The exact etiology of placental abruption is unknown. Clearly, abruption may result from a number of different etiologies and pathways.¹ The mechanism of an abruption following acute trauma or rapid uterine decompression is different from that which follows a long-standing process such as preeclampsia or uteroplacental insufficiency, the latter being one of the clinical manifestations of ischemic placental disease.²⁵ There is an increasing body of evidence that abruption is often the end result of long-standing defective placentation (Chapter 6), as it is associated with abnormal trophoblastic invasion and remodeling of the spiral arteries.^25,26 Rupture of maternal decidual vessels leads to dissection of the placental-decidual interface. Pathological findings consistent with abruption include indentation of the maternal surface of the placenta and a retroplacental clot. Other findings may include intravillous or intervillous hemorrhage, hemosiderin deposition, decidual inflammation, and placental infarction.^27,28 Nath and colleagues found histologic evidence of inflammation (chorioamnionitis) in pregnancies complicated by placental abruption.²⁹ Although this association was strongest in term pregnancies with abruption, it was present, to a lesser degree, in preterm abruptions.²⁹

Importantly, whereas the diagnosis of abruption is primarily a clinical one, histopathologic findings consistent with abruption are found in a percentage of normal pregnancies. When placentas of pregnancies in preterm deliveries are examined by a pathologist, there is a higher rate of such findings than in pregnancies delivered at term.³⁰ These findings support the well-documented association of placental abruption with spontaneous preterm birth.³⁰ Abruption results in thrombin production from tissue decidual factors, provoking preterm contractions and labor. Furthermore, this may lead to degradation of metalloproteins in the membranes^30,31 and result in preterm premature rupture of the membranes.³² In fact, at least 20% of spontaneous preterm births are the consequence of placental abruption (Chapter 49).³⁰

Placental abruption may be revealed or concealed (Figure 47.1). In revealed abruption, the blood tracks between the membranes and exits from the vagina (Figure 47.1A).¹ In concealed abruption, blood accumulates between the placenta and the uterine wall (Figure 47.1B).

Although in the past abruption was regarded as an acute event, there is now an ample body of evidence that suggests that the pathophysiological processes that lead to most abruptions have their origins early in pregnancy.^25,26 A study by Ananth and colleagues found that a first-trimester pregnancy-associated plasma protein A less than the 5th percentile was associated with an increased risk of abruption.³³ Similarly, elevated maternal serum alpha-fetoprotein was found more commonly in pregnancies complicated by abruption compared with those without abruption. Furthermore, in a previous study, our group found that a high risk for abruption occurred in pregnancies that had both bleeding in the first half of pregnancy and placental histologic lesions.²⁶