Pathophysiology

During labor the fetus follows a series of stereotypic movements known as the cardinal movements of labor. Although the specifics have little bearing on the emergency physician’s approach to labor, the final movement typically leaves the baby with the occiput anterior (relative to the maternal pelvis) and the head sharply flexed. This position offers the smallest fetal head diameter and is therefore optimal for passage through the pelvis. Any deviation from this position is by definition a malpresentation, and these different presentations are all associated with increasing morbidity and mortality. The overwhelming majority of births, however, will require little physician intervention beyond timely encouragement and vigilance for complications.

For a description of potential malpresentation, along with management recommendations, see www.expertconsult.com

Presenting Signs and Symptoms

Labor is classically heralded by shedding of the mucous plug that was occluding the cervix (the “bloody show”), passage of clear fluid from the vagina from ruptured membranes (the “water breaking”), and contractions. True contractions are organized and detectable by tocometry; tend to increase in pain, frequency, and strength with time; and have associated cervical changes. Braxton-Hicks contractions, commonly called false labor, are characterized by unorganized myometrial activity without cervical changes. Other common symptoms at labor onset include abdominal pain and back pain.

In the emergency department (ED), the majority of patients seen in labor are in the latter part of stage I or stage II.¹ Precipitous delivery is a common occurrence because most patients whose labor progresses more slowly will have time to get to their designated obstetric facility.

Follow-Up, Next Steps in Care, and Patient Education

After the placenta is delivered and the neonate is stabilized, the mother should be evaluated for bleeding—the causes and treatment of which are covered next. If hemodynamically stable after the first postpartum hour, the mother may be transferred to the postpartum floor.

Epidemiology

Hemorrhage is a significant cause of maternal morbidity and is the second most common cause of peripartum deaths (following amniotic fluid embolism). Hemorrhage was a direct cause of more than 18% of 3201 pregnancy-related maternal deaths in the United States from 1991 to 1997.³ Worldwide, hemorrhage has been identified as the single most important cause of maternal death and is responsible for almost half of all postpartum deaths in developing countries.⁴

Postpartum hemorrhage is the term used to describe excessive blood loss after delivery. Classically, it is defined as more than 500 mL of blood loss in a vaginal delivery or more than 1000 mL of blood loss in a cesarean delivery; however, careful quantitative measures reveal that blood loss in the range of 500 to 1000 mL is actually average for both types of delivery. Of note, practitioners often underestimate blood loss by as much as 50%.⁵ For the ED physician, the most important causes of hemorrhage in the postpartum period are birth trauma, uterine atony, uterine rupture, and uterine inversion.

Pathophysiology

Separation and delivery of the placenta constitute the third stage of labor. With separation of the placenta, there is also severance of the numerous uterine arteries and veins that carry 600 mL/min of blood through the intervillous space. The most important factor for hemostasis is contraction and retraction of the myometrium to compress and obliterate the open lumens of the vessels.

Uterine atony, the most common cause of postpartum hemorrhage, is the result of a hypotonic uterus after delivery. Factors that lead to uterine overdistention or that interfere with uterine contractility can cause uterine atony and are associated with postpartum hemorrhage. Although it is important to keep these associations in mind, most cases of postpartum hemorrhage occur without any known predisposing factors.

Trauma to the genital tract during labor and delivery (lacerations of the perineum, vagina, vulva, or cervix) is the second most common cause of postpartum hemorrhage. Abnormal placentation (placenta accreta, increta, or percreta) can contribute to postpartum hemorrhage in different ways: (1) an adherent placenta or large blood clots prevent effective contraction of the myometrium, thereby impairing hemostasis at the implantation site, and (2) significant bleeding from the implantation site is more likely with placental separation of abnormally adherent tissue.

Uterine inversion is prolapse of the uterine corpus to or through the cervix. Uterine inversion may be incomplete (inverted but does not go through the cervix) or complete (the fundus protrudes through the cervix). In the more extreme cases, the entire uterus may prolapse out of the vagina. Most cases are acute and occur immediately after delivery and before the cervical ring constricts. If inversion occurs (or is noted) after cervical contraction, the inversion is termed subacute. Chronic inversion takes place weeks after delivery. The majority of cases of uterine inversion occur as a result of traction on the umbilical cord during removal of the placenta. Acute, significant hypotension is common.

Uterine rupture is classified by the degree (complete or incomplete) and cause (spontaneous or traumatic) of the defect. A complete uterine rupture is defined as a full-thickness tear of the uterine wall and overlying serosa; it is associated with life-threatening maternal and fetal compromise. After complete rupture, the uterine contents may escape or partially extrude from the uterus and into the peritoneal cavity. An incomplete uterine rupture is defined as uterine muscle separation with an intact visceral peritoneum (often from uterine scar dehiscence). In an incomplete rupture, hemorrhage frequently extends into the broad ligament, which has a tamponading effect.

Presenting Signs and Symptoms

Peripartum patients may lose a substantial amount of blood before becoming hypotensive or feeling symptomatic. Immediate postpartum hemorrhage should be recognized as a potential complication of a precipitous delivery. The classic clinical manifestation is a woman with sudden massive vaginal bleeding who is tachycardic, pale, and possibly diaphoretic or hypotensive. However, three factors make this classic manifestation flawed. First, an elevated pulse and decreased blood pressure are insensitive indicators until large amounts of blood have been lost. Second, many patients will have steady bleeding that, although moderate in appearance, may escape notice until serious hypovolemia develops. Third, intrauterine, intravaginal, intraperitoneal, and retroperitoneal accumulation of blood can be overlooked.

In a reported case series on uterine inversion, the most common signs were shock and hemorrhage.⁶ With a complete inversion, the prolapsed uterus may be visible as a large, dark red polypoid mass within the vagina or protruding through the introitus. If the fundus remains within the vagina, the diagnosis may be suspected because of dimpling, indentation, or absence of the uterine fundus on abdominal examination or because a mass is palpated in the cervix on bimanual examination. Establishing the diagnosis of incomplete inversion can be quite difficult; severe hypotension, postpartum hemorrhage, and subtle abnormalities on abdominal examination may be the only clues.

Uterine rupture is also a difficult clinical diagnosis and should be considered in any patient with unexplained peripartum hemorrhage or hypotension. The classic findings of uterine rupture are “ripping” or “tearing,” suprapubic pain and tenderness, absence of fetal heart sounds, recession of the presenting parts, and vaginal hemorrhage. Signs and symptoms of hypovolemic shock and hemoperitoneum may follow. This classic manifestation is actually rare; 87% of patients with uterine rupture have no pain and 89% have no vaginal bleeding. Pain is also an unreliable finding because of the altered response to noxious intraperitoneal stimuli by a stretched abdominal wall. Fetal distress is the most consistent finding (80% to 100%), with fetal bradycardia being the most common sign.⁷ Most reports of uterine rupture describe patients with normal blood pressure or even elevated blood pressure without tachycardia. Abnormal maternal vital signs are late indicators of severe hemorrhage. The most important risk factor for uterine rupture is a previous uterine scar; other factors are listed in Box 122.1.

Differential Diagnosis and Medical Decision Making

Postpartum hemorrhage is a sign, not a diagnosis; it is important to consider the cause of the postpartum hemorrhage because it will often direct the treatment. The key to identifying the cause of postpartum hemorrhage is the physical examination. Because uterine atony is the most common cause of postpartum hemorrhage, accurate assessment of uterine tone is essential. To assess uterine tone, a hand is placed on the anterior wall of the uterus (over the fundus) to palpate it. If a soft, boggy, or very large uterus is felt, the diagnosis of uterine atony is established. At this point, management of uterine atony should be a priority over inspection for secondary causes of bleeding. If a firm, contracted uterus is felt, a search for other causes should be initiated promptly.

Without palpation or visualization of a frankly prolapsed uterus, it may be difficult to differentiate uterine inversion from severe atony. Heavy bleeding may make visualization of the cervix impractical. In addition, accurate abdominal palpation for a uterine fundus may be impossible in an obese patient. Depending on factors such as patient stability, resources, and diagnostic uncertainty, ultrasonography or laparotomy may be necessary. In stable patients in whom the diagnosis is uncertain and resources are available, prompt ultrasound scanning may be helpful.⁹ Ultrasonography may be able to identify retained products or clot in the uterus, but manual exploration is still needed. Ultrasound can also help detect peritoneal free fluid suggestive of uterine rupture. In selected circumstances in stable patients, a computed tomography scan can be useful in making the diagnosis in those with postpartum hemorrhage (retroperitoneal hematoma). If the accompanying hemorrhage or shock is sufficiently alarming to require immediate exploration, the correct diagnosis may be established only at laparotomy.

Although congenital coagulation defects may be relatively rare, consumptive, dilutional, and disseminated intravascular coagulopathies are important considerations. Depletion of platelets and soluble clotting factors after blood loss and subsequent crystalloid and packed red blood cell replacement is difficult to distinguish clinically from disseminated intravascular coagulopathy. Placental abruption, amniotic fluid embolism, HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count), and intrauterine demise are pregnancy-related risk factors for disseminated intravascular coagulation. Initial laboratory studies include a complete blood count, coagulation studies, disseminated intravascular coagulation panel, liver function tests, and basic metabolic panel.

Treatment

The most important aspects of managing postpartum hemorrhage are obtaining hemostasis and treating shock, including supplemental oxygen, placement of two large-bore intravenous (IV) lines, hemodynamic monitoring, and volume replacement. In addition, blood should be typed and crossmatched and 4 to 6 units of packed red blood cells should be available. Consultation with the obstetrics service should be arranged. Along with the initial resuscitation, bimanual massage and IV oxytocin should be initiated (Fig. 122.1 and Table 122.1). A Foley catheter should be placed.

Fig. 122.1 Algorithm for postpartum hemorrhage management strategies.

ABCs, Airway, breathing, and circulation; AFE, amniotic fluid embolism; CT, computed tomography; CV, cardiovascular; DIC, disseminated intravascular coagulation; IR, interventional radiology; OB, obstetrics; OR, operating room; UI, uterine inversion; UR, uterine rupture.

If the placenta has been delivered, manual uterine exploration may reveal uterine rupture or retained products or clots (which should be removed manually to improve uterine contraction). If the placenta is still in place and bleeding is ongoing, the placenta should be removed if a distinct cleavage plane is palpated on exploration. If an indistinct cleavage plane is revealed, the diagnosis of placenta accreta is likely. In this case the placenta should not be removed in the ED. Bimanual uterine compression should continue, with the goal being to stabilize patients until they can be taken to the operating room.

Trauma to the genital tract can be diagnosed by careful inspection of the labia, vagina, and cervix for laceration or hematoma. Noncomplex (first or second degree), easily accessible lacerations can be repaired with absorbable suture. Cervical lacerations and third- and fourth-degree lacerations should be repaired by an obstetrician. Temporary hemostasis may be achieved by direct pressure or, in the case of cervical lacerations, by gentle application of ring forceps to the bleeding point.

Retroperitoneal hematoma is a potentially life-threatening condition that may be manifested as hypotension, cardiovascular shock, or flank pain. Once a diagnosis is made, treatment should be supportive until the obstetrician, interventional radiology, or the operating room is available.

First-line interventions for atony are part of the initial management of postpartum hemorrhage—namely, initiation of bimanual uterine compression, IV oxytocin, and clearing of products of conception and clots from the uterus. If bleeding persists after the initial interventions, additional uterotonic medications should be given (see Table 122.1). The choice of agent may be influenced by the side effect profile, but the best drug is probably the agent that is the most quickly available in the ED. Interventional radiology may be beneficial because embolization may control the bleeding. In any case, temporizing measures may be required until definitive intervention (Table 122.2).

Table 122.2 Temporizing Measures for Hemostasis of Postpartum Hemorrhage

Uterine tamponade with sterile gauze and balloon tamponade are commonly used temporizing measures. Uterine balloon tamponade has been described with large Foley catheters, Sengstaken-Blakemore tubes, condom catheters, sterile gloves, and Rusch urologic catheters, as well as with catheters specifically designed to be used for uterine tamponade in patients with postpartum hemorrhage (SOS Bakri tamponade balloon).¹⁰

Uterine Inversion

Management of uterine inversion has two important components: treatment of hemorrhagic shock and immediate repositioning of the uterus (Fig. 122.2). Resuscitation should be initiated immediately and continued while attempts are made to reposition the uterus manually. If oxytocin is being infused, it should be stopped once uterine inversion is suspected.

Fig. 122.2 Algorithm for uterine inversion management strategies.

ABCs, Airway, breathing, and circulation; IV, intravenous; OB, obstetrics; UI, uterine inversion.

The success of nonsurgical replacement depends on completion before the myometrium regains its tone. The reported rate of successful immediate reduction is between 40% and 80%.¹¹ If initial measures are delayed or fail to relieve the condition, the inversion may progress to the point at which operative treatment or even hysterectomy is necessary.

The most common nonsurgical replacement method is a variation of the Johnson maneuver.¹² The prolapsed uterus is cupped in the operator’s palm, and firm upward pressure is applied to move the uterus up through the cervix along the natural curve of the pelvis toward the umbilicus until it is in place. Usually when the inverted mass is pushed upward, the uterus automatically reverts, with the fundus returning to its anatomic position. If the placenta has not separated, it should not be removed.

If initial repositioning is unsuccessful, myometrial relaxation with pharmacologic agents should be attempted. Magnesium sulfate, terbutaline, and nitroglycerin (attractive because of its easy availability and short half-life) are the agents most commonly used (see Table 122.1).¹³ Attempts at manual repositioning of the uterus should continue.

After successful reduction, the uterus should be supported for several minutes to allow the ligaments to return to their original state while uterotonics are administered. If magnesium sulfate was administered as a tocolytic, calcium gluconate can be given to reverse the tocolytic effect. Fluid and blood replacement and manual uterine massage should be maintained until the uterus is well contracted and the bleeding has stopped. Antibiotics should be started as soon as practical. Uterotonics are continued for at least 24 hours.

If all other efforts have failed to reposition the inverted uterus, operative intervention is required. If the uterus was repositioned with the placenta attached, manual removal can be attempted once the use of relaxants is stopped. Uterotonics should be initiated, and if the placenta cannot be removed easily, it should be left in place.