Gynaecology 6th year 2015

By Brendon Govender

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 Contents
1) AUB(4-26) 12)Bartholin’s Cyst &
2) PMB(27-34) Abscess
3) Amenorrhoea(35-55) 13)STIs
4) Dysmenorrhoea I. Syphilis
5) Menopause & HRT II. Gonorrhoea
6) Ectopic Pregnancy III. Chancroid
7) Miscarriages + EVAC IV. LGV
8) Infertility V. Chlamydia
9) Contraception VI. Genital Warts
10)Fibroids VII. HSV
11)PID VIII.Trichomonas
IX. Candidiasis 2
 Contents continued…
14)Ca cervix
15)Ca endometrium
16)Ca ovary
17)PCOS
18)Endometriosis
19)Chronic Pelvic Pain
20)Genital Prolapse
21)Urinary Incontinence
22)GTD
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Abnormal Uterine Bleeding

By Brendon Govender

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 Definitions
• Menorrhagia: Excessively prolonged (> 7days)or profuse
menses(>80ml) (regular cyclical)

• Metorrhagia: irregular acyclic bleeding

• Menometrorrhagia - Prolonged or excessive uterine

bleeding occurring irregularly and more frequent than
normal

• Polymenorrhoea: Occurrence of menstrual cycles of

greater than normal frequency (<21 days)

• Oligomenorrhoea: Scanty menstrual cycles (>35 days) 5

 Aetiology
• Pregnancy-related causes
– vaginal bleeding early in pregnancies due to abnormal placentation
– miscarriage or an ectopic (tubal) pregnancy
• Reproductive tract problems
– Uterine fibroids and polyps (growths)
– Uterine infections.
– Precancer or cancer in the uterus, cervix (opening of the uterus), or vagina
• Medical conditions
– obesity
– thyroid problems
– blood clotting problems
– liver disease
• Medications
– Hormones
– Warfarin
– Birth control methods such as pills, implants, shots, and intrauterine devices (IUDs
• Dysfunctional uterine bleeding
– No organic cause can be found for abnormal bleeding, it is called dysfunctional uterine
bleeding.

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 Aetiology cont.
• P-Polyp(cervical & endometrial polyps)
• A-Adenomyosis (enlarged uterus approx 14 wks)
• L-Leiomyomata(clinical)
• M-Malignancy+ hyperplasia(Pap Smear + Pipelle)
• C-Coagulopathy(Hx + Exam + coag screen)
• O-Ovulatory dysfunction
• E-Endometrial(prod of prostaglandins)
• I-Iatrogenic(COC,HRT,steroidal)
• N-Not yet classified
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 Dysfunctional Uterine Bleeding
• Definition
– Abnormal Uterine bleeding in the absence of
organic disease

• It is a diagnosis of exclusion

• 60% of abnormal uterine bleeding will be

diagnosed as dysfunctional uterine bleeding

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 Pathophysiology:
Ovulatory Dysfunctional Uterine Bleeding
• Usually due to local factors originating in the
endometrium
• Patients present with :
– menorrhagia with regular, cyclic bleeding
– PMS symptoms, often have structural abnormality
– Abnormal progesterone ratios

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Pathophysiology:

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 Ovulatory DUB
• Poor function of the Corpus Luteum
– ↑ bleeding due to corpus insufficiency (↓ secretion of
progesterone)
– Short luteal phase and irregular endometrial ripening
• Persistence of the Corpus Luteum
– Persistant progesterone secretion
– ↑luteal phase therefore bleeding is prolonged and
intermittent
– Irregular shedding of endometrium

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 Anovulatory Dysfunctional Uterine
Bleeding
• Abnormality of the H-P-O axis
• Bleeding is not preceeded by ovulation
• Usually occurs early after menarche or in
perimenopausal women
• Present with:
– irregular, prolonged and excessive bleeding
(menometrorrhagia)
– Absence of cyclic progestin causes fragile unstructured
endometrium prone to breakage and bleeding

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Pathophysiology:

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 Anovulatory DUB
• Excessive Oestrogen Stimulation of the Endometrium
– Graafian follicle forms but doesnt rupture
• Progressive ↑ in oestrogen level
• Endometrial hyperplasia
• When oestrogen level fluctuate and fall below a critical level this
results in heavy menstrual bleed

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• Inadequate stimulation of the endometrium
– Low levels of oestrogen
– Thin endometrium
– Levels fall too low to maintain the endometrial
lining resulting in irregular acyclical bleeding

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 History
• Reproductive history
– Age of menarche
– Last menstrual period
– Menstrual history (cycle length, duration of flow, amount of
blood loss, passage of clots)
– Postcoital bleeding

• Full Gynae History

– Previous abortion or recent termination of pregnancy
– Sexually transmitted diseases (STDs) or ectopic pregnancy
– Contraception
– Pap smears
– Gynae Surgery
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• Medical History
– Symptoms of anaemia or hypovolaemia (including
fatigue, dizziness, and syncope)
– Symptoms indicating bleeding disorders
– Diabetes mellitus
– Endocrine problems, pituitary tumours, Thyroid
disease, liver disease
• Drug history
• Family History
– Bleeding disorders

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 Examination
• General
– Vitals
– Patients haemodynamic status (exclude shock due to excessive
bleeding)
– Anaemia,
• Signs of endocrine disease:
– goitre, obesity, striae, hirsutism, acne
• Evidence of haemaological abnormalities:
– petechiae, purpura, mucosal bleeding, bruising
• Signs of liver disease
• Abdominal examination:
– masses, uterine enlargement, abdominal tenderness
• Speculum, bimanual, and rectovaginal examination
– Inspect vulva, vagina, cervix for infection or lesions

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 Investigations
• Pregnancy test
• Check Haemoglobin
– If patient anaemic do FBC
• If coagulopathy suspected, do coagulation screen
• Pelvic Ultrasound:
– identification of intrapelvic and adnexal disease
(hyperplasia, polyps, fibroids)
• Cervical Cytology
• Endometrial Sampling-For patients >45 yrs/patients
with failed medical therapy
• Hysteroscopy
– Direct visualisation of endometrium, and allows for biopsy
• Laparoscopy for organ pelvic disease
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 General Approach of Mx
• Stop Bleeding (Hormonal-COC,POP,Oestrogens
/Non-Hormonal)
• Clinical Picture (Hypovolaemia?Resus?)
• When acute bleeding stops →Treat causes- PALM
COEIN
1st line @ KEH→IV Cyclokapron à PALM COEIN àIf pt
still bleeding àgive high doses of COC every 6hrs
for 3-5 days /can give high doses POP for 3-5 days
20-30mg/Oestrogen IMI 25mg
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 Medical Management
Type Drug Name Dose Uses Side Effects Contra-
indications
Antifibrinolytic Tranexamic Acid 1,5 g orally, TDS, Useful in acute Nausea, dizziness, Patients with
Therapy (Cyklokapron) for 1st 3-4 days of bleeding and long tinnitus, rash, history of
bleeding term; abdominal cramps thromboembolism
For patients where
oestogen and
progesterone are
contraindicated
Hormonal Progestogens 5mg orally, TDS, Anovulatary DUB; Weight gain,
Therapy 1. Medroxy- prescribed from When oestrogens bloating, oedema,
progesterone day 16-25 of cycle are contraindicated headache
(Provera)
2. Norethisterone
(Primolut)
Hormonal Intra-uterine 20µg Ovulatory; Few S/E since little
Therapy System levonorgestrel Also reliable absorbed
Mirena (releases realeased every method of systemically
levonorgestrel) 24 hrs contraception
Hormonal Combined Oral Anovulatory or Weight gain, CVD, CAD, Hx of
Therapy Contraceptive Pill Ovulatory Bleeding; abdominal DVT, CCF,
Also reliable discomfort, untreated HT,
method of spotting breast cancer,
Contracerptin suspected
pregnancy21
Type Drug Name Dose Uses Side Effects

Hormonal Danazol-Not 200mg daily for 12 Reserved for Weight gain, acne,
Therapy commonly used weeks patients where hirsutism. Breast
oestogen and atropy, greasy skin,
progesterone are headaches,
contraindicated depression

Hormonal GnRH analogues Anovulatory or Hot flushes, vaginal

Therapy 1. Leuprolide Ovulatory Bleeding; dryness, mood
acetate Also useful for swings,
2. Goserelin alleviating osteoporosis
associated
dysmenorrhoea

NSAIDs 1.Mefenamic acid 1. 500mg TDS Reduce menstrual Dyspepsia, nausea,

2.Ibuprofen 2. 400mg TDS flow by 30% vomitting diarhoea
Also useful for
dysmenorrhoea

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 Surgical Management
— Endometrial Ablation
◦ Destruction of the stratum basalis layer of the
endometrium
◦ Prevents endometrial regeneration
◦ Pre-operative medication: Danazol or GnRH analogues to
produce a thin atrophic endometrium
◦ Procedure done as outpatient under local anaesthesia or
under general anaesthesia as an inpatient
– Necesary to ablate endometrium to a depth of 5mm to be
effective
– Methods : laser ablation, endometrial resection, various balloon
techniques
– *Make sure you have excluded endometrial malignancy &
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Pregnancy before Endometrial Ablation!
24
 Hysterectomy
• Definitive Management for:
– Patients who have completed their families and
are over the age of 45
– Failed medical treatment
– Premalignant conditions of the cervix or
endometrium
– Failed endometrial ablation

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AGE CAUSE MANAGEMENT
Adolecence Usually Dyfunctional Usually self limiting
(anovulatory) • Mild
reassure, counsel, menstrual
calendar, haematinics

• Severe
1. Check FBC, exclude blood dyscrasia
2. Blood Transfusion only if necessary
3. Hormone therapy
Low dose COC or progestogens
4. Haematinics

Reproductive Phase (20 – 40) Usually pathological: Full exam and Investigations (hysteroscopy and endometrial
-Polyps, PID, abnormal pregnancy sampling if necessary)
states (e.g. Abortion, ectopic)
Treat underlying pathological cause
If Dysfunctional usually ovulatory
DUB – combined oestrogen/progesterone therapy in last 5-
10days of cycle

Perimenopausal Organic cause : NB exclude Full exam and Investigations (hysteroscopy and endometrial
malignacy sampling)

DUB: anovulatory Treat underlying pathological cause

(may be hyperplastic)
DUB
Hysteroscopy and Curettage
-(if bleeding settles + histology benign the not further
treatment)
-If continues COC (low dose) or Mirena
-If histology show atypical hyperplasia- hysterectomy
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-Simple hyperplasia progestogens if fails - hysterectomy
 PMB

DEFINITION
Any bleeding from the female genital tract in;
1) the appropriate aged woman not using hormonal
replacement therapy at least 6 months after the
cessation of menstruation (or 1 year if previous cycles
were oligomenorrhoeic) or
2)Acyclical bleeding in post menopausal women on
hormone replacement therapy

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 Aetiology
• SYSTEMIC • LOCAL

•Bleeding disorders: BENIGN

-Thrombocytopaenia •Vulva-dystrophy, dermatitis, trauma
-Von Willebrands disease •Vagina-atrophy, inflammation, trauma, polyps
-anticoagulants •Cervix- cervicitis, polyps, trauma
•Endometrium- endometritis, atrophy, polyps
•Exogenous estrogens: •Uterine fibroids
-Hormone therapy
-Natural products e.g. soy MALIGNANT
•Vulval carcinoma
•Endogenous estrogens: •Vaginal carcinoma
-peripheral conversion of androgens •Cervical carcinoma
-oestrogen producing tumours •Endometrial hyperplasia
•Endometrial carcinoma
•Uterine sarcoma
•Fallopian tube carcinoma
•Secondary tumours

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 History

• Exact nature of bleeding

• Exclude bleeding from urethra, bladder, rectum,
anus
• Bleeding tendencies
• Medication (hormone therapy,
anticoagulants,tamoxifenand natural products )
• Associated symptoms: pain, malodourous
discharge, post coital bleeding (all suggestive of
cervical Ca)
• Fertility hx, menstrual hx
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 Examination
4. CERVIX
1.GENERAL EXAMIANTION • -inflammation, ulceration, polyps
• -BMI • -consistency, surface, excitation and
• -Blood pressure mobility
• -lymph nodes (esp virchows trousier node) • -smear for cytological evaluation
• -signs of bleeding tendency • -sample endo and ecto-cervix
• -anaemia • -biopsy suspicious lesions
• -wet mount examination when discharge or
2. ABDOMINAL EXAM inflammation present
• -organomegaly
• -masses 5.UTERUS AND ADNEXAE
• -ascites • -document any masses palpable on
bimanual examination
3. VULVA AND VAGINA
6. RECTUM
• -inspect for lesions
• -exclude rectal involvement of palpable
• -palpatefor Bartholinsglands mass
• -on speculum exam-no any bleeding or • -assess parametria
discharge
• -look for lesions of vaginal walls
• -ulceration around ring pessaries 30
 Investigations
• FBC: Hb, WCC, platelets
• U&E
• Urine: Dipstix (haematuria)
• Pap smear: Rule out Ca cervix
• Transvaginal U/S: Mass, endometrial thickness
• Pipelle biopsy
• Hysteroscopy: directly visualise intrauterine pathology
• Transvaginal sonography: measure endometrial thickness, presence of polyps,
fibroids, adnexal mass
• Saline hysterosonography: used when intra cavity polyps or fibroids are suspected.
Endometrial calcification indicates TB

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 Management-Benign conditions
Endometrial atrophy/Normal endometrium Endometrial hyperplasia without atypia
•usually does not require treatment •Progesterone (10-20mg daily x 3months)
•Then sample to confirm regression of
•Counsel on reporting recurrence of bleeding hyperplasia

•If recurrent bleeding-exclude all possible

causes, then do hysterectomy

Vaginal atrophy Endometrial and cervical polyps

•Oestrogen application in cream/tablet form •Remove to stop bleeding and exclude
(endometrial hyperplasia with prolonged malignant change
use!!)
Bleeding associated with Hormone therapy Fibroids
•Treat after exclusion of other causes •resect
•Depends on dose, regimen etc
Endometrial hyperplasia with atypia Trauma
•TAH with bilateral salping-oophorectomy •Usually due to coitus
as risk of endometrial Ca is high (48%) •Treat as for vaginal atrophy
•Exclude sexual abuse with thorough history
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 Management-Malignant conditions
ENDOMETRIALCARCINOMA CERVICAL CARCINOMA

•Surgery involves TAH and BSO with peritoneal •Cone biopsy/ simple hysterectomy
lavage or radical hysterectomy and bilateral pelvic
node dissection in patients fit for surgery for
•Pelvic and para-aortic lymphadenectomy for stage 1
deep Grade 1 or 2 and for grade 3
•Radical surgery or chemo radiationfor stage 2
•Individualised surgery and adjuvant chemo or
radiotherapy for grade 4 •Radiation for stage 3

•Palliative care for stage 4

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Algorithm

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 Amenorrhoea
•Amenorrhoea: absence of menses
•Classification:
•Primary(delayed menarche): failure to initiate
menstruation by age of 16 years or later
•Secondary(post menarchal): absence of menses
when menstruation has previously occurred.
Absence of at least 6 months if regular menses and
12 months if infrequent.

Symptom and not a diagnosis

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 Normal menstrual cycle
• Requirements:
– Intact intergrated Hypothalamic- pituitary- ovarian
axis(HPO)
– Responsive endometrium
– Patent outflow tract

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 Aetiology
• Endocrine dysfunction- 99%
• Anatomical defect- 1%

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 Physiological causes
• Pregnancy:
– associated with raised prolactin levels- inhibit HPO axis
• Lactation:
– also associated with raised prolactin levels
• Perimenarchal amenorrhoea
– upper limit of normal age of menarche is 16 years
– the first ovarian cycles after menarche are often anovulatory,
and oligomenorrhoea and amenorrhoea are common
• Perimenopausal amenorrhoea
– ovary becomes less sensitive to FSH and LH stimulation towards
end of reproductive life anovulation and oligomenorrhoea may
occur

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 CNS and Hypothalamus
• Psych-neuroendcrinological factors:
– Stress- Increased circulating endorphins, prolactin levels and weight
loss- inhibit HPO axis at hypothalamic level
– Pseudocyesis(Phantom pregnancy)
• women with intense desire for pregnancy/ overwhelming fear of becoming
pregnant.
• Usual pregnancy induced changes
• Hypersecretion of LH and prolactin caused by decreased central dopaminergic
activity
– Under nutrition-
• adequate nutrition & normal body composition essential for HPO axis
• Decreased gonadotrophin secretion with reduced pulse amplitude, decreased
ovarian stimulation and eventualy the loss of normal folliculogenesis and
steroidgenesis
– Exercise- same as undernutrition but intake normal, energy
consumptions is increased

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• Psych-neuroendcrinological factors cont…
– GnRH deficiency
• uncommon cause
• Idiopathic hypothalamic failure
– Compression/destruction of hypothalamus
• Tumours eg. Craniopharyngioma- most common
• Non- neoplastic: TB, Sarcoidosis
• Decreased GnRH release & production resulting in
hypopituitarism

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 CNS and Hypothalamus cont…
• Pituitary gland
– Hyperprolactinaemic states
• Prolactin: under tonic inhibition by hypothalamus
• Major prolactin inhibitory factor- Dopamine
• Stimulants of release of prolactin: Oestrogen,
endogenous opiods, TRH
• Interruption of hypothalamic-pituitary system-
disinhibition and elevation of prolactin

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• Pituitary gland cont…
– Cellular and anatomic defects causing
hypopirtuitarism
• Empty-sella syndrome: elevated prolactin, low
gonadotropins
• Non- neoplastic intracellular masses: TB, Sarcoidosis
– Acromegaly and Cushing’s syndrome

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• Pituitary gland cont…
– Disruption of hypothalamic-pituitary connections
• Pituitary stalk lesions- result- no stimulation by
hypothalamus- no stimulation by releasing hormone-
decreased secretion by anterior pituitary
• Elevated prolactin
• Sheehan’s syndrome: necrosis of anterior pituitary
following massive PPH with infarction and interruption
of the vascular links of pituitary gland

43
 Gonadal Causes
• Primary ovarian failure
– Gonadal dysgenesis
• Gonads don’t develop- appear as streaks of white
tissue without follicles, lying adjacent to fallopian tubes
• Gonadal sex hormone production at puberty doesn’t
occur- no secondary sexual characteristics and primary
amenorrhoea
• FSH and LH elevated
• Cause- Turner’s syndrome, Swayer syndrome

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• Primary ovarian failure cont…
– Premature ovarian failure
• ovarian function fails before 40 years
• failure of folliculogenesis and inadequate
steroidogenesis
• Low oestrogen, elevated FSH & LH (negative feedback)
• Causes:
– Iatrogenic
– Autoimmune diseases
– Idiopathic

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 Gonadal Causes cont…
• Gonadal dysfunction
– Functional ovarian tumours
• follicular cysts, persistent luteal cyst & hormone producing
tumours
• Abnormal hormone production
– Polycystic ovary syndrome(PCOS)
• unknown cause
• Presentation:
– Menstrual abnormalities Hirsutism & acne
– Alopecia Obesity
– Anovulatory infertility Insulin resistence
– Endometrial hyperplasia Dyslipidemia
• ultrasound: large ovaries with multiple cysts distributed evenly
around ovarian periphery and increased stroma

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 End-organ defects
• Congenital abnormalities
– Mullerian agenesis
• caused by intrauterine insult at critical time of development
• Ovarian function is normal- normal secondary sexual
characteristics
• Primary amenorrhoea
– Mullerian anomalies
• cervical & vaginal atresia, tranverse vaginal septa,
imperforated hymen
• Presentation: pelvic mass, cryptomenorroea(hidden
menstruatruation)

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• Congenital abnormalities cont…
– Errors in genital differentiation
• Acquired abnormalities
– Endometrial fibrosis: obstruction of the cavity
• cause: TB, Bilharzia or traumatic curatage, childbirth
– Cervical stenosis
• causes: surgery: cone biopsy

48
• Thyroid
– occurs in hyper and hypothyroidism
– primary hypothyroidism- increased TRH- increase
prolactin
– Hyperthyroidism- weight loss
• Metabolic conditions
– DM, Liver cirrhosis and vegan diet
• Medication
– Contraceptives, drugs that cause hyperprolactanaemia

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 Approach
• History
• Exam
• Investigation
• Management

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 History
• Presenting complaint
• Gynaecological :
– menstrual history
– pubertal development & history
– contraceptive history
– possibility of pregnancy
• Previous Obstetric:
postpartum haemorrhage, abortion , sepsis
and curettage, lactation
• Past medical & surgical :
– medication

51
 History cont…
– symptoms indicating possible hypothalamic causes-
weight, stress, anosmia
– symptoms indicating possible hyperprolactinaemia-
galactorrhoea, visual disturbances, loss of libido,
vaginal dryness, mastalgia
– symptoms of hyperandrogenism- hirsutism, acne,
alopecia, voice changes
– symptoms of ovarian failure -hot flushes, sweat
– symptoms of diabetes and thyroid disease-polyuria,
polydipsia, weight changes, temp preference,
tachycardia
– Family history- PCOS
– Social History- Stress, career, domestic life

52
 Examination
Examination
• General
features of chromosomal abnormalities
hair distribution & acne
height , weight & BMI
Pubertal staging ( if indicated)

• Gynaecological
internal & external genitalia

53
 Investigations
• First exclude pregnancy- urine- Beta hCG/ serum hCG
• Any women presenting with amenorrhoea who fulfils the following
criteria should be investigated:
– 14 year old without secondary sexual characteristics
– 16 year old with normal secondary sexual characteristics
– Amenorrhoea for 3 – 6 months
– Signs of hyperandrogenism and any endocrinopathy
– Dysmorphic features

• FSH & LH , TSH, Testosterone levels

• Karyotype
• TFT , Prolactin concentration
• Progestogen withdrawal test (Provera 10 mg daily for 5 days)
• Ultrasound of pelvis (uterus present, Polycystic ovarian syndrome)

54
 Management
• Manage underlying pathology

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 DYSMENORRHOEA
• Painful menstrual cramps of uterine origin
• Most young adolescents experience it in a few
years after menarche, with the peak onset
happening between the ages 19 and 24
• It declines with oral contraceptive use and
childbirth
• Leading cause of short term absenteeism
from school and work

56
 Epidemiology
One of the most common complaints in women of reproductive age
- Varied prevalence estimates: 45-95% in different age groups
- Incidence of primary dysmenorrhoea: 75%
- Peak onset found to be between 19 and 24 years of age
- Family history significant- increase in prevalence of dysmenorrhoea in
individuals with a positive family history of presence in 1st degree relatives

57
 Classification
• PRIMARY DYSEMENORRHOEA
• Spasmodic painful menstrual cramps without an underlying organic
pathology

• SECONDARY DYSMENORRHOEA
• Based on the underlying pathology

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PRIMARY DYSMENORRHOEA SECONDARY DYSMENORRHOEA
Onset shortly after menarche Onset occurs any time after menarche
(usually after 25 yrs of age)
Lower pelvic / abdominal pain is Women may complain of change in
usually associated with onset of time of pain onset during menstrual
menstrual flow and lasts 8-72 hrs cycle or in intensity of pain
Back and thigh pain, headache, Other gynae symptoms ( like
diarrhoea, nausea and vomiting may dyspareunia, menorrhagia) may be
be present present
No abdominal findings on exam Pelvic abnormality on physical exam

59
 AETIOLOGY
Theory postulated; aetiology largely unknown
1. Nausea, Vomiting, Cramping, Bloating
• Symptoms attributed to action of uterine prostaglandin PGF2
• Progesterone levels decrease because of the regression of the
corpus luteum
• triggers an increase in fatty acid content in phopsholipid layer of cell
membrane
• Before menstruation, there is progesterone withdrawal
• Following withdrawal of progesterone omega6 fatty acids are
released
• In response, prostaglandins and leukotrienes are activated and
released; inflammatory response
2. Pain
• Prostaglandin E2, F2a, COX, Artachadonic Acid Metabolites cause
vasoconstriction in vessels of the myometrium;
• During contraction, results in ischaemia and subsequently pain

60
Primary Dysmenorrhoea

61
 Risk Factors
• Heavy menstrual flow
• Young age <20 yrs
• Nulliparity
• Early menarche
• Smoking
• Obesity
• Family history
• High levels of stress, anxiety and depression

62
 Clinical Presentation
• Lower abdominal pain
• Pain 2-3 hours prior to menstrual flow
(variable)
• Cramping, spasmodic pain
• Radiation to lower back and thighs
• Associated with systemic symptoms

63
 Clinical Presentation
• Detailed gynaecological history essential

• May reveal Lower Abdominal Pain

• Suprapubic tenderness

• PV Examination reveals no abnormalities usually-

• Avoid in young patients that have never been sexually active

• Full systems examination

• Exclude Pregnancy and Ectopic pregnancy

• Assess severity of dysmenorrhoea

64
Verbal multidimensional scoring
system for assessment of
dysmenorrhoea

65
 Diagnosis and Investigations
• Focused history
• Pregnancy testing
• Imaging- has limited value if no pelvic pathology
suspected
• Chronic intractable pain/ severe dysmenorrhoea-
abdominal ultrasound
• Beta-hCG studies for suspected ectopic
pregnancies
• Laparosopy indicated for suspected secondary
dysmenorrhoea

66
 Management
NON PHARMACOLOGICAL AGENTS
• Acupuncture
• Heat therapy: use of a hot water bottle over the
suprapubic region.
• Lifestyle modification: low fat vegetarian diet
decreases the duration and intensity of
dysmenorrhoea
• Aerobic exercise
• Psychological therapy: reassurance, support and
explanation

67
 Pharmacological Agents
• NSAIDs
• Cyclo-oxygenase II inhibitors – cardiovascular
side effects led to the withdrawal from the
market
• combined oral contraceptives
• Levonorgestrel – releasing intrauterine system
• vitamin supplements

68
 NSAIDs
•first line treatment
•there are two classes of NSAIDs – carboxylic acids and enoloic acids
•the carboxylic acid are the first choice, they include
• Propionic acids – Ibuprofen 400-800mg po6 hrly, Naproxen
250-500mg po 6hrly
• Fenamates – Mefanamic acid 250-500mg 6hrly
• Acetic acid – Indomethacin 25-50mg po 8hrly
• salycylic – asprin is not routinely used
•the enoloic acids include
– oxicam – Piroxicam, has bone marrow toxicity
– Pyrazolones – Phenylbutazone

69
 NSAIDs
•Method of action of NSAIDs – inhibits endometrial
prostaglandin (PG) production and release
•onset – 30-90 mins
•duration – prescribed at the onset of menstruation and
continued for 3 days
•adverse effects
– GI ulcers
– Hepatotoxicity
– Nephrotoxicity
– bronchospasm

70
 Combined Oral Contraceptives
• second line treatment
• it inhibits ovulation leading to thinning of the
endometrium
• causes decreased menstrual fluid volume and
decreased PG release, resulting in pain relief
• both the monophasic and triphasic are
equally effective
• other hormonal treatment include Depo
Provera
71
Levonrgestrel- Releasing Intrauterine
System

• releases levonorgestrel 20ug/day into the

uterine cavity
• results in thinning of the endometrium

72
 Vitamin Supplements
• vitamin B1
• Vitamin E 2500 IU taken for 5 days
• thiamine 100mg daily
• Mg supplements
• Glyceryl Trinitrate – a source of nitric oxide
that causes uterine relaxation
• transdermal nitroglycerine

73
 Surgical Intervention
• Reserved for those patients that don't respond to medical therapy
• LUNA (Laparoscopic Uterosacral Nerve Ablation) and
presacral neurectomy
• LUNA- complete transection of the uterosacral ligaments by CO2
laser or electrosurgical thermal energy
• Laparoscopic presacral neurectomy- disrupts the sensory pathway
from the uterus in the hypogastric nerve plexus. High risk of
complications and no guarantee to work
• Dilatation of the cervix
• For cervical stenosis in cases of congenital abnormalities.
• Not routinely done unless obstruction is proven
• Hysterectomy
• Not done in patients in their reproductive years
• Adenomyosis or endometriosis must be ruled out

74
 Summary of Approach to Primary
Dysmenorrhoea
• NSAIDs are the first line of treatment
• hormonal therapy may be used as a second line of therapy
• a monophasic low dose combined oral contraceptive is
recommended in young patients, and Depo Provera in the
older patient
• Alternatively, non pharmacological agents such as lifestyle
modifications may also be used. Vitamin supplements may
also be used

75
 SECONDARY DYSMENORRHOEA
• it is menstrual pain due to secondary
underlying pelvic pathology
• the onset is usually after 2 years of menarche
or after the age of 25 yrs without a previous
history of spasmodic dysmenorrhoea

76
 Causes
EXTRAUTERINE INTRAMURAL INTRAUTERINE
Endometriosis Adenomyosis Submucous fibroids
Tumours Leoimyomata Polpys
PID IUCD
Pelvic congestion Cervical stenosis
syndrome
Adhesions Infection
Psychogenic factors
Mullerian tract
anomalies

77
• pain occurs as a result of inflammation, ischaemia, distension
or haemorrhage caused by the underlying disease
• the above process causes irritation to the peritoneum and
pelvic congestion

78
 Clinical presentation
• pain may be constant and diffuse
• onset – precedes menses
• duration – throughout the menstrual cycle
• the pain may improve with time or get worse
• heavy menstrual flow with dysmenorrhoea may suggest adenomyosis,
myoma or polyp
• pain that increase in severity with menses with associated infertility and
history of dyspareunia maybe due to endometriosis
• if there is tenderness and excitation on pelvic examination with a fixed
retroverted uterus , pelvic infection must be considered.

79
 Investigations
• pelvic ultrasound
• cervical and urine cultures
• hysteroscopy or hysterography for uterine
abnormalities
• the gold standard is laparoscopy under
general anaesthesia especially if
endometriosis or pelvic infection are
suspected

80
 Management
• treatment is based on the underlying cause, which maybe medical or
surgical
endometriosis – perform a laparoscopic incision using laser or
electrosurgery. Laparoscopic Uterosacral Nerve Ablation maybe used in
stage 1-2 endometriosis
PID – medical management with NSAIDs and systemic antibiotics. Stage 3-4
surgery is required. For recurrent, unresponsive severe chronic PID, a
total abdominal hysterectomy and bilateral salpingo – oopherectomy
with adhesiolysis is indicated

81
 Management
pelvic congestion syndrome
• engorgement of the pelvic vasculature
• The associated pain is described as throbbing or burning,
its worse at night and after standing.
• Diagnosis is to perform a laparoscopy which shows
congestion of the uterus and the pelvic wall veins.
• It maybe attributed to psychomatic problems.
• Management requires a careful history, of the patients past
and present social situation and counselling.
• In severe cases, if the patient is non responsive to
counselling and medical management than a hysterectomy
may be performed

82
 Management
ovarian cyst – an ovarian cystectomy is performed by either
stripping or excisional surgery
leiomyomata and polyps –
– there may be an underlying PID.
– Management options include a
– laparoscopic myomectomy,
– hysteroscopic removal,
– transcervical endometrial resection,
– hysterectomy (especially in patients with severe
dysmenorrhoea unresponsive to NSAIDs)

83
Menopause & HRT

84
 Definitions: (WHO)
• Menopause:
• permanent cessation of menstruation
• Result of loss of ovarian follicular function
• Determined retrospectively after 12 consecutive months of amenorrhoea following the FMP
• without any other pathological or physiological cause
• Spontaneous or Induced

• Natural menopause :- permanent cessation of menstruation determined after 12 consecutive

months of amenorrhea without any other pathological/physiological cause.
• Induced menopause :- the cessation of menses due to removal of both ovaries with /without
removal of the uterus or iatrogenic ablation of ovarian fx.

• Premenopause:
• The entire reproductive period prior to FMP- this term is not really used because causes
confusion

• Perimenopause:
• period just prior to FMP til 1st year after the FMP
• Starts @ onset of endocrinological & menstrual changes
85
• Premature Menopause:
– Natural menopause <40 yrs old
– PrematureOvarianFailure
– All characteristics of menopause BUT may not be permanent
• Postmenopause:
– all the time in the woman’s life after FMP
• Early:1st 5 years ffg menopause
• Late: From 5 yrs after menopause until demise

86
• Menopausal Transition:
• Early & Late
• Transition begins with variation in menstrual cycle and ends
with FMP
• Incr. FSH but LH & oestradiol where the follicular phases are
longer there making cycle length longer
• Early:
• Variable menstrual cycle
• Differing by >7days from normal
• Late:
• 2/more skipped cycles
• Interval of amenorrhoea of at least 60 days
• Climacteric:
• phase during the ageing of the women that marks the transition
from reproductive phase to non-reproductive phase
• waning ovarian function
• May be ass. symptoms 87
• Early menopause
• NAMS define this as a natural or induced menopause
that occurs well before the average age of natural
menopause ie at or under 45
• Temporary Menopause:
– Normal ovarian function is interrupted and temporary
amenorrhoea results
– Examples:
• Following chemo / pelvic radiation
• Women who over-exercise / over diet = hypo-oestrogenic state
• Drug therapy – GnRH Analogues

88
 Physiology of Menopause

• Age of Menopause:Influenced by
– Familial factors
– Genetic polymorphism of the oestrogen receptor
– Not related to race, socio-economic status, education, ht,
wt, age @ menarche, prior ovulations, age @ last preg
– Ave. age:51 yrs, range: 40 – 58 yrs

89
• Results from loss of ovarian sensitivity to
gonadotropin stimulation – directly related to
follicular decline & dysfunction

• Oocytes in ovaries undergo atresia throughout a

womans life cycle – quantity & quality of follicles
decrease approx. 20-25 yrs after menarche

• Around 45 yrs only a few primordial follicles still

remain to be stimulated by FSH & LH

• Production of oestrogen by primordial follicles also

decreases as the number of primordial follicles
approaches zero

90
• When oestrogen production falls below a critical
level – oestrogens can no longer inhibit
production of FSH & LH sufficiently to cause
regular cycles(via feedback loop)

• Consequently – FSH & LH (mainly FSH) are

produced in large & continuous quantities

• Oestrogens continue to be produced in

subcritical quantities for a short time after
menopause but over a few yrs – as primordial
follicles become atretic – production of
oestrogens by ovaries falls almost to zero 91
 Ageing follicles =
resistant to gonadotroph

Physiology: stimulation

FSH & LH

Derived from ovarian stromal Stromal stimulaton of

& adrenal secretion of
ovary
androstenedione (androgen)
– aromatized to oestrone in
peripheral circulation Oestrone Inhibin
Oestradiol

Without a follicular source of Failure of

oestrogen- this is the main endometrial
source of oestrogen for development &
menopausal women absence of
uterine
bleeding
This form of oestrogen is
unapposed by progesterone
prodxn (corpus luteum) -
therefore women often Clinically
exposed to unopposed observed as
oestrogen for long periods – menopause
can lead to endometrial
hyperplasia
92
 Endocrinology
• Endocrine changes @ climacteric:
– Phase 1:
• Hypothalamic-pituitary hyperactivity
– Phase 2:
• Ovulation & corpus luteum failure
– Phase 3:
• Ovarian follicular failure

93
 Phase 1:
Hypothalamic-pituitary hyperactivity
• Starts 10-15 yr before menopause
• Compensatory for increased resistance of
ovarian follicles & decreased follicular
hormone secretion
• Evidenced by raised FSH & later LH (pituitary
may become exhausted late postmenopausal)

94
 Phase 2:
Ovulation & Corpus Luteum failure
• Occurs in most women with increasing
frequency as menopause approaches;
anovulatory cycles or shortened luteal phase
• Deficient dysfunctional uterine bleeding,
endometrial hyperplasia & adenocarcinoma

95
 Phase 3:
Ovarian Follicular failure
• Failure of follicular development causes fall in
oestradiol secretion & cessation of menses
• Ovarian stroma remains active; with adrenal cortex,
produces androstenedione & testosterone
• Oestrone, produced by extraglandular conversion of
androgens, is the main postmenopausal oestrogen
(only 10-15% of women are truly oestrogen
deficient)

96
 Symptoms / Complications of
Menopause:
• Due to oestrogen deficiency
• Acute / Intermediate / Long term

Vasomotor Neuro- Lower Uro- Connective Arterial Skeletal

endocrine genital Tract Tissue

ACUTE - - - - mnths - - - - Menstruation ceases - - - - - - - - mnths - - - - - - - - yrs - - - - CHRONIC

97
 1. Vasomotor:
• Hot flushes (50-85%)
• ? Decreasing oestrogen or rapid withdrawal of oestrogen
• Feeling of extreme heat that come on unexpectedly,
lasting 30 sec’s to 5 min’s
• More freq & severe in 1st 2-3 yrs of perimenopause
• Affects thermoregulation in brain
• Women who suffer hot flushes = smaller
thermoregulatory zone than women w/out hot flushes
• Flush – preceded by increase in digital perfusion – ffd by
increase in:
• Periph skin Temperature
• Circulating norephinephrine
• LH levels
• Heart rate
• Mx: oestrogen replacement / non-oestrogen Tx options
• Night sweats
• Insomnia
98
 2. Neuroendocrine:

– Mood changes
Controversy exists:
– Anxiety • Oestrogen relieves
these symptoms directly
– Irritability
• Oestrogen prevents
– Poor memory hot flushes & allows
women to sleep better
– Poor concentration = symptoms relieved
indirectly
– Loss of self-esteem

99
 3. Lower Urinary Tract:

– Genital tract atrophy Can produce senile

vaginitis / atrophic
– Dyspareunia vaginitis

Itching, burning,
– Urethral Syndrome discomfort, bleeding
• Urinary urge incontinence
• Urinary frequency, dysuria, nocturia
• Shortening & shrinking of distal urethra
– increased risk of UTI

100
 4. Connective tissue:

– Skin thinning
• Oestrogen deprivation decreases collagen content (main
protein which forms skin)
• Amount of collagen in skin diminishes rapidly – esp in 1st
5 yrs of menopause
• Skin = thin & wrinkly
– Tooth Loss
• More common in women who don’t take oestrogen
replacement
– Joint aches & pains
– Prolapse
• Pelvic organ prolapse – collagen loses its strength –
cystocele, rectocele, enterocele
– Incontinence
• With decreased synthesis of collagen in endopelvic
fascia – decreased support of urethrovescical jxn & with
increased abdominal pressure = urinary stress
incontinence 101
 5. Arterial:

– Cerebrovascular accident
– Coronary Heart disease
– Atherosclerosis
ØDecreased levels of oestrogen with menopause = high risk of
developing Cardiovascular disease:
•Oestrogen stimulates liver to produce increased HDL
Cholesterol
•Oestrogen relaxes blood vessels and causes vasodilatation
in peripheral & coronary arteries

102
 6. Skeletal:

• Osteoporosis
– compromised bone strength – increased risk of
fracture
– Dependant on:
– Bone quality
– Bone mineral density
– Post-menopausal bone loss – more in trabecular bone
(eg. Spine, distal radius) than cortical bone
– Process begins 2-3 yrs before menopause
– lower circulating oestradiol – loss of oestrogen
mediated inhibition of bone resorption w/out
compensatory increase in bone formation
– @ least 25% of bone needs to be lost before
osteoporosis is diagnosed by routine X-ray exam
– Bone mineral Density = measured by DEXA (Dual
Energy X-ray Absorptiometry)
– Only performed when high risk factors or cinical decisions will be
influenced by information gained
103
 7. Other:

– Ocular changes:
• Dry eye syndrome – dryness, pressure, foreign body
sensation, scratchiness, burning, light & cold
intolerance
– Body Mass:
• Many menopausal women gain wt – ageing &
lifestyle
• After menopause:
– Lean body mass decreases
– Abd fat increases
– Result: greater ratio of waist-to-hip circumference
– This shift of fat distribution = risk factor for CVS dx 104
 Management of Menopause:

• Counselling & Education

– Need to educate women about menopause and what to
expect
– lifestyle modification Stop smoking, decrease alcohol
intake, regular exercise, stress reduction, healthy diet, vit
& mineral supplements, weight Mx
• Provide Options
• Individualize Mx
• Hormone Replacement Therapy (HRT)

105
 Symptomatic Tx:
• Hot flushes
– Oestrogen:
• 0.625mg CEE/ oestrone sulphate or 1mg E2 orally or 0.o5mg E2 transderm
– tibolone
• GUT
– Oestrogen
– tibolone
• Osteoporosis:
– Oestrogen
• For women @ risk – optimal means of preventing postmenopausal bone loss
• If C/I – potent bisphosphonate (alendronate, risendronate, ibandronate) is useful
– Other alternatives:
• Vit D & Calcium supplements – slows done post-menopausal bone loss
• Calcitonin – admin in a nasal spray, an option
• Selective Oestrogen Receptor Modulator (SERM) – Raloxifen – dissociates bone remodelling,
stimulating the formation of new bone tissue & decreasing bone resorption
• Teriparatide (Recombinant Human PTH), anabolic, directly stimulates osteoblastic bone
formation
– Restricted to patients with severe osteoporosis @ high risk of fractures
• Tibolone
– Prevent OP

106
 Lifestyle:

• Diet:
• Avoiding spicy foods, alcohol & caffeine – gives relief of
hot flushes
• Low fat, high calcium diet – lowers risk of heart disease
& osteoporosis
• Exercise:
• Wt-bearing & strength training – retards bone loss
• Aerobic exercise – decreases risk of heart disease
• In general – helps relieve stress, improves self-image &
self esteem
107
Hormone Replacement Therapy (HRT)
• Hormone replacement therapy (HRT) is a system of
medical treatment for surgically menopausal,
perimenopausal and postmenopausal women, based
on the assumption that it may prevent discomfort and
health problems caused by diminished circulating
oestrogen and progesterone hormones.
• The treatment involves a series of drugs designed to
artificially boost hormone levels.
• The main types of hormones involved are oestrogens,
progesterone/ progestins
• Indications
• Relief of peri- & postmenopausal symptoms
• Tx of atrophic changes
• Prevention of OP
108
 HRT:

• Oestrogen therapy should be given in the

lowest effective dose that:
– Relieves vasomotor symptoms (hot flushes)
– Prevents vaginal & urethral epith. Atrophy
– Maintains collagen content of skin
– Reduces amount of bone absorption
– Benefits atherosclerosis
• Progesterone – mandatory in women with
intact uterus to prevent endometrial
hyperplasia
– May have adverse effect on vaginal & urethral
mucosa, may produce undesired CNS symptoms &
adversely affect mood & sense of well-being (PMS)
109
 HRT – Single vs. Combination:
• Single:
– Oestrogen replacement only

• Combination/continuos:
– Oestrogen replacement & Progestogen

110
 HRT – Regimens:
• Cyclic:
– Unopposed oestrogen regimen
– Recommended for women who have undergone
hysterectomy (no risk for endometrial cancer)

Day 1 Day 21 Day 25 Day 30

Oestrogen

Oestrogen

111
 HRT – Regimens:
• Sequential:
– Oestrogen & Progestogen
– Postmenopausal women who have a uterus Oestrogen
= given everyday of the mnth in a continuous fashion
– Progestogen daily for first 10 – 14 days/mnth

Day 1 Day 21 Day 25 Day 30

Oestrogen

Progestogen 5 mg of medroxyprogesterone acetate

112
 HRT – Regimens:
• Continuous/combined:
– Oestrogen & Progestogen
– Postmenopausal women who have a uterus
– Both Oestrogen & Progestogen administered every day of
the mnth

Day 1 Day 21 Day 25 Day 30

Oestrogen

Progestogen 2,5 mg of medroxyprogesterone acetate

113
 Examples of HRT:
• Oestrogen:
– Natural:
• Oestrone sulphate
• Conjugated equine oestrogen
• Micronised oestradiol
– Synthetic
• Diethyl stilboestrol
• Ethinyl oestradiol
• Progesterone:
– Dydrogesterone & Medrogestone
– Medroxyprogesterone
– Norethisterone

114
 Routes of Administration:
• Oral
• Percutaneous – gel
• Transdermal – patch
• Subcutaneous – implant
• Vaginal
• Nasal spray
• Injections
• Intrauterine device
Each route of administration has benefits & disadvantages

115
 Benefits of HRT:
• Systemic treatment of moderate to severe
menopause symptoms
• Improvement of uro-genital atrophy
• Prevention of osteoporosis
• Enhancement of quality of life

116
 Risks associated with HRT:
• Metabolic effects:
– Liver globulins
• Increase serum globulins
• increase in BP (Angiotensin)
• Hypercoaguable state
– Venous Thrombosis
• 3x more likely
• Risk greater 1st 12mnths of Rx
– Cholelithiasis
• Increase biliary cholesterol saturation – cholesterol
gallstone formation

117
 Risks associated with HRT:
• Neoplastic effects:
– Breast Cancer
• assoc. with increased risk of Breast Ca
• <5yrs – little effect on breast ca
• Risk increases with duration of use
• Risk may be decreased with Oestrogen therapy only –
controversial
• Risk declines after cessation of HRT (baseline after +/- 5 yrs)

– Endometrial Cancer
• Increased risk in women ingesting oestrogen w/out progestogen
• Risk persists for many yrs after Tx discontinued
• Risk can be decreased by using oestrogen & progestogen

118
 Contra-indications to HRT:
• Absolute: • Relative:
• Breast / endometrial Ca • Endometriosis
• Active thrombophlebitis • Fibroids
• Undiagnosed abnormal • Prev. Coronary heart disease
uterine bleeding • ? Otosclerosis
• Acute liver disease • ? Focal migraine
• Acute intermittent porphyria • ? SLE
• Active venous thrombo- • ? Malignant Melanoma
embolism • ? Seizure disorders
• Pregnancy
• Desmoid tumours
• Patient refusal

119
 Other options:
• Gonadomimetics
• SERMS
• Non-steroidal Selective Oestrogen Receptor Modulator
• Act as weak oestrogen agonist (bone)in some organs &
antagonists in others (breast & uterus)
• 1st gen. Tamoxifen
• 2nd gen. Raloxifene

• Androgens

120
 Conclusion:
• HRT is not needed by all menopausal women & it is
not the single-most important element of
menopause Mx

• Consider patients preference

• Sishi is da bomb

121
 Ectopic Pregnancy
Ectopic pregnancy occurs when the developing
blastocyst implants anywhere other than in the
endometrial lining of the uterus.
( *Implants in the Ampullary 70% of the time

122
 Risk Factors
• 1)Prev. Tubal Ligation
• 2)Prev. Ectopic
• 3)Prev. Induced Abortion
• 4) Prev. Miscarriage
• 5) Prev. PID
• 6) IUCD
• 7) Tubal Ligation performed
• 8)Prev. genital infection confirmed
• 9) Age >40 years
• 10)Current/Past Smoker
123
 Pathology & Pathophysiology
• Natural progression is one of the following:
1) Tubal Rupture
2) Tubal Abortion
3) Spontaneous resolution
4) Chronic Ectopic (>12 weeks)
• Factors leading to Ectopic
1)Tubal factors
2)Chromosomal
3)Exogenous Hormones= Progesterone ↓ SM
contractility
4)IUCD
124
 Clinical Presentation
• On History look for:
1) Pain
2) Bleeding- decidual shedding
3) Collapse?-Ruptured
• On Examination look for:
• Abdominal
1) Distended
2) Peritionitis
• Vaginal
1) Unfavourable Cervix (long and closed)
2) CET
3) Adnexal Mass
125
 Diagnosis
• Classic Triad of:
1) Amenorrhoea/ Recent irregular menstrual
period
2) Vaginal bleeding
3) Abdominal pain
(HCG and U/S if still uncertain)

126
 Investigations
• Bloods
1) FBC, U&E, cross match
2) Serum HCG
• Urine
1) Pregnancy test
• Imaging
1) TV U/S= Picks up @ 5-6 weeks (look for 1) Empty
Uterus 2)Free fluid in pouch 3) Donut sign)
2) TA U/S= Picks up at 7-8 weeks
*Progesterone levels? (<20mmol/l= failing preg vs
>60mmol=ongoing preg- both irrespective of
location)
127
 Management-Unruptured
• Expectant
1) ß-HCG ≤ 1000 IU/l
2) Declining ß-HCG within 48h
3) Patient is in close proximity to hospital
4) Repeat ß-HCG & TV U/S in 48h
• Medical
1) ß-HCG ≤ 3000 IU/l + small <3cm?
2) ß-HCG rising at 48h
3) Normal FBC and Liver enzymes (Methotrexate
C/I)
128
 Management-Unruptured Cont…
4)No Fetal cardiac activity on U/S
5) Methotrexate (folate antagonist) 1mg/kg IM
(Day 1, 3, 5, 7)- Continue until ß-HCG falls >15 %
/4 doses given.
• Surgical
1) ß-HCG >3000 IU/l
2) Fetal cardiac activity present
Salpingectomy (Opp. tube is fine) vs Salpingotomy
(Opp. Tube diseased) & Laparoscopy vs
Laparotomy.
129
 Management-Ruptured
• Surgical
1) Salpingectomy
• Resus Immediately
1) O₂ face mask
2) IV lines-infuse 2L rapidly @200ml/hr
3) FBC and clotting profile
4) Type & cross-match 2-4 units of bloos
5) Preg test?

130
 Management-Ruptured Cont…
• Treatment goals
1) Hb 7-10g/dl, platelets > 100 000/mm³
2) INR <1.5
3) Avoid Hypothermia, Hypocalcaemia,
Metabolic alkalosis & Hyperkalaemia
4) MAP 70-80mmHg
5) U/O ≥ 30ml/hr

131
 Miscarriages
Definition
A miscarriage is the ending of a pregnancy before the
fetus is viable

Viability:
South Africa: Before 28 weeks from LNMP or under 1 kg
Before 26 weeks from conception

WHO: before 22wks or under ½ kg

132
 Miscarriage
• Incidence
– Early pregnancy loss (EPL) = miscarriage before 13
weeks
– Most common complication of human
reproduction
– Affects about 50 –70% of all conceptions, with
majority before implantation & the missed period.
– EPL rate: 15 %
– Once fetal♥= risk 4 %
– After first trimester = risk only 1 %
133
Classification

134
First Trimester Spontaneous Miscarriage

135
Causes of Spontaneous Miscarriage
Early Late

Chance Occurrence Poor Placentation Inability 2 hold Preg Poor Placentation

1. Chromosomal 1. Uterine septum, 1. Congenital abn of 1. Inadequate

Abn (60%) etc uterus trophoblastic
invasion

2. Environmental 2. AI Dxs 2. Incompetent 2. Maternal PE

factors: toxins, viral cervix
infxs, smoking,
cocaine, alcohol,
caffeine.

3. HLA similarity 3. Submucous fibroid

136
 Aetiology cont
• Miscellaneous factors:
– TORCHS
– Chlamydia and mycoplasma infx
– Hypothyroidism
– Uncontrolled DM

137
 Recurrent Miscarriages
Definition
• Recurrent pregnancy loss is the miscarriage
of three or more consecutive pregnancies in
the first trimester.
• After 3 miscarriages, risk of 4 is 45%
th

• Can have recurrent early pregnancy loss

• And recurrent loss in early 2 trimester
nd

• Women who suffer from recurrent

pregnancy loss require referral for specialist
care.
138
Recurrent Miscarriages - Aetiology
Genetic Abn Structural Infx AP Ab Syndrome Thrombophylic
d/o
1. Balanced 1.Incompetent 1. Syphylis 1. Clinical criteria: 1. Factor V
reciprocal cervix - >= 3 consec Leiden Def
translocation unexpl MC
<10wks GA.
- >=1 unexpl
death of a
morphologically
norm fetus
>10wks GA
- >=1 PT delivery
of
norm<34weeks
2. 2. Uterine Abn 2. BV 2. Activated
Robertsonian septae/bicorn- Protein C/S def
translocation uate)
3. Prothrombin
139
G def
 Antiphospholipid Syndrome
• An important and treatable cause of recurrent miscarriage.
• Prevalence is about 15% in women who have recurrent miscarriage and the rate of
miscarriage is 90% in untreated women.
What is it ?
• AP antibodies are directed against phospholipid binding plasma proteins.
• Lupus anticoagulant and anticardiolipin antibodies are the important ones in
recurrent miscarriage.
• The presence of these antibodies and the ffg Clinical criteria are necessary to make
the diagnosis.

Clinical criteria
• 3 or more consecutive unexplained miscarriages before the 10thweek of gestation;
• One or more unexplained deaths of a morhologically normal fetus older than
10weeks gestation;
• One or more premature births of a morphologically normal fetus younger than 34
weeks with severe pre-eclampsia or placental insufficiency.

Treatment
• combo heparin + low dose aspirin = best outcome.
140
 Diagnosis of Miscarriage:

• Patient presents with:

1. PV bleed +/- clots
2. +/- LAP TRIAD
3. Following period of amenorrhea

• Use TVUS & Clinical features to diagnose

• In less obvious cases e.g. irregular menses or adnexal

masses, may need urine+serumB-HCG and U/S to
exclude ectopic pregnancy

141
Threatened Miscarriage

142
Inevitable Miscarriage

143
 Incomplete Miscarriage
• Hx
• Pain relief after some products passed (amniotic fluid/fetus/placental tissue)
• PV Bleed after amenorrhea

• Exam
• Pt either stable or bleeding profusely (pale & +/-shock)
• Abdominal palpation: uterus smaller than expected for gestational age
• Cervical os open
• Retained products may be visible/felt at the os
• TVUS shows endometrial thickness > 15 mm = confirms RPOC àEvac!

• Mx
• If RPOC are visible at osàremove with ovum forceps

• (this will allow the uterus to contract& ↓ bleeding & will ↓ pt’s pain)
• Surgical curettage for any gest age
144
• Evac by MVA if under 12 weeks
 Incomplete Miscarriage

Transvaginal ultrasonography, with some products of

conception in thecervix (to the left in the image) and
remnants of a gestational sac by thefundus (to the right in
the image), indicating an incomplete miscarriage
145
Complete Miscarriage

146
 Complete Miscarriage

Transvaginal ultrasonography after an episode of heavy bleeding in an

intrauterine pregnancy that had been confirmed by a previous
ultrasononography. There is some widening between the uterine walls, but no
sign of any gestational sac, thus in this case being diagnostic of a complete
miscarriage
147
Missed Miscarriage (Early fetal demise)

148
Summary types & management

149
 Subsequent Management
• Emotional support:
• Miscarriage is a traumatic experience.
• Stages of Grief:
• Shock
• Denial
• Anger
• Denial
• Acceptance
• Encourage the patient to talk about the event.
• During follow up consultation, ascertain how she and her partner have adjusted to
the circumstances.
• Refer patient to a psychologist if she is unable to cope.
• The next pregnancy- it is suggested that the couple should wait until both feel that
they have come to terms with the miscarriage.

• Subsequent pregnancy Management:

• Women who have had recurrent mid-trimester miscarriages run an increased risk
of the following.:
ü Pre-eclampsia.
ü IUGR .
ü Perinatal loss in subsequent pregnancies.
• Therefore, she should be followed up as a patient with high risk pregnancy. 150
 Septic Miscarriage
• Abortion that is complicated by fever >38°C
• Site of sepsis is located in the lower genital tract
or uterine cavity
• Critically ill
• Commonly d/t unsafe abortions
• Pt will usually deny interference
• Requires emergency medical attention =>
potentially life threatening
• Septic abortion carries a 15% mortality risk

151
152
 Definitive Mx: Septic abortion
• Indications for Hysterectomy (H)Septic shock
• Multiple organ dysfunction
• Necrotic appearance of cervix speculum exam
• Pus in abdomen detected via colpopuncture at evac
• Perforation of the uterus

• If there is no indication for H then pt req EVAC of the septic uterine

contents in theatre under GA

– Must have colpopuncture at the same time to exclude indication for H

– Consent must be taken for hysterectomy
– Systemic evaluation continued for 24 hours to ensure tx was effective
– IV Antiobiotics: 2nd gen cephalosporin (Augmentin 1,2g 8hrly IV)
– Gentamycin (no renal impairment) (240mg IV daily)

153
 Other complications of abortion
• Bleeding d/t:
– Uterine atony
– Trauma
– RPOC
– DIC
• Trauma
– Overzealous dilation of the cervix
• Infertility
– Over vigorous curettage of the uterus => Asherman’s
syndrome = Inner uterine surfaces can become attached to
one another => obliterate the uterine cavity
• Psychological
– Emotional crisis => grief counselling
154
Methods of Evacuation of the Uterus

155
Methods of Evacuation of the Uterus

156
 Methods of Evacuation of the Uterus

• Repeat bimanual palpation

• Suspicious products should be sent for histo
• Anti-D prophylaxis
• Post op Temp
– PR
– BP
– Counsel on contraception/STDs
– If well after 24 hours -FFD

157
Second Trimester Induced abortion
Unsafe abortion: self induced abortion
• Performed under unsterile conditions
• Substance may be used to induce abortion
• High risk of Maternal M&M

• TOP
• Any pregnant woman irrespective of age
• Only the consent of the preg woman is needed
• The patient must be counselled before the TOP about
alternatives to TOP, complications of the procedure and
future family planning
• Indications....

158
 Indications for TOP
<12 wks: Any reason

13-20wks: medical practitioner (MP) is in the opinion that

• Continued pregnancy poses a risk of injury to the mothers physical or
mental health
• Risk that fetus would suffer from a severe physical or mental abn
• Preg is a result of rape or incest
• Socio-economic reason

>20 wks: medical practitioner after consultation with another medical

practitioner or midwife is of the opinion that continued preg would
• Endanger the mothers life
• Result in severe malformation of the fetus
• Pose a risk of injury to the fetus
159
 TOP
WHO CAN PERFORM A TOP?
• <13 wks TOP can be performed by Midwife or MP
• >13 wks TOP can only be performed by a MP
• Involvement of MP in TOP is voluntary
• If a woman requests TOP, MP is bound by law to
advise the woman how to gain access to an
institution where TOP is performed

WHERE ARE TOPs PERFORMED?

• Can only be performed at designated institutions
and must be reported to the DOH 160
Methods of TOP

161
 Medical management
• Exclusion criteria
• Unable to attend outpatient visits
• Haemodynamically unstable
• Anaemia
• History of clotting disorder or use of
anticoagulants
• allergy to PG or NSAID
• Severe asthma
• Mitral stenosis
• Severe infection
• Suspicion of ectopic pregnancy 162
Differential Diagnosis for Miscarriage

163
 Infertility

1.Infertility: The inability to achieve a pregnancy after one year

of adequate sexual exposure (regular intercourse (at least 3-4
times/week) without the use of contraception).
2.Reproductive Failure: Repeated failure to carry a pregnancy to
viability.
3.Primary Infertility: Implies that the woman has never been
able to conceive.
4.Secondary Infertility: Indicates that at least one previous
conception has occurred.
5.Sterility: Presence of a condition/absolute factor preventing
conception. Implies irreversibility of the condition.

164
 Causes
Female Infertility
1. Anovulation
– Obesity, maternal age >35, Hyperprolactinaemia, hypothyroidism, polycystic
ovarian syndrome, injectable contraception, stress, adrenal gland disorders,
2. Anatomical Factors:
– Vaginal Factors
• Anatomical defects (e.g. high vaginal septum), infections, lubricants,
psychosomatic manifestations, Changes in vaginal pH can reduce sperm
motility, vaginismus, vaginal obstruction.
– Cervical Factors
• Problems with cervical mucus
blocking sperm entry, Sperm
agglutinisation (allergic reaction,
antisperm antibodies),
anatomical defects (cervical stenosis),
infections
– Uterine Factors
• Anatomical defects (e.g. Mullerian
Agenesis), infections, surgery
e.g. curettage (Asherman’s
syndrome), uterine fibroids. 165
 – Tubal Factors
• Anatomical defects e.g. Fibroids (obstruct fallopian tubes or interfere with
implantation, placental formation), Infections e.g pelvic inflammatory disease,
Endometriosis, tubal occlusion, tubal dysfunction (e.g. decreased cilia motility),
previous ectopic pregnancy.
• Surgery: adhesions(previous surgery), previous tubal ligation.
– Ovaries
• Functional disorders, infection, surgery, endometriosis, Polycystic ovary syndrome,
ovarian cancer, gonadal dysgenesis, luteal dysfunction, premature menopause,
chemotherapy, diminished ovarian reserve, menopause
– Pelvic Peritoneum
• Adhesions, endometriosis, infection (e.g. appendicitis), ulcerative colitis
2. Systemic factors
Hypothalamic dysfunction, pituitary
Gland dysfunction, thyroid gland,
adrenal glands, cardiovascular system,
liver, kidney
3. Immunological factors
– Antisperm antibodies, allergy to semen
4. Pharmacological Factors
– Opioids, antiprostaglandins,
– chemotherapy, antidepressants,
– Injectable contraceptives 166
5. Environmental Factors
– Smoking
– Drugs: Antidepressants, clomiphene citrate, drugs causing
hyperprolactinaemia, chemotherapy
– Recreational Drugs: cocaine, marijuana. etc
– Previous Surgery: intra-abdominal or pelvic
6. Genetic Factors
– Turner syndrome :There is a loss or abnormality of the second X
chromosome. The ovaries are usually just streaks. This condition
may be a mosaic.
– Klinefelter's syndrome (46XXY) appears as a male.
– The XXX karyotype: fertility in women with trisomy X is generally
considered normal, however there is an increased risk for
premature ovarian failure.

167
 Causes
Male Infertility

1. Pretesticular/Pregerminal causes
o Central Gonadotropin deficiency
ü Hypothalamic: tumour, congenital GnRH deficiency, infection, head trauma
ü Pituitary: congenital FSH/LH deficiency, tumour, infection, infarction, trauma
ü Other: Sarcoidosis, haemochromatosis
o Endocine excess syndromes
ü Oestrogen: functional tumour of adrenal gland, cirrhosis
ü Androgen: congenital adrenal hyperplasia, androgen producing tumour
ü Glucocorticoid: Cushing’s syndrome, Steroid treatment (Ulcerative Colitis,
asthma)
o Other
ü Hypothyroidism
ü Diabetes Mellitus

168
2. Testicular Causes
o Chromosomal Abnormalities: Klinefelter’s Syndrome (47,XXY)
o Cryporchidism (unilateral or bilateral)
o Radiation and chemotherapy
o Trauma
o Sertoli-cell-only Syndrome
o Mumps,Viral orchitis
o Idiopathic maturation arrest
o Androgen receptor abnormality – Androgen insensitivity syndrome
3. Post Testicular Causes
o Congenital ductal obstruction
ü Vas deferens, epididymis
o Acquired ductal block
ü Infection: Gonorrhoea, Tuberculosis
ü Vas Ligation
o Impaired motility
ü Enzyme deficiencies
ü Immotile cilia syndrome
ü Kartagener’s syndrome
ü Protein carboxymethylase
4. Genitourinary Infections
5. Immunological Causes
169
 Risk Factors
Female
• Age: > 35
• Weight (Overweight, Obese, Underweight) – abnormalities of
hypothalamic GnRH and pituitary gonadotropin secretion.
• Smoking
• Substance abuse: marijuana (affects ovulatory function); cocaine
(increases risk of tubal disease)
• Alcohol abuse
• Poor diet
• stress
• Sexually transmitted infections
• Perchlorethylene exposure in dry cleaning industry, toluene in
printing industry and ethylene oxide exposure.
• Environmental exposure to herbicides and fungicides

170
 Male Risk Factors
• Alcohol Abuse
• Cigarette Smoking
• Marijuana use (inhibits secretion of GnRH and suppresses
reproductive function.
• Overweight
• Past or present Sexually Transmitted Disease
• Radiation exposure
• Toxin exposure e.g. pesticides, mixed solvents
• Heat exposure, e.g. overheating in long distance drivers.
• Previous vasectomy or orchidectomy
• Trauma or previous major abdominal or pelvic surgery
• Congenital disorders, e.g. undescended testes, hydrocoele
171
 Evaluation
– Involves the taking of a careful history, including the identification of risk factors,
followed by a physical examination, baseline investigations and counselling if the
couple.
– Infertility relates to a couple and not to a single person, both partners should be
involved in the investigation and management.

History
1. Infertility Related History:
– Age of each partner
– Determine whether Primary or secondary infertility
– Previous marital and reproductive history (including live births, abortions, ectopic
pregnancies and puerperal infections)
– Menstrual history: age at menarche, regularity, length of cycle, dysmenorrhoea.
(ovulation indicated by normal and regular menstrual cycle)
– Previous contraception and complications
– Previous pelvic infections
– Breasts: thelarche, development, galactorrhoea and premenstrual tenderness
– Skin abnormalities: acne, abnormal hair growth
– Mass: sudden increase or decrease

172
 Evaluation
2. History from the couple
General History:
• History of abdominal surgery and other diseases or infections
• Occupational History

Sexual history:
• Perception of the fertile period and whether adequate intercourse is taking
place during that time.
• Frequency of intercourse and sexual problems e.g. Dyspareunia; lack of libido;
ejaculatory/erectile dysfunction.

Psychosocial:
• Impact of involuntary childlessness on psychological and social wellbeing.
Depression, loss of self esteem, anger, loneliness, marital conflict.
• High incidence of verbal and physical abuse, abandonment, stigmatisation,
ostracism and lack of social security
• Couples should be asked what they believe to be the cause of their
childlessness*

Previous infertility investigations or management:

• To prevent unnecessary investigations 173
 Evaluation:
3. History from the female:
Gynaecological history:
• Irregular menstrual cycles (anovulation)
• Galactorrhoea (anovulation)
• Excessive menstrual blood loss (uterine fibroids or polyps)
• Severe dysmenorrhea (endometriosis)
• Previous pelvic infections or symptoms (tubal damage)

Obstetric history :
• Number of previous pregnancies, outcomes and whether or not conception
occurred spontaneously or after infertility treatment
• Women with recurrent miscarriage

Medical/surgical history :
• Pre-existing medical conditions e.g. Diabetes Mellitus, cardiac disease, epilepsy,
need be optimised. Any regular medication should be compatible with
pregnancy

Social history :
• Alcohol and smoking history needs to be noted
• Socioeconomic factors 174
 Evaluation
4. History from the male:
Previous fertilisations:
• Should be recorded in current and previous relationships

Medical and surgical history:

• Thyrotoxicosis, Diabetes Mellitus (erectile dysfunction), cystic fibrosis
• Drug therapy: Antineoplastic and psychoactive drugs may affect sperm
production and function

Genital pathology:
• Orchitis, surgery, trauma, torsion

Social history:
• Alcohol, tobacco, drug use

Occupational history:
• Exposure to heat or environmental toxins (insecticides, other chemicals)
175
 Physical Examination
A Comprehensive Physical Exam should include:
1. Examination of the Female
ü Assessment of stature, body length and mass, BMI.
ü Assessment of secondary sexual characteristics and hair distribution.
ü Assessment of breast development and exclusion of galactorrhoea.
ü Abdominal Examination: Note surgical scars, tenderness and any intra-
abdominal masses.
ü Complete gynaecological examination.
ü Rectovaginal examination to exclude possible endometriosis.

2. Examination of the Male

ü Normal secondary sexual characteristics
ü Abdominal and inguinal pathology
ü Urogenital examination: presence and size of testis, epididymis, vas
deferens
ü Scrotal swellings or varicocoeles, penile pathology
176
 Investigations
• Aims to classify patients into one of two categories, ovulatory or
anovulatory.
• Investigations are directed in order to identify the cause of the infertility
and assist with the management.

1. Mandatory investigations:
i. Pap smear
ii. Syphilis serology
iii. HIV status and whether on treatment.

2. Mid Luteal Phase Serum Progesterone:

– To assess whether there is ovulation.
– Usually recorded on day 21 if cycle is 28 days (female records menstrual cycle
to validate day 21 progesterone result).
– Progesterone on day 21 > 30nmol/l indicates ovulation
3. Serum Prolactin: Exclude hyperprolactinaemia (if present investigate and
treat).
4. Serum TSH: Exclude hypothyroidism.
177
 Imaging (Tubal Patency)
1. Hysterosalpingogram
– Primary investigation used to exclude provide
information about the:
ü endocervical canal;
ü diameter and configuration of the internal os;
ü endometrial cavity;
ü uterine/tubal junction (cornual ostium); diameter,
location, and direction of the fallopian tubes;
ü status of the fimbriae and spill into the endometrial
cavity.
– Also provides indirect evidence of pelvic adhesions
and uterine, ovarian, or adnexal masses.
– Non-invasive procedure, can be done as
outpatient.
– Disadvantages – causes pain during the procedure,
and provides no information concerning the
presence of peritoneal disease such as
endometriosis and adnexal adhesions, and the
motility of Fallopian tube and fimbrial ends cannot
be evaluated.
– Exclude cervicitis before doing HSG to prevent
introduction of infection in upper genital tract.
178
2. Laparoscopic Chromopertubation (Lap & dye)
– Gold standard in tubal evaluation
– Evaluate for pelvic disease, e.g. endometriosis and check the patency
of the tubes.
– Involves the inspection of the inside of the abdomen and pelvis
including the outside of the womb, the tubes and ovaries using a
laparoscope inserted into the abdomen
– A coloured dye, methylene blue is injected through the cervix. If the
tubes are patent the dye should pass along them and spill into the
abdomen.
– Allows management of the problem if an abnormality is found during
laparoscopy for example opening of blocked tubes, cutting of
adhesions to free the tubes

179
 Male Factor
Semen Analysis
1. Volume(ml): 1.5ml – 6ml
2. Concentration(million/ml): >15 million/ml
3. Motility(% motile): >40%
4. Forward progression or motility grade, where the motility of sperm
are divided into four different grades:
– Grade a: Sperm with progressive motility. These are the strongest and
swim fast in a straight line.
– Grade b: (non-linear motility): These also move forward but tend to
travel in a curved or crooked motion.
– Grade c: These have non-progressive motility because they do not
move forward despite the fact that they move their tails.
– Grade d: These are immotile and fail to move at all.
5. Morphology(% normal): >15%
6. pH: 7.4 – 8.2

180
Classification of Male Fertility Potential
Semen parameter Infertile Subfertile Fertile

Concentration <2.0 <15 >15

(million/ml)
Motility (% motile) <10 <30 >30

Forward <1.0 1.0 - 1.9 >2

progression (0-4)
Motility index <20.0 20.0 – 49.9 >50

Morphology (% <5 <5 >5

normal)
Volume (ml) <1.0 <1.5 >1.5

181
 Semen Analysis
1. Normospermia: Normal semen parameters, ejaculate likely to be fertile (>5%
normal morphology).
2. Oligozoospermia: Sperm count less than 10 million/ml.
3. Asthenozoospermia: Less than 30% motile spermatozoa with forward
progression <2.
4. Teratozoospermia: <5% spermtozoa with normal morphology.
5. Oligoastheno-teratozoospermia: Disturbance of all 3 variables (amount,
motility, morphology).
6. Azoospermia: No spermatozoa in ejaculate.
7. Globozoospermia: Sperm with a round head and no visible acrosome.
8. Aspermia: No ejaculate.

182
 Obtaining Semen Sample
1. Counselling of the patient and the partner is essential
2. The patient should abstain from sexual intercourse for >3 days but
not more than 5 days
3. The patient should abstain from smoking and alcohol use for at
least 1 week prior to specimen collection.
4. The patient should be accompanied by the partner to the clinic
5. The partner should help stimulate the patient
6. The patient should ejaculate in a specimen bottle
7. The sample should reach the lab within 1 hour.

A second sample can be taken if there is an abnormality with the first

analysis.

183
 Other Investigations
Assessment of ovulation
1. Mid-Cycle Cervical Mucus
During the peri-ovulatory period, cervical mucous secretion should be examined
on a daily basis. Adequate mucous has the following characteristics:
ü There should be a sufficient amount (speculum examination)
ü Spinnbarkeit (ability of the mucous to stretch) should be 8 – 10 cm or more.
ü The macroscopic appearance should be watery, thin, clear and transparent.
ü Ferning pattern when dried on a slide.

184
2. Basal body temperature
– There is an increase in basal body temperature at Day 14 (immediately after
ovulation) by 0.5 – 1° C.
– Basal body temperature charts can be used to predict ovulation.
– A basal body thermometer measures the slight rise in temperature.

3. FSH and LH
• FSH levels only done if there is secondary amenorrhoea or if progesterone
levels are low in luteal phase.
• If >30 IU on two occasions, indicates ovarian insufficiency.
185
4. Urine LH
– LH kits are used to detect mid-cycle LH surge in urine.
– Ovulation predictor kits turn positive when the urinary LH concentration exceeds threshold level
normally only seen during the LH surge.
– The surge usually lasts for up to 48 hours.

Tests for the male

1. Mixed Agglutination Reaction Test
– Screening method for sperm antibodies which may impair male reproduction.
– Detection of IgG antibodies in the semen sample.
– Routinely used to demonstrate membrane-bound antibodies on sperm.
– Abnormal if the values are >50%.
2. Immunobead Test
– Performed if the MAR test is positive.
– Demonstrates the presence antibodies and indicates the region of binding on the surface of the
sperm and determines the class and subclass of immunoglobulin involved.
3. Sperm Penetration Assay
– Test for assessing the sperm penetration ability using hamster oocytes.
– Fertile if penetration rate is more than 10%, infertile if <10%.
4. Hemizona Assay
– Assessment of tight binding of spermatozoa to human zona pellucida.
– Oocytes cut into halves (hemizona), one hemizona is used to assess the patient’s spermatozoa
binding ability and the other is used for comparison to a proven fertile male.
– Promising ability to predict the chances of fertilisation in vitro.

186
 Management of the Female
1. Ovulation disorders
– Medical induction of ovulation is the treatment of choice.
Ø Clomiphene 25mg/day for 5 days (day 5 – 9 of menstrual cycle)
Ø Ovulation usually occurs between the 5th and 8th day after the last tablet.
Ø During the periovulatory period (days 13 – 16) follow up daily on the amount and quality
of cervical mucous and if adequate repeat clomiphene for 3 menstrual cycles.
Ø If the mucous is inadequate or no pregnancy results, refer for specialist treatment.
Ø Clomiphene citrate may lead to multiple pregnancies or have a contraceptive effect
(antioestrogenic action of clomiphene causing thickening of cervical mucous and
reduction of sperm penetration).

– Obese patients are advised to lose weight, it may be the cause of anovulation and resistance
to clomiphene.
– Patients with Polycystic Ovarian Syndrome must be treated cautiously, they may be sensitive
to clomiphene and may react with hyperstimulation.
– Other agents include Human menopausal gonadotropin (HMG), HMG injection acts directly on
the ovaries to stimulate ovulation and is used for women who don't ovulate due to problems
with their pituitary gland.
– Follicle-stimulating hormone (FSH) causes the ovaries to begin the process of ovulation.
– Human Gonadotropin-releasing hormone (GnRH) and GnRH analogues are also used for
women who don't ovulate regularly each month. 187
2. Surgery
– Surgery for tubal disease is the most successful if the disease is
localised to the distal portion of the tube.
– Fimbrioplasty: lysis of fimbrial adhesions or dilation of fimbrial
structures.
– Neosalpingostomy: creation of a new tubal opening in a fallopian tube
with a distal occlusion.
– Microsurgical re-anastomosis of fallopian tubes after surgical
sterilisation is one of the most successful surgical procedures for
infertility.
– Clinical characteristics for high success rate for surgical re-anastamosis:
ü Female partner <40 years old
ü Tubal length > 4cm
ü Falope ring, Filshie clip or Pomeroy tubal ligation
ü Absence of associated pelvic disease

188
 Specialist Treatments
1. Artificial insemination
– Artificial insemination with the husband’s washed spermatozoa is mainly
indicated in patients with a cervical factor e.g. thick mucous.

2. In vitro fertilisation (IVF)

– Patients are hyperstimulated with various ovulation induction agents.
– Indictions:
ü Absent or irreparably damaged Fallopian tubes (main indication)
ü Idiopathic infertility
ü Endometriosis causing infertility
ü Male factor
ü Female antisperm antibodies

3. Gemete Intrafallopian Transfer (GIFT)

– Can only be performed if at least one fallopian tube is patent
– 2 – 3 oocytes with washed spermatozoa are transferred into the fallopian tube
immediately after oocyte retrieval.
– Indications:
ü Idiopatic infertility
ü Infertility associated with endometriosis
ü Male factor infertility
ü Adhesions to the Fallopian Tubes 189
4. Pronuclear Stage Transfer (PROST) and Zygote Intrafallopian Transfer (ZIFT)
– Combination of features of IVF (transvaginal oocyte retrieval, fertilisation in vitro)
and GIFT (transfer of gametes to fallopian tubes).
– ZIFT has the advantage of providing direct observation of the success of the
fertilisation process in vitro (not possible with GIFT)

5. Cryopreserved Embryos
– Embryos can be frozen and stored for future use if fertilisation and cleavage up to
8 cell stage occurs.
– Thawed embryos can be placed into the uterine cavity or laparoscopically into the
fallopian tubes.

6. Gamete Donation
– Oocyte donation is an option in cases of ovarian failure.
– IVF or GIFT procedure is used.

190
 Management of the male
1. Azoospermia
– Always exclude retrograde ejaculation: Ask the patient to pass urine after the
semen sample is obtained to ensure there is no spermatozoa in the bladder
due to retrograde ejaculation.
– Intracytoplasmic sperm injection following testicular biopsy is the treatment of
choice.
– Intrauterine insemination is offered in cases with retrograde ejaculation.
– Donor sperm may also be a consideration.

2. Asthenozoospermia
– Repeat semen analysis, if confirmed by at least 3 samples, refer for further
treatment.
– Sperm manipulation procedures can be used.
– Treatment methods include Intrauterine insemination, gamete intrafallopian
transfer (GIFT), in vitro fertilisation (IVF), and in severe cases using sperm
microinjection techniques (ICSI).

3. Teratozoospermia
– If infertility is present >2 years IVF or GIFT can be offered.
– IUI is also attempted, if not successful after 3 – 4 attempts ICSI is attempted.
191
4. Antisperm Antibodies
– Artificial insemination can be attempted if antisperm antibodies are present.
– ICSI is the treatment of choice.
– Sperm manipulation procedures are used to improve the sample and motility.

5. Micromanipulation (ICSI)
– Involves the injecting of selected spermatozoa into the oocyte.
– Indications:
ü Oligozoospermia
ü Severe asthenozoospermia
ü Severe teratozoospermia
ü Azoospermia (spermatozoa can be obtained and injected after testicular biopsy)
ü Micromanipulation may be applied in conjunction with IVF to try to achieve a
pregnancy.

4. Gamete Donation
– Artificial insemination with donor sperm is
considered in cases with azoospermia,
oligo-, terato-, and/or asthenozoospermia.

192
 HIV Discordant Couples
• Female Positive and Male Negative:
üArtificial Insemination

• Male Positive and Female Negative:

üArtificial Insemination with washed spermatozoa
from the male

193
CONTRACEPTION GUIDELINES

194
 COCs
• Low dose COCs
• Low-dose COCs contain 35 μg or less of the synthetic
oestrogen ethinyl estradiol and one of a range of
synthetic progestogens (for example levonorgestrel).
• They are very effective in preventing pregnancy when
taken regularly every day, and are safe for most clients.
• Many conditions that restrict the use of high-dose COCs
do not apply to the low-dose formulations, but screening
and careful instructions are required to ensure correct
and consistent use.

195
Characteristics of low dose COCs

196
 Procedures required for the initiation
of COCs
• Screening for medical eligibility

• The vast majority of women can use COCs safely. Most of the conditions
that may preclude women from the safe use of COCs are not very common
in women of reproductive age and usually can be ruled out by taking
appropriate medical history.
• Thorough medical history taking is essential before the initiation of COCs.
• Whenever possible, blood pressure should be measured before initiating
COCs; but a woman should not be denied COCs if her blood pressure
cannot be measured, provided she has never been diagnosed with high
blood pressure. Where possible, blood pressure should be measured
within three months of commencing the method

197
 Timing of initiation
• COCs may be initiated at any time, as long as it is reasonably
certain that the client is not pregnant.
• If pregnancy cannot be ruled out, the client should be
advised to avoid sex or use condoms until her next period
starts, and start taking COCs on day 1 of her period.
• If her next period is late, she should come back for a
pregnancy test.

198
199
 Method-specific counselling
• Appropriate method-specific counselling is essential.
• Provide the necessary information on key characteristics of
the method, answer the client’s questions, address fears and
concerns respectfully, and instruct the client on correct
method use.
• Explain routine pill taking
• Discuss what to do if pills are missed
• Discuss STI and HIV

200
 Follow-up
• Schedule
Routine follow-up visits:
• first follow-up visit should be scheduled before the end of the
third packet of COCs;
• at the first follow-up visit and at subsequent visits, 6–12-
month supplies of COCs can be
• provided to clients in WHO MEC Category 1 and 2. (Category 3
clients should only receive
• COCs if prescribed by a doctor and they require careful
medical follow-up.)

201
• Content
• Counselling should cover client’s questions, experiences
with the method, satisfaction, side effects and health
concerns.
• Where possible, blood pressure and weight should be
measured and recorded at every visit.
• Management of side effects if needed.
• Invite the client to return again at any time if she has
difficulties and ensure easy appointment system.
• Discuss STI and HIV risk, the need for dual protection and
HCT.
• If the client is HIV-positive, monitor her CD4 count, assess
her eligibility for ART and initiate or refer as appropriate
202
 Combined hormonal methods not yet available
in the public sector in South Africa
• Combined hormonal transdermal contraceptive patches
(Evra®)
• Combined hormonal vaginal ring
• Combined injectables

203
Drug interactions and combined
hormonal contraceptives

204
205
 Progesterone-Only Contraceptives
• Progesterone-Only pills (POP’s)
• oestrogen-free oral contraceptives containing very low doses of synthetic
progestogen.
• taken approximately at the same time every day.
• No inactive pills in the POP pack and no break required between packs.
• appropriate for : breastfeeding women
use as an alternative for women who experience
oestrogen-related side effects with COCs
have health conditions that may preclude safe use
of COCs.
• In common use, POP effectiveness is slightly less than that of COCs in non-
breastfeeding women but, when compliance is good, POPs are very
effective.

206
 Key Characteristics of POP’s
Effectiveness In non-breastfeeding women: 90–92% as commonly used; when used
consistently and correctly, POPs are more than 99% effective. In
breastfeeding women: ≥99% effective
Age limitations No restrictions on use for women from menarche to menopause
Parity No restrictions
limitations
Mode of action Primarily thickens cervical mucus and so prevents sperm penetration (after
2 days of use). Also inhibits ovulation in 60% of cycles
Common side Changes in menstrual bleeding (irregular bleeding, spotting or
effects amenorrhoea), mild headaches, nausea, dizziness, mood changes and
breast tenderness
Effect on STI Not protective
and HIV risk
Duration of Can be used throughout the reproductive years
use
Return to Fertility returns without a delay
fertility

207
 Initiation
• POPs have fewer contraindications than COCs.

• Most of the conditions that may preclude safe use of POPs are not
common in women of reproductive age and usually can be ruled out by
taking appropriate medical history.

• Timing : Initiated anytime provided it is certain patient not pregnant

If pregancy is suspected the patient should wait for her
next menstrual period and begin pill from day 1 of the cycle.
• Patient is counselled and a follow up is arranged.

208
 Progestogen-only injectables
• Highly effective method of reversible contraception suitable for most
women.
• Contain synthetic progestogens administered by deep intramuscular
injection.
• Two available and widely used in S A :
1. Depot medroxyprogesterone acetate (DMPA)
2. Norethisterone enanthate (NET-EN).
• Highly effective, easy to comply with, require only periodic clinic visits, are
private and no supplies need to be kept at home.

209
 Key characteristics of progestogen-only injectables
Effectiveness As commonly used, injectables are 94% effective. If used correctly (for example woman
comes for reinjection on time), the effectiveness is as high as 99.7%
Age limitations Overall no restrictions, but some caution may be warranted in adolescents younger than
18 years and women older than 45 years due to concerns about reduced bone mineral
density.
Parity limitations No restrictions

Mode of action Primarily inhibits ovulation but also thickens cervical mucus and thereby prevents sperm penetration

Common side effects Changes in menstrual bleeding (irregular, prolonged or/and heavy bleeding,
amenorrhoea) and weight gain, are important issues to cover during counselling. Other
possible side effects include headaches, dizziness, mood changes and decrease in sex
drive
Effect on STI and HIV risk Not protective.

Duration of use Can be used throughout a woman’s reproductive years but perimenopausal women may
not have enough time until menopause to regain bone density. Switching to another
method after reaching 45 years may be considered
Return to fertility Average delay of about 4–6 months depending on type of injectable. No permanent
damage to fertility has been associated with injectables. Cover this issue when counselling

210
 Initiation
• Injectables can be used safely, provided condoms are used correctly and
consistently to prevent HIV and STIs. Most of the conditions which may preclude
safe use of injectables are not common in women of reproductive age and usually
can be ruled out by taking appropriate medical history.

Timing of initiation
• If the first injection is given within the first seven days of the menstrual cycle,
protection is immediate and no backup contraception is needed.
• The first injection can also be given at any other time during the menstrual cycle if
it is reasonably certain that the client is not pregnant .If injectables are started
after day 7, the client should avoid sex or use condoms for the next seven days
after the injection.
• Counselling
• Follow up - every 12 weeks forDepot medroxyprogesterone acetate (DMPA)
and every 8 weeks for Norethisterone enanthate (NET-EN).

211
 Administering the injection

Injection procedure
• Administer by deep intramuscular injection into the buttock or upper arm
depending on client’s preference.
• The degree of obesity may make it difficult to inject the drug into the
muscle of the buttocks and the arm would be the preferred site of
injection in such cases.
• Aseptic injection technique should be followed (the use of a sterile needle
and syringe for each injection and their safe disposal).

212
 Subdermal Implants
• Long-acting progestogen subdermal implants
• Systems consisting of single rods containing etonorgestrel (Implanon
NXT®) – effect lasts for 3 years
• Other types
Two rods containing levonorgestrel (Jadelle® and Sino-plant®) effective for 5
and 4 years respectively.
An older, six-rod system Norplant®, effective for 5 years, but is no longer on
the market.

213
 Single-rod implant (Implanon NXT)

• Consists of a small plastic rod, about the size of a matchstick, which placed
just under the skin of the upper arm that releases small amounts of
progestogen into the body.
• Contains no oestrogen
• Implants have been shown to be the most effective form of contraception,
with extremely low failure rates and high continuation rates.
• They have been shown to be the most effective form of contraception,
with extremely low failure rates and high continuation rates. Despite high
initial costs they have proved to be cost effective compared with pills and
injections at one year.
• A trained health care provider (doctor or nurse) is required to insert and
remove implants.

214
 Key characteristics of progesterone-only implants
Effectiveness Implants are almost 100% effective. (With Implanon, one pregnancy occurs
in 1000 women over a 3-year period)

Age limitations No restrictions from menarche to menopause

Parity limitations No restrictions

Mode of action Primarily inhibits ovulation and thickens cervical mucus and thereby prevents
sperm penetration

Common side effects Changes in menstrual bleeding are common, including lighter bleeding,
irregular bleeding, infrequent bleeding and amenorrhoea. Other side effects
include headaches, nausea, dizziness, breast tenderness, mood changes and
abdominal
pain due to enlarged ovarian follicles

Non-contraceptive Prevention of symptomatic PID and iron-deficiency anemia

benefits
Effect on STI and HIV Not protective
risk
Duration of use Can be used throughout the reproductive years

Return to fertility No delay

215
INTRAUTERINE CONTRACEPTION

216
 COPPER INTRAUTERINE DEVICE
Definition:
Small, flexible contraceptive device made of
plastic and copper that prevent pregnancy when
fitted into the uterus.

217
• 99,2-99,4% effective in the first year of use
• No age and parity limitations
• No drug interactions
• Not protective against HIV and STIs
• The device only needs to be replaced every 10
years (Cu T380)
• Women return to fertility immediately upon
removal

218
 Mode of action
• Primarily prevents fertilisation by inhibiting
sperm migration into the upper female genital
tract
• Secondary action prevents implantation
through endometrial changes

219
Procedure for initiation of Copper IUDs

• Counsel patient on all available methods of

contraception
• History- medical, obstetric, menstrual,
gynaecological, contraceptive and sexual
• Abdominal Examination
• Pelvic Examination

220
 Timing of insertion
• Can be inserted within the first 12 days of the
menstrual cycle.
• Can also be inserted at any other time of the cycle as
long as pregnancy is excluded
• Following uncomplicated first or second trimester
miscarriage, it may be inserted immediately or within
the first 12 days after miscarriage
• Following normal vaginal delivery after full term, it can
be inserted 4-6weeks postpartum
• Can be inserted at the time of Caesarean section or 6
weeks after by experienced staff only
• If a cervical discharge or a pelvic inflammatory disease
is suspected, treat the patient and her partner before
insertion of the device. Provide with another method
during that time.
221
 Follow-up
• 3-6 weeks after insertion
• Return at any time if there are problems
related to the copper IUCD, wishes to
discontinue because of the side effects or to
plan a pregnancy
• When the device needs to be replaced
• Annual check-ups are not required

222
 Complications
• Irregular or heavy vaginal bleeding
• Cramping and pain
• Missing strings
• Vaginal discharge and lower abdominal pain

223
 Levonorgestrel Releasing Intrauterine
System
Definition:
The system releases a constant, small amount of
progestogen directly into the uterine cavity.

Marketed under the brand name Mirena.

224
• Failure rate of 0,2%
• As effective as male and more effective than
female sterilisation
• No age or parity limitations
• Not protective against HIV and STIs
• No drug interactions
• Duration of use is 5 years
• Following removal return to fertility is
immediate

225
 Mode of action
• Thickens cervical mucus and suppresses
endometrial development

226
 Side effects
• Light irregular bleeding
• Headaches
• Nausea
• Breast tenderness
Usually settle within a few months

• Development of amenorrhoea later

227
 Non-contraceptive benefits
• Reduces menstrual blood loss
• Protects against ectopic pregnancy
• Reduces menstrual cramps and symptoms of
endometriosis, such as pelvic pain and
excessive bleeding

228
 Availability
• Registered in South Africa for:
§ Contraception
§ Management of heavy menstrual bleeding
§ Endometrial protection during hormone therapy
• This method is only available in private sector
and some secondary and tertiary institutions

229
EMERGENCY CONTRACEPTION

230
 Definition
• The use of a contraceptive method following
an episode of unprotected sexual intercourse
(before pregnancy is established) in order to
reduce the risk of pregnancy.

231
• Can be used within 5 days of unprotected
sexual intercourse
• 2 types are currently available in South Africa:
§ Hormonal, emergency contraceptive pill
§ Copper IUCD
• The copper IUCD is the most effective
emergency contraceptive and the efficacy
remains high for the 5 days
• The emergency contraceptive pill is simpler
and less invasive however the pills are more
effective the sooner they are taken

232
 Emergency Contraceptive Pills (ECPs)
• ECPs are oral contraceptive pills taken at a
higher dose and in a different way to the
regular contracpetives
• The combined oral contraceptives (COC) and
the progestogen only (POP)regimens are used
• The POP is more effective and has fewer side
effects
• POP is 58-95% effective
• COC is 31-77% effective
233
 Mode of action
• Primarily inhibit or delay ovulation
• May also interfere with implantation
• No evidence that ECPs cause abortion

Side effects
• Nausea and vomiting
• Dizziness, headaches and fatigue
• Cycle irregularities
234
 Recommended ECP Regimens
Content of ECP 1st dose within 120 2nd dose 12 hours
hours (5 days) later
Combined oral contraceptive
50ug ethinyl estradiol, 250ug levonorgestrel (eg. 2 pills 2 pills
Ovral/ Famynor)
30ug ethinyl estradiol, 150ug levonorgestrel (eg. 4 pills 4 pills
Nordette/Oralcon)

Progestogen only pills

1,5mg levonorgestrel (eg. Escapelle) 1 pill, single dose
0,75mg levonorgestrel (eg. Norlevo) 2 pills, single dose
30ug levonorgestrel (eg. Microval/ Hy-an) 50 pills as a single 25 pills if divided
dose or 25 pills as a dose
divided dose

235
 Counselling of the patient
• Correct regimen- when to take the pills and
how many to take
• Possible side effects and how to manage
• Future family planning
• Expect menstruation to occur a few days
earlier or later than usual
• Information and counselling regarding
termination of pregnancy in case of failure
236
 Emergency copper IUCD
• Treatment fails in <0,1% of cases
• It can remain as a long term contraceptive
device or can be removed during the following
menstruation
• Mode of action: prevents fertilisation or
implantation depending on ovulation

237
 BARRIER METHODS
• Male condom

• Female condom

• Diaphragm and spermicides

238
 Male condom
• Provides a physical barrier preventing sperm entering
the female genital tract
• Provides DUAL PROTECTION (pregnancy and infection)
• And part of DUAL METHOD(if used with another
effective contraceptive)
• Single most effective contraceptive method and
protection against HIV & STIs 2nd to abstinence
• Is 85-98% effective if used correctly & consistently
• Virtually any male can use it and has close to none
disadvantages or contraindications. Requires no follow
up, is mostly free and available everywhere

239
Eligibility
• almost everyone can use it and requires no screening,
limitations come in if there is erectile dysfunction or
latex allergy(which can be checked & enquired about) –
may require change in make of condom
Counselling
• Emphasize correct use and must demonstrate and
remember not to use oil based lubricants rather water
based
• Consistency must be reiterated. Must be every time,
with other contraceptive method, know what to do
when breaks and know availability and supply is always

240
 Female condom
• Provides physical barrier preventing sperm from
entering female genital tract
• Virtually anyone can use it unless presence of latex
allergy(in partner) but is polyurethene and synthetic
rubber so little worry about latex and used if male
partner refuses using a male condom and is great
because no need for follow up, is free and available
• DUAL PROTECTION & DUAL METHOD
• 79-95% effective if used correctly and consistently –
has higher failure rate therefore Dual method must
be advocated 241
Eligibilty – every female is legible therefore no
need for screening
Counselling – emphasize correct use and to use
it consistently

242
 Diaphragm and spermicide
• These are methods but are not included or
discussed in the guidelines due to the fact that
they are not readily found in the public health
sector
• Diaphragm – has some prevention over cervical
infections and pelvic inflammatory disease but
not STIs
• Spermicide – no protection against infection and
1 of the least effective contraceptive and if
recurrent use makes you more prone to HIV
acquisition

243
• Definition: Permanent removal of an individual’s ability to reproduce with their free
and informed consent.
• Proper counselling prior to the procedure is required to enable the user to make a fully
informed decision for themselves.
• Patients must fully understand the sterilisation procedure, risks, and the consequences
thereof before they are able to give informed consent.
• The Sterilisation Act 44 of 1998 (Section 2) prohibits the sterilisation of people without
their informed consent.
• The Sterilisation Amendment Act (Act No 3 of 2005) makes provision for clients not
considered competent to make an informed decision and consent to surgery.

244
245
Effectiveness
Effectiveness -99.5–99.8%
-99.5–99.8%inin thethe
firstfirst
yearyear
afterafter
the procedure; 98.2% over
the procedure; 10 over
98.2% years 10
of use
years
Age limitations of usea medical perspective, no restrictions for age or parity. However, incidence
-From
Age limitations -From
of regreta is
medical
highest perspective,
amongst women nounder
restrictions
30 yearsfor ageand/or
of age or parity. However,
of low parity,
incidence
so of regret is
careful counselling is essential
highest amongst women under 30 years of age
Mode of action -Blocking
and/or ofoflow the fallopian
parity, sotubes prevents
careful the ovum
counselling is and sperm from uniting. The
essential
Mode of action woman
-Blockingis of the fallopian tubes prevents the ovum and sperm from
sterile
uniting. Thefrom
womanthe time the procedure
is sterile from theis time
completed
the procedure is completed
Common immediate -Post-operative pain for a few days, wound infection, haematoma
Common immediate -Post-operative pain for a few days, wound infection, haematoma
problems/complications
problems/complicatio
ns
Non-contraceptive -Female sterilisation may provide some protection against PID and ovarian cancer
Non-contraceptive
benefits -Female sterilisation may provide some protection against PID and
benefits
Effect on STI and HIV risk ovarian cancer
-Not protective
Effect on STI and HIV -Not protective
Drug interaction -None
risk
Duration of use -Considered to be permanent and irreversible
Drug
Returninteraction
to fertility -None
-Never, unless the tubes are reconnected (either spontaneously or surgically,
Duration of use -Considered to beand
which is expensive permanent andguaranteed)
success is not irreversible
Return to fertility -Never, unless the tubes are reconnected (either spontaneously or
surgically, which is expensive and success is not guaranteed)
246
A- Pomeroy technique
B-Falope ring technique
C-Filshie clip technique
D-Essure Micro-Insert.

247
Effectiveness -Over 99.8% in the first year after the procedure
Age limitations -From a medical perspective, no restrictions for age ((although
Effectiveness young men haveinathe
-Over 99.8% higher chance
first year after theof regret later in life, so careful
procedure
Age limitations counselling-From aismedical perspective, no restrictions for age
essential)
((although young men have a higher chance of regret
Mode of action -Surgical closure
later in life, soof both
careful vas deferens
counselling is essential)(two tubes that carry the
Mode of action sperm to ejaculatory
-Surgical duct)
closure of both to prevent
vas deferens sperm
(two tubes that from mixing with
carry the sperm to ejaculatory duct) to prevent sperm
ejaculate. Not effective immediately. Takes on average three
from mixing with ejaculate. Not effective
monthsimmediately.
for vas deferens to bethree
Takes on average cleared
months of sperm
for vas
Common immediate -Minor deferens to be cleared of sperm
post-operative short-term effects (e.g. discomfort for a
Common immediate -Minor post-operative short-term effects (e.g.
problems/complications few days
problems/complications and scrotal
discomfort for a fewbruising andbruising
days and scrotal swelling),
and bleeding from
wound,swelling),
haematoma, wound
bleeding from wound,infection
haematoma,and, woundless frequently,
infection and, less frequently, chronic scrotal pain.
Non-contraceptive chronic-None
scrotal
otherpain.
than protection for man’s partner from
Non-contraceptive benefits
benefits -None other than protection
risks associated with pregnancy for man’s partner from risks
Effect on STI and HIV risk -Not protective
associated with pregnancy
Drug interaction -None
Effect on STI and HIVDuration
risk of use -Not protective
-Considered to be permanent and irreversible
Drug interaction Return to fertility-None -Never, unless the vas deferens is reconnected (either
spontaneously or surgically, which is expensive and
Duration of use -Considered
success istonotbeguaranteed)
permanent and irreversible
Return to fertility -Never, unless the vas deferens is reconnected (either
spontaneously or surgically, which is expensive and success is not
guaranteed)
248
249
• Can be used for both planning and avoiding pregnancy
• They are based on the identification of naturally occurring signs and symptoms of the
fertile and infertile phases of the menstrual cycle and the abstinence or use of condoms
during the fertile phase
• FAB methods are effective when both partners are motivated to abstain consistently from
coitus (or use condoms) during the fertile phase of each cycle.
• The Billing’s Ovulation Method and the sympto-thermal method are the most frequently
used FAB methods in South Africa.
• These are based on observing the signs and symptoms of ovulation and have replaced
methods that are based on keeping track of days in the menstrual cycle, such as the
rhythm/ calendar method.

250
Abstinence or the avoidance of sexual intercourse is the most effective way to prevent pregnancy, STIs and
HIV.
-other forms of sexual expression are permissible during sexual abstinence, such as hugging, kissing, ETC.

Effectiveness -73% during first year of typical use, 96% if used

consistently and correctly
Age limitations - No restrictions
Mode of action - Prevents sperm from entering the vagina
Common side effects -None
Non-contraceptive benefits -None

Effect on STI and HIV risk -Not protective

Drug interaction -None
Duration of use - Can be used throughout the reproductive years
Return to fertility - Fertility never affected 251
Effectiveness -98–99% among amenorrhoeic, fully breast-feeding women during the first six
months after
childbirth

Age limitations - No restrictions

Mode of action -Suppresses ovulation
Common side effects -No side effects
Non-contraceptive benefits - The use of LAM provides the following additional health benefits for mother and
infant:
• Provision of the best source of nutrition for the infant
• Protection of the infant from life-threatening diarrhoea
• Provision of passive immunisation to diseases such as measles and pneumonia
• Reduction in postpartum bleeding
• Decreased risk of breast cancer

Effect on STI and HIV risk -Not protective

Drug interaction -None, but to protect infant health, breastfeeding is not recommended for women
who are on the following drugs: antimetabolites, bromocriptine, certain
anticoagulants, high doses of corticosteroids, cyclosporin, ergotamine, lithium,
mood altering drugs, radioactive drugs
and reserpine
Duration of use - First six months after childbirth, effectiveness falls thereafter
Return to fertility - Once any one out of the three LAM criteria is not met, an additional method of
contraception should be added to prevent pregnancy 252
• Traditional methods for the prevention of pregnancy include herbal mixtures, intercrural
sex, breastfeeding and abstinence after childbirth.
• There has been very little research conducted and documentation of the traditional
methods used by the different cultural groups in South Africa.
• Providers should be aware that clients may be using a variety of different traditional
methods of contraception, which are specific to their locality.

253
 Contraception and HIV
• Conducted studies showed inconclusive
evidence of disease progression of HIV with
females on hormonal or oral contraception
and contraception does not increase
transmission chance nor does it increase
acquisition
• DUAL METHOD IS BEST FOR MOST EFFECTIVE
CONTRACEPTIVE METHOD

254
 TYPES AND EFFECTIVENESS
• HORMONAL CONTRACEPTION ie progestogen
only injectables and implants
• Interaction of ART drug ritonovir and NNRTIs and
TB drugs rifampicin and rifabutin with implants &
norethisterone enanthate
• Even though interaction, significant effectiveness
of either is not affected therefore can be used by
HIV positive patients on ARTs and TB treatment
but dual protection always recommended
255
• DMPA does not have drug interactions
• Drug interactions occur with Combined oral,
combined injectables and progestogen only
pills because of blood level hormones are
significantly reduced due to interactions with
Ritinovir and TB drugs rifampicin and rifabutin
• Lesser interactions with NNRTIs therefore dual
method always recommended

256
Emergency contraceptive
• HIV positive patients on ARTs or TB treatment can use it unlikely to
reduce effectiveness
IUD
• Copper or levonorgestrel releasing intrauterine system safe use in
HIV positive and AIDS patients as long as they are clinically well on
ART
• If developed AIDS during IUD It can be continued safely even when
not on ART
Sterilization
• Can be done as long as appropriately counselled
Condoms
Suitable for all but dual method always recommended especially HIV
positive or at risk

257
 Fibroids
Leio=Smooth
Myo =muscle
Oma= tumour
Benign smooth muscle neoplasm often occurring in
the myometrium

258
RISK FACTORS

• Age 30-45
• Race
• Obesity
• Low parity
• Hormones(eostrogen,
progesteron & growth
factors)
• Early menarche or
Infertility
259
 Clinical Features
— 50% asyptomatic
q AUB
— Menorrhagia (excessive menses) due to:
— Increased bleeding surface
— Abnormal blood vessels stretched over tumour
— Endometrial glandular hyperplasia on margins
— Metrorrhagia- necrosis & infection of endometrium on leiomyomatous
polyp
— Iron-deficiency anaemia

q Pain
— Concurrent PID
— Torsion of penduculated fibroid- acute abdomen
— Dysmenorrhea- active myometrium trying to expel fibroid polyp
— Increased concentration of prostaglandin receptors

260
 Clinical Features cont…
qInfertility
— Common sx
— Submucosal and intramural types may be responsible for
unfavourable IU enviroment>> reccurent abortion and infertility
— They usually occlude the interstitial portion of fallopian tube
— Distortion of uterine contour: impair implantation, cause
dysfunctional uterine contractility ,interfere with sperm migration,
ovum transport

qVaginal discharge
— Infection usually of submucous fibroid
— Poor drainage of endometrial cavity> endometritis + pyometra (pus
in the uterus)

261
 Pressure effects
qPressure effect
• Urinary tracts:
urine retention,
overflow
incontinence,
hydroureter
and
hydronephrosis
• Gastric tract: :
Constipation
262
 Complications
• Pregnant Pt
• Enlarges during pregnancy
• L/t large for dates pregnancy
• Can lead to necrobiosis w localised pain-exclude abruptio
• Usually settles with no effect on pregnancy
• Labor cxrd: Uterine inertia; Malpresentation; Obstructed birth
Canal; 3 stage of labour
• C/S
• Ectopic Preg, Haemoperitoneum, PROM
• Non Pregnant Pt
• Anaemia
• Infection
• Torsion
• Ascites

263
 Differential Diagnosis
• Pregnancy
• Ovarian tumours
• Inflammatory masses
• Ca endometrium
• Adenomyosis
• Endometriosis
• Bladder masses
• Kidney masses

264
 Diagnosis
– Most common combination
§ Infertility
§ Abnormal menses
§ Abdominal mass
– Abdominal mass
§ Single: regular and symmetrical
§ Multiple: irregular
§ Mass moves with the uterus
– On PV exam
§ Cervix displaced upwards, usually under pubic symphysis

265
 Investigations
— FBC- assess the Hb for anaemia
— Pregnancy test (rule out pregnancy as cause of mass)
— X-ray: shows calcified leiomyoma
— Ultrasonography
Ø number, size, and shape of most fibroids.
Ø shows a homogeneously enlarged uterus or a solid mass with the same
texture as a normal uterus

— MRI: Better than U/S for diagnosis and evaluation of leiomyomata in

different sites of the uterus but expensive
— Hysteroscopy and hysterosalpingography
Ø Usually combined when pt. presents with infertility
Ø Indicated for diagnosis of small submucous tumours

266
 Management

• Conservative

• Medical

• Surgical

267
 Conservative Treatment
• Fibroid is small

• Symptomless

• Discovered incidentally in perimenopausal women

• The exact nature of the fibroid must be known before treating in

this manner!!!!!!

• Patients are seen at 3 month intervals to assess the state of the

tumour.

• If symptoms develop or there is progressive growth intervention

required.

268
 Medical Treatment
— assessed at 6 monthly intervals clinically and with U/S

Indications:
— Asymptomatic /Mildy sx
— Size of uterus <12 weeks
— Small fibroid perimenopausally
— Many small fibroids/Single solitary fibroid

269
— NSAIDs for pain, dysmenorrhoea and menorrhagia:
­ Eg. Mefenamic acid 500mg TDS
­ Decrease prostaglandin synthesis by COX inhibition
­ Taken at the time of menstruation
­ S/E’s- headaches, GI symptoms, diarrhoea, N&V
• Antifibrinolytics for excessive bleeding
­ Tranexamic acid (Cyclokapron) 1.5 g tds
­ Prevent activation of plasminogen to plasmin
­ S/Es- nausea, dizziness, tinnitus, rashes, abdominal cramps, thrombosis
• Oral contraceptive pills- cycle control
- eg. Nordette
§ Intra-uterine systems- Mirena
• Androgens (Danazol )(17alpha-ethinyl testosterone) has been associated with a
reduction in volume of the fibroid in the order of 20% to 25%. Although the long-term
response to danazol is poor, it may offer an advantage in reducing menorrhagia.
oral dose of 200-800mg (max of 9 months)
­ Induces endometrial atrophy.
­ not routinely used because of androgenic side effects such as hirsutism, acne,
voice changes

270
 GnRH agonists
• Available in nasal spray, subcutaneous injections, and slow release injections
• Goserelin (Zoladex)
• 3.6mg subcut
Decrease
size of fibroids up to 50% of their initial volume within 3 months of therapy.
menstrual blood flow
Pelvic pain/dysmenorrhoea
• preoperatively to shrink fibroids and to reduce menstrual related anemia
• GnRH agonist treatment should be restricted to a 3- to 6-month interval, following
which regrowth of fibroids usually occurs within 12weeks
Side effects
Hot flushes (>80% of patients). Headaches, depressive mood changes, sleeping
disturbances,joint and muscle stiffness, decreased libido, vaginal dryness and
dyspareunia and hair loss are reported in 5-15% of cases.

271
 Mifepristone
• This is a synthetic
antiprogestogenic steriod. The
clinical effect is similiar to that of
Gonadotropin-releasing hormone
analogue.
• C/I in Pregnancy as it may induce
Labour and/or terminate
intrauterine pregnancy.
• Oral dose of 200mg. 272
 Non-Invasive Surgical Treatment
• Uterine Artery embolisation:
uterine artery selectively
embolised leading to shrinkage
and improvement of
symptoms. Post procedure
complications-fever and pain.
Adv: shorter hospital stay and
fewer adverse effects.
• Magnetic resonance guided
focussed ultrasound surgery:
thermo-ablative technique

273
 Surgical Management
Indications

• Uterus size >14 wks gestation

• Distortion of the uterine cavity in a patient who desires
fertility
• Leiomyoma in the lower part of uterus with potential
to obstruct labour
• Doubt about nature of the leiomyoma
• Presence of complications – severe menorrhagia, pain,
pressure on neighbouring organs
• Sudden enlargement* =6 weeks in 6 months

274
 Preoperative precautions
• Preoperative evaluation (history, systemic exam, pelvic
exam)
• Investigations: Urinalysis, pregnancy test, Hb, FBC, U/E,
cytology in hysterectomy, X-ray, ECG
• Counselling and Informed consent
• Correct Anaemia if present
• GnRHa to reduce blood loss (but may make fibroid
capsule difficult to identify)
• Prophylactic antibiotics
• Restriction of food and drink on the day of operation
• Horizontal incisions- parallel to muscle fibres

275
 Invasive Surgical Treatment

Invasive
— Abdominal myomectomy
— Laparoscopic myomectomy
— Hysterscopic myomectomy
— Vaginal myomectomy
— Abdominal/ vaginal hysterectomy

276
 Myomectomy
• Young patients
• Desire for fertility
• Small fibroid uterus(<20 weeks)
• Few tumours with healthy fallopian tubes
• Complications:
• Asherman’s syndrome
• Uterine rupture in subsequent pregnancies

277
Abdominal myomectomy

278
 Hysterectomy
• Abdominal hysterectomy: prevents recurrence of
tumours and ensures that symptoms are relieved.
There is said to be less blood loss and post-op
morbidity compared to a myomectomy
• Vaginal hysterectomy: for smaller tumours
Advantages over myomectomy
• Prevents recurrence
• Absolute certainty that symptoms will be relieved
• Less blood loss
• Less post-op morbidity

279
 Hysterectomy
• Complications
• Intra operative: haemorrhage, bladder,
ureteric and bowel injury
• Post op: vault haematoma, infection,
prolonged paralytic ileus, vaginal vault
granulation, vaginal vault prolapse, pulmonary
embolus, incisional hernia, bowel obstruction,
early menopause.

280
 Post operative care
• Vitals
• Remove catheter as soon as patient can be
mobilized
• Vaginal bleeding
• Fever(does not necessarily indicate infection)
• Early ambulation
• Diet
• NO tampons, douche, sex, or anything in the
vagina for at least 4-6 weeks after surgery

281
 PID

Acute infection of the upper genital tract

structures in women, involving any or all of
the uterus, fallopian tubes & ovaries

282
 Organisms involved in PID
• Primary Infecting Agents
1) Neisseria Gonorrhoea
2) Chlamydia Trachomatis
3) Gardnerella Vaginalis
• Seconary Invaders
1) Streptococcus
2) Staph
3) E.coli
4) Haemophilus Influenza
5) Klebsiella
283
 High Risk Factors
1) Early Sexual debut
2) Women <25 years
3) New, multiple or symptomatic partners
4) Low Parity
5) Hx of prev PID attac/STD
6) Sex during menses
7) Bacterial vaginosis
8) Low Socio-economic status

284
 History & Exam
• LAP
• Deep Dyspareunia
• Abnormal Vaginal bleeding
• Abnormal Vaginal/Cervical discharge
• Hx of STI in the past

• Pyrexia >38°C
• Lower abdominal Tenderness-bilateral
• Adnexal tenderness on bimanual vaginal exam
• CET on vaginal exam-equivalent to rebound tenderness
in the abdomen. 285
 Clinical Diagnosis
• A triad of:
1) LAP/Tenderness
2) CET
3) Adnexal/Uterine tenderness (uni/bi-lateral)
Plus 1 of the following should be present:
1)Temp >38,3°C
2)Abundant WBCs on saline microscopy of vaginal
secretions
3)Mucopurulent discharge from the cervix
4) ESR >15mm/hr
5)↑ CRP 286
 Gainesville Classification
• Stage 1= Early Salpingitis + Tenderness localised to
adnexa →outpatient tx + oral antibiotics
• Stage 2= Late Salpingitis + Pelvic Peritonitis→ inpatient
tx with parenteral antibiotics
• Stage 3= Evidence of 1)Pyosalpinx 2)Tubo-ovarian mass
3) Tubal Occlusion 4)ESR >60mm/hr→ inpatient tx with
parenteral antibiotics
• Stage 4= 1) Ruptured tubo-ovarian complex
2)Generalised peritonitis 3)Septicaemia→Laparotomy +
triple antibiotics
• Stage 5=
ARDS;;&&&&&&&&&;&&&&&&&&&&&&&&&&8 287
 Differential Diagnosis
1) Ectopic Pregnancy
2) Acute Appendicitis
3) Bleeding/ torsion of ovarian cyst
4) Endometriosis
5) UTI

288
 Investigations
• Bloods=
1)FBC, U&E, RPR, HIV + CRP,ESR + Blood culture
2) Pregnancy Test (urine/serum)
• Microscopy= Swab +→supports -→ doesn’t exclude
1) High Vaginal Swabs( trichomonas vaginalis, candidiasis,bacterial vaginosis)
2) Endocervical swabs (gonorrhoea,chlamydia)
• Imaging=
1)TV U/S
2)Doppler TV U/S
3) CT & MRI (not cost effective)
• Surgical=
-Laparoscopic Indications
1) Sick pt with diagnostic uncertainty (appendicitis)
2) Acutely ill pt that has failed outpatient tx (stage 1)
3) Failure to respond within 48-72 hrs of inpatient antibiotic therapy
-Laparotomy indications
1) Generalised Peritonitis
2) Pt > 40 years old
3) Recurrent PID attacks
4) Hx of tubal ligation
289
 Management
• Outpatient
1)Cefixime 400mg oral stat/Cefoxitin 2g IM stat
+ 2) Doxycycline 100mg oral bd for 14 days
+ 3) Metronidazole 400mg oral bd for 14 days
• Inpatient
-Regimen 1
1) Cefixime 400mg IV 8 hrly
2) Doxycycline 100mg IV/Orally 12 hrly
3)Gentamycin -Loading dose (2-3mg/kg body weight)
-Maintenance dose (1,5mg/kg 8 hrly)- continue
for 48 hrs after the patient is well.
-Doxycycline 100mg oral bd-send home with patient for
prolonged eradication of chlamydia trachomatis.
290
Bartholin’s Cyst and Abscess

291
 Anatomy and Function
• Pea-sized, usually <1cm
• Homologues of Bulbourethral/Cowpers glands in males

• Location:
- Gland – on each side, posterior to bulb of vestibulum
- In labia minora, 4 and 8 ‘o’ clock positions
- Duct- 2 – 2.5cm opens into vestibulum, between labia minora and
margin of hymen.
Opposite junction of anterior 2/3 and posterior 1/3 of labia majora.
• Function:
• Begin to function at puberty
• Mucus secretion
• Lubricates vaginal opening and canal
• Especially during coitus
292
293
 Pathology
• OBSTRUCTION OF DUCT :
• reason not clear, possibly –
1) trauma,
2) swelling
3) infection
- CYST any age, more common in
- ABCESS reproductive age group
• MALIGNANCY } postmenopausal women/ >40 years

294
 BARTHOLINS CYST
Ducts prone to obstruction at vestibular orifice/distal end

Retention of fluids

Dilatation of the duct and gland

Formation of cyst

• Cyst contains sterile mucoid liquid

MANAGEMENT
- Asymptomatic: <1cm – no treatment
- Symptomatic : Marsupialization 295
296
 BARTHOLINS ABCESS
• 3 times more common than cysts

• Occurs when:
- Bartholin’s cyst becomes infected
- Bartholin’s gland becomes infected

AETIOLGY
• Sexually transmitted infections
• Vulvovaginal surgery

• Polymicrobial
297
 PATHOLOGICAL AGENTS
Aerobic organisms

1. Neisseria gonorrhoeae #
2. Staphylococcus aureus
3. Streptococcus faecalis
4. Escherichia coli
5. Pseudomonas aeruginosa
6. Chlamydia trachomatis #

Anaerobic organisms#
1. Bacteroides fragilis
2. Clostridium perfringens
3. Peptostreptococcus species
4. Fusobacterium species

# COMMON AGENTS
298
 PRESENTATION
• Patient presents with:
- Acutely painful
- Throbbing
- Tender swelling in vulva
• Patient may complain of Vulvar pain during activity – walking, sitting, sexual
activity
• Fever

EXAMINATION
• Normally: gland NOT palpable unless disease or infection
• Gland/mass palpable
• Unilateral

• EXTERNALLY: protrudes into labia Majora (posterior 2/3)

• VAGINAL EXAM:
• Medially protruding mass, in posterior introitus, in region were duct enters
vestibule
• Local tenderness, inflammation, warmth, Induration around gland
• Explore extent of cyst
299
 DIFFERENTIAL DIAGNOSIS
CONDITION DIFERENTIATING SIGNS/SYMPTOMS

1. MUCUS CYST OF VESTIBULE < 2cm diameter, superficial, soft,

smooth

2. MALIGNANCY Irregular nodular mass, +/-

ulcerations, biopsy to confirm

3. VULVAL HAEMATOMA Following trauma. Extravastated

blood expand into areolar tissue of
labia. Cause tender swelling

4. VULVAL FIBROMA Firm, non-cystic, asymptomatic

300
301
Inflammed

302
303
 MANAGEMENT
INCISION DRAINAGE MARSUPIALISATION
Indications:
• Abscess/cysts > 1 cm
• Symptomatic: tender, inflammation, fever

Procedure:
• Informed consent
• In theatre or in office
• Lithotomy position, clean and drape area
• General or local anaesthesia

• Incision : cruciate or longitudinal incision on inner/vestibular aspect of abscess, mucosal surface

• Drainage: a pus swab sample may be taken for investigation
• Marsupialisation:
- Abcess wall is everted, centre of flaps sutured to edge of Skin
- Petal-shaped manner
- Permanent fistulisation of gland
- This decreases the risk of recurrence

• Guaze (Jelonet) packing placed overnight 304

CRUCIATE INCISION
305
LONGITUDINAL
INCISION

306
Excision of gland
• Recurring episodes, patient did not respond to previous
management
• Perform when no active infection – empiric broad-spectrum
antibiotic
• Over 40 years :To exclude malignancy

Post-operative
• Antibiotics (optional) – e.g. Doxycylin (400mg BD);
metranidazole (400mg TDS)
• 1 week follow up
• Avoid sexual intercourse until pain or discharge subsides
• Sitz baths: sitting in a tub of water up to the hip – keeps
area clean, increase blood flow to it

307
Sexually transmitted infections

308
Syndrome Symptoms Signs Most common
causes
Vaginal Unusual vaginal discharge Abnormal vaginal VAGINITIS:
discharge Vaginal itching discharge – Trichomoniasis
Dysuria (pain on urination) – Candidiasis
Dyspareunia (pain during CERVICITIS:
sexual Intercourse) – Gonorrhoea
– Chlamydia
Urethral Urethral discharge Urethral discharge Gonorrhoea
discharge Dysuria (if necessary ask patient Chlamydia
Frequent urination to milk urethra)
Genital ulcer Genital sore Genital ulcer Syphilis
Chancroid
Genital herpes
Lower Lower abdominal pain Vaginal discharge Gonorrhoea
abdominal Dyspareunia Lower abdominal Chlamydia
pain tenderness on palpation Mixed anaerobes
Temperature >38°
Scrotal swelling Scrotal pain and Scrotal swelling Gonorrhoea
swelling Chlamydia
Inguinal Painful enlarged Enlarged inguinal lymph LGV
bubo inguinal lymph nodes nodes Chancroid
Fluctuation
Abscesses or fistulae
Neonatal Swollen eyelids Oedema of the eyelids Gonorrhoea
conjunctivitis Discharge Purulent discharge Chlamydia
309
Baby cannot open eyes
Lecture Outline:
Family Condition Causative Agent
Bacterial • Syphillis • Treponema pallidum
• Gonorrhoea • Niessieria gonorrhoeae
• Chancroid • Haempilus Ducreyi
• Genital Tuberculosis • Mycobacterium
tuberculosis

Viral • Genital Warts • Human Papilloma virus

• Herpes Simplex Viral • Herpes simplex virus’
Infections
• AIDS • Human immunodeficiency
virus (HIV)

Chlamydial • Chlamydial infections (Often • Chlamydia hominis

non-specific genital
infections)

Fungal • Candiadisis • Candida albicans

Protozoal • Trichomoniasis • Trichomonas vaginalis

Parasites • Scabies • Sarcoptes scabiei 310

Syphilis

311
Pathophysiology:
• Caused by bacterium: Treponema pallidum.
• Spread by sexual contact; close contact with lesions; or by vertical
transmission.
• Incubation period: 9-90 days.
• Primary syphilis:
– Chancre formation.
– Ulceration at inoculation site; usually genitals, perineal area or mouth.
– Solitary purple papule due to lymphocytic infiltration on dermis.
– Inflammatory changes lead to necrosis; ulcer forms; highly infectious.
• Secondary syphilis:
- Condylomata lata; wart-like growth on labia majora; labia minora;
perineum.
- 6-8 weeks after primary chancre manifests.
- Systemic illness.

312
Pathophysiology:
• Early latent syphilis: asymptomatic; <2 years duration.
• Late latent syphilis: asymptomatic; >2 years duration.
• Tertiary syphilis:
– Gummatous syphilis: necrotic nodules or plaques which develop 3-12
years after primary infection.
– Neurosyphilis: 10-20 years after primary infection.
– Meningovascular syphilis
– Cardiovascular syphilis: angina; aortic regurgitation; aneurysms; occurs
10-40 years after infection.

313
Presentation:
• Primary:
-solitary painless ulcer
-inguinal lymphadenopathy: rubbery and non-tender
-patients may not notice the lesion
• Secondary:
– generalized lesions affecting skin and mucous membranes
– symmetrical: macular, popular, rarely pustular.
– Systemic involvement:
• Fever; malaise
• Generalized lymphadenopathy
• Meningitis; paralysis of cranial nerves
• Iritis
• Pharyngitis
• Arthritis
• Hepatoslpenomegaly
• Anaemia
314
Investigations:
• Dark-field microscopy
• Non-specific serology tests:
– VDRL (venereal disease research laboratory)
– RPR (rapid plasma reagin)
– Detect antibody (regain) in serum.
– False positives; retest in 6 months.
• Specific serology tests:
-EIA (enzyme immunosorbent assay)
-FTA-Abs ( fluorescent treponemal antibody absorption test)
-TPHA ( treponema pallidum haemaglutination)

315
Management:
• Full sexual health screen including HIV testing
• Partner notification and treatment.
• Avoid intercourse until clear and partner has been treated.
• Counsel on contraceptive use.
• Early syphilis:
-Benzyl penicillin 2.4 mu IM STAT
-Erythromycin 500mg 4 times a day; oral for 15 days.

• Late syphilis:
-Benzyl penicillin 2.4 mu IM 3 weeks
-Erythromycin 500mg 4 times a day; oral for 15 days.
• Pregnancy: weekly Benzyl penicillin; 3 doses.
• Follow-up: treatment of partner and other STIs.

316
Gonorrhoea

317
Pathophysiology:
• Neisseria gonorrhoea: gram negative diplococcus.
• Incubation period: 2 weeks or more.
• Uncomplicated gonorrhoea:
-Urethritis
-Cervicitis
-Proctitis
-Pharyngitis
• Complicated gonorrhoea:
-Bartholin’s duct abscess
-Salpingitis

318
Presentation:
• Majority asymptomatic.
• Commonest symptom: mucopurulent discharge.
• Dysuria.
• Lower abdominal pain.
• Intermenstrual bleeding; postcoital bleeding.
• Pelvic or lower abdominal tenderness.

319
Investigations:
• Microscopy:
- Gram stain
-directly visualize gram negative diplococcic.
-identified extracellularly or intracellularly within leukocytes.
-provisional diagnosis; need confirmation by culture.
• Culture
• PCR

320
Management:
• Full sexual health screen including HIV testing
• Partner notification and treatment.
• Avoid intercourse until clear and partner has been treated.
• Counsel on contraceptive use.
• Treat uncomplicated gonorrhoea:
– Amoxicillin 3g PO plus probenicid 1g PO
– Procaine penicillin 3g IM plus probenicid 1g PO
– Cefixime 400mg PO stat
– Ceftriaxone 125 mg IM stat
– Ciprofloxacin 500mg stat
• Amoxicillin and penicillin not first line treatment due to high prevalence of
penicillin strains.
• Follow-up: treatment of partner and other STIs.

321
Complications:
• PID
• Haematogenous spread:
-bacteraemia (chills, fever, dermatitis)
-arthritis
-gonococcal emboli (vesicles; pustules; petechial)

322
Chancroid

323
Pathology:
• Caused by Haemophilus Ducreyi.
• Non-motile; gram negative rod with rounded edges.
• Most common cause of genital ulceration.

324
Presentation:
• Multiple papules develop at the labia majora; cervix; vagina; perineum.
• Develop into pustules and eventually form ulcers.
• Soft consistency therefore called a chancre or chancroid.
• Inguinal lymphadenopathy.
• Nodes may become confluent and form a fluctuating abscess: BUBO.
• Bubo may break by forming a sinus; large ulcer.

325
Investigations:
• Usually diagnosed based on clinical presentations.
• Other causes of ulcers ruled out e.g. RPR to rule out syphilis.
• No suitable serological test.
• Bacteriological identification through selective media.
• Culture:
– Swabs from ulcers or aspirates from bubo.

326
Management:
• Recommended single dose regimen:
-Azithromycin 1 g PO stat
or
-Ceftriaxone 250 mg IM stat
• Multiple dose regimen:
– Ciprofloxacine 500mg PO twice a day for 3 days
or
-Erythromycin 500mg PO three times a day for 7 days.

327
Lymphogranuloma venereum

328
Presentation:
• Caused by Chlamydia trachomatis; serotypes L1-L3.
• Incubation period: 1-6 weeks.

• Primary painless lesion on vulva; vaginal wall and cervix.

• Painful inguinal or femoral lymphadenopathy.
• Lymph nodes become matted: BUBO.
• Genital oedema.
• Rectal complications: proctitis; perirectal abscess; rectal stricture.
• Systemic symptoms: fever; headache; nausea; arthralgia; weight loss;
backache; general malaise.

329
Diagnosis:
• Clinical presentation; history; laboratory examination.
• Serological tests.
• Culture.
• Cytology.
• ELISA
• Fluorescent monoclonal antibody staining.
• PCR:
- urine specimens
-cervical and vulval swabs.

330
Management:
• Doxycycline 100 mg (p.o.) b.d. for 21 days
Alternative regimens:
• Erythromycin 500 mg (p.o.) q.d.s. for 21 days
• Aspirate fluctuant buboes
• Incision & drainage or LN excision are
• contra-indicated
• Late sequelae may require surgery

331
Chlamydia

332
Pathogenesis:
• Chlamydia trachomatis.
• Obligate intracellular bacterium.
• Attaches to and in internalised by endocytic vesicles.
• Infect the: cervix; urethra; rectum; Bartholin’s gland; pharynx; eye.
• Incubation period: 1 day – 6 weeks.

333
Presentation:
• Asymptomatic 70%
• Lower abdominal pain.
• Dysuria.
• Purulent vaginal discharge.
• Postcoital bleeding.
• Intermenstrual bleeding.

334
Investigations:
• NAATs (nuclei acid amplification tests): gold standard.
• If unconfirmed result, treat and retest.
• Endocervical swab.
• Vulvovaginal swab.
• Urine sample: first catch specimen.

335
Management:
• Full sexual health screen including HIV testing
• Partner notification and treatment.
• Avoid intercourse until clear and partner has been treated.
• Counsel on contraceptive use.
• Uncomplicated infection:
-Azithromycin 1 g PO stat
-Doxycycline 100mg PO BD for seven days
• Complicated infection:
-PID
-Outpatient treatment; hospitalisation may be required.
• Follow-up:
- treatment of partner and other STIs.
-urethritis persists or recurs.
-retest after 6 weeks; especially in pregnant or breastfeeding women.

336
Complications:
• PID
• Tubal pathology
• Ectopic pregnancy
• Chronic pelvic pain
• Reactive arthritis

337
Genital Warts

338
Pathology:
• Caused by Human papillomaviruses; group of DNA viruses.
• Benign genital disease: Types 6; 11.
• Cervical neoplasia: Types 16; 18; 31; 33.
• Transmission: sexual contact; also by autoinoculation.
• Commonly found: introitus; vulva; also at the cervix; perianal areas; anus
and rectum.
• Incubation period: 3 weeks – 8 months.

339
Presentation:
• Usually painless lumps.
• Solitary or multiple.
• Condylomata accuminata: red/ pink/ brown swellings aboves skin
surface; become pedunculated.

340
Investigations:
• Cytology:
-Pap smear
• Colposcopy
• Cone biopsy

341
Management
• Podophyllotoxin:
-0.5% applied twice a day for 3 days; repeated once a week.
-cytotoxic agent
-washed out 4 hours later; may cause burns of healthy skin.
-S/E: peripheral neuropathy; hypokalemia; coma.
-safety during pregnancy not established
• Imiquimod:
-5% cream; OD three times a week for 16 weeks.
-immune response modifier; induces a cytokine response.
• Electrocauterisation
• Laser therapy: shorter healing time; safe use during pregnancy.
• Surgery
• Cryotherapy: retreatment required at intervals of one to two weeks.

342
Complications:
• Cervical neoplasia.
• Recurrence common.
• Warts often increase in pregnancy.

343
Herpes Simplex

344
Pathophysiology:
• HSV type 1: orolabial herpes; occurs in childhood.
• HSV type 2: commonly affects the genitals.
• Incubation period 1 -2 weeks.
• Highly contagious; latent in sacral dorsal root ganglia; recurrent infections
may occur.

345
Presentation:
• Primary:
– Fever; myalgia; malaise.
– Headache; photophobia; neck stiffness.
– Dysuria
– Vaginal discharge
– Painful ulceration; multiple blisters and ulcers of vulva; cervix; anal
area.
– Inguinal lymphadenopathy.

• Secondary:
- Asymptomatic
-Single or multiple painful ulcers; less painful than primary lesions;
affect same area.
-Prodromal symptoms: tingling in area.

346
Investigations:
• Pap smear: identify virus infected cells; large with intranuclear inclusions.
• Electronmicroscopy
• Culture:
-swab base of the lesion; taken immediately to lab.
• PCR
• Serology:
-one sample at time of infection usually negative; repeat at 3
months.
-exposed in the past; both tests positive.

347
 Management:
• PRIMARY OCCURRENCE:
• Full sexual health screen.
• Partner notification.
• Counselling on contraception use.
• Counselling is important about natural history; transmission; asymptomatic
shedding and protection of partners.
• Oral antivirals:
-Acyclovir 400mg PO three times a day for 7-10 days.
-Acyclovir 200mg PO five times a day for 7-10 days.
-Famciclovir 250 mg PO three times a day for 7-10 days.
-Valacyclovir 1g PO twice a day for 7-10 days.
• Extend treatment after 10 days of therapy if healing incomplete.
• Symptomatic treatment: analgesics; application of 2% lignocaine hydrochloride on
genital ulcers.
• Antibiotics indicated if secondary bacterial infection.
• If vomiting or unable to swallow; consider IV treatment.

348
Management:
• SECONDARY OCCURRENCE:
• COCP tricycle to avoid menstruation as it triggers recurrences.
• Suppressive continuous low dose treatment:
-Acyclovir 400mg BD for maximum 1 year.

349
Complications:
• Aseptic meningitis.
• Autonomic neuropathy; urinary retention.

350
Trichomonas

351
Pathophysiology:
• Caused by protozoan parasite: Trichomonas vaginalis.

• Incubation period: 4 days -4 weeks.

• Found in: vagina; urethra; Bartholins gland; Skene’s ducts; bladder;

endocervix; rare cases organism isolated from uterus and fallopian tubes.

352
Presentation:
• 10-50% asymptomatic.
• Vaginal discharge: yellow-greenish; malodorous.
• Vaginal pruritus.
• Dysuria.
• Frequency.
• Lower abdominal pain.
• Dyspareunia.
• Postcoital bleeding.
• “Strawberry cervix”

353
Investigations:
• Smears:
-Wetmount smear
-sample of discharge taken from posterior fornix/ lateral fornix.
-examined under microscope: typical jerky movements of flagella
- Cytological smear
-grey-green pap smear stained oval structures.
• Culture

354
Management:
• Full sexual health screen including HIV testing
• Partner notification and treatment.
• Avoid intercourse until clear and partner has been treated.
• Counsel on contraceptive use.

• Metronidazole 2 g PO stat or 400-500mg BD PO for 7 days.

• Contraindicated in first trimester of pregnancy; Clotrimazole vaginal cream
indicated instead.
• In lactating mothers; breastfeeding should be withheld for 24 hours.
• Avoid alcohol for 48 hours after treatment; may cause abdominal cramps;
nausea; vomiting; headaches; sweating; flushing.

355
Complications:
• Enhanced HIV transmission.
• Problems in pregnancy: preterm delivery; low birth weight babies.

356
Candidiasis

357
Pathophysiology:
• Candida is a yeast; commensal of intestinal tract.
• Overgrow or colonize vagina from the perineum and perianal areas.
• Especially if normal flora of vagina affected by anitbiotics.
• Most common: Candida albicans.

358
Presentation:
• Vulval pruritus
• Vaginal discharge: white; cheese-like and thick.
• Dyspareunia.
• Dysuria.

• Speculum examination:
– Vulva: erythema; oedematous; fissuring.
– Satellite lesions; small white plaques.

359
Diagnosis:
• Wetmount smear:
- potassium hydroxide used
-dissolves bacteria and leucocytes.
-pseudohyphae and blastocysts detected
• Culture

360
Management:
• Avoid local irritants.
• Counsel on contraceptive use: abstain or use alternative to barrier method
as pessaries reduce effect.
• Intravaginal administration of agents inserted at night:
– Clotrimazole 500mg
– Econazole 1g/100g for 14 days
– Miconazole 100mg/5gg for 7 days.

• Oral administration:
- Itraconazole 200mg 12 hourly for one day.
- Fluconazol 150 mg stat

361
Ca cervix

362
 Risk factors & Aetiology
• Cervical Cancer is currently seen as a cancer which is caused by a carcinogen
and mediated by host factors
• Human Papilloma Virus: carcinogen
– High-risk viral types (16,18,31,33,39, 45,51) associated with cancer
– Predominantly but not exclusively a sexually transmitted virus – survives inside
epithelial cells in episomal form
– When host factors are favourable viral DNA integrates into host DNA leading to
the formation of dysplastic cells , this process is termed “cervical
carcinogenesis”

– Host Genetic Factors:

• Deficiency of cellular P53 (“mop-up protein”) in cervical cancer ® d/t
mutation or suppression from the virus itself, or unknown factors

– Host Infectious factors:

• HPV infection and pre-malignant cervical disease much higher in HIV
positive patients
• invasive cancer is however not higher in HIV positive patients as compared
to the general public.( invasive ca takes years to develop, most patients
have AIDS related demise before true malignant changes develop)
– Risk factors for exposure to HPV:
• Coital factors ® sexual intercourse most important rf; Age at
1st coitus (adolescence - ­ risk); multiple sexual partners;
– Women with high-risk HPV infection after age > 30 years
® @ risk for cervical cancer
– Chlamydia Trachomatis ® risk factor for cervical
neoplasia

• Male factors ® sexual transmission, semen may contain

oncogenic protein
• Racial & Cultural Factors ® low socio-economic status,
differences in sexual behaviour
• Smoking ® 2-fold increased risk ® effect on P53
function.
• Oral Contraceptive Pills ® slightly increased risk but
influenced by other- especially sexual- factors
 PRIMARY PREVENTION
• Vaccine now available against HPV
Gardasil (6, 11, 16, 18)
Cervarix (16, 18)
• Target group- pubertal females, similar
aged males may also be vaccinated
• Not yet part of governmental policy in SA
Preinvasive (Premalignant) Lesions
of the cervix
Transformation zone: is of utmost importance. During the
transformation from columnar to squamous epithelium
(metaplastic transformation) exposure to carcinogens may
lead to dysplasia. Foci of atypical cells are found. They may
overcome host defence mechanisms, multiply and replace
normal cells to form a clinically detectable lesion that is a
precursor of invasive cervical carcinoma.
 Screening for carcinoma of the cervix
• AIMS:
– Decrease the incidence of cervical cancer.
– Detect precursor lesions.
– Prevent progression of abnormal cells to cancer

SCREENING METHOD
Ø Papanicolaou smear- send for cytology and classified according to the
Bethesda classification
- Sample cells from the transformation zone (junction of the endocervix
and ectocervix)
• Alternatives to cytology:
– Macroscopic inspection of the cervix with or without the application
of acetic acid and cervicography using close up photographs-
sensitivity acceptable and specificity is low.
– HPV PCR screening test-100 % sensitivity. not available due to the cost
of the test.
 S.A. National Guidelines
• 3 smears per lifetime, with 10 yr interval
between each smear, commencing at age 30
(Preinvasive phase lasts 10yrs)
• First smear at age 55yrs, only one more smear
if first smear is negative
• Additional smears patients own cost
• HIV positive- initial pap on diagnosis then 6
months later, if both are negative then annual
pap smears
 Bethesda Classification (2001)
• Squamous Cell
• Atypical squamous cells (ASC)
– Undetermined Significance (ASC-US)
– Cannot exclude High Grade SIL (ASC-H)
• Low Grade Squamous Intraepithelial lesion (LSIL)
• High Grade Squamous Intraepithelial lesion (HSIL)
• Squamous Cell Carcinoma

• Glandular Cell
• Atypical Glandular cells (AG)
– Undetermined Significance (AG-US)
– Favors Neoplasm
• Adenocarinoma In Situ (AIS)
• Adenocarcinoma
Causes of false positive cervical
smears
Management according to Papsmear results
• Repeat papsmear in 6months :
– LSIL
– HPV
– ASCUS

• Colposcopy
– Abnormal PAP smear
– Persistent ASC-US
– AGUS
– ASC-US + high risk HPV (16,18)
– Persistent LSIL
– HSIL( CIN1/ CIN2)
 Diagnosis
• Counsel the patient on the results of the papsmear and the
need for colposcopy .
• Precise diagnosis of a pre-malignant condition is made
histologically on cervical biopsy

COLPOSCOPY
• Colposcopy- allows the clinician to view the cervix under
magnification, with the use of acetic acid and Lugol’s iodine.
• must ensure the entire TZ is visualized (satisfactory
colposcopy). Biopsies can be taken from the most abnormal
areas.
• Therapeutic measures (eg. Large loop excision of the
transformation zone) can be done at the same time for high
grade lesions.
• If colposcopy is unavailable or unsatisfactory: cone biopsy is
done under general or local anaesthesia.
 Colposcopy
• Explain the procedure to the patient and obtain consent
• Place her in the lithotomy position
• Need a good light source and all the equipment ready including speciman
bottle and form,thigh pad and tbe connected to the graves speculum to
suck out the smoke
• Pass the graves speculum (coated speculum to prevent burning they
patient). Visualise the cervix and the TZ looking at the bloodvessels, any
discharge, obvious leisons, leukoplakia.
• Note: Leukoplakia is abnormal white patch and should be biopsied. Unable
to see through these cells and dysplastic cells may be behind them.
• Also looking for Epithelial changes (aceto white areas,hpv and glandular
involvment) and vascular changes like punctation,mosaicism and
abnormal branching
• Stain cervix with 3-5% acetic acid,this picks up the dysplastic cells as it
denatures its proteins-that area will be white. Can also use iodine-the
normal cells will take up the iodine.
• Once stained,pass Koogens speculum and look to see the extent of the
lesion,if you cant see the upper border- can do LLETZ, if you cant see the
upper border, need to do Cone biopsy
• Fig. 1. (A) and (B) Normal cervix, nulliparous patient. The opened
speculum has exposed the columnar epithelium surrounding the os
and is in the endocervical canal. Higher magnification shows the
junction between columnar and squamous epithelia. The faint
white line is the transformation zone, which is quite narrow in this
patient.
• (C) Acetowhite epithelium surrounding an area of columnar
epithelium. The border, with the surrounding squamous epithelium
is irregular.
• (D) Atypical transformation zone showing an area of punctation in
the center of the photograph and a separate island of mosaic in the
upper right corner. Note the varying size of the mosaic tiles, but
uniform size of the punctate vessels. Biopsy showed CIN 2.
• (E) Atypical transformation zone showing mosaic tiles. The border is
distinct, but irregular. Biopsy showed CIN 1.
• (F) Large acetowhite lesion showing predominantly mosaic changes.
Note the distinct border in the upper right as well as the varying
intercapillary distances and punctate vessels within the mosaic tiles
(“umbilication”). Biopsy showed CIN 3.
 Large Loop excison of the TZ ( LLETZ)
• Must tell the patient what you plan on doing
• Give local –lignocaine at 12,6,3,9 oclock with a dental
syringe.
• Choose the loop according to the size of the lesion
• Cut a piece of tissue and send in the specimen bottle
for histopathology.
• Then use a ball co-agulator to achieve haemeostasis
 Post Colposcopy
• Counsel the patient on stopping sex for
6weeks
• That there might be spotting and some
bleeding
• Come back in 1month for the results
 Cone Biopsy:
The TZ and part of the endocervical canal are excised as a cone-
shaped tissue specimen
• Unsatisfactory colposcopy
• LSIL on cytology and colposcopy unavailable
• Colposcopy directed biopsy shows a lower grade abnormality than seen on
cytology and colposcopy
• Microinvasive carcinoma on directed biopsy- C.B. to rule out more
advanced invasion in the cervix
• Suspected endocervical adenocarcinoma
• Lesion extends into endocervical canal and the furthest extent exceeds
colposcopy/LETTZ capacity
• Endocervical curettage reveals abnormal histology
• CIS
• Repeatedly abnormal cytology suggesting neoplasia but no corresponding
abnormality seen on cervix/vagina on colposcopy
• Cervix too short for LETTZ
• To preserve fertility in a patient with stage 1a1 carcinoma of the cervix
 HISTOLOGICAL CLASSIFICATION
cervical intraepithelial neoplasia (CIN)
• Potentially cancerous precursor lesions found on the uterine cervix
are referred to as cervical intraepithelial neoplasia (CIN).
• CIN 1: Dysplastic cells are present in the lower third of the cervical
epithelium
• CIN 2: Dysplastic cells are present in the lower two-thirds.
• CIN 3: Dysplastic cells are found in the full thickness of the
epithelium.
Ø LSIL equivalent to histological diagnosis CIN1 and or HPV
Ø HGSIL equivalent to histological diagnosis CIN 2 and 3

• Most lesions either persist or progress to more severe grades. It is

unlikely that CIN lesions will regress.
• HPV lesions can regress spontaneously or persist. 50% of such lesions
will progress to CIN.
 Management
• ASC and low grade SIL can be followed up with a
repeat smear 3 to 9 months later.
Persistent low grade SIL for more than 1 year needs
to be treated.
• High grade SIL , CIN2 & CIN3- best option is local
destructive therapy.
• Large loop excision of the transformation zone
(LLETZ) is the standard of care for precancerous
lesions. It is quick, safe & removes the TZ, allows
for healing and has a success rate of >95 % in
immunocompetent patients.
• CO2 laser is an alternative- costly and difficult to perform.
• LSIL cryotherapy can be done.
• Definitive treatment -Vaginal or total abdominal
hysterectomy can be performed for CIN 2 and 3. (Patients
who have completed their families, other gynaecological
pathology such as fibroids or abnormal uterine bleeding,
and for patients in whom follow up will be problematic.)
• Following LLETZ follow up with cytology and colposcopy
after 4- 6months. Thereafter, annual pap smears. Vault
smears should be taken annually if a hysterectomy was
performed.

** follow up is important because treated patients are still at

high risk for recurrent CIN lesions. Hysterectomised
patients may develop vaginal intraepithelial neoplasia
INVASIVE CARCINOMA OF
CERVIX
 SQUAMOUS CARCINOMA
• New cases frequently diagnosed despite
screening for pecursor phase with cytology
• Western world- diagnosis made in early
stages- improved prognosis
• Third world- late presentation- poor
prognosis- pattern seen in South Africa
 CLINICAL PRESENTATION:
-History
} Mean age at diagnosis- 50 years, patients < 30
not infrequent
} Triad of: postcoital bleeding, profuse offensive
watery discharge, lower abdominal pain
} Early lesions may be asymptomatic
• Advanced ®
v backache, leg pain, leg oedema, haematuria,
alteration in bowel habit, general malaise, weight
loss, anaemia
 Examination:
• General: vital signs for haemodynamic stability,
pallor, jaundice, lymphadenopathy
• CNS: exclude brain metastasis
• Chest: exclude lung metastases
• CVS: important due to blood loss
• Abdomen: hepatosplenomegaly, ascites
• Pelvic examination: mass
• Speculum: lesion on cervix
• PV: lesion and size, extension to vaginal wall &
amount of vagina involved
• PR: parametrial involvement, rectal involvement
 Examination:
} Colposcopy
} Atypical blood vessels, irregular surface contour,,loss of surface epithelium, colour tone
changes

} Exophytic lesion = commonest

} Usually on the ectocervix – often produces a large friable polypoid mass which bleeds easily
} Also arises from within the endocervical canal ® canal becomes distended and “barrel-
shaped”

} Infiltrating tumour
} Shows little ulceration or exophytic growth but tends to produce hard indurated cervix

} Ulcerative Tumour
} Erodes part of the cervix and vaginal vault
} Produces a crater with local infection and seropurulent discharge

In older patients may grow occult in endocervical canal

 Differential diagnosis
• MALIGNANT: primary cervical malignancy or
metastases

• BENIGN:
– Infective: TB, amoebiasis, schistosomiasis, HPV
related condyloma
– Non infective: polyps, fibroids (cervical or
prolapsed uterine)
 Investigations:
• Haematological:
– Full blood count
– Urea and electrolytes
– Liver function test
– HIV & CD4
– RPR

• Imaging:
– Ultrasound abdomen (hsm, ascites, lymphadenopathy, hydroureter,
hydronephrosis)
– Chest X ray
– Cystoscopy- from stage II

• Other:
– GFR (chemotherapy), ascitic tap, FNAC lymph nodes where indicated
 DIAGNOSIS AND STAGING
• Histological diagnosis- usually from
colposcopy and directed biopsy/LLETZ, cone
biopsy, punch biopsy
• Staging is done according to FIGO, and is a
clinical staging, which directs treatment and
suggests prognosis.
• Investigations may be used to plan therapy for
individual patients.
FIGO Staging of Cervical Cancer

Stage Invasion Management: Management:

Radical Fertility sparing

IA1 Confined to the cervix. Simple hysterectomy Cone biopsy

Diagnosed only by
microscope. Depth of
Invasion £ 3mm and width £
7mm (includes early stromal
invasion of upto 1mm)
IA2 Confined to the cervix. Radical hysterectomy and Radical trachelectomy and lymph
Diagnosed only by pelvic lymph node node dissection
microscope. Depth of dissection
invasion 3.1-5mm and width
£ 7mm
IB1 Tumour confined to cervix Radical hysterectomy and Radical trachelectomy and lymph
and diameter less than 4cm pelvic lymph node node dissection
dissection

IB2 Tumour confined to cervix Radical hysterectomy and

and diameter more than pelvic lymph node
4cm dissection
Stage Invasion Management - radical

IIA1 Upper two-thirds of vagina without Radical hysterectomy and pelvic

parametrial invasion, <4cm lymph node dissection

IIA2 > 4cm in dimension Radiotherapy + chemotherapy

IIB Upper two-thirds of vagina plus Radiotherapy + chemotherapy

parametrial disease

IIIA Lower third of vagina Radiotherapy + chemotherapy

IIIB Pelvic side wall and / or Radiotherapy + chemotherapy

hydronephrosis

IVA Bladder/ rectum Palliative radiotherapy

IVB Beyond pelvis, distant organs Palliative radiotherapy

 Different types of procedures
Total hysterectomy :Includes the removal of the entire uterus, including the fundus
(the part of the uterus above the openings of the fallopian tubes) and the cervix,
but not the ovaries. This is the most common type of hysterectomy.
• Hysterectomy with bilateral oophorectomy :Includes the removal of one or both
ovaries, and sometimes the fallopian tubes, along with the uterus.
• Radical hysterectomy:Includes the removal of the uterus, cervix, the top portion
of the vagina, most of the tissue that surrounds the cervix in the pelvic cavity,
and may include the removal of the pelvic lymph nodes.
• Supracervical hysterectomy (partial or subtotal hysterectomy). Removal of the
body of the uterus while leaving the cervix intact.
• Abdominal hysterectomy. The uterus is removed through the abdomen via a
surgical incision .
• Vaginal hysterectomy. The uterus is removed through the vaginal opening. This
procedure is most often used in cases of uterine prolapse, or when vaginal
repairs are necessary for related conditions. No external incision is made, which
means there is no visible scarring.
• Laparoscope-assisted vaginal hysterectomy (LAVH).
Vaginal hysterectomy is performed with the aid of a
laparoscope, a thin, flexible tube containing a video
camera. Thin tubes are inserted through tiny
incisions in the abdomen near the navel. The uterus
is then removed in sections through the laparoscope
tube or through the vagina.

• Trachelectomy : removal of the cervix. Can be simple

or radical.
• Simple:specific type of biopsy
• Radical: total removal of cervix and adjacent tissue.
 PATTERNS OF SPREAD
• DIRECT- uterine corpus, vagina, parametria, uterine
ligaments, bladder & rectum (muscle, then mucosa)

• LYMPHATIC-
– Primary- external and internal iliac, obturator, presacral
– Secondary- common iliac, para-aortic

• HAEMATOGENOUS- lungs, bone and brain

• INTRAPERITONEAL- in advanced carcinoma

 MANAGEMENT:
• Counselling

• Acute: manage bleeding and optimise haemodynamic status

• All patients receive symptomatic treatment for ca cervix

– Haematinics: FeSO4
– Antibiotics: Flagyl 400mg daily, Bactrim 2 tablets daily
– Betadine douche
– Analgesia according to pain ladder: paracod/NSAIDS → tramadol → morphine
– Tranexamic acid 1g tds → qid

• Definitive rx depends on stage, performance status of pt and surgical/anaesthetic

fitness
 MANAGEMENT:
} Treat primary lesion and potential first sites of spread

} Available treatments:

} Surgery- stage 1 and II a- advantages of removal of primary

lesion, tissue available for histopathological analysis, lower
incidence sexual dysfunction and chronic bowel and bladder
problems vs radiotherapy

} Radiotherapy- external beam or brachytherapy

} Chemotherapy- platinum based

• TERMINAL CARE
– Input of clinician, nurse, social worker, spiritual
leaders
– Reassure patient of concern and that comfort can
be offered
– Conult and support relatives
– Care at home or hospice
– Pain relief NB- morphine
 ADENOCARCINOMA OF THE CERVIX
} Incidence is 18% of all invasive carcinomas
} Less favourable prognosis at all stages
} Most likely due to endophytic growth pattern- large
barrel shaped cervix
} Lesion within endocervical canal- may lead to delayed
dignosis, when there is already a large tumour volume.
} Management follows same criteria as squamous
} Stage 1- radical surgery preferred
} Stage II-postradiation hysterectomy to ↓ recurrence
} Adenosquamous carcinoma is usually high in the
endicervical canal and may have a poorer prognosis
than either adeno or squamous carcinoma
 All patients receive the ffg:

• Haematinics FESO4 200mg BD-TDs

• Antibiotics:Flagyl 400mg dly and Bactrim 2 tabs daily
• Betadine douche
• Analgesia according to pain ladder:Paracord/NSAIDs-Tramadol-Morphine-Tranexamic acid
1g TDs QID

400
 Ca in preganancy

Preinvasive neoplasia

• All pregnant patients without prior normal cervical cytology should have a smear taken at first antenatal visit
• Abnormal smears-refer for colposcopy and directed biopsy-CIN 1&/HPV=follow –up postponed tillpuerperium
• CIN 2/3 reassess at the start of 3rd trimester with cytology and biopsy to exclude invasive carcinoma
• Definitive treatment to be performed 6-12 wks postpartum

Invasive carcinoma

• 1:2000 cases
• Diagnosis by wedge or punch biopsy
• Positive but no visible lesion –cone biopsy can be done
• Management
• Stage 1a-allow progress until fetal amturity is achived,allow NVD and 6 wks postpartum simple hysterectomy/
for C/S caesarean hysterectomy
• Stage 1a2-1b-non viable fetus=radical hysterectomy and pelvic node dissection
• Viable matured fetus=C/S followed by radical hysterectomy and pelvic node dissection
• Via ble immature fetus-administer corticosteroids and delivery-chemoradiation therapy
• Counsel and support patient at all times

401
 Special Problems
Cancer of the cervical stump

Invasive Ca found at the time of simple hysterectomy

PID

Coexistent pelvic mass

Pyometra

Acute haemorrhage

Recurrences

Terminal care

402
 Prevention
HPV Vaccination

Single partner

Protection during intercourse

ARV’s

Stop smoking
403
Ca Endometrium

404
ENDOMETRIAL
CARCINOMA
405
 AETIOLOGY
• Physiological and histological changes in the
endometrium during the menstrual cycle occur due to
ovarian sex hormones
• Oestrogen stimulates endometrial proliferation
resulting in a proliferative phase of the endometrium
• Progesterone stimulates secretory changes in the
endometrium subsequent to ovulation
• Unopposed oestrogen (endogenous / exogenous) leads
to continued stimulation and proliferation of the
endometrium with the eventual development of
carcinoma

406
 RISK FACTORS
1) Obesity:
- ↑peripheral fat conversion of androgens to oestrogens &
concomitant anovulation predisposes them to further oestrogen
production.
2) Parity
- Infertility d/t anovulation ↑’s exposure time to unopposed
oestrogens. Therefore nulliparous infertile females are at a
greater risk
3) Family history
- Positive hx of ca endometrium found in 15% of cases
- Genetic predisposition to development of (nonpolyposis) colon
cancer, pancreatic, ovarian, breast & uterine ca occurs in an AD
condition – Lynch Type II Syndrome

407
 RISK FACTORS CONT.
4) Delayed menopause
– 4 fold ­ in females who menstruate age > 52
(compared to those at 49)
5) Exogenous oestrogen
– Unopposed oestrogen ↑’s risk of ca endometrium
– Postmenopausal oestrogen hormone replacement in
women with intact uterus must thus be opposed with
progesterone for a minimum of 11 days out of every 28
day cycle.
– Tamoxifen (Rx breast cancer) ↑’s ca endometrium risk.
– Use of oral contraceptives has a protective effect(d/t
progesterone component of pill)

408
 RISK FACTORS CONT.
6) Endogenous oestrogen
– Women with PCOS are anovulatory, thus ↑’d risk
of ca endometrium
– Ovarian granulosa cells assoc with endometrial
hyperplasia & carcinoma d/t their oestrogen
producing effect

7) Medical disorders
– Previous pelvic irradiation, HPT, DM risk of ca
endometrium

409
 PATHOLOGY
• Normal menstrual cycle: proliferative phase
(oestrogen) followed by secretory phase
(progesterone)
• A state of hyper-oestrogenism leads to
hyperplasia and cellular atypia within the
endometrium
• These changes have a definitive relationship to
the eventual development of carcinoma
• 15% of endometrial ca, tumour occurs without
evidence of hyperplasia and hyperoestrogenism
410
 HISTOLOGICAL CLASSIFICATION
• Adenocarcinoma
– Most common cell type of endometrial Ca (60-
80%)
– Degree of differentiation is defined by % of solid
growth patterns occurring in the tumour
– d/t oestrogenic aetiology, various degrees of
hyperplasia occur concomitant with the carcinoma
– Carcinomatous invasion of the myometrium
correlates with LN mets

411
 HISTOLOGICAL CLASSIFICATION
• Adenocarcinoma with squamous metaplasia
– Simultaneous occurrence of areas of squamous
metaplasia in endometrial adenocarcinoma
– Prognosis defined by degree of differentiation of
adenomatous part

• Adenosquamous carcinoma
– Presence of malignant glandular and squamous
elements in the tumour

412
 HISTOLOGICAL CLASSIFICATION
• Clear cell carcinoma
– Arises from the Mullerian structure
– Most frequently seen in elderly patients

• Uterine papillary serous adenocarcinoma

– Malignant condition
– Deep myometrial invasion and spread to ovaries
and omentum at the time of diagnosis

413
 PATTERNS OF SPREAD
• Direct invasion
– Direct myometrial invasion by ca provides access to
venous & lymphatic channels resulting in lymphatic &
haematogenous dissemination of
– tumour
– Advanced dx – continuous spread to ovaries, fallopian
tube and pelvic viscera
• Haematogenous Spread
– Late phenomenon
– Predilection for lungs, liver, bone, brain(rare)

414
 PATTERNS OF SPREAD
• Lymphatic Spread
– Lymphatic drainage of the uterus is a complex system,
draining to the pelvic (obturator, external iliac &
common iliac groups) & para-aortic LN’s
– Primary site of the tumour usually determines
anatomical drainage site of tumour
– Fundal tumours- para-aortic LN’s
– Cervical tumours – pelvic LN’s
– Retrograde LN spread may result in spread to vagina
with tumour deposits
– Occasional groin node involvement d/t spread via
round ligament

415
 CLINICAL PRESENTATION
• Postmenopausal bleeding
– Any postmenopausal bleeding should be regarded as
malignant until proven otherwise
• Vaginal discharge
– Purulent discharge d/t secondary infection of tumour
– Pyometra
• Pain
– Late sign, usually d/y metastatic spread
• Signs of risk factors
– Obesity, HPT, vaginal lesions, vaginal atrophy
– Pelvirectal exam N.B – rule out parametrial invasion, barrel
shaped cervix = possible cervical invasion, thus formal
conisation of cervix done.
416
 FIGO STAGING
• Stage 1a : Tumour limited to endometrium
• Stage 1b : Invasion to <1/2 of the myometrium
• Stage 1c : Invasion equal to >1/2 the myometrium

• Stage 2a : Endocervical glandular involvement only

• Stage 2b : Cervical stromal invasion

• Stage 3a : Tumour invades the serosa of the corpus uteri and/or

positive abd lavage cytological findings
• Stage 3b : Vaginal mets
• Stage 3c : mets to the pelvis and/or para-aortic LN’s

• Stage4a : tumour invasion of the bladder and/or bowel mucosa

• Stage 4b : distant mets, including intra-abd mets and/or inguinal
LN’s

417
418
 INVESTIGATIONS & DIAGNOSIS
• Cervical cytology
- can’t be used in suspected endometrial
adenocarcinoma either as screening or
diagnostic method
- Combination of endo+ectocervical cytology or
VCE smear (vagina,cervix,ectocervix) has poor
results with proven ca endometrium
• U/S
– Transvaginal U/S – primary assessment for pt
presenting postmenopausal bleeding 419
 INVESTIGATIONS & DIAGNOSIS
• Outpt endometrial sampling
– Technique involves transcervical intro of a cannula
with vacuum aspiration of endometrial tissue using
endorette/accurette
• Hysteroscopy and D&C
– Directed biopsy of suspicious endometrial pathology
• Hysteroscopy and D&C under GA
– Indicated if cervical stenosis, poor pt co-op, severe
med conditions eg. HT, DM

420
 TREATMENT
• Surgery
– Primary sx – initial Rx of choice in all cases of histologically
confirmed endometrial Ca
– Aim of Sx: adeq stage dx, debulk dx, in selective cases
palliative role.
– Sx involves aTAH, BSO & peritoneal lavage as initial
procedures
– Advanced cases involves a radical hysterectomy and pelvic
node resection OR omentectomy and debulking may also be
indicated
– Extreme obesity/medical disorders: vaginal hysterectomy +
oophorectomy procedure of choice.
– Laparoscopic hysterectomy, BSO, L/N dissection = acceptable
alternatives to laparotomy

421
 TREATMENT
• Radiation therapy
– Post-op (adjuvant) OR palliative in advanced dx
• Chemotherapy
– Hormonal – well differentiated tumours treated
with high doses progesterone (s/e: fluid retention,
labile emotions)
– Chemotherapeutic agents – adariamycin &
epiadariamycin. (cardiotoxic agents, thus use in
hypertensive diabetics with ca endometrium
questionable)

422
 FOLLOW UP

• Detect dx recurrence – palliation

• Therapy related complications

– Pelvic irradiation causes bowel and bladder
complications – diarrhoea and dysuria

423
UTERINE SARCOMAS

424
• Rare malignancy
• Occurs in the soft tx components of the corpus

• Aetiology: previous pelvic radiotherapy is assoc with the dev of

uterine sarcomas

• Classified according to histopathological cell type

• Most common sarcomas : leiomyosarcoma, MMMT,
endometrial stromal sarcomas (ESS)

• Clinical Features: lower abd mass, postmenopausal bleeding/

abN menstruation
• Peak incidence between 45-55 yrs

• Diagnosis by histology
• Rx – sx with adjuvant radio- and chemotherapy
• Poor prognosis
425
Ovarian Cancer

426
 Classification
• Ovarian neoplasms are classified according to tissue
of origin:

– Epithelial
– Stromal
– Germ cell
Benign: Teratoma
Malignant: Dysgerminoma
– Metastatic
427
 Risk Factors
• Reproductive factors:
q Low parity
q Long ovulatory age
q Use of oral contraception and multiparity are considered protective

§ Genetic factors
q Family history of ovarian cancer
q BRCA 1 and BRCA 2
q Lynch II Syndrome
q History of breast cancer
§ Previous hormone therapy
q Fertility drugs

428
 Hx:

• Irregular menses (premenopausal Px)

• Pelvis mass
• Gynae sxs-urinary frequency
• Lower abdominal discomfort/bloating
• RS sxs:-SOB due to pleual effusion
• GI sxs:- constipation, indigestion

429
 O/E
Ò Clinically ill-looking and wasted
Ò Vitals: Stable or shock (tachycardia, hypotension,
hypothermia), tachypnoea.
Ò General exam: Pallor, inguinal lymph enlargement,
oedema, jaundice
Ò Gynae:
-Abdomen:-mass (solid, fixed and irregular)
:-ascites or a nodular cul-de-sac
- speculum-might be normal
-PV exam-might be normal
-Bimanual-adnexal tenderness
Ò RS: Pleural effusion

430
 Possible Malignancy
• If suspect Ca Ovary- bld taken for βHCG & CA 125
Levels
• If pt young and germ cell tumour suspected-LDH and
AFP measured.
• All suspected malignancy
• Haem&Biochem Assessment
• Chest X-ray

• CT/MRI/Laparotomy

431
 Ix:
• Bloods-FBC/U&E/LFT/RPR/HIV (CD4 count); Anaemic:
type and screen
• Tumour markers: Assist in the diagnosis of specific
tumours
– Ca125( cancer antigen 125): Epithelial tumours
– Alpha fetoprotein: Embryonal carcinoma and germ cell
tumours.
– HCG: Choriocarcinoma and germ cell tumours
• U/S-pelvic (solid or cystic mass) and abdomen (ascitic
fluid, liver, kidneys)
• CXR-metastatic lesions in the lung
• Colonoscopy/barium enema: if hx indicates GIT
involvement. 432
U/S Criteria to differentiate Benign ovarian
cyst and Malignancy
Benign Ovarian Cyst Malignancy

Unilocularity Multilocular cysts

Clear contents Solid or cystic/solid
mass
Thin cyst walls Thick cyst wall
Smooth cyst wall Papillary growth
Size<8cm in diameter Size>8cm
Unilaterality Bilaterality
No ascitic fluid present Ascitic fluid present
433
 The FIGO Staging System
Stage Description
I Growth limited to ovaries
Ia Growth limited to 1 ovary; neither
ascites nor washings contain malignant
cells. Intact ovarian capsule with no
surface disease
Ib Growth limited to both ovaries; neither
ascites nor washings contain malignant
cells. Intact ovarian capsule with no
surface disease
Ic Tumour of either stage Ia or Ib but with
a ruptured capsule, surface involvement
or malignant cells in the ascites or
washings

434
 The FIGO Staging System
Stage Description
II Growth involving 1 or both ovaries with
pelvic extension
IIa Extension and/or metastases to the
uterus or fallopian tubes
IIb Extension to other pelvic tumours
IIIc Tumour of either stage IIa or IIb but with
a ruptured capsule, surface involvement
or malignant cells in the ascites or
washings

435
 The FIGO Staging System
Stage Description
III Tumour involving 1 or both ovaries with
histologically confirmed peritoneal implants
outside the pelvis and/or retroperitoneal or
inguinal nodes. Superficial liver metastases
equals stage III
IIIa Tumour grossly limited to the pelvis with
negative nodes but with histologically
confirmed microscopic seeding of abdominal
peritoneal surfaces (e.g. Omentum, small
bowel, mysentry)
IIIb Tumour involving 1 r both ovaries with
histologically confirmed peritoneal implants
outside the pelvis, none exceeding 2cm in
diameter; negative nodes
IIIc Peritoneal metastases outside the pelvis >
2cm in diameter and positive retroperitoneal
or inguinal nodes 436
 The FIGO Staging System
Stage Description
IV Growth involving 1 or both ovaries with
distant metastases. If pleural effusion is
present there must be positive cytology
to allot a case to stage IV. Parenchymal
liver metastases equals stage IV.

437
 Mx:

• Staging: Laparotomy
• Stage <1b surgical resection
• Stages 2-4 chemotherapy

438
 Managment
• Surgical staging laparotomy
qMidline incision to allow for full examination of the
entire peritoneal cavity
qAny free fluid is collected for cytological
examination. If there is no free fluid then a
washing of the pelvis, paracolic gutters and lower
surface of diaphragm is performed
qIf a distinct tumour is present it must be removed
intact

439
 Management
• Surgical staging continued...
qThe definitive operation for ovarian ca is a TAH and a
bilateral salpingo-oopherectomy with infracolic
omentectomy and resection of visible intraperitoneal
metastases
qThe exception to this is a young patient with unilateral
epithelial tumours in whom future fertility is desired-a
unilateral salpingo-oopherectomy, omentectomy and
intraperitoneal staging can be performed
qConservative management can also be applied to germ
cell and stromal tumours
qBiopsies are also taken
440
 Gross Characterisitics of Ovarian
Tumours
• Benign • Malignant
– Usually unilateral – Frequently bilateral
– Mobile – Fixed
– Cystic and thin walled – Solid
– Unilocular – Multilocular
– Smooth surface – Surface papillary
– Intact capsule growths
– Normal blood vessels – Capsule ruptured
– Increased vasculartiy
– Ascites
– Peritoneal seeding

441
 Management
• Surgical debulking
qUsed for fixed tumours with multiple adhesions
qAll the bulky tumour should be resected if possible
qAim is to not leave behind any tumour or nodule of >
1. 5cm therefore improving the prognosis

442
 Management
• Subsequent Management
• Stage Ia and Ib with well-differentiated
tumours
qSurgical resection

• Stage Ia, Ib (poorly differentiated tumours)

and Ic
qChemotherapy-given for a limited number of cycles
and frequently with a single agent

443
 Managment
• Subsequent Management continued...
• Stage II, III and IV
qChemotherapy for 6-8 cycles over a period of 6-8
months
qDuring chemotherapy the patient is monitored
clinically and with U/S or CT
qSerial CA 125 levels should be monitored. If
increasing could suggest recurrence

444
 Management
• Interval cytoreduction
qPatients with large, fixed tumours thought to be
inoperable
qPlatinum-based chemotherapy is used as first-line
treatment for 3 courses
qCytoreductive therapy is then performed
q3 more courses of chemotherapy are given

445
 PCOS

oCommon hormonal disorder among women of

reproductive age. The women have enlarged
ovaries containing numerous small cysts located
along the periphery of each ovary.

o1st described by Irving Stein and Michael

Leventhal as a triad of amenorrhea, obesity and
hirsutism (1935)
446
• NIH-Sponsored Conference on PCOS (1990 Criteria)
Diagnosis of PCOS-chronic anovulation with biochemical evidence of
hyperandrogenism. Ovarian morphology on sonar not included in this criteria

• Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group (2003

Criteria)
•Two of the following symptoms required for diagnosis:
–Polycystic ovaries (PCO)
–Hyperandrogenism (clinical/biochemical)
–Anovulation (menstrual irregularities)
ØNo single criteria is sufficient for clinical diagnosis

447
 Pathogenesis:
• Remains unclear
• Complex Genetic Disorder(familial basis)
• Ovarian Genetic Trait that interacts with other
congenital or cellular environment factors
(obesity, exposure to excess androgens in
childhood).
• Chronically elevated LH(unknown genetic
cause or result of ovarian dysfunction),
hyperandrogenism and insulin resistance.
448
 Pathophysiology:
• The pathophysiology of PCOS, although still
not entirely clear, is mainly due to the
hormone imbalance caused by both
hyperandrogenism and hyperinsulinemia,
which are also effects of PCOS.

449
Pathophysiological role of hyperandrogenism and the insulin resistance-
hyperinsulinemic state in determining the PCOS phenotype

450
 Clinical presentation
Symptoms: Signs:
• Menstrual irregularity • Hirsutism, acne, alopecia
• Infertility • Obesity
• Hirsutism, acne, alopecia • Ovarian enlargement
• Obesity • Acanthosis nigricans

451
 Menstrual irregularities
• Caused by anovulation , which is defined
by a history of eight or fewer menstrual
cycles in a year, that are shorter than 26
days or longer than 35 days. Women with
PCOS typically have cycles lasting longer
than 35 days.
• Chronic anovulation can lead to
endometrial carcinoma due to unopposed
estrogen.

452
 Metabolic problems
• Higher prevalence of metabolic problems
associated with PCOS. Women will experience
obesity, an increased risk of
hyperinsulinaemia, impaired glucose tolerance
and diabetes.

453
 Clinical hyperandrogenism:
• Hirsutism
• Acne
• Seborrhea
• Male-pattern Balding
• Increased Muscle Mass
• Deepening Voice
• Clitoromegaly

454
 Differential diagnosis of PCOS:
• Congenital Adrenal Hyperplasia
• Androgen-Secreting Ovarian or Adrenal Tumors
• Idiopathic Hyperandrogenism
• Idiopathic Hirsutism
• Syndromes of Severe Insulin Resistance
• Hyperprolactinomia
• Thyroid Abnormalities
• Cushing’s Syndrome
• Androgenic Anabolic Steroid Usage
• Other Medications Usage :Danazol,
Phenothiazines, Corticotropin or ACTH analogues,
?Valproate

455
 Diagnosis
1. Ultrasonography

The transabdominal ultrasound is used to detect

the poly cystic ovary
Sonographic features
presence of multiple cysts, 2-18mm in
diameter, all distributed evenly around the
ovary, with an increased ovarian stroma(10
cubic centimetres).

456
457
 2. Biochemical/Lab:
• One may see the following:
– Increased free testosterone/N testosterone, increased
androstenedione
– Increased LH, normal FH; Inc. LH/FSH
– Increased estradiol, estrone
– hyperinsulinaemia
– Decreased SHBG
– Mildly elevated prolactin

458
2. Biochemical diagnosis
insulin resistance

459
• Insulin resistance is a subnormal biological
response to a given level of insulin
• Increased androgen production suppress the sex
hormone binding globulin(SHBG), thereby further
increasing the bioavailability of free testosterone
• Homeostatic measurements of fasting glucose or
insulin ratios such as the homeostatic model
assessment(HOMA) are used to test for the
insulin resistance
460
 3.Endocrine diagnosis
• An increased mean concentration of
luteinizing hormone- androgen production by
the ovarian theca cells is LH dependent, so the
excess androgen production is subsequent to
elevated LH levels
• FSH levels also are monitored
• Testosterone , serum levels of testesterone
and SHBG are monitored

461
 PCOS IN ADOLESCENCE
• “Polycystic ovarian syndrome is the most common
endocrinopathy in adult women, and is emerging as a common
cause of menstrual disturbances in the adolescent population”
• Most of adolescents with menstrual irregularity or persistent
acne will have PCOS, particularly if associated with a raised
BMI.

462
 Management of PCOS in young
women
• Weight loss
• Combined oral contraceptive + anti-
androgenic
• Insulin sensitizer (metformin)

463
PCOS and anovulatory infertility

• Women with PCOS have an increased

World Health Organisation (WHO)
group 2 anovulatory infertility.
• Increased serum levels of androgens
and impaired folliculogenesis
associated with PCOS lead to
anovulatory infertility

464
 Management
methods to induce ovulation
1. weight loss
• Frequency of obesity in women with anovulation
and PCO: 30%-75%

• Weight loss benefits to women with PCOS

– Decreased fasting insulin and testosterone
levels
– resumed ovulation
– 85% can become pregnant

465
 Anti estrogen treatment
• First line method for inducing ovulation in WHO
group 2 anovulatory infertility is Clomiphen
Citrate:Stimulates the release of hormones
needed for ovulation.

• Clomiphene and dexamethasone

Supress adrenal androgen secretion

• Insulin sensitisers
-Metformin
-Thiazolidinediones

466
 Other treatment options:
• Gonadotropin therapy: 2nd line, if not
responding to anti-oestrgens.
• Laparoscopic ovarian diathermy:if not
responsive to clomiphene citrate, can be
offered as 2nd line.

467
Endometriosis

468
DEFINITION
• Is the presence of tissue, histologically similar to
endometrium, at the site outside uterine cavity
• A definite histological diagnosis requires two of
the following features: endometrial glands,
stroma and haemosiderin pigment
• G- Glands (endometrium)
• P- Pigment (Haemosiderin)
• S- Stroma

469
 Aetiology
• Mechanism by which endometriosis occur is unknown
• Many theories exist
1. Transplantation of shed endometrium
• Sampson proposed that the menstrual effluent contained viable stromal and
glandular endometrial cells that could be transplanted to ectopic sites
• He concluded that endometrial cells regurgitate through the fallopian tube at
the time of of mentruatiom

2. Halbans theory
• spread of endometrial tissue outside the uterus by lymphatic drainage
• Micro. Deposits of endometrial tisuue have been found lymphatic channels, LN,
and umbilicus
3. Coelomic metaplasia
• Postulate that repeated irritation of the mesothilium is ass. With variety of
factorssuch as hormonal or infectious stimuli, can induce the pluripotentia
coelomic cells to transform into endometrial tissue

470
 Other factors contributing to the
development of endometriosis
GRIMC
• Familial and genetic factors- multi fact. mode
of inheritance and occurs in 1st degree
relatives
• Race –rare in blacks
• Menstrual factors
• Delayed child bearing
• Immunological factors ass. With incr. in anti
nuclear ab’s, lupus anticoagulant, IgG & IgM
471
 Clinical presentation
• Dysmenorrhoea
• Pelvic pain
• Infertility
• Dyspareunia
• Menstrual irregularities
• Cyclic dysuria/haematuria
• Dyschesia
• Rectal bleeding
• M- Menstrual abn, Dysmenorrhea
• I- Infertility
• B- Bleeding –rectal
• P- Pain- Dyspareunia, pelvic pain, cyclic dysuria /haematuria

472
 Diagnosis (BLAU)
• Bimanual exam

1. Tender uterosacral ligaments

2. Cobblestone/”shotty” feel in Pouch Of Douglas
3. Tender nodules
4. Thickened retro vaginal septum
5. Enlarged tender ovaries
6. Generalised or localised pelvic tenderness
T- tenderness
N- nodules
C- cobblestone
S- septum (thick retrovaginal septum)
O- ovaries enlargened and tender

473
 Diagnosis
• Laparoscopy with biopsy
1. Typical or atypical lesion
• Ovarian tumour ass. Antigen (CA 125)
1. Because of overlapping range in ovarian cancer and
endometriosis, this test cannot be used clinically to
differentiate the two
• U/S
1. Not diagnostic may only give additional and
confirmatory info.

474
 CLINICAL APPEARANCE

Refer to text book From the history, clinical exam

and laparoscopic exam, three differrent forms
of pelvic endometriosis can be recognised:
• Peritoneal(1)- red à2 blackàwhite
• Ovarian (superficial and intraovarian)
• Endometriosis of the rectovaginal septum
(similar to uterine adenomyosis)

475
 Classification
View table in text book
• AMERICAN SOCIETY FOR REPRODUCTIVE MEDICINE
1. It is based on the natural progression of the
disease, with considerations made for unilateral or
bilateral involvement, differentiation between
superficial and invasive (deep) endometriosis of
the peritoneum or ovaries, and stratification for
severity as minimal (stage I), mild (stage II),
moderate (stage III), or severe (stage IV), as well as
quantification of tubo-ovarian adhesions

476
• Management depends on
• FADE P2
• F- fertility requirement
• A- age
• D- duration
• E- extent
• P- pain
• P- primary or recurrent

477
 management
• Medical
1. Danazol
Derivative of 17-ethyl testosterone
MOA :partially supp. gonadotropin levels by ablating the midcycle LH surge but
preserving basal secretion
Long term use : androgenic side effects e.g. hirsutism and deepening of the voice
2. Gestrinone
weak progestin and androgen agonist/antagonist
MOA: acts on the hypothalamic- pituitary system to suppress midcycle surges of LH
AND FSH
Dose 1.5 mg 2 x wk x 6/12
3. Medroxyprogesterone acetate
results in amelioration of pain
Dose 30-50 mg/day
S/E break through bleeding, nausea and breast tenderness

478
 Management

Surgical treatment of endometriosis

Treatment of choice for endometriosis ass.
infertility
This can be accomplished by :
• Laparoscopy
• Laparotomy :conservative and complete

479
Chronic Pelvic pain

480
 Chronic pelvic pain
• Chronic pelvic pain is defined as intermittent or
constant pain in the lower abdomen or pelvis of
at least 6 months duration not occurring
exclusively with menstruation, intercourse or
pregnancy
• It is a symptom not a diagnosis

481
 Definition of pain
• Pain is “an unpleasant sensory and emotional experience
associated with actual or potential tissue damage”
• The experience of pain is affected by physical psychological and
social factors
• Acute pain reflects tissue damage and resolves with tissue
healing.
• Chronic pain is more complex involving changes in afferent and
efferent nerve pathways in central and peripheral systems.
Descending info from CNS shaped by previous experiences and
current circumstances modifies visceral function and pain
perception

482
 Differentials of chronic pelvic pain
GYNAE CAUSES UROLOGICAL CAUSES
— Fibroids — Interstitial cystitis
— Endometriosis — Detrussor over activity
— Adenomyosis — Chronic infection
— Adhesions — Urethral diverticulum
— Pelvic inflammatory disease MUSCULOSKELETAL
— Pelvic venous congestion — Scoliosis
GI CAUSES — Lumbar disc disorders
— Irritable bowel syndrome — Spondylolisthesis
— Diverticular disease — Osteitis pubis
— Inflammatory bowel disease OTHERS
— Constipation — Fasciitis
— Adhesions — Muscle spasm
— Nerve entrapment
— Hernia

483
 Assessment
• Many women present because they want an
explanation for their pain. Often they already have a
theory or a concern about the origin of the pain.
These ideas should be discussed in the initial
consultation

• Eliciting women’s own ideas will result in better doctor

patient relationship and improved concordance with
investigations and treatment

484
 History
• Pattern and nature of pain
• Association with menstruation
• Bladder symptoms
• Bowel symptoms
• Effect of movement and posture on pain
• Symptoms of depression/sleep disorders
• Psychological/social/sexual issues

485
 Menstrual pain
• Cardinal symptoms of dysmenorrhoea,
dyspareunia and chronic pelvic pain =
endometriosis but not always!
• Irritable bowel and pain perception worsens
with menstrual cycle!
• GENEALLY CYCLICAL PAIN IS GYNAE IN NATURE

486
 Adhesions
• Adhesions may cause pain particularly on organ
distension or stretching.
• Dense adhesions or vascular adhesions if
released cause relief of symptoms
• Adhesions may be asymptomatic
• Adhesions are caused by endometriosis,
previous surgery, PID
• Trapped ovarian syndrome is well recognised
cause of pain post TAH
487
 Urological causes
• Take bladder history-
• Frequency, haematuria, pain, incomplete
emptying,burning,stress/urge incontinence

488
 Musculoskeletal pain
• Posture based
• History or family history of arthritis
• Pain worse on leg raising

489
 Nerve entrapment
• Nerve entrapment in scar tissue, fascia, or a
narrow foramen results in pain and dysfunction
in the distribution of that nerve
• Pain described as localised, sharp, stabbing,
worse with movement- often after a
pfannenstiel incision

490
 Irritable bowel
• Symptom based diagnostic criteria can be used
with confidence to make the diagnosis of
irritable bowel with positive predictive value of
98%
• Attempt to detect presence of psycholgocial
comorbidity- ie sleep/appetite disturbance
tearfulness etc

491
 Rome II criteria for diagnosis of IBS
• At least 12 weeks of continuous or recurrent
abdominal pain with at least 2 of the following
– Pain relieved with defecation
– Associated with change in frequency of stool
– Associated with change in appearance or form of stool

– Abdominal bloating, passing mucus, also common

– Extraintestinal symptoms of lethargy, backache, urinary
frequency and dyspareunia also common

492
 Psychological and social issues
• Depression and sleep disorders are common in
women with chronic pelvic pain
• Association with current or previous sexual
abuse is well recognised
• Child sexual abuse may initiate a cascade of
events or reactions which makes an individual
more vulnerable to the development of chronic
pelvic pain as an adult

493
 examination
• General examination
• Abdominal examination
• Examination of the lumbosacral area, the external genitalia, the
vagina, the tubes and the ovaries( bimanual and rectovaginal
examination)
• Patient should be examined standing for hernias, both
abdominal and pelvic

494
 Management /investigations
• Aim for the integrated/multidisciplinary team
approach from the outset- including patient
involvement- immediate diagnostic laparoscopy
for all is unnecessary
• Multidisciplinary team includes- urologist,
physicians, physiotherapist ,psychologist,
psychosexual counselor, pain specialist.

495
 investigations
• Pap smear
• Screen for STI especially chlamydia and
gonorrhea +-HIV
• Mid stream urine- assessing for blood cells/pus
cells and culture
• Transvaginal scan- useful for assessment of
adnexal mass and effective for
endometriosis/useful for adenomyosis

496
 Diagnostic laparoscopy
• The gold standard in the diagnosis of chronic
pelvic pain
• BUT
– risks
– death rate 1/10,000
– Risks to bowel, bladder/ blood vessels of 2.4/10000
of which 2/3rds will require laparotomy

497
 Diagnostic laparoscopy
• Only test available for identifying peritoneal
endometriosis and adhesions
• BUT
• No good for IBS/adenomyosis
• 1/3rd to ½ diagnosis laps are negative and much
pathology identified is NOT the cause of the pain

498
 management
• Medical:
– oral NSAIDS: ibrufen,
– Antibiotics for infection
– Psychotropic agents fro depression
– Hormonal preparations for ovarian cycle suppression- long term
progesterone e.g. medroxyprogetsterone acetate as depot injection or
monophasic pills
• Physiotherapy- musculoskeletal problems
• Psychotherapy
• Surgery:
– Lap adhesiolysis
– Lap ablation or excision endometriosis
– Hysterectomy- only after failed conservative management

499
Genital Prolapse

500
anatomy

501
 The three layers of the pelvic floor:

• The pelvic organs are kept in place by ligaments, connective tissue

and muscles.
• They are grouped into three layers which make up the pelvic floor.
• Layer 1: uterosacral ligaments
transverse cervical ligament
condensations of endopelvic fascia
Attached to the cervix and suspend the uterus from the pelvic
sidewall and sacrum respectively.
Layer 2: endopelvic fascia
minor contribution from the levator ani
Layer 3 : levator ani muscle
perineal body
Damage occuring at these levels of vaginal support may cause
prolapse.
502
 Definition

• A prolapse is a protrusion of the uterus and/or

vagina beyond normal anatomical confines .
The bladder, urethra , rectum and bowel are
also involved.

503
 Types of prolapse.

Ø Anterior vaginal wall prolapse: urethrocoele

cystocele
Ø Apical vaginal wall prolapse : vault prolapse
uterine prolapse
Ø Posterior vaginal wall prolapse: enterocele
rectocele
Ø Perineal body defect: stretched out perineal body
Ø Perineal body descent: associated with enterocele
Ø Rectal prolapse : The rectum prolapses through the
anus
504
 Risk factors:
Ø Pregnancy: The placenta and ovaries secrete
relaxin which is believed to be
responsible for the contribution
of pregnancy towards prolapse.
Ø Vaginal childbirth: the most important
contributing factor.
The severe stretching of the muscles may result in:
§ Levator ani muscle trauma
§ endopelvic fascia laceration
§ Perineal body damage, resulting in a thin perineal body
( forceps delivery and prolonged second stage of labour)
Ø Hysterectomy: it will disrupt the upper layer of the pelvic floor, the
uterosacral ligament will retract, leaving a weak spot where
the cervix was and thus cause prolapse. ( enterocoele)
Ø Menopause : Pelvic organ prolapse doubles every decade of life and even more after
the age of 50. The main reason is weakening of the muscles and connective tissue in the
pelvic floor.
Ø Chronically increased intra- abdominal pressure ( coughing, constipation)
Ø Obesity: causes weakening of the pelvic muscles, the heavy bowel and omentum exerting increased pressure on
the pelvic floor and it may limit the success of surgery.
Ø Genetic factors : they deal with the quality of the endopelvic fascia: the stronger the fascia, the less the prolapse(
(black race)
Ø neuropathy: if the nerves are damaged, the muscles will be weakened .

505
 Prevention
Ø Healthy lifestyle ( it will discourage the
development of prolapse, it may not prevent it
but it may control to such a point that surgery
remains unnecessary )
Ø Good obstetrical practice
Ø Avoid unnecessary hysterectomy ( a prolapse may
be an indication for hysterectomy but if that’s not
the case then preservation of the uterus and
upper pelvic floor should be considered).
506
 Grading
1. The pelvic organ prolapse quantification(POP-Q)
2. Baden-Walker halfway system
The hymen is used as a landmark in both these systems.
The POP-Q
STAGE DESCRIPTION
0 No prolapse is demonstrated
1 Prolapse is noticed, with the most
distal portion >1 cm above the hymen
2 The most distal portion of the prolapse is
1cm or less proximal or distal to the plane of
the hymen
3 The most distal portion of the prolapse is >1cm below the
plane of the hymen(max 7 cm)
4 Complete eversion of the total length of the vagina is demonstrated (>7cm)
The baden-Walker halway system
Stage description
0 no prolapse is demonstrated
1 Descent halfway to the hymen
2 descent to the hymen
3 descent halfway past the hymen
4 maximum possible descent for each site

507
 Pathophysiology
• Pelvic organ support is maintained by the muscles and
connective tissue . Damage to any of these will cause a
prolapse.
• In a normal standing female, the upper vagina lies
horizontally creating a flap valve effect in which the
upper vagina is compressed against the levator ani
during periods of increased intra-abdominal pressure.
When the levator ani loses tone, the vagina becomes
semi-vertical. This opens the uterogenital hiatus(
opening in the levator ani through which the three
pelvic organs pass: urethra, vagina and rectum) thus
promoting prolapse.

508
 Mechanism of levator ani damage
Ø Stretch injury: happens in vaginal delivery
Ø Nerve damage(neuropraxia): when the levator ani’s
nerve supply is damaged, the muscle will lose its tone
and the hiatus genitalis ( distance from the midpoint of
the external urethral opening to the hymenal ring on
the posterior vaginal wall) will widen and prolapse will
occcur.
§ Labour and delivery may result in this damage and
chronic constipation may results in damage of the
pudendal nerve with susequent levator ani loss of
tone.
Ø Levator ani tears will also lead to prolapse.

509
 Connective tissue injury
• Endopelvic tissue damage.
• Three theories:
1. Fascial breaks
2. Paravaginal defects: if the endopelvic facia that
suspends the lateral aspects of the vagina and
bladder to the pelvic sidewall is torn, it will
jeopardise the support of these organs and lead
to prolapse.
3. Distention and displacement of organs:
cystocele

510
 Evaluation
Ø Assess Quality Of Life( physical, social and mental well
being)
§ Bladder( overactive detruser(urge), stress urinary
incontinence, frequency, nocturia, poor stream, incomplete
emptying, position change to urinate)
§ Vagina( dyspareunia, coital obstruction, sexual problems)
§ Bowel( constipation, manual assistance for defecation,
incontinence of flatus or stool)
§ General (lower abdominal pain, lower back pain, pressure
or heaviness in the pelvis, something protruding through
the introitus or anus)
Ø Physical examination
Ø Ultrasound examination
511
 Details on physical examination
1. General and abdominal examination
2. Part the labia minora with two fingers: look
obvious prolapse, severe perineal defects and
anal pathology such as haemarrhoids. Measure
the genital hiatus while the patient is pushing
down.
3. Do a pap smear, if the uterus is intact
4. Measure the total vaginal length and evaluate
the anterior compartment by pushing it down
512
 Treatment
• The aim is two-fold:
1. To relieve symptoms and improve quality of life
2. To anatomically correct the prolapse of the affected organs
Ø Can be surgical or non-surgical
Non-surgical: improvement of general well- being
physiotherapy( stage 1-3)
vaginal pessaries ( at all stages)
Surgical: can be done with or without mesh ( synthetic gauze like material fixed itno the pelvis to suspend prolapsed
organs and to restore them in their original locations)
Vaginally
Without mesh
1. Perineal body repair
2. Posterior repair
3. Anterior repair
4. Paravaginal repair
5. STAAR procedure( stapled trans-anal resection of rectocele)
with mesh
Anterior repair
Posterior repair
Sacrospinous fixation(the cervix and vaginal vault is fixed to the sacrospionous ligament with a nonabsorbale stitch.

513
 Treatment continued
Abdominally
ØWith mesh ( sacrocolpexy which is the golden standard for the repair
of severe pelvic organ prolapse. It is fixation of the vaginal vault to the
sacrum)
ØLaparoscopic

514
 Investigations
• Mid stream urine for culture and sensitivity
• Transperineal ultrasound
• Conoloscopy (mainly in patients above 50)
• Pre-operatively: FBC,U&E

515
Urinary Incontinence

516
 Definitions
§ UI: complaint of any involuntary leakage of urine
§ Stress UI: urinary incontinence on effort, or exertion,
or sneezing or coughing
§ Urge UI: urinary incontinence accompanied by or
immediately preceded by urgency
§ Detrusor overactivity: urodynamic observation
characterized by involuntary detrusor contractions,
which can lead to UUI
§ Mixed UI: urinary incontinence with urgency and also
with exertion, effort, coughing or sneezing (SUI).
§ Continuous UI: complaint of continuous leakage
§ Extra urethral incontinence: urine leakage through
channels other than the urethra. 517
518
 Physiology of Micturition
§ Filling phase:
-Bladder is relaxed, with low intravesical pressure
-Sphincter unit contracts and close the urethra
§ Voiding phase:
-Stretch receptors respond to 300-500ml of urine in the
bladder
-P∑ signals detrusor muscle to contract & internal urinary
sphincter to open (also inhibits ∑ pathways that would
prevent urination)
-Voluntary contraction of abd wall muscles increases
abdominal pressure
-Voluntary relaxation of ext urethral sphincter, urethra opens
-Complete emptying of bladder.
-Normal sensation is dependent on intact detrusor neural
function,spinal cord reflexes and cortical control and
awareness. 519
 Risk factors for UI
§ Age
-Delirium
-Infection
-Atrophic changes
-Pharmacological
-Psychological
-Excess urinary output
-Restricted mobility
-Stool impaction
520
§ Obesity – Increased intra-abdominal pressure
§ Family history
§ Childbirth- NVD is associated with pudendal
nerve injury and CT injury. Pregnancy also results
in increased intra-abdominal pressure. Assisted
or forceps delivery is also a risk factor
§ Surgery- Ureteric or bladder injuries leading to
fistulae are fortunately rare.
§ Medications – Diuretics (overactive bladder), β
blockers(inhibits bladder relaxation), alpha
blockers(decrease urethral resistance), ACE-
inhibitors (cough leading to SUI)

521
 Clinical Features
§ Stress UI
-triggered by activities associated with an
increase in intra-abdominal pressure such as
coughing, sneezing, lifting, exercise, jumping
-In severe cases, leakage occur with minimal
effort

522
 Clinical Features cont…
§ Urge UI
-sudden and severe desire to pass urine
-associated with frequency and nocturia,
-described as overactive bladder syndrome
-triggered by coughing, sneezing, and laughing,
-and therefore can imitate Stress UI

523
 Clinical Features cont…
§ Mixed UI
-women present with symptoms of both SUI and
UUI
-found in approximately 40% of women with UI

524
 Clinical Features cont…
§ Overflow incontinence
-chronic urinary retention and leakage from an over
distended bladder
-caused by hypoactive detrusor muscle or bladder
outlet obstruction
-patient presents with reduced sensation of fullness
and feeling of incomplete emptying.
-occurs when the postvoid residual volumes are
above 300ml
-patients tend to leak continuously.

525
 Clinical Features cont…
§ Urinary Fistula
-mostly in a form of vesicovaginal or
uretovaginal connection
-most common causes are injury at the time of
hysterectomy or obstructive labour
-lower genital tract malignancies can also be the
cause
-patients present with continuous leakage from
vagina.
526
 Clinical Features cont…
§ Functional Incontinence
-occurs in situation where there are certain
limitations
-secondary to physical or mental impairment

527
 Clinical Examination
§ Abdominal- a palpable bladder suggest chronic
retention if palpable after voiding
§ Pelvic- genital atrophy d/t oestrogen deficiency might
contribute to symptoms of UUI and require treatment.
Cough test to exclude SUI, pelvic floor strength and
pelvic mass must be examined
§ Rectal- constipation and anal tone
§ Neurological- perianal sensation, anal tone, lower limb
neurological examination
§ Cardiac- signs of cardiac failure and volume status
§ Sideroom- urine dipstick, urine culture

528
 Investigations
§ Postvoid measurement of the residual volume
-a residual volume of <50 ml is normal
§ The voiding diary
-objective measure of woman’s symptoms, monitor
progress of the treatment, and allows for diagnosis
of polyuria.
§ Urodynamic studies
-used to better define bladder dysfunction
-contraindicated in patients with UTI

529
 Management
§ Conservative therapy
-first line of treatment for patients who are
unfit for surgery
-includes lifestyle intervention(weight reduction,
reduction of strenuous exercise and physical
work, smoking cassation and relief of
constipation), physical therapies(pelvic floor
muscle training, intravaginal weighted cones and
electric and magnetic stimulation)

530
 Management
§ Medical therapy
-For SUI Duloxetine is used
-combined serotonin-and-noradrenalin-reuptake
inhibitor
-MoA: increases sphencteric muscle activity
during both the filling and storage phase

531
 Management
§ Surgical therapy
-minimal invasive vaginal surgery
-various types of surgery are selected for a
specific type of urinary incontinence.

532
Gestational trophoblastic disease

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 Gestational trophoblastic disease (GTD)
(GTD) comprises a spectrum of disorders of the trophoblast, ranging from
benign to malignant forms of the disease.
Classification
Ø Hydatidiform mole( HM) (benign)
-complete
-partial
Ø invasive mole (IM) (malignant)
Ø Choriocarcinoma (CC) ( malignant)
Ø Placental site trophoblastic tumour
Ø Miscllaneous trophoblastic lesions
Ø Unclassified trophoblastic lesions
Most of this conditions produce human chorionic gonadotropin (hCG)

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 RISK FACTORS
• Age: less than 20 and more than 40
• Racial
• Parity: past obs losses are associated with higher rates of GTD
• Blood group: group B
• Diet
• Smoking: increased risk in women who smoke more than 15
cig a day
• Past molar pregnancy: complete mole 20%, 2,9-9% for partial
mole

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 Pathology
• Normal placenta has trophoblasts classified according to their
location aand ytological features.
• Villous trophoblasts grows with chorionic villi
• Extravillous trophoblastic, trophoblasts that inflitrates the
decidua, myometrium and blood vessels of the placenta.
• These 3 distict types of trophoblasts are described as:
cytotrophoblast (CT), syncytrophoblast (ST) and intermediate
trophoblast (IT)

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 Hydatidiform mole( HM)

• Hydatidiform moles represent placenta with abnormal

development of the chorionic villi.
• Features of HM includes the presence of enlarged,
oedematous and vesicular villi with variable amounts of
abnormal proliferation of trophoblast.
COMPLETE MOLE
• Mole without embryo or fetus. Oedematous chorionic villi are
grouped into clusters of vesicles “bunch of grapes”
• Microscopic features include enlarged oedematous villi and
abnormal proliferation of trophoblast.
• Central cistern pattern in some of enlarged viili.

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 PARTIAL MOLE
• Macroscopic features of PM are variable and incl
placental tissue which is bulky with variable
propotions of vesicles.
• There may be fetal parts, umbilical cord or
membranes present. If a fetus is present, it ussually
has congenital and chromosomal abnormalities.
• PM has fewer enlarged villi and fewer masses of
grape like villi
• Central cistern pattern is less developed

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 INVASIVE MOLE
• CM or PM may invade into the myometrium, blood vessels, adnexae and
infrequently spread to distant sites such as the lungs.
• Diag ussually made on hysterectomy specimen but it can be detected on
u/s and colour doppler showing molar preg within the uterus invading into
uterine wall.
• Macroscopically IM appear as haemorrhagic masses of tissue. Invading the
myometrium and or adnexae
• Clinically it is difficult to distinguish IM fro choriocarcinoma since both
result in elevated hCG levels and can have lesions on distant site.
• But in IM, villi are present, in contrast to CC which has no chorionic villi.

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 Choriocarcinoma (CC)

• Gestational Choriocarcinoma represents a highly malignant tumour and

must be distinguished from non-gestational cc
• 50% of CCs are preceded by molar gestations,25% by spontaneous
abortions, 22.5% by normal preg and 2.5% by an ectopic preg.
• Metastases to the lungs, brain and liver are very common.
• Macroscopically, well-circumscribed, haemorrhagic, nodular
lesions.
• In most cases the tumour is composed of mainly blood with a
thin rim of viable tumour around the periphery.
• Microscopically, biphasic pattern with central cores of
mononuclear cytotrophoblast surrounded by rim of
multinucleated syncytiotrophoblast.
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 Clinical features
• Symptoms
-vaginal bleeding- cm present btwn the 11th and 25th week of preg.
-hyperemesis gravidarum-due to high levels of serum hCG levels.
-miscellaneous presentation-due to metastases
• Signs
-pre-eclampsia
-hyperthyroidism

• Abd xm- greater height of fundus than expected

• Pelvic xm- vaginal metastases

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 Diagnosis
• Positive urine and serum hCG levels
• Radiological features-cystic appearance of molar preg
• Ultrasound- myometrial and or adnexal invasion, theca lutein
cysts or abdominal metastasis
• CXR- metastases, pleural effusion or consolidation.
• When there is a platue of hcg lasting for 4 measurements over
a period of 3wks
• When hcg levels remain elevated for 6 months or more

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 Management
• Ressuscitation
• Invasive mole- management = chemotherapy
-low risk pt tx with single agent (methotrexate oractinomycinD)
-high risk pt-combination chemo
• Non-invasive- management = evacuation of the uterine contents by suction
curettage.
• Patient should be advised not to conceive for 12 months. contraception
• Surgery is reserved for:-removal of focus of chemoresistant
-life threatening haemorrhage
-tx of infection.
Prognosis: low risk GTD cure rate 100% with chemo, high risk 70%
Follow up; monthly hCG and clinical xm for 6 months, and thereafter every 3 month
for the next 6 months, if values are negative pt is followed up every 6-12months.

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