O&G Case 8, 15, 17, 18 Flashcards
Whats the DDX for preterm labour?
● Preterm labour
● APH
pregnancy
● Placental abruption
● Uterine rupture
What is preterm birth and how common is it?
● Defined as “delivery before completion of 37+0 weeks gestation”
○ Later preterm: 34-37
○ Early preterm: <34
○ Very preterm: 28-<32
○ Extremely preterm: <28
● Apprxomimately 8% of births
● Threatened <3cm cervical dilation
What are the relative contributions of iatrogenic and spontaneous preterm birth?
● 2⁄3 spontaneous
○ Can have ROM without labour and can labour without ROM
○ Preterm prelabour rupture of membranes (PPROM)
● 1⁄3 iatrogenic preterm delivery for maternal or fetal indications
○ Preeclampsia
○ IUGR
○ Placenta praevia
Whatcan preterm birth cause in terms of morbidity (particularly neurodevelopmental) and perinatal mortality?
● Neurosensory issues
● Respiratory distress
○ Apnea of prematurity (cessation of breathing for >20s)
○ Transient tachypnoea of the newborn (TTN)
○ Bronchopulmonary dysplasia (BPD)
● Feeding intolerance and necrotising enterocolitis (NEC)
● Hypoglycaemia
● Hypothermia
● Jaundice at birth
What factors prior to pregnancy increase the risk of preterm birth?
- Prev preterm and/or PPROM
- Prev late miscarriage
- Cervical incompetance / fibroids
- Previous surgery i.e lETZ
- Hx of termination <1cm, or C-section at full dilation
What factors during a pregnancy increase risk of preterm birth?
- Maternal age <20 or >40
- Low or high BMI
- Polyhydraminos
- Infection
- Smoking
- Placental abruption
- ART
What are the common causes of preterm labour?
● Any stimulus for inflammation can precipitate preterm labour:
○ Infection
○ Bleeding
○ Uterine distension (due to multiple pregnancy or polyhydramnios)
● Premature activation of maternal or fetal hypothalamic-pituitary-adrenal axis
● Decidual haemorrhage
How can preterm labour be predicted?
● Risk scoring
● Cervical length (TVUS)
○ Shorter cervix → higher risk
● Vaginal biomarker swabs (mostly fFN)
○ Elevated fFN from 22-37 weeks gestation associated with higher risk of preterm labour
○ Can also use placental alpha macroglobulin-1 and phosphorylated insulin like growth factor binding protein 1 (Never heard of this in clincial practice)
How can preterm labour be prevented?
● Cervical cerclage
(between 12-14 weeks)
● Rescue cerclage
○ Already dilated cervix but no contractions yet
● Progesterone
○ For high risk woman
● Antibiotics
● Prophylactic tocolysis
○ Use to buy time for steroids to be taken and take effect or to transfer them to
appropriate centre for care
○ Nifedipine
○ Suppress premature labour
○ Calcium channel blocker
■ Stops influx of calcium which prevents uterine contractions
What must you give to a women with suspected preterm labour?
● Steroids
○ To prevent respiratory distress by accelerating pulmonary surfactant production
○ 11.4mg betamethasone x 2 24 hours apart
○ Give to women;
■ Increases risk of delivery <34+6 weeks gestation
■ When preterm birth is planned or expected within next 7 days (even within 24
hours)
What is the role of administering magnesium sulphate to women at preterm delivery?
● Magnesium sulphate
○ Usually in more preterm woman
○ Neuroprotection for infant
○ Reduces risk of cerebral palsy
○ Given as IV infusion over 4 hours just before birth
How would your management of a woman in preterm labour differ in a rural vs a tertiary hospital setting?
● Rural hospitals may not have NICU so need to factor in transfer of women to tertiary centre
● Tocolysis (nifedipine) will delay delivery by >48 hours to allow for transfer and administration
of antenatal corticosteroids and magnesium sulphate
What is the fetal fibronectin test and what is its role in assessing a woman in suspected preterm labour?
● fFN test detects the fFN (glue that attaches the fetal membranes to the decidua basalis) in the cervicovaginal fluid
● Elevated levels from 22-37 weeks associated with risk of preterm labour
● Strong negative predictive value → >99% of women with negative test will not delivery in next
10 days
● Do test before vaginal examination, ROM, or >48 hours from last sexual intercouse, if cervical
dilation <3cm → false positives (but can still be reassuring if negative)
What is tocolysis? What drug is commonly used for tocolysis in New Zealand?
● Tocolytics = medications used to suppress labour
● Nifedipine most common in NZ
○ Calcium channel blocker
■ Stops influx of calcium which prevents uterine contractions
○ Side effects
■ Transient palpitations
■ Headache
■ Flushing ○ Contraindications
■ Suspected or confirmed IU infection
■ Placental abruption
■ Significant hypotension
■ Maternal shock
What investigations might be useful when assessing a woman in suspected preterm labour?
● Blood test
○ FBC
○ CRP
○ G&h
● MSU
● High vaginal swab
● fFN (<34+6weeks)
● TVUS
○ Cervical length >30mm = negative
○ Cervical length <15mm = positive
● CTG (cardiotocography)
● Other vaginal biomarkers (PAMG-1)
● Ferning
○ Vaginal secretions mixed with amniotic fluid make a “fern-like” pattern under microscope
● Nitrazine test
○ Paper strips that detect pH changes in the vagina (amniotic fluid has higher pH than
vaginal fluid) ● USS
○ Fetal height and measurements
○ Liquor volume
○ Measurement of amniotic fluid volume to determine PPROM
What are the general principles of management for women in preterm labour?
Admit
- Confirm reg contractions
- FFN
- Cervical length and dilatation
Monitoring
● IV line → FBC, CRP, G&H, blood cultures if suspicious of infection
● Confirm fetal presentation by USS
● Continuous CTG (if in labour)
Give medicines
What medicines do you give for a preterm labour?
○ Administer corticosteroids
○ Magnesium sulphate (<30weeks)
○ Tocolysis (Nifidipine)
○ Prophylactic antibodies for threatened labour → UTI etc (to settle uterus down)
○ Prophylactic antibodies for group B (if in labour)
During labour what do you for a preterm?
Delayed cord clamping (if in labour)
● Prolongation of the time between the delivery of a newborn and the clamping of the umbilical
cord
● 60 seconds at birth
● Reduces neonatal mortality
How do you manage PPROM?
● Same management +
○ 10/7 oral erythromycin (reduce preterm birth)
○ Conservative management until >37 weeks gestation then IOL
How do you treat stress and urge incontinence?
- Pelvic floor training
- Estrogen cream
- Bladder training
- Surgical intervention
- Duloxetine, Oxybutinin
- Botox
What are the surgical interventions for incontinence?
○ Suspension/sling operations to elevate bladder neck and support urethra
○ Mid-urethral slings
■ Mesh tape is placed under the urethra through two to three small incisions in order to support the urethra
■ Increases sub-urethral support
○ Intramural urethral bulking agents
■ Bulking materials injected into the urethra and bladder neck which helps to close the lumen of the urethra
■ Increasing tissue mass increases outflow resistance
■ Evidence limited
What is prolapse?
Prolapse = muscles and tissues supporting pelvic organs become weak or loose Traditional terms describing pelvic organ prolapse
What is the new descriptive terms for prolapse?
● Anterior prolapse
○ Front wall of the vagina has herniated inward
○ Usually caused by the bladder or/and urethra shifting position and placing
pressure on the vaginal wall
○ This term includes the possibility of a cystocele, urethrocele and cystourethrocele.
● Posterior
○ Rectum to herniate into the vagina
○ Due to weakening of the musculature and connective tissue or damage to the
rectovaginal septum
○ This term includes the possibility of a rectocoele or enterocoele
● Apical
○ Tissue supporting the uterus weakens and the uterus slips downward, placing pressure on the vagina
○ Usually associated with trauma in childbirth
● Vaginal vault prolapse
○ Roof of the vagina collapses
○ Usually following hysterectomy
■ Will also have an enterocoele present
What are the symptoms and signs of prolapse?
● Feels like something is “coming down”
● Backache, urinary problems, dyspareunia
● Difficulty with micturition or defecation
● Discharge and bleeding (procidentia)
● Symptoms often less apparent in the morning
How do you assess prolapse?
● Introitus inspected
● Woman asked to bear down (with the labia separated and the anus supported with a swab)
○ Vaginal wall prolapse will be evident ● Sim speculum exam in left lateral position
○ Examine vaginal walls and assess descent of cervix
● Bimanual exam
○ Assess uterine mobility and descent
○ Assess perineum and pelvic floor muscle tone
● If symptoms worse when standing → assess while standing
● May need neurological exam
○ Consider MS or neuropathy as cause for incontinence (urge)
Whats the treatment for prolapse?
● Elicit from history (as it may impact management)
○ Menorrhagia?
○ Is family complete?
○ Normal sexual function?
● Address modifiable lifestyle factors that can contribute to the problem
● Consider and treat lack of estrogen (topical estrogen therapy)
● Physiotherapy for pelvic floor exercises
● Pessary (ring or cube)
● Surgery (repair +/- hysterectomy)
Pessaries
Which investigations may be useful in assessing a patient with incontinence?
- Urine dipstick
- Serum creatinine
- Bladder diary
- Post void residual vol
- Urodynamic testing
What meds can exacerbate incontinence?
- Diuretics
- Alpha blockers,
- Anti psychotics
- Opioids
- Sedatives
What is the climacteric in the context of menopause?
Refers to the physical and emotional symtpoms of menopause
What is menopause?
‘Menopause’ is referring to a specific event, the cessation of menses, and ‘climacteric’ to gradual changes of ovarian function that start before the menopause and continue thereafter for a while
Describe the changes in the function of the hypothalamic-pituitary-ovarian axis which occur at menopause?
● Inhibin B levels begin to decline in perimenopause
○ Inhibin B is produced by granulosa cells in primary follicles (which are becoming
lower)
● Decreased ovarian feedback of inhibin (and estradiol) results in reduced negative feedback on pituitary for FSH release
● Higher plasma levels of FSH (increase 10-20x) stimulate a greater level of primordial follicles
and accelerates depletion of primordial reserve
○ LH also increases x 4-5
● Estrogen levels decrease by 80-90%
○ Oestradiol bigger reduction than oestrone
● Androgen decreases by 15%
What symptoms are attributable to the physiological changes of the perimenopause?
Vasomotor changes → changes in level of estrogen and progesterone
● Hot flushes
● Night Sweats
● Palpitations
● Weakness
● Faintness
GU → due to reduction in estrogen
● Vaginal dryness
○ Atrophic changes
○ Reduction in vaginal lubrication
○ Rise in pH of vaginal fluids
Reduction in uterus size → due to reduction in estrogen Reduction of breast density → due to reduction in estrogen Osteoporosis → due to reduction in estrogen
Blood lipid changes
Behavioural and psychological changes → hormonal changes
What tx or advice is given to women experiencing hot flushes, atrophic vaginal symptoms, prevention of osteoporosis?
● Hot flashes
- Avoid triggers
- Environmental temperature regulation
● Atrophic vaginal symptoms
- Vaginal estrogen creams
- Rings
- Tablet estrogen therapy
- Estrogen can reduce incidence of UTIs and features of overactive bladder
● Prevention of osteoporosis
- Smoking cessation
- Vitamin D
- Regular weight-bearing exercise
What is the non-hormonal therapy for menopause?
● Selective estrogen receptor modulators
○ Tamoxifen
○ Ospemifene
○ Raloxifene
● Paroxetine (for vasomotor symptoms)
● Clonidine and/or gabapentin
What are the types of HRT for menopause?
● Estrogen therapy (women without uterus)
● Estrogen + progestin (women with uterus)
○ Perimenopausal → cyclical
○ Postmenopausal → continous
● Oral or transdermal
What are the risks associated with HRT in menopause?
○ Cancer
■ Unopposed estrogen therapy → endometrial cancer risk
■ Estrogen + progestin → breast cancer risk
○ CVD risk → DVT, PE, stroke
○ Gallbladder disease
○ Stress urinary incontinence
What are the contraindications to HRT in menopause?
Cancer:
○ Undiagnosed vaginal bleeding
○ Breast cancer
○ Endometrial cancer
CVD:
○ Chronic liver disease
○ Hyperlipidaemia
○ Recent DVT/stroke
○ Coronary artery disease
pregnancy
What are the important ddx for pevlic masses in children, adults of child baring and non-baring ages?
Urgent - childbearing age
● Ectopic (?rupture)
● Adnexal torsion
Urgent - non childbearing age(cancer)
● Primary malignancy in pelvic organs
● Metastases
Children (cysts)
● Physiological cysts as newborn
● Follicular ovarian cysts
What are the potential other causes of pevlic masses in pre-menopausal women?
Hormonally driven
● Fibroid
● Endometrioma
● Physiological cyst
● Cysts
● PCOS
Non-hormonal
● Cysts adenoma
● Teratoma
Inflammatory
● Abscess
● Tubo Ovarian abscess
● Hydrosalpinx (often present with pain rather than mass)
○ Adhesions causing a backlog of fluid (expands fallopian tube)
What are the post menopausal causes of pelvic masses?
Post-menopausal
● Same conditions as younger women
○ Hormonally driven things → present smaller
● Malignancy
● Metastatic disease
Whats the trick for remembering different causes of pelvic masses?
Fetus
Flatus
Fibroids Flipping tumour
● Benign
○ Dermoid
○ Cystadenoma
○ Mucinous cystadenoma
○ Fibroma
● Malignant
○ Any organ
○ Leiomyosarcoma
○ Ovarian malignancy
■ Premenopausal
● Germ and stromal
■ Post-menopausal
● Epithelial
○ Serous
○ Mucinous
What are the post menopausal tumor markers?
● CA 125 → serous cystadenoma, endometriosis, PID, pregnancy, pancreatitis
● Ca 19.9 → mucinous cystadenoma
● CEA
What are the pre-menopausal tumor markers?
● AFP
● Beta HCG → germ cell tumours of ovary
● Lactate dehydrogenase
● CA 15-3 → breast cancer marker but also for benign ovarian masses
What is the ‘risk of malignancy index’, and how is it useful in triage of women with ovarian masses?
RMI
● USS findings
● Clinical findings → such as ascites
● Menopausal status
● CEA marker finding
What are the epidemiological features of and risk factors for ovarian cancer?
● Malignancy of older people ○ <55 years
● Genetic risk factors
○ BRCA1
○ BRAC2
○ HNPCC/lynch syndrome
● Hormonal
○ HRT
○ Nulliparity
○ Early menarche/late menopause
○ Infertility
○ Endometriosis
Arises from fallopian tubes → that’s why it is epithelial
What are the main histological types of ovarian cancer?
● Epithelial
○ Serous
○ Mucinous
○ Endometrioid
● Germ cell
What are the common presenting symptoms of ovarian cancer?
● In most cases, there are no early symptoms
● In advanced stages, the size and growth of the tumor can lead to:
○ Abdominal pain and ascites
○ Cancer cachexia
○ Possible disruption of menstrual cycle
○ Dyspnea due to malignant pleural effusion
○ Abdominal or pelvic mass
● Complication: tumor can cause ovarian torsion→ tissue infarction → surgical emergency
● The first symptom is often increasing abdominal girth (clothes no longer fit at the waist)
How is ovarian cancer staged?
FIGO staging
Stage 1 → confined to ovaries Stage 2 → into pelvis
Stage 3 → into abdomen Stage 4 → distant mets
What are the general principles of treatment for ovarian cancer?
Pelvic USS
CT chest/abdo/pelvis
If defined to ovary with no spread → surgical debulking
Most ovarian cancers present late and have spread → histology first (biopsy)
● Then chemotherapy first
● Stage 3 or less → chemo shrinks it down and can do interval debunking therapy
Krukenberg tumour
● Sister mary joseph nodule
What are the common and important causes of postmenopausal bleeding?
Consider:
- Vulvovaginal atrophy
● Exogenous oestrogen
● Polyps
● Endometrial hyperplasia
● Endometrial cancer
● Cervical cancer
What investigations may be indicated for a patient with postmenopausal bleeding?
○ FBC
○ Ferritin
● Smear and STI check
● Pelvic TVUSS
○ Endometrial thickness
■ <5mm unlikely to be endometrial cancer
■ Check ovaries, for polyps, fluid in endo cavity.
● Pipelle
○ Suctions/scrapes out some of endometrium
○ If 5mm-10mm on USS and get negative pipelle can discharge
○ If they have risk factors do a hysteroscopy anyway
● Hysteroscopy
○ Do straight away if >20mm
○ Directly visualises the endometrium with a microscope
○ Dilation and curettage
○ Outpatient or short GA
What is the epidemiology of endometrial cancer?
● Most common gynae cancer in NZ and developed world
● Maori and pacific patients diagnosed at younger ages than NZ european
● Increasing → associated with high estrogen states (obesity is estrogen producing)
● Usually diagnosed early due to bleeding as common symptom
● Older demographic (<55 years) → mostly post-menopausal women
What are risk factors for endometrial cancer?
● Age (mean age = 65)
● Unopposed estrogen therapy
○ PCOS
○ Tamoxifen (estrogen receptor modulator)
○ Anovulation
○ Nulliparity
○ Oestrogen only HRT
● Obesity (BMI >30)
● HTN
● Diabetes
● Previous endometrial polyps
● HNPCC
● Family history
How does endometrial cancer typically present?
● Post-menopausal bleeding
● Intermenstrual bleeding (if perimenopausal)
What are the general principles of treatment for endometrial cancer?
Treatment for endometrial cancer is surgical (unless otherwise contraindicated) with adjuvant
therapy (radiotherapy, chemotherapy, or hormonal therapy)
- Check for spread (imaging)
- Adjuvant use is determined by risk of recurrence
How is endometrial cancer graded?
Type 1 = low grade oestrogen dependent/endometrioid = good prognosis ● Endometrioid adenocarcinomas = 80% of endometrial cancers
Type 2 = high grade oestrogen independent / non endometrioid cancers = poor prognosis
How is endometrial cancer staged?
FIGO staging
● Stage 1: confined to uterus
● Stage 2: involves the cervix
● Stage 3: pelvic mets (spread to ovaries, fallopian tubes, vagina, or nearby lymph nodes)
● Stage 4: mets outside pelvis (bladder, rectum, abdomen)
How is endometrial cancer treated?
(1) Low risk = Stage IA endometrial carcinoma without myometrial invasion => hysterectomy & BSO + post-operative observation + no adjuvant
(2) Stage IA endometrial carcinoma with myometrial invasion, 1B, or II => Intermediate risk => surgery + vaginal brachytherapy
● Stage IB and II higher risk so might offer EBRT
○ Brachytherapy = internal radiation treatment = radiation source placed close to the cancer through the vagina
● +/- chemotherapy (Paclitaxel and carboplatin)
High risk => stages III-IV and all non-endometrioid carcinomas => external beam radiotherapy + chemotherapy
Write some notes on endometrial hyperplasia
● Hyperplasia divided into simple or complex (further divided into with or without atypia)
● Endometrial cancer may be preceded by, or co-exist with, premalignant hyperplasia =
complex endometrial hyperplasia with atypia
● Complex atypia = 80% risk of development of cancer ⇒ hysterectomy
● Simple <5% chance of developing into cancer
● Progesterone (high dose) treatment
