Managing postpartum hemorrhage: establish a cause
Although postpartum hemorrhage may be both sudden and massive, this condition has only 4 causes: uterine atony, genital-tract lacerations, retained placenta, and coagulopathy. Thus, the first step in management is determining the cause of bleeding.
- The most widely used agent for both prevention and management of postpartum hemorrhage is misoprostol.
- The primary contraindications to 15 methyl prostaglandin F2αre asthma and cyanotic cardiac disease.
- In most cases of failed medical management of uterine atony, hysterectomy is necessary.
- Although routine inspection of the placenta for completeness is essential following every delivery, portions may remain behind even when the delivered placenta appears to be complete.
While even optimal management may not prevent all maternal deaths, a reasoned and scientific approach to postpartum hemorrhage can dramatically improve maternal outcome.
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.
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).
Causes of postpartum hemorrhage
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.
15 methyl prostaglandin F2α (carboprost tromethanine). Of all the prostaglandins used in the United States today, this 1 has the longest track record in managing uterine atony. Administer it into a peripheral muscle or directly into the uterus itself. In general, I prefer the first approach. If the patient is hypotensive, however, peripheral muscular perfusion will be diminished, and direct injection into the myometrium may be more effective.
One vial of 15 methyl prostaglandin F2α (PGFα) contains 250 μg. The medical literature suggests the use of 2 to 6 vials before considering the intervention a therapeutic failure.1 My own approach, generally, is to inject 2 vials initially in cases of serious uterine atony, then move on to other drugs if this proves ineffective. In most cases, however, it is entirely appropriate to repeat this 500-μg dose once or twice. (There is no evidence supporting the routine initial administration of 500 μg as opposed to 250 μg.) Patients generally respond within 5 minutes.
The primary contraindications to 15 methyl PGF2 α re asthma and cyanotic cardiac disease. Since this drug is a general bronchoconstrictor, clinically insignificant desaturation occurs in all women. Because asthmatic women are more sensitive to these bronchoconstrictive effects, the use of this agent in an asthmatic patient may have disastrous results. For the same reason, a woman with cyanotic heart disease—who may be only marginally oxygenated—might be unable to tolerate a degree of oxygen desaturation that would be insignificant in most patients.
Methylergonovine maleate. This drug has the longest history of use in the management of uterine atony. It is a potent smooth muscle constrictor, affecting not only smooth muscle of the uterus but vascular smooth muscle as well. In the vast majority of cases, the drug, dosed at 0.2 mg, should be given intramuscularly (IM). As with 15 methyl PGF2α, the patient generally responds within 5 minutes. Most physicians give 1 to 2 doses of methylergonovine at 5-minute intervals before abandoning the therapy. However, if the atony is slow, chronic, or intermittent, additional doses at longer intervals may be appropriate, as may oral therapy.
Because it may lead to hypertensive crisis and cerebral vascular accident, the drug is contraindicated in hypertensive patients.
Misoprostol. The most widely utilized agent in the world for both prevention and management of postpartum hemorrhage is misoprostol. It was not commonly used in the United States until recently, but is increasingly valued for its effects against postpartum atony. The drug comes in 100-μg pills. Although very small doses (25 μg) are used in labor induction, much larger quantities are needed for postpartum atony—generally in the range of 600 to 800 μg. Misoprostol is readily absorbed through any mucous membrane and may be given rectally, buccally, or orally, as the situation demands. (Avoid the vaginal route in patients with hemorrhage because the pills will wash out.)
While neither the obstetrician nor the patient wants to go from a normal spontaneous vaginal delivery to peripartum hysterectomy, such lifesaving decisions must occasionally be made.
Misoprostol generally takes effect within 10 to 15 minutes. There are no known contraindications to its use. In such high doses, however, violent shivering is a relatively frequent occurrence. This may be frightening for both patient and physician, but is transient and requires no treatment.
Surgery. When pharmacologic therapy fails, laparotomy is indicated. A number of surgical approaches to uterine atony have been described.3-5 Although some clinicians advocate uterine and hypogastric artery ligation, most series touting the effectiveness of these techniques do not include patients for whom medical management has failed.6 In my experience, these women are extremely unlikely to respond to either uterine or hypogastric artery ligation. Indeed, any technique that causes further ischemia of an organ would seem to stand little chance of improving the function of that organ and increasing contraction.
In most instances of failed medical management, hysterectomy is necessary. While neither the obstetrician nor the patient wants to go from a normal spontaneous vaginal delivery to peripartum hysterectomy, such life-saving decisions must occasionally be made. Death due to uterine atony alone is almost always preventable.
Uterine atony: predisposing factors
Genital-tract lacerations are the second most common cause of postpartum bleeding. When the palpated uterus is found to be firm in a hemorrhaging patient, a thorough search for lacerations is indicated. Begin this process with careful inspection of the vagina and cervix. Adequate anesthesia often is essential for such exploration. In some instances, it may be necessary to move the patient to the operating room (OR), as surgical assistance may be needed to obtain appropriate exposure.
Lacerations should be surgically repaired. Unless the patient has undergone a vaginal birth after cesarean (VBAC) or the bleeding is observed to originate in the uterus, it is not necessary initially to inspect the uterine cavity manually.
After delivery, inspection of the placenta helps to determine if all cotyledons have been expelled intact. Be aware, however, that portions may remain behind even when the delivered placenta appears to be complete. When the uterus is firm and careful inspection of the lower genital tract reveals no bleeding sites, uterine exploration is necessary.
Manually explore the uterine cavity and remove any retained placenta that is encountered. Adequate anesthesia—even, at times, general anesthesia—is crucial under these circumstances. In some cases, postpartum curettage performed with a specially designed curet may help. Complete removal of all portions of the placenta generally leads to the prompt cessation of bleeding.
When the preceding methods fail to resolve bleeding due to retained placenta, prompt exploratory laparotomy is mandatory. On occasion, broad-ligament hematomas may be detected, the laceration corrected, and hysterectomy avoided. In other instances, hysterectomy is performed as a lifesaving measure without exact knowledge of the source of the bleeding. This is often followed by the pathologic diagnosis of placenta accreta.
When the uterus is firm and careful inspection of the lower genital tract reveals no bleeding sites, uterine exploration is necessary.
Other surgical approaches. Ligation of the uterine or internal iliac arteries is more likely to be effective in cases of uterine rupture. The classic approach to treating placenta accreta is hysterectomy. While a theoretical benefit exists for hypogastric artery ligation in some cases, the rarity of indications for this procedure means that very few recently trained obstetricians will be proficient enough to perform it under emergent conditions. A lack of such knowledge does not indicate inadequate training or technique. Rather, internal artery ligation has limited clinical value and is never required by the standard of care. With an experienced operator, however, the technique may occasionally make uterine conservation possible.
There are only 2 causes of acute consumptive coagulopathy in obstetrics: massive placental abruption and amniotic fluid embolism. Most chronic coagulation defects are uncovered long before pregnancy, usually during a workup for menorrhagia. Thus, in most cases of acute disseminated intravascular coagulopathy (DIC), such clotting abnormalities will be readily apparent.