A systematic clinical evaluation of an abnormal mass in the pelvis using history, physical examination, imaging, and laboratory studies to determine its origin (gynecologic, gastrointestinal, or urologic), nature (benign versus malignant), and appropriate management.

Exam domain	One-glance essentials
Definition / diagnosis	*A pelvic mass is an abnormal structure arising from gynaecological, gastrointestinal, urinary, retroperitoneal, or pregnancy-related tissue* ^[1]^[2] The task is to determine origin, urgency, and likelihood of malignancy rather than name every possible lesion ^[1]
Epidemiology / risks	Age, pregnancy status, menopausal status, family cancer history, prior surgery, and endometriosis alter the differential ^[1]^[2] Postmenopausal status, persistent complex morphology, ascites, or constitutional symptoms raise malignancy concern ^[1]
Core mechanism	Uterine, adnexal, bowel, or urinary lesions enlarge through cyst formation, solid proliferation, inflammation, torsion, haemorrhage, or obstruction ^[1] Mass effect can compress bladder, bowel, ureters, pelvic veins, or nerves ^[2]
Clinical picture	*Pain suggests torsion, rupture, haemorrhage, infection, or pressure; bloating, early satiety, weight loss, or PMB suggest malignancy* ^[1]^[2] On examination decide whether the mass is uterine or adnexal, mobile or fixed, tender or non-tender, and associated with ascites or nodularity ^[1]
Investigations	Pregnancy test and pelvic ultrasound, usually TVUS, are first-line ^[1]^[2] Use CBC and targeted tumour markers or cross-sectional imaging when morphology and clinical context justify them; tumour markers are not stand-alone screening tests ^[1]
Management	Unstable pain or suspected torsion, rupture, ectopic pregnancy, or sepsis needs urgent intervention ^[1]^[2] Observe selected simple benign cysts; refer suspicious masses to gynaecological oncology for planned staging and surgery without rupture ^[1]
Complications	Complications include torsion, rupture, haemorrhage, infection, obstruction, infertility, venous thrombosis, and malignant spread ^[1]^[2] Unplanned surgery on an unsuspected cancer can spill tumour and compromise staging ^[1]
Prevention / follow-up	Use age-appropriate cancer-risk assessment and follow imaging pathways for incidental masses ^[1] Safety-net new pain, increasing abdominal distension, bleeding, or pressure symptoms during surveillance ^[2]
Exam traps	*CA-125 is neither specific for ovarian cancer nor suitable as a stand-alone screening test* ^[1]^[2] A large mass is not necessarily ovarian, and benign-appearing imaging does not override acute torsion symptoms ^[1]

References

^[1] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (pp. 2, 21, 23, 66, 71) ^[2] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (pp. 10, 18)

Approach to Pelvic Mass

A pelvic mass is any abnormal growth or swelling arising from structures within or adjacent to the pelvis that is detected clinically (on abdominal/bimanual vaginal/rectal examination) or incidentally on imaging. The pelvis is a confined bony space packed with gynaecological, urological, and gastrointestinal organs, so the differential diagnosis is broad and requires a systematic organ-based approach.

Breaking the term down:

Pelvis (Latin: pelvis = basin) — the bony basin formed by the sacrum, coccyx, and two hip bones.
Mass (Latin: massa = lump) — any space-occupying lesion.

The lecture slide (GC 118, p2) frames the approach around: History taking → Physical exam → DDx → Management, covering ovarian masses (cysts and cancer), uterine fibroids, and pelvic imaging. ^[1]

2. Epidemiology & Risk Factors (Hong Kong Context)

Pelvic masses are extremely common in women of reproductive age. The most frequent pelvic mass in a premenopausal woman is a functional ovarian cyst (follicular or corpus luteum), which is physiological and usually self-resolves.
Uterine fibroids (leiomyomas) affect up to 20–40% of women of reproductive age and are the single most common benign pelvic tumour.
Ovarian cancer is a major concern because it is the leading cause of death from gynaecological malignancy — in Hong Kong, epithelial ovarian cancer is the 6th most common cancer in women (crude incidence ~9–10 per 100,000) ^[1]^[2].
In men, pelvic masses most commonly represent bladder pathology, colorectal tumours, or prostatic enlargement (BPH/carcinoma) ^[3].

Condition	Important Risk Factors (HK-relevant)
Functional ovarian cysts	Reproductive age, ovulation induction (e.g. clomifene, IVF)
Endometriotic cysts ("chocolate cysts")	Nulliparity, early menarche, short menstrual cycles, family history
Benign ovarian tumours (dermoid/mature cystic teratoma)	Peak 20–40 years
Epithelial ovarian cancer	Age > 50, nulliparity, early menarche/late menopause, family history (BRCA1/2, Lynch syndrome), HRT, infertility, endometriosis
Uterine fibroids	African descent, unopposed oestrogen, early menarche, nulliparity, obesity, family history, age 30–50
Colorectal cancer	Age > 50, family history, IBD, dietary (red/processed meat), obesity — HK has the highest incidence in Asia for CRC ^[4]
Ectopic pregnancy	PID history, previous ectopic, tubal surgery, IUD, infertility treatment

Protective Factors for Ovarian Cancer

Combined oral contraceptive pill (COCP) use, multiparity, breastfeeding, tubal ligation, and hysterectomy are all protective against epithelial ovarian cancer — the common thread is suppression of ovulation (the "incessant ovulation" hypothesis) ^[1].

3. Relevant Anatomy & Function

Understanding where things are in the pelvis is the key to generating a sensible differential for a pelvic mass.

The true pelvis (lesser pelvis) lies below the pelvic brim (arcuate line of ilium, pectineal line of pubis, sacral promontory).
It contains: bladder (anterior), uterus and adnexa (middle), rectum (posterior) in females; bladder (anterior), rectum (posterior), prostate (inferior to bladder) in males.

Structure	Position	Key Relations	Typical Masses
Uterus	Midline, anteverted and anteflexed (normally)	Bladder anteriorly, rectum posteriorly, broad ligaments laterally	Fibroids, adenomyosis, endometrial cancer, pregnancy
Ovaries	Lateral pelvis in ovarian fossa (below external iliac vessels, anterior to ureter & internal iliac vessels)	Attached to uterus by utero-ovarian ligament, to pelvic sidewall by suspensory (infundibulopelvic) ligament containing ovarian vessels	Functional cysts, endometriomas, dermoids, serous/mucinous cystadenomas, ovarian cancer
Fallopian tubes	Within superior free edge of broad ligament	Open into peritoneal cavity at fimbrial end	Ectopic pregnancy, tubo-ovarian abscess, hydrosalpinx, fallopian tube carcinoma
Bladder	Behind pubic symphysis	Uterus posterosuperiorly	Distended bladder (retention), bladder cancer
Rectum/Sigmoid	Posterior pelvis	Uterus anteriorly	Colorectal cancer, diverticular phlegmon/abscess

Pouch of Douglas (rectouterine pouch): the most dependent part of the peritoneal cavity in the upright position → fluid, blood, and transcoelomic metastases (e.g. Krukenberg tumours) collect here.
Broad ligament: a double layer of peritoneum extending from the lateral uterine wall to the pelvic sidewall. Contains the fallopian tube (in its superior free edge, the mesosalpinx), the round ligament (anteroinferiorly), and uterine/ovarian vessels.
Suspensory (infundibulopelvic) ligament: carries the ovarian artery, vein, lymphatics, and nerve supply — this is what must be ligated during oophorectomy and is at risk of ureteric injury during surgery.

Uterus: uterine artery (branch of internal iliac) — "water under the bridge" (uterine artery crosses over the ureter at the level of the internal os ~2 cm lateral to the cervix).
Ovary: dual supply from ovarian artery (directly from aorta at L2 level) and ovarian branch of uterine artery.
Venous drainage: right ovarian vein → IVC; left ovarian vein → left renal vein (analogous to left testicular vein; explains why left varicocele is more common).

Ovary: para-aortic lymph nodes (because the ovary is an intra-abdominal organ embryologically).
Uterine body: external iliac and para-aortic nodes.
Cervix: obturator, internal/external iliac, presacral nodes.
This matters because ovarian cancer spreads transcoelomically along peritoneal surfaces AND to para-aortic nodes, which is why staging laparotomy includes omentectomy and para-aortic lymph node sampling.

The ureter crosses the pelvic brim at the bifurcation of the common iliac artery, runs along the lateral pelvic wall, then passes under the uterine artery ("water under the bridge") ~2 cm from the cervix before entering the bladder. It is vulnerable to injury during hysterectomy, oophorectomy, and any pelvic surgery.

4. Aetiology & Pathophysiology

The most useful way to classify causes of a pelvic mass is by organ of origin. This is exactly how you should think on a ward round or in an exam when you encounter a pelvic mass.

4.1 Gynaecological Causes

A. Ovarian Masses

Follicular cyst: occurs when a developing follicle fails to rupture at ovulation and continues to enlarge, filled with follicular fluid. Usually < 5 cm, thin-walled, unilocular, anechoic on USS. Self-resolves within 1–3 menstrual cycles.
Corpus luteum cyst: forms when the corpus luteum fails to regress and fills with blood (haemorrhagic corpus luteum). Can cause acute pain if it ruptures → haemoperitoneum. May mimic ectopic pregnancy.
Theca lutein cysts: bilateral, multiloculated cysts from excessive hCG stimulation (e.g. molar pregnancy, multiple pregnancy, ovulation induction). Regress when hCG falls.

The pathophysiological basis is simple: normal follicular development or luteinisation goes too far and too long, producing a fluid-filled structure that is not neoplastic.

Tumour	Origin	Features	Pathophysiology
Serous cystadenoma	Surface epithelium	Unilocular, thin-walled, clear straw-coloured fluid. Most common benign ovarian neoplasm	Epithelial proliferation without invasion
Mucinous cystadenoma	Surface epithelium	Can become VERY large (even filling the whole abdomen), multiloculated, mucin-filled	Mucin-secreting epithelium proliferates
Mature cystic teratoma (dermoid cyst)	Germ cells	Most common ovarian tumour in young women (20–40 yrs). Contains teeth, hair, sebaceous material, fat. Characteristic calcification on X-ray	Arise from totipotent germ cells that differentiate into ectoderm (skin/hair/teeth), mesoderm, endoderm
Fibroma	Sex cord-stromal	Solid ovarian tumour. A/w Meigs' syndrome (ovarian fibroma + ascites + pleural effusion)	Fibrous tissue proliferation; fluid accumulates by unclear mechanism (possibly peritoneal irritation)
Brenner tumour	Surface epithelium (transitional)	Rare, usually benign, solid	Resembles bladder transitional epithelium

Ovarian cancer is subdivided into three main categories by cell of origin: ^[1]

Category	%	Subtypes	Key Features
Epithelial (surface epithelium)	~90%	High-grade serous (most common, ~70%), low-grade serous, endometrioid, clear cell, mucinous	Most important. Usually presents late (stage III/IV). Spreads transcoelomically (peritoneal seeding, omental cake). Marker: CA-125
Germ cell	~5%	Dysgerminoma, immature teratoma, yolk sac tumour, choriocarcinoma, embryonal carcinoma	Young women (10–30 yrs). Often unilateral. Markers: AFP, βhCG, LDH
Sex cord-stromal	~5%	Granulosa cell tumour, Sertoli-Leydig cell tumour, fibroma	May produce hormones (oestrogen → endometrial hyperplasia/cancer; androgens → virilisation)

Pathophysiology of Epithelial Ovarian Cancer (Key Theories):

"Incessant ovulation" hypothesis: Each ovulation causes micro-trauma to the ovarian surface epithelium, requiring repair and cell division → increased chance of DNA mutations → malignant transformation. This explains why COCP (suppress ovulation), multiparity, and breastfeeding are protective ^[1].
"Tubal origin" hypothesis (modern, now dominant for high-grade serous): Many high-grade serous ovarian cancers actually originate from the fimbrial epithelium of the fallopian tube (serous tubal intraepithelial carcinoma, STIC), not from the ovary itself. The fimbrial cells implant on the ovary and grow. This is why prophylactic bilateral salpingectomy (not just oophorectomy) is now recommended in BRCA carriers, and opportunistic salpingectomy at time of hysterectomy for benign disease is increasingly practiced.
Endometriosis-associated pathway: Clear cell and endometrioid subtypes are strongly associated with endometriosis (endometriotic cyst → atypical endometriosis → carcinoma).

Two-Pathway Model of Epithelial Ovarian Cancer

Type I tumours: Low-grade serous, endometrioid, clear cell, mucinous — slow-growing, often confined to ovary at diagnosis, arise from identifiable precursor lesions (e.g. borderline tumours, endometriosis). Mutations: KRAS, BRAF, PTEN, ARID1A.

Type II tumours: High-grade serous (the majority!) — aggressive, usually presents at advanced stage, arises de novo from tubal epithelium or surface epithelium. Key mutation: TP53 (in virtually all), BRCA1/2 dysfunction. ^[1]

Endometriosis = presence of functional endometrial tissue (glands + stroma) outside the uterine cavity.
When endometriotic deposits involve the ovary, they form cysts filled with old, dark, haemolysed blood → the characteristic "chocolate" appearance.
On ultrasound: homogeneous low-level internal echoes ("ground glass" appearance) ^[5].
Pathophysiology: ectopic endometrial tissue responds to cyclical hormonal changes (oestrogen-driven proliferation → progesterone-driven secretory phase → menstruation with no outflow) → repeated bleeding into a confined space → cyst formation.
Endometriomas carry a small risk (~1%) of malignant transformation, particularly to clear cell or endometrioid ovarian carcinoma.

B. Uterine Masses

Fibroids (leiomyomas/myomas) are benign monoclonal tumours of uterine smooth muscle ^[1].

Epidemiology: The most common pelvic tumour. Prevalence 20–40% by age 35, up to 70–80% by age 50 (higher in women of African descent). HK prevalence follows the general Asian pattern (~20–30% of reproductive-age women).

Pathophysiology:

Fibroids are oestrogen- and progesterone-dependent → they grow during reproductive years, enlarge in pregnancy, and shrink after menopause ^[1].
Each fibroid is monoclonal (arises from a single smooth muscle cell that acquires a somatic mutation, e.g. MED12 mutation in ~70% of fibroids).
The tumour produces excessive extracellular matrix (collagen, fibronectin) → the characteristic firm, whorled, white appearance on cut section.

Classification by Location (FIGO System): ^[1]

FIGO Type	Location	Clinical Significance
0	Pedunculated submucosal (intracavitary)	Highest impact on fertility and bleeding
1	Submucosal, < 50% intramural	Heavy menstrual bleeding
2	Submucosal, ≥ 50% intramural	Heavy menstrual bleeding
3	Contacts endometrium, 100% intramural
4	Intramural (entirely within myometrium)	Bulk symptoms when large
5	Subserosal, ≥ 50% intramural	Bulk symptoms, pressure effects
6	Subserosal, < 50% intramural	May be palpable abdominally
7	Pedunculated subserosal	Can undergo torsion
8	Other (e.g. cervical, parasitic, broad ligament)

The key teaching point: submucosal fibroids cause the most menstrual bleeding (because they distort the endometrial cavity and increase surface area), while subserosal fibroids cause the most bulk/pressure symptoms (because they project outwards). ^[1]

Degeneration of Fibroids: Fibroids can outgrow their blood supply, leading to various types of degeneration:

Type of Degeneration	Pathophysiology	Clinical Features
Hyaline degeneration	Most common. Replacement of smooth muscle by hyaline material	Softening of fibroid
Cystic degeneration	Liquefaction of hyaline material	Fluid-filled spaces within fibroid
Red (carneous) degeneration	Venous thrombosis → haemorrhagic infarction. Classically occurs in pregnancy	Acute pain, tenderness over fibroid, low-grade fever, leukocytosis
Calcification	End-stage dystrophic calcification (post-menopausal)	Visible on X-ray/CT
Sarcomatous (malignant) degeneration	Extremely rare (< 0.5%). Transformation to leiomyosarcoma	Rapid growth, esp. postmenopausal — should raise suspicion

Definition: Presence of endometrial glands and stroma within the myometrium, with surrounding smooth muscle hypertrophy.
Pathophysiology: Invagination of the basal endometrium into the myometrium → ectopic endometrial tissue responds to hormones → cyclical bleeding within the myometrium → reactive smooth muscle hypertrophy → diffusely enlarged, boggy uterus.
Clinical features: Dysmenorrhoea, menorrhagia, uniformly enlarged tender uterus. Often coexists with fibroids and endometriosis.

Endometrial carcinoma: Most common gynaecological malignancy in developed countries. Presents with post-menopausal bleeding. The uterus may be enlarged.
Cervical carcinoma: May present as a pelvic mass only in advanced disease (bulky tumour).
Uterine sarcoma (leiomyosarcoma, endometrial stromal sarcoma): Rare. Suspect when a "fibroid" grows rapidly, especially post-menopausally.

Ectopic pregnancy: The most important emergency cause of a pelvic mass in a woman of reproductive age. Any woman of reproductive age with a pelvic mass + abdominal pain + missed period → must exclude ectopic pregnancy (serum βhCG + TVUSS).
Tubo-ovarian abscess (TOA): Complication of pelvic inflammatory disease (PID). Tender, complex adnexal mass with fever and raised inflammatory markers. Organisms: Neisseria gonorrhoeae, Chlamydia trachomatis, polymicrobial.
Hydrosalpinx: Chronic tubal obstruction (post-PID, post-surgery) → fallopian tube distends with serous fluid.
Paraovarian/paratubal cyst: Arises from Wolffian duct remnants (mesonephric) in the broad ligament. Usually small, incidental, benign.

The Gynaecological Emergency You Must Not Miss

In any woman of reproductive age presenting with a pelvic mass, lower abdominal pain, or vaginal bleeding — ALWAYS perform a urine pregnancy test (or serum βhCG) FIRST to exclude ectopic pregnancy. This is a potentially life-threatening emergency. ^[2]

Organ	Pathology	Key Features
Bladder	Distended bladder (urinary retention), bladder cancer	Midline, arising from pelvis, can't get below it, dull to percussion. Uterine fibroid and gravid uterus are the most common DDx for a midline suprapubic mass ^[3]^[6]
Colon/Rectum	Colorectal cancer, diverticular abscess, faecal loading	Faecal loading can mimic a pelvic mass! Always do PR exam
Appendix	Appendiceal abscess/mucocele	RLQ mass, post-appendicitis
Retroperitoneal	Lymphoma, sarcoma, retroperitoneal fibrosis	Fixed, non-mobile
Kidney	Pelvic kidney (congenital), transplant kidney
Peritoneum	Mesenteric cyst, pseudomyxoma peritonei
Bone/Soft tissue	Sacral chordoma, pelvic sarcoma

Gravid uterus (intrauterine pregnancy): The most common cause of a midline pelvic mass in a reproductive-age woman! Always exclude pregnancy first.
Ectopic pregnancy: As above — tubal (most common), ovarian, cervical, abdominal.
Gestational trophoblastic disease (molar pregnancy): Enlarged uterus, markedly elevated βhCG, "snowstorm" appearance on USS.

5. Classification of Pelvic Masses

Multiple classification systems exist; the most clinically useful ones are:

As laid out in Section 4 above.

Nature	Features	Examples
Physiological	Self-limiting, cycle-related	Functional ovarian cysts, early pregnancy
Benign neoplastic	Well-defined, slow-growing, no invasion	Fibroids, dermoid cysts, cystadenomas
Malignant neoplastic	Irregular, solid components, rapid growth, ascites	Ovarian cancer, endometrial cancer, CRC
Inflammatory/Infective	Tender, fever, raised WCC/CRP	TOA, appendiceal abscess, diverticular abscess
Functional/Non-neoplastic	Cycle-related or obstruction-related	Follicular cyst, distended bladder, haematometra

This is extremely high-yield for exams — distinguishing benign from malignant ovarian masses: ^[1]

Feature	Suggests Benign	Suggests Malignant
Age	Premenopausal	Postmenopausal
Laterality	Unilateral	Bilateral
Size	< 5 cm	> 5-10 cm (but mucinous cystadenomas can be huge and benign!)
Consistency	Cystic, smooth, mobile	Solid or complex (mixed solid-cystic), irregular, fixed
Growth	Slow	Rapid
Ascites	Absent	Present
Peritoneal deposits	Absent	Present (omental cake)
USS features	Unilocular, thin septae, no solid component, no blood flow to wall	Multilocular, thick septae (> 3 mm), solid components with blood flow (on Doppler), papillary excrescences
CA-125	Normal (< 35 U/mL)	Elevated (but non-specific — also raised in endometriosis, PID, pregnancy, cirrhosis)

6. Clinical Features

6.1 Symptoms

The symptoms of a pelvic mass depend on: (a) the organ of origin, (b) the size, (c) whether it is benign vs. malignant, and (d) complications.

Symptom	Mechanism (Pathophysiological Basis)
Lower abdominal/pelvic heaviness or fullness	Physical mass effect — the mass occupies space and stretches the peritoneum or pelvic structures
Urinary frequency, urgency, or retention	Anterior compression of the bladder (e.g. large fibroid, ovarian mass). A large cervical fibroid can kink the urethra → acute urinary retention (AROU) ^[6]
Constipation or tenesmus	Posterior compression of the rectum/sigmoid
Abdominal distension	Large mass (e.g. giant mucinous cystadenoma) or associated ascites (malignancy)
Lower limb oedema	Compression of iliac veins or lymphatics by the mass → impaired venous/lymphatic return
Deep vein thrombosis (DVT)	Same mechanism — venous compression → stasis → Virchow's triad
Ureteric obstruction → hydronephrosis	Lateral extension of mass or advanced malignancy compressing the ureter at the pelvic brim
Dyspnoea	Massive ascites (malignant) or very large mass splinting the diaphragm; or pleural effusion (Meigs' syndrome)

Symptom	Pathophysiological Basis	Think of...
Abnormal uterine bleeding (menorrhagia, intermenstrual bleeding, postmenopausal bleeding)	Submucosal fibroids distort endometrial cavity → increase surface area → disrupt normal haemostatic mechanisms at menstruation; endometrial cancer causes friable neovascularised tissue that bleeds irregularly	Fibroids, adenomyosis, endometrial cancer
Dysmenorrhoea (painful periods)	Adenomyosis: ectopic endometrium within myometrium bleeds cyclically → swelling, inflammation within the muscle wall; Endometriotic cysts: cyclical bleeding within cyst → stretching of cyst wall and peritoneal irritation	Adenomyosis, endometriosis
Pelvic pain (chronic)	Stretching of capsule (ovarian cyst), peritoneal inflammation (endometriosis), degeneration of fibroid	Endometriosis, fibroids (degeneration), ovarian cysts
Acute pelvic pain	Ovarian cyst accident: torsion (vascular compromise → ischaemia), rupture (chemical peritonitis from cyst contents), haemorrhage; Ectopic pregnancy rupture; Red degeneration of fibroid	See Gynaecological Emergencies ^[2]
Dyspareunia (deep)	Mass in Pouch of Douglas, endometriosis involving uterosacral ligaments, retroverted uterus with adenomyosis	Endometriosis, TOA, ovarian cyst
Infertility	Submucosal fibroids distort cavity → impair implantation; Endometriomas → peri-ovarian adhesions → impaired ovum pick-up; Tubal damage from PID → hydrosalpinx → tubal factor infertility	Fibroids (submucosal), endometriosis, PID
Vaginal discharge (abnormal)	Cervical carcinoma (offensive, blood-stained); infected/necrotic fibroid (purulent)	Cervical cancer, infected fibroid
Postmenopausal bleeding	Endometrial atrophy, endometrial cancer, cervical cancer. Any postmenopausal bleeding is endometrial cancer until proven otherwise	Endometrial cancer
Virilisation (hirsutism, voice deepening, clitoromegaly)	Androgen-secreting ovarian tumour (Sertoli-Leydig cell tumour) → excess testosterone	Sex cord-stromal tumour
Precocious puberty / postmenopausal vaginal bleeding from oestrogen	Granulosa cell tumour secretes oestrogen → endometrial stimulation	Sex cord-stromal tumour
Bowel symptoms (change in bowel habit, rectal bleeding)	Colorectal cancer, compression by mass	CRC, advanced ovarian cancer

Symptom	Mechanism
Abdominal distension / bloating	Ascites from peritoneal carcinomatosis (transcoelomically spread ovarian cancer)
Early satiety, nausea	Omental cake/peritoneal deposits → mechanical compression of stomach/bowel
Constitutional symptoms (weight loss, fatigue, anorexia)	Cancer cachexia (cytokine-mediated: TNF-α, IL-6)
Increasing abdominal girth with weight loss	Classic "paradox" of ovarian cancer: gaining waist circumference (ascites) while losing weight (cachexia)
New onset urinary symptoms or change in bowel habit in older woman	Should raise alarm for ovarian cancer — symptoms are often vague and non-specific, contributing to late diagnosis

Why is Ovarian Cancer Called the 'Silent Killer'?

Ovarian cancer presents late because the ovary is deep in the pelvis with room to grow, and early symptoms (bloating, vague discomfort, urinary frequency) are non-specific and easily dismissed as IBS or normal ageing. By the time ascites or a palpable mass appears, ~75% of patients are already stage III/IV ^[1].

These are essential to know for the approach to acute pelvic pain: ^[2]

Emergency	Key Symptoms	Mechanism
Ovarian torsion	Sudden onset severe unilateral pelvic pain, nausea/vomiting (due to peritoneal irritation and autonomic reflex), may have history of known ovarian cyst	The ovary (± tube) twists on its pedicle (infundibulopelvic + utero-ovarian ligament) → venous outflow obstruction first → congestion → if persists, arterial compromise → ischaemic necrosis
Ruptured ovarian cyst	Sudden sharp pelvic pain, may have haemodynamic instability if significant haemoperitoneum (ruptured haemorrhagic corpus luteum)	Cyst wall ruptures → fluid/blood spills into peritoneal cavity → peritoneal irritation and potential hypovolaemia
Ruptured ectopic pregnancy	Acute pelvic pain, amenorrhoea/missed period, vaginal bleeding (usually dark, scanty), shoulder tip pain (diaphragmatic irritation from haemoperitoneum), syncope/collapse	Trophoblastic invasion through the tubal wall → rupture → intra-abdominal haemorrhage
Red degeneration of fibroid	Acute/subacute pain localised over fibroid, often in pregnancy (2nd trimester), low-grade fever	Venous thrombosis within the fibroid → haemorrhagic infarction → necrosis with release of inflammatory mediators
Torsion of pedunculated fibroid	Acute lower abdominal pain	Pedunculated subserosal (FIGO 7) or submucosal (FIGO 0) fibroid twists on its pedicle → ischaemia

6.2 Signs

Sign	What It Suggests	Mechanism
Pallor	Anaemia — chronic blood loss (menorrhagia from fibroids) or acute blood loss (ruptured ectopic, ruptured ovarian cyst)	Iron deficiency from chronic menstrual loss; acute hypovolaemia
Cachexia / wasting	Malignancy	Cytokine-mediated catabolic state
Virchow's node (left supraclavicular lymphadenopathy)	Gastrointestinal or pelvic malignancy with metastasis	Thoracic duct drains into left subclavian-jugular confluence; tumour cells travel via lymphatics
Leg oedema (bilateral or unilateral)	Pelvic mass compressing iliac veins/lymphatics	Impaired venous/lymphatic return
Signs of hyperoestrinism	Oestrogen-secreting ovarian tumour (granulosa cell)	Exogenous oestrogen effect on target tissues
Virilisation (hirsutism, acne, male-pattern balding, deep voice)	Androgen-secreting tumour (Sertoli-Leydig cell tumour)	Excess androgens

Systematic approach to examining a pelvic mass on abdominal examination: ^[3]^[6]

Sign	Interpretation	Mechanism / Explanation
Abdominal distension	Large mass or ascites. If ascites + pelvic mass in postmenopausal woman = ovarian cancer until proven otherwise	Tumour bulk or malignant peritoneal effusion
"You cannot get below the mass" (cannot palpate the lower border)	The mass arises from the pelvis — this is the hallmark finding of a pelvic mass on abdominal examination. Unlike liver/spleen/kidney where you can usually get below the mass, a pelvic mass extends down into the pelvis beyond the examining hand	The mass is arising from below the pelvic brim
Midline suprapubic mass	Think: uterus (fibroid, pregnancy), distended bladder	These are midline structures
Lateral pelvic mass	Think: ovarian mass, tubo-ovarian abscess, appendiceal mass	Ovaries are lateral structures
Mass moves with respiration	NOT a pelvic mass — likely liver, spleen, kidney, gallbladder (these move down with diaphragmatic descent on inspiration)	Diaphragmatic excursion pushes intra-abdominal organs downward
Mass moves with palpation (side-to-side) but NOT with respiration	Uterine origin (e.g. fibroid) — because the uterus is tethered by the cardinal and uterosacral ligaments but has some lateral mobility	Uterine attachments allow side-to-side movement ^[3]^[6]
Mass is fixed	Retroperitoneal mass OR advanced malignancy with fixation to surrounding structures	Invasion or retroperitoneal location
Shifting dullness, fluid thrill	Ascites — think malignancy (ovarian cancer) or Meigs' syndrome	Free peritoneal fluid
Mass is dull to percussion	Solid or fluid-filled pelvic mass	Solid/fluid attenuates sound
Tympanitic above the mass	Bowel displaced superiorly by the mass	Gas-containing bowel loops pushed up

How to distinguish an abdominal wall mass from an intra-abdominal mass: ^[3]

Ask the patient to cross arms and lift head + shoulders off the pillow (contracts rectus abdominis):
- If the mass disappears or becomes smaller → intra-abdominal (now hidden behind the tensed abdominal wall)
- If the mass remains the same or becomes more prominent → abdominal wall origin (e.g. rectus sheath haematoma, desmoid tumour)

This is the most important examination for characterising a pelvic mass: ^[1]

Finding	Interpretation
Uterus enlarged, firm, irregular, mobile	Uterine fibroids
Uterus uniformly enlarged, tender, boggy	Adenomyosis
Uterus bulky with cervical mass	Cervical carcinoma
Separate from uterus, unilateral, cystic, mobile	Ovarian cyst (likely benign)
Separate from uterus, bilateral, solid, fixed, nodular	Ovarian cancer (advanced)
Tender adnexal mass with cervical excitation tenderness	Ectopic pregnancy (if βhCG +ve) or tubo-ovarian abscess (if febrile with raised CRP)
Fixed mass in Pouch of Douglas	Advanced pelvic malignancy (ovarian, colorectal, endometrial), frozen pelvis
Cervical excitation tenderness (Chandelier sign)	Peritoneal irritation — ectopic pregnancy, PID, ruptured ovarian cyst — moving the cervix stretches the peritoneum via the uterosacral ligaments

Cardinal Rule

Never perform a vaginal examination in a patient with suspected placenta praevia or active heavy vaginal bleeding until ultrasound has been performed first. And never forget: pregnancy test first in any woman of reproductive age with a pelvic mass! ^[2]

Per rectal examination (PR): Essential to assess the posterior pelvic compartment. Can feel a rectal mass, bulging Pouch of Douglas (blood/fluid/tumour), frozen pelvis from advanced malignancy, or rectal involvement by tumour.
Speculum examination: Visualise the cervix — look for cervical mass (cervical cancer), cervical polyp, vaginal discharge, bleeding from os.

7. Summary of Clinical Approach (History & Examination Framework)

The approach to a pelvic mass follows a structured clinical method: ^[1]

Domain	Key Questions	Rationale
Age	Premenopausal vs. postmenopausal	Functional cysts common premenopausal; malignancy more likely postmenopausal
Menstrual history	Last menstrual period (LMP), regularity, menorrhagia, dysmenorrhoea, intermenstrual/postcoital/postmenopausal bleeding	Fibroids → menorrhagia; endometrial cancer → PMB; ectopic → missed period
Obstetric history	Parity, mode of delivery, complications	Nulliparity → risk for ovarian cancer; multiparity → protective; ectopic pregnancy history
Contraception	COCP (protective for ovarian Ca), IUD (risk for ectopic, PID)
Sexual history	STI risk (PID → TOA)
Associated symptoms	Pain (acute vs. chronic, character, radiation), urinary, bowel, constitutional	Guides DDx
Family history	Breast/ovarian cancer (BRCA), CRC (Lynch syndrome)	Hereditary cancer syndromes
Past medical/surgical history	Previous pelvic surgery, endometriosis, PID, cancer
Drug history	HRT, tamoxifen (risk for endometrial cancer/ovarian cysts)

General: Vitals, BMI, pallor, cachexia, lymphadenopathy (Virchow's node), leg oedema
Abdomen: Inspection (distension, scars, visible mass), palpation (mass characteristics — site, size, shape, surface, edge, consistency, mobility, tenderness), percussion (shifting dullness for ascites, dull vs. tympanitic), auscultation (bowel sounds)
Pelvic: Speculum examination → bimanual vaginal examination
Rectal: PR examination
Breast: In cases of suspected ovarian cancer (exclude primary breast cancer with ovarian metastasis)

High Yield Summary

1. Definition: A pelvic mass is any space-occupying lesion arising from structures within or adjacent to the pelvis.

2. Epidemiology: Functional ovarian cysts and uterine fibroids are the most common pelvic masses. Ovarian cancer is the leading cause of death from gynaecological malignancy. In HK, CRC is the most common cancer overall and can present as a pelvic mass.

3. Anatomy: The pelvis contains the uterus (midline), ovaries (lateral), fallopian tubes, bladder (anterior), and rectum (posterior). The ovary drains to para-aortic nodes. The ureter runs under the uterine artery ("water under the bridge").

4. Aetiology (Think by Organ):

Ovary: Functional cysts, endometriomas, benign neoplasms (dermoid, cystadenoma), malignant neoplasms (epithelial 90%, germ cell, sex cord-stromal)
Uterus: Fibroids (most common pelvic tumour), adenomyosis, endometrial cancer
Tube: Ectopic pregnancy, TOA, hydrosalpinx
Non-gynae: Distended bladder, CRC, appendiceal mass

5. Pathophysiology Highlights:

Ovarian cancer: Incessant ovulation → epithelial trauma → mutation accumulation; tubal origin hypothesis for high-grade serous
Fibroids: Oestrogen/progesterone-dependent monoclonal smooth muscle tumours; submucosal → bleeding, subserosal → bulk
Endometriomas: Ectopic endometrium → cyclical bleeding in ovary → chocolate cyst

6. Classification: By organ, by nature (physiological/benign/malignant/inflammatory), by USS features (benign vs. malignant criteria).

7. Clinical Features:

Bulk symptoms: Urinary frequency (bladder compression), constipation (rectal compression), abdominal distension
Organ-specific: Menorrhagia (submucosal fibroid), PMB (endometrial cancer), acute pain (torsion/rupture/ectopic)
Malignancy red flags: Ascites, weight loss, bilateral fixed mass, postmenopausal, raised CA-125

8. Examination:

"Cannot get below it" = pelvic origin
Side-to-side mobility = uterine
Fixed, bilateral, nodular with ascites = suspect malignancy
Always do pregnancy test first in reproductive-age women

Active Recall - Approach to Pelvic Mass

^[1] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[2] Lecture slides: Block C - Gyanecological Emergency Notes to Students.pdf ^[3] Senior notes: Ryan Ho Fundamentals.pdf (Section 7: Approach to Palpable Mass, p76) ^[4] Senior notes: Ryan Ho GI.pdf (Section 3.3.6: Colorectal Tumours, p163) ^[5] Senior notes: Ryan Ho Radiology.pdf (p34) ^[6] Senior notes: Ryan Ho Urogenital.pdf (Section 8.1: Approach to Urinary Incontinence, p159; AROU section p164)

Differential Diagnosis of a Pelvic Mass

The ability to construct a structured, prioritised differential diagnosis list is the most critical clinical skill when approaching a pelvic mass. As the Gynaecological Emergency lecture notes explicitly state: "The most important part is the ability to formulate the list of differential diagnoses and to prioritise them according to the clinical condition and NOT just to give the right diagnosis" ^[2].

The philosophy is straightforward: think by organ of origin first, then refine by clinical context (age, menopausal status, acuity, associated symptoms). The pelvis is a "shared space" — gynaecological, gastrointestinal, and urological structures all live here, so you must consider all three systems.

1. Master Differential Diagnosis List (By Organ System)

The lecture slides (GC 118, p23) explicitly list the DDx for pelvic mass classified as gynaecological vs. non-gynaecological: ^[1]

Organ	Condition	Why It Presents as a Pelvic Mass
Uterus	Uterine fibroid (leiomyoma)	Monoclonal smooth muscle tumour; oestrogen/progesterone-dependent → grows progressively → can become enormous (fills pelvis and abdomen). Midline mass, mobile side-to-side
	Adenomyosis	Diffuse myometrial thickening from ectopic endometrial glands/stroma within the muscle wall → uniformly enlarged boggy uterus (less likely to be palpable abdominally unless severe)
	Uterine sarcoma (leiomyosarcoma)	Rare malignant counterpart of fibroid; suspect when a "fibroid" grows rapidly, especially in postmenopausal women when it should be shrinking (no oestrogen drive)
Pregnancy-related	Undiagnosed pregnancy (gravid uterus)	Most common physiological cause of a midline pelvic mass in a reproductive-age woman. Uterus becomes palpable abdominally from ~12 weeks' gestation
	Molar pregnancy (gestational trophoblastic disease)	Abnormal trophoblastic proliferation → uterus larger than expected for gestational age, markedly elevated βhCG
	Ectopic pregnancy	Trophoblast implants outside endometrial cavity (95% tubal) → adnexal mass ± haemoperitoneum. This is a life-threatening emergency
Ovary	Ovarian cyst (functional or neoplastic)	Fluid-filled structure expanding the ovary; functional cysts (follicular, corpus luteum) are cyclical and self-limiting; neoplastic cysts (serous/mucinous cystadenoma, dermoid) persist and grow
	Ovarian cancer	Surface epithelial malignancy (90%) → solid-cystic mass, often bilateral, with ascites and peritoneal deposits in advanced disease
	Metastatic ovarian tumour (Krukenberg)	Transcoelomic/haematogenous spread from GI tract (especially stomach, CRC) to ovary → bilateral solid ovarian masses. Named after pathologist Friedrich Krukenberg; histology shows signet-ring cells
Tube / Adnexa	Paraovarian cyst	Arises from mesonephric (Wolffian) duct remnants in the broad ligament → separate from the ovary, usually unilocular and benign
	Hydrosalpinx	Chronic tubal obstruction (post-PID, post-surgery) → fallopian tube distends with serous fluid → sausage-shaped cystic mass
	Tubo-ovarian abscess (TOA)	Complication of ascending PID → mixed inflammatory mass encasing tube + ovary, tender, febrile

The lecture slide (GC 118, p23) separates non-gynaecological causes into gastrointestinal, urological, retroperitoneal, and others: ^[1]

System	Condition	Why It Presents as a Pelvic Mass
Gastrointestinal	Colorectal tumour (sigmoid/rectal cancer)	Annular or polypoid lesion in the rectosigmoid region → palpable on PR or as a left-sided pelvic mass
	Mesenteric cyst	Cystic lymphatic malformation within the mesentery → mobile mass, may transilluminate. Moves perpendicular to mesenteric root
	Diverticular abscess/phlegmon	Complicated sigmoid diverticulitis → inflammatory mass in left lower quadrant/pelvis, tender, febrile
	Dilated bowel (obstruction)	Distal large bowel obstruction → massively distended sigmoid or caecum palpable as "mass"
	Hernia (obturator, femoral, inguinal)	Herniated bowel can present as a groin/pelvic mass
	Appendiceal mass/abscess	Walled-off acute appendicitis → RLQ inflammatory mass ^[7]
Urological	Distended bladder (urinary retention)	Failure to empty → progressive distension → midline suprapubic mass, dull to percussion, disappears after catheterisation. The most common "pseudo-mass" that catches students out!
	Bladder diverticulum	Outpouching of bladder mucosa through muscular wall (from chronic outlet obstruction)
	Pelvic kidney	Congenital malposition — kidney fails to ascend during embryological development → remains in pelvis
	Transplanted kidney	Allografted kidney is placed in the iliac fossa → palpable mass (normal finding post-transplant!)
Retroperitoneal	Retroperitoneal sarcoma	Rare soft tissue malignancy arising from retroperitoneal mesenchymal tissue → usually very large before detection because the retroperitoneum is a "silent" space. Usually not palpable ^[1]
	Retroperitoneal lymphadenopathy (lymphoma)	Bulky para-aortic/pelvic lymph nodes from lymphoma or metastatic disease → fixed, non-tender
Others	Pseudocyst (related to previous surgery)	Post-surgical peritoneal fluid collections enclosed by adhesions → can mimic cystic pelvic mass ^[8]
	Abscess (pelvic abscess from any cause)	Post-operative, post-PID, perforated appendicitis/diverticulitis → walled-off collection in the pelvis

Don't Forget Pregnancy!

The lecture slide explicitly warns: "Don't forget about pregnancy → especially for teenage girls" ^[8]. A gravid uterus is the most common midline pelvic mass in reproductive-age women. Failure to perform a pregnancy test before further investigation (especially before CT scan or surgery) is a classic and dangerous error.

Don't Forget Post-Surgical Pseudocysts!

The lecture slide also specifically mentions "pseudocyst related to previous surgeries" ^[8] — these are peritoneal inclusion cysts (fluid trapped between adhesions) that can mimic ovarian cysts on imaging. A thorough surgical history is essential.

2. Clinical Approach to Narrowing the DDx

The key clinical discriminators are age/menopausal status, acuity of presentation, mass characteristics, and associated features. Let's work through these systematically.

Age Group	Most Likely Diagnoses	Why
Adolescent / Young reproductive age (< 30)	Pregnancy (always!), functional ovarian cyst, dermoid cyst (mature cystic teratoma), ectopic pregnancy, germ cell tumour	Ovulation is active → functional cysts common. Dermoids peak at 20–40. Germ cell tumours peak 10–30
Reproductive age (30–50)	Uterine fibroids, endometriotic cyst, ovarian cysts (functional + neoplastic), ectopic pregnancy, TOA, adenomyosis	Fibroids are oestrogen-driven → peak prevalence. Endometriosis is active while menstruating
Perimenopausal (45–55)	Fibroids (should stabilise/shrink), ovarian neoplasms (borderline/early malignant), endometrial cancer	Transition period — benign conditions should be "burning out" while malignant risk rises
Postmenopausal (> 55)	Ovarian cancer, endometrial cancer, colorectal cancer, metastatic disease	Oestrogen withdrawal means fibroids and endometriotic cysts should shrink — any NEW or GROWING pelvic mass in a postmenopausal woman is malignant until proven otherwise

This age-based thinking is the single most powerful discriminator. A 25-year-old with a smooth, mobile, unilateral cystic adnexal mass almost certainly has a benign cyst. A 65-year-old with the same finding needs urgent investigation for malignancy.

Presentation	Think of...	Distinguishing Features
Acute pain + pelvic mass	Ovarian torsion, ruptured ovarian cyst, ruptured ectopic pregnancy, red degeneration of fibroid, TOA	History of known cyst (torsion), missed period (ectopic), fever (TOA), pregnancy (red degeneration) ^[2]
Subacute / progressive	Growing fibroid, ovarian neoplasm (benign or malignant), endometrioma, hydrosalpinx	Progressive bulk symptoms, menstrual disturbance
Chronic / incidental	Fibroid, dermoid, paraovarian cyst, pelvic kidney	Found incidentally on imaging or routine examination

The approach to palpable mass (from Ryan Ho Fundamentals, p76) provides a framework for differentiating masses: ^[3]

Characteristic	Likely Diagnosis	Reasoning
Midline, arising from pelvis ("cannot get below"), mobile side-to-side but NOT with respiration	Uterine origin: fibroid, gravid uterus	Uterus is a midline pelvic structure tethered by cardinal/uterosacral ligaments but with some lateral mobility ^[3]
Midline, arising from pelvis, dull to percussion, disappears after catheterisation	Distended bladder	Urine is fluid → dull to percussion; resolves when emptied
Lateral pelvic mass, cystic, mobile, separate from uterus	Ovarian cyst (benign), paraovarian cyst	Ovaries are lateral structures
Lateral pelvic mass, solid-cystic, fixed, bilateral, with ascites	Ovarian cancer	Malignant features: bilateral, fixed (peritoneal invasion), ascites (transcoelomic spread)
Tender, ill-defined, febrile	Inflammatory: TOA, appendiceal/diverticular abscess	Infection → oedema, pus, ill-defined borders ^[3]
Hard, irregular, nodular, fixed	Malignancy (advanced)	Infiltrative growth → irregular surface, fixation to surrounding structures ^[3]
Completely fixed, does not move with inspiration or palpation	Retroperitoneal mass or advanced tumour with fixation	Retroperitoneal structures are tethered against the posterior abdominal wall ^[3]

Associated Feature	Points Towards	Mechanism
Menorrhagia + dysmenorrhoea	Fibroid (submucosal), adenomyosis	Cavity distortion → increased surface area → heavier bleeding
Postmenopausal bleeding	Endometrial cancer (must exclude), cervical cancer	Friable neoplastic tissue bleeds spontaneously
Amenorrhoea + positive βhCG	Pregnancy (intrauterine or ectopic)	hCG produced by trophoblast
Fever + vaginal discharge + cervical excitation	PID / TOA	Ascending polymicrobial infection
Ascites + weight loss + bloating	Ovarian cancer	Peritoneal carcinomatosis + cancer cachexia
Change in bowel habit + PR bleeding	Colorectal cancer	Mucosal invasion/ulceration → bleeding; luminal narrowing → altered bowel habit
Virilisation / precocious puberty	Sex cord-stromal tumour	Hormone-secreting tumour (androgens or oestrogens)
Raised CA-125	Epithelial ovarian cancer (but non-specific)	CA-125 is a glycoprotein expressed by coelomic epithelium — also raised in endometriosis, PID, pregnancy, liver disease

The following algorithm integrates the clinical discriminators above into a practical decision tree:

4. Differential Diagnosis by Clinical Scenario

To make this exam-ready, here are high-yield clinical scenarios with the most likely differential:

Priority	DDx	Key Distinguishing Feature
1	Ectopic pregnancy	Amenorrhoea, positive βhCG, adnexal mass ± free fluid
2	Ovarian cyst torsion	Sudden unilateral pain, nausea/vomiting, known cyst, absent Doppler flow
3	Ruptured ovarian cyst	Mid-cycle pain, free fluid, βhCG negative
4	Acute appendicitis	RLQ pain, migration from periumbilical, fever, raised WCC ^[7]
5	PID / TOA	Bilateral pain, vaginal discharge, cervical excitation tenderness, fever

Priority	DDx	Key Distinguishing Feature
1	Uterine fibroid	Midline firm irregular mass, mobile side-to-side, heavy regular periods
2	Adenomyosis	Uniformly enlarged tender uterus, dysmenorrhoea, "boggy"
3	Ovarian cyst/neoplasm	Separate from uterus on bimanual, lateral
4	Pregnancy	Always exclude with βhCG

Priority	DDx	Key Distinguishing Feature
1	Ovarian cancer	Bilateral, complex solid-cystic mass, ascites, raised CA-125, omental cake on CT
2	Colorectal cancer with pelvic extension	Change in bowel habit, PR bleeding, mass on PR exam
3	Metastatic disease (Krukenberg)	History of GI primary, bilateral solid ovarian masses
4	Uterine sarcoma	Rapidly enlarging uterine mass post-menopause
5	Endometrial cancer	PMB, thickened endometrium on USS

Priority	DDx	Key Distinguishing Feature
1	Tubo-ovarian abscess	Sexually active, vaginal discharge, cervical excitation, raised CRP
2	Appendiceal abscess	History of RLQ pain → localised → mass, raised WCC ^[7]
3	Ectopic pregnancy (subacute)	Positive βhCG
4	Ovarian cyst complication	Known cyst, sudden pain onset

The lecture summary slide (GC 118, p71) states: "Uterine fibroid, ovarian mass and cancer are important differential diagnoses of pelvic mass" ^[1]. Here is how to tell them apart:

Feature	Uterine Fibroid	Benign Ovarian Cyst	Ovarian Cancer
Age	30–50 (reproductive)	Any reproductive age	Postmenopausal (peak 60s)
Position	Midline, continuous with uterus	Lateral, separate from uterus	Lateral or fills pelvis, separate from uterus
Mobility	Side-to-side (uterine mobility)	Mobile	Fixed
Consistency	Firm, rubbery	Cystic, smooth, tense	Solid-cystic, irregular, hard
Laterality	N/A (uterine)	Usually unilateral	Often bilateral
Ascites	Absent	Absent (unless Meigs' syndrome with fibroma)	Present
USS	Hypoechoic solid mass within myometrium	Unilocular, anechoic, thin wall	Complex: thick septae, solid components, papillary excrescences, vascularity on Doppler
Tumour markers	Normal	Normal (CA-125 may be mildly elevated in endometrioma)	CA-125 elevated (often > 200 U/mL)
Menstrual symptoms	Menorrhagia, dysmenorrhoea	Usually asymptomatic or cyclical pain	Non-specific (bloating, early satiety)

6. Special Considerations for Non-Gynaecological DDx

Why it fools you: A chronically retaining bladder can reach the umbilicus and feel like a large smooth midline mass — exactly mimicking a fibroid uterus or gravid uterus.
How to differentiate: It is dull to percussion (like uterus), but it disappears after catheterisation. Always catheterise (or get a post-void residual USS) before taking a patient to theatre for a suspected pelvic mass.
Common causes in women: organ prolapse (cystocele), gynaecological tumours (fibroid compressing urethra), neurogenic bladder ^[9].

Sigmoid and rectal cancers can present as pelvic masses, especially when locally advanced.
The key discriminator is change in bowel habit, PR bleeding, and findings on PR examination.
CRC is the most common cancer overall in Hong Kong ^[4] — always consider it in the pelvic mass DDx, especially in older patients.

Appendiceal abscess after perforated appendicitis presents as a tender RLQ mass with fever ^[7].
Appendiceal mucocele (mucinous cystadenoma of the appendix) can present as an asymptomatic RLQ mass and may rupture to cause pseudomyxoma peritonei.

Integrating the physical examination approach from Ryan Ho Fundamentals (p76): ^[3]

Examination Finding	DDx	Reasoning
Cannot get below the mass	Pelvic origin: fibroid, ovarian mass, pregnancy, distended bladder	Mass extends into the bony pelvis below the examiner's reach
Moves with respiration	NOT pelvic → liver, spleen, kidney, gallbladder	Descends with diaphragm on inspiration
Moves side-to-side but not with respiration	Uterine origin: fibroid, gravid uterus	Uterine ligamentous attachments permit lateral mobility ^[3]
Fixed, does not move at all	Retroperitoneal mass, advanced malignancy with invasion	Tethered to posterior abdominal wall or invaded into surrounding structures
Cystic, regular, smooth, tense	Ovarian cyst, mesenteric cyst, distended bladder	Fluid-filled structures have uniform tension and smooth wall ^[3]
Hard, irregular, nodular	Malignancy: ovarian cancer, CRC, sarcoma	Infiltrative growth pattern with surface irregularity ^[3]
Solid, ill-defined, tender	Inflammatory: TOA, appendiceal abscess, diverticular phlegmon	Oedema and pus create ill-defined borders; active inflammation causes tenderness ^[3]

High Yield Summary — Differential Diagnosis of Pelvic Mass

1. Classify DDx as gynaecological (uterine, ovarian, tubal/adnexal, pregnancy-related) vs. non-gynaecological (GI, urological, retroperitoneal, other) ^[1].

2. Rule of Three — Always exclude first:

Pregnancy (βhCG — especially in teenage girls ^[8])
Distended bladder (catheterise or post-void residual)
Malignancy (especially in postmenopausal women)

3. Age is the best discriminator:

Young → functional cyst, dermoid, ectopic, germ cell tumour
Reproductive → fibroid, endometrioma, ectopic, cystadenoma
Postmenopausal → malignancy until proven otherwise (ovarian cancer, endometrial cancer, CRC)

4. Mass characteristics guide diagnosis:

Midline + side-to-side mobility = uterine (fibroid, pregnancy)
Lateral + cystic + mobile = benign ovarian cyst
Lateral + solid-cystic + fixed + bilateral + ascites = ovarian cancer
Tender + ill-defined + febrile = inflammatory (TOA, abscess)

5. Uterine fibroid, ovarian mass, and ovarian cancer are the three most important DDx of a pelvic mass ^[1].

Active Recall - Differential Diagnosis of Pelvic Mass

References

^[1] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p2, p23, p71) ^[2] Lecture slides: Block C - Gyanecological Emergency Notes to Students.pdf (p1) ^[3] Senior notes: Ryan Ho Fundamentals.pdf (Section 7: Approach to Palpable Mass, p76) ^[4] Senior notes: Ryan Ho GI.pdf (Section 3.3.6: Colorectal Tumours, p163) ^[7] Senior notes: Maksim Surgery Notes.pdf (Section 4.6: Acute appendicitis, p89) ^[8] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p17) ^[9] Senior notes: Ryan Ho Urogenital.pdf (Section 8: Voiding Complaints, p164)

Investigations and Diagnostic Approach to Pelvic Mass

There is no single "diagnostic criterion" for a pelvic mass the way there is for, say, rheumatoid arthritis or diabetes. Instead, the approach is an investigative algorithm — a sequence of bedside tests, blood tests, imaging, and (when needed) histopathology that progressively narrows the differential diagnosis from "pelvic mass" to a specific tissue diagnosis.

The logic flows from simple → complex and non-invasive → invasive:

Bedside tests (pregnancy test, urinalysis) — to immediately exclude emergencies and common mimics
Blood tests (tumour markers, CBC, biochemistry) — to stratify risk and guide imaging
Imaging (ultrasound → CT/MRI) — to characterise the mass and assess extent
Histopathology (biopsy or surgical specimen) — to provide definitive tissue diagnosis when needed

The lecture slide (GC 118, p2) structures the approach as: History taking → Physical exam → DDx → Management, with pelvic imaging forming a core component ^[1]. A separate section of the lecture (Block C, p18) explicitly identifies "Part 4: Investigations / Pelvic imaging" and notes that "some indications require emergency management" — i.e., certain findings on investigation must trigger immediate action (e.g., ectopic pregnancy, torsion). ^[10]

The following algorithm represents the standard clinical approach in Hong Kong to a woman presenting with a pelvic mass:

3. Step-by-Step Investigation Modalities

Test	What It Tells You	Why It's Done First	Key Interpretation
Urine pregnancy test (or serum βhCG)	Detects pregnancy (intrauterine or ectopic)	Must be the FIRST investigation in ANY woman of reproductive age with a pelvic mass — failure to do so risks missing ectopic pregnancy (life-threatening) and exposes a potential fetus to harmful investigations (CT radiation, contrast) ^[10]^[11]	Positive → USS to locate pregnancy. Negative → proceed with workup
Urinalysis + dipstick	Screens for UTI, haematuria, glycosuria	May reveal urological cause (haematuria → bladder CA; pyuria → infection/TOA)	Haematuria + pelvic mass → consider bladder cancer, renal pathology ^[12]
Vital signs	Identifies haemodynamic instability	Ruptured ectopic, ruptured ovarian cyst, sepsis from TOA	Tachycardia + hypotension = haemorrhagic shock → emergency

The Pregnancy Test Is Non-Negotiable

Never skip the pregnancy test. Even if the patient "can't be pregnant" — always test. Ectopic pregnancy kills, and a positive test completely changes the diagnostic pathway. This is emphasised on the lecture slide: "Don't forget about pregnancy → especially for teenage girls" ^[8].

Category	Tests	Rationale and Interpretation
Haematology	CBC with differential	Anaemia (Hb ↓) → chronic blood loss from menorrhagia (fibroids) or malignancy. Leukocytosis (WCC ↑) → infection (TOA, appendiceal abscess) or haematological malignancy. Thrombocytosis → reactive (malignancy, inflammation) ^[11]
Biochemistry	RFT, electrolytes	Ureteric obstruction from pelvic mass → obstructive uropathy → ↑creatinine. Also baseline before contrast CT
	LFT	Liver metastases (ovarian cancer, CRC) → ↑ALP, ↑GGT, ↑bilirubin
	CRP / ESR	Inflammatory causes: TOA, diverticular abscess, appendiceal abscess. Also elevated in malignancy
	Glucose, HbA1c	DM is a risk factor for endometrial cancer and affects surgical fitness
Tumour Markers	CA-125	The most important tumour marker for epithelial ovarian cancer. Normal < 35 U/mL. Elevated in ~80% of advanced epithelial ovarian cancer (especially high-grade serous). BUT non-specific: also elevated in endometriosis, PID, liver cirrhosis, pregnancy, peritonitis, fibroids, menstruation ^[1]
	HE4 (Human Epididymis Protein 4)	Newer marker, more specific than CA-125 (not elevated by endometriosis or benign cysts). Used in combination with CA-125 in the ROMA (Risk of Ovarian Malignancy Algorithm)
	CEA	Elevated in colorectal cancer, mucinous ovarian cancer, other GI malignancies. Useful when GI origin suspected
	CA 19-9	Mucinous ovarian tumours, pancreatic/biliary cancers. Also elevated in endometriosis and mature cystic teratomas
	AFP (α-fetoprotein)	Germ cell tumours: yolk sac tumour (↑↑AFP), embryonal carcinoma. Also hepatocellular carcinoma
	βhCG (quantitative)	Germ cell tumours: choriocarcinoma (↑↑βhCG), embryonal carcinoma. Also ectopic/molar pregnancy
	LDH	Germ cell tumours: dysgerminoma (↑↑LDH). Non-specific; also elevated in any tissue damage/turnover
	Inhibin	Granulosa cell tumour (sex cord-stromal)
Other	Clotting profile, Group & Save	Pre-operative or if haemorrhage suspected

Understanding Tumour Markers from First Principles:

Tumour markers are proteins or glycoproteins produced by tumour cells (or by the body in response to cancer) that can be detected in blood. They are not diagnostic on their own — they are used for:

Risk stratification (pre-operative: is this likely benign or malignant?)
Monitoring treatment response (post-treatment: is the marker falling?)
Surveillance for recurrence (rising marker = possible recurrence)

The key problem is specificity — many benign conditions elevate the same markers. This is why CA-125 alone is insufficient for diagnosis and must always be interpreted in clinical context.

A useful mnemonic for ovarian tumour markers by cell type:

Epithelial → CA-125, HE4

Germ cell → AFP, βhCG, LDH (think "the same markers as testicular tumours" — because germ cells are germ cells regardless of sex)

Sex cord-stromal → Inhibin, oestradiol, testosterone

3.3 Step 3 — Pelvic Ultrasound (First-Line Imaging)

Pelvic ultrasound is the cornerstone investigation for a pelvic mass ^[1]. It is the first-line imaging modality because it is readily available, non-invasive, no radiation, and provides excellent resolution for pelvic structures.

The lecture and radiology notes distinguish two complementary approaches: ^[5]

Feature	Trans-abdominal USS (TAUS)	Transvaginal USS (TVUSS)
Probe frequency	4–5 MHz (lower frequency → deeper penetration)	Up to 10 MHz (higher frequency → better resolution)
Bladder	Requires full bladder (as an acoustic window — urine transmits sound well, displaces bowel gas)	Full bladder NOT required
Field of view	Panoramic — good for large masses that extend above the pelvis	Smaller field of view
Resolution	Lower	Higher — improved resolution and contrast, better anatomical detail, reduced attenuation
When preferred	First-line (less invasive); essential for large masses; provides overview	Second-line complementary — for detailed assessment of ovarian/uterine/adnexal pathology; cannot visualise large masses in their entirety
Patient acceptability	Better (external probe)	Requires vaginal probe (may not be appropriate for virgins, children)

Exam pearl (from Ryan Ho Radiology Q23, M19 Rotation 3): When a patient has a left adnexal mass detected on PV examination with urinary incontinence, the most appropriate investigation is transabdominal ultrasound (not TVUSS) — because you need the panoramic view and the full bladder as an acoustic window for a mass that may be large, and you need to assess the urinary tract as well ^[5].

USS Finding	Diagnosis Suggested	Why
Unilocular, anechoic, thin-walled cyst < 5 cm	Functional cyst (follicular or corpus luteum)	Simple fluid-filled structure with no solid components — reflects physiological ovarian activity
Homogeneous low-level internal echoes ("ground glass")	Endometriotic cyst (endometrioma / "chocolate cyst")	Old haemolysed blood has uniform fine echogenicity — the "ground glass" or "chocolate" pattern. Often causes cyclical pain in young patients ^[5]
Hyperechoic mass with posterior acoustic shadowing, containing calcification/teeth/fat	Mature cystic teratoma (dermoid cyst)	Ectodermal tissue (hair, teeth, fat) produces strong echogenic reflections. Fat-fluid level may be visible ("dermoid plug")
Large multiloculated cystic mass	Mucinous cystadenoma (if benign) or mucinous cystadenocarcinoma (if malignant)	Multiple compartments filled with mucin of varying viscosity → different echogenicity in each locule
Solid hypoechoic mass within the myometrium, with whorled texture	Uterine fibroid (leiomyoma)	Smooth muscle + fibrous tissue creates the characteristic "whorled" hypoechoic pattern. May show calcification (shadowing) in degenerated fibroids
Diffusely enlarged uterus with heterogeneous myometrium, myometrial cysts, ill-defined endo-myometrial junction	Adenomyosis	Ectopic endometrial glands within myometrium → small foci of bleeding → tiny cystic spaces within a thickened, heterogeneous myometrium
Anechoic cyst with mixed content, solid components with vascularity (on Doppler)	Ovarian cancer	"Mixed solid-cystic lesion" in a 70-year-old with pelvic mass → likely malignant ^[5]

These USS features should raise the suspicion of ovarian malignancy: ^[1]^[5]

Feature	Rationale
Solid component within a cystic mass	Benign cysts are usually entirely cystic; solid elements suggest neoplastic tissue
Thick septations (> 3 mm)	Thin septae are benign; thick, irregular septae suggest tumour growth along septae
Papillary excrescences (projections into the cyst)	Represent tumour growth protruding into the cyst lumen
Increased vascularity on Doppler (low resistance flow)	Malignant neovascularisation — tumours recruit new blood vessels (angiogenesis) that lack normal smooth muscle → low resistance to flow
Bilateral	Epithelial ovarian cancer frequently seeds the contralateral ovary
Associated ascites	Peritoneal carcinomatosis → fluid accumulation

Exam Question Pattern

From Ryan Ho Radiology (Q20, M18 Rotation 3): "F/75 complained of increasing abdominal girth. PE found abdominal mass arising from pelvis and ascites. USG found mixed solid-cystic lesion at pelvis and ascites. Uterus cannot be visualised. Most likely diagnosis? → Ovarian cancer" ^[5]. The reasoning: postmenopausal + mixed solid-cystic + ascites + cannot identify uterus separately (mass obscures it or is very large) = ovarian cancer until proven otherwise.

3.4 Step 4 — Advanced Imaging

When ultrasound alone is insufficient (equivocal findings, suspected malignancy requiring staging, complex anatomy), further imaging is pursued:

Aspect	Detail
When	Suspected malignancy (staging), equivocal USS, assessment of lymphadenopathy, peritoneal disease, distant metastases
Strengths	Excellent for staging: detects peritoneal deposits, omental cake, lymphadenopathy (para-aortic, pelvic), liver/lung metastases, ascites. Fast acquisition. Available in emergency
Findings in ovarian cancer	Large mass with multiple septation, solid and cystic components, peritoneal thickening/nodularity, omental cake (thickened, enhancing omentum), ascites, retroperitoneal lymphadenopathy ^[5]
Limitations	Radiation exposure. Less soft tissue contrast than MRI for pelvic organs. Should not be used in pregnancy. Requires IV contrast (check renal function)
Role in emergencies	CT abdomen and pelvis with contrast is used for acute abdomen workup — e.g., appendiceal abscess, diverticular abscess, perforated viscus ^[13]^[11]

Aspect	Detail
When	Fibroid mapping (pre-operative planning for myomectomy or uterine artery embolisation), characterisation of indeterminate adnexal masses, endometriosis staging, local staging of cervical/endometrial cancer
Strengths	Superior soft tissue contrast — the gold standard for characterising uterine and adnexal pathology. No radiation. Can distinguish fibroid subtypes, map their relationship to the endometrial cavity, differentiate adenomyosis from fibroids
Fibroid on MRI	Well-circumscribed, low T2 signal (because of dense fibrous/smooth muscle tissue — low water content). Degenerated fibroids may show variable signal
Endometrioma on MRI	"Shading sign" on T2-weighted images — high T1 signal (blood products), low T2 signal (concentrated old blood with high protein content causing T2 shortening)
Ovarian cancer on MRI	Solid enhancing tissue, peritoneal deposits, lymphadenopathy. MRI is particularly useful for assessing resectability and involvement of adjacent structures

Aspect	Detail
What	Fluoroscopic imaging after injecting radio-opaque contrast through the cervix into the uterine cavity and fallopian tubes
When	Infertility workup — to demonstrate patency of the fallopian tubes and outline the endometrial cavity ^[5]
Findings	Contrast fills the uterine cavity (can show submucous fibroids as filling defects, congenital anomalies), flows along the fallopian tubes, and spills into the peritoneal cavity if tubes are patent
NOT used for pelvic mass workup per se	But worth knowing as it is a pelvic imaging modality tested in exams

Exam pearl (Ryan Ho Radiology Q23, M18 Rotation 3): "33/F Ix for infertility, what imaging exam confirms fallopian tube patency? → Hysterosalpingogram" ^[5].

3.5 Step 5 — Risk Stratification Scoring Systems

Once you have clinical data, blood results, and imaging, you need to decide: is this mass likely benign or malignant? Several scoring systems exist to help:

The RMI is the most widely used scoring system in clinical practice for pre-operative assessment of ovarian masses: ^[1]

Formula: RMI = U × M × CA-125

Where:

U = Ultrasound score
- 0 points if no suspicious features
- 1 point if one suspicious feature
- 3 points if ≥ 2 suspicious features
- (Suspicious features: multilocular, solid areas, bilateral, ascites, metastases)
M = Menopausal status
- 1 if premenopausal
- 3 if postmenopausal
CA-125 = serum CA-125 level (U/mL)

Interpretation:

RMI < 200 → low risk of malignancy → can be managed by general gynaecologist
RMI ≥ 200 → high risk of malignancy → should be referred to a gynaecological oncology centre for surgery

Why does this formula work? It elegantly combines the three key risk factors: (1) ultrasound morphology (structural concern), (2) menopausal status (age-related risk), and (3) CA-125 (biochemical signal). The postmenopausal weighting (×3) and multiple USS feature weighting (×3) heavily penalise the combination of postmenopausal status + complex mass + elevated CA-125, which is exactly the high-risk combination for ovarian cancer.

Sensitivity ~78%, Specificity ~87% at a cut-off of 200.

More modern approaches developed by the International Ovarian Tumor Analysis (IOTA) group:

IOTA Simple Rules: Use 5 "B-features" (benign) and 5 "M-features" (malignant) on USS. If only B-features → benign; if only M-features → malignant; if mixed or no features → indeterminate (need expert USS or MRI).
- B-features: unilocular, solid component < 7 mm, acoustic shadows, smooth multilocular < 10 cm, no blood flow
- M-features: irregular solid tumour, ascites, ≥ 4 papillary structures, irregular multilocular-solid > 10 cm, very strong blood flow
ADNEX model: A multivariate logistic regression model that gives a percentage risk of malignancy (and even the subtype — borderline, stage I, stage II–IV) based on age, CA-125, and six USS parameters.

Combines HE4 + CA-125 + menopausal status into a predictive algorithm.
Particularly useful when CA-125 is equivocal (e.g., mildly elevated in a premenopausal woman who may have endometriosis).

The definitive diagnosis of a pelvic mass — especially when malignancy is suspected — requires histopathological examination.

Method	When Used	Key Points
Surgical excision and histopathology	The gold standard for ovarian masses. Suspicious ovarian masses should be removed INTACT (not biopsied in situ) to avoid tumour spillage and upstaging	If RMI > 200 or suspicious imaging → laparotomy with full staging (midline incision, peritoneal washings, TAH + BSO + omentectomy + lymph node sampling). If low risk → laparoscopic cystectomy or oophorectomy
Ascitic fluid cytology (paracentesis)	When ascites is present and tissue diagnosis is needed pre-operatively (e.g., patient unfit for surgery)	Peritoneal fluid sent for cytology. Can identify malignant cells but sensitivity is variable (~60–90%)
Image-guided biopsy (CT or USS-guided)	Rarely used for primary ovarian masses (risk of spillage). May be used for: (1) suspected recurrent disease, (2) non-ovarian pelvic masses (e.g., retroperitoneal sarcoma, lymphoma), (3) liver/omental metastases for tissue confirmation	Percutaneous biopsy of an ovarian mass is generally AVOIDED because of the risk of tumour seeding along the needle tract and intraperitoneal spillage (which can upstage the cancer)
Frozen section (intra-operative)	During surgery, a sample is sent for rapid histological assessment. Guides the extent of surgery (if benign → conservative; if malignant → proceed to full staging)	Accuracy ~90–95% for distinguishing benign vs. malignant. Less accurate for borderline tumours
Endometrial sampling (Pipelle biopsy or hysteroscopy)	When the pelvic mass is uterine and endometrial cancer is suspected (e.g., PMB + thickened endometrium)	Pipelle biopsy is an office procedure; hysteroscopy allows direct visualisation + targeted biopsy
Cervical biopsy (colposcopy-directed)	When cervical cancer is suspected

Never Biopsy a Suspicious Ovarian Mass Percutaneously

Unlike many other solid organ tumours where biopsy precedes treatment, ovarian masses suspected of malignancy should NOT be biopsied percutaneously. The reasons: (1) Risk of tumour spillage into the peritoneal cavity, which worsens prognosis and upstages the cancer from stage IC (capsule ruptured) to requiring more aggressive chemotherapy; (2) The entire specimen is needed for accurate histological diagnosis (ovarian tumours are heterogeneous). The principle is: remove it intact, examine it all.

Diagnosis	Pregnancy Test	Key Bloods / Markers	USS Findings	Advanced Imaging
Functional cyst	Negative	CA-125 normal	Unilocular, anechoic, thin-walled, < 5 cm	Not needed. Repeat USS 6–8 weeks → should resolve
Endometrioma	Negative	CA-125 mildly ↑	"Ground glass" homogeneous low-level echoes, no solid component ^[5]	MRI: "shading sign" on T2
Dermoid (mature cystic teratoma)	Negative	AFP normal, CA 19-9 may be ↑	Hyperechoic, calcification/teeth, fat-fluid level, "dermoid plug"	CT: fat density (-20 to -120 HU) + calcification is pathognomonic
Serous/mucinous cystadenoma	Negative	CA-125 normal/mildly ↑	Unilocular (serous) or multilocular (mucinous), thin walls, no solid component	CT/MRI if large or indeterminate
Epithelial ovarian cancer	Negative	CA-125 ↑↑ (often > 200), HE4 ↑	Complex: solid + cystic, thick septae, papillary excrescences, bilateral, Doppler vascularity, ascites ^[5]	CT staging: peritoneal deposits, omental cake, lymphadenopathy, pleural effusion
Germ cell tumour	Negative (unless choriocarcinoma → βhCG ↑↑)	AFP ↑ (yolk sac), βhCG ↑ (choriocarcinoma), LDH ↑ (dysgerminoma)	Solid or mixed, unilateral, in young woman	CT staging
Uterine fibroid	Negative	CBC (anaemia), CA-125 normal	Solid hypoechoic mass within myometrium, whorled texture, calcification in degenerated fibroid	MRI: T2 low signal, well-circumscribed. Gold standard for mapping fibroids pre-operatively
Ectopic pregnancy	Positive	Serum βhCG: positive but lower than expected for gestational age, may show abnormal doubling	Empty uterus + adnexal mass (may see "tubal ring" sign) + free fluid in Pouch of Douglas	Not usually needed; if USS indeterminate → serial βhCG + repeat USS
TOA	Negative	WCC ↑, CRP ↑↑	Complex adnexal mass with thick wall, internal debris, surrounding inflammation	CT if USS equivocal: rim-enhancing collection
Distended bladder	Negative	RFT may be deranged (if obstructive uropathy)	Fluid-filled structure in midline, resolves post-catheter	Not needed if confirmed by catheter

Scenario	Investigation	Rationale
Suspected ovarian torsion	USS with Doppler (TVUSS)	Absent or reduced ovarian blood flow on Doppler. Enlarged oedematous ovary ("whirlpool sign" of twisted pedicle). However, normal Doppler does NOT exclude torsion (dual blood supply may maintain some flow)
Suspected appendiceal mass	CT abdomen pelvis with contrast	Distended appendix > 6 mm, wall thickening, periappendiceal fat stranding ± appendicolith, abscess collection ^[14]
Suspected CRC	Colonoscopy (gold standard) + CT staging	Direct visualisation + biopsy of colonic lesion; CT for staging
Infertility workup with pelvic mass	Hysterosalpingogram (HSG)	Demonstrates tubal patency and uterine cavity shape ^[5]
Pre-operative fibroid mapping	MRI pelvis	Best modality for number, size, location (FIGO classification), relationship to endometrial cavity, degeneration type
Suspected endometrial cancer	Transvaginal USS (endometrial thickness) + Pipelle endometrial biopsy	Postmenopausal endometrial thickness > 4 mm is abnormal → requires histological sampling

The power of the diagnostic approach lies in combining clinical, biochemical, and imaging data — no single test is diagnostic in isolation.

Example 1: 65-year-old with CA-125 of 450, bilateral complex masses on USS, and ascites → RMI = 3 (USS) × 3 (postmenopausal) × 450 (CA-125) = 4,050 → very high risk → refer to gynae-oncology for staging laparotomy.

Example 2: 28-year-old with CA-125 of 60, unilateral 4 cm cyst on USS, regular periods → RMI = 0 (USS) × 1 (premenopausal) × 60 = 0 → very low risk → likely endometrioma or functional cyst. Repeat USS in 6–8 weeks.

The lesson: CA-125 of 60 in a premenopausal woman is almost certainly benign (endometriosis, luteal cyst). CA-125 of 60 in a postmenopausal woman with a complex mass demands urgent investigation.

High Yield Summary — Diagnostic Approach to Pelvic Mass

1. Always start with a pregnancy test — in ANY woman of reproductive age, regardless of history.

2. Pelvic ultrasound (TAUS + TVUSS) is the first-line imaging modality for all pelvic masses. TAUS gives the panoramic view (good for large masses); TVUSS gives superior resolution for adnexal and uterine detail.

3. Key USS features of malignancy: solid components, thick septae, papillary excrescences, bilateral, Doppler vascularity, ascites.

4. CA-125 is the most important tumour marker for epithelial ovarian cancer, but is non-specific. Interpret in context: age, menopausal status, USS findings. Use RMI scoring (U × M × CA-125). RMI ≥ 200 → refer to gynae-oncology.

5. CT is for staging when malignancy is suspected (peritoneal disease, lymphadenopathy, distant metastases). MRI is for soft tissue characterisation (fibroid mapping, endometriosis, indeterminate adnexal masses).

6. Do NOT percutaneously biopsy a suspicious ovarian mass — risk of spillage and upstaging. Remove it intact surgically.

7. Frozen section intra-operatively guides surgical extent (conservative vs. radical).

8. For fibroids: USS is first-line for diagnosis; MRI is gold standard for pre-operative mapping.

9. For endometrial cancer: TVUSS for endometrial thickness + Pipelle biopsy for histology.

10. Germ cell tumour markers: AFP (yolk sac), βhCG (choriocarcinoma), LDH (dysgerminoma) — same as testicular tumour markers.

Active Recall - Investigations for Pelvic Mass

References

^[1] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p2, p21) ^[5] Senior notes: Ryan Ho Radiology.pdf (p32, p34, p39, p40) ^[8] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p17, p18) ^[10] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p18) ^[11] Senior notes: Ryan Ho Fundamentals.pdf (p76, p279) ^[12] Senior notes: Ryan Ho Urogenital.pdf (p133, p134) ^[13] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p36, p39, p81) ^[14] Senior notes: Ryan Ho GI.pdf (p150)

Management of Pelvic Mass

The lecture summary slide (GC 118, p71) states the key principle: "Management will depend on the age, symptom, condition and wish of the patient" ^[1]. This single sentence captures the four pillars of management decision-making:

Age — reproductive vs. postmenopausal; fertility desires; life expectancy
Symptoms — is the mass causing problems (pain, bleeding, pressure), or is it an incidental finding?
Condition — what is the mass? Benign vs. malignant? Emergency vs. elective?
Wish of the patient — fertility preservation, desire to avoid surgery, cultural preferences

The lecture also notes: "Some indications require emergency management — ovarian cyst complications, pregnancy complications" ^[10]. So the very first branch in any management algorithm is: is this an emergency?

The management approach is best understood by condition, since each type of pelvic mass has its own specific treatment pathway. However, there is a unifying master algorithm that applies to all pelvic masses.

3. Management by Condition

Understanding the rationale from first principles: Functional cysts (follicular and corpus luteum) are by-products of normal ovarian physiology. A follicular cyst forms when a follicle fails to rupture; a corpus luteum cyst forms when the corpus luteum fails to regress. Since these structures are driven by the menstrual cycle, they almost always resolve spontaneously within 1–3 cycles as hormone levels change.

Approach	Detail	Rationale
Conservative observation	Repeat USS in 6–8 weeks	Most functional cysts < 5 cm resolve spontaneously. The 6–8 week interval spans 1–2 menstrual cycles, allowing the cyst to regress if it is physiological
COCP	May be offered to prevent new functional cysts (by suppressing ovulation)	Does NOT accelerate resolution of an existing cyst — this is a common misconception. COCP prevents future cysts by suppressing the HPO axis
Surgical excision	Laparoscopic cystectomy or oophorectomy	Indicated if: (1) persistent > 3 cycles, (2) enlarging, (3) becoming symptomatic, (4) suspicious features develop, (5) postmenopausal (no "functional" explanation)

Common Exam Misconception

The COCP does NOT treat an existing functional ovarian cyst — it only prevents new ones from forming. An existing cyst resolves on its own because the hormonal milieu changes naturally with the next cycle. If the cyst persists beyond 2–3 cycles, it is probably not functional and needs further evaluation.

Tumour	Management	Why
Mature cystic teratoma (dermoid cyst)	Laparoscopic ovarian cystectomy (preferred if < 10 cm and fertility desired) or oophorectomy	Dermoids do not resolve spontaneously (they are neoplastic, not functional). Risk of complications: torsion (due to heavy cyst acting as a pendulum), rupture (chemical peritonitis from sebaceous content), and rare malignant transformation (< 2%, usually in > 40 yr). Fertility-sparing surgery is standard in young women
Serous/mucinous cystadenoma	Laparoscopic cystectomy or oophorectomy	These are true neoplasms — they will not regress. Mucinous types can become enormous. Risk of malignancy increases with age and complexity. Surgical excision removes the mass and provides histological diagnosis
Ovarian fibroma	Oophorectomy	Solid tumour; important to differentiate from malignancy on histology. If Meigs' syndrome present (ascites + pleural effusion), both resolve after tumour removal

Key surgical principles for benign ovarian masses:

In young women desiring fertility → ovarian cystectomy (preserve ovarian tissue)
In older women or if malignancy suspected → oophorectomy (remove entire ovary)
Avoid spillage — endometriomas (chocolate cyst content causes peritoneal irritation and adhesions), dermoids (sebaceous material causes severe chemical peritonitis), and potentially malignant cysts (spillage can upstage cancer)
Use an endobag to retrieve specimens laparoscopically and prevent spillage into the peritoneal cavity

3.3 Suspected or Confirmed Ovarian Cancer

This is the most critical management pathway. Ovarian cancer management requires a multidisciplinary team (MDT) approach led by a gynaecological oncologist. ^[1]

The cornerstone of ovarian cancer management is primary debulking surgery (PDS) — the goal is to remove as much tumour as possible (optimal cytoreduction), ideally to no visible residual disease (R0).

Component of Staging Laparotomy	Purpose	Explanation
Midline vertical incision	Allows complete access to the entire abdomen and pelvis	A transverse incision is inadequate — you need to inspect the diaphragm, paracolic gutters, omentum, and all peritoneal surfaces
Peritoneal washings / ascitic fluid for cytology	Cytological staging — identifies malignant cells in peritoneal fluid	Positive washings upstage the cancer (stage IC/IIIA)
Total abdominal hysterectomy + bilateral salpingo-oophorectomy (TAH + BSO)	Remove the primary tumour and uterus	The contralateral ovary frequently harbours microscopic disease; uterus is removed to facilitate complete clearance
Infracolic omentectomy	Remove the greater omentum	Omentum is the most common site of peritoneal metastasis ("omental cake" on CT). Contains milky spots rich in macrophages where tumour cells preferentially seed
Pelvic and para-aortic lymph node dissection/sampling	Lymphatic staging	Ovarian cancer spreads to para-aortic nodes (following the ovarian vessels to the aorta at L2). Pelvic nodes may also be involved
Appendicectomy	Particularly in mucinous tumours	To exclude a primary appendiceal mucinous tumour masquerading as ovarian (pseudomyxoma peritonei)
Peritoneal biopsies	Multiple biopsies from paracolic gutters, diaphragm, pelvic peritoneum	Detects microscopic peritoneal implants not visible to the naked eye
Maximum cytoreductive effort	Resection of all visible tumour deposits — may include bowel resection, diaphragmatic stripping, splenectomy, peritoneal stripping	The single most important prognostic factor in advanced ovarian cancer is the amount of residual disease after surgery — patients with no visible residual (R0) have significantly better survival than those with > 1 cm residual

In young women with early-stage (IA), low-grade ovarian cancer and desire for fertility, conservative surgery may be offered:
- Unilateral salpingo-oophorectomy (USO) + comprehensive staging (peritoneal washings, omentectomy, LN sampling, contralateral ovarian biopsy)
- Followed by completion surgery (TAH + contralateral BSO) after childbearing is complete
This is ONLY for: stage IA, unilateral, non-clear cell histology, no extra-ovarian disease

Adjuvant platinum-based chemotherapy is the standard of care for epithelial ovarian cancer:

Regimen	Indication	Mechanism
Carboplatin + Paclitaxel (first-line)	Standard adjuvant for all epithelial ovarian cancer except very early stage (IA, grade 1)	Carboplatin (a platinum compound) cross-links DNA strands → prevents DNA replication and transcription → tumour cell apoptosis. Paclitaxel (a taxane, from Taxus = yew tree) stabilises microtubules → prevents mitotic spindle disassembly → arrests cell division in M phase
Neoadjuvant chemotherapy (NACT)	When primary debulking surgery is not feasible (e.g., extensive peritoneal disease, poor performance status, unresectable tumour bulk)	3 cycles of chemotherapy → interval debulking surgery (IDS) → 3 more cycles. This "sandwich" approach reduces tumour burden before surgery
Bevacizumab (anti-VEGF)	Added to first-line chemotherapy in advanced stage (FIGO IIIB–IV) or high-risk stage III	Monoclonal antibody against VEGF (vascular endothelial growth factor) — "beva" = antibody targeting angiogenesis. Blocks new blood vessel formation by the tumour → starves tumour of oxygen and nutrients
PARP inhibitors (olaparib, niraparib)	Maintenance therapy after response to platinum-based chemo, especially in BRCA-mutant tumours	PARP (poly ADP-ribose polymerase) is a DNA repair enzyme. In BRCA-mutant cells, homologous recombination repair is already defective. Blocking PARP eliminates the "backup" repair pathway → synthetic lethality → tumour cell death. Normal cells with intact BRCA can still repair DNA, so they survive

Why platinum-based? Ovarian cancer (especially high-grade serous) is remarkably chemo-sensitive to platinum compounds. The initial response rate is ~80%. However, most patients eventually relapse — the platinum-free interval determines subsequent treatment (platinum-sensitive relapse if > 6 months; platinum-resistant if < 6 months).

Feature	Approach	Rationale
Surgical	Fertility-sparing USO + staging (even in advanced disease, as they are chemo-sensitive)	Germ cell tumours are usually unilateral and occur in young women. Excellent response to chemotherapy means aggressive surgical debulking of the contralateral ovary is unnecessary
Chemotherapy	BEP regimen: Bleomycin + Etoposide + Cisplatin	Same regimen as testicular germ cell tumours (because germ cells are germ cells). Cure rates > 90% even in advanced disease

3.4 Uterine Fibroids

Fibroid management is nuanced and highly individualised. The key question is: does the patient have symptoms, and what is her reproductive plan?

Treatment	Mechanism	Indications	Key Points
Tranexamic acid	Anti-fibrinolytic: blocks plasminogen → plasmin conversion, thereby reducing breakdown of fibrin clots at the endometrial surface → ↓menstrual blood loss	First-line for menorrhagia ^[15]	Taken only during menstruation (not continuous). Reduces menstrual blood loss by ~50%. Contraindicated with concurrent COCP use (thrombotic risk) ^[15]
Non-steroidal anti-inflammatory drugs (NSAIDs)	Inhibit cyclooxygenase → ↓prostaglandin synthesis → ↓endometrial blood flow and uterine contractility → ↓menstrual blood loss and dysmenorrhoea	Menorrhagia + dysmenorrhoea	Mefenamic acid is commonly used. Also taken only during menstruation
Combined oral contraceptive pill (COCP)	Suppresses ovarian steroid production → thin, atrophic endometrium → less menstrual bleeding. Also provides regular withdrawal bleeds	Menorrhagia, cycle regulation	Contraindicated if uncontrolled CV risk factors or active smoking ^[15]
Levonorgestrel-releasing intrauterine system (LNG-IUS / Mirena)	Local progesterone effect → endometrial decidualisation and atrophy → dramatically ↓menstrual blood loss	Effective for menorrhagia, especially in women not planning pregnancy	Not ideal if large submucosal fibroid distorting the cavity (risk of expulsion). May also cause fibroid volume to decrease slightly via progesterone effect
GnRH agonists (e.g. leuprolide / goserelin)	Initially stimulate GnRH receptors → then cause receptor downregulation ("medical menopause") → ↓↓ oestrogen and progesterone → fibroid shrinkage (40–60% volume reduction)	Short-term pre-operative use to shrink fibroids before surgery (3–6 months max) or as bridge-to-menopause	Cannot be used long-term (> 6 months) due to hypoestrogenic side effects: bone density loss, vasomotor symptoms (hot flushes), vaginal dryness. Fibroids regrow after stopping. "Add-back" therapy (low-dose oestrogen + progestogen) can mitigate side effects
GnRH antagonists with add-back (e.g. relugolix + E2/NETA)	Direct competitive blockade of GnRH receptors → rapid ↓ oestrogen → fibroid shrinkage. Combined with add-back hormones (oestradiol + norethindrone acetate) to prevent bone loss and vasomotor symptoms	Newer option for long-term medical management of fibroids (FDA-approved 2021)	Oral medication (unlike injectable GnRH agonists). Can be used for up to 24 months with add-back
Ulipristal acetate (selective progesterone receptor modulator, SPRM)	Binds progesterone receptors → blocks progesterone action on fibroid → ↓fibroid growth and ↓endometrial bleeding	Previously used for pre-operative fibroid management	Currently restricted/withdrawn in many countries (including EU) due to risk of severe liver injury. Important to know for exams but unlikely to be first-line in current clinical practice

Procedure	Approach	Indications	Contraindications / Limitations
Myomectomy	Hysteroscopic (FIGO 0–2 submucosal): resected transcervically using resectoscope. Laparoscopic or open (FIGO 3–7): enucleation of fibroid from myometrium with closure of uterine defect	Fertility desired, symptomatic fibroids	Higher risk of recurrence (~15–30% over 5 years — fibroids are multifocal). May need to convert to open if multiple/large. Uterine rupture risk in subsequent pregnancy (especially if endometrial cavity entered)
Hysterectomy	Total abdominal hysterectomy (TAH), laparoscopic hysterectomy, or vaginal hysterectomy	Definitive treatment — when fertility no longer desired, severe symptoms, failed other treatments, suspected malignancy	Irreversible — loss of fertility. Surgical risks (bleeding, infection, ureteric/bladder injury — remember "water under the bridge"). Not appropriate if fertility desired
Uterine artery embolisation (UAE)	Interventional radiology procedure: catheter inserted via femoral artery → bilateral uterine arteries selectively embolised with particles (PVA particles or gelfoam) → devascularisation of fibroids → ischaemic necrosis and shrinkage ^[13]	Symptomatic fibroids in women who wish to avoid surgery or are poor surgical candidates	Contraindicated if fertility desired (concerns about uterine blood supply and endometrial/ovarian damage affecting future pregnancy). Also contraindicated if infection suspected, if pedunculated subserosal fibroid (risk of detachment and peritonitis), or suspected malignancy
MR-guided focused ultrasound surgery (MRgFUS / HIFU)	High-intensity focused ultrasound beams converge on the fibroid under MRI guidance → thermal ablation → coagulative necrosis	Selected fibroids (favourable location, not too large, not too many)	Limited by fibroid number, size, and location. Not widely available. Fertility data limited
Radiofrequency ablation (RFA, e.g. Acessa)	Laparoscopic or transcervical insertion of RF probe into fibroid → thermal destruction	Symptomatic, intramural or subserosal fibroids	Newer technique; growing evidence base. May preserve uterus for future fertility

UAE is specifically mentioned in the radiology notes as a key interventional radiology procedure: "Uterine fibroid embolisation" using embolic agents (Gelfoam, PVA particles, coil, glue) to block the uterine artery ^[13].

Hysterectomy Routes — How to Choose

Vaginal hysterectomy is preferred when technically feasible (shortest recovery, fewest complications) — best for normal-sized or moderately enlarged uterus with adequate vaginal access.

Laparoscopic hysterectomy (total or laparoscopic-assisted vaginal) is preferred for larger uteri or when concurrent procedures are needed (adhesiolysis, oophorectomy).

Abdominal hysterectomy is reserved for: very large uteri (> 12–14 weeks' size), suspected malignancy (need midline incision for staging), complex pelvic pathology (severe adhesions, endometriosis).

Approach	Treatment	Mechanism and Rationale
Medical	LNG-IUS (Mirena), COCP, GnRH agonists, progestogens	All reduce oestrogenic stimulation of ectopic endometrial tissue within the myometrium → ↓ cyclical bleeding and inflammation → ↓ pain and menorrhagia
Surgical	Hysterectomy (definitive)	Adenomyosis is diffuse throughout the myometrium and cannot be "excised" the way a fibroid can. Hysterectomy is the only cure. Fertility-sparing adenomyomectomy is experimental

Approach	Treatment	Indications
Medical	COCP (continuous), progestogens (dienogest), GnRH agonists, LNG-IUS	Pain management, suppression of ectopic endometrial tissue, prevention of recurrence after surgery
Surgical	Laparoscopic excision/drainage of endometrioma (cystectomy preferred over drainage alone — lower recurrence rate); excision/ablation of peritoneal deposits	Symptomatic endometrioma > 4 cm, failed medical therapy, fertility (endometrioma may impair ovum pickup and ovarian reserve), suspicious features
Fertility	Surgery to restore anatomy + ART (IVF) if needed	Endometriosis impairs fertility through adhesions (mechanical distortion), inflammatory peritoneal fluid (toxic to sperm/embryo), and reduced ovarian reserve (from cysts and surgery)

Approach	Treatment	Indications
Expectant	Close monitoring with serial βhCG measurements	Small ectopic, declining βhCG, haemodynamically stable, no symptoms, βhCG < 1000–1500. Many tubal ectopics will undergo tubal abortion and resolve. Patient must be reliable for follow-up
Medical	Methotrexate (single or multi-dose IM injection)	Unruptured ectopic, βhCG < 5000 (some centres < 3000), no fetal heartbeat, haemodynamically stable, no contraindication to methotrexate (e.g., liver/renal disease, thrombocytopaenia). Methotrexate inhibits dihydrofolate reductase → blocks DNA synthesis in rapidly dividing trophoblast cells → regression of ectopic pregnancy
Surgical	Laparoscopic salpingectomy (preferred) or salpingotomy	Ruptured ectopic (emergency), haemodynamic instability, βhCG > 5000, fetal heartbeat seen, contraindication/failure of methotrexate. Salpingectomy (removing the tube) is preferred over salpingotomy (opening the tube and removing the pregnancy) because of lower risk of persistent trophoblast and future ectopic in the same tube. However, salpingotomy may be preferred if the contralateral tube is absent/damaged (to preserve any chance of natural conception)

Stage	Treatment	Rationale
Mild / unruptured	Broad-spectrum IV antibiotics (e.g., ceftriaxone + doxycycline + metronidazole — covers N. gonorrhoeae, C. trachomatis, anaerobes, and Gram-negatives)	Polymicrobial ascending infection; initial antibiotic therapy is successful in ~75% of cases
No response to antibiotics (48–72 hours)	Image-guided percutaneous or transvaginal drainage (interventional radiology or USS-guided)	Antibiotics cannot penetrate a walled-off abscess effectively; drainage + antibiotics is synergistic
Ruptured TOA / septic shock / no response	Emergency laparoscopy or laparotomy — drainage, unilateral or bilateral salpingo-oophorectomy (if extensive destruction)	Ruptured TOA causes diffuse peritonitis → life-threatening sepsis. Definitive source control is required

Step	Action	Rationale
Emergency laparoscopy	Detorsion (untwisting the pedicle) ± oophoropexy (fixing the ovary to prevent re-torsion)	The priority is to save the ovary — even if it appears dusky/necrotic at first, it often recovers after detorsion (reperfusion). Ovarian conservation is especially important in young women
Oophorectomy	If the ovary is clearly non-viable after detorsion, or if the mass is suspicious for malignancy	Non-viable tissue will necrose and become a source of infection. Malignant masses should not be left in situ
Cystectomy	Often performed at the same time if a cyst was the lead point for torsion	Removing the cyst (which acts as a pendulum causing torsion) reduces the risk of recurrence

Exam point: do NOT delay surgery to confirm diagnosis with Doppler — clinical suspicion alone is sufficient to proceed to emergency laparoscopy. Normal Doppler does NOT exclude torsion (dual blood supply may maintain some flow initially).

Condition	Management	Referral Pathway
Distended bladder	Catheterisation (urethral or suprapubic) → investigate and treat underlying cause	Urology
Colorectal cancer	Surgical resection ± neoadjuvant/adjuvant chemo/RT	Colorectal surgery + oncology
Appendiceal abscess	IV antibiotics → interval appendicectomy (6–8 weeks)	General surgery
Retroperitoneal sarcoma	Surgical resection (often requires multidisciplinary approach) ± RT	Surgical oncology
Pelvic lymphoma	Chemotherapy ± RT (tissue biopsy for subtyping first)	Haematology-oncology

Treatment	Indications	Contraindications / Limitations
Conservative observation	Functional cysts < 5 cm in premenopausal women; asymptomatic small fibroids	Postmenopausal cyst (higher malignancy risk); enlarging/symptomatic mass
COCP	Menorrhagia (fibroids), cycle regulation, prevention of new functional cysts, endometriosis suppression	Uncontrolled CV risk factors, active smoking (> 35 yr), history of VTE, migraine with aura, concurrent tranexamic acid ^[15]
Tranexamic acid	First-line for menorrhagia	Concurrent COCP use (↑thrombotic risk) ^[15]; active thromboembolic disease
LNG-IUS (Mirena)	Menorrhagia (fibroids, adenomyosis, DUB)	Large submucosal fibroid distorting cavity (risk of expulsion); uterine anomaly; active PID
GnRH agonists	Pre-operative fibroid shrinkage; bridge-to-menopause; endometriosis	Long-term use > 6 months (bone loss); pregnancy; undiagnosed vaginal bleeding
Myomectomy	Symptomatic fibroids with desire for fertility preservation	Very high risk of recurrence; may not be feasible if too many/large fibroids
Hysterectomy	Definitive for fibroids, adenomyosis, endometrial cancer; completed family	Fertility desired; unfit for surgery
UAE	Symptomatic fibroids, not desiring fertility, poor surgical candidate	Fertility desired; pedunculated subserosal fibroid; suspected malignancy; active infection ^[13]
Staging laparotomy	Suspected or confirmed ovarian cancer	Medically unfit (→ NACT first); very early favourable disease in young woman (→ fertility-sparing USO)
Platinum-based chemotherapy	Adjuvant for epithelial ovarian cancer (most stages)	Very early, low-grade stage IA (may not need chemo); contraindications to platinum (renal failure, allergy)
PARP inhibitors	Maintenance after platinum response, especially BRCA-mutant	Non-BRCA, platinum-resistant disease (less benefit); myelosuppression
Methotrexate (ectopic)	Unruptured ectopic, βhCG < 5000, no fetal heartbeat, stable	Ruptured ectopic, haemodynamic instability, high βhCG, fetal heartbeat, hepatic/renal disease, immunodeficiency, breastfeeding
Laparoscopic salpingectomy	Ruptured ectopic, failed methotrexate, high βhCG	Relative: absent contralateral tube (may prefer salpingotomy)
Emergency detorsion	Ovarian torsion	Mass highly suspicious for malignancy (risk of tumour dissemination during manipulation)

5. Special Considerations

Red (carneous) degeneration is the classic fibroid complication in pregnancy (typically 2nd trimester). The rapidly growing uterus causes venous thrombosis within the fibroid → haemorrhagic infarction.

Aspect	Management
Treatment	Conservative: rest, IV fluids, analgesia (paracetamol first-line; NSAIDs avoided in pregnancy, especially after 28 weeks due to premature closure of ductus arteriosus)
Surgery	AVOID myomectomy during pregnancy — the uterus is extremely vascular and surgery risks catastrophic haemorrhage. Exception: torsion of pedunculated fibroid
Delivery	Fibroids in the lower segment may obstruct vaginal delivery → caesarean section. Myomectomy at caesarean is controversial (risk of haemorrhage from highly vascular myometrium)

For young patients with early-stage, unilateral, non-clear-cell ovarian cancer: unilateral salpingo-oophorectomy + comprehensive staging preserves contralateral ovary and uterus
For germ cell tumours: fertility-sparing USO standard even in advanced disease (excellent chemo-sensitivity)
Oocyte or embryo cryopreservation should be discussed before starting chemotherapy (gonadotoxic agents)
GnRH agonists during chemotherapy may offer some ovarian protection (controversial but increasingly used)

Management of ovarian cancer should be discussed at an MDT meeting involving:

Gynaecological oncologist (surgery)
Medical oncologist (chemotherapy)
Radiologist (imaging interpretation)
Pathologist (histological typing/grading)
Clinical nurse specialist
Genetic counsellor (for BRCA testing)

High Yield Summary — Management of Pelvic Mass

1. Management depends on 4 factors: age, symptoms, diagnosis, and patient's wishes ^[1].

2. Emergency management first: ruptured ectopic → emergency laparoscopy/laparotomy; ovarian torsion → emergency detorsion; ruptured cyst with haemodynamic instability → surgical haemostasis.

3. Functional ovarian cysts: observe + repeat USS in 6–8 weeks. COCP prevents NEW cysts but does NOT treat existing ones.

4. Benign ovarian neoplasms: surgical excision (cystectomy if fertility desired; oophorectomy if not).

5. Ovarian cancer: staging laparotomy (TAH + BSO + omentectomy + LN sampling + washings) → adjuvant carboplatin + paclitaxel. Goal = R0 (no visible residual). PARP inhibitors for BRCA-mutant maintenance.

6. Fibroids: medical first (tranexamic acid, LNG-IUS, GnRH agonists) → surgical if failed (myomectomy if fertility desired; hysterectomy if definitive). UAE is an alternative in selected patients not desiring fertility.

7. Ectopic pregnancy: expectant (low βhCG, declining), methotrexate (unruptured, βhCG < 5000), salpingectomy (ruptured/failed/high βhCG).

8. TOA: IV antibiotics first → drainage if no response → surgery if ruptured/no improvement.

9. Ovarian torsion: emergency detorsion — try to save the ovary.

10. UAE contraindicated if fertility desired, pedunculated fibroid, suspected malignancy.

Active Recall - Management of Pelvic Mass

References

^[1] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p2, p71) ^[5] Senior notes: Ryan Ho Radiology.pdf (p32, p34) ^[10] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p18, p59) ^[13] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p78, p85) ^[15] Lecture slides: Block C - O&G Theme Case 2.docx.pdf (p5)

Complications of Pelvic Masses

Complications of pelvic masses can be divided into two broad categories: (A) complications arising from the mass itself (the natural history of an untreated pelvic mass) and (B) complications arising from treatment (surgical, medical, and interventional). Both are equally important for exams and clinical practice.

The lecture slides explicitly highlight that ovarian cyst complications and pregnancy complications require emergency management ^[1]^[10], and that the pelvic mass DDx should always prompt the clinician to "attend patients who need URGENT management — shock, severe pain (peritoneal signs) — may require straight laparotomy — exclude ovarian cyst complications, pregnancy complications" ^[16].

Part A: Complications of the Mass Itself (By Condition)

1. Ovarian Cyst Complications

These are acute gynaecological emergencies. They can occur with any ovarian cyst — functional, endometriotic, or neoplastic.

Aspect	Detail
What happens	The ovary (± fallopian tube) twists on its vascular pedicle (infundibulopelvic ligament + utero-ovarian ligament)
Pathophysiology	Cysts, especially those 5–10 cm, act as a pendulum weight → movement causes the pedicle to twist → venous outflow obstruction first (thin-walled veins occlude before thick-walled arteries) → venous congestion → oedema → if persistent, arterial compromise → ischaemic necrosis → gangrenous ovary → peritonitis if untreated
Why 5–10 cm?	Too small (< 5 cm) and the ovary is stable; too large (> 10 cm) and the mass is relatively immobile due to crowding. The "Goldilocks zone" of 5–10 cm has enough weight to swing but enough room to twist
Risk factors	Known ovarian cyst/mass (especially dermoid — heavy, pendulous), ovulation induction, pregnancy (corpus luteum), long utero-ovarian ligament (paediatric/adolescent — prepubertal ovaries have longer pedicles)
Clinical features	Sudden severe unilateral pelvic pain, nausea/vomiting (vagal stimulation from peritoneal irritation), low-grade fever (if necrotic)
Consequence if missed	Irreversible ovarian necrosis → loss of ovary → reduced fertility (especially if contralateral ovary is also compromised); gangrenous tissue → peritonitis, sepsis

Aspect	Detail
What happens	The cyst wall breaks → contents spill into the peritoneal cavity
Pathophysiology	Depends on the cyst contents: (a) Follicular/serous fluid → chemical peritonitis (usually mild, self-limiting); (b) Blood (haemorrhagic corpus luteum) → haemoperitoneum → hypovolaemic shock if significant; (c) Sebaceous material (ruptured dermoid) → severe chemical peritonitis and dense adhesion formation → granulomatous peritonitis; (d) Endometriotic "chocolate" fluid → chemical peritonitis, adhesion formation; (e) Malignant contents → peritoneal seeding → upstaging of cancer (IA → IC)
Clinical features	Sudden sharp pelvic pain, may have signs of peritonism (guarding, rebound), signs of haemodynamic compromise if haemoperitoneum (tachycardia, hypotension, pallor)
Consequence	Haemorrhagic shock (corpus luteum rupture), adhesion formation (dermoid/endometrioma), cancer dissemination (if malignant cyst ruptures intra-operatively or spontaneously)

Aspect	Detail
What happens	Bleeding into the cyst cavity without rupture
Pathophysiology	Most commonly in corpus luteum cysts (highly vascular structure → vessels within the cyst wall bleed into the cyst lumen → enlargement → stretching of capsule → pain). Anticoagulation increases risk
Clinical features	Subacute onset unilateral pelvic pain, enlarging tender cyst on USS
Consequence	Usually self-limiting; may progress to rupture → haemoperitoneum

Aspect	Detail
Pathophysiology	Secondary bacterial infection of a pre-existing cyst (usually from ascending PID or haematogenous spread) → abscess formation
Clinical features	Fever, worsening pain, raised WCC/CRP, complex cyst on USS
Consequence	Tubo-ovarian abscess, sepsis, adhesion formation → tubal damage → infertility

Emergency Complications of Ovarian Cysts

The lecture slide (GC 118, p24) states: "Attend patients who need URGENT management — shock, severe pain (peritoneal signs) — may require straight laparotomy — exclude ovarian cyst complications, pregnancy complications." ^[16] The three acute cyst complications to always consider are: torsion, rupture, and haemorrhage. All three can present identically with acute pelvic pain — the key differentiators are USS findings, Doppler flow, and the presence/absence of free fluid.

Fibroids, despite being benign, cause a wide range of complications through their sheer bulk, location, and blood supply demands.

Complication	Pathophysiology	Clinical Presentation
Menorrhagia and iron-deficiency anaemia	Submucosal fibroids distort the endometrial cavity → increased endometrial surface area + disruption of normal endometrial haemostatic mechanisms (compression of myometrial spiral arteries, impaired contractility of overlying myometrium) → heavier, prolonged menstrual bleeding → chronic iron loss	Heavy menstrual bleeding, fatigue, pallor, microcytic hypochromic anaemia
Infertility and subfertility	Submucosal fibroids distort the uterine cavity → impair embryo implantation. Intramural fibroids may obstruct the tubal ostia or alter uterine contractility, impairing sperm transport. Large fibroids may compress the fallopian tubes	Difficulty conceiving, recurrent miscarriage
Pregnancy complications	Fibroids enlarge in pregnancy (oestrogen/progesterone-driven) → red degeneration (venous thrombosis within the fibroid → haemorrhagic infarction, typically 2nd trimester); malpresentation (fibroid displaces fetus); obstructed labour (lower segment fibroid blocks birth canal); placenta praevia (fibroid distorts lower segment); preterm labour (uterine irritability); postpartum haemorrhage (impaired uterine contraction at fibroid site)	Acute pain over fibroid, premature contractions, abnormal lie, need for caesarean
Acute urinary retention (AROU)	Large cervical or lower segment fibroid compresses or kinks the urethra → inability to void ^[17]	Suprapubic pain, inability to pass urine, palpable distended bladder
Ureteric obstruction → hydronephrosis	Large lateral fibroids or broad ligament fibroids compress the ureter at the pelvic brim → impaired urine drainage → back-pressure on kidney	Often asymptomatic (chronic compression); may present as loin pain, recurrent UTI, or incidental finding on imaging. Bilateral obstruction → obstructive uropathy → renal failure
Constipation / bowel symptoms	Posterior fibroids compress the rectosigmoid	Difficulty with defecation, tenesmus
Deep vein thrombosis (DVT)	Large pelvic mass compresses iliac veins → venous stasis → Virchow's triad → thrombus formation	Unilateral leg swelling, pain, warmth
Torsion of pedunculated fibroid	Pedunculated subserosal (FIGO 7) or submucosal (FIGO 0) fibroid twists on its stalk → vascular compromise → ischaemia → necrosis → peritoneal irritation	Acute onset severe lower abdominal pain, peritonism
Degeneration	Fibroid outgrows its blood supply → various degeneration types: hyaline (most common, softening), cystic (liquefaction), red/carneous (haemorrhagic infarction, pregnancy), calcification (post-menopausal, dystrophic), myxoid, fatty	Pain (especially red degeneration), incidental finding on imaging (calcification)
Sarcomatous (malignant) transformation	Extremely rare (< 0.5%) — transformation to leiomyosarcoma. Whether this is truly "transformation" or a de novo sarcoma arising independently is debated	Rapidly enlarging "fibroid" in a postmenopausal woman (when it should be shrinking due to oestrogen withdrawal) should raise suspicion

Why does postmenopausal growth raise alarm? Fibroids are oestrogen- and progesterone-dependent. After menopause, they should shrink. If a uterine mass is growing in a postmenopausal woman without HRT, it suggests either a sarcoma or a different pathology entirely.

Ovarian cancer is described as an "insidious disease → 'silent killer', usually diagnosed at a late stage" ^[10]. Its complications arise from both local spread and distant metastasis.

Complication	Pathophysiology	Clinical Manifestation
Malignant ascites	Peritoneal carcinomatosis → tumour implants on the peritoneal surface produce excess fluid (both transudative from increased peritoneal permeability and exudative from tumour VEGF secretion causing capillary leak) + impaired lymphatic drainage (tumour blocks diaphragmatic lymphatic stomata that normally reabsorb peritoneal fluid)	Progressive abdominal distension, discomfort, dyspnoea (splinting diaphragm), early satiety
Bowel obstruction	Peritoneal deposits form adhesions and compress/infiltrate bowel loops → mechanical obstruction (especially small bowel); omental cake can encase bowel in a "cocoon"	Abdominal pain, vomiting, distension, constipation. Can be multifocal (multiple sites of obstruction simultaneously — makes surgical management very challenging)
Pleural effusion	(a) Direct transcoelomically: malignant cells track through diaphragmatic defects (especially right hemidiaphragm) → malignant pleural effusion; (b) Meigs' syndrome (benign ovarian fibroma + ascites + right pleural effusion — resolves after tumour removal); (c) Lymphatic obstruction	Dyspnoea, reduced breath sounds, stony dull percussion at base
Venous thromboembolism (DVT/PE)	Malignancy-associated hypercoagulability (Trousseau's syndrome: tumour procoagulant factors, tissue factor expression, cancer-associated inflammation) + venous stasis from pelvic mass compressing iliac veins + immobility	Leg swelling (DVT), acute dyspnoea/chest pain (PE). Ovarian cancer has one of the highest rates of VTE among all cancers
Lymphoedema / lower limb swelling	Lymphatic invasion by tumour impedes lymphatic return ^[10]	Bilateral or unilateral lower limb oedema
Ureteric obstruction → obstructive uropathy	Tumour encases or compresses the ureters in the pelvis → hydronephrosis → progressive renal impairment if bilateral	Loin pain, rising creatinine, hydronephrosis on imaging. May require percutaneous nephrostomy
Cachexia and malnutrition	Cancer cachexia: tumour-derived cytokines (TNF-α, IL-6, proteolysis-inducing factor) → skeletal muscle wasting, lipolysis, anorexia. Additionally, bowel obstruction/ascites → reduced oral intake	Weight loss, muscle wasting, fatigue, hypoalbuminaemia
Paraneoplastic syndromes	Rare but recognised: hypercalcaemia (PTHrP secretion, especially small cell/clear cell); cerebellar degeneration (anti-Yo antibodies, especially in serous ovarian cancer); dermatomyositis; Trousseau's syndrome	Variable depending on syndrome
Recurrence	Despite initial response to platinum-based chemotherapy (~80% response rate), most advanced epithelial ovarian cancers recur (platinum-sensitive recurrence if > 6 months; platinum-resistant if < 6 months). Recurrence typically involves peritoneal disease, lymph nodes, or distant organs	Rising CA-125, new symptoms, imaging findings

Complication	Pathophysiology	Consequence
Tubal rupture	Trophoblast invades through the thin muscular wall of the fallopian tube → erosion of tubal arteries → rupture → massive intra-abdominal haemorrhage	Hypovolaemic shock, haemoperitoneum, death if not treated emergently
Persistent trophoblastic tissue	After conservative treatment (salpingotomy or methotrexate), residual trophoblastic tissue may persist and continue to grow/bleed	Rising or plateauing βhCG post-treatment → requires further methotrexate or salpingectomy
Recurrence	After salpingectomy, risk of ectopic in the contralateral tube is ~10%. After salpingotomy, risk of ipsilateral ectopic recurrence is ~15%	Future ectopic pregnancy
Tubal damage → infertility	Ectopic pregnancy itself and its treatment (salpingectomy) reduce the number of functional tubes → reduced fertility	Future fertility impairment

Complication	Pathophysiology
Chronic pelvic pain	Cyclical inflammation and bleeding within ectopic endometrial deposits → fibrosis, nerve irritation, peritoneal inflammation
Infertility	Adhesion formation (mechanical distortion of tubo-ovarian anatomy → impaired ovum pick-up); inflammatory peritoneal fluid (toxic to sperm and embryos); reduced ovarian reserve (endometriomas destroy normal ovarian cortex)
Adhesion formation	Repeated cyclical bleeding → inflammatory response → fibrous adhesion formation between pelvic organs (ovary to tube, tube to pelvic sidewall, uterus to bowel)
Malignant transformation	Endometriomas carry a small but real risk (~1%) of transformation to clear cell or endometrioid ovarian carcinoma. Atypical endometriosis is the histological precursor
Bowel/urinary tract involvement	Deep infiltrating endometriosis can involve the rectosigmoid (cyclical rectal bleeding, dyschezia, bowel obstruction), bladder (cyclical haematuria), or ureter (hydronephrosis)
Chocolate cyst rupture	Endometrioma rupture → release of "chocolate" (old blood) content into the peritoneal cavity → severe chemical peritonitis and adhesion formation

Complication	Pathophysiology
Rupture → peritonitis and sepsis	Abscess wall breaks down → purulent material spills into peritoneal cavity → generalised peritonitis → septic shock. This is a surgical emergency
Tubal damage → infertility	Inflammatory destruction of the tubal epithelium and fimbrial architecture → tubal occlusion, hydrosalpinx → tubal factor infertility
Chronic pelvic pain	Post-inflammatory adhesions → chronic pain, dyspareunia
Recurrence	Damaged tubes are susceptible to re-infection → recurrent PID/TOA
Ectopic pregnancy	Tubal damage from PID → abnormal ciliary function and narrowed tubal lumen → fertilised ovum cannot pass through → tubal ectopic pregnancy

Part B: Complications of Treatment

7. Surgical Complications

Timing	Complication	Mechanism
Intra-operative	Haemorrhage	Pelvic vasculature is rich and tortuous (uterine artery, ovarian vessels, internal iliac branches, presacral venous plexus). Adhesions from previous surgery or endometriosis increase bleeding risk
	Ureteric injury	The ureter passes 2 cm lateral to the cervix, under the uterine artery ("water under the bridge"). It is at risk during hysterectomy, oophorectomy, and any pelvic dissection. Injury can be transection, ligation, thermal, or kinking
	Bladder injury	The bladder is adherent to the anterior uterine wall, especially after previous caesarean sections (bladder flap adhesions). Risk during anterior dissection in hysterectomy
	Bowel injury	Risk increases with adhesions (previous surgery, endometriosis), advanced malignancy, and laparoscopic entry
	Nerve injury	Pelvic autonomic nerves (hypogastric plexus, splanchnic nerves) may be damaged during radical surgery → urinary dysfunction (retention), sexual dysfunction, bowel dysmotility ^[7]
Early post-operative	Wound infection	Bacterial contamination of surgical site. Risk factors: DM, obesity, immunosuppression, prolonged surgery
	Venous thromboembolism (DVT/PE)	Pelvic surgery is a major risk factor for VTE: venous stasis (immobility), endothelial injury (surgical trauma), hypercoagulability (surgical stress response, malignancy). Ovarian cancer surgery carries one of the highest VTE risks of any surgery
	Ileus	Post-operative bowel handling → transient inhibition of bowel motility. Prolonged ileus more common after extensive debulking surgery with bowel manipulation
	Urinary retention (AROU)	Post-operative pain, analgesics (opioids), pelvic dissection near autonomic nerves → temporary detrusor dysfunction → retention ^[17]
	Pelvic abscess / collection	Haematoma or seroma becomes secondarily infected, or contamination from bowel surgery
Late post-operative	Adhesion formation → bowel obstruction	Surgical peritoneal trauma → inflammatory response → fibrous adhesion formation between bowel loops, pelvic sidewall, and abdominal wall → can cause small bowel obstruction (years later)
	Vault prolapse (after hysterectomy)	Loss of uterine support → vaginal vault descends. Risk factors: poor pelvic floor, obesity, chronic cough
	Lymphoedema	After pelvic/para-aortic lymph node dissection → disruption of lymphatic drainage → chronic lower limb or genital lymphoedema
	Incisional hernia	Especially after midline laparotomy incisions. Risk: obesity, poor wound healing, infection, repeated surgery
	Sexual dysfunction	Loss of ovaries → surgical menopause (vasomotor symptoms, vaginal dryness, loss of libido). Nerve damage during radical surgery → altered sensation
	Premature menopause (after BSO)	Bilateral salpingo-oophorectomy in premenopausal women → abrupt loss of oestrogen → vasomotor symptoms (hot flushes), vaginal atrophy, osteoporosis, cardiovascular risk, mood changes, cognitive effects. Consider HRT if no contraindication

Complication	Mechanism
Trocar/Veress needle injury	Entry into the abdomen can injure bowel or major vessels (aorta, iliac vessels, inferior epigastric artery). Risk higher with adhesions from previous surgery. Open (Hasson) technique reduces but does not eliminate risk
Gas embolism	CO₂ insufflation → if gas enters an open vein → gas embolism → cardiovascular collapse. Extremely rare but potentially fatal
Subcutaneous emphysema	CO₂ tracks into subcutaneous tissue planes. Usually self-limiting
Port-site metastasis	In malignant cases, tumour cells can implant at trocar insertion sites. This is why suspected ovarian cancer should ideally undergo midline laparotomy rather than laparoscopy for staging
Cyst rupture/spillage	Laparoscopic removal of ovarian cysts risks intra-operative rupture → spillage of contents. For dermoids → chemical peritonitis; for malignant cysts → peritoneal seeding and upstaging

Complication	Mechanism
Post-embolisation syndrome	Most common (> 50%): pelvic pain, fever, nausea, malaise for 1–2 weeks after procedure. Caused by ischaemic necrosis of fibroid tissue → release of inflammatory mediators and necrotic debris. Managed with analgesia and NSAIDs
Fibroid expulsion	Necrotic submucosal fibroid detaches and passes through the cervix → can cause pain, bleeding, infection. Sometimes requires hysteroscopic removal
Premature ovarian failure	Non-target embolisation of the ovarian artery (which may arise from or anastomose with the uterine artery) → ovarian ischaemia → premature menopause. Risk increases with age > 45. This is why UAE is contraindicated in women desiring future fertility
Endometritis / uterine infection	Necrotic tissue within the uterus becomes infected. Rare but may require hysterectomy if septic
Amenorrhoea	Endometrial damage from ischaemia → Asherman's-like adhesions → amenorrhoea. Another reason fertility is a contraindication

Drug	Key Complications	Mechanism
GnRH agonists (e.g. leuprolide)	Bone density loss (osteopenia → osteoporosis), vasomotor symptoms (hot flushes, night sweats), vaginal dryness, mood changes, headache	Creates a hypoestrogenic state ("medical menopause") → oestrogen withdrawal effects on bone (↑osteoclast activity), hypothalamic thermoregulatory centres (vasomotor instability), vaginal epithelium (atrophy)
Tranexamic acid	VTE risk (rare), nausea, diarrhoea	Anti-fibrinolytic → if systemic effect → hypercoagulability. Generally very safe when used cyclically
Methotrexate (for ectopic)	Abdominal pain ("separation pain" — can mimic rupture), nausea/vomiting, stomatitis, transient LFT derangement, bone marrow suppression (rare at single-dose), alopecia (rare)	Dihydrofolate reductase inhibitor → blocks DNA synthesis → affects rapidly dividing cells (trophoblast, but also GI mucosa, bone marrow, hair follicles). "Separation pain" occurs as the trophoblast undergoes necrosis and separates from the tube
Platinum-based chemotherapy (carboplatin)	Nephrotoxicity (cisplatin >> carboplatin), ototoxicity, peripheral neuropathy, bone marrow suppression (thrombocytopaenia with carboplatin), nausea/vomiting, alopecia	Platinum cross-links DNA → cell death in rapidly dividing cells. Nephrotoxicity from tubular damage (cisplatin); ototoxicity from cochlear hair cell damage; neuropathy from dorsal root ganglion neurotoxicity
Paclitaxel	Peripheral neuropathy (dose-limiting), alopecia, bone marrow suppression (neutropaenia), hypersensitivity reactions, myalgia/arthralgia	Microtubule stabilisation → prevents mitotic spindle disassembly → arrests cell division. Also affects microtubule-dependent neuronal transport → peripheral neuropathy
PARP inhibitors (olaparib)	Myelodysplastic syndrome / acute myeloid leukaemia (rare but serious, ~1–2%), fatigue, nausea, anaemia	Long-term PARP inhibition → impaired DNA repair in normal haematopoietic stem cells → genomic instability → myeloid malignancy
Bevacizumab	Hypertension, proteinuria, GI perforation (rare), impaired wound healing (must stop 6 weeks before surgery), thromboembolic events, haemorrhage	Anti-VEGF → impaired angiogenesis → vascular endothelial dysfunction → hypertension, proteinuria. Loss of VEGF-mediated vascular maintenance in the GI tract → bowel wall weakening → perforation

When a pelvic mass (fibroid, ovarian mass) causes urinary retention, catheterisation itself can cause complications ^[17]:

Complication	Mechanism
Post-obstructive diuresis	Tubular damage from prolonged back-pressure → impaired concentrating ability → rapid fluid and solute loss (> 200 mL/h for ≥ 2 hours or > 3 L in 24 hours). Can cause hyponatraemia, hypokalaemia, hypovolaemia. Must monitor I/O closely and replace fluids appropriately
Haemorrhage ex vacuo	Sudden decompression of a greatly distended bladder → bladder mucosal disruption → transient haematuria. Usually self-limiting
Transient hypotension	Vasovagal response to rapid bladder decompression, or relief of compression on pelvic veins

Don't Decompress Too Fast

When catheterising a patient with chronic urinary retention and a hugely distended bladder, some clinicians advocate intermittent clamping (draining 500 mL at a time, then clamping for 15 minutes) to reduce the risk of ex vacuo haemorrhage and post-obstructive diuresis. However, evidence for this practice is weak — the most important thing is to monitor urine output closely (Q2h) and replace fluids if post-obstructive diuresis develops ^[17].

Condition	Must-Know Complications
Ovarian cyst	Torsion, rupture, haemorrhage, infection
Uterine fibroid	Menorrhagia/anaemia, infertility, red degeneration (pregnancy), torsion of pedunculated fibroid, AROU, ureteric obstruction, sarcomatous change (rare)
Ovarian cancer	Malignant ascites, bowel obstruction, VTE, pleural effusion, lymphoedema, cachexia, recurrence
Ectopic pregnancy	Tubal rupture → haemoperitoneum/shock, persistent trophoblast, recurrence, infertility
Endometrioma	Chronic pain, infertility, adhesions, malignant transformation (clear cell/endometrioid), rupture
TOA	Rupture → sepsis, tubal damage → infertility, chronic pain, ectopic pregnancy
Pelvic surgery	Haemorrhage, ureteric/bladder/bowel injury, VTE, adhesions, premature menopause (BSO), lymphoedema
UAE	Post-embolisation syndrome, premature ovarian failure, fibroid expulsion, infection
Chemotherapy	Myelosuppression, nephrotoxicity, neuropathy, nausea, alopecia, secondary malignancy (PARP inhibitors)

High Yield Summary — Complications of Pelvic Masses

1. Acute ovarian cyst complications (torsion, rupture, haemorrhage) are gynaecological emergencies requiring urgent surgical intervention. Torsion causes ischaemia via venous outflow obstruction first; rupture causes peritonitis ± haemoperitoneum.

2. Fibroid complications are driven by location: submucosal → menorrhagia/anaemia/infertility; subserosal → pressure effects/torsion; any large fibroid → AROU, ureteric obstruction, DVT. Red degeneration is classic in pregnancy (2nd trimester).

3. Ovarian cancer complications arise from its biology: transcoelomic spread → malignant ascites, bowel obstruction, omental cake; hypercoagulability → VTE; lymphatic invasion → lower limb oedema.

4. Surgical complications: always remember ureteric injury ("water under the bridge"), VTE risk (especially in cancer surgery), adhesion-related bowel obstruction (years later), and premature menopause after BSO.

5. UAE complications: post-embolisation syndrome (pain, fever — most common), premature ovarian failure (why fertility is a contraindication), fibroid expulsion.

6. Chemotherapy toxicity: platinum → nephrotoxicity, neuropathy; paclitaxel → neuropathy; bevacizumab → GI perforation, hypertension, impaired wound healing; PARP inhibitors → MDS/AML (rare but serious).

7. Post-catheterisation for AROU: watch for post-obstructive diuresis (monitor I/O Q2h, replace fluids), ex vacuo haematuria, and vasovagal hypotension.

Active Recall - Complications of Pelvic Masses

References

^[1] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p23, p66, p71) ^[7] Senior notes: Maksim Surgery Notes.pdf (p108 — post-operative complications of pelvic surgery) ^[10] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p10, p18) ^[16] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p24) ^[17] Senior notes: Ryan Ho Fundamentals.pdf (p351, p353 — AROU complications and management)

High Yield Summary

Definition: A pelvic mass is any space-occupying lesion arising from pelvic or adjacent structures. Approach it by organ of origin: ovarian, uterine, tubal/adnexal, pregnancy-related, gastrointestinal, urological, or retroperitoneal.

Most important causes:

Ovarian: functional cyst, dermoid, cystadenoma, endometrioma, ovarian cancer.
Uterine: fibroid, adenomyosis, endometrial cancer.
Tubal/adnexal: ectopic pregnancy, tubo-ovarian abscess, hydrosalpinx.
Non-gynae: distended bladder, colorectal cancer, appendiceal mass, retroperitoneal tumour.

First exclusions: In any reproductive-age patient, do beta-hCG first to exclude pregnancy/ectopic pregnancy. Also exclude a distended bladder and look actively for malignancy, especially postmenopause.

Age discriminator:

Young: functional cyst, dermoid, ectopic pregnancy, germ cell tumour.
Reproductive age: fibroid, endometrioma, ectopic pregnancy, cystadenoma.
Postmenopausal: malignancy until proven otherwise.

Clinical clues:

Midline, moves side-to-side, continuous with cervix = uterine origin.
Lateral, cystic, mobile = likely benign ovarian mass.
Fixed, irregular, bilateral, solid-cystic mass with ascites/cachexia = suspect ovarian cancer.
Tender ill-defined mass with fever = inflammatory mass/TOA.

High Yield Summary — Diagnosis

First-line imaging: Pelvic ultrasound with TAUS + TVUS. TAUS gives the panoramic view for large masses; TVUS gives better adnexal and uterine detail.

Ultrasound malignancy features: solid areas, thick septae, papillary projections, bilateral masses, ascites, irregular margins, and increased Doppler vascularity.

Tumour markers:

CA-125 for suspected epithelial ovarian cancer, interpreted with age, menopausal status, and ultrasound findings.
AFP, beta-hCG, and LDH for suspected germ cell tumours.
Inhibin/oestradiol/testosterone for sex cord-stromal tumours when clinically suggested.

Risk stratification: RMI = U x M x CA-125. RMI >= 200 should prompt gynae-oncology referral.

Advanced imaging: CT abdomen/pelvis for staging suspected malignancy. MRI pelvis for fibroid mapping, endometriosis, or indeterminate adnexal masses.

Tissue diagnosis pitfall: Do not percutaneously biopsy a suspicious ovarian mass because spillage may upstage disease. Preferred diagnosis is intact surgical removal with histology/frozen section when appropriate.

High Yield Summary — Management

Management depends on age, symptoms, likely diagnosis, malignancy risk, fertility wishes, and emergency features.

Emergencies first:

Ruptured ectopic pregnancy: resuscitation + emergency surgery.
Ovarian torsion: urgent laparoscopy and detorsion, with ovarian conservation where possible.
Ruptured/bleeding cyst with instability: urgent surgical haemostasis.
TOA rupture or sepsis: antibiotics + drainage/surgery as needed.

Condition-specific approach:

Functional ovarian cyst: observe and repeat ultrasound in 6-8 weeks.
Benign ovarian neoplasm: cystectomy if fertility desired; oophorectomy if appropriate.
Ovarian cancer: gynae-oncology staging/debulking surgery aiming R0 + carboplatin/paclitaxel, with maintenance therapy when indicated.
Fibroid: medical treatment for bleeding/pain first; myomectomy if fertility desired; hysterectomy if definitive treatment desired; UAE only for selected patients not pursuing fertility.
Ectopic pregnancy: expectant, methotrexate, or surgery depending on stability, beta-hCG, rupture risk, and fertility context.

High Yield Summary — Complications

Mass complications:

Ovarian cyst: torsion, rupture, haemorrhage, infection.
Fibroid: menorrhagia/anaemia, infertility, pressure symptoms, AROU, ureteric obstruction, red degeneration in pregnancy.
Ovarian cancer: ascites, bowel obstruction, omental cake, VTE, lymphoedema, cachexia.
Ectopic pregnancy: rupture, haemoperitoneum, shock.
TOA: rupture, sepsis, infertility, chronic pelvic pain.

Treatment complications:

Pelvic surgery: haemorrhage, infection, adhesions, bowel/bladder/ureteric injury, VTE, premature menopause after BSO.
UAE: post-embolisation syndrome, fibroid expulsion, premature ovarian failure.
Chemotherapy/targeted therapy: neuropathy, nephrotoxicity, myelosuppression, bevacizumab-related hypertension/GI perforation, PARP inhibitor-associated MDS/AML.

Exam pearl: Remember the ureter during pelvic surgery: "water under the bridge" at the uterine artery.

Approach To Pelvic Mass

1. Definition

2. Epidemiology & Risk Factors (Hong Kong Context)

2.1 General Epidemiology

2.2 Key Risk Factors by Aetiology

3. Relevant Anatomy & Function

3.1 Bony Pelvis

3.2 Female Pelvic Organs

3.3 Key Ligaments and Peritoneal Reflections

3.4 Blood Supply

3.5 Lymphatic Drainage

3.6 The Ureter — The Surgeon's Nightmare

4. Aetiology & Pathophysiology

4.1 Gynaecological Causes

A. Ovarian Masses

(i) Functional (Physiological) Cysts

(ii) Benign Ovarian Neoplasms

(iii) Malignant Ovarian Neoplasms (Ovarian Cancer)

(iv) Endometriotic Cyst ("Chocolate Cyst" / Endometrioma)

B. Uterine Masses

(i) Uterine Fibroids (Leiomyomas)

(ii) Adenomyosis

(iii) Uterine Malignancy

C. Tubal/Adnexal Masses

4.2 Non-Gynaecological Causes

4.3 Pregnancy-Related Causes

5. Classification of Pelvic Masses

5.1 By Organ of Origin (Most Practical for DDx)

5.2 By Nature

5.3 Ovarian Masses: Benign vs. Malignant (Clinical Distinction)

6. Clinical Features

6.1 Symptoms

A. Symptoms Related to Mass Effect ("Bulk Symptoms")

B. Symptoms Related to Organ of Origin

C. Symptoms Suggestive of Malignancy

D. Symptoms of Acute Complications (Gynaecological Emergencies)

6.2 Signs

A. General Examination

B. Abdominal Examination

C. Pelvic Examination (Bimanual Vaginal Examination)

D. Other Examinations

7. Summary of Clinical Approach (History & Examination Framework)

7.1 History

7.2 Examination Checklist

Active Recall - Approach to Pelvic Mass

References

1. Master Differential Diagnosis List (By Organ System)

1.1 Gynaecological Causes

1.2 Non-Gynaecological Causes

2. Clinical Approach to Narrowing the DDx

2.1 Age and Menopausal Status

2.2 Acuity of Presentation

2.3 Mass Characteristics on Examination

2.4 Associated Features as Discriminators

3. Algorithmic Approach to Differential Diagnosis

4. Differential Diagnosis by Clinical Scenario

Scenario 1: Young woman (17 yr) with acute pelvic pain [2]

Scenario 2: 35-year-old woman with gradually enlarging pelvic mass + menorrhagia

Scenario 3: 60-year-old postmenopausal woman with abdominal distension + pelvic mass

Scenario 4: 25-year-old woman with RLQ mass + pain + fever

5. Key Differentiating Features Between the "Big Three" Pelvic Masses

6. Special Considerations for Non-Gynaecological DDx

6.1 Distended Bladder Masquerading as a Pelvic Mass

6.2 Colorectal Cancer

6.3 Appendiceal Pathology

7. DDx by Examination Finding — Quick-Reference Table

Active Recall - Differential Diagnosis of Pelvic Mass

1. Overarching Principles

2. Diagnostic Algorithm — Master Flowchart

3. Step-by-Step Investigation Modalities

3.1 Step 1 — Bedside Tests

3.2 Step 2 — Blood Investigations

3.3 Step 3 — Pelvic Ultrasound (First-Line Imaging)

Two Approaches: TAUS vs TVUSS

Key USS Findings and Their Interpretation

Features Suspicious for Malignancy on USS

3.4 Step 4 — Advanced Imaging

CT Abdomen and Pelvis (with contrast)

MRI Pelvis

Hysterosalpingogram (HSG)