The prevalence of placental abruption (PA) ranges from 0.4 to 1 % of all pregnancies and depends on the population. In Nordic countries, approximately 0.38–0.51 % of all pregnancies are complicated by placental abruption. This rate tends to be higher in the USA (0.6–1 %). In the developing areas, e.g., in some African countries, PA incidence can reach up to 2 %. According to epidemiological reports, the incidence of PA has been steadily increasing. The recurrence rate of placental abruption is 8.8 and 25 % after one and two events, respectively [1–8, 11].

Preterm detachment of the placenta is potentially disastrous, especially for the fetus, with perinatal mortality of 25 %. The incidence of PA is the highest at 24–26 weeks of gestation and decreases with advancing gestation. Over 50 % of the cases occur before 37 completed weeks of gestation. In the developed countries, almost 10 % of preterm deliveries are caused by placental abruption [9, 10]. High neonatal mortality is mainly related to prematurity, low birth weight, IUGR, and asphyxia. A 25-fold higher mortality is present even in term pregnancies complicated by PA. Although the stillbirth rate due to abruption has declined, it remains an important cause of neurological deficits in the first year of life. Approximately 20 % of the survivors delivered between 26 and 36 weeks present cerebral palsy [12].

Maternal morbidity and mortality associated with PA include massive blood loss, disseminated intravascular coagulation, emergency hysterectomy, the need for blood transfusion, renal failure, and maternal death. In Western Europe and the USA, PA-related maternal mortality is 0.4 per 1,000 births. The rate of maternal deaths depends on the level of medical care, ranging from 1 to 4.7 in the developing countries [10, 13, 14].

The underlying pathomechanism of placental abruption remains unclear. PA seems to be a multifactorial disease, with different causative patterns in preterm and term gestations. Several risk factors, i.e., abdominal trauma, hypertension, or coagulopathy, have been defined as strongly related to placental abruption. However, there are still many cases which occur without any perceptible causes [15].

The placenta is fixed to the uterine wall by the anchoring villi. When spiral arteries lack the physiologic trophoblast invasion, abruption might occur. Infusion of thromboplastic material induces disseminated intravascular coagulation. Hypertonicity of the uterus occurs probably to prevent the entrance of further thromboplastic material into the maternal circulation. The conditions which contribute to the avulsion of the anchoring placental villi from the expanding lower uterine segment, which in turn leads to bleeding into the decidua basalis, can be explained by a number of hypotheses [16–20].

Lack of one hypothesis about the mechanism which leads to placental abruption is the reason why identification of the most frequent risk factors for this severe pregnancy complication is a subject of much heated debate. The literature offers reports on numerous multicenter analyses which have been conducted to identify the most common risk factors (Table 3.1) [38].

Advanced maternal age (>35 years) and parity have the strongest correlation with placental abruption out of the sociodemographic and behavioral risk factors. Some authors also mention maternal age of <20. In general analyses, black ethnic origin, marital status (unmarried), and lower socioeconomic status are related to higher prevalence of placental abruption [24, 25].

Several studies have demonstrated that maternal smoking during pregnancy increases the risk for abruption even by 2.5-fold. Interestingly, paternal smoking doubles the risk. Probably, quitting smoking before pregnancy reduces the risk to the level of nonsmokers. Among drug-using women, cocaine use is the strongest risk factor for abruption, increasing the risk even by 8.6-fold [5, 23, 25, 26].

Among pregnancy-related risk factors, pregnancy-induced hypertension and preeclampsia have been demonstrated to have the strongest correlation with PA (2.5 and 4.4, respectively). Many studies have shown that the more severe the hypertension, the higher the risk for abruption [2, 6, 28, 29]. Other pregnancy complications which can increase the incidence of placental abruption include placenta previa, vaginal bleeding in the early pregnancy, and multiple gestations. The risk for PA in case of premature rupture of membranes is 5.9 % and is related to sudden changes of intrauterine pressure and increased risk for chorioamnionitis [1, 2, 6, 29].

Chronic hypertension is one of the most frequent maternal risk factors for PA. Chronic hypertension complicates 0.3–0.8 % of all pregnancies and often corresponds with other risk factors, including advanced maternal age, black race, smoking, and parity. According to the literature, chronic hypertension increases the risk for abruption by 2.4-fold [2, 27, 28]. Also, thrombophilia and hyperhomocysteinemia are strongly related with the risk for PA. Hyperhomocysteinemia is associated with folate and vitamin B12 deficiency, which can be the direct cause of the abruption. In most studies, homozygous methylenetetrahydrofolate reductase point mutation 677 is related to an even sevenfold increase of PA. Literature data about the wide range of thrombophilia are insufficient, but a Swedish study of Prochazka failed to show a correlation between factor V Leiden carrier rate and placental abruption [30–33].

In the group of history-related risk factors, special attention should be paid to patients after previous cesarean section. According to the literature, the first cesarean delivery increases the risk for abruption by 30–40 % in the next pregnancy, as compared to the first vaginal delivery. The risk increases to 52 % if the inter-pregnancy interval is <1 year [4, 34, 35].

Approximately 6 % of all trauma cases in pregnancy and 20–25 % of major traumas are associated with PA. The first manifestation of placental abruption after abdominal trauma occurs mainly within 6–48 h. In rare cases, placental abruption can manifest even up to 5 days after the initial trauma [21, 36, 37].

Depending on the extent of the separation, placental abruption can be partial or complete. Due to localization of the detachment, abruption can be classified as marginal or central.

Clinical classification contains 0–3 classes and is based on the severity of the clinical symptoms.

Class 0 – asymptomatic:

The diagnosis is made retrospectively by finding an organized blood clot or a depressed area on a delivered placenta.

Class 1 – mild (48 % of the cases); the characteristics include the following:

Class 2 – moderate (27 % of all cases); the characteristics include the following:

Class 3 – severe (28 % of all cases); the characteristics include the following:

Placental abruption should be taken into consideration in each case of vaginal bleeding in the second and third trimester of pregnancy. The presence of a large retroplacental hematoma in most cases results in typical signs such as abdominal pain, contractions, and uterine tenderness. In case of strong suspicion of PA and signs of fetal distress, immediate management should be initiated, without any delay caused by an additional examination. Regardless, numerous hematomas do not reach significant size and remain asymptomatic. If the course of the events is not rapid, an ultrasound examination could be performed. According to the literature, sensitivity of ultrasound diagnosis of a hematoma is not higher than 50 %. Nevertheless, due to its availability and short time required for the exam, ultrasound examination of the placenta is considered very helpful and can be useful in the differential diagnosis between PA and placenta previa (Fig. 3.6a, b).

Placental abruption results in a wide variety of sonographic findings, e.g., preplacental fluid collection (between the placenta and the amniotic fluid); jellylike movements of the chorionic plate induced by fetal activity; presence of marginal, subchorionic, or intra-amniotic hematoma; and increased heterogeneous placental thickness (>5 cm in the perpendicular plane) (Figs. 3.7, 3.8, 3.9, and 3.10). Most of them depend on the location of the bleeding and its duration. The locations of the hemorrhage can be categorized as follows: most frequent, subchorionic (between the myometrium and the placental membranes), retroplacental (between the placenta and the myometrium), and preplacental (between the myometrium and the amniotic fluid). Most subchorionic hematomas are contiguous with the placental margin. However, in some cases the majority of the blood separates from the placenta and forms a hematoma on the myometrial surface, opposite the placenta.

Echogenicity of a hematoma strictly correlates to the time of the bleeding. Acute bleeding (<48 h) can be presented as a hyperechoic area, defined as equal to or greater than the adjacent placenta. Acute hematoma often imitates placental tissue, making the correct diagnosis challenging even for experienced sonographers (Fig. 3.11a, b). In order to avoid misdiagnosis, the examination may need to be repeated in the next 24 h. In the next 3–7 days, the hematoma is presented as a hypoechogenic area similar to the myometrium. After 2 weeks, the major part of the hematoma becomes sonolucent (anechoic) and can be compared to the amniotic fluid.

The volume of the hematoma and the size of the detached area of the placenta are the most appropriate prognostic factors in a sonographic examination. Three perpendicular diameters (D) need to be measured and put into the following formula:0.52 × (D1 × D2 × D)3, to estimate the volume of the hemorrhage (Figs. 3.12 and 3.13). In cases when the detachment exceeds 50 % of the placenta or the hematoma volume is over 50 ml, the prognosis is very poor [40, 42–44].

Color Doppler flow images add a considerable value to sonographic examination by excluding, i.e., placental vascular abnormalities, adhesive disorder, or vasa previa (Fig. 3.14).

Importantly, lack of sonographic confirmation does not exclude placental abruption and should never delay management .