Managing postpartum hemorrhage: establish a cause

Still, even with modern blood-banking techniques and effective medical and surgical approaches for combating bleeding, this common obstetric dilemma remains a significant cause of maternal morbidity and, occasionally, mortality—even in developed nations.¹

Postpartum hemorrhage is not a medical condition in and of itself, but rather a clinical sign of other conditions that differ widely in both pathophysiology and treatment. For that reason, when excessive bleeding occurs, the clinician’s first step should be to establish a cause. In most cases, the appropriate treatment then becomes apparent.

Defining hemorrhage

Traditionally, postpartum hemorrhage has been defined as blood loss exceeding 500 cc in a vaginal delivery.¹ This definition persists in a number of textbooks despite the fact that it has been well established that mean blood loss during vaginal delivery is 500 cc.² Thus, there is no uniformly accepted volume of bleeding that defines postpartum hemorrhage. In general, the diagnosis should be considered whenever experienced observers perceive blood loss to exceed the norm, or when otherwise unexplained drops in maternal blood pressure (BP) occur in the postpartum period.

Because many gravidas have BPs significantly lower than the general population (80/50 mm Hg is by no means unusual in a pregnant woman at term), the traditional definition of hypotension—a systolic BP below 90 mm Hg—is not always applicable in pregnancy. Because epidural anesthesia also may cause hypotension, it sometimes is difficult to determine whether the hypotension is a result of hemorrhage. Clinicians therefore may need to compare a gravida’s pre- and intrapartum BP measurements and consider maternal pulse to determine the significance of “low” readings obtained during labor and delivery.

While sudden massive hemorrhage can be associated with maternal bradycardia, most young, healthy patients tend to respond to hemorrhage with progressive tachycardia—another meaningful sign of developing hypovolemia.

All told, however, there are only 4 causes of postpartum hemorrhage (TABLE 1).

TABLE 1

Causes of postpartum hemorrhage

Uterine atony

The most common cause of excessive post-partum bleeding is uterine atony, which is linked to several predisposing factors (TABLE 2). While a knowledge of these factors may help the clinician identify patients at increased risk, many women—even some with severe atony—have no risk factors at all. In 1 review of women with atony that was unresponsive to medical therapy and required hysterectomy, 20% lacked any identifiable risk factors.³ Thus, the obstetrician needs a clear understanding of the management of uterine atony and should be prepared to quickly initiate a sequence of well-defined steps aimed at its elimination. While there likely are a number of ways to appropriately address this condition, I tend to take the following approach.

Uterine compression. By manually manipulating the uterus in a serious case of uterine atony, we aim to mimic the firm, steady contraction seen in the normal postpartum uterus. After all, direct pressure is an effective means of stopping most bleeding—at least temporarily. The uterus is no exception. Note that this is a separate entity from fundal massage, which can help a clinician express postpartum clots.

For serious uterine atony, place 1 hand in the vagina toward the posterior fornix and the other on the patient’s abdomen, trapping the uterus between the 2. Apply firm pressure. As long as this pressure continues, bleeding will be significantly reduced. In some instances, this pressure is all that is needed to stop the bleeding, as the uterus eventually responds and contracts on its own. In other cases, manual compression may simply buy the clinician some time to obtain additional intravenous (IV) access, administer pharmacologic agents, arrange for blood transfusion, or summon assistance.

Oxytocin infusion. This step generally is carried out at the same time as uterine compression. Resist the temptation to administer oxytocin as an IV bolus; this can lead to paradoxical hypotension in a small percentage of women. Instead, infuse a dilute solution (20 to 40 U per liter).

Medical treatment. The combination of simple compression and oxytocin infusion resolves most cases of uterine atony. When these measures are insufficient, additional pharmacologic therapy is necessary. While each of the following agents is often effective in combating atony, there is no established order for their administration. In some instances, maternal medical conditions may contraindicate some medications. In others, the clinician’s personal preference and experience will guide management. It usually is possible to go through a series of these additional medications within 15 to 20 minutes while maintaining fundal compression to decrease the bleeding.