Adenomyosis vs Endometriosis

• Junctional zone (JZ) thickening ≥12 mm on T2-weighted images for adenomyosis
• T1-hyperintense endometrioma with T2 'shading' on fat-saturated sequences for endometriosis
• Ill-defined low-T2 myometrial signal with small T1-hyperintense hemorrhagic foci within the uterine wall (adenomyosis) versus implants at extrauterine sites such as uterosacral ligaments, pouch of Douglas, or rectovaginal septum (endometriosis)

• Adenomyosis is characterized by junctional zone thickening ≥12 mm, representing hypertrophied smooth muscle responding to ectopic endometrial glands within the myometrium.
• Adenomyotic myometrium shows ill-defined low T2 signal (reflecting fibrosis and smooth-muscle hypertrophy) interspersed with small T2-hyperintense and T1-hyperintense (hemorrhagic) foci representing ectopic glandular and blood-containing spaces.
• Adenomyosis causes globular uterine enlargement with radiating striations extending from the endometrium into the myometrium, best seen on T2-weighted imaging.
• Endometrioma appears as a complex ovarian cyst with T1-hyperintense content that does not suppress on fat-saturated sequences (distinguishing it from fat or gadolinium), combined with characteristic T2 'shading' (peripheral bright T2 signal with central dark T2 signal) and possible hemosiderin deposits.
• Deep infiltrating endometriosis (DIE) manifests as low-T2 spiculated or stellate soft-tissue nodules and fibrosis at the uterosacral ligaments, rectovaginal septum, bowel wall, and bladder, best appreciated on multiplanar imaging with dedicated pelvic protocol.
• Endometriosis causes secondary findings including pelvic adhesions, tethering, angulated or kinked bowel loops, and 'kissing ovaries' (opposed adnexa due to adhesive traction), findings not typical of isolated adenomyosis.
• Adenomyosis is best assessed on T2-weighted and T1-weighted (with fat saturation) imaging focused on the uterine body and junctional zone, whereas endometriosis requires a comprehensive pelvic survey to detect peritoneal, ligamentous, and ovarian implants.
• Adenomyosis typically presents in multiparous women aged 40–50 years with menorrhagia and dysmenorrhea, while endometriosis typically presents in reproductive-age women with cyclic pain, dyspareunia, and infertility, though both are estrogen-dependent and often coexist.

• Uterine leiomyoma (fibroid) versus adenomyosis: fibroids are well-circumscribed, often homogeneously low T2, cause mass effect distorting the junctional zone, and may show degeneration or cystic change; adenomyosis shows ill-defined junctional zone thickening without a discrete nodule.
• Endometrial cancer versus adenomyosis: endometrial cancer presents as an echogenic or heterogeneous endometrial mass with abnormal junctional zone disruption and often elevated T2 signal; adenomyosis is diffuse myometrial involvement with preserved, though thickened, junctional zone.
• Ovarian cyst with hemorrhage versus endometrioma: hemorrhagic ovarian cysts may show T1 hyperintensity but typically resolve over time and lack the characteristic T2 shading pattern and persistent T1-bright non-fat-suppressing content of endometrioma.
• Bowel pathology (Crohn disease, malignancy) versus deep infiltrating endometriosis: bowel inflammation or neoplasm shows enhancement, wall thickening, and clinical/endoscopic correlation; DIE typically causes wall thickening without mucosal involvement or enhancement and is associated with peritoneal findings.
• Adenomyosis versus diffuse myometrial edema from infection or inflammation: myometritis shows acute T2 hyperintensity, clinical fever, and elevated inflammatory markers; adenomyosis is chronic with low T2 foci and no acute systemic symptoms.
• Normal thick junctional zone (reproductive age) versus pathologic adenomyosis: the junctional zone normally measures up to 10–12 mm in reproductive-age women and may transiently thicken with hormonal changes; adenomyosis is diagnosed when JZ ≥12 mm persists with associated T2 hyperintense and T1 hyperintense foci.

Clearly separate adenomyosis from endometriosis in your report by stating the precise location of findings: "Junctional zone thickening (≥12 mm) with myometrial foci consistent with adenomyosis" for intrauterine disease, versus "T1-hyperintense ovarian cyst with T2 shading and non-fat-suppressing content consistent with endometrioma" or "Low-T2 nodular fibrosis at the uterosacral ligament/rectovaginal septum consistent with deep infiltrating endometriosis" for extrauterine disease, and explicitly note whether both entities are present, as this impacts counseling and treatment.

• Mistaking a normal junctional zone (which can measure up to 10–12 mm in reproductive-age women) for pathologic adenomyosis; adenomyosis requires both JZ thickening ≥12 mm and associated T2-hyperintense and T1-hyperintense myometrial foci rather than isolated JZ measurement.
• Failing to perform dedicated fat-saturated sequences; without fat saturation, T1-hyperintense endometriomas cannot be confidently distinguished from fat, and endometriotic implants at peritoneal or ligamentous sites may be missed.
• Overlooking the characteristic T2 'shading' pattern (peripheral bright, central dark signal) of endometrioma; absence of shading should prompt consideration of other hemorrhagic cystic lesions and correlation with imaging over time.
• Finding adenomyosis and assuming this excludes endometriosis (or vice versa); substantial proportion of patients have both, so identification of one should trigger systematic evaluation of extrauterine sites and careful assessment of the myometrium.