Placental Abruption at Near-Term and Term Gestations: Pathophysiology, Epidemiology, Diagnosis, and Management

Abstract

Placental abruption is the premature separation of the placenta from its uterine attachment before the delivery of a fetus. The clinical manifestations of abruption typically include vaginal bleeding and abdominal pain with a wide variety of abnormal fetal heart rate patterns. Clinical challenges arise when pregnant people with this condition present with profound vaginal bleeding, necessitating urgent delivery, especially when there is concern for maternal and fetal compromise and coagulopathy. Abruption occurs in 0.6–1.2% of all pregnancies, with nearly half of abruption occurring at term gestations. An exposition of abruption at near-term (defined as the late preterm period from 34 to 36^6/7 weeks’ gestation) and term gestations (defined as ≥37 weeks’ gestation) provides unique insights into its direct effects, as risks associated with preterm birth do not impact outcomes. In this review, we explore the pathophysiology, epidemiology, and diagnosis of abruption. We discuss the interaction of chronic processes (decidual and uteroplacental vasculopathy) and acute processes (shearing forces applied to the abdomen) that underlie the pathophysiology. Risk factors for abruption and strengths of association are summarized. Sonographic findings of abruption and fetal heart rate tracings are presented. In addition, we propose a management algorithm for acute abruption that incorporates blood loss, vital signs, and urine output, among other factors. Finally, we discuss blood component therapy, viscoelastic post-of-care testing, disseminated intravascular coagulopathy, and management of abruption complicated by fetal death. The review seeks to provide comprehensive, clinically focused guidance during a gestational age range when neonatal outcomes can often be favorable if rapid and evidence-based care is optimized.

Condensation

A review of placental abruption at near-term and term gestations, when preterm birth does not contribute significantly to risk, provides insight into the direct effects of this complication. In this article, we provide a comprehensive, clinically focused review of abruption after 34 weeks’ gestation, focusing on pathophysiology, epidemiology, diagnosis, and management.

Introduction

Placental abruption is the premature separation of the placenta from its uterine attachment before the delivery of a fetus. Although the clinical manifestations are myriad, abruption is classically associated with vaginal bleeding and abdominal pain, with or without uterine contractions, and is often accompanied by abnormal fetal heart rate (FHR) patterns. Clinical challenges arise when pregnant people with this condition present with profound vaginal bleeding, necessitating urgent delivery, especially when there is concern for maternal and fetal compromise and coagulopathy.

The management of preterm abruption has received significant attention in the obstetrical literature (1, 2). This is because much of the perinatal morbidity and mortality associated with preterm abruption is impacted by gestational age at delivery, which is a mediating variable that features on the causal pathway between abruption and adverse perinatal outcomes (3). Yet approximately half of abruption occurs at term gestations, when preterm delivery has less impact on neonatal outcomes (4–7). The discussion of abruption at near-term (defined as the late preterm period from 34^0/7 to 36^6/7 weeks’ gestation) and term gestations (defined as ≥37 weeks’ gestation) therefore gives unique insight into the direct effects of abruption.

In this review, we focus on abruption after 34 weeks’ gestation and seek to provide clinical guidance when perinatal outcomes can often be favorable if rapid and evidenced based care is optimized. We review the pathophysiology, epidemiology, and diagnosis of abruption. We also review clinical management, focusing on associated challenges encountered by obstetricians, including obstetrical hemorrhage, coagulopathy, and delivery in the setting of fetal death. Finally, we propose a management algorithm and other clinical pearls that are intended to assist obstetric clinicians in their daily clinical practices when they encounter abruption and obstetric hemorrhage.

Pathophysiology

The pathophysiology of abruption includes both long-standing chronic processes and acute “triggers” as well as the interaction between the two processes (FIGURE 1) (8, 9). Chronic processes that predispose to abruption include thrombosis, inflammation, infection, and decidual and uteroplacental vasculopathy. These processes lead to placental hypoperfusion and defective spiral artery remodeling, placental infarction, and shallow trophoblast invasion (10). The relative hypoxia also promotes expression of vascular endothelial growth factor, which may alter the inflammatory response to decidual bleeding (11). These chronic changes predispose to abruption as well as other placentally mediated pathologies, including fetal growth restriction (FGR) and preeclampsia (12), often occurring weeks or months before the manifestations of these complications become clinically evident (8).

Figure 1. Pathophysiology of placental abruption.

Placental abruption is the end-result of an acute process (“acute pathway”) or the culmination of long-standing chronic processes (“chronic pathway”) or both. The acute pathway is driven by mechanical and shearing forces applied to the abdomen, causing premature placental separation. The chronic pathway includes thrombosis, infection, and decidual and uteroplacental vasculopathy as well as other inflammatory processes.

Figure adapted from “Pathogenesis of abruption” figure created by Cande Ananth, used with permission from UpToDate, Inc., Waltham, MA.

Acute processes leading to abruption are largely the consequence of mechanical and shearing forces applied to the abdomen. There may be an inciting event that precipitates abruption, such as abdominal trauma (13). Abruption may also be precipitated by rapid decompression of the uterine cavity following amniotomy or after vaginal delivery of a first twin (FIGURE 2) (14). Rupture of maternal decidual vessels leads to bleeding at the decidual-placental interface (10). Blood accumulates in this space, and detachment of the placenta from the uterus occurs, often accompanied by vasospasm of small vessels (10).

Figure 2. Electronic fetal monitoring of acute abruption with tachycardia and prolonged decelerations, preceding a terminal bradycardia.

A para 1 pregnant patient with cephalic-cephalic presenting dichorionic-diamniotic twins at 36 weeks’ gestation had a vaginal delivery of fetus A. Immediately after delivery of the first fetus, there was a large gush of bright red vaginal bleeding. The fetal heart rate of fetus B revealed fetal tachycardia and prolonged decelerations, which forecasted the acute abruption and preceded a terminal bradycardia. Due to the severe abruption with FHR changes, the patient subsequently underwent urgent cesarean delivery, which was notable for bloody amniotic fluid and complete placental separation.

Decidual bleeding that results in dissection and laceration along the decidual plane may lead to retroplacental, subchorionic, and subamniotic bleeding (15). Intraplacental accumulation of blood may also occur due to disruption of vasculopathic decidual arterioles in a setting of maternal vascular hypoperfusion (16). Inadequate myometrial contractions are unable to constrict bleeding vessels and sinuses at the placental bed due to uterine distension from the fetus. Consequently, the bleeding continues and intravascular channels for thromboplastic materials remain open.

The clinical sequelae of abruption are thought to be mediated by thrombin, which plays a critical role in inflammation and vascular response to endothelial injury. Decidual bleeding leads to release of excess thrombin, which is generated by tissue factor expressed on decidual cells to promote hemostasis (17, 18). Higher levels of vascular endothelial growth factor stimulate decidual endothelial cells to generate more tissue factor and more thrombin (11). This results in degradation of extracellular matrix and further endothelial injury from enhanced expression of matrix metalloproteinases (17) as well as the release of pro-inflammatory cytokines, such as interleukin-8 (19). These factors, coupled with the uterotonic effects of thrombin (20), may lead to rupture of membranes and uterine contractions. When significant amounts of thrombin become intravascular, consumptive coagulopathy, or disseminated intravascular coagulation (DIC), may ensue with potential for maternal morbidity and mortality (21).

Epidemiology

Abruption complicates 0.6–1.2% of pregnancies (4–7). Among singleton deliveries at term gestations in the United States (US) Collaborative Perinatal Project (CPP, 1959–66), the rate of clinical abruption was 1.4% (589 of 42,821) (22). Pregnant people with an abruption in one pregnancy carry up to a 10-fold increased risk of recurrence in a subsequent pregnancy; the recurrence risk is 25-fold higher in a third pregnancy when two prior pregnancies are complicated by abruption (23–26). The prevalence of abruption has been increasing in the US and Canada, but declining in other European countries, including Finland, Denmark, Norway, Sweden, and Spain (27). The reason for this divergence is unclear, but may be related to different risk factor profiles of these distinct populations. Differences in the prevalence rates of tobacco smoking, obesity, and multivitamin use, as well as differences in the implementation of universal folate fortification programs across these countries, may help explain some of the differences in the temporal changes in abruption rates across countries (27).

The risk of abruption is 3 to 4-fold higher among pregnant people with chronic hypertension, and 4 to 6-fold higher among those with preeclampsia, particularly preeclampsia with severe features and superimposed preeclampsia (28–31). Other clinical risk factors for abruption include pregestational and gestational diabetes, preterm prelabor rupture of membranes (PROM), chorioamnionitis, and oligohydramnios (31–33). Pregnant people with iron deficiency anemia, infection and other inflammatory states, as well as folate deficiency and hyperhomocysteinemia are also at increased risk (33–36). Increased circulating folate levels in pregnancy are associated with reduced levels of homocysteine, and increased levels of homocysteine are directly implicated in methylenetetrahydrofolate reductase (MTHFR) gene mutation (36–38). A large population-based study from Norway showed that the risk of abruption was 19% lower (odds ratio [OR] 0.81, 95% confidence interval [CI] 0.68, 0.98) among pregnant people who took folic acid supplementation compared to non-users.

Tobacco smoking is associated with a 1.7 to 2-fold increased risk of abruption, with a strong dose-response association between the number of cigarettes smoked per day (39–41). In a systematic review and meta-analysis of observational studies that included 1,358,083 pregnancies, smoking during pregnancy was associated with a 90% increased odds of abruption (OR 1.9, 95% CI 1.8–2.0) and up to a quarter of all abruptions were attributable to smoking (42). The risk of abruption is also increased among pregnant people who consume illicit drugs, particularly cocaine and marijuana (43, 44).

People who suffer from mental stress or depression, especially in the latter half of pregnancy, also have an increased risk of abruption (45, 46). However, the process through which maternal mental stress and affective disorders are associated with the risk of abruption is not well understood. It is believed that altered plasma cortisol, β-endorphin corticotrophin releasing hormone, and serotonin concentrations are higher in pregnant people with mood and/or anxiety disorders. This abnormally elevated hormone profile, in turn, increases the inflammation at the maternal-fetal interface, leading to higher abruption risk (45).

Risk factor assessments for term versus preterm abruption reveals significant overlap (9). In a large retrospective cohort study of over 30 million births in the US from 1995–2002 that sought to distinguish causal pathways of abruption at term versus preterm gestations, the authors found that chronic clinical processes associated with oxidative stress, vascular reactivity, and platelet activation, such as FGR and preeclampsia, were associated with increased risk for abruption across all gestations whereas acute inflammatory conditions (e.g., chorioamnionitis and PROM) were more significant drivers of risk in preterm gestations (9). This overlapping profile was also seen by Sheiner and colleagues who found that pregnancy-induced hypertension and nonvertex presentations were associated with abruption across all gestations whereas previous second-trimester bleeding was strongly associated with term abruption and polyhydramnios was strongly associated with preterm abruption (47, 48).

Clinical and non-clinical risk factors and their strength of associations with abruption are summarized in TABLE 1. Although many factors are associated with abruption, the factors that have the greatest risk include prior abruption, chronic hypertension, preeclampsia, cocaine and drug use, and intimate partner violence.

Table 1.

Risk factors and strength of associations with placental abruption

	Range of relative risk/odds ratio	Strength of association
Medical/obstetrical risk factors
Chronic hypertension	1.8–5.1	+++
Pregestational diabetes	2.5–3.0	++
Gestational diabetes	0.7–0.8	+/−
Gestational hypertension	1.5–2.5	++
Preeclampsia	2.0–4.5	+++
Eclampsia	3.0–5.5	+++
Polyhydramnios	2.0–3.0	++
Oligohydramnios	2.0–2.5	++
Prelabor rupture of membranes	1.8–5.1	++
Chorioamnionitis	2.0–2.5	++
Multiple gestation	2.0–2.5	++
Genetic risk factors
Thrombophilia	1.5–7.0	+++
MTHFR gene mutation	1.1–1.2	+/−
Hyperhomocysteinemia	1.5–4.0	++
Obstetrical history
Previous preeclampsia	1.5–2.0	++
Previous FGR/SGA	1.4–2.0	++
Previous abruption	6.0–12.0	++++
Behavioral risk factors
Cocaine and drug abuse	4.0–8.0	+++
Tobacco smoking during pregnancy	1.7–2.0	++
Alcohol use	1.5–2.5	++
Infertility	1.5–2.0	++
Iron deficiency anemia	2.2	++
Folic acid supplementation	0.8	++
Multivitamin supplementation	0.7–0.8	++
Vitamin C or E supplementation	0.6–0.7	++
Depression/anxiety	1.2–5.0	++
Anger/outbursts	2.8	++
Intimate partner violence	5.0–6.0	+++
Sociodemographic factors
Advanced maternal age (≥35 years)	1.5–2.5	+
Parity ≥3	1.1–1.6	+
Single marital status	1.2–1.4	+
African-American (Black) race/ethnicity	1.5	+

Since associations of risk factors near-term and term abruption are unavailable, we present the associations for all abruption, regardless of gestational age at diagnosis or delivery.

MTHFR: methylenetetrahydrofolate reductase; FGR: fetal growth restriction; SGA: small for gestational age

Clinical presentation

Acute versus chronic abruption

Acute abruption is characterized by the sudden onset of vaginal bleeding, and chronic abruption is characterized by recurrent episodes of light to moderate vaginal bleeding. The clinical manifestations of abruption are influenced by the caliber and location of maternal decidual vessels as well as the chronicity of bleeding. Bleeding from centrally located, larger arteries may lead to acute manifestations including hemorrhage and fetal distress (and potentially demise), necessitating urgent clinical interventions to minimize associated morbidity. Bleeding from peripherally located, smaller veins may not require urgent clinical evaluation and management, even though these abruptions warrant additional fetal surveillance and appropriately timed delivery to prevent fetal death (49).

Diagnosis

Classic symptoms of abruption include vaginal bleeding and abdominal pain. Uterine contractions are often present, but contractions are not a specific abruption characteristic since painful uterine contractions are also present in normal labor. Although there is potential for bleeding from fetal sources, associated vaginal bleeding is typically of maternal origin. Abruption is ultimately a clinical diagnosis that requires the exclusion of other causes of vaginal bleeding such as placenta previa and cervical dilation with labor, often termed “bloody show.”

Ultrasound may identify findings concerning for abruption, especially when abnormal blood collections adjacent to and within the placenta are large (FIGURE 3–5) (50). Due to limitations of third trimester ultrasound and the similar echotexture of hemorrhagic products and placenta, sonographic findings of abruption may not be evident. In a study of ultrasound characteristics among 30 patients with abruption, ultrasound had sensitivity of 57.0% (CI 37.2–75.6), specificity of 100% (CI 15.8–100.0), positive predictive value of 100% (CI 79.4–100.0), and negative predictive value of 14.0% (CI 1.8–42.8) (51). Another prospective study of 73 pregnant people who presented with vaginal bleeding reported a higher sensitivity to detect abruption of 80% (14). Classic ultrasound findings were described by Yeo and colleagues and include the following: (1) preplacental collection (2) “jello-like” movement of the chorionic plate with fetal activity; (3) retroplacental collection; (4) marginal collection; (5) subchorionic collection; (6) placentomegaly or intraplacental echogenicity; and (7) intra-amniotic hematoma (14).

Figure 3. Intraamniotic hematoma status post motor vehicle accident at 36 weeks’ gestation.

A pregnant patient was a restrained passenger in a motor vehicle accident at 35 weeks’ gestation. An ultrasound performed at 36 weeks’ gestation revealed an intraamniotic hematoma with layering. The patient had an uncomplicated induction of labor at 37 week’s gestation with favorable maternal and neonatal outcomes.

Image courtesy of Susan Egan, RDMS

Figure 5. Placentomegaly associated with catastrophic acute abruption.

A pregnant patient had an ultrasound at 33^4/7 weeks’ gestation that was notable for placentomegaly. The placenta was bulky and contained intraplacental heterogenicities. As a gestational diabetic (class A2), the patient was compliant with twice weekly fetal surveillance with alternating biophysical profiles and non-stress tests. In the 36^th week, she experienced heavy vaginal bleeding at home. She was transported by emergency medical services to a local hospital in hemorrhagic shock with disseminated intravascular coagulopathy and fetal death.

Concealed abruption may manifest in pregnant people with symptoms of abdominal pain and uterine contractions, but without overt vaginal bleeding or with small quantities of bleeding. Concealed abruption can be severe and lead to fetal death and coagulopathy (52). Clinicians should have high index of suspicion in cases of spontaneous tachysystole, even if there are normal ultrasound findings, especially with rapid labor progress. Approximately 10% of spontaneous preterm labor has been attributed to concealed abruption (53), but the impact of concealed abruption on labor at near-term and term gestations is less clear.

In some cases of abruption, there is extravasation of blood into the myometrium, known as uteroplacental apoplexy or Couvelaire uterus (FIGURE 6). This condition is typically not evident sonographically (54), but may be ascertained through direct external inspection of the uterus at cesarean delivery or hysterectomy. Uteroplacental apoplexy is not an absolute indication for hysterectomy.

Figure 6. Couvelaire uterus.

Image courtesy of Aileen Baffo, MD

Clinical management of abruption

Acute near-term and term abruption, whether mild or severe, is typically managed by maternal stabilization followed by delivery. Delivery is recommended to minimize the risks of ongoing vaginal bleeding and the potential for fetal compromise and maternal injury. An algorithm for the management of abruption is described in FIGURE 7.

Figure 7. Algorthim to guide the management of obstetrical hemorrhage associated with placental abruption with acute hemorrhage.

The algorithm for management of placental abruption with acute hemorrhage employs the ATLS classification of hypovolemic shock, which has not been validated in pregnancy and does not consider various factors that may impact physiologic compensatory changes. The staging system is presented here as a theoretic framework to guide the clinical approach to resuscitation in the context of obstetrical hemorrhage due to placental abruption.

Labs include complete blood count and coagulation studies (including PT, aPTT, and fibrinogen) and/or point-of-care tests (including arterial blood gas assessment, thromboelastography, and rotational thromboelastometry)

T&S: type and screen; NICU: neonatal intensive care unit; PRBC: packed red blood cells; FFP: fresh frozen plasma; IUFD: fetal death

There is lack of evidence to guide delivery timing for chronic abruption (55). There is also lack of data to guide management strategies such as inpatient versus outpatient care for these complicated pregnancies. After diagnosis and a period of observation in inpatient settings, outpatient management may be reasonable for preterm patients with chronic abruption who can comply with additional fetal surveillance, including serial fetal growth assessments and antenatal testing. Once or twice weekly fetal surveillance, such as fetal non-stress testing and biophysical profiles, should be initiated at the time of diagnosis (56). Multivessel Doppler velocimetry should also be employed when there is concurrent FGR (57) or when fetal anemia is suspected (58). Patients with chronic abruption also require close monitoring for recurrent episodes of vaginal bleeding. In our opinion, it is reasonable to deliver pregnant patients with chronic abruption during the 36^th and 37^th weeks of gestation. However, the decision should be individualized in situations where there are complicating factors, such as FGR, oligohydramnios, and ongoing vaginal bleeding. Development of any FHR abnormalities in chronic cases should be an indication for delivery in all near-term or term gestations.

At initial evaluation of new onset vaginal bleeding in near-term and term gestations, abruption severity should be ascertained though thorough history, evaluating the inciting event (if any) and quantifying estimated blood loss. The amount of vaginal bleeding, which may be difficult to quantify due to concealed bleeding, does not correlate with clinical sequelae (50). Clinical evaluation should therefore also incorporate assessment of vital signs, urine output, and mental status. The Advanced Trauma Life Support (ATLS) Classification of Stages of Hemorrhagic Shock incorporates these parameters to create a profile of clinical findings associated with various degrees of hemorrhage (59). The staging system has not been validated in pregnancy and does not consider factors that may impact physiologic compensatory changes. Given the high prevalence of hypertension and preeclampsia among pregnant people with abruption at near-term and term gestations, for example, the ATLS classification may underestimate the amount of intravenous fluid and blood products that are required for resuscitation in some cases. Despite these potential limitations, the ATLS classification is presented as a theoretic framework to guide the clinical approach to resuscitation (TABLE 2).

Table 2.

The Advanced Trauma Life Support classification of hypovolemic shock

	Class 1	Class 2	Class 3	Class 4
Estimated blood loss, percent	<15	15–30	30–40	>40
Heart rate, beats per minute	<100	100–120	120–140	>140
Blood pressure	Normal	Normal	Decreased	Greatly decreased
Pulse pressure	Normal or increased	Decreased	Decreased	Decreased
Respiratory rate, breaths per minute	14–20	20–30	30–40	>35
Mental status	Slightly anxious	Mildly anxious	Anxious, confused	Confused, lethargic
Urine output, cc per hour	>30	20–30	5–15	Minimal

Table adapted from: Committee on Trauma, American College of Surgeons. Advanced trauma life support for doctors–student course manual. 8th ed. American College of Surgeons, Chicago 2008.

Caveat: The ATLS classification of hypovolemic shock has not been validated in pregnancy and does not consider various factors that may impact physiologic compensatory changes, such as maternal age, medical comorbidities, and medications (e.g. beta blockers). The staging system is presented here as a theoretic framework to guide the clinical approach to resuscitation in the context of obstetrical hemorrhage due to placental abruption.

The initial management focuses on maternal stabilization including placement of large bore intravenous catheters (eg. 16 or 18 gauge) and fluid resuscitation with crystalloids (60). Stat laboratory tests to evaluate hemoglobin and platelet count as well as coagulation parameters, including prothrombin time (PT) and fibrinogen, and a blood type and antibody screen for red blood cell cross matching, should be obtained. Kleihauer-Betke testing is indicated in patients with vaginal bleeding who are Rh(D)-negative to guide the appropriate administration of Rh(D) immune globulin and does not provide insight into abruption severity. Blood products and coagulation factors may be needed with uncrossed type O-negative blood immediately available and activation of massive transfusion protocols (MTP) when clinically indicated (61).

Fetal status should be assessed after initiating maternal stabilization efforts. A wide array of abnormal FHR patterns is possible (62–65), reflecting the underlying pathophysiology of this condition (TABLE 3). In acute and severe abruption, there is often marked fetal bradycardia with absent variability, which is a pre-terminal FHR pattern. This fetal bradycardia can occur suddenly or can be heralded by variable, late, or prolonged decelerations (FIGURE 8). Fetal tachycardia and minimal or absent variability may or may not be present. In cases of decreased fetoplacental blood flow and hypoxia, sinusoidal FHR patterns can be seen prior to the terminal bradycardia (FIGURE 9) (66–68). Abnormalities in the uterine contraction pattern, such as tetanic or high frequency, low amplitude contractions, may also be present (69–71). In chronic abruption, there may be normal FHR patterns and tocodynamometry allowing conservative management initially. However, when the fetus is becoming compromised, variable or late decelerations with or without fetal tachycardia and minimal or absent variability are frequently present.

Table 3.

Fetal heart rate patterns associated with acute and chronic placental abruption

Abruption Type	Fetal Heart Rate Patterns	Tocodynometry
Acute	• Variable, late, or prolonged decelerations • Fetal tachycardia with minimal and/or absent variability • In cases of profound hypoxia and/or anemia, sinusoidal pattern prior to terminal bradycardia • Fetal bradycardia with absent variability prior to terminal bradycardia	• Increased resting tone • Tetanic or high frequency, low amplitude contractions
Chronic	• Normal patterns • When fetus is becoming compromised, variable or late decelerations with or without fetal tachycardia and minimal and/or absent variability	• Normal patterns

Figure 8. Electronic fetal monitoring of acute abruption with recurrent variable decelerations and minimal variability.

A para 2 pregnant patient presented with crampy abdominal pain for one day at 37 weeks’ gestation. On examination, her abdomen was tender and firm, described by the evaluating physician as “rock hard.” She denied vaginal bleeding. Electronic fetal heart rate monitoring revealed recurrent variable decelerations and minimal variability. The patient underwent urgent cesarean delivery under general anesthesia for presumed concealed abruption with category 2 fetal heart rate pattern. The amniotic fluid was noted to be meconium stained and blood tinged. The umbilical artery gas revealed pH of 7.02, PC02 of 79.0 mmHg, and standard base excess of −11.9 mmol/L, indicating mixed metabolic and respiratory acidosis.

Figure 9. Example of a sinusoidal fetal heart rate pattern associated with marked fetal hypoxia due to decreased fetoplacental blood flow.

A para 1 pregnant patient was admitted to the intensive care unit with hypoxic respiratory failure, sepsis, and hypotension refractory to multiple vasopressors at 28 week’s gestation. The patient was severely acidotic despite resuscitation with bicarbonate. Fetal monitoring revealed a sinusoidal pattern (sometimes referred to as a pseudosinusoidal pattern in this context), a pre-terminal pattern associated with decreased fetoplacental blood flow and severe hypoxia. The patient underwent urgent cesarean delivery, but the fetus was profoundly acidotic and died in the operating room.

A majority of abruption will have FHR changes, though It is not clear if abruption at near-term and term gestations have different profiles of abnormal FHR patterns compared to abruption at preterm gestations. In a retrospective cohort study of 355 patients who had clinical abruption in 2009 and delivered in a consortium of 94 centers in Japan, and after excluding 89 fetal deaths on presentation, 166 (62.4%) FHR tracings were abnormal (72). Severity of FHR changes also correspond with severity of abruption. In an analysis of 40 pregnant people in Japan with abruption, absent variability and bradycardia were associated with 5 minute Apgar <7, arterial umbilical cord blood pH <7.1, and larger abruption (64). Several studies suggest that acute abruption is a significant contributor to category III FHR patterns due to terminal bradycardia and sinusoidal FHR patterns (62, 64–68).

Intrauterine resuscitative measures such as maternal position changes and supplemental oxygen may be of limited benefit. Antenatal corticosteroids to promote fetal maturation may be considered prior to 36^6/7 weeks (when delivery is anticipated in 7 days and prior to 37 weeks’ gestation), but delivery should not be deferred to administer steroids in the late preterm period (34^0/7to 36^6/7 weeks) (73). Tocolytics should not be utilized during this gestational age range. Magnesium sulphate is also not used during this range for neuroprotection, though it should be utilized for seizure prophylaxis in cases of preeclampsia with severe features.

After delivery, there may be evidence of an adherent clot on the fetal surface of the placenta (FIGURE 10) (74). If an intraplacental hematoma forms and self-limits the amount of bleeding, the abruption may be detected at delivery with observation of an organized hematoma in an area of infarcted placenta. The histologic finding that appears to be most strongly associated with acute abruption is hemorrhage in the decidua basalis with underlying parenchymal indentation (FIGURE 11) (75). In the absence of this indentation (e.g. if the abruption is acute and blood passes vaginally or into the amniotic fluid) and in chronic abruption, other nonspecific histologic features may be present on postpartum pathologic evaluation of the placenta, including intravillous and intervillous hemorrhage, early trophoblastic necrosis, and decidual inflammation (74). A retrospective study of 305 cases of abruption that characterized placental histopathology found that abruption ≥34 week’s gestation were characterized by fewer placental maternal vascular malperfusion lesions, maternal inflammatory response lesions, and placental hemorrhages compared to abruption <34 weeks (76).

Figure 10. Placenta with large adherent retroplacental hematoma.

Image courtesy of Catherine W. Chan, MD

Figure 11. Histology of acute placental abruption.

Retroplacental hemorrhage extending into the decidua and indenting the placental parenchyma, consistent with placental abruption. Retroplacental hemorrhage is shown at the bottom of the image, indenting the decidua and placental parenchyma (marked by X). Chorionic villi are above the indenting hemorrhage. Magnification is 2x.

Image courtesy of Debra Heller, MD

Clinical challenges associated with abruption

Obstetrical hemorrhage

Abruption with heavy vaginal bleeding at near-term and term gestations requires prompt evaluation and management. Several principles guide this care, such as identifying the cause of bleeding, expediting delivery to control bleeding, providing supportive care, and early recognition of DIC. The administration of packed red blood cells (PRBC) and coagulation factors, termed blood component therapy, is an essential part of this supportive care (77, 78). Transfusion of ≥4 units is a marker of significant obstetrical morbidity (79). The risk of massive transfusion, defined as ≥10 units of PRBC, is uncommon. In a large retrospective cohort study that included all delivery hospitalizations for hospitals that reported at least one delivery-related transfusion per year in New York (1998–2007), massive transfusion occurred in 6 per 10,000 deliveries, and abruption was a strong independent risk factor (occurring in 1 per 10,000 deliveries; adjusted OR 14.6, 95% CI 11.2–19.0) (80).

Blood component therapy

The main purpose of PRBC transfusion is to improve oxygen carrying capacity. If effective fluid resuscitation ensures adequate intravascular volume, oxygen extraction at the tissue level can compensate for the reduction in arterial oxygen content until anemia becomes very severe (81, 82). In stable pregnant patients with self-limited episodes of acute vaginal bleeding (as well as postpartum patients), restrictive approaches to blood transfusion may be considered. Clinical trials suggest that a hemoglobin of <6–7 g/dL is appropriate for many patients (83), but consideration of potential additional bleeding during labor and at delivery is necessary. Transfusion in the context of active and heavy bleeding should not be based on specific hemoglobin thresholds and rather should be guided by vital signs, the amount of current and anticipated bleeding, and the projected length of time until delivery (e.g. when bleeding potential is highest, but when active bleeding may conclude).

Fresh frozen plasma (FFP) contains all coagulation factors and fibrinogen. Its use is indicated when a pregnant patient with abruption is thought to have multiple acquired coagulation factor deficiencies, such as in cases of obstetrical hemorrhage treated with massive transfusion and in cases of DIC. Although FFP can provide some volume expansion, it should not be used for this purpose. Rather, intravenous fluids such as crystalloids and albumin and other plasma derivatives may restore circulating blood volume without exposing patients to the potential risks associated with FFP. Cryoprecipitate is a plasma derived product that contains fibrinogen and other coagulation factors including factor VIII, factor XIII, and von Willebrand factor. Although its use is declining in favor or specific coagulation factor concentrates that have more favorable risk profiles, cryoprecipitate remains a mainstay for treatment of acquired hypofibrinogenemia. Cryoprecipitate should be administered to ensure the patient with abruption has fibrinogen levels of >50–100 mg/dL. In the context of active bleeding, platelets should be transfused to a goal of >50 × 10³ per mL. Often platelets are transfused in the setting of massive transfusion, accompanying PRBC and FFP transfusions. TABLE 4 describes characteristics of blood components, including PRBC, FFP, cryoprecipitate, and platelets.

Table 4.

Blood component therapy to guide management of obstetrical hemorrhage due to placental abruption

Component	Volume	Contents	Time to prepare	Risks*	Effect**	ABO cross matching required?	Indications
Packed red blood cells	250–300 cc per unit; hematocrit is typically 55%	Red blood cells, white blood cells, plasma	30 minutes (stored frozen)	Infection, transfusion reactions, volume overload, hyperkalemia	1 unit increases hemoglobin by 1 g/dL	Yes, but can use O-negative uncrossed PRBCs in emergencies	• Hemoglobin <6–7 g/dL (unless medical comorbidities warrant higher threshold) • Hemoglobin <9 g/dL in active bleeding
Fresh frozen plasma	200–250 cc per unit; INR of FFP is 1.1	All coagulation factors, including fibrinogen	30 minutes (stored frozen)	Infection, transfusion reactions, volume overload	1 unit increases factor concentrations by 30% and increases fibrinogen by 10–15 mg/dL	Yes, but Rh(D) status does not need to be considered and can use type AB FFP in emergencies	• Hemorrhage and/or active bleeding in patients with (or at risk for) multiple acquired coagulation factor deficiencies (eg. INR >2.0, aPTT >1.5× normal, or abnormal clotting factor activity by TEG/ROTEM) • FFP should not be used for volume expansion
Cryoprecipitate	10–20 cc per unit; typically administered in 5 or 10 unit pools	Fibrinogen, Factor VIII, Factor XIII, and von Willebrand factor	30 minutes (stored frozen)	Infection, transfusion reactions	1 unit increases fibrinogen by 10–15 mg/dL; 5-unit pool increases fibrinogen by 50 mg/dL	No	• Hemorrhage and/or active bleeding in patients with acquired hypofibrinogenemia, defined as fibrinogen <50–100 mg/dL
Platelets	250–300 cc per unit of apheresis*** derived platelets or per 5–6 units of pooled platelets	Platelets, plasma, small numbers of RBCs and WBCs	Rapidly available (stored room temperature)	Risks may be higher for whole blood derived platelets; infection, transfusion reactions	Increases platelets by 30–50×103/mL	ABO compatible platelets are preferred, but ABO incompatible platelets can be used with minimal risk	• Platelets <50 ×103/mL with active bleeding and/or massive transfusion

PRBC: packed red blood cells; FFP: fresh frozen plasma; INR: international normalized ratio; TEG/ROTEM: thromboelastography/rotational thromboelastometry

^*Risks greatest in those receiving massive transfusions; strategies to reduce risks include use of leukoreduced products, volume reduced products, saline washed products, and pathogen inactivated products

^**Assumes no bleeding

^***Apheresis: process whereby one or more blood component is collected, and other components are returned to donor

Note: Pre-thawed PRBC and FFP may be immediately available in many high-volume centers and most Level I trauma centers

Point-of-care viscoelastic testing

Coagulation studies have limitations to guide decision making related to blood transfusion in the context of abruption with significant hemorrhage (84). These tests were developed to monitor the degree of coagulation conferred by exogenous anticoagulants, not to ascertain the bleeding risk of obstetrical patients. These limitations as well as potential for delayed results have driven interest in point-of-care testing that can characterize viscoelastic hemostatic properties, such as thromoboelastography (TEG) and rotational thromboelastometry (ROTEM) (85–88). These tests evaluate the viscoelastic properties of clot, such as time to initiate clot, time to amplify clot, clot strength, and the degree of fibrinolysis, among other properties (TABLE 5, FIGURE 12-A). The main advantages are in rapid results and goal directed therapy. TEG/ROTEM results are typically available in 15–20 minutes, which is much faster than coagulation studies (88). Additionally, these point-of-care tests may direct resuscitative efforts to avoid over treatment (89–91). Several simplified examples of TEG temograms are illustrated in FIGURE 12. In 12-B, the normal temogram suggests an adequate hemostatic profile; uterotonic medications, intrauterine tamponade balloon, and other surgical approaches may be helpful to control bleeding. Temogram 12-C reflects prolonged R and K times, which suggests that acquired coagulation deficiencies are present and should be addressed with FFP. Temogram 12-D has slightly prolonged R time, but the K time is prolonged, the alpha angle is decreased, and the maximum amplitude is decreased. The viscoelastic properties suggest hypofibrinogenemia is responsible for bleeding and cryoprecipitate is indicated. Finally, in temogram 12-E, the K time is prolonged and the maximum amplitude is decreased, suggesting thrombocytopenia is the underling etiology and platelet transfusion is indicated.

Table 5.

Thromboelastography and the viscoelastic properties of clot formation

TEG variable	ROTEM equivalent	Derivation	Main determinants	Interpretation	Main corrective components	Approximate normal values
Reaction time (R time)	Clotting time (CT)	Time for clot initiation from start of test to the first detectable fibrin strands (amplitude of 2 mm); minutes	Activity of coagulation factors	Prolongation may indicate deficiency of procoagulants or presence of anticoagulants	FFP	4–8 minutes
Kinetics time (K time)	Clot formation time (CFT)	Time from clot initiation to reach clot width of 20 mm amplitude, reflects amplification; minutes	Activity of coagulation factors	Possible early indicator of clot deficiency or hypercoagulability	FFP	1–4 minutes
∝ angle	Clot formation time	Thrombin burst or propagation (speed at which the fibrin builds up and crosslinking takes place); slope of line between R and K, formed by the slope of the TEG tracing from the horizontal line; degrees	Presence and interactions of fibrinogen	Prolongation may suggests platelet dysfunction or deficiency, fibrinogen deficiency, or both; shortening may indicate hypercoagulability	Cryoprecipitate	47–74 degrees
Maximum amplitude (MA)	Maximum clot firmness (MCF)	Strength of the clot (stability) as measured by maximum curve width; mm	Platelets (80%) and fibrin (20%)	Reduced MA may represent reduce platelet number and function, as well as impaired fibrin cross-linking	Platelets	55–73 mm
Clot lysis time at 30 and 60 minutes (CL30, CL60) after maximum clot strength	LY30, LY60	Amount of clot lysis at 30 and 60 minutes after MA is achieved; percent decrease in amplitude	Activity of fibrinolytic factors	Indicates possible need for antifibrinolytic agents	Tranexamic acid	0–8% at CL30

TEG: thromboelastography; ROTEM: rotational thromboelastometry; FFP: fresh frozen plasma

Table adapted from: Pavord S, Maybury H. How I treat postpartum hemorrhage. Blood. 2015;125(18)2759–70.

Nelson DB, Ogunkua O, Cunningham FG. Point-of-Care Viscoelastic Tests in the Management of Obstetric Hemorrhage. Obstet Gynecol 2022;139:463–72

Figure 12. Examples of thromoboelastography temograms that may be encountered in obstetric hemorrhage.

A. Normal temogram that illustrates the various viscoelastic properties of clot formation; B. Normal hemostasis: the R time, K time, α angle, and maximum amplitude are normal; C. Clotting factor deficiency: the R and K time are prolonged, and α angle and maximum amplitude are decreased; D. Hypofibrinogenemia: the R time is normal or prolonged, and the K time is prolonged, the alpha angle is decreased, and the maximum amplitude is decreased; E. Thrombocytopenia: the R time is normal, but the K time is prolonged and the maximum amplitude is decreased.

An example of obstetrical hemorrhage protocol that employs TEG to guide blood component therapy is illustrated FIGURE 13. An alternative protocol that employs ROTEM and was utilized in a cohort of 521 subjects who had moderate and severe postpartum hemorrhage and evaluated the test characteristics of ROTEM compared with routine coagulation studies was recently published (92). Cases of abruption with FHR changes, where urgent cesarean delivery may be indicated and there is insufficient time to wait for routine coagulation studies, call for further studies to ascertain whether the adoption of these point-of-care tests and incorporation into clinical management algorithms improves outcomes.

Figure 13. Example of obstetric hemorrhage protocol that employs thromoboelastography.

Protocol courtesy of Sue Pavord, MBChB Leicester, FRCP, FRCPath

Coagulopathy

Abruption is the most common cause of DIC in pregnancy (93, 94). Compared to other causes of obstetrical hemorrhage, pregnant people with significant abruption experience greater decreases in platelets, require more platelet transfusions, and have more acquired hypofibrinogenemia (95–97). In severe abruption, the infusion of collagen and tissue components into maternal circulation leads to the release of tissue factor through the extrinsic clotting pathway. Tissue factor complexes with factor VII and activates factors IX and X (98). Systemic activation of coagulation ensues, leading to the widespread formation of microvascular thrombi in small vessels and endothelial injury with concomitant fibrinolysis, a process that consumes platelets and clotting factors (98). The process is also associated with increased production of fibrin split products and D-dimer and reduction in natural anticoagulants (98).

DIC may be suspected based on clinical presentation and laboratory findings, but no single laboratory test is sufficient to make the diagnosis (99). The classic laboratory findings of DIC are low platelets, prolonged PT and aPTT, and low fibrinogen levels. There may be mild reduction in platelet counts or thrombocytopenia, defined as platelet count less than 150 × 10³ per mL (99). Clinically significant DIC may have normal or mildly reduced fibrinogen levels as it is an acute phase reactant, which limits its sensitivity as test for DIC severity (99). However, early hypofibrinogenemia is highly predictive of severe postpartum hemorrhage (100). Prolongation of the PT and PTT may be a relatively late finding; these tests become prolonged when there is depletion of more than 50% of clotting factors, and clinical bleeding may occur when depletion is >50–75% (99). Scoring systems such as the International Society of Thrombosis and Hemostasis DIC Score (101) was modified for pregnancy (93)(TABLE 6). Although not widely used, a score of ≥26 has a sensitivity of 88% and a specificity of 96% for the diagnosis of DIC.

Table 6.

The International Society for Thrombosis and Hemostasis Scoring System, including modified pregnancy score

	Third trimester values	Modified ISTH DIC Score ≥26: DIC present		ISTH DIC Score ≥5: DIC present
			Assigned weight		Assigned weight
Platelets	146–429×103/mL	<50×103/mL	1	<50×103/mL	3
		50–100×103/mL	2	50–100×103/mL	2
		100–185×103/mL	1	>100×103/mL	0
		>185×103/mL	0
Prothrombin time	9.5–13.4 seconds	PT difference <0.5 seconds	0	PT difference >3 seconds	0
		PT difference 0.5–1.0 seconds	5	PT difference 3–6 seconds	1
		PT difference 1.0–1.5 seconds	12	PT difference >6 seconds	2
		PT difference >1.5 seconds	25
Fibrinogen	373–619 mg/dL	<300 mg/dL	25	<100 mg/dL	1
		300–400 mg/dL	6	>100 mg/dL	0
		400–450 mg/dL	1
		>450 mg/dL	0
D-dimer	483–2256 ng/mL			<400 ng/mL	0
				400–4,000 ng/mL	2
				>4,000 ng/mL	3

PT difference: the difference between the prothrombin time result of the patient and the normal control value

Abbassi-Ghanavati M, Greer LG, Cunningham FG. Pregnancy and laboratory studies: a reference table for clinicians. Obstet Gynecol. 2009;114(6):1326–31.

Aldona Siennicka et al. Reference Values of D-Dimers and Fibrinogen in the Course of Physiological Pregnancy: the Potential Impact of Selected Risk Factors—A Pilot Study. Biomed Res Int. 2020; 3192350.

Erez O, Novack L, Beer-Weisel R, et al. DIC Score in Pregnant Women – A Population Based Modification of the International Society on Thrombosis and Hemostasis Score. PLOS One. 2014;9(4):e93240.

Taylor FB, Jr., Toh CH, et al. Towards definition, clinical and laboratory criteria, and a scoring system for disseminated intravascular coagulation. Thromb Haemost. 2001; 86: 1327–30.

Observational studies suggest that administration of fibrinogen concentrate may result in reduced blood loss in hemorrhage associated hypofibrinogenemia associated with abruption (102, 103). In cases of active bleeding, the use of fibrinogen concentrates as an adjunctive treatment of obstetrical hemorrhage may reduce the need for massive transfusion (104, 105). However, a randomized, placebo-controlled trial explored the preemptive use of fibrinogen concentrates in bleeding pregnant patients with hypofibrinogenemia (106). The study, which included 249 subjects, found that preemptive use did not reduce the risk of blood transfusion. Similar results were also observed in a recent double-blind, randomized placebo-controlled trial, which included 437 patients (107).

Fetal death

Approximately 5–10% of fetal deaths have been attributed to abruption (108). Although some of these cases may not manifest with heavy vaginal bleeding, abruption associated with fetal death should be categorized as severe abruptions that may also be associated with increased risk for maternal morbidity.

Vaginal delivery is the preferred mode of delivery as it avoids the risks of operative bleeding that may be exacerbated by coagulopathy and the potential sequelae associated with multiple repeat cesarean deliveries. In a single center retrospective cohort study of fetal deaths associated with abruption (1995–2015), vaginal delivery was successful in 14 of 15 (93.3%) cases that underwent trial of labor. Patients with Bishop scores >3 had shorter labors (3:37 hours versus 7:58 hours) and larger blood loss (3605 cc versus 1788 cc) compared to patients with Bishop scores ≤3 (109), which reflects the observation that pregnancies complicated by severe abruption may have rapid labors.

The management of patients with fetal death and prior uterine surgery and risk factors for uterine rupture, such as multiple cesarean deliveries, prior classical hysterotomy, and prior uterine rupture, should be individualized (110). Induction of labor in patients with one prior cesarean delivery via low transverse hysterotomy may be considered. For some patients who are at increased risk of uterine rupture, an induction and trial of labor may be reasonable approach, though early recognition of uterine rupture is imperative. Some patients may require laparotomy if there is clinical concern for uterine rupture. A repeat cesarean delivery may be performed for patients who have risk factors for uterine rupture and in whom the associated risks of trial of labor are perceived to be prohibitive (110).

Adverse outcomes among pregnant people

Short-term risks

Short term risks of abruption are often driven by hemorrhage. Pregnant people who experience abruption have increased risks of hemorrhagic shock, DIC, need for blood transfusion, and hysterectomy. Risks in the postpartum period also include intensive care unit admission and maternal death (4).

Long-term effects

Recent evidence suggests that pregnant people who experience clinical abruption are at increased risk of mortality from cardiovascular disease (CVD) and cerebrovascular disease, as well as non-fatal morbidity, pointing to long-term consequences of this condition. A recent systematic review and meta-analysis of 11 studies comprising 6,325,152 pregnancies suggested that the risk of combined CVD and stroke mortality was 2.65-fold (95% CI 1.55–4.54) higher among pregnant people with abruption compared to those without abruption (111). Similarly, the risk of non-fatal CVD and stroke complications was 1.32-fold (95% CI 0.91–1.92) higher among pregnant people with abruption compared to those without abruption. Importantly, there is evidence of increasing risks of CVD and stroke mortality with increasing number of abruptions across successive pregnancies. To the extent that abruption is associated with increased risk of preterm birth as well, it remains unknown whether increased CVD risks are shaped by abruption that occur at preterm versus term gestations (53, 112–114).

There are several pathways through which abruption may confer increased risks of CVD. It is thought that obstetrical complications, particularly ischemic placental disease, serve as a “stress test” that unmasks preexisting CVD. These obstetrical complications induce uteroplacental ischemia, resulting in oxidative stress, vascular damage, and thrombosis (49). Abruption and CVD share similar pathways from disruption of the vascular system and hemostatic defects, suggesting that the factors that contribute to abruption also continue to future CVD (115).

Perinatal outcomes

Short-term effects

Pregnancies complicated by abruption end, on average, about 3–4 weeks earlier than otherwise normal pregnancies. Among non-abruption births, the perinatal mortality rate is about 8 per 1000, which is in sharp contrast to the mortality rate among abruption births (15-fold greater, 120 per 1000) (116). Well over half of the increased perinatal mortality risk that accompanies abruption is attributed to preterm delivery and an additional 9% to FGR (116).

Long-term effects

There is evidence of increased risks of an array of neurological complications and neurodevelopmental deficits in the offspring of subjects that develop abruption. Neonates exposed to abruption, particularly those that complicate pregnancies at preterm gestations, are at increased risk for cystic periventricular leukomalacia and intraventricular hemorrhage (117, 118). Abruption is associated with 6 to 10-fold increased risk of cerebral palsy and 2 to 4-fold increased risk of developmental disorders in infants born of abruption pregnancies (62, 118–121). Data from the US CPP (1959–66 with follow-up to 1974) showed that the risk ratio of abnormal motor and mental assessments at 8-months of life were 2.35 (95% CI 1.39–3.98) and 2.03 (95% CI 1.13–3.64), respectively, in relation to abruption. The associations at 4 years were attenuated and resolved fully at 7 years (22). These findings provide compelling evidence that some neurodevelopmental effects of abruption may be transient. Importantly, this study showed that preterm birth mediated up to three-fourths of this association at 8-months, with progressively decreasing proportions at 4 and 7 years of the abruption-neurodevelopmental associations (22). A large cohort study of 217,910 deliveries with 1003 cases of abruption reported no increased risk of non-fatal CVD in the offspring (hazard ratio 1.12, 95% CI 0.60–2.11) (122).

Conclusions

In this review, we focus on abruption at near-term and term gestations, when the impact of preterm birth is reduced and we can glean insights into the direct effects of abruption. When pregnant people present to labor and delivery with vaginal bleeding due to abruption—abdominal pain, vaginal bleeding, and abnormal FHR patterns—urgent evaluation and management is required. Although abnormal FHR patterns and coagulopathy pose clinical challenges, early recognition of DIC, the administration of blood component therapy, and expediting delivery are essential components of abruption. This review seeks to provide comprehensive, clinically focused guidance during a gestational age range when neonatal outcomes can often be favorable if rapid and evidence-based care is optimized.

Figure 4. Evolution of a large subchorionic hematoma from 32 to 35 weeks gestation.

A pregnant patient with vaginal spotting was observed to have a large subchorionic hematoma at 32 weeks’ gestation (A). In this context, she was diagnosed with a placental abruption. After a period of inpatient surveillance, she was discharged home with outpatient fetal surveillance, including twice-weekly fetal assessments of wellbeing and serial growth ultrasounds. (B) At 35 weeks’ gestation, she had repeat evaluation of the subchorionic hematoma. The hematoma appeared slightly smaller, but its appearance was similar to adjacent placental tissue.

Images courtesy of Susan Egan, RDMS