Gynaecology

Gynaecology

INTRODUCTION AND OVERVIEW

Gynaecology is a large part of any general practice, and the conditions described below are part of a general practitioner’s everyday experience. While we owe our female patients effective care in their own right, society also benefits when women are healthy and happy in their daily lives. Women are central to the mental, physical, nutritional, educational and, frequently, economic health of their families and communities. By managing the woman’s care effectively, we also benefit the health of her children, her partner and, often, her parents.

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FIGURE 52.1 The female reproductive system

ANATOMY AND DEVELOPMENT OF THE UTERINE CERVIX

The ectocervix is covered by pink squamous epithelium, which changes suddenly to the red columnar (glandular) epithelium of the endocervix at the squamocolumnar junction (SCJ) (Fig 52.2). The columnar epithelium is shorter in height than squamous epithelium and appears red because the thin cell layer allows the underlying blood vessels to be easily seen. Columnar epithelium invaginations into the cervical stroma form endocervical glands.

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FIGURE 52.2 The uterine cervix

Before puberty, the squamocolumnar junction lies close to the external cervical os. As oestrogen levels rise after menarche and during pregnancy, the columnar epithelium everts further out onto the ectocervix to form an ‘ectropion’. Older terms including ‘erosion’ or ‘ulcer’ should not be used. Over time, the columnar epithelium exposed to the acid environment of the vagina is replaced by squamous epithelium (squamous metaplasia) and a new SCJ closer to the external os is formed. The area between the old and new SCJs where squamous metaplasia occurs is called the transformation zone. This is where most carcinogenesis occurs.

Newly formed immature metaplastic epithelium may develop into either:

• normal mature squamous metaplastic epithelium or, occasionally,
• atypical, dysplastic epithelium if persistent human papillomavirus (HPV) infection is present—this dysplastic epithelium may regress to normal, persist as dysplasia or progress into invasive cancer.

As oestrogen levels fall at menopause, the cervix shrinks and the new SCJ moves back towards the external os and into the endocervical canal. The epithelium becomes thin, pale and atrophic, with subepithelial petechial haemorrhagic spots.

The external os is small and circular in nullipara or in women who have delivered only by caesarean section, and gaping and transverse in parous women. Nabothian cysts are retention cysts that develop when endocervical crypt openings are occluded by the overlying metaplastic squamous epithelium.

Endocervical polyps can form at any age after menarche, and arise from the endocervix. They may cause intermittent vaginal or postcoital bleeding, a discharge or, in older women, postmenopausal bleeding.

CERVICAL CANCER SCREENING

Routine screening:

• begins at 1–2 years after first sexual contact with a male or female partner
• is not necessary for women who have never been sexually active
• continues 2-yearly for asymptomatic women with normal smear histories
• may cease at age 70 with two normal smears within the past 5 years
• should continue after hysterectomy if the smear history or histology of the cervix was abnormal, or the cervix was retained.

Technique:

• Examine the vulva, vagina and cervix for visible abnormalities. Suspicious lesions should be referred for colposcopy regardless of the cervical cytology result.
• Sample from the SCJ using the tools most applicable to the site of the transformation zone, e.g. broom for most women, brush where the SCJ is inside the canal, or spatula where the SCJ is on the outer ectocervix.
• Correct sampling requires both endocervical and ectocervical cells to be present on the smear.
• Liquid-based cytology screening may reduce false negatives and avoid unsatisfactory collection where blood is present.

Cytological signs of dysplasia (cervical intraepithelial neoplasia, CIN) include nuclear enlargement, increased nuclear–cytoplasmic ratio, hyperchromasia, irregular chromatin distribution and increased mitotic figures.

Koilocytes are atypical cells with perinuclear cytoplasmic cavitation (halo) typical of HPV infection.

Histological signs of dysplasia (CIN) are categorised according to the proportion of the epithelium showing undifferentiated (dysplastic) cells:

• CIN 1—undifferentiated cells confined to the lower third of the epithelium
• CIN 2—undifferentiated cells in the lower two-thirds of the epithelium
• CIN 3—differentiation may be absent or present only in the superficial quarter of the epithelium.

Since 1990, a simplified two-grade histological system using the term ‘squamous intraepithelial lesion’ (SIL), known as The Bethesda System, has been used.

• Low-grade squamous lesion (LSIL)—includes koilocytic atypia (HPV infection) and CIN 1 lesions.
• High-grade squamous lesion (HSIL)—includes CIN 2 and 3; considered a true precursor of invasive cancer.

MANAGEMENT OF ABNORMAL SMEARS

The NHMRC booklet, ‘Screening to prevent cervical cancer: guidelines for the management of asymptomatic women with screen detected abnormalities’ (see Resources list) contains information on:

• management of women with abnormal cytology
• the Australian Modified Bethesda system (AMBS 2004)
• less common cytological descriptions and their interpretation.

In general:

• Low-grade lesions may be transient. Their management varies and is discussed in the NHMRC booklet. However, women with low-grade lesions on cytology may have high-grade lesions found at colposcopy. CIN or any repeat low-grade lesions should be referred for colposcopy.
• High-grade lesions, including ‘possible high grade lesion’, may indicate an underlying invasive carcinoma and should be referred immediately for colposcopy.
• Invasive squamous cell carcinoma or adenocarcinoma should be referred immediately to a gynaecological oncologist.

Abnormal cytology results frequently cause significant fear and anxiety for the woman, including:

• embarrassment—at her condition, at having a ‘sexually transmitted disease’, at the diagnostic procedures involved or lack of privacy
• fear—of infertility, pain, putting her partner at risk or the outcome of investigations.

An explanation of the procedure, reassurance and information to read will help allay her fears and allow her to relax during the procedure. There are no specific symptoms that indicate dysplasia.

Colposcopy

A colposcope is a stereoscopic, binocular microscope with a powerful light source used to view the cervix:

• with green light to show the vascular pattern, and
• after 3–5% acetic acid solution, which stains dysplastic cells or squamous metaplasia ‘acetowhite’ by coagulating their higher nuclear protein content

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FIGURE 52.3 Colpophotograph after cervical biopsy

• after Lugol’s iodine solution, which stains the glycogen in normal oestrogenised squamous epithelium brown/black. Abnormal, oestrogen-deficient or columnar epithelium lacks glycogen and does not stain.

Neoplastic lesions are ‘acetowhite’ and ‘iodine-negative’ with abnormal vasculature. Any abnormal areas may be biopsied for histological confirmation.

Colposcopy during pregnancy requires skill and experience, due to progressive oedema, increased eversion, increased vascularity and the risk of significant bleeding with biopsy.

HUMAN PAPILLOMAVIRUS INFECTION

Human papillomavirus (HPV) infection is common. Most infections are transient and resolve over 12–18 months. However, persistent infection with an oncogenic serotype of HPV increases the risk of invasive cancer. Types 16 and 18 cause 70% of cervical cancer cases, and types 31, 33, 35, 39, 45, 51, 52, 56, 58, 59 and 68 are also oncogenic. HPV types 6 and 11 cause 90% of genital warts.

Oncogenic HPV infection is also associated with:

• adenocarcinoma in situ (AIS) of the cervix and invasive adenocarcinoma
• vulval intraepithelial neoplasia (VIN) and invasive cancer
• vaginal intraepithelial neoplasia (VAIN) and invasive cancer
• anal intraepithelial neoplasia (AIN) and invasive cancer.

PREVENTION OF CERVICAL DYSPLASIA

Prevention options include:

• minimising partner numbers
• consistent condom usage, which lowers the risk of HPV infection
• vaccination against HPV prior to infection—there are currently two commercially available recombinant vaccines, both involving a series of three injections over 6 months:
• Gardasil® (Merck) against HPV 6, 11, 16 and 18. TGA approval covers females aged 9–26 years (subsidised) and males aged 9–15 years (unsubsidised)
• Cervarix® (GlaxoSmithKline) against HPV 16, 18, 45 and 31
• optimising co-factors such as smoking and chronic inflammation, and correcting micronutrient deficiencies, which may affect disease progression.

TREATMENT OF CONFIRMED CERVICAL DYSPLASIA

Treatment options include:

• colposcopic review only, with treatment if the lesion persists or progresses over 18–24 months
• cryotherapy—healing occurs over 6 weeks, with a watery discharge for 3–4 weeks. No specimen is available for histology and lesions in glandular crypts may be missed. Can be performed without analgesia
• large loop excision of transformation zone (LLETZ, or LEEP)—provides a histological specimen. Severe postoperative bleeding occurs occasionally and must be managed promptly
• cold knife conisation where significant lesions inside the endocervical canal are suspected.

After surgery, women should avoid strenuous exercise, vaginal douche, tampons or intercourse until the vaginal discharge has settled (usually 2–4 weeks). Recurrent lesions occur in 5–10% of women.

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FIGURE 52.4 Vulval warts

Treatment on the day of colposcopy without confirmatory biopsy may be considered in women who may fail to return for follow-up. This risks over-treatment of lesions.

Post-procedure follow-up depends on the severity of the lesion, the completeness of excision and other individual features.

Treatment can remove dysplasia but not cure HPV infection. HPV testing 12 months after treatment of a high-grade lesion may be useful as a ‘test of cure’.

Other measures include:

• Avoid tobacco smoke.
• The few studies of HPV persistence showed a possible protective effect of fruits, vegetables, vitamins C and E, beta- and alpha-carotene, lycopene, luterin/zeaxanthin and cryptoxanthin.1 Evidence for a protective effect of cervical neoplasia was probable for folate, retinol and vitamin E, and possibly for vegetables, vitamins C and B12, alpha-carotene, beta-carotene, lycopene, lutein/zeaxanthin and cryptoxanthin. Evidence for an increased risk of cervical neoplasia associated with high blood homocysteine was probable, although the evidence is still inconclusive. Patients with an abnormal Pap smear should be advised to eat a diet rich in beta-carotene, vitamin C and folate (vitamin B9) from fruits and vegetables.
• Exercise regularly.
• Reduce avoidable stress. Higher levels of perceived stress have been associated with impaired HPV-specific immune response in women with cervical dysplasia.2

ABNORMAL UTERINE BLEEDING

A normal menstrual cycle occurs every 21–35 days, with bleeding for 2–7 days. Normal blood loss is 20–60 mL per period, with > 80 mL described as heavy.

The process of normal regular menstruation requires:

• sufficient oestrogen to induce ‘follicular phase’ endometrium
• ovulation with formation of a corpus luteum, production of progesterone and induction of ‘secretory phase’ in the endometrium
• withdrawal of progesterone as the corpus luteum declines. Declining progesterone is the trigger for menstruation
• synchronous breakdown and repair of the endometrium at menses
• breakdown factors including prostaglandins, interleukin-1, matrix metalloproteinase (MMP)-1 and MMP-7
• endometrial repair factors including epidermal growth factor-alpha, endothelins and vascular endothelial growth factor (VEGF).3

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FIGURE 52.5 The menstrual cycle and hormonal levels

TERMINOLOGY

Terms such as menorrhagia, metrorrhagia, polymenorrhoea, oligomenorrhoea and metropathia haemorrhagica should be replaced by descriptions of the frequency, heaviness and length of bleeding.

Abnormal uterine bleeding (AUB) covers all vaginal bleeding apart from regular ovulatory normal menses.

AETIOLOGY

Abnormal uterine bleeding is most common soon after menarche or in the years before menopause. It may be:

• anovulatory—without ovulation, a corpus luteum does not form. The resulting lack of progestogen and unopposed oestrogen stimulates the endometrium. Bleeding occurs when oestrogen levels fall or the endometrium becomes unstable:
• post-menarche—oestrogen levels rise but the immature hypothalamic-pituitary axis is unable to trigger ovulation. Menses may be infrequent but very heavy, often resulting in anaemia
• perimenopausal—ovarian follicle quality declines, resulting in variable oestrogen levels and variable menstrual flow. A dyssynchronous endometrium with irregular menstrual shedding results in prolonged menses with eventual amenorrhoea
• chronic anovulation—e.g. polycystic ovarian syndrome or hypothalamic dysfunction associated with low body weight, excessive exercise or stress. Oestrogen levels are variable. The corpus luteum does not form or is inadequate to maintain endometrial stability. Unopposed oestrogen stimulates the endometrium, which ultimately becomes unstable and bleeds irregularly
• ovulatory—periods are heavy but regular, due to:
• uterine pathology, e.g. fibroids
• abnormal endometrial function4 or
• systemic causes, e.g. obesity (endogenous oestrogen), clotting disorders (including von Willebrand’s disease), hypothyroidism
• iatrogenic—an imbalance between oestrogen and progestogen associated with the oral contraceptive pill (OCP), hormone replacement therapy (HRT) or progestins results in abnormal bleeding:
• light or absent periods, often with irregular bleeding due to excess progestogen effect
• premenstrual bleeding with inadequate progestogen
• intermenstrual bleeding with triphasic contraceptives
• heavier periods with excess oestrogen effect
• midcycle bleeding with inadequate oestrogen.

Medications associated with bleeding include anticoagulants, selective serotonin reuptake inhibitors, antipsychotics, corticosteroids, tamoxifen.

Medications that interact with the OCP/HRT, including liver enzyme inducers, antibiotics, anti-tuberculous drugs and antifungals, may also cause bleeding.

Herbal substances associated with bleeding include ginseng, ginkgo and soy supplements.

Causes of abnormal uterine bleeding are listed in Box 52.1.

BOX 52.1 Causes of abnormal uterine bleeding

Endocrine:

• immature hypothalamic–pituitary axis
• menopause
• obesity
• polycystic ovarian syndrome
• premature ovarian failure
• Cushing’s disease
• hyperprolactinaemia
• hypothyroidism
• weight loss

Infections:

• chlamydia
• gonorrhoea
• PID
• cervicitis

Uterine lesions:

• adenomyosis
• endometrial or cervical polyps
• endometrial or cervical malignancy
• leiomyomas

Pregnancy:

• ectopic pregnancy
• incomplete abortion

Medications:

• oral contraceptive pill (especially low dose, missed pills or drug interactions)
• progestogen-only contraceptives
• intrauterine devices
• tamoxifen
• warfarin

Other conditions:

• bleeding disorders (including thrombocytopenia, von Willebrand’s disease)
• endometriosis
• trauma
• excessive exercise
• stress

HISTORY

The history should include:

• menstrual history—last menstrual period (LMP), flow, ‘accidents’, ‘flooding’, length of cycle, number of days of bleeding, frequency of pad/tampon changes (more than 2-hourly is heavy), limitations on daily activities, use of double pads, changing at night
• features of polycystic ovarian syndrome
• reproductive history—contraceptive use, pregnancies, fertility plans
• lifestyle factors—change in exercise, stress, weight
• symptoms of anaemia—tiredness, palpitations
• medical history—thyroid function, bleeding disorders
• drug history—anticoagulants, hormone use, aspirin, anticonvulsants, SSRIs, antibiotics, alternative and complementary therapies.

EXAMINATION

Examination may be normal but should include:

• signs of anaemia, thyroid disease, bleeding disorder, hyperprolactinaemia

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FIGURE 52.6 Main causes of uterine bleeding: A Anovulatory endometrium with stromal breakdown; B Chronic endometriosis with numerous plasma cells (arrow); C Endometrial polyp; D Submucosal leiomyoma with attenuation of the endometrial lining (arrow)

• signs of polycystic ovarian syndrome (i.e. hyperandrogenism, hirsutism, acne, obesity and palpable enlarged ovaries; see Fig 7.7)
• speculum examination to exclude cervical and vaginal causes, especially if bleeding is post-coital
• bimanual examination to exclude fibroids and adnexal masses.

INVESTIGATIONS

Investigations include:

• pregnancy test
• Pap smear, STD screen
• haematology where loss is heavy:
• complete blood picture
• iron studies
• prothrombin time, activated partial thromboplastin time, von Willebrand screen—if bleeding heavy since menarche or suggestive history
• follicle-stimulating hormone, prolactin, thyroid-stimulating hormone
• transvaginal ultrasound—uterine lesions, polycystic ovarian syndrome (PCOS), retained products of conception, ovarian tumours. An endometrial thickness ≤ 4 mm virtually excludes endometrial cancer5
• endometrial biopsy—does not allow visual inspection of cavity and will not allow removal of polyps, resection of fibroids or endometrial ablation
• hysteroscopy and curettage, if required—exclusion of malignancy, removal of endometrial polyp, resection of submucosal fibroid.

MANAGEMENT

Management depends on the cause of bleeding, the woman’s plans for fertility and the impact that periods have on her life. In addition to bleeding, periods may involve dysmenorrhoea, sore breasts, mood disorder, migraines or an aggravation of pelvic symptoms.

Some women may request minimal treatment. Others may wish to avoid periods entirely. Different women may choose very different treatment options.

Teenagers presenting acutely with prolonged heavy bleeding (anovulatory cycles):

• Exclude anaemia, iron deficiency, pregnancy, bleeding disorders (including von Willebrand’s disease).
• Consider options including:
• Vitex agnus castus (chaste tree) 1000 mg daily.6 Although few randomised controlled trials (RCTs) exist, Vitex is commonly prescribed for menstrual irregularities, based on data collected by the German Commission E.7 Menstrual cycle irregularities due to hyperprolactinaemia, corpus luteum insufficiency, oligomenorrhoea and secondary amenorrhoea have been effectively treated with Vitex extract in open-label, uncontrolled studies
• combined 30–35 μg OCP q.d. with antiemetic until bleeding stops (within 72 hours). Follow with 1 tablet daily without placebo for 3–6 weeks, then withdrawal bleed for 5 days, then OCP8
• norethisterone 5–15 mg daily until bleeding stops, then 5–10 mg daily for 3–6 weeks
• IV conjugated oestrogen (Premarin®) 25 mg. Repeat 4-hourly until bleeding stops, usually within three doses. Follow with a combined OCP or progestin for 3–6 weeks9

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FIGURE 52.7 Polycystic ovaries: A Operative findings of classical enlarged polycystic ovaries. The uterus is located adjacent to the two enlarged ovaries. B Sectioned polycystic ovary with numerous follicles. C Histological section of a polycystic ovary with multiple subcapsular follicular cysts and stromal hypertrophy (low power, left). At higher power (×100, right), islands of luteinized theca cells are visible in the stroma.

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FIGURE 52.8 Pathology of polycystic ovarian syndrome

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FIGURE 52.9 Cervical polyp

• intracavity tamponade with 30–50 mL Foley catheter for 2–48 hours10
• Iron therapy until ferritin level is in normal range and for 3 months after bleeding becomes normal.

Ovulatory, regular, heavy periods:

• Exclude anaemia, hypothyroidism, iatrogenic causes, uterine disease (ultrasound).
• Where dysmenorrhoea is present, consider endometriosis or adenomyosis.
• Consider options including:
• Vitex agnus castus 1000 mg daily
• progestogen-dominant OCP
• NSAIDs (e.g. naproxen 500 mg b.i.d. or mefenemic acid 2 capsules t.d.s. during menses)
• tranexamic acid (i.e. 1–2 capsules q.i.d. during menses. Reduce dose if nauseated)
• levonorgestrel IUD—will also treat dysmenorrhoea
• danazol (i.e. 200 mg daily continuously). Treatment beyond 6 months is controversial. Treats mastalgia effectively
• endometrial ablation—less effective for pain. Contraception is required
• hysterectomy.

Perimenopausal women with frequent irregular periods and variable flow:

• Exclude anaemia, hypothyroidism, hyperprolactinaemia, iatrogenic causes.
• Exclude uterine and cervical disease—ultrasound and cervical smear.
• Consider the woman’s general wellbeing—oestrogen/testosterone deficiency symptoms, increased exercise, dietary review, weight loss assistance, psychological support.
• Consider options:
• Vitex agnus castus 1000 mg daily
• low-dose OCP—if low risk, non-smoker < 50 years
• cyclical progestins, e.g. norethisterone 5 mg day 1–12 each calendar month until menses cease
• sequential HRT—especially with menopausal symptoms
• levonorgestrel IUD—will reduce volume but not change timing of periods
• hysterectomy.

DYSMENORRHOEA

Dysmenorrhoea can be considered ‘normal’ if:

• it is only present on day 1–2 of the cycle
• it resolves with the OCP, or anti-inflammatory medications, and
• the woman is nulliparous.

MANAGEMENT

Management options for ‘normal period pain’ include:

• acupuncture and acupressure
• vitamin B1, 100 mg daily11
• magnesium supplement
• strenuous physical exercise.

Herbal

Common herbal treatments include:

• Chinese herbal therapies12
• chaste tree (Vitex agnus castus) 1000 mg daily before breakfast.

Diet

• Reduce red meat, to reduce levels of arachidonic acid.
• Increase consumption of omega-3 fatty acids, including fish and fish oil supplements.

Pharmacological

• Monophasic progestogen-dominant OCP (e.g. 30–35 μg ethinyl oestradiol with 500–1000 mg norethisterone or 150 mg levonorgestrel)—continuous-use OCP with menses every 2–3 months (skipping periods) may be beneficial.
• NSAID medications taken early in the pain, then regularly with food—consider suppositories for longer duration of action. The most effective NSAID varies between individuals. Can be taken with an H2-antagonist where there is a risk of gastritis.
• A levonorgestrel-releasing IUCD (Mirena®)—frequently most effective. Suitable for nulliparae, virgins and teens, after consideration of risks/benefits. Consider insertion under general anaesthesia. Three months of irregular bleeding ± crampy pain is common while it settles.
• Etonorgestrel implant (Implanon®)—less effective than levonorgestrel IUCD.

Dysmenorrhoea that does not resolve with the OCP or anti-inflammatories requires investigation. Common causes include endometriosis and adenomyosis. Any woman old enough to have periods is old enough to have endometriosis. While pregnancy frequently improves day 1–2 period pain in normal nulliparae, it seldom improves dysmenorrhoea in women with endometriosis and is inappropriate to recommend outside a suitable social setting.

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FIGURE 52.10 Pathology of endometriosis

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FIGURE 52.11 Intraoperative photo of endometriosis

ENDOMETRIOSIS

DEFINITION

Endometriosis is the presence of endometrial glands and stroma outside the uterus.

AETIOLOGY

The aetiology of endometriosis is unknown. It is increasing in prevalence. A tendency to develop endometriosis is inherited as a complex genetic trait influenced by environmental factors.13 Established lesions include inflammatory cells, fibrosis, neovascularisation and aberrant innervation. It has been associated with environmental toxins including organochlorines (polychlorinated biphenyls and dioxin-like compounds).14

Risk is increased with nulliparity and early menarche.15

SYMPTOMS

In the past, endometriosis was considered an uncommon condition of women in their thirties and forties. We now know it to be a common condition (5–10%) of women in their teens and twenties.

While some women are asymptomatic, common symptoms include:

• period pain resistant to OCP or anti-inflammatories
• period pain present for more than 1–2 days
• period pain felt on one side or in the lower back
• period-like pain during the month
• ovulation pain always felt on one side
• deep dyspareunia
• progression to chronic pelvic pain
• infertility—this is variable; many women become pregnant easily, so contraception is required
• fatigue.

Dysmenorrhoea is usually a combination of pain from the endometriosis and pain from the uterus. The endometrium of women with endometriosis has nerve fibres (pain receptors) not present in women without endometriosis.16 Optimal outcome requires management of both endometriotic lesions and the uterine component of pain.

HISTORY

Typical histories include:

• a teenager in whom periods have always been painful. Initial improvement on the OCP is followed by worsening pain resistant to NSAIDs
• a young woman with period pain on more than 1–2 days of a period, pain leading up to a period or pain that feels like period pain at other times of the cycle
• a woman who has had period pain for some time, but now has pain on most days (chronic pain), often with several different pain symptoms
• a woman whose severe period pain as a young woman did not resolve after pregnancy.

DIAGNOSIS

Reliable diagnosis requires laparoscopy. Diagnostic delay averages 6 years in Australia, due to a mixture of:

• Late presentation to a doctor. The woman or her family may believe that severe pain is normal. Her pain may be considered unimportant or exaggerated.
• Lack of investigation by the woman’s doctor, who may:
• fail to recognise a suggestive history
• believe she is too young for endometriosis
• underestimate the severity of her pain
• persist with failed treatments, or
• believe that a normal ultrasound excludes endometriosis.
• Lack of a non-invasive test for endometriosis.
• Missed diagnosis at laparoscopy. Lesions may be subtle, clear blebs in teenagers. White lesions may be misdiagnosed as scar tissue of unknown cause. The diagnosis of endometriosis requires a skilled laparoscopist.

INVESTIGATIONS

CA 125

• Rarely used. Not useful for screening.
• Mildly elevated in some cases.

Ultrasound

• Usually normal unless endometriomas are present.
• Transvaginal ultrasound is preferred, except in virgins or where the vaginal probe would cause pain or distress.
• An endometrioma has a grey, homogeneous, ‘ground glass’ appearance.
• The differential diagnosis of an endometrioma is a haemorrhagic corpus luteum. Repeat scan in 2–3 months will show persistence of an endometrioma or resolution of a corpus luteum.
• 99% of women with an endometrioma on ultrasound will have additional peritoneal deposits found at laparoscopy.17
• An endometrioma may be a marker for severe peritoneal or rectosigmoid disease.

MRI

Rarely required. May be used to investigate rectosigmoid disease or diagnose coexistent adenomyosis.

Laparoscopy

• Required for definitive diagnosis and treatment.
• Lesions may be clear, pink, yellow, brown, white, red or bluish black. May show only as increased vascularity, white scarring or adhesions. Frequently under-diagnosed.
• Histological confirmation of lesions is required.
• Areas of inflammatory tissue are common, but rare in women without pain.

TREATMENT OPTIONS

The treatments chosen will depend on the woman’s individual symptoms, preference, desire for fertility and coexistent conditions.

Explanation and support

• Ensure she knows you believe in her pain. Many women have been told that their pain is exaggerated, it is all in their head or their pain is normal.
• Provide education regarding endometriosis, her specific situation and the treatment options.
• Provide a management plan for when pain is severe, to allow her to control her pain. Anticipation of severe uncontrolled pain causes distress and anxiety as the period approaches.
• Involve a psychologist/counsellor where possible. The psychological, educational, financial, employment and relationship sequelae of pain, low self-esteem and self-doubt are common.

Laparoscopy

Once the diagnosis has been made, options include:

• excision of the endometriosis lesions if an experienced laparoscopic surgeon is present. Conservation of the uterus and ovaries is usual unless the woman is older and removal of these organs has been discussed
• documentation of the lesions and referral to a laparoscopic surgeon for repeat laparoscopy with excision
• diathermy to the endometriosis lesions—this is suitable for superficial ovarian lesions and some superficial peritoneal lesions. It is less effective than excision as deep lesions are incompletely removed and lesions close to the bowel or ureter cannot be safely diathermied
• no surgical treatment, with consideration of medical therapies.

Dietary and complementary therapies

These aim to:

• reduce oestrogen dominance
• reduce inflammation
• block aromatase activity in the endometriosis lesion.

Management includes:

• reducing dietary saturated fats
• avoiding trans fats (found in many processed foods)18
• maintaining healthy weight range
• reducing caffeine and alcohol intake
• engaging in regular strenuous exercise.

Herbs and supplements:19

• Vitex agnus castus 1000 mg daily
• anti-inflammatory—Boswellia, cat’s claw, turmeric, bromelain
• magnesium
• vitamin C 500 mg daily, vitamin E 400 IU daily20
• fish oil 1–2 g daily
• traditional Chinese medicine21—herbs often prescribed include corydalis, cnidium, bupleurum, dong quai and perilla, sometimes accompanied by acupuncture.

Medical treatments

Medical treatments do not improve fertility, will not divide adhesions or remove scar tissue, will not resolve an endometrioma and will not resolve deep endometriotic lesions. They may improve symptoms in the short term. Medical treatments are not required where excision of endometriotic lesions is complete. However, endometriosis surgery is challenging and requires advanced laparoscopic surgical skills and equipment. Medical treatments include:

• gonadotrophin-releasing hormone (GnRH) analogues—by daily nasal spray or monthly depot injection, for 3–6 months. Hypo-oestrogenic side effects include hot flushes, poor sleep, tiredness, dry vagina and loss of bone density. May be used with combined HRT to minimise side effects without decreased efficacy
• progestins (e.g. norethisterone 5–10 mg daily)—can be used in the long term if effective
• danazol or dimetriose—used less now due to androgenic side effects
• aromatase inhibitors.

Consider treatment of coexistent causes of pelvic pain at the laparoscopic procedure. For example:

• insertion of levonorgestrel IUCD to manage uterine aspect of dysmenorrhoea
• cystoscopy with hydrodistension to diagnose interstitial cystitis
• starting a medication for neuropathic pain
• providing photographs to allay fears and increase understanding.

A full discussion of the management of endometriosis is available in textbooks on this topic.22

MANAGEMENT OF OVARIAN ENDOMETRIOMAS / SEVERE ENDOMETRIOSIS

Effective treatment of endometriomas requires removal of the cyst wall from inside the ovary, by either ‘stripping’ cystectomy or diathermy (less effective). Drainage alone is rapidly followed by recurrence. Where endometriosis is severe, the pouch of Douglas may be obliterated, and endometrosis may invade the muscularis of the rectum.

Where laparoscopy does not help her pain

Either the endometriosis was incompletely removed, or the pain is due to another condition (e.g. uterine pain, pelvic muscle pain, interstitial cystitis or neuropathic pain). Even when present, the endometriosis may not be the main cause of pain.

Recurrent pain after previously successful surgery

Where the current pain is the same as the pain that resolved with surgery, review laparoscopy is reasonable. Where the pain is different, consider other causes of pain (e.g. uterine pain, interstitial cystitis, neuropathic pain).

ADENOMYOSIS

Adenomyosis is the presence of endometrial glands and stroma in the myometrium with adjacent smooth muscle hyperplasia. It is generally diffuse but may form an adenomyoma locally. The aetiology is unknown, but it is more common in women with endometriosis.

SYMPTOMS

Symptoms where present include:

• dysmenorrhoea, often with back pain
• heavy periods
• dyspareunia.

Suggestive histories include:

• dysmenorrhoea due to endometriosis as a young woman, few problems during childbearing years, then increasing dysmenorrhoea due to adenomyosis once childbearing complete
• trouble-free periods when young, with worsening dysmenorrhoea after the birth of a child.

DIAGNOSIS

Diagnosis requires histology but is likely with:

• suggestive symptoms and the absence of endometriosis at laparoscopy
• a bulky uterus on vaginal examination
• ultrasound features of:
• bulky, rounded uterus with asymmetrical thickness of the anterior and posterior myometrium
• subendometrial myometrial microcysts
• subendometrial echogenic linear striations
• poor definition of the endometrial myometrial junction
• heterogeneous myometrium
• MRI changes consistent with adenomyosis.

TREATMENT

If asymptomatic, no treatment is required. Treatment options include:

• levonorgestrel-releasing IUCD
• NSAIDs with back-up narcotic-based analgesia for dysmenorrhoea
• progestogens, e.g. norethisterone 5 mg daily continuously or progestogenic OCP
• treatment of coexisting menorrhagia, to minimise the contribution from ‘clot colic’. Endometrial ablation may worsen adenomyosis
• treatment of coexisting menstrual symptoms, to minimise the number of symptoms the woman must cope with during menses (e.g. premenstrual mood disorder, menstrual migraine, bloating, lethargy)

image

FIGURE 52.12 Pathology of adenomyosis: Sagittal (A) and axial (B) MR images through the pelvis show focal junctional zone widening and characteristic thickened areas (*); Sagittal (C) and axial (D) MR images in a different patient show widening of the entire junctional zone (*) which contains endometrial rests

• hysterectomy.
• A danazol-loaded IUCD has been investigated in Japan.23

CHRONIC PELVIC PAIN

While some women with endometriosis improve over time and others persist with dysmenorrhoea over the long term, a proportion progress to chronic pelvic pain. Pain becomes a mixture of pelvic symptoms and central sensitisation with neuropathic pain. Symptoms include some or all of:

• dysmenorrhoea present before the chronic pain began, that now affects more days per month
• urinary symptoms of frequency, urgency, nocturia and bladder pain
• variable bowel symptoms, often with food intolerance and bloating
• sharp, stabbing, burning or aching pains that occur spontaneously, often at night
• painful pelvic muscles with dyspareunia
• other pain conditions, including migraine, muscle trigger points, generalised muscle aches or vulvodynia
• hypersensitivity of the abdomen or pelvis
• poor sleep, fatigue, anxiety and diminished quality of life.

These symptoms may develop even when all her endometriosis has been removed and after hysterectomy. In women with pain on most days, a central chronic pain process is likely, and management usually includes neuropathic pain medications, cognitive behavioural lifestyle changes, and management of the local pelvic symptoms.24

MANAGEMENT

Pain is now complex. No single treatment and no surgery will resolve all the woman’s pain. While complete cure is unlikely, substantial improvement can be achieved by managing local pain symptoms, treating central sensitisation and rehabilitation of the sequelae of her chronic pain condition.

• Make a list of each pain she has, what it feels like, where it is and when it happens. Ask specifically about sharp pains, bladder function, bowel function, dyspareunia and pain in other areas of the body.

Related posts:

  1. disease
  2. Menopause
  3. Episiotomy
  4. Adnexal Masses

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Nov 4, 2016 | Posted by in OBSTETRICS | Comments Off on Gynaecology

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