Placenta accreta: Pathogenesis of a 20th century iatrogenic uterine disease

Abstract

Placenta accreta refers to different grades of abnormal placental attachment to the uterine wall, which are characterised by invasion of trophoblast into the myometrium. Placenta accreta has only been described and studied by pathologists for less than a century. The fact that the first detailed description of a placenta accreta happened within a couple of decades of major changes in the caesarean surgical techniques is highly suggestive of a direct relationship between prior uterine surgery and abnormal placenta adherence. Several concepts have been proposed to explain the abnormal placentation in placenta accreta including a primary defect of the trophoblast function, a secondary basalis defect due to a failure of normal decidualization and more recently an abnormal vascularisation and tissue oxygenation of the scar area. The vast majority of placenta accreta are found in women presenting with a previous history of caesarean section and a placenta praevia. Recent epidemiological studies have also found that the strongest risk factor for placenta praevia is a prior caesarean section suggesting that a failure of decidualization in the area of a previous uterine scar can have an impact on both implantation and placentation. Ultrasound studies of uterine caesarean section scar have shown that large and deep myometrial defects are often associated with absence of re-epithelialisation of the scar area. These findings support the concept of a primary deciduo-myometrium defect in placenta accreta, exposing the myometrium and its vasculature below the junctional zone to the migrating trophoblast. The loss of this normal plane of cleavage and the excessive vascular remodelling of the radial and arcuate arteries can explain the in-vivo findings and the clinical consequence of placenta accreta. Overall these data support the concept that abnormal decidualization and trophoblastic changes of the placental bed in placenta accreta are secondary to the uterine scar and thus entirely iatrogenic.

Introduction

Placenta accreta is a novel pathological entity. Unlike many other placental disorders, such as hydatidiform mole, which have been known for centuries, placenta accreta was first described in the 20th century. In 1937, Irving and Hertig defined placenta accreta as “the abnormal adherence, either in whole or in part, of the afterbirth to the underlying uterine wall [1]. The fact that it was not described by the anatomists and pathologists of the 18th and 19th century who describe most of the pathological lesions that we know today, suggests that the condition did not exist or was so rare that it was not diagnosed before the 1930s. Within this context and due to the severe clinical complications associated with the abnormal adherence of the placenta at birth, it is very unlikely that placenta accreta would have avoided detection for so long.

The general term “placenta accreta” refers to different grades of abnormal placental attachment to the uterine wall, which are characterised by invasion of trophoblast into the myometrium (Fig. 1). The term placenta increta is sometimes used to describe deep myometrial invasion of trophoblast villi and placenta percreta refers to accreta villi perforating through the full thickness of the myometrium and uterine serosa with possible involvement of adjacent organs [2], [3]. Placenta increta and percreta are rare representing less than 20% of the cases of placenta accreta [4]. Before the development of imaging techniques, it was not often easy to assess clinically the exact depth of placental invasion and the term placenta accreta has been used to describe all types of abnormally adherent placentae. Placenta accreta has also been subdivided into total, partial or focal, depending on the amount of placental tissue involved. This sub-classification is rarely used on the basis that in case of placenta accreta the microscopic examination of the hysterectomy specimen is rarely complete and that attempts at manual removal often distort the placental anatomy [2].

Where placenta accreta is present, the failure of the placenta to separate normally from the uterus after delivery is typically accompanied by severe post-partum haemorrhage. Attempts to remove the adherent tissue may provoke further bleeding and a cascade of ongoing haemorrhage, shock and coagulation disorders requiring complex clinical management. Not surprisingly, a recent study has shown that women managed by a multidisciplinary care team are less likely to require large-volume blood transfusion, re-operation within seven days of delivery for bleeding complications and to experience prolonged maternal admission to the intensive care unit, large-volume blood transfusion, coagulopathy, urethral injury and early re-operation than women managed by standard obstetric care [5].

There has been a substantial increase in the occurrence of placenta accreta over the last 50 years with as much as a 10 fold rise in the prevalence to around 1 in 2500 deliveries in many Western countries [11], [12], [13], [14], [15], [16], [17]. Thus placenta accreta can be no longer considered as a rare obstetric pathology and has become a complication that an average obstetrician is likely to encounter several times during a practicing lifetime. It is rapidly becoming recognised as a major cause of obstetric complications worldwide, including in developing countries. With the development of high quality ultrasound and colour Doppler imaging it is now possible to diagnose abnormal trophoblast invasion into the myometrium early in the first trimester of pregnancy As most cases of placenta accreta continue to be diagnosed during the second and third trimester of pregnancy little is known about the natural evolution of this placentation disorder. We have reviewed current literature on the aetiology, pathophysiology and early prenatal diagnosis of this placental abnormality which is rapidly becoming one of the main placental-related obstetric problems around the world.