Adenomyosis is the presence of endometrial glands and stroma within the myometrium, causing diffuse uterine enlargement, dysmenorrhea, and menorrhagia.

Exam domain	One-glance essentials
Definition / diagnosis	*Adenomyosis is endometrial glands and stroma within the myometrium with reactive smooth-muscle hypertrophy* ^[1]^[2] It may be diffuse or form a focal adenomyoma and commonly coexists with endometriosis ^[2]
Epidemiology / risks	Typical patients are 35–50 years, multiparous, or have prior uterine surgery, although younger patients are increasingly diagnosed by imaging ^[2] Risk is associated with childbirth and disruption of the endomyometrial junction ^[2]
Core mechanism	Endomyometrial invagination → cyclic intramyometrial bleeding → inflammation and prostaglandin release → pain and diffuse uterine enlargement ^[2] Impaired myometrial contraction and increased endometrial surface contribute to HMB ^[2]
Clinical picture	*HMB plus progressive dysmenorrhoea with a uniformly enlarged, globular, boggy, tender uterus is classic* ^[1]^[2] A firm irregular uterus suggests fibroids; deep dyspareunia and pouch-of-Douglas nodularity suggest endometriosis ^[1]
Investigations	TVUS is first-line: heterogeneous myometrium, myometrial cysts, fan-shaped shadowing, and an irregular junctional zone ^[1]^[2] MRI helps when ultrasound is equivocal or focal disease mimics fibroid; histology after hysterectomy is definitive ^[2]
Management	*LNG-IUS is a preferred uterus-preserving treatment; NSAIDs, tranexamic acid, other progestogens, combined hormonal contraception, or short-course GnRH therapy may help ^[2] Hysterectomy is definitive* when symptoms are severe and fertility is complete because adenomyosis lacks a clean enucleation plane ^[1]^[2]
Complications	Iron-deficiency anaemia, chronic pelvic pain, subfertility, and adverse pregnancy outcomes are important ^[2] Conservative surgery may recur; subsequent pregnancy after adenomyomectomy carries uterine-rupture risk ^[2]
Prevention / follow-up	Treat anaemia, review symptom control, and reassess new or persistent abnormal bleeding for coexisting pathology ^[2] Shared decisions should address fertility, recurrence risk, and the consequences of definitive surgery ^[2]
Exam traps	*Adenomyosis produces diffuse boggy enlargement; fibroids produce discrete firm irregular masses* ^[1] A normal or non-specific ultrasound does not exclude disease; MRI can clarify equivocal cases ^[2]

References

^[1] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (pp. 6, 14 — adenomyosis and fibroid distinction) ^[2] Senior notes: Adrian Lui Gynecology Notes.pdf (pp. 50–51 — adenomyosis)

Adenomyosis

Adenomyosis (子宮腺肌症) — breaking down the term: "adeno-" = gland, "myo-" = muscle, "-osis" = condition/process. So literally: a condition where glandular tissue is found within muscle.

Adenomyosis is the invasion of endometrial glands and stroma into the myometrium, with surrounding smooth muscle hyperplasia ^[1]. This is the key defining feature — ectopic endometrial tissue is not just sitting passively in the myometrium, it actively induces the surrounding smooth muscle to hypertrophy and hyperplase, leading to a diffusely enlarged uterus.

Histologically, the formal criterion is: presence of endometrial tissue within myometrium ≥1 low-power field from the endomyometrial junction ^[1]. This threshold exists because the normal endometrial-myometrial border is somewhat irregular, and you need to distinguish true adenomyosis from normal undulations of the junction.

Key Distinction from Endometriosis

Adenomyosis = endometrial tissue within the myometrium (i.e., the uterine wall itself). Endometriosis = endometrial tissue outside the uterus entirely (ovaries, peritoneum, pouch of Douglas, etc.). They are pathogenetically distinct although they commonly co-occur ^[1]. Think of adenomyosis as an "inward" invasion and endometriosis as an "outward" seeding.

Affects ~1% of women ^[1] — though this figure likely underestimates true prevalence, as definitive diagnosis historically required hysterectomy specimens. With improved imaging (MRI, high-resolution TVUS), reported prevalence in some studies ranges from 20–35% of hysterectomy specimens.
Usually presents in the 35–50 year age group ^[1] — this makes sense because:
- These women have had decades of menstrual cycling, providing repeated stimulus for endometrial invagination into the myometrium.
- The condition is oestrogen-dependent; it tends to regress after menopause when oestrogen levels drop.
More common in multiparous women — repeated pregnancies and deliveries may disrupt the endomyometrial junction, facilitating glandular invasion.
Associated with prior uterine surgery (e.g., caesarean section, D&C, myomectomy) — surgical disruption of the endomyometrial border may allow endometrial tissue to penetrate into the myometrium.

Risk Factors

Risk Factor	Mechanism
Age 35–50 years	Cumulative exposure to oestrogen-driven menstrual cycling
Multiparity	Disruption of endomyometrial junction during pregnancy/delivery
Prior uterine surgery (C-section, D&C, myomectomy)	Iatrogenic breach of the endomyometrial barrier
Early menarche	Longer lifetime oestrogen exposure
Short menstrual cycles	More frequent endometrial cycling → more invagination opportunities
Obesity	Peripheral aromatisation of androgens → excess oestrogen
Tamoxifen use	Acts as a partial oestrogen agonist on the uterus
Coexisting endometriosis	Shared risk factors and possibly shared pathogenetic mechanisms

3. Anatomy and Relevant Functional Considerations

Understanding adenomyosis requires understanding the normal uterine wall architecture:

Endometrium (innermost): The mucosal lining. Composed of:
- Stratum functionalis — shed during menstruation, hormonally responsive.
- Stratum basalis — the regenerative layer; does NOT shed during menstruation. This is the layer from which adenomyosis is thought to originate.
Myometrium (middle): Thick smooth muscle layer. Subdivided into:
- Junctional zone (JZ) — the innermost layer of the myometrium, directly abutting the endometrium. This zone is critical in adenomyosis:
  - It has a different embryological origin (Müllerian) compared to the outer myometrium.
  - It is hormonally responsive and contracts during menstruation to aid in endometrial shedding.
  - On MRI, thickening of the junctional zone > 12 mm is highly suggestive of adenomyosis ^[1].
- Outer myometrium — the bulk of the muscle wall.
Serosa/Perimetrium (outermost): Visceral peritoneum covering the uterus.

The junctional zone (JZ) is the "battleground" in adenomyosis. Think of it as the gatekeeper between endometrium and myometrium. When this zone is disrupted — whether by surgery, repeated pregnancies, or intrinsic factors — endometrial glands can breach through and invade the myometrium. The JZ is the key structure visualised on MRI when assessing for adenomyosis.

4. Aetiology and Pathogenesis

The exact cause of adenomyosis is unknown ^[1], but several theories exist:

The endometrium directly invaginates from the endomyometrial junction into the myometrium ^[1].

How? The stratum basalis of the endometrium herniates through the junctional zone into the myometrium. This is facilitated by:
- Repeated mechanical trauma (menstruation, pregnancy, surgery).
- High local oestrogen levels driving glandular proliferation and invasion.
- Altered expression of matrix metalloproteinases (MMPs) that break down the extracellular matrix at the endomyometrial interface.
Why the basalis? Because the basalis does not shed — it persists cycle after cycle, and if it starts growing "downward" instead of "upward," it invades into muscle.
This theory is supported by the observation that adenomyosis is continuous with the endometrial surface in most cases.

Alternatively, adenomyosis may arise from de novo metaplasia from Müllerian rests within the myometrium ^[1].

During embryological development, remnants of Müllerian duct tissue may persist within the myometrium.
Under hormonal stimulation (oestrogen), these rests could undergo metaplasia into endometrial-type tissue.
This theory explains cases where adenomyotic foci are found deep within the myometrium, completely disconnected from the endometrial surface.

This is a more recent and integrative theory:

Repeated tissue injury at the endomyometrial junction (from uterine peristalsis during menstruation, or from surgical trauma) triggers a repair process.
This repair process involves local oestrogen production, activation of stem cells, and epithelial-mesenchymal transition (EMT).
Over time, this leads to progressive invagination and establishment of ectopic endometrial tissue within the myometrium.

Once endometrial glands/stroma are within the myometrium, they induce hypertrophy and hyperplasia of the surrounding smooth muscle ^[1].

This is the hallmark pathological process:

This results in a diffusely enlarged uterus, analogous to the concentric enlargement of a pregnant uterus ^[1] — because the muscle is hypertrophying concentrically around the ectopic glands, rather than a focal mass pushing things aside (as in a fibroid).

Adenomyosis is Oestrogen-Dependent

Like endometriosis, adenomyosis depends on oestrogen for growth. This is why:

It presents in the reproductive years (peak 35–50).
It regresses after menopause.
GnRH agonists (which suppress oestrogen) provide symptomatic relief.
Pregnancy can sometimes worsen symptoms (high oestrogen state).

5. Classification

Type	Description	Clinical Implication
Diffuse adenomyosis (typical) ^[1]	Widespread involvement of the myometrium; no discrete mass	The classic presentation: uniformly enlarged, boggy uterus
Focal adenomyosis (adenomyoma) ^[1]	Localised collection of ectopic endometrial tissue forming a discrete mass within the myometrium	Often confused with leiomyomas (fibroids) ^[1]; requires MRI for differentiation

Some classification systems grade adenomyosis by how deeply the ectopic glands penetrate:

Superficial: Limited to the inner third of the myometrium (junctional zone).
Deep: Extends into the outer two-thirds of the myometrium.
Deeper invasion tends to correlate with more severe symptoms.

This is a standardised ultrasound-based classification system proposed by international consensus:

Location: Anterior, posterior, lateral, fundal.
Type: Diffuse vs. focal.
Extent: Percentage of myometrial involvement.
Features: Presence of cysts, echogenic islands, fan-shaped shadowing, etc.

Diffuse vs. Focal — Why It Matters Clinically

Diffuse adenomyosis → hysterectomy is often the definitive treatment because the disease is everywhere in the myometrium and cannot be "excised."
Focal adenomyosis (adenomyoma) → may be amenable to surgical excision (adenomyomectomy) in women wishing to preserve fertility, though it is technically challenging.

6. Clinical Features

6.1 Symptoms

Asymptomatic in 33% of cases ^[1] — adenomyosis is often found incidentally on imaging or in hysterectomy specimens.

For the symptomatic majority, the cardinal symptoms are:

Heavy menstrual bleeding (60%): due to increased endometrial surface area of the enlarged uterus ^[1].

Pathophysiological basis:

The uterus is diffusely enlarged due to myometrial hypertrophy → the endometrial cavity is also stretched and expanded → more endometrial surface area to shed → heavier bleeding.
Ectopic endometrial glands within the myometrium also bleed during menstruation → this blood has nowhere to go and contributes to prolonged oozing.
The hypertrophied, adenomyotic myometrium has impaired contractility — normal myometrial contraction is critical for haemostasis after endometrial shedding (it compresses the spiral arterioles). Adenomyotic tissue disrupts the coordinated contraction → poor haemostasis → prolonged and heavy bleeding.
Increased local prostaglandin and inflammatory mediator production → vasodilation of endometrial vessels → more bleeding.

High Yield: The mechanism is similar to why fibroids cause HMB — both increase endometrial surface area and impair myometrial contraction. The key difference is that fibroids cause focal enlargement while adenomyosis causes diffuse enlargement.

Dysmenorrhoea (25%): due to bleeding and swelling of endometrial islands confined by myometrium ^[1].

Pathophysiological basis:

During menstruation, the ectopic endometrial glands within the myometrium undergo the same cyclical changes as the normal endometrium — they proliferate, secrete, and then bleed.
Unlike the endometrial cavity (which has an exit through the cervix), blood from these ectopic glands is trapped within the myometrium. This causes local swelling and pressure.
The surrounding myometrium is being stretched and distended by this trapped blood → this activates pain receptors (nociceptors) in the myometrium.
Inflammatory mediators (prostaglandins, particularly PGF2α and PGE2) are released from the ectopic endometrial tissue → these cause myometrial smooth muscle spasm and sensitise nerve endings → pain.
The dysmenorrhoea is typically secondary dysmenorrhoea — i.e., it starts later in life (30s–40s) and worsens progressively, unlike primary dysmenorrhoea which starts at menarche.

Character of pain:

Cramping, often midline, deep pelvic pain.
Starts before menstruation and continues throughout (sometimes extending beyond the period).
May worsen with each cycle as the disease progresses.

Generally NOT associated with dyspareunia (but may have deep pelvic pain) ^[1].

Why not dyspareunia?

Dyspareunia (pain during intercourse) is more characteristic of endometriosis (especially deep infiltrating endometriosis involving the uterosacral ligaments or pouch of Douglas, or ovarian endometriomas).
In adenomyosis, the pathology is within the myometrial wall — it doesn't typically involve the pelvic peritoneum or pouch of Douglas, so deep thrust dyspareunia is not a hallmark feature.
However, the diffusely enlarged, tender uterus may cause a vague deep pelvic heaviness or ache, especially premenstrually.

Infertility: controversial ^[1].

Possible mechanisms (debated):

Disrupted junctional zone peristalsis → impaired sperm transport toward the fallopian tubes.
Altered endometrial receptivity → defective implantation.
Chronic inflammatory milieu within the endometrium and myometrium → hostile environment for embryo implantation.
Increased uterine contractility → may expel the embryo.
Association with other conditions that cause infertility (e.g., endometriosis).

Current evidence suggests adenomyosis likely does negatively impact fertility and IVF outcomes, but the data are not as robust as for endometriosis. It is increasingly recognised as a factor in recurrent implantation failure.

Intermenstrual bleeding — ectopic glands may bleed at times outside the menstrual period.
Iron deficiency anaemia — secondary to chronic HMB.
Menstrual clots and flooding — from the heavy flow.
Chronic pelvic pain — from ongoing low-grade inflammation in the myometrium.
Bladder/rectal pressure symptoms — from an enlarged uterus pressing on adjacent structures (less common than with large fibroids, since adenomyotic uteri rarely exceed 12 weeks' size ^[1]).

6.2 Signs

Physical examination findings ^[1]:

Typically mobile ^[1] — the uterus is not fixed (unlike in endometriosis with dense adhesions). This is because adenomyosis is an intrinsic disease of the myometrium, not a peritoneal disease.
Diffusely enlarged ^[1] — the uterus is symmetrically enlarged (contrast with fibroids, which cause asymmetric/irregular enlargement).
Globular ^[1] — the uterus has a round, ball-like shape (rather than the normal pear shape). This is because the concentric myometrial hypertrophy expands the uterus in all directions.
Boggy (soft) ^[1] — the uterus feels softer than expected. This is because:
- The myometrium is infiltrated with glandular tissue and microcysts, making it less firm than normal muscle.
- Contrast with fibroids, which feel firm/hard because they are composed of dense fibrous tissue and smooth muscle.
Rarely exceeds 12 weeks' size ^[1] — i.e., usually < 12 cm. This is a useful clinical pearl to distinguish from fibroids (which can grow much larger).
Tenderness ^[1] — especially during menstruation, due to active bleeding within the myometrial glands. The uterus may be tender on palpation, particularly in the premenstrual/menstrual phase.

Boggy vs. Firm — The Key Exam Distinction

Adenomyosis = Diffusely enlarged, boggy/soft, globular, tender uterus. Fibroids = Irregularly enlarged, firm/hard, non-tender, may have discrete lumps. This is a favourite exam question! If the uterus is uniformly enlarged and soft → think adenomyosis. If it's irregular and firm → think fibroids.

Cervix usually appears normal.
There may be heavy menstrual flow seen at the os during menstruation.

This is a critical comparison for exams:

Feature	Adenomyosis	Fibroids (Leiomyomas)
Pathology	Endometrial glands/stroma within myometrium	Benign smooth muscle tumour
Distribution	Diffuse (or focal = adenomyoma)	Discrete, encapsulated masses
Uterine enlargement	Diffuse, symmetrical, globular	Irregular, asymmetric, lobulated
Consistency	Boggy/soft	Firm/hard
Size	Rarely > 12 weeks	Can be very large (> 20 weeks)
Tenderness	Yes, especially menstrual	Usually non-tender
Mobility	Mobile	Mobile (unless pedunculated/broad lig.)
Peak age	35–50 years	30–50 years
Key symptom	Dysmenorrhoea + HMB	HMB ± pressure symptoms
Dyspareunia	Not typical	Not typical
Imaging	Ill-defined, JZ thickening, no capsule	Well-defined, encapsulated, may calcify
Definitive diagnosis	Histology (hysterectomy)	Histology
Definitive treatment	Hysterectomy	Myomectomy or hysterectomy

8. Approach to Evaluation

Initial evaluation ^[1]:

HMB and dysmenorrhoea are the most characteristic symptoms ^[1].
Ask about:
- Menstrual pattern: duration, flow volume (number of pads/tampons, passing clots, flooding), impact on daily activities.
- Dysmenorrhoea: onset, severity, timing relative to menses (typically starts before and continues through menstruation).
- Fertility history and desire for future fertility (crucial for management decisions).
- Previous uterine surgery (C-section, D&C, myomectomy).
- Symptoms of anaemia (fatigue, breathlessness, palpitations).
- Rule out red flags: postmenopausal bleeding, intermenstrual bleeding in women > 45 (need to exclude endometrial cancer).

PE: typically mobile, diffusely enlarged, globular, boggy (soft) uterus (rarely exceed 12w) ± tenderness ^[1].
Bimanual pelvic examination is the key clinical assessment.

Endometrial assessment (EA) may be indicated in the case of AUB > 45 years to rule out endometrial carcinoma ^[1].
Methods: Pipelle endometrial biopsy (office-based, first-line), hysteroscopy with directed biopsy if Pipelle is inadequate.

D. Imaging

TVUS is the 1st line imaging ^[1].

Key sonographic features:

Feature	Description	Pathological Basis
Subendometrial echogenic linear striations/nodules ^[1]	Bright lines or dots just beneath the endometrium extending into the myometrium	Ectopic endometrial glands within the inner myometrium
Anechoic cysts (myometrial cysts) ^[1]	Small dark (fluid-filled) areas within the myometrium, typically 1–7 mm	Dilated ectopic endometrial glands filled with old blood or secretions
Focal or diffuse myometrial bulkiness (esp. fundal and posterior wall) ^[1]	Asymmetric thickening of the myometrium, often more prominent posteriorly	Smooth muscle hypertrophy/hyperplasia in response to ectopic glands
Increased vascularity corresponding to adenomyosis lesions ^[1]	On colour Doppler, increased blood flow within the thickened areas	Angiogenesis driven by ectopic endometrial tissue
Heterogeneous myometrial echotexture	The myometrium loses its normal homogeneous appearance	Intermixed glandular tissue and hypertrophied muscle
Fan-shaped acoustic shadowing	Shadows radiating from the lesion	Different acoustic impedance between glandular tissue and muscle
Irregular/indistinct endometrial-myometrial border	The normally sharp endomyometrial junction becomes blurred	Direct extension of endometrial tissue into the myometrium

Sensitivity of TVUS: Approximately 72–89% sensitive and 65–98% specific for adenomyosis, especially when performed by experienced sonographers.

Pelvic MRI is the most sensitive (sensitivity 78–88%, specificity 67–93%), reserved for focal adenomyosis confused with fibroids ^[1].

Key MRI features:

Thickening of the junctional zone (JZ) of the uterus > 12 mm is associated with adenomyosis ^[1].
Foci of increased T1W and increased T2W density ^[1]:
- High T1W signal = haemorrhagic foci (blood within ectopic glands).
- High T2W signal = glandular tissue and oedema within the thickened JZ.
The junctional zone appears as a band of low T2 signal on MRI (because it is compact smooth muscle). When it is thickened and contains high-signal foci, this is diagnostic of adenomyosis.
MRI can distinguish adenomyoma from leiomyoma:
- Adenomyoma: Ill-defined borders, no capsule, high T1 foci (blood), within thickened JZ.
- Leiomyoma: Well-defined borders, pseudocapsule, low T2 signal (dense fibrous tissue), may calcify.

MRI Junctional Zone Thickness — The Key Number

JZ < 8 mm = normal
JZ 8–12 mm = equivocal (correlate clinically)
JZ > 12 mm = highly suggestive of adenomyosis ^[1] Remember: 12 mm is the magic number for JZ thickening on MRI.

The gold standard for definitive diagnosis is histopathological examination of a hysterectomy specimen.
This is why adenomyosis was historically under-diagnosed — you couldn't confirm it without removing the uterus.
With modern high-resolution TVUS and MRI, clinical/radiological diagnosis is now standard for management purposes, and histological confirmation is obtained when hysterectomy is eventually performed.

9. Gross and Histological Pathology

Grossly: uterus uniformly enlarged and boggy, classically crisscross appearance upon sectioning the uterus ^[1].

On cut section, the myometrium shows a trabeculated, whorled, "Swiss cheese" appearance with small haemorrhagic or cystic areas scattered throughout.
The classic "crisscross" pattern reflects the interwoven bands of hypertrophied smooth muscle surrounding islands of ectopic endometrial tissue.
There is no capsule or clear boundary (unlike fibroids).
The endometrial-myometrial junction is indistinct.

Endometrial glands and stroma are found deep within the myometrium (≥1 low-power field from the endomyometrial junction).
The surrounding myometrium shows smooth muscle hyperplasia and hypertrophy.
The ectopic glands may show various phases of the menstrual cycle (proliferative, secretory) or may be inactive.
Old haemorrhage (haemosiderin-laden macrophages) may be seen around the ectopic glands.

High Yield Exam Points:

Adenomyosis = endometrial glands + stroma in myometrium + smooth muscle hypertrophy

Peak age 35–50, affects ~1% women

Pathogenetically distinct from endometriosis but commonly co-occur

Cardinal symptoms: HMB (60%) + dysmenorrhoea (25%); 33% asymptomatic

Examination: mobile, diffusely enlarged, globular, boggy, tender uterus, rarely > 12 weeks

TVUS first line; MRI for equivocal/focal cases (JZ > 12 mm diagnostic)

Definitive diagnosis = histology from hysterectomy specimen

Diffuse (typical) vs. focal (adenomyoma — confused with fibroids)

High Yield Summary

Definition: Invasion of endometrial glands and stroma into myometrium with surrounding smooth muscle hyperplasia.

Epidemiology: ~1% women, peak 35–50 years, multiparous, prior uterine surgery.

Aetiology: Unknown — endomyometrial invagination (most accepted) or de novo metaplasia from Müllerian rests. Pathogenetically distinct from but commonly co-occurs with endometriosis.

Pathology: Diffusely enlarged, boggy uterus with crisscross pattern on cut section. Histology: endometrial tissue ≥1 low-power field from endomyometrial junction.

Classification: Diffuse (typical) vs. focal (adenomyoma — mimics fibroids).

Symptoms: HMB (60%, due to ↑endometrial surface area), dysmenorrhoea (25%, due to bleeding/swelling of ectopic glands confined by myometrium), NOT typically dyspareunia, ?infertility (controversial), 33% asymptomatic.

Signs: Mobile, diffusely enlarged, globular, boggy/soft, tender uterus, rarely > 12 weeks' size.

Approach: History (HMB + dysmenorrhoea) → PE (boggy uterus) → TVUS 1st line (subendometrial striations, myometrial cysts, ↑vascularity) → MRI if equivocal (JZ > 12 mm, T1/T2 bright foci) → EA if AUB > 45y → Definitive Dx = histology.

Active Recall - Adenomyosis (Definition, Aetiology, Clinical Features)

^[1] Senior notes: Adrian Lui Gynecology Notes.pdf (Section 2.3.3 Adenomyosis, p. 50)

Differential Diagnosis of Adenomyosis

When a woman aged 35–50 presents with heavy menstrual bleeding (HMB), dysmenorrhoea, and an enlarged uterus, adenomyosis is one of several diagnoses to consider. The differential is built around two cardinal presenting features — the symptom complex (HMB + dysmenorrhoea ± pelvic pain) and the examination finding (enlarged uterus). Let's work through each differential systematically, explaining why each condition mimics adenomyosis and how to distinguish them.

The differentials can be organised by which feature of adenomyosis they share:

Key Differentials — Detailed Comparison

This is the most important differential — fibroids and adenomyosis are the two most common causes of an enlarged uterus with HMB in premenopausal women, and they frequently coexist.

Similarities: Heavy menstrual bleeding, enlarged uterus ^[1].

Difference: Uterine enlargement is irregular and focal ^[1].

Feature	Adenomyosis	Fibroids
Type of enlargement	Diffuse, symmetrical, globular ^[1]	Irregular and focal ^[1]; discrete lumps/lobules palpable
Consistency	Boggy/soft ^[1] — because glandular tissue infiltrating muscle is softer than dense fibrous tumour	Firm/hard — fibroids are composed of densely packed smooth muscle + collagen
Tenderness	Tender, especially perimenstrually ^[1] — due to active bleeding within myometrial glands	Usually non-tender — fibroids are inert masses unless degenerating
Size	Rarely exceeds 12 weeks ^[1]	Can grow very large ( > 20 weeks); pedunculated fibroids can be enormous
Dysmenorrhoea	Prominent (25%) — ectopic glands bleed and swell within trapped myometrium	Less prominent; pressure symptoms (urinary frequency, constipation) more typical
TVUS	Ill-defined myometrial changes, no capsule, myometrial cysts, fan-shaped shadowing	Well-defined hypoechoic mass with a pseudocapsule, may show calcifications
MRI	JZ thickening > 12 mm, T1/T2 bright foci, no capsule	Well-circumscribed mass, low T2 signal, pseudocapsule, whorled pattern
Cut section	Crisscross/trabeculated, no plane of cleavage	Whorled, well-demarcated, can be "shelled out" (enucleated)
Response to hormonal Rx	Hormonal treatment generally similar to endometriosis (unlike fibroids, where they are generally ineffective) ^[2]	Hormonal treatments (OCPs, progestins) generally ineffective for fibroids; GnRH agonists temporarily shrink them

Why does this distinction matter clinically?

Fibroids can be enucleated (myomectomy) because they have a pseudocapsule and a clear surgical plane.
Adenomyosis has no surgical plane for simple enucleation (even in adenomyoma) ^[2] — the disease is diffusely infiltrating the myometrium, so the only definitive surgical treatment is hysterectomy.

High Yield: Focal adenomyosis (adenomyoma) is often confused with leiomyomas ^[1]. MRI is the key differentiator — adenomyoma has ill-defined borders, no capsule, and high T1 foci (blood), while fibroids have well-defined borders and a pseudocapsule.

The 'Boggy vs. Firm' Exam Question

This is a classic clinical examination question. If the stem says "uniformly enlarged, soft/boggy, tender uterus" → adenomyosis. If it says "irregularly enlarged, firm, non-tender uterus with discrete lumps" → fibroids. Don't mix them up!

Similarities: Dysmenorrhoea, infertility ^[1].

Difference: Usually associated with dyspareunia; uterus is usually not enlarged ^[1].

Feature	Adenomyosis	Endometriosis
Location of ectopic tissue	Within the myometrium (intrinsic uterine disease)	Outside the uterus (ovaries, peritoneum, uterosacral ligaments, pouch of Douglas)
Uterine size	Diffusely enlarged ^[1]	Usually not enlarged ^[1] — the pathology is extra-uterine
Dyspareunia	Generally NOT associated ^[1] — pathology is within the uterine wall, not touching pelvic peritoneum	Usually associated with dyspareunia ^[1] — especially deep dyspareunia from involvement of uterosacral ligaments / pouch of Douglas
Dysmenorrhoea	Present (25%) — bleeding within myometrium	Present — peritoneal irritation from ectopic endometrial bleeding
Infertility	Controversial ^[1]	Well-established — distorted anatomy, adhesions, inflammatory milieu, impaired oocyte quality
Examination	Bulky, globular, mildly tender uterus ^[3]	Cervical displacement or stenosis, adnexal mass (endometrioma), palpable tender nodules in adnexa or pouch of Douglas ^[3]
HMB	60% ^[1] — due to increased endometrial surface	Not a typical feature (unless coexisting adenomyosis/fibroids)
Key imaging	TVUS: myometrial changes; MRI: JZ thickening	TVUS: "chocolate cysts" (endometriomas); MRI: deep infiltrating endometriosis; diagnostic laparoscopy is definitive
Age at presentation	35–50 years	25–40 years (tends to present younger)

Why do they commonly coexist?

Although pathogenetically distinct, adenomyosis commonly co-occurs with endometriosis ^[1].
Shared risk factors: prolonged oestrogen exposure, retrograde menstruation, Müllerian duct abnormalities, possible shared stem cell origins.
If one is found, always look for the other.

The key clinical tip: If a woman has dysmenorrhoea + HMB + enlarged uterus → think adenomyosis. If she has dysmenorrhoea + dyspareunia + infertility + normal-sized uterus → think endometriosis. If she has all of the above → both may coexist.

This is the "can't miss" diagnosis — you must exclude malignancy, especially in older women with abnormal uterine bleeding.

Endometrial assessment (EA) may be indicated in the case of AUB > 45 years (d/dx CA endometrium) ^[1].

Feature	Adenomyosis	Endometrial Cancer
Age	35–50 years	Typically postmenopausal (peak 55–65 years), but can occur in younger women with risk factors
Bleeding pattern	HMB (cyclical, predictable)	Postmenopausal bleeding (PMB), or irregular/intermenstrual bleeding in premenopausal women
Pain	Dysmenorrhoea	Pain is a late feature (advanced disease)
Uterine size	Enlarged, boggy	May be normal or enlarged (if advanced/myoinvasive)
Risk factors	Multiparity, prior surgery	Obesity, diabetes, PCOS, tamoxifen, unopposed oestrogen, nulliparity, HNPCC (Lynch syndrome)
Key investigation	TVUS + MRI	Endometrial biopsy (Pipelle) — the definitive diagnostic step
TVUS	Myometrial changes, JZ thickening	Thickened endometrium ( > 4 mm postmenopausal), irregular endometrial outline, increased vascularity

Why must we consider this?

Both adenomyosis and endometrial cancer cause abnormal uterine bleeding.
A woman over 45 with AUB could have both — adenomyosis does not protect against endometrial cancer.
EA is indicated for AUB > 45 years ^[1] to exclude endometrial pathology before attributing bleeding to adenomyosis alone.

Don't Be Complacent

Never assume AUB in a woman over 45 is "just adenomyosis" without performing endometrial assessment. Endometrial cancer must be actively excluded. A Pipelle biopsy is simple, office-based, and potentially life-saving.

A rare but dangerous differential — uterine sarcomas account for 3–9% of all uterine malignancies ^[4].

Feature	Adenomyosis	Uterine Sarcoma
Growth	Stable or slowly progressive	Rapidly enlarging uterine mass — this is the red flag
Age	35–50	Leiomyosarcoma peak 52y; carcinosarcoma median 65y ^[4]
Consistency	Boggy/soft	May be soft (necrotic areas) or firm
Pain	Cyclical dysmenorrhoea	Persistent pain (not cyclical), often severe
Bleeding	Cyclical HMB	May have PMB, foul-smelling discharge ^[4]
Imaging	Diffuse myometrial changes	Irregular heterogeneous mass, necrosis, rapid growth on serial imaging
Definitive Dx	Histology (hysterectomy)	Histology — often diagnosed only after myomectomy/hysterectomy for "presumed fibroids" ^[4]

Leiomyosarcoma arises from smooth muscles of myometrium but is genetically and histologically distinct from leiomyomas (progression from leiomyoma is rare) ^[4].

Stromal sarcomas can be found in association with adenomyosis and endometriosis ^[4] — so there is a direct pathological link. This is why persistent or worsening symptoms in a woman with known adenomyosis should prompt re-evaluation.

Red flags suggesting sarcoma over benign disease:

Rapidly growing "fibroid" (especially postmenopausal).
New or worsening pain.
Postmenopausal bleeding with an enlarging uterus.
Abnormal imaging features (necrosis, heterogeneity).

Feature	Adenomyosis	Chronic PID / Endometritis
Pain	Cyclical dysmenorrhoea	Lower abdominal pain and tenderness, deep dyspareunia ^[5]
Discharge	Normal	Abnormal vaginal or cervical discharge ^[5]
Fever	Absent	Fever > 38.3°C ^[5] (acute PID)
Examination	Boggy, enlarged uterus	Cervical excitation and adnexal tenderness ^[5]; uterus may be tender but not typically enlarged
Causation	Non-infectious	STI or ascending infection
Imaging	Myometrial changes	TVUS/MRI showing tubo-ovarian complex, thickened fluid-filled tubes ± free pelvic fluid ^[5]
Lab	Normal WBC, may have anaemia	Raised WBC, raised CRP/ESR

Chronic endometritis (not to be confused with endometriosis) can cause HMB and pelvic pain, mimicking adenomyosis. Endometrial biopsy showing plasma cells in the stroma confirms chronic endometritis.

Condition	Key Distinguishing Features
Pregnancy (including ectopic)	ALWAYS excluded by pregnancy test ^[5]. Amenorrhoea → AUB may be confused with LMP. Must be excluded in any reproductive-age woman with pelvic pain + bleeding.
Endometrial polyps	Focal endometrial thickening on TVUS; causes intermenstrual bleeding or HMB; diagnosed by hysteroscopy. Does NOT cause uterine enlargement or dysmenorrhoea.
Coagulopathy / Bleeding disorders	e.g., von Willebrand disease. Causes HMB from menarche. Normal uterine size. No dysmenorrhoea. Family history. Investigate with coagulation screen.
Ovarian cyst complications	Sudden onset of severe pain ^[5] — torsion or rupture. Acute presentation, not chronic cyclical pain. Adnexal mass, not uterine enlargement.
Haematometra / Cervical stenosis	Retained menstrual blood from outflow obstruction. Cyclical pain. Enlarged uterus (blood-filled). Diagnosed by ultrasound showing distended endometrial cavity.

This table is the highest yield comparison for exams, taken directly from lecture material:

	Adenomyosis	Fibroids	Endometriosis
Shared feature	—	HMB, enlarged uterus ^[1]	Dysmenorrhoea, infertility ^[1]
Key difference	Diffuse, boggy, tender	Irregular and focal ^[1] enlargement	Dyspareunia; uterus usually not enlarged ^[1]
Uterine consistency	Boggy/soft	Firm/hard	Normal
Typical symptom	HMB + dysmenorrhoea	HMB + pressure symptoms	Dysmenorrhoea + dyspareunia + infertility
Hormonal Rx	Effective (similar to endometriosis) ^[2]	Generally ineffective ^[2]	Effective
Definitive surgical Rx	Hysterectomy (no plane for enucleation)	Myomectomy or hysterectomy	Laparoscopic excision/ablation

The Lecture Slide Differential — Memorise This Table

From the lecture slides ^[1], the differential for adenomyosis is presented as:

	Similarities	Difference
Fibroids	HMB, enlarged uterus	Uterine enlargement is irregular and focal
Endometriosis	Dysmenorrhoea, infertility	Usually a/w dyspareunia; uterus usually not enlarged

This is the minimum you must know for the exam.

High Yield Differential Points:

Focal adenomyoma is often confused with leiomyomas — MRI differentiates (JZ thickening, no capsule vs. pseudocapsule).

Hormonal treatment works for adenomyosis (like endometriosis) but NOT for fibroids — this is a key pharmacological distinction.

Always exclude pregnancy in any reproductive-age woman with pelvic pain and bleeding.

Always perform endometrial assessment in AUB > 45 years to exclude endometrial cancer.

Stromal sarcomas can be found in association with adenomyosis — keep in mind if symptoms are atypical or rapidly worsening.

Active Recall - Differential Diagnosis of Adenomyosis

References

^[1] Senior notes: Adrian Lui Gynecology Notes.pdf (Section 2.3.3 Adenomyosis, p. 50–51) ^[2] Senior notes: Adrian Lui Gynecology Notes.pdf (Section 2.3.3 Adenomyosis – Management, p. 51) ^[3] Senior notes: Adrian Lui Gynecology Notes.pdf (Section on Dysmenorrhoea – Approach and Evaluation, p. 44) ^[4] Senior notes: Adrian Lui Gynecology Notes.pdf (Section 4.3.5 Uterine Sarcoma, p. 105) ^[5] Senior notes: Adrian Lui Gynecology Notes.pdf (Section on PID – Diagnosis and Differential Diagnosis, p. 66)

Diagnostic Criteria, Algorithm and Investigation Modalities for Adenomyosis

Unlike many conditions with crisp diagnostic criteria (e.g., rheumatic fever's Jones criteria), adenomyosis does not have universally accepted, codified diagnostic criteria in the way that, say, endometrial cancer does. This is because:

The diagnosis is generally histological, based on hysterectomy specimen ^[1] — i.e., the gold standard has historically required removing the uterus entirely.
You cannot biopsy the myometrium easily in a living patient (unlike the endometrium, which can be sampled with a Pipelle).
Therefore, clinical practice relies on a clinical-radiological diagnosis — a combination of suggestive history, examination findings, and imaging.

This creates a practical tension: the definitive diagnosis requires tissue you can only get by doing the definitive treatment (hysterectomy). So we work with clinical diagnostic criteria and imaging criteria for the living patient, reserving histological confirmation for when hysterectomy is performed.

1. Diagnostic Criteria

The definitive histological criterion:

Presence of endometrial glands and stroma within the myometrium ≥1 low-power field from the endomyometrial junction ^[1].

Why ≥1 low-power field? The normal endomyometrial junction is not a perfectly smooth line — it has natural undulations and minor irregularities. Endometrial glands sitting right at the junction could simply reflect normal anatomy. The threshold of ≥1 low-power field (approximately 2.5 mm) ensures you are identifying genuinely ectopic tissue that has invaded into the myometrium, not just a normal junction irregularity.
Additional histological features:
- Surrounding smooth muscle hypertrophy and hyperplasia — the reactive change induced by the ectopic glands.
- Haemosiderin-laden macrophages — evidence of old bleeding from cyclically active ectopic endometrial glands.
- The ectopic glands may show proliferative, secretory, or inactive phases.

In clinical practice, a presumptive diagnosis of adenomyosis is made when the following triad is present:

Component	Criteria
1. Suggestive symptoms	HMB and dysmenorrhoea are the most characteristic ^[1]; secondary dysmenorrhoea in a woman 35–50 years
2. Suggestive examination	Mobile, diffusely enlarged, globular, boggy (soft) uterus (rarely exceed 12w) ± tenderness ^[1]
3. Supportive imaging	TVUS or MRI features consistent with adenomyosis (see below)

There is no formal "scoring system" or checklist — the diagnosis is a clinical-radiological synthesis.

Key Lecture Point — Adenomyosis as a DDx of Secondary Dysmenorrhoea

If a lady has a baseline of no dysmenorrhoea, and suddenly develops dysmenorrhoea → considered secondary. Secondary dysmenorrhoea — remember to ask for associated symptoms of menorrhagia / subfertility, associated pelvic mass → think adenomyosis ^[6].

Adenomyosis = endometrial glands growing into muscularis / myometrium of uterus. Whenever there is menstruation, the contraction of the myometrium stimulates the glands, resulting in dysmenorrhoea ^[6].

C. Imaging Diagnostic Criteria

TVUS is the 1st line imaging ^[1].

The MUSA (Morphological Uterus Sonographic Assessment) consensus criteria standardise the sonographic features. A diagnosis of adenomyosis on TVUS is supported when ≥2 of the following features are present:

TVUS Feature	Description	Pathological Basis
Subendometrial echogenic linear striations/nodules ^[1]	Bright lines or nodules just beneath the endometrium extending into the myometrium	Columns of ectopic endometrial glands penetrating through the junctional zone
Anechoic myometrial cysts ^[1]	Small dark (fluid-filled) areas within the myometrium, typically 1–7 mm	Dilated ectopic endometrial glands filled with old menstrual blood or secretions
Focal or diffuse myometrial bulkiness (esp. fundal and posterior wall) ^[1]	Asymmetric thickening of the myometrium	Smooth muscle hypertrophy/hyperplasia in response to ectopic endometrial tissue
Increased vascularity corresponding to adenomyosis lesions ^[1]	Colour Doppler showing increased blood flow within affected areas	Angiogenesis driven by ectopic endometrial tissue and inflammatory mediators
Heterogeneous myometrial echotexture	Loss of the normal homogeneous myometrial echo pattern	Intermixed glandular tissue, cysts, and hypertrophied muscle creating acoustic heterogeneity
Fan-shaped acoustic shadowing	Shadows radiating outward from the affected area	Difference in acoustic impedance between glandular tissue and surrounding muscle
Irregular/poorly defined endometrial-myometrial border	Blurring of the normally sharp junction between endometrium and myometrium	Direct invasion/extension of endometrial tissue into the myometrium
Asymmetric myometrial wall thickening	One wall (usually posterior) thicker than the other without a discrete mass	Preferential involvement of the posterior wall (the most common site)

Sensitivity of TVUS: Approximately 72–89% sensitive, 65–98% specific in experienced hands. Performance is highly operator-dependent.

Pelvic MRI is the most sensitive (sensitivity 78–88%, specificity 67–93%), reserved for focal adenomyosis confused with fibroids ^[1].

MRI Feature	Criterion	Explanation
Junctional zone thickening	> 12 mm ^[1]	The JZ (inner myometrium) is normally < 8 mm on T2W. Thickening reflects smooth muscle hypertrophy driven by ectopic glands. The 12 mm threshold has high specificity.
JZ thickness ratio	JZ max / myometrial thickness > 40%	An alternative criterion that accounts for overall uterine size
Foci of increased T1W signal	Bright spots within the JZ/myometrium ^[1]	Represent haemorrhagic foci — blood products within ectopic endometrial glands (T1 shortening from methaemoglobin)
Foci of increased T2W signal	Bright spots within the thickened JZ ^[1]	Represent ectopic endometrial glands and surrounding oedema (glands are fluid-filled → high T2)
Ill-defined myometrial lesion without capsule	No pseudocapsule around area of abnormality	Distinguishes adenomyoma from leiomyoma (which has a well-defined pseudocapsule)
Low T2 signal of the thickened JZ	The bulk of the thickened JZ is dark on T2	This is the hypertrophied smooth muscle component — smooth muscle is T2-dark

JZ Thickness Interpretation:

JZ Thickness on MRI	Interpretation
< 8 mm	Normal
8–12 mm	Equivocal — correlate with symptoms and other features
> 12 mm ^[1]	Highly suggestive of adenomyosis

MRI — When to Use It

MRI is NOT first-line for adenomyosis. Use it when:

Focal adenomyosis (adenomyoma) is confused with fibroids ^[1] — MRI can distinguish (no capsule, high T1 foci = adenomyoma; pseudocapsule, low T2 = fibroid).
TVUS is equivocal or technically limited.
Pre-surgical planning (mapping the extent of disease before considering conservative surgery).
HIFU treatment planning — requires contrast-enhanced MRI to assess localised adenomyotic lesion or adenomyoma < 10 cm in diameter, involving only anterior or posterior uterine wall, and not both ^[7].

3. Investigation Modalities — Detailed Breakdown

Why first? Always exclude pregnancy in any reproductive-age woman presenting with pelvic pain and/or abnormal bleeding. A pregnancy (intrauterine or ectopic) can mimic adenomyosis with uterine enlargement, pain, and bleeding.
Modality: Urine βhCG (rapid, point-of-care) or serum βhCG (quantitative, more sensitive).
Interpretation: Positive → evaluate for intrauterine pregnancy, ectopic pregnancy, miscarriage. Negative → proceed with workup.

Investigation	Purpose	Expected Findings in Adenomyosis
Complete blood count (CBC)	Assess for anaemia from chronic HMB	Microcytic hypochromic anaemia (low Hb, low MCV, low MCH) — iron deficiency pattern
Iron studies	Confirm iron deficiency	Low ferritin, low serum iron, high TIBC
Coagulation screen	Exclude coagulopathy as cause of HMB (especially if HMB since menarche)	Normal in adenomyosis
TFT	Hypothyroidism can cause HMB	Normal in adenomyosis (but should be checked to exclude a treatable cause)
CA-125	May be elevated in adenomyosis	Can be mildly elevated (typically < 100 U/mL); not specific — also elevated in endometriosis, ovarian cancer, PID, pregnancy. Not routinely used for diagnosis but may support clinical suspicion.

TVUS is the 1st line imaging ^[1].

Why TVUS first?

Non-invasive, widely available, no radiation, relatively inexpensive.
Can be performed in the clinic setting.
Experienced operators achieve high sensitivity (72–89%) and specificity (65–98%).
Can simultaneously assess for fibroids, endometrial pathology, adnexal masses.

Systematic approach to TVUS interpretation in suspected adenomyosis:

What to Assess	Normal	Adenomyosis
Uterine size and shape	Normal pear-shaped, symmetric walls	Globular enlargement, asymmetric wall thickening (posterior > anterior)
Myometrial echotexture	Homogeneous, uniform	Heterogeneous, with echogenic linear striations, nodules
Myometrial cysts	Absent	Anechoic cysts 1–7 mm ^[1] within the myometrium
Endomyometrial junction	Sharp, well-defined	Irregular, blurred, ill-defined
Subendometrial region	Smooth interface	Echogenic linear striations/nodules ^[1] extending from the endometrium into the myometrium
Colour Doppler	Normal vascularity	Increased vascularity corresponding to adenomyosis lesions ^[1] — this distinguishes from myometrial cysts of other aetiology
Shadowing	Absent	Fan-shaped acoustic shadowing — characteristic of adenomyosis (cf. posterior shadowing in fibroids which is more defined)
Discrete masses	Absent	If present: adenomyoma (ill-defined, no capsule) vs. fibroid (well-defined, pseudocapsule)

Fibroids are generally asymmetric and irregular → if the uterus is globally enlarged symmetrically, may suggest adenomyosis instead ^[8].

TVUS: Adenomyosis vs. Fibroid — The Sonographic Distinction

Feature	Adenomyoma (focal adenomyosis)	Fibroid (leiomyoma)
Borders	Ill-defined, blends into myometrium	Well-defined, pseudocapsule
Shape	Elliptical or irregular	Round/oval
Echogenicity	Heterogeneous with cysts	Hypoechoic, may have calcifications
Shadowing	Fan-shaped, radiating outward	Edge shadowing or posterior attenuation
Vascularity	Vessels penetrating through the lesion	Peripheral feeding vessels ("ring sign")
Effect on endometrium	May distort endomyometrial junction	Displaces/compresses endometrium

Fibroids have a pseudo-capsule surrounding it, whereas adenomyosis does not have one → adenomyosis thus cannot be enucleated like fibroids ^[6].

Pelvic MRI: most sensitive (sensitivity 78–88%, specificity 67–93%), reserved for focal adenomyosis confused with fibroids ^[1].

When to order MRI:

Focal lesion on TVUS — is it adenomyoma or fibroid?
Equivocal TVUS findings.
Pre-treatment planning (especially before HIFU or uterus-conserving surgery).
Young woman desiring fertility — need precise mapping of disease.

MRI Protocol for Adenomyosis:

T2-weighted (T2W) sequences are most important:
- The junctional zone appears as a dark band (low T2 signal) between the bright endometrium and intermediate-signal outer myometrium.
- Thickening of the junctional zone > 12 mm ^[1] = adenomyosis.
- High T2 foci within the dark JZ = ectopic endometrial glands (fluid-filled → bright on T2).
T1-weighted (T1W) sequences:
- Foci of increased T1W signal ^[1] = haemorrhagic deposits within ectopic glands (methaemoglobin shortens T1 → appears bright).
- T1W with fat saturation helps distinguish blood (remains bright) from fat (suppressed).
Post-gadolinium (contrast-enhanced) sequences:
- Used for HIFU planning.
- Helps delineate the extent of adenomyosis and distinguish from fibroid (fibroids enhance more uniformly).

MRI Findings Summary:

Sequence	Adenomyosis Finding	Interpretation
T2W	JZ thickening > 12 mm, dark band with bright foci	Hypertrophied muscle (dark) with ectopic glands (bright)
T1W	Bright foci within myometrium	Haemorrhagic deposits in ectopic glands
T1W fat-sat	Bright foci persist after fat suppression	Confirms blood (not fat)
Post-gadolinium	Heterogeneous enhancement of thickened JZ	Active endometrial tissue with surrounding inflammation

MRI: Adenomyoma vs. Leiomyoma:

Feature	Adenomyoma	Leiomyoma
Borders	Ill-defined, no capsule	Well-defined, T2-dark pseudocapsule
T2 signal	Low signal JZ with high T2 foci (glands)	Uniformly low T2 signal (dense muscle/collagen)
T1 signal	High T1 foci (blood)	Usually isointense; no T1 bright foci unless degenerated
Location	Within thickened JZ	Any myometrial location; may be pedunculated
Enhancement	Heterogeneous, less than normal myometrium	Variable; may enhance less or more than myometrium

EA may be indicated in the case of AUB > 45 years (d/dx CA endometrium) ^[1].

Why is this important?

Adenomyosis causes HMB. So does endometrial cancer.
In women over 45, you cannot simply attribute HMB to adenomyosis without first excluding malignancy.
Even if TVUS confirms adenomyotic features, the endometrium must be assessed independently.

Methods of Endometrial Assessment:

Method	Description	When to Use
Pipelle endometrial biopsy	Office-based, blind sampling of the endometrium using a thin flexible catheter	First-line for women > 45 with AUB or any woman with risk factors for endometrial cancer
Hysteroscopy with directed biopsy	Direct visualisation of the endometrial cavity with targeted biopsy	When Pipelle is inadequate, failed, or TVUS shows a focal endometrial lesion (e.g., polyp)
Dilatation and curettage (D&C)	Under anaesthesia, systematic scraping of the endometrial cavity	Rarely first-line now; used when hysteroscopy is unavailable or for therapeutic purposes

Important: Endometrial assessment does NOT diagnose adenomyosis (which is in the myometrium, not the endometrium). It is done to exclude coexisting endometrial pathology.

Not routinely indicated for adenomyosis — the pathology is within the myometrial wall and not visible on the serosal surface.
However, it may be performed when:
- Coexisting endometriosis is suspected (to directly visualise peritoneal implants).
- Persistent/progressive pain unresponsive to medical treatment — to exclude other causes.
- As part of surgical management (e.g., laparoscopic hysterectomy).
Adenomyosis may be suspected at laparoscopy if the uterus appears diffusely enlarged and bluish-purple discolouration is seen on the serosal surface (from subsersoal ectopic glands), but this is unreliable.

Investigation	Indication	Relevance
USG pelvis ^[9]	Evaluation of amenorrhoea or pelvic mass	Screen for uterine and adnexal pathology
Saline infusion sonography (SIS)	Suspected endometrial polyp or submucosal fibroid	Distends the cavity with saline to delineate intracavitary lesions; not specific for adenomyosis
FSH, LH, E2, PRL, TFT, testosterone ^[9]	Evaluation of amenorrhoea	If amenorrhoea coexists — exclude hormonal causes
Hysterosalpingography (HSG)	Infertility workup	May show "spiculated" or "stippled" appearance of the endometrial cavity (contrast entering ectopic glands); largely superseded by MRI

Here is how you would approach a real clinical scenario:

Scenario: A 42-year-old multiparous woman (G3P3) with progressively worsening dysmenorrhoea for 3 years and increasing menstrual flow, now using 8–10 pads per day with clots. She feels tired and breathless on exertion. She had one previous caesarean section.

Step-by-step approach:

βhCG → Negative (exclude pregnancy).
CBC → Hb 9.2 g/dL, MCV 72 fL → microcytic anaemia → likely iron deficiency from chronic HMB.
Iron studies → Ferritin 8 µg/L (low) → confirmed iron deficiency.
Pelvic examination → uterus is 10 weeks' size, diffusely enlarged, globular, soft/boggy, mildly tender, mobile. No adnexal masses. → Suggestive of adenomyosis.
TVUS → globular uterus, heterogeneous myometrium with multiple small anechoic cysts in the posterior wall, echogenic linear striations at the endomyometrial junction, increased vascularity on Doppler. No discrete mass. Endometrial thickness 8 mm (normal for Day 14). → Consistent with diffuse adenomyosis.
Age < 45 → endometrial assessment not mandated, but if any atypical bleeding pattern (e.g., intermenstrual), consider Pipelle.
Diagnosis: Clinical-radiological diagnosis of diffuse adenomyosis with secondary iron deficiency anaemia.

Feature	Adenomyosis	Fibroid	Endometrial Cancer
TVUS	Heterogeneous myometrium, myometrial cysts, linear striations, no capsule	Hypoechoic mass, pseudocapsule, calcification	Thickened irregular endometrium, increased vascularity
MRI - T2W	JZ > 12 mm, dark band + bright foci	Low T2 mass with pseudocapsule	Intermediate T2 endometrial mass invading myometrium
MRI - T1W	Bright foci (blood)	Usually isointense	Variable
Borders	Ill-defined	Well-defined	Irregular endometrial-myometrial interface
Capsule	No capsule ^[6]	Pseudocapsule ^[6]	None
Enucleation	Cannot be enucleated ^[6]	Can be enucleated ^[6]	Not applicable (requires staging surgery)

Exam Pearl: The Fibroid vs. Adenomyosis Distinction on Imaging

Fibroids classically do NOT cause dysmenorrhoea ^[6] — a pure fibroid will seldom cause dysmenorrhoea (exceptions: clot expulsion from heavy bleeding, or pedunculated intracavitary fibroid acting as a foreign body). If a patient has HMB + significant dysmenorrhoea, think adenomyosis or coexisting adenomyosis + fibroids.

Menstrual flow change → DDx: fibroid, adenomyosis ^[10]. Both cause HMB, but the mechanism differs — fibroids increase surface area focally and distort the cavity, while adenomyosis increases surface area diffusely and impairs myometrial contractility.

High Yield Diagnostic Points:

Gold standard = histology from hysterectomy specimen (endometrial tissue ≥1 LPF from endomyometrial junction)

Working diagnosis = clinical-radiological (symptoms + examination + TVUS/MRI)

TVUS first-line: myometrial cysts, echogenic striations, heterogeneous myometrium, increased vascularity, irregular endo-myometrial junction

MRI second-line: JZ > 12 mm on T2W, T1/T2 bright foci, no capsule

Always exclude pregnancy (βhCG) and endometrial cancer (EA if > 45 years)

Key imaging distinction: adenomyosis = no capsule, ill-defined; fibroid = pseudocapsule, well-defined

High Yield Summary

Diagnostic Criteria:

Histological (gold standard): Endometrial glands/stroma within myometrium ≥1 low-power field from endomyometrial junction.
Clinical-radiological (working diagnosis): Suggestive symptoms (HMB + dysmenorrhoea) + examination (diffusely enlarged, boggy uterus) + imaging (TVUS or MRI features).

Investigation Modalities:

βhCG — exclude pregnancy first.
CBC + iron studies — assess for iron deficiency anaemia from chronic HMB.
TVUS (1st line) — myometrial cysts, echogenic striations, heterogeneous echotexture, increased vascularity, irregular endomyometrial junction.
Pelvic MRI (2nd line) — JZ > 12 mm, T1 bright foci (blood), T2 bright foci (glands), no capsule. Reserved for focal disease confused with fibroids.
Endometrial assessment — Pipelle biopsy for AUB in women > 45 to exclude endometrial cancer.

Key Distinction: Adenomyosis = no capsule, cannot be enucleated. Fibroid = pseudocapsule, can be enucleated. MRI is the differentiator.

Active Recall - Diagnosis and Investigations for Adenomyosis

References

^[1] Senior notes: Adrian Lui Gynecology Notes.pdf (Section 2.3.3 Adenomyosis, p. 50–51) ^[6] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p. 6 — Dysmenorrhoea, adenomyosis vs fibroid distinction) ^[7] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p. 65 — HIFU indications) ^[8] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p. 14 — Specific findings, fibroid vs adenomyosis) ^[9] Lecture slides: GC 114. Climacteric symptoms menopause and related illness; amenorrhoea.pdf (p. 19 — Amenorrhoea evaluation investigations) ^[10] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p. 8 — Menstrual flow DDx)

Management of Adenomyosis

Before diving into specifics, let's establish the logical framework. Management decisions in adenomyosis hinge on three key questions:

Is the patient symptomatic? — Asymptomatic adenomyosis incidentally found does not require any treatment ^[1].
Does the patient desire future fertility? — This determines whether uterus-conserving approaches are needed.
How severe are the symptoms? — This guides the escalation from medical → procedural → surgical treatment.

The fundamental management challenge is this: adenomyosis has no surgical plane for simple enucleation (even in adenomyoma) ^[1] — unlike fibroids, you cannot simply "shell out" the disease. The ectopic endometrial tissue is diffusely infiltrating the myometrium. Therefore:

Medical treatment aims to suppress the hormonally-active ectopic glands.
Hysterectomy is the only truly definitive cure.
Uterus-conserving procedures offer intermediate options but have significant recurrence/failure rates.

Asymptomatic adenomyosis incidentally found does not require any treatment ^[1].

Who qualifies:

Women with adenomyosis discovered incidentally on imaging performed for another indication.
Women approaching menopause with minimal symptoms (the disease will regress naturally once oestrogen levels decline post-menopause).

Rationale: Adenomyosis is a benign condition — it does not undergo malignant transformation (though stromal sarcomas can rarely be found in association with adenomyosis ^[4]). There is no indication to treat the radiological finding if it is not causing symptoms or functional impairment.

What to do:

Reassure the patient.
Monitor symptoms at routine gynaecological reviews.
Advise to return if symptoms develop (HMB, dysmenorrhoea, anaemia).

2. Medical Treatment

Hormonal treatment: generally similar to endometriosis (unlike fibroids, where they are generally ineffective) ^[1].

This is a critical pharmacological distinction: adenomyosis is composed of hormonally-responsive ectopic endometrial tissue (just like endometriosis), so hormonal suppression works by causing decidualisation and atrophy of those glands. Fibroids, by contrast, are smooth muscle tumours — hormonal treatments have little effect on their bulk or bleeding.

Medical treatment is the first-line approach for symptomatic adenomyosis, especially in women who:

Desire future fertility.
Are not yet candidates for surgery.
Are approaching menopause (bridging to natural resolution).

These treat the consequences of adenomyosis (bleeding, pain, anaemia) without addressing the underlying disease:

Drug	Dose	Mechanism	Role in Adenomyosis
Tranexamic acid (Transamin)	1g TDS PO up to 4 days per cycle, max 4g daily ^[11]	Anti-fibrinolytic: inhibits plasminogen activation → prevents clot breakdown → reduces menstrual blood loss	Reduces volume of HMB. Does not affect pain. Used as adjunct to hormonal therapy or for women who cannot take hormones.
NSAIDs (e.g., mefenamic acid / Ponstan)	250–500 mg TDS PO PRN ^[11]	Inhibits cyclooxygenase (COX) → reduces prostaglandin synthesis → decreases myometrial contractions and pain	Targets the dysmenorrhoea component. Fenamates may have a slight advantage as they also block PG action ^[3] (i.e., they inhibit both synthesis AND receptor binding of prostaglandins).
Iron supplementation (Ferrous sulphate)	300 mg TDS PO × 6 months if Hb < 10 g/dL ^[11]	Replaces iron stores depleted by chronic HMB	Essential supportive treatment for iron deficiency anaemia. Continue until Hb and ferritin normalise.

NSAIDs in Adenomyosis vs. Fibroids

NSAIDs do NOT appear to reduce blood loss in fibroids but can reduce painful menses ^[11]. In adenomyosis, NSAIDs address the dysmenorrhoea (by reducing prostaglandin-mediated myometrial spasm) but have limited effect on HMB. For bleeding control, tranexamic acid is more effective.

B. Hormonal Medical Treatment

Hormonal treatment is generally similar to endometriosis ^[1]. The overarching principle: suppress oestrogen-driven cyclical stimulation of the ectopic endometrial glands.

Progestin-only treatment: e.g., Mirena ^[1].

Aspect	Detail
Mechanism	Releases levonorgestrel locally within the uterine cavity → causes decidualisation and atrophy of the endometrium (both eutopic and ectopic glands within the inner myometrium) → reduces bleeding and pain. Also suppresses endometrial prostaglandin production.
Why first-line?	Delivers progestin directly to the target organ (uterus) with minimal systemic side effects. Proven efficacy in reducing HMB (up to 90% reduction in menstrual blood loss). Also provides contraception. Duration of action: 5 years (up to 8 years for contraception in newer data).
Efficacy in adenomyosis	Reduces menstrual blood loss significantly. Reduces dysmenorrhoea. May reduce uterine volume modestly. Best evidence of any medical treatment for adenomyosis-related HMB.
Limitations	Requires insertion (may be technically challenging in a distorted or enlarged cavity). May be expelled if the cavity is significantly enlarged/distorted. Initial irregular spotting/bleeding for 3–6 months.
Contraindications	Active PID, current STI, unexplained vaginal bleeding (until evaluated), uterine anomaly precluding insertion, current breast cancer. Mirena is suitable if fibroids < 3 cm with no cavity distortion ^[11] — by extension, if adenomyosis has significantly distorted/enlarged the cavity, it may not be appropriate.

Progestin-only treatment: e.g., depot Provera ^[1].

Aspect	Detail
Mechanism	Systemic progestin → suppresses HPG axis → anovulation + endometrial atrophy → reduces bleeding and pain. Also causes decidualisation of ectopic endometrial glands.
Dose	150 mg IM every 12 weeks
Efficacy	Effective for HMB and dysmenorrhoea. May induce amenorrhoea in ~50% of women by 12 months.
Side effects	Weight gain, mood changes, irregular bleeding (especially initially), delayed return of fertility (average 10 months after last injection), bone density loss with prolonged use ( > 2 years — especially relevant in young women).
Contraindications	Current breast cancer, severe liver disease, unexplained vaginal bleeding.

Oral contraceptive pills: little data on efficacy but still commonly used ^[1].

Aspect	Detail
Mechanism	Provide exogenous ovarian hormones → suppress HPG axis → provide manual control over menstrual cycles ^[12]. The progestin component causes endometrial atrophy; the oestrogen component stabilises the endometrium and prevents breakthrough bleeding.
Regimens	Cyclic (monthly withdrawal bleed), extended (one bleed every 3 months), continuous ^[12] — extended/continuous regimens may be more beneficial in adenomyosis as they reduce the frequency of withdrawal bleeds (and thus the frequency of painful menstruation).
Efficacy	Associated with 30% reduction in average monthly blood loss ^[12]. Makes bleeding more regular, lighter (cycle + flow control). Reduces dysmenorrhoea ^[12]. However, little data on efficacy specifically for adenomyosis ^[1] — most evidence is extrapolated from dysmenorrhoea and AUB studies.
Side effects	Minor: N/V, dizziness, breast tenderness, fluid retention, weight gain. Breakthrough bleeding. CVS risk: increased risk of MI, stroke, thromboembolism. Minimal increased risk in breast and cervical CA ^[12].
Contraindications	Full breastfeeding (oestrogen affects milk production). Thromboembolic risk: Hx of VTE, major surgery, prolonged immobilisation, first 21 days postpartum ^[12]. Also: migraine with aura, uncontrolled hypertension, current breast cancer, active liver disease, age > 35 and smoking > 15 cigarettes/day.

COCP in Adenomyosis — The Oestrogen Paradox

COCPs contain oestrogen, which theoretically could stimulate adenomyotic tissue. However, in practice, the net effect of COCPs is suppressive because: (1) the progestin component dominates and causes endometrial atrophy, and (2) ovulation suppression eliminates the natural cyclical oestrogen peaks that drive adenomyotic growth. Nevertheless, in severe adenomyosis, progestin-only methods may be preferred to avoid any oestrogen exposure.

GnRH agonists ^[1].

Aspect	Detail
Mechanism	Desensitisation of the pituitary GnRH receptors → medically induce menopause → reduce size of adenomyotic tissue, reduce menstrual-related symptoms ^[11]. Initially causes a "flare" effect (transient increase in FSH/LH for 1–2 weeks) before down-regulation.
Examples	Goserelin (Zoladex) 3.6 mg SC monthly, Leuprolide (Lupron) 3.75 mg IM monthly
Efficacy	Highly effective — induces amenorrhoea, significantly reduces uterine volume and symptoms.
Limitations	Rapid relapse following discontinuation. Significant climacteric symptoms with menopause-related side effects (e.g., bone density loss) → therefore NOT for long-term use ^[11]. Typically limited to 6 months without add-back therapy.
Add-back therapy	Low-dose oestrogen/progestin "add-back" can mitigate menopausal side effects (hot flushes, bone loss) while maintaining efficacy. Allows longer use (up to 12–24 months).
Role in adenomyosis	Pre-operative shrinkage before hysterectomy (makes surgery easier). Bridging in perimenopausal women (bridge symptoms until natural menopause). Pre-IVF in women with adenomyosis-related subfertility (2–3 months pre-treatment to reduce uterine volume and improve implantation rates).
Side effects	Irregular bleeding, URTI symptoms ^[11], hot flushes, vaginal dryness, mood changes, headache, bone density loss.

Aspect	Detail
Mechanism	Competitive blockade of GnRH receptors → immediate suppression of FSH/LH (no initial flare, unlike agonists)
Examples	Elagolix, Relugolix (oral preparations — a major advantage over injectable GnRH agonists)
Advantage	Dose-dependent suppression — can be titrated to partially suppress oestrogen (maintaining some bone protection) rather than inducing complete menopause. No flare effect. Oral administration.
Current status	Emerging evidence for use in adenomyosis. Relugolix combination therapy (with add-back) is approved in some jurisdictions for uterine fibroids and is being studied for adenomyosis.

Aromatase inhibitor ^[1].

Aspect	Detail
Mechanism	Blocks aromatase enzyme → prevents peripheral conversion of androgens to oestrogens → reduces systemic and local oestrogen levels. Particularly targets local aromatase within adenomyotic tissue (which produces its own oestrogen via local aromatase expression — a self-sustaining paracrine loop).
Examples	Letrozole 2.5 mg daily, Anastrozole 1 mg daily
Efficacy	Limited but promising data. May be effective as second-line or adjunct therapy.
Side effects	Bone density loss, hot flushes, arthralgia, ovarian stimulation (can cause multiple follicle development in premenopausal women → must co-administer with progestin or GnRH agonist to prevent this).
Role	Reserved for refractory cases or when other hormonal options are contraindicated/ineffective.

Drug	Mechanism	Notes
Dienogest (2 mg daily)	Selective progestin → decidualisation of ectopic endometrial tissue, suppresses ovulation, anti-inflammatory	Specifically studied and approved in some countries for endometriosis; growing evidence for adenomyosis. Well-tolerated. May become first-line progestin of choice.
Cyclical oral progestogens (e.g., Primolut N / norethisterone 5 mg TDS on day 5–26) ^[11]	Suppresses endometrial proliferation during luteal phase	Less effective than continuous progestin methods. Used mainly for cycle control.
Danazol	Androgenic steroid → suppresses HPG axis + causes endometrial atrophy	Effective but poorly tolerated (androgenic side effects: acne, hirsutism, voice deepening, weight gain, liver toxicity). Rarely used now.

Treatment	HMB	Dysmenorrhoea	Uterine Volume	Fertility-Compatible	Duration
LNG-IUS (Mirena)	+++	++	±	Reversible (remove for conception)	Up to 5 years
DMPA	+++	++	±	Delayed return (10 months)	Ongoing injections
COCP	++	++	–	Reversible	Ongoing
GnRH agonist	+++	+++	↓↓	Used pre-IVF	Max 6 months (or with add-back)
Aromatase inhibitor	+	++	↓	No (use with GnRH agonist)	Short-term
Dienogest	++	+++	↓	Reversible	Ongoing
Tranexamic acid	++	–	–	Yes	Per cycle
NSAIDs	±	++	–	Yes	Per cycle

3. Surgical Treatment

A. Hysterectomy — The Definitive Treatment

Definitive treatment: only way to excise as there is no surgical plane for simple enucleation (even in adenomyoma) ^[1].

Why is hysterectomy definitive?

The ectopic endometrial glands are diffusely infiltrating the myometrium with no capsule, no plane of cleavage, and no clear boundary.
You cannot "peel out" adenomyosis the way you can enucleate a fibroid (which has a pseudocapsule).
Removing the entire uterus removes all the diseased tissue.
Cure rate: virtually 100% for symptom resolution.

Indications for hysterectomy:

Symptomatic adenomyosis refractory to medical treatment.
Completed childbearing or no fertility wish.
Severe symptoms significantly impacting quality of life.
Acute haemorrhage not responding to other therapies ^[11].
Coexisting indications: increased risk for CA cervix, endometrium, ovaries (e.g., CIN, endometrial hyperplasia) ^[11].
Patient preference.

Extent: subtotal hysterectomy as cervix and ovaries are not affected ^[1].

This is an important point. Let's break it down:

Structure	Affected by Adenomyosis?	Include in Surgery?
Uterine body (corpus)	Yes — the site of disease	Must be removed
Cervix	Not affected ^[1]	Can be preserved (subtotal/supracervical hysterectomy) ^[1] — preserving the cervix may be associated with better pelvic floor support and sexual function
Ovaries	Not affected ^[1]	Should be preserved ^[1] — especially in premenopausal women, to avoid surgical menopause. Bilateral salpingo-oophorectomy (BSO) is only added if there are separate indications (e.g., BRCA mutation, endometriosis of ovaries, perimenopausal age with ovarian pathology)
Fallopian tubes	Not directly affected	Opportunistic bilateral salpingectomy is increasingly recommended for ovarian cancer risk reduction (most high-grade serous ovarian cancers originate in the fimbriae)

Subtotal vs. Total Hysterectomy for Adenomyosis

The lecture notes state subtotal hysterectomy ^[1] (i.e., preserving the cervix). However, in clinical practice, total hysterectomy (removing cervix) is more commonly performed because:

It eliminates the need for ongoing cervical screening (Pap smears).
It removes any risk of cervical stump pathology.
Some adenomyosis can extend to the isthmus/upper cervix.

The choice between subtotal and total hysterectomy is individualised — discuss with the patient. If cervical preservation is desired (for pelvic floor support), subtotal is acceptable as long as there is no cervical pathology.

Route: vaginal, laparoscopic, open, robotic — indications as in other cases ^[1].

Route	When Preferred	Advantages	Limitations
Vaginal	Uterus < 12 weeks, mobile, adequate vaginal access	Shortest recovery, no abdominal incision, lowest complication rate	Limited by uterine size, access, and need for adnexal surgery
Laparoscopic (TLH / LAVH)	Most cases; gold standard approach in many centres	Minimally invasive, shorter recovery than open, good visualisation	Requires laparoscopic expertise; may be limited by very large uterus
Open (abdominal)	Very large uterus ( > 16–20 weeks), suspected malignancy, extensive adhesions	No size limitation, allows thorough exploration	Longer recovery, larger incision, more pain
Robotic	Similar to laparoscopic with added dexterity	Wristed instruments, 3D visualisation, ergonomic for surgeon	Expensive, longer setup time, limited availability

B. Uterus-Conserving Surgical Options

For women who desire fertility or wish to avoid hysterectomy:

Concept: Excise the focal adenomyotic lesion (adenomyoma) and reconstruct the myometrium.
Feasibility: Only possible for focal adenomyosis (adenomyoma). Diffuse adenomyosis cannot be excised without removing the entire uterus.
Techniques:
- Laparoscopic or open excision of the adenomyoma.
- Wedge resection of affected myometrial wall.
- "Triple-flap" technique for deep posterior adenomyosis.
Challenges:
- No capsule or clear surgical plane — margins are poorly defined.
- High risk of incomplete excision → symptom recurrence.
- Risk of uterine rupture in subsequent pregnancy (weakened myometrial wall at the repair site).
- Technically demanding.
Outcomes: Symptom improvement in 50–80%, but recurrence rates of 30–40% at 5 years.

Uterine artery embolization (UAE): reserved for failure or C/I to medical + surgical therapy ^[1].

Aspect	Detail
Mechanism	Fluoroscopy-guided catheterisation of the uterine arteries (via femoral artery approach) → injection of embolic agents (e.g., PVA particles, gelfoam, coils ^[13]) → occlusion of the uterine arteries → ischaemia of the adenomyotic tissue (and the entire uterus to some extent) → necrosis and shrinkage of the ectopic glands
Indication	Reserved for failure or C/I to medical + surgical therapy ^[1]. Also used when patient refuses hysterectomy.
Efficacy	~2/3 had long-term decrease in symptom severity ^[1]
Limitations	High rate of additional intervention for persistent or recurrent symptoms ^[1]. Less predictable than for fibroids (where UAE is more established). The diffuse nature of adenomyosis means ischaemia may be incomplete.
Side effects	Post-embolisation syndrome (pain, fever, nausea — self-limiting, 24–72 hours), infection, uterine necrosis (rare), ovarian failure (if ovarian arteries are inadvertently embolised — more common in women > 45), amenorrhoea
Fertility	Generally not recommended for women desiring fertility — risk of impaired uterine perfusion, endometrial damage, and uterine rupture in subsequent pregnancy

UAE works better for fibroids than adenomyosis because fibroids have a well-defined vascular supply that can be selectively targeted, whereas adenomyosis is diffusely supplied by the myometrial vasculature.

Ablative techniques: e.g., RFA, HIFU (investigational) ^[1].

Aspect	Detail
Mechanism	Non-invasive. Focused ultrasound waves converge on the adenomyotic lesion → generate heat at the focal point → thermal ablation (coagulative necrosis) of the tissue → shrinkage over weeks to months
Guidance	MRI-guided (MRgFUS) or ultrasound-guided
Indication	Women with significant symptoms related to adenomyosis, intractable to standard medical therapy, or patient considering radiological intervention (UAE) or surgery ^[7]
Selection criteria	Localised adenomyotic lesion or adenomyoma identified of less than 10 cm in diameter as judged by contrast-enhanced MRI, involving only anterior or posterior uterine wall, and not both ^[7]
Efficacy	Emerging evidence: symptom improvement in 60–80%, but long-term data still accumulating
Limitations	Investigational status. Requires specific equipment and expertise. Not available in all centres. Not suitable for diffuse adenomyosis involving both walls. Limited long-term follow-up.
Advantages	Non-invasive (no incision), outpatient procedure, short recovery, can be repeated
Fertility	Limited data; some case reports of successful pregnancy after HIFU, but not yet recommended as a fertility-preserving standard

Aspect	Detail
Mechanism	Percutaneous or laparoscopic insertion of an RFA needle into the adenomyotic lesion → radiofrequency energy generates heat → thermal ablation of the lesion
Status	Investigational ^[1]
Indication	Focal adenomyosis refractory to medical treatment in women wishing to avoid hysterectomy
Advantages	Minimally invasive (laparoscopic or ultrasound-guided)
Limitations	Limited evidence base. Risk of incomplete ablation. Not suitable for diffuse disease.

Scenario	Recommended Approach
Asymptomatic, incidental finding	No treatment required ^[1]. Reassure. Monitor.
Mild symptoms, reproductive age, fertility desired	LNG-IUS (if cavity not distorted) or dienogest. NSAIDs for dysmenorrhoea. Tranexamic acid for HMB. Iron supplementation.
Moderate symptoms, fertility desired	GnRH agonist pre-IVF (2–3 months). Consider adenomyomectomy if focal disease.
Severe symptoms, fertility desired	GnRH agonist + IVF. Adenomyomectomy if focal. HIFU if available and criteria met ^[7].
Mild-moderate symptoms, family complete	LNG-IUS or COCP or DMPA. NSAIDs + tranexamic acid.
Severe symptoms, family complete	Hysterectomy (subtotal, preserving ovaries ^[1]). Route: vaginal or laparoscopic preferred.
Failed medical + not fit for surgery	UAE (reserved for failure or C/I to medical + surgical therapy ^[1]).
Perimenopausal (approaching menopause)	Medical treatment to bridge until natural menopause. GnRH agonist with add-back. Conservative management.
Acute severe HMB	Resuscitation → tranexamic acid IV → hormonal haemostasis (high-dose progestins or IV conjugated oestrogen) → if refractory: hysterectomy for acute haemorrhage not responding to other therapies ^[11].

Treatment	Key Contraindications
LNG-IUS	Active PID/STI, unexplained vaginal bleeding, current breast cancer, significantly distorted/enlarged cavity
COCP	VTE history, major surgery, prolonged immobilisation, first 21 days postpartum, full breastfeeding ^[12], migraine with aura, uncontrolled HTN, age > 35 + heavy smoking, current breast cancer
DMPA	Current breast cancer, severe liver disease, unexplained vaginal bleeding
GnRH agonists	Pregnancy, osteoporosis (relative — can use with add-back), duration > 6 months without add-back
Tranexamic acid	Active thromboembolic disease, history of VTE (relative), severe renal impairment, subarachnoid haemorrhage
NSAIDs	Peptic ulcer disease, aspirin-sensitive asthma, severe renal/hepatic impairment, third trimester pregnancy
Hysterectomy	Desire for future fertility, unfit for anaesthesia/surgery, patient preference
UAE	Desire for future fertility (relative), active PID, allergy to contrast, uncorrected coagulopathy, suspected malignancy
HIFU	Diffuse disease involving both walls, lesion > 10 cm ^[7], proximity to bowel/bladder, suspected malignancy

High Yield Management Points:

Asymptomatic = no treatment

Medical treatment is first-line and works because adenomyosis is hormonally responsive (like endometriosis, unlike fibroids)

LNG-IUS is the best-studied medical option for HMB

GnRH agonists are highly effective but time-limited (6 months without add-back)

Hysterectomy is the only definitive cure — subtotal, preserving ovaries

UAE is second-line with ~2/3 long-term improvement but high re-intervention rate

HIFU and RFA are investigational

High Yield Summary

Management Framework:

Asymptomatic → No treatment. Reassure and monitor.
Medical (1st line) → Hormonal treatment similar to endometriosis (unlike fibroids). Options: LNG-IUS (Mirena, 1st choice), DMPA, COCP (little data but commonly used), GnRH agonists (short-term or pre-IVF), aromatase inhibitors (2nd line). Non-hormonal adjuncts: tranexamic acid + NSAIDs + iron.
Hysterectomy (definitive) → Only way to excise; no surgical plane for enucleation. Subtotal hysterectomy as cervix and ovaries not affected. Routes: vaginal, laparoscopic, open, robotic.
Uterus-conserving procedures → UAE (reserved for failure/CI to medical + surgical; ~2/3 improve but high re-intervention). HIFU/RFA (investigational; localised lesion < 10 cm, one wall only).

Key Pharmacological Principle: Adenomyosis responds to hormonal suppression (ectopic endometrial tissue is hormonally responsive). Fibroids do NOT respond to hormonal treatment (smooth muscle tumour, not endometrial tissue).

Active Recall - Management of Adenomyosis

References

^[1] Senior notes: Adrian Lui Gynecology Notes.pdf (Section 2.3.3 Adenomyosis — Management, p. 51) ^[3] Senior notes: Adrian Lui Gynecology Notes.pdf (Section on Dysmenorrhoea — Management, p. 44) ^[4] Senior notes: Adrian Lui Gynecology Notes.pdf (Section 4.3.5 Uterine Sarcoma, p. 105) ^[7] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p. 65 — HIFU indications) ^[11] Senior notes: Adrian Lui Gynecology Notes.pdf (Section on Fibroids — Medical and Surgical Treatment, p. 91–92) ^[12] Senior notes: Adrian Lui Gynecology Notes.pdf (Section on AUB/COCP management, p. 15) ^[13] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p. 85 — Transcatheter Embolization, embolic agents and UAE)

Complications of Adenomyosis

Adenomyosis is a benign condition — it does not undergo malignant transformation per se. However, it causes significant morbidity through several important complications. Let's think about these systematically, categorising them by mechanism.

The complications of adenomyosis arise from three pathological processes:

Chronic heavy menstrual bleeding → haematological consequences
The disease process itself (ectopic endometrial glands in myometrium) → structural and functional uterine consequences
Coexisting conditions and associations → related pathology

The most common complication.

Heavy menstrual bleeding (60%): due to increased endometrial surface area of the enlarged uterus ^[1].

Pathophysiological chain:

Adenomyosis → myometrial hypertrophy → diffuse uterine enlargement → increased endometrial surface area → more endometrium to shed per cycle → heavier menstrual blood loss → chronic iron loss exceeds dietary iron absorption → depleted iron stores (low ferritin) → reduced haemoglobin synthesis → microcytic hypochromic anaemia.

Additionally, the adenomyotic myometrium has impaired contractility (the normal "living ligature" mechanism where myometrial contraction compresses spiral arterioles after endometrial shedding is disrupted) → prolonged bleeding per cycle → further iron loss.

Clinical consequences of anaemia:

Fatigue and lethargy — reduced oxygen-carrying capacity → tissues receive less oxygen → compensatory mechanisms (increased heart rate, increased cardiac output) are insufficient at rest.
Exertional dyspnoea — exercise increases oxygen demand beyond the diminished delivery capacity.
Palpitations and tachycardia — compensatory increase in cardiac output.
Pallor — reduced haemoglobin in dermal and mucosal capillaries.
Koilonychia, glossitis, angular stomatitis — iron deficiency affects rapidly dividing cells (nails, tongue epithelium, oral mucosa).
Pica (craving non-food substances like ice, clay) — mechanism poorly understood but well-documented in iron deficiency.
Reduced work productivity and quality of life — the "hidden" burden of adenomyosis.

Pallor due to menorrhagia ^[14] is listed as a key finding in the evaluation of pelvic masses causing HMB. Always check conjunctival pallor and nail beds.

Management:

Iron supplementation: oral ferrous sulphate 300 mg TDS × 6 months if Hb < 10 g/dL ^[11].
Treat the underlying cause (reduce HMB with hormonal therapy or surgery).
In severe anaemia (Hb < 7 g/dL or symptomatic): consider IV iron infusion or blood transfusion.

2. Subfertility and Infertility

Infertility: controversial ^[1].

This is one of the most actively debated areas in reproductive medicine. While the association between adenomyosis and subfertility is increasingly recognised, the causal relationship is not definitively established. Let's examine the proposed mechanisms:

The normal junctional zone (inner myometrium) undergoes coordinated peristaltic contractions that facilitate sperm transport from the cervix toward the fallopian tubes.
In adenomyosis, the JZ is thickened, infiltrated with ectopic glands, and hyperplastic → dysperistalsis (disorganised contractions) → impaired sperm transport → reduced fertilisation.

The endometrium overlying adenomyotic foci may have altered gene expression, including:
- Reduced expression of implantation markers (e.g., HOXA10, LIF, integrin αvβ3).
- Altered local immune milieu (increased pro-inflammatory cytokines).
- Defective decidualisation.
This creates a hostile endometrial environment for embryo implantation.

The ectopic endometrial glands within the myometrium undergo cyclical bleeding → chronic low-grade inflammation → release of prostaglandins, cytokines (IL-6, TNF-α), and reactive oxygen species.
These inflammatory mediators diffuse into the endometrial cavity → impair embryo implantation and early embryo development.

The hypertrophied, adenomyotic myometrium may have increased uterine contractility → premature expulsion of the embryo before implantation can be established.

Adenomyosis is increasingly recognised as a factor in recurrent implantation failure after IVF.
Women with adenomyosis undergoing IVF have lower clinical pregnancy rates, lower live birth rates, and higher miscarriage rates compared to controls.
Pre-treatment with GnRH agonists (2–3 months before IVF) to suppress adenomyotic activity and reduce uterine volume may improve IVF outcomes — this is current best practice.

When women with adenomyosis do conceive (spontaneously or via ART), they face increased obstetric risks. The mechanisms are directly related to the structural and functional abnormalities of the adenomyotic myometrium:

Complication	Mechanism
Miscarriage (increased risk)	Impaired decidualisation of the endometrium overlying adenomyotic foci → defective trophoblast invasion → placental insufficiency → early pregnancy loss. Analogous to how submucosal fibroids adversely affect implantation and placentation ^[14].
Preterm labour (increased risk)	Chronic inflammation in the myometrium → increased prostaglandin production → premature uterine contractions → preterm birth. The ectopic glands continue to respond to hormones during pregnancy, causing local irritation.
Preterm premature rupture of membranes (PPROM)	Inflammatory mediators from the adenomyotic myometrium may weaken the fetal membranes overlying affected areas.
Small for gestational age (SGA) / Fetal growth restriction (FGR)	Impaired uteroplacental blood flow through the adenomyotic myometrium → reduced nutrient and oxygen delivery to the fetus.
Pre-eclampsia (increased risk)	Defective deep trophoblast invasion into the spiral arteries (adenomyotic tissue disrupts normal spiral artery remodelling) → uteroplacental insufficiency → the shared pathway to pre-eclampsia.
Placenta praevia (increased risk)	The altered endomyometrial junction may affect normal placental implantation site selection → increased chance of low-lying placenta.
Placenta accreta spectrum (PAS)	Disrupted endomyometrial junction → absence of normal decidua basalis → abnormally deep trophoblast invasion into the myometrium. This is the same mechanism as PAS after caesarean section — the boundary between endometrium and myometrium is compromised.
Postpartum haemorrhage (PPH)	Adenomyotic myometrium has reduced force and coordination of uterine contractions → increased risk of uterine atony ^[14]. The infiltrating glands disrupt the smooth muscle's ability to contract uniformly around placental-site vessels after delivery.
Uterine rupture (rare but serious)	Particularly after adenomyomectomy — the surgically weakened myometrial wall may rupture during labour. Also theoretically possible in severe adenomyosis where the myometrium is extensively replaced by glandular tissue.

Adenomyosis and PPH — The Mechanism

The mechanism is identical to why fibroids cause PPH: decreased force and coordination of uterine contractions → increased risk of atony ^[14]. In adenomyosis, the ectopic glandular tissue interspersed within the myometrium physically disrupts the "woven basket" of smooth muscle fibres that must contract circumferentially to compress the open blood vessels at the placental site. The result is uterine atony → PPH.

Dysmenorrhoea (25%): due to bleeding and swelling of endometrial islands confined by myometrium ^[1].

Over time, the cyclical pain of adenomyosis can evolve into chronic pelvic pain through:

Peripheral sensitisation — repeated nociceptive input from monthly bleeding within the myometrium → upregulation of pain receptors in the myometrium → lower pain threshold → pain at progressively lower stimuli.
Central sensitisation — chronic nociceptive input to the spinal cord → wind-up phenomenon → the CNS amplifies pain signals → even non-painful stimuli (e.g., bladder filling, bowel distension) are perceived as painful (visceral cross-sensitisation).
Psychosocial impact — chronic pain leads to anxiety, depression, sleep disturbance, impaired sexual function, and reduced work capacity. This creates a vicious cycle where psychological distress lowers pain thresholds further.

Clinical features of chronic pelvic pain in adenomyosis:

Non-cyclical dull aching pelvic pain (superimposed on cyclical dysmenorrhoea).
May have bladder and bowel symptoms (due to visceral cross-sensitisation, not direct invasion).
Generally NOT associated with dyspareunia ^[1] — but deep pelvic pain may be triggered by intercourse in some cases.

Pathogenetically distinct from endometriosis although it commonly co-occurs with endometriosis ^[1].

Coexistence rate: up to 70–80% of women with adenomyosis also have endometriosis.
Shared risk factors: prolonged oestrogen exposure, retrograde menstruation, possible common stem cell origins.
The clinical significance is that when adenomyosis is diagnosed, you should actively look for endometriosis (and vice versa), as coexisting endometriosis will add:
- Dyspareunia (which adenomyosis alone does not typically cause).
- Additional infertility burden.
- Ovarian endometriomas ("chocolate cysts").
- Deep infiltrating endometriosis (bowel, bladder, uterosacral ligaments).

Stromal sarcomas can be found in association with adenomyosis and endometriosis ^[4].

Endometrial stromal sarcoma (ESS) is a rare malignancy that arises from the stroma of the endometrium ^[4].
It can develop within foci of adenomyosis — the ectopic endometrial stroma undergoes malignant transformation.
Stromal sarcomas tend to present in a younger age group (45–50y) ^[4] — overlapping with the peak age of adenomyosis.
Usually presents with AUB ± foul-smelling vaginal discharge and a uterine mass ^[4].

Red flags that should raise suspicion for sarcoma in a woman with known adenomyosis:

Rapidly increasing uterine size (especially postmenopausal).
New-onset or worsening persistent (non-cyclical) pain.
Postmenopausal bleeding in a woman with previously stable adenomyosis.
Heterogeneous, necrotic-appearing lesion on imaging.
Foul-smelling vaginal discharge.

Adenomyosis Does NOT Undergo Malignant Transformation — But...

Adenomyosis itself is benign and the ectopic endometrial glands do not become malignant. However, the stromal component of the ectopic endometrial tissue can (rarely) give rise to endometrial stromal sarcoma. This is not "transformation" of adenomyosis but rather a de novo malignancy arising in the ectopic stromal cells. The clinical implication: a rapidly changing uterus in a woman with known adenomyosis warrants re-evaluation and should not be dismissed as "just adenomyosis getting worse."

Important to consider iatrogenic complications from the treatments used for adenomyosis:

Treatment	Potential Complications
LNG-IUS (Mirena)	Expulsion (higher risk in enlarged/distorted cavity), perforation (rare), irregular bleeding (first 3–6 months), hormonal side effects (acne, mood changes), infection
GnRH agonists	Significant climacteric symptoms ^[11]: hot flushes, vaginal dryness, mood swings, bone density loss (critical if > 6 months without add-back), initial flare effect (transient worsening of symptoms in first 1–2 weeks)
COCP	CVS risk: increased risk of MI, stroke, thromboembolism ^[12]. Breakthrough bleeding.
Hysterectomy	Surgical risks: bleeding, infection, visceral injury (bladder, ureter, bowel), VTE, anaesthetic complications. Long-term: surgical menopause (if ovaries removed), vaginal cuff dehiscence (rare), pelvic floor changes
UAE	High rate of additional intervention for persistent or recurrent symptoms ^[1]. Post-embolisation syndrome (pain, fever). Ovarian failure (especially > 45y). Uterine necrosis/infection (rare). Non-target embolisation.
Adenomyomectomy	Uterine rupture in subsequent pregnancy (weakened wall). Incomplete excision → symptom recurrence (30–40% at 5 years). Adhesion formation.
HIFU/RFA	Investigational ^[1]. Skin burns (HIFU), thermal injury to adjacent structures, incomplete ablation, recurrence.

Often underestimated but arguably the most significant "complication" from the patient's perspective:

Domain	Impact	Mechanism
Physical functioning	Fatigue, exercise intolerance	Anaemia + chronic pain
Work productivity	Absenteeism, presenteeism	Monthly debilitating pain and heavy bleeding
Sexual function	Reduced desire, avoidance of intercourse	Pain, heavy bleeding, psychological burden
Mental health	Anxiety, depression, frustration	Chronic pain, unpredictable bleeding, fertility concerns
Social functioning	Avoidance of activities, social isolation	Fear of heavy bleeding episodes, need for frequent pad changes
Financial burden	Healthcare costs, time off work	Repeated consultations, medications, potential surgery

Category	Complication	Pathophysiological Basis
Haematological	Iron deficiency anaemia	Chronic HMB → iron depletion
Reproductive	Subfertility / infertility	JZ dysperistalsis, impaired endometrial receptivity, inflammation, altered contractility
	Miscarriage	Defective decidualisation and trophoblast invasion
	Preterm labour	Chronic myometrial inflammation → prostaglandins → premature contractions
	FGR / SGA	Impaired uteroplacental blood flow
	Pre-eclampsia	Defective spiral artery remodelling
	Placenta accreta spectrum	Disrupted endomyometrial junction → abnormal trophoblast invasion
	PPH	Impaired myometrial contractility → uterine atony
Pain	Chronic pelvic pain	Peripheral and central sensitisation from repeated nociceptive input
Associations	Coexisting endometriosis	Shared risk factors, common co-occurrence
	Endometrial stromal sarcoma (rare)	Malignancy arising in ectopic endometrial stroma within adenomyotic foci
Iatrogenic	Treatment complications	See table above for each modality
Psychosocial	Reduced QoL, depression, anxiety	Chronic pain + HMB + fertility concerns

High Yield Complications Points:

Anaemia is the most common complication — always check Hb and ferritin.

Infertility is controversial but increasingly recognised; adenomyosis is a factor in recurrent IVF implantation failure.

Adverse pregnancy outcomes: miscarriage, preterm labour, FGR, pre-eclampsia, PAS, PPH — all related to disrupted myometrial/endometrial function.

Stromal sarcoma can arise in association with adenomyosis — red flag if rapid uterine growth.

Treatment complications: GnRH agonists → bone loss; UAE → high re-intervention rate; COCP → VTE risk.

High Yield Summary

Key Complications of Adenomyosis:

Iron deficiency anaemia — from chronic HMB due to increased endometrial surface area and impaired myometrial contractility. Treat with iron supplementation (FeSO4 300 mg TDS × 6 months if Hb < 10).
Subfertility — controversial but increasingly recognised. Mechanisms: JZ dysperistalsis, impaired endometrial receptivity, chronic inflammation, altered contractility. Consider GnRH agonist pre-treatment before IVF.
Adverse pregnancy outcomes — miscarriage, preterm labour, FGR, pre-eclampsia, placenta accreta spectrum, PPH (from uterine atony due to disrupted myometrial contraction).
Chronic pelvic pain — from peripheral and central sensitisation due to repeated cyclical bleeding within myometrium.
Association with endometriosis — co-occurs frequently; look for both when one is found.
Association with stromal sarcoma — rare but important. Red flags: rapidly growing uterus, postmenopausal bleeding, atypical symptoms.
Treatment-related complications — GnRH agonists: bone loss, menopausal symptoms. UAE: high re-intervention rate. Hysterectomy: surgical risks. Adenomyomectomy: uterine rupture risk in future pregnancy.

Active Recall - Complications of Adenomyosis

References

^[1] Senior notes: Adrian Lui Gynecology Notes.pdf (Section 2.3.3 Adenomyosis, p. 50–51) ^[4] Senior notes: Adrian Lui Gynecology Notes.pdf (Section 4.3.5 Uterine Sarcoma, p. 105) ^[11] Senior notes: Adrian Lui Gynecology Notes.pdf (Section on Fibroids — Medical and Surgical Treatment, p. 91–92) ^[12] Senior notes: Adrian Lui Gynecology Notes.pdf (Section on AUB/COCP management, p. 15) ^[14] Senior notes: Adrian Lui Gynecology Notes.pdf (Section on Pelvic Mass Evaluation and Fibroid Clinical Features, p. 70, 90)

High Yield Summary

Definition: Endometrial glands and stroma invading the myometrium with surrounding smooth muscle hyperplasia. Histology: endometrial tissue ≥1 low-power field from endomyometrial junction. Distinct from endometriosis (ectopic tissue outside uterus) but commonly co-occurs.

Epidemiology: ~1% (likely underdiagnosed); peak 35–50 years; multiparous; prior uterine surgery (C-section, D&C). 33% asymptomatic.

Pathophysiology:

Endomyometrial invagination (most accepted) or de novo Müllerian metaplasia / TIAR.
Cyclic bleeding of ectopic glands trapped in myometrium → inflammation, prostaglandins, smooth muscle hypertrophy → diffusely enlarged boggy uterus.

Classification: Diffuse (typical) vs focal adenomyoma (mimics fibroid).

Cardinal symptoms:

HMB (60%): ↑ endometrial surface area + impaired myometrial contractility (poor haemostasis).
Dysmenorrhoea (25%): bleeding/swelling confined by myometrium.
NOT typically dyspareunia (disease is intramural, not peritoneal).
Infertility: controversial but increasingly recognised (JZ dysperistalsis, ↓ receptivity).

Exam — exam favourite: Mobile, diffusely enlarged, globular, boggy/soft, tender uterus; rarely > 12 weeks. Contrast fibroids: irregular, firm, discrete lumps.

Key distinction: Hormonal treatment works (like endometriosis); fibroids generally do NOT. Adenomyosis has no capsule → cannot enucleate.

High Yield Summary — Differential Diagnosis

The "Big Three" for HMB + dysmenorrhoea + enlarged uterus:

	Adenomyosis	Fibroids	Endometriosis
Enlargement	Diffuse, globular	Irregular, focal	Usually normal
Consistency	Boggy/soft	Firm/hard	Normal
HMB	60%	Most common symptom	Uncommon
Dysmenorrhoea	Yes	Rare (exceptions: clots, pedunculated submucous)	Yes + dyspareunia
Hormonal Rx	Effective	Ineffective	Effective
Surgery	Hysterectomy (no plane)	Myomectomy (pseudocapsule)	Lap excision

Must exclude:

Endometrial cancer — EA (Pipelle) if AUB > 45 years (adenomyosis does not protect).
Uterine sarcoma — rapidly enlarging uterus, PMB, foul discharge (stromal sarcoma can arise in adenomyosis).
Pregnancy (β-hCG).
PID — discharge, fever, cervical excitation.

Focal adenomyoma vs fibroid: MRI — adenomyoma = ill-defined, no capsule, T1 bright foci (blood); fibroid = pseudocapsule, low T2, whorled.

High Yield Summary — Diagnosis

Gold standard: Histology from hysterectomy specimen.

Working (clinical-radiological) diagnosis: HMB + dysmenorrhoea + boggy uterus + supportive imaging.

Algorithm: β-hCG → history/exam → TVUS (1st line) → MRI if equivocal/focal → EA if AUB > 45.

Modality	Key findings
TVUS	Heterogeneous myometrium, subendometrial striations, myometrial cysts (1–7 mm), ↑ vascularity, irregular endo-myometrial junction; no pseudocapsule
MRI	JZ thickness > 12 mm on T2W; T1/T2 bright foci (blood/glands); ill-defined, no capsule. JZ: < 8 normal, 8–12 equivocal, > 12 diagnostic

Adenomyoma vs leiomyoma on MRI: No capsule vs T2-dark pseudocapsule.

Secondary dysmenorrhoea clue: New dysmenorrhoea + menorrhagia → think adenomyosis.

Laparoscopy: Not routine — disease is intramural; may suggest coexisting endometriosis.

High Yield Summary — Management

Asymptomatic incidental: No treatment — observe.

Medical (1st line) — hormonal suppression like endometriosis:

LNG-IUS (Mirena) — best evidence for HMB.
DMPA, COCP (continuous preferred), dienogest, GnRH agonist (short-term/pre-IVF).
Adjuncts: tranexamic acid, NSAIDs (dysmenorrhoea), iron if anaemic.

Definitive: Hysterectomy — only true cure; no surgical plane for enucleation. Extent: subtotal acceptable (cervix/ovaries unaffected); preserve ovaries if premenopausal.

Uterus-conserving (fertility desired):

Adenomyomectomy (focal only) — high recurrence, uterine rupture risk in pregnancy.
UAE: ~2/3 improve long-term; high re-intervention; avoid if fertility desired.
HIFU/RFA: investigational; localised lesion < 10 cm, one wall only.

Acute severe HMB: Resuscitation → tranexamic acid → high-dose progestins → hysterectomy if refractory.

Scenario	Approach
Mild, wants fertility	Mirena ± tranexamic acid/NSAIDs
Severe, family complete	Hysterectomy
Perimenopausal	Bridge with GnRH agonist + add-back
Failed medical, not surgical candidate	UAE

High Yield Summary — Complications

Haematological: Iron deficiency anaemia from chronic HMB — most common complication; check Hb/ferritin.

Reproductive:

Subfertility/implantation failure — JZ dysperistalsis, ↓ receptivity, inflammation; consider GnRH agonist 2–3 months pre-IVF.
Adverse pregnancy: miscarriage, preterm labour, FGR, pre-eclampsia, placenta accreta spectrum, PPH (impaired myometrial contraction).

Chronic pain: Peripheral/central sensitisation from repeated intramyometrial bleeding.

Associations:

Endometriosis (co-occurs up to 70–80%) — look for both.
Endometrial stromal sarcoma (rare) — rapidly enlarging uterus, atypical symptoms.

Treatment-related:

GnRH agonist: bone loss, menopausal symptoms.
UAE: ovarian failure (> 45y), re-intervention.
Adenomyomectomy: uterine rupture in subsequent pregnancy.

Psychosocial: ↓ QoL from HMB, pain, fertility concerns.

Adenomyosis

1. Definition

2. Epidemiology

3. Anatomy and Relevant Functional Considerations

The Uterine Wall — Three Layers

The Junctional Zone — Why It Matters

4. Aetiology and Pathogenesis

Theory 1: Endomyometrial Invagination (Most Accepted)

Theory 2: De Novo Metaplasia from Müllerian Rests

Theory 3: Tissue Injury and Repair (TIAR) — Modern Concept

Downstream Consequence — The Vicious Cycle

5. Classification

By Distribution Pattern

By Depth of Invasion

MUSA Classification (Morphological Uterus Sonographic Assessment)

6. Clinical Features

6.1 Symptoms

A. Heavy Menstrual Bleeding (HMB) — 60%

B. Dysmenorrhoea — 25%

C. Deep Pelvic Pain

D. Infertility

E. Other Symptoms

6.2 Signs

A. Bimanual Pelvic Examination

B. Speculum Examination

7. Summary Table — Adenomyosis vs. Fibroids (Leiomyomas)

8. Approach to Evaluation

A. History

B. Physical Examination

C. Endometrial Assessment

D. Imaging

Transvaginal Ultrasound (TVUS) — First Line

Pelvic MRI — Gold Standard Imaging

E. Definitive Diagnosis

9. Gross and Histological Pathology

Gross Appearance

Histological Appearance

Active Recall - Adenomyosis (Definition, Aetiology, Clinical Features)

References

Conceptual Framework for the Differential

Key Differentials — Detailed Comparison

1. Uterine Fibroids (Leiomyomas)

2. Endometriosis

3. Endometrial Carcinoma / Endometrial Hyperplasia

4. Uterine Sarcoma

5. Chronic Pelvic Inflammatory Disease (PID) / Endometritis

6. Other Differentials (Less Common but Important)

Diagnostic Differentiation Algorithm

Summary Comparison Table — The "Big Three" Differentials

Active Recall - Differential Diagnosis of Adenomyosis

The Diagnostic Challenge — Why Adenomyosis Is Tricky

1. Diagnostic Criteria

A. Histological Criteria (Gold Standard — Post-Hysterectomy)

B. Clinical Diagnostic Criteria (Working Diagnosis)

C. Imaging Diagnostic Criteria

i. TVUS Criteria (First-Line Imaging)

ii. MRI Criteria (Second-Line — Gold Standard Imaging)

2. Complete Diagnostic Algorithm

3. Investigation Modalities — Detailed Breakdown

Step 1: Exclude Pregnancy — βhCG

Step 2: Blood Tests

Step 3: Transvaginal Ultrasound (TVUS) — First-Line Imaging

Step 4: Pelvic MRI — Second-Line (When TVUS Is Equivocal)

Step 5: Endometrial Assessment (EA)

Step 6: Diagnostic Laparoscopy (Rarely Needed)

Additional Investigations — Special Situations

4. Putting It All Together — The Diagnostic Approach in Practice

5. Key Diagnostic Distinctions on Imaging — High-Yield Summary Table

Active Recall - Diagnosis and Investigations for Adenomyosis

Guiding Principles — How to Think About Management

Management Algorithm

1. Conservative Management (Observation)

2. Medical Treatment

A. Non-Hormonal Medical Treatment (Symptomatic Relief)

B. Hormonal Medical Treatment

i. Levonorgestrel-Releasing Intrauterine System (LNG-IUS / Mirena)

ii. Depot Medroxyprogesterone Acetate (DMPA / Depot Provera)

iii. Combined Oral Contraceptive Pills (COCPs)

iv. GnRH Agonists

v. GnRH Antagonists (Newer Option)