Key Abbreviations
Bilevel positive airway pressure BiPAP
Continuous positive airway pressure CPAP
Fresh frozen plasma FFP
Packed red blood cells pRBCs
Obstetric hemorrhage is one of the leading causes of maternal morbidity and mortality throughout the world. Hemorrhage following delivery is the leading reason for an obstetric admission to the intensive care unit (ICU), and it is responsible for one third of all pregnancy-related deaths in both high- and low-income countries. Therefore it is critical for the obstetrician to have a thorough understanding of the hemodynamic changes that accompany pregnancy, the maternal adaptations that occur with excessive blood loss, and the management principles for obstetric hemorrhage.
Pregnancy-Related Hemodynamic Changes
Pregnancy is associated with five significant hemodynamic changes (see Chapter 3 ). The first of these changes is plasma volume expansion. The average singleton pregnancy is accompanied by a 40% to 50% increase in plasma volume by the thirtieth week of gestation. This increase in plasma volume occurs along with the second change, an increase in red blood cell (RBC) mass . With appropriate substrate availability, RBC mass can be expected to increase 20% to 30% by the end of pregnancy. Third, maternal cardiac output rises with normal pregnancy owing to both increased stroke volume and increased heart rate. According to consensus, the average rise in cardiac output is 30% to 50% above nonpregnant levels, and the peak occurs in the early third trimester. Fourth, systemic vascular resistance falls in parallel with this rise in cardiac output and blood volume expansion. Fifth, fibrinogen and the majority of procoagulant blood factors (II, VII, VIII, IX, and X) increase during pregnancy. These five changes are protective of maternal hemodynamic status and thus allow for certain physiologic adaptations that accompany obstetric hemorrhage.
Physiologic Adaptation to Hemorrhage
During pregnancy and the puerperium, a defined sequence of physiologic adaptations occurs with hemorrhage ( Fig. 18-1 ). When 10% of the circulatory blood volume is lost, vasoconstriction occurs in both the arterial and venous compartments in order to maintain blood pressure and to preserve blood flow to essential organs. As blood loss reaches 20% or more of the total blood volume, increases in systemic vascular resistance can no longer compensate for the lost intravascular volume, and blood pressure decreases with a commensurate rise in heart rate. Cardiac output falls in parallel because of a loss in preload that results in poor end-organ perfusion. If the intravascular volume is not appropriately replaced, shock will ensue.
In severe preeclampsia (PE), these physiologic adaptations are altered. Unlike in most pregnant women, the protective mechanism of blood volume expansion is diminished with severe PE. It is estimated that plasma volume expansion is 9% lower in the setting of PE. In addition, because of the significant vasoconstriction that accompanies PE, blood loss in these patients may be underestimated because blood pressure is often maintained in the normotensive range. Finally, oliguria may not be as reliable an indicator of poor end-organ perfusion secondary to hemorrhage because reduced urine output is often a manifestation of the severity of PE.
Classification of Hemorrhage
A standard classification for acute blood loss is illustrated in Table 18-1 . Understanding the physiologic responses that accompany varying degrees of volume deficit can assist the clinician when caring for hemorrhaging patients. Determination of the hemorrhage class reflects the volume deficit, which may not be the same as the volume loss. The average 70-kg pregnant woman maintains a blood volume of 6000 mL by 30 weeks of gestation (85 mL/kg).
| CLASS | ACUTE BLOOD LOSS (mL) | % LOST | PHYSIOLOGIC RESPONSE |
|---|---|---|---|
| 1 | 1000 | 15 | Dizziness, palpitations, minimal blood pressure change |
| 2 | 1500 | 20-25 | Tachycardia, tachypnea, sweating, weakness, narrowed pulse pressure |
| 3 | 2000 | 30-35 | Significant tachycardia and tachypnea, restlessness, pallor, cool extremities |
| 4 | ≥2500 | 40 | Shock, air hunger, oliguria or anuria |
Class 1 hemorrhage corresponds to approximately 1000 mL of blood loss. This blood loss correlates to a 15% volume deficit. Women with this amount of volume deficit exhibit mild physiologic changes such as dizziness and palpitations owing to the hemodynamic adaptations that accompany normal pregnancy.
Class 2 hemorrhage is characterized by 1500 mL of blood loss, or a 20% to 25% volume deficit. Early physical changes that occur during a hemorrhage of this class include tachycardia and tachypnea . Although tachycardia is usually recognized as a compensatory mechanism to increase cardiac output, the significance of tachypnea is unclear and is often unappreciated clinically. Tachypnea can represent a sign of impending clinical decompensation. Narrowing of the pulse pressure is another sign of a class 2 hemorrhage. The pulse pressure represents the difference between the systolic and diastolic blood pressures. Systolic blood pressure is a good representation of stroke volume and β 1 stimulation. Diastolic blood pressure is a reflection of systemic vasoconstriction; therefore the pulse pressure represents the interrelationship between these entities. With a class 2 volume deficit, the sympathoadrenal system is activated, which results in a diversion of blood away from nonvital organs (skin, muscle, and kidney) and a redistribution of the circulation to vital body organs, including the brain and heart. The end result is increased vasoconstriction, increased diastolic blood pressure, maintenance of systolic blood pressure, and a narrowing of the pulse pressure. With greater narrowing of the pulse pressure, more compensatory vasoconstriction occurs to accommodate for a loss in stroke volume. A final physiologic response of class 2 hemorrhage is orthostatic hypotension. Although blood pressure comparisons can be made in the supine, sitting, and standing positions to document this response, a practical approach is to assess the time needed to refill a blanched hypothenar area on the patient’s hand. Typically, a patient with normal volume status can reperfuse this area within 1 to 2 seconds after pressure is applied. A patient with a class 2 hemorrhage and orthostatic hypotension will have significant reperfusion delay.
Class 3 hemorrhage is defined as a blood loss of 2000 mL and corresponds to a volume deficit of 30% to 35%. Within this hemorrhage class, the physiologic responses noted in class 2 hemorrhage are exaggerated. Patients demonstrate significant tachycardia (120 to 160 beats/min), tachypnea (30 to 50 breaths/min), overt hypotension, restlessness, pallor, and cool extremities.
Class 4 hemorrhage is characterized by more than 2500 mL of blood loss. This amount of blood loss exceeds 40% of the patient’s total blood volume. The clinical manifestations of this volume deficit include absent distal pulses, shock, air hunger, and oliguria or anuria. When significant hemorrhage occurs, renal blood flow is reduced and is redirected from the outer renal cortex to the juxtamedullary region. In this region, increased water and sodium absorption occur and result in decreased urine volume, lower urinary sodium concentration, and increased urine osmolarity. A urine sodium concentration less than 10 to 20 mEq/L or a urine/serum osmolar ratio greater than 2 indicates significantly reduced renal perfusion in the face of hemorrhage.
Antepartum Hemorrhage
Placental Abruption
Definition and Pathogenesis
Placental abruption, or abruptio placentae, refers to the premature separation of a normally implanted placenta from the uterus prior to delivery of the fetus. The diagnosis is typically reserved for pregnancies at greater than 20 weeks of gestation. Abruption is characterized by defective maternal vessels in the decidua basalis, which rupture and cause the separation. On rare occasions, the separation may be caused by a disruption of the fetal-placental vessels. These damaged vessels cause bleeding, which results in a decidual hematoma that may promote placental separation, destruction of placental tissue, and a loss of maternal-fetal surface area for nutrient and gas exchange.
Whereas some placental abruptions may occur acutely after a sudden mechanical event (e.g., blunt trauma, sudden uterine decompression, or motor vehicle accident), most cases result from more chronic processes. Abnormal development of the spiral arteries can lead to decidual necrosis, inflammation, infarction, and bleeding due to vascular disruption. Thrombin, which is released in response to decidual hemorrhage or hypoxia, appears to play an active role in the pathogenesis of placental abruption. Thrombin acts as a direct uterotonic, enhances the action of matrix metalloproteinases, upregulates apoptosis genes, increases the expression of inflammatory cytokines, triggers the coagulation cascade, and initiates functional progesterone withdrawal. These thrombin-mediated events initiate a cyclic pathway of vascular disruption, hemorrhage, inflammation, contractions, and rupture of membranes.
Incidence
The overall incidence of placental abruption is approximately 1 in 100 births ; however, a range of 1 in 80 to 1 in 250 deliveries has been reported. The range in incidence likely reflects variable criteria for diagnosis as well as an increased recognition in recent years of milder forms of abruption. About one third of all antepartum bleeding can be attributed to placental abruption, which peaks in the third trimester; 40% to 60% of abruptions occur prior to 37 weeks of gestation.
Clinical Manifestations
Several factors determine the clinical manifestations of placental abruption. These factors include (1) the temporal nature of the abruption (acute vs. chronic), (2) clinical presentation (overt vs. concealed), and (3) severity. An acute, overt abruption typically presents with vaginal bleeding, abdominal pain, and uterine contractions. As the placental separation worsens, uterine tenderness, tachysystole, fetal heart rate (FHR) patterns consistent with hypoxia, and fetal death may occur. The amount of vaginal bleeding correlates poorly with the extent of placental separation and its potential for fetal compromise. In fact, concealed abruption occurs in 10% to 20% of cases. With severe abruptions, more than 50% of the placental surface area separates. With extensive abruption, a significant risk for fetal death exists, and maternal compromise in the form of consumptive coagulopathy may result from the triggering of the clotting cascade by hemorrhage and extensive thrombin deposition.
Chronic abruption may be insidious in its presentation and is often associated with ischemic placental disease. Typically, these cases present with intermittent, light vaginal bleeding and evidence of chronic placental inflammation and dysfunction, such as oligohydramnios, fetal growth restriction, preterm labor, premature preterm rupture of membranes (PPROM), and PE.
Risk Factors
Although the exact etiology of placental abruption is unclear, a variety of risk factors have been identified ( Box 18-1 ).
Increasing parity and maternal age
Maternal substance use
- •
Cigarette smoking
- •
Cocaine abuse
- •
Trauma
Maternal diseases
- •
Hypertension
- •
Hypothyroidism
- •
Asthma
- •
Preterm premature rupture of membranes
Rapid uterine decompression associated with multiple gestation and polyhydramnios
Uterine and placental factors
- •
Anomalies
- •
Synechiae
- •
Fibroids
- •
Cesarean scar
- •
Abnormal placental formation
- •
Chronic ischemia
- •
Prior abruption
Hyperhomocysteinemia
Increasing Parity and Maternal Age
Several studies have noted a higher incidence of placental abruption with increasing parity . Among primigravid women, the frequency of placental abruption is less than 1%; however, 2.5% of grand multiparas experience placental abruption. Theories suggest that damaged endometrium, impaired decidualization, and aberrant vasculature may have causal roles with increasing parity or age.
Maternal age is often cited as an associated risk factor for placental abruption. Although a 15-year population-based study in Norway was able to demonstrate a strong relationship between maternal age and placental abruption for all levels of parity, others studies suggest that there is no increased risk for placental abruption among older women when parity and hypertensive disease are excluded.
Maternal Substance Abuse
Cigarette smoking is associated with a significantly increased incidence of placental abruption and fetal death. There appears to be a dose-response relationship with the number of cigarettes smoked and the risks for placental abruption and fetal loss. Compared with nonsmokers, smokers have a 40% increased risk for fetal death from placental abruption with each pack of cigarettes smoked. In addition, smoking and hypertensive disease appear to have an additive effect on the likelihood of placental abruption. Proposed etiologies include placental hypoperfusion with resulting decidual ischemia and necrosis.
Cocaine abuse in the third trimester has been associated with as high as a 10% placental abruption rate . The pathogenesis appears to be related to cocaine-induced vasospasm with subsequent decidual ischemia, reflex vasodilation, and vascular disruption within the placental bed.
Trauma
Blunt or penetrating trauma to the gravid abdomen has been associated with placental abruption. After a minor trauma, the risk for placental abruption is between 7% and 9%, whereas the risk may be as high as 13% after severe injury. The two most common causes of maternal trauma are motor vehicle crashes and domestic abuse. With motor vehicle crashes, uterine stretch, direct penetration, and placental shearing from acceleration-deceleration forces are the primary etiologies of trauma-related placental abruption (see Chapter 26 ).
Maternal Diseases
Maternal hypertension has been the most consistently identified risk factor for placental abruption. This relationship has been observed with both chronic and pregnancy-related hypertensive disease. Compared with normotensive women, hypertensive women have a fivefold increased risk for placental abruption. Unfortunately, antihypertensive therapy has not been shown to reduce the risk for placental abruption in women with chronic hypertension.
Maternal subclinical hypothyroidism and asthma have also been associated with placental abruption in some studies.
Preterm Premature Rupture of Membranes
Placental abruption occurs in 2% to 5% of pregnancies with PPROM. Intrauterine infection and oligohydramnios significantly increase the risk for placental abruption, and nonreassuring FHR patterns occur in nearly half of these pregnancies.
It is unclear whether placental abruption is the cause or consequence of PPROM. Hemorrhage and associated thrombin generation may stimulate cytokine and protease production, which results in membrane rupture. Alternatively, the cytokine-protease cascade that follows ruptured membranes may cause damage to the decidual vasculature, which predisposes the placenta to separation.
Rapid Uterine Decompression Associated with Multiple Gestations and Polyhydramnios
Rapid decompression of an overdistended uterus can precipitate an acute placental abruption. This may occur in the setting of multiple gestations or with polyhydramnios. Compared with singletons, twins have been reported to have nearly a threefold increased risk for placental abruption. Although the exact timing of placental abruption in multiple gestations is difficult to ascertain, it has been attributed to rapid decompression of the uterus after the delivery of the first twin. Likewise, rapid loss of amniotic fluid in pregnancies complicated by polyhydramnios has been implicated in placental abruption. This can occur with spontaneous rupture of membranes or may follow therapeutic amniocentesis. For this reason, controlled artificial rupture of membranes with induction of labor may be advisable if significant polyhdramnios complicates pregnancy.
Uterine and Placental Factors
Suboptimal placental implantation in patients with uterine anomalies, synechiae, fibroids, and cesarean scars is associated with abruption. In addition, abnormal placental formation (e.g., circumvallate placenta) or chronic ischemia associated with PE and fetal growth restriction have been implicated in placental abruption.
Prior Abruption
Women who have had a previous abruption are at significant risk for recurrent abruption. After one abruption, the recurrence risk is 5% to 15%, whereas the risk increases to 20% to 25% after two abruptions. The risk of recurrence is greater after a severe abruption. When an abruption is associated with fetal demise, there is a 7% incidence of the same outcome in a future gestation.
Thrombophilia
Inconsistent data exist regarding an association among thrombophilias and placental abruptions. Hyperhomocysteinemia (a fasting homocysteine level >15 µmol/L) may be associated with recurrent abruption.
Diagnosis
Placental abruption is primarily a clinical diagnosis that is supported by radiographic, laboratory, and pathologic studies. Any findings of vaginal bleeding, uterine contractions, abdominal and/or back pain, or trauma should prompt an investigation for potential placental abruption. Vaginal bleeding may range from mild to severe. Unfortunately, bleeding may be underestimated because it can be retained behind the placenta. The typical abruption contraction pattern is high frequency and low amplitude; however, it may simulate labor in some circumstances.
Radiology
Although early studies that evaluated the use of ultrasound for the diagnosis of placental abruption identified less than 2% of cases, recent advances in imaging and its interpretation have improved detection rates. Early hemorrhage is typically hyperechoic or isoechoic, whereas resolving hematomas are hypoechoic within 1 week and sonolucent within 2 weeks of the abruption. Acute hemorrhage may be misinterpreted as a homogeneous thickened placenta or fibroid.
Ultrasound can identify three predominant locations for placental abruption. These are subchorionic (between the placenta and the membranes), retroplacental (between the placenta and the myometrium), and preplacental (between the placenta and the amniotic fluid). Figure 18-2 illustrates the classification of hematomas in relation to the placenta. Figure 18-3 demonstrates a sonographic representation of a subchorionic abruption.
The location and extent of the placental abruption identified on ultrasound examination is of clinical significance. Retroplacental hematomas are associated with a worse prognosis for fetal survival than subchorionic hemorrhage. The size of the hemorrhage is also predictive of fetal survival. Large retroplacental hemorrhages (>60 mL) have been associated with a 50% or greater fetal mortality, whereas similarly sized subchorionic hemorrhages are associated with a 10% mortality risk.
Magnetic resonance imaging (MRI) has been used occasionally for the diagnosis of placental abruption when sonography is equivocal.
Laboratory Findings
Few laboratory studies assist in the diagnosis of placental abruption. Hypofibrinogenemia and evidence of consumptive coagulopathy may accompany severe abruption ; however, clinical correlation is necessary. Moreover, most abruptions are not accompanied by maternal coagulopathy.
Abnormal serum markers early in pregnancy, such as an unexplained elevated maternal serum α-fetoprotein (MSAFP) or human chorionic gonadotropin (hCG) and decreased pregnancy-associated plasma protein A (PAPP-A) or estriol, have been associated with an increased risk for subsequent placental abruption.
Pathologic Studies
Macroscopic inspection of the placenta may demonstrate adherent clot and depression of the placental surface. Fresh or acute placental abruptions may not have any identifiable evidence on gross pathologic examination, but histologic analysis may show preservation of the villous stroma, eosinophilic degeneration of the syncytiotrophoblast, and scattered neutrophils with villous agglutination. Chronic abruptions may demonstrate histologic signs of chronic deciduitis, maternal floor decidual necrosis, villitis, decidual vasculopathy, infarction, intervillous thrombosis, villous maldevelopment, and hemosiderin deposition.
Management
Both maternal and fetal complications may occur with placental abruption. Maternal complications include blood loss, consumptive coagulopathy, need for transfusion, end-organ damage, cesarean delivery, and death. Fetal complications include intrauterine growth restriction (IUGR), oligohydramnios, prematurity, hypoxemia, and stillbirth. Although maternal complications are related to the severity of the abruption, fetal complications are related to both the severity and timing of the hemorrhage.
Despite its relative frequency, no randomized trials and few studies have examined management approaches for placental abruption. Typically, management of placental abruption depends on the severity, gestational age, and maternal-fetal status. Once the diagnosis of placental abruption has been made, precautions should be taken to anticipate the possible life-threatening consequences for both mother and fetus. These precautions include baseline laboratory assessment (hemoglobin, hematocrit, platelet count, type and screen, fibrinogen, and coagulation studies), appropriate intravenous (IV) access (large-bore catheter), availability of blood products, continuous FHR and contraction monitoring, and communication with operating room (OR) and neonatal personnel.
Small placental abruptions remote from term (<34 weeks) may be managed expectantly. With cases of chronic abruption, clinical circumstances that include gestational age and the extent of the abruption influence the need for prolonged hospitalization until delivery. In many cases, a cyclic event of bleeding, thrombin generation, contractions, and further placental separation occurs. Tocolysis may help prevent contractions and thus may break the abruption cycle. If the maternal-fetal status is stable, a trial of tocolysis for documented preterm labor and administration of antenatal corticosteroid therapy can be considered. Whereas the choice of tocolysis should be individualized, magnesium sulfate administration may confer an added benefit of fetal neuroprotection. Reported series of expectant management in preterm gestations with placental abruption have shown a significant prolongation of the pregnancy (>1 week) in more than 50% of patients without adverse maternal or fetal outcomes. In a large series of preterm patients who presented with placental abruption and received tocolysis, about one third delivered within 48 hours of admission, one third delivered within 7 days, and one third delivered more than 1 week from initial presentation. No cases of intrauterine demise were reported in women who presented with a live fetus. Although these results are encouraging, the clinician must always keep in mind that placental abruption can result in both maternal and fetal morbidity. Any attempt to arrest preterm labor in a known or suspected placental abruption must be weighed against the likelihood of neonatal survival and morbidity, the severity of the abruption, and the safety of the mother.
Women who present at or near term with a placental abruption should undergo delivery. Induction or augmentation of labor is not contraindicated in the setting of an abruption; however, close surveillance for any evidence of maternal or fetal compromise is advised. Continuous FHR monitoring is recommended because 60% of fetuses may exhibit intrapartum heart rate patterns consistent with hypoxia. Intrauterine pressure catheter (IUPC) placement and internal FHR monitoring can assist the clinician during the intrapartum course. IUPC monitoring may demonstrate elevated uterine resting tone, which can be associated with fetal hypoxia. Maternal hemodynamic and clotting parameters must be followed closely to detect signs of evolving coagulopathy. Although vaginal delivery is generally preferable, operative delivery is often necessary owing to fetal or maternal decompensation. When cesarean delivery is required, a rapid decision-to-delivery time is optimal because an interval of less than 20 minutes from the onset of fetal bradycardia is associated with improved outcomes. A Couvelaire uterus, also known as uteroplacental apoplexy, is characterized by extravasation of blood into the myometrium; it may be noted in some cases and is often associated with significant uterine atony. Administration of uterotonic therapy usually improves the condition. Hysterectomy should be reserved for cases of atony and hemorrhage unresponsive to conventional uterotonic therapies and replacement of blood products.
The management of women with consumptive coagulopathy and fetal demise requires a thorough knowledge of the natural history of severe placental abruption. Nearly five decades ago, Pritchard and Brekken noted several clinically important observations: (1) about 40% of patients with placental abruption and fetal demise will demonstrate signs of consumptive coagulopathy; (2) within 8 hours of initial symptoms, hypofibrinogenemia will be present; (3) severe hypofibrinogenemia will not recover without blood product replacement; and (4) the time course for recovery from hypofibrinogenemia is roughly 10 mg/dL per hour after delivery of the fetus and placenta.
When managing women with severe placental abruptions and fetal demise, maintenance of maternal volume status and replacement of blood products is essential. Although operative delivery may appear to lead to the most rapid resolution of the problem, it may pose significant risks to the patient. Unless the consumptive coagulopathy is corrected, surgery can result in uncontrollable bleeding and an increased need for hysterectomy. The uterus does not need to be evacuated before coagulation status can be restored. Blood product replacement and delayed delivery until hematologic parameters have improved are generally associated with good maternal outcomes.
Neonatal Outcome
Placental abruption is associated with increased perinatal morbidity and mortality. When compared with normal pregnancies, pregnancies complicated by abruption have a tenfold increased risk for perinatal death. A case-control study has also shown a greater risk for adverse long-term neurobehavioral outcomes in infants delivered after placental abruption. Neonates at risk for abnormal outcomes had higher incidences of abnormal FHR tracings (45%) and emergency cesarean deliveries (53%) compared with controls (10% and 10%, respectively). Finally, hypoxia-associated periventricular leukomalacia and sudden infant death syndrome (SIDS) are more common in newborns delivered after placental abruptions.
Placenta Previa
Definition and Pathogenesis
Placenta previa is defined as the presence of placental tissue over or adjacent to the cervical os. Traditionally, four variations of placenta previa were recognized: 1) complete, 2) partial, 3) marginal, and 4) low lying. Although complete placenta previa has been the term used to refer to the total coverage of the internal cervical os by placental tissue, the differences among the terms partial (placental edge partially covering the internal cervical os), marginal (placental edge at the margin of the internal cervical os), and low lying (placental edge within 2 cm of the interval cervical os) were often subtle and varied by the timing and method of diagnosis. Improved ultrasound technology and precision have allowed for more accurate assessments of the placental location in relation to the cervical os. Recent revised classification of placenta previa consists of two variations: true placenta previa, in which the internal cervical os is covered by placental tissue, and low-lying placenta, in which the placenta lies within 2 cm of the cervical os but does not cover it. Although not a true placenta previa, low-lying placentas are associated with increased risks for bleeding and other adverse pregnancy events.
Incidence
The overall reported incidence of placenta previa at delivery is 1 in 200 births. In the second trimester, placenta previa may occur in up to 6% of pregnancies. The term placental migration has been used to explain this “resolution” of placenta previa that is noted near term. Three theories have been suggested to account for this phenomenon. The first hypothesis proposes that as the pregnancy advances, the stationary lower placental edge relocates away from the cervical os with the development of the lower uterine segment. Indeed, the lower uterine segment has been noted to increase from 0.5 cm at 20 weeks to more than 5 cm at term. Secondly, the placenta-free uterine wall has been proposed to grow at a faster rate than the uterine wall covered by the placenta. A final hypothesis suggests that trophotropism, the growth of trophoblastic tissue away from the cervical os toward the fundus, results in resolution of the placenta previa.
Clinical Manifestations
Placenta previa typically presents as painless vaginal bleeding in the second or third trimester. The bleeding is believed to occur from disruption of placental blood vessels in association with the development and thinning out of the lower uterine segment. Between 70% and 80% of patients with placenta previa will have at least one bleeding episode. About 10% to 20% of patients present with uterine contractions before bleeding, and fewer than 10% remain asymptomatic until term. Of those with bleeding, one third of women will present before 30 weeks of gestation, one third between 30 and 36 weeks, and one third after 36 weeks. Early-onset bleeding (<30 weeks) carries with it the greatest risk for blood transfusion and associated perinatal morbidity and mortality.
Risk Factors
Several risk factors for placenta previa have been noted ( Box 18-2 ). Additionally, some reports have documented a higher association of fetal malpresentation, preterm labor, PPROM, IUGR, congenital anomalies, and amniotic fluid embolism with placenta previa.
Intrinsic maternal factors
- •
Increasing parity
- •
Advanced maternal age
- •
Maternal race
- •
Extrinsic maternal factors
- •
Cigarette smoking
- •
Cocaine use
- •
Residence at higher elevation
- •
Infertility treatments
- •
Fetal factors
- •
Multiple gestations
- •
Male fetus
- •
Prior placenta previa
Prior uterine surgery and cesarean delivery
Intrinsic Maternal Factors
Studies have reported more cases of placenta previa with increasing parity . Grand multiparas have been reported to have a 5% risk for placenta previa compared with 0.2% among nulliparous women. Maternal age also seems to influence the occurrence of placenta previa. Women older than 35 years of age have more than a fourfold increased risk for placenta previa, and women older than 40 years of age have a ninefold greater risk. Finally, maternal race has been associated with placenta previa. In a large population-based cohort, the rate of placenta previa among white, black, and other races was 3.3, 3, and 4.5 per 1000 births, respectively. Asian women appear to have the highest rates of placenta previa.
Extrinsic Maternal Factors
Cigarette smoking has been associated with as high as a threefold increased risk for previa formation. Likewise, a case-control study has demonstrated that maternal cocaine use increases the risk of placenta previa fourfold. Residence at higher elevations may also contribute to previa development. The need for increased placental surface area secondary to decreased uteroplacental oxygenation may play a role in this association. Finally, prior infertility treatment is statistically associated with higher rates of placenta previa.
Fetal Factors
Controversy exists regarding an increased risk for placenta previa with multiple gestations. Although some studies have shown a higher incidence of placenta previa among twins, others have not documented a significantly increased risk. A consistently higher proportion of offspring in women with placenta previa are male. This association is unexplained; however, two theories suggest larger placental sizes among male fetuses and delayed implantation of the male blastocyst in the lower uterine segment.
Prior Placenta Previa
Having had a prior placenta previa increases the risk for the development of another previa in a subsequent pregnancy. This association has been reported to be as high as an eightfold relative risk. The exact etiology for this increased risk is unclear.
Prior Uterine Surgery and Prior Cesarean Delivery
Prior uterine surgery has been associated with placenta previa formation. Although a history of curettage and/or myomectomy attends a slightly elevated previa risk, prior cesarean delivery has been the most consistent risk factor. In the pregnancy following a cesarean delivery, the risk for placenta previa has been reported to range from 1% to 4%. A linear increase is seen in placenta previa risk with the number of prior cesarean deliveries. Placenta previa occurs in 0.9% of women with one prior cesarean delivery, in 1.7% of women with two prior cesarean deliveries, and in 3% of those with three or more cesarean deliveries. In patients with four or more cesarean deliveries, the risk for placenta previa has been reported to be as high as 10%. Endometrial scarring is thought to be the etiologic factor for this increased risk.
Diagnosis
The timing of the diagnosis of placenta previa has undergone significant change in the past four decades. Painless third-trimester bleeding was a common presentation for placenta previa in the past, whereas most cases of placenta previa are now detected antenatally with ultrasound prior to the onset of significant bleeding.
Radiology
Transabdominal and transvaginal ultrasound provide the best means for diagnosing placenta previa. Although transabdominal ultrasound can detect at least 95% of placenta previa cases, transvaginal ultrasound has a reported diagnostic accuracy that approaches 100%. Typically, a combined approach can be used in which transabdominal ultrasound is the initial diagnostic modality, followed by transvaginal ultrasound for uncertain cases. Transvaginal ultrasound is safe and is not contraindicated in these circumstances. Of note, quality images can be obtained using transvaginal ultrasound without the probe contacting the cervix ( Fig. 18-4 ).
If a placenta previa or low-lying placenta is diagnosed in the second trimester, repeat sonography should be obtained in the early third trimester at 32 weeks. More than 90% of the cases of placenta previa diagnosed in the second trimester resolve by term. The potential for placenta previa resolution is dependent on the timing of the diagnosis, extension over the cervical os, and placental location. For example, one study of 714 women with an ultrasound diagnosis of placenta previa noted that the earlier the diagnosis, the more likely the previa would resolve by term ( Table 18-2 ). In addition, complete placenta previa diagnosed in the second trimester will persist into the third trimester in 26% of cases, whereas a low-lying placenta will persist in only 2.5% of cases. Finally, anterior placenta previa is less likely to migrate away from the cervical os than posterior placement.
| GESTATIONAL AGE AT DIAGNOSIS (WK) | PREVIA AT TERM (%) |
|---|---|
| 15-19 | 12 |
| 20-23 | 34 |
| 24-27 | 49 |
| 28-31 | 62 |
| 32-35 | 73 |
Occasionally, MRI may be used to diagnose placenta previa. MRI is particularly helpful with posterior placenta previa identification and assessment of invasive placentation (see below).
Management
General management principles for patients with placenta previa in the third trimester include serial ultrasounds to assess placental location and fetal growth, avoidance of cervical examinations and intercourse, activity restrictions, counseling regarding labor symptoms and vaginal bleeding, dietary and nutrient supplementation to avoid maternal anemia, and early medical attention if any vaginal bleeding occurs.
Asymptomatic Placenta Previa
A recent working group has given specific recommendations for management of asymptomatic placenta previa at varying gestational ages. For pregnancies at greater than 16 weeks of gestation with a low-lying placenta (placental edge within 2 cm from the internal cervical os) or a placenta previa, repeat ultrasound to assess placental location is recommended at 32 weeks. If a low-lying placenta or placenta previa persists at 32 weeks, repeat sonography is again obtained at 36 weeks.
Asymptomatic women with placenta previa may be managed expectantly as outpatients. Although some sonographic features have been associated with a higher likelihood of bleeding—such as complete placental coverage of the cervical os, a thickened placental edge, echo-free placental space over the cervical os, and cervical length less than 3 cm—it is not possible to predict all cases of bleeding that result from placenta previa. With this in mind, asymptomatic patients should be instructed to avoid activities that may stimulate uterine contractions and/or cervical irritation, such as strenuous exercise, intercourse, and digital cervical examinations. Several studies have documented the safety, efficacy, and cost savings of outpatient management for asymptomatic placenta previa. Candidates for outpatient management must (1) be compliant, (2) live within a short commute from the hospital, (3) have 24-hour emergency transportation to the hospital, and (4) verbalize a thorough understanding of the risks associated with placenta previa.
Bleeding Placenta Previa
Women with placenta previa who present with acute vaginal bleeding require hospitalization and immediate evaluation to assess maternal-fetal stability. They should initially be managed in a labor and delivery unit with hemodynamic surveillance of the mother and continuous FHR monitoring. Large-bore IV access and baseline laboratory studies (hemoglobin, hematocrit, platelet count, blood type and screen, and coagulation studies) should be obtained. If the pregnancy is less than 34 weeks of gestation, administration of antenatal corticosteroids should be undertaken as well as an assessment of the facility’s emergency resources for both the mother and the neonate. In some cases, maternal transport and consultation with a maternal-fetal medicine specialist and a neonatologist may be warranted. Finally, tocolysis may be used if the vaginal bleeding is preceded by or associated with uterine contractions. Whereas various agents have been used, magnesium sulfate is often preferred as a first-line agent because of its limited potential for hemodynamic-related maternal side effects and its added benefit for fetal neuroprotection.
Once stabilized, most women with symptomatic placenta previa can be maintained on hospitalized bed rest and expectantly managed. In several observational studies, 50% of women with bleeding placenta previa were undelivered in 4 weeks, including those with initial bleeding episodes of more than 500 mL. Minimizing maternal anemia by using blood conservation techniques is recommended. Although some patients may require transfusion, many patients can be supplemented with iron replacement (oral or IV), vitamin C to enhance oral iron absorption, and B vitamins. Erythropoietin may be used in selected cases to hasten red cell formation. Lastly, autologous donation may be considered in patients with hemoglobin concentrations greater than 11 g/dL.
Although maternal hemorrhage is of the utmost concern, fetal blood can also be lost during the process of placental separation with a bleeding placenta previa. Rh0(D) immune globulin should be given to all Rh-negative unsensitized women with third-trimester bleeding from placenta previa. A Kleihauer-Betke preparation of maternal blood should be considered. Occasionally, a fetomaternal hemorrhage of greater than 30 mL occurs that necessitates additional doses of Rh0(D) immune globulin. One study noted that 35% of infants whose mothers received an antepartum transfusion were also anemic and required a transfusion following delivery.
Delivery
Cesarean delivery is indicated for all women with sonographic evidence of placenta previa and most women with low-lying placenta. When the placental distance is between 1 and 20 mm from the internal cervical os, the rate of cesarean delivery ranges from 40% to 90%. If a vaginal trial of labor is attempted for a low-lying placenta, precautions should be taken for the possibility of an emergent cesarean delivery and need for blood transfusion.
A consensus panel has given delivery-timing guidelines for uncomplicated placenta previa, which includes cases with normal fetal growth and no other pregnancy-associated complications. Cesarean delivery of asymptomatic placenta previa should occur between 36 0/7 and 37 0/7 weeks of gestation. In cases of complicated placenta previa, delivery should occur immediately regardless of gestational age. Complicated placenta previa includes bleeding associated with a nonreassuring fetal heart pattern despite resuscitative measures, life-threatening maternal hemorrhage, and/or refractory labor.
When performing a cesarean delivery for placenta previa, the surgeon should be aware of the potential for rapid blood loss during the delivery process. Blood products that are cross-matched should be readily available for delivery. In addition, before incising the lower uterine segment, the surgeon should assess the vascularity of this region. Although a low transverse incision is not contraindicated in patients with placenta previa, performing a vertical uterine incision may be preferable in some cases. This is particularly true with an anterior placenta previa. Ideally, the placenta should not be disrupted when entering the uterus. If disruption occurs, expedited delivery is essential. Given the potential for invasive placentation, the physician should allow the placenta to spontaneously deliver. If it does not separate easily, precautions should be taken for placenta accreta management (see below). Once the placenta separates, bleeding is controlled by the contraction of uterine myometrial fibers around the spiral arterioles. Because the lower uterine segment often contracts poorly, significant bleeding may occur from the placental implantation site. Aggressive uterotonic therapy, surgical intervention, and/or tamponade techniques should be undertaken to rapidly control bleeding. Finally, some studies have shown reduced bleeding at the placental site with the injection of subendometrial vasopressin after delivery of the fetus.
Associated Conditions
Placenta Accreta
Definition and Pathogenesis
Placenta accreta represents the abnormal attachment of the placenta to the uterine lining due to an absence of the decidua basalis and an incomplete development of the fibrinoid layer. Variations of placenta accreta include placenta increta and placenta percreta, in which the placenta extends to or through the uterine myometrium, respectively ( Fig. 18-5 ).
Incidence and Risk Factors
The overall incidence of placenta accreta or one of its variations is 3 per 1000 deliveries. Based on histologic diagnosis, placenta accreta is the most common form of invasive placentation (79%) followed by placenta increta (14%) and placenta percreta (7%), respectively. The two most significant risk factors for placenta accreta are placenta previa and prior cesarean delivery. The risk for placenta accreta in patients with placenta previa and an unscarred uterus is approximately 3%. This risk dramatically increases with one or more cesarean deliveries ( Table 18-3 ). Even without a coexisting placenta previa, placenta accreta is more common in women with a prior cesarean delivery.
| NO. OF PRIOR CESAREAN DELIVERIES | PLACENTA ACCRETA RISK (%) |
|---|---|
| 0 | 3 |
| 1 | 11 |
| 2 | 40 |
| 3 | 61 |
| ≥4 | 67 |
Other reported risk factors include increasing parity and maternal age, submucosal uterine fibroids, prior uterine surgery, cesarean scar, and endometrial defects. Unlike placenta previa, a female fetus is more common with invasive placentation.
Clinical Manifestations
The clinical manifestations of placenta accreta are often similar to those of placenta previa; however, profuse bleeding usually follows attempted manual placental separation. Hematuria can be a feature of placenta percreta with bladder invasion.
Diagnosis
Most cases of placenta accreta are now diagnosed antenatally by advanced radiographic techniques. Prenatal diagnosis has been shown to improve maternal outcomes, resulting in less blood loss and decreased transfusion requirements.
Radiographic Techniques
Ultrasound is the preferred radiographic modality for the diagnosis of placenta accreta. Findings suggestive of placenta accreta include a loss of the normal hypoechoic retroplacental-myometrial zone, thinning and disruption of the uterine serosa–bladder wall interface, focal exophytic masses within the placenta, and numerous intraplacental vascular lacunae ( Fig. 18-6 ). A recent systemic review and meta-analysis of 23 studies that used prenatal sonographic identification of placenta accreta demonstrated a sensitivity of 90%, a specificity of 97%, a positive likelihood ratio of 11, and a negative likelihood ratio of 0.16.
Color Doppler ultrasound is also useful as an adjunctive tool in diagnosing placenta accreta. Specific color Doppler findings that differentiate placenta accreta from normal placentation include diffuse and focal intraparenchymal placental lacunar blood flow, hypervascularity of the bladder and uterine serosa, prominent subplacental venous complexes, and loss of subplacental Doppler vascular signals. Some color-flow mapping studies suggest that a myometrial thickness less than 1 mm with large intraplacental venous lakes is highly predictive of invasive placentation (sensitivity, 100%; specificity, 72%; positive predictive value, 72%; and negative predictive value, 100%).
In addition to the above ultrasound modalities, three-dimensional ultrasound has been used successfully to identify invasive placentation. Diagnostic criteria include irregular intraplacental vascularization and hypervascularity of the uterine serosa–bladder wall interface.
Finally, MRI can be used in conjunction with sonography to assess abnormal placental invasion. MRI is particularly helpful when ultrasound findings are equivocal, the placenta is in a posterior location, and for determination of the extent of placental invasion within surrounding tissue, such as the parametrium and bladder. In a review and meta-analysis of 1010 pregnancies at risk for placenta accreta, MRI had a diagnostic sensitivity of 94% and a specificity of 84%.
Laboratory Findings
Placenta accreta has been associated with unexplained elevations in maternal serum α-fetoprotein (MSAFP).
Pathologic Studies
Placenta accreta is confirmed by the pathologic examination of a hysterectomy specimen . Histologic evaluation demonstrates placental villi within the uterine myometrium and absence of a decidual plate. In focal accreta cases in which the uterus is not removed, curettage specimens may show myometrial cells adherent to the placenta.
Management
Because of its associated risk for massive postpartum hemorrhage, placenta accreta accounts for a large percentage of peripartum hysterectomies. A multidisciplinary team approach is the ideal way to manage these cases. Preoperative assessments by maternal-fetal medicine specialists, neonatologists, blood conservation teams, anesthesiologists, advanced pelvic surgeons, and urologists —especially for a suspected placenta percreta—are recommended. Timing of delivery depends upon clinical circumstances; however, most authorities favor delivery at 34 0/7 to 35 6/7 weeks with or without antenatal corticosteroid administration. Ideally, the delivery should be scheduled at a time with optimal personnel availability at a facility prepared to manage significant obstetric hemorrhage. Adequate IV access with two large-bore catheters and ample blood product availability are mandatory. Cell-saver technology, donor-directed or autologous blood donation, and recombinant VIIa should be considered. Placement of ureteral stents preoperatively or intraoperatively can assist in maintaining urinary tract integrity. When performing the surgery, it is recommended that the uterus be incised above the placental attachment site and that the placenta be left in situ after clamping the cord because disruption of the implantation site may result in rapid blood loss. Finally, adjuvant use of aortic and/or internal iliac artery balloon occlusion catheters with postsurgical embolization has been shown to reduce blood loss, transfusion requirements, and duration of surgery in some studies.
In specific circumstances, uterine conservation may be attempted. These situations include focal accreta, desired future fertility, and fundal or posterior placenta accreta. Uterine conservation techniques typically include leaving the placenta in situ at the delivery with subsequent expectant management, delayed manual placental removal, wedge resection or oversewing of the placental implantation site, tamponade of the lower uterine segment, curettage, uterine artery embolization, hemostatic sutures, arterial ligation, and/or administration of methotrexate. Although each of these techniques has reported success, each is also associated with potential complications, including delayed hemorrhage, infection, fistula formation, subsequent surgery and/or hysterectomy, uterine necrosis, and even death. Data are limited regarding long-term reproductive outcomes in women treated conservatively for invasive placentation. Although most women are able to conceive after conservative management, they remain at risk for spontaneous abortion, uterine synechiae and rupture, preterm delivery, recurrent placenta accreta, and peripartum hysterectomy.
Vasa Previa
Definition and Pathogenesis
Vasa previa is defined as the presence of fetal vessels over the cervical os. Typically, these fetal vessels lack protection from Wharton jelly (velamentous cord insertion) and are prone to rupture and compression. When the vessels rupture, the fetus is at high risk for exsanguination. Velamentous cord insertion may occur without vasa previa and can occasionally exist as fetal vessels that run between a bilobed or succenturiate-lobed placenta.
Incidence and Risk Factors
The overall incidence of vasa previa is 1 in 2500 deliveries; however, data have shown a range from 1 in 2000 to 1 in 5000 deliveries. Reported risk factors for vasa previa include bilobed and succenturiate-lobed placentas; pregnancies that result from assisted reproductive technology (ART); multiple gestations; and history of second-trimester placenta previa or low-lying placenta.
Clinical Manifestations
In the past, most cases of vasa previa presented after rupture of membranes with acute onset of vaginal bleeding from a lacerated fetal vessel. If immediate intervention was not provided, fetal bradycardia and subsequent fetal death occurred. Today, many cases of vasa previa are diagnosed antenatally by ultrasound. In rare cases, pulsating fetal vessels may be palpable in the membranes that overlie the cervical os.
Diagnosis
Vasa previa is often diagnosed antenatally by ultrasound with color and pulsed Doppler mapping. Transabdominal and transvaginal approaches are most often used. The diagnosis is confirmed by documenting umbilical vessels over the cervical os using color and pulsed Doppler imaging ( Fig. 18-7 ).
Management
When diagnosed antenatally, vasa previa should be managed similarly to placenta previa . Some authorities have recommended twice-weekly nonstress testing at 28 to 30 weeks of gestation to assess for cord compression; others have favored hospitalization in the third trimester with administration of antenatal corticosteroids, serial antepartum testing, and cesarean delivery between 34 0/7 to 36 0/7 weeks of gestation . If an intrapartum diagnosis of vasa previa is made, expeditious delivery is needed. Immediate neonatal blood transfusion is often required in these circumstances.
Postpartum Hemorrhage
Postpartum hemorrhage is an obstetric emergency that complicates between 1 in 20 and 1 in 100 deliveries. In the past decade, reported postpartum hemorrhage has increased 26% within the United States. Because it is a major cause of maternal morbidity and mortality, obstetricians need to have a clear understanding of normal delivery-related blood loss so that postpartum hemorrhage can be efficiently recognized and managed.
Normal Blood Loss and Postpartum Hemorrhage
Normal delivery-related blood loss depends on the type of delivery. Based on objective data, the mean blood losses for a vaginal delivery, cesarean delivery, and cesarean hysterectomy are 500, 1000, and 1500 mL, respectively. These values are often underestimated and unappreciated clinically owing to the significant blood volume expansion that accompanies normal pregnancy.
Postpartum hemorrhage has been variably defined in the literature. Definitions have included subjective assessments greater than the standard norms, a 10% decline in hemoglobin concentration, and the need for blood transfusion. A more practical definition is excessive delivery-related blood loss that causes the patient to be hemodynamically symptomatic and/or hypovolemic.
Postpartum Hemorrhage Etiologies
The etiologies of postpartum hemorrhage can be categorized as primary (early) or secondary (late). Primary postpartum hemorrhage refers to excessive bleeding that occurs within 24 hours of delivery, whereas secondary postpartum hemorrhage refers to bleeding that occurs from 24 hours until 12 weeks after delivery. Box 18-3 lists the most common causes of primary and secondary postpartum hemorrhage. Because primary postpartum hemorrhage is more common than the secondary kind, the remainder of this discussion focuses on its etiology and management ( Fig. 18-8 ).
Early
Uterine atony
Lower genital tract lacerations (perineal, vaginal, cervical, periclitoral, periurethral, rectum)
Upper genital tract lacerations (broad ligament)
Lower urinary tract lacerations (bladder, urethra)
Retained products of conception (placenta, membranes)
Invasive placentation (placenta accreta, placenta increta, placenta percreta)
Uterine rupture
Uterine inversion
Coagulopathy
Late
Infection
Retained products of conception
Placental site subinvolution
Coagulopathy
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