INTRODUCTION — Placental abruption (also referred to as abruptio placentae) refers to partial or complete placental detachment prior to delivery of the fetus. The diagnosis is typically reserved for pregnancies over 20 weeks of gestation. The major clinical findings are vaginal bleeding and abdominal pain, often accompanied by uterine 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 pathophysiology, etiology, clinical features, diagnosis, and consequences of placental abruption. Management of patients with abruption is reviewed separately. (See "Placental abruption: Management and long-term prognosis".)

INCIDENCE — Placental abruption complicates approximately 2 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, Canada, and several Nordic countries [1], possibly due to increases in the prevalence of risk factors for the disorder and/or to changes in case ascertainment [3,4].

Two-thirds of abruptions are classified as severe, based on the presence of associated maternal, fetal, and neonatal morbidity/mortality [5]. (See 'Severe abruption' below.).

In one large series of over 500 abruptions with a live birth, 60.4 percent occurred at term, 25.3 percent occurred at 32 to 36 weeks, and 14.3 percent occurred before 32 weeks [6]. However, gestational age-specific incidence rates vary considerably depending on the etiology [7,8].

PATHOPHYSIOLOGY — 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. Complete or nearly complete placental separations are caused by high pressure arterial hemorrhage in the central area of the placenta that extensively dissect through the placental-decidual interface. This leads to rapid development of potentially life-threatening clinical manifestations of abruption (eg, severe bleeding, maternal disseminated intravascular coagulation [DIC], fetal heart rate abnormalities). Low pressure venous hemorrhage, typically at the periphery of the placenta (marginal abruption), tends to be self-limited and results in a small area of separation. The clinical manifestations occur over time (eg, light intermittent bleeding, oligohydramnios, and fetal growth restriction associated with redistribution of cerebral blood flow [decrease in the middle cerebral artery pulsatility index [9]]).

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 [10]. 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 [11]. The production of thrombin can lead to the following clinical sequelae:

●Uterine hypertonus and contractions, as thrombin is a potent, direct uterotonic agent [12].

●Enhanced expression of matrix metalloproteinases [10,13], up-regulation of genes involved in apoptosis [11], and induced expression of inflammatory cytokines (predominantly interleukin-8), leading to tissue necrosis and degradation of extracellular matrix [11,14,15]. A vicious cycle then ensues, resulting in further vascular disruption, and often leading to initiation of labor and rupture of membranes (algorithm 1).

In women with prelabor rupture of membranes, the risk of placental abruption increases with increasing latency, which suggests that inflammation subsequent to membrane rupture can induce rather than result from the cascade of events leading to placental separation [16-20].

●Triggering of coagulation. 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 of time [21]. 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 [22].

ETIOLOGY — The etiology of bleeding at the decidua basalis remains speculative in most cases, despite extensive clinical and epidemiologic research. Most abruptions appear to be related to a chronic placental disease process. In these cases, abnormalities in the early development of the spiral arteries lead to decidual necrosis, placental inflammation and possibly infarction, and ultimately vascular disruption and bleeding [7,8,23-25].

A small proportion of all abruptions are related to sudden mechanical events (eg, blunt abdominal trauma [26]) or rapid uterine decompression (eg, after delivery of the first twin). The sudden stretching or contraction of the underlying uterine wall caused by these events causes shearing of the inelastic placenta [7,8]. In motor vehicle crashes, an additional factor is rapid acceleration-deceleration of the uterus, which causes uterine stretch without 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, but even minor trauma can result in abruption [27].

RISK FACTORS

Clinical — Previous abruption is the strongest risk factor for abruption, with recurrence risks of 10- to 15-fold higher [28], and as high as 93-fold higher (95% CI 62-139) than in women with no previous abruption [2]. Other major risk factors are described in the table (table 1) [29].

Cocaine use and smoking are important, but less common risk factors for abruption. 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 women using cocaine in the third trimester will develop placental abruption [30-32].

Smoking is one of the few modifiable risk factors for abruption [33]. Smoking is associated with a 2.5-fold increased risk of abruption sufficiently severe to result in fetal death, and the risk increases by 40 percent for each pack per day smoked [34]. 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 [35,36]. Vitamin C-E supplementation appeared to mitigate the risk of abruption among smokers in one study [37], but this finding must be cautiously interpreted given the small number of events and wide confidence interval.

Hypertensive women have a fivefold increased risk of severe abruption compared with normotensive women. Antihypertensive therapy does not appear to reduce this risk in women with chronic hypertension [38]. The combination of cigarette smoking and hypertension has a synergistic effect on risk [39].

Uterine anomalies (eg, bicornuate uterus), uterine synechiae, and leiomyoma are modest risk factors for abruption [40]. They represent mechanically and biologically unstable sites for placental implantation; abruption at these sites may be due to inadequate decidualization and/or shear.

Additional modest risk factors for abruption include asthma [41,42], a sister who had an abruption [43], major fetal congenital anomalies (especially when the fetus is growth restricted) [44], prior cesarean delivery [45], pregnancy-related acute kidney injury [46], air pollution exposure [47-49], and conception as a result of assisted reproductive technology [50]. In addition, mothers of short stature and those born small for gestational age (SGA) are more likely to experience a severe abruption; the risk is further increased if her siblings were also SGA (relative risk 2.4, 95% CI 1.7-3.3), supporting a familial preponderance to ischemic placental disease [51,52].

There are insufficient data to support a recommendation for limiting physical activity for the purpose of reducing the risk of placental abruption, although it is common for women with a history of abruption to avoid strenuous activity in fear of a recurrence. A case-crossover study of women who delivered in Peruvian hospitals reported an increased risk of placental abruption in the hour following moderate or heavy physical exertion (odds ratio 7.8, 95% CI 5.5-11.0), especially in those with a sedentary lifestyle [53]. Physical exertion was assessed through a 15-point visual analog Borg scale, with scores ranging from 6 to 20. Women were asked to define the level of physical exertion based on intensity of episodes categorized as light (eg, mopping), moderate (eg, dancing), or heavy (eg, sprinting). Despite the strong associations between physical exertion very close to delivery and abruption, 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 placental abruption.

Laboratory — 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 [54-60]. 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. Women with multiple abnormal biochemical markers are at highest risk [59].

In women 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 [61].

Research studies have also implicated early maternal serum metabolomics, placenta-specific microRNAs [62,63], and subclinical hypothyroidism as biomarkers of future placental abruption [64].

CLINICAL FEATURES

Acute abruption

Patient presentation — Women with an acute abruption classically present with the abrupt onset of vaginal bleeding, mild to moderate abdominal and/or back pain, and uterine contractions. Back pain is prominent when the placenta is on the posterior wall of the uterus. The uterus is often firm, and may be rigid and tender.

Contractions are usually high frequency and low amplitude, but a contraction pattern typical of labor is also possible, and labor may proceed rapidly.

Vaginal bleeding ranges from mild and clinically insignificant to severe and life-threatening. Blood loss may be underestimated because the blood may be retained behind the placenta and thus difficult to quantify. The amount of vaginal bleeding correlates poorly with the degree of placental separation and does not serve as a useful marker of impending fetal or maternal risk.

By contrast, abdominal pain [65], hypotension, and fetal heart rate abnormalities suggest clinically significant separation that could result in fetal death and severe maternal morbidity [65,66]. When the presenting symptom is abdominal pain, the incidence of preeclampsia, preterm birth, maternal hemorrhage, and neonatal compromise is increased compared with women whose presenting symptom is vaginal bleeding, highlighting the point that the degree of bleeding correlates poorly with outcomes [66].

When placental separation exceeds 50 percent, acute disseminated intravascular coagulation (DIC) and fetal death are common [67,68].

In 10 to 20 percent of placental abruptions, patients present with only preterm labor, and no or scant vaginal bleeding. 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 [67]. Therefore, in pregnant women with abdominal pain and uterine contractions, even a small amount of vaginal bleeding should prompt close maternal and fetal evaluation for placental abruption. In other cases, a small concealed abruption may be asymptomatic and only recognized as an incidental finding on an ultrasound.

Occasionally, the signs and symptoms of abruption develop after rapid uterine decompression, such as after uncontrolled rupture of membranes in the setting of polyhydramnios or after delivery of a first twin. Signs and symptoms of abruption also may occur after maternal abdominal trauma or a motor vehicle crash. In these cases, placental abruption generally presents within 24 hours of the precipitating event and tends to be severe. The clinical presentation and obstetric evaluation of pregnant trauma victims are described in detail separately. (See "Initial evaluation and management of major trauma in pregnancy", section on 'Initial evaluation and management of major trauma'.)

Laboratory findings — Mild separation/hemorrhage may not be associated with any abnormalities of commonly used tests of hemostasis.

Severe abruption can lead to DIC. DIC occurs in 10 to 20 percent of severe abruptions with death of the fetus. (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults", section on 'Diagnostic evaluation'.)

The fibrinogen level has the best correlation with severity of bleeding [69], presence of overt DIC, and the need for transfusion of multiple blood products [70]. 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 [71]. Diagnosis of DIC in pregnant women is reviewed separately. (See "Disseminated intravascular coagulation (DIC) during pregnancy: Clinical findings, etiology, and diagnosis", section on 'Diagnosis'.)

The Kleihauer-Betke test or flow cytometry is positive in a small proportion of abruptions. There is poor correlation between the results of these tests and the presence or absence of abruption [67,72-74]; sensitivity is only 4 percent [75].

Imaging

●Ultrasound – Identification of a retroplacental hematoma is the classic ultrasound finding of placental abruption (image 1). 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 2).

The sensitivity of ultrasound findings for diagnosis of abruption is only 25 to 60 percent [76-79], but the positive predictive value is high (88 percent) when ultrasound findings suggestive of abruption are present in symptomatic patients [76,79,80]. A thorough search for other findings in symptomatic patients may improve the sensitivity and specificity of ultrasound. These findings include subchorionic collections 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) [80].

Sonographic findings consistent with placental abruption are associated with the worst maternal and perinatal outcomes. However, whether a hematoma is identified depends on the extent of hemorrhage, chronicity of the bleeding, and extent that blood has escaped through the cervix (image 3A-B and image 4A-B). Although the worst outcomes appear to occur when there is sonographic evidence of a retroplacental hematoma [79,81], the absence of retroplacental hematoma does not exclude the possibility of severe abruption because blood may not collect behind the placenta.

●Magnetic resonance imaging – Magnetic resonance imaging can detect abruptions missed by ultrasound examination, but increased diagnostic certainty is unlikely to change management or be cost-effective [82,83].

●Computed tomography (CT) – Although contrast enhanced CT is rarely used as a first-line imaging test in pregnancy, it may be performed after maternal trauma to rule out an internal injury. In this setting, it has high sensitivity but low specificity for identifying placental abruption [84]. CT can also estimate the extent (<25 percent, 25 to 50 percent, >50 percent) of placental separation.

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 delivery occurs [7,8,67,68,85-90]. 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 [67,68,85,86,91]. In a retrospective cohort study, the frequency of serious maternal complications among women with no abruption, mild abruption, and severe abruption was 15, 33, and 142 per 10,000 women, respectively [5].

●Maternal consequences – Serious maternal consequences of abruption include:

•Excessive blood loss and DIC, which generally necessitate blood transfusion and can lead to hypovolemic shock, renal failure, adult respiratory distress syndrome, multiorgan failure, peripartum hysterectomy and, rarely, death [6,67].

•Emergency cesarean delivery for fetal or maternal indications.

In addition to these acute consequences, the mother is at increased long-term risk of premature cardiovascular disease and doubling of the risk of death after coronary artery revascularization [92-95]. 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 women without abruption has also been noted [96].

●Fetal/neonatal consequences – Serious fetal and neonatal consequences of abruption include:

•Increased perinatal morbidity and mortality related to hypoxemia, asphyxia, low birth weight, and/or preterm delivery [68,85-88,91,97-100].

•Fetal growth restriction (with chronic abruption) [68,85-87,91,101]. (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) [85,97,100,102,103]. 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 [6,104]. Deaths in the postnatal period are primarily related to preterm birth [85,97,102,103,105].

Placental abruption is implicated in up to 10 percent of preterm births [67,68,91]. 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 [67]. Of note, perinatal mortality associated with abruption appears to be decreasing [97].

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 [106]. Long-term neurodevelopmental deficits among children born after placental abruption appear to be mediated largely through preterm birth [107]. (See "Short-term complications of the preterm infant" and "Perinatal asphyxia in term and late preterm infants" and "Infants with fetal (intrauterine) growth restriction" and "Long-term outcome of the preterm infant".)

Placental pathology — Abruptio placentae is considered a clinical diagnosis: Only half of revealed, acute abruptions will demonstrate histologic confirmation. The most common findings are indentation of the maternal surface of the placenta and intravillous hemorrhage [108].

In less acute cases, an organizing retroplacental hematoma indenting the parenchyma may be noted [24]. 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. There does not, however, appear to be a clear stepwise progression of histologic lesions that would allow accurate timing of abruption [108].

Histological findings, such as diffuse retromembranous and/or intradecidual hemorrhages, pigmented histiocytes, irregular basal intervillous thrombi, and recent villous stromal hemorrhage, are not specific for the diagnosis. Histologic evidence of decidual hemorrhage is noted in 2 to 4 percent of deliveries; most cases are associated with preterm prelabor rupture of membranes or preterm labor and delivery rather than a clinical diagnosis of abruption [67,109].

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) [68].

Recurrence — Women with placental abruption are at severalfold higher risk of abruption and other manifestations of ischemic placental disease in a subsequent pregnancy. (See "Placental abruption: Management and long-term prognosis", section on 'Recurrence risk' and "Placental abruption: Management and long-term prognosis", section on 'Other pregnancy-related risks'.)

Chronic abruption — Women with chronic abruption experience relatively light, chronic, intermittent bleeding. They are at risk of developing clinical manifestations of ischemic placental disease over time, such as oligohydramnios (termed chronic abruption-oligohydramnios sequence [110]), fetal growth restriction, and preeclampsia [17,18,101]. They are also at risk of preterm prelabor rupture of membranes.

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.

Abruption in the second trimester accompanied by oligohydramnios has a dismal prognosis, including high rates of fetal death, preterm birth, and serious neonatal morbidity or death [110-113].

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 [24].

DIAGNOSIS — The diagnosis of abruptio placentae is primarily clinical, but findings from imaging, laboratory, and postpartum pathologic studies can be used to support the clinical diagnosis. Women with an acute abruption classically present with the abrupt onset of mild to moderate vaginal bleeding and abdominal and/or back pain, accompanied by uterine contractions. The uterus has increased tone/rigidity and may be tender both during and between contractions. In patients with classic symptoms, fetal heart rate abnormalities or intrauterine fetal demise and/or maternal disseminated intravascular coagulation (DIC) strongly support the clinical diagnosis and indicate extensive placental separation. (See 'Patient presentation' above and 'Chronic abruption' above.)

Ultrasound examination is useful for identifying a retroplacental hematoma and for excluding other disorders associated with vaginal bleeding and abdominal pain (see 'Differential diagnosis' below). A retroplacental hematoma is the classic ultrasound finding and strongly supports the clinical diagnosis, but is absent in many patients with abruption. (See 'Imaging' above.)

Postpartum, the absence of characteristic placental findings does not exclude the diagnosis. In a multicenter case-control study, standardized gross and histopathological evaluation of the placenta was only able to confirm a strong clinical diagnosis in 30 percent of cases (49/162) [24]. (See 'Placental pathology' above.)

Severe abruption — Severe abruption has been defined as an abruption with ≥1 of the following complications in the mother, fetus, or newborn [5]:

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

●Fetal – Nonreassuring status, growth restriction, death.

●Newborn – Preterm birth, small for gestational age, death.

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

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".)

The characteristic clinical presentation of placenta previa is painless vaginal bleeding after 20 weeks of gestation; however, 10 to 20 percent of women 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 women 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 is most common in women with a prior hysterotomy, and usually occurs during labor. Signs of uterine rupture may include the sudden onset 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 is believed 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 [114]. 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 [115]. 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 [116]. Women with subchorionic hematomas have a greater than fivefold increased risk of developing an abruption, as well as other pregnancy complications (eg, preterm labor, premature rupture of membranes) [116].

DETERMINING THE CAUSE OF ABRUPTION — In the absence of a preceding traumatic or mechanical event, the cause of most abruptions cannot be determined with certainty. (See 'Etiology' above.)

A thorough history and physical examination may identify risk factors for the disorder (see 'Risk factors' above). A standardized interview to screen for misuse of substances is part of this review; some examples are shown in the table (table 2). (See "Clinical assessment of substance use disorders" and "Substance use during pregnancy: Screening and prenatal care".)

Laboratory screening for underlying conditions, such as subclinical hypothyroidism, at the time of presentation is not recommended, as it provides little assistance in the acute assessment or management of abruption.

MANAGEMENT — (See "Placental abruption: Management and long-term prognosis".)

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".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

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

SUMMARY AND RECOMMENDATIONS

●Placental abruption refers to partial or complete separation of the placenta prior to delivery of the fetus. (See 'Introduction' above.)

●Most placental abruptions are related to a chronic pathologic vascular process, but some are due to acute events, such as trauma or vasoconstriction. The immediate cause of placental separation is rupture of maternal blood vessels in the decidua basalis. The subsequent release of tissue factor and generation of thrombin lead to many of the clinical sequelae of acute abruption. (See 'Etiology' above.)

●A prior abruption is the major risk factor. Risk factors for placental abruption are listed in the table (table 1). (See 'Risk factors' above.)

●The classic symptoms and signs of acute placental abruption are vaginal bleeding, abdominal pain, contractions, uterine rigidity and tenderness, and possibly a nonreassuring fetal heart rate (FHR) tracing. In 10 to 20 percent of placental abruptions, patients present with only preterm labor, and no vaginal bleeding. 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 premature placental separation. FHR abnormalities suggest clinically significant separation that could result in fetal death. (See 'Patient presentation' above.)

●A retroplacental clot is the classic ultrasound finding of placental abruption, but is not always present. (See 'Imaging' above.)

●When placental separation exceeds 50 percent, acute disseminated intravascular coagulation (DIC) and fetal death are common. (See 'Laboratory findings' above and 'Consequences' above.)

●In contrast to acute abruption, patients with chronic placental abruption experience relatively light, chronic, intermittent bleeding and exhibit clinical manifestations that develop over time, such as oligohydramnios, fetal growth restriction, and preeclampsia. (See 'Chronic abruption' above.)

●The diagnosis of acute abruption 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 with abruption. In patients with classic symptoms, FHR abnormalities or intrauterine fetal demise and/or DIC strongly support the clinical diagnosis and indicate extensive placental separation. (See 'Diagnosis' above.)

●Severe abruption has been defined as an abruption with ≥1 maternal complication (DIC, hypovolemic shock, blood transfusion, hysterectomy, renal failure, in-hospital death), fetal complication (nonreassuring status, growth restriction, death), or newborn complication (preterm birth, small for gestational age, death). (See 'Severe abruption' above.)

●Women with placental abruption are at severalfold higher risk of abruption in a subsequent pregnancy, especially if the abruption was severe. (See 'Recurrence' above.)