Diseases of the Uterus

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Chapter 11 Diseases of the Uterus

Uterine Polyps 196

Endometrial Polyp 196

Placental Site Trophoblastic Tumour 196

Fibroids 197

Fibroids (Leiomyoma) 197

Pressure Symptoms 198

Diagnosis 199

Complications 199

Treatment 200

Endometrial Hyperplasia 201

Clinical Findings 201

Simple Hyperplasia 201

Complex Hyperplasia 201

Atypical Hyperplasia 201

Aetiology 202

Investigation 202

Treatment 202

Carcinoma of the Endometrium 203

Presentation 203

Diagnosis 203

Histology 204

Staging of Endometrial Carcinoma 205

Spread of Endometrial Carcinoma 206

Local Spread 206

Lymphatic Spread 206

Aetiological Factors in Endometrial Carcinoma 207

Prognosis of Endometrial Carcinoma 208

Treatment of Endometrial Carcinoma 209

Stage I 209

Stage II 209

Stage III/IV 209

Recurrence of Endometrial Carcinoma 210

Sites 210

Treatment for Recurrence 210

Sarcoma of the Uterus 211

Clinical Features 211

Histological Appearances 211

Endometrial Stromal Sarcomas 212

Carcinosarcoma (Malignant Mixed Mesodermal Tumour) 212

Leiomyosarcoma 212

Uterine polyps

Endometrial polyp

Symptoms

Symptoms are heavier but regular periods, postmenopausal bleeding, and irregular bleeding on hormone replacement therapy (HRT).

Cramping pain occurs as the uterus tries to expel the polyp.

Intermenstrual bleeding – usually occurs due to congestion or necrosis, but a malignant change must always be considered.

The polyp may be visible in the external os and there may be more than one polyp. Endometrial polyps may be identified by transvaginal scan but hysteroscopy will allow direct visualisation.

Placental site trophoblastic tumour

This is due to the survival of chorionic tissue from a recent pregnancy. The tissue remains adherent to the uterine wall and enlarges with the accretion of fibrin and fibrous tissue. This can produce either high or low grade disease.

Symptoms

Menorrhagia and intermenstrual bleeding may present some time after the pregnancy has terminated or miscarried. Examination can reveal an enlarged uterus.

Treatment

All polyps must be removed and submitted to pathology. The final treatment will depend upon the histology, malignant potential and patient’s symptoms. Surgery, including hysterectomy, may be required in some cases, especially where malignant transformation is known or is suspected.

Fibroids

Fibroids (leiomyoma)

Fibroid is the gynaecological term for a leiomyoma of the uterus or, occasionally, of the cervix.

It is a circumscribed tumour of non-striped muscle with supporting fibrous tissue.

Fibroids develop in the myometrium and are not encapsulated, but they develop a false capsule of compressed myometrial tissue.

The location of the fibroid describes the type.

They are sometimes conglomerate and multiple, and vary in size from tiny (millet seed) to large, which may be many centimetres in diameter.

Some fibroids develop a long pedicle and present as polyps.

Fibroids are common tumours found in 15–20% of women. They may make the uterus bulky and irregular and may enlarge the cavity so that there is a greater area of endometrium to be shed at menstruation. Menstruation tends to be heavy but the cycle is usually regular. Fibroids are associated with infertility and nulliparity.

A fibroid polyp starts as a submucous fibroid and develops a pedicle. It causes dysmenorrhoea as the uterus tries to expel it. It may be extruded through the cervix and become necrotic, giving a foul discharge with irregular staining, and may even be mistaken for cervical cancer.

Pressure symptoms

The bulk of fibroids in the uterus gives

A palpable abdominal tumour
Urinary frequency
A growth filling the pelvis leading to bladder displacement, retention and overflow and difficulty with defecation.

Diagnosis

Symptoms and Signs

Menstrual disorders, pressure related symptoms and abdominal distension are all potential symptoms. A palpable mass per abdomen and/or on bimanual examination may be elicited during examination. The mass is usually firm, smooth and can be irregular.

Investigations

Patients may be anaemic if suffering from menorrhagia and investigations for this should be undertaken with full blood count and possibly assessment of ferritin, folate and B12 levels, where appropriate.

The suspicion of a fibroid on clinical assessment should be confirmed with imaging. Imaging will assess the size, site and nature of the fibroid. While rare, some fibroids can show signs of malignant change (leiomyosarcoma). Ultrasound will suffice for the assessment of most but further information may be gained by the use of magnetic resonance imaging (MRI), especially when the nature of the mass is being considered.

Complications

Sarcomatous change. This is rare but can occur, and large or complex asymptomatic fibroids must be kept under observation if not being removed surgically.

Degeneration. Fibroids tend to outgrow their blood supply and are subject to various forms of degeneration.Necrobiosis (‘red degeneration’) occurs in pregnancy and is a cause of pain. Usually, this remits and no treatment is needed.

Hyaline, mucoid, cystic degeneration. These changes may produce soft or hard fibroids, confusing the diagnosis. Torsion of the pedicle. This can arise in the case of a polypoid subserous fibroid, and will give rise to acute abdominal symptoms. If the torsion is subacute and the blood supply is gradually reduced, the fibroid may develop a new vascularity through adhesions (parasitic tumour).

Treatment

Conservative management.

Small, asymptomatic fibroids need not be treated.

Medical treatment

Gonadotropin releasing hormone (GnRH) analogues may give 50% reduction in 6 months, but rapid return to former size may follow cessation of therapy. Treatment for longer than 6 months can lead to osteoporosis.

Surgical treatment

Uterine artery embolisation – radiologically guided arterial embolisation

Myomectomy – conserving the uterus but removing the fibroid may preserve fertility.

Hysterectomy – removal of uterus with the fibroids.

Myomectomy

The approach to the tumour is made through the uterine wall following an injection of a vasopressor to minimise blood loss. The fibroid is shelled out by sharp and blunt dissection. The false capsule may make the plane of dissection difficult to identify. It can be performed by open or laparoscopic techniques.

The resultant cavity is obliterated by buried sutures and the uterine wall flapped over to bring the suture line as low on the uterine wall as possible to reduce the risk of adhesions to the bowel.

The disadvantages of myomectomy are possible blood loss and the recurrence of fibroids. Hysterectomy is the treatment of choice unless the patient wishes to retain fertility potential.

Endometrial hyperplasia

Being less accessible than lesions of the vulvar, vaginal or cervical epithelium, endometrial premalignant conditions are less easily diagnosed and followed up. Any hyperplastic condition raises the question of development of cancer and assessment of risk is important. Hyperplasia and carcinoma may coexist.

Endometrial hyperplasia may be classified as simple, complex or atypical.

Clinical findings

Most patients are in the 3rd and 4th decades of life, but hyperplasia is not confined to these age groups. It may be found in association with anovulation in teenage girls and in postmenopausal women. Heavy and/or irregular vaginal bleeding are the presenting symptoms but its severity or frequency is not related to the degree of pathological change.

Simple hyperplasia

This is the most common type. The endometrium has a characteristic appearance, often termed ‘Swiss cheese’ or cystic glandular hyperplasia.

At low power magnification the pattern is a mixture of glands of varying sizes, a significant proportion of them being cystic. There is no crowding of the glands which are lined by cubical or columnar epithelium. Mitotic figures are present in small numbers. A similar gross picture may be seen in atrophic endometria but the mitotic activity is absent. Other associated pathology is rare.

Complex hyperplasia

In this grade of hyperplasia the most striking feature is the quite obvious hyperplasia – crowding of glands so that they are back-to-back, the epithelium is stratified and mitoses are relatively frequent. There is, however, no epithelial atypia.

Atypical hyperplasia

At this stage nuclear atypia is present. Intra-glandular polypoid formations and abnormal mitotic figures are seen. Severe cases may be indistinguishable from a carcinoma and adjacent areas of endometrial carcinoma may occur.

Aetiology

Exogenous or endogenous unopposed oestrogens are primarily implicated in the pathogenesis of hyperplasia. Anovulatory cycles in perimenopause, obesity, polycystic ovarian disease, oestrogen secreting ovarian tumours (granulosa cell tumours), tamoxifen therapy (selective oestrogen receptor modulator) and unopposed oestrogen hormone replacement therapy can cause hyperplasia of endometrium.

Investigation

Imaging of the uterus with ultrasound to assess the endometrium is indicated. To obtain a diagnosis, an endometrial biopsy, with or without hysteroscopic assessment, will be required. Investigation will usually be in an outpatient setting but inpatient general anaesthetic assessment may also be needed.

Treatment

This depends principally on the types of hyperplasia. The age of the patient and a desire to retain fertility are factors to be considered.

Simple hyperplasia, with 1% risk of progression to carcinoma requires no routine follow-up. Symptomatic patients can be treated with progestogenic agents such as oral preparations or, increasingly, with the levonorgestrel releasing intrauterine device (IUD) (Mirena®). Recurrent abnormal bleeding would, of course, merit investigation.

Complex hyperplasia is not thought to merit hysterectomy. Progestin therapy, such as levonorgestrel releasing IUD, is again indicated for symptomatic management. Subsequent care after diagnosis can reasonably be dictated by the presenting symptoms.

Atypical hyperplasia, with estimated risks of co-existence of, or progression to, endometrial carcinoma of between 20% and 50% merits hysterectomy and a bilateral salpingo-oophorectomy in most cases. Women who wish to remain potentially fertile may be treated with oral progestogens or by levonorgestrel releasing IUD but long-term data is lacking. Recurrence on cessation of therapy has been reported and long-term surveillance with repeated endometrial sampling is mandatory.

Carcinoma of the endometrium

One of the commonest gynaecological cancers, it occurs most often in postmenopausal women (up to 80% of cases) with less than 5% diagnosed under 40 years of age. Its association with obesity, diabetes and polycystic ovarian syndrome is common. Postmenopausal American women may run a 1 in 1000 risk of endometrial carcinoma each year. There is no effective screening programme, but postmenopausal bleeding may be a cardinal symptom prompting urgent investigation.

Presentation

The usual presenting symptom of endometrial carcinoma is postmenopausal bleeding which carries a 10% risk of associated malignancy. However, patients may also present in the perimenopause with frequent, irregular bleeding or before the menopause with irregular vaginal bleeding. An awareness of the risk factors will prompt appropriate investigation. Pyometra also carries a high risk of underlying carcinoma

Increased risk is associated with obesity, nulliparity, late menopause, tamoxifen, polycystic ovarian disease, oestrogen secreting tumours.

Diagnosis

Transvaginal scan showing thickened endometrium

Patients presenting with postmenopausal bleeding should be reviewed urgently and investigated with an abdomino-pelvic ultrasound including a transvaginal ultrasound. This will allow an assessment of the ovaries and the endometrium. Where the endometrial thickness is measured to be less than 3 mm in women not on HRT and less than 5 mm in women taking HRT, there is an extremely low incidence of endometrial cancer and the patient can be reassured. Recurrent bleeding should prompt further investigation.

Patients with abnormal scans and all women with irregular bleeding on tamoxifen should undergo hysteroscopy and endometrial biopsy. In addition, careful inspection of the cervix, vulva and vagina should be undertaken to exclude these as a source of bleeding due to malignant change.

Spread of endometrial carcinoma

Magnetic resonance imaging is preferable to an ultrasound for the assessment of myometrial invasion and pelvic spread. To assess distal metastases, a computerised tomography (CT) scan of the chest, abdomen and pelvis may also be of value.

Local spread

Invasion of the myometrium and cervix is the commonest spread. It may produce considerable uterine enlargement.

Lymphatic spread

Lymphatic spread is more likely to occur when the tumour is poorly differentiated and the uterine wall is deeply invaded. The incidence of pelvic nodal metastases is in the region of 10%.

Most metastases occur in the adjacent structures and in the peritoneum. In advanced cases, distant metastases do occur, most commonly in lung, but occasionally in liver, vertebrae or other bones and in the supraclavicular lymph nodes.

Aetiological factors in endometrial carcinoma

There are two suggested types of endometrial carcinoma, based on aetiology.

Type 1 – arising in patients with a background history of oestrogen excess.

Type 2 – arising without evidence of oestrogenic stimulation.

Type 1 tumours would appear to have a better prognosis with a better differentiation pattern and a less invasive component. They would appear to be derived from a hyperoestrogenic stimulus. Type 2 tumours, including serous and clear cell cancers, arise from a atrophic type endometrium and have a more aggressive phenotype with greater invasion, poorer differentiation, more metastatic disease and, as such, they carry a poorer prognosis. Type 2 tumours have been associated with abnormalities in tumour suppressor genes.

Obesity, in particular, appears to be a developing issue in terms of the risk of endometrial carcinoma. Obese patients convert peripheral androgens to oestrogens via the action of the aromatase enzyme in adipose cells. Countries where the incidence of obesity is rising have started to also see an increase in the incidence of endometrial carcinoma. In some countries, it is now the commonest cancer of the female genital tract, overtaking ovarian carcinoma.

Hereditary non-polyposis colorectal cancer (Lynch II) syndrome is an inherited mutation in DNA mismatch repair genes. In those affected, the endometrial carcinoma occurs more frequently, together with breast and colon cancer.

Prognosis of endometrial carcinoma

The overall 5-year survival rate is approximately 80%. Fortunately, over 80% of cases are diagnosed at Stage I. The survival is affected by multiple prognostic factors including:

Stage at diagnosis

Histological grade

Depth of myometrial invasion

Lympho-vascular space involvement (LVSI)

Non-endometrioid type

5-year survival rates according to clinical staging are as follows:

Stage	5-year survival (%)
I	85
II	75
III	45
IV	25

Assessing 5-year survival rates according to International Federation of Gynecology and Obstetrics (FIGO) histological grading is reported as follows:

Grading	5-year survival (%)
G1	92
G2	90
G3	81

Using both methods on similar cases, we find that the 5-year survival rates for Stage I are the only ones altered significantly:

Stage and histology	5-year survival (%)
I, G1 and 2	80
I, G3	60

Treatment of endometrial carcinoma

This is essentially surgical, with postoperative adjuvant radiotherapy added when unfavourable prognostic features are found at surgery. Adjuvant therapy for endometrial cancer is a contentious, evolving field. To date, it provides improved local control but without improved survival. Many believe that the addition of adjuvant chemotherapy may add a survival advantage and research is underway.

Progestogen therapy is probably only of value in recurrent disease, but has been studied in early stage, well-differentiated, disease where fertility preservation is an issue and in patients not fit for radical therapy. If a woman is unfit for surgery then radiotherapy may be used alone, but it is less effective.

Stage I

Surgery for total abdominal hysterectomy and bilateral salpingo-oophorectomy without partial removal of vagina is the treatment of choice. Peritoneal saline washings are taken for cytology on opening the abdomen during surgery and the abdominal contents are carefully examined. The procedure can also be performed laparoscopically with equivalent 5-year survival and a lower operative morbidity. Evidence from randomised trials does not support lymphadenectomy as a therapeutic intervention.

Stage II

Stage II carries a prognosis that is similar to Stage I, and is usually treated as for Stage I and diagnosed by pathology. Where preoperative assessment suggests obvious cervical involvement then a radical hysterectomy with pelvic lymphadenectomy may be undertaken.

Stage III/IV

Treatment of this stage is designed to control tumour growth and alleviate symptoms. Treatment will depend upon tumour burden at the preoperative assessment and imaging. Many cases may only be identified as Stage III, following surgical management. Surgery, radiation therapy, chemotherapy and adjuvant progestogen therapy all have a place.

Recurrence of endometrial carcinoma

The majority of recurrences appear within 3 years of treatment. Early recurrence has a poor prognosis.

Sites

Recurrence can be local but endometrial carcinoma can also recur outside the pelvis. Vault recurrence is less common after adjuvant vaginal vault irradiation but distal recurrence is found more frequently if vault irradiation has been performed.

Treatment for recurrence

Where recurrence is localised to the central pelvis, its salvage with radiotherapy and/or surgery can be successful. Progestogens have been used as part of a combined primary treatment, as well as for recurrent or metastatic growths. Between 15% and 50% of recurrences will respond to therapy. Tumour response is especially noted in those patients with progesterone receptors in the tumour. Medroxyprogesterone acetate is most commonly employed and the addition of tamoxifen may improve the response. Chemotherapy also has a place in recurrent disease. Combination treatment with adriamycin and cisplatin gives response rates between 20% and 40%.

Sarcoma of the uterus

These are rare tumours and include:

Endometrial stromal sarcomas

Leiomyosarcomas

Carcinosarcomas

This group of cancers has undergone changes in nomenclature and even now some consider that uterine sarcomas are best described as high or low grade uterine sarcomas. They share a common presentation with other uterine cancers, with irregular and/or postmenopausal bleeding.

Clinical features

The patient is usually over 50 years old and presents with a complaint of fairly heavy bleeding of recent origin, accompanied by pain. Pelvic examination reveals a large intrauterine mass with friable tissue palpable through the os. The tumour may originate from the vagina in younger women and from the cervix in the child; but these are, indeed, very rare conditions. Sarcomatous change may occur in 0.1% of fibroids.

Histological appearances

Tumour tissue may infiltrate the whole myometrium and fill the uterine cavity or arise from a pedicle. This type often presents as a cervical or vaginal polyp. The tissues of origin are the connective tissue and muscle of the myometrium or leiomyoma, or the endometrial stroma.

These are composed of undifferentiated round- or spindle-cell masses. In children, striated muscle is often a feature and a characteristic polypoidal growth occurs – sarcoma botryoides.

High power appearance of round-cell sarcoma

Low power view of spindle-cell sarcoma

High power view of smooth muscle sarcoma

Endometrial stromal sarcomas

These are tumours of the endometrial stromal cells and form two groups:

Low Grade Stromal Sarcomas

The clinical course is often uncomplicated and cure may follow surgery. They can recur, often years later, and recurrence up to 25 years later has been reported.

High Grade Stromal Sarcoma

This type of stromal tumour shows numerous mitoses and is infiltrative from the start. There is early recurrence and widespread metastases occur even if there has been little local invasion of the myometrium. The prognosis is poor.

Carcinosarcoma (malignant mixed mesodermal tumour)

In this variant, both epithelial and stromal elements are malignant. It forms a soft polypoid mass that is usually haemorrhagic. Microscopically, most of the growth is sarcomatous but there are foci of carcinoma – adeno, squamoid, undifferentiated or various mixtures of these. The prognosis is poor. Treatment is surgical with hysterectomy, bilateral salpingo-oophorectomy and pelvic lymphadenectomy.

Leiomyosarcoma

Usually these cases do not present with postmenopausal bleeding and are found in patients thought to have a uterine fibroid. Fibroids of a very large size or those which increase rapidly in size should be suspected as having a higher chance of malignant change.

Treatment is usually hysterectomy and bilateral salpingo-oophorectomy. It is often not suspected at diagnosis. If detected postoperatively, then CT scan of chest, abdomen and pelvis should be undertaken to look for metastases. 10% of cases at diagnosis may have pulmonary metastases. Haematogenous spread is most common.

Pelvic examination, in this case, would suggest a cervical origin.

A diffuse infiltrating sarcoma.

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