Uterine fibroids are benign smooth muscle tumors (leiomyomas) of the myometrium that can cause abnormal uterine bleeding, pelvic pain, and reproductive dysfunction.

Exam domain	One-glance essentials
Definition / diagnosis	*Uterine fibroids are benign monoclonal smooth-muscle tumours of the myometrium* ^[1]^[2] Classify by location: submucosal, intramural, subserosal, cervical, or FIGO type ^[1]
Epidemiology / risks	Risk is associated with reproductive age, family history, Black ethnicity, early menarche, obesity, and nulliparity ^[1]^[2] Fibroids are oestrogen and progesterone responsive and often shrink after menopause ^[1]
Core mechanism	Hormone-responsive smooth-muscle proliferation plus extracellular matrix deposition → a well-circumscribed mass with a pseudocapsule ^[1]^[2] Location determines effects: submucosal lesions distort the cavity; subserosal lesions cause pressure ^[1]
Clinical picture	*HMB and a firm, irregularly enlarged uterus are classic* ^[1]^[2] Pressure, pelvic mass, urinary or bowel symptoms, infertility, and pregnancy complications vary with size and site; many fibroids are asymptomatic ^[1]
Investigations	Pelvic ultrasound is first-line to map number, size, and location ^[1]^[2] Hysteroscopy evaluates intracavitary disease; MRI helps complex mapping or procedural planning; sample the endometrium when bleeding risk warrants it ^[1]
Management	Observe asymptomatic disease; control bleeding with medical therapy and correct anaemia ^[1]^[2] Use hysteroscopic resection, myomectomy, UAE, other selected procedures, or hysterectomy according to symptoms, cavity distortion, fertility, age, and preference ^[1]
Complications	Complications include iron-deficiency anaemia, pressure or obstruction, degeneration, torsion of a pedunculated lesion, infertility, miscarriage, malpresentation, and PPH ^[1]^[2] Treatment may cause adhesions, reduced fertility, uterine scar, ovarian impairment after UAE, or surgical morbidity ^[1]
Prevention / follow-up	Review growth or new symptoms after menopause, optimise iron before procedures, and plan pregnancy care when fibroids distort the cavity or lower segment ^[1]^[2] Safety-net rapid enlargement, PMB, severe pain, or systemic symptoms for reassessment ^[1]
Exam traps	*Fibroids are firm, discrete, and irregular; adenomyosis is diffuse, globular, boggy, and has no enucleation plane* ^[1]^[2] A rapidly growing mass is not proof of sarcoma, but postmenopausal growth or atypical features require investigation ^[1]

References

^[1] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (uterine fibroids and pelvic imaging) ^[2] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (fibroid presentation, differentiation and management)

Uterine Fibroid (Leiomyoma)

Uterine fibroids — medically termed leiomyomata (singular: leiomyoma) — are benign monoclonal neoplasms arising from the smooth muscle cells (myocytes) of the myometrium ^[1]^[2].

Let's break down the name:

"Leio-" (Greek leios) = smooth
"-myo-" (Greek mys) = muscle
"-oma" = tumour/mass

So a leiomyoma literally means "a tumour of smooth muscle." The common name "fibroid" comes from the firm, fibrous cut-surface appearance due to abundant extracellular matrix (collagen, fibronectin, proteoglycans) deposited between the neoplastic smooth muscle cells. Despite the name, these are not primarily fibrous tissue tumours — they are smooth muscle tumours with a heavy fibrous stroma ^[1].

Key Distinction

Fibroids are benign. Malignant transformation to leiomyosarcoma is exceedingly rare ( < 0.1–0.5%) and is now thought to arise de novo rather than from pre-existing fibroids in most cases. Do not confuse fibroid with leiomyosarcoma ^[1]^[2].

Each fibroid is monoclonal — meaning each individual fibroid arises from a single progenitor myocyte that acquires a somatic mutation (most commonly in MED12, HMGA2, or other driver genes), then proliferates. A single uterus can harbour multiple fibroids, each genetically distinct (i.e., each fibroid is an independent clonal proliferation) ^[2].

Fibroids are the most common pelvic tumour in women ^[1]^[2].

2. Epidemiology

Fibroids are extremely common — affecting up to 70–80% of women by age 50 ^[1]^[2].
Clinically significant (symptomatic) fibroids occur in approximately 25–30% of reproductive-age women.
Many fibroids are asymptomatic and found incidentally on imaging or at surgery.

Peak incidence in the reproductive years, particularly ages 30–50 ^[1].
Uncommon before menarche (because they are oestrogen-dependent).
Tend to shrink after menopause due to declining oestrogen levels ^[1]^[2].
Fibroids that persist or enlarge post-menopause should raise concern for leiomyosarcoma (red flag).

African and Afro-Caribbean women have a 2–3× higher incidence, earlier onset (younger age), and tend to develop larger and more numerous fibroids compared to Caucasian and Asian women.
In Hong Kong, fibroids remain a very common gynaecological condition, though specific local prevalence data are less well-characterised. They are a leading indication for hysterectomy and myomectomy in the Chinese population ^[1].

Factor	Effect	Mechanism
Oestrogen exposure	↑ risk	Oestrogen is a major mitogen for fibroid growth (see Pathophysiology)
Early menarche	↑ risk	Longer lifetime oestrogen exposure
Nulliparity	↑ risk	No pregnancy-related amenorrhoea → more cumulative oestrogen cycles
Obesity (BMI > 25)	↑ risk	Adipose tissue converts androgens → oestrogens via aromatase; also ↓SHBG → ↑free oestrogen
Family history (1st degree)	↑ risk (2–3×)	Genetic predisposition (MED12, HMGA2 mutations)
African ethnicity	↑ risk (2–3×)	Genetic and possibly epigenetic factors
Hypertension	↑ risk	Likely related to smooth muscle cell injury and cytokine milieu
Tamoxifen	↑ risk of fibroid growth	Tamoxifen has oestrogenic activity on uterine tissue (partial agonist at uterine oestrogen receptors)
Parity	↓ risk	Each pregnancy provides months of anovulation + remodelling of myometrium
Combined OCP	Variable	May be protective if started early; but exogenous oestrogen can promote growth in some
Smoking	Slightly ↓ risk	Anti-oestrogenic effect (↑hepatic oestrogen metabolism + ↓aromatase); note: smoking is harmful overall
Progesterone	Complex role	Progesterone can stimulate fibroid growth (hence why GnRH agonists alone, which suppress both E2 and P4, are effective)
Diet high in red meat, alcohol	↑ risk	Possibly via oestrogen metabolism; vitamin D deficiency may also contribute

High Yield — Oestrogen Dependence

The single most important concept to understand about fibroid biology: fibroids are oestrogen (and progesterone) dependent. This explains why they appear after menarche, enlarge during pregnancy (high E2/P4), enlarge with obesity/HRT, and shrink after menopause or with GnRH agonist treatment ^[1]^[2].

3. Anatomy and Function: The Uterus

To understand fibroids, you need to know the anatomy of the uterus — because the location of the fibroid within the uterine wall determines its symptoms.

The uterus is a thick-walled, hollow, pear-shaped muscular organ located in the pelvis between the bladder (anteriorly) and rectum (posteriorly). It has:

Fundus: the dome-shaped upper portion above the level of the tubal ostia
Body (corpus): the main bulk
Isthmus: the narrow transitional zone between body and cervix
Cervix: the lower cylindrical portion opening into the vagina

Layer	Structure	Relevance to Fibroids
Endometrium (innermost)	Mucosal lining; functional layer sheds during menstruation	Submucosal fibroids distort this layer → abnormal uterine bleeding
Myometrium (middle)	Thick layer of smooth muscle arranged in interlacing bundles; the layer from which fibroids arise	Intramural fibroids reside here
Serosa / Perimetrium (outermost)	Peritoneal covering (visceral peritoneum)	Subserosal fibroids project outward from here

Uterine artery (branch of the internal iliac artery) — the dominant blood supply
Ovarian artery (branch of the aorta) — provides collateral supply via tubo-ovarian anastomosis
The uterine artery is the target vessel in uterine artery embolisation (UAE) ^[3]

The myometrium contracts during labour to expel the fetus, and during menstruation to help shed the endometrium. Fibroids distort the normal myometrial architecture and can:

Impair contractility → heavy menstrual bleeding (failure to compress spiral arterioles)
Distort the endometrial cavity → abnormal implantation / infertility
Compress adjacent organs (bladder, ureters, rectum) → urinary/bowel symptoms

4. Aetiology and Pathophysiology

Each fibroid begins as a single mutated myometrial stem cell that gains a proliferative advantage:

MED12 mutations — found in ~70% of fibroids; MED12 is a subunit of the Mediator complex involved in transcriptional regulation. Mutations here lead to dysregulated cell proliferation.
HMGA2 rearrangements — HMGA2 (High Mobility Group AT-hook 2) is a chromatin architectural protein; its overexpression promotes cell growth.
Fumarate hydratase (FH) mutations — seen in hereditary leiomyomatosis and renal cell cancer (HLRCC) syndrome; loss of this Krebs cycle enzyme leads to pseudohypoxia and growth factor activation.
Other less common drivers: COL4A5/COL4A6 deletions (Alport syndrome-associated)

4.2 Promotion (Growth — the role of sex steroids)

Once initiated, oestrogen and progesterone are the key promoters of fibroid growth:

Oestrogen stimulates fibroid growth by:
- Upregulating growth factors (EGF, IGF-1, TGF-β)
- Promoting extracellular matrix (ECM) deposition
- Increasing progesterone receptor expression (priming the fibroid for P4 effects)
Fibroids overexpress aromatase (CYP19A1), allowing local conversion of androgens to oestrogen within the fibroid itself — creating an autocrine/paracrine loop that sustains growth even when systemic oestrogen is relatively low.

Progesterone's role is now recognised as equally important (if not more so in promoting mitotic activity):
- Progesterone stimulates cell proliferation (mitotic activity peaks in the secretory/luteal phase, not the follicular/oestrogenic phase)
- Upregulates anti-apoptotic factors (Bcl-2)
- This is why selective progesterone receptor modulators (SPRMs) like ulipristal acetate can shrink fibroids

Why do fibroids enlarge during pregnancy?

During pregnancy, both oestrogen and progesterone levels rise dramatically. The combined mitogenic effect drives fibroid enlargement. Additionally, the increase in blood flow to the uterus provides more nutrients. However, fibroids may also undergo red/carneous degeneration during pregnancy due to outgrowing their blood supply (see Degeneration below) ^[1].

Fibroids produce a disproportionately large amount of ECM (collagen types I and III, fibronectin, proteoglycans). This gives them their characteristically firm, whorled, white cut surface and contributes to bulk symptoms. The ECM also acts as a reservoir for growth factors (TGF-β, bFGF) that promote further fibroid growth.

When fibroids outgrow their blood supply, they undergo degenerative changes. This is clinically important because degeneration can cause acute pain:

Type of Degeneration	Pathophysiology	Clinical Significance
Hyaline degeneration	Most common (60%); homogeneous acellular areas replace smooth muscle	Usually asymptomatic; fibroid becomes softer
Cystic degeneration	Liquefaction of hyalinised areas → cyst formation	Mimics ovarian cyst on imaging
Calcification (calcific degeneration)	Calcium deposition, especially post-menopause with poor blood supply	Visible on X-ray / AXR as "popcorn" calcification ^[4]; usually asymptomatic
Red (carneous) degeneration	Venous thrombosis at fibroid periphery → haemorrhagic infarction; classically occurs in pregnancy (2nd trimester) or with OCP use	Acute pain, tenderness, low-grade fever; managed conservatively with analgesia ^[1]
Fatty degeneration	Rare; lipid deposition	Usually incidental
Sarcomatous change	Extremely rare ( < 0.5%); likely represents de novo leiomyosarcoma	Suspect if rapid growth post-menopause; needs surgical excision

Red Degeneration in Pregnancy

A pregnant woman (typically 2nd trimester) presenting with acute localised uterine tenderness, low-grade fever, and mild leukocytosis with a known fibroid should be suspected of red/carneous degeneration. Management is conservative — rest, hydration, analgesia (paracetamol, NSAIDs avoided in late pregnancy). Surgery is almost never needed ^[1].

5. Classification

Fibroids are classified by their location within the uterine wall, which directly determines the symptom profile. The FIGO leiomyoma subclassification system (FIGO classification / PALM-COEIN system for AUB) is the standard ^[1]^[2]:

FIGO Type	Location	Key Clinical Feature
0	Pedunculated submucosal (entirely intracavitary)	Heavy bleeding; may prolapse through cervix
1	Submucosal, < 50% intramural component	Heavy bleeding; affects fertility
2	Submucosal, ≥ 50% intramural component	Heavy bleeding; harder to resect hysteroscopically
3	Intramural, contacts endometrium	May cause bleeding
4	Entirely intramural	Bulk symptoms; may affect bleeding if large
5	Subserosal, ≥ 50% intramural	Bulk symptoms
6	Subserosal, < 50% intramural	Bulk symptoms, pressure effects
7	Pedunculated subserosal	Torsion risk; may mimic adnexal mass
8	Cervical, parasitic, broad ligament, round ligament	Site-specific symptoms

Clinical Pearl — Location Determines Symptoms

Submucosal fibroids (Types 0–2) → most likely to cause abnormal uterine bleeding (AUB) and infertility even when small, because they distort the endometrial cavity ^[1]^[2].
Intramural fibroids (Types 3–4) → cause both bleeding (if large/close to endometrium) and bulk symptoms.
Subserosal fibroids (Types 5–7) → primarily cause bulk/pressure symptoms; unlikely to cause bleeding unless very large distorting the cavity.

Pedunculated: attached to the uterus by a stalk (pedicle). Can be submucosal (intracavitary, Type 0) or subserosal (Type 7). The stalk can twist → torsion → acute pain from ischaemia ^[1].
Parasitic fibroid: a fibroid that has detached from the uterus and gained an alternative blood supply (e.g., from the omentum or bowel mesentery). Increasingly recognised post-laparoscopic morcellation.
Broad ligament fibroid: grows laterally between the layers of the broad ligament. Can displace the ureter → hydroureter/hydronephrosis. Can be mistaken for an ovarian mass.
Cervical fibroid: arises from the cervix; can obstruct labour or cause urinary retention.
Intraligamentary fibroid: within the broad or round ligament.

6. Clinical Features

The majority (50–80%) of fibroids are asymptomatic and discovered incidentally ^[1]^[2]. When symptomatic, the clinical features depend on the size, number, and location of the fibroids.

6.1 Symptoms

The "P" in PALM-COEIN stands for Polyp, Adenomyosis, Leiomyoma, Malignancy — fibroids are a structural cause of abnormal uterine bleeding ^[5].

Heavy menstrual bleeding (HMB / menorrhagia) — the single most common presenting complaint
- Prolonged periods (> 7 days) and/or increased volume
- Characteristically regular cycle (as opposed to anovulatory bleeding which is irregular) — because fibroids do not disrupt the hypothalamic-pituitary-ovarian axis
- Patients may report flooding, passage of large clots, needing to change pads/tampons every 1–2 hours, and soaking through clothes or bedsheets

Why do fibroids cause heavy bleeding? Multiple mechanisms:

Increased endometrial surface area: submucosal and large intramural fibroids enlarge the uterine cavity → more endometrium to shed → more bleeding
Distortion of the subendometrial venous plexus: fibroids compress and dilate the venous sinuses underlying the endometrium → venous ectasia → heavy bleeding
Impaired myometrial contractility: the myometrium normally contracts after menstruation to compress spiral arterioles and stop bleeding (similar to how it contracts post-partum). Fibroids disrupt the normal architecture, preventing effective contraction around blood vessels → failure of haemostasis
Altered local prostaglandin/growth factor production: fibroids increase local production of PGE2, PGI2 (vasodilators and anti-platelet) and decrease PGF2α (vasoconstrictor) → impaired vasoconstriction and platelet aggregation → ongoing bleeding
Ulceration of overlying endometrium: submucosal fibroids can cause pressure necrosis and ulceration of the overlying endometrium → bleeding from a raw surface

Intermenstrual bleeding (IMB) — less common; can occur if submucosal fibroid causes endometrial ulceration
Postcoital bleeding — if cervical fibroid present
Iron deficiency anaemia — consequence of chronic heavy menstrual blood loss

Fibroid vs. Adenomyosis

Both fibroids and adenomyosis cause HMB and dysmenorrhoea, and they frequently coexist. Key clinical differences: adenomyosis causes a uniformly enlarged, boggy, tender uterus (often described as "globular"), whereas fibroids cause an irregularly enlarged, firm, non-tender uterus with discrete nodules. On USS, adenomyosis shows a heterogeneous myometrium with poor junctional zone definition, whereas fibroids appear as well-circumscribed round lesions. MRI is the gold standard to differentiate them.

As fibroids enlarge, they exert mass effect on adjacent pelvic structures:

Pelvic pressure / heaviness / discomfort — from the sheer mass of the fibroid(s) in the pelvis
Urinary symptoms — from compression of the bladder (anterior to uterus):
- Urinary frequency — reduced bladder capacity
- Urgency
- Nocturia
- Acute urinary retention — particularly with a large cervical fibroid or anterior wall fibroid impacting the bladder neck ^[6]
- Hydroureter / hydronephrosis — large broad ligament or laterally placed fibroids can compress the ureter at the pelvic brim, causing obstruction. If bilateral or in a solitary kidney, this can lead to renal impairment (obstructive uropathy)
Bowel symptoms — from compression of the rectum (posterior to uterus):
- Constipation
- Tenesmus (sensation of incomplete evacuation)
- Rectal pressure
Abdominal distension — very large fibroids (can reach up to the xiphisternum in extreme cases; uterine size often described in "weeks" like a pregnant uterus, e.g., "20-week size")

Fibroids per se are often painless. When pain occurs, consider:

Dysmenorrhoea (painful periods) — due to:
- Abnormal myometrial contractions trying to expel submucosal fibroids
- Distortion of the uterine cavity
- Concomitant adenomyosis (common co-pathology)
Acute pain — suggests:
- Red (carneous) degeneration — especially in pregnancy (2nd trimester); localised tenderness over the fibroid, low-grade fever
- Torsion of a pedunculated fibroid — sudden onset severe pain, peritonism
- Acute urinary retention — suprapubic pain
Dyspareunia (deep) — if fibroid is in the posterior wall or cervix, pressing on the pouch of Douglas or vaginal fornices
Chronic pelvic pain — less specific; may be due to degeneration, pressure, or associated conditions

Subfertility / infertility — fibroids may impair fertility through several mechanisms:
- Submucosal fibroids distort the endometrial cavity → impaired implantation
- Intramural fibroids near the tubal ostia → mechanical tubal obstruction
- Altered endometrial receptivity (local cytokine/growth factor changes)
- Altered uterine contractility → impaired sperm transport
- However, fibroids are the sole cause of infertility in only ~2–3% of cases
Recurrent pregnancy loss — submucosal fibroids associated with increased miscarriage risk
Pregnancy complications — if fibroids are present during pregnancy:
- Red degeneration (as above)
- Malpresentation (e.g., transverse lie, breech) — fibroid distorts uterine cavity
- Preterm labour
- Placental abruption — if fibroid is at the placental site
- Obstructed labour — particularly cervical or lower segment fibroids
- Postpartum haemorrhage (PPH) — fibroids are a risk factor for uterine atony (the most common cause of PPH) because the fibroid-laden uterus cannot contract effectively to compress the placental bed blood vessels ^[7]

Fibroid and PPH

Fibroids cause abnormal myometrium — this is listed as a risk factor for PPH under the "Tone" category (the 4 T's: Tone, Tissue, Trauma, Thrombin). The upper segment of the uterus is the main contractile force in PPH prevention; fibroids in the upper segment are therefore particularly problematic ^[7].

Polycythaemia (secondary erythrocytosis) — rare paraneoplastic phenomenon; some fibroids produce erythropoietin (EPO) → secondary erythrocytosis (this is listed under "inappropriate EPO production" alongside RCC, HCC, and cerebellar haemangioblastoma) ^[8]
Ascites + pleural effusion — Meigs-like syndrome (pseudo-Meigs syndrome): very rare; large subserosal fibroids can produce a triad of pelvic mass + ascites + pleural effusion, mimicking ovarian cancer

6.2 Signs (Physical Examination)

Palpable pelvic/abdominal mass — arising from the pelvis (you cannot "get below it" on abdominal palpation, i.e., the lower margin is continuous with the pelvis)
- Firm to hard in consistency (due to smooth muscle and collagen)
- Irregular / lobulated surface if multiple fibroids
- Non-tender (unless undergoing degeneration)
- Mobile side to side but not up and down if connected to the uterus (transmits movement with cervical excitation — see bimanual exam)
- Dull to percussion (as opposed to tympanitic for bowel)
- The mass moves with respiration (if intraperitoneal) — actually, a pelvic mass typically does not move with respiration because it is fixed in the pelvis (contrast with hepatomegaly or splenomegaly)

How to differentiate a pelvic mass from an ovarian mass on examination: A fibroid uterus is typically a midline mass; you cannot feel a plane of separation between it and the uterus on bimanual exam; it moves when the cervix is moved (i.e., transmitted mobility on bimanual exam). An ovarian mass tends to be more lateral, with a palpable groove between it and the uterus.

Enlarged uterus — often described in terms of gestational weeks
Irregular contour — multiple fibroids give a "knobbly" or lobulated feel
Firm consistency
Non-tender (unless degeneration)
Cervical fibroid — may be palpable as a mass at the cervix; a pedunculated submucosal fibroid may prolapse through the cervical os and be visible/palpable on speculum examination (polypoidal mass protruding through cervix — fibroid polyp)
Uterus may be retroverted and fixed if posterior wall fibroids are present

Fibroid polyp protruding through the cervical os (pedunculated submucosal fibroid, FIGO Type 0)
Cervix may appear displaced by cervical or lower uterine segment fibroids

Pallor — suggesting iron deficiency anaemia from chronic HMB
Signs of iron deficiency: koilonychia, angular stomatitis, glossitis (smooth tongue)

What if the fibroid grows rapidly postmenopausally?

A fibroid that enlarges after menopause is a red flag for leiomyosarcoma. In the absence of HRT or other oestrogen sources, fibroids should be regressing. Rapid growth (especially with pain) warrants urgent investigation (MRI +/- surgical excision for histological assessment). However, note that "rapid growth" alone has poor predictive value for sarcoma — the overall risk remains very low ^[2].

Beyond local effects, fibroids can rarely cause systemic phenomena:

Effect	Mechanism
Iron deficiency anaemia	Chronic heavy menstrual blood loss → depleted iron stores
Secondary erythrocytosis	Inappropriate EPO production by the fibroid ^[8]
Pseudo-Meigs syndrome	Large fibroid → peritoneal irritation → ascites; sympathetic pleural effusion (usually right-sided)
Hypercalcaemia	Extremely rare; production of PTHrP
Venous thromboembolism	Large fibroids can compress pelvic veins → venous stasis → DVT/PE

This will be covered in more detail in the Diagnosis section, but for completeness of clinical features:

USS (transabdominal +/- transvaginal) — first-line imaging ^[1]^[4]:
- Well-defined, hypoechoic, round mass within the myometrium
- May show posterior acoustic shadowing (due to dense fibrous tissue)
- Very vascular on Doppler (peripheral and intralesional vascularity) ^[4]
- Submucosal fibroids indent/distort the endometrial stripe
- Calcified fibroids → hyperechoic foci with shadowing
AXR — "popcorn" or amorphous calcification in the pelvis may indicate calcific degeneration of a fibroid ^[4]
MRI — gold standard for mapping fibroid number, location, and type; essential for surgical planning
- T1: iso- to hypointense
- T2: typically hypointense (dark) due to dense fibrous tissue; degenerated fibroids may show heterogeneous or hyperintense signal
Uterine artery embolisation (UAE) — both diagnostic and therapeutic; demonstrates the vascular supply on angiography before embolisation ^[3]

Fibroids are classified under the "L" (Leiomyoma) of the PALM-COEIN system for abnormal uterine bleeding (AUB) ^[5]. The FIGO system further subclassifies the fibroid based on its relationship to the endometrial cavity:

AUB-L (SM) — submucosal component present (FIGO 0–2) → most likely to cause AUB
AUB-L (O) — other types without submucosal component (FIGO 3–8)

This distinction is important because only submucosal fibroids are strongly associated with AUB, and the management approach differs (hysteroscopic resection is possible for submucosal fibroids).

High Yield Summary

Uterine Fibroid (Leiomyoma) — Key Points for Exams:

Most common pelvic tumour in women — benign, monoclonal, smooth muscle neoplasm of the myometrium
Oestrogen AND progesterone dependent — appears after menarche, grows in pregnancy, shrinks after menopause
Risk factors: early menarche, nulliparity, obesity, African ethnicity, family history, hypertension
Location determines symptoms — Submucosal (bleeding/infertility), Intramural (bleeding + bulk), Subserosal (bulk/pressure)
Heavy menstrual bleeding (HMB) is the most common symptom — due to ↑endometrial surface area, venous ectasia, impaired myometrial contractility, altered prostaglandins
Bulk symptoms: urinary frequency/retention, constipation, abdominal distension
Red degeneration — acute pain in pregnancy (2nd trimester); manage conservatively
Fibroid is a risk factor for PPH — abnormal myometrium → uterine atony
Pedunculated subserosal fibroid can mimic adnexal mass; pedunculated submucosal fibroid can prolapse through cervix
Rapid enlargement post-menopause → suspect leiomyosarcoma
USS is first-line imaging; MRI is gold standard for mapping
"L" in PALM-COEIN (AUB classification); FIGO leiomyoma subclassification Types 0–8
Rare: secondary erythrocytosis (EPO production), pseudo-Meigs syndrome
On AXR: "popcorn" calcification (calcific degeneration)

Active Recall - Uterine Fibroid (Definition to Clinical Features)

^[1] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[2] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[3] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p85 — Transcatheter Embolization: uterine fibroid embolization) ^[4] Senior notes: Ryan Ho Radiology.pdf (p33 — Uterine mass, leiomyoma on USS) ^[5] Lecture slides: GC 112. Abnormal vaginal bleeding Gynaecological cancer.pdf ^[6] Senior notes: Ryan Ho Urogenital.pdf (p164 — gynaecological tumours e.g. fibroid as cause of female AROU) ^[7] Lecture slides: Block C - Postpartum Haemorrhage.pdf (p5 — risk factors for PPH: abnormal myometrium including fibroid) ^[8] Senior notes: Maksim Medicine Notes.pdf (p170 — uterine fibroma as cause of inappropriate EPO production / secondary erythrocytosis)

Differential Diagnosis of Uterine Fibroid

The differential diagnosis of uterine fibroid is best approached from two angles:

The patient presents with a pelvic mass — what else could it be?
The patient presents with abnormal uterine bleeding (AUB) — what else could cause it?

These are two distinct clinical presentations, and the DDx list differs for each. We will cover both systematically.

Uterine fibroid, ovarian mass and cancer are important differential diagnoses of pelvic mass ^[1]^[2]. The key principle is to classify by organ of origin and then use history, examination, and imaging to narrow down.

A. Differential Diagnosis of a Pelvic Mass

Classify according to gynaecological, and non-gynaecological. Non-gynaecological: separate into gastrointestinal, urological, retroperitoneal ^[2].

I. Gynaecological Causes

Condition	Key Differentiating Features from Fibroid	Why it mimics fibroid
Adenomyosis	Uniformly enlarged, globular, boggy, tender uterus (vs. fibroid: irregular, firm, non-tender). Less mobile on PE since inflammation may cause adhesions dragging it down to the Pouch of Douglas ^[9]. Dysmenorrhoea is typically more prominent and progressive. MRI shows diffuse junctional zone thickening ( > 12 mm) rather than a discrete mass	Both cause HMB, dysmenorrhoea, and an enlarged uterus. They frequently coexist (up to 20–35% of cases)
Uterine sarcoma / Leiomyosarcoma	Rapid growth especially postmenopausally. Often heterogeneous on imaging with areas of necrosis and haemorrhage. Irregular margins. LDH may be elevated. Definitive diagnosis is histological	A necrotic fibroid and a leiomyosarcoma can look identical on imaging — both show heterogeneous signal on MRI. Key red flag is rapid enlargement without oestrogen exposure ^[2]
Endometrial cancer	Typically presents with postmenopausal bleeding (PMB) or irregular/heavy bleeding in premenopausal women. USS shows thickened endometrium ( > 4 mm in PMB). Diagnosed by endometrial biopsy (pipelle or hysteroscopy). Risk factors: unopposed oestrogen, obesity, Lynch syndrome ^[5]	Both can cause AUB. A large endometrial mass can mimic a submucosal fibroid

Adenomyosis vs Fibroid on Examination

Adenomyosis: less mobile on PE since the inflammation may cause adhesions dragging it down to the Pouch of Douglas. Fibroid: mobile, irregular, firm mass ^[9]. This is a classic clinical exam question. On bimanual, the adenomyotic uterus feels diffusely enlarged and tender whereas the fibroid uterus is irregularly enlarged with discrete nodules and non-tender.

Condition	Key Differentiating Features	Why it mimics fibroid
Ovarian cyst (functional, dermoid, endometrioma)	Mobile cystic mass arising from the pelvis. On bimanual: ovarian-origin mass is more apparent when palpating the sides (lateral to uterus), and there is a palpable groove between mass and uterus. USS: unilocular, smooth-walled, mainly fluid component, no free fluid for benign cysts ^[9]	A large ovarian cyst can fill the pelvis and be difficult to distinguish from a fibroid clinically. A pedunculated subserosal fibroid (FIGO Type 7) can mimic an adnexal mass
Ovarian cancer	Fixed and hard mass, constitutional symptoms (weight loss, fatigue), ascites, nodular deposits in Pouch of Douglas on PR exam. USS: heterogeneous with solid component, irregular wall, papillary projections, increased vascularity, multilocular, free abdominal fluid ^[9]. Elevated CA-125	A solid ovarian mass can mimic a pedunculated fibroid. However, ovarian cancer typically has constitutional symptoms, ascites, and peritoneal disease
Paraovarian cyst	Arises from mesosalpinx (embryological remnant). Typically unilocular, smooth, separate from ovary on USS	Large paraovarian cysts can be mistaken for ovarian or uterine masses
Hydrosalpinx	Fluid-filled fallopian tube (often from PID sequelae). Tubular shape on USS with "cogwheel" sign on cross-section	Usually identifiable on USS; can be confused with cystic adnexal mass

How to differentiate uterine mass from ovarian mass on bimanual examination: Uterine origin → central and more apparent; entire mass moves up with cervical palpation (transmitted mobility). Ovarian origin → more apparent when palpating the sides (lateral), and there is a plane of separation between it and the uterus ^[9].

Condition	Key Features
Undiagnosed intrauterine pregnancy	Don't forget about pregnancy — especially for teenage girls ^[2]. A gravid uterus is soft, symmetrically enlarged, and the patient has amenorrhoea. Always do a urine pregnancy test (UPT) in any woman of reproductive age presenting with a pelvic mass or AUB. LMP history is critical
Molar pregnancy (hydatidiform mole)	Markedly elevated β-hCG, "snowstorm" appearance on USS, uterus large for dates, hyperemesis, possibly pre-eclampsia in first trimester
Ectopic pregnancy	Positive pregnancy test, adnexal mass/tenderness, PV bleeding, acute pain. Not a pelvic "mass" per se but must be excluded in acute presentations

Never Forget Pregnancy

Always exclude pregnancy first in any reproductive-age woman with a pelvic mass or abnormal bleeding. A simple urine pregnancy test takes 5 minutes and can be life-saving (e.g., ruptured ectopic). This is consistently emphasised in both lecture slides and clinical practice ^[2]^[9].

II. Non-Gynaecological Causes

Mesenteric cyst — rare, thin-walled cystic mass within the mesentery; typically mobile perpendicular to mesenteric axis
Colorectal tumour — especially a sigmoid/rectal tumour; may present with altered bowel habit, PR bleeding, weight loss. CEA may be elevated
Diverticular abscess / mass — history of diverticulitis, LIF pain, fever, leukocytosis. CT shows pericolic abscess
Hernia — inguinal or femoral hernia extending into pelvis; reducible on examination, cough impulse positive
Dilated bowel / faecal loading — constipated patients can have palpable faecal masses; AXR shows loaded colon. Distinguish by the "indentable" nature on palpation

Distended bladder — midline, smooth, dull to percussion, tender. Disappears after catheterisation. Always catheterise before assuming a mass is uterine!
Bladder diverticulum — can form a palpable mass; cystoscopy diagnostic
Pelvic kidney / transplanted kidney — important to remember in patients with unusual anatomy or post-renal transplant. USS/CT clarifies

Retroperitoneal sarcoma — usually not palpable ^[1] as these are deep; when large enough to be palpable, they are typically fixed and hard. CT/MRI diagnostic

Pseudocyst — related to previous surgeries ^[2]; lymphocele, seroma, or peritoneal inclusion cyst
Pelvic abscess — post-surgical, post-PID, or post-appendicitis. Tender, fluctuant, patient is febrile. CT shows rim-enhancing collection

When the presenting complaint is heavy menstrual bleeding rather than a pelvic mass, the DDx broadens. The PALM-COEIN classification (FIGO system) is the standard framework for AUB ^[5]:

Category	Structural (PALM)	Non-structural (COEIN)
P	Polyp (endometrial)	C — Coagulopathy (e.g., von Willebrand disease, platelet disorders)
A	Adenomyosis	O — Ovulatory dysfunction (e.g., PCOS, hypothyroidism, hyperprolactinaemia)
L	Leiomyoma (Fibroid)	E — Endometrial (primary endometrial disorder, e.g., chronic endometritis, AVM)
M	Malignancy and hyperplasia (endometrial cancer, sarcoma, cervical cancer)	I — Iatrogenic (e.g., anticoagulants, IUD, hormonal)
		N — Not yet classified

Key differentiators for the common structural DDx of AUB:

Feature	Fibroid	Adenomyosis	Endometrial Polyp	Endometrial Cancer
Typical age	30–50	35–50	Any; more common peri/postmenopausal	Postmenopausal (mostly)
Bleeding pattern	Regular, heavy periods	Heavy, painful periods	IMB, postmenstrual spotting, PMB	PMB, irregular bleeding
Dysmenorrhoea	Variable	Prominent, progressive	Uncommon	Uncommon
Uterine size	Enlarged, irregular	Enlarged, globular, boggy	Usually normal	Usually normal (or enlarged if advanced)
USS finding	Well-defined hypoechoic mass, pseudocapsule, vascular on Doppler ^[4]	Heterogeneous myometrium, poor JZ definition, myometrial cysts	Echogenic focal lesion within endometrium	Thickened endometrium, irregular
Diagnostic test	USS / MRI	MRI (gold standard)	Hysteroscopy + polypectomy	Endometrial biopsy (pipelle) or hysteroscopy

If a patient with a known fibroid presents with sudden onset of severe abdominal pain, the DDx includes ^[9]:

Degeneration of fibroid — outgrowing blood supply and becoming necrotic
- Red/haemorrhagic degeneration (especially during pregnancy)
- Other types of degeneration (hyaline, cystic)
Torsion/twisting of a pedunculated fibroid on its stalk — ischaemic pain, peritonism
Non-gynaecological causes must also be excluded:
- Acute appendicitis
- Renal colic (ureteric stone)
- Bowel obstruction
- Ruptured ovarian cyst / ovarian torsion (if concurrent adnexal pathology)

Two DDx for a Necrotic-Looking Fibroid

A very brown, necrotic fibroid has 2 DDx: (1) malignant — leiomyosarcoma; (2) benign — growth of fibroid faster than growth of blood supply (degeneration) ^[2]. Always consider sarcoma if the clinical picture is atypical (postmenopausal, rapid growth, systemic symptoms).

History and physical examination usually help to suggest a diagnosis ^[1]^[2].

Feature	Uterine Fibroid	Ovarian Cyst	Ovarian Cancer	Pregnancy
Menstrual history	Menorrhagia, regular cycles	Usually normal cycles	May have irregular bleeding	Amenorrhoea
Pressure symptoms	Frequency, constipation	Usually not unless large	Bloating, early satiety	Urinary frequency
Constitutional symptoms	Absent (unless anaemia)	Absent	Weight loss, fatigue, anorexia	Nausea/vomiting (1st trimester)
Abdominal examination	Mobile, irregular, firm mass	Mobile, cystic mass	Fixed, hard, ascites	Soft, symmetrical
Bimanual exam	Central, moves with cervix	Lateral, separate from uterus	Fixed to pelvis	Soft enlarged uterus
USS appearance	Solid, hypoechoic, pseudocapsule, vascular on Doppler	Unilocular, anechoic, smooth	Solid/mixed, papillary projections, multilocular, vascularity, free fluid	Gestational sac, fetal pole
Key investigation	USS / MRI	USS ± tumour markers	CA-125, CT staging, surgical biopsy	UPT, β-hCG, USS

This is a favourite exam question (both written and OSCE):

Feature	Uterine Mass (Fibroid)	Ovarian Mass
Position	Central / midline	Lateral
Relationship to uterus	Continuous with uterus; no plane of separation	Separate from uterus; palpable groove between mass and uterus
Cervical excitation	Entire mass moves when cervix is moved (transmitted mobility)	Mass does not move with cervical excitation
Consistency	Firm, irregular	Variable (cystic if benign cyst, solid/hard if malignancy)
Mobility	Mobile side to side	Mobile in all directions (if not fixed by adhesions or malignancy)

Broad ligament fibroid — can be lateral and mimic an adnexal mass. MRI helps by showing myometrial tissue continuous with the mass
Pedunculated subserosal fibroid (FIGO Type 7) — hangs off the uterus on a stalk; can be indistinguishable from a solid ovarian tumour on initial imaging. Doppler may show a feeding vessel from the uterine artery (the "bridging vessel sign")
Endometriosis with ovarian endometrioma — can cause a pelvic mass and dysmenorrhoea/AUB. Endometriosis also causes nodular deposits in the Pouch of Douglas ^[9], potentially mimicking ovarian cancer
Distended bladder — an embarrassingly common cause of a "pelvic mass." Always ask about last void and catheterise if in doubt

High Yield Summary — DDx of Uterine Fibroid

When presenting as a pelvic mass, the key DDx categories are:

Gynaecological: adenomyosis, ovarian cyst, ovarian cancer, undiagnosed pregnancy, molar pregnancy, uterine sarcoma, endometrial cancer
GI: colorectal tumour, diverticular abscess, mesenteric cyst, faecal loading
Urological: distended bladder, pelvic kidney
Retroperitoneal: sarcoma (usually not palpable)
Others: pseudocyst (post-surgical), pelvic abscess

When presenting as AUB, use PALM-COEIN: Polyp, Adenomyosis, Leiomyoma, Malignancy — Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not classified.

Clinical differentiation keys:

Fibroid: firm, irregular, central, moves with cervix, non-tender
Adenomyosis: globular, boggy, tender, less mobile
Ovarian cyst: lateral, cystic, separate from uterus, does not move with cervix
Ovarian cancer: fixed, hard, ascites, constitutional symptoms
Always exclude pregnancy (UPT) in reproductive-age women

Active Recall - Differential Diagnosis of Uterine Fibroid

References

^[1] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[2] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[4] Senior notes: Ryan Ho Radiology.pdf (p33 — Uterine mass, leiomyoma on USS) ^[5] Lecture slides: GC 112. Abnormal vaginal bleeding Gynaecological cancer.pdf ^[9] Lecture slides: Block C - O&G Theme Case 3.pdf (p3–5 — DDx of pelvic mass, clinical differentiation of fibroid vs adenomyosis vs ovarian pathology)

Diagnosis of Uterine Fibroid

Unlike many medical conditions, there are no formal consensus "diagnostic criteria" for uterine fibroids in the way that exist for, say, rheumatoid arthritis or SLE. The diagnosis of uterine fibroid is primarily a clinico-radiological diagnosis — made by correlating clinical features with imaging findings.

In the past, investigation for fibroid was based solely on clinical (examination). But now, patient expectation is higher so you have to use USG ^[2].

The diagnosis rests on:

Clinical suspicion — based on symptoms (HMB, pressure symptoms) and examination findings (firm, irregular, non-tender pelvic mass that moves with the cervix)
Imaging confirmation — pelvic ultrasound is commonly performed and is the first-line imaging modality ^[1]^[2]
Exclusion of differentials — particularly pregnancy, ovarian pathology, adenomyosis, and malignancy (endometrial cancer, leiomyosarcoma)
Histological confirmation — only obtained when the fibroid is surgically removed (myomectomy/hysterectomy specimen); pre-operative tissue diagnosis is not routinely performed because biopsy of a myometrial mass is impractical and carries risks

No Biopsy Needed for Most Fibroids

Unlike many tumours where tissue diagnosis is mandatory before treatment, fibroids are diagnosed by imaging and confirmed only after surgical excision. The reason: (1) USS/MRI have high sensitivity and specificity for typical fibroids; (2) a needle biopsy of a myometrial mass is technically difficult, may not be representative, and carries bleeding risk; (3) the distinction between fibroid and leiomyosarcoma cannot be reliably made by needle biopsy — the entire specimen is needed for assessment of mitotic rate, necrosis pattern, and atypia.

The diagnostic approach follows a logical sequence: Clinical assessment → Exclude pregnancy → First-line imaging → Further imaging if needed → Exclude co-pathology → Additional investigations for complications.

Investigation Modalities — Detailed

Step 1: Clinical Assessment

Menstrual history: cycle length, duration, volume (number of pads/tampons, flooding, clots), regularity — fibroids typically cause regular, heavy periods ^[9]
Pressure symptoms: urinary frequency, urgency, retention, constipation, tenesmus
Pain: dysmenorrhoea (also think adenomyosis), acute pain (degeneration, torsion)
Reproductive history: subfertility, recurrent miscarriage
Red flags for malignancy: postmenopausal bleeding, constitutional symptoms (weight loss, anorexia), rapid enlargement
Don't forget about pregnancy — especially for teenage girls ^[2]

Key examination findings were covered in the Clinical Features section. To summarise the diagnostic value:

Finding	Significance
Pallor	Due to menorrhagia caused by fibroid → iron deficiency anaemia ^[1]^[2]
Usually non-tender	Except for red degeneration (bleeding within the fibroid, can occur during pregnancy) ^[1]^[2]
Asymmetric/irregular enlargement	Typical of fibroid; if the uterus is globally enlarged symmetrically, may suggest adenomyosis instead ^[2]
Firm mass arising from pelvis, rubbery consistency	Classic fibroid feel ^[1]
Mass moved with the cervix	Confirms uterine origin; if you feel this upon digital examination, could be a cervical fibroid ^[1]^[2]
Special locations	Pedunculated/subserosal fibroids, fibroid polyps — hard to determine based on physical examination alone → imaging needed ^[2]

Bimanual Palpation — Uterine vs Ovarian Origin

Uterine origin → central and more apparent; entire mass moves up with palpation. Ovarian origin → more apparent when palpating the sides ^[9]. This distinction on bimanual exam is a fundamental clinical skill and frequent OSCE station.

Urine pregnancy test (UPT) — mandatory in every woman of reproductive age with a pelvic mass, AUB, or pelvic pain before any further investigation or treatment
Why? Because a gravid uterus can feel like a fibroid (soft, enlarged), and treating a pregnant uterus as a fibroid (e.g., attempting myomectomy) would be catastrophic
Serum β-hCG — if ectopic pregnancy is suspected or UPT is equivocal

Pelvic ultrasound is commonly performed ^[1]^[2] and is the first-line investigation for suspected uterine fibroid. It is widely available, non-invasive, inexpensive, and radiation-free.

Two approaches are used, often combined:

Modality	Technique	Advantages	Limitations
Transabdominal USS (TAS)	Probe placed on abdomen; requires a full bladder as acoustic window	Better for large masses that extend out of the pelvis; gives overview of pelvic/abdominal anatomy	Lower resolution; limited by body habitus (obesity)
Transvaginal USS (TVS)	Probe inserted into vagina; higher frequency, closer to target	Higher resolution for uterine detail; better for submucosal fibroids and endometrial assessment	Limited field of view; cannot visualise very large masses that extend above the pelvis

Typical USS Findings of a Fibroid ^[4]^[9]:

Feature	Description	Explanation
Well-defined, round/oval hypoechoic mass	Appears darker than surrounding myometrium with clear margins	Dense smooth muscle and collagen reflect sound differently from normal myometrium
Pseudocapsule	Thin echogenic rim surrounding the fibroid	Compressed normal myometrium and connective tissue forms a false capsule around the fibroid — important surgical landmark for myomectomy ^[9]
Posterior acoustic shadowing	Dark shadow behind the fibroid	Dense fibrous tissue attenuates the ultrasound beam, preventing passage to deeper structures — a hallmark of solid, collagenous lesions
Whorled internal echo pattern	Heterogeneous internal echoes in a swirled pattern	Corresponds to the interlacing bundles of smooth muscle and fibrous tissue
Very vascular on Doppler	Peripheral and intralesional blood flow on colour Doppler	Fibroids have a rich blood supply, predominantly from the uterine artery via peripheral feeding vessels ^[4]
Endometrial distortion	Submucosal fibroids indent or distort the endometrial echo (stripe)	Mass effect on the cavity — correlates with AUB and infertility
Calcification	Hyperechoic foci with dense posterior acoustic shadowing	Calcific degeneration of longstanding fibroids
Cystic areas	Anechoic spaces within the fibroid	Cystic or hyaline degeneration

A classic USS case: 50/F, menorrhagia with clots, referred by GP for USG. Transabdominal ultrasound: uterine mass noted, very vascular on Doppler. Impression: leiomyoma ^[4].

USS — Pseudocapsule is a Key Finding

The pseudocapsule on USS is a thin echogenic halo around the fibroid ^[9]. This is the compressed myometrium that the surgeon dissects along during myomectomy. Its presence on USS is a reassuring sign of a benign fibroid (leiomyosarcomas tend to have irregular, ill-defined margins without a true pseudocapsule).

Saline Infusion Sonohysterography (SIS)

Also called sonohysterogram or saline-infused sonography
Technique: sterile saline is infused through a catheter into the uterine cavity during TVS → the fluid distends the cavity and provides contrast, delineating intracavitary and submucosal lesions
Indications: better assessment of submucosal fibroids (FIGO Types 0–2), endometrial polyps, and endometrial cavity distortion
Particularly useful for pre-surgical planning of hysteroscopic myomectomy — to determine how much of the fibroid is intracavitary vs intramural
More sensitive than TVS alone for detecting submucosal fibroids

Step 4: Second-Line Imaging

MRI is not the first-line investigation (it is expensive and not always readily available), but it is the gold standard for:

Precise fibroid mapping — number, size, location (FIGO type) of every fibroid
Surgical planning — especially before myomectomy (deciding approach: hysteroscopic, laparoscopic, or open)
Differentiating fibroid from adenomyosis — MRI is superior to USS for this
Differentiating fibroid from leiomyosarcoma — though not 100% reliable
Pre-treatment assessment for HIFU and UAE — contrast-enhanced MRI is required to assess fibroid vascularity, necrosis, and suitability for these modalities ^[1]

Typical MRI Findings of a Fibroid:

Sequence	Appearance	Explanation
T1-weighted	Iso- to hypointense (similar to or darker than normal myometrium)	Dense fibrous tissue has low signal on T1
T2-weighted	Hypointense (dark) — this is the hallmark	Dense fibrous and smooth muscle tissue has very low water content → low T2 signal. This is in contrast to most other soft tissue tumours which are bright on T2
T2 — degenerated fibroid	Heterogeneous or hyperintense areas	Hyaline/cystic degeneration → increased water content → bright on T2; red degeneration → haemorrhagic areas with variable signal
Contrast-enhanced T1	Homogeneous enhancement (non-degenerated); poor/absent enhancement in degenerated areas	Enhancement reflects vascularity; non-enhancing areas suggest necrosis/degeneration

MRI — Red Flags for Leiomyosarcoma (as opposed to benign fibroid):

Irregular, ill-defined margins (no pseudocapsule)
Heterogeneous signal on T2 with areas of haemorrhage and necrosis
High T1 signal (haemorrhage) and high T2 signal (necrosis/oedema) — more heterogeneous than typical fibroid
Central unenhanced areas on contrast (necrosis)
Rapid growth on serial imaging
Restricted diffusion on DWI (high cellularity)
However: no single MRI feature reliably distinguishes fibroid from leiomyosarcoma — histology remains the definitive test

Not routinely used for fibroid diagnosis (USS and MRI are superior for soft tissue characterisation)
May be useful when:
- Evaluating a pelvic mass of uncertain origin (CT gives a broader view of abdominal/pelvic anatomy)
- Assessing for ureteric obstruction / hydronephrosis from large fibroids
- Incidental finding: calcified fibroid on CT performed for another indication
- Staging of suspected malignancy
CT findings: well-defined soft tissue mass with the same density as myometrium; calcification appears as dense foci ("popcorn" calcification)

Not a diagnostic tool for fibroids, but calcified fibroids may be seen incidentally as "popcorn" calcification in the pelvis on AXR ^[4]
Also relevant: the tooth-shaped radiodensity is not a fibroid — it's an ovarian teratoma (dermoid cyst) ^[4]

Step 5: Assess for Complications and Co-pathology

These investigations are not for diagnosing the fibroid itself, but for evaluating its impact and excluding co-existing pathology:

Test	Purpose	Expected Findings
CBC	Assess for anaemia related to menorrhagia ^[2]	Microcytic, hypochromic anaemia (low MCV, low MCH) from iron deficiency
Iron studies (ferritin, serum iron, TIBC, transferrin saturation)	Confirm iron deficiency	Low ferritin ( < 30 μg/L), low serum iron, high TIBC
Blood group and screen / crossmatch	Pre-operative preparation	Needed before myomectomy/hysterectomy (risk of significant blood loss)
RFT (renal function tests)	If large fibroid — assess for obstructive uropathy	Elevated creatinine/urea if bilateral ureteric obstruction
Coagulation screen	If AUB is severe or suspect coagulopathy	Usually normal in fibroid-related AUB; abnormal suggests coagulopathy (the "C" in PALM-COEIN)
TFTs	Exclude hypothyroidism as cause of AUB	Hypothyroidism can cause menorrhagia via anovulation
LDH	If suspecting leiomyosarcoma	May be elevated in sarcoma (non-specific)
β-hCG	Exclude pregnancy	Must be negative before any intervention
CA-125	If ovarian pathology cannot be excluded	Elevated in ovarian cancer; can also be mildly elevated in fibroids, adenomyosis, endometriosis (low specificity)

Endometrial sampling (pipelle biopsy) — indicated in women with AUB to exclude endometrial hyperplasia or cancer, especially if:
- Age ≥ 40 (or ≥ 35 with risk factors)
- Irregular bleeding (not just regular heavy menses)
- Postmenopausal bleeding
- Failed medical treatment
- Thickened endometrium on USS ( > 4 mm postmenopausal)
Why? Because fibroid and endometrial cancer can coexist, and HMB attributed to fibroids may actually be from co-existing endometrial pathology
Hysteroscopy — direct visualisation of the uterine cavity with a camera:
- Diagnostic: visualise submucosal fibroids, polyps, endometrial abnormalities
- Therapeutic: hysteroscopic myomectomy (resection of submucosal fibroids, FIGO 0–2), polypectomy, directed biopsy
- "See and treat" — the advantage of hysteroscopy over blind pipelle biopsy

When to Biopsy the Endometrium

Do not assume that HMB in a 45-year-old woman is "just fibroids." Endometrial cancer and endometrial hyperplasia must be excluded with endometrial sampling, especially in women with risk factors for endometrial cancer (obesity, unopposed oestrogen, nulliparity, PCOS, tamoxifen, Lynch syndrome) ^[5]. A fibroid and endometrial cancer can coexist.

Hysterosalpingogram (HSG) — visualises uterus and fallopian tubes under fluoroscopy ^[3]:
- Technique: water-soluble contrast injected into cervix under fluoroscopic guidance; movement of contrast up genital tract observed
- Indication: assess patency of fallopian tubes and uterine anatomy in infertility, recurrent abortions, following tubal surgery ^[3]
- Can show: filling defects from submucosal fibroids distorting the cavity; tubal obstruction near fibroid-distorted cornua
- Contraindicated in pregnancy ^[3]
- Patent fallopian tubes show free spill of contrast into the peritoneal cavity ^[3]
Saline infusion sonohysterography (SIS) — as described above; increasingly used as an alternative to HSG for cavity assessment
3D USS — provides a coronal view of the uterus (not possible with conventional 2D USS) → useful for mapping submucosal fibroids and assessing cavity distortion

Renal USS — to assess for hydronephrosis if a large fibroid (especially broad ligament or lateral wall) is suspected of compressing the ureter
IVU (intravenous urogram) — largely replaced by CT urogram but can show ureteric displacement/obstruction

Uterine artery embolisation (UAE) requires pre-procedural MRI with gadolinium contrast to:
- Confirm the fibroid is suitable for embolisation (not pedunculated — risk of detachment and peritonitis)
- Assess vascularity and degree of degeneration (poorly vascular fibroids respond poorly)
- Exclude adenomyosis (which can also be treated with UAE but outcomes differ)
- Exclude leiomyosarcoma (relative contraindication)
HIFU (High-Intensity Focused Ultrasound) — also requires contrast-enhanced MRI for selection:
- One dominant fibroid of less than 12 cm in diameter without significant areas of necrosis as judged by contrast-enhanced MRI ^[1]
- Non-pedunculated fibroid
- Fibroid not suspicious of malignancy ^[1]

Investigation	Purpose	Key Finding
UPT / β-hCG	Exclude pregnancy	Must be negative
Pelvic USS (TAS + TVS)	First-line imaging	Well-defined hypoechoic mass, pseudocapsule, vascular on Doppler, posterior shadowing
SIS (sonohysterogram)	Submucosal fibroid assessment	Intracavitary component delineated by saline
MRI Pelvis	Gold standard for fibroid mapping; pre-HIFU/UAE	T2-hypointense, well-defined; heterogeneous if degenerated
CT	Not routine; for uncertain masses or staging	Soft tissue mass ± calcification
AXR	Incidental finding	Popcorn calcification in pelvis
CBC + iron studies	Assess anaemia	Microcytic hypochromic anaemia, low ferritin
RFT	Obstructive uropathy	Elevated creatinine if ureteric obstruction
Endometrial sampling (pipelle)	Exclude endometrial cancer/hyperplasia	Histology: normal, hyperplasia, or malignancy
Hysteroscopy	Direct visualisation of uterine cavity	Submucosal fibroid, polyp; allows "see and treat"
HSG	Tubal patency + cavity assessment in infertility	Filling defect from submucosal fibroid; tubal patency
Renal USS	Hydronephrosis from ureteric compression	Dilated collecting system
CA-125	If ovarian pathology not excluded	Mildly elevated possible in fibroids; markedly elevated in ovarian Ca
LDH	Suspecting sarcoma	Elevated (non-specific)

While histology is not a diagnostic investigation (it is post-hoc), knowing the pathological features is important for understanding and exams:

Feature	Description
Gross	Whorl (whorled) appearance on cut section ^[9]; firm, well-circumscribed, white/grey
Microscopic	Interlacing bundles of uniform spindle-shaped smooth muscle cells; low mitotic rate ( < 5 mitoses per 10 HPF); no cellular atypia; no tumour cell necrosis
Leiomyosarcoma features (contrast)	≥ 10 mitoses per 10 HPF, moderate-to-severe atypia, coagulative tumour cell necrosis ("Stanford criteria" — need 2 of 3 features)

Typical internal gross appearance of bisected fibroid: whorl appearance ^[9]. This is a classic pathology viva/exam image.

High Yield Summary — Diagnosis of Uterine Fibroid

Diagnosis is clinico-radiological — no formal diagnostic criteria; clinical suspicion + imaging confirmation
Always exclude pregnancy first (UPT) in reproductive-age women
Pelvic USS (TAS + TVS) is the first-line imaging — look for hypoechoic mass, pseudocapsule, vascular on Doppler
MRI is the gold standard for fibroid mapping and surgical planning, and is required pre-HIFU and pre-UAE
SIS/hysteroscopy — for submucosal fibroid assessment and endometrial cavity evaluation
HSG — for tubal patency assessment in infertility workup
Always assess for anaemia (CBC + iron studies) — anaemia from HMB is extremely common
Endometrial sampling (pipelle/hysteroscopy) — mandatory in women ≥ 40, irregular bleeding, PMB, or risk factors for endometrial cancer; fibroid and endometrial cancer can coexist
No pre-operative biopsy is routine — histology is obtained from the surgical specimen
Red flags for leiomyosarcoma on MRI: heterogeneous signal, irregular margins, no pseudocapsule, restricted diffusion, rapid growth post-menopause
AXR: "popcorn" calcification — calcific degeneration of longstanding fibroid

Active Recall - Diagnosis of Uterine Fibroid

References

^[1] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[2] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[3] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p23 — Hysterosalpingogram; p85 — Transcatheter Embolization / UAE) ^[4] Senior notes: Ryan Ho Radiology.pdf (p33 — USS findings of leiomyoma; AXR calcification) ^[5] Lecture slides: GC 112. Abnormal vaginal bleeding Gynaecological cancer.pdf ^[9] Lecture slides: Block C - O&G Theme Case 3.pdf (p3–5 — clinical differentiation, USS findings, pathological specimen)

Management of Uterine Fibroid

Before diving into specific treatments, you need to understand the core philosophy that guides fibroid management:

Management will depend on the age, symptom, condition and wish of the patient ^[1]^[2].

This single sentence from the lecture slides captures everything. Unlike cancer management where you have relatively standardised protocols, fibroid management is highly individualised. The key decision-making factors are:

Is the patient symptomatic? — Asymptomatic fibroids can still be observed ^[2]. Even very large fibroids ("I have seen a fibroid up to the epigastric area", but if the patient is asymptomatic and it is her choice, observation is still fine) ^[2]
What are the dominant symptoms? — If menorrhagia alone, then medical treatment should be sufficient. But if there are pressure symptoms, then surgical removal may be better ^[2]
What is the patient's age and reproductive wish? — A 28-year-old wanting children requires a completely different approach from a 52-year-old nearing menopause
Fibroid characteristics — size, number, location (FIGO type), presence of degeneration
Patient preference — some patients wish to avoid surgery entirely; others want definitive treatment

Treatment principle is to rule out acute conditions first → since those can deteriorate quickly and threaten life ^[2].

Who is this for?

Asymptomatic fibroids — regardless of size ^[2]
Perimenopausal women with mild symptoms (fibroids will likely shrink after menopause as oestrogen declines)
Small fibroids discovered incidentally

What does it involve?

Reassurance and patient education
Serial USS monitoring every 6–12 months to track growth
Monitoring haemoglobin if any bleeding symptoms develop
Prompt reassessment if symptoms develop or fibroid grows rapidly (red flag for sarcoma post-menopausally)

Why does it work? Fibroids are benign, slow-growing, and oestrogen-dependent. After menopause, they shrink. Many women live with fibroids their entire reproductive lives without needing intervention. The risk of malignant transformation ( < 0.5%) is negligible.

Observation Even for Large Fibroids

Size alone is not an indication for treatment. A large asymptomatic fibroid reaching the epigastrium can still be observed if the patient is well-informed and chooses not to intervene ^[2]. However, you must ensure no complications are developing (e.g., ureteric obstruction → check RFT, renal USS).

II. Medical Treatment

Medical treatment primarily targets abnormal uterine bleeding (menorrhagia) and, to some extent, pain/dysmenorrhoea. Medical therapy does not significantly reduce fibroid size (except GnRH agonists/antagonists). It is therefore most useful when bleeding is the dominant complaint, not bulk/pressure symptoms.

Approach to fibroid can be conservative vs. surgical, based on what symptoms there are. E.g. menorrhagia alone, then medical treatment should be sufficient ^[2].

A. Symptomatic Relief [1]

Mechanism: Releases levonorgestrel (a potent progestogen) directly into the uterine cavity → causes endometrial atrophy (thinning of the endometrium) → less endometrium to shed → dramatically reduced menstrual blood loss (up to 90% reduction)
Indication: First-line treatment for HMB in women who do not want immediate fertility; works well for small-to-moderate fibroids
Duration: Licensed for 5 years; also provides contraception
Limitations:
- May be difficult to insert if the uterine cavity is significantly distorted by submucosal or large intramural fibroids
- Higher expulsion rate with submucosal fibroids (the fibroid can push it out)
- Does not shrink fibroids — only controls bleeding
- Not suitable if cavity is > 12 cm (device may not sit properly)
Why it works so well: The progestogen acts locally on the endometrium with minimal systemic absorption → maximal endometrial effect, minimal systemic side effects

Mechanism: Anti-fibrinolytic agent — inhibits plasminogen activation → prevents clot breakdown → clots persist longer over bleeding endometrial vessels → reduced blood loss
"Trans-" = across; "examic" from "aminocaproic" family — blocks the lysine-binding sites on plasminogen, preventing its conversion to plasmin
Dose: 1g TDS–QDS during menstruation only (not taken continuously)
Reduction: ~40–50% reduction in menstrual blood loss
Advantages: Non-hormonal; taken only during periods; can be combined with other therapies
Contraindications: History of thromboembolic disease (because anti-fibrinolytic → theoretically pro-thrombotic, though evidence for this is weak at standard doses)
Does not affect fibroid size or reduce pressure symptoms

Mechanism: Inhibit cyclooxygenase (COX) → reduced prostaglandin synthesis → reduced PGE2 (vasodilator) and PGI2 (anti-platelet) → relative ↑ in vasoconstriction and platelet aggregation → reduced blood loss. Also analgesic → helps with dysmenorrhoea
Dose: Mefenamic acid 500mg TDS during menstruation
Reduction: ~20–30% reduction in menstrual blood loss
Often used in combination with tranexamic acid
Does not shrink fibroids

Mechanism: COCP provides exogenous oestrogen + progestogen → suppresses endogenous HPO axis → thinner, more stable endometrium → lighter withdrawal bleeds. Cyclical progestogens (e.g., norethisterone, medroxyprogesterone) also stabilise the endometrium
Limitation: May theoretically promote fibroid growth due to the oestrogen component (though in practice, low-dose COCPs rarely cause significant fibroid enlargement). Not first-line for fibroid-related HMB but used in younger women who also need contraception
Cyclical norethisterone (5mg TDS, days 5–26) can regulate bleeding but is less effective than LNG-IUS

B. Agents That Shrink Fibroids (Pre-Operative / Short-Term)

These are generally used pre-operatively to shrink fibroids before surgery, making the operation technically easier and reducing blood loss. They are not used long-term (with one exception).

Mechanism: GnRH agonists initially stimulate the pituitary (flare effect), then cause downregulation of GnRH receptors → pituitary desensitisation → ↓FSH, ↓LH → profound ↓oestrogen (to postmenopausal levels / "medical castration") → fibroid shrinkage (up to 50% volume reduction over 3–6 months)
"GnRH agonist" = mimics GnRH but given continuously (the pituitary normally responds to pulsatile GnRH; continuous exposure paradoxically shuts it down)
Indications:
- Pre-operative — to shrink large fibroids before myomectomy or hysterectomy (makes surgery easier, reduces blood loss, may allow laparoscopic approach instead of open)
- To correct severe anaemia before surgery (cessation of menses allows Hb to recover)
- Bridge therapy for perimenopausal women (shrink fibroid until menopause occurs naturally)
Duration: Maximum 6 months continuous use
Side effects: Menopausal symptoms (hot flushes, vaginal dryness, mood changes, decreased libido), and critically — bone mineral density loss (because oestrogen is essential for bone metabolism). This is why they cannot be used long-term without "add-back therapy" (low-dose HRT to protect bones while still keeping oestrogen low enough to maintain fibroid shrinkage)
Limitation: Fibroids regrow rapidly after cessation → must proceed to surgery while on treatment, or transition to another therapy
Flare effect: Initial 2-week stimulation can worsen bleeding → may need to cover with progestogen or start mid-luteal phase

Mechanism: Directly block GnRH receptors on the pituitary → immediate suppression of FSH/LH (no flare effect!) → ↓oestrogen → fibroid shrinkage
Advantage over GnRH agonists: No initial flare, oral formulation available, can be combined with add-back therapy from the start
Relugolix combination therapy (Myfembree®): Relugolix 40mg + estradiol 1mg + norethindrone acetate 0.5mg — approved for long-term use (up to 2 years) because the add-back therapy mitigates bone loss and menopausal symptoms while maintaining fibroid control
This represents a newer approach (approved 2021–2023) that allows longer-term medical management of fibroids

Mechanism: Modulates the progesterone receptor → inhibits progesterone's mitogenic effect on fibroids → induces fibroid cell apoptosis + amenorrhoea (via endometrial effect) → fibroid shrinkage (comparable to GnRH agonists) WITHOUT causing hypoestrogenism (oestrogen levels remain in mid-follicular range → no hot flushes, no bone loss)
Advantage: Can achieve amenorrhoea (stops bleeding) AND shrink fibroid without menopausal symptoms
Limitation: SERIOUS SAFETY CONCERN — reports of severe liver injury (including cases requiring liver transplantation) led to EMA restriction in 2020. Currently restricted to pre-operative use in specific circumstances with mandatory liver function monitoring (LFTs before, during, and after treatment). Not available/recommended in many centres
Previously considered a game-changer but safety profile has limited its use

GnRH Agonist vs Antagonist vs SPRM

Feature	GnRH Agonist	GnRH Antagonist	SPRM (UPA)
Route	SC/IM injection (monthly/3-monthly)	Oral (newer) or SC	Oral
Onset	Delayed (2–4 weeks, after flare)	Immediate	Rapid
Flare	Yes	No	No
Oestrogen effect	Profound suppression	Partial suppression (with add-back)	Maintained mid-follicular
Bone loss	Yes (limits to 6 months)	Mitigated by add-back (up to 2 years)	Minimal
Fibroid shrinkage	~35–50%	~40%	~40%
Liver risk	Minimal	Minimal	Serious (rare)
Current status	Established; widely used pre-op	Increasingly first-line for long-term medical Rx	Restricted due to hepatotoxicity

III. Surgical Treatment

Surgical removal (myomectomy vs hysterectomy), approach (open / laparoscopic / vaginal / hysteroscopic) ^[1].

Surgery is indicated when:

Medical treatment fails or is not appropriate
Pressure/bulk symptoms (medical treatment does not help)
Subfertility attributed to fibroids
Suspicion of malignancy (leiomyosarcoma)
Patient preference for definitive treatment

A. Myomectomy — Uterus-Preserving Surgery

"Myo-" = muscle, "-ectomy" = surgical removal. Myomectomy removes the fibroid(s) while preserving the uterus.

Symptomatic fibroids in women who wish to preserve fertility or wish to retain their uterus
Submucosal fibroids causing HMB or infertility (hysteroscopic approach)
Failed medical treatment

Approach	Indication	Technique	Advantages	Limitations
Hysteroscopic myomectomy	Submucosal fibroids (FIGO 0, 1, 2)	Resectoscope inserted through cervix → fibroid shaved/resected under direct vision	No abdominal incision; outpatient/day case; rapid recovery; preserves uterus and fertility	Limited to submucosal fibroids ≤ 4–5 cm; Type 2 may require staged procedure; risk of fluid overload (glycine absorption), uterine perforation
Laparoscopic myomectomy	Subserosal or intramural fibroids, ≤ 3–4 fibroids, size ≤ 8–10 cm	Keyhole surgery; fibroid enucleated from pseudocapsule, uterine defect sutured laparoscopically, fibroid removed via morcellation or colpotomy	Minimally invasive; less pain, shorter hospital stay, faster recovery	Technically demanding; risk of morcellation spreading occult sarcoma (see below); limited by fibroid number/size
Open (abdominal) myomectomy	Large fibroids ( > 10 cm), multiple fibroids, deep intramural location	Laparotomy; fibroid(s) enucleated through uterine incision	Can handle any size/number; suturing of myometrium under direct vision → more secure closure (important for future pregnancy)	Major surgery; longer recovery (4–6 weeks); larger scar; more adhesion formation

Morcellation Controversy

Power morcellation (using a device to cut the fibroid into small pieces for extraction through a laparoscopic port) has been controversial since 2014 when the FDA issued a safety communication. The concern: if the "fibroid" is actually an occult leiomyosarcoma (which cannot be reliably excluded pre-operatively), morcellation will disseminate malignant tissue throughout the abdomen → upstaging and worsening prognosis. Current practice:

Contained morcellation (within a bag) is now preferred if morcellation is used
Informed consent must include discussion of this risk
Pre-operative MRI to assess for atypical features is recommended

Pseudocapsule is the surgical plane — the compressed myometrium around the fibroid provides a natural dissection plane. The surgeon incises the myometrium, identifies the pseudocapsule, and "shells out" the fibroid
GnRH agonist pre-treatment (3 months) can be given to shrink the fibroid and reduce vascularity → less intra-operative blood loss. However, it can obscure the pseudocapsule plane (fibroids become softer and harder to identify)
Recurrence: ~15–30% recurrence rate at 5 years (because myomectomy removes existing fibroids but does not address the underlying predisposition to form new ones)
Uterine rupture risk in future pregnancy: after myomectomy (especially open, with full-thickness myometrial incision), there is a small risk of uterine rupture during labour → elective caesarean section may be recommended (similar to the concept of a high segment uterine scar having 10% rupture risk for subsequent vaginal delivery ^[7])

B. Hysterectomy — Definitive Treatment

"Hyster-" (Greek hystera) = uterus, "-ectomy" = surgical removal. Hysterectomy removes the entire uterus and is the only treatment that guarantees no recurrence.

Symptomatic fibroids in women who have completed their family and desire definitive treatment
Failed medical treatment and myomectomy
Suspicion of malignancy
Very large/multiple fibroids making myomectomy impractical
Co-existing uterine pathology (e.g., adenomyosis, endometrial hyperplasia)

Type	What is removed	When to choose
Total hysterectomy	Uterus + cervix	Standard; most common. Cervix removed to eliminate risk of cervical stump cancer
Subtotal (supracervical) hysterectomy	Uterus only; cervix retained	May preserve pelvic floor support and sexual function (controversial); requires continued cervical screening
Total hysterectomy with BSO	Uterus + cervix + bilateral ovaries + tubes	If concurrent ovarian pathology, or as risk-reducing surgery (e.g., BRCA carriers); causes surgical menopause if premenopausal

Approach	Indication	Advantages
Vaginal hysterectomy	Smaller uterus (≤ 12-week size); uterine prolapse	No abdominal incision; fastest recovery; preferred route if feasible
Laparoscopic hysterectomy (TLH)	Moderate-sized uterus; no prolapse	Minimally invasive; good visualisation; shorter recovery than open
Abdominal (open) hysterectomy	Very large uterus; suspected malignancy; extensive adhesions	Handles any size; allows complete staging if cancer suspected

Definitive — no recurrence (obviously, since uterus is removed)
Irreversible — loss of fertility; significant psychological impact for some women
Ovaries: should be conserved in premenopausal women unless there is a specific indication for removal (e.g., endometriosis, BRCA mutation, concurrent ovarian pathology). Removing ovaries causes immediate surgical menopause with increased cardiovascular and osteoporosis risk
Decision between myomectomy and hysterectomy depends on the age, symptom, condition and wish of the patient ^[1]^[2]

IV. Other Modalities [1]

These are alternatives to surgery for women who wish to avoid an operation.

What it is: An interventional radiology procedure where the uterine arteries are selectively catheterised (via femoral artery puncture) and embolic agents (e.g., Gelfoam, PVA particles, coil, glue) are injected to occlude the blood supply to the fibroids ^[3]
"Embol-" = plug/block; "-isation" = the process of blocking
Mechanism: Fibroids have a disproportionately high blood supply relative to normal myometrium. Embolisation preferentially infarcts the fibroids (which depend on end-artery supply) while normal myometrium recovers via collateral circulation → fibroids undergo ischaemic necrosis and shrink (40–70% volume reduction over 6 months)
Advantages:
- Minimally invasive — percutaneous (small groin puncture), LA/conscious sedation, no abdominal incision ^[3]
- Suitable for patients who may not be suitable for surgery ^[3]
- ↓hospital stay + faster recovery ^[3]
- Preserves the uterus
- Can treat multiple fibroids simultaneously
Indications:
- Symptomatic fibroids (HMB and/or bulk symptoms) in women who wish to avoid surgery
- Women who are poor surgical candidates (significant comorbidities)
- Failed medical treatment
Contraindications:
- Pregnancy or desire for future fertility (effects on fertility and pregnancy outcomes are uncertain; UAE may damage ovarian reserve, especially in women > 40, due to non-target embolisation of ovarian vessels)
- Active pelvic infection (risk of infected fibroid → abscess)
- Pedunculated subserosal fibroid (risk of fibroid detachment post-embolisation → free intraperitoneal body → peritonitis)
- Pedunculated submucosal fibroid (risk of infarcted fibroid detaching into cavity → expulsion, infection)
- Known or suspected malignancy (leiomyosarcoma)
- Severe contrast allergy or renal impairment (contrast used for angiography)
Complications: Post-embolisation syndrome (pain, fever, nausea — occurs in most patients for 1–2 weeks; managed with analgesia); infection/abscess; premature ovarian failure (especially > 45 years); fibroid expulsion (submucosal); failure requiring subsequent surgery (~15–20%)

Uterine fibroid embolisation and uterine artery embolisation (UAE) for post-partum haemorrhage are both clinical indications for transcatheter embolisation, but they are different procedures with different contexts ^[3].

What it is: A non-invasive procedure where focused ultrasound waves (guided by either MRI or USS) are directed at the fibroid → thermal ablation (heating to > 55°C) → coagulative necrosis of fibroid tissue → fibroid shrinks
Think of it as using a magnifying glass to focus sunlight — except with ultrasound energy focused on the fibroid
Two modalities:
- MRgFUS (MRI-guided Focused Ultrasound Surgery) — uses MRI for real-time temperature monitoring and targeting. More precise but more expensive and time-consuming
- USgHIFU (Ultrasound-guided HIFU) — uses USS for guidance. Faster, more widely available (especially in Asia/China), less expensive
Advantages: Completely non-invasive (no incision, no puncture); outpatient; preserves uterus; rapid recovery (return to work within 1–2 days)
Selection criteria (as assessed by contrast-enhanced MRI) ^[1]:
- One dominant fibroid of less than 12 cm in diameter
- Without significant areas of necrosis (non-enhancing fibroid does not absorb ultrasound energy effectively)
- Non-pedunculated fibroid (pedunculated fibroids may detach after treatment)
- Fibroid not suspicious of malignancy ^[1]
- Fibroid should be accessible (not obscured by bowel or behind a surgical scar that could cause skin burn)
- T2 signal intensity matters: T2-dark fibroids (dense, fibrous) respond better to HIFU than T2-bright fibroids (degenerated, high water content — absorb less energy)
Limitations: Not suitable for multiple large fibroids; recurrence possible (~20% may need re-treatment); limited availability in some centres; treatment time can be long (several hours per session)

Technique	Principle	Status
Radiofrequency ablation (RFA) — e.g., Acessa®	Laparoscopic or transcervical insertion of a radiofrequency probe into the fibroid → thermal destruction	Emerging; FDA-approved; limited data on long-term outcomes and fertility
Microwave ablation	Similar to RFA but uses microwave energy	Used in some centres in Asia
Laparoscopic uterine artery occlusion	Surgical clipping/coagulation of uterine arteries laparoscopically	Alternative to UAE but requires GA; limited adoption

V. Management of Specific Clinical Scenarios

Most fibroids do not cause problems during pregnancy
Red degeneration (2nd trimester): conservative management — rest, analgesia (paracetamol), hydration. Surgery is almost never needed ^[2]
Fibroids at lower uterine segment: may cause malpresentation or obstruct labour → planned caesarean section
Myomectomy during pregnancy: generally avoided (high risk of bleeding), unless there is torsion of a pedunculated fibroid causing acute abdomen
Myomectomy at caesarean section: traditionally avoided (increased bleeding risk), but selective removal of pedunculated fibroids during CS is increasingly practiced in experienced hands
Fibroid is a risk factor for PPH (abnormal myometrium → uterine atony) ^[7] → active management of third stage of labour; be prepared with uterotonics and blood products

Assess whether the fibroid is the sole or contributing factor for infertility (it is the sole cause in only ~2–3%)
Submucosal fibroids (FIGO 0–2): hysteroscopic myomectomy is recommended — evidence shows improved pregnancy rates after resection
Intramural fibroids ≥ 4 cm distorting the cavity: consider myomectomy, though evidence is less clear
Subserosal fibroids: generally do not affect fertility → usually no intervention needed
GnRH agonist: can be used pre-operatively to shrink fibroids before myomectomy in the infertility context, but should not delay fertility treatment unduly (GnRH agonist suppresses ovulation → cannot conceive while on treatment)
UAE and HIFU: generally not recommended for women desiring pregnancy (uncertain effects on uterine integrity and ovarian reserve)

If symptoms are manageable → expectant management with medical treatment (LNG-IUS, tranexamic acid) until menopause, when fibroids will shrink naturally
GnRH agonist can be used as a bridge to menopause — shrink fibroid and control symptoms until natural oestrogen decline takes over
Avoids the need for surgery in many perimenopausal women

Scenario	Management
Severe acute menorrhagia with haemodynamic instability	Resuscitation (large bore IV access, crystalloid, blood transfusion if needed) ^[10]; high-dose IV tranexamic acid; IV conjugated oestrogen (stops acute bleeding); emergency hysteroscopic/surgical intervention if unresponsive
Red degeneration	Conservative: rest, analgesia, hydration
Torsion of pedunculated fibroid	Surgical excision (laparoscopic or open)
Acute urinary retention	Catheterisation; definitive management of fibroid

Patient Profile	First-Line Treatment	Alternatives
Asymptomatic	Observation	—
HMB only, small fibroids, fertility not desired	LNG-IUS (Mirena) / Tranexamic acid / NSAIDs	COCP; GnRH antagonist
HMB from submucosal fibroid	Hysteroscopic myomectomy	LNG-IUS if Type 2 with small intracavitary component
Bulk/pressure symptoms, fertility desired	Myomectomy (open or laparoscopic)	GnRH agonist pre-op to shrink
Bulk/pressure symptoms, family complete	Hysterectomy	UAE; HIFU
Fertility desired, submucosal fibroid	Hysteroscopic myomectomy	—
Fertility desired, intramural/subserosal	Open/laparoscopic myomectomy	GnRH agonist pre-op
Perimenopausal, mild symptoms	Medical Rx + expectant (bridge to menopause)	GnRH agonist bridge
Wishes to avoid surgery, not suitable for surgery	UAE	HIFU
Suspected malignancy	Total hysterectomy + BSO (via laparotomy)	—

High Yield Summary — Management of Uterine Fibroid

Management depends on age, symptoms, condition, and patient wish — highly individualised
Asymptomatic fibroids → observation regardless of size
Menorrhagia alone → first try medical treatment: LNG-IUS (Mirena) is first-line; tranexamic acid, NSAIDs, COCP as adjuncts
Pressure/bulk symptoms → surgical or procedural treatment (medical Rx does not help bulk symptoms)
GnRH agonists shrink fibroids (up to 50%) but limited to 6 months (bone loss). Used pre-operatively
GnRH antagonists (relugolix combination) — newer, oral, no flare, can be used longer-term with add-back therapy
Surgical removal: myomectomy vs hysterectomy; approach: open / laparoscopic / vaginal / hysteroscopic ^[1]
Myomectomy preserves uterus and fertility; 15–30% recurrence rate
Hysterectomy is definitive (no recurrence); only for completed family or suspected malignancy
Other modalities: UAE and HIFU ^[1] — non-surgical uterus-preserving options
UAE: embolic agents occlude uterine artery → fibroid ischaemia/shrinkage; CI: fertility desired, pedunculated, suspected malignancy
HIFU: thermal ablation; requires contrast-enhanced MRI for selection (one dominant fibroid < 12 cm, non-pedunculated, no necrosis, not suspicious of malignancy) ^[1]
Fibroids in pregnancy → conservative for red degeneration; fibroids are a risk factor for PPH ^[7]
Power morcellation carries risk of disseminating occult sarcoma → use contained morcellation and inform patient

Active Recall - Management of Uterine Fibroid

References

^[1] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[2] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[3] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p78, p85 — Interventional Radiology; Transcatheter Embolization including uterine fibroid embolisation and UAE) ^[7] Lecture slides: Block C - Postpartum Haemorrhage.pdf (p5 — fibroid as risk factor for PPH due to abnormal myometrium) ^[10] Senior notes: Ryan Ho Critical Care.pdf (p21 — Management of hypovolemic shock including uterine haemorrhage)

Complications of Uterine Fibroid

Complications of uterine fibroids can be organised into two major categories: (A) complications of the fibroid itself (disease-related) and (B) complications of treatment (iatrogenic). Understanding these from first principles — why each complication occurs — is far more useful than memorising a list.

These arise from the natural behaviour of the fibroid: its growth, its location, its hormonal responsiveness, and the fact that it can outgrow its blood supply.

Anaemia related to menorrhagia ^[2] — this is the most common complication of symptomatic fibroids
Why? Chronic heavy menstrual bleeding (HMB) depletes iron stores faster than dietary intake can replenish them → negative iron balance → depleted ferritin → microcytic hypochromic anaemia
Iron is essential for haemoglobin synthesis (each haem group requires one iron atom). When stores are exhausted, the bone marrow produces RBCs with less haemoglobin and smaller volume (microcytic, hypochromic)
Can be severe — Hb < 7 g/dL is not uncommon in women who normalise heavy bleeding ("I've always had heavy periods") and only present when symptomatic with fatigue, dyspnoea on exertion, palpitations, dizziness
Manifestations on exam: pallor ^[11], koilonychia, angular stomatitis, glossitis, tachycardia, flow murmur
Management: oral iron supplementation (ferrous sulphate 300 mg TDS × 6 months if Hb < 10 g/dL ^[11]); treat the underlying fibroid to stop ongoing blood loss; IV iron infusion if oral iron not tolerated or rapid correction needed pre-operatively; blood transfusion if haemodynamically significant

Degeneration occurs when the fibroid outgrows its blood supply — the tumour mass increases but its vasculature cannot keep up, leading to ischaemia and necrosis of central regions. Think of it like a city growing too fast for its infrastructure.

Degeneration: breakdown of fibroid tissue due to outgrowth of blood supply ^[11].

Type	Pathophysiology	Clinical Features
Hyaline degeneration	Most common (60%); gradual loss of blood supply → asymptomatic softening and liquefaction when the fibroid gradually outgrows its blood supply ^[11]	Usually asymptomatic; fibroid becomes softer on exam; may mimic cystic mass on USS
Cystic degeneration	Progression of hyaline degeneration to central necrosis → formation of a cystic space in centre → later may have calcification ^[11]	Cystic appearance on USS may mimic ovarian cyst; usually asymptomatic
Calcific degeneration	Calcium deposition in longstanding fibroids with poor perfusion, especially post-menopause	"Popcorn" calcification on AXR/CT; usually asymptomatic
Red (carneous) degeneration	Haemorrhage into fibroid and necrosis; occurs in mid-2nd trimester when there is an acute disruption of blood supply during active growth ^[11]. The rapid uterine enlargement in pregnancy redirects blood away from the fibroid. Venous thrombosis at the fibroid periphery → haemorrhagic infarction → the cut surface appears red/beefy	Acute pelvic pain, low-grade fever, ↑WBC, tender uterus ^[11]. Dx: pain when USS probe is directly over fibroid; contrast MRI pelvis for characteristic loss of contrast in degenerating fibroid ^[11]. Mx: Panadol or other analgesics (note NSAIDs C/I for > 32 weeks) ^[11]
Sarcomatous change (leiomyosarcoma)	Can occur but only in < 1/200 cases ^[11]. Now thought to arise de novo rather than from true transformation of a benign fibroid (genetically and histologically distinct entities) ^[12]	Should be suspected in post-menopausal women with rapid ↑size of fibroid ^[11]. May present with pain, PMB, rapidly growing mass. Diagnosis is post-operative (histological)

Red Degeneration — Exam Favourite

A pregnant woman in the 2nd trimester with a known fibroid presenting with acute localised uterine pain, low-grade fever, and leukocytosis — the diagnosis is red degeneration until proven otherwise. Management is conservative (analgesia, rest). Surgery is almost never needed. Remember: NSAIDs are contraindicated after 32 weeks (risk of premature closure of the ductus arteriosus and oligohydramnios) ^[11].

Large fibroids exert mass effect on adjacent pelvic organs. The complication depends on which structure is compressed:

Structure Compressed	Complication	Mechanism
Bladder (anterior)	Urinary frequency (most common pressure symptom); urgency; nocturia	Reduced bladder capacity due to extrinsic compression → bladder fills to smaller volume before stretch receptors trigger urge to void
Urethra / bladder neck	Acute urinary retention (AROU)	Classically a 12-week uterus with a cervical fibroid or a posterior fibroid pushing onto a retroverted uterus → kinking of urethra ^[11]^[6]. Mechanical obstruction of urethral outflow
Ureter (lateral)	Hydroureter → hydronephrosis → obstructive uropathy	Broad ligament or lateral wall fibroids compress the ureter at the pelvic brim. If bilateral or in a solitary kidney → renal failure. Often silent ("silent kidneys") until renal function deteriorates
Rectum (posterior)	Constipation, tenesmus	Extrinsic compression reduces rectal lumen → impaired passage of stool; sensation of incomplete evacuation
Inferior vena cava / iliac veins	Venous compression → ↑risk of VTE (DVT/PE); lower limb oedema	Very large uteri may compress vena cava → ↑risk of VTE ^[11]. Venous stasis (one of Virchow's triad) from extrinsic compression of major pelvic veins

Silent Hydronephrosis

Ureteric obstruction from fibroids can be bilateral and painless (unlike ureteric colic from stones which is acute and unilateral). This means the patient can develop significant renal impairment without knowing. Always check RFT and consider renal USS in patients with large fibroids, especially those situated laterally or in the broad ligament.

Pregnancy-related complications of fibroids are clinically important and are frequently examined:

Complication	Mechanism	Clinical Significance
Red degeneration	Rapid growth during pregnancy outgrows blood supply → haemorrhagic infarction ^[11]	Acute pain in 2nd trimester; managed conservatively
Miscarriage and preterm labour	Adverse effect by submucosal fibroids on implantation, placentation and increase in uterine contractility ^[11]	Higher miscarriage rate with submucosal fibroids
Malpresentation and obstructed labour	Distortion of shape of birth canal ^[11]; lower segment fibroids physically block fetal descent	May necessitate caesarean section
Difficult caesarean section	May be difficult when fibroid is located in lower uterine segment ^[11]	Increased blood loss; difficulty accessing the lower segment
Postpartum haemorrhage (PPH)	↑risk by ↓force and coordination of uterine contractions → ↑risk of atony ^[7]^[11]	PPH is the leading cause of maternal mortality worldwide; fibroid is a recognised risk factor under "Tone" (the 4 T's)
Infertility	Association is controversial but appears to be ↑in those distorting the cavity ^[11]. Submucosal fibroids impair implantation; intramural fibroids near ostia can obstruct tubes	Fibroid is the sole cause of infertility in only ~2–3% of cases
Large SFH	Fibroid adds to uterine bulk → large SFH on obstetric examination ^[13]	Must differentiate from other causes (macrosomia, polyhydramnios, multiple pregnancy)

Why? A pedunculated fibroid (subserosal Type 7, or submucosal Type 0) hangs from the uterus on a stalk (pedicle). Movement or gravity can cause the pedicle to twist → occlusion of the feeding blood vessels → ischaemic infarction → acute pain
Torsion of pedunculated fibroid: associated with acute pain ± fever ^[11]
Management: Surgical excision (laparoscopic or open) is usually required — unlike red degeneration, torsion does not resolve with conservative management

A pedunculated submucosal fibroid (Type 0) can elongate and prolapse through the cervical os into the vagina → a fibroid polyp
Fibroid polyp ± prolapse: due to uterine contractions in attempt to expel the fibroid polyp ^[11]
The uterus recognises the intracavitary mass as "foreign" and contracts rhythmically to try to push it out — similar to labour contractions
Clinical features: profuse bleeding if fibroid polyp protrudes through cervix ^[11]; cramping lower abdominal pain; visible mass at the introitus or on speculum exam
Management: Hysteroscopic resection; if prolapsed, may be amenable to vaginal removal (twist and cut the pedicle under anaesthesia)

Meigs syndrome classically refers to the triad of ascites, pleural effusion, and benign ovarian tumour (fibroma/thecoma). When a fibroid causes the same triad, it is technically called pseudo-Meigs syndrome ^[2]
Why does this happen? Large fibroids (especially subserosal) can irritate the peritoneum → transudative ascites → sympathetic right-sided pleural effusion (fluid tracks through diaphragmatic lymphatics)
Important diagnostic criteria is that Meigs syndrome resolves after the resection of the tumour ^[2]

Rare paraneoplastic complication — some fibroids produce erythropoietin (EPO) → stimulates bone marrow to produce excess RBCs → secondary erythrocytosis ^[8]
Listed alongside RCC, HCC, cerebellar haemangioblastoma as a cause of inappropriate EPO production ^[8]
Resolves after fibroid removal

B. Complications of Treatment (Iatrogenic)

Complication	Mechanism	Frequency
Haemorrhage	Myometrium is highly vascular; enucleation of fibroid disrupts feeding vessels	Significant; may require transfusion; vasopressin injection and misoprostol pre-op help reduce blood loss ^[11]
Conversion to hysterectomy	Uncontrollable bleeding or unexpected findings	1–2% ^[11]
Adhesion formation	Peritoneal injury and inflammation from surgery → fibrinous adhesions form during healing	Adhesions affecting fertility ^[11]; particularly after open myomectomy. Anti-adhesion barriers can be used
Recurrence	Myomectomy removes existing fibroids but does not address the underlying predisposition to form new ones	30% require surgery for recurrence in 10 years ^[11]
Uterine rupture in subsequent pregnancy	Full-thickness myometrial incision weakens the wall; during labour, the scar may fail under the pressure of contractions	Uterine scarring requiring C/S if cavity entered ^[11]; risk higher with deep intramural and posterior wall myomectomy
Uterine perforation	During hysteroscopic myomectomy, the resectoscope can perforate the uterine wall	More common with deep intramural component (FIGO Type 2); requires laparoscopy to assess damage
Fluid overload / hyponatraemia	Hysteroscopic myomectomy uses glycine or saline for uterine distension; excessive absorption → dilutional hyponatraemia	Manifest as nausea, confusion, seizures; prevented by monitoring fluid deficit (limit to < 1000–1500 mL)

Complication	Mechanism
Bleeding / haematoma	Vascular pedicles; pelvic vascularity
Ureteric injury	The ureter runs 1–2 cm lateral to the cervix ("water under the bridge" — ureter passes under the uterine artery). During hysterectomy, the ureter can be ligated, kinked, or transected
Bladder injury	Bladder sits anterior to the cervix; dissection of the vesicouterine fold can damage the bladder dome
Bowel injury	Particularly if adhesions from previous surgery or endometriosis
Vault prolapse	Loss of uterine support → weakening of pelvic floor → vaginal vault descends post-hysterectomy ^[11]
Primary ovarian insufficiency	For 2–4 years due to disruption of blood supply ^[11] — the ovarian blood supply partly comes from the uterine artery via the tubo-ovarian anastomosis; hysterectomy may compromise this even if ovaries are conserved
Wound infection / VTE	Standard surgical complications
Psychological impact	Loss of fertility; body image; sense of femininity — important to counsel pre-operatively

3. Complications of Uterine Artery Embolisation (UAE) [11]

Complication	Details
Anaesthetic and contrast-related complications	< 0.7% ^[11]
Access-related	Groin haematoma, arterial thrombosis, pseudoaneurysm ^[11] — from femoral artery puncture
Pelvic pain	Almost universal but usually resolves in 14–17 days ^[11] — due to ischaemia and necrosis of fibroid tissue
Vaginal discharge	60%; can last for months but usually self-limiting unless febrile or purulent → evaluate for pelvic infections ^[11]
Post-embolisation syndrome	< 40%; fever, nausea, pain, malaise, leukocytosis ^[11] — inflammatory response to fibroid necrosis. Managed with analgesia, anti-emetics, and hydration. Self-limiting (1–2 weeks)
Vaginal expulsion of fibroid/fibroid tissue	10%; usually managed expectantly but may need D&C or hysteroscopic removal ^[11] — submucosal fibroids that undergo necrosis can detach and be expelled through the cervix

Complication	Details
Amenorrhoea	2% if < 45 years, 8% if > 45 years; may be due to ovarian insufficiency or endometrial atrophy ^[11]. Non-target embolisation of ovarian artery branches → premature ovarian failure. This is why UAE is generally not recommended for women desiring future fertility
Pelvic inflammatory disease	< 2%; may require IV antibiotics or even hysterectomy ^[11] — infected necrotic fibroid acts as a nidus for infection
Recurrence of symptoms requiring intervention	25% if < 40 years, 10% if 40–50 years ^[11] — incomplete fibroid infarction or growth of new fibroids

UAE — Amenorrhoea Risk Increases with Age

Amenorrhoea after UAE occurs in 2% of women under 45 but 8% of women over 45 ^[11]. This is because older women have a smaller ovarian reserve to begin with, and any non-target embolisation of the ovarian vessels causes disproportionate damage. This is a critical counselling point when discussing UAE with women in their 40s who still desire fertility.

Skin burns — if the ultrasound beam path traverses a surgical scar (scars absorb more energy) or if the fibroid is too superficial
Bowel injury — if bowel loops interpose between the transducer and the fibroid
Sciatic nerve injury — if the fibroid is close to the sacrum and heat dissipates posteriorly
Incomplete treatment — T2-bright (degenerated) fibroids absorb energy poorly → inadequate necrosis → recurrence
Generally very safe with a low complication rate compared to surgery

Risk of disseminating occult leiomyosarcoma — if the "fibroid" is actually a sarcoma (cannot be reliably excluded pre-operatively), cutting it into pieces and distributing fragments throughout the abdomen upstages the cancer and dramatically worsens prognosis
This led to the 2014 FDA safety communication and the shift toward contained morcellation (within a specimen retrieval bag)

Category	Complications
Haematological	Iron deficiency anaemia; secondary erythrocytosis (rare)
Degenerative	Hyaline, cystic, calcific, red (carneous), sarcomatous change
Pressure/Compression	Urinary frequency, AROU, hydroureter/hydronephrosis, constipation, VTE
Obstetric	Red degeneration, miscarriage, preterm labour, malpresentation, obstructed labour, difficult CS, PPH, infertility
Mechanical	Torsion of pedunculated fibroid; prolapse of fibroid polyp
Systemic (rare)	Pseudo-Meigs syndrome; secondary erythrocytosis
Post-myomectomy	Haemorrhage, adhesions, recurrence (30% at 10y), uterine rupture in pregnancy, conversion to hysterectomy (1–2%)
Post-hysterectomy	Vault prolapse, ureteric/bladder/bowel injury, ovarian insufficiency (2–4y), VTE
Post-UAE	Post-embolisation syndrome, pelvic pain, vaginal discharge, fibroid expulsion (10%), amenorrhoea (2–8%), PID, recurrence
Post-HIFU	Skin burns, bowel/nerve injury, incomplete treatment
Morcellation	Dissemination of occult sarcoma

High Yield Summary — Complications of Uterine Fibroid

Iron deficiency anaemia is the most common complication — from chronic HMB
Degeneration — red degeneration in pregnancy (2nd trimester); manage conservatively with analgesia; NSAIDs C/I after 32 weeks
Sarcomatous change ( < 1/200 cases) — suspect in postmenopausal rapid growth; leiomyosarcoma is genetically distinct from fibroid
Pressure complications — urinary frequency (anterior), AROU (cervical fibroid), hydronephrosis (lateral), constipation (posterior), VTE (IVC compression)
Obstetric complications — red degeneration, miscarriage, malpresentation, obstructed labour, difficult CS, PPH from uterine atony
Torsion of pedunculated fibroid → acute pain, requires surgical excision
Fibroid polyp prolapse through cervix → profuse bleeding, cramping pain
Pseudo-Meigs syndrome — ascites + pleural effusion + fibroid; resolves after resection
Myomectomy complications — haemorrhage, adhesions (affect fertility), 30% recurrence at 10y, uterine rupture in future pregnancy, 1–2% conversion to hysterectomy
UAE complications — post-embolisation syndrome (fever/pain/nausea), fibroid expulsion (10%), amenorrhoea (2% < 45y, 8% > 45y), PID ( < 2%), recurrence (25% if < 40y)

Active Recall - Complications of Uterine Fibroid

References

^[2] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[6] Senior notes: Ryan Ho Urogenital.pdf (p164 — gynaecological tumours e.g. fibroid as cause of female AROU) ^[7] Lecture slides: Block C - Postpartum Haemorrhage.pdf (p5 — fibroid as risk factor for PPH due to abnormal myometrium) ^[8] Senior notes: Maksim Medicine Notes.pdf (p170 — uterine fibroma as cause of inappropriate EPO production / secondary erythrocytosis) ^[11] Senior notes: Adrian Lui Gynecology Notes.pdf (p89–94 — fibroid clinical features, degeneration, complications, treatment complications including myomectomy, hysterectomy, and UAE) ^[12] Senior notes: Adrian Lui Gynecology Notes.pdf (p105 — uterine sarcoma; leiomyosarcoma is genetically distinct from leiomyoma) ^[13] Senior notes: Ryan Ho Fundamentals.pdf (p191 — large SFH causes including fibroid)

High Yield Summary

Definition: Leiomyoma — benign monoclonal smooth muscle tumour of myometrium ("fibroid" = firm fibrous cut surface).

Epidemiology: Most common pelvic tumour in women; up to 70–80% by age 50; symptomatic ~25–30%; peak 30–50 years; shrink post-menopause.

Oestrogen/progesterone dependent: grow after menarche, in pregnancy, with obesity/HRT; shrink with menopause/GnRH agonists.

Risk factors ↑: nulliparity, early menarche, obesity, African ethnicity (2–3×), family history, tamoxifen.

FIGO location (determines symptoms):

Submucosal (0–2): HMB, subfertility — worst for bleeding/fertility
Intramural (3–4): HMB, bulk symptoms
Subserosal (5–7): pressure; pedunculated → torsion
Cervical (8): urinary retention (kink urethra)

Exam: Firm, irregular, non-tender mass; moves with cervix; very vascular on Doppler. Contrast adenomyosis: diffuse boggy uterus.

Malignant transformation: < 0.1–0.5% — leiomyosarcoma usually de novo; suspect if postmenopausal rapid growth.

High Yield Summary — Differential Diagnosis

Pelvic mass DDx: fibroid vs adenomyosis (boggy, hormonal Rx works) vs ovarian mass (separate from uterus) vs pregnancy vs uterine sarcoma/endometrial cancer.

AUB DDx (if presenting with bleeding): structural (PALM) — fibroid, polyp, adenomyosis; non-structural (COEIN) — coagulopathy, ovulatory dysfunction, endometrial, iatrogenic, not classified.

Fibroid vs adenomyosis (exam favourite):

	Fibroid	Adenomyosis
Uterus	Irregular, firm lumps	Diffuse, boggy
HMB	Common	Common
Hormonal Rx	Ineffective	Effective
Surgery	Myomectomy (pseudocapsule)	Hysterectomy (no plane)

Red flags: postmenopausal enlargement, PMB, rapid growth → exclude leiomyosarcoma and endometrial cancer (pipelle if AUB).

High Yield Summary — Diagnosis

Clinico-radiological diagnosis — no routine pre-op biopsy (cannot reliably distinguish fibroid vs sarcoma on needle biopsy).

Algorithm: history/exam → pregnancy test → pelvic USS (TAS ± TVS) → MRI if atypical → assess complications.

USS features: well-defined hypoechoic myometrial mass, pseudocapsule, very vascular on Doppler, shadowing (calcification).

MRI: gold standard for mapping before myomectomy/UAE; T2-hypointense well-defined mass.

Additional tests:

CBC/ferritin — anaemia from HMB
RFT/renal USS — if large fibroid (?ureteric obstruction)
Endometrial assessment (pipelle/hysteroscopy) if AUB >45 or risk factors
HSG/SIS if subfertility (cavity distortion)

High Yield Summary — Management

Principle: Age + symptoms + fibroid characteristics + patient wish.

Asymptomatic: observe — even large fibroids if patient chooses; serial USS 6–12 months.

HMB alone (no bulk symptoms): medical first — LNG-IUS (Mirena), tranexamic acid, NSAIDs, COCP/progestogens.

Pressure/bulk symptoms or failed medical Rx:

Fertility desired → myomectomy (hysteroscopic for submucosal FIGO 0–2; lap/open for intramural/subserosal)
No fertility wish → hysterectomy (definitive) or uterus-sparing (UAE, HIFU)

Subfertility: remove cavity-distorting submucosal fibroids; consider GnRH agonist pre-myomectomy to shrink.

Acute pain:

Red degeneration in pregnancy → conservative (analgesia, rest); NSAIDs CI >32 weeks
Pedunculated fibroid torsion → surgical excision

Rule out acute emergencies first (torsion, severe anaemia, urinary retention).

High Yield Summary — Complications

Most common: iron deficiency anaemia from chronic HMB — pallor, fatigue; treat iron + underlying fibroid.

Degeneration (outgrow blood supply):

Hyaline (commonest, asymptomatic)
Red (carneous) — pregnancy 2nd trimester: acute localised pain, fever, ↑WCC; USS tender over fibroid; conservative management
Sarcomatous change — suspect if postmenopausal rapid growth (< 1/200)

Pressure effects:

Bladder → frequency, urgency
Ureter → silent hydronephrosis → renal failure
Cervical/posterior fibroid → acute urinary retention (kinked urethra)
Rectum → constipation
IVC compression → ↑ VTE risk, leg oedema

Pregnancy-related: red degeneration, malpresentation, preterm labour, placental abruption (rare), obstructed labour (cervical/low fibroid).

Treatment complications: haemorrhage (myomectomy), adhesion formation, recurrence after myomectomy (~15–30% at 5 years), UAE amenorrhoea/Ovarian failure, hysterectomy surgical risks.

Uterine Fibroid

1. Definition

2. Epidemiology

Prevalence

Age

Ethnicity

Risk Factors

3. Anatomy and Function: The Uterus

3.1 Gross Anatomy of the Uterus

3.2 Layers of the Uterine Wall

3.3 Blood Supply

3.4 Functional Significance

4. Aetiology and Pathophysiology

4.1 Initiation (Tumourigenesis)

4.2 Promotion (Growth — the role of sex steroids)

Oestrogen

Progesterone

4.3 Extracellular Matrix (ECM)

4.4 Degeneration

5. Classification

5.1 By Location (FIGO Subclassification)

5.2 Other Descriptors

6. Clinical Features

6.1 Symptoms

A. Abnormal Uterine Bleeding (AUB) — the most common symptom [1][2]

B. Bulk/Pressure Symptoms

C. Pain

D. Reproductive Symptoms [1][2]

E. Other Symptoms

6.2 Signs (Physical Examination)

Abdominal Examination

Pelvic (Bimanual) Examination

Speculum Examination

General Examination

7. Secondary Effects (Paraneoplastic and Systemic)

8. Imaging Appearances (Preview)

9. Relation to the PALM-COEIN System

Active Recall - Uterine Fibroid (Definition to Clinical Features)

References

Approach to the Differential Diagnosis

A. Differential Diagnosis of a Pelvic Mass

I. Gynaecological Causes

1. Uterine Origin

2. Ovarian / Adnexal Origin

3. Pregnancy-Related

II. Non-Gynaecological Causes

1. Gastrointestinal [1][2]

2. Urological [1][2]

3. Retroperitoneal [1][2]

4. Others [1][2]

B. Differential Diagnosis of Abnormal Uterine Bleeding (AUB)

C. Causes of Acute Pain in a Patient with Known Fibroid

D. Clinical Approach to Differentiating Fibroid from Key Mimics

E. Key Differentiating Points — Fibroid vs. Ovarian Pathology on Examination

F. Rare Mimics and Pitfalls

Active Recall - Differential Diagnosis of Uterine Fibroid

Diagnostic Criteria

Diagnostic Algorithm

Investigation Modalities — Detailed

Step 1: Clinical Assessment

History

Examination

Step 2: Exclude Pregnancy

Step 3: First-Line Imaging — Pelvic Ultrasound (USS)

Step 4: Second-Line Imaging

MRI Pelvis — Gold Standard for Fibroid Mapping

CT Abdomen/Pelvis

Abdominal X-ray (AXR)

Step 5: Assess for Complications and Co-pathology

A. Blood Investigations

B. Endometrial Assessment

C. Assessment of Uterine Cavity for Fertility

D. Assessment of Urinary Tract

E. Diagnostic Radiology for Treatment Planning

Summary Table — Investigations for Uterine Fibroid

Special Pathological Findings (Post-Excision Histology)

Active Recall - Diagnosis of Uterine Fibroid

Guiding Principles

Management Algorithm

I. Expectant Management (Observation / Watchful Waiting)