genital tract lacerations. Finally, given the relative maternal hypervolemia that is present near term, clinical signs of hemorrhage, such as hypotension and tachycardia, do not present until substantial blood loss (i.e., more than 1,500 mL) has occurred, often just before the patient becomes hemodynamically unstable.


Postpartum hemorrhage can be classified as early or late. Early postpartum hemorrhage occurs within the first 24 hours after delivery, and late postpartum hemorrhage occurs 24 hours to six weeks postpartum.[7]

The causes of early postpartum hemorrhage are listed in Table 1. Since uterine atony is responsible for over 90 percent of cases of postpartum hemorrhage,[4] this condition should be suspected whenever continued bleeding occurs after delivery. The risk factors for uterine atony are given Table 2.


Causes of Early Postpartum Hemorrhage


Uterine atony Lower genital tract lacerations Retained placental products

Less common

Hematoma Uterine inversion Uterine rupture Placenta accreta/increta/percreta Coagulopathy


Risk Factors for Uterine Atony

Prolonged labor Retained placental products Chorioamnionitis Oxytocin use in labor Preeclampsia/eclampsia Multiple gestation Hydramnios Halogenated anesthesia Previous episode of uterine atony

The relative risks for postpartum hemorrhage associated with various maternal and fetal factors are presented in Table 3.[3] Several explanations for the strong association between postpartum hemorrhage and a prolonged third stage of labor (i.e., delivery of the placenta) have been proposed.[3] One is that some degree of placenta accreta may have occurred. Another is that manual extraction of the placenta is often performed in women with a prolonged third stage of labor. Finally, a prolonged third stage may be the result of undetected uterine atony Other factors strongly associated with significant bleeding following delivery are preeclampsia, episiotomy and a history of postpartum hemorrhage.

TABLE 3Risk Factors for Postpartum Hemorrhage OddsRisk factor ratioProlonged third stage of labor (more than 7.6 30 minutes)Preeclampsia 5.0Mediolateral episiotomy 4.7Previous postpartum hemorrhage 3.6Multiple gestation 3.3Arrest of descent 2.9Lacerations (cervical/vaginal/perineal) 2.1Active-phase arrest of labor 1.9Maternal ethnic group: Asian or Hispanic 1.7Forceps/vacuum delivery 1.7Augmented labor 1.7Midline episiotomy 1.6Nulliparity 1.5

Episiotomies can be an obvious source of hemorrhage. A recent study[3] confirmed that the risk of hemorrhage is greater with mediolateral episiotomies than with midline episiotomies.


Pelvic hematomas are a source of blood loss that can be difficult to detect. Bleeding may be unnoticed because these lesions often produce little or no external blood loss but instead cause profuse bleeding into the retroperitoneal space.[2,4] Patients who complain of severe rectal or perineal pain after delivery should be evaluated for the presence of a hematoma. Large hematomas (greater than 3 cm in diameter) usually require operative intervention, with some authorities recommending the empiric use of postoperative antibiotic therapy.[10]

Pelvic hematomas may be vaginal, vulvar or retroperitoneal. Although vaginal hematomas are commonly associated with forceps delivery, they can also occur spontaneously. Patients with vaginal hematomas frequently complain of rectal pressure, and inspection of the vagina demonstrates a bulging vaginal mass. Vaginal hematomas require incision and evacuation, but they are usually left open. While vulvar hematomas are usually associated with vulvar pain, they may also present as hemorrhoidal pain. Vulvar hematomas should be incised and evacuated, and the dead space should be closed.[11] Retroperitoneal hematomas are rare, but they are the most dangerous hematomas. A large amount of blood can be lost with no significant clinical symptoms occurring until the patient goes into shock. When these hematomas are diagnosed, immediate exploratory surgery is indicated.


Uterine inversion is another rare but life-threatening cause of postpartum hemorrhage. Immediate recognition and action are necessary to avoid a catastrophic outcome. Patients with inversion classically have profuse bleeding and severe pain. As many as 40 percent of such patients go into shock.[4]

Complete inversion of the uterus should be obvious, with a bluish-gray mass observed in the vagina. Incomplete inversion of the uterus may be less apparent. Palpation of the abdomen may reveal a fundal defect.

When a uterus is found to be inverted, it should be repositioned immediately, and intravenous fluid resuscitation should be initiated. Several methods of repositioning the uterus have been reported. In the Johnson maneuver, the physician grasps the inverted fundus in one hand and presses it back through the cervix, aiming toward the umbilicus.[4] In another method, the physician inserts one hand under the inverted fundus and through the cervix, while the other hand is positioned on top of the uterus and through the cervix. With palms opposed, the physician compresses the -uterus and gradually moves it back into position, beginning with the area that was last inverted.[8]

If the placenta is still attached, it should be left in place until the uterus has been successfully repositioned.[4] Oxytocin is then administered, and the placenta is removed manually. The physician's hand remains in the uterus until the organ begins to contract. If initial attempts at uterine repositioning are unsuccessful, a tocolytic agent should be administered to relax the uterus. Satisfactory results have been obtained with intravenous administration of 0.25 mg of terbutaline or intravenous infusion of 2 g of magnesium sulfate over 10 minutes. General anesthesia may be required in some patients.[4]

Unsuccessful maneuvers occur more often with prolonged inversions. Preparations for surgical intervention should not be delayed while the physician tries to reposition the uterus manually. If attempts to reposition the uterus fail, prompt surgical intervention is necessary.[4]


Patients with a ruptured uterus usually have severe abdominal pain, with external bleeding varying from minimal to profuse. Risk factors for uterine rupture include previous cesarean section, prior uterine curettage and multiple gestations. Hemorrhage may occur into the peritoneal cavity or into the broad ligaments. Thus, the blood loss may not be detected until the patient becomes symptomatic from hypovolemia.

When rupture is suspected, the uterus must be inspected manually. With uterine rupture, prompt surgical intervention is required, and patients often need fluid resuscitation and/or blood transfusion.


Coagulopathies should be considered when a patient has prolonged bleeding with no identifiable source. Disorders of blood coagulation may be present before pregnancy, or they may be acquired as a complication of pregnancy. The prenatal history should identify preexisting coagulopathies, von Willebrand's disease, idiopathic thrombocytopenic purpura, and other such disorders. Consumptive coagulopathies may develop as a result of amniotic fluid embolism, sepsis, preeclampsia or eclampsia, abruptio placentae, prolonged intrauterine fetal demise or excessive blood loss.[2,4]

Clinical signs, such as oozing from the site of an intravenous line or the development of petechiae, should alert the physician to the possibility that the patient has a disorder of blood coagulation. Laboratory tests can be helpful in detecting a coagulopathy. Tests that should be performed include a prothrombin time, a partial thromboplastin time, a platelet count, a fibrinogen level, and fibrin degradation product or D-dimer levels.[8] Although these evaluations are quite useful, test results often are not available for a substantial period of time. While awaiting the laboratory results, the physician can perform a simple clot retraction test. For this test, a red top tube is drawn, set aside for five minutes and then examined. A firm clot indicates that the patient's fibrinogen level is greater than 100 mg per dL (1.0 g per L). A soft clot indicates a fibrinogen level between 50 and 100 mg per dL (0.5 to 1.0 g per L). If no clot is present, the fibrinogen level is less than 50 mg per dL.[8]

The management of coagulopathies includes treatment of the underlying cause and replacement of fluids and clotting factors as indicated. Depending on the needs of the individual patient, treatment may also include fresh frozen plasma, cryoprecipitate and platelets.


While postpartum hemorrhage most often occurs within hours of delivery, a patient may have this complication up to six weeks postpartum. Infection, subinvolution of the placental bed and retained placental products are the major causes of late postpartum hemorrhage.

Signs of endometritis include fever, uterine tenderness and foul-smelling lochia. Endometritis complicated by postpartum hemorrhage is managed with fluid resuscitation, either oxytocin (20 to 40 U per L of normal saline or lactated Ringer's solution administered at a rate of 250 to 500 mL per hour) or methylergonovine (0.2 mg administered intramuscularly), and appropriate antibiotic therapy.[4]

While curettage may be needed, it increases the risk of intrauterine adhesions. For retained placental products, curettage is necessary.


Surgical intervention is required for patients who do not respond to medical management or who have extensive lacerations, large hematomas or a ruptured uterus. The procedure that is performed is determined in part by the urgency of the situation, the skill and experience of the surgeon and the patient's desire to have more children.

Every effort should be made to stabilize the patient before surgery is performed. Fluid and blood replacement is essential to maintain intravascular volume and to prevent shock. Two large-bore intravenous lines should be placed to provide adequate access for the rapid administration of fluids. An indwelling urinary catheter is recommended so that urine output can be measured accurately. A minimum urine output of 30 mL per hour (0.5 mL per kg per hour) is necessary to demonstrate adequate renal perfusion.[2]

Most patients have a substantial increase in blood volume during pregnancy and can usually tolerate a blood loss of 1,000 mL with little change in blood pressure or urine output. Since patients with preeclampsia or eclampsia do not have this blood volume reserve, they are less able to tolerate losing a large amount of blood.[12]

Patients with signs or symptoms of hypovolemia should be considered to have lost more than 1,000 mL. These patients should receive prompt fluid resuscitation, in which each milliliter of lost blood is replaced with 3 mL of crystalloid solution. If a patient fails to respond to the administration of 3,000 mL of crystalloids, a blood transfusion should be given.[2] Antishock garments and uterine packing may be required in the patient who is in shock and does not respond to fluid or blood infusion.

A variety of surgical procedures can be used in the rare patient whose bleeding is not controlled by medical therapy. Step-wise uterine devascularization is effective, especially in the patient who wants to maintain her ability to bear more children. In this procedure, the uterine and ovarian arteries are ligated sequentially until bleeding is controlled.[13] Other possible procedures include hypogastric artery ligation, infundibulopelvic vessel ligation and hysterectomy.

If interventional radiography is available, arterial embolization may be a surgical alternative. This technique is probably better suited for the hemodynamically stable patient with delayed-onset bleeding that is not profuse.[8] In this procedure, catheters are used to place absorbable gelatin foam or some other material in the artery supplying the area of bleeding.


[1.] Kaunitz AM, Hughes JM, Grimes DA, Smith JC, Rochat RW, Kafrissen ME. Causes of maternal mortality in the United States. Obstet Gynecol 1985;65:605-12.

[2.] Roberts WE. Emergent obstetric management of postpartum hemorrhage. Obstet Gynecol Clin North Am 1995;22:283-302.

[3.] Combs CA, Murphy EL, Laros RK Jr. Factors associated with postpartum hemorrhage with vaginal birth. Obstet Gynecol 1991;77:69-76.

[4.] Druelinger L. Postpartum emergencies. Emerg Med Clin North Am 1994;12:219-37.

[5.] Gilstrap LC 3d, Ramin SM. Postpartum hemorrhage. Clin Obstet Gynecol 1994;37:824-30.

[6.] Advanced Life Support in Obstetrics. Postpartum hemorrhage. 3d ed. Kansas City, Mo.: American Academy of Family Physicians, 1996.

[7.] Diagnosis and management of postpartum hemorrhage. ACOG technical bulletin number 143. Washington, D.C.: American College of Obstetricians and Gynecologists, 1990.

[8.] Varner M. Postpartum hemorrhage. Crit Care Clin 1991;7:883-97.

[9.] Khong TY, Khong TK. Delayed postpartum hemorrhage: a morphologic study of causes and their relation to other pregnancy disorders. Obstet Gynecol 1993;82:17-22.

[10.] Zahn CM, Yeomans ER. Postpartum hemorrhage: placenta accreta, uterine inversion, and puerperal hematomas. Clin Obstet Gynecol 1990;33:422-31.

[11.] Benedetti TJ. Postpartum hemorrhage. In: Gabbe SG, Niebyl JR, Simpson JL, eds. Obstetrics: normal and problem pregnancies. New York: Churchill Livingstone, 1991:589-604.

[12.] Robson SC, Boys RJ, Hunter S, Dunlop W. Maternal hemodynamics after normal delivery and delivery complicated by postpartum hemorrhage. Obstet Gynecol 1989;74:234-9.

[13.] AbdRabbo SA. Stepwise uterine devascularization: a novel technique for management of uncontrolled postpartum hemorrhage with preservation of the uterus. Am J Obstet Gynecol 1994;171:694-700.

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