Vaginal Bleeding During the Second 20 Weeks of Pregnancy: Emergency Department Evaluation and Management Strategies for Maximizing Fetal and Maternal Outcomes
Vaginal Bleeding During the Second 20 Weeks of Pregnancy: Emergency Department Evaluation and Management Strategies for Maximizing Fetal and Maternal Outcomes
Author: Gary Hals, MD, PhD, Attending Physician, Department of Emergency Medicine, Palmetto Richland Memorial Hospital, Columbia, SC.
Peer Reviewers: David E. Manthey, MD, FAAEM, Director, Undergraduate Medical Education, Department of Emergency Medicine, Wake Forest University Baptist Medical Center, Winston-Salem, NC; and Gwen M. Allen, MD, Associate Professor, Department of OB/GYN, Wake-Forest University Winston-Salem, NC.
We have all been there, and the clinical decision-making process can be daunting: "Doctor," the nurse informs us, "the new patient in the OB-GYN room is having severe vaginal bleeding. She’s 26 weeks pregnant." This is a presentation that will quicken the pulse and raise the anxiety level of most emergency department (ED) physicians, even the most seasoned clinicians who fully appreciate the differential diagnosis and possible complications. Pregnant women with this chief complaint are especially stressful for the ED physician for a number of reasons. First, the clinician will be concerned that the mother may deliver a premature, but potentially viable child. Once a pregnancy has reached about 24 weeks, the fetus is potentially viable, but it may require critical, invasive interventions. In such cases, survival of the fetus may depend on appropriate, life-supporting interventions administered by the ED physician and/or neonatologist caring for the child during the first few minutes, or hours, of life.
Even in the absence of fetal delivery, the ED physician will usually simultaneously have to manage the care of two "patients," one of which (the fetus) primarily can be assessed only by data obtained from the fetal monitor or ultrasonographic evaluation. Another complicating factor is that although most ED physicians have adequate "book knowledge" about such cases, they often lack sufficient hands-on clinical experience. In this regard, most ED physicians are comfortable with precipitous term deliveries, but emergency resuscitation of a preterm infant presents an unfamiliar challenge. Most emergency medicine residency programs are based at medical centers with active obstetrical residencies; as a result, these patients oftentimes bypass the ED, entirely depriving the ED physician of first hand experience with these patients.
Although pregnancy is classically divided into 13-week trimesters, the approach to vaginal bleeding in pregnancy is to divide the pregnancy into the first half (< 20 weeks) and second half (> 20 weeks) of gestation. One factor justifying such a division is that conditions associated with late second-trimester bleeding are similar to that are produced during the third trimester. First-trimester bleeding is common, occurring in about 40% of pregnancies. In contrast, bleeding during the last half of gestation occurs in only 3-4% of all pregnancies, and is associated with a perinatal mortality rate of 23-32%.1
The purpose of this article is to review the current evidence-based recommendations related to the diagnosis and management of vaginal bleeding that occurs during the second half of pregnancy. Finally, the relative lack of experience and high risk nature of these patients—and their associated conditions—demand that the ED physician keep abreast of clinical advances in this area in order to provide state-of-the-art care for these ED patients.
— The Editor
Introduction
From a practical, clinical perspective, causes of vaginal bleeding during the second half of pregnancy can be divided into obstetrical and non-obstetrical causes. Obstetrical causes of vaginal bleeding during this period include the following: 1) placental abruption; 2) placenta previa; 3) uterine rupture; 4) vasa previa (or isolated fetal hemorrhage); and 5) the "bloody show" associated with onset of labor. Each of these conditions will be discussed, highlighting risk factors, diagnosis, and ED management.
Nonobstetrical causes of bleeding during the last 20 weeks of pregnancy rarely cause significant bleeding. Nevertheless they may occur, and entities that should be considered include lesions of the vagina, cervical polyps or cancer, friable condyloma acuminata, hemorrhoids, and postcoital trauma. It should be emphasized that because the cervix is much more vascular during the later phases of pregnancy, there may be more bleeding than is typically associated with these cervical lesions. As a result, biopsies of cervical lesions should be performed only by an experienced obstetrician. If bleeding is minor (simple spotting), if there is a verifiable history of recent trauma (speculum exam or intercourse), and if a bleeding site is identified on exam that does not originate from the os, then the patient can be reassured that the bleeding is not serious. Nevertheless, any patient with a diagnosis of non-obstetrical vaginal bleeding should be cautioned about warning signs that indicate more serious bleeding, and these women should be referred directly to their obstetrician for urgent follow-up in the event of more serious hemorrhage.
Finally, it is important to stress that basic physiological changes occur in pregnancy that protect the mother from natural blood loss associated with delivery. For example, by 40 weeks gestation, plasma volume dramatically increases by 33% (450 mL), and total blood volume increases by an average of 45% above pre-pregnancy levels. This augmentation of blood volume occurs gradually and mirrors the growth of the fetus. However, the red cell mass expands at a slightly slower rate, producing a dilutional anemia that is most pronounced in early pregnancy. Consequently, the mean hemoglobin level during pregnancy is 10.2 g/dL to 11.6 g/dL.2 As a result, from a physiological perspective, the mother may tolerate blood loss slightly better than a non-pregnant patient with the same degree of hemorrhage, but on the other hand, the resulting anemia may be more profound as a result of fluid shifts and resuscitation with saline. Fibrinogen levels are also increased in pregnancy, rising up to three times the pre-pregnancy level by term.
Placental Abruption
Placental abruption (or abruptio placenta) is defined as premature separation of a normally implanted placenta from its attachment to the uterus before birth of the fetus. Abruption occurs most frequently during the third trimester; about 80% of all cases will occur shortly before the onset of labor, although this complication may occur at any time after 20 weeks of gestation.3 Placental separation during the first 20 weeks is considered part of the process of spontaneous abortion.4 The incidence of abruption is between 1 in 86 and 1 in 200 live births, and therefore, complicates approximately 1% of all pregnancies.3 Even so, abruption is the most common cause of intrapartum fetal death, with an associated mortality rate of 25-50%. The majority of these deaths are due to complications of premature birth (respiratory distress syndrome, intraventricular hemorrhage, and necrotizing enterocolitis). As a result, placental abruption accounts for up to 15% of all perinatal deaths.5 Morbidity also is significant, with permanent neurological deficits reported in up to 14% of surviving infants.6 Abruption can also produce significant complications in the mother, among them, life-threatening maternal hemorrhage, severe coagulopathies, and the need for emergency Cesarean section (C-section); these complications account for significant maternal morbidity and mortality.
Placental separation occurs in varying degrees of severity, and is generally classified according to the following schemata: 1) complete or Grade 3; 2) partial or Grade 2; and 3) mild or Grade 1, in which case separation involves only the placental margin. (See Figure 1.) These classes of placental abruption correlate reasonably well with clinical findings and prognostic outcomes for both mother and fetus. Fortunately, Grade 3 (severe) abruptions are the least common, occurring in only 15-24% of clinically recognized cases of abruption.1,7 Grade 2 (moderate) abruptions account for about 27-45% of cases, and Grade 1 (mild) abruptions are seen in 40-48% of cases.1,7 A key point to remember is that the amount of external bleeding associated with abruption may not correlate with the extent or severity of the abruption and this may create a sense of false security. In this regard, for example, concealed hemorrhage occurs when the bleeding is contained inside the uterus, and these abruptions may be as dangerous to the mother and fetus as those characterized by severe external bleeding. Important and characteristic clinical findings for each class of abruption are summarized in Table 1.
| Table 1. Clinical Findings in Placental Abruption: Grade-Dependent Maternal and Fetal Profiles | |
| Grade 1: | |
| Slight or minimal vaginal bleeding (spotting) and limited uterine irritability (no organized contractions) are typically present. Maternal blood pressure is unchanged, and maternal serum fibrinogen level is normal (normal maternal fibrinogen concentration is 450 mg/percent). Fetal heart rate is normal, between 120 bpm and 160 bpm. | |
| Grade 2: | |
| External uterine bleeding is mild to moderate, similar to that of a heavy period. Uterine irritability is evident, with tetanic contractions at times. Maternal hypotension is absent in supine position, but orthostatic symptoms may be present. Resting maternal pulse rate may be elevated. Fibrinogen levels are lowered to the range of 150 mg/percent to 250 mg/percent. Fetal distress is evident as manifested by compromised fetal heart rate patterns. | |
| Grade 3: | |
| Bleeding is moderate to severe but may be underestimated by external losses. Painful uterine contractions are present and they are often tetanic in nature. Hemodynamic instability is evident by maternal hypotension and tachycardia. Fibrinogen levels are often reduced to less than 150 mg/percent, representing a blood loss of approximately 2000 mL. Maternal coagulopathies (thrombocytopenia, clotting factor, and fibrinogen depletion) are often present. Fetal death is common. | |
Clinical Pathophysiology. In placental abruption, bleeding is thought to initiate from abnormal small vessels in the basal layer of the decidua or from fetoplacental vessels. As bleeding progresses, a hematoma enlarges beneath the placenta, sheering it from the uterus. Bleeding may be seen vaginally, or it may be concealed entirely inside the uterus. (See Figure 1.) As a result, the amount of visible or external bleeding may not necessarily correlate with maternal blood loss or grade of abruption.
Fetal compromise in abruption results from fetal hypoxia associated with the placenta’s decreased ability to perform gas exchange. Additional risks include fetal blood loss through the disrupted placenta, maternal Rh sensitization, amniotic fluid embolism, and maternal disseminated intravascular coagulation (DIC). In severe abruption, microvascular coagulation is thought to stimulate the maternal fibrinolytic system, resulting in critical depletion of platelets and clotting factors, a serious clinical event that places the mother at risk for additional bleeding.
When a concealed abruption occurs, intrauterine pressures rise and, as a result, uterine muscles are unable to contract sufficiently around fractured vessels in order to inhibit further bleeding. Blood may also dissect into the fetal membranes or into the wall of the uterus. The clinical, disruptive effects of abruption on the fetus depend almost entirely upon the degree of separation of the placenta. Marginal separation from the uterus may produce no notable effects, whereas in complete abruption, fetal death is almost unavoidable. In almost 50% of cases characterized by severe abruption, the fetus is dead by the time the mother is admitted to the hospital.8 As would be expected, varying degrees of separation between marginal and complete separation will have variable effects on the fetus.
The precise etiology of placental abruption currently remains unclear, but several risk factors have been identified. The most important risk factor appears to be maternal hypertension. Hypertension in pregnancy is defined as a blood pressure 140/90 mmHg, an increase in systolic pressure of greater than 30 mmHg, or an increase in diastolic pressure of greater than 15 mmHg as compared to pre-pregnancy values. Although hypertension is a risk factor for all types of abruption, the correlation is most striking with Grade 3 abruption where 50% of cases are associated with either pregnancy-induced or chronic maternal hypertension.4 Transient rises in blood pressure precipitated by cocaine use also can increase risk of abruption.9 Furthermore, any condition that predisposes the mother to vascular disease (i.e., preeclampsia, diabetes, collagen vascular diseases, and chronic renal disease) is associated with increased risk for abruption. Finally, a variety of other conditions also are associated with increased risk for abruption. (See Table 2.)
| Table 2. Risk Factors for Placental Abruption | |
| • Maternal hypertension | |
| • Eclampsia and preeclampsia | |
| • History of previous abruption | |
| • Uterine distension (multiple gestations, hydramnios, or tumors) | |
| • Vascular disease (collagen vascular disorders, diabetes) | |
| • Tobacco smoking | |
| • Cocaine use | |
| • Microangiopathic hemolytic anemia | |
| • Premature rupture of membranes | |
| • Uterine blunt trauma (domestic abuse, automobile collisions) | |
| • Short umbilical cord | |
It should be stressed that a previous placental abruption greatly increases the risk for abruption in subsequent pregnancies by more than 10-fold.10 Because blunt abdominal trauma is also a risk factor for abruption, this etiology should be considered in any trauma evaluated during the second half of pregnancy. A history of trauma, especially from domestic abuse, also should be elicited in any pregnant woman presenting with abdominal pain or bleeding. Data now confirms that physical trauma currently complicates one out of every 12 pregnancies, and that spousal abuse is a leading cause in these cases.1 Several, newer studies have identified maternal cigarette use, advanced maternal age, and male fetal gender as additional risk factors for abruption.11 A link between intrauterine growth retardation and increased risk for abruption also has been proposed.12
Clinical Presentation. The classical presentation of placental abruption is characterized by sudden onset of abdominal pain, uterine contractions, and vaginal bleeding. In clinical practice, however, the presentation of abruption is highly variable. This variability results from the various degrees of placental separation. Typically, patients with more severe placental separation will present with more severe and "classical" symptoms. For example, in Grade 3 abruption, severe and abrupt abdominal and/or back pain is common. Although the pain is constant, painful uterine contractions will be superimposed. When uterine tetany occurs, there will be no cyclical nature to the patient’s pain. Frequently, by the time an exam is performed, the fetus will be in severe distress (bradycardic) or even dead.
Severe abruptions also can cause maternal cardiovascular shock that is accompanied by hypotension and tachycardia. Complications of shock (adult respiratory distress syndrome and acute tubular necrosis) may be apparent at the time of ED presentation. Hematuria, easy bruising, and continued bleeding at puncture sites are signs of DIC that may be seen early in the clinical course. Patients with severe abruption are suffering from hypovolemic shock and should be viewed as hypotensive multi-trauma patients in terms of their complications. Accordingly, aggressive fluid resuscitation and early transfusion should be instituted. (Please see Patient Management section.) Finally, any patient presenting with vaginal bleeding during the second half of pregnancy should never have a vaginal or rectal exam done until the possibility of placenta previa has been ruled out by ultrasonographic studies.
Patients with Grade 1 abruption usually will present with more subtle findings and may be difficult to diagnose. In this regard, pain may not be present with smaller separations, although in most cases uterine irritability (mild contractions) is present. Vaginal bleeding is seen in only 80% of cases because bleeding is concealed in the intrauterine space in the remaining 20% of patients.1 Patients with concealed hemorrhage have a higher maternal mortality rate, perhaps because of failure to recognize the severity of maternal blood loss during the initial patient encounter. As smaller abruptions will not affect the fetal heart rate, a common misdiagnosis in these patients is early onset labor. Although these patients may not require any intervention if their abruption remains small, they should be carefully monitored for signs of worsening separation. A significant number of patients with mild abruption will have no signs or symptoms. Almost 30% will be diagnosed at the time of delivery when a small retroplacental clot is identified.1
Patients with Grade 2 abruptions typically present with more classic symptoms, but may not manifest symptoms of hypovolemic shock as early as patients with severe abruptions. However, the onset of symptoms may be gradual or sudden. Several significant findings can alert the ED physician that this is not simply a case of early onset labor. The uterus is often tender and fails to relax between contractions. Vaginal bleeding, when not concealed, is moderate by abruption standards but is much more pronounced than the typical "bloody show" of labor. Once again, it should be emphasized that the amount of vaginal bleeding is often misleading, and that if the patient presents with symptoms of more extensive blood loss, appropriate intervention is required. Fetal distress is common in Grade 2 abruptions, a finding that should prompt urgent obstetric consultation.
Laboratory Studies. From a practical, clinical perspective, the take-home message is that placental abruption, for the most part, is a clinical diagnosis. There are no pathognomonic laboratory studies that accurately establish the diagnosis. Given that premise, research is being conducted to identify serum markers for abruption. Thrombomodulin (a marker of endothelial cell damage) has been reported to be a sensitive marker for abruption, and may prove to be clinically useful in the future.13 Currently, useful laboratory markers center are associated with the appearance of complications, most notably DIC.
DIC can be triggered by massive hemorrhage, which in turn stimulates production of tissue thromboplastin, resulting in extensive microvascular clotting (hence the name disseminated intravascular coagulation). These clots stimulate the fibrinolytic cascade, which leads to extensive consumption of platelets, fibrinogen, and other clotting factors. Maternal fibrinogen levels are normally in the range of 450 mg/percent, and the volume of blood lost roughly correlates with the decrease in fibrinogen levels. The majority of patients experiencing a significant drop in fibrinogen level will ultimately require transfusion of blood products. At levels of 300 mg/percent, maternal coagulation abnormalities begin to manifest themselves with spontaneous bleeding at puncture sites. A fibrinogen level of 150 mg/percent correlates with a maternal hemorrhage of more than 2 liters. As the average blood loss in a Grade 3 abruption is 2.5 liters or more, the fibrinogen level may provide a rough estimate of the severity of placental separation, as well as fetal prognosis.
As there may be a delay in obtaining a fibrinogen level in some centers, another "crude" alternative may be used.14 In the "poor man’s fibrinogen assay," a red top tube of blood is allowed to sit at room temperature. If a clot does not form within 6 minutes or forms and lyses within 30 minutes, a coagulation defect is probably present and the fibrinogen level is less than 150 mg/percent.14 Other lab values related to DIC include low platelets, prolonged PT or PTT, and raised D-dimer levels (released in fibrin degradation).
Finally, placental separation may introduce fetal blood into the maternal circulation, which can be detected by the Kleihauer-Betke test. While this test also can be used to dose Rhogam in these patients, a major disadvantage of this test is the long processing time. Clinical decisions, therefore, should be based on other data and this test should be limited to use as a screening tool for identifying patients with minimal or Grade 1 abruption, especially in cases where there is no other evidence for abruption except clinical suspicion.
Imaging Studies. During the first 20 weeks of pregnancy, imaging studies provide a reliable modality for clinical diagnosis. Unfortunately, this is not the case for placental abruption. Initial studies evaluating the usefulness of this technique found that ultrasound missed a surprising 98% of placental separations.14 More advanced ultrasound technology, however, has greatly reduced the false-negative diagnosis rate, but ultrasonographic evaluation will still fail to detect up to 50% of abruptions.14
When present, a number of ultrasonographic findings are consistent with the diagnosis of placental abruption. Hematomas may be seen either in the subchorionic (between the placenta and the membranes), retroplacental (between placenta and uterine wall), or preplacental (between the placenta and amniotic fluid) compartments. (See Figure 2.) Interestingly, the precise location of the hematoma can affect the prognosis of the fetus. In particular, large retroplacental hematomas (> 60 mLs or greater than 50% of placental surface affected) will produce fetal death in about 50% of cases, whereas an equivalent subchorionic hemorrhage will cause fetal death in only 10% of cases.15 Therefore, the primary purpose of ultrasound in diagnosis of abruption is to rule out other causes of vaginal bleeding in late pregnancy, most notably placenta previa. In these cases, ultrasound also can be used to assess for the fetal heartbeat.
Magnetic resonance imaging (MRI) is the only other diagnostic modality currently used to identify abruption. It has the advantage of high sensitivity. However, the lack of access to the test, as well as time and expense involved, do not make MRI a viable option in most emergency departments. At present, its use is relegated to clinically stable patients in whom the diagnosis is suspected, but in whom the diagnosis cannot be established by other means.
Patient Management. Treatment of patients with placental abruption depends, in part, on the degree of placental separation and the hemodynamic stability of mother and fetus. Stable patients with suspected or proven Grade 1 abruption (mild) should be admitted for observation and, in some cases, elective delivery. Patients with a higher grade abruption will manifest, or will unpredictably manifest, signs of hemorrhagic shock. The fetus may show signs of distress, or in the most severe cases, they will already have lost a heartbeat by the time of presentation to the ED.
Hence, all patients should have a fetal monitor placed, regardless of their initial presentation. They should be treated with close monitoring, two large-bore IV lines, and a type and cross for 2-4 units of blood should be obtained. Coagulation studies (CBC, PT/PTT, fibrinogen level, D-dimer) should be ordered STAT and repeated if the patient’s condition deteriorates. Blood products should be utilized for anemia or as the patient’s condition dictates. Correction of coagulopathy caused by DIC also is recommended. Immediate consultation with an obstetrician is mandatory, as no patient with a suspected abruption should ever be discharged to home.
Patients with large, concealed hemorrhages are at risk for uterine rupture, and decompression of the uterine cavity may be done by amniotomy (rupture of membranes). As a rule, ED physicians should not perform this procedure, but if consultation is unavailable, remember that it may improve the mother’s condition. A small incision is made in the membranes bulging through the os, but should only be performed in patients with suspected concealed hemorrhage when all other resuscitative measures are failing.
Resuscitation of the mother takes priority over all clinical contingencies, and when required, type O negative blood may be used for resuscitation if time does not permit type and crossmatch. Transfusion of platelets and fresh frozen plasma can also be used to treat coagulopathies associated with DIC. While it is true that there are two patients involved in patient management, the mother’s hemodynamic stability takes precedence. Improvement of the mother’s circulation will often improve that of the fetus if distress is present, and therefore, resuscitation of the mother is the first step in fetal resuscitation. Second, the fetus may not have reached sufficient maturity to permit survival outside of the mother and saving the mother will be the only way for the fetus to survive to maturity. Accordingly, accurate and early establishing of fetal gestational age is another goal in these patients. Often, this is as easy as asking the mother, but it becomes critical information at certain times in gestation. When the fetus is near term (36 weeks and up), emergent C-section is a more likely option than in patients in whom fetal viability is in question.
A fetus younger than 23-24 weeks is considered non-viable for survival outside the mother. Consequently, from a practical clinical perspective, it is of paramount importance to establish the age of the fetus. If the mother is unsure of dates, an urgent ultrasound will help clarify gestational age. If the fetus is clearly preterm, most obstetricians use magnesium sulfate or subcutaneous terbutaline to control uterine contractions and prevent actual labor. When the fetus is potentially viable, fetal monitoring and urgent consultation with a neonatal team or pediatrician also should be performed early. Although considerable controversy exists about the management of patients with abruption and a preterm fetus, most authors recommend trying to prevent labor until the fetus is clearly viable. When delivery is indicated, the method of choice is also debated in the obstetric literature. C-section may be the fastest method of delivery, but it also will increase blood loss and the risk of complications, especially when DIC is present. Alternatively, vaginal delivery may be associated with decreased blood loss, but can take a prolonged course with additional stress on the fetus.
Likewise, management of patients with fetal demise and coagulopathy is also controversial, since emergent C-section will considerably increase maternal blood loss and risk. Therefore, C-section should only be performed as a last resort in those patients in whom maternal hemorrhage is uncontrollable by any other means. With so much debate on the most outcome-effective approach, the primary goal of the ED physician should be to stabilize the patient(s) and deliver them to the care of obstetricians and pediatricians who can make these controversial decisions.
Once the patient is stabilized, she may need to be transferred to an appropriate center for further evaluation and treatment. However, transfer should not be attempted until the patient is sufficiently stabilized to undergo transport without additional risk. Finally, Rh-negative mothers should be treated with Rhogam. Recommendations are for 50 microgram IM injection in patients less than 12 weeks and 300 micrograms IM for those 12 weeks or more. Alternatively, one may simply use 300 micrograms for all Rh-negative patients, as gestational dates can be inaccurate and there is no additional risk with the higher dose.
Placenta Previa
Placenta previa is another important cause of bleeding during the later half of pregnancy. This condition is defined as the improper implantation of the placenta over the cervical os; in other words, the placenta is inappropriately positioned between the cervix and the presenting fetal part, thereby impairing unencumbered descent of the fetus. The incidence of previa is similar to abruption, occurring in approximately one in 200 live births.4
Three different types of previa have been identified and are characterized as follows: marginal, partial, and total. (See Figure 3.) They are defined according to the extent to which the placenta encroaches on the cervix. Marginal previa occurs when the placenta extends up to the os, but does not cover it. Partial previa is defined by partial occlusion of the os by the placenta, with an incidence reported to be as high as 3% of all cases of previa.14 Total previa, as the name suggests, occurs when the placenta completely covers the os. The incidence of total previa is estimated to occur in 20-43% of all cases of previa.16 In contrast to abruption, the classification of previa neither predicts mortality of mother or fetus nor forecasts management approaches. Any patient with any type of previa can develop life-threatening hemorrhage during labor. The preferred method of management for all patients with previa is delivery by C-section.
Pathophysiology. The mechanism by which placenta previa causes serious—and potentially life-threatening—vaginal bleeding during the later half of pregnancy is relatively clear. Hemorrhage results from early separation of the placenta from the uterus. (See Figure 4.) This typically occurs from gradual thinning of the cervix in anticipation of delivery. Bleeding can also be induced from physical exertion, labor, local trauma (intercourse or digital examination by a physician), or it may have no apparent trigger.
Regardless of the cause, the comparative lack of muscle tissue in the lower uterine segment is predisposed to bleeding from the placenta as it separates from the uterine wall. The lower the attachment of the placenta, and the earlier in pregnancy that the lower uterus begins to change, the earlier bleeding occurs. The first bleeding episode typically ceases on a self-limited basis, but recurs as cervical changes become more pronounced. Nearly 33% of patients are diagnosed before 30 weeks gestation, but up to another 33% are not diagnosed until after 36 weeks gestation.1 In one study, 5-15% of patients were diagnosed at 17 weeks.16 However, almost 90% of these patients had resolution of the previa by term.17 In contrast to abruption, the fetus is generally compromised from the bleeding unless a larger portion of the placenta detaches or maternal blood loss is extensive. The primary danger to the fetus is from preterm delivery precipitated by the bleeding episodes. As one would expect, the earlier in pregnancy that bleeding begins, the worse the perinatal risk. Interestingly, there is an association between fetal growth retardation and congenital abnormalities and children born to mothers with placenta previa.18,19
Although the mechanism of bleeding is clear, the reasons for improper placental implantation in these patients are not well characterized. Most authors agree that a host of factors are involved and some may be more important in the individual patient. Risk factors most commonly cited are multiparity (large number of previous pregnancies), prior C-section, prior placenta previa, multiple gestation (twins, etc.), and prior abortion with curettage.4 A common theme among the risk factors is the scarring of the uterus. Uterine scars are formed by surgical procedures, such as C-section or elective abortion, or they may result from previous placental implantation.
Some authors suggest the placenta implants in the lower uterine segment to "avoid" previously damaged uterine muscle, where implantation may be more difficult or may impair subsequent placental function. Whatever the explanation, the presence of a scar from previous C-section increases the mother’s risk for previa by about six-fold, yielding a 1-4% risk for previa in any pregnancy after C-section.20 The risk increases in direct correlation to the number of uterine surgeries. In patients with a history of four or more C-sections, there is nearly a 10% risk of placenta previa.21 This risk is not affected by the orientation of the C-section incision (transverse vs vertical), and appears to be a result of the presence of previous uterine trauma alone. The evidence for multiparity as a risk factor for previa also is strong. Placenta previa is seen in 1 out of 20 grand multiparas and only 1 in 1500 nulliparas.1 In the uncommon case of multiple gestations, the larger surface area of the placenta (or placentas) gives rise to an increased risk of previa simply by the relatively decreased surface area of the uterus. As with abruption, male fetal sex and maternal cigarette use also have been found to increase risk for placenta previa.12,22
Clinical Presentation. In contrast with placental abruption, patients with previa typically present with painless vaginal bleeding; in fact, almost 70% of patients with previa will present in this fashion.14 Another 20% will have uterine contractions associated with pain. Clearly, this can be a source of confusion for the physician as painful bleeding is the classical presentation of placental abruption. It is important to note that the pain associated with previa is usually milder than pain in patients with significant placental abruption. The remaining 10% of patients will be incidentally diagnosed at time of C-section or during the course of a routine ultrasound.14
Even though the majority of patients with previa present with painless vaginal bleeding, less than 50% of patients who present with these signs and symptoms are ultimately diagnosed with previa.1 In previa, the blood noted usually is bright red in color. It will be necessary to verify that blood is coming from the os and not from another vaginal source, and a speculum exam is required to verify this. However, it is very important for the ED physician to be clear about the risks of performing a vaginal exam in any patient with bleeding in the second half of pregnancy. While placenta previa does not often cause life-threatening hemorrhage on its own (in the absence of labor), iatrogenic trauma of the cervix can produce bleeding that is dangerous both to mother and child. Therefore, any patient with vaginal bleeding in the later half of pregnancy where previa is in question should not undergo any invasive exam of the vagina until previa is ruled out.
When an exam is performed by the obstetrician, it is performed as a "double set-up" exam. The patient undergoes vaginal exam in the OR with all the necessary equipment and personnel to proceed immediately with an emergency C-section in the event dangerous bleeding is induced by the exam. Obviously, the exam is performed in this fashion if the fetus is considered viable for delivery. In the absence of these conditions, it is never "safe" to perform any invasive vaginal exam (speculum or digital) in a patient with previa. The only possible exception to this may be in an ED where there is no access to an obstetrician or ultrasound. A very gentle and limited speculum exam may be indicated to verify the bleeding is coming from the os and not from another, less worrisome source. Even in this setting, it can be argued that if no consultant is available, the patient should be transferred to an ED where appropriate consultation exists before attempting a potentially dangerous maneuver.
Imaging Studies. Apart from standard laboratory tests used to guide resuscitative efforts in a mother with significant hemorrhage, ultrasound is virtually the only test required for evaluation of a patient suspected of having placenta previa. (See Figure 5.) As with abruption, MRI is being investigated as a tool for diagnosis, but currently is not recommended for ED use.23 As mentioned above, ultrasound should be done to rule out previa as a diagnosis before any invasive vaginal exams are performed. Therefore, in stable patients with bleeding during the second half of pregnancy, ultrasound should be performed as rapidly as possible to clarify the patient’s diagnosis. With a hemodynamically unstable patient, resuscitation and emergency C-section may be the only treatment indicated.
Because it is completely non-invasive, transabdominal ultrasound is the technique of choice to rule out previa. This is not to say that transvaginal exams are not potentially safe and more accurate when performed by appropriately trained individuals. Several authors report that transvaginal exams are safe and provide better data in these patients.24-26 Recommendations are that the probe be inserted no more than 3 cm into the vagina, and that no contact is made with the cervix or lower uterine segment in order to avoid iatrogenic bleeding. Images obtained by transvaginal ultrasound are of superior quality, and this approach avoids poor images that frequently are produced in obese patients and those with full urinary bladders. When using the transabdominal approach, it is recommended that a second scan be obtained with an empty bladder to increase accuracy. Likewise, when the placenta is implanted posteriorly or laterally in the uterus, diagnostic transabdominal images are difficult to obtain. Overall, the accuracy of transabdominal ultrasound is reported to be in the 93-97% range, with 2-6% false-positive and 2% false-negative rates.25,27 Comparison to previous ultrasound studies is very useful, but not always available when the patient presents to the ED.
It should be stressed that up to 90% of patients diagnosed with placenta previa before 20 weeks gestation will resolve by term delivery.17 The term "placental migration" has been used to explain this fact. The term is somewhat of a misnomer, as it is improbable that the placenta actually separates and re-implants to account for this observation. A more likely explanation is that the lower uterine segment structure changes with time and grows disproportionately. Another possibility is that the placenta may also undergo relatively more growth away from the cervix. Whatever the exact mechanism, it is surprising to find that 73% of patients with total previa diagnosed in the second trimester will regress to a lesser degree of previa.28 Marginal previa will be found at term in only 2.5% of cases diagnosed in the second trimester.28 Another author reports that up to 5% of all pregnant women will have evidence of some type of placenta previa on ultrasound in the second trimester.1 Furthermore, 95% of these patients will have no symptoms, no previa at term, and a normal ultrasound by 28 weeks.1 Therefore, a history of previa diagnosed early in the patient’s pregnancy does not mean that the condition will still present at the time of their ED visits.
Finally, it should be noted that the other important function of ultrasound in these patients is to establish fetal gestational age and potential fetal viability outside the mother. As will be seen in the next section, management of patients with placenta previa is greatly influenced by whether a viable or near-term fetus exists at time of the mother’s presentation.
Patient Management. Care of the patient with documented or suspected placenta previa and late term vaginal bleeding can be complex. As with abruption, management is determined by the severity of maternal hemorrhage and fetal viability as judged by gestational age and current vital signs. Patients who present with bleeding complications of previa often do so late in their pregnancy. As maternal blood volume has increased by 20-40% by term, the mother may tolerate substantial blood loss (500 mLs) without affecting vital signs. Therefore, when the vital signs show evidence of hypovolemia, one should assume that blood loss has been catastrophic and treat the patient accordingly. Consequently, any "sick" patient with bleeding and previa requires full efforts at maternal volume resuscitation, including large bore IVs (or central access) and early transfusion of appropriate blood products. Urgent consultation in these cases is required inasmuch as emergency C-section may be life-saving for the mother and the fetus.
The general approach to a stable patient with vaginal bleeding in the second 20 weeks of gestation requires an accurate, relevant history of the event, including history of complications during the current as well as during previous pregnancies, an overview of general medical conditions, and a history of potential trauma (intercourse, recent medical exams, etc.). A physical exam—excluding a vaginal or rectal exams—should be performed. Reportedly, placenta previa is more likely when a "high presenting part" of the fetus is palpated on abdominal exam. The physician is reminded not to forget a "5th vital sign" in these patients (i.e., fetal heart monitoring, which is the standard of care in any patient with late trimester bleeding). (See Fetal Assessment supplement inserted in this issue.)
A transabdominal ultrasound exam should be obtained early in the work-up of any patient in whom placenta previa is suspected. If evidence of previa is obtained on ultrasound, the obstetrician will proceed with a C-section or expectant management, depending on the condition of mother and fetus, fetal gestational age, and the severity of maternal bleeding. When the fetus is clearly viable, significant improvements in perinatal mortality have been noted with early use of C-section.1 A recent evaluation of C-section in previa, however, found that regional anesthesia is associated with lower blood loss and may be a safer alternative than general anesthesia for delivery in these patients.29 In patients in whom the fetus is clearly not viable outside the mother, the pregnancy is supported in the hospital until fetal maturity can be established. Use of tocolytics in this setting remain controversial, and up to 33% of patients will fail expectant management.30 Such complications as DIC and renal failure less frequently are seen in cases of previa as compared to abruption. Maternal mortality is now less than 1%, and perinatal mortality is less than 5% with current therapies.1
Vasa Previa
Although rare, vasa previa is a potentially important cause of painless late trimester bleeding. The condition is distinguished by the fact the vaginal bleeding in vasa previa is completely of fetal origin. Consequently, in contrast to other causes of obstetrical hemorrhage, the mother, for all practical purposes, is not physically endangered by this type of hemorrhage. This condition results from a defect in placental formation. Typically, the umbilical cord is inserted in a lateral (velamentous) position on the placenta. The umbilical vessels travel through the placental membranes unsupported by other placental tissue. As these vessels travel across the cervix, in advance of the presenting fetal anatomy, they are at risk of rupture and isolated, fetal hemorrhage.
Vasa previa can also be caused by presence of an extra lobe on the placenta. Most often, the umbilical vessels are torn at time of labor or during artificial rupture of the membranes, but bleeding also may occur spontaneously late in pregnancy. As the fetal blood volume is quite small (up to 500 mLs), seemingly insignificant amounts of vaginal bleeding can result in fetal exsanguination. While vasa previa complicates only 1 in 2000-5000 pregnancies, perinatal fetal mortality from rupture of these vessels approaches 75%.31
As might be expected, diagnosis of this condition can be difficult in the ED setting. If the condition is not detected prior to ED presentation, the fetus may expire before the diagnosis is confirmed. Ultrasound findings of a bi-lobed placenta will certainly heighten suspicion, but are not diagnostic. Transvaginal color-flow Doppler has been used to diagnose vasa previa, but the technique is still being developed and transvaginal ultrasound is not yet the standard of care to rule out placenta previa.32 Most authors still recommend first ruling out placenta previa before pursuing other diagnoses. Vaginal instrumentation (the best way to diagnose vasa previa) in patients with potential placenta previa is currently contraindicated.
Laboratory tests are available that will detect the presence of fetal hemoglobin or nucleated red blood cells in the expelled blood. However, the lack of availability of these tests when needed, the length of time required to perform them, and their inaccuracy render them less useful clinically. The ED physician, however, should be aware, though, of the "Apt" test.33 The "Apt" test is used to distinguish fetal from maternal red blood cells in vaginal blood, based on the higher resistance of fetal hemoglobin to alkaline conditions.
Clinical suspicion for this condition should be heightened when the mother presents with a small volume, bleeding episode, and absence of other maternal symptoms (significant uterine pain, signs of large volume blood loss), but the fetal monitor shows significant fetal distress. (See special supplement on Fetal Assessment inserted with this issue.) Specifically, one should search for fetal tachycardia, sinusoidal fetal heart rate pattern, or variable decelerations that coincide with membrane rupture. The presence of any of these fetal distress patterns combined with "minor" vaginal bleeding and lack of maternal symptoms suggest vasa previa. Emergency C-section is virtually the only method of fetal salvage in these cases, and delays in obtaining an emergent obstetrical consultation will increase an already high fetal mortality.
Uterine Rupture
Uterine rupture is a devastating event. Maternal mortality approaches 40% in the worst cases, and the fetal mortality is even higher.4 Risk factors for this condition have two themes in common: weakness of the uterine wall (typically associated with surgical scars), and increased intrauterine pressures. The most common causes of uterine scarring are previous C-section, fibroid removal, or other procedures that divide the uterine wall. Increased intrauterine pressures can be seen with concealed placental abruption, blunt abdominal trauma, and other placental abnormalities. Placenta acreta/increta/percreta are conditions where the placenta invades the uterine wall from just below the surface (acreta) to completely through it (percreta). Invasive moles and chroiocarcinoma are also risk factors for uterine rupture.
Clinical signs of uterine rupture include a sudden increase in uterine pain or irritability, loss of previously normal contraction patterns, and fetal heart rate abnormalities. At times, the physician may be able to palpate fetal parts on abdominal exam. As expected, intra-abdominal bleeding can vary from small to clinically significant volumes, depending on the extent of the uterine tear. True maternal blood loss is often much greater than the amount of vaginal bleeding. Both mother and fetus often suddenly decompensate during "normal" labor and emergent action is required. The severity of the patient’s condition will usually preclude any attempt at imaging or other diagnostic maneuvers. In the worst case scenario, it may also mean that definitive treatment is needed before consultants arrive. Obviously, this is a disastrous situation, and only an emergent C-section will possibly salvage the fetus (or just to control maternal hemorrhage).
Summary
Pregnancy is an important but potentially stressful time in a woman’s life. When an unexpected, potentially dangerous event such as vaginal bleeding occurs, it is extremely upsetting for the expectant mother and father. While the ED physician may not always be able to bring good news to these patients, in many cases early intervention can make the difference between life and death for the fetus, and at times the mother as well.
Placental abruption and placenta previa are the two most common causes of vaginal bleeding in the second half of pregnancy. Therefore, any patient presenting to the ED with bleeding in later pregnancy may be suffering from one of these conditions until proven otherwise. The ED physician must first recognize the potential danger, and realize that patients may be more ill than they first appear. Resuscitation of the mother, fetal monitoring, fetal gestational age estimates, an ultrasound to rule out previa as a cause, and obstetrical consultation should be performed in all cases. Early pediatric consultation is also essential when dealing with a viable fetus. The ED physician must recognize that early delivery is essential in cases of severe bleeding.
References
1. Scott JR. Placenta previa and abruption. In: Scott JR, et al, eds. Danforth’s Obstetrics and Gynecology. 8th ed. Philadelphia: Lippincott Williams & Wilkins; 1999:407-418.
2. Hansen WF, Hansen AR. Problems in pregnancy. In: Tintinalli JE, Ruiz E, Krome RL, eds. Emergency Medicine: A Comprehensive Study Guide, 4th Ed. New York: McGraw-Hill; 1996:564-575.
3. Pritchard J. Obstetric hemorrhage. In: Pritchard J, MacDonald P, eds. Williams Obstetrics. New York: Appleton-Century-Crofts; 1980:485.
4. VanDeKerkhove KM, Johnson TRB. Bleeding in the second half of pregnancy: Maternal and fetal assessment. In: Pearlman MD, Tintinalli JE. eds. Emergency Care of the Woman. New York: McGraw Hill; 1998:303-312.
5. Pritchard JA, Cunningham G, Pritchard SA, et al. A prospective controlled study of outcome after trauma during pregnancy. Am J Obstet Gynecol 1990;162:1502-1505.
6. Abdella TN, Sibai BM, Harp JM, et al. Perinatal outcome in abruptio placentae. Obstet Gynecol 1984;63:365-370.
7. Hurd W, Miodovnik M, Hertzberg V, et al. Selective management of abruptio placentae: A prospective study. Obstet Gynecol 1983;61:467-473.
8. Knab DR. Abruptio placentae. An assessment of the time and method of delivery. Obstet Gynecol 1978;52:625-629.
9. Landy HJ, Hinson J. Placental abruption associated with cocaine use: A case report. Repro Toxicol 1987;1:203-205.
10. Ananth CV, Savitz DA, Williams MA. Placental abruption and its association with hypertension and prolonged rupture of membranes: A methodologic review and meta-analysis. Obstet Gynecol 1996;88:309-318.
11. Kramer MS, Usher RH, Pollack R, et al. Etiologic determinants of abruption placentae. Obstet Gynecol 1997;89:221-226.
12. Andres RL. The association of cigarette smoking with placenta previa and abruptio placentae. Semin Perinatol 1996;20:154-159.
13. Magriples U, Chan DW, Bruzek D, et al. Thrombomodulin: A new marker for placental abruption. Thromb Haemost 1999;81:32-34.
14. Benedetti TJ. Obstetric hemorrhage. In: Gabbe SG, Niebyl JR, Simpson JL, eds. Obstetrics: Normal and Problem Pregnancies, 3rd Ed. New York: Churchill Livingstone; 1996:499-532.
15. Nyberg DA, Mack LA, Benedetti TJ, et al. Placental abruption and placental hemorrhage: Correlation of sonographic findings with fetal outcome. Radiology 1987;358:357-361.
16. Cotton D, Ead J, Paul R, et al. The conservative aggressive management of placenta previa. Am J Obstet Gynecol 1987;168:1424-1429.
17. Rizos N, Doran T, Miskin M, et al. Natural history of placenta previa ascertained by diagnostic ultrasound. Am J Obstet Gynecol 1979;133:287-291.
18. Brar HS, Platt LD, DeVore GR et al. Fetal umbilical velocemetry for the surveillance of pregnancies complicated by placenta previa. J Reprod Med 1988;33:741-744.
19. McShane PM, Heyl PS, Epstein MF. Maternal and perinatal morbidity resulting from placenta previa. Obstet Gynecol 1985;65:176-182.
20. Chattopadhyay S, Kharif H, Sherbeeni J. Placenta previa and accreta after previous cesarean section. Eur J Obstet Gynecol Reprod Biol 1993;52:151-156.
21. Clark S, Koonings P, Phelan J. Placenta previa/accreta and prior cesarean section. Obstet Gynecol 1985;66:89-92.
22. Demissie K, Breckenridge MB, Joesph L, et al. Placenta previa: A preponderance of male sex at birth. Am J Epidemiol 1999;149:824-830.
23. Thorp JM Jr, Wells SR, Wiest HH, et al. First trimester diagnosis of placenta previa by magnetic resonance imaging. Am J Obstet Gynecol 1998;178:616-618.
24. Thorp JM, Councell RB, Sandridge DA, et al. Antepartum diagnosis of placenta previa percreta by magnetic resonance imaging. Obstet Gynecol 1992;80:506-508.
25. Tan NH, Abu M, Woo JLS, et al. The role of transvaginal ultrasonography in the diagnosis of placenta previa. Aust NZ J Obstet Gynecol 1995;35:42-45.
26. Farine D, Fox, HE, Jakobson S, et al. Vaginal ultrasound for the diagnosis of placenta previa. Am J Obstet Gynaecol 1988;159:566-569.
27. Leerentveld, RA, Gilberts EC, Arnold M, et al. Accuracy and safety of transvaginal sonographic placental localization. Obstet Gynecol 1990;76:759-762.
28. Zelop C, Bromley B, Frigoletto FJ, et al. Second trimester sonographically diagnosed placenta previa: Prediction of persistent previa at birth. Int J Gynaecol Obstet 1994;44:207-210.
29. Fredericksen MC, Glassenberg R, Stika CS. Placenta previa: A 22-year analysis. Am J Obstet Gynecol 1999;180:1432-1437.
30. Watson WJ, Defalo RC. Magnesium sulfate tocolysis in selected patients with placenta previa. Am J Perinatol 1990;7:251-253.
31. Kouyoumkjian A. Velamentous insertion of the umbilical cord. Obstet Gynecol 1980;56:737.
32. Harding JA, Lewis DF, Major CA, et al. Color flow Doppler—A useful instrument in the diagnosis of vasa previa. Am J Obstet Gynecol 1990;163:1566-1568.
33. Odunski K, Bullough CH, Henzel J, et al. Evaluation of chemical tests for fetal bleeding from vasa previa. Int J Gynaecol Obstet 1996;55:207-212.
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