Obs + gynae Flashcards
Ectropion overview
(previously cervical ectopy, cervical erosion or abrasion)
Under the influence of oestrogen the columnar epithelium of the endocervix is displayed beyond the os.
Dx: It is seen on examination as a red ring around the os and is so common.
Cause/epidemiology: It is most commonly seen in teenagers, during pregnancy and in women on combined oral contraception (COC).
Presentation: asymptomatic (occasionally, bleeding or excessive discharge)
Mx:
Cervical smear (Pap smear) for all.
Stopping any oestrogen-containing contraceptive
If asymptomatic»_space; conservative management. Over time, vaginal acidity promotes metaplasia to squamous epithelium.
4. If there are symptoms»_space; treatment options:
Diathermy, Cryotherapy, Laser Treatment, Microwave therapy
Bartholin’s cyst/abscess
Background:
Common in ages 20-30 in roughly 3% of women
Most common in women of childbearing age
If they present after age 40 must consider a malignant cause (although rare)
Pathology:
Two small glands located slightly posteriorly at both sides of the vaginal introitus (vaginal opening), secreting mucus to lubricate the vagina
Normally cannot be palpated and pea sized
Damage or infection of the ostium of the duct causes a blockage or cyst, which can become infected resulting in an abscess
Aetiology:
abscess - Infection, most commonly E. coli, gonorrhoea or chlamydia
Bartholin’s cyst risk factors and presentation
Risk factors:
STI
Ages 20-30
Presentation:
Typically unilateral presentation
Small cyst - soft painless lump, may be fluctuant
Large cyst - uncomfortable when mobilising, sitting and dyspareunia
Abscess - erythematous, hot to touch, hard, tender mass arising over 1-2 days
Bartholin’s cyst diagnosis and management
Diagnosis:
Swab from contents of cyst/abscess
STI screening
+/- biopsy (women >40 should have excisional biopsy to rule out carcinoma)
Management:
Small and asymptomatic - warm compresses, good hygiene
Large and uncomfortable/abscess:
Sitz baths (warm baths helping drain abscess)
Antibiotics and analgesia
Surgical incision and drainage (avoided if possible as increases risk of recurrence)
Marsupialisation (incision and drainage under general anaesthetic and sides of abscess are sutured open for continuous drainage preventing recurrence
Word catheter (bartholin’s gland balloon - tube with balloon on the end, incision and drainage, word catheter inserted into abscess space and inflated <3ml under local anaesthetic) insertion for a few weeks to epithelialize new tract
Imperforate hymen overview
Hymen is the membrane at the mouth of the vagina where the Mullerian and urogenital systems fuse
The normal hymen has multiple variations of perforation, including an imperforate hymen
Aetiology:
Normal anatomical variation of fusion of the mullerian and urogenital systems during development
Presentation:
Apparent/false primary amenorrhea
History of monthly abdominal pain and swelling
Membrane bulging under pressure of hematocolpos (build up of menstrual blood)
Possible complication - hematometra and hematosalpinx (rare) blood builds up reaching uterus and ovaries
Investigation/diagnosis:
Genital examination
USS to assess for hematometra/hematocolpos
Management:
Relieved by cruciate incision into the hymen forming opening/perforation
Vaginal Genesis or atresia
Agenesis - Vagina and uterus are absent but ovaries are present (rare)
Atresia - lower portion of the vagina consists of fibrous tissue with a well differentiated uterus (rare)
Transverse vaginal septa overview
Background:
Relatively common, often missed on examination
Pathology:
Can be single or multiple, in the upper, mid or lower vagina
Can be patent or perforated
Aetiology:
Congenital anomaly during development
Presentation:
Transverse connective tissue within the vaginal canal
Investigation/diagnosis:
Vaginal examination
Management:
Surgery if needed
Cervical/uterus duplication overview
Background:
Common - duplication of uterus or cervix
Rare - condition present with primary amenorrhoea
Pathology:
Duplication of the cervix and/or uterus
Bi-cornuate uterus - partially divided
Unicornuate uterus - one side of uterus has failed to develop
Aetiology:
Congenital anomaly
Presentation:
May be missed on examination
Varies depending on duplications/divisions
Two asymptomatic smaller uteri/cervix
Recurrent miscarriage (particularly second trimester)
Labour difficulties
Based on type - dysmenorrhoea, haematometra, recurrent miscarriage, pregnancy and labour complications
Fertility usually not affected
Investigation/diagnosis:
MRI
3D USS
Hysterosalpingogram (HSG)
Management:
referral to gynaecology
Female genital mutilation background and risk factors
Background:
Partial or total removal of the female external genitalia or other injury to the female genital organs for non-medical reasons
In the UK the majority of affected women are from Somalia, Kenya, Eritrea, Ethiopia, Yemen
It is also common in Mali, Guinea and Egypt
Estimated around 137,000 females in the UK have been affected
Around 60,000 girls under age 15 are at risk of FGM in the UK (2015)
Risk factors:
Coming from a community that practices FGM
Family history of FGM
FGM classification
type I - Partial or total removal of clitoral glands (external and visible part of clitoris, very sensitive) and/or prepuce
type II - Partial or total removal of the clitoral glans and labia minora (inner folds of vulva) +/- labia majora
type III - AKA infibulation - narrowing of the vaginal opening through the creation of a covering seal. Seal is formed via cutting and repositioning the labia minora or majora sometimes with stitching. +/- removal of the clitoral prepuce and glans (type I FGM)
type IV - Includes all other harmful procedures to female genitalia for non-medical purposes (pricking, piercing, incising, scraping and cauterising the genital area
FGM complications
Immediate - death, shock, pain, haemorrhage, infection, adjacent organ damage, acute urinary retention
Long term reproductive - AIDS, HIV, blood borne disease, problems with pregnancy and childbirth, psychological and psychiatric problems
Long term pelvic organ complications - failure to heal, recurrent UTI, renal/bladder calculus formation, urethral obstruction/urinary retention, pelvic infections, abscesses, menstrual abnormalities and infertility, sexual dysfunction (VERY COMMON), fistulae
FGM investigations and management
Investigation/diagnosis:
FGM guidelines from the royal college of obs and gynae (RCOG) state every pregnant women must be asked if she has been cut and all those attending maternity, family planning, gynae, urology clinics should be routinely asked aboout FGM
Genital assessment
Must record:
If they have FGM
If there is a family history of FGM
If an FGM related procedure has been carried out on a woman
Management:
As of 2015, all FGM in girls under 18 must be reported to the police. Should also contact social services and safeguarding, paediatrics, specialist gynae/FGM services and counselling
In those >18 a risk assessment is used to determine if police/social services should be contacted: includes risk to other family members. (Gov.uk website)
Record grade of mutilation after consent for genital assessment
Refer to MDT for psychological and educational support (FGM clinic)
Infection, adjacent organ damage, fistulae to be managed PRN
Deinfibulation should be offered after a full assessment by an FGM specialist if: Intercourse problem Micturition problem Delivery problem Patients wish
Reinfibulation (performed after childbirth to re-close the vaginal orifice) is illegal
cervical cytology and NHS screening
NHS cervical screening programme (NHSCSP) aims to reduce incidence of and mortality from cervical cancers through a systematic quality assured population-based screening programme for eligible women
Testing:
Training is needed to ensure clinicians are competent to visualise the cervix and take a sample from the whole transformation zone
HPV triage and liquid based cytology that looks for abnormal cells
Primary high risk HPV (HR-HPV) testing now takes precedence
Reduction in inadequate tests and improved sensitivity compared to Papanicolaeou (PAP) smears
Cervical/LBC brush:
Enables simultaneous collection of endocervical, ectocervical and transformation zone cells with single device
Hairs are flexible so mucosal surface is well sampled but not damaged
Criteria for cervical screening and reasons to delay screening
Criteria for screening in the UK:
Screening for all women (transgender men or non-binary who have retained a cervix included) before between the ages of 24.5-64 years
Invitation sent to those aged 24.5 to ensure they can be screened before age 25
Screening from ages 25-49 every 3 years
Screening form ages 50-64 every 5 years
65< invited if: a recent cervical cytology sample is abnormal or they have not had cervical screening since age 50 and they request one
Delayed screening:
Avoid if:
Menstruating
<12 weeks postnatal
<12 weeks after pregnancy termination
Has vaginal discharge or pelvic infection - treat first
If pregnant (seek specialist advice if they have had a recent abnormality)
Those with any sexual contact/sexual orientation are at risk and should be screened
Women should be ceased from the programme where they no longer have a cervix or have undergone pelvic radiotherapy (they should have vault cytology)
Voluntary withdrawal: Must be done in writing
Reasons include
Low risk of cervical cancer (no sexual contact)
Physical or learning disability making process difficult or distressing
Terminally ill/will not benefit from screening
Unable to give adequate samples - FGM (gynae referral instead)
Those who do not want to participate (must be made aware of the risks)
HPV overview and vaccines available
Very common sexually transmitted virus
Most infectious are transient, usually the immune system clears the virus
If it persists, can cause genetic mutation predisposing to carcinogenic changes (responsible for 99% of cervical cancers)
13 high risk strains - 16 and 18 account for 80%
Vaccination programme from ages 12-13 both sexes
High negative predictive value of HR-HPV test raises prospect that HPV can become primary screening at more regular intervals
Vaccines:
Gardasil: protects against 4 types of HPV (6, 11, 16 and 18)
Gardasil 9: prevents infection from the same 4 strains plus 5 additional cancer causing types (31, 33, 45, 52 and 58)
Cervarix: discontinued, vaccinated against types 16 and 18
Liquid based cytology sampling, results and actions
Inadequate:
Sample taken but cervix not fully visualised
Taken inappropriately (using unapproved devices etc.)
Contains insufficient cells
Contains obscuring elements (lubricant, inflammation, blood etc.)
Incorrectly labelled
Samples must be repeated after 3 months (time taken for cells to regrow)
Two consecutive inadequate samples warrant referral to colposcopy to exclude invasive cancer
Results:
Negative: no abnormality detected
Abnormal:
Borderline changes in squamous or endocervical cells (cells seen with abnormal nuclei) - 1
Low grade dyskaryosis (abnormal nuclei and cell morphology) - usually CIN1. 1
High grade dyskaryosis (moderate) - usually CIN2. 2
High grade dyskaryosis (severe) - usually CIN3. 2
Invasive squamous cell carcinoma. 2
Glandular neoplasia. 2
1 - Colposcopy in 6 weeks
2 - Colposcopy in 2 weeks (2WW)
Colposcopy
Those who are HPV positive/present with abnormal cytology are referred to colposcopy allowing direct observation using a colposcope and staining of the cervix for either a punch biopsy or excisional treatment.
Acetic acid is applied to the cervix using cotton wool ball or spray to show cell changes by turning them white
Schiller’s iodine test uses iodine solution to stain normal cervical tissue dark brown. Cell changes may not stain
Excisional biopsy may be recommended for:
Most of endocervix is replaced with high grade abnormality
Low grade colposcopy change associated with high grade dyskaryosis (severe) or worse
Lesion extends into the canal - sufficient canal must be removed with endocervical extension of abnormality
Cervical intraepithelial neoplasia (CIN)
Premalignant lesion detected by colposcopy
Three stages dependent on how deep cell changes go into the OUTER surface of the cervix
CIN1: ⅓ thickness of the surface layer of the cervix is affected
CIN2: ⅔ thickness of the surface layer of the cervix is affected
CIN3: sometimes called high grade or severe dysplasia or stage 0 cervical carcinoma in situ. Full thickness of surface layer is affected
Left untreated, CIN2 or 3 (CIN2+) may progress to cervical cancer
Usually for all three grades only a small part of the cervix has abnormal changes
Cervical glandular intraepithelial neoplasia (CGIN)
Changes to the glandular cells that line the INSIDES of the cervix
Without treatment these cells can develop into adenocarcinoma
CGIN is less common than CIN but treated similarly
CIN and CGIN management
Large loop excision of the transformation zone (LLETZ)
Needle excision of transformation zone (NETZ/SWETZ)
Cone biopsy
Laser therapy ablation
Cold coagulation (thermoablation)
Cryotherapy
follow up spec exams on case by case basis and smear usually 1 year after treatments.
Invasive cancer - triage onto 2 week pathway for additional treatments
Large loop excision of transformation zone (LLETZ) and needle excision of transformation zone (NETZ/SWETZ) therapy
LLETZ
Uses a thin wire loop with an electrical current to remove the affected area of the cervix
Most common treatment for abnormal cells
Usually requires local anaesthetic although general can be requested
Risks of bleeding, change in vaginal discharge, cervical stenosis, premature birth or late miscarriage
NETZ
Straight wire excision of the transformation zone (SWETZ) and NETZ are similar to LLETZ but a thin wire is strength rather than looped
Treatment usually reserved for cell changes INSIDE the cervical canal (CGIN)
Cone biopsy treatment
Minor operation to remove a cone shaped piece of tissue of the cervix
Carried out under general anaesthesia usually taking about 15 minutes but may need overnight stay depending on complications
Usually use a medical “plug” tampon to help stop any initial bleeding
Advise to avoid menstruation tampons, sexual intercourse or contact and swimming for at least 4 weeks
Abnormal vaginal bleeding terminology
Polymenorrhea: frequent periods within the calendar month (<21 day interval between 2 consecutive periods)
Oligomenorrhea: less frequent periods or delayed periods >35 days
Dysmenorrhoea: pain before and with periods lasting 1-3 days from onset of bleeding
Menorrhagia: heavy menstrual bleeding and usually for longer duration >7 days
Intermenstrual bleeding: vaginal bleeding (other than postcoital) at any time during the menstrual cycle other than normal menses. May indicate underlying cervical/uterine pathology such as fibroids, endometriosis or cancers
Postcoital bleeding: non-menstrual bleeding occurring immediately after sexual intercourse. Following vaginal sex, may indicate cervical pathology or PID
Dyspareunia
Pain during or after sexual intercourse, can affect men but more common in women
Can be superficial (localised to vulva or vaginal entrance) while deep pain is often inside the vagina or lower pelvis
Causes are vaginal or genital infections, vaginal dryness, menopause (atrophic vaginitis), vigorous activity
Menorrhagia
Background:
Excessive (heavy) menstrual blood loss occurring regularly (every 24-35 days) interfering with a women’s physical, emotional, social and material quality of life
The average blood loss during menses is 30-40mL, 90% of women have losses <80mL
Excessive blood loss is classified at >80mL and/or a duration of >7 days - direct measurement is accurate but difficult to undertake in clinical practice
It is also defined as the need to change a menstrual product every 1-2 hours, passage of clots >2.54cm and/or “very heavy” periods as reported by women
Can occur alone or in combination with associated symptoms
One of the most common causes of referral to gynaecologist, especially in women aged 30-49
Up to 25% of women suffer at least one episode of dysfunctional uterine bleeding during reproductive years and around 20% will have a hysterectomy before age 60 to alleviate heavy bleeding
Pathology:
As the corpus luteum regresses the concentrations of oestrogen and progesterone decrease. At their lowest concentrations, spiral arteries collapse and the functional endometrial layer of the uterus “sloughs off” for menstruation
Bleeding occurs for an average of 5 days (>7 days menorrhagia)
Menorrhagia cause and presentation
Aetiology:
50% idiopathic (dysfunctional uterine bleeding)
Uterine and ovarian pathologies - fibroids, endometriosis, adenomyosis, PID and infection, endometrial polyps or hyperplasia, PCOS
Systemic diseases - coagulation disorders (willebrand disease), hypothyroidism, diabetes, hyperprolactinaemia, liver/renal disease
Iatrogenic - anticoagulant, chemotherapy, herbal supplements (ginseng, ginkgo, soya), IUD
Presentation:
Heavy bleeding during menstruation
Associated symptoms of underlying cause (dysmenorrhoea, pelvic pain, vaginal discharge, postcoital bleeding, menstrual irregularity)
Complications - iron deficiency anaemia (⅔ cases), increased risk of endometrial pathology, negative impacts on psychosocial, emotional or material quality of life
Menorrhagia investigations and diagnosis
Investigation/diagnosis:
No associated symptoms - consider pharmacological treatment without examination
Associated symptoms - genital examination
FBC (iron def. anaemia)
Hysteroscopy/pelvic USS/transvaginal USS - Suspected fibrous, polyps, endometrial pathology
Vaginal or cervical swab - infection
TFTs
Coagulation studies/genetic testing - coagulation disorders
Management:
Provide information and reassurance of natural variability of menstrual blood loss and information of possible treatments (NHS on heavy periods - https://www.nhs.uk/conditions/heavy-periods/)
Idiopathic/fibroids <3cm or adenomyosis -
LNG-IUS first line
2nd line Tranexamic acid or NSAIDs (non-hormonal) or combined oral contraceptive/cyclical oral progesterone (hormonal) prescription
Progesterone only contraception may suppress menstruation
Fibroids >3cm diameter -
Tranexamic acid and/or NSAIDs, advise to continue for as long as is beneficial
LNG-IUS, CHC or cyclical oral progesterone 2nd line
Uterine artery embolisation
Surgery (myomectomy, hysterectomy, 2nd generation endometrial ablation)
Vaginal concern history taking
Nature of bleeding and impact on quality of life
Age - first year after menarche and perimenopause are associated with irregular cycles and anovulatory bleeding
Cervical screening history, previous abnormal results and treatments
Details of normal cycles (length, frequency, intermenstrual bleeding, postcoital bleeding, pains between periods, vaginal discharge, dyspareunia, pain in rectum, days of menses and variation from normal pattern)
Sexual history (current contraception, future family plans, partners, STI screening, type of sex, pain with sex/associated symptoms)
Medical history (endometriosis, family history of coagulation disorders, PID, willebrand disease, comorbidities
Drug history including previous menorrhagia treatments
Smoking history
Obstetric history
Related symptoms (intermenstrual bleeding, pelvic pain, pressure symptoms)
Referrals:
Urgent - ascites and/or pelvic/abdominal mass + weight loss using 2WW pathway, no weight loss - 4 week wait referral
Compressive symptoms from large fibroids (dyspareunia, pelvic pain, discomfort, constipation, urinary symptoms)
Iron deficiency anaemia failed to respond to treatment and other causes excluded (2WW)
Menorrhagia has not improved despite treatment
menorrhagia management advise on treatment
- levonorgestrel-releasing IUS - warn of changes in bleeding pattern, particularly first few cycles maybe >6 months and it is advisable to wait at least 6 cycles to see benefits of treatment*
- uterine artery embolisation - cannulating femoral artery and identifying uterine arteries to inject embolic agents to impair blood supply to fibroids. May potentially allow them to retain fertility*
- myomectomy - inform it may potentially allow retained fertility and may increase pregnancy rate compared to UAE in women with fibroids*
- hysterectomy - can be vaginal, abdominal or laparoscopic. May include removal or preservation of ovaries/cervix. Should be informed of risk of haemorrhage, organ damage, loss of ovarian function/menopause. Should discuss the psychological impact, alternative surgery, expectations, complications, further treatments needed, bladder function, impact on fertility*
- endometrial ablation - destroys endometrial lining and superficial myometrium of uterus (muscle). Inform them to avoid subsequent pregnancy (must be on effective contraception)*
dysmenorrhoea
Background:
Painful cramping, usually in the lower abdomen occurring shortly before and/or during menstruation (pain lasting >3 days from period onset)
Can be primary (alone) occurring in young females with no pelvic pathology, 90% of women at reproductive age report this
Secondary occurring in association with pelvic pathology, less common
Childbirth reduces dysmenorrhoea and severity diminishes with age
Pathology:
Thought to be from an excess/imbalance of prostaglandins and leukotrienes in the menstrual fluids producing vasoconstriction in uterine vessels
This causes uterine contractions causing pain and may also be responsible for diarrhoea, nausea, headache, light-headedness
dysmenorrhea aetiology and risk factors
Aetiology:
Primary: thought to be caused by prostaglandin production during menstruation (from progesterone drop) stimulating uterine myometrial contractions leading to decreased blood flow, uterine hypoxia and pain
Secondary: Pelvic disorders (endometriosis, fibroids, PID, ovarian cancer, IUD)
Risk factors: Longer duration of menses Early menarche Smoking Alcohol Obesity Depression or poor social support networks Risk factors for more severe symptoms: Earlier age of menarche Menorrhagia Nulliparity Family history
Presentation for dysmenorrhea
Painful cramping, usually in the lower abdomen occurring shortly before and/or during menstruation
Primary - often begins with onset of ovulatory cycles, six months-1 year after menarche in absence of underlying pathology. Pain with onset of period lasting 24-72 hours. Often associated with non-pelvic symptoms such as N+V, dizziness, headaches, lower back pain, emotional symptoms
Secondary - more likely years after menarche, associated dyspareunia, pelvic pain, evidence of underlying pathology (fibroids, endometriosis, PID, adhesions, developmental abnormalities. May be present with associated symptoms such as dyspareunia, vaginal discharge, rectal pain, bleeding, postcoital bleeding etc.
Cu-IUCD recent application can cause dysmenorrhoea
Dysmenorrhea investigations
History taking - exclude secondary causes
Clinical diagnosis
Abdominal and vaginal examination if sexually active
Speculum exam
High vaginal swab, STI screening
Cervical smear
Pelvic USS for masses or uterine enlargement
Transvaginal USS
Dysmenorrhea management
Information and reassurance of normal variation of menses cycles (NHS on period pains or women’s health concerns www.womens-health-concern.org)
Primary often improves with age, parity and use of oral contraceptives
Lifestyle changes - smoking cessation and local heat application, tea (regular, camomile or mint), abdominal/back massages, lying supine. Dietary supplements and herbal remedies can be tried but have insufficient evidence (calcium, Mg, thiamine, ginger, fish oil, toki-shakuyaku-san), acupuncture and acupressure
Primary:
NSAIDs/paracetamol
3-6 months trial of hormonal contraceptive (COC)/oral progestins (desogestrel), parenteral (Depo-Provera) or LNG-IUS
Combination of NSAIDs and contraceptive if ineffective alone
Transcutaneous electrical nerve stimulation (TENS)
Surgery - laparoscopic uterine nerve ablation (LUNA) for severe cases or hysterectomy
Secondary:
Refer for red flags:
Ascites and/or pelvic/abdominal mass
Abnormal cervix
Persistent intermenstrual or postcoital bleeding without associated features of PID (pelvic pain, deep dyspareunia, abnormal vaginal/cervical discharge)
USS suggestive of cancer
Investigation/management of underlying cause
Endometriosis
Background:
One of the most common gynae disorders in women of reproductive age (2nd after fibroids)
Affects approx 10% of women in the UK however variance of clinical presentation means prevalence is not well known
Infertility affects 30% of sufferers
Pathology:
Chronic oestrogen-dependent condition characterised by growth of endometrial tissue in sites other than the uterine cavity, most commonly the pelvic cavity (including ovaries), uterosacral ligaments, pouch of douglas, rectosigmoid colon, bladder and distal ureter
Other sites are rarely involved but include umbilicus, scar sites, pleura, pericardium and CNS
Cause and risk factors for endometriosis
Idiopathic but may be a result of a combination of:
Retrograde menstruation (cells flow backwards from uterine cavity through fallopian tubes implanting in pelvic organs
Lymphatic or circulatory dissemination (may travel to distant sites via lymphatic/blood system)
Genetic predisposition
Metaplasia (cells in pelvic/abdo area change into endometrial type cells)
Environmental factors (toxins)
Immune dysfunction
Risk factors: Early menarche Late menopause Later first sexual encounter Delayed childbearing Nulliparity Obstruction of vaginal outflow - FGM, hypercolpos etc. Family history Caucasian ethnicity Low BMI Smoking
Endometriosis presentation and investigations
Presentation:
Dysmenorrhoea
Dysparenuia
Cyclical or chronic pelvic pain
Subfertility
Other - bloating, lethargy, low back pain, cyclic rectal bleeding, asymptomatic
Complications - risk of ovarian cancer, infertility, adhesions, IBD
Investigation/diagnosis: Laparoscopy GOLD STANDARD Transvaginal USS MRI to assess extent/severity CA 125, FBC, urinalysis and microscopy, cervical swabs, beta-HCG to exclude differentials acutely
Endometriosis Management and referrals
Management:
Based on nature, severity and future fertility plans
Suppression of ovarian function for at least 6 months via COC, medroxyprogesterone acetate, GnRH agonists
Levonorgestrel IUS effective after 3 years of use
Surgery - removing infiltrating lesions, ovarian cystectomy, adhesiolysis and bilateral oophorectomy +/- hysterectomy
Uterine artery embolisation for adenomyosis - short/medium term relief
Pain management (NSAIDs, paracetamol, danazol, GnRH agonists for 3-6 months) and clinical psychology referrals
AVOID medical treatment for women trying to conceive
Referral:
Severe, persistent or recurrent symptoms
Pelvic signs of endometriosis
Initial management not effective/not tolerated or CI
adenomyosis pathology, cause and risk factors
Background:
Occurs in around 10% of women
Pathology:
The invasion of myometrium by endometrial tissue causing inflammation, pain, formation of adhesions, enlargement of uterine wall and can lead to chronic pelvic pain, dyspareunia and infertility
Aetiology:
Not well understood but thought to have a multifactorial cause (hormones, trauma, inflammation)
Risk factors:
Later reproductive years
Multiparous women (multiple pregnancies)
Presentation of adenomyosis
Dysmenorrhoea
Menorrhagia
Dyspareunia
Infertility or pregnancy related complications
⅓ are asymptomatic
Associated with - infertility, miscarriage, preterm birth, small for gestational age, malpresentation, C section and postpartum haemorrhage
Adenomyosis investigation and management
Investigation:
Bimanual exam - enlarged, tender uterus, feels softer than fibroids
Transvaginal USS first line
MRI/transabdominal USS
Histological exam (GOLD STANDARD after a hysterectomy)
Management:
Symptoms tend to resolve after menopause as the condition is hormone dependent
Does not want contraception: Tranexamic acid (no associated pain) Mefenamic acid (with associated pain)
Contraceptive:
Mirena coil first line
COC
cyclical oral progesterone
Premenstrual symptoms PMS
Background:
Most common type is called Core PMDs (premenstrual disorders), must have no other underlying cause to be found
Premenstrual dysmorphic disorder (PMDD): a severe form of PMS, occurring when a woman suffers from at least 5 out of 11 distinct psychological premenstrual symptoms, one of which must include mood
Variants of PMD: do not meet PMD criteria:
Premenstrual exacerbation of underlying disorder (Diabetes, depression, migraine)
Non-ovulatory PMDs (symptoms result from ovarian activity other than ovulation)
Progesterone-induced PMD (symptoms result from exogenous progesterone administration like HRT, COC etc.)
PMDs with absent menstruation (symptoms arise from continued ovarian activity even though menstruation has been suppressed (hysterectomy, ablation, LNG-IUS etc.)
Pathology:
Symptoms are present during the luteal phase and resolve as menstruation begins, then followed by a symptom free week
Aetiology:
Hormonal changes during the luteal phase of the menstrual cycle
PMS presentation
Core PMDs: timing starts 1-2 weeks before menstruation, symptoms are nonspecific and recur in ovulatory cycles
Symptoms can be severe enough to affect daily functioning or interfere with work, school performance or interpersonal relationships
Psychological - Irritability, labile affect/mood swings, anxiety, lassitude (lack of energy), fatigue, low mood, changes in appetite, sex drive, sleep disturbance
Physical - breast tenderness/pain, joint pain, muscle pain, back pain, abdominal swelling or bloating, headaches/migraines, skin disorders (acne), swelling of extremities, weight gain
Symptoms vary in severity from person to person and time to time
Investigation/diagnosis:
Clinical diagnosis and exclusion of other possible causes
Daily symptoms diary for 2 or 3 cycles and review (daily record of severity of problems)
PMS management
Inconclusive symptoms diary - refer to hospital secondary care
Lifestyle advice - diet, exercise, stress reduction, vitamin and dietary supplements
Pain management (NSAIDs)
Moderate PMS - new COC (Yasmin)
Severe PMS - SSRI (sertraline 50-100mg OD) for 3 months- 1 year continuously or during luteal phase or CBT
Spironolactone may be used to treat physical symptoms - breast swelling, water retention and bloating
Review after 2 months to assess treatment effectiveness
Vaginitis
Background:
Bacterial vaginosis - change in normal bacteria - overgrowth of other organisms
Atrophic vaginitis/genitourinary syndrome of menopause - very common in postmenopausal women due to decreasing oestrogen
Pathology:
Inflammation of the vagina that can result in discharge, itching and pain
Usually caused by an imbalance of normal vaginal bacteria or infection
Reduced oestrogen levels especially after menopause (increases vaginal dryness) and some skin disorders may also cause
Atrophic - Epithelial lining and mucus thickens in response to oestrogen, when oestrogen is lower the cells are more prone to inflammation and there are changes in vaginal pH and microbial flora contributing to local infections.
vaginitis causes and presentation
Aetiology/risk factors:
Most common cause is bacterial vaginosis
Yeast infection (candida albicans)
Trichomoniasis (commonly transmitted via sexual intercourse)
Atrophic vaginitis
Menopausal changes in oestrogen
Presentation:
Bacterial vaginosis - 50% asymptomatic, foul/fishy-smelling vaginal discharge
Atrophic - dry vagina, burning/itching vagina/vulva, dyspareunia, vaginal discharge (white/yellow), postcoital bleeding
Vaginitis investigation and management
Investigation/diagnosis:
Genital exam
Speculum exam - atrophic will show pale mucosa, think skin, reduced skin folds, erythema and inflammation, dryness and sparse pubic hair
Management:
BV - non-pregnant women with asymptomatic BV usually need no treatment. For symptomatic/pregnant women oral metronidazole is 1st line or intravaginal metronidazole gel/clindamycin cream alternatives
Atrophic - lubricants (short relief) such as Sylk, Replens and YES. Topical vaginal oestrogen (long term use) such as oestriol cream (syringe application at night time), oestriol pessaries (nighttime), tablets (vagifem) taken OD, vaginal ring (Estring) replaced every three months
Contraindications for topical oestrogens - breast cancer, angina, venous thromboembolism, women should be monitored at least annually with a view of stopping treatment whenever possible
Cervicitis, causes and risk factors
Background:
Can be acute onset (usually severe) or chronic lasting months+
Pathology:
Irritation or infection of the cervix
Aetiology:
Gonorrhoea, chlamydia
Herpes
HPV
Risk factors:
Previous STI
Multiple/new change in sexual partner
Unprotected sex
Cervicitis presentation, Ix and management
Presentation: Purulent discharge Pelvic pain Intermenstrual and postcoital bleeding Urinary symptoms
Investigation/diagnosis:
Cervical smear +/- biopsy (cytology)
Cervical and vaginal swabs (culture)
Management:
Antibiotics for specific identified organism (doxycycline chlamydia, ceftriaxone gonorrhea)
Superficial lesions - cervical cautery (outpatient procedure) via electrocautery or cryosurgery for chronic cases
Deep lesions - deeper cauterisation or conisation under general anaesthesia
Fibroids
Background:
Very common, affecting 40-60% of women in later reproductive years and in black women
Types:
Intramural: within the myometrium (the muscle of the uterus). As they grow they change shape and distort the uterus
Subserosal: just below the outer layer of the uterus. These fibroids grow outwards and can become very large, filling the abdominal cavity
Submucosal: just below the endometrium
Pedunculated: on a stalk
Pathology:
Benign tumours of the smooth muscle in the uterus (uterine leiomyomas)
They are oestrogen sensitive and grow in response to high concentrations
aetiology:
unknown but thought to be related to genes increasing uterine growth
Fibroids risk factors and presentation
Risk factors:
Later reproductive years
Black ethnicity
Presentation: Often asymptomatic Menorrhagia is most common symptoms Abdominal pain, worse around menses Bloating or feeling full in abdomen Urinary or bowel symptoms due to pelvic pressure of fullness Deep dyspareunia Reduced fertility Palpable pelvic masses or enlarged non-tender uterus on abdominal or bimanual exam
Fibroid complications
Menorrhagia and iron deficiency anaemia
Reduced fertility
Constipation
Urinary outflow obstruction and UTIs
Red degeneration of fibroid
Torsion of fibrosis (usually pedunculated)
Malignant change to a leiomyosarcoma (<1% very rare)
Fibroid investigations
Abdominal exam Bimanual exam Hysteroscopy (submucosal fibroids with menorrhagia) Pelvic USS MRI (before surgery)
Management of fibroids
Fibroids <3cm/no uterine distortion: Mirena coil first line NSAIDs COC or cyclical oral progestogens Endometrial ablation, resection (during hysteroscopy) or hysterectomy for severe small
fibroids/menorrhagia
>3cm fibroids/uterine distension:
NSAIDs and tranexamic acid
Mirena coil (depending on size, shape and type)
COC or cyclical oral progestogens
Surgery: uterine artery embolisation, myomectomy, hysterectomy (may use GnRH agonists like Goserelin or leuproelin to reduce fibroid size before surgery)
Red degeneration of fibroids:
Ischaemia, infarction and necrosis of the fibroid due to disrupted blood supply
More likely in larger fibroids (>5cm) during 2nd or 3rd trimester of pregnancy
May occur if a fibroid rapidly enlarges during pregnancy, outgrowing blood supply causing ischaemia
Or due to kinking in blood vessels as the uterus changes shape and size during pregnancy
Presents with severe abdominal pain, low grade fever, tachycardia, vomiting
Management is supportive with rest, fluids and analgesia
TOM TIP: Look out for the pregnant woman with a history of fibroids presenting with severe abdominal pain and a low-grade fever in your exams. The diagnosis is likely to be red degeneration.
Normal pregnancy overview
Full-term lasts 40 weeks
Preterm/early labour is <37 weeks
Consists of 3 trimesters (Tri 1 - weeks 1-12; tri 2 - weeks 13-27 and tri 3 - weeks 28-40)
Age of viability - infants born very early are not considered to be viable until after 24 weeks gestation (less survival chance)
Antepartum haemorrhage (APH), bleeding during pregnancy during 1st 24 weeks can end in miscarriage
Obstetric terminologies
Gravidity: defined as the number of times that a woman has been pregnant (e.g. gravida 2 or G2)
Parity: the number of times that she has given birth to a foetus with gestational age of >24 weeks, regardless of if the child was born alive or stillborn (Para 2 or P2)
Nulliparous women: (nullip) has not previously given birth >24 weeks gestation
Primigravida: first pregnancy (Primi)
Multiparous: patient who has given birth after 24 weeks gestation two or more times regardless of outcome
Primiparous: technically refers to patient that has never given birth after 24 weeks gestation
Gestational age: duration of pregnancy starting from date of last menstrual period
Last menstrual period: date of first day of their last (most recent) period
E.g. G2 P0 - pregnant twice, no births. G1 P1 - one pregnancy and birth
Gestational age is described in weeks and days e.g. 5+0 = 5 wks since LMP, 13+6 = 13 wks 6 days gestational age
Prenatal/antenatal care
Regular forms of check-ups for pregnant women by a midwife or specialist doctor to prevent and treat potential health problems throughout the course of pregnancy
During follow ups women are encouraged to follow healthy lifestyle for the benefit of her and the baby
Provides health promotion, risk reduction and disease prevention
WHO - All women should have 8 contacts with a health provider
Screening and diagnosis helps to reduce: Maternal death Miscarriages Birth defects Low birth weight Neonatal infections
Uncomplicated pregnancy/routine care
Health promotion and identifying those at risk
Screening for haematological conditions - anaemia, thalassaemia
Screening for foetal abnormalities (NHS programme)
Screening for infections
Screening for clinical conditions (gestational diabetes, HTN)
Assessment of foetal growth and well-being
Appointments:
Managed by midwives, GPs and obstetricians
10 appointments (nullipara) 7 appointment (parous)
Each appointment is different depending on stage of gestation
Advise on supplements - vit D 10mcg OD, folic acid 400mcg OD
Lifestyle advice - smoking cessation, diet, exercise
Key pregnancy appointment and milestones
Gestational age:
<10 weeks
Booking clinic
Offer baseline assessments, lifestyle advice and plan pregnancy (booking bloods, risk assessments)
Gestational age:
10-13+6
Dating scan
Accurate gestational age is calculated from the crown rump length (CRL), confirmed intrauterine pregnancy, check development and multiple pregnancies identified
Gestational age:
16 weeks
Antenatal appointment
Discuss results and plan future appointments
Gestational age:
18-20+6
Anomaly scan
USS to identify 11 specific rare anomalies, heart conditions etc.
Gestational age:
25, 28, 31, 34, 36, 38, 40, 41, 42 wks
Antenatal appointments
Monitor pregnancy and discuss future plans
First pregnancy appointment
10 wks pregnant
Given a green book documenting pregnancy progress
Initial assessment of weight, BMI, BP, urinalysis for proteinuria
Identify those at risk and additional care needed with current/past medical history, discuss FGM, domestic violence
Lifestyle advice on diet, alcohol, smoking, exercises, education on what to expect at each stage, screening tests, antenatal classes, breastfeeding classes, mental health discussion.
Discussion or offering screening tests for blood group and Rh status, anaemia screening, IDA, sickle cell, thalassaemia (family history questionnaire) also offered HIV, Hep B and syphilis.
Offer foetal screening for chromosomal abnormalities (down’s, edward’s, pataus’s syndrome) and screening for other anomalies by USS at 18-20 wks
12 week pregnancy appointment
Checking how many weeks in pregnancy, calculating due date (estimated delivery date (EDD))
Number of foetus’
Confirm intrauterine pregnancy
Check foetal development
Detect some health conditions such as spina bifida
Mid-pregnancy anomaly scan (20 weeks)
Scan looks in detail at the bones, heart, brain , spinal cord, face, kidneys and abdomen of the baby
Allows screening for 11 rare conditions: Anencephaly Open spina bifida Diaphragmatic hernia Gastroschisis Serious cardiac abnormalities Bilateral renal agenesis Lethal skeletal dysplasia Edwards syndrome (T18) Plateau syndrome (T13)
Edwards syndrome presentation
Congenital heart defects growth retardation dysmorphic features facial clefts spina bifida severe developmental delay
Down’s syndrome screening
Combination of USS and blood tests taken over weeks 11-14
USS screening showing nuchal translucency (thickness of back of neck) Downs is indicated if thickness >6mm
Serum screening - blood sample from mother for protein markers PAPP-A (lower result = higher risk) and beta-HCG (higher result = high risk)
These combined between 10-14 weeks of pregnancy are the “combined test”
Triple test performed between weeks 14-20 weeks involving blood tests only (beta-HCG high, alpha-fetoprotein low and serum oestriol lower indicate a higher risk)
Quadruple test between 14-20 weeks is identical to the triple test but also looks at maternal inhibin-A (higher = greater risk)
Results are a statistical chance and sometimes classed as “increased chance” or “low chance”. When risk is greater than 1 in 150 women are offered amniocentesis (USS guided aspiration of amniotic fluids later in pregnancy) or chorionic villus sampling (USS guided biopsy of placental tissue done before 15 weeks gestation).
Involves sampling foetal cells for karyotyping to confirm diagnosis
Non-invasive prenatal testing is a new maternal blood test looking for DNA fragments from placental tissue, not a definitive test but gives a good indication, can be used for women with high risk (1 in 150)
Additional test for Edwards’ syndrome (trisomy 18) and Pataus’ syndrome (trisomy 13) offered at 18-20 weeks
Screening for gestational diabetes
Gestational diabetes (24-28 weeks), develops in 2 or 3rd trimester due to hormonal and other lifestyle risk factors. May develop symptoms of hyperglycemia Screening test - oral glucose tolerance test (OGTT) - 2 hours
NICE recommends test should be offered if:
BMI >30
Given birth to large babies previously
Previous gestational diabetes
Family history of diabetes
Family origin of south asia, black caribbean or middle eastern
Gestational diabetes management and complications overview
Management:
Usually improves with diet and exercise
tablets/insulin therapy may be needed to help control diabetes if lifestyle changes are ineffective
Monitoring and interventions during pregnancy and labour
Complications:
Macrosomia (big baby) may make birth complicated/difficult
Polyhydramnios - too much amniotic fluid around the baby in the womb
Type 2 DM long term
HTN in pregnancy screening
BP and urinalysis regularly throughout pregnancy
Can have HTN pre-pregnancy or diagnosed within the first 20 weeks (chronic HTN)
New onset occurring in second half of pregnancy (gestational HTN) or new HTN with features of multi-organ involvement (Pre-eclampsia)
Additional milestones for complicated pregnancies
Higher risk pregnancies need more app.
Oral glucose tolerance test (gest. diabetes)
anti-D injections in Rh -ve women at weeks 28 and 34
USS at 32 weeks for women with placenta praevia on anomaly scan
Serial growths scans are offered to increased risk of fetal growth restriction
Routine antenatal discussions and vaccines
Discuss plans for pregnancy and delivery
Symphysis-fundal height measured from 24 weeks onwards
Fetal presentation assessment from 36 weeks onwards
Urine dipstick for proteinuria and BP (pre-eclampsia)
Urine for microscopy and culture for asymptomatic bacteriuria
Vaccines: Whooping cough (pertussis) from 16 weeks gestation Influenza in autumn or winter when available
General pregnancy lifestyle advise
Folic acid 400mcg before pregnancy to 12 weeks (reduced neural tube defects)
Vitamin D supplements (10mcg/400 IU daily)
AVOID vitamin A, liver or pate (teratogenic in high doses)
AVOID alcohol (miscarriage, small for gestation, preterm birth, foetal alcohol syndrome, risk is greatest within first 3 months of pregnancy)
AVOID smoking (foetal growth restriction, miscarriage, stillbirth, preterm labour, placetal abruption, pre-eclampsia, cleft palate/lip, sudden infant death syndrome (SIDS)
AVOID unpasteurised dairy or blue cheese (risk of listeriosis)
AVOID undercooked or raw poultry (salmonella)
Continue moderate exercise but AVOID contact sports
Sex is safe
Flying increases the risk of VTE. RCOG advises flying is generally ok in uncomplicated pregnancy up until 37 weeks (single pregnancy) or 32 weeks (twins). After 28 weeks most airlines ask for a note from a healthcare professional to state it’s going well with no additional risks
Place car seatbelts above/below bump NOT across
fetal alcohol syndrome overview
refers to certain characteristics that can occur in children of mothers that consumed alcohol during pregnancy.
The features include: Microcephaly (small head) Thin upper lip Smooth flat philtrum (the groove between the nose and upper lip) Short palpebral fissure (short horizontal distance from one side of the eye to the other) Learning disability Behavioural difficulties Hearing and vision problems Cerebral palsy
Vulval neoplasms
Background:
Primary malignancy is very rare (1% UK cancers)
Usually starts as a premalignant lesion - VIN
Benign neoplasms (lipoma etc.) are less common
90% are SCC
10% are BCC, adenocarcinomas (glandular cells - Paget’s disease of vulva, bartholin’s cancer), sarcomas and melanomas
Labia majora are most common site - 50%, labia minora in 20% cases and the clitoris and bartholin’s glands are less commonly involved
5 year survival rate is >80%
Pathology:
Mutated cells proliferate forming undifferentiated/partially differentiated mass of cells - tumour
Usually spreads slowly, locally (vagina, urethra, anus) then metastasises to the groin lymph nodes, then pelvic lymph nodes
Aetiology:
Cellular mutation, environmental factors
vulval neoplasm risk factors
> 60 (70% cases)
Smoking
HIV/immunodeficiencies
HPV - especially 16, 18 (50% of SCC are in relation to HPV infection)
Vulvar intraepithelial neoplasia (VIN) - premalignant state
Lichen sclerosus (4% risk which may not be reduced with treatment)
Paget’s disease of the vulva (adenocarcinoma in situ) has risk of invasive cancer
Atypical mole - malignant melanoma
vulval neoplasms presentation
Vulval lump Ulceration with bleeding Bleeding or blood stained discharge Wart-like lesion in postmenopausal women Suspicious lesions - chronic, insufficient response to treatments Vulval pruritus and pain/tenderness Burning while urinating 75% on labia majora Presentation is often delayed Melanoma - dark brown lesions (ABCDE rule)
vulval neoplasm investigation and staging
Investigation/diagnosis:
Vaginal examination - look for spread to local or lymph node areas
Biopsy (punch or excisional) +/- vulvoscopy for subclinical lesions
Staging - cystoscopy, proctoscopy, CXR, MRI
Grading of non-invasive cancers:
Low grade squamous intraepithelial lesions (LSIL): equivalent to anogenital warts, treated with podophyllotoxin or imiquimod creams, cryotherapy or surgical excision
High grade squamous intraepithelial lesions (HGIL): topical treatment, ablation, wide local excision, skinning vulvectomy
TNM staging for Invasive vulvar cancer:
stage I - <2cm local lesion, no lymph node or distant metastases
stage II - invasion into lower 1/3 urethra, vagina and/or anus with no lymph or distant metastases
stage III - above but with lymph node metastases
stage IV - any form of vulval neoplasm with distant metastases
vulval cancer management
2WW referral for women with UNEXPLAINED vulval lump, vulval ulceration or bleeding
Pruritus or pain without suspected vulvar cancer - treat suspected cause, watch and wait, refer any persistent symptoms to gynae (2WW or routine depending on presentation)
Radical or wide local resection of cancer
Advanced - sentinel lymph node biopsy (SLNB) or groin node dissection, radiotherapy +/- chemotherapy
Reconstructive surgery after resection
Women with uncomplicated lichen sclerosus do NOT need routine hospital based follow up but must be informed of risk of cancer
vulval intraepithelial neoplasia (VIN) overview
Background:
Premalignant lesions
May start independently or as a transformation of already existing vulval disorders (lichen sclerosus, squamous cell hyperplasia)
Pathology:
VIN 1: ⅓ thickness dysplasia
VIN 2: ⅔ thickness dysplasia
VIN 3: full thickness dysplasia
Presentation:
Most pruritus
Asymptomatic
White, grey, red or raised patches of skin
Indurated, ulcerated nodules
White, multifocal pearly lesions in peri-clitoridian and labia regions
Investigation/diagnosis:
Vaginal examination
Biopsy (multiple for large lesions)
Management: Laser therapy Wide local excision Imiquimod cream (Zyclara, Aldara) Lifelong follow up - close association with HPV infection and risk of recurrence
vaginal neoplasms
Background:
Rare
80% of vaginal carcinoma is metastatic spread from the cervix, endometrium or ovary
Primary malignancy are SCC mostly and adenocarcinomas (melanoma and sarcoma are very rare)
SCC 85% cases - Upper posterior vaginal wall, postmenopausal women
Adenocarcinoma - peak incidence 17-21 years
Vaginal intraepithelial neoplasia (VAIN) is associated with other genital neoplasia (CIN, VIN) etc so should always be examined for this too
Pathology:
Cancerous cell proliferation and growth to form tumours
SCC usually spreads superficially within the vaginal wall and later invades the paravaginal tissues (bladder or rectum) and then parametria. Distant metastases most often to the lungs and liver
Adenocarcinoma - more pulmonary metastases and supraclavicular, pelvic node involvement
Aetiology:
Genetic, environmental multifactoral cell changes
vaginal neoplasms risk factors and presentation
Risk factors:
HIV (have more VIL)
HPV
Vaginal intraepithelial lesions
Presentation:
SCC - ulcerative or exophytic lesions. Some Bleeding
Adenocarcinoma - bleeding
vaginal neoplasms investigation and staging
Investigation/diagnosis:
Colposcopy - screen for other neoplasia
Multiple biopsies (vaginal, cervical, endometrial)
CT, PET, CXR, cystoscopy, sigmoidoscopy for staging
Staging FIGO system:
Stage O: SCC in situ, usually multifocal and at vaginal vault
Stage I: limited to vaginal wall mucosa
Stage II: subvaginal tissue not not pelvic wall
Stage III: extends to the pelvic wall
Stage IV: extends beyond true pelvis or involves the bladder/rectal mucosa
Stage IVA: spread to adjacent organs (bladder/rectum)
Stage IVB: spread to distant organs
vaginal neoplasm management
2WW referral for women with unexplained palpable mass in or at entrance to the vagina
Dependent on stage
Carbon dioxide laser - safe and effective in premalignant condition
Surgery and radiotherapy - early stages of disease (stage I and II some cases may need a radical hysterectomy with removal of upper vagina)
Radiation therapy - advanced stages
pelvic organ prolapse
Background:
Can be classified according to compartment affected
Anterior vaginal wall prolapse - cystocele, urethrocele (most common)
Posterior vaginal wall prolapse - rectocele, enterocele (prolapse of bowel into top part of vagina)
Prolapse of the cervix or uterus
Apical prolapse - Prolapse of the uterus or vaginal vault (least common)
Prolapse of the vaginal vault (occurs after hysterectomy)
40-60% of parous women experience prolapse
Several types may coexist in the same patient
Pathology:
Falling, slipping or downward displacement of pelvic organ(s) or structure beyond its normal confines
Caused by weakness of the supporting structures (levator ani muscles and endopelvic fascia) allowing pelvic organs (bladder, rectum, uterus, vaginal vault etc.) to sag into the vagina
pelvic organ prolapse cause and risk factors
Aetiology: Congenital weakness (rare) Childbirth Menopausal atrophy (coughing and straining exacerbating condition) Likely a multifactorial cause
Risk factors: Increasing age Obesity Increasing parity Vaginal delivery Previous hysterectomy
pelvic organ prolapse presentation and investigation
Presentation:
Based on type, may cause urinary, bowel, sexual, local pelvic symptoms
Vaginal symptoms - common in all types - sensation of heaviness, fullness, bulging, difficulty retaining tampons, spotting (ulceration)
Urinary symptoms - incontinence, frequency, urgency, tenesmus, weak/prolonged stream, need to manually reduce/change position prolapse before voiding/to completely void
Coital difficulty - dyspareunia, loss of sensation, flatus, loss of arousal, change in body image
Bowel symptoms - constipation, urgency, incontinence, flatus, tenesmus, needing to apply digital pressure or digital evacuation
Investigation/diagnosis: Clinical diagnosis Vaginal examination Bimanual examination In standing and LLD positions, Sims’ speculum - ask to strain/cough
pelvic organ prolapse management
Conservative:
Regularly assess for symptoms and complications until treatment is needed
Lifestyle - decrease weight, avoid heavy lifting, prevent constipation, smoking cessation, pelvic floor exercises (Kegel’s for supervised 16 week course of training, continue if beneficial)
Topical oestrogen: For postmenopausal women with vaginal atrophy Estriol cream 0.1% twice weekly Oestrogen releasing ring Estradiol vaginal tablets
Vaginal pessary:
Silicone or plastic ring shaped device into the vagina to provide support and relieve pressure on bowel or bladder (FIRST LINE usually)
Can be used short term prior to surgery or long term if surgery is not wanted or CI
Should be removed and changed every 6 months to avoid complications
Common types: ring, Gellihorn, Doughnut pessaries
Treat vaginal atrophy BEFORE fitting
May affect sexual intercourse
Complications: bleeding, discharge, difficulty removing, expulsion
CI: active pelvic infection, ulceration, silicone allergy
Surgery:
Failure or other treatments, presence of voiding/bowel symptoms, recurrence of prolapse after surgery, ulceration, irreducible, or preferred treatment
Choice based on if they’re sexually active, family plans, general fitness, past hysterectomy, nature of prolapse
Can be abdominal or transvaginal surgery
Surgery indicated for POP-Q stage 2+
Needs follow ups annually for 5 years
cystocele overview
Prolapse of the bladder into the vagina (anterior wall prolapse)
Presentation:
Small isolated cystocele - asymptomatic/few symptoms
Larger - frequency, recurrent UTI, sensation of pressure, mass
Investigation/diagnosis: Vaginal examination Standing and Sim’s speculum exam - ask to strain/cough Urinalysis and MSU Urodynamic studies Urea and creatinine Renal USS
Management: conservative (lifestyle) vaginal pessaries topical Oestrogens Surgery - anterior colporrhaphy + Mesh reinforcement
rectocele overview
Prolapse of the rectum into the vagina (posterior wall prolapse)
Presentation:
Asymptomatic
Splinting (applying digital pressure to perineum or posterior vaginal wall to defecate)
Digital rectal evacuation
Investigation/diagnosis:
Vaginal examination
Standing and Sim’s speculum exam - ask to strain/cough
Anal manometry
Defecography
Endo-anal USS (if fecal incontinence to assess anal sphincter)
Management: conservative vaginal pessaries topical Oestrogens Surgery - posterior colporrhaphy + mesh reinforcement
history taking for breast complaint
Examination:
Ask them to remove clothes from the waist up, including bra, go behind curtain for privacy
Use paper towel to cover self up while waiting
History taking:
When did you notice it?
Is it painful?
When was the last menstrual period? Could you be pregnant? Is the condition premenstrual?
Are you currently breastfeeding?
Does the lump size change?
Have you noticed nipple changes? Discharge, inverted?
Changes to the colour of the skin?
Any trauma to the breast? (haematoma)
Any previous breast lumps or diagnoses?
History of breast surgeries? Scarring, fibrosis, much more difficult to feel a lump
Family history of breast cancer?
Taking any regular medications? Allergies?
fibroadenosis
Background:
More common in women of childbearing age, can occur unilaterally or bilaterally
More than 50% of women have fibroadenosis/fibrocystic disease at some point in their lives
Do not increase the risk of cancers
Pathology:
Fibrosis: similar to scar tissue
Cyst - fluid filled sacs
Aetiology:
Usually as a result of hormonal changes during menstrual cycle
fibroadenosis presentation, Ix and Mx
Presentation:
COC, HRT and pregnancy can make the lump tender/worse
Fibrosis - feels rubbery, firm, hard to touch
Cysts - >2.5cm, can become tender before periods, mobile, smooth, fluctuant lumps
Much more common to be bilateral
Investigation/diagnosis: Breast examination (ask them where they felt it to help locate)
Management:
Reassurance and education as to cyclical nature
Supportive bra
NSAIDs, review of contraceptive (if it is impacting them significantly)
If after 3 months and impacts on quality of life - refer to specialist team for further management
Larger cysts - needle aspiration or local excision
fibroadenoma
Background: Common in puberty and younger girls AKA the breast mice - small and mobile 25% self-resolve Simple fibroadenomas - 1-3cm size Complex - can be >5cm Other types - giant and juvenile
Pathology:
Benign tumour developed from a lobule within the breast tissue forming a solid lump
Aetiology:
Unknown aetiology - thought to be an increased sensitivity to oestrogens causing growth
fibroadenoma presentation, Ix and Mx
Presentation:
Lump developing from lobule (usually <3cm)
Smooth, rubbery textured unilateral lump (raisen like)
Highly mobile
Common in puberty
Hormone dependent, regress after menopause
Usually painless but can cause pain/deformity
Investigation/diagnosis:
Breast examination
Mammography/USS
Excisional biopsy (not needed if <25 YO with confirmed diagnosis)
Management:
Asymptomatic, simple fibroadenomas - no treatment needed and no follow-ups (should report/have all new fibroadenomas checked individually)
Symptomatic - usually removed surgically or by vacuum-assisted mammotome (GA or LA)
lipoma in breast overview
Background:
Benign breast lesions
Painless, fatty lump caused by overgrowth of adipose cells
Pathology:
Benign mesenchymal tumours composed of mature adipose tissue
Aetiology:
Multifactoral
Presentation: Soft and doughy Slow growing Up t0 20cm size Painless most often
Investigation/diagnosis:
Breast examination
Mammography/USS
Management:
Refer to 2WW if diagnosis is uncertain
Diagnosis certain and asymptomatic - leave alone
Diagnosis uncertain - imaging +/- surgical intervention
Patient symptomatic - surgically removal
mastitis
Background:
Painful, inflammatory condition which can be accompanied by an infection
It is not clinically possible to differentiate between infected and non-infected mastitis
Pathology:
Non-infectious - milk stasis irritated breast tissue causing inflammation
Infectious - milk stasis leads to infection, spreading through breast tissue causing inflammation
Aetiology:
Lactating women - milk stasis usually primary cause
Soft tissue infection via break in skin integrity
Risk factors:
Breastfeeding (weaning baby off breast milk or within first few weeks of starting especially)
Smoking - damage to ducts in breast
mastitis presentation, ix and mx
Typically develops within first few weeks of breastfeeding
Very tender breast
Red, swollen breast sometimes with hard areas
Can present with fever and general malaise
Investigation/diagnosis:
Clinical
Breast exam
Management:
Antibiotics (flucloxacillin soft tissue infection)
NSAIDs
Continue breastfeeding/expression of milk if possible to avoid milk stasis
breast abscess overview
Collection of pus within the breast tissue
Aetiology:
Can be complication of mastitis (infected mastitis)
Soft tissue infection - commonly staphylococcus aureus and strep pyogenes
Presentation: Extremely painful May be visible on skin surface Can present as very tender lump May be very afebrile and unwell (fever, tachycardia, hypotensive)
Investigation/diagnosis:
Clinical
Breast exam
Culture of fluid
Management:
Refer urgently for diagnostic USS, drainage (USS guided needle aspiration/surgical drainage)
Antibiotics (IV if needed)
Advise lactating women to try to continue breastfeeding or express if too painful to avoid milk stasis
breast carcinoma
Background:
Most common form is ductal carcinoma in situ (DCIS) for invasive and non-invasive types
Most types are invasive, inflammatory carcinoma only occurs in a minority of cases
Approximately 4-6% of breast cancers are metastatic when diagnosed
Second most common cause of death from cancer in the UK
Pathology:
Cancerous mass
Aetiology:
Multifactoral
breast carcinoma risk factors
Previous breast cancer Family history Genetics - BRCA1, 2 and TP53 mutations Nulliparity or giving birth after 30 Early menarche and late menopause Radiation to chest Western style diet Obesity Alcohol HRT COC Breast augmentation does NOT increase the risk but can make diagnosis difficult
breast carcinoma presentation
Lump/craggy feeling lumps (walnut consistency), bumpy, hard, no defined borders, less mobile
Nipple changes, discharge - bloody discharge in intraductal carcinoma
Skin dimpling
Skin changes
Breast pain
breast carcinoma Ix and staging
Breast examination
Mammograms >30 years OR USS <30 years
Biopsy (FNA)
TNM Staging - CXR, CT, bloods (LFTs), PET, bone scans
staging:
N0-N3: no lymph node - metastases to one+ lymph nodes
M0-M1: no distant metastases - distant metastasis
breast carcinoma management
Management:
Stop systemic HRT, offer counselling about early menopause risk and fertility preservation
Surgery
Radiotherapy (can be preoperative to shrink large tumours)
Chemotherapy
Hormone therapy
Biological agents
Follow up - no screening needed for total mastectomy, yearly mammography for 5 years in those with early BC, after 5 years frequency based on risk for individuals. All patients should have care plans with contact details, treatment review dates, surveillance dates, safety netting advice and support service details
NICE breast referral guidelines
NICE 2WW referral guidelines for breast lumps:
30+ with unexplained breast lump with/without pain
Skin changes suggestive of breast cancer
50+ with any of the following:
Discharge from nipple
Retraction of nipple
Other changes of concern
Consider non-urgent referral in those aged <30 with an unexplained breast lump with/without pain
inflammatory breast carcinoma overview
Background:
Poor prognosis, 50% 5 year survival rate with lymph node involvement
50% 2 year survival with metastatic rate
More common in younger population
Pathology:
Rapidly growing, painful mass causing enlargement of the breast and overlying skin to become erythematous and hot
May have diffuse infiltration of tumour
Aetiology:
Multifactoral
Risk factors:
As for breast carcinoma
Presentation: NOT TENDER Red, swollen breast Hot and firm to touch Ridges/thickening of skin Pitted skin like orange peel Lump in breast Discharge from nipple Inverted nipple
Investigation/diagnosis and management:
as for breast carcinoma
breast self examination guide
look for: thick mass indentation skin sores or rashes erythema or heat new fluid dimpling bump growing vein retracted nipple new shape/size orange peel skin (textured) hidden lumps pain in breast or armpit all of the time swelling in the armpits or around the collar bone
breast cancer radiotherapy advice/info
- anyone receiving radiotherapy for breast cancer receives targeted radiotherapy just to the breast tissue
- does not cause any pain or discomfort
- patient must not move at all
- teats 2% of the lungs - possibly may get lung fibrosis (small amount) as complication
- 2 week treatment everyday OR every 4 days go in for treatment
- often causes fatigue
- big lump of vaseline like substance put on top of directed breast (BOLUS) and used to bring therapy away from the lung closer to the skin - causes a burn in shape of bolus (square red mark on chest)
- large masses may need radiotherapy before surgery to shrink the tumour - needs a two week gap between radiotherapy and surgery
fungating breast cancer
extensive breast cancer with fungal growths
usually problematic and very high risk to remove due to extensive blood supply - needs radio +/- chemo to shrink the tumour and then remove more safely
male breast cancer overview
Background:
Rare (1% all breast cancers)
Prognosis largely depends on staging
Staging identical to female breast cancer
Most common type is infiltrating ductal carcinoma
Pathology:
Cancerous mass
Aetiology:
Multifactoral
Risk factors: Increasing age BRCA1, 2 genes Elevated oestrogen (gynaecomastia) Prior radiation Family history of breast cancer
Presentation: Painless or tender lump, hard knot, thickening of breast/chest area Change in size/shape of breast Dimpling, puckering, redness of skin Itchy, scaly, sore rash Inverted nipple Nipple discharge
Investigation/diagnosis:
Breast examination
Mammography or USS
Tissue biopsy (FNA)
Management:
Surgery (radical mastectomy or simple mastectomy)
Hormone therapy (tamoxifen)
Radiotherapy +/- chemotherapy
Gynaecomastia
Background:
Can occur from neonates to elderly
⅓ of men experience in their lifetime
Most commonly ages 50-69
Breast cancer only detected in 1% of male breast enlargement
Common in puberty and old age and is most often entirely reversible
Pseudogynecomastia - breast enlargement mainly due to excess adipose tissue formation
Pathology:
Benign proliferation of male breast glandular tissue, resulting from a relative decrease in androgen effect/increase in oestrogen effect
May be associated with chronic liver disease/drug induced due to altered oestradiol/testosterone ratio
Aetiology/risk factors: Obesity Oestrogen surge (neonates) Puberty Drop in testosterone in old age Medication - oestrogens, digoxin, metronidazole, ketoconazole, spironolactone, chemotherapy, GnRH, anabolic steroids, antiretrovirals etc. Alcohol Illicit drugs - cannabis Chronic liver disease
Gynaecomastia presentation and red flags
Presentation:
Mass around >2cm size, firm
Palpable, subareolar gland and ductal breast tissue
Evidence of palmar erythema, bruising, spider naevi, hepatosplenomegaly (liver disease)
Red flags: Unilateral enlargement Hard or irregular breast tissue Rapidly enlarging Recent onset Fixed mass Nipple or skin abnormalities Painful breast Axillary LAP
gynaecomastia Ix and Mx
Investigation/diagnosis: Breast exam Bloods - eGFR, LFTs, TFTs, hormone profile USS/mammography CXR for suspected lung lesions Biopsy (FNA)
Management:
Refer if any red flags on 2WW pathway
Neonates - leave, reassurance and education
Reassurance, education, Diet and lifestyle advice (weight loss, alcohol decrease)
Surgery (exceptional case funding)
Drugs to reduce oestrogen
causes of retracted nipples
Injury to breast, surgery
Breast cancer
Breast infections (mastitis)
Rapid and substantial weight loss
galactorrhea
Background:
Lactation can begin during second trimester and can continue up to 2 years post-breastfeeding in pregnancy
Can also be idiopathic hyperprolactinemia - elevated prolactin levels with absence of underlying cause, usually self limiting and benign
Prolactinomas - pituitary gland tumour, most common between ages 20-40
Pathology:
Milk production from breasts in response to the hormone prolactin (produced in anterior pituitary, breast and prostate)
Dopamine blocks prolactin secretion
Aetiology: Pregnancy Idiopathic hyperprolactinemia Prolactinomas Drugs - contraceptives, SSRIs, antipsychotics, methyldopa, digoxin, spironolactone etc. Endocrine disorders - hypothyroid, acromegaly, Cushing’s, PCOS Liver failure CKD
Risk factors:
Prolactinomas are associated with MEN1 syndrome
galactorrhea presentation, Ix and mx
Presentation:
Idiopathic hyperprolactinemia - galactorrhoea
Prolactinomas - gynaecomastia, sexual dysfunction, amenorrhea, infertility, bitemporal hemianopia, galactorrhea
Investigation/diagnosis:
Pregnancy test
Medication review
Cranial nerve exam (bitemporal hemianopia)
Bloods - hormone profile, LFTs, TFTs, eGFR
Management:
Prolactinomas - bromocriptine (dopamine agonist) and surgery to remove tumour
Idiopathic hyperprolactinemia - bromocriptine to reduce prolactin concentration
Identify and treat underlying cause
menopause
Background:
Women periods cease for >12 months and are no longer able to become pregnant naturally
Permanent end to menstruation
On average occurs at age 51 although this varies significantly
Menopause is the point at which menstruation ceases
Postmenopase - period from 12 months after final menstrual period onwards
Perimenopause - time around the menopause, women often experience vasomotor symptoms, irregular periods etc. and are typically >45 YO
Premature menopause - menopause before age 40.
Pathology:
Primordial follicles mature into primary and secondary follicles within the ovaries, meaning the numbers deplete throughout our lifetime.
Without the growth of follicles there is reduced production of oestrogen
As oestrogen declines in perimenopausal period there is an absence of negative feedback on the pituitary gland, therefore increased levels of LH and FSH
The failing follicular development results in anovulation, irregular menstrual cycles and amenorrhoea (due to endometrium not developing)
Lowered oestrogen also causes perimenopausal symptoms
Aetiology:
Premature - premature ovarian insufficiency
natural decline in primordial follicles via ovulation during reproductive years
perimenopause/menopasue presentation
7 dwarfs of menopause: Sleepy Bitchy Itchy Psycho Forgetful Sweaty Bloaty
Hot flushes Emotional lability or low mood Premenstrual syndrome Irregular periods Joint pains Heavier or lighter periods Vaginal dryness and atrophy Reduced libido
postmenopause - absence of menses for >12 months
risks associated with oestrogen decline
CVD and stroke increase
Osteoporosis
Pelvic organ prolapse
Urinary incontinence
menopause Ix and management
Investigation/diagnosis:
Clinical (Perimenopause and menopause diagnosis can be made in women >45 with typical symptoms without performing investigations)
NICE guidelines state to use FSH blood test to aid diagnosis in women <40 with suspected premature menopause and women aged 40-45 with menopausal symptoms or change in their menstrual cycle
Management:
Vasomotor symptoms are likely to resolve after around 2-5 years without treatment
HRT
Tibolone (synthetic steroid hormone can only be used 12 months after menopause)
Clonidine (alpha adrenergic agonist and imidazoline receptor agonist)
CBT
SSRIs (fluoxetine or citalopram)
Testosterone (for reduced libido) usually cream or gel
Vaginal oestrogen cream/tablets for vaginal dryness or atrophy (can be used alongside systemic HRT)
Vaginal moisturisers (Sylk, Replens and YES)
HRT
HRT:
Small doses of an oestrogen (plus progesterone in women with a uterus) used to counter decreasing hormone levels and associated symptoms of menopause
Come in various forms: tablets, patches, gels
Can use vaginal products if symptoms are limited to that region (vaginal atrophy) or systemic products for vasomotor symptoms etc.
Has increased risk of endometrial cancer, ovarian cancer, thrombosis, CVD (stroke, CAD)
Patch:
Apply once weekly continuously
Women with uterus going through PERIMENOPAUSE have cyclical progesterone (e.g. medroxyprogesterone acetate 10mg daily for last 14 days of 28 day HRT cycle) containing patch to induce menstrual bleed and reduce risk of abnormal cells developing
POSTMENOPAUSAL women have continuous oestrogen (non-cyclical)
contraception and perimenopause
Fertility gradually declines after 40, however women should still consider themselves fertile.
Pregnancy after 40 is associated with increased risks and complications.
Women need to consider contraception for:
Two years after the last menstrual period in women under 50
One year after the last menstrual period in women over 50
Hormonal contraceptives do not affect the menopause, when it occurs or how long it lasts, although it may suppress symptoms
UKMEC 1 contraceptive choices for women approaching menopause:
Barrier methods
Mirena or copper coil
POP
Progesterone implant
Progesterone depot injection (under 45 - not suitable for over age 45 due to osteoporosis risk)
Sterilisation
UKMEC 2:
COC (ages 40-50 if no CI)
Norethisterone or levonorgestrel containing pills in women >40 have lower VTE risk
anovulation overview
Background:
Chronic anovulation is a common cause of infertility (30% female infertility)
Pathology:
Lack or absence of ovulation caused by an imbalance of FSH increase to stimulate follicle growth and LH surge needed to cause ovulation
Aetiology: PCOS Obesity Stress Low body weight/excessive exercise Thyroid dysfunction Physiological - before menarche and postmenopausal
Presentation: Irregular menstruation Amenorrhea Presentation of underlying cause Lack of physiological changes from ovulation - temperature increase etc.
Investigation/diagnosis:
Clinical
Bloods - progesterone, TFTs, SHBG, free testosterone
Pelvic USS
Management:
Lifestyle - healthy weight/BMI, alter exercise habits, stress management, CBT
Clomiphene citrate
Aromatase inhibitors
Insulin sensitising agents
Gonadotrophins
IVF or intrauterine insemination (IUI) for infertility
oligomenorrhoea
Background:
Very common can be physiological variation in cycles
Can be pathological
Very common in adolescence and perimenopause
Pathology:
Infrequent menstrual periods >35 days in length
Aetiology: Physiological variance, perimenopause and puberty, Pregnancy Hormonal birth control (IUS/POP/implant/injection) Excessive exercise Anorexia and bulimia Thyroid dysfunction Diabetes Hyperprolactinemia
Presentation:
Oligomenorrhea
Symptoms of underlying cause (if present)
oligomenorrhoea Ix and Mx
Investigation/diagnosis: History/clinical Pelvic/transvaginal USS Bloods - FSH/LH, prolactin, SHBG, free testosterone, TFTs, glucose/insulin Medication review
Management:
Lifestyle - healthy BMI, alter exercise as needed
Hormonal birth control to induce regular cycles (and reduce risk of endometrial hyperplasia and cancer in cases of severe oligomenorrhea)
Identify and treat cause
PCOS
Background:
5-15% of women of reproductive age are affected
Causes metabolic and reproductive problems, characterised by multiple ovarian cysts, infertility, oligomenorrhea, hyperandrogenism and insulin resistance
Pathology:
Multiple follicles fill with fluid appearing like a cyst instead of having normal follicle anatomy
Essential changes include hyperandrogenism from ovary production (due to hyperinsulinemia or LH levels)
Reduced production of sex hormone-binding globulin (SHBG) in the liver (may subsequently raise levels of free testosterone)
LH:FSH ratio increased due to raised LH levels (>2)
Oestrogens may be normal or slightly raised and may have hyperinsulinemia due to insulin resistance which can lead to glucose intolerance
Aetiology:
Cause unknown but likely multifactorial.
Genetic link (family clustering)
Risk factors:
Family history
PCOS presentation
Asymptomatic (33%) Oligomenorrhea (<9 periods per year) Fertility difficulty Acne Hirsutism (60%) Male pattern balding, alopecia Obesity or difficulty losing weight Acanthosis nigricans CVD, hypercholesterolemia Endometrial hyperplasia/cancer risk increased Obstructive sleep apnea Sexual issue Depression and anxiety
PCOS ix and diagnosis
Investigation/diagnosis:
History to exclude other causes
Pelvic/transvaginal USS (cysts and endometrial thickness)
Bloods - LH, FSH, insulin, free testosterone, oestrogens, SHBG, OGTT
QRISK and CVD factors
PCOS does not have to be present on USS, and this finding alone does not establish a diagnosis.
Both hyperandrogenism and irregular menstrual cycles are needed to diagnoses PCOS, especially in adolescence girls
Two of the following needed for diagnosis (Rotterdam criteria):
Polycystic ovaries (either 12+ peripheral follicles or increased ovarian volume >10cm3)
Oligomenorrhea or anovulation (amenorrhea)
Clinical or biochemical signs of hyperandrogenism, including hirsutism, male balding, elevated testosterone etc.
PCOS management
There is no treatment to reverse hormonal disturbances, medical management is targeted on individual symptoms and only in association with lifestyle changes Patient education (oligomenorrhea/amenorrhea known to increase risk of endometrial hyperplasia and cancer in untreated cases - encourage progesterones to induce withdrawal bleed at least every 3-4 months to reduce risk of cell changes) Lifestyle - weight reduction, address psychological problems (CBT, therapy), smoking cessation
Prolonged oligo/amenorrhea (less than one period/3 months), abnormal bleeding or excessive weight
Cyclical progesterone for 14 days to induce withdrawal bleeding,
COC/LNG-IUS long term
Manage long term complications (diabetes - regular OGTT tests, CVD risk assessments)
Metformin used off-licence (specialist). Orlistat to assist with weight loss and may improve testosterone and insulin sensitivity
Antihypertensives and statins if needed (QRISK)
Infertility - Clomiphene, laparoscopic ovarian drilling or IVF if weight loss does not improve symptoms/fertility
Hirsutism - weight loss, dianette COC, topical eflornithine (facial hair usually takes 6-8 weeks), electrolysis, laser hair removal, spironolactone, finasteride, flutamide, cyproterone acetate
Acne - COC first line, topical adapalene, topical antibiotics, topical azelaic acid 20%, oral tetracycline antibiotics (lymecycline first line)
primary amenorrhea
Background:
Menses have not occurred by age 15, this can vary depending on other secondary sexual characteristics present
Not starting menstruation by age 13 where there is NO other evidence of puberty development
By age 15 where there ARE other signs of puberty (breast buds etc.)
Pathology:
Puberty usually starts between ages 8-14 in girls and takes about 4 years. Begins with development of breast buds, then pubic hair and finally menarche (from about 2 years pubertal onset)
Before puberty there is a state of hypogonadism (lack of sex hormones) and a lack in these hormones (FSH and LH) for longer than usual can delay puberty, leading to an absence or cessation of menstruation
Hypogonadotropic hypogonadism - deficiency in LH and FSH from anterior pituitary gland, resulting in lack of stimulation to produce oestrogens. Results in low FSH, LH and oestrogens.
Hypergonadotropic hypogonadism - gonads fail to respond to FSH and LH resulting in lack of oestrogen production. No negative feedback on pituitary leads to excess LH and FSH levels. Results in high levels of FSH and LH and low oestrogens
Aetiology/risk factors:
Hypogonadotropic hypogonadism - hypopituitarism, damage to HPG axis (radio or chemotherapy), cystic fibrosis, IBD, excessive exercise/dieting, constitutional delay in growth and development, thyroid disorders, Cushing’s, hyperprolactinemia, Kallman syndrome
Hypergonadotropic hypogonadism - previous damage to gonads (torsion, cancer, infections - mumps), congenital absence of ovaries, Turner syndrome
Structural pathology - imperforate hymen, transvaginal septae, vaginal agenesis, absent uterus, FGM
primary amenorrhea presentation, Ix and Mx
Presentation:
Absence of menses either before menarche
Kallman syndrome - failure to start puberty associated with anosmia (loss of smell)
Congenital adrenal hyperplasia - family history (autosomal recessive), electrolyte disturbances at birth, hypoglycemia, tall for their age, facial hair, amenorrhea, deep voice, early puberty
Androgen insensitivity syndrome - female phenotype with male internal pelvic organs
Investigation/diagnosis:
Threshold for investigating is NO evidence of pubertal changes in a girl aged 13, or can be considered if there is some evidence but no progression after two years
Bloods - FBC, ferritin, U+E (CKD), anti-TTG or anti-EMA (coeliac), LH, FSH, TFTs, IGF-1, prolactin, testosterone
Genetic testing - Turner’s syndrome (XO)
Wrist XR - bone age for constitutional delay diagnosis
Pelvic USS
MRI brain - pituitary pathology and olfactory bulbs (Kallman syndrome)
Management:
Identify and treat underlying cause
Healthy diet, BMI, altered exercise regimens, stress management (CBT)
Constitutional delay in growth and development - reassurance and observation
Hypogonadotropic hypogonadism - pulsatile GnRH to induce ovulation and menstruation and can potentially induce fertility. If pregnancy is not wanted then replacement sex hormones (COC) to induce regular menstruation and prevent oestrogen deficiency
Ovarian cause - (PCOS, damage) - COC to induce menstruation and releve oestrogen deficiency
secondary amenorrhea
Background:
Secondary - menstruation has previously occurred but has stopped (usually at least 3 with previously normal menstruation or 6-12 consecutive months with previous oligomenorrhea)
Pathology:
GnRH production is inhibited in response to significant physiological and psychological stress, leading to hypogonadotropic hypogonadism and amenorrhea.
This is the body’s response to prevent pregnancy when the body may not be fit for it e.g. excessive exercise, low body weight, chronic disease, psychological stress
Pituitary tumours (prolactinoma - high prolactin negatively feeds back to inhibit GnRH) or pituitary failure from trauma, radiotherapy, surgery or Sheehan syndrome may also lead to secondary amenorrhea
Aetiology:
Physiological - pregnancy, menopause, POP and IUS-mirena coil
Pathological with no androgen excess - primary ovarian failure, chemotherapy, irradiation, Turner syndrome, hypothalamic dysfunction, pituitary disease, hyperprolactinemia, thyroid disease,
Pathological with androgen excess - PCOS, Cushing’s, adrenal/ovarian carcinoma
secondary amenorrhea presentation, Ix and Mx
Presentation:
Previous menses ceased for 3-6 months
Evidence of underlying pathology
Investigation/diagnosis:
Pregnancy test
Bloods - FSH, LH, prolactin, testosterone and sex hormone-binding globulin, TFTs
Pelvic USS
Management:
Pituitary adenoma - no treatment, dopamine agonists to reduce prolactin
Lifestyle advice - excessive exercise, obesity/anorexia can cause amenorrhea
Secondary - investigate and manage underlying cause
Replacement hormones to induce menstruation and improve symptoms - COC/POP
Associated with low oestrogen levels - vitamin D and calcium, HRT or COC to prevent osteoporotic effects
primary ovarian insufficiency
Background:
Menopause before the age of 40
Pathology:
Decline in normal activity of the ovaries at an early age
Characterised by hypergonadotropic hypogonadism - under activity of the gonads to produce oestrogen resulting in excess LH and FSH with low oestrogen levels
Aetiology:
Idiopathic (50%)
Iatrogenic - chemotherapy, radiotherapy, surgery
Autoimmune - coeliac disease may be associated, adrenal insufficiency, T1DM, thyroid disease
Genetic - family history or Turner’s syndrome
Infection - mumps, TB, cytomegalovirus
primary ovarian insufficiency presentation, Ix and Mx
Presentation:
Early onset presentation of perimenopausal symptoms (hot flushes, night sweats, vaginal dryness, low libido, irritable mood swings, bloating etc.)
Irregular menstrual periods or amenorrhea
Menopause
Associations - CVD, stroke, osteoporosis, cognitive impairment, dementia, parkinsonism
Investigation/diagnosis:
Can be diagnosed in women younger than 40 with typical menopausal symptoms and elevated FSH levels (persistently >25 IU/l on 2 consecutive samples with more than 4 week gap) for diagnosis
Bloods - hormone profile
Management:
HRT until the age of expected natural menopause (52) to reduce low oestrogen risks and symptoms associated - can be traditional hormone replacement or COC pill
Traditional associated with lower BP compared to COC but the COC additionally acts as a contraceptive
Extramammary Paget disease of the skin overview
Uncommon intraepithelial adenocarcinoma usually of the anogenital or axillary skin
Classified into primary (cutaneous origin) and secondary disease (associated with primary adenocarcinoma elsewhere in the body)
Generally affects >50 YO more common in caucasian females or asian males
Poorly understood aetiology but most commonly located in the apocrine gland rich skin
Usually itchy, excoriations and lichenification can present
Burning pain, irritation, hyperpigmentation and/or leukoplakia
Erosions, maceration, crusting, nodules (indicate later invasive disease)
Diagnosed clinically and via skin biopsy for conformation
Surgical treatment for wide local excision and Mohs micrographic surgery is the standard treatment, consider lymph node biopsy if it has extended into reticular dermis or within lymphatics or vascular spaces - this can impact quality of life significantly
Imiquimod cream may be good non-surgical management for initial or recurrent presentation
Radiotherapy
High recurrence rate, long term follow-ups are recommended to monitor for recurrence.
lichen sclerosis overview
Common chronic skin disorder most often affecting genital and perianal areas
Can begin at any age although often diagnosed after 50 YO
10x more common in women and 15% patients know a family member with this condition or often have personal/family history of another autoimmune disease like thyroid, pernicious anaemia or alopecia areata.
May coexist or follow another skin condition (most often lichen simplex, psoriasis, erosive lichen planus, vitiligo or morphea)
Cause is poorly understood, thought to be multifactorial but often classified as autoimmune
Is associated with ECM-1 antibodies
Presents as white crinkled or thickened patches of skin that tend to scar
Complications include infection and SCC
Diagnosed clinically and via dermoscopy/skin biopsy
Treatment general: wash once or twice daily, non-soap cleanser, avoid tight clothing, rubbing and scratching, activities like biking, horse riding can aggravate symptoms, if incontinent seek medical advice, apply emollients to relieve dryness and itching
Topical steroid then reassess after few weeks to see response
Intravaginal oestrogen cream/pessaries in postmenopausal women
Topical calcineurin inhibitors (tacrolimus and pimecrolimus) creams in addition or instead of steroids
Topical retinoids may reduce scaling and dryness
Surgery for high grade squamous intraepithelial lesions or cancers
drugs and pregnancy
First trimester (weeks 1-12) drugs can produce congenital malformations (teratogenesis) with the greatest risk period being weeks 3-11 Second and third trimester drugs can affect growth or functional development or can have toxic effects on foetal tissues Drugs given shortly before term or during labour can have adverse effects on labour or neonate after delivery Intrauterine exposure to drugs is not always present immediately after birth, it can include late onset effects such as malignancy (adenocarcinoma of the vagina after puberty in females exposed to diethylstilbestrol in the womb)
baby movements
When the baby is small, he has enough room to move around within the womb, however with growth, the space constraint restricts freedom of movement
Normally baby kicks can be felt between weeks 16-25 of the pregnancy, if it is a first time pregnancy then expect to feel movements closer to 25th week mark
Often observe babies move more after meals due to energy surge
Baby kicks indicate they are fine and active, not hyperactivity
It is always good to keep track of the baby’s movements
estimated delivery date
Gestational age is estimated at early USS (weeks 10-14) by comparing size of the embryo/foetus to that of a reference group of pregnancies of known gestational age and using the mean age of the same size
EDD calculated by Naegele’s rule assuming a gestational age of 280 days at childbirth
Take the last menstrual period (LMP), add 7 days, subtract 3 months and add 1 year.
Another method is to add 9 months and 7 days to the first day of the LMP
Variation is +/- 14 days usually
choosing place of birth
Low risk of complications:
Advise multiparous women that labour is generally safe for the mother and baby, they my choose a home setting or midwifery-led unit as the rate of interventions is lower and outcome for the baby is no different compared with an obstetric unit
Advising nulliparous women planning to give birth in a midwifery-led unit is particularly suitable as rate of interventions are lower and baby outcome is no different to obstetric unit. If they have a home birth there is a small increased risk of adverse outcome (4 per 1000 birth increase)
There are higher rates of spontaneous vaginal delivery in midwifery-led units and higher rates of interventions in obstetric units
always give information on likelihood of receiving one-to-one care, a familiar midwife, access to medical staff, pain relief and likelihood of being transferred to an obstetric unit
always ask about their wants, concerns and expectations for labour - has she written a birth plan (discuss with them), ask permission before all procedures and observations, let them know they can have available help and support whenever needed
indications for obstetric led delivery
CV
Cardiac disease
Hypertensive disorders
Respiratory
Asthma requiring increased treatment or hospital treatment
Cystic fibrosis
Haematological SCD Beta-thalassaemia History of Thromboembolic disorders Immune thrombocytopenia purpura or platelet disorder or platelet count <100x10(9)/L Von Willebrand’s disease Bleeding disorders in mother or baby Atypical antibiotics with risk of haemolytic disease of newborn
Endocrine
Hyperthyroidism
Diabetes
Infective Risk factors of group B strep Hepatitis B/C with abnormal LFTs carrier/infected with HIV Toxoplasmosis (receiving treatment) Current active infection of chickenpox/rubella/genital herpes TB (under treatment)
Immune: SLE Scleroderma Renal Abnormal renal function Renal disease needing supervision by renal specialist
Neurological: Epilepsy Myasthenia gravis Previous CVA GIT Liver disease associated with current abnormal LFTs Psychiatric Psychiatric disorder requiring current inpatient care
Previous complications:
Unexplained stillbirth/neonatal death or previous death related to intrapartum difficulty
Previous baby with neonatal encephalopathy
Preeclampsia requiring preterm birth
Placental abruption with adverse outcome
Eclampsia
Uterine rupture
Primary postpartum haemorrhage requiring additional treatment or blood transfusion
Retaining placenta requiring manual removal in theatre
C section
Shoulder dystocia
Current pregnancy: Multiple birth Placenta praevia Preeclampsia or pregnancy induced HTN Preterm labour or prelabour rupture of membranes Placental abruption Anaemia - Hb <85g/L at labour onset Induction of labour Confirmed intrauterine death Substance misuse Alcohol dependency requiring assessment of treatment Onset of gestational diabetes Malpresentation - breech or transverse lie BMI >35 Recurrent antepartum haemorrhage Small for gestational age (less than 5th centile or reduced growth velocity on USS) Abnormal foetal HR/doppler studies USS diagnosis of oligo-polyhydramnios
Previous gynaecological history:
Myomectomy
Hysterectomy
guiding through labour
always ask about their wants, concerns and expectations for labour - has she written a birth plan (discuss with them), ask permission before all procedures and observations, let them know they can have available help and support whenever needed
Encourage and help women to move and adopt whatever position she finds most comfortable throughout labour
Encourage having the birth companion of her choice
Tap water used for cleansing before vaginal examination
Standard hand hygiene and non-sterile single use gloves to prevent cross contamination
PPE based on risk of transmission and contamination
information for nulliparous women about labour
What to expect in latent stages of labour
How to work with pain
How to contact their midwifery care team and what to do in an emergency
How to differentiate between Braxton Hicks and active labour
Expected frequency of contractions and duration
Recognition of amniotic fluids
Description of normal vaginal loss
Guidance and support to women’s birth companion
Ask about baby’s movements and any changes there may have been
Advise of breathing exercises, immersion in water can reduce pain in latent labour - do NOT offer aromatherapy, yoga, acupressure for pain relief during latent stage but respect wishes if they wish to do this
Explain the reasoning for assessments
Explain risks, benefits and limitations of CTG and support choice, explain that having a CTG will require transfer to obstetric led care if not available where her planned choice is
Consider an early face to face assessment for all low risk nulliparous women either at home or in facility of planned place of birth
antenatal assessment at labour
Review antenatal notes and discuss with woman
Ask about length, strength and frequency of contractions
Ask about any pain and discuss options for relief
Record pulse, BP, temperature, urinalysis
Record if there has been any vaginal loss
Ask about baby’s movement within the last 24 hours
Palpate abdomen to determine fundal height, baby’s lie, presentation, position, engagement, frequency and duration of contractions
Auscultate foetal HR for 1 minute minimum immediately after a contraction (doppler USS or Pinard stethoscope).
Palpate woman’s pulse to differentiate between heartbeats
Offer a vaginal examination if uncertainty of labour status or if woman appears to be in established labour
Respect consent, dignity, privacy and comfort
maternal red flags for transfer to obstetric led care
Pulse >120/minute on 2 occasions 30 minutes apart
Single reading of raised diastolic >110 or systolic >160mmHg
Raised diastolic >90 or systolic >140mmHg on more than 2 consecutive readings taken 30 minutes apart
Reading of 2+ protein on urinalysis and single reading either raised diastolic BP >90 or systolic >140mmHg
Temperature >38 on single reading or >37.5degrees on 2 consecutive readings 1 hour apart
Rupture of membranes more than 24 hours before onset of established labour
Presence of significant meconium (dark green/black thick/tenacious amniotic fluid)
Pain reported differing from normal contraction pain
Any risk factors recorded in women’s notes indicating need for obstetric led care
foetal red flags for obstetric led care
Any abnormal presentation, including cord presentation
Transverse or oblique lie
High (4/5-5/5 palpable) or free floating head in nulliparous woman
Suspected foetal growth restriction or macrosomia
Suspected anhydramnios or polyhydramnios
Foetal HR below 110 or above 160 bpm
Deceleration in fetal HR heard on intermittent auscultation
Reduced foetal movements in last 24 hours reported by mum
care of women during established labour
Supportive one-to-one care, do not leave alone aside from short periods of time or at womans request
Controlling gastric acidity - consider H2RA or antacids for women receiving opioids or with risk factors making general anaesthetic more likely
Inform her she may drink during established labour and isotonic drinks may be more beneficial than water
She may eat a light diet unless she has received opioids or develops risk factors making GA more likely
pain relief in labour
Give information on all types available and support her decision
Breathing and relaxation techniques
Massage techniques
Paracetamol +/- codeine in early labour can be effective (avoid NSAIDs)
Labour in water (monitor temperature of women and water hourly to avoid pyrexia - should not be above 37.5degrees)
Do NOT offer acupuncture, acupressure or hypnosis but do not prevent women who wish to use this
Offer choice of music
Entonox (50:50 mix of nitrous oxide and oxygen) available in all birth settings for short term relief - side effect of nausea and dizziness
IV and IM opioids (pethidine, diamorphine) provide limited pain relief - side effects of drowsiness, N+V, short term respiratory depression and drowsiness for babies, may also interfere with breastfeeding. Should also administer an antiemetic and should NOT enter birthing pool within 2 hours of opioid dose or with drowsiness
IV remifentanil patient controlled analgesia - needs careful monitoring and input from an anaesthetist/facilities in place if adverse events occur including access to naloxone for respiratory depression and atropine for bradycardia
Epidural - only available in obstetric units, more effective pain relief than opioids. Adverse effects - headache, hypotension, motor weakness, nerve damage, prolonged second stage, increased probability of instrumental delivery. Will be accompanied by a more intensive level of monitoring and IV access so mobility may be reduced. Needs urgent review if develop significant motor weakness (cannot straight leg raise) as catheter may be incorrectly sited in subarachnoid space rather than epidural space
epidural
Epidural or spinal-epidural analgesia for establishing regional analgesia in labour
If rapid analgesia is needed used combined spinal-epidural with bupivacaine and fentanyl
Local anaesthetic and opioid solution to establish epidural
Use low concentration local anaesthetic and opioid solutions for maintaining epidural analgesic in labour
Do not use high concentrations of local anaesthetic solutions (>0.25% of bupivacaine or equivalent) routinely
Can be patient controlled or intermittent bolus given by HCP
measuring foetal HR
Offer intermittent auscultation of FHR to women at low risk of complications in established first stage of labour, immediately after contraction for at least 1 minute at least every 15 minutes and record as single rate
Palpate maternal pulse hourly (more if concerns)
Carry out more frequent FHR measurement if FHR decelerations or rising foetal baseline HR detected, consider asking for help from senior or transfer to obstetric led care if safe to do so
Advice for CTG if any red flags for mother or foetus are suspected
first stage of labour
Background:
The process by which the foetus is delivery after the 24th week of gestation
Onset of labour is defined as the point when uterine contractions become regular and cervical, effacement and dilatation of the cervix becomes progressive (>4cm dilatation).
Rupture of membranes/passage of show (mucus plug) may not be associated with labour and does not suggest labour themselves
Strength of contractions increases in frequency, duration and strength over time
Advise women that the length of first stage of labour varies between women, first labours last on average 8 hours (unlikely to last over 18 hours) and second/subsequent labours last on average 5 hours (unlikely to last over 12)
First stage of labour has three stages:
Latent: 0-3cm dilated. Progresses at around 0.5cm/hour with irregular contractions
Active: 37cm dilation. Progresses at around 1cm/hour with regular contractions
Transition phase: 7-10cm dilated. Progresses at around 1cm/hour with strong regular contractions
Pathology:
First stage: true contractions increasing in intensity and duration until the cervix is fully dilated to 10cm
Involves cervical dilation (opening) and effacement (thinning)
The show (mucus plug) prevents bacteria entering the uterus during pregnancy - falls out during labour creating space for the baby to pass through
first stage of labour presentation and Ix
Latent: Show Rupture of membranes Painful, irregular contractions Changes to the cervix with effacement and dilation up to 4cm
Established:
Regular, painful contractions
Dilatation up to 4cm of cervix
Investigations/monitoring:
Vaginal exam
Cardiotocography (CTG)
Partogram (FHR, contractions, maternal pulses, BP, temperature, vaginal exam, urinalysis)
Uterine contractions are measured in contractions per 10 minutes (2 in 10 means 2 contractions in 10 minutes)
partogram
Background:
Women are monitored for progress during the first stage of labour using a partogram
What is recorded:
Cervical dilatation (4 hourly)
Descent of foetal head in relation to ischial spines
Maternal pulse, BP, temperature and urine output
Foetal HR
Frequency of contractions]status of membranes, presence of liquor and whether it is stained by blood or meconium
Drugs and fluids given
Timings:
FHR should be monitored every 15 minutes (or continuously with a CTG)
Contractions should be assessed every 30 minutes
Maternal pulses should be checked hourly
BP and temperature should be checked 4 hourly
Vaginal exam should be offered every 4 hours to assess progress
Maternal urine is tested 4 hourly or when passed for ketones and protein
Interpreting:
Two lines indicating progression labelled alert and action
Cervical dilatation is plotted against duration of labour, if these plots cross the alert or action lines then it must be escalated
Alert line indicates an amniotomy to artificially rupture the membranes and repeat examination in 2 hours
Action line means escalate to obstetric led care and senior HCPs for appropriate action
cardiotocography CTG and indications
CTG/electronic foetal monitoring is used to monitor the FHR and uterine contractions
Explain it may restrict mobility
Explain a normal trace indicates the baby is coping well with the labour and give details to types of findings that may occur
Explain changes to the FHR pattern are common and not necessarily cause for concern
Explain if the trace is abnormal there is less certainty about the condition of the baby so continuous monitoring will be advised
Explain the decisions of care during labour and birth are based on assessment of several factors including her preferences, condition and foetal condition as well as CTG findings
If the CTG is started due to concerns but the trace is normal for 20 minutes return to intermittent auscultation unless the women requests staying on CTG
Always offer telemetry to any women with CTG
Operation:
Two transducers placed on the abdomen (one above foetal heart for FHR using a doppler USS and one near fundus of the uterus using USS to assess tension of uterine wall to monitor contractions)
Indications: Sepsis Maternal tachycardia >120 Significant meconium Preeclampsia Fresh antepartum haemorrhage Delay in labour Use of oxytocin Disproportionate maternal pain
baseline variability on CTG
Reassuring
Variability 5-25 is reassuring. Continue care as normal
Non-reassuring
<5 for 30-50 mins OR >25 for 15-25 mins is concerning.
Correct underlying causes, perform full maternal obs, start 1 or more conservative measures, inform obstetrician or senior midwife, document plan for reviewing whole clinical picture and CTG findings, discuss with woman and birth companion about what is happening and take her preferences into account
Abnormal
<5 for >50 mins OR >25 for >25 mins OR sinusoidal is abnormal
baseline FHR values
reassuring
110-160 continue as normal
non-reassuring
100-109 or 161-180 is concerning: continue normal care if there is normal baseline variability and no variable or late decelerations
abnormal
<100 or >180 is abnormal
Always differentiate between maternal and foetal HR by palpating maternal pulse
decelerations CTG values
Reassuring - no or early decelerations or variable with no concerning characteristics for <90 mins
Non-reassuring - variable with no concerning characteristics for >90 mins. Variable with any concerning characteristics up to 50% of contractions for >30mins. Variable with concerning characteristics in up to 50% of contractions for <30mins. Late decelerations in over 50% contractions for <30 mins with no maternal or foetal clinical risk factors
Abnormal - variable with any concerning characteristics in over 50% contractions for 30 mins (less if maternal or foetal RFs present)
Late decelerations for 30 mins (less if maternal or foetal RFs)
Acute bradycardia or single prolonged deceleration lasting >3mins. Immediately seek senior help, correct underlying causes, start one+ conservative measures, make preparation for urgent birth, discuss with women and companions as to what is happening and preferences. Expedite birth if acute bradycardia persists >9 mins, if FHR recovers during this time reassess any decisions to expedite birth with woman and HCP.
conservative measures during labour
Encourage mobilisation or alternate position (avoid supine), offer IV fluids, if hypotensive, reduce contraction frequency/reduce or stop oxytocin or offer tocolytic drug
deceleration interpretation on CTG (variable, late, early decelerations etc)
Timing in relation to contractions Duration If FHR returns to baseline How long have they been present for Do they occur with 50% contractions Presence or absence of biphasic W shape Presence or absence of shouldering Presence of absence of reduced variability within deceleration Concerning characteristics - lasting >60 seconds. Failure to return to baseline. Biphasic W shape and no shouldering
Terminology:
Early deceleration - lowest point of deceleration corresponds to peak of contraction, normal noon-pathological.
Late deceleration, gradual fall in FHR after contraction has begun, delay resulting in lowest point of deceleration being after peak of contraction, caused by hypoxia in foetus from excessive uterine contractions, maternal hypotension or maternal hypoxia).
Variable decelerations are abrupt decelerations that may be unrelated to uterine contractions (fall of >15bpm from baseline) lowest point occurs within 30 seconds and deceleration lasts less than 2 minutes in total. Often indicate intermittent compression of umbilical cord causing foetal hypoxia. Brief accelerations before and after decelerations are known as SHOULDERS and are a reassuring sign of coping
Prolonged decelerations last between 2-10 minutes with a drop of more than 15bpm from baseline. Often indicates compression of the umbilical cord causing foetal hypoxia. Abnormal and concerning findings.
CTG result categories and management
Result categories:
Normal
Suspicious: single non-reassuring feature
Pathological: two non-reassuring features or a single abnormal feature
Need for urgent intervention: acute bradycardia or prolonged deceleration >3 minutes
Management:
The outcome of the CTG will guide management, such as:
Escalating to a senior midwife and obstetrician
Further assessment for possible causes, such as uterine hyperstimulation, maternal hypotension and cord prolapse
Conservative interventions such as repositioning the mother or giving IV fluids for hypotension
Fetal scalp stimulation (an acceleration in response to stimulation is a reassuring sign)
Fetal scalp blood sampling to test for fetal acidosis
Delivery of the baby (e.g. instrumental delivery or emergency caesarean section)
foetal scalp stimulation and foetal blood sampling
Foetal scalp stimulation for pathological CTG trace - if this leads to acceleration in FHR only continue with foetal blood sampling if CTG trace is still pathological
Foetal blood sampling (do not carry out in acute events, expedited birth, risk of maternal-foetal transmission or infection, bleeding disorders). Explain why, risks, benefits - sample of blood taken from baby’s head making small scratch on scalp which heals quickly but has risk of infection. Do NOT take during or immediately after prolonged deceleration. Use pH or lactate to interpret results
pH >7.25 is normal. Borderline is 7.21-7.24. Abnormal is <7.20
Lactate <4.1mmol/l normal. Borderline 4.2-4.8. Abnormal >4.9mmol/l
Expedite birth for abnormal results
foetal prolonged bradycardia rule of 3s
3 minutes: call for help
6 minutes: move to theatre
9 minutes: prep for delivery
12 minutes: delivery baby (by 15 minutes)
sinusoidal CTG
Rare pattern indicating severe foetal compromise
Gives pattern similar to a sine wave with smooth regular waves up and down with amplitude of 5-15bpm
Usually associated with severe foetal anaemia e.g. caused by vasa praevia with foetal haemorrhage
how to interpret and report CTG findings DR C BRaVADO
DR C BRaVADO DR: Define Risk (based on individual women and pregnancy before assessing CTG) Contractions BRa: baseline rate Variability Accelerations Delecerations Overall impression (clinical picture, women's preference and CTG)
failure to progress
Background:
Slow progress in the active phase of labour (primary dysfunctional labour)
Cessation of cervical dilatation following a normal portion of active phase is termed “secondary arrest” of labour
Delay in first stage is considered when there is either: <2cm dilatation in 4 hours OR slowing progress in a multiparous women
Delay in the second stage is defined as lasting over 2 hours in a nulliparous woman, or 1 hour in a multiparous woman.
Delay in the third stage is defined as >30 minutes with active management OR >60 minutes with physiological management
Aetiology:
Power problem - Inefficient uterine activity (most common)
Passenger problem - malposition, malpresentation or macrosomia (large baby)
Passage problem - inadequate pelvis (narrow, abnormality)
Combination of above
Second stage - weak uterine contractions, macrosomia, incorrect lie, presentation or attitude, poor pelvic passage
failure to progress presentation, Ix and Mx
Presentation:
First stage - slow cervical dilatation, lack of ROM
Second stage - lasting >2 hours in nulliparous or >1 hour in multiparous women
Investigation/diagnosis:
Poor progression approach:
Review history
Abdominal palpation, frequency and duration of contractions
Review fetal condition, HR, colour/quantity of amniotic fluid
Review maternal condition including hydration and analgesia
Vaginal assessment, cervical effacement, dilatation, caput, moulding, position, station of the head
Management:
First stage:
Amniotomy (AROM) and reassess in 2 hours
Amniotomy + oxytocin infusion and reassess in 2 hours (always consider in nulliparous women)
Second stage: Changing positions Encouragement Analgesia Oxytocin infusion and reassess (multiparous women and those with previous C section: an experienced obstetrician should review before starting oxytocin) Episiotomy Instrumental delivery Caesarean section (foetal distress)
Third stage:
Active management: IM oxytocin and controlled cord traction
Physiological management: pain relief
oxytocin in labour
First line to stimulate uterine contractions during labour
Started low rate and titrated up at intervals of at least 30 mins PRN
Aim for 4-5 contractions/10 minutes (4-5 in 10)
Too many contractions can result in foetal compromise from lack of recovery in between contractions
Shown to increase cervical prostaglandin levels
Most receptors are in the myometrium so it is more suitable for initiating uterine contractions
Best used where membranes have ruptured (spontaneously or after amniotomy)
second stage labour and delays
If they have an epidural and the CTG is reassuring, 1 hour is allowed for passive descent before active pushing is commenced
During this hour it is important to ensure good contractions are maintained and oxytocin may be given PRN
Form the start of the second stage, birth should take place within 3 hours for nulliparous women and 2 hours for a multiparous women
Delay in nulliparous:
If delivery is not imminent after 1 hour of active pushing: vaginal examination should be offered and amniotomy recommended
If not delivered within 2 hours requires review by obstetrician to consider instrumental delivery or C section
Delay in multiparous women:
If delivery is not imminent after 1 hour of active pushing a review by obstetrician to consider instrumental delivery or CS is needed
Delay in the second stage in a multiparous woman must always raised suspicion of foetal malposition
en caul
In most cases the amniotic sac breaks down during delivery causing the “waters to break” Rare cases (1 in 80,000 births) the sac remains fully in tact and babies are born “en caul” This is completely harmless and easily removed by HCP
third stage labour physiological management
On average lasts 5-30 minutes
Physiological management:
No oxytocin or syntometrine given
Cord allowed to stop pulsating before it is clamped and cut
Placenta is delivered by maternal effort alone
Must NOT pull the cord and uterus not pushed in any direction
Examination of placenta:
Thorough inspection of the placenta must be done to ensure no parts of the placenta or membranes have been retained as this can result in postpartum haemorrhage and/or infection
third stage labour active management overview
Active management is needed in the event of:
Haemorrhage
Failure to deliver placenta within 1 hour
Maternal desire to shorten the 3rd stage
Active management:
Use of uterotonics (Must exclude multiple pregnancies before uterotonics are given)
Syntometrine IM (ergometrine 0.5mg + oxytocin 5IU) or oxytocin 10 IU IM given as anterior shoulder of the baby is born (NICE recommends oxytocin 10 IU instead of syntometrine as it appears to have similar efficacy but fewer side effects)
Clamping and cutting of the cord within 5 mins of birth (delay of 1-3 mins to allow blood flow to baby unless resus needed)
Palpate abdomen to assess for contractions
Dish is placed at the introitus to collect placenta and blood loss.
Controlled cord traction applied with the right hand, whilst supporting the fundus pushing upwards with the left (Brandt-Andrew’s technique)
As the uterus contracts to 20 week size, the placenta separates from the uterus and will feel firmer, the cord will lengthen and often there is a fresh trickle of blood (separation bleeding)
After delivery the uterus is massaged until contracted and firm, placenta is examined to ensure no retained parts within the uterus
Benefits:
Reduced rate of postpartum haemorrhage by >1000mL
Reduced mean blood loss of postnatal anaemia
Reduced need for blood transfusion
Examination of placenta:
Thorough inspection of the placenta must be done to ensure no parts of the placenta or membranes have been retained as this can result in postpartum haemorrhage and/or infection
cord prolapse
Pathology:
Umbilical cord descends below the presenting part of the foetus and through the cervix into the vagina, after rupture of the foetal membranes
Significant risk of cord compression in presenting part resulting in foetal hypoxia
Aetiology:
Abnormal lie providing space for the umbilical cord to prolapse below presenting part (in cephalic lie the head typically descends into the pelvis without room for the cord)
Risk factors:
Abnormal lie after 37 weeks gestation (anything but cephalic)
cord prolapse presentation, Ix and Mx
Presentation:
Prolapsed cord on vaginal exam
CTG abnormality indicating foetal hypoxia/distress
Investigation/diagnosis:
CTG - signs of foetal distress
Vaginal examination
Speculum exam to confirm
Management:
Emergency CS due to high risk of cord compression and hypoxia
Keep cord warm and wet, minimal handling whilst awaiting delivery (handling may cause vasospasm)
Lie the women in the left lateral position (pillow under hip or knee to chest position on all fours) to use gravity to draw away the foetus and reduce cord compression
Tocolytic medication (terbutaline) to minimise contractions whilst awaiting CS delivery
post delivery care
Most complications occur in the first 2 hours after delivery including PPH, uterine inversion and haematoma formation at the episiotomy site
Continuous observation in the delivery unit of pulse, BP, temperature, uterine size, contractions, fresh bleeding etc.
Monitoring of those with high risk of complications (multiple pregnancies) and a prophylaxis of oxytocin 40 IU in 500mL saline can be given over 3-4 hours if needed
Skin to skin contact should occur ASAP and mother and baby should not be separated for the 1st hour
Support for breastfeeding which should be initiated within the 1st hour
If there are no complications during these 2 hours, the mother may then be transferred to the postnatal ward
dystocia
Background:
Causes difficulty during labour
Types: cervical and shoulder dystocia
Cervical dystocia: cervix fails to dilate during labour
Shoulder dystocia:
Pathology (shoulder dystocia):
During final stage labour the infant’s head is delivered first. In dystocia, usually the anterior shoulder is impacted (stuck) against the pubic symphysis after delivery of the head, often due to failure to internally rotate the shoulders
Foetal deterioration is rapid, largely due to cord compression and trauma
Aetiology:
Can result due to “The Powers, Passenger and the Parts” (uterus, foetus and pelvis)
Often caused by macrosoma secondary to gestational diabetes
Uterine factors: insufficiency, uncoordinated contractions, primigravida
Foetal factors: position or lie (transverse/breech), macrosomia (birth weight >4.5kg), shoulder dystocia (combination of foetal and pelvic factors)
Pelvic passage factors: pelvis with a round brim is very favourable in labour however some women have long oval brims
shoulder dystocia complications and risk factors
Complications: Foetal hypoxia and neurological injury (cerebra) Brachial plexus injury and Erb’s palsy Fracture of clavicle or humerus Intracranial haemorrhage Cervical spine injury Foetal death (rare) Maternal PPH, genital tract trauma including 3rd and 4th degree perineal tears
Risk factors (Shoulder dystocia):
Previous shoulder dystocia (10x risk)
Maternal diabetes (2-4x risk)
Foetal macrosomia (though 48% infants weight <4kg)
Maternal obesity
Induction of labour
Prolonged labour (1st or 2nd stage or secondary arrest)
Assisted vaginal delivery (forceps or ventouse)
shoulder dystocia presentation, Ix
Presentation:
Difficulty delivery the face and head
Obstruction in delivery of the shoulder after delivery of the head
May show failure of restitution - head remains face down and does not turn sideways as expected after head delivery
Turtle neck sign - head delivery but retracts back into the vagina after contraction
Investigation/diagnosis:
Clinical diagnosis
shoulder dystocia management
Management:
Obtain help form senior obstetrician and midwife immediately, call anaesthetist and paediatrician
Stop the mother pushing as this can worsen impaction and risk of brachial plexus injury
Avoid downward traction on foetal head
Episiotomy to reduce risk of tearing
McRoberts’ maneuver - hyperflexion of the mother at hip (knees to abdomen) giving posterior pelvic tilt lifting the pubic symphysis up and out of the way
Pressure to anterior shoulder - pressing on suprapubic region putting pressure on posterior shoulder of baby to encourage it down
Rubins manoeuvre - reaching into the vagina to put pressure on posterior aspect of baby’s anterior shoulder to help move it
Wood’s screw manoeuvre - performed during Rubins, other hand used to reach in the vagina and put pressure on the anterior aspect of the posterior shoulder. Top shoulder pushed forwards and bottom shoulder pushed backwards (rotating and helping delivery) can try reverse motion if this fails
Zavanelli manoeuver - pushing baby’s head back into the vagina to enable an emergency CS
Do not apply fundal pressure (associated with high neonatal complication rate and can result in uterine rupture)
At all times consider the need for C section and do not delay this if necessary
operative/assisted vaginal delivery
Forceps and ventouse are complementary to one another and the operators skill and experience as well as clinical findings should decide which is best to use
10% of births in the UK are assisted with instrumental delivery
Can usually be carried out in a labour ward however if there are concerns it can be moved to theater so an emergency CS can be done if needed
Single dose of co-amoxiclav is recommended after instrumental delivery to reduce risk of maternal infection
Indications: Failure to progress Foetal distress Maternal exhaustion Control of head in various foetal positions
ventouse suction cup
Creates negative pressure to allow scalp tissues to be sucked into the cup ventouse
Creates artificial caput called a chignon
Should NOT be used <34 weeks gestation
Vertex presentation
Requires less analgesia than forceps, usually with episiotomy and aseptic technique
Maternal explanation and consent should be taken
Forceps delivery
Curved blades that sit around the foetal head and allows traction of the head and rotation
Usually used to speed up delivery, usually with episiotomy
Can cause complications - shoulder dystocia, postpartum haemorrhage so experience and skill is needed
Aseptic technique
operative vaginal delivery
Term used when it is not possible to determine with sufficient confidence that an instrumental delivery will be successful
Takes place in theatre where it is possible to move to immediate CS, avoiding failed delivery in the delivery room and subsequent delay in performing CS which may compromise foetal wellbeing
The woman should b fully informed of likely success and sign a consent form for “trial of instrumental vaginal delivery +/- emergency CS”
If instrumental delivery is unsuccessful, assistance may be needed to push head up from vagina during CS as head may be impacted on the pelvis
Senior obstetric input is recommended in 2nd stage CS, especially after failed trial of instrumental delivery
maternal and foetal risk of assisted vaginal delivery
Maternal Risks: Postpartum haemorrhage Episiotomy Perineal tears Anal sphincter injury Incontinence of bladder or bowel Nerve injury (obturator or femoral nerve - usually resolves around 6-8 weeks, or lateral cutaneous, lumbosacral plexus or common peroneal nerve - foot drop)
Foetal risks: Ventouse - cephalohaematoma Forceps - facial nerve palsy, bruising, fat necrosis Subgaelea haemorrhage Intracranial haemorrhage Skull fracture Spinal cord injury
episiotomy
Surgical incision to enlarge vaginal opening, made in the perineum tissue between vaginal opening and the anus
The decision to perform an episiotomy is made by the birth attendant
It is done to reduce risk of perineal tearing, however evidence recommends restricted use of episiotomies
More than 85% of women delivery vaginally in the UK will sustain some degree of perineal trauma
Indications (WHO):
Complicated vaginal delivery (shoulder dystocia, forceps, ventouse)
Extensive lower genital tract scarring (FGM, poorly healed 3rd/4th degree tears
When there is foetal distress
Indications of extensive previous perineal trauma
perineal tears
Background:
Third degree can be sub categorised as 3A (<50% external AS affected), 3B (>50% external AS affected) and 3C (internal and external AS affected)
Classification:
First degree: injury limited to frenulum of labia minora (posterior meeting) and superficial skin
Second degree: including perineal muscles but not affecting anal sphincter
Third degree: including anal sphincter but not affecting rectal mucosa
Fourth degree: including the rectal mucosa
Pathology:
Skin and tissues within the external vaginal area tearing as the baby’s head passess through
Range from grazes to large tears involving the anal sphincter (3rd degree)and rectal mucosa (4th degree)
Aetiology:
Occurs when the external vaginal opening is too narrow to accommodate the baby
perineal tears risk factors, presentation and Ix
Risk factors: Nulliparity Macrosoma >4kg Shoulder dystocia Asian ethnicity Occipito-posterior position Instrumental delivery
Presentation:
Complications - urinary or anal incontinece and altered bowel habits, fistula formation, sexual dysfunction and dyspareunia, psychological and mental health consequences
Investigation/diagnosis:
Clinical diagnosis
Rectal exam recommended before starting to ensure no trauma to anal sphincter
perineal tears management, prevention and complications
Management:
First degree - no sutures needed
Second degree and above - Suture ASAP to reduce bleeding and infection risk (3/4th degree likely to need repair in theatre)
Rectal exam recommended before starting to ensure there is no trauma to anal spincter
Attendant should have adequate training for type of tear: difficult trauma should be repaired in theatre by experienced operator
Use of rapid absorption polyglactin suture material is associated with significant pain reduction
Rectal examination after completion ensures no suture has accidentally passed into the rectum or anal canal
Broad spectrum antibiotics to reduce infection risk
Laxatives to reduce constipation and wound dehiscence
Physiotherapy to reduce risk and severity of incontinence
Follow up to monitor long standing complications
Complications after repair: Pain Infection Bleeding Wound dehiscence or breakdown
Prevention: Episiotomy under LA made 45 degrees diagonally from vaginal opening down and laterally to avoid anal sphincter damage (mediolateral episiotomy) and is sutured after delivery Perineal massage (massaging skin/tissue of perineum in a structured way from 34 weeks gestation to stretch and prepare for delivery)
Cesarean section
Background:
Surgical operation to delivery the baby via incision in the abdomen and uterus
Pfannenstiel incision is a curved incision two fingers above pubic symphysis
Joel-cohen incision is a straight incision slightly higher (recommended incision)
Vertical incision down middle of abdomen is also possible but rarely used
Blunt dissection is used after initial incision with a scalpel to separate remaining layers of abdominal wall and uterus. Using fingers and instruments and traction to tear tissue apart rather than cutting, results in less bleeding, shorted operating times and less risk of injury
Spinal anaesthetic given as is safer and leads to fewer complications and faster recovery than GA
Risks: anaphylaxis, hypotension, headache, urinary retention, nerve damage, haematoma, sore throat (GA), damage to teeth or mouth (GA)
CS indications and layers to cut through
Pathology layers to cut through: Skin Subcut tissue Fascia/rectus sheath Rectus abdominis Peritoneum Vesicouterine peritoneum Uterus Amniotic sac
Main indications: Foetal compromise/distress Failure to progress in labour Breech presentation Placenta praevia (low placenta) Preventing transmission of infection (genital herpes/HIV)
CS types
Immediate crash CS (emergency): immediate threat to life of woman or foetus:
Decision to delivery time is 30 minutes
Placental abruption with abnormal FHR or uterine irritability
Cord prolapse
Uterine scar rupture
Prolonged foetal bradycardia
Scalp pH <7.20
Urgent: maternal or foetal compromise, not immediately life threatening
Decision to delivery time is 75 mins
Failure to progress with pathological CTG
Scheduled: no maternal or foetal compromise but needs early delivery:
Severe preeclampsia
Intrauterine growth restriction (IUGR) with poor foetal function tests
Failed induction of labour
Elective:
Delivery time to suit woman and staff,
No medical reason but upon request (discussion, risk/benefit, consultation must be provided before decision)
Indications include previous CS, symptomatic after previous perineal tear, placenta praevia, vasa praevia, breech presentation, multiple pregnancy, uncontrolled HIV infection, cervical cancer
CS complications
Emergency has higher risk
Bleeding, infection, pain,
VTE (prophylaxis with LMWH): likely to lead to decreased mobility after operation so VTE risk assessment must be performed to determine type and duration of VTE prophylaxis, early mobilization, anti-embolism stockings or intermittent pneumatic compression of legs and LMWH
PPH, Oxytocin during procedure to reduce PPH risk
Wound infection, Prophylactic antibiotics for infection
Wound dehiscence, endometritis
Aspiration pneumonitis from prolonged supine posture: give H2RA or PPI
Damage to uterus, bladder, bowel, blood vessels
Ileus, adhesions, hernias
Future pregnancy risk: repeat CS, uterine rupture, placenta praevia, stillbirth
Risk to baby: lacerations, transient tachypnoea of newborn
vaginal birth after CS (VBAC)
It is possible to have a vaginal birth after CS provided cause of CS is unlikely to recur
Assessment of likelihood of success should be made in each case
Success rate of VBAC is around 75% with risk of uterine rupture around 0.5%
CI: previous uterine rupture, vertical CS incision, other usual CI to vaginal delivery (placenta praevia)
postpartum haemorrhage
Background:
Can be primary (within 24 hours) or secondary (24hours - 12 weeks after birth)
Women at risk should be identified earlier and place of delivery planned accordingly
Most common cause of significant obstetric haemorrhage
Must be >500mL loss after vaginal delivery OR >1000mL loss after CS
Minor PPH - <1000mL
Major PPH >1000mL
Moderate PPH 1000-2000mL
Severe PPH >2000mL
Pathology:
Continuous bleeding which fails to stop after delivery of the placenta (third stage with loss of >1000mL) may be accompanied by clinical shock (tachycardia, hypotension)
Aetiology: 4 Ts
Primary - Most commonly is uterine atony
Secondary - most common from retained placenta or infection (endometritis)
Tone - uterine atony, distended bladder
Trauma - lacerations of the uterus, cervix or vagina
Tissue - retained placenta or clots
Thrombin - preexisting or acquired coagulopathy
PPH risk factors and presentation
Risk factors:
Antepartum haemorrhage in this pregnancy
Placenta praevia (12x risk)
Suspected or proven placental abruption
Multiple pregnancy (5x risk) and other causes of uterine overdistension (polyhydramnios or macrosomia)
Preeclampsia or pregnancy induced HTN (4x risk)
Grand multiparity (4+ pregnancies)
Previous PPH (3x risk) or history of retained placenta
Asian ethnicity (2x risk)
Emergency CS (4x risk)
Elective CS (2x risk especially if >3 repeat procedures)
Retained placenta (5x risk)
Mediolateral episiotomy (5x risk)
Induction of labour (2x risk)
Operative vaginal delivery (2x risk)
Labour >12 hours (2x risk)
>4kg baby (2x risk)
Maternal pyrexia in labour (2x risk)
Presentation:
Blood loss excessive of 1000mL
Bleeding does not cease with placental delivery
Most likely to occur within 2 hours postpartum
Complications - hypovolemic shock, DIC, AKI, liver failure, death
PPH Ix
Ix:
Primary:
ABCDE approach
Bloods - FBC, Group and save 4 units, clotting screen
Modified obstetric early warning system (MEOWS) monitoring
Secondary:
USS for retained products
Endocervical and high vaginal swabs for infection
PPH Mx and prevention
Management:
Keep them lying flat, ABCDE approach
IV fluid resus and oxygen
Fresh frozen plasma (clotting abnormality) or 4 units blood transfusion PRN
Record all parameters on flow charts (modified obstetric early warning system (MEOWS) chart
Oxytocin 5 units slow IV infusion (can repeat)
Ergometrine 0.5mg slow IV or IM unless history of HTN
Mechanical intervention - rub uterus through abdomen to stimulate contraction (rubbing up the fundus) and catheterisation of bladder to prevent distension interfering
Surgery - intrauterine balloon tamponade, B-Lynch suture (compress uterus with suture around it), uterine artery ligation or hysterectomy (last resort to save life)
Secondary:
Surgical evaluation for retained products
Antibiotics for infection
Prevention:
Treating anaemia during antenatal period
Empty bladder before birth (full bladder reduces uterine contraction)
Active management of 3rd stage of labour
Prophylactic oxytocin 5 or 10 IU IM/infusion to reduce risk of PPH by 60% - first line
Misoprostol 1000mcg rectal/oral as alternative prophylaxis
Ergometrine 0.5mg slow IV or IM unless history of HTN
IV tranexamic acid during CS in 3rd stage in higher risk patients
attending a birth outside of hospital
Call for help
Catch the baby
Place skin to skin, dry baby and keep warm
Leave the cord and placenta, clamp if possible
Rupture of membrane (ROM)
Can be spontaneous (early or during labour)
Early rupture is termed premature rupture of membranes (PROM)
Artificial rupture of membranes (AROM) is performed by the midwife at time of labour
Spontaneous rupture of membrane (SROM)
Prelabour rupture of membrane (PROM) - ruptures before onset of labour
Preterm prelabour rupture of membranes (P-PROM) - rupture before 37 weeks gestation
Prolonged rupture of membranes (PROM) - amniotic sac ruptures >18 hours before delivery
prelabour rupture of membrane at term (PROM) pathology, presentation, Ix, Mx
Background:
Occurs in 6-19% of term pregnancies
Prelabour rupture of membrane (PROM) - ruptures before onset of labour
Prolonged rupture of membranes (PROM) - amniotic sac ruptures >18 hours before delivery
Pathology:
Rupture of the amniotic sac before true labour contractions have begun
Aetiology:
Unknown
Presentation:
Waters breaking - gushing of watery fluid from vagina (low rupture)
Trickling of watery fluid from vagina (high rupture)
Investigation/diagnosis:
If certain diagnosis - do not perform speculum examination
Uncertain - offer examination to determine rupture, avoid digital vaginal examination in absence of contractions
PROM management
Advise of risk of serious infection is 1% rather than 0.5%
60% of women with prelabour rupture will go into labour within 24 hours
Induction of labour is appropriate approximately 24 hours after membrane rupture
Advise taking temperature every 4 hours whilst awake to spot infection and report any change in colour or smell of vaginal loss immediately
Bathing or showering is not associated with increased infection but sexual intercourse may be
Assess foetal movement and HR at initial contact, then every 24 hours after rupture while they are not in labour, advice to report any decrease in foetal movements immediately
If labour has not started after 24 hours, advise the woman to give birth where there is access to neonatal services and to stay in hospital for at least 12 hours after birth
Advised women should be induced to labour within 96 hours due to infection risk
premature birth
Background:
Prematurity defined as <37 weeks gestation
The more premature, the worse the outcomes
Babies are considered non-viable <23 weeks gestation, generally resus is not considered in those aged 23-24 weeks that do not show signs of life. From 24 weeks onwards full resus is offered and survival chance increases
Babies born at 23 weeks have around 10% chance of survival
Fewer than 1 in 5 cases of suspected premature labour actually result in
WHO classification:
<28 weeks extreme preterm
28-32 weeks very preterm
32-37 weeks moderate to late preterm
Pathology:
Regular, painful contractions from oxytocin sensitisation of uterus and production of oxytocin from pituitary in response to positive feedback from excessive oestrogen and progesterone
Aetiology:
Unknown
Preterm labour risk factors and presentation
Preeclampsia Multigravida, multiple foetus’ Smoking Maternal stress Vaginal bleeding after 14 weeks gestation Uterus abnormalities Polyhydramnios (excess fluid around baby) Cervical insufficiency Placenta previa Fertility treatments <6 months between pregnancies Foetal abnormalities (rare) UTI Alcohol or drug use Domestic violence
Presentation:
Water breaking
Show - mucus plug
True contractions
Preterm labour Ix and Mx
Investigation/diagnosis: Bloods - CRP, ESR, cultures, Urinalysis USS Vaginal exam Speculum exam Foetal fibronectin (<34 weeks gestation - 1 in 5 with +ve test will go into labour within 10 days)
Management:
Oxytocin to induce labour, emergency CS if labour is concerning/maternal or foetal health at risk
Delaying delivery for 48 hours for transfer to specialist units, steroid doses etc. using tocolytics
Delaying delivery for as long as possible
Steroids to promote foetal lung development, magnesium sulfate to protect brain development
>34 weeks or more - Allowing natural labour
Prophylaxis: Vaginal progesterone gel or pessary to help maintain pregnancy and prevent labour by decreasing myometrial activity and cervix remodelling. Offered to women with cervix length <25mm on vaginal USS between 16-24 weeks gestation Cervical cerclage (stitch) to add support and keep it closed under GA or spinal anaesthetic. Stitch is removed when labour or term is reached. Offered to women with cervix length <25mm on vaginal USS between 16-24 weeks gestation who have had previous premature birth or cervical trauma (colposcopy and cone biopsy) Rescue cervical cerclage can be offered between weeks 16-27+6 weeks when there is cervical dilatation without ROM to prevent progression and premature delivery
preterm prelabour rupture of membranes (P-PROM)
Background:
Occurs in 2% of all pregnancies
Associated with 40% of preterm deliveries and can lead to significant morbidity and mortality
Pathology:
Rupture of amniotic membranes before labour onset in preterm pregnancy (<37 weeks gestation)
Most women will go into labour within 24 hours of ROM, but 6% will not be in labour within 96 hours
The earlier in gestation P-PROM occurs, the less likely the labour onset will be within a specified time period.
Aetiology:
Unknown
Risk factors:
Heavy smoking, greatest risk <28 weeks gestation
Previous preterm delivery
Vaginal bleeding at any time during pregnancy
Lower genital tract infection
P-PROM presentation and Ix
Presentation:
Popping or gushing sensation
Continuous watery liquid draining thereafter
Signs of ascending infection - foetal tachycardia, maternal temperature, vaginal discharge
Investigation/diagnosis:
Sterile speculum exam after lying down for 30 minutes
Bloods - Insulin-like growth factor binding protein-1 (IGFBP-1) and placental alpha-microglobulin-1 (PAMG-1), if infection suspected: FBC, CRP, MSU and cultures
Regular pad checks/Vision amniotic leak detector (ALD) diagnostic liner attached to underwear used in community
USS
CTG/foetal monitoring
Temperature and vital obs at least 12 hourly for ascending infection
High vaginal swab
DO NOT routinely perform digital vaginal examination - increases risk of ascending infection
P-PROM Mx and complications
Management:
Prophylactic antibiotics to prevent chorioamnionitis (erythromycin 250mg QDS)
Antenatal steroids given if gestation between 24-34+6 weeks gestation
Admitted to hospital for the first 48 hours for monitoring then discharged home for regular (4-8 hourly) temperature assessments etc.
Labour induction offered from 34 weeks onwards to initiate labour onset
Prevention: Intravaginal progesterone (women with no history of preterm birth or pregnancy loss between 16-34 weeks and women who have previously had a preterm birth/pregnancy loss between 16-34 weeks) Cervical cerclage (women who have previously had a preterm birth/pregnancy loss between 16-34 weeks and women who have had a PPROM in a previous pregnancy or history of cervical trauma)
Complications:
Three causes of neonatal mortality: prematurity, sepsis and pulmonary hypoplasia
Umbilical cord prolapse
Placental abruption
Oligohydramnios (early in pregnancy)
Increased incidence of retained placenta and secondary postpartum haemorrhage
Preterm labour with intact membranes overview
Pathology:
Regular painful contractions and cervical dilatation without rupture of amniotic sacs
Investigation/diagnosis:
Speculum exam (<30 weeks gestation this is enough to diagnose)
Transvaginal USS to assess cervical length (<15mm preterm labour management offered, >15mm preterm labour is unlikely) given to women of >30 weeks gestation
Foetal fibronectin (alternative to vaginal USS) <50ng/ml considered negative and indicates unlikely preterm labour
Management:
Foetal monitoring (CTG or intermittent auscultation)
Tocolysis with nifedipine (or atosiban if CI) to suppress labour/contractions, can only be used between 24-33+6 weeks
Maternal corticosteroids (can be given before 35 weeks) to reduce neonatal morbidity and mortality by promoting foetal lung development usually used in those <36 weeks
IV Mg sulphate given before (can be given before 34 weeks) helps protect baby’s brain
Delayed cord clamping or cord milking to increase circulating blood volume and haemoglobin in baby at birth
Rhesus incompatibility
Pathology:
Rhesus antigens on RBC surface in maternal blood stream - does not matter if the foetus has rhesus antigens
Rhesus negative pregnant women may still have rhesus positive babies. It is possible for the foetal and maternal blood to mix during pregnancy/at birth and when this happens the rhesus antigens from the foetus RBCs will be detected and recognised as foreign, antibodies will be produced against rhesus-D antigen and the mother will become “immune”
This does not usually cause a problem during first pregnancy however in subsequent pregnancies these maternal antibodies can cross the placenta, these antibodies may then cause an immune response to the foetus RBCs resulting in haemolysis, called haemolytic disease of the newborn
Aetiology:
Negative Rh status of mother and positive Rh status of baby
Risk factors for haemolytic disease of the newborn:
Previous Rh sensitisation from previous pregnancy
Presentation:
Asymptomatic
Rh -ve mother/presence of anti-D antibodies detected by indirect Coombs test
Infants - mild cases can be clinically normal or can include jaundice, pallor, hepatosplenomegaly, bilirubin encephalopathy, hydrops fetalis, pericardial effusion, pleural effusion, ascites, petechiae
Rhesus incompatibility Ix and management
Investigation/diagnosis:
Kleihauer test - after 20 weeks gestation
Indirect Coombs test - maternal antibodies
Doppler UD can show foetal anaemia
Foetal blood sampling to confirm anaemia
Management:
Prevention of sensitisation is the only treatment as once sensitised there is no way to reverse the process
All rhesus negative women who have not been sensitised - anti-D prophylaxis using anti-D Ig (given as two doses of Ig, 500 IU at 28 and 34 weeks OR large single dose 1500 IU at 28 weeks) OR given at birth if baby’s blood group found to be rhesus positive
Should be given at any time where sensitisation may occur: antepartum haemorrhage, amniocentesis procedures, abdominal trauma, premature births, miscarriages, terminations given within 72 hours of a sensitisation event
After 20 weeks the Kleinhauer test is performed to see how much foetal blood has passed into the mother’s blood to determine whether further doses of anti-D are required
Works by attaching to rhesus-D antigens of FRBCs preventing recognition in maternal circulation therefore preventing antibody production
Kleihauer test
Checks how much foetal blood has passed into the mother’s blood during sensitisation event
Used after 20 weeks gestation to assess if further doses of anti-D are required
Involves adding acid to a sample of mother’s blood, foetal Hb is naturally more resistant to acid, so that they are protected against acidosis that occurs around childbirth
Therefore, foetal Hb persists in response to added acid, while the mothers Hb is destroyed
Number of cells still containing Hb can then be calculated
Multiple gestation
Background:
16 per 1,000 births in the UK currently
Pathology:
Two or more ova are fertilised to form dizygotic (non-identical) twins or a single egg divides to form monozygotic (identical) twins
Aetiology:
Dizygotic - two eggs released during ovulation both are fertilised
Monozygotic - single egg fertilised, splits during beginning stage of cell division and begins to form two foetus’
Risk factors: Previous multiple pregnancy Family history (maternal side) Increasing maternal age IVF/assisted conception
Presentation:
Multiple foetus’ seen on USS
Investigation/diagnosis:
Antenatal USS
Multiple pregnancy management
Refer to obstetricians for shared care due to higher risk
Inform of greater likelihood of Down’s syndrome in twin and triplet pregnancies before screening as well as maternal complications such as preeclampsia
Monitor carefully for intrauterine growth restriction (IUGR) and for foetal transfusion syndrome (FFTS)
Women with uncomplicated monochorionic (shared placenta) twin pregnancies - offer elective birth from 36 weeks after course of antenatal steroids
Women with dichorionic (two sacs two placentas) twin pregnancies - offer elective birth from 37 weeks
Women with triplet pregnancies - offer birth from 35 weeks
Choice of delivery depends on case, CS usually preferred if there is moniamniocity, non-cephalic presentation of first twin or other risk factors
When there is cephalic presentation of the first twin, vaginal delivery and CS have similar outcomes
Ectopic pregnancy
Background:
A pregnancy of unknown location (PUL) is when a woman has a +ve pregnancy test and there is no evidence of the pregnancy on USS, meaning ectopic cannot be excluded
Pathology:
Blastocyst implants outside of the uterus, most commonly in the fallopian tube but can also implant in the fallopian tube entrance (cornual region), ovary, cervix or abdomen
Aetiology:
Unknown aetiology
Risk factors: Previous ectopic pregnancy Previous PID Previous surgery to fallopian tubes IUD/IUS Increased age Smoking
ectopic pregnancy presentation and Ix
Presentation:
Usually presents around 6-8 weeks gestation
Missed periods
Recent unprotected sex
Lower abdominal pain (RIF or LIF)
Vaginal bleeding
Cervical motion tenderness (pain moving the cervix during bimanual exam)
Dizziness/syncope
Peritonitis (shoulder tip pain)
Gestational sac seen in fallopian tube (blob sign) that will move SEPARATELY to the ovary (corpus luteum moves WITH the ovary) seen on transvaginal USS
Empty uterus but +ve pregnancy test
Fluid in the uterus (pseudogestational sac)
Investigation/diagnosis:
Bimanual exam
Transvaginal USS first line for miscarrriage
Serum hCG over time to monitor pregnancy of unknown location (repeat in 48 hours)
ectopic pregnancy management
Pregnancy test in all women with abdominal or pelvic pain that may be caused by ectopic pregnancy
Refer women with pelvic pain and tenderness AND a positive pregnancy test to the early pregnancy assessment unit (EPAU) or gynae service
All ectopic pregnancies must be terminated as they are not a viable pregnancy this is done by expectant management (awaiting natural termination), medical management (methotrexate) or surgical management (salpingectomy or salpingotomy)
expectant and surgical management of ectopic pregnancy
Follow up needs to be possible as close monitoring of hCG and quick, easy access to health services needed in case of deterioration Ectopic needs to be unruptured Adnexal mass <35mm No visible heartbeat No significant pain hCG <1500 IU/L
Surgical management:
Anyone not meeting the criteria for expectant or methotrexate needs surgical intervention
Most patients with ectopic pregnancy will need surgical management, including those with pain, adnexal mass >35mm, visible heartbeat and hCG >5000 IU/L
Laparoscopic salpingectomy is first line, removal of ectopic and affected fallopian tube.
Laparoscopic salpingotomy is used to remove only the ectopic and reclose the fallopian tube in cases where infertility is likely, but up to 1 in 5 women may need further treatment with methotrexate or salpingectomy
Anti-rhesus D prophylaxis is given to rhesus negative women having surgical management of ectopics
methotrexate management of ectopic pregnancy
Highly teratogenic substance given as IM injection to the buttock, halting pregnancy resulting in spontaneous termination
Advise women not to become pregnant within 3 months following treatment due to harmful effects
Common side effects: vaginal bleeding, N+V, abdominal pain, stomatitis (mouth inflammation)
Criteria: Follow up needs to be possible as close monitoring of hCG and quick, easy access to health services needed in case of deterioration Ectopic needs to be unruptured Adnexal mass <35mm No visible heartbeat No significant pain hCG <5000 IU/L Confirmed absence of intrauterine pregnancy on USS
hCG monitoring for pregnancies
Repeat hCG measurements at 48 hours
Should double every 48 hours in normal pregnancy but this is not the case in micarriage or ectopic
A rise of >63% after 48 hours indicates intrauterine pregnancy is likely and repeat USS required after 1-2 weeks to confirm intrauterine pregnancy (should be visible with hCG levels >1500 IU/L
Rise of <63% after 48 hours may indicate ectopic pregnancy - needs close monitoring and review
Fall of >50% is likely to indicate miscarriage. Urine pregnancy test should be performed after 2 weeks to confirm miscarriage is complete
Reviewed in early pregnancy assessment unit within 24 hours if b-hCG results between these parameters
Termination of pregnancy
Background:
An elective procedure to end a pregnancy
The 1967 abortion act is the legal framework for abortion and the 1990 human fertilisation and embryology act altered and expanded the criteria for abortion and reduced latest gestational age where abortion is legal from 28 weeks to 24 weeks
Abortion services can be accessed by self-referral or by GP/family planning clinic.
Marie Stopes UK is a charity offerening abortion services to <10 weeks gestation with telephone consultations and medication issued remotely to be taken home
Criteria:
An abortion can be performed before 24 weeks gestation is continuing the pregnancy involves greater risk to the physical or mental health of the women or existing children of the family (clinical judgment of medical practitioners)
An aboriton can be performed at ANY time during pregnancy if continuing is likely to risk life of the mother, terminating will prevent “grave permanent injury” to the physical or mental health of the woman or there is substantial risk the child would suffer physical or mental abnormalities making it seriously handicapped
termination of pregnancy methods
Medical abortion:
Mifepristone (anti-progesterone) halting pregnancy and relaxation of cervix
Misoprostol (prostaglandin analogy) prescribed 1-2 days after mifepristone dose to activate prostaglandin receptors, softening cervix and stimulating uterine contractions. From 10 weeks gestation, additional misoprostol doses (every 3 hours) are needed until expulsion
Rhesus negative women with gestational age >10 weeks should have anti-D prophylaxis
Surgical abortion:
Can be performed under LA, GA or LA+sedation
Misoprostol, mifepristone or osmotic dilators (inserted into cervix, gradually expand as fluid is absorbed) are given for cervical priming prior to surgery
Cervical dilatation and suction of contents of uterus (usually performed up to 14 weeks)
OR cervical dilatation and evacuation using forceps (14-24weeks gestation)
Rhesus negative women should have anti-D prophylaxis
termination of pregnancy and Ix, Mx and complications
Investigation/diagnosis:
Must be signed by 2 trained doctors
Management:
Offer counselling and information to help make an informed decision from a trained practitioner
Medical abortion is most appropriate earlier in pregnancy but can be used at any gestation
Surgical abortion with suction usually up to 14 weeks
Surgical abrotion with forcep evacuation usually between 14-24 weeks
May experience vaginal bleeding and abdominal cramps intermittently for up to 2 weeks after procedure
Urine pregnancy test performed 3 weeks after abortion to confirm it is complete
Contraception discussed and started where appropriate
Complications:
Bleeding, pain, infection
Failure of abortion
Damage to cervix, uterus or other structures
Molar pregnancy
Background:
Hydatidiform mole - tumour growth within the uterus like a pregnancy, called a molar pregnancy
Two types: complete mole and partial mole
Pathology:
Complete mole occurs when two sperm cells fertilise an ovum containing no genetic material (empty ovum), the sperm combine genetic material and cells divide and grow into a complete mole tumour. No foetal material will form
Partial mole occurs when two sperm cells fertilize a normal ovum at the same time (polyspermy). New cell has three sets of chromosomes, begins dividing and multiplies into a tumour called a parietal mole. This may form some foetal material
Aetiology:
Complete - two sperm fertilising empty ovum
Partial - two sperm fertilising ovum
molar pregnancy risk factors, presentation and Ix
Risk factors: More common in ages >45 and <16 Multiple pregnancies Previous molar pregnancy Menarche >12, light menstruation, history of COC Asian women
Presentation:
Behaves like a normal pregnancy - amenorrhea, hormonal changes, morning sickness etc.
More severe morning sickness
Vaginal bleeding
Increased uterus enlargement
Abnormally high hCG
Thyrotoxicosis (hCG can mimic TSH and stimulate thyroid to produce excess T3 and T4)
Investigation/diagnosis:
Pelvic USS - snowstorm appearance
Biopsy of mole after evacuation to confirm
molar pregnancy Mx
Evacuation of uterus to remove the mole and histological examination of contents
Refer to gestational trophoblastic disease centre for management and follow up
hCG monitored until returned to normal levels (partial mole - confirmed 4 weeks after, if values are normal then no further follow up. Complete mole - until normal, continue monthly testing for 6 months after evacuation or normalised levels)
Occasional the mole can metastasise and patient may need systemic chemotherapy
Twins with viable pregnancy and molar pregnancy - allow pregnancy to proceed if mother wishes, appropriate counselling of around 25% chance of viability, no increased risk of persistent GTD and outcome after chemotherapy is unaffected
Advise women to wait until hCG returns to normal before becoming pregnant again
miscarriage
Background:
Relatively common experience (1 in 5 women will experience)
Early miscarriage - before 12 weeks gestation
Late miscarriage - between 13-24 weeks gestation
Missed miscarriage - foetus no longer alive but no symptoms occurred
Threatened miscarriage - vaginal bleeding with closed cervix and a foetus that is alive
Inevitable miscarriage - vaginal bleeding with open cervix
Incomplete miscarriage - retained products of conception remain in the uterus after the miscarriage
Complete miscarriage - full miscarriage has occured and no products of conception left in the uterus
Anembryonic pregnancy - gestational sac is present but contains no embryo
Pathology:
Spontaneous termination of pregnancy
Three features a sonographer looks for in early pregnancy, each appear sequentially with the previous becoming less important to assess viability
Mean gestational diameter
Foetal pole (expected once mean gestational sac diameter is >25mm) and crown-rump length
Foetal heartbeat - pregnancy is considered viable and is only experienced once the crow-rump length is >7mm
Aetiology:
Varying causes and pathology
miscarriage risk factors and presentation and Ix
Risk factors: Maternal age >35 Previous miscarriage Foetal abnormality Infection (toxoplasma, rubella, malaria) Maternal illness (diabetes, thrombophilia, thyroid disease) APS Uterine abnormality Cervical insufficiency
Presentation:
Asymptomatic (missed miscarriage)
Vaginal bleeding
Abdominal cramps
Lower back pains
Vaginal discharge - bright red, brown, spotting, passing clots
Red flags - lower abdominal pain, positive pregnancy test MUST be investigated for ectopic pregnancy until proven otherwise
Investigation/diagnosis:
Transvaginal USS first line
Crown-rump length <7mm with no heartbeat - repeat USS after at least one week to ensure heartbeat develops
Crown-rump length >7mm without heartbeat - repeat USS and if no heartbeat heard then confirmed non-viable pregnancy
Mean gestational sac diameter >25mm with no foetal pole - repeat scan after one week before confirming anembryonic pregnancy
Urinalysis - b-hCG
Assess bleeding
Speculum examination - is cervix open or closed?
Bloods - b-hCG, FBC, coagulation, G+S
Miscarriage Mx
<6 weeks gestation with bleeding but no pain/other complications - expectant management awaiting miscarriage without Ix or Mx (USS unlikely to be helpful as pregnancy too small to see). Repeat urine test performed after 7-10 days to confirm miscarriage
Refer for continued bleeding or if pain occurs
> 6 weeks gestation with bleeding and positive pregnancy test - refer to early pregnancy assessment unit (EPAU). USS scan to confirm location and viability of pregnancy (exclude ectopic). Use expectant management, medical or surgical management
Expectant management is the first line for women without risk factors for heavy bleeding or infection. 1-2 weeks given to allow a spontaneous miscarriage with repeat pregnancy test 3 weeks after bleeding and pain settle to confirm. Persistent or worsening bleeding needs further Ix and Mx
Medical management of misoprostol to stimulate uterine contractions (vaginal suppository or oral dose). Can cause heavier bleeding, pain, vomiting and diarrhoea.
Surgical management under LA/GA to perform manual evacuation aspiration (LA as outpatient - tube attached to syringe inserted through cervix into uterus to aspirate contents, woman must consent and be <10 weeks gestation, usually more appropriate for parous women) or electric vacuum aspiration (GA - performed through vagina and cervix with no incisions. Cervix widened with dilators and conception products removed using vacuum). Given misoprostol before procedures and anti-rhesus D prophylaxis given to rhesus negative women after ectopic pregnancy
Incomplete miscarriage:
Medical management with misoprostol
Surgical management (evacuation of retained products of conception - ERPC. GA procedure using aspiration and curettage) potential complication of endometritis
Prevention:
Encourage smoking and drug cessation, alcohol reduction
Vitamin supplementation prior to/early pregnancy does not prevent miscarriage but iron and folic acid dose reduce risk of stillbirth
Recurrent miscarriage
Background:
Miscarriage is relatively common
Recurrent miscarriages are classed as three or more consecutive miscarriages
Investigations initiated after three or more first trimester miscarriages OR one or more second trimester miscarriages
Aetiology:
Idiopathic (particularly in older women)
Antiphospholipid syndrome
Hereditary thrombophilias - factor V leiden (most common), factor II (prothrombin) or protein S deficiency
Uterine abnormalities - uterine septum, unicornuate uterus, bicornuate uterus, didelphic uterus, cervical insufficiency, fibroids
Genetic factors (balanced translocations in parental chromosomes)
Chronic histiocytic intervillositis - rare, particularly second trimester miscarriages
Other diseases - diabetes, untreated thyroid disease, SLE
Risk factors: Increasing age (10% in ages 20-30, 15% ages 30-35, 25% ages 35-40, 50% in ages 40-45)
Recurrent miscarriage presentation, Ix and Mx
Presentation:
Recurrent first term miscarriages
One or more second term miscarriages
Investigation/diagnosis:
Bloods - coagulation status, haematinics, factors V (leiden), II (prothrombin), VII, IX, X, protein S, VWF, APS autoantibodies
Pelvic USS
Genetic testing of products of conception from third or future miscarriages
Parental genetic testing
Management:
APS - low dose aspirin and LMWH (antiplatelet and anticoagulant)
Manage underlying cause
PRISM trial suggests vagina progesterone pessaries in early pregnancy for recurrent miscarriages presenting with bleeding
Toxic shock syndrome
Background:
Multisystemic inflammatory response to presence of bacterial exotoxins
Rate of cases has declined with increased awareness and change in tampon manufacture
Mortality rate around 5-15% for TSS with fatality rate up to 64% for streptococcal toxic-shock like syndrome TSS (STSS)
Pathology:
Infecting staphylococcal or streptococcal exotoxin acts as a superantigen, setting off a reactive inflammatory cascade, mediated mainly by TNF alpha and IL-1
Aetiology:
Associated with tampon use and Group A strep infections (streptococcal toxic shock-like syndrome [STSS])
Group C and G strep have been reported to cause invasive disease similar to group A
TSS risk factors and presentation
Risk factors: S. aureus after mosquito bites Wounds and burns Tampon use (less relevant now) or gynaecological infection Puerperal sepsis Postoperative infections Packed wounds (nasal) Sinusitis Tracheitis Recreational IV drug use HIV Allergic contact dermatitis Influenza A virus
Presentation:
High fever
Diffuse macular, erythrodermic rash or widespread fine, red, papular sandpaper like with flexural accentuation
Hypotension
Multiorgan dysfunction
Desquamation of palms and soles of feet 1-2 weeks after onset
Palms, soles of feet and tongue may be bright red
N+V and diarrhoea
Myalgia and muscle weakness
Confusion and disorientation may indicate encephalopathy
TSS Ix and Mx
Investigation/diagnosis: ABCDE assessment Close examination of skin Check for tampons - gynaecological exam Respiratory examination Bloods cultures, FBC, U+Es, CK, LFTs Urinalysis Throat swabs CXR
Management:
Remove persisting focus of infection (abscess, wound pack, slough, tampon)
Aggressive haemodynamic resus with central fluid volume monitoring and regular U+Es monitoring and correction
Vasopressor agents to manage shock
Monitor and correct glucose as needed
Antibiotics - penicillinase-resistant penicillin, cephalosporin or vancomycin with clindamycin or linezolid
Steroids low dose
Cervical incompetence
Background:
AKA cervical insufficiency
Pathology:
Cervical shortening and softening during the second trimester of pregnancy(>12 weeks) causes opening of the cervix without any signs/symptoms of labour, often causing second trimester miscarriage or premature birth via bulging and breaking of amniotic sac/fluids
Aetiology:
Unknown thought to be weakened cervix, possible infection or inflammation may have a role also
Risk factors: Inherited collagen synthesis disorders Cervical surgery such as cone biopsy Cervical injury, dilatation or curettage Congenital womb abnormalities Previous miscarriages in 2nd trimester Known cervical incompetence in previous pregnancy DES medication taken in mothers pregnancy
cervical incompetence presentation and Ix
Presentation: Painless dilatation of the cervix +/- ROM Miscarriage >14 weeks (second trimester) Pelvic pressure Cramping Vaginal discharge changes Losing mucus plug
Investigation/diagnosis:
TVUS
Vaginal examination
Speculum examination
cervical incompetence Mx
Indication for treatment - Hx of >3 spontaneous preterm births/second trimester miscarriages or patients with short cervix (high risk) in second trimester
Prophylactic placement of cervical stitch (cerclage) aiming to prevent miscarriage (strong band of thread around the cervix usually done between 12-24 weeks)
Rescue cerclage to prevent premature birth in patients with cervix opening
Shortening seen in weeks 16-24 - vaginal progesterone
Antibiotics for infection
Arabin pessary (soft silicone bowl shaped pessary inserted into the vagina to sit around the cervix)
Antepartum haemorrhage
Background:
Any vaginal bleeding from the 24th week of gestation until delivery
Pathology:
Depends on underlying cause, results in haemorrhage within uterine cavity causing varying degrees of blood loss
Aetiology:
Most important causes - placenta previa, abruption and vasa praevia
Risk factors: Placenta previa Vasa previa Placental abruption Placenta accreta
Presentation:
Vaginal bleeding any time after 24th week gestation
Abdominal pain (uterine rupture/placental abruption)
Painless bleeding (vasa previa, placenta previa)
Antepartum haemorrhage Ix and Mx
Investigation/diagnosis: Clinical diagnosis Antenatal USS Transvaginal USS ABCDE (severe blood loss)
Management:
Depends on underlying condition
Diagnosed antenatally - steroids after 24-32 weeks gestation to improve foetal development, planned CS (+/- hysterectomy etc.)
Emergency CS, blood transfusion, IV fluids, maternal intensive care, neonatal intensive care
Placenta previa
Background:
Obstetric emergency (potentially)
Means “placenta going first”
Occurs in around 1% of pregnancies and is a notable cause of antepartum haemorrhage
Can be complete - completely covers the internal cervical Os
Partial - partially covers the internal Os
Marginal/low lying placenta - edge of the placenta extends to within 2cm of the internal cervical Os
Associated with placenta accreta (placenta invades myometrium)
Pathology:
Normally the placenta implants on the upper cervix, above the foetus
In placenta previa it implants in the lower uterine cavity, below the presenting part of the foetus and sometimes covering the cervical opening (internal cervical Os)
As the uterine segment grows, it disrupts placental vessels and causes easy bleeding, usually after 20 weeks gestation
Aetiology:
Unknown but thought to be due to upper endometrium not being well vascularised
Causes of decreased vascularisation - damage from previous CS, abortion/miscarriage, uterine surgery or multiparity
placenta previa risk factors, complications and presentation
Risk factors:
Multiple placentas (twins/multi pregnancy)
Placenta has larger than normal surface area (twins/multi pregnancy)
Maternal age >35
Intrauterine fibroids
Smoking
Presentation: Bright red, painless bleeding Usually after 20 weeks gestation Intermittent or continuous May increase during labour due to contractions
Complications: Antepartum haemorrhage Emergency CS Emergency hysterectomy Maternal anaemia and transfusions VTE from prolonged inpatient care Foetal hypoxia and preterm delivery Stillbirth
placenta previa Ix and Mx
Investigation/diagnosis:
Clinical diagnosis as USS cannot exclude abruption
ABCDE for severe bleeding
Prenatal USS (20 week anomaly scan assesses placenta position)
Transvagainal USS
Bloods - FBC, U+E, iron and haematinic studies
Management:
Diagnosed at 20 week anomaly scan - recommended repeat scans at 32 and 36 weeks to help delivery decisions, advise against penetrative intercourse and avoid vaginal examinations
Corticosteroids given between 34 and 35+6 weeks to enhance foetal lung development (surfactant) in case of preterm birth
Consider planned delivery between 36-27 weeks to reduce risk of spontaneous labour and bleeding (planned CS)
Minor bleeding - bed rest
Major bleeding - blood transfusion and IV fluids
Signs of foetal distress, premature labour or antenatal haemorrhage - emergency CS +/- blood transfusions, intrauterine balloon tamponade, uterine artery occlusion and emergency hysterectomy
Vasa praevia
Background:
Obstetric emergency (potentially)
Menas “vessel going before”
Type I - foetal vessels are exposed as a velamentous umbilical cord
Type II - vessels exposed as they travel to an accessory placental lobe
Pathology:
Foetal vessels (umbilical arteries and umbilical vein) are within the foetal membranes (chorioamniotic membranes) and travel across the internal cervical Os, placed before the foetus
Normally, the umbilical cord (containing two arteries and a single vein) inserts directly into the placenta and foetal vessels are always protected by the umbilical cord (contains Wharton’s jelly) or the placenta
Velamentous umbilical cord - umbilical cord inserts into the chorioamniotic membrane and foetal vessels travel unprotected through the membranes before joining the placenta
OR an accessory lobe of the placenta (succenturiate lobe) is connected by foetal vessels that travel through the chorioamniotic membranes between placental lobes
The vessels are exposed and prone to bleeding, particularly when membranes rupture during labour and can lead to foetal blood loss and death
Vasa prevue risk factors, presentation and Ix
Risk factors:
Low lying placenta (praevia)
IVF pregnancy
Multiple pregnancy
Presentation:
Seen on USS
Antepartum haemorrhage during second or third trimester
Vaginal examination during labour (pulsating vessels seen through dilated cervix)
Foetal distress during labour and dark red bleeding following membrane rupture (high foetal mortality even with emergency CS)
Investigation/diagnosis:
Antenatal USS
Vaginal examination during labour (pulsating vessels seen through dilated cervix)
Vasa praaevia management
Asymptomatic women - corticosteroids given from 32 weeks to mature foetal lungs
Elective CS planned for weeks 34-36 gestation to avoid spontaneous labour or haemorrhage
Antepartum haemorrhage - emergency CS
After stillbirth or unexplained compromise during delivery - examine placenta for evidence of vasa praevia
Placental abruption
Background:
Obstetric emergency
Can be classified as partial (section separates) or complete (total separation)
Severity graded as spotting, minor, major and massive hemorrhage
Spotting - spots of blood noticed on underwear
Minor - <50mL blood loss
Major - 50-100mL blood loss
Massive - >100ml blood loss with signs of shock
Concealed abruption - cervical Os remains closed and any bleeding remains within the uterine cavity. Severity of bleeding can be significantly underestimated.
Releavel abruption - blood loss observed via the vagina
Pathology:
Either whole or part of the placenta (decidua basalis) separates from the uterus wall during pregnancy
Site of attachment can bleed extensively after separation and is a significant cause of antepartum haemorrhage
If the site is close to the edge of the placenta can cause vaginal bleeding but if it is in the centre of the placenta a pool of blood within the uterine cavity can form without much external presentation
Aetiology:
Unknown
placental abruption risk factors and presentation
Risk factors: Previous placental abruption Preeclampsia Bleeding in early pregnancy Trauma Multiple pregnancy Foetal growth restriction Multigravida Increased maternal age Smoking Cocaine or amphetamine use
Presentation:
Sudden onset, continuous severe abdominal pain
Vaginal bleeding (antepartum haemorrhage)
Shock (hypotension and tachycardia)
Abnormalities on CTG (foetal distress)
“Woody” abdomen on palpation (suggests large haemorrhage)
Sheehan syndrome - prenatal pituitary necrosis
Foetal hypoxia and preterm birth
placental abruption Ix
Investigation/diagnosis:
Clinical diagnosis (no reliable diagnostic tests)
Abdominal exam
CTG
Bloods - G+S, FBC, U+Es, iron studies, coagulation studies
USS to exclude placenta previa
Kleihauer test - determine how much foetal blood is mixed with maternal blood to determine dose of anti-D prophylaxis
placental abruption Mx
Management:
Major or massive haemorrhage:
Urgent involvement of senior obstetrician, midwife and anaesthetist
IV fluids +/- blood transfusions to maintain circulation and prevent DIC
Bloods - FBC, U+Es, LFT, coagulation, G+S 4 units blood
CTG monitoring of foetus and close maternal observations
Antenatal steroids offered between 24-34+6 weeks to mature foetal lungs in anticipation of preterm delivery
rhesus-D negative women require anti-D prophylaxis when bleeding occurs
Emergency CS for maternal or foetal distress/instability
Active management of third stage recommended
Monitor for signs of postpartum haemorrhage (common complication)
placenta succenturiata and membranacea
Placenta succenturiata:
There is a separate (succenturiate) lobe away from the main placenta which may fail to separate normally an cause PPH or puerperal sepsis
Placenta membranacea:
1 in 3000 pregnancies. A thin placenta surrounds the baby, some in the lower segment predisposes to antepartum haemorrhage.
May fail to separate during third stage of labour
placenta accreta
Background:
Referred to as placenta accreta spectrum due to spectrum of severity in how deep and broad the abnormal implantation extends
Superficial PA - implants in the surface of the myometrium
Placenta increta - attached deeply into the myometrium
Placenta percreta - invades past the myometrium and perimetrium, potentially reaching other organs such as the bladder
Pathology:
The placenta implants past the endometrium into the myometrium and beyond, making placental separation difficult after delivery of the baby and often leading to extensive bleeding (postpartum haemorrhage)
Aetiology:
Endometrial defect from previous uterine surgery (CS or curettage procedures)
placenta accreta risk factors and presentation
Risk factors: Previous PA Previous endometrial curettage procedures (miscarriage or abortion) Previous CS Multigravida Increased maternal age Low lying placenta
Presentation: Asymptomatic in pregnancy Antepartum haemorrhage during third trimester Delayed/difficult third stage of labour Postpartum haemorrhage
placenta accreta Ix and Mx
Investigation/diagnosis:
Antenatal USS
MRI to assess depth and width of invasion
Management:
Antenatal diagnosis:
MRI scans
MDT specialists management for complex uterine surgery, blood transfusions, intensive care for mother and neonatal intensive care
Delivery planned between 35-36+6 weeks - CS +/- hysterectomy with placenta remaining in the uterus (recommended), uterus preserving surgery (resection of myometrium) or expectant management (leaving placenta in place to be reabsorbed over time)
Antenatal steroids for foetal lung development
*expectant management has significant risks (bleeding, infection most commonly)
After delivery diagnosis:
Recommended hysterectomy
Breech presentation overview
Background:
Refers to the presenting part of the foetus being the legs and bottom, opposed to cephalic presentation where the head presents first
Occurs in less than 5% pregnancies by 37 weeks gestation
Pathology:
Complete breech - legs fully flexed at hips and knees
Incomplete breech - one leg flexed at hip and extended at knee
Extended breech - AKA frank breech, both legs flexed at hips and extended at knees
Footling breech - foot presenting through the cervix with leg extended
Aetiology:
Foetal movement and rotation during pregnancy allows for the baby to change positions continually, eventually ending in cephalic presentation >37 weeks gestation, however sometimes this does not occur as the baby may have restricted movement or move incorrectly
Presentation: Breech presentation on USS Breech on vaginal examination/during labour Difficult/slow progressing second stage labour Foetal distress Investigation/diagnosis: Vaginal examination USS
Management:
Before 36 weeks - often turn spontaneously, no Mx advised
At 37 weeks - external cephalic version can be used to attempt to turn the foetus, if ECV fails given choice of vaginal delivery or elective CS (vaginal safer for mother, CS safer for baby)
Vaginal delivery needs access to emergency theatre PRN (40% chance of needing emergency CS)
If first baby in twin pregnancy is breech - CS required
External cephalic version
50% successful
Used after 36 weeks gestation for nulliparous women and after 37 weeks parous women
Given tocolysis to relax uterus before procedure (subcut terbutaline)
Rhesus-D negative women require anti-D prophylaxis when ECV is performed
Kleihaur test used to quantify how much foetal and maternal blood has mixed to assess dose needed
Nabothian cysts
Background:
Aka nabothian follicles or mucinous retention cysts
Unrelated to cervical cancer
Pathology:
Fluid filled cysts on the surface of the cervix
Columnar epithelium of the endocervix produces cervical mucus
When squamous epithelium of the ectocervix slightly covers the mucus secreting columnar epithelium, the mucus becomes trapped and forms a cyst
Aetiology/risk factors:
Childbirth
Mild trauma to the cervix
Cervicitis secondary to infection
Nabothian cysts presentation, Ix and Mx
Presentation:
1-30cm in size, white or yellowish colour
Smooth, rounded bumps usually near the Os
Often asymptomatic, found incidentally
If very large may cause feeling of pelvic fullness
Investigation/diagnosis:
Speculum examination
Colposcopy - uncertain diagnosis
Management:
Reassurance and education that they are harmless and self resolving
Symptomatic - colposcopy biopsy or excision to treat symptoms (rare)
Ovarian cysts
Background:
Functional ovarian cyst - related to fluctuating hormones of menstrual cycle (most commonly follicular cysts)
Very common in premenopausal women
Vast majority are benign
Cysts in postmenopausal women always need further investigation as are higher risk of cancer
Patients with multiple ovarian cysts (string of pearls on USS) cannot be diagnosed with PCOS unless they also show features of the condition (anovulation, hyperandrogenism and PCO on USS)
ovarian cyst pathology
Follicular cyst - Developing follicles may fail to rupture and release egg during ovulation, resulting in a cyst that can persist to grow in response to hormones
Corpus luteum cysts - corpus luteum fails to break down and fills with fluid (often seen in early pregnancy)
Serous cystadenoma - benign tumours of epithelial cells
Mucinous cystadenoma - benign tumours of epithelial cells, can grow to take up lots of space in the pelvis/abdomen
Endometrioma - lumps of endometrial tissue within the ovary, occurring in patients with endometriosis
Dermoid cysts/germ cell tumours - benign ovarian tumours (teratomas) and may contain various tissues types (skin, teeth, hair and bone) and are particularly associated with ovarian torsion
Sex cord stromal tumours - benign or malignant tummours arising from the stroma or sex cords.
Ovarian cyst risk factors and presentation for malignancy
Risk factors for malignancy: Increasing age Postmenopausal Increased number of ovulations Obesity Smoking HRT Breastfeeding (protective) Family history BRCA1 and BRCA2 genes
Presentation: Asymptomatic Bloating Pelvic pain Abdominal fullness Palpable pelvic mass Acute pelvic pain - ovarian torsion, haemorrhage or rupture of the cyst Tumours - weight loss, ascites, LAP Meigs syndrome - triad of ovarian fibroma (ovarian mass), pleural effusion and ascites
Ovarian cysts Ix and Mx
Investigation/diagnosis:
Ovarian USS
Bloods - CA125, LDH, alpha-fetoprotein, HCG
Risk of malignancy index (RMI) - menopausal status, USS findings and CA125 level
Management:
Premenopausal women with simple ovarian cyst <5cm on USS need no further Ix, usually resolves within 3 menstrual cycles, monitor via USS every 4-6 months
5-7cm - routine referral to gynae and yearly USS to monitor progression
>7cm - consider MRI or surgical evaluation
Possible ovarian cancer (complex cysts/raised CA125) - 2WW
Dermoid cysts - refer to gynae for surgery
Persistent of large cysts may need surgery, ovarian cystectomy and possibly oophorectomy
Meigs syndrome - removal of benign tumour should resolve all symptoms
causes of raised CA125
Ovarian cancer
Endometriosis
Fibroids
Adenomyosis
Pelvic infection
Liver disease
Pregnancy
Ovarian torsion
Background:
Medical emergency
Pathology:
Ovary twists in relation to the surrounding connective tissue, fallopian tube and blood supply (the adnexa)
Leads to tissue ischaemia and eventually necrosis if the twisting persists which can lead to loss of ovarian function
The other ovary can usually compensate for loss of one ovary function but if this was the only viable ovary, infertility and menopause will follow
Aetiology:
Usually from an ovarian mass >5cm such as a cyst or tumour
Can occur in girls before menarche when girls have longer infundibulopelvic ligaments allowing easier twisting
Risk factors:
More likely to occur with benign tumours
Pregnancy
Ovarian torsion presentation
Presentation:
Sudden onset severe unilateral pelvic pain
Constant and progressively worsening pain
Nausea and vomiting
Can be more mild twisting - mild pain longer persistence/intermittent pain
Localised tenderness
Palpable mass in pelvis
Necrotic ovary - may become infected, develop an abscess or lead to sepsis, or could rupture resulting in peritonitis and adhesions
ovarian torsion Ix and Mx
Investigation/diagnosis:
Pelvic USS
Transvaginal or transabdominal USS (whirlpool sign and oedema of ovary)
Doppler studies - blood flow
Laparoscopic surgery is definitive diagnosis
Management:
Admission to gynae for urgent Ix and surgical management
Detorsion or oophorectomy needed immediately, decision is made during surgery
Endometritis
Background:
Infection or inflammation of the endometrium
Can be obstetric or non-obstetric as well as acute or chronic
Acute - presence of >5 neutrophils in 400 power field in endometrial glands
Chronic - presence of >1 plasma cell and lymphocytes in 120 power field in endometrial stroma
Postpartum endometritis occurs following 1-3% of vaginal births and up tp 27% CS
Pathology:
Infection usually from the lower genital tract travels up and attacks the endometrium resulting in inflammation and damage
Can then spread to the ovaries (salpingo-oophoritis) and is debated as to weather it may contribute to PID
Aetiology:
Infection likely of multiple organisms most commonly staph, group A and B strep, E. col etc.
Endometritis risk factors
5-20x more common after CS Prolonged ROM Severe meconium Long labour with multiple examinations Retained products of conception Manual removal of placenta Maternal age very young/very old Home delivery in poor hygiene environment Maternal anaemia Obesity Diabetes Prolonged surgery Internal foetal monitoring Pre Existing infection, PID, bacterial vaginosis etc.
endometritis presentation and Ix and Mx
Presentation: Fever Abdominal pain and tenderness around uterine area/may radiate to adnexae Offensive smelling lochia (normal discharge after birth) Abnormal vaginal bleeding/PPH Dysparenuia Dysuria Malaise
Investigation/diagnosis: Bloods - cultures, FBC MSU High vaginal swab/STI screening Endometrial biopsy is diagnostic
Management:
Antibiotics guided by swab results and infection source
Hospitalization for unstable or deteriorating patients
Foetal distress
Background:
Compromised to the foetus due to hypoxia or inadequate nutrient supply
Can occur due to maternal, foetal or placental factors
Can lead to neonatal brain injury or stillbirth
Pathology:
Main cause is uteroplacental insufficiency, reduced uterine perfusion, intrauterine sepsis, reduced foetal reserves and cord compression can be involved alone or in combination
Gestational and antepartum factors can modify the foetal response to them
Aetiology/Risk factors: Dehydration Maternal hypovolemia Foetal growth restriction (IUGR) Preeclampsia Stillbirth Oligohydramnios or polyhydramnios Multiple pregnancies Rhesus sensitisation HTN Obesity Smoking Diabetes and chronic disease Decreased foetal movement Recurrent antepartum haemorrhage Post-term pregnancy Maternal age >35
Foetal distress presentation, Ix and Mx
Presentation:
Clinical suspicion - decreased foetal movements
Abnormal sonographic biometric parameters
Signs of underlying pathology
Investigation/diagnosis: Maternal and foetal observations Doppler USS CTG Biophysical profile Foetal scalp blood sampling
Management:
More intensive monitoring
Emergency CS or delivery
Amnioinfusion may be beneficial for cord compression
Gestational trophoblastic disease
Background:
Group of disorders which range from molar pregnancies to malignant such as choriocarcinoma
If there is any evidence of persistence of GTD it is referred to as gestational trophoblastic neoplasia
Very good prognosis and cure rates due to central registration and monitoring within the UK using b-hCG as a biomarker and effective treatments
Classification:
Premalignant: hydatidiform mole (complete or parietal)
Malignant: GTN (invasive mole, choriocarcinoma, placental site trophoblastic tumour [PSTT], epithelioid trophoblastic tumour [ETT])
Pathology:
Invasive mole - develops from complete mole and invade the myometrium
Choriocarcinoma - most often follows molar pregnancy but can follow normal pregnancy, ectopic, abortion and should always be considered with continued vaginal bleeding after end of pregnancy
Placental site trophoblastic tumours - most often follow normal pregnancy but occasionally arise from molar pregnancies and may also be metastatic
Aetiology:
Varies on underlying cause
Gestational trophoblastic disease risk factors and presentation
Risk factors: More common in ages >45 and <16 Multiple pregnancies Previous molar pregnancy Menarche >12, light menstruation, history of COC Asian women
Presentation: Vaginal bleeding in first trimester Uterine evacuation around 10 weeks gestation Hyperemesis Abnormal uterine enlargement Hyperthyroidism Anaemia Respiratory distress
Gestational trophoblastic disease Ix, staging and Mx
Investigation/diagnosis: Urinalysis - hCG Bloods - hCG Histology USS (snowstorm appearance)
Staging:
Confined to uterus
Extends outside uterus but limited to genital structures
Extends to lungs +/- genital tract involvement
All other metastases
Management:
Oral and written information of condition and follow up, screenings
Hydatidiform moles - suction curettage first line, pregnancy test 3 weeks after, anti-D prophylaxis, follow up biweekly hCG until normal values
Chemotherapy - plateaued or rising hCG, histological evidence of choriocarcinoma, evidence of metastases, heavy vaginal bleeding or intraperitoneal haemorrhage, serum hCG greater than 20,000 IU/L, raised hCG for 6 months after evacuation
If received chemotherapy - life long follow up monitoring hCG (initially weekly, then monthly, then 6 monthly from year 6) as highest risk of recurrence is within the first year
Advise women not to conceive until hCG levels are normal again, women undergoing chemotherapy advice to wait for at least a year
Cervical cancer
Background:
3rd most commonly diagnosed cancer worldwide
4th leading cause of death in women
More common between the ages of 25-34
⅓ of cases are detected through cervical screening
Pathology:
Cervical carcinoma
70% are SCC, 15% adenocarcinoma, 15% mixed
Bulky tumour - ectocervical tumours filling the upper vagina
Invasive - fills the lower pelvis
Destructive - invasive tumour that erodes tissues, ulceration, necrotic cavities, excavation with infected abscesses
The transformation zone is the main site of growth (where squamous and columnar cells meet from endo to ecto cervix. Metaplasia of cells near this zone can lead to ectropion (transformation of ectocervical cells to present endocervical cells) which can then develop onto carcinogenic changes of more cells
HPV inserts its DNA into the DNA of transformation zone cells and causes genetic mutations leading to carcinogenic traits of cells (if the infection persists)
Aetiology:
Multifactoral
cervical cancer risk factors
HPV is biggest risk factor Heterosexual Multiple sexual partners Smoking Lower social class Immunosuppression COC (slight increase) Non-attendance at cervical screening programme
cervical cancer presentation and Ix
Asymptomatic
Abnormal vaginal bleeding (most common) - scanty or severe, spontaneous, post-coital, micturition or defecation
Vaginal discharge - intermittent or continuous
Vaginal discomfort
Urinary symptoms
Painless haematuria
Chronic frequency
Painless fresh rectal bleeding, altered bowel habits
Leg oedema, pain, hydronephrosis
CKD
Examination - normal, white/red patches on cervix, erosion, ulcers or tumour on cervix and vagina, pelvic mass on bimanual exam
PR examination - mass or bleeding
Investigation/diagnosis: Speculum examination Bimanual exam PR examination (rectal symptoms) Smear test - colposcopy STI screening Bloods - FBC, eGFR, LFTs Staging - examination under anaesthesia (abdominal, vaginal and rectal), CT, MRI, colposcopy, cystoscopy, sigmoidoscopy + biopsies, PET scans
cervical cancer staging, management and referrals
Staging:
0: no evidence of primary tumour
Tisb: carcinoma in situ (pre-invasive)
1: confined to uterus
2: Invades beyond uterus but NOT pelvic wall or lower ⅓ vagina
3: invades into pelvic wall and/or lower ⅓ vagina or causes hydronephrosis of kidneys
4: Further metastases
Management:
Depends on family plans of females and staging
Surgery - conisation or wertheim’s radical hysterectomy
Radiotherapy
Combination of radio and chemotherapy
Prevention - smear testing and HPV vaccination
Referral red flags:
All postmenopausal women who have not received HRT and have vaginal bleeding or have persistent/unexplained vaginal bleeding after cessation of HRT for 6 weeks
Premenopausal women with persistent intermenstrual, postcoital bleeding or blood stained vaginal discharge AND polyp, ectropion, cervicitis or warts AND infection has been excluded/treated but symptoms persist 6-8 weeks post Tx
Consider urgent referral for women with persistent intermenstrual bleeding and negative pelvic examination
Consider in women not participating in cervical cancer screening, bleeding continues beyond 3 months (6 months IUS), has new symptoms or changed bleeding pattern or tried contraceptive modification but bleeding persists
ovarian cancer
Background:
Leading cause of death from gynaecological cancer in the UK
Lifetime risk of around 2% of women in england and wales
Most common in postmenopausal women
Complications - torsion, rupture or infection
Epithelial ovarian tumours are most common (90%) mostly in >50YOs. Subtypes include serous, endometrioid, clear cell tumours, mucinous tumours, brenner (transitional cell) and undifferentiated tumour.
Germ cell tumours - 5-10% cases, mostly in women <35 YOs. dysgerminoma is the most common type.
Sex cord stromal tumours - less than 5% cases. Types include fibroma, fibrosarcoma, seroli-leydig and granulosa cell tumours
Metastatic tumours - from breast, GI, hematopoietic, uterus and cervix.
Borderline tumours - malignant tumours but very well differentiated (low grade). 10-15% of ovarian tumours. Types include serous, mucinous and endometrioid
Pathology:
Malignant ovarian tumours can be solid or cystic
Epithelial ovarian tumours (90% cases), germ cell tumours, sex cord stromal tumours and metastatic tumours
Epithelial ovarian tumours - Arise from the epithelial surface of the ovary.
Germ cell tumours - from primitive embryonic gonad
Sex cord stromal tumours - from connective tissue cells,
Aetiology:
Multifactorial
ovarian cancer risk factors and protective factors
Risk factors:
>50YOs
Smoking
Obesity
Lack of exercise
Talcum powder
Asbestos
Infertility and use of fertility drugs (clomifene)
Early menarche, late menopause
HRT
Family history
BRCA1 and 2 genes
History of ovarian, breast or bowel cancer
History of endometriosis
Protective factors:
Childbearing
Breastfeeding
Early menopause
Oral contraceptive pill
ovarian cancer presentation and red flags
Germ cell tumours - rapidly enlarging abdominal mass, causes considerable pain, often ruptures or undergoes torsion
Early symptoms - abdominal discomfort, distension, bloating, urinary frequency, dyspepsia
B symptoms - weight loss, anorexia, depression
Pelvic or abdominal mass
Torsion, rupture, infection - pain
Late signs - abdominal, pelvic or back pain
Meigs syndrome: triad of benign ovarian tumour (fibroma), Ascites and pleural effusion that resolves after tumours removal
Red flags:
Persistent abdominal distension or bloating
Early satiety or loss of appetite
Pelvic or abdominal pain
Increased urgency and/or frequency
Unexplained weight loss, fatigue, changes in bowel habit
>50YO with IBS symptoms over the last 12 months
ovarian cancer ix and staging
Investigation/diagnosis:
Bloods - CA125, genetic testing (BRCA1/2), in women <40YOs arrange alpha fetoprotein (AFP) and b-hCG
Measure CA125 in primary care for those with symptoms or examination suggesting ovarian Ca - if >35 IU/ml arrange USS of abdomen and pelvis, if >250, refer to specialist MDT
If USS suggestive of Ca, urgent referral to gynae cancer service
CT, MRI
Risk of malignancy index - menopausal status x ultrasound score x CA125 value
USS score - 0-3 based on multilocular cysts, solid areas, metastases, ascites and bilateral lesions
Menopausal status score 1: premenopausal, 3: postmenopausal
Staging:
Limited to ovaries
Involving one/both ovaries with pelvic extension
Involving one/both ovaries with microscopically confirmed peritoneal implants outside of the pelvis
Distant metastasis
ovarian cancer Mx and referrals
Management:
Explorative laparotomy + chemotherapy
Bevacizumab - biological therapy in advanced tumours
Germ cell tumours - often curable with high survival rates
Borderline tumours - often need surgery as don’t respond well to chemotherapy
Monitor CA125, beta-hCG and AFP throughout Tx and during recovery
Referrals:
Refer 2WW to gynae cancer service with ascites and/or pelvic/abdominal mass that is not obviously uterine fibroids.
USS suggestive of ovarian cancer
Krunkenberg tumours
Malignancy in the ovary that has metastasised from a primary site
Classically from the stomach or colon although can arise from the breast
Gastric adenocarcinoma is most common source
This metastases can be larger or more symptomatic than the original tumours
endometrial cancer
Background:
>90% of cases are women >50 YOs
Most common in western societies
4th most common cancer in women in the UK
Two subtypes: oestrogen dependent endometrioid (type 1) and oestrogen independent non-endometrioid (type 2)
Pathology:
80% are adenocarcinomas from mucosa of the uterus
Unopposed oestrogen - when oestrogen is not modified by effects of progesterone from medication or anovulatory cycles (corpus luteum does not mature and secrete progesterone)
This oestrogen can lead to more mitotic growth of endometrium and long term increases the risk of mutation and carcinogenic changes.
Aetiology:
multifactorial
endometrial cancer risk factors and presentation
Risk factors: Unopposed oestrogen is the biggest risk factor (as medication) Nulliparous Menopause >52 YOs Obesity T2D Endometrial hyperplasia PCOS Tamoxifen in women >50 YOs Hereditary nonpolyposis colon cancer (HNPCC)
Presentation:
Abnormal uterine bleeding
Postmenopausal bleeding - must always screen for endometrial cancer
Irregularities of menstrual cycle
Usually only advanced disease has abnormal examination
endometrial cancer ix and staging
Investigation/diagnosis:
Cervical smear
Transvaginal USS - thickening of endometrium
Hysteroscopy + endometrial biopsy (curettage) confirms diagnosis
Staging - Laparoscopy, total abdominal hysterectomy + bilateral salpingo-oophorectomy (also treatment), CT, MRI, EUA, endoscopies, PET scan
Bloods - FBC, eGFR, LFTs
Staging: TNM, FIGO
Confined to corpus uteri
Involves corpus and there is invasion into cervical stroma but not outside of the uterus
Local or regional spread beyond the uterus
Involvement of the bladder or bowel mucosa or distant metastases
endometrial cancer Mx and referrals
Management:
Based on staging
Stage IA type 1 (endometrioid endometrial cancer) without invasion in women who want to preserve fertility - progesterone
Stage I - total abdominal hysterectomy + bilateral salpingo-oophorectomy +/- lymphadenectomy
Stage II - radical hysterectomy + pelvic node clearance
Stage III and IV - de-bulking surgery + radiation + chemotherapy
Referrals:
Age >55 with postmenopausal bleeding (consider also in postmenopausal women <55YO)
Consider direct access to USS in women aged 55+ with unexplained vaginal discharge, have thrombocytosis or haematuria OR have visible haematuria AND low Hb, thrombocytosis or high blood glucose levels
Gestational diabetes
Background:
Most significant complication is macrosomia increasing the risk of shoulder dystocia and longer term risk is of long term diabetes postpartum
Pre-existing diabetics who become pregnant must carefully monitor their glucose control throughout
Pathology:
During pregnancy, maternal levels of insulin production increase in order to supply the foetus with insulin, however this can damage maternal insulin receptors if risk factors such as obesity already exist and have previously caused loss of insulin sensitivity. This leads to loss of insulin sensitivity and causes a loss of blood glucose control
Possible adverse effects to the baby are: neonatal hypoglycemia, polycythaemia, jaundice, congenital heart disease and cardiomyopathy
Aetiology:
Reduced insulin sensitivity during pregnancy
gestational diabetes risk factors and Ix
Risk factors: Previous gestational diabetes Previous macrosomia (>4.5kg) BMI >30 Ethnic origin black caribbean, middle eastern and south asian Family history of diabetes
Investigation/diagnosis:
Oral glucose tolerance test at 24-28 weeks gestation for anyone with risk factors/presenting symptoms
OGTT should be done in the morning after fasting - patient BG is measured before, then drinks 75g glucose drink and BG checked again and then once more at 2 hours post drink.
Normal results for fasting <5.6mmol/l, at 2 hours is <7.8mmol/l, higher than these diagnose gestational diabetes
TOM TIP: cutoff for gestational diabetes as 5 – 6 – 7 – 8.
gestational diabetes management
Monitoring BG levels several times daily with target levels 5.3 fasting, 7.8 1 hour post meal, 6.4 for 2 hours and must avoid levels <4mmol/l
Four weekly USS to monitor foetal growth and amniotic fluid volume from 28-36 weeks gestation
Fasting glucose <7mmol/l a trial of diet and exercise for 1-2 weeks followed by metformin then insulin if these fail to control BG
Fasting glucose >7mmol/l start insulin and metformin combined therapy
Fasting glucose >6mmol/l AND macrosomia or other complications - insulin and metformin combination therapy
Glibenclamide suggested for those who decline insulin or cannot tolerate metformin
Women with gestational diabetes can give birth up to 40+6 weeks (full term)
Can stop medications immediately after birth as gestational diabetes should improve
pre-existing diabetes in pregnancy management
5mg folic acid from preconception until 12 weeks gestation
Type 1 and 2 diabetics should both aim for same BG levels as gestational diabetics
Type 2 managed with insulin and metformin and additional oral medication should be stopped
Type 1 diabetics managed with sliding scale insulin, dextrose and insulin infusion titrated to BG levels according to local guidelines (also considered for type 2 poorly controlled)
Retinopathy screening should be performed at beginning and at 28 weeks gestation (refer to ophthalmology)
Planned delivery between 37-38+6 weeks
Lower insulin doses and be aware of hypoglycemia in postnatal period
Babies:
Need close monitoring for neonatal hypoglycemia with regular BG monitoring and frequent feeds
If BG falls below 2mmol/l commence IV dextrose and nasogastric feeding
pregnancy induced HTN
Background:
Chronic HTN is HTN existing <20 weeks gestation and is longstanding, not caused by placental dysfunction and is not classed as preeclampsia
Pregnancy induced HTN/gestational HTN is HTN occurring after 20 weeks gestation without proteinuria
Pathology:
Occurs after 20 weeks gestation when spiral arteries of the placenta form abnormally leading to high vascular resistance
The trophoblast should send signals during endometrial invasion to spiral arteries, reducing their vascular resistance and increasing blood flow, eventually these break down forming lacunae which pool maternal blood.
At 20 weeks in preeclampsia the lacunae do not form properly or are inadequate and this predisposes preeclampsia development caused by high vascular resistance in spiral arteries and poor perfusion of the placenta
This causes oxidative stress in the placenta and release of inflammatory chemicals into the systemic circulation, causing systemic inflammation and impaired endothelial function in blood vessels
Poorly understood pathophysiology
Aetiology:
Spiral artery dysfunction and lacunae malformation during pregnancy
pregnancy induced HTN risk factors and presentation
High risk: Pre-existing HTN Previous HTN in pregnancy Existing autoimmune conditions Diabetes CKD
Moderate risk: >40 BMI >35 >10 years since previous pregnancy First or multiple pregnancy Family history
Presentation:
BP >135/85 during pregnancy
pregnancy induced HTN Ix and management
Investigation/diagnosis: BP Urinalysis Bloods - eGFR, creatinine, LFTs Doppler USS scans for foetal growth
Management:
Aim for BP 135/85mmHg
Admission for BP >160/110mmHg
Urinalysis at least weekly (creatinine:protein, albumin:creatinine ratios)
Monitoring bloods weekly (FBC, LFTs, eGFR, creatinine)
Monitoring foetal growth by doppler scans
PlGF testing on one occasion
If HTN cannot be controlled consider planned early birth, corticosteroids for baby’s development
After birth, BP should return to normal once placenta is removed
preeclampsia
Background:
Refers to new hypertension in pregnancy with end organ dysfunction, notably proteinuria.
Significant cause of maternal and foetal morbidity and mortality
Can lead to maternal organ damage, foetal growth restriction, seizures, early labour and death
Preeclampsia is pregnancy induced HTN associated with organ damage
Eclampsia is when seizures occur as a result of preeclampsia
HELLP syndrome - haemolysis, elevated liver enzymes and low platelets, complications of preeclampsia and eclampsia
Pathology:
Occurs after 20 weeks gestation when spiral arteries of the placenta form abnormally leading to high vascular resistance
The trophoblast should send signals during endometrial invasion to spiral arteries, reducing their vascular resistance and increasing blood flow, eventually these break down forming lacunae which pool maternal blood.
At 20 weeks in preeclampsia the lacunae do not form properly or are inadequate and this predisposes preeclampsia development caused by high vascular resistance in spiral arteries and poor perfusion of the placenta
This causes oxidative stress in the placenta and release of inflammatory chemicals into the systemic circulation, causing systemic inflammation and impaired endothelial function in blood vessels
Poorly understood pathophysiology
Aetiology:
Spiral artery and lacunae malformation/dysfunction during pregnancy
preeclampsia risk factors and presentation
High risk: Pre-existing HTN Previous HTN in pregnancy Existing autoimmune conditions Diabetes CKD
Moderate risk: >40 BMI >35 >10 years since previous pregnancy First or multiple pregnancy Family history
Presentation: Triad of HTN, proteinuria and oedema Headaches Visual disturbance N+V Upper abdominal or epigastric pain Oedema Reduced urine output Brisk reflexes
preeclampsia Ix and diagnosis
Investigation/diagnosis:
Vitals - BP, oxygen, temperature, capillary refill
Urinalysis - Proteinuria
Bloods - creatinine, LFTs, platelets, FBC
Doppler USS for foetal growth
Diagnostic: BP >140/90mmHg PLUS any of following:
Proteinuria protein:creatinine ratio >30mg/mmol/ or albumin:creatinine ratio >8mg/mmol/l on 1+ dipstick Organ dysfunction (thrombocytopenia or haemolytic anaemia, LFTs, creatinine) Placental dysfunction (IUGR or abnormal doppler studies)
preeclampsia management
Prophylaxis for women with single high risk factor or two or more moderate RFs - aspirin given from 12 weeks gestation-birth
All women are monitored every appointment BP and urinalysis
fullPIERS or PREP-S score to determine need for hospital admission
BP monitored closely at least every 48 hours
USS monitoring of foetus, amniotic fluid and dopplers performed two weekly
Labetalol first line antihypertensive
Nifedipine second line
Methyldopa 3rd line (must be stopped within 2 days of birth)
IV hydralazine may be used in critical care with severe preeclampsia or eclampsia
IV Mg sulphate during labour and in 24 hours postpartum to prevent seizures (als given during eclampsia)
Fluid restriction in severe preeclampsia/eclampsia during labour to avoid fluid overload
After 3rd stage labour BP should return to normal overtime, consider switching to combination of enalapril (1st line), nifedipine or amlodipine (1st line black african/caribbean) or labetalol or atenolol (3rd line)
