Acute placental abruption: Pathophysiology, clinical features, diagnosis, and consequences

INTRODUCTION — Placental abruption is defined as the premature separation of the placenta from the decidua at or after 20 weeks gestation. The major clinical findings are vaginal bleeding and abdominal pain, often accompanied by uterine contractions (including tachysystole), uterine tenderness, and a nonreassuring fetal heart rate pattern. Abruption is a significant cause of both maternal morbidity and neonatal morbidity and mortality, particularly when it occurs preterm.

This topic will discuss the epidemiology, pathophysiology, etiology, clinical features, diagnosis, and consequences of placental abruption. Management and long-term prognosis of patients with abruption is reviewed separately. (See "Acute placental abruption: Management and long-term prognosis".)

INCIDENCE — The overall incidence of placental abruption is approximately 3 to 10 per 1000 births [1,2]. The United States and Canada are at the upper end of this range, while the Netherlands, Spain, Finland, Sweden, Denmark, and Norway are at the lower end. The incidence appears to be increasing in the United States and Canada and declining in Nordic countries [1]. Changes in incidence may be related to changes in the prevalence of risk factors for the disorder and/or to changes in case ascertainment [3,4].

DISTRIBUTION OF CASES BY TIMING AND SEVERITY

●Mild versus severe – Two-thirds of abruptions are severe, which is defined by ≥1 of the following maternal, fetal, or neonatal complications in a patient diagnosed with abruption [5]:

•Maternal – Disseminated intravascular coagulation (DIC), hypovolemic shock, blood transfusion, hysterectomy, renal failure, in-hospital death

•Fetal – Nonreassuring fetal status, fetal growth restriction, death

•Newborn – Preterm birth, small for gestational age (SGA), death

●Gestational age – The gestational age at diagnosis in a series of over 500 abruptions with a live birth was as follows [6]; however, gestational age-specific incidence rates vary considerably depending on the etiology [7,8]:

•Term – 60 percent

•32 to 36 weeks – 25 percent

•<32 weeks – 14 percent

●Antepartum versus intrapartum – The proportion of abruptions diagnosed antepartum versus intrapartum in another series was [2]:

•Antepartum – 56 percent

•Intrapartum – 44 percent

PATHOPHYSIOLOGY

Overview — The immediate cause of the premature placental separation is rupture of maternal vessels in the decidua basalis. Rarely, the bleeding originates from the fetal-placental vessels. The accumulating blood splits the decidua, separating off a thin layer of decidua with its placental attachment.

The ruptured maternal vessel may be an artery or a vein.

●In acute severe abruption, high-pressure arterial hemorrhage in the central area of the placenta extensively dissects through the placental-decidual interface and causes complete or nearly complete placental separation. This leads to rapid development of the potentially life-threatening clinical manifestations of abruption, such as severe maternal bleeding, maternal disseminated intravascular coagulation (DIC), and category III fetal heart rate patterns.

A small proportion of these cases are caused by sudden mechanical events (eg, blunt abdominal trauma,) or by rapid uterine decompression (eg, after birth of the first twin or rapid release of polyhydramnios). These acute events can strain the interface between the pliable myometrium and the inelastic placenta. In motor vehicle crashes, an additional factor is rapid acceleration-deceleration of the uterus, which causes uterine stretch exceeding concomitant placental stretch, leading to a shearing force between the placenta and the uterine wall. Severe maternal trauma is associated with a sixfold increase in abruption, while minor blunt trauma is unlikely to result in abruption [9,10]. In the absence of a preceding traumatic or mechanical event, the trigger for acute abruption cannot be determined with certainty.

●In chronic abruption, early abnormal spiral artery development leads to decidual necrosis, placental inflammation (and possibly infarction), and ultimately low-pressure venous hemorrhage, typically at the periphery of the placenta (ie, marginal abruption). This process tends to be self-limited and results in a small area of separation. The clinical manifestations occur over time and include light intermittent bleeding, oligohydramnios, and fetal growth restriction associated with redistribution of cerebral blood flow (decrease in the middle cerebral artery pulsatility index [11]) [7,8,12-14].

Role of thrombin — Thrombin plays a key role in the clinical consequences of placental abruption, and may be important in its pathogenesis, as well. It is formed via two pathways: in one pathway, decidual bleeding leads to release of tissue factor (thromboplastin) from decidual cells, which generates thrombin [15]. In the other pathway, decidual hypoxia induces production of vascular endothelial growth factor, which acts directly on decidual endothelial cells to induce aberrant expression of tissue factor, which then generates thrombin [16]. The production of thrombin can lead to the following clinical sequelae:

●Uterine hypertonus and contractions, as thrombin is a potent, direct uterotonic agent [17].

●Enhanced expression of matrix metalloproteinases [15,18], up-regulation of genes involved in apoptosis [16], and induced expression of inflammatory cytokines (predominantly interleukin-8), leading to tissue necrosis and degradation of extracellular matrix [16,19-21]. A vicious cycle then ensues, resulting in further vascular disruption, and often leading to initiation of labor and membrane rupture (algorithm 1).

In patients with prelabor rupture of membranes, the risk of placental abruption increases with increasing latency, which suggests that inflammation subsequent to membrane rupture can also induce rather than simply result from the cascade of events leading to placental separation [22-26].

●Bleeding diathesis. If a massive amount of tissue factor (thromboplastin) is released, a massive amount of thrombin is generated and enters the maternal circulation over a brief period [27]. This overwhelms hemostatic control mechanisms without allowing sufficient time for recovery of compensatory mechanisms. The clinical consequence is a profound systemic bleeding diathesis and, due to widespread intravascular fibrin deposition, ischemic tissue injury and microangiopathic hemolytic anemia (ie, DIC).

●Functional progesterone withdrawal by reduced expression of progesterone receptors in decidual cells, which initiates or contributes to uterine contractility [28].

RISK FACTORS

●Previous abruption – Previous abruption is the strongest risk factor for abruption, with recurrence risks of 10- to 15-fold higher [29]. Patients with a placental abruption in their first pregnancy have a greatly increased risk of placental abruption, as much as 93-fold higher (95% CI 62-139) in a subsequent pregnancy [30]. Abruption at term in the first pregnancy appears to be associated with a greater risk for recurrence (adjusted odds ratio [aOR] 188, 95% CI 116-306) than preterm abruption (<37 weeks: aOR 52, 95% CI 25-111) or early preterm abruption (<32 weeks: aOR 39, 95% CI 13-116) in the first pregnancy.

Recurrent abruption is associated with earlier gestational ages at delivery compared with first episodes, although perinatal mortality rates are similar [31]. Other major risk factors are described in the table (table 1) [3,32].

●Hypertension – Patients with hypertension have a fivefold increased risk of severe abruption compared with normotensive patients. Antihypertensive therapy in patients with chronic hypertension appears to reduce the risk of abruption, probably as a result of reducing hydrostatic pressure and spiral arterial wall damage accruing from severe hypertension [33].

●Structural uterine abnormalities – Structural uterine abnormalities include congenital anomalies, synechiae, and leiomyoma [34]. They represent mechanically and biologically unstable sites for placental implantation; abruption at these sites may be due to inadequate decidualization and/or shear. Congenital anomalies are associated with a fivefold odds of placental abruption [35], with uterine septae associated with a greater risk compared with fusion defects (such as bicornuate and didelphys uteri) [36].

●Behavioral factors

•Cocaine use – The pathophysiological effect of cocaine in the genesis of abruption is unknown but may be related to cocaine-induced vasoconstriction leading to ischemia, reflex vasodilatation, and disruption of vascular integrity. As many as 10 percent of pregnant individuals using cocaine in the third trimester will develop an abruption [37-39].

•Cigarette smoking – Smoking is one of the few modifiable risk factors [40] and associated with a fourfold increased risk of abruption [41]. The mechanism(s) that underlie the relationship between smoking and abruption are unclear. One hypothesis is that the vasoconstrictive effects of smoking cause placental hypoperfusion, which could result in decidual ischemia, necrosis, and hemorrhage leading to premature placental separation [42,43]. Vitamin C-E supplementation appeared to mitigate the risk of abruption among smokers in one study [44], but this finding must be cautiously interpreted given the small number of events and wide confidence interval.

The combination of cigarette smoking and hypertension has a synergistic effect on risk [45].

●Genetic factors – The risk of abruption is increased in patients whose sister had an abruption [46]. Pregnant individuals who were born small for gestational age (SGA) are more likely to experience a severe abruption; the risk is further increased if their siblings were also SGA (relative risk 2.4, 95% CI 1.7-3.3), supporting a familial preponderance to ischemic placental disease [47].

●Other

•Miscellaneous associations – Additional modest risk factors for abruption that have been reported include asthma [48,49], subclinical hypothyroidism [50], major fetal congenital anomalies (especially when the fetus is growth restricted) [51], prior cesarean birth [52], pregnancy-related acute kidney injury [53], air pollution exposure [54-56], conception as a result of assisted reproductive technology [57,58], marginal placental cord insertion, grand multiparity [59,60], and short maternal stature [61].

A strong association between physical exertion very close to delivery and abruption were observed in one study [62]; however, many confounders in this study remain unknown (such as altitude, dietary habits, and other forms of physical exertion). Prospective studies should be performed to confirm this finding in other populations and, if confirmed, to determine which types of physical exertion may be associated with abruption. Although it is common for patients with a history of abruption to avoid strenuous activity in fear of a recurrence, there are insufficient data to support a recommendation for limiting physical activity for the purpose of reducing the risk of placental abruption.

•COVID-19 – A link between COVID-19 infection during pregnancy and adverse obstetrical outcomes, including abruption, has been investigated with inconsistent findings [63,64]. A case-control study of stillbirths among those with and without COVID-19 infections identified an increase in abruption among cases and a second study found an increased odds of abruption in the setting of COVID-19 (odds ratio [OR] 1.86) [65]. However, in a large retrospective cohort of over 800,000 deliveries, no difference in the rate of abruption was identified in pregnant individuals who tested positive compared with those who tested negative for COVID-19 [64].

•Incidental biomarkers – Abnormalities of maternal serum biochemical markers used for Down syndrome or neural tube defect screening carry up to a 10-fold increase in risk of subsequent abruption [66-71]. These markers include increased alpha fetoprotein or human chorionic gonadotropin, decreased pregnancy-associated plasma protein A or unconjugated estriol, and inhibin A ≤5^th or ≥95^th percentile, not explained by fetal abnormalities. Patients with multiple abnormal biochemical markers are at highest risk [70].

In patients who underwent first-trimester cell-free DNA screening for Down syndrome, a low fetal fraction was associated with a 2.5-fold increased risk of composite obstetric morbidity, including placental abruption, in one study [72].

Some early maternal serum metabolomics and placenta-specific microRNAs have been implicated as markers of future abruption [73,74].

CLINICAL FEATURES OF ACUTE ABRUPTION

Patient presentation

●Classic presentation – Patients with an acute abruption classically present with the abrupt onset of vaginal bleeding, mild to moderate abdominal pain, and uterine contractions. Back pain may be an additional prominent symptom when the placenta is on the posterior wall of the uterus. The uterus is often firm and may be rigid and tender. If a substantial volume of blood has extravasated into the myometrium, it can become "woody hard," with fetal parts no longer palpable. Contractions are often high frequency and low amplitude, but a typical labor pattern is also possible and may result in rapid labor progress. However, not all signs may be present simultaneously. In patients who have experienced abdominal trauma or a motor vehicle crash, symptoms generally develop within 24 hours of the precipitating event. (See "Initial evaluation and management of major trauma in pregnancy", section on 'Initial evaluation and management of major trauma'.)

The severity of abdominal pain is a useful marker of the severity of the abruption and in turn, maternal and fetal/newborn risk of morbidity and mortality [75]. In particular, the combination of abdominal pain, hypotension, and fetal heart rate abnormalities suggest clinically significant separation that could result in severe maternal morbidity and fetal death [75-78]. By comparison, the amount of vaginal bleeding correlates poorly with the degree of placental separation: A severe abruption may be associated with mild/clinically insignificant vaginal bleeding when a large volume of blood is retained behind the placenta.

●Other presentations – In 10 to 20 percent of abruptions, patients present for care only because of uterine contractions/irritability with no or minimal vaginal bleeding and no abdominal pain. In these cases, termed concealed abruption, all or most of the blood is trapped between the fetal membranes and decidua rather than escaping through the cervix and vagina [77]. A nonreassuring fetal heart rate pattern may be present.

In a few cases, a small, concealed abruption may be asymptomatic and only recognized as an incidental finding on an ultrasound examination.

Laboratory findings — Laboratory findings correlate with the degree of placental separation. A small degree of placental separation may not be associated with any abnormalities of commonly used tests of hemostasis, whereas >50 percent separation can result in disseminated intravascular coagulation (DIC). DIC is present in 10 to 20 percent of abruptions with death of the fetus. Coagulation defects appear to develop rapidly, within a few hours or even in minutes [79].

The fibrinogen level is the test that correlates best with severity of bleeding [80], presence of overt DIC, and the need for transfusion of multiple blood products [81]. Initial fibrinogen levels ≤200 mg/dL are reported to have 100 percent positive predictive value for severe postpartum hemorrhage, while levels of ≥400 mg/dL have a negative predictive value of 79 percent [82].

Although abruption may result in fetomaternal bleeding, the Kleihauer-Betke test or flow cytometry is not useful diagnostically since it is positive in only 4 percent of patients and correlates poorly with the presence or absence of abruption [77,83-86]. However, if fetal anemia is suspected, testing may be useful in patients who are RhD-negative since fetal blood in the maternal circulation may lead to alloimmunization and the test results can help identify patients who need additional doses of anti-D immune globulin to avoid alloimmunization. (See "RhD alloimmunization: Prevention in pregnant and postpartum patients".)

Ultrasound findings — During the acute phase of abruption, the blood is isoechoic or similar to the surrounding placental tissue. Thus, it can be difficult to differentiate a concealed hemorrhage from the surrounding placental tissue.

The three most common locations for placental abruption are subchorionic (between the placenta and the membranes), retroplacental (between the placenta and the myometrium), and preplacental (between the placenta and the amniotic fluid) [87]. A retroplacental hematoma is the classic ultrasound finding (image 1A-B and image 2A-C). Retroplacental hematomas have a variable appearance; they can appear solid, complex, and hypo-, hyper-, or isoechoic compared with the placenta. Hypoechogenicity and sonolucency are features of resolving rather than acute hematomas (image 3). A retroplacental hematoma is more likely to be seen with more extensive placental separation and in patients who go on to have adverse maternal and perinatal outcomes [88-90], but its absence does not exclude the possibility of abruption, including a severe abruption, because blood may not collect and remain behind the placenta.

Other findings suggestive of abruption include a subchorionic collection of fluid (even remote from the placental attachment site), echogenic debris in the amniotic fluid, or a thickened placenta, especially if it shimmers with maternal movement ("Jello" sign) [91].

CONSEQUENCES — For the mother, the potential consequences of abruption are primarily related to the severity of the placental separation, while the risks to the fetus are related to both the severity of the separation and the gestational age at which birth occurs [7,8,77,78,92-97]. With mild placental separation, there may be no significant adverse effects. As the degree of placental separation increases, the maternal and perinatal risks also increase [5,77,78,92,93,98]. In one large series, gross examination of the placenta at delivery revealed the following estimated frequencies of placental separation: less than 25 percent placental separation (54 percent); 25 to 49 percent placental separation (16 percent); 50 to 74 percent placental separation (13 percent); over 75 percent placental separation (17 percent) [78].

Maternal — Serious maternal consequences of abruption include:

●Excessive blood loss and disseminated intravascular coagulation (DIC), which can lead to hypovolemic shock, acute kidney injury, adult respiratory distress syndrome, multiorgan failure, peripartum hysterectomy and, rarely, death [6,77].

●Emergency cesarean birth for fetal or maternal indications.

In addition to these acute consequences, the mother is at increased long-term risk of premature cardiovascular disease [99,100] and doubling of the risk of death after coronary artery revascularization [101-104]. These increased risks may reflect underlying maternal vascular abnormalities that manifest during pregnancy as abruption. Increased overall mortality and at an earlier age compared with patients without abruption has also been noted [105].

Fetal — Serious fetal and neonatal consequences of abruption include:

●Increased perinatal morbidity and mortality related to hypoxemia, asphyxia, low birth weight, and/or preterm birth [2,78,92-95,98,106-109].

●Growth restriction/small for gestational age (SGA) birthweight (when abruption is chronic) [78,92-94,98,110]. (See 'Chronic abruption' below.)

In population-based studies, the perinatal mortality rate ranged from 3 to 12 percent (versus 0.6 percent in births without abruption) [92,106,109,111,112]. More than 50 percent of abruption-related perinatal deaths are stillborns due to intrauterine asphyxia, which generally occurs when over 45 percent of the placenta detaches, particularly central detachment [6,113]. Deaths in the postnatal period are primarily related to preterm birth [92,106,111,112,114].

Abruption is implicated in up to 10 percent of preterm births [77,78,98]. Preterm birth may be iatrogenic due to the nonreassuring fetal or maternal condition, or it may be related to preterm labor or preterm prelabor rupture of membranes [77]. Neonatal morbidities are strongly linked to preterm birth [2]. Of note, perinatal mortality associated with abruption appears to be decreasing [106].

Fetal asphyxia, preterm birth, and growth restriction can be associated with short- and long-term sequelae, and abruption appears to compound the risk. A study of 29 neonates from pregnancies complicated by abruption at a median of 29 weeks of gestation reported a 10-fold increase in periventricular leukomalacia compared with matched neonates in pregnancies without abruption; the rate of periventricular leukomalacia was 34 percent [115]. Long-term neurodevelopmental deficits among children born after placental abruption appear to be mediated largely through preterm birth [116]. (See "Overview of short-term complications in preterm infants" and "Perinatal asphyxia in term and late preterm infants" and "Infants with fetal (intrauterine) growth restriction" and "Overview of the long-term complications of preterm birth".)

DIAGNOSIS

Clinical — Acute abruption should be suspected in a pregnant patient with the abrupt onset of vaginal bleeding (any) plus abdominal and/or back pain and contractions, especially when associated with uterine tenderness and increased uterine tone. In patients with these classic symptoms, fetal heart rate abnormalities or fetal demise and/or maternal disseminated intravascular coagulation (DIC) strongly support the diagnosis and indicate extensive placental separation. (See 'Patient presentation' above.)

Ultrasound examination is useful for identifying a retroplacental hematoma, which strongly supports the clinical diagnosis in symptomatic patients (positive predictive value 88 percent) [89,91,117], but it is absent in many patients (sensitivity 25 to 60 percent [89,117-119]) (see 'Ultrasound findings' above). Ultrasound is also useful for excluding other disorders associated with vaginal bleeding and abdominal pain, since abruption is often a diagnosis of exclusion in a patient with vaginal bleeding and no other identified etiology. (See 'Differential diagnosis' below.)

Acute abruption should also be suspected in a pregnant patient with uterine irritability and a nonreassuring fetal status, as a small percentage of patients with severe abruption present without vaginal bleeding.

Patients undergoing evaluation after abdominal trauma may undergo contrast enhanced computed tomography (CT) of the abdomen to rule out an internal injury. In this setting, CT has high sensitivity but low specificity for identifying abruption and can estimate the extent (<25 percent, 25 to 50 percent, >50 percent) of placental separation [120]. Likewise, magnetic resonance imaging (MRI) can detect abruption and may be more sensitive than ultrasound examination, but increased diagnostic certainty is unlikely to change management or be cost effective [121,122].

Placental pathology — Acute abruption is considered a clinical rather than a histologic diagnosis. Only 30 to 50 percent of acute abruptions with vaginal bleeding are associated with diagnostic histologic findings [13,123]: Grossly, blood accumulation on the maternal surface with congestion and/or hemorrhage within or compression of the overlying parenchyma; microscopically, blood accumulation beneath and dissecting the decidua and compression of the overlying intervillous space, with villous crowding, congestion, and/or intravillous hemorrhage with touching villi [124]. Histologic evidence of decidual bleeding alone is a nonspecific finding noted in 2 to 4 percent of births; most cases are associated with preterm prelabor rupture of membranes or preterm labor and birth rather than a clinical diagnosis of abruption [77,125].

In less acute cases, an organizing retroplacental hematoma indenting the parenchyma may be noted [13]. Recent infarcts may be present and are characterized by preservation of villous stromal architecture, eosinophilic degeneration of the syncytiotrophoblast, and villous agglutination with scattered intervillous neutrophils. These infarcts take approximately four to six hours to develop. However, there is no clear stepwise progression of histologic lesions that allow accurate timing of the placental separation [123].

DIFFERENTIAL DIAGNOSIS — In pregnant patients with suspected abruption, the differential diagnosis of vaginal bleeding accompanied by abdominal pain and contractions includes labor, placenta previa, uterine rupture, and subchorionic hematoma.

●Labor – The signs and symptoms of labor have a more gradual onset than those of abruption. The onset of labor (preterm or term) is characterized by mild uterine contractions at infrequent and/or irregular intervals; the contractions become more regular and painful over time and are accompanied by cervical dilation and/or effacement. Mucus that has accumulated in the cervix may be discharged as clear, pink, or slightly bloody secretions (ie, mucus plug, bloody show), sometimes several days before labor begins. Early labor is usually associated with less bleeding, less uterine rigidity, less abdominal pain, and fewer high frequency contractions compared with abruption; however, there is an overlap in symptoms since abruption may trigger labor or occur intrapartum. (See "Preterm labor: Clinical findings, diagnostic evaluation, and initial treatment".)

●Placenta previa – The characteristic clinical presentation of placenta previa is painless vaginal bleeding after 20 weeks of gestation; however, 10 to 20 percent of patients present with uterine contractions associated with the bleeding. Thus, abruption and placenta previa can be difficult to distinguish clinically since abruption may not be associated with significant pain and placenta previa may not be painless. In pregnant patients with vaginal bleeding, an ultrasound examination should be performed to determine whether placenta previa is the source. (See "Placenta previa: Epidemiology, clinical features, diagnosis, morbidity and mortality", section on 'Diagnosis'.)

●Uterine rupture – Uterine rupture is most common in patients with a prior hysterotomy, and usually occurs during labor. Signs of uterine rupture may include the sudden onset of fetal heart rate abnormalities, vaginal bleeding, constant abdominal pain, cessation of uterine contractions, recession of the presenting part, and maternal hypotension and tachycardia. Many of these symptoms are also seen with abruption because uterine rupture often leads to placental separation; however, cessation of uterine contractions and recession of the presenting part, when present, are strongly associated with rupture and would be unusual during an abruption. (See "Uterine rupture: After previous cesarean birth" and "Uterine rupture: Unscarred uterus".)

●Subchorionic hematoma – Subchorionic hematoma is thought to result from partial detachment of the chorionic membranes from the uterine wall, in contrast to abruption, which is due to detachment of the placenta from the uterine wall [126]. Patients are asymptomatic or experience light vaginal bleeding. In contrast to abruption, abdominal pain is typically absent, a minority of patients experience cramping or contractions, and the diagnosis is usually made before rather than after 20 weeks of gestation [127]. The diagnosis is based on ultrasound findings of a hypoechoic or anechoic crescent-shape area behind the fetal membranes, which may also elevate the edge of the placenta [128]. Patients with subchorionic hematomas have a greater than fivefold increased risk of developing an abruption, as well as other pregnancy complications (eg, preterm labor, prelabor rupture of membranes) [128].

CHRONIC ABRUPTION

●Clinical findings and course – Patients with chronic abruption experience relatively light, chronic, intermittent bleeding. They are at risk of developing placental ischemia, resulting in oligohydramnios (termed chronic abruption-oligohydramnios sequence [129]), fetal growth restriction, and/or preeclampsia [23,24,110]. They are also at risk of developing preterm prelabor rupture of membranes, which is another cause of oligohydramnios.

●Laboratory and imaging – Coagulation studies are usually normal. Ultrasound examination may identify a placental hematoma (retromembranous, marginal, or central), and serial examinations may reveal fetal growth restriction and/or oligohydramnios.

●Outcome – Chronic abruption-oligohydramnios sequence has a dismal prognosis, including high rates of fetal death, serious neonatal morbidity from preterm birth, and neonatal death [129-132].

●Placental pathology – Histological examination of the placenta may show chronic lesions, such as chronic deciduitis (lymphocytes with or without plasma cells), decidual necrosis, villitis, decidual vasculopathy (specifically, in the vessels of the extraplacental membrane roll), placental infarction, intervillous thrombosis, villous maldevelopment, and hemosiderin deposition [13].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Obstetric hemorrhage".)

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●Basics topic (see "Patient education: Placental abruption (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Terminology and pathophysiology – Placental abruption (ie, abruptio placentae) refers to partial or complete separation of the placenta from the decidua occurring at any time after 20 weeks of gestation and before fetal expulsion. It may be classified as mild or severe. Rupture of maternal arterial or venous vessels in the decidua basalis is the direct cause of the separation. (See 'Introduction' above and 'Pathophysiology' above.)

●Risk factors – Risk factors are listed in the table (table 1). In patients who smoke cigarettes and/or have chronic hypertension, smoking cessation and antihypertensive therapy to prevent severe hypertension appear to reduce risk. (See 'Risk factors' above.)

●Patient presentation – The classic presentation is abrupt onset of vaginal bleeding, mild to moderate abdominal pain and/or back pain, and uterine contractions, which may be high frequency and low amplitude or a normal labor pattern. The uterus is often firm and may be rigid and tender. The fetal heart rate pattern may be nonreassuring. In patients who have experienced abdominal trauma or a motor vehicle crash, symptoms generally develop within 24 hours of the precipitating event. In 10 to 20 percent of abruptions, patients present with only preterm labor with or without a nonreassuring fetal heart rate pattern; some abruptions are asymptomatic. The amount of bleeding does not correlate well with the extent of maternal hemorrhage and cannot be used as a marker to gauge the severity of placental separation. (See 'Patient presentation' above.)

●Laboratory findings – A small degree of placental separation may not be associated with any abnormalities of commonly used tests of hemostasis, whereas >50 percent separation can result in disseminated intravascular coagulation (DIC), which is present in 10 to 20 percent of abruptions with death of the fetus. A fibrinogen level ≤200 mg/dL correlates well with severe bleeding. (See 'Laboratory findings' above and 'Role of thrombin' above.)

●Diagnosis – The diagnosis is clinical and based on the abrupt onset of mild to moderate vaginal bleeding and abdominal and/or back pain, accompanied by uterine contractions. A retroplacental clot is the classic ultrasound finding and strongly supports the clinical diagnosis but is absent in many patients. In patients with classic symptoms, fetal heart rate abnormalities or fetal demise and/or DIC strongly support the clinical diagnosis and indicate extensive placental separation. (See 'Diagnosis' above and 'Ultrasound findings' above and 'Laboratory findings' above and 'Consequences' above.)

●Shortterm consequences – Two-thirds of abruptions are severe, which is defined by ≥1 of the following findings (see 'Distribution of cases by timing and severity' above and 'Consequences' above):

•Maternal – DIC, hypovolemic shock, blood transfusion, hysterectomy, renal failure, in-hospital death

•Fetal – Nonreassuring fetal status, fetal growth restriction, death

•Newborn – Preterm birth, small for gestational age birth weight, death

●Chronic abruption – Patients with chronic abruption experience relatively light, chronic, intermittent bleeding. They may develop oligohydramnios (termed chronic abruption-oligohydramnios sequence), fetal growth restriction, and preeclampsia. They are also at risk of preterm prelabor rupture of membranes (See 'Chronic abruption' above.)