Swellings of all kinds that involve the ovary.
The adnexal mass could be:
I] Functional cysts
Differential diagnosis from:
I)Pedunculated uterine fibroids,2)Colonic
masses,3)Peritoneal or UT lesions.
Ovarian masses are:
Cystic, solid or partially cystic/solid
Benign or malignant
Unilocular or multilocular
Having thick or thin septa
Freely , strictly mobile or fixed
Unilateral or bilateral.
Functional or organic
Aetiology & Epidemiology
Aetiology is unknown
Ca ovary is commoner in developed world
Most ovarian tumours are epithelial in origin
Incidence: rare at <35 yrs. Peak at 50-70 yrs
Only 3% of ovarian Ca are seen at < 35 yrs.The vast
majority are non-epithelial [germ cell tmrs].
Contributory factors ; 1) Early menarche
2) Late menopause
3) Years of ovulation
Now, reproductive factors – like parity and the use of oral
contraceptives are considered most influential.
1. Parity: Smoothly decreasing risk of Ca ovary with
2. Oral contraceptives: protective role is evident even
for ten yrs after stopping them.
3. Years of ovulation: Fathalla’s hypothesis- active
ovulation time increases the risk.
4. Other environmental factors: Alcohol and tobacco,
coffee – have weak evidence.
5. Genetic factors: play an important role. First –
degree relative, having the disease under the age
of 50, the risk will increase by 6 – 10 fold. If > 2
relatives are affected the life-time risk rises to
WHO (Serov et al 1973) – morphological,
based on the relation of cell types of tmrs to
tissues normally present in the ovary.
surface epitheliumsurface epithelium
1. History; [a] 2/3 present too late, [b] poor prognosis, [c] 5-yr survival is ~
2. Metastasis; [a] direct-- to pelvic peritoneum + pelvic organs,to diaphragm
& omentum, to surfaces of bowel + liver.[b] lymphatic- via ovarian vessels
to renal & para-aortic region,via broad ligament to pelvic nodes, to neck
and groin. [c] blood – to liver and lung .
3. Clinical staging; is redefined by FIGO in 1889, by adding 3 substages to
stage III etc.
Stage I: Growth limited to ovaries ( Ia, Ib, Ic)
Stage II: Growth involving one or both ovaries (IIa,b,c)
+ pelvic extension.
Stage III: Growth involving one or both ovaries (IIIa,b,c)
+ extension outside the pelvis.
Stage IV: Growth involving one or both ovaries
+ distant metastasis.
Symptoms:1] Abd.pain & discomfort
2] Distension or feeling a lump
3] indigestion,urinary symptoms
4] weight loss and AUB.
Examination: Feeling a pelviabdominal mass
Investigations:1} Hb,grouping,urea & electrolytes liver function tests. 2}
Chest X-ray & barium enema. 3} IVU
Imaging techniques: USS,CAT and MRI.
Cytology:From pleural effusion or ascites. FNA from lymph nodes .
Tumour markers: None of them is accurate;
1) CA 125 – rises in endometriosis,rapidly falls after chemotherapy.
2) CEA [carcinoembryonic antigen rises in mucinous cystadenoCa.
3) OCCA & OCA – tumour-associated a. :rises in both serous & mucinous.
Screening: routine USS, colour Doppler, Serum CA 125, Family history.
Surgery: the mainstay of both diagnosis and treatment.Vertical incision is
required. A sample of ascitic f. is taken.Exploration of omentum, bowels and
other organs. The therapeutic objective is to remove the tumour completely.
Cytoreduction to<1.5c may have the same prognosis.TAH+BSO+ Omentectomy
Radiotherapy: is indicated in st.(I+II).In st.(III) – irradiation to the whole abdomen
& pelvis is needed.In st. (IV) radiotherapy is ineffective.
Chemotherapy: plays major role ;
a) Stage Ia -------------- surgery alone.
b) Stage Ib–IIIa ------ Chemotherapy+ Radiotherapy.
c) > minimal residuum-------- Chemotherapy.
Single + combination therapy can be used: Alkylating agents --- ( Melphan,
Cyclophosphamide). Antimetabolites (5-fluorouracil, Methotrexate). Antibiotics
Other treatments: 1) Hormonal – Tamoxifen + LHRH agonists and others have
been used with little success. 2) Immunotherapy – has no proven benefit.
Combination of BCG (Bacille Calmette-Guerin) + alpha-interferon +
chemotherapy showed some encouraging results.