Placental bed disorders in the genesis of the great obstetrical syndromes
Book Chapter
Romero, R, Kusanovic, JP, Kim, CJ. (2010). Placental bed disorders in the genesis of the great obstetrical syndromes
. 271-289. 10.1017/CBO9780511750847.025
Romero, R, Kusanovic, JP, Kim, CJ. (2010). Placental bed disorders in the genesis of the great obstetrical syndromes
. 271-289. 10.1017/CBO9780511750847.025
Recognition of the placental bed as a key interface in normal and abnormal human gestation The recognition of the placental bed as a distinct anatomical site for the physiology and pathology of pregnancy began in 1958 after the pioneering studies of Dixon and Robertson [1] and the seminal contributions of Brosens [2] in 1964. The term ‘placental bed’ was purposely chosen to emphasize that the area of study was not the decidua basalis attached to the floor of the placenta, but rather the uterine tissues (endometrium and myometrium) underneath the placenta. This was important because the myometrium contains the origins of the spiral arteries. The investigators believed that these vessels were the target of lesions in preeclampsia on the basis that decreased uteroplacental blood flow had been reported using a number of experimental techniques [3, 4, 5] coupled with the belief that the increased frequency of infarcts in the placenta of women with preeclampsia was due to interference with the maternal blood supply. However, instead of finding the lesions associated with hypertension in target organs, Brosens discovered the lack of physiological transformation of the spiral arteries in the myometrium of women with preeclampsia [6, 7, 8]. These lesions were also found in pregnancies with intrauterine growth restriction [9] and subsequently, in patients with spontaneous abortion [10, 11], placental abruption, [12], antiphospholipid syndrome [13], preterm labor with intact membranes leading to preterm delivery [14], and preterm premature rupture of membranes [15].
