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Chapter 3: Gynaecology 47
https://t.me/med1917
Disorders of the vulva & vagina
Vulval symptoms
• Pruritus – dermatological disease, neoplasia, infections
• Soreness/burning
• Superficial dyspareunia
Candida
HSV
Viral warts
Syphilis
Benign disorders
LICHEN SIMPLEX CHRONIC VULVAL DERMATITIS
→ chronic inflammatory skin condition
• RFs: sensitive skin/eczema, stress
• Sx: severe pruritus (worse at night), inflamed/thickened labia
• Dx: biopsy if unsure
• Mx: emollients, moderate potency steroid creams,
antihistamines; avoid irritants
LICHEN PLANUS
→ dermatological disease commonly affecting mucosal surfaces
• RFs: ?autoimmune link
• Sx: flat papular purple lesions, pain
• Mx: high potency steroid creams
LICHEN SCLEROSUS → thinning of vulval epithelium due to collagen loss
• RFs: ?autoimmune link e.g. thyroid disease, vitiligo
• Sx: severe pruritus (worse at night), pain/dyspareunia, pink–white papules,
parchment-like skin with fissures
• Dx: biopsy to exclude carcinoma
• Mx: ultra-potent topical steroids
VULVODYNIA VULVAL PAIN
→ can be provoked/spontaneous, local/generalised
• RFs: genital tract infections, use of OCP
• Sx: burning pain (generalised), superficial dyspareunia (localised)
• Mx: amitriptyline, gabapentin
Vulva: External anterior view Vulva: Internal anteriolateral view
Superficial dyspareunia = pain on initial
penetration during intercourse
Deep dyspareunia = pain felt within the pelvis on
deep penetration during intercourse
Prepuce
Glans clitoris
Labia minora
Corpus cavernosum
Bulb of vestibule
Urethral opening
Labia majora
Vaginal opening
Opening of right
Bartholin’s gland
Anus
Fig. 3.3 Anatomy of the vulva.
Bartholin’s glands
BARTHOLIN’S GLAND CYST/ABSCESS
→ CYST: blocked duct causes mucus build-up
→ ABSCESS: infected cyst (E. coli / Staphylococcus)
• Sx: acutely painful red swelling
• Mx: incision & drainage
VAGINAL CYSTS → congenital
• Sx: smooth white lump ± superficial dyspareunia
• Mx: excision if symptomatic
VAGINAL ADENOSIS → columnar epithelium found in the normally squamous
epithelium of vagina
• RFs: mother was given DES (diethylstilboestrol) during pregnancy (1940–70)
• Mx: usually resolves spontaneously BUT can become malignant (clear cell
carcinoma)
VULVAL INTRAEPITHELIAL NEOPLASIA VIN
→ presence of atypical cells in vulval epithelium
• RFs: HPV 16, smoking, immunosuppression
• Sx: pruritus/pain, nodules/warts/papules/plaques
• Mx: emollients, mild topical steroids
Give ABX
Drainage with Word catheter or marsupialisation
(sutures to keep cyst open)
48 Chapter 3: Gynaecology
https://t.me/med1917
Conditions of the cervix
Cervical screening
Frequency of screening
25–49y = every 3y
50–65y = every 5y
>65y = only if recent abnormal smear
Risk factors for cervical cancer
• HPV 16 & 18 ( sexual contacts)
• Smoking
• Immunosuppressed/HIV
• Long-term OCP use (v. small risk)
Symptoms of cervical cancer
• bleeding between periods, after sex, after
menopause
• change in vaginal discharge
AIMS
1. Reduce incidence of cervical cancer by detecting pre-cancerous changes
2. Reduce mortality from invasive cervical carcinoma
METHOD: cervical smear test
• Insert Cusco’s speculum
• Use brush to sweep around transformation zone
• Liquid-based cytology of cells collected (centrifuge + microscopy)
• HPV also tested for in this sample
Transformation zone = area of metaplasia between squamous and columnar epithelium
Oestrogen causes columnar epithelium to evert onto endocervix
→ exposure to acidic vagina causes metaplasia to squamous epithelium
HPV PRIMARY SCREENING
Screen for high risk HPV (16 & 18) in smear before cytology for dyskaryosis
• high risk HPV present in 99.7% cervical cancers
• more sensitive test (fewer false negatives)
5
Preventing cervical cancer:
HPV vaccine, barrier contraception, screening
CIN = cervical intraepithelial neoplasia
→ pre-cancerous changes to cells
Grade depends on amount of dyskaryosis
(abnormal nuclei)
CIN I = atypical cells in / epithelium
CIN II = atypical cells in / epithelium
CIN III = atypical cells throughout
Negative
Positive
Abnormal
High grade
dyskaryosis
Fig. 3.4
HR HPV TEST
Normal
LIQUID CYTOLOGY
Low grade dyskaryosis
COLPOSCOPY
CIN II/III → LLETZ
Return to screening programme
Repeat screening in 12m
CIN I → Punch biopsy &
repeat screening in
12m
Colposcopy
METHOD
• speculum to open vagina & colposcope to examine cervix
• acetic acid added to stain cells → abnormal cells turn white
• biopsies taken for histological examination & definitive diagnosis
(CIN I, II, III or rarely cervical cancer)
Fig. 3.5 Abnormal
cells stained white with
acetic acid.
5
PHE (2021) Cervical screening: programme and colposcopy management
LLETZ = large loop excision of transformation zone
https://t.me/med1917
Chapter 3: Gynaecology 49
METHOD
• excision of abnormal cells under local anaesthetic
• diathermy (heat) can stop bleeding vessels
COUNSELLING POST-PROCEDURE
• avoid tampons & intercourse for 4w
• one treatment of LLETZ doesn’t reduce fertility
• may have some bleeding / brown discharge (if offensive get ABX from GP)
Benign conditions of the cervix
Ectropion/erosion: area of eversion at transformation zone appears red
• Sx: may present with vaginal discharge or post-coital bleeding
• Tx of bleeding: cryotherapy*
Acute cervicitis: due to STIs (rare)
Chronic cervicitis: inflammation/infection usually of ectropion
• Sx: vaginal discharge
• Tx: cryotherapy ± ABX
Polyps: benign tumours of endocervical epithelium
• Sx: asymptomatic/IMB/PCB
• Tx: avulsion & histology
Cervical intraepithelial neoplasia (CIN)
Complications/risks of LLETZ
• post-op haemorrhage (1–2%)
• cervical stenosis
• small increased risk preterm labour & PROM
→ pre-malignant changes to cervical epithelium due to HPV (16 & 18)
Epidemiology: peak 25–29y
RF: same as for cervical cancer
Pathology: exposure of cells at transformation zone to HPV results in
incorporation of viral DNA into cells
Symptoms: asymptomatic but risk of cervical malignancy
Diagnosis: cervical smear screening programme
Management: if HPV positive refer to colposcopy
Reassure women with CIN that these are
pre‑malignant changes & colposcopic
treatment is straightforward and very successful
50 Chapter 3: Gynaecology
https://t.me/med1917
Gynae-oncology
PALLIATIVE CARE: MDT of GP, cancer nurses,
specialist gynae unit
1. PAIN CONTROL – analgesic ladder
2. N&V – antiemetics/antihistamines
3. HEAVY VAGINAL BLEEDING – high dose
progesterones/radiotherapy (advanced
cervical/endometrial cancers)
4. ASCITES/BOWEL OBSTRUCTION –
paracentesis, antiemetics, stool softeners,
antispasmodics (advanced ovarian cancers)
Indications for radiotherapy
Stage 1:
Hysterectomy + BSO
+
Stage >1:
Radiotherapy
Total hysterectomy
+ BSO + partial
omentectomy
≥Stage 2:
+ LN dissection
+ post-op chemo
Advanced / unfit for
surgery: palliative
1. Primary therapy: if unfit for surgery or
gross metastases
2. Adjunct therapy: used pre- or post-op
3. Recurrent disease
Hysterectomy complications/risks
• Small bowel obstruction
• Bladder dysfunction
• Ureteral strictures
• Damage to other structures
• Blood loss
• Infection
• VTE/PE
• Fistulae
Definitions
PMB: post-menopausal bleeding
EUA: examination under anaesthetic
Trachelectomy: removal of 80% cervix + upper
vagina
Pre‑malignant: atypical hyperplasia
Stage 1: uterus only
TV USS
Endometrial biopsy
a) Pipelle
Post‑menopausal
• Bleeding
• Discharge
obesity
oestrogen >
progesterone
•
Stage 2: + cervix
Stage 3: through uterine wall/ LN
b) hysteroscopic
=
Pre‑menopausal
• IMB
• PCOS
• nulliparous
• late menopause
involvement
Stage 4: bladder/bowel or distant mets
Hysteroscopy
=
• recent onset HMB
• atrophic vaginitis
(oestrogen/tamoxifen)
• unopposed therapy
• Spreads via pelvic + para-aortic LNs
MRI/CXR
=
DM, HTN, Lynch type 2
PROTECTIVE:
COCP & pregnancy
Stage 1: ovaries only
Stage 2: pelvis only
Women >50y
CA125 levels
USS abdo/pelvis
abdo distension
Initially asymp.
•
• abdo/pelvic mass
early menarche
ovulations
•
• late menopause
Stage 3: abdomen only
Stage 4: beyond abdo
• Mostly direct spread
Women <40y
+ AFP & hCG
• early satiety
• weight loss
• pelvic/abdo pain
• urine urge/freq.
• nulliparous
• FHx BRCA1 or 2
• FHx HNPCC (Lynch)
• Also via para-aortic LNs
CT abdo/pelvis
=
• altered bowels
• ascites
PROTECTIVE:
COCP, lactation,
pregnancy
Peak 60y
90% adenocarcinoma
Type Pathology Epidemiology RFs Symptoms Investigation Staging Treatment
Endometrial
85% post-menopause
75% 5y survival
10% adenosquamous
carcinoma
Most common
(
Uterine sarcomas
=
Peak 70–80y
<35% 5y survival as
presents late
90% epithelial
carcinomas
If <30y:
Ovarian
germ cell tumours
most common
https://t.me/med1917
1b–2a AND –ve LNs:
1a: cone biopsy
Radical hysterectomy
OR
Trachelectomy
≥2b OR +ve LNs:
Chemo-radiotherapy
Stage 1:
wide local excision
Stage >1:
wide local
excision + groin
Chapter 3: Gynaecology 51
lymphadenectomy
+ radiotherapy if LN
+ve
Intravaginal
radiotherapy
OR radical surgery
Pre‑malignant: CIN (1–3)
Stage 1: cervix only
VE/DRE & EUA
Biopsy
=
• PCB
• IMB
• PMB
HPV 16 & 18
• sexual contacts
• unvaccinated
Stage 2: + upper / vagina
Stage 3: + lower / vagina or pelvic
=
• offensive discharge
Later signs:
Other
• smoking
MRI
wall or ureteric obstruction ± LNs
Stage 4: bladder/rectum or further
t
=
Pelvic pain, anaemia,
uraemia, haematuria,
rectal bleeding
HIV
• immunosuppressed/
• long-term OCP use
Stage 1: vulva/perineum only
Biopsy Premalignant: VIN
• Pruritus
• Bleeding
• Discharge
• Lichen sclerosus
• Paget’s disease of vulva
• Immunosuppression
Stage 2: adjacent spread (urethra/
vagina) but no LNs
Stage 3: +ve LNs
clitoris
• Ulcer/mass on labia/
• Lymphadenopathy
• Smoking
Stage 4: upper vagina, rectum/bladder,
distant mets
Superficial & deep inguinal LNs →
femoral & external iliac
Stage 2: through vaginal wall
Stage 3: reached pelvic wall or LNs
Stage 4: bladder/rectum/ beyond pelvis
Biopsy Stage 1: vagina only
Bleeding
• Discharge
• Mass/ulcer
2 peaks: 30y & 80y
65% 5y survival
carcinomas
10% columnar cell
adenocarcinomas
Cervical 90% squamous cell
(
Peak at >60y
Vulval 95% squamous cell
Stage 1:
>90% 5y survival
carcinoma
5% melanoma,
Stage 3–4:
40% 5y survival
basal cell carcinoma,
adenocarcinoma
50% 5y survival Older women •
cell carcinoma
Vaginal Usually squamous
52 Chapter 3: Gynaecology
Ovulation
Anterior
https://t.me/med1917
The menstrual cycle
cycle
Ovarian
Growing follicle Ovulation Corpus luteum Corpus albicans
37° C
Body
temp.
Features of normal menstruation
Menarche <16y
Menopause >45y
Menstruation <8d
Cycle length 23–35d
No intermenstrual
bleeding (IMB)
Blood loss <80ml
Stages of female puberty
>8y = GnRH = LH/FSH = oestrogen
9–11y: oestrogen causes development of
2° sexual characteristics
11–13y: menarche (onset of menstruation)
Fig. 3.6
36° C
pituitary
hormones
Ovarian
hormones
cycle
Uterine
Menses
0 days14 days
Estradiol
Luteinizing hormone (LH)
Follicle-stimulating
hormone (FSH)
Luteal phaseFollicular phase
Progesterone
Menses
28 days
breasts → pubic hair → growth spurt →
menarche
Oestrogen causes proliferative changes
(thickening
Progesterone causes secretory changes
(stromal cells , glands swell, blood supply )
1. FOLLICULAR PHASE (DAYS 1–14)
A) Menstruation (days 1–4): endometrium shedding + myometrial contractions
B) Proliferative phase (days 5–13):
• GnRH pulses from hypothalamus stimulate LH & FSH release
• FSH stimulates follicle development → follicles produce oestrogen &
inhibin
• Low level oestrogen + inhibin = –ve feedback to inhibit >1 follicle developing
• Graafian (dominant) follicle continues to grow & produce oestrogen
• Oestrogen levels peak → +ve feedback occurs → LH SURGE
2. OVULATION DAY 14/MIDCYCLE:
• 36h after LH surge = follicle rupture
• Graafian follicle becomes corpus luteum
3. LUTEAL/SECRETORY PHASE (DAYS 14–28)
• Corpus luteum produces progesterone > oestrogen = –ve feedback so FSH/LH
• If no fertilisation: corpus luteum degenerates after 14d = progesterone
→endometrial degeneration & menstruation
Hormone Gland Effects
FSH Anterior
Pituitary
LH Anterior
Pituitary
Acts on follicle granulosa cells in ovary:
1.
Follicle development
→ oestrogen & inhibin production
1.
LH surge causes ovulation
2. Maintenance of corpus luteum
Oestrogen Ovaries
(follicle/CL)
Progesterone Ovaries
(CL)
1. Endometrial proliferation
2. Thinning of cervical mucus (better for sperm)
1. Stimulates secretory phase
2. Inhibits LH & FSH
Menorrhagia (HMB)
https://t.me/med1917
>80ml blood loss interfering with physical, social, emotional quality of life
CAUSES
• Idiopathic/dysfunctional uterine
bleeding (majority)
• Uterine fibroids (30%)
• Polyps (10%)
• Adenomyosis
• Coagulopathies (rare)
• Consider IUD as cause
Chapter 3: Gynaecology 53
INVESTIGATIONS
• History: amount & timing of bleeding
• Examination: signs of anaemia, palpation of masses, pelvic tenderness
• FBC: Hb (TFTs & clotting if history suggests necessary)
• TV USS: exclude masses, detect polyps
• Endometrial Pipelle biopsy: exclude malignancy
• Hysteroscopy: allows biopsy & inspection of uterine cavity
MANAGEMENT
1st-line: IUS – not suitable if want to conceive
2nd-line:
• Tranexamic acid = antifibrinolytic
• NSAIDs – useful if + dysmenorrhoea
• COCP
6
+ may need iron supplements
if anaemic
Surgical:
• Hysteroscopic polyp removal
• Endometrial ablation – destroy
endometrium to bleeding
• Myomectomy – fibroid removal
3rd-line:
• Progesterones
(GnRH first to size)
• Hysterectomy – last resort
• GnRH agonist – limited to 6m use
Inter-menstrual bleeding (IMB)*
→ common in early or late reproductive years
CAUSES
• Fibroids, polyps, ovarian cysts
• Adenomyosis
• Chronic pelvic infection
• Malignancy – recent onset/older
INVESTIGATIONS: same as for HMB
→ detect anaemia, exclude local
pathology & malignancy
MANAGEMENT
Medical: if no anatomical cause detected
• IUS/COCP – lighter bleeding
• Progesterones – cause amenorrhoea
• HRT – if irregular bleeding during
menopause
Surgical: same as for HMB
• Polyp removal, myomectomy,
hysterectomy
Indications for endometrial biopsy
(Pipelle/hysteroscopic)
• endometrial thickness >10mm
(or >4mm post-menopausal)
• polyp suspected
• >40y with recent onset HMB/IMB/
treatment resistant
• RFs for cancer: PCOS, FHx, HNPCC,
obesity/DM
reduces fertility & pregnancy would be high risk
→ permanent contraception recommended
Dysmenorrhoea
→ high prostaglandin levels cause painful uterine contraction & ischaemia
PRIMARY7:**
• Cause: no organic cause
• Tx: NSAIDs/ COCP
SECONDARY:***
• Cause: pelvic pathology – fibroids, adenomyosis, endometriosis, PID,
malignancy
• Sx: ± deep dyspareunia, HMB
• Ix: pelvic USS, hysteroscopy
• Tx: depends on cause
6
NICE (2018, updated 2021) Heavy menstrual bleeding [NG88]
7
NICE (2018) CKS Clinical management scenario – Dysmenorrhoea
**With start of menstruation
50% women (esp. adolescents)
***Precedes & relieved by menstruation
54 Chapter 3: Gynaecology
https://t.me/med1917
*Always abnormal (unless 1st intercourse)
Causes cyclical lower abdo pain
Physiological causes of amenorrhoea
Post-coital bleeding*
→ vaginal bleeding after intercourse that is not menstrual loss
CAUSES
• Endometrial instability – most common cause, especially with use of hormonal
contraception
• Cervical carcinoma: <1% but MUST EXCLUDE
• Cervical ectropions/eversion – Tx with cryotherapy
• Benign cervical polyps – Tx with avulsion & biopsy
• Cervicitis, atrophic vaginitis
INVESTIGATIONS
• Cervical inspection (speculum) & smear
• Colposcopy if abnormal appearance of cervix
Amenorrhoea/oligomenorrhoea
→ absent/infrequent menstrual bleeding
PRIMARY:
1. Delayed puberty: secondary sexual characteristics not present by 14y
2. Menstrual outflow problem: imperforate hymen, transverse vaginal septum
3. Congenital: Turner syndrome (1 missing X chromosome), congenital adrenal
hyperplasia
• Pregnancy/lactation
• Menopause
• Drugs
Investigations
• History & examination
• PREGNANCY TEST (urine hCG)
• FSH/LH, prolactin, testosterone
• TFTs
• Pelvic USS for PCOS
• MRI/CT if suspect tumours
Management: treat underlying cause & bone
protection (HRT)
Stimulates dopamine release which inhibits
prolactin
SECONDARY:
1. Hypothalamic hypogonadism = FSH/LH & therefore oestrogen
• Causes: psychological (stress), anorexia, excess exercise
• Tx: oestrogen replacement (COCP/HRT)
2. Hyperprolactinaemia = inhibits GnRH
• Causes: pituitary hyperplasia, benign adenoma (prolactinoma),
medications (methyldopa, opiates, heroin)
• Tx: bromocriptine, cabergoline + endocrine referral
3. Hyper-/hypothyroidism
4. PCOS – often oligomenorrhoea + subfertility
5. Premature menopause 1 in 100 women
Premenstrual syndrome (PMS)
→ psychological, behavioural & physical symptoms experienced
regularly in luteal phase of cycle
Cause:
Unknown – progesterone involved
Symptoms:
Psychological/behavioural: irritability,
aggression, depression
Physical: bloated, GI upset, breast pain
Investigations:
Management8:
• SSRIs – continuous or intermittent
• Oral contraception – continuous
• HRT – oestrogen patches
• GnRH agonists + add‑back HRT
(if severe/Tx-resistant)
+ Non‑pharmacological: diet, exercise, CBT
Menstrual diaries: record mood & symptoms
most common cause
95% women
5% = severely debilitating
8
RCOG (2016) Management of premenstrual syndrome [GTG48]
Subfertility
https://t.me/med1917
Chapter 3: Gynaecology 55
Where conception has not occurred after 1y of UPSI
15% couples
Causes of subfertility
1. Anovulation (30%) = egg not produced
2. Male factor problem (25%) = inadequate sperm
3. Disorders of fertilisation (30%) = sperm doesn’t reach egg
4. Unexplained (15%) = large proportion may result from defective implantation
Anovulation
DETECTING OVULATION
• Serum progesterone – day 21 (mid-luteal) increase
• LH detecting kits (over the counter) – detect LH surge
• Temperature – 0.2°C pre-ovulation & 0.5°C after
• USS to detect follicle size/rupture – not often used
• Anti-Müllerian hormone (AMH) – indicator of ovarian reserve
CAUSES OF ANOVULATION
1. PCOS*
• Causes: disordered LH production () & insulin resistance
• RFs: genetics, high BMI, T2DM
• Symptoms: infertility, oligomenorrhoea, hirsutism
• Investigations
▶ Bloods
▶ TV USS: for PCO
▶ DM screen: fasting glucose & lipids
• Management
▶ Clomifene citrate (anti-oestrogen) – triggers –ve feedback to LH & FSH
for follicle development
▶ Metformin, diet & weight advice – insulin sensitisation
▶ Laparoscopic ovarian diathermy
▶ COCP/anti-androgens – regulate menstruation/hirsutism
2. Hyperprolactinaemia = prolactin = GnRH
• Causes: benign pituitary adenoma, pituitary hyperplasia, PCOS,
hypothyroidism, psychotropic drugs
• Symptoms: oligo-/amenorrhoea, galactorrhoea, headaches, bitemporal
hemianopia
• Investigations: bloods ( prolactin), CT scan
• Management: dopamine agonist (bromocriptine/cabergoline), surgery
3. Hypothalamic hypogonadism = GnRH release = LH/FSH & oestrogen
• Causes: anorexia nervosa / BMI, athletes, stress, Kallmann syndrome
• Symptoms: amenorrhoea
• Investigations: bloods ( GnRH, LH, FSH & oestrogen)
• Management: GnRH pump + bone protection (COCP/HRT), restore weight
4. Pituitary damage – causes include tumours & infarction
5. Premature ovarian failure
6. Gonadal dysgenesis
7. Hypo-/hyperthyroidism
9
Important to involve a trained counsellor /
provide psychological support for the
couple
FSH interpretation re anovulation
Raised: ovarian failure
Low: hypothalamic disease
Normal: PCOS
*See notes on disorders of the ovaries
Pre‑ovulation: FSH, LH, oestrogen
(& progesterone)
Post‑ovulation: fall in hormones if not
fertilised
Blood test results in PCOS
• Raised LH
• Raised testosterone
• Raised AMH
• Normal FSH/prolactin/TSH
• Low 21-d progesterone
if fertility not required
Diagnostic criteria for PCOS
PCO = ≥12 small follicles in an enlarged ovary
PCOS = ≥2 of:
• PCO on TV USS
• irregular menstrual periods (>35d apart)
• hirsutism ( acne/hair or serum
testosterone)
9
NICE (2013, updated 2017) Fertility problems [CG156]
56 Chapter 3: Gynaecology
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Ovarian hyperstimulation syndrome (OHSS)
• Sx: large, painful follicles (± oedema, ascites,
SOB, hypovolaemia)
• RF: gonadotrophins, IVF, <35y, PCO
• Ix: FBC, U&Es/renal func, CXR, PV USS
• Mx: supportive – watch & wait (monitor
closely) ± fluid tap
• Prevent: lowest dose gonadotrophins + USS
monitoring
electrolyte imbalance
Drugs to induce ovulation
→ First treat underlying cause
1st‑line: clomifene citrate (anti-oestrogens)
2nd‑line:
• Gonadotrophins (FSH ± LH) – daily SC injections
• GnRH pump – in hypothalamic hypogonadism
Risks of ovulation induction:
>1 follicle develops = multiple pregnancy
Before offering ovulation stimulation:
1.
Confirm anovulation with low 21-d progesterone
2. Ensure no tubal problems
3. Ensure no male factor problems
Male factor problem
SPERMATOGENESIS: takes 70d
• LH causes testosterone production in Leydig cells
• Testosterone & FSH control synthesis and transport of sperm in Sertoli cells
CAUSES OF INADEQUATE SPERM
• Idiopathic
• BMI
• Drugs – alcohol, smoking, anabolic
steroids
• Industrial chemicals/solvents
• Varicocele – in 25% cases
• Anti-sperm antibodies – common
after vasectomy reversal
INVESTIGATIONS
1. Semen analysis
• produced by masturbation after 2–7d abstinence
• analysed within 1–2h
• repeat for abnormal results in 12w
• persistent abnormalities = scrotal exam &
further investigations (see below)
2. Blood tests: FSH, LH, TSH, testosterone,
prolactin
3. Serum karyotype: e.g. for Klinefelter’s (XXY)
MANAGEMENT
1. Lifestyle advice
• reduce smoking/alcohol/drug exposure; weight loss
• testicles below body temperature
2. Assisted conception
• Mild oligospermia: intrauterine insemination (IUI)
• Mod.–severe oligospermia: IVF ± intracytoplasmic sperm injection (ICSI)
• Azoospermia: sperm retrieval from testes + ICSI–IVF
10
• Infections – epididymitis, mumps,
orchitis
• Congenital abnormalities / genetics,
e.g. Klinefelter’s (XXY), CF
• Hypothalamic problems /
hypogonadotrophic hypogonadism
Azoospermia + absent vas deferens
= investigate for cystic fibrosis
Normal semen analysis
Volume: >1.5ml
Sperm count: >15million/ml
Progressive motility: >32%
Azoospermia: no sperm
Severe oligospermia: <5million/ml
Asthenospermia: low motility
10
NICE (2013, updated 2017) Fertility problems [CG156]
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