- •Contents
- •Contributors
- •1 Introduction
- •2.1 Posterior Compartment
- •2.2 Anterior Compartment
- •2.3 Middle Compartment
- •2.4 Perineal Body
- •3 Compartments
- •3.1 Posterior Compartment
- •3.1.1 Connective Tissue Structures
- •3.1.2 Muscles
- •3.1.3 Reinterpreted Anatomy and Clinical Relevance
- •3.2 Anterior Compartment
- •3.2.1 Connective Tissue Structures
- •3.2.2 Muscles
- •3.2.3 Reinterpreted Anatomy and Clinical Relevance
- •3.2.4 Important Vessels, Nerves, and Lymphatics of the Anterior Compartment
- •3.3 Middle Compartment
- •3.3.1 Connective Tissue Structures
- •3.3.2 Muscles
- •3.3.3 Reinterpreted Anatomy and Clinical Relevance
- •3.3.4 Important Vessels, Nerves, and Lymphatics of the Middle Compartment
- •4 Perineal Body
- •References
- •MR and CT Techniques
- •1 Introduction
- •2.1 Introduction
- •2.2.1 Spasmolytic Medication
- •2.3.2 Diffusion-Weighted Imaging
- •2.3.3 Dynamic Contrast Enhancement
- •3 CT Technique
- •3.1 Introduction
- •3.2 Technical Disadvantages
- •3.4 Oral and Rectal Contrast
- •References
- •Uterus: Normal Findings
- •1 Introduction
- •References
- •1 Clinical Background
- •1.1 Epidemiology
- •1.2 Clinical Presentation
- •1.3 Embryology
- •1.4 Pathology
- •2 Imaging
- •2.1 Technique
- •2.2.1 Class I Anomalies: Dysgenesis
- •2.2.2 Class II Anomalies: Unicornuate Uterus
- •2.2.3 Class III Anomalies: Uterus Didelphys
- •2.2.4 Class IV Anomalies: Bicornuate Uterus
- •2.2.5 Class V Anomalies: Septate Uterus
- •2.2.6 Class VI Anomalies: Arcuate Uterus
- •2.2.7 Class VII Anomalies
- •References
- •Benign Uterine Lesions
- •1 Background
- •1.1 Uterine Leiomyomas
- •1.1.1 Epidemiology
- •1.1.2 Pathogenesis
- •1.1.3 Histopathology
- •1.1.4 Clinical Presentation
- •1.1.5 Therapy
- •1.1.5.1 Indications
- •1.1.5.2 Medical Therapy and Ablation
- •1.1.5.3 Surgical Therapy
- •1.1.5.4 Uterine Artery Embolization (UAE)
- •1.1.5.5 Magnetic Resonance-Guided Focused Ultrasound
- •2 Adenomyosis of the Uterus
- •2.1 Epidemiology
- •2.2 Pathogenesis
- •2.3 Histopathology
- •2.4 Clinical Presentation
- •2.5 Therapy
- •3 Imaging
- •3.2 Magnetic Resonance Imaging
- •3.2.1 Magnetic Resonance Imaging: Technique
- •3.2.2 MR Appearance of Uterine Leiomyomas
- •3.2.3 Locations, Growth Patterns, and Imaging Characteristics
- •3.2.4 Histologic Subtypes and Forms of Degeneration
- •3.2.5 Differential Diagnosis
- •3.2.6 MR Appearance of Uterine Adenomyosis
- •3.2.7 Locations, Growth Patterns, and Imaging Characteristics
- •3.2.8 Differential Diagnosis
- •3.3 Computed Tomography
- •3.3.1 CT Technique
- •3.3.2 CT Appearance of Uterine Leiomyoma and Adenomyosis
- •3.3.3 Atypical Appearances on CT and Differential Diagnosis
- •4.1 Indications
- •4.2 Technique
- •Bibliography
- •Cervical Cancer
- •1 Background
- •1.1 Epidemiology
- •1.2 Pathogenesis
- •1.3 Screening
- •1.4 HPV Vaccination
- •1.5 Clinical Presentation
- •1.6 Histopathology
- •1.7 Staging
- •1.8 Growth Patterns
- •1.9 Treatment
- •1.9.1 Treatment of Microinvasive Cervical Cancer
- •1.9.2 Treatment of Grossly Invasive Cervical Carcinoma (FIGO IB-IVA)
- •1.9.3 Treatment of Recurrent Disease
- •1.9.4 Treatment of Cervical Cancer During Pregnancy
- •1.10 Prognosis
- •2 Imaging
- •2.1 Indications
- •2.1.1 Role of CT and MRI
- •2.2 Imaging Technique
- •2.2.2 Dynamic MRI
- •2.2.3 Coil Technique
- •2.2.4 Vaginal Opacification
- •2.3 Staging
- •2.3.1 General MR Appearance
- •2.3.2 Rare Histologic Types
- •2.3.3 Tumor Size
- •2.3.4 Local Staging
- •2.3.4.1 Stage IA
- •2.3.4.2 Stage IB
- •2.3.4.3 Stage IIA
- •2.3.4.4 Stage IIB
- •2.3.4.5 Stage IIIA
- •2.3.4.6 Stage IIIB
- •2.3.4.7 Stage IVA
- •2.3.4.8 Stage IVB
- •2.3.5 Lymph Node Staging
- •2.3.6 Distant Metastases
- •2.4 Specific Diagnostic Queries
- •2.4.1 Preoperative Imaging
- •2.4.2 Imaging Before Radiotherapy
- •2.5 Follow-Up
- •2.5.1 Findings After Surgery
- •2.5.2 Findings After Chemotherapy
- •2.5.3 Findings After Radiotherapy
- •2.5.4 Recurrent Cervical Cancer
- •2.6.1 Ultrasound
- •2.7.1 Metastasis
- •2.7.2 Malignant Melanoma
- •2.7.3 Lymphoma
- •2.8 Benign Lesions of the Cervix
- •2.8.1 Nabothian Cyst
- •2.8.2 Leiomyoma
- •2.8.3 Polyps
- •2.8.4 Rare Benign Tumors
- •2.8.5 Cervicitis
- •2.8.6 Endometriosis
- •2.8.7 Ectopic Cervical Pregnancy
- •References
- •Endometrial Cancer
- •1.1 Epidemiology
- •1.2 Pathology and Risk Factors
- •1.3 Symptoms and Diagnosis
- •2 Endometrial Cancer Staging
- •2.1 MR Protocol for Staging Endometrial Carcinoma
- •2.2.1 Stage I Disease
- •2.2.2 Stage II Disease
- •2.2.3 Stage III Disease
- •2.2.4 Stage IV Disease
- •4 Therapeutic Approaches
- •4.1 Surgery
- •4.2 Adjuvant Treatment
- •4.3 Fertility-Sparing Treatment
- •5.1 Treatment of Recurrence
- •6 Prognosis
- •References
- •Uterine Sarcomas
- •1 Epidemiology
- •2 Pathology
- •2.1 Smooth Muscle Tumours
- •2.2 Endometrial Stromal Tumours
- •3 Clinical Background
- •4 Staging
- •5 Imaging
- •5.1 Leiomyosarcoma
- •5.2.3 Undifferentiated Uterine Sarcoma
- •5.3 Adenosarcoma
- •6 Prognosis and Treatment
- •References
- •1.1 Anatomical Relationships
- •1.4 Pelvic Fluid
- •2 Developmental Anomalies
- •2.1 Congenital Abnormalities
- •2.2 Ovarian Maldescent
- •3 Ovarian Transposition
- •References
- •1 Introduction
- •4 Benign Adnexal Lesions
- •4.1.1 Physiological Ovarian Cysts: Follicular and Corpus Luteum Cysts
- •4.1.1.1 Imaging Findings in Physiological Ovarian Cysts
- •4.1.1.2 Differential Diagnosis
- •4.1.2 Paraovarian Cysts
- •4.1.2.1 Imaging Findings
- •4.1.2.2 Differential Diagnosis
- •4.1.3 Peritoneal Inclusion Cysts
- •4.1.3.1 Imaging Findings
- •4.1.3.2 Differential Diagnosis
- •4.1.4 Theca Lutein Cysts
- •4.1.4.1 Imaging Findings
- •4.1.4.2 Differential Diagnosis
- •4.1.5 Polycystic Ovary Syndrome
- •4.1.5.1 Imaging Findings
- •4.1.5.2 Differential Diagnosis
- •4.2.1 Cystadenoma
- •4.2.1.1 Imaging Findings
- •4.2.1.2 Differential Diagnosis
- •4.2.2 Cystadenofibroma
- •4.2.2.1 Imaging Features
- •4.2.3 Mature Teratoma
- •4.2.3.1 Mature Cystic Teratoma
- •Imaging Findings
- •Differential Diagnosis
- •4.2.3.2 Monodermal Teratoma
- •Imaging Findings
- •4.2.4 Benign Sex Cord-Stromal Tumors
- •4.2.4.1 Fibroma and Thecoma
- •Imaging Findings
- •4.2.4.2 Sclerosing Stromal Tumor
- •Imaging Findings
- •4.2.5 Brenner Tumors
- •4.2.5.1 Imaging Findings
- •4.2.5.2 Differential Diagnosis
- •5 Functioning Ovarian Tumors
- •References
- •1 Introduction
- •2.1 Context
- •2.2.2 Indications According to Simple Rules
- •References
- •CT and MRI in Ovarian Carcinoma
- •1 Introduction
- •2.1 Familial or Hereditary Ovarian Cancers
- •3 Screening for Ovarian Cancer
- •5 Tumor Markers
- •6 Clinical Presentation
- •7 Imaging of Ovarian Cancer
- •7.1.2 Peritoneal Carcinomatosis
- •7.1.3 Ascites
- •7.3 Staging of Ovarian Cancer
- •7.3.1 Staging by CT and MRI
- •Imaging Findings According to Tumor Stages
- •Value of Imaging
- •7.3.2 Prediction of Resectability
- •7.4 Tumor Types
- •7.4.1 Epithelial Ovarian Cancer
- •High-Grade Serous Ovarian Cancer
- •Low-Grade Serous Ovarian Cancer
- •Mucinous Epithelial Ovarian Cancer
- •Endometrioid Ovarian Carcinomas
- •Clear Cell Carcinomas
- •Imaging Findings of Epithelial Ovarian Cancers
- •Differential Diagnosis
- •Borderline Tumors
- •Imaging Findings
- •Differential Diagnosis
- •Recurrent Ovarian Cancer
- •Imaging Findings
- •Differential Diagnosis
- •Value of Imaging
- •Malignant Germ Cell Tumors
- •Dysgerminomas
- •Imaging Findings
- •Differential Diagnosis
- •Immature Teratomas
- •Imaging Findings
- •Malignant Transformation in Benign Teratoma
- •Imaging Findings
- •Differential Diagnosis
- •Sex-Cord Stromal Tumors
- •Granulosa Cell Tumors
- •Imaging Findings
- •Sertoli-Leydig Cell Tumor
- •Imaging Findings
- •Ovarian Lymphoma
- •Imaging Findings
- •Differential Diagnosis
- •7.4.3 Ovarian Metastases
- •Imaging Findings
- •Differential Diagnosis
- •7.5 Fallopian Tube Cancer
- •7.5.1 Imaging Findings
- •Differential Diagnosis
- •References
- •Endometriosis
- •1 Introduction
- •2.1 Sonography
- •3 MR Imaging Findings
- •References
- •Vagina and Vulva
- •1 Introduction
- •3.1 CT Appearance
- •3.2 MRI Protocol
- •3.3 MRI Appearance
- •4.1 Imperforate Hymen
- •4.2 Congenital Vaginal Septa
- •4.3 Vaginal Agenesis
- •5.1 Vaginal Cysts
- •5.1.1 Gardner Duct Cyst (Mesonephric Cyst)
- •5.1.2 Bartholin Gland Cyst
- •5.2.1 Vaginal Infections
- •5.2.1.1 Vulvar Infections
- •5.2.1.2 Vulvar Thrombophlebitis
- •5.3 Vulvar Trauma
- •5.4 Vaginal Fistula
- •5.5 Post-Radiation Changes
- •5.6 Benign Tumors
- •6.1 Vaginal Malignancies
- •6.1.1 Primary Vaginal Carcinoma
- •6.1.1.1 MRI Findings
- •6.1.1.2 Lymph Node Drainage
- •6.1.1.3 Recurrence and Complications
- •6.1.2 Non-squamous Cell Carcinomas of the Vagina
- •6.1.2.1 Adenocarcinoma
- •6.1.2.2 Melanoma
- •6.1.2.3 Sarcomas
- •6.1.2.4 Lymphoma
- •6.2 Vulvar Malignancies
- •6.2.1 Vulvar Carcinoma
- •6.2.2 Melanoma
- •6.2.3 Lymphoma
- •6.2.4 Aggressive Angiomyxoma of the Vulva
- •7 Vaginal Cuff Disease
- •7.1 MRI Findings
- •8 Foreign Bodies
- •References
- •Imaging of Lymph Nodes
- •1 Background
- •3 Technique
- •3.1.1 Intravenous Unspecific Contrast Agents
- •3.1.2 Intravenous Tissue-Specific Contrast Agents
- •References
- •1 Introduction
- •2.1.1 Imaging Findings
- •2.1.2 Differential Diagnosis
- •2.1.3 Value of Imaging
- •2.2 Pelvic Inflammatory
- •2.2.1 Imaging Findings
- •2.3 Hydropyosalpinx
- •2.3.1 Imaging Findings
- •2.3.2 Differential Diagnosis
- •2.4 Tubo-ovarian Abscess
- •2.4.1 Imaging Findings
- •2.4.2 Differential Diagnosis
- •2.4.3 Value of Imaging
- •2.5 Ovarian Torsion
- •2.5.1 Imaging Findings
- •2.5.2 Differential Diagnosis
- •2.5.3 Diagnostic Value
- •2.6 Ectopic Pregnancy
- •2.6.1 Imaging Findings
- •2.6.2 Differential Diagnosis
- •2.6.3 Value of Imaging
- •3.1 Pelvic Congestion Syndrome
- •3.1.1 Imaging Findings
- •3.1.2 Differential Diagnosis
- •3.1.3 Value of Imaging
- •3.2 Ovarian Vein Thrombosis
- •3.2.1 Imaging Findings
- •3.2.2 Differential Diagnosis
- •3.2.3 Value of Imaging
- •3.3 Appendicitis
- •3.3.1 Imaging Findings
- •3.3.2 Value of Imaging
- •3.4 Diverticulitis
- •3.4.1 Imaging Findings
- •3.4.2 Differential Diagnosis
- •3.4.3 Value of Imaging
- •3.5 Epiploic Appendagitis
- •3.5.1 Imaging Findings
- •3.5.2 Differential Diagnosis
- •3.5.3 Value of Imaging
- •3.6 Crohn’s Disease
- •3.6.1 Imaging Findings
- •3.6.2 Differential Diagnosis
- •3.6.3 Value of Imaging
- •3.7 Rectus Sheath Hematoma
- •3.7.1 Imaging Findings
- •3.7.2 Differential Diagnosis
- •3.7.3 Value of Imaging
- •References
- •MRI of the Pelvic Floor
- •1 Introduction
- •2 Imaging Techniques
- •3.1 Indications
- •3.2 Patient Preparation
- •3.3 Patient Instruction
- •3.4 Patient Positioning
- •3.5 Organ Opacification
- •3.6 Sequence Protocols
- •4 MR Image Analysis
- •4.1 Bony Pelvis
- •5 Typical Findings
- •5.1 Anterior Compartment
- •5.2 Middle Compartment
- •5.3 Posterior Compartment
- •5.4 Levator Ani Muscle
- •References
- •Evaluation of Infertility
- •1 Introduction
- •2 Imaging Techniques
- •2.1 Hysterosalpingography
- •2.1.1 Cycle Considerations
- •2.1.2 Technical Considerations
- •2.1.3 Side Effects and Complications
- •2.1.5 Pathological Findings
- •2.1.6 Limitations of HSG
- •2.2.1 Cycle Considerations
- •2.2.2 Technical Considerations
- •2.2.2.1 Normal and Abnormal Anatomy
- •2.2.3 Accuracy
- •2.2.4 Side Effects and Complications
- •2.2.5 Limitations of Sono-HSG
- •2.3 Magnetic Resonance Imaging
- •2.3.1 Indications
- •2.3.2 Technical Considerations
- •2.3.3 Limitations
- •3 Ovulatory Dysfunction
- •4 Pituitary Adenoma
- •5 Polycystic Ovarian Syndrome
- •7 Uterine Disorders
- •7.1 Müllerian Duct Anomalies
- •7.1.1 Class I: Hypoplasia or Agenesis
- •7.1.2 Class II: Unicornuate
- •7.1.3 Class III: Didelphys
- •7.1.4 Class IV: Bicornuate
- •7.1.5 Class V: Septate
- •7.1.6 Class VI: Arcuate
- •7.1.7 Class VII: Diethylstilbestrol Related
- •7.2 Adenomyosis
- •7.3 Leiomyoma
- •7.4 Endometriosis
- •References
- •MR Pelvimetry
- •1 Clinical Background
- •1.3.1 Diagnosis
- •1.3.2.1 Cephalopelvic Disproportion
- •1.3.4 Inadequate Progression of Labor due to Inefficient Contraction (“the Powers”)
- •2.2 Palpation of the Pelvis
- •3 MR Pelvimetry
- •3.2 MR Imaging Protocol
- •3.3 Image Analysis
- •3.4 Reference Values for MR Pelvimetry
- •5 Indications for Pelvimetry
- •References
- •MR Imaging of the Placenta
- •2 Imaging of the Placenta
- •3 MRI Protocol
- •4 Normal Appearance
- •4.1 Placenta Variants
- •5 Placenta Adhesive Disorders
- •6 Placenta Abruption
- •7 Solid Placental Masses
- •9 Future Directions
- •References
- •Erratum to: Endometrial Cancer
MR Imaging of the Placenta |
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Table 1 Summary of MR imaging parameters |
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T2-weighted |
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Sagittal |
Sagittal |
|
True FISPa |
|
half-Fourier RAREb |
T1-weighted |
diffusion- |
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Coronal/ |
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Coronal/ |
three-dimensional |
weighted |
Parameter |
Transverse |
sagittal |
Transverse |
sagittal |
imagingc |
imagingd |
TR/TE (ms)e |
4.3/2.2 |
4.3/2.2 |
1000/90 |
1000/90 |
4.1/1.1 |
3200/75 |
Flip angle |
50° |
50° |
150° |
150° |
10° |
10° |
Field of view (mm) |
320–400 |
320–400 |
320–400 |
320–400 |
320–400 |
320–400 |
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Matrix |
256 × 224 |
256 × 224 |
256 × 224 |
256 × 224 |
256 × 224 |
256 × 192 |
Parallel imaging factor |
2 |
2 |
2 |
2 |
3 |
2 |
Section thickness (mm) |
5 |
5 |
4 |
4 |
2.5 |
5 |
Intersection gap (mm) |
0 |
0 |
0 |
0 |
0 |
0 |
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No. of signals acquired |
1 |
1 |
1 |
1 |
1 |
6 |
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Receiver bandwidth (kHz) |
125 |
125 |
200 |
200 |
310 |
1930 |
Acquisition time (s) |
19 |
21 |
15–20 |
15–20 |
15–18 |
180 |
aFISP fast imaging with steady-state precession bRARE rapid acquisition with relaxation enhancement
cImaging was performed with dynamic volumetric interpolated breath-hold examination with fat saturation. Fat saturation was achieved with the chemical shift–selective fat suppression technique
dDiffusion-weighted MR images were acquired with b values of 50, 400, and 800 s/mm2 eTR/TE repetition time/echo time
sequences as needed, including fat-suppressed and opposed-phase imaging if a fat containing lesion is suspected, and time-of-flight imaging if further evaluation of a vascular structure is indicated.
Parallel imaging reconstruction algorithms GRAPPA with iPAT factor 2 are used to decrease the MR data acquisition time of the sequences therefore reducing fetal and maternal motion artifacts.
To minimize the deposition of radiofrequency energy in the pregnant patient and optimize temporal resolution, a 256 × 224 matrix is used with a partial-phase field of view of 0.75 in applicable rectangular geometries, such as the axial plane.
An attempt is made to confirm all suspected abnormalities in at least two imaging planes because the normal curvature of the uterus can potentially lead to a false-positive examination in a single imaging plane. When higher-resolu- tion imaging is required to maintain a satisfactory signal-to-noise ratio, additional images can be obtained in the desired plane using a T2-weighted fast spin-echo sequence. This sequence can be performed over a limited area during a breath-hold using some type of flip back pulse to shorten the repetition and acquisition times.
The use of fat suppression in conjunction with T1-weighted sequences improves the conspicuity of blood products.
Some investigators have advocated the use of gadolinium-based contrast agents to improve the specificity of MRI for diagnosis of placenta accreta by better defining the outer placental surface and myometrium and distinguishing placenta accreta from percreta (Palacios Jaraquemada and Bruno 2000; Tanaka et al. 2001).
Therefore, in clinical practices, gadoliniumbased contrast agents are not used in pregnancy, except when the potential risks to the patient are outweighed by the potential benefits of contrastenhanced imaging.
Clinical experience with diffusion-weighted placental imaging is likewise limited (Bonel et al. 2010; Morita et al. 2009), but this sequence has been recently demonstrated to be very useful in the detection of placental hematoma (Masselli et al. 2011b).
4\ Normal Appearance
Before interpreting images for pathologic findings, it is necessary to understand the normal anatomy and the normal findings of the placenta at multiplanar MR imaging (Nguyen et al. 2012).
470 |
G. Masselli |
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The gravid uterus should be pear shaped, with the fundus and body being wider than the lower uterine segment. The uterine contour is usually smooth, and focal bulging should not be present.
Typically, the placenta is located along the anterior or posterior uterine wall, extending onto the lateral walls.
Placental size is expressed in terms of thickness in the midportion of the organ and should be between 2 and 4 cm. Placental thinning has been described in systemic vascular and hematologic diseases that result in microinfarctions. Thicker placentas (>4 cm) are seen in fetal hydrops, antepartum infections, maternal diabetes, and maternal anemia. Placental thickening can be simulated by myometrial contractions and underlying fibroids (Victoria et al. 2011).
The MR signal of the placenta varies according to the utilized imaging sequence (Leyendecker et al. 2012; Levine and Pedrosa 2005). With the most commonly utilized fetal pulse sequence, HASTE, the placenta demonstrates intermediate signal, hypoor isointense with respect to the surrounding myometrium. A fine line of separation between the myometrium and the placenta may be visualized, most likely representing the placental-myometrial interface. The placenta is predominantly homogeneous in signal in the early second trimester and has a relatively flat and smooth surface (Fig. 1).
On steady-state free-procession or true FISP images, the placenta is hypoto isointense with respect to the myometrium and homogeneous in appearance during the second trimester, becoming more heterogeneous as maturation occurs. The placental-myometrial interface may be seen, although it was less distinct than in HASTE images.
On T1 FLASH images, the placenta demonstrates a homogeneous signal, isointense to myometrium.
As the placenta matures, particularly in the third trimester, cotyledons become easier to discern as round, high-signal structures seen in fluid-sensitive sequences, delineated by a subtle peripheral low signal line, likely representing the normal placental septa (Fig. 2). The placenta also
becomes more complex appearing, with gentle lobulations seen on its fetal surface and fine vascular channels becoming more distinct as they traverse the placental tissue.
Placental septa and the cotyledons are more often seen when imaging with a 3 T system (Fig. 3).
The normal subplacental vascularity can be seen as numerous flow voids just under the placenta. A few flow voids can also be seen within the placenta and are usually in the region of the insertion point of the umbilical cord.
The myometrium has a variable thickness and thins as the pregnancy progresses.
It can be seen as three distinct layers of signal intensity; the inner and outer layers of the myometrium are seen as thin bands of decreased T2 signal intensity (Fig. 4). The middle layer is thicker, has intermediate T2 signal intensity, and often contains multiple flow voids representing the normal myometrial vascularity.
As the pregnancy progresses, the myometrium can become quite thin and should be visualized as a continuous band of soft tissue low intensity signal surrounding the placenta (Fig. 5).
However, the myometrium may blend into the placenta, and it can be difficult to visualize even at technically adequate examinations in patients with prior cesarean section.
One problem with MR imaging of placenta adhesive disorders is that distinction between the myometrium and the placenta can be difficult on the types of sequences typically used (Kim and Narra 2004; Lax et al. 2007).
If placenta accreta is suspected, additional imaging planes are chosen that best show the placenta-myometrium interface in the region of suspected abnormality or other structures of interest, such as the bladder dome. Such imaging is typically best accomplished in an angled scan plane perpendicular to the placenta-myometrium interface or myometrium-bladder interface (Masselli et al. 2008).
4.1\ Placenta Variants
Most placentas are round or discoid in shape, but other shapes should be described when present;
MR Imaging of the Placenta |
471 |
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a |
b |
c |
d |
Fig. 1 Normal placenta in this 26-week-old fetus. (a) Sagittal T2-weighted half-Fourier RARE T2-weighted MR image shows a placenta (P) with intermediate signal intensity. (b) Sagittal T1-weighted fat saturation sequence
demonstrates a homogeneous placenta, isointense to myometrium. (c) Sagittal DWI sequence (B = 800) and ADC map (d) demonstrates a homogeneous placenta
472 |
G. Masselli |
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a |
b |
Fig. 2 Coronal T2-weighted half-Fourier RARE (a) and true FISP (b) MR images show a homogeneous placenta with thin linear areas of decreased signal intensity in a
Fig. 3 Coronal T2-weighted half-Fourier RARE at 3 Tesla MR scanner shows the cotyledon structure of the placenta (arrows)
regular pattern (arrows) representing normal placental septa
Fig. 4 Axial T2-weighted MR image of healthy secondtrimester placenta shows the three layers of the normal myometrium. The hypointense outer (short arrows) and inner (arrows) layers surround the more hyperintense middle layer, which contains the vasculature
MR Imaging of the Placenta |
473 |
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Fig. 5 Axial T2-weighted MR image of healthy thirdtrimester placenta shows the placenta has homogeneous intermediate signal intensity and the myometrium is visible as a low-signal-intensity line external to the placenta (arrows)
Fig.6 Sagittal T2-weighted half-Fourier RARE MR image shows a normal placenta with a succenturiate lobe. The main body of the placenta is located along the posterior uterine wall (arrow). A second soft tissue structure with similar signal intensity is seen along the anterior uterine wall and represents the succenturiate lobe (small arrow)
variant placental shapes include bilobed, succenturiate, circumvallate, and placenta membranacea (Huppertz 2008).
Usually discoid in shape, the placenta can exhibit various morphologies. The placenta can have a separate lobule that is not contiguous with the main placental body, which is called a succenturiate placenta (Fig. 6) (Elsayes et al. 2009).
A small lobule of placenta separate from the main bulk of the placenta is referred to as a succenturiate lobe. This is important to describe when present because of the risk of connecting vessel rupture or retention of the lobe at delivery, both potentially resulting in significant hemorrhage (Bernirschke and Kaufmann 2000).
If there are two lobes of placenta, similar in size, the placenta can be described as bilobed. Circumvallate placenta is best described as having a rolled-up edge. In a retrospective review of 7666 deliveries, the odds ratio of placental abruption in patients with circumvallate placenta was 13.10 (95% confidence limits: 5.65–30.20) (Elsayes et al. 2009). A placenta membranacea or “placenta diffusa” occurs when villous atrophy fails to occur early in gestation. As a result, fetal membranes remain covered with chorionic villi. This rare entity presents with a thinned diffuse placenta covering the uterine cavity, and is associated with placental invasion (Linduska et al. 2009). Annular placenta may be a variant of placenta membranacea, presents with a ring-shaped placenta, and has similar risks of hemorrhage and growth restriction (Derwig et al. 2011).
Lastly, in placenta fenestrata, the placenta may also demonstrate a central defect in which placental tissue is nonexistent, leaving only a membranous sheath.
The normal umbilical cord measures 50–60 cm long, contains two umbilical arteries and one vein, and typically inserts centrally within the placenta (Palacios Jaraquemada and Bruno 2000). A marginal cord insertion, also known as a battledore placenta, occurs within 1–2 cm of the placental edge. With a velamentous cord insertion, the placental vessels insert separate from the placenta and traverse between the amnion and chorion before entering the placenta (Tanaka et al. 2001). Umbilical vessels crossing the internal os of the cervix in the setting of velamentous insertion, a condition known as vasa previa, predispose to catastrophic hemorrhage of the fetal umbilical artery (Palacios Jaraquemada and Bruno 2000). Undiagnosed vasa previa has a fetal mortality rate nearing 60% (Bardo and Oto 2008).
Placenta previa refers to abnormal implantation of the placenta in the lower uterine segment,