Epidemiology

The incidence of placenta previa varies throughout the world but is estimated to be 1 in 200 pregnancies at term, corresponding to a prevalence of 4.0 per 1000 births. The exact cause is unclear, but prior uterine trauma (e.g., scar from prior cesarean delivery) is a common finding. The placenta may implant in the scarred area, which typically includes the lower uterine segment. Conditions associated with placenta previa include multiparity, advanced maternal age, smoking history, male fetus, previous cesarean delivery or other uterine surgery, and previous placenta previa. Asian-American women are at increased risk for placenta previa compared with white women in the United States. The presence of placenta previa increases the likelihood of fetal anomalies, neurodevelopmental delay, sudden infant death syndrome, and the risk that the mother will require a peripartum hysterectomy.

Diagnosis

Transvaginal ultrasonography is the “gold standard” for diagnosis of placenta previa. Routine assessment of the relationship between the placenta and cervix has nearly eliminated the need for double setup examination (i.e., vaginal examination with all clinicians prepared for immediate cesarean delivery). Measuring the distance from the placental edge to the internal os predicts the likelihood of antepartum hemorrhage and need for cesarean delivery. Magnetic resonance imaging (MRI) is also useful for the diagnosis of placenta previa, but its use is not practical in most cases of antepartum hemorrhage.

The classic clinical sign of placenta previa is painless vaginal bleeding during the second or third trimester. All parturients with painless vaginal bleeding after 20 weeks’ gestation should be assumed to have placenta previa until proven otherwise. Digital or speculum examination should be avoided until ultrasonography excludes abnormal placentation. Placenta previa diagnosed in asymptomatic patients before the third trimester frequently resolves as pregnancy progresses. In fact, ninety percent of placentas identified as low lying in early pregnancy will normalize by the third trimester. The lack of abdominal pain and/or absence of abnormal uterine tone helps distinguish placenta previa from placental abruption. The absence of these factors does not exclude abruption, however, and patients with placenta previa are at risk for coexisting placental abruption.

Obstetric Management

Obstetric management is based on the severity of vaginal bleeding and the maturity and status of the fetus. Active labor, persistent bleeding, a mature fetus (gestational age 36 weeks or greater), or nonreassuring fetal status should prompt delivery. The fetus is at risk from two distinct pathophysiologic processes: (1) progressive or sudden placental separation that causes uteroplacental insufficiency and (2) preterm delivery and its sequelae. The first episode of bleeding characteristically stops spontaneously and rarely causes maternal shock or fetal compromise. Expectant management in the hospital has been shown to prolong pregnancy by an average of 4 weeks after the initial bleeding episode. Maternal vital signs are assessed frequently, and the hemoglobin concentration is checked at regular intervals. Fetal evaluation involves frequent performance of a nonstress test or biophysical profile, and ultrasonographic assessment of fetal growth. Hemorrhage may be prevented by limitations on physical activity and avoidance of vaginal examinations and coitus, although the evidence supporting these measures is limited.

Outpatient management has resulted in good outcomes in carefully selected patients. Outpatient management is reserved for stable patients without bleeding in the previous 48 hours who have both telephone access and the ability to be transported quickly to the hospital. Expectant management requires immediate access to a medical center with 24-hour obstetric and anesthesia coverage and a neonatal intensive care unit.

In most cases of placenta previa diagnosed between 24 and 34 weeks’ gestation, a corticosteroid (e.g., betamethasone) is administered to accelerate fetal lung maturity. A significant number of patients with placenta previa have preterm labor, which may provoke bleeding. The use of tocolysis in women with placenta previa is controversial. Some obstetricians may administer tocolytic therapy to decrease preterm uterine contractions with the goal to stabilize antepartum bleeding. Ritodrine has been shown to prolong pregnancy in women with placenta previa, but no studies have confirmed any decrease in the frequency or severity of vaginal bleeding. Obstetricians must balance the potential cardiovascular consequences of tocolytic therapy in the event of maternal hemorrhage against the consequences of preterm delivery. Tocolytic therapy is not recommended for patients with uncontrolled hemorrhage or those in whom placental abruption is suspected. Although expectant management reduces the risk for prematurity, it does not eliminate it from occurring.

Fetuses of women with placenta previa may be at risk for other complications, including fetal growth restriction (previously known as intrauterine growth restriction). Several factors may account for the association between placenta previa and fetal growth restriction. First, the lower uterine segment may be less vascular than normal sites of placental implantation. Second, the placenta often is adherent to an area of fibrosis tissue. Third, patients with placenta previa have a higher incidence of first-trimester bleeding, which may promote a partial placental separation, reducing the surface area for placental exchange. Fourth, although the blood loss from placenta previa is almost entirely maternal, trauma to the placenta with vaginal examination or coitus may result in some fetal blood loss, which could restrict fetal growth. Additionally, a higher incidence of congenital anomalies in the fetuses of women with placenta previa may occur.

Experts recommend that women with a placental edge–to–internal os distance greater than 1 cm be offered a trial of labor because the risk for antepartum hemorrhage and need for cesarean delivery during labor are low in this setting. Parturients with a total previa, placental edge–to–internal os distance less than 1 cm, and/or significant bleeding will require abdominal delivery, as will some patients with nonreassuring fetal status.

Anesthetic Management

All patients admitted with vaginal bleeding should be evaluated by an anesthesia provider on arrival. Special consideration should be given to the airway examination, intravascular volume assessment, and history of previous cesarean delivery or other procedures that create a uterine scar. Volume resuscitation should be initiated using a non–dextrose-containing balanced salt solution (e.g., lactated Ringer’s, normal saline). Women with placenta previa may remain hospitalized for some time before delivery, and at least one intravenous catheter should be maintained if bleeding is recurrent or imminent delivery is anticipated. Hemoglobin concentration measurement may be indicated after a bleeding episode. Availability of cross-matched blood should be ensured. The American Association of Blood Banks (AABB) recommends repeating such tests every 3 days in pregnant women because of the small but finite risk for developing a new alloantibody during pregnancy. The use of lower-extremity sequential compression devices may decrease the risk for venous thromboembolism in patients on bed rest. Pharmacologic prophylaxis may be withheld because of the risk for bleeding.

The choice of anesthetic technique depends on the indication and urgency for delivery, the severity of maternal hypovolemia, and the obstetric history (e.g., prior cesarean delivery and risk for placenta accreta). Few reliable data exist to guide anesthetic choice in the context of abnormal placentation. Survey data reveal that obstetric anesthesia providers prefer neuraxial anesthesia in patients with placenta previa without active bleeding or intravascular volume deficit. A randomized controlled trial comparing epidural with general anesthesia for cesarean delivery in women with placenta previa in the absence of active bleeding demonstrated that epidural anesthesia was associated with (1) more stable blood pressure after delivery and (2) lower transfusion rates and transfusion volumes with similar hematocrit measurements the day after surgery. Operative times, estimated blood loss, urine output, and Apgar scores were similar in the two groups. Combined spinal-epidural anesthesia, or even single-shot spinal anesthesia, is considered acceptable for patients without active bleeding.

Patients who have placenta previa—even without active preoperative bleeding—remain at risk for increased intraoperative blood loss for at least three reasons. First, the obstetrician may injure an anteriorly located placenta during uterine incision. Second, after delivery, the lower uterine segment implantation site, lacking uterine muscle compared with the fundus, does not contract as well as the normal fundal implantation site. Third, a patient with placenta previa is at increased risk for placenta accreta, especially if there is a history of previous cesarean delivery (see later discussion) ( Table 37.1 ). For these reasons, it may be advisable to place two large-bore intravenous catheters before the start of either elective or emergent cesarean delivery. No consensus exists on the need for blood product availability in these patients, but it seems prudent to order a blood type and screen and ensure blood product availability. If preoperative imaging indicates the possibility of a placenta accreta, preparation for massive blood loss should be undertaken.

Patients with placenta previa and active preoperative bleeding represent a significant challenge for the anesthesia care team. Frequently, such patients have just presented to the hospital and there is minimal time for evaluation. In these cases, patient evaluation, resuscitation, and preparation for operative delivery all proceed simultaneously. Because the placental site is the source of hemorrhage, the bleeding may continue unabated until the placenta is removed and the uterus contracts. Preoperative evaluation requires careful assessment of the parturient’s airway and intravascular volume. Two large-bore intravenous catheters should be placed, and blood products should be ordered as necessary. Blood administration sets, fluid warmers, and equipment for invasive monitoring should be immediately available. Initially, non–dextrose-containing crystalloid or colloid is infused rapidly. In some cases, the patient requires transfusion before cross-matched blood is available, and type-specific blood or type O, Rh-negative blood must be administered.

Rapid-sequence induction of general anesthesia is the preferred technique for bleeding patients. The choice of intravenous induction agent depends on the degree of cardiovascular instability. In patients with severe hypovolemic shock, tracheal intubation may be accomplished without an induction agent, although this situation is rare. A low dose of propofol should be administered in women with ongoing hemorrhage. Ketamine and etomidate are useful alternative induction agents for hemodynamically unstable patients. Ketamine 0.5 to 1.0 mg/kg has an excellent record of safety and efficacy in obstetric anesthesia practice. Emergence phenomena such as hallucinations and nightmares are uncommon when the dose does not exceed 1 mg/kg. Ketamine may cause direct myocardial depression, which can result in hypotension in patients with severe hypovolemia. Etomidate 0.3 mg/kg causes minimal cardiac depression and is safe for use in obstetric patients. A low dose is appropriate in patients with severe hemorrhage. Disadvantages of etomidate include pain on administration, myoclonus, and possible adrenocortical suppression.

The agent(s) chosen for maintenance of anesthesia depends on maternal cardiovascular stability. In patients with modest bleeding and no fetal compromise, 50% nitrous oxide in oxygen can be administered with a low concentration of a volatile halogenated agent before delivery to prevent maternal awareness. The concentration of nitrous oxide or halogenated agent can be reduced or omitted in cases of severe maternal hemorrhage or fetal compromise. In these cases, a benzodiazepine such as midazolam may be administered to provide amnesia.

Oxytocin should be administered by intravenous infusion immediately after delivery. The relatively amuscular lower uterine segment implantation site does not contract as efficiently as the uterine fundus. If bleeding continues, it may be best to discontinue the volatile halogenated agent completely after delivery and to substitute 70% nitrous oxide and an intravenous opioid or ketamine. These drugs, along with small doses of midazolam, can be administered without causing significant uterine relaxation or cardiovascular depression. A low-dose infusion of propofol and/or ketamine may be considered, with the caution that propofol causes decreased uterine contractility in a dose-dependent manner. Some anesthesia providers contend that bispectral index (BIS) monitoring may be useful in lowering the risk for intraoperative awareness in cases in which the volatile anesthetic agent has been discontinued, although this issue is a matter of some dispute.

If the placenta does not separate easily, placenta accreta may exist. In such cases, massive blood loss and the need for cesarean hysterectomy should be anticipated (see later discussion). The need for invasive hemodynamic monitoring varies among patients. An indwelling arterial catheter is useful for patients with hemodynamic instability or for those who require frequent determination of hematocrit and blood gas measurements.

Epidemiology

Placental abruption complicates 0.4% to 1.0% of pregnancies. The United States incidence increased through the 1990s, particularly among African-American women, and then stabilized after 2000. The causes of abruption are not well understood, but several conditions are known risk factors for abruption ( Box 37.1 ).

Diagnosis

The classic presentation of abruption consists of vaginal bleeding, uterine tenderness, and increased uterine activity, but not all symptoms are always present. In cases of concealed abruption, vaginal bleeding may be absent, and gross underestimation of maternal hypovolemia can occur. Bleeding may be painless. In some cases, abruption may manifest as idiopathic preterm labor. Patients may have a variety of nonreassuring fetal heart rate (FHR) patterns, including bradycardia, late or variable decelerations, and loss of variability. The diagnosis of placental abruption is primarily clinical, but in a subset of cases, ultrasonography may help confirm it. Ultrasonography is highly specific for placental abruption (96%), but it is not very sensitive (24%). It is also useful for determining placental location, which can exclude placenta previa as a cause of vaginal bleeding. The ultrasonographic examination can ascertain whether a retroplacental or subchorionic hematoma is present. Normal findings do not exclude the diagnosis of placental abruption.

Pathophysiology

Complications of placental abruption include hemorrhagic shock, coagulopathy, and fetal compromise or demise. One-third of coagulopathies in pregnancy are attributable to abruption, and coagulopathy is associated with fetal demise. Placental tissue displays tissue factor and other procoagulant substances on cell membranes, and it is surmised that when bleeding at the decidual-placental interface (i.e., abruption) occurs, these thromboplastic substances are released into the central circulation, resulting in consumptive coagulopathy and disseminated intravascular coagulation (DIC).

Although some cases of abruption occur acutely (e.g., in the setting of trauma), many abruptions complicate chronic, long-standing placental abnormalities. Investigators have noted strong associations between abruption, fetal growth restriction, and preeclampsia, and all three conditions share similar risk factors. Histologic evidence of shallow trophoblastic invasion of the spiral arteries supports the conclusion that “ischemic placental disease” may underlie chronic placental hypoxia, leading to preeclampsia, fetal growth restriction, and abruption. Decidual necrosis at the placental margin and large placental infarcts are the most common abnormalities among patients who suffer placental abruption and fetal demise. Infants who die typically have 14% less placental weight, 8% less body weight, and 3% shorter body length than surviving control infants of the same gestational age. The major risks for the fetus are hypoxia and prematurity. Separation of all or part of the placenta reduces gas exchange surface area and can lead to fetal death. The risk for intrauterine fetal demise increases as the detachment area increases, particularly when the location of bleeding is retroplacental rather than subchorionic. Inadequate transplacental oxygen exchange is exacerbated by maternal hypotension, which decreases uteroplacental blood flow. The increased perinatal mortality rate associated with placental abruption reflects both a high risk for fetal death and the consequences of preterm birth.

Obstetric Management

The definitive treatment is delivery of the infant and placenta, but the degree of maternal and fetal compromise and estimated gestational age determine the timing and route of delivery. If the fetus is at or near term and both maternal and fetal status are reassuring, vaginal delivery may be appropriate. If the patient is preterm, the extent of abruption is minimal, and the mother and fetus show no signs of compromise, the patient may be hospitalized and the pregnancy allowed to continue to optimize fetal maturation. The obstetrician may administer a corticosteroid to promote fetal lung maturity. If the mother develops hemodynamic instability or coagulopathy, or the fetal status becomes nonreassuring, urgent cesarean delivery may become necessary. Vaginal delivery is preferred for patients with intrauterine fetal demise.

Anesthetic Management

If abruption is suspected, the anesthesia provider should insert a large-bore intravenous catheter and assess hemoglobin, coagulation status, and blood product preparation. When gauging volume status, the clinician must remain aware of the possibility of hemorrhage concealed behind the placenta. Placement of a urethral catheter to monitor urine output may help the physician assess adequacy of renal perfusion.

Epidemiology

Fortunately, uterine rupture occurs very rarely in the woman with an unscarred uterus, but it does occur. Previous uterine surgery (e.g., cesarean delivery or myomectomy) increases the risk, but the incidence of true uterine rupture after cesarean delivery is still low, occurring at a rate of less than 1%. Box 37.2 lists additional conditions that have been associated with uterine rupture.

Although rupture of a previous uterine scar may occur in the absence of labor, it occurs more commonly during labor (see Chapter 19 ). A population-based retrospective analysis of more than 20,000 women who had undergone one previous cesarean delivery demonstrated the risk for uterine rupture among nonlaboring women was 1.6 per 1000, whereas among women in spontaneous labor the risk increased approximately threefold to 5.2 per 1000. Among women undergoing induction of labor, the risk increased nearly fivefold to 7.7 per 1000, and among women undergoing prostaglandin induction the risk increased almost 16-fold to 24.5 per 1000. This apparent risk escalation may not result from the induction/augmentation process per se, but may reflect the fact that prolonged labor increases rupture risk, and induced/augmented labors are longer than those not induced/augmented. Additional risk factors for uterine rupture during a trial of labor after cesarean (TOLAC) include an interdelivery interval of less than 12 to 16 months, multiple previous cesarean deliveries, postterm gestation, birth weight greater than 4000 g, maternal age older than 35 years, and previous delivery with severe postpartum hemorrhage. Previous vaginal delivery and prior successful vaginal delivery after cesarean confer decreased rupture risk. Evidence of decreased lower uterine segment thickness on ultrasound examination increases rupture risk, but a precise clinically applicable threshold value below which a TOLAC should not be offered has not been determined.

The rupture of a classical uterine incision scar (a vertical incision involving the muscular uterine fundus) is associated with greater morbidity and mortality than rupture of a low transverse uterine incision scar because the anterior uterine wall is highly vascular and may include the area of placental implantation. Lateral extension of the rupture can involve the major uterine vessels and is typically associated with massive bleeding. Maternal death secondary to uterine rupture is rare, although there were three deaths attributed to uterine rupture in the 2006 to 2008 triennial report from the United Kingdom. Rupture-associated neonatal hypoxic-ischemic encephalopathy or mortality occurs at rates of less than one per 1000 trials of labor after cesarean delivery in the United States.

Diagnosis

The variable presentation of uterine rupture may cause diagnostic difficulty. An FHR abnormality is the first sign of uterine rupture in more than 80% of patients (see Chapter 19 ). The triad of abdominal pain, abnormal FHR pattern, and vaginal bleeding is seen less frequently (9% of patients with rupture). Other presenting signs include vaginal bleeding, uterine hypertonia, cessation of labor, maternal hypotension, loss of the fetal station, decrease in cervical dilation, or a change in fetal presentation. Breakthrough pain and need for frequent redosing during neuraxial labor analgesia may also indicate impending or evolving uterine rupture.

Obstetric Management

Treatment options for uterine rupture include repair of the uterus, arterial ligation, and hysterectomy. Uterine repair is appropriate for most cases of separation of a prior low transverse uterine scar and for some cases of rupture of a classical incision. However, the risk for rupture in a future pregnancy remains. A disadvantage of arterial ligation is that it may not control the bleeding and may delay definitive treatment. Hysterectomy may become necessary, albeit rarely.

Anesthetic Management

Patient evaluation and resuscitation are initiated while the patient is being prepared for emergency laparotomy. If rupture has occurred antepartum, fetal compromise is likely. General anesthesia may be necessary, but surgery can proceed under neuraxial anesthesia in stable patients with preexisting epidural labor analgesia. Aggressive volume replacement is essential, and transfusion may be necessary. Urine output should be monitored. Focused cardiac ultrasound monitoring may be appropriate whenever there is uncertainty about the intravascular volume status.

Epidemiology

Vasa previa occurs rarely (1 in 2500 to 1 in 5000 deliveries). Because it involves the loss of fetal blood, vasa previa is associated with a high fetal mortality rate (nearly 60% if vasa previa is unrecognized). The blood volume of the fetus at term is approximately 80 to 100 mL/kg. Therefore, the amount of blood that can be lost without leading to fetal death is small. In addition, the presence of vasa previa exposes the vulnerable fetal vessels to compression by the fetal presenting part, resulting in fetal hypoxia and death. Risk factors for vasa previa include the presence of velamentous cord insertion, placenta previa or low-lying placenta in the second trimester, placental accessory lobes, in vitro fertilization, and multiple gestation.

Diagnosis

Ultrasonography can be used to visualize the velamentous insertion of the vessels, but vasa previa should be suspected whenever bleeding occurs with rupture of membranes, particularly if the rupture is accompanied by FHR decelerations or fetal bradycardia. Hemorrhage can also occur without rupture of membranes, making the diagnosis more difficult.

Obstetric Management

Prenatal diagnosis confers a neonatal survival benefit: neo­natal mortality is 3% when vasa previa is diagnosed antenatally but increases to 56% when it is not. Any woman at risk for vasa previa should have an ultrasonographic examination with transvaginal color Doppler. The management of vasa previa is directed toward ensuring fetal survival.

Timing of delivery reflects a balance between the risks associated with preterm delivery and the risk for vessel rupture if the pregnancy is allowed to continue. Experts advocate antenatal steroid administration between 30 and 32 weeks’ gestation to promote fetal lung maturity, and hospitalization of the patient between 30 and 34 weeks’ gestation to ensure prompt delivery should rupture of membranes occur. Mathematical modeling comparing delivery timing strategies for women with vasa previa reveals that the best fetal outcomes will occur with elective delivery between 34 and 35 weeks’ gestation. Amniocentesis to evaluate fetal lung maturity is not recommended because delaying delivery is typically not an option.

Ruptured vasa previa is a true obstetric emergency that requires immediate delivery of the fetus by cesarean delivery. Neonatal resuscitation requires attention to neonatal volume status.

Anesthetic Management

The choice of anesthetic technique depends on the urgency of the cesarean delivery. In many cases, general anesthesia is necessary for prompt delivery.

Epidemiology

Uterine atony is the most common cause of severe postpartum hemorrhage, accounting for approximately 80% of cases; the incidence is increasing in the United States. Box 37.3 lists conditions associated with uterine atony. In addition to normal hemostatic mechanisms, postpartum hemostasis involves the release of endogenous uterotonic agents—primarily oxytocin and prostaglandins—that contract the uterus and constrict uterine vessels. Uterine atony represents a failure of this process. In addition, parturients with obstetric hemorrhage may have uterine arteries that are relatively unresponsive to vasoconstrictor substances.

Diagnosis

An atonic, poorly contractile uterus and vaginal bleeding are the most common findings in patients with uterine atony. The absence of vaginal bleeding does not exclude this disorder because the atonic, engorged uterus may contain more than 1000 mL of blood. Unrecognized bleeding may manifest initially as tachycardia; worsening hypovolemia eventually leads to hypotension ( Table 37.2 ).

Obstetric and Anesthetic Management

Prophylaxis.

The ACOG recommends active management of the third stage of labor, including uterine massage and prophylactic oxytocin administration to decrease blood loss and transfusion requirements compared with expectant management. Oxytocin is the first-line drug for prophylaxis of uterine atony after delivery of a third-trimester pregnancy. (The number of high-affinity receptors for oxytocin increases greatly near term; alternative uterotonics are more effective in the first and second trimesters of pregnancy.) Endogenous oxytocin is a nine–amino acid polypeptide produced in the posterior pituitary gland. The exogenous form of the drug (Pitocin, Syntocinon) is a synthetic preparation with a rapid onset and short half-life.

Unfortunately, exogenous oxytocin can be associated with serious side effects, including vasodilation, tachycardia, hypotension, coronary vasoconstriction, myocardial ischemia, and, rarely, even death, especially in hypovolemic or other hemodynamically compromised women. Many of these adverse effects are directly related to the dose of oxytocin. Administration of phenylephrine with oxytocin can mitigate the adverse hemodynamic consequences of oxytocin, but phenylephrine may not be necessary as long as an oxytocin bolus dose is avoided and the infusion rate is maintained below 1 IU/min, the threshold at which hemodynamic consequences become apparent. High doses of oxytocin administered concomitantly with large volumes of intravenous fluids, especially those containing free water, can lead to hyponatremia, seizures, and coma because of oxytocin’s structural similarity to vasopressin.

Oxytocin is rapidly metabolized by hepatic oxytocinases and cleared in the urine and bile, resulting in a half-life of less than 6 minutes. Consequently, a prolonged intravenous infusion is more effective than bolus administration in preventing uterine atony. Administering a 5-IU bolus of oxytocin before an infusion does not provide benefit compared with an infusion without a bolus, and may cause more hemodynamic perturbations. The dose of oxytocin required to generate satisfactory uterine tone after delivery is lower than previously thought (see Chapter 26 ). The ED ₉₀ of bolus-dose oxytocin for satisfactory uterine tone within 3 minutes of cesarean delivery in nonlaboring women is 0.35 IU ; the ED ₉₀ is almost ten times higher, approximately 3 IU, in women undergoing cesarean delivery for labor arrest after labor augmentation or induction with oxytocin. Similarly, the ED ₉₀ of oxytocin administered via infusion without a bolus dose is approximately 0.3 IU/min in nonlaboring women, but approximately 0.7 IU/min in women exposed to oxytocin during labor before cesarean delivery.

Munn et al. randomized women undergoing intrapartum cesarean delivery to receive a prophylactic infusion of oxytocin at 2.67 IU/min or 0.33 IU/min for 30 minutes after delivery. The higher dose was associated with less need for secondary uterotonics (19% versus 39%, respectively; P < .001); however, this high dose of oxytocin may be associated with clinically significant tachycardia and hypotension, and other authors have not demonstrated any differences in bleeding-related outcomes after introducing protocols that employ oxytocin doses in the lower range. Awareness of the dangers of high-dose administration and data demonstrating the effectiveness of lower oxytocin doses than used historically call into question the safety of the practice of injecting 10 to 40 IU of oxytocin into a 1-liter crystalloid solution and infusing the solution at an unspecified rate, often “wide open” (i.e., gravity-dependent flow). The doses administered with this method may approach those achieved with bolus administration. Box 37.4 contains a suggested protocol for third-stage oxytocin administration.

Box 37.4

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