Obstetrics Flashcards
Antenatal visit frequency
> 28/40: monthly
28-36: biweekly
36: weekly
Medications that cross the placenta so should be changed in pregnancy are
Medical conditions advised AGAINST getting pregnant
Anti-epileptic drugs
Warfarin (swap for LMW hep)
Pulm HTN Renal failure (until on dialysis or receive a transplant)
SX of pregnancy
Nausea
Tender breasts
Missed period
Urinary frequency
Naegle’s rule
Date of conception is first day of last normal period + 9 months and 7 days
- When does the uterus first become palpable?
2. When do fetal movements first become noticeable?
- 12 weeks
2. ~20 weeks
What supplements should pregnant women be taking?
Folate
Vitamin D
Iron
Ca
Routine bloods at first antenatal visit (12 weeks)
FBE Blood group and antibody screen (ABO, Rh) HIV, HBV, HCV, syphilis Rubella immunity MSU for MCS (?asymptomatic bacteriuria)
+/- VZV immunity
+/- Down syndrome serum screen (free betaHCG, PAPP-A)
Components of combined down syndrome serum screen
12 week ultrasound - gestational age and nuchal translucency
Serum free bHCG + PAPP-A
OR as an alternative, non-invasive pre-natal screen for cell-free DNA from 9 weeks. tests for aneuploidies. 99% NPV. If pos, refer for invasive testing. Takes 3 days but costs $450.
IF a women’s combined serum screen comes back as high risk, what is the next step in investigations for diagnosis?
Refer her for diagnostic invasive testing (chorionic villus sampling at 10-13 weeks or amniocentesis at 15-18 weeks) anti-D if mum is Rh neg
+ FISH and full karyotype
when do routine USS in low-risk pregnancies typically occur.
Ultrasound @ 12 weeks: gestational age and down syndrome screen
18-20weeks: morphology and wellbeing
What bloods get done in the second trimester and when?
28 week bloods:
- FBE
- Oral glucose challenge
- AB screen in Rh neg women (will need anti-D injections if no Anti-D detected)
Who needs anti-D injections and when are these given?
Rh neg women who are negative for anti-D antibodies
Given at 28 and 36 weeks
To Rh(neg) women with M/C, invasive procedures, abruption, trauma etc
What 2 medical conditions do we screen for every visit and how do we do this?
Placental insufficiency - ask about fetal movements + SFH
Pre-Eclampsia - HTN (BP), proteinuria (urine dipstick) , oedema (exam/Hx)
When should women stop working?
34 weeks onwards
What routine Inx get done in the third trimester and when?
36 weeks:
- FBE
- AB screen in Rh neg women (will need anti-D injections if no Anti-D detected)
- GBS swab! (lower vaginal)
Physiological changes in third trimester
Breast enlargement, colostrum production
Uterine contractions/tightenings, painless at first and becoming more painful closer to labour
Cervical ripening (effacement and dilation), evidenced by incr loss of D/C or mucus plug
Advise to women in third trimester as to when to come to hospital
Contractions are regular and painful, occurring ~1x5min (2:10) OR:
- DFM
- Bleeding
- SROM
- Psychological distress
When does the GBS swab get done?
36 weeks, lower vaginal and anal swab
When does the oral glucose challenge test get done?
28 weeks
How do you assess fetal wellbeing antenatally (5)
- fetal movements
- maternal SFH
- USS
- Infection screen +/- karyotype (aneuploidy screen)
- CTG
Assessing fetal wellbeing in labour
- CTG
- fetal movement
- Doppler
- Fetal scalp blood sampling
At what gestation does the uterus sit at the
- umbi
- xiphisternum
- 20 weeks
2. 38 weeks
Causes of:
- Oligohydramnios
- Polyhydramnios
- Decr fetal urine production (kidney or urinary tract problems) or ruptured/leaking membranes
- Placental insufficiency
- Post-date pregnancy
- Maternal problems (HTN, PE, dehydration, GDM) - Fetal inability to swallow or excess amniotic fluid production (polyuria in GDM)
What arteries does the doppler measure blood flow in and what is the clinical significance of each?
Umbilical arteries: fetal blood flow to placenta. Placental resistance to flow should be low and cardiac activity high so good flow in diastole.
Placental insufficiency or cardiac impairment can lead to absent or reversed diastole flow and high resistance to flow.
MCA: blood from circle of willis to brain. Resistance to flow should be HIGH. Fetal hypoxia -> MCA dilates -> reduces resistance to flow.
Uterine arteries: reflects maternal perfusion of uterus and normal placental implantation. Resistance should start high and reduce after 23 weeks.
what growth scan patterns do you see in IUGR babies?
GDM babies?
asymmetrically small: HC is relatively larger than AC
Asymmetrically large: AC to HC ratio high (due to glycogen deposits in liver)
What doppler USS features do you see in IUGR babies?
Umbilical arteries: increased resistance and reduced end diastolic flow (incr SDR, PI and RI). OR absent end diastolic slow (RI=1) OR reversal of end diastolic flow
MCA: decr resistance
Differentials for small fetus
- Normal
- Incorrectly diagnosed (earlier in gestation than thought)
- Abnormally small (chromosomal/structural/genetic syndrome)
- IUGR
Management of IUGR
Maternal CS administration if expected pre-term
NVD w continuous CTG monitoring if near term
If v small and v preterm, may need elective LUSCS
Maternal and fetal condition dictates need/timing of delivery
Differential causes of macrosomia
Normal
Incorrectly diagnosed
Maternal GDM
Beckwith-Wiedemman Syndrome
Indications for elective C/S delivery for large babies
If EFW >97th centile
GDM
High AC: HC ratio (risk of shoulder dystocia)
Risk factors for ovarian cancer
Protective factors
- Age
- Obesity
- Incr # ovulations (nulliparity)
- Family HX ovarian/breast/colorectal cancer:
Lynch syndrome (HNPCC) - 10% risk
BRCA1 (50% risk)
BRCA2 (20% risk) - HRT/unopposed oestrogen
Protected: OCP, multiparty, breast feeding
Most common histo subtype of ovarian cancer
Serous adenocarcinoma
Clinical présentation of ovarian cancer
Bloating, abdo swelling Abdo pain Dyspepsia Urinary freq Weight change Irreg bleeding SX metastatic disease: ascites, pleural effusions, SBO/LBO
Inx for suspected ovarian cancer
TVUSS
Bloods: CA125 and CEA ; hcG, LDH, alpha fetoprotein
Management of ovarian cancer
- Pre-op CT or MRI
- Surgical staging and debunking (aim for <1cm residual) - laparotomy or hysterectomy + bilateral salpingo-oophrectomy
OR Chemo if disease is widespread/metastatic at diagnosis - Post-op: 6 cycles cytotoxic chemo
- Regular monitoring: imaging and CA125 levels
Stages of ovarian cancer
- limited to ovaries
- ovaries + pelvic spread (uterus, tubes, bowel, bladder etc)
- disease outside pelvis +/- positive retroperitoneal or inguinal lymph nodes
- distant mets /liver parenchymal disease
Risk factors uterine cancer
- Age
- Caucasian
- nulliparity
- early menarche, late menopause
- Hx infertility
- HRT/tamoxifen
- Obesity
- Diabetes
- PCOS
- Endometrial hyperplasia
- HNPCC
- Endometrial polyps
screening for ovarian cancer
NOT Recommended in asymptomatic women.
Only in women w Lynch syndrome - are high risk so annual endometrial sampling is recommended
Main histo subtypes for endometrial cancers
-prognosis
endometriod and mucinous adenocarcinoma
2 types of uterine cancers and he relative proportions of each
What are the prognoses of each?
95% Endometrial (good prognosis)
5% Sarcoma (myometrial cancer) - aggressive, younger onset and poor prognosis
How do you diagnose endometrial cancer?
Endometrial biopsy for histology, via D&C, O/P pipelle, or hysteroscopy
+ Evidence of spread via CT or MRI abdo, chest, pelvis
Management of uterine cancer
REFER TO GYNAE ONC
Pre-op CT/PET/MRI to assess for risk of lymph node mets - may need lymphadenectomy for high risk tumours (ex: Lynch)
Total hysterectomy + bilateral salpingooophrectomy +/- pelvic and para-aortic lymphadenectomy
NEED To assess involvement of ovaries via histopath- determines stage and prognosis
Younger women: want to conserve fertility so trial progesterone therapy (high dose oral or IUD)
If this fails, need hysterectomy + conservation of ovarian reserve
Long-term follow up evaluating for recurrence (13% risk overall, higher if metastatic spread at DX)
2 main Histological subtypes of cervical cancers
80% SCC
20% Adenocarcinoma
Presentation of cervical cancer
Early stage:
Asymptomatic
Post-coital bleeding, AUB, PMB, vaginal D/C
Late stage:
- pelvic or back pain
- Sciatica/neuropathy
- enlarged groin nodes
- bladder/bowel SX, lower limb oedema
How does cervical cancer spread?
What nodes does it spread to first?
Local extension (perineum, vagina bladder, bowel, Lymphatics
Nodes: Pelvic -> common iliac -> Paraaortic nodes (rarely inguinal nodes involved)
How is staging of cervical cancer performed?
Clinically at first (spec, bimanual, cystoscopy, PR etc).
Further accuracy based on PET/MRI/CT +/- surgery.
FIGO Staging of cervical cancer
0 - carcinoma in situ (full thickness but no stromal invasion)
1 - confined to cervix
2 - spread beyond uterus but not to pelvic wall or lower 1/3 of vagina
3 - extends to pelvic wall and/or to lower 1/3 vagina
4 - involves mucosa of bladder/bowel OR mets in distant organs
Treatment of cervical cancer
MANAGED by gynae onc! REFER!
Stage 1-2a: surgery (cone biopsy or trachelectomy or hysterectomy +/- staging lymphadenectomy) or chemoradiation
Stage 2b-4A (bladder/bowel): chemoradiation
Stage 4b: systemic chemotherapy
What is a trachelectomy?
Remove cervix, parametric with cuff of vagina and suture uterus back to top of vagina
Fertility-sparing measure in treatment of cervical cancer for young patients with stage 1-2a disease
The different ‘layers’ of the cervix (endo/exo/trans zone etc)
Endocervix: columnar mucus -secreting epithelium
Transformation zone: squamo-columnar junction, area of active cellular change! cells constantly changing over from columnar to squamous when exposed to acidic pH of vagina (undergoing metaplasia), hence are prone to making mistakes and becoming dysplastic (esp w infected w HPV).
Ectocervix: non-keratinising squamous epithelium
Risk factors for cervical cancer
SMOKING Long term OCP use HIV, immune suppression High parity Chlamydia trachoma's, HSV infection Uncircumcised male partner
What can HPV virus cause?
Genital warts (warts elsewhere too, like plantar warts etc) Cervical cancer Vulval/vaginal cancer Anal cancer Penile cancer
Natural history of HPV infection of cervix
Normal cervix HPV infected cervix with mild-cytological abnormalities. This can be cleared by the immune system so the cervix goes back to normal, or can progress to a precancerous lesion (CIN 1 and 2 which are LGSIL or CIN3 which is HGSIL). Most LGSIL regress without treatment.
Most HGSIL will progress over 7-10 years, if not treated, to invasive cancer (carcinoma in situ)
When is the guardasil vaccine given and what HPV strains does it protect against?
Given at 0, 2, 6 months of age
HPV 16,18,11
What is the screening process for cervical cancer?
Currently women aged 18-70 who have ever been sexually active need 2 yearly pap tests
Options:
- Smear test
- Liquid based cytology (thin prep or sure pap)
- HPV test (detects HPV DNA presence, 99% NPV)
Management of LGSIL found on pap test
Mostly acute/transient HPV infection that the body clears within 12 months
NO TREATMENT. Repeat smear yearly until 2 consecutive neg results, then return to normal bi-yearly screening.
If a second LGSIL -> colposcopy and biopsy -> if confirmed normal or LGSIL, screen again in 12 months; if confirmed HGSIL, treat.
If any progression to HGSIL on repeat smears, straight to colposcopy and biopsy
Management of HGSIL found on pap
Colposcopy and biopsy Confirmation on biopsy needs tx: Conservative - Diathermy - Laser - Cryotherapy - LLETZ (most common tx mode) = large loop excision of transformation zone - Cone biopsy (only used for adenocarcinoma in situ due to incr risk profile)
Definitive
- Hysterectomy (fertility not desired)
Follow up protocol post HGSIL dx and tx
- 4-6 monthly pap test and colposcopy
- 12 monthly pap test, HPV test (test of cure as 99% NPV). Repeat annually until woman has tested negative to both tests on 2 consecutive occasions, then return to normal 2 yearly screening.
Risks to pregnancy w LLETZ procedure
If > 2x LLETZ, incr risk of cervical incompetence -> preterm labour
Ovarian germ cell tumours
- which type are most common?
-when is their peak incidence?
most common - 95% benign, mature cystic teratomas (dermoid cysts)
Other types can be malignant
peak incidence in fertile years (young women and teens)
How might an ovarian germ cell tumour present?
Non specific abdo sx
- abdo distension and pain (? ruptured cyst or torsion)
- mass effects (bladder, bowel sx)
- Menstrual irregularities
- SX of pregnancy
- SX of metastatic disease (ascites, lymphadenopathy)
Investigating suspected germ cell tumour
Tumour markers (AFP, LDH, CA125, CA19.9, bHCG) TV USS CT abdo pelvis if malignancy suspected
MX of ovarian germ cell tumours
Surgery
- cystectomy w ovarian preservation (dermoid cysts only)
- Unilat salpingooophrectomy +/- …
Adjuvant chemotherapy
Follow up (Hx, exam, tumour markers) for 10 years after
Any recurrence gets chemo, not surgery!
What is GTD?
tumours arising from the fetal trophoblast -> abnormal proliferation of trophoblast, capable of invasion and metastatic spread
How does GTD present?
Usually presents as miscarriage <10weeks and is diagnosed on post-mortem histopath
Sx of pregnancy
Early pregnancy PV bleeding
irregular vaginal bleeding
What hormone does GTD produce and how is this helpful clinically?
produces hCG, used as a tumour marker for diagnosis (serial hCG) and follow-up/monitoring
Types of GTD
Benign (hydatidiform mole=molar pregnancy)
- partial or complete
Malignant or persistant = gestational trophoblastic neoplasm
- diagnosed after attempted evaluation of molar pregnancy, when it persists/hCG levels fail to decrease
Which type of benign molar pregnancy has a higher risk of progression to neoplasia?
Complete mole
How do complete vs partial moles originate/their genotypes?
Complete: sperm fertilises an empty egg and then duplicates it’s genetic material to form a full set -> 46XX or 46XY (YY not seen)
Partial: 2 sperm fertilise a normal egg -> 69XXY (triple karyotype)
Treatment benign moles
Suction curette with simultaneous US exam, oxytocic support and D&C
Anti-D to Rh neg women (risk of haemmhorage)
Spread of malignant GTD
Local spread
+ via blood to liver, lungs, brain
Treatment and prognosis of malignant GTD
Treatment: chemo +/- surgery (if no desire for future fertility or chemo-resistant mets)
Follow up via serial HCG and early surveillance in future pregnancies due to risk of recurrence
Prognosis - 100% cure rate if caught before metastatic stage
complications of genital prolapse
Hydronephrosis (obstruction of ureters in severe cases)
Urinary retention (outflow obstruction)
Faecal incontinence
Rectal prolapse
Haemmharoids
Risk factors for prolapse
Age Smoking Obesity Incr post-menopausal status (decr oestrogen) Incr parity Incr birthweight
CLD
types of genital prolapse
cystocoele (anterior compartment collapse)
Rectocele (posterior compartment collapse)
Enterocoele (Small intestine)
SX of genital prolapse to ask about
Dragging/heavy sensation in vagina Lump/bulge in vagina Difficulty emptying bladder/bowels Difficulty inserting tampons Urinary/fecal incontinence Haemmharoids lower back pain DC/bleeding from ulceration
Management of genital prolapse
Reassurance
Reversible risk factor identification and lifestyle changes (weight loss, stop smoking, constipation)
Pelvic floor exercises - liase w physio and continence nurse
Vaginal oestrogen supplements (topical creams)
Vaginal pessaries!
Surgery last line
Side effects of pessaries
Ulceration, bleeding incr rates infection and D/C Expulsion Constipation Pain
causes of urinary incontinence
Pregnancy
Injury/trauma (pregnancy/malignancy/direct trauma/pelvic radiotherapy, complications following surgery )
Medications
Medical conditions (DM, UTI, MS,
Excessive fluid intake
Causes of Fecal incontinence
Most common cause is childbirth!
- traumatic delivery causing nerve damage or direct trauma to anal sphincter
- fetal macrosomia
- 3rd and 4th deg perineal tear/epis
- instrumentation
types of incontinence
- Stress incontinence: loss of urine with IAP incr
- Urge incontinence: loss of urine assoc w uncontrollable desire to void
- Detrusor overactivity: urodynamic dx made when detrusor contraction is assoc w strong desire to void in a person trying NOT to
- Overactive bladder - urinary freq and urgency +/- urge incontinence
- Voiding dysfunction
How do you assess the progress of a woman in labour?
- Abdo palpation hourly
- Contractions - duration, freq, intensity
- VE - 4 hourly (as long as membranes are NOT ruptured)
Indications for giving Abx intrapartum (and what antibiotic?)
GBS positive mum or GBS status unknown (i.e. preterm)
Maternal fever
Prolonged ROM >18 hours
Previous baby with widespread GBS disease
Options for intrapartum pain relief
Support person
NO mask
PCA Narcotics (morphine has longer half life than fentanyl or pethidine)
Regional anaesthesia using lignocaine or bupivicaine (epidural for labour ward; spinal for theatre, faster onset action but shorter t1/2)
How do you assess the mother and baby during labour?
Mother:
- Vitals (BP, temp, HR) hourly
- contractions (should be ~4:10)
- Urine 4 hourly
- PV loss?
Baby:
- Doppler USS if no risk factors
- CTG if high risk
- Amniotic fluid - colour and vol
Criteria for incr risk baby needing additional monitoring
DM, HTN/PE, IUGR, bleeding, mea stained liquor, abnormal FHR
SE of regional analgeisa
Hypotension
Pruritus, headache
URinary retention (req IDC)
Paralysis (rare)
Explain the mechanics of 2nd stage of labour
- maternal effort (urge to push)
- gravity
- uterine contractions
baby
- head moulding to change shape
- flexion of head onto chest (OE smallest diameter)
- rotation (baby undergoes internal rotation, head extension then external rotation of head)
active management of third stage
- oxytocin/syntocinon to stimulate uterine contraction to deliver placenta/prevent PPH
- controlled cord traction
- fundal pressure
- cord clamping within 5 min
Causes of PPH
Tone
Tissue
Trauma
Thrombin (rare)
when is the foetus most susceptible to teratogens?
first trimester, when organogenesis occurs
Effects of smoking on fetus
Prematurity IUGR/LBW Miscarriage Stillbirth Placental abruption SIDs Premature rupture of membranes
What defines Hyperemesis gravidarum. What complications do you have to watch for?
Excessive pregnancy related vomiting and nausea that prevents adequate food and fluid intake and is assoc w >5% LOW, usually peaking mid-first trimester
Complications: dehydration, malnutrition, electrolyte imbalance, mallory-weiss tear with prolonged/severe vomiting, hyperthyroid (due to cross-reactivity between TSH and HCG)
RF for hyperemesis gravidarum
Previous HG Multi-pregnancy Molar pregnancy Female embryos Increase free beta HCG (molar pregnancies)
Investigations for vomiting in pregnancy and why
UEC, LFTs, TFTs, FBE +/- CRP
urine MCS and dipstick
Exclude UTI, gastro/other infection, biliary disease, appendicitis, Addison’s disease, Thyroid disease, electrolyte disturbances from extreme dehydration
What is pre-eclampsia?
De novo HTN (>140/90, or >30/50 over baseline) arising after 20/40 and returning to normal within 3 months postpartum + evidence of dysfunction in at least one other organ (kidney, liver, neuro, haem, fetus)
Pathyphys of PE
Placental disorder! Placenta demands more O2 and nutrients that the mother can provide, so becomes hypoxic.
Hypoxic placenta releases toxic products which damage mum’s vasculature, causing vasospasm, and vasoconstriction -> HTN and ischaemia to other organs
RF for PE
First pregnancy or new paternity Age extremes (teens and >40) Obesity Smoking Previous PE Family HX Assisted reproduction
Medical conditions: essential HTN, GDM, RA, SLE, renal disease etc
Large placenta - Multi pregnancies, GDM, GTD
Clinical features of PE
Stage 1: isolated HTN
Stage 2: + Proteinuria + Generalised swelling (facial and lower limb)
Stage 3 = Eclampsia
Signs of multi system dysfunction…
Neuro: SEIZURES!! Headaches +/- visual changes; hyper-reflexia and/or clonus
Renal: Oliguria, renal failure
Hepatic dysfunction: Epigastric/RUQ pain/lower abdo pain
CV: CCF, Pulm oedema (SOB)
Haem: thrombocytopenia, haemolysis, DIC
Uteroplacental: decr FM, IUGR, abruption, FDIU
Investigations for PE
FBE (plt, Hb)
UEC (renal function and uric acid)
LFTs (ALT deranged w liver dysfunction)
24 hour urine collection or spot Cr:urea ratio
CTG and USS (assess growth, AF, UA)
Definition of Eclampsia
Seizures assoc w PE due to hypo perfusion of brain
Prevention of PE.
Which women should get this?
Low-dose Aspirin and Ca supplements in high risk women
High dose folate
Diet (antioxidants, Mg, zinc, fish oil), exercise, bed rest
Salt restriction
+/- LMWH for women with genetic/acquired thrombophilias
High risk: HTN, renal disease, obesity, insulin resistance, GDM, assisted reproduction, and a history of preeclampsia in a previous pregnancy,
MX of (pre-)eclampsia
DELIVERY of placenta is curative (but not necessarily right away)
- timing and ode of delivery depends on stage
Stage 1: monitor, educate, antiHTN If >160/100, wait until >38 weeks
Stage 2: Close monitoring - bidaily CTG, 2 weekly USS; education; labetalol if >160/100; IOL or C/S past 34-36 weeks
Stage 3: immediate delivery once mum stable
Admit!
Monitor fluid balace/renal function (replace if necessary)
4 hourly bloods (FBE, UEC, LFTs)
Fetal surveillance (CTG)
Stabilise mother
- IV MgSO4 if they have had a convulsion (bolus + infusion) - will help to bring down BP (vasodilation)
- Epidural and anaesthetics R/V - will help to bring down BP
- Antihypertensives if SBP>=160 and DBP >=100 despite MgSo4 and epidural ( IV labetalol)
- Steroids if preterm
Surveillance postpartum (fluid-balance) and F/U post-delivery
When is the highest risk for VTE?
peri-puertum (6 weeks post delivery)
Inx for suspected VTE
Doppler for VTE
VQ scan or CTPA for PE
Treatment of PE
LMWH for 6 weeks post part and for remaining duration of pregnancy
Can change to warfarin postpartum
+ needs LMWH throughout next pregnancy up to 6 weeks postpartum for prevention
Consequences of GDM
Fetal
- Macrosomia
- Shoulder dystocia
- Birth Trauma (fractures)
- Birth asphyxia
- Polyhydramnios (polyuria)
- Congenital abnormalities
- Stillbirth
Maternal
- HTN disorders
- Infection
- Caesarian/instrumental delivery
- ?PPH and Perineal trauma
- 50% incr lifetime risk of developing T2DM
Neonatal:
- hypoglycaemia
- hypocalcaemia
- RDS
- jaundice
- NICU/SCN admission
- perinatal mortality and morbidity (incr risk obesity, DM)
Clinical presentation of GDM
Asymptomatic, picked up on routine 28 week GTT
SX of hyperglycaemia (polyuria, polydipsia)
Incr SFH
MX of GDM
Multidisciplinary care
1. Education. Diabetic education nurse, dietician, endocrinologist, obs/gynae input
2. Frequent self monitoring of capillary BSL (fasting <5mmol, 1hr post prandial <8mmol)
3. Diet and exercise daily
Add insulin and/or sulfonyelurea/metformin if targets not met
4. Antenatal Fetal monitoring
- Additional routine growth scans
- Regular clinical assessments of growth (SFH)
5. Consider IOL/electice LUSCUS after 38 weeks if poorly controlled /evidence of fetal involvement
6. Close fetal monitoring intrapartum
7. Postpartum neonatal follow-up monitoring for jaundice, RDS, hypoglycaemia, hypocalcaemia
8. Screening GCT early in future pregnancies
What is the definition of a miscarriage?
When is the risk of this highest?
Spontaneous loss of pregnancy <20weeks gestation
Highest risk <12/40
Definition of recurrent miscarriage.
What investigations would you perform?
> 3 consecutive miscarriages
Inx:
Cytogenic analysis on products of conception
Karyotypes of parents
Inx for thrombophilia, structural abnormalities, medical disorders etc
Aetiology for miscarriage
Advancing maternal age -> chromosomal (aneuploidy, 45XO etc)
Chronic disease (thrombophilia, APLS, SLE, Coeliac, GDM etc)
Structural abnormalities of uterus (bicornuate, subseptate)
Incompetent cervix
Toxins (smoking, cytotoxic drugs, high dose radiation)
TORCH infections
How does M/C present?
PV bleeding
Lower abdo pain
What is a threatened MC?
MX
Ongiong/live pregnancy but PV bleed/spotting +/- lower abdo pain in 1st trimester
MX: reassurance and follow up
What is an inevitable MC?
MX
A miscarriage that will definitely happen. PV bleed/lower abdo pain in presence of an open internal os in first trimester (means the body is already in process of expelling the embryo).
But POC still present, yet to be passed.
MX: Nothing can be done about it.
Psychol support, close follow up and expectant management
What is an incomplete MC?
MX
PV bleeding and lower abdo pain have have passed some POC but some POC yet to be passed, and are visible on USS.
Cervix still open.
MX: expectant MX or can use Misoprostol (PGE analogue) or Mifepristone (anti-progesterone) to help expel products
What is a complete MC?
MX
All POC have been passed; the cervix is now closed and the uterine cavity is empty on USS
MX: f/u with serum HCG measurements
What is a missed MC?
MX
No SX of miscarriage - it is picked up on routine AN care due to lack of FHR, small for dates. May be complete or incomplete.
MX: expectant MX or can use Misoprostol (PGE analogue) or Mifepristone (anti-progesterone) to help expel products
When would you do surgical D&C as treatment for miscarriage?
If the woman is haemodynamically unstable (heavy bleeding etc)
Advice after a M/C
Pain and bleeding similar to a period is normal for ~2 weeks, treat w over the counter analgesia
Strong pain/heavy bleeding/abnormal DC/fever -> see doctor or ED
Avoid sex until bleeding stops, pain lessens
Use pads, NOT tampons until bleeding stops
Need anti-D injection if Rh(D)neg and Ab neg.
Wait until after next normal pregnant to try getting pregnant again (slightly incr risk of m/C again if you get pregnant within 4-6 weeks)
What is the leading cause of maternal death in the first trimester?
Ectopic pregnancy
Risk factors for ectopics
STIs Smoking Prior ectopic Incr age Prior tubal surgery/ligation IVF Progestogens Contraceptive failures (pregnant with IUD)
Presentation of ectopic pregnancy
Pelvic pain (unilateral or generalised)
Delayed period
Abnormal bleeding
Pallor, hypotension, tachycardia, guarding/peritonism indicate ruptured ectopic -> shock
On exam: PV bleeding, closed cervix, adnexal mass, Localised tenderness
Inx for suspected ectopic
TVUSS (free fluid, adnexal or fallopian tube mass, absence of IU gestational sac)
Serial betaHCG high (>1000) but rising less than 60% over 48 hours
FBE, blood group and cross match
MX of ectopic
If in shock: emergency laparotomy
Not in shock:
- If HCG<1000: Admit for Observation, await natural resolution (betaHCG and USS monitoring)
- If HCG>1000 or keeps rising:
Medical (for small tubal ectopics and minimal bleeding): Methotrexate IM
Surgical (for large ectopics or IU bleeding): laparoscopy and salpingectomy/salpingostomy
Follow up: serum B-HCG on days 4 and 7, should decr to ensure complete removal
Psych support
Impact of ectopic on future pregnancies
Incr risk of future ectopic so future pregnancies require early TVUSS at 5-6 weeks to ensure they are intra-uterine
Take folate when trying to get pregnant in future.
Wait 2 months post surgery and 4 months post medication to try for another baby
CI to the COCP
Women with IHD Previous stroke, VTE Breast cancer Severe liver/biliary disease Breast feeding with infants <6mo Migraine with aura
Mechanism of action of the COCP
Progesterone
- prevents LH surge which prevents ovulation
- thickens the cervical mucus impeding sperm passage
- thins endometrium making it less favourable for implantation
- decr motility within fallopian tubes
Oestrogen
- stabilises endometrium to reduce irreg bleeding
- prevents follicular maturation
What happens if you miss one COCP pill?
What happens if you miss 2 or more?
1 missed pill: take it as soon as you remember
2+ missed pills: take the last missed pill as soon as you remember even if it means taking 2 on one day. Don’t worry about other missed pills. Then use condoms/abstinence in conjunction with active pills for another 7 days, even if this means skipping the placebo pills and running 2 packs together.
Advice for starting the COCP
Start on days 1-5 of menstrual cycle (period) and you will be protected immediately, OR use back-up contraception until you have taken 7 active pills
You can start at any time if you are SURE you aren’t pregnant (abstinent etc)
Risks vs benefits of the COCP
Benefits:
- reversible contraception
- decr PMS SX, can help w acne and PCOS
- decr painful/heavy bleeding
- predictable, regular bleeding
- controls vasomotor SX around menopause
Risks:
- hormonal SE
- user dependent
- incr risk VTE, stroke, breast cancer, cervical cancer
Which women is the progesterone only mini pill good for?
Breast feeding women (COCP CI for babies <6mo)
Women in whom oestrogen is CI (breast cancer, risk of VTE etc)
How does the mini pill work?
SE
Continuous release of low dose progesterone keeps the lining thin and thickens cervical mucus, can also prevent ovulation.
SE - unpredictable bleeding and spotting because there are no scheduled withdrawal bleeds.
How does the nuva ring work?
Soft vinyl ring placed in vagina that releases constant dose of oestrogen and progesterone to vessels underlying vaginal skin
Stays in place 3 weeks then is removed for a week, in which a withdrawal bleed occurs. Put a new one in after that.
Advantages and disadvantages of nuvaring
Adv: avoids first pass hepatic metabolism
- low dose local release of hormone means fewer side effects
Disadv: expensive!
How does Depot Provera work?
Adv and disadv?
Injectable (IM) progesterone-only contraceptive lasting 3 months.
Adv: only need it 4x year; can lighten periods (not in everyone though)
Disadv: Irregular bleeding/spotting, irreversible, delay in return of ovulation after sensation by ~8mo, weight gain, not for long-term use due to risk of osteopenia/osteoporosis with lack of oestrogen
What is implanon and it’s advantages and disadvantages
rod-implant that releases progesterone
adv: efficacy ~99.9%, no decr in bone density, is immediately reversible, not user dependent
disadv: intermittent bleeding and hormonal SEs
How does the copper IUD work and what are side effects
Cu is toxic to sperm
Acts as a IU foreign body which interferes with implantation
Lasts 10 years or 5 years
SE: incr bleeding and pain with periods after insertion
Expulsion, perforation, infection, bleeding, pain on insertion
How does the progesterone IUD work and what are advantages and disadvantages?
Delivers progesterone to uterus at constant rate, thickens cervical mucus and thins endometrium
Adv: minimal systemic SEs, 90% women report lighter or no periods after 6 months
lasts 5 years, cheap
Disadv: risk of perf, infection, pain, bleeding, expulsion, vasovagal on/soon after insertion
Incr relative risk of ectopic or miscarriage if you get pregnant with it in situ (but 99.7% protection)
Advice on natural family planning
Most fertile from day 8-19 inclusive (5 days either side of day 14) so avoid unprotected sex on these days to avoid getting pregnant (only reliable in women w regular cycles)
- Thin fertile mucus and 0.3C rise in temp during ovulation are other indicators
- only 75% accurate
How does a female diaphragm work?
Individually fitted silicone done-shaped cup attached to flexible circular springs. Sit in front of cervix and vaginal vault and held in place by pelvic muscles.
Insert anytime before sex but must remove within 6 hours after.
Note: only 94/84 perfect/typical use efficacy
explain the pathophys behind GDM and fetal growth
GDM is a state of insulin resistance: blood glucose isn’t taken up into maternal tissues due to factors released by placenta (CRH, GH, placental lactogen).
Leads to maternal hyperglycaemia -> fetal hyperglycaemia -> fetal pancreas produces it’s own insulin -> incr fetal insulin -> incr glucose uptake into fetal tissues -> incr fetal grwoth
Resp physiological changes
20% incr O2 consumption via incr tidal volume (not RR)
Diaphragmatic breathing (uterus pushes up on diaphragm and increases IAP)
Decr functional residual volume, exp and insp volume due to displacement of diaphragm. Mild decr in TLC.
Incr central resp drive -> relative hyperventilation (incr O2 and decr CO2) -> mild compensated resp alkalosis
CV physiological changes
Increase CO by 40% (to supply placenta) from incr HR and SV
Decr systemic vasc resistance due to widespread vasodilation
Decr BP
Supine hypotension effect of position in late pregnancy
Haem physiological changes
40% incr plasma volume -> periph oedema, pulm oedema
20% incr in RBC volume
Anaemia common (due to haemodilution)
Haemodiluition -> decr [albumin] -> oedema
Incr clotting factors -> Pro-thrombotic state
MSK physiological changes
Incr BMI by 10-14kg lower back pain Lordosis Carpal tunnel due to oedema Sciatica due to oedema Calf cramp
Derm physiological changes
Incr skin pigmentation Distension and proliferation of blood vessels Spider nivae Striae gravidarum Facial flushing
Gynae physiological changes
Breast enlargement (oestrogen causes incr adipose tissue and in ductal system; progesterone causes enlargement of breast lobule)
Areola pigmentation
Cervical gland hypertrophy and formation of mucus plug
Vaginal lactobacilli proliferation
Uterine hypertrophy and hyperplasia
Endocrine physiological changes
Anterior pituitary
- incr prolactin
- fish and lh suppressed
- decr TSH in first trim due to HCG levels
Posterior pituitary: incr oxytocin
Pregnancy hormones
- BetaHCG
- Oestrogen and progesterone released by implanted embryo
- Human placental lactogen (released by placenta, implicated in GDM)
Physiological insulin resistance and relative glucose intolerance
Incr maternal lipolysis (mother uses fats for fuel and preserves carbs for fetes)
Renal physiological changes
Incr renal blood flow -> incr renal size; and incr GFR -> incr urinary frequency and incr clearance of creatinine, glucose and aa -> glycosuria and aminoaciduria
Ureteric dilation/enlargement (smooth muscle relaxation due to progesterone)
Uterine enlargement compresses bladder -> urinary frequency
Compression of ureter may lead to hydronephrosis - generally asymptomatic
GI physiological changes
GORD due to relaxation of smooth muscle sphincter by progesterone, and incr IAP
Incr aspiration risk under anaesthesia
Haemmharoids due to incr IAP
Constipation due to smooth muscle relaxation by progesterone
Gallstones (decr gallbladder motility)
Thyroid physiological changes
Incr levels T3 and T4
TSH levels decr in Trim1 due to thyrotrophic effects of beta HCG but incr again in Trim2 and 3
Incr HCG levels assoc w hyperthyroid
Pregnancy aggravates I deficiency (transported to fetes and lost in urine) -> goitre can result in I-deficient women
What factors does O2 delivery to placenta and fetes depend on?
Maternal O2 saturation Hb concentration Uterine blood flow (10% of CO) LEFTWARD shift of Hb sat curve -> allowing higher Hb saturation at lower pO2 O2 has higher affinity for HbF than HbA
Breast milk production physiology
Anterior pituitary produces prolactin which stimulates milk production.
During pregnancy the embryo/placenta releases oestrogen and progesterone which inhibit the production of prolactin. Oestrogen and progesterone levels decrease after delivery, prolactin is no longer inhibited so milk production begins.
Sensory signals from baby suckling stimulate release of oxytocin from posterior pituitary which causes release of milk
Role of umbilical artery and vein
Umbilical vein transports O2 and nutrients from placenta to fetal circulation (x1)
Umbilical arteries (x2) transport deoxy blood from fetus to placenta
Uterine artery is from mother to placenta
Uterine vein is from placenta to mother
DDX genital itch (females)
Infection
- candida albicans
- Bacterial vaginosis
- Trichomonas vaginosis
- Genital warts
- Pinworms (night time itch)
- Pubic lice
Inflammation
- irritant contact dermatitis
- lichen sclerosis
- psoriasis
- allergic dermatitis
- allergic urticaria
Neoplasm
- VIN
- vulval cancer (SCC)
Atrophic vaginitis in post-menopausal women
What is bacterial vaginosis?
SX
Diagnosis
Tx
Disturbance of normal bacterial equilibrium in the vagina - overgrowth of anaerobic bacteria
SX: abnormal vaginal discharge (alkaline white-grey discharge with fishy odour) + EXTREME ITCH in women of reproductive age
DX: high vaginal swab -> microscopy and culture
Tx: oral metronidazole; topical in pregnant women to reduce systemic side effects.
How does trichmononas vaginalis present?
What sort of bug is it?
How do you diagnose it?
How do you treat it?
Males - asymptomatic
Females - malodorous vaginal (frothy yellow-green fishy) discharge + ITCH
Protozoan parasite
Dx: high vaginal swab for microscopy and culture
Tx: oral metronidazole
Chlamydia Trachomatis:
SX
What sort of bug is it?
How do you diagnose it?
How do you treat it?
SX: Males - urethritis
females - asymptomatic but may get vaginal d/c, dysuria, dyspareunia, post-coital bleed
Long-term can result in PID, ectopic, infertility, pain
Bacteria
DX: endocervical swab (women) or urine (males) for PCR
tx: single dose azithromycin OR doxycycline 7 days bd + test for cure 2-3 months post-treatment
Gonorrhoea
SX
What sort of bug is it?
How do you diagnose it?
How do you treat it?
SX: males are 75% asymptomatic
females - dyspareunia, irregular bleeding, abnormal discharge, bartholin’s abscess, infertility/ectopic, chronic pelvic pain (but can be asymptomatic)
Bacteria
DX: endocervical swab for PCR and MCS
Tx: single dose IM ceftriaxone
What are notifiable STIs?
Chlamydia Gonorrhoea HBV HCV HIV Syphilis
What HPV strains cause genital warts?
6 and 11
Candida albicans
SX
DX
TX
Cottage cheese DC + itchy, irritated vulva
RF: immunosuppression, diabetes, pregnancy, use of broad-spectrum abx or exogenous steroids
High vaginal swab for MCS
Tx - fluconazole for 1 week
HSV
SX
How do you diagnose it?
How do you treat it?
type 1 causes oral lesions and type 2 causes genital ulcers
Tiny punched out extremely painful ulcers with discharge
Primary episode is severe +/- flu-like illness, with recurrent episodes more mild
Dx- swab lesions for viral PCR, and serology (IgM and IgG)
MX - acyclovir within 2-3 days of sx, especially in third trimester of pregnancy (+ LUSCS)
+/- topical lignocaine for pain
When is the HIV virus first detectable in the blood?
what factors indicate progression of disease?
2-3 months post infection HIV Ab is detectable
Incr viral load and decr CD4 count indicates progression
Management of pregnant patients w HIV
Antiretrovirals antenatally to suppress viral load
Antiretrovirals to mama and bub postpartum
Elective LUSCS
Avoid breast feeding
What do the various HBV serum markers indicate:
- HBsAg
- ABsAb
- HBcAb
- HBeAg
- HBsAg - ACTIVE infection (Acute or chronic)
-> persisting beyond 6 month indicates chronic HBV which is more common when infected in infancy -> likely to progress to chronic disease and incr risk of transmission
If this is positive, no immunity has been developed yet. Should be NEGATIVE in vaccinated individuals - ABsAb (immunity following vaccine or infected)
- positive in vaccinated individuals or in individuals with resolved past infection. - HBcAb (only follows natural infection-past or current)
- HBeAg (highly infectious carrier)
What is the risk of syphilis in pregnancy?
Tx for syphilis
Spread transplacentally to fetes -> 40% risk of prematurity and perinatal death
tx: Penicillin
What is the supine hypotensive effect of pregnancy?
How do you prevent/treat this?
Due to vena caval compression by gravid uterus, which can decr CO by ~30% and result in hypotension -> collapse
Position mother in left lateral tilt to reduce aortocaval compression
Preterm birth risk factors
Previous preterm birth Polyhydramnios Multi pregnancy Antepartum haemmhorage Low SES Smoking, drugs Young maternal age 2x previous LLETZ /cone biopsy resulting in cervical incompetence Poor antenatal care Chorioamnionitis
Definition and Treatment of cervical incompetence
Cervical length of <1.5cm at <24 weeks gestation
Prostaglandins (pessary/local vaginal)
Cerclage suture
how do you diagnose preterm birth?
Clinical (uterine activity + cervical effacement and dilatation)
+/- posterior vaginal swab for fetal fibronectin test (99% NPV but only 20% PPV)
Management of preterm birth
Admit Analgesia Tocolysis (nifedipine, other Ca channel blockers) to buy time for: - 2 doses steroids over 48 hours - Transfer to tertiary centre if <32/40
ABX (oral erythromycin) if PPROM or chorioamniotitis (maternal fever, pain/tender, looks septic, mec stained liquor)
Delivery immediately if chorioamnionitis suspected!
Otherwise try to buy time and D/C if contractions settle
Prevention of preterm birth
Stop smoking
Vaginal progesterone or cerclage/cervical suture if cervical incompetence or previous preterm birth (Former only)
Treatment of asymptomatic bacteriuria
Triggers for preterm birth
Infection (ascending, UTI, dental)
Ruptured membranes
Cervical insufficiency (note - painless and brief!)
Stretching of uterus - multi pregnancy, polyhydramnios
Antepartum haemmhorage
Definition and Causes of antepartum haemmhorage
Defintion: Bleeding PV from 20 weeks gestation onwards
Causes:
placental abruption and placenta praaevia most common
Also Placenta accreta, vasa praevia, infection, malignancy
How do you diagnose placental abruption?
Clinical diagnosis - USS is not sensitive for this.
Features: VAGINAL BLEEDING +/- ABDO PAIN in 2nd 1/2 of pregnancy +/- uterine tightenings
OE: Uterine tenderness on palpation, increase uterine tone (woody/hard)
RF for abruption
PE/eclampsia, smoking/cocaine, PPROM, previous abruption, multi pregnancy, polyhydramnios, trauma to abdo/cervix, low lying placenta
Management of suspected abruption
Aim to buy time if pre-term!
- Admit for Steroid loading (2 doses over 48 hours)
- AntiD if Rhneg and Abneg
- MgSO4 if <30weeks (prevent CP)
- FBE and iron-> IV infusion if significant/ongoing bleeding
- D/C once not bleeding for 24 hours and mum and bub are stable
- F/U: Monitor via freq growth scans, SFH for IUGR
If term and no fetal compromise -> Induce
If fetal or maternal compromise -> immediate delivery via emergency LUSCS
Definition of placenta praevia
Implantation of placenta within 2cm of os (lower segment)
Dx - routine 20week morph USS with follow up scans to see if it has moved (90% move away on their own)
RF for placenta praecia
INCR number previous caesarians incr age and multiparty smoking IVF uterine surgery
Mx of placenta praevia
DO NOT do VE
Expectant management if mum and bub are well -> ELECTIVE LUSCS ~37 weeks with regional anaesthesia (don’t want them going into labour - NVD Ci if <2cm from os). If recurrent bleeds, deliver at 34 weeks.
If presenting with bleed, follow routine antepartum haemmhorage care (admit, steroid load, +/- anti-D, +/- volume resus, deliver if mum or bub are unstable otherwise D/C once not bleeding and stable for 24 hours)
What is placenta accreta? RF DX Risk Management
Placenta morbidly adherent to uterine wall
RF - incr # C/S (esp. classical), placenta praaevia, previous intrauterine procedures
Dx: USS +/- MRI
Risk: life-threatening PPH or APH
Mx: transfer to tertiary centre for elective caesarian hysterectomy (NVD CI!!)
What is vasapraevia? RF DX Risk Management
Fetal blood vessels run in amniotic membranes below presenting part of fetes in front of the cervix
RF - IVF, abnormal placenta, low-lying placenta, multi pregnancy
Dx- clinical palpation of fetal vessels on VE or visualisation with an amnioscope. TV colour Doppler USS can confirm if suspected.
Risk - fetal haemmhorage and death
MX - Immediate LUSCS if bleeding and maternal or fetal compromise.
If confirmed vasa praaevia but not bleeding, admit between 28-32 weeks for steroids, observation and elective LUSCS between ~37 weeks. If labour or ROM -> LUSCS.
Inx and MX of antenatal haemmhorage
CTG, USS FBE Anti-D and antibody status for Rhneg women Group and hold Kleihauer test for Rhneg women
MX: Admit for anti-D and Steroids.
IV infusion (Hartmans if stable; RBC if deteriorating) if significant/ongoing bleed
if in labour -> continuous CTG monitoring
If maternal or fetal compromise -> emergency C/S
If at term or close to full dilation, can try for NVD (as long as placenta accreta, praaevia vasa praaevia are ruled out)
Home if just light spotting and USS has ruled out praevia and abruption
Home once bleeding has stopped and mum and bub are stable for 24 hours
F/U - monitor for IUGR
What other compilations of labour are associated with placenta praaevia?
Placenta accreta, vasa praaevia, abruption
Malpresentation
RF of cord prolapse
breech and other malpresentation disengaged fetal head and beginning of labour multi pregnancy grand multi instrumentation preterm
Risk associated w cord prolapse
Perinatal mortality due to umbilical artery vasospasm or cord compression
Management of cord prolapse
IMMEDIATE delivery
- call for help
- try to displace cord manually above presenting part, or dislodge the presenting part to relieve pressure on cord and re-place cord
- emergency caesarian if NVD not possible
How do you diagnose amniotic fluid embolism
Diagnosis of exclusion!
Diagnosed post-mortem - fetal Saumes found on biopsy
RF for shoulder dystocia
Maternal obesity Previous SD GDM Fetal macrosomia Post-date pregnancy Prolonged 1st and 2nd stages labour IOL
Risks associated w shoulder dystocia (5)
1 .Cord compression, perinatal death
- Fracture of humerus or clavicle
- Damage to brachial plexus
- Maternal soft tissue trauma/damage to bladder, rectum, urethra
- PPH
MX of shoulder dystocia
Early identification!
Call for help
Discourage maternal pushing - may exacerbate impaction
McRobert’s position (extended lithotomy) is 1st line +/- Suprapubic pressure
Internal manoeuvres (may need episiotomy to gain access)
- Delivery of posterior arm
- rotational manœuvres
2nd line: reposition to all 4s (slim, mobile women without epidural)
POST DELIV: neonatal assessment of baby and pay attention to blood loss! (PPH)
Definition of PPH
> 500ml blood loss during 3rd stage or within 24 hours of delivery (primary)
24hr-6 weeks is secondary PPH
Prevention of PPH
Placenta out within 20 min!
Active management of 3rd stage
- syntometrin (syntocinon +ergometrine) as prophylactic uterotonic
- controlled cord traction
- fundal massage after placental delivery
2 large bore cannulas on admission for high-risk women
Management of PPH
Early recognition - call for help!
Freq/ongoing vital monitoring - signs of shock?
RESUS- ABCs
- O2 - high flow (10L/min)
- IV fluid replacement via 2 large bore cannulas (crystalloids, or blood products if going to theatre, Hb<70 or unstable despite 2-3L crystalloids)
Bloods - FBE, UEC, coag screen, cross match
Check placenta for completeness
Check perineum for trauma, stitch any 3-4deg tears
Treat underlying cause
- fundal massage
- uterotonics (syntocinon IV, ergometrine IM, PR misoprostol)
- IDC to empty bladder
- Tranexamic acid (coag abnormalities)
May need surgical exploration for retained productions (PGF2alpha in theatre)
- brace suture, IU balloon, embolisation or ligation
- hysterectomy last-line
Stage 1 of labour
regular painful uterine contractions with cervical effacement and dilation
stage 1 - passive (up to 3-4cm dilation); oxytocin and prostaglandins cause uterine contractions which help baby’s head to defend and stretch the cervix leading to its effacement and dilation
stage 2 -active (4cm-10cm); contractions continue under oxytocin and PGE2; also increase IAP which lead to rupture of amniotic sac (SROM)
Complications of labour and their respective management
Failure of SROM
- amniotomy to artificially rupture membranes
Premature ROM
- rupture before 37 weeks, will need antibiotics (erythromycin)
- if term, admission for observation and IOL
- if preterm, also give corticosteroids and deliver at 34 weeks
Failure to progress
- try amniotomy, oxytocin infusion +/- ECV if malpresentation
Fetal distress (CTG or doppler auscultation) - do a fetal scalp lactate -> acidosis is indication for immediate delivery (C/S if in S1 or instrumental if fully dilated and head engaged)
Perineal trauma
- incidental trauma or episiotomy
- repair second-fourth degree tears with sutures, in layers.
Malpresentation
- OP or OT usually spontaneously revert but may need instrumentation
- Face and brow: emergency C/S may be necessary
- Breech - supported NVD w manoeuvres or elective C/S
- Transverse/oblique - stabilise lie w ECV and IOL, or C/S
Complications of instrumentation
Perineal trauma
Subgaleal haemorrhage
Cephalohematoma
Things done in third stage of labour
- syntometrine injection
- deliver placenta (prolonged >1hr)
- check placenta - membranes and cotyledons, insertion and vessels for completeness
- check uterine tone and fundal massage
- Umbilical cord bloods
- Check pack and pad need count
Indications for C/S
Failure to progress
Fetal distress
Abnormal lie or malpresented at onset of labour
Elective if NVD poses significant risk to mother and/or fetes
Complications of C/S
Surgical risks
prolonged recovery time
Risk of uterine dehiscence and rupture with future pregnancies
Incr risk of placenta accreta, vasa praaevia, placenta praaevia
How do you induce labour?
- VE to assess fetal engagement and cervical ripeness (Bishop’s score)
- BS<6: Cervix is Unfavourable and needs to be primed:
- PGE2 or mechanical balloon
- takes 1-2 days - BS>6: Cervix IS favourable -> amniotomy and oxytocin to stimulate uterus
- takes <16hours - Continuous fetal CTG monitoring
Risks of IOL
fetal distress due to hyper stimulation of uterus -> may need to revert to C/S
Initial investigations for infertility
Hormones (FSH, Lh, oestrogen, androgens) Genetic karyotype +/- CF screen (males) Semen analysis (men) Imaging - USS testes; ovaries, uterus
Causes of female infertility
Egg factors - Advanced maternal age is #1!; aneuploidy
Anovulation
Endocrine - hypothyroid, hyperprolactinoma
Anatomy - Mullein abnormalities - Endometriosis - Chronic infection (PID), scarring - Fibroids (distortion) Idiopathic
Causes of male infertility
Sperm - poor sperm count or abnormal sperm Genetics - CF or Kleinfelter Hypo-Monadism Vasectomy/testicular removal previously Varicocele, torsion, undescended testes Anabolic steroids
Causes of anovulation
and management of each
Normal FSH (MX: lifestyle - weight loss, diet +/- ovulation induction)
- obesity
- PCOS (+/- metformin)
Incr FSH (ovarian failure) - MX: IVF
- Age >45
- iatrogenic (radio/chemo)
- autoimmune (SLE, RA)
- Genetic (45XO, fragile X etc)
Decr FSH (HPO failure) - MX: lifestyle +/- ovulation induction
- anorexia, stress, chronic illness, over-exercising
- Pituitary tumour
- infiltrative disease (sarcoid)
Idiopathic (Mx: IVF)
management - male infertility
Lifestyle - stop smoking, drinking, increase exercise and dietary antioxidants
Intra-cytoplasmic sperm injections (donor sperm)
Management of infertility
- Lifestyle - weight loss, exercise and diet (PCOS, obesity and incr sperm count)
- Ovulation induction (for PCOS, obesity, HPO failure)
- Clonifine first line for PCOS; Letrozol; FSH; pulse dose LH/GnRH analogue/HCG triggers ovulation - IVF (for ovarian failure)
- Serum AMH predicts response to IVF - Cryopreservation (if <35years old)
- Consider male-infertility and Tx for that
What is HELLP syndrome?
A complication/variant of pre-eclampsia
Features: Haemolysis
Elevated liver enzymes
Low plt count
Sx - malaise, epigastric pain, ROQ tenderness (from liver dysfunction and capsular distention) \+Ft of PE: N and V Headache Swelling, oedema HTN, proteinuria
RF for malpresentation
Pre-term
Placenta praaevia
Fetal anomaly
Polyhydramnios
MX of malpresenation
CONFIRM presentation - abdo palpation + bedside USS
options:
- NVD
- Admit and await labour if >=37 weeks
- ok for breech, req CTG monitoring and senior obstetrician skilled in breech deliveries available - ECV (with IOL and ROM if >=37 weeks)
- Emergency LUSCS if fetal distress or ECV unsuccessful
PLUS all need IV access, continuous C TG monitoring +/- epidural
Risks and CI to ECV
Risks: fetal distress, placental abruption, cord prolapse, ROM, APH
CI: recent APH, abnormal CTG, Ruptured membranes, multi pregnancy, major uterine abnormalities
Mx of breech via NVD
CTG monitoring and IV access
skilled senior obstetrician present
Position: dorsal lithotomy
+/- episiotomy
- Lovset monoeuvre to deliver arms + suprapubic pressure to assist head flexion
- Head delivery with forceps, Marceiu-Smellie-Velt or Burns-Marshall method
NOTE: if above fails, -> emergency c/s
Causes of reduced variability on CTG
4 Ss: Sick Sleeping Sedated Sub-mature
What does absent variability indicate on CTG. what next?
hypoxia -> confirm w scalp pH - metabolic acidosis confirms
cause of variable decels
Types of variable decelerations
Cord compression
Simple - rapid onset and recovery, occurring with contractions; shouldering present (reassuring)
Compound - increased baseline; slow to return to baseline; prolonged (>15s) = broad-based (bad!)
MX of variable decels
- Conservative
- fluid resus
- change position
- decr syntocinon IV rate
Fetal scalp electrode
Terbutaline (beta agonist)
- Do nothing
- Deliver!
- lower threshold for intervention if known IUGR or thick mea-stained liquor
Early vs late vs prolonged decels
Early and late are both repetitive and persistent with slow onset and recovery
Early: occur with contraction (due to head compression in labour)
Late: peak AFTER contraction (indicate fetal hypoxia and acidosis)
Prolonged: Last >2min duration = sustained bradycardia = sustained hypoxia
RED FLAGS on fetal CTG monitoring
Lack of accelerations
Rising baseline
Persistent prolonged decels with prolonged recovery
REduced/absent variability -> fetal hypoxia
Contractions >5:10 despite decr synt infusion
Criteria for diagnosis of PCOS
Rotterdam criteria: 2 of the following
- Oligomenorrhoea reflecting an ovulation
- Hyperandrogenism (clinical or biochemical with incr free testosterone and decr SHBG)
- Polycystic ovaries on USS
SX of PCOS
Obesity Acne Hirsutism Sub fertility Oligo or anovulation
Risks assoc w PCOS
Glucose intolerance and insulin sensitivity -> T2DM Hyperlipidaemia Obesity OSA Depression, anxiety Endometrial hyperplasia -> endometrial cancer CVD NAFLD
Screening of women with PCOS
Lipid profile and OGTT every 2years
BP every year
Mental wellbeing and desire for pregnancy
Management of PCOS
Diet and exercise firstling
Rest of MX depends on SX
- Oligomenorrhoea/anovulation (COCP to restore ovulation; cyclic progestins ex: IUD; metformin)
- Hirsutism (Diane trial for 6 mo 1st line; Spironolactone 2nd line; laser therapy, creams, doxycycline)
- Subfertility (diet and exercise, smoking cessation, folate supplement; ovulation induction ex: clomiphene +/- metformin)
- Cardiometabolic risk (metformin)
Which type of twin is more risky and what are some of the complications/associated risks?
TTTS Conjoined twins Death of a co-twin Discordant fetal anomalies TOPS - Twin oligohydramnios polyhydramnios syndrome Perinatal mortality Preterm LBW, IUGR NICU admission, NEC etc GDM
What additional antenatal care considerations do women pregnant w twins need?
Education/counselling around additional risks (fetal + maternal GDM, PE, APH, PPH, depression, anaemia, marital problems) and support services
Nutritional advice - incr requirements of energy, protein, folate, Ca, iron,
Aspirin from 12-36 weeks as PE prevention
Early GTT at 12 weeks if other RFs for GDM
When should twins be delivered?
DCDA: ~37 weeks
MCDA: no later than 37+6
MCMA: 32+0 to 33+6 with daily CTG monitoring after 26 weeks (MOST RISKS)
MX of labour of twins
NVD fine as long as twin 1 is cephalic. if not -> LUSCS
Presence of skilled doctors (senior obstetrician, paeds, anaesthetics) IV access Epidural MANDATORY (for easy manipulation of twin 2 if necessary) Deliver twin 1 then ensure long. lie of twin 2 (breech or vertex both ok)
Start syntocinon to restart contractions
ARM when twin 2 is in pelvis
Vaginal delivery of twin 2`
What is TTTS
Consequences
Twin-twin transfusion syndrome
- net shunt of blood from donor to recipient in MC twins
Donor: anaemia, oliguria, hypovolaemia, oligohydramnios, IGUR, FDIU
Recipient: Polycythaemia, polyuria, hypervolaemia, polyhydramnios, cardiomyopathy
Mx of TTTS
- amniodrainage - 70% survival but poor long term outcomes.
2. laser photocoagulation - creates functionally DC (only in severe cases)
What features does USS look at?
Fetal biometry (AC, HC, FL, HC:AC)
Liquor volume
Fetal activity
Doppler USS -> umbilical artery waveform, uterine artery, MCA
What umbilical artery waveforms are associated with placental gas exchange abnormalities
Raised Systolic diastolic ratio
Absent end-diastolic flow
Management of pregnant women with influenza
Empiric antiviral (tamiflu etc) therapy for pregnant women exposed to influenza virus or within 2 weeks either side of delivery (pre and postpartum) Infection control measures
Antibiotics for UTI in pregnancy
Empiric cephalexin or augmentin
Risks of Rubella infection in pregnancy
SX
Highest risk with maternal viraemia in 1st trimester
Infx <16 wks -> congenital rubella syndrome (blind, deaf, CP, heart abnormalities)
Infx>16wks -> growth restriciotn
SX - asympt or may have mild febrile illness and fleeting rash
MX of a women NOT immune to rubella antenatally
Paired IgM and IgG testing 14-21 days apart
Confirmed infection in first 12 weeks, offer termination
Confirmed infection > 16 weeks: fetal growth surveillance
Vaccine post-partum (live attenuated)
CMV
SX
Risks associated with this?
SX - mum asymptatomic
Risks - congenital non-genetic deafness, blindness, intellectual disability/neurodegenerative problems
Diagnosis and management of CMV
DX: no routine screening;
CMV IgG and avidity of IgG if high-risk or if USS or neonatal abnormalities have been detected.
Amniocentesis and serial USS if IvIg positive antenatally.
MX- insider termination if picked up early. no tx exists.
SX of maternal and congenital VZV
maternal: vesicular rsh +/- varicella pneumonia several days after rash onset
congenital: cicatricial skin lesions, limb hypoplasia, microcephaly, eye lesions (evident on USS)
Mx of a mother seronegative for VZV
If exposed:
VZVIg (ZIG) within 96 hours of exposure
Oral Acyclovir if you miss the 96hr window
IV Acyclovir if complications present (varicella pneumonia)
Babies born to infected mothers: ZIG +breastfeeding
If not exposed: postpartum vaccination
Mx of syphilis in pregnancy. when is risk of transmission greatest?
Penicillin!
risk of perinatal transmission highest in primary, secondary syphillis, followed by early latent syphilis.
What does listeria infection in pregnancy cause?
How do you prevent this infection?
Maternal sepsis and chorioamnionitis with intact membranes
Miscarriage
Transmitted by food so prevent via:
- safe food hygeine/handling; avoid high risk foods (unpasteurised diary, pre-prepared salads, uncooked seafood and chicken, processed meats)
When does GBS sepsis present and what are risk factors for the congenital infection?
First 24 hours of life
RF: premature, PROM >18 hours, maternal fever, GBS positive mother (carries it in her GI/GU tract)
MX of a GBS positive mother
IV intrapartum antibiotics: 2 doses 4 hours apart, starting at onset of labour (IV benpen or cephazolin if allergic)
Neonatal obs for 24 hours following delivery +/- neonatal abx if clinical suspicion of sepsis
outcomes of maternal toxoplasmosis infection
How do you test for this?
10% of intrapartum infection -> miscarriage, still birth, congenital birth defects ( chorioretinitis, intracranial calcification and hydrocephaly )
Inx: not routine but can order serum IgM and IgG -> if positive, amniocentesis for confirmation
What infection are child-care workers predisposed to in pregnancy?
SX
CMV infection (asymptomatic) and parvovirusB19 (slapped-cheek/lacy trunkal rash)
Consequences of maternal parvovirus B19 infection in pregnancy
If primary infection in pregnancy, small risk (3-5% of maternal infections) of fetal hydrous and intrauterine death secondary to fetal anaemia
Diagnosis and MX of parvovirus B19
DX: paired parvovirus B19 IgG and IgM serology in mum.
MX:
Close USS surveillance for development of fetal anaemia and hydrous in bub (polyhydramnios, ascites, incr SDR)
No tx for mum.
If fetal anaemia detected, refer to tertiary centre for care -> intrauterine infusion (O-neg blood) via umbilical cord
Mx of intrapartum HSV
Highest risk of neonatal transmission with primary infection in 3rd trimester of pregnancy with viral shedding at time of vaginal delivery
Late primary infection: Antivirals (acyclovir) and C/S to reduce neonatal risk
Early primary infection: antivirals from 36 weeks, can try NVD unless there are active lesions at labour onset (in which case LUSCS is necessary)
Risk factors for chorioamniotis
PROM
Prolonged labour
Multiple intrapartum VEs
Internal fetal HR monitoring (scalp electrode)
Genital tract infections (STIs, GBS positive)
Clinical features of chorioamnionitis
Maternal fever or fetal tachycardia Uterine pain/tenderness PV blood loss Preterm labour Malodorous or purulent amniotic fluid FBE: Incr WCC + incr CRP
Management of chorioamnionitis
Erythromycin for 10 days + steroids
Immediate delivery if baby is unstable (even if preterm, if infected - i.e. baby tachycardia, offensive D/C, pain, bleeding)
Management of pROM
If baby is stable, buy more time!
Antibiotics (10days erythromycin) and discharge with biweekly O/P appointments and at-home vital monitoring
IOL at 37 weeks
IOL pre-term if ?Chorio/unstable baby
Pathophys of menopause
how do hormones change with this?
Physiological - loss of ovarian function from exhaustion of primordial follicles due to atresia/atrophy
Iatrogenic - gynae surgery (bilateral oophorectomy; chemo, radiation to pelvis)
Decr Estrogen and progesterone
Incr FSH
Symptoms of menopause and what do they relate to?
SX Related to decr oestrogen
Vasomotor SX (hot flushes, night sweats, palpitations)
Sleep problems
Urogenital problems (dry vaginal, atrophic vaginitis, urinary frequency)
Locomotor sx (joint pain, backache, muscle aches)
Psychological SX (anxiety, depression, feeling unloved etc)
Loss of libido
Osteoporosis and incr fracture risk
Common sites for osteoporotic fractures
Vertebral
Hip
Wrist
Definition of osteoporosis
Bone density (DEXA scan) <2.5 SD below mean
Osteopenia is 1.5 - 2.5 SD below the mean
Management of osteoporosis in menopause
All women with risk factors get 2 yearly DEXA scans
T-scores <2.5 get treatment:
Lifestyle/conservative: Ca, vit D supplements and daily exercise
<60: HRT
>60: Bisphosphonates (SE: GORD, osteonecrosis of the jaw)
Risk factors for osteoporosis
Low BMI Smoking Family Hx excessive caffeine steroids IBD/malabsorption Decr VitD
Definition of menopause
normal age range
final menstrual period, determined after 12 months of amenorrhoea
normal age range: 45-57
Non-hormonal management of menopause
Lifestyle:
- stop smoking
- weight mx (exercise and diet)
- <2SD alcohol
- Decr caffeine
SX-treatment Vasomotor SX - SNRI (Venlafaxine, fluoxetine, citalopram) - GABApentin - Clonidine/nifedipine (Ca ch blocker)
Vaginal dryness
- vaginal oestrogen pessary
- lubricants and gels, moisturisers and oils
Locomotor SX: analgesia, NSAIDs, exercise
Psych SX: Antidepressants, anxiolytics, counselling
Hormonal management of menopause
- HRT (only for women <60 to limit risks of CVD, VTE, stoke etc)
Relieves menopausal SX and incr bone density
With uterus: Oestrogen and progesterone (protects from incr risk of endometrial cancer)
Method: local cream/pessary/tablet if vaginal dryness (no need for prog)
- tablets, patches, subcut implant, skin gel (combined preparations)
Without uterus: oestrogen alone
- Tibolone: synthetic steroid with weak oestrogen, progesterone and anti androgen effects (helps w vasomotor SX, vaginal lubrication and libido; incr bone mass density and decr fracture risk; no incr risk endometrial cancer)
SE of HRT and CI
SE:
incr risk stroke, VTE, CVD (oestrogen)
incr risk breast cancer (combined - prog)
incr risk endometrial, ovarian cancer and cholecystitis w unopposed estrogen
CI: HX breast, ovarian, endometrial cancer HX VTE or thrombophilia HX stroke or heart disease Uncontrolled HTN Active liver or cholestatic disease Migraine w aura Abnormal vaginal bleeding
Investigations for premature menopause (<45)
FSH (elected on 2 occasions is diagnostic)
Decr E2
Inx for other causes
prolactin, TFTs, betaHCG
Karyotype (turner’s) and fragile X screen
pelvic USS
Differentials deep dyspaerunia
Endometriosis Adenomyosis Adhesions PID Fibroid Neoplasia
Differentials superficial dyspareunia
Vulvovaginitis (inflammation) - thrush, STIs, herpes, UTI
Dermatological - lichen sclerosis, eczema, psoriasis, contact dermatitis, atrophic vaginitis
Inadequate lubrication - menopause, oestrogen deficiency, radio/chemotherapy, drugs
Trauma
Vaginismus (spasm of vaginal muscles)
Vulvodynia
Rigid hymen
Neoplasia
Aetiology post-menopausal bleeding
Anovulatory cycles (lack of ovulation leads to endometrial build up that outgrows blood supply)
Endometrial cancer until proven otherwise! Cervical cancer (70% SCC due to HPV; 30% adenocarcinoma)
Benign causes :
- Urogenital atrophy (due to lack of oestrogen, thinning of vaginal and cervical epithelium and endometrium)
- Endometrial polyps
- Fibroids
- Endometrial hyperplasia (simple; atypical - 40% progress to carcinoma)
Inx and Mx of post-menopausal bleeding
Inx: TVUSS and hysteroscopy D&C or O/P pipelle for endometrial sampling (colposcopy if pap spec and pap smear abnormal)
MX:
Medical
- vaginal oestrogen therapy for urogenital atrophy
- Progesterones (mirena, depot provera injections) for SIMPLE endometrial hyperplasia
- COCP if <60 and low risk for CVD, VTE
Surgical
- Hysterectomy for atypical endometrial hyperplasia (+/- bilateral sapling-oophrectomy with lymph node sampling for endometrial cancer; +/- pelvic lymph node sampling for cervical cancer)
- Endometrial ablation + contraception or tubal ligation
Complications in the puerperium
Secondary PPH (retained products or endometritis) Infection - Sepsis (GAS) - Endometritis - Wounds (C/S, Epis/perineal tears) - epidural or IV site - UTI - Mastitis, other lactation problems
VTE risk
Urinary retention or incontinence (urethral damage etc)
Constipation or faecal incontinence
Mood disorders
Time course of breastfeeding
Exclusive breastfeeding for up to 6 months post delivery with gradual introduction of solids and continued (non-exclusive) breastfeeding into 2nd year
CI to breastfeeding
HIV
Methotrexate, cyclosporin
Benefits of breast feeding
Infant - Decr risk of RTIs, gastro illness, DM, obesity, HTN, CV disease, NEC, SIDS; incr IQ
Mother - contraception, decr risk of ovarian cancer, breast cancer, osteoporosis, faster return to pre-pregnancy weight
Complications of breast feeding
Mastitis (staph infection) +/- Breast abcess
Cracked/grazed/bleeding nipples - due to incorrect attachment
Engorgement
Low supply
Presentation of mastitis
Red, hot, tender breast lump; Fever, pain, malaise +/- systemic SX
MX: encourage mum to keep feeding to drain the breast
AbX (fluxclox) only if SX unresolved for 12 hours -> if unstable, admit for IV antis + breast milk culture
Risk factors for T21
age >= 37 is high risk
Prev chromosomal abnormalities (T21, T18, T13, 45XO)
2 or more minor or 1 major abnormality on USS
Chrom. abnormality in either partner
MX of termination of pregnancy
- offer SW and psych referral
- Inx: blood group and Ab (if Rh neg give antiD); STI swabs
If 1st trim: Surgical D&C (day procedure but surgical risks)
Medical: Misoprostil/mifepristone (painful, takes 3 days; 15% fail and need D&C)
2nd trim: Surgical: D&C or hysterotomy
-Medical: IOL + KCL + Mifepristone + Misoprostil
At what point does a terminal panel and 2 doctors need to agree on performing a termination?
24 weeks onwards
Features of trisomy 21
1/2 are FDIU Low IQ Congenital abnormalities Dysmorphic features Heart, hearing problems Short stature
