Placental abruption (abruptio placentae) is the premature separation of a normally implanted placenta from the uterus after the 20th week of gestation prior to fetal delivery. It occurs in approximately 1% of pregnancies. The pathophysiology of placental abruption involves rupture of a decidual spiral artery. The resulting hemorrhage dissects between layers of the decidua basalis with loss of corresponding placental area for fetal gas exchange. If >50% of placenta is involved, fetal death is likely, representing the distinction between a "total" abruption and a "partial" abruption. The dissection can be self-limited and can self-tamponade without any external signs of its occurrence, called a "concealed" abruption. Alternatively or additionally, it can progress to the placental edge and track down between fetal membranes resulting in external vaginal bleeding and stimulating pain and uterine contractions, called an "acute" abruption. In some cases, chronic placental separation occurs with slowly expanding retroplacental blood clot called "chronic" abruption.

Severity is variable. Classic presentation is acute-onset vaginal bleeding and abdominal (uterine) pain with physical exam findings of uterine tenderness and contractions and fetal compromise on external fetal heart rate monitoring (late or variable decelerations, prolonged bradycardia, sinusoidal pattern). The majority of affected patients will have stable vital signs. Other patients will show severe, potentially life-threatening bleeding (overt or concealed), uterine contractions, hypovolemic shock, consumptive coagulopathy, and fetal death in 1 out of every 420 pregnancies. A patient who is stable upon presentation may quickly destabilize as abruption evolves.

Etiology of placental abruption is variable. Traumatic abruption may occur secondary to acute shearing forces resulting from motor vehicle accident or blunt abdominal trauma, or from sudden decompression of an overdistended uterus such as with membrane rupture in the setting of polyhydramnios (elevated amniotic fluid levels) or after delivery of multiple gestation. Primary placental disorders such as preeclampsia and intrauterine growth restriction (IUGR) predispose to abnormal trophoblastic invasion and abruption. Preterm premature ruptures of membranes (PPROM) is strongly associated with abruption both as causal and consequential.

The strongest risk factor is a history of abruption in a prior pregnancy, which increases the risk of recurrence 20-fold. Chronic hypertension, preeclampsia, tobacco use, drug use (especially cocaine and resulting cocaine-induced hypertension), multiparity, major congenital fetal anomalies, uterine leiomyomas near mucosal surface at implantation site, and subchorionic hematoma are also risk factors. Catastrophic abruption with fetal death is most common in African American and white women (incidence 0.5%), less common in women of Asian descent, and least common in Latina women. The incidence of abruption peaks between 24 and 26 weeks of gestation and contributes to 10% of all preterm deliveries.