Abstract
Introduction
Placenta accreta spectrum (PAS) is characterized by abnormal implantation of chorionic villi directly onto the myometrium due to defective decidua basalis formation. The main risk factors include placenta previa and prior cesarean delivery, which are widely recognized. The incidence has increased nearly tenfold over the past five decades, largely attributed to rising cesarean rates. Accurate prenatal diagnosis is crucial to ensure maternal safety and surgical planning. 1 Ultrasound is the first-line modality in the diagnosis of PAS; however, MRI provides additional diagnostic and preoperative information. According to the Society of Abdominal Radiology (SAR) and the European Society of Urogenital Radiology (ESUR) joint consensus statement, the recommended MRI features of PAS include T2 dark bands, placental bulge, loss of T2 hypointense interface, myometrial thinning, bladder wall interruption, focal exophytic mass, and abnormal vascularization of the placental bed. 2
Recently, diffusion lacunae (DL) were reported as a novel finding on diffusion-weighted imaging (DWI) in PAS evaluation. 3 DL are characterized by intraplacental ovoid or irregular hypointense areas equivalent in signal to amniotic fluid on DWI, with corresponding hyperintensity on apparent diffusion coefficient (ADC) maps. They are presumed to correspond to placental lacunae—the most recognized ultrasound feature of PAS—but their histopathologic basis remains uncertain. Similarly, T2 dark bands—seen as irregular or linear hypointense areas on T2-weighted imaging (T2WI) and balanced steady-state free precession sequence (SSFP)—have been attributed to fibrin deposition due to repetitive intraplacental hemorrhage or infarction,4,5 although supportive pathologic evidence has been limited. We present a hysterectomy case with precise MR–pathologic correlation to clarify the histopathologic origins of DL and T2 dark bands.
Case history
A 41-year-old woman (gravida 2, para 1) with one prior cesarean delivery was referred for evaluation of suspected PAS with marginal placenta previa. At 26 weeks and 3 days of gestation, she presented with antepartum bleeding and underwent MRI the following day. MRI included T2WI in three orthogonal planes; axial and sagittal SSFP; axial fat-saturated T1-weighted imaging; and axial and sagittal DWI. Irregular hypointense areas were observed on both T2WI and SSFP, corresponding to T2 dark bands suggestive of PAS (Figures 1(a) and (b)). At 34 weeks and 3 days, she experienced sentinel bleeding. Although cesarean delivery had been scheduled for the following week, an emergency cesarean hysterectomy was performed at 34 weeks and 4 days with prophylactic bilateral internal iliac artery balloon occlusion in place. Intraoperatively, placental invasion into the myometrium was suspected. The entire placenta and uterine wall were formalin-fixed and sectioned through close collaboration between pathologists and radiologists to match the axial MRI slice plane. The uterine serosa was intact, and histopathology confirmed a diagnosis of placenta increta (FIGO classification, Grade 2). (a) T2-weighted imaging (T2WI); (b) balanced steady-state free precession imaging (SSFP); (c) diffusion-weighted imaging (DWI); (d), (e) hematoxylin and eosin (H&E) staining at low magnification. An intraplacental irregular hypointense area (T2 dark bands) is observed on T2WI and SSFP (a, b arrows). Posterior to this area, there is a lesion demonstrating low signal on T2WI but high signal on SSFP, consistent with flow voids (a, b arrowheads). On DWI with b value of 800, a hypointense area larger than the T2 hypointense region is identified (c, arrowhead) and considered to correspond to diffusion lacunae (DL). H&E staining at low magnification demonstrates that the region corresponding to DL (d, arrows) lacks chorionic villi (e, arrows) and contains recently formed thrombi (e, arrowheads).
MR–pathologic correlation was performed using representative axial MRI and histopathologic findings (Figure 1). An intraplacental irregular hypointense area corresponding to T2 dark bands was observed on T2WI and SSFP (Figures 1(a) and (b)). Posterior to this area, there was a lesion showing low signal intensity on T2WI but high signal intensity on SSFP, indicative of flow voids (Figures 1(a) and (b)). On DWI with b value of 800, a hypointense area larger than the T2 hypointense region was identified and considered to correspond to DL (Figure 1(c)). Histopathology demonstrated that the corresponding area lacked chorionic villi and contained recently formed thrombi (Figures 1(d) and (e)). Thus, the DL were considered to correspond to villous-devoid regions. Meanwhile, another section demonstrated irregular shaped T2 dark bands on T2WI (Figure 2(a)). Histopathology revealed that the bands were composed predominantly of thrombi with lines of Zahn (Figures 2(b) and (c)) and partial villous infarction (Figures 2(c) and (d)). (a) T2-weighted imaging (T2WI); (b), (c) hematoxylin and eosin (H&E) staining at low magnification; (d) H&E staining at high magnification. Another section demonstrates irregularly shaped T2 dark bands on T2WI (a, arrows). H&E staining reveals that the bands are composed predominantly of thrombi (b, arrows) with lines of Zahn (c, arrows) and partial villous infarction (c, d arrowheads).
Discussion
DL represent a novel MRI finding defined as intraplacental hypointense areas ≥1 cm on DWI and are presumed to correspond to placental lacunae seen on ultrasound. 3 Understanding mechanisms underlying lacunar formation is essential for elucidating the pathophysiology of PAS. In normal placentation, remodeled spiral arteries deliver low-velocity, high-volume maternal blood to the intervillous space. In PAS, radial arteries instead deliver high-velocity blood directly into the intervillous space, thereby disrupting the lobular structure and enlarging intervillous spaces to form lacunae. 6 The mechanism supports the concepts that lacunae correspond to villous destruction or loss. However, microscopic alterations of the villous architecture overlying the abnormally attached areas with placental lacunae on ultrasound imaging have not been demonstrated. 7
In this present case, whole-uterus sectioning enabled precise MR–pathologic correlation, demonstrating that DL corresponds to villous-devoid areas consistent with the proposed pathophysiology of PAS. The low-echogenicity appearance of placental lacunae on ultrasound has been reported to reflect villous-free regions within the placental parenchyma. 7 Therefore, the hypointensity observed as DL on DWI likely corresponds to villous-free areas, consistent with their pathological basis.
Similarly, T2 dark bands have been attributed to fibrin deposition due to repetitive intraplacental hemorrhage or infarction.4,5 However, Jauniaux et al. reported fibrin deposition at the utero–placental interface was only 0.5–2 mm thick, 8 insufficient to explain MR-visible bands. Moreover, large intervillous thrombi have been found in about half of PAS cases. 9 This supports the further evidence that T2 dark bands primarily represent thrombus formation. Additionally, several lines known as “lines of Zahn” were identified in the thrombus. These lines commonly occur in thrombi formed in the presence of blood flow. Therefore, we propose that such thrombi gradually develop under conditions of blood stasis with residual blood flow. Moreover, large, recent intervillous thromboses in direct contact with the basal plate that extend to at least half of the placental tissue thickness have been identified at delivery in most PAS cases with six or more lacunae on ultrasound. 9 In the present case, recent thrombi were also found within the lacunae, although not visible on MRI. We speculate that villous loss was likely present within the DL region, followed by progressive thrombus formation due to blood stasis. If MRI had been obtained nearer to delivery, the area initially identified as DL might have fully evolved into a thrombus, manifested as visible T2 dark bands. These findings may suggest a possible pathological continuum between DL and T2 dark bands, reflecting sequential stages from villous destruction to thrombus formation in some cases.
Meanwhile, a previous case report suggested that infarct-associated fibrosis corresponded to placental T2 dark bands. 10 However, the contribution of infarction to T2 dark bands formation was minimal in this present case.
Regarding the gestational age at the time of MRI, the examination in this case was performed earlier than the 28–32 weeks recommended in the SAR–ESUR joint consensus statement. However, the original article referenced in that statement does not mandate MRI at 28–32 weeks, but instead indicates that placental MRI examinations performed before 24 weeks’ gestation may be unreliable in detecting abnormal placentation. 11 In addition, another article recommends performing the examination at 24–30 weeks. 12 Taken together, these reports suggest that the MRI findings obtained at 26 weeks’ gestation in the present case are likely to be reliable.
Conclusion
Diffusion lacunae represent intraplacental areas devoid of chorionic villi, consistent with lacunar formation in PAS. T2 dark bands primarily consist of thrombi formed under blood stasis. These two MR findings likely reflect sequential stages of a single pathophysiologic process, and recognizing their continuum may refine MRI interpretation in PAS.
Footnotes
Ethical considerations
This case report was approved by the Institutional Review Board (25J006), and the requirement for written informed consent was waived.
Funding
The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study was supported by Japan Society for the Promotion of Science, Grant No. 25K10912.
Declaration of conflicting interests
The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
