- •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
Endometriosis
Vera Schreiter and Karen Kinkel
Contents
1 Introduction\
2 Imaging Techniques and Findings\
2.1 Sonography\
2.2 MRI\
3 MR Imaging Findings\
3.1 Endometriosis of the Ovaries: Endometriotic
Cysts or Endometriomas\
3.2 Endometriosis of the Vesicouterine Pouch
and the Urinary Bladder\
3.3 Endometriosis of the Vaginal Wall
and in Particular the Posterior Fornix
of the Upper Vaginal Wall\
3.4 Endometriosis of the Uterine Ligaments
Including the Uterosacral Ligaments
and the Round Ligaments, the Lateral
and Anterior Pelvic Wall,
and the Parametrium and the Peritoneum\
3.5 Endometriosis of the Bowel, Specifically
the Anterior Rectum and the Sigmoid,
the Cecum, the Ileum, and the Appendix\
3.6 Endometriosis in Rare Localizations,
Special Types, and Associated
Complications\
References\
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mapping of endometriotic lesion localization. |
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The interpretation of MR images should use |
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a checklist to search for lesions based on the |
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most common locations of endometriosis and |
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typical changes in MRI signal intensity. |
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1\ |
Introduction |
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V. Schreiter, MD, PD (*) Department of Radiology, Charité – Universitätsmedizin Berlin,
Augustenburger Platz 1, 13353 Berlin, Germany e-mail: vera.schreiter@charite.de
K. Kinkel, MD, PD
Institut de Radiologie, Clinique des Grangettes,
ch. des Grangettes 7, 1224 Chêne-Bougeries, Geneva, Switzerland
e-mail: karen.kinkel@grangettes.ch
With an estimated prevalence of 10–15%, endometriosis is the third most common benign disease in women of premenopausal age after adenomyosis and fibroids of the uterus (Houston 1984). Endometriosis affects young women, peaking at age 28 (Bloski and Pierson 2008). Premenarchal onset and occurrence in men have been reported (Oliker and Harris 1971; Pinkert et al. 1979; Schrodt et al. 1980). Most women present with abdominal and pelvic pain, dysmenorrhea, dyschezia or other bowel-related symptoms, dysuria
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or back pain, and fertility-related problems (Bloski and Pierson 2008). Many of these symptoms are attributable to the aggressive infiltrative nature of endometriosis. Endometrial tissue can occur anywhere in the body. Completely asymptomatic forms of endometriosis also exist (Balasch et al. 1996; Fedele et al. 2004).
The etiology of endometriosis has not been fully elucidated. Six different theories about the underlying mechanism exist, which are in part complementary and in part additive. Currently, the tissue injury and repair (TIAR) theory is considered the most plausible and most widely accepted explanation. This theory was proposed by Leyendecker and assumes that underlying microinjury and repair of the fundocornual raphe lead to enhanced hyperand dysperistalsis with retrograde expulsion of basal endometrial tissue through the fallopian tubes into the abdominal cavity (Leyendecker et al. 2009). Leyendecker’s explanation is a sensible supplement to the older transplantation theory of J. A. Sampson, known as retrograde menstruation (1927). The metaplasia theory proposed by R. Meyer (1919) assumes that endometrial tissue outside the uterus is composed of dedifferentiated celomic cells, which have undergone transformation under various influences and thus lead to extrauterine endometrial implants (Matsuura et al. 1999). Generally, there appears to be a strong association with estrogen (Da Costa e Silva Rde et al. 1992). This phenomenon plays a role in the aromatase theory, which assumes an increased formation of estrogen from C19 androgens, and in personalized treatment approaches (Zeitoun and Bulun 1999). The invasiveness and multifocal ectopic occurrence of the condition are explained by the cellular and molecular biological concepts with disturbed tissue integrity. Explanations for the lack of intrinsic defense mechanisms of the body against the invasive growth of endometriosis are proposed by immunological concepts involving cytokines, growth factors, and various hormones (Khorram et al. 1993; Halme et al. 1988; Vinatier et al. 1996).
The diagnosis of endometriosis is difficult and takes on average 6 years or even longer (Hadfield et al. 1996). Laparoscopy, combining visual inspection with the option of obtaining tissue for histology, remains the gold standard for the diagnosis of endometriosis (Dunselman et al. 2014). Besides the initial diagnosis comprising a gyneco-
logic history and pelvic examination, laboratory testing (CA 125), and an ultrasound examination, magnetic resonance imaging (MRI) is gaining an increasing role, especially for preoperative mapping in women with extensive involvement and for diagnosis of recurrent endometriosis.
2\ Imaging Techniques
and Findings
2.1\ Sonography
Vaginal ultrasound is the first-line diagnostic imaging modality in women with endometriosis; however, because of its limited range, it should be supplemented by additional examinations such as transrectal and/or transabdominal ultrasound and MRI, as well as endoscopic examinations including rectosigmoidoscopy and cystoscopy.
Vaginal ultrasound allows identification of ovarian manifestations of endometriosis as well as involvement of directly adjacent organs such as the urinary bladder and intestine and also provides information for differentiation of endometriosis from adenomyosis of the uterus (Lazzeri et al. 2014). Ovarian manifestations of endometriosis are known as endometriomas, chocolate cysts, or endometriotic cysts. They are categorized as benign cystic and cyst-like ovarian lesions and must be differentiated from other ovarian cystic lesions: functional ovarian cysts (follicular and corpus luteum cysts), surface epithelial inclusion cysts, ovarian dermoid cysts, ovarian cyst mimics (paraovarian cyst, paratubal cyst), cyst-like lesions (hydrosalpinx, tubo-ovarian abscess, lymphocele), benign epithelial ovarian tumors (serous cystadenomas, cystadenofibromas, mucinous cystadenomas), borderline tumors, and carcinoma of the ovary (Fleischer et al. 1978; Atri et al. 1994; Ekici et al. 1996). Sonographically, ovarian endometriotic cysts are hypoechoic cysts with lowlevel internal echoes and no demonstration of intralesional flow signals by color Doppler ultrasound (Patel et al. 1999). There is no hyperechoic solid node on the wall. In up to 30% of cases, small hyperechoic foci consistent with cell debris, cholesterol deposits, or small hemorrhages are seen within the lesion (Savelli 2009). Such hyperechoic internal foci must be differentiated from
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wall-related hyperechoic structures with maximum diagnostic confidence to rule out a possible malignant component (ovarian cancer). This may necessitate an additional MRI examination since even additional functional assessment by color Doppler imaging often provides no reliable diagnosis either (Wu et al. 2004). With its high soft tissue contrast, MRI appears to be a valuable noninvasive diagnostic imaging modality for further evaluation of extragenital endometriotic lesions and second-line evaluation of some genital lesions: MRI primarily offers advantages in the characterization of nongenital endometric lesions, which often have a noncystic appearance (Bazot et al. 2004a).
Supplementary abdominal ultrasound should focus on the morphologic evaluation of both kidneys for ruling out possible secondary urinary stasis, evaluation of the filled bladder to rule out bladder endometriosis (supplemented by cystoscopy as needed), and on ruling out endometriosis of the appendix (Carmignani et al. 2010; Vercellini et al. 1996; Halis et al. 2010). When rectovaginal endometriosis is suspected, diagnostic workup should be supplemented by MRI and transrectal ultrasound and, possibly, followed by rectosigmoidoscopy (Halis et al. 2010; Fedele et al. 1998).
2.2\ MRI
Based on current knowledge, MRI has the following indications: second-line imaging modality for pelvic endometriosis following ultrasound examination, patients with clinical symptoms and negative and/or indeterminate sonographic findings (Guerriero et al. 2015, 2016), and as a staging investigation prior to surgery in patients with multifocal deep infiltrating endometriosis (Medeiros et al. 2015).
Despite qualitative differences in terms of spatial resolution (Hottat et al. 2009; Rousset et al. 2014; Manganaro et al. 2012) and fat suppression (Manganaro et al. 2012; Cornfeld and Weinreb 2008), both 1.5 T and 3.0 T MRI appear to be suitable for examining women with endometriosis. The use of a pelvic phased-array coil is recommended because of the higher signal-to-noise ratio (McCauley et al. 1992; Kier et al. 1993). Patients should be examined supine; claustrophobic patients
may be examined in prone position. Good bowel preparation is essential when looking for deep endometriotic nodules. Peristalsis should be eliminated to a maximum by administration of antiperistaltic medication (e.g., 1 mg glucagon (GlucaGen ®, Novo Nordisk ®; Bagsværd, Denmark) or 20 mg butylscopolamine (Buscopan ®, Boehringer Ingelheim GmbH; Ingelheim, Germany)) (Manganaro et al. 2014). Additional fasting for 3–6 h before the MRI examination is recommended (Manganaro et al. 2012; Saba et al. 2012; Abrao et al. 2007; Bazot et al. 2009; Fiaschetti et al. 2012; Bazot et al. 2004b; Chamie et al. 2011a). Expert consensus about the best time of the menstrual cycle to perform MRI does not exist according to the new ESUR guidelines (Bazot et al. 2016).
Further measures to be taken before the MRI examination depend on the clinical symptoms and suspected sites of endometriosis. For example, if bladder endometriosis is suspected, the patient should have a moderately filled urinary bladder, which can be accomplished, for example, by having the patient drink 1.5 l of water 45 min before the examination (Grasso et al. 2010; Takeuchi et al. 2005). Filling the rectum with ultrasound gel or water can potentially improve detection of endometrial lesions in the pouch of Douglas and the rectosigmoid junction (Fiaschetti et al. 2012; Takeuchi et al. 2005; Faccioli et al. 2010; Kikuchi et al. 2014) but is not mandatory. This should be done after prior bowel rinsing which is strongly recommended by several authors including the new ESUR guidelines (Chamie et al. 2011a; Bazot et al. 2016; Takeuchi et al. 2005; Yoon et al. 2010) and may possibly be supported by dietary measures starting up to 3 days before the MRI examination (Faccioli et al. 2010).
Vaginal filling with ultrasound gel is another optional measure and can potentially improve detection of endometriotic implants in the posterior vaginal fornix (Fiaschetti et al. 2012; Kikuchi et al. 2014).
The following MRI protocol is recommended for endometriosis mapping:
A T2-weighted (T2w) sequence is the sequence of choice for the detection of pelvic endometriosis, especially of the deep infiltrating type. At least two 2D T2w sequences – fast spin echo (FSE) and turbo spin echo (TSE) – in sagittal and axial planes (Hottat et al. 2009; Manganaro et al. 2012; Saba et al. 2012; Fiaschetti et al. 2012; Bazot