Approach To Pelvic Mass
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.
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.
Pelvic Organ Prolapse (pop)
Pelvic organ prolapse is the descent of one or more pelvic organs (bladder, uterus, or rectum) from their normal anatomical position due to weakening of the pelvic floor support structures.
Cervical Cancer
Cervical cancer is a malignant neoplasm arising from the cervical epithelium, most commonly the squamocolumnar junction, predominantly caused by persistent high-risk human papillomavirus (HPV) infection.