The incidence of placenta previa varies worldwide, with rates ranging from 2 to 12 per 1000 pregnancies. 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. There is a “dose-response” relation between the risk of placenta previa and the number of prior cesarean deliveries; the relative risk (RR) increases from 4.5 (95% confidence interval [CI], 3.6 to 5.5) with one prior cesarean to 44.9 (95% CI, 13.5 to 149.5) with four prior cesarean deliveries. In the United States, Asian patients are at increased risk for placenta previa compared with White patients. Placenta previa can lead to antepartum hemorrhage and PPH, and it is associated with perinatal and neonatal morbidities, including preterm birth, fetal anomalies, neurodevelopmental delay, and sudden infant death syndrome.

Most patients are initially diagnosed during routine transabdominal ultrasonography. Due to its superior diagnostic accuracy, transvaginal ultrasonography is typically performed for diagnostic confirmation. Measuring the distance from the placental edge to the internal os predicts the likelihood of antepartum hemorrhage and the need for cesarean delivery. Magnetic resonance imaging (MRI) may be 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 examination may cause catastrophic hemorrhage and should be avoided. Placenta previa diagnosed in asymptomatic patients before the third trimester frequently resolves as pregnancy progresses; 90% of low-lying placentas diagnosed in early pregnancy normalize by the third trimester. The lack of abdominal pain does not exclude placental abruption, and patients with placenta previa are at risk for coexisting placental abruption.

Obstetric management is based on the severity of vaginal bleeding, the gestational age, and fetal status. Active labor, persistent bleeding, a mature fetus (gestational age ≥ 36 weeks), or nonreassuring fetal status should prompt delivery. The fetus is at risk for 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 reported to prolong pregnancy by an average of 4 weeks after the initial bleeding episode. Maternal vital signs and hemoglobin concentration should be assessed frequently. Fetal evaluation involves nonstress tests, biophysical profiles, and ultrasonographic assessments of fetal growth (see Chapter 6 ). Traditionally, limited physical activity and avoidance of vaginal examinations and coitus has been recommended, although the evidence supporting these measures is limited.

Outpatient management is associated with favorable outcomes in select patients, such as 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 ICU.

For patients with placenta previa diagnosed between 24and 34 weeks’ gestation, a corticosteroid (e.g., betamethasone) is typically administered. This is done to accelerate fetal lung maturity due to concern for preterm delivery. To mitigate this concern, short-term tocolytic therapy may be used to treat patients with preterm uterine contractions. Tocolytic therapy is not recommended for patients with uncontrolled hemorrhage or those with evidence of maternal or fetal compromise.

If the placental edge–to–internal os distance is greater than 1 cm, patients may be offered a trial of labor—the risk of antepartum hemorrhage and the need for cesarean delivery during labor are low. Conversely, patients require cesarean delivery if the placental edge–to–internal os distance is less than 1 cm, total placenta previa is present, fetal status is nonreassuring, or if significant bleeding is present.

Typically, stable patients with a placenta previa without significant antepartum vaginal bleeding or uterine contractions will undergo a scheduled cesarean delivery between 36 and 37 weeks’ gestation.

All patients presenting with antepartum vaginal bleeding or uterine contractions should undergo urgent anesthesia evaluation in anticipation of expedited delivery. 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. Large-bore intravenous access should be obtained. For patients with significant or active bleeding, hematologic and coagulation indices should be urgently evaluated, red blood cells (RBCs) ordered, and intravenous fluid resuscitation initiated. Activation of a massive transfusion protocol (MTP) is advised for patients with severe or massive antepartum hemorrhage (see later discussion).

Patients without significant vaginal bleeding may require antepartum hospitalization. Vascular access with at least one intravenous catheter should be maintained if bleeding is recurrent or imminent delivery is anticipated. The use of lower-extremity sequential compression devices may decrease the risk for venous thromboembolism in patients on bed rest.

The choice of anesthetic technique depends on the indication and urgency for delivery, the severity of maternal hypovolemia, laboratory indices, and the obstetric history (e.g., prior cesarean delivery, risk for placenta accreta). Few reliable data exist to guide anesthetic choice in the context of abnormal placentation. Survey data reveal that most anesthesia providers prefer neuraxial anesthesia in patients with placenta previa without active bleeding or intravascular volume deficit. A large cohort study examined the mode of anesthesia in patients with placenta previa and reported outcomes for 1234 patients. Neuraxial anesthesia and general anesthesia were performed in 59.7% and 40.3% of cases, respectively. Blood transfusion was less common in the neuraxial anesthesia group (19.8% versus 76.7%). After adjustment for confounders, findings from regression analyses suggested that neuraxial anesthesia was associated with less blood loss, a lower transfusion requirement, and less neonatal morbidity (neonatal asphyxia and neonatal ICU admission). However, these findings may be explained by residual confounding.

Patients who have placenta previa—even without active preoperative bleeding—remain at risk for increased intraoperative blood loss for three reasons. First, an anteriorly located placenta may be surgically transected during a 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 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 ( Table 37.1 ). Therefore, anesthesia providers should be prepared for severe or massive intraoperative hemorrhage in all patients with placenta previa (see later discussion). Before delivery, intravenous access should be established with at least two large-bore intravenous catheters and two cross-matched RBC units should be immediately available.

If the placenta does not separate easily from the uterine wall, placenta accreta should be suspected, and massive blood loss and cesarean hysterectomy should be anticipated.

Placental abruption complicates 0.6% to 1.2% of pregnancies, with an incidence of 3 to 10 per 1000 births worldwide. The causes of abruption are not well understood, but several conditions are known risk factors for abruption ( Box37.1 ). Patients with abruption are also at risk for PPH from uterine atony and coagulopathy.

For an acute revealed abruption, the classic clinical features are vaginal bleeding in 70% to 80% of cases, abdominal pain or uterine tenderness in two-thirds of cases, and increased uterine contractions in one-third of cases. In cases of concealed abruption (20% of cases), vaginal bleeding and pain may be absent, but fetal death and coagulopathy can still occur. In nearly a third of concealed cases, abruption may manifest as idiopathic preterm labor. Uterine contractions may be difficult to distinguish from the pain associated with placental abruption. Patients may have a variety of nonreassuring fetal heart rate (FHR) patterns, including late or variable decelerations, fetal tachycardia, and loss of variability. The severity of FHR changes may correspond with the severity of abruption. For example, with profound fetal hypoxia, sinusoidal patterns can occur before terminal bradycardia. For a chronic abruption, the clinical features include light to moderate vaginal bleeding only.

In a subset of cases, ultrasonography may help confirm the diagnosis, which appears as large abnormal blood collections close to or within the placenta. Ultrasonography is highly specific for placental abruption (96% to 100%) but assessment of sensitivity varies between studies, ranging from 24% to 57%. Ultrasonography is also useful for determining placental location to exclude placenta previa, a retroplacental hematoma, and subchorionic hematoma. However, normal ultrasonographic findings do not exclude placental abruption.

The initial management of placental abruption should focus on maternal stabilization and appropriate resuscitation. Delivery may be necessary, especially in patients presenting with severe bleeding, to minimize the risks of severe hemorrhage, coagulopathy, fetal compromise, and maternal hypoperfusion.

Current evidence is insufficient to guide the timing of delivery for patients with acute or chronic abruption. A suggested obstetric management algorithm has been published ( Fig. 37.1 ). After an initial period of observation for noncompromised patients, decision-making regarding the need and timing of delivery versus inpatient or outpatient management is necessary. These decisions should consider the patients’ gestational age and other complicating factors (e.g., oligohydramnios, ongoing vaginal bleeding, FHR abnormalities). A course of corticosteroids may be administered to promote fetal lung maturity for patients presenting preterm, but delivery should not be deferred to administer corticosteroids in the late preterm period. Vaginal delivery is preferred for patients with intrauterine fetal demise unless they are at increased risk for uterine rupture.

Management Algorithm for Placental Abruption.

The algorithm for the management of placental abruption with acute hemorrhage employs the Advanced Trauma Life Support classification of hypovolemic shock, which has not been validated in pregnancy. FFP , Fresh frozen plasma; IUFD , intrauterine fetal death; IV , intravenous; MFM , maternal-fetal medicine; MTP , massive transfusion protocol; NICU , neonatal intensive care unit; PRBCs , packed red blood cells; T&S , type and screen. Placental abruption at near-term and term gestations.

From Brandt JS, Ananth CV. Placental abruption at near-term and term gestations: pathophysiology, epidemiology, diagnosis, and management. Am J Obstet Gynecol . 2023;228(5S):S1313–S1329.

If abruption is suspected, initial interventions should focus on maternal stabilization, including large-bore intravenous access, intravenous fluid resuscitation, and assessment of hemoglobin, coagulation status, and the need for blood products. Clinicians must be vigilant for hypovolemic shock, even in the absence of external blood loss (presence of concealed abruption).

Neuraxial techniques for labor analgesia or cesarean anesthesia may be offered for patients who are hemodynamically stable without coagulopathy. Intravenous patient-controlled opioid analgesia should be considered for patients in labor, and general anesthesia should be administered for cesarean delivery in patients with severe thrombocytopenia or coagulopathy. General anesthesia (see Chapter 26 ) may also be necessary for emergency cesarean delivery in the setting of severe fetal compromise or severe antepartum hemorrhage.

Uterine rupture is rare (1:16,849) among patients with an unscarred uterus. Previous uterine surgery (e.g., cesarean delivery, myomectomy) increases the risk (<1% for patients with one previous cesarean delivery, 3.9% for those with more than one cesarean delivery). Box 37.2 lists other conditions associated with uterine rupture.

Among patients who have undergone a prior cesarean delivery, the presence or absence of labor influences their risk of uterine rupture (see Chapter 20 ). A population-based retrospective analysis of more than 20,000 patients demonstrated that the risk among nonlaboring versus laboring patients was 1.6 per 1000 versus 5.2 per 1000. Among patients undergoing induction of labor, the risk increased nearly fivefold to 7.7 per 1000 and was highest among those undergoing prostaglandin induction (24.5 per 1000). 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 > 4000 g, maternal age > 35 years, and previous delivery with severe PPH. Decreased thickness of the lower uterine segment on ultrasonographic examination increases rupture risk, but a precise threshold value below which TOLAC should not be offered because the risk of rupture is too high is unclear.

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 a rate of less than one per 1000 TOLACs in the United States.

An FHR abnormality is the first sign of uterine rupture in more than 80% of patients (see Chapter 20 ). Breakthrough pain and need for frequent neuraxial labor analgesia redosing may also indicate impending or evolving uterine 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.

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.

Patient evaluation and resuscitation should be initiated while the patient is being prepared for emergency laparotomy. If antepartum rupture has occurred, fetal compromise is likely. Rapid induction of general anesthesia is likely to be necessary, but neuraxial anesthesia may be possible in stable maternal patients with a functioning epidural catheter that allows timely conversion from labor analgesia to surgical anesthesia. In many cases, major hemorrhage requiring massive transfusion and hemostatic support may be required (see later discussion).

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 and the unprotected vessels tear). The blood volume of the fetus at term is approximately 80 to 100 mL/kg; thus, the loss of small amounts of blood can have devastating fetal consequences. 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.

Prenatal ultrasonography can be used to visualize the velamentous insertion of the vessels and leads to improved perinatal outcomes. Vasa previa should be suspected whenever bleeding occurs with intrapartum rupture of membranes, particularly if the rupture is accompanied by FHR decelerations (e.g., a sinusoidal pattern, fetal bradycardia). Hemorrhage can also occur without the rupture of membranes, making the diagnosis challenging.

Prenatal diagnosis is critical for neonatal survival. Antenatal diagnosis reduces neonatal mortality to 3%, while undiagnosed cases have a mortality rate of 56%. Any patient 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.

The 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. Cesarean delivery should occur before labor or membrane rupture to prevent vessel rupture. Experts advocate antenatal corticosteroid administration between 30 and 32 weeks’ gestation to promote fetal lung maturity, and antepartum maternal hospitalization between 30 and 34 weeks’ gestation to ensure prompt delivery in the event of rupture of membranes. Findings from a decision analysis suggest scheduling a cesarean delivery between 34 and 35 weeks’ gestation. This overlaps with the Society for Maternal-Fetal Medicine guidelines for delivery between 34 and 37 weeks’ gestation. However, recommendations for delivery at 34 weeks were made prior to published data, highlighting the perinatal morbidity risks of preterm delivery. Recent expert opinion suggests that delivery be considered at 36 to 37 weeks in asymptomatic patients. Amniocentesis to evaluate fetal lung maturity is not recommended because delaying delivery is typically not an option.

Ruptured vasa previa in the presence of FHR abnormalities (bradycardia, late decelerations, sinusoidal pattern) is an obstetric emergency that requires immediate cesarean delivery. Neonatal resuscitation requires attention to neonatal blood volume status.

The choice of anesthetic technique depends on the urgency of the cesarean delivery. Patients with prenatally diagnosed vasa previa will typically undergo scheduled cesarean delivery before labor or rupture of membranes, with a lower-segment transverse uterine incision. Assuming no contraindications, neuraxial anesthesia is recommended for these patients. Neuraxial anesthesia may also be considered for patients in labor or with membrane rupture but without vessel rupture or fetal compromise. In these scenarios, continuous fetal monitoring in the case of vessel rupture and fetal compromise is required before, during, and after the initiation of neuraxial anesthesia. General anesthesia may be necessary for emergency cesarean delivery if there is acute, potentially life-threatening fetal compromise from a vessel rupture.

Uterine atony is the most common cause of PPH, accounting for 80% of all PPH events. Atony is associated with other causes of PPH, such as genital tract trauma, placenta previa, and placental abruption. The mechanism of this association is unclear but suggests that atony may not always be the primary cause of PPH, but rather an exacerbating complication ( Box 37.3 ).

Although molecular phenotypes or signatures for uterine atony are not fully known, studies have improved our understanding of the pathophysiology of uterine atony. In cultured human uterine smooth muscle cells, decreased oxytocin receptor mRNA and a 50% to 60% reduction in oxytocin-induced calcium occur after 48 hours of oxytocin pretreatment. In addition, oxytocin-induced desensitization of smooth muscle cells occurred after 4 hours of oxytocin exposure, although the cells continued to respond to prostaglandin F _2α stimulation. In an in vitro study of contractility patterns in isolated human myometrium from nonlaboring patients undergoing elective caesarean delivery, decreased contractility was observed in response to oxytocin when preexposed to a higher versus lower oxytocin concentration (10 ⁻⁵ to 10 ⁻⁸ M versus 10 ⁻¹⁰ M).

Based on the totality of these research findings, oxytocin pretreatment attenuates increases in intracellular Ca ²⁺ and myometrial contractility in response to exogenous oxytocin in a dose- and duration-dependent manner. Oxytocin receptor desensitization may not impair the pre- or postreceptor signaling of other drugs that potentiate myometrial contractility, such as prostaglandins or ergot alkaloids. These findings provide a scientific rationale for the association between prolonged or augmented labor and poor uterine responsiveness to oxytocin after delivery.

A poorly contractile uterus and excessive blood loss are the most common clinical features of uterine atony. The diagnosis is typically based on bimanual uterine assessment after vaginal delivery or direct evaluation of uterine tone during cesarean delivery. The absence of vaginal bleeding does not exclude this disorder because an atonic, engorged uterus may contain more than 1000 mL of blood. Unrecognized bleeding may manifest initially as tachycardia, with worsening hypovolemia eventually leading to hypotension.

The prophylactic administration of oxytocic agents, most commonly oxytocin or carbetocin, is a critical component of the active management of the third stage of labor. When uterine atony occurs, additional oxytocic supplementation can be considered. In the setting of refractory uterine atony, prostaglandins and ergot alkaloids are recommended for second-line treatment ( Table 37.2 ). Based on data from a nationwide sample of US delivery hospitalizations between 2007 and 2011, the median hospital-level frequency of second-line uterotonic use was 7.1%; the most frequently used second-line uterotonics were methylergonovine maleate, misoprostol, and carboprost.

The natural ergot alkaloids are produced by a fungus that commonly infests rye and other grains. Ergonovine and methylergonovine (a semisynthetic preparation with an identical pharmacologic profile) are the two ergot alkaloids currently available for use. Their uterotonic effect is most likely mediated by serotonergic agonism; the ergot alkaloids are also weak dopamine and alpha-adrenergic receptor agonists. Both drugs have similar pharmacologic properties and are dispensed in ampules containing 0.2 mg. When administered via the intramuscular route, both drugs have a rapid onset (1 to 3 minutes), long half-lives (30 to 120 minutes), and reach maximal plateau concentrations in 40 minutes. Ergot alkaloids are stable at room temperature for prolonged periods.

Prostaglandins of the E and F families have gained wide acceptance as second-line therapy when high-dose oxytocin is inadequate for the treatment of uterine atony. Concentrations of endogenous prostaglandins increase during labor, and levels peak at the time of placental separation. It is hypothesized that uterine atony may represent a failure of prostaglandin concentrations to increase during the third stage of labor in some women. Prostaglandins increase myometrial intracellular free calcium concentration, ultimately leading to an increase in myosin light-chain kinase activity. Common side effects noted after prostaglandin administration include fever, chills, diarrhea, nausea, and vomiting.

Choice of anesthetic technique for the repair of genital lacerations and evacuation of pelvic hematomas depends on the affected area, surgical requirements, the patient’s intravascular volume and hemodynamic status, and urgency of the procedure. Local infiltration and a small dose of intravenous opioid may suffice for the drainage of small vulvar hematomas; however, repair of extensive lacerations and drainage of large vaginal hematomas require a greater depth of surgical anesthesia. A pudendal nerve block may not be technically feasible because of anatomic distortion or severe pain from the hematoma. Spinal or epidural anesthesia may be indicated for patients requiring surgical anesthesia beyond a localized area. However, clinicians should exercise caution initiating (or extending) a neuraxial block in a patient with significant hypovolemia due to concern for precipitating cardiovascular collapse. For patients with severe hemodynamic instability or severe and evolving hemorrhage, general anesthesia with tracheal intubation may be necessary. Exploratory laparotomy for a retroperitoneal hematoma typically requires general anesthesia with anticipation for severe or massive intrabdominal hemorrhage requiring a massive transfusion and hemostatic support (see later discussion).

Treatment of retained placenta during the early postpartum period often involves gentle cord traction, uterine massage, manual removal, and inspection of the placenta. If manual extraction is not successful, curettage may be required. The clinician may need to discontinue oxytocin during curettage and then, once the placenta has fully delivered, restart it to augment uterine tone. The eventual removal of the placenta typically promotes uterine contraction and reduces bleeding. However, close observation for signs of recurrent hemorrhage is warranted. Because manual extraction of the placenta increases the risk for endometritis, the WHO recommends prophylactic antibiotic administration, but published studies neither support nor refute this recommendation.

Manual extraction of the placenta is painful and requires analgesia. In some cases, intravenous analgesia may be adequate to allow examination and manual placental extraction by a skilled obstetrician. However, in many cases, administration of local anesthetic through an indwelling epidural catheter provides better quality analgesia. In the absence of an indwelling epidural catheter, de novo spinal anesthesia should be considered in patients who are not bleeding severely and are hemodynamically stable in the operating room. General anesthesia with a rapid sequence induction may be necessary for patients experiencing severe breakthrough pain or who are hemodynamically unstable. Caution should be exercised in using sedation or “monitored anesthesia care” because many patients will not meet “nil by mouth” precautions and thus be at risk for pulmonary aspiration. Additionally, the depth of analgesia with sedatives and/or opioids is typically not sufficient to ensure that patients can safely experience manual placental removal without incurring significant periprocedural pain and psychological distress.

To facilitate manual placental removal, nitroglycerin may be administered for uterine relaxation. Nitroglycerin provides a rapid onset of smooth muscle relaxation and a short plasma half-life (2 to 3 minutes). Successful removal of retained placenta was observed in 15 parturients after administration of intravenous nitroglycerin 500 µg. Others have used substantially lower doses of nitroglycerin (50 to 100 µg) with similar results. Nitroglycerin may also be administered sublingually via spray or tablet. A double-blind, randomized controlled study compared sublingual nitroglycerin with a placebo for management of retained placenta; the placenta was delivered successfully within 5 minutes in all 12 of the parturients who received nitroglycerin compared with only 1 of the 12 who received a placebo. Nitroglycerin most likely produces uterine smooth muscle relaxation by releasing nitric oxide, which temporarily decreases systemic blood pressure. Because of its short plasma half-life, sustained hypotension after bolus administration is rare. Nevertheless, administration of nitroglycerin necessitates vigilant blood pressure monitoring and treatment when indicated.

Uterine inversion should be suspected when severe hemorrhage occurs in the presence of a mass in the vagina and a nonpalpable fundus. Inversion should be suspected in all cases of PPH. Ultrasonographic examination may show characteristic findings, such as an echolucent zone within an echogenic mass filling the uterine cavity on transverse view. Historically, obstetricians have observed that the shock is out of proportion to the blood loss, which may be mediated by parasympathetic stimulation caused by tissue stretching. An incomplete inversion not protruding through the introitus is more likely to result in missed or delayed diagnosis.

Replacement of the uterus and resuscitation, even before removal of the placenta, are the immediate treatment goals. All uterotonic drugs should be discontinued immediately. The obstetrician should attempt to reduce the inversion by applying pressure through the vagina to the uterine fundus; ring forceps may be used on the cervix to apply countertraction. Once the uterus is repositioned, uterine atony often follows, especially if tocolytics have been used. It is therefore important to treat uterine atony early and establish uterine contractility to avoid any likelihood of reinversion. Therapeutic measures to treat uterine atony include fundal massage and second-line uterotonic agents. Insertion of an intrauterine balloon may prove useful during treatment to prevent reinversion.

Hemorrhage in the setting of uterine inversion can be abrupt, severe, and life threatening. Immediate resuscitation is needed by the anesthesia team. Closure of the cervical os and uterine smooth muscle contraction precludes reducing the uterus. Thus, relaxation of both the cervical ring and uterus is a prerequisite for successful treatment. Nitroglycerin can facilitate uterine relaxation and replacement, with reports describing an intravenous bolus dose between 200 and 250 μg. Given that the vasodilatory effect of nitroglycerin can compound maternal hemodynamic instability, the anesthesia provider should closely support the maternal circulation with intravenous fluids and vasopressors. If early attempts to reposition the uterus fail following tocolysis, general anesthesia with a volatile halogenated agent is indicated to facilitate uterine relaxation and/or a laparotomy.

The incidence of PAS has increased over the last several decades in association with increasing rates of cesarean delivery. In the United States, the incidence has increased from 1 in 30,000 pregnancies in the 1960s to 1 in 300 pregnancies in the 2010s. In a systematic review of PAS in general population studies, the pooled prevalence was 0.17% (95% CI, 0.14 to 0.19).

Previous cesarean delivery or other uterine surgery increases the risk for both placenta previa and PAS. The combination of placenta previa with previous cesarean delivery increases the risk for PAS, particularly if the placenta is anterior and overlies the uterine scar. A prospective multicenter observational study found that for patients with a placenta previa and prior cesarean delivery, the risk of PAS was 3%, 11%, 40%, 61%, and 67% for the first, second, third, fourth, and fifth or more prior cesareans, respectively (see Table 37.1 ). A systematic review of 3889 patients with one or more prior cesarean deliveries with placenta previa or low-lying placenta in the index pregnancy (identified by ultrasonography) found that the incidence of placenta accreta was 4.1% in patients with one prior cesarean and 13.3% in patients with two or more prior cesareans. Based on data from pathologic studies, the distribution of accreta subtype in descending order of frequency is accreta (69.5%), increta (23.7%), and percreta (6.8%).

Ultrasonography is the primary diagnostic modality for the antenatal diagnosis of placenta accreta. Ideally, patients with risk factors for placenta accreta should be evaluated by obstetricians experienced in the ultrasonographic diagnosis of placenta accreta. Features of placenta accreta may be visible on ultrasonography as early as the first trimester. However, in most cases, the diagnosis is made in the second or third trimesters. Placenta previa is typically detected in more than 80% of PAS cases in the second and third trimesters. Other key ultrasonographic features include multiple placental vascular lacunae, loss of the normal hypoechoic zone between the placenta and myometrium, reduced retroplacental myometrial thickness (<1 mm), an abnormal uterine serosa-bladder interface, and extension of the placenta into myometrium, serosa, or bladder. No clear ultrasonographic features reliably predict the depth of placental invasion or PAS subtype.

Ultrasonography has very high sensitivity (91%) and specificity (97%) in the diagnosis of PAS. MRI is another well-described modality for identifying PAS. Findings from a systematic review indicate MRI has comparable predictive accuracy to ultrasonography, with high sensitivity (94%) and moderate-to-high specificity (84%). The accuracy of these modalities may be overestimated because studies typically involve patients with risk factors for PAS who undergo imaging in high-volume specialist centers. Although patients with indeterminate ultrasonographic findings or who are at high risk for more invasive accreta subtypes may undergo MRI, the extent to which MRI improves the diagnostic accuracy of ultrasonography is unclear. Prediction models that incorporate clinical, radiologic, and/or biologic data have been explored. However, their widespread integration into clinical practice has been limited by heterogeneity across studies in terms of the selected potential predictors for PAS, the classification of PAS, and the variable accuracy of prediction models upon external validation.

While antenatal identification of PAS is crucial for optimizing outcomes, a 2011 survey of ACOG members revealed that only one in four general obstetricians refered patients with suspected PAS to a specialist center. Therefore, all facilities that provide obstetric care should have an action plan or checklist for the delivery care of patients with suspected or unexpected PAS. In such cases, mobilization of essential resources and experienced staff is critical. Numerous studies have shown that antenatal compared to intrapartum diagnosis of PAS leads to less blood loss at delivery and optimized maternal outcomes.

The ACOG and the Society for Maternal-Fetal Medicine (SMFM) recommend that patients with PAS be referred to and managed at a center with available resources of a Maternal Level of Care III (subspecialty) or IV facility (see Table 11.3 ). Observational data suggest that patients who deliver in centers with a multidisciplinary team that includes a 24-hour in-house obstetrician and anesthesia provider, immediate availability of a gynecologic oncologist, a fully stocked blood bank, and interventional radiology services, experience less morbidity than those treated at hospitals without these services. Criteria for a PAS center of excellence have been described ( Box 37.4 ).

Antenatal bleeding may necessitate emergency preterm delivery, although some cases of vaginal bleeding remote from term resolve spontaneously, and expectant management may prolong the duration of pregnancy into the third trimester. The risk for severe antenatal bleeding increases as gestational age increases. The timing of delivery involves balancing the risk of emergency delivery for hemorrhage against the neonatal risks associated with preterm delivery. Decision analysis suggests that 34 weeks’ gestation is the preferred time for planned delivery. Professional organizations, including the ACOG and SMFM, recommend delivery between 34 0/7 and 35 6/7 weeks’ gestation in a stable patient without additional medical, surgical, or fetal comorbidity and in the absence of labor or bleeding.

Most patients with known PAS should undergo planned preterm cesarean delivery and hysterectomy with the placenta left in situ . Manual attempts to remove the placenta are strongly discouraged. For patients with an uncertain antenatal diagnosis, spontaneous placental separation may be appropriate if resources are available to manage severe hemorrhage. Preoperative placement of ureteral stents may minimize urinary tract injury. Preoperative cystoscopy may also be considered to visualize placental involvement in the bladder wall. A midline vertical skin incision can improve surgical exposure. To avoid cutting through the placenta, surgeons may modify the uterine incision, such as selecting a fundal location to avoid a low-lying accreta.

Patients diagnosed with PAS should receive anesthetic management in specialist centers (ACOG Maternal Level of Care III or IV), with 24-hour availability of anesthesia providers. However, consensus on best approaches to anesthetic management is lacking because most studies of anesthesia practices are based on small samples from single obstetric centers. Further, sparse information is available on the level of subspecialist experience of anesthesia staff that manage PAS cases, as well as the location for delivery, whether an operating room on the labor and delivery unit, the main operating room complex, or a hybrid room in the interventional radiology suite.

Options for the primary mode of anesthesia for cesarean delivery include neuraxial anesthesia, general anesthesia, or both ( Table 37.4 ). A review of anesthetic practices from published studies revealed a wide range in the reported frequency of general anesthesia (5% to 100%), neuraxial anesthesia (0% to 72%), and intraoperative conversion from neuraxial to general anesthesia (7% to 70%).

Nearly half of patients with suspected PAS experience hemorrhage requiring blood transfusion. Therefore, anticipatory planning for massive intraoperative hemorrhage is critical. Key considerations for hemorrhage management include location and size of intravenous access (peripheral and/or central), blood product ordering (number and types of blood components), resources for facilitating massive transfusion (e.g., institution-specific MTP, rapid infusion devices, intraoperative use of cell salvage), and point-of-care devices (e.g., transthoracic echocardiography for assessing intracardiac volume and contractility, viscoelastic testing devices). Based on a metaanalysis of studies that reported transfusion volumes in the surgical management of patients with PAS, a minimum of six units of RBCs should be available.

In all cases, anesthesia providers should prepare for the potential for massive hemorrhage. The SMFM has developed an emergency checklist, planning worksheet, and system preparedness bundle to assist anesthesia and obstetric providers in system and team preparedness for peripartum management. For all PAS cases, the anesthesia care should be directed by an experienced obstetric anesthesiologist, and preparations made for large volume blood loss ( Box37.5 ). In our current practice, we prefer neuraxial anesthesia (combined spinal-epidural anesthesia or single-shot spinal and thoracic epidural catheter placement) for the cesarean delivery, with planned conversion to general anesthesia for patients requiring hysterectomy.

Limited information exists regarding postpartum outcomes and analgesia use after cesarean hysterectomy. In a single-center study of 39 patients with suspected PAS who underwent cesarean delivery, postoperative opioid consumption varied according to anesthesia mode. Compared to patients who received general anesthesia only, mean-adjusted postoperative opioid consumption was lower (at least 150 oral morphine mg equivalents) for patients who had neuraxial anesthesia only, or neuraxial anesthesia with conversion to general anesthesia following delivery.

Postoperative analgesia options include long-acting neuraxial opioids, an epidural infusion of local anesthetic with or without opioids, intravenous patient-controlled analgesia, abdominal wall field blocks, and intravenous or oral analgesia (see Chapter 27 ). Because patients who undergo cesarean hysterectomy typically have a midline vertical skin incision, multimodal postoperative analgesia is suggested.

Fibrinogen levels increase during pregnancy up to 4 to 6 g/L by term. Observational studies have reported an inverse nonlinear relationship between the magnitude of blood loss and nadir plasma fibrinogen level. Among patients with 1000- to 1500-mL blood loss, the incidence of hypofibrinogenemia is between 4% and 5%. In a cohort of patients with major PPH (≥5-unit RBC over 4 hours or ≥8-unit total RBC transfusion), 40% to 50% have a fibrinogen level < 200 mg/dL.

In cohorts of patients who experience moderate-to-severe PPH, retrospective and prospective studies have shown that the fibrinogen level is a predictive biomarker for morbidity or progression to more severe PPH. A landmark study from France first reported that a fibrinogen level < 200 mg/dL during the early phase of PPH had a 100% positive predictive value for subsequent RBC transfusion greater than four units or a reduction in hemoglobin levels by 4 g/dL or more. Subsequent observational studies have confirmed that a fibrinogen level < 200 mg/dL is an important predictor of severe PPH.

Thrombocytopenia is a less common abnormality, occurring in 1% to 5% of patients with mild to moderate PPH. The incidence increases up to 50% during severe or life-threatening PPH. In a cohort study of patients with PPH, investigators observed that a platelet transfusion was only required with large-volume blood loss (>5 L) or if hemorrhage was associated with placental abruption or a preexisting thrombocytopenia.

The presence, type, and severity of coagulopathy vary according to the primary hemorrhage etiology and the volume of blood lost. Coagulopathy is very uncommon when PPH is due to uterine atony or genital tract trauma, unless there is massive hemorrhage. Observational data indicate that hypofibrinogenemia occurs in only 2% to 3% of cases of hemorrhage of approximately of 1000 mL caused by uterine atony or genital tract trauma. For a hemorrhage greater than 2500 mL, the incidence was approximately 14%. In patients with PAS, large-volume hemorrhage is more common, but the presence of coagulopathy correlates with the severity of blood loss. For example, in one observational study, 60% of PAS cases with massive hemorrhage (median blood loss, 6 L) had fibrinogen levels < 200 mg/dL at the time of initial blood sampling. For hemorrhage due to uterine atony and birth trauma, the incidence of a prolonged PT or aPTT is rare with blood loss < 3000 mL, and correlates with the volume of bleeding (see Table 37.5 ). In a prospective cohort study of 518 patients with PPH, a linear fall in nearly all clotting factors levels, except platelets and factor VIII, was reported with increasing volume of blood loss.

In contrast, for PPH associated with placental abruption and amniotic fluid embolism, coagulopathy can occur early, is severe, and is unrelated to blood loss severity; severe hypofibrinogenemia and hyperfibrinolysis are common features. Several observational studies have found that cases with placental abruption or amniotic fluid embolism had the greatest proportion of patients with hypofibrinogenemia. Acute obstetric coagulopathy , a distinct coagulopathic phenotype, is characterized by markedly elevated markers of fibrinolysis, hypofibrinogenemia, dysfibrinogenemia, and reduced factor V and VIII levels. This particular phenotype is rare, is not correlated with blood loss volume, is most commonly seen with placental abruption and amniotic fluid embolism, but can occur with any PPH etiology, and often requires massive hemostatic support.

In summary, the likelihood of coagulopathy is most common with placental abruption and amniotic fluid embolism, but can still occur regardless of hemorrhage etiology, and is usually related to the severity of blood loss. Therefore, patients with a known coagulopathy, suspected abruption, amniotic fluid embolism, or a PPH greater than 2000 mL should undergo an evaluation for coagulopathy, especially during the setting of ongoing severe blood loss.