Placenta accreta spectrum (PAS) disorders are 2/2 pathologic implantation of the placenta into the myometrium.
Thought to be 2/2 defects in the endometrial-myometrial interface leading to failure of normal decidualization.
This results in trophoblastic migration and abnormal attachment / invasion of the placental chorionic villi directly to the underlying myometrium, with subsequent failure of placental separation from the uterus at time of delivery.
Major RFs: Placenta previa, Prior C-section, H/o prior PAS disorder
Additional RFs: multiparity, prior uterine surgery (D&C, myomectomy), endometrial ablation, pelvic irradiation, uterine artery embolization, advanced maternal age, infertility, and use of assisted reproductive technologies.
The common feature is uterine scarring or injury
The marked increase in the incidence of PAS disorders is 2/2 increasing C-section deliveries, no 1/3 or all deliveries.
Repeat C-section is assoc w/ progressively increased risk of PASD
Risk
Sonographics findings of PASD include:
Abnormal placental lacunae*
Loss of retroplacental clear zone
Myometrial thinning
Placental bulge
Bladder wall interruption*
Focal exophytic mass
Abnormal vascularity
*most specific findings
Color doppler US helps assessment by showing bridging vessels perpendicular through the placenta and toward the bladder considered highly indicative of PASD.
MRI depicts the depth and topography of invasion.
Very valuable in assessment of posterior placenta.
Accuracy of MRI can be affected by the timing of imaging as the myometrium naturally becomes thinner w/ progression of pregnancy which can mimic pathologic thinning.
Optimal time to evaluate for PASD is 28-32 weeks
<28 wks is limited 2/2 incomplete placental maturity
>32 wks is challenging 2/2 overlapping features of normal late gestation and PASD.
Goals of imaging are to
Identify findings supportive of PASD
Identify the presence/absence of myoinvasion
Outline the topography of myoinvasion.
Depth and topography are the main determinants of surgical outcome in patients with PASD
Topography - spatial delineation and anatomic location of myoinvasion, extrauterine spread, and adjacent organ invasion. It is the more reliable predictor of surgical morbidity.
SAR-ESUR consensus statement recommends seven features for diagnosing PASD:
Intraplacental T2-dark bands
Placental / uterine bulge
Myometrial thinning
Bladder wall interruption
Focal exophytic mass
Loss of T2-hypointense retroplacental line
Abnormal vascularization of the placental bed
It is the combination of features in the context of clinical RFs that increases the likelihood of underlying PASD.
IPBs
Irregular T2-dark bands
Ranging in size from 6 to 20 mm
Typically extend from the maternal surface
Represent fibrin deposition from hemorrhage and infarct
The most sensitive feature MRI feature for PASD (high sensitivity, moderate specificity)
Easily distinguished from BVs on SSFP
IPBs are T2 dark on SSFP
BVs are T2 bright on SSFP
A normal placenta has thin T2 septa.
Correlate with T1WI to exclude hemorrhage mimicking bands.
If performed late in gestation, small focal placental infarcts can be considered normal.
Large areas of placental infarcts, particularly those not overlying the cervix, should raise suspicion and alert you of additional features of PASD.
UPG involves deviation of the uterine serosa from the expected plane due to abnormal bulging of the placenta toward adjacent organs.
The uterine serosa remains intact but uterine shape is morphologically distorted.
There is often a widening of the lower uterine segment due to myometrial remodeling, resulting in an hourglass configuration as opposed to the normal inverted pear-shaped uterus.
Placental bulge has been shown to be an independent predictor of myoinvasive severe PAS disorder
Sensitivity of 76.7%, specificity of 62.5% for placenta increta
Sensitivity of 77.4%, specificity of 64.7% for placenta percreta.
UPG in conjunction with other findings of PAS disorder is 100% predictive of myometrial invasion; however, the uterine bulge sign alone without other features can lead to false-positive results, particularly given the reported fair to moderate interobserver variability for this feature.
Myometrial vascular congestion is seen in both normal pregnancies and PASD can make dilineation of the placental contour difficult and can mimic a bulge.
Myometrium may appear mildly T2 bright, blending in w/ the adjacent placenta and creating the appearance of a bulge.
In this setting, DWI can help at delineating the myometrial-placental interface cmpared w/ T2WI taking advantage of the intrinsic SI differences b/n high SI placenta and low SI myometrium on high B-value images.
Defined as thinning of the myometrium over the placenta to <1 mm or not visible at all.
Loss of normal trilaminar appearance can be present in a normal placenta, especially late in gestation, however, the T1 dark line at the serosal margin should remain intact (figure D).
This sign should only be used in conjunction with other findings supportive of PASD, particularly if imaging is performed >32 weeks gestation.
Focal myometrial interruption has good sensitivity/specificity for PASD
Several pitfalls
Nonpathologic myometrial thinning can often be seen in areas of myometrial compression such as b/n the uterus and maternal spine.
Patients who have undergone repeat C-sections can have widening of the old thin scar during pregnancy 2/2 dehiscence of the lower uterine segment. In such cases, the placenta extends to the expected serosal margin at imaging, mimicking myometrial thinning which can be mistaken for myoinvasive PAS disorder.
At delivery, the placenta may be visualized intraoperatively through this "uterine window" however at pathologic examination there is no true villous invasion into the serosa or residual myometrium.
Focal interruption or irregularity of the normal T2 dark bladder wall is concerning for involvement. The bladder should be moderately distended for optimal evaluation.
Direct nodular placental invasion into the bladder is diagnostic of placenta percreta but is RARELY seen.
The presence of bladder tenting is highly associated w placenta percreta.
The bladder vessel sign and serosal vessel sign which refer to flow voids in the bladder wall and serosa or vesicouterine space are highly suspicious for bladder wall involvement.
FEM refers to invasion of placental tissue into the myometrium, breaking through the T2 dark uterine serosal margin w/ variable extension beyond the serosal surface.
Most often seen along the anterior aspect of the uterus toward the bladder or into the parametrium.
Highly specific for percreta when it extends towards the bladder
Focal interruption or diffuse loss of the T2 dark placental inner myometrial interface can be seen in PASD.
This is often seen in conjunction w/ myometrial thinning and correlates w/ loss of the retroplacental clear zone at sono.
As with myometrial thinning, this line may be difficult to visualize in late gestation and should be interpreted in conjunction w/ other findings.
The retroplacental bed consists of normal vessels, decidua, and adjacent myometrium.
Owing to vascular placental changes in PASD these vessels lose their uniform appearance of T2 dark flow voids and become heterogeneous in size, w/ disruption of the uteroplacental interface.
This network of abnormal vessels may extend into the myometrium and course along the serosa, appearing hypertrophied around the bladder, uterus, and vagina.
The presence of vessels w/n the vesicouterine space is highly suspicious for bladder wall involvement.
Vessels extending from uterine surface into the parametrial fat is an independent predictor of parametrial invasion.
Normal increase in periuterine vascularity late in gestation is a known pitfall, emphasizing the need for the presence of other signs to support the diagnosis of PASD.