Pathophysiology of Placenta Percreta
Placenta percreta develops when defects in the endometrial-myometrial interface from uterine scarring lead to failure of normal decidualization, allowing abnormally deep anchoring of placental villi that invade through the full thickness of the myometrium and into extrauterine structures. 1, 2
Core Pathophysiologic Mechanism
The fundamental defect in placenta percreta involves loss of the decidua basalis layer that normally separates the placenta from the myometrium. 1 This protective barrier is disrupted in areas of prior uterine trauma, most commonly from cesarean delivery, creating vulnerable zones where trophoblastic tissue can penetrate abnormally deep. 1
Two Competing Theories
Defective decidualization theory: The primary mechanism is failure of normal decidual formation at sites of endometrial-myometrial interface damage from scarring, which removes the natural barrier to deep placental anchoring. 1, 2
Abnormal trophoblast invasion theory: Some evidence suggests abnormalities in the invasive properties of extravillous trophoblast (EVT), with interstitial EVT adjacent to damaged smooth muscle driving the deep invasion seen in percreta. 1
The consensus view favors a combination of both mechanisms, where uterine scarring creates the permissive environment and altered trophoblast behavior drives the invasion. 1, 2
Anatomic Progression to Percreta
Placenta percreta represents the most severe end of the placenta accreta spectrum, characterized by invasion through the entire myometrial thickness with less than 25% preservation of normal uterine wall, disruption of the uterine serosa, and extension into extrauterine structures. 1, 3
Histologic Hallmarks
Complete absence of decidua basalis at the placental-myometrial interface is the diagnostic feature. 1
Chorionic villi or extravillous trophoblast (EVT) must be documented in extrauterine tissues such as perivesical adipose tissue, parametrial fat, bladder wall, or other pelvic organs for definitive diagnosis. 1, 3
The placental-myometrial interface shows an irregular, infiltrative pattern rather than smooth separation. 1
Two Distinct Invasion Patterns
Direct infiltrative invasion: Cancer-like penetration through myometrium showing abrupt transition from normal myometrial thickness to placental parenchyma. 1, 3
Cesarean scar dehiscence pattern: Implantation overlying areas of scar with gradual wedge-shaped transition from myometrium to extremely thin fibrous tissue. 1, 3
Critical Risk Factors Driving Pathophysiology
Prior cesarean delivery is the primary risk factor in developed countries, with incidence increasing from 0.24% after one cesarean to 6.74% after six or more cesareans. 1 The mechanism involves surgical disruption creating full-thickness endometrial-myometrial defects that fail to decidualize properly in subsequent pregnancies. 2
Placenta previa overlying a cesarean scar creates the highest risk scenario (present in 49% of all accreta cases), as the placenta implants directly over the most vulnerable scarred area. 4
Other uterine surgeries including myomectomy with endometrial cavity entry, curettage, and Asherman syndrome create similar endometrial-myometrial interface disruption. 1, 2
Important Pathophysiologic Controversies
Recent evidence challenges whether true "percreta" with villous tissue penetrating through intact serosa actually exists. 5 A 2022 prospective cohort found that most cases classified clinically as percreta showed only histologic evidence of placenta creta or increta, with apparent serosal penetration actually representing uterine rupture or surgical disruption rather than primary placental invasion. 5
This explains why expert pathology panels now require microscopic confirmation of EVT in extrauterine adipose tissue for percreta diagnosis, rather than accepting surgeon's intraoperative impression or villi at specimen margins alone. 1, 3
Clinical Implications of the Pathophysiology
The invasive nature of percreta creates high maternal morbidity (82.1%) and mortality (1.4%) because attempting placental removal results in catastrophic hemorrhage from the deeply invaded myometrium and extrauterine structures. 6 The pathophysiology explains why cesarean hysterectomy with placenta left in situ is standard management—the abnormal vascular remodeling and lack of decidual plane make separation impossible without life-threatening bleeding. 4, 6