Women's Health Flashcards
Epidemiology of subfertility/infertility
1 in 7 women
50% are due to females
25% due to males
25% are unknown
Increases with age
No family history
Risk factors for subfertility/infertility
Increasing female age Depression Stress STIs Smoking Alcohol intake (even moderate) Overweight or underweight
Causes of infertility (general)
25% ovulatory 20% tubular damage 10% uterine or peritoneal disorders 30% male 25% unknown
What are the 3 WHO classifications for disorders of ovulation
Group 1 - hypothalamic-pituitary failure (low oestrogen, low gonadatrophin)
Group 2 - hypothalamic-pituitary-ovarian failure (normal oestrogen, high or low gonadatrophin)
Group 3 - ovarian failure (raised gonadatrophin, low oestrogen)
Causes of ovulatory dysfunction causing infertility
PCOS
- Pituitary tumours
- Panhypopituitarism (Simmond’s disease)
- Sheehan’s disease (pituitary infarction following PPH)
- Hyperprolactinaemia
- Chromosomal disorders (Turners XO, Klinefelter’s XXY) XXX (increased premature ovarian failure)
- Premature ovarian failure/ menopause
Role of FSH
Follicle stimulating hormone
Stimulates follicle development and oestrogen production
Role of LH
Midcycle LH surge causes ovulation.
Maintains corpus luteum and stimulates progesterone and estradiol production
Causes of infertility - tubes/uterus/cervix
STI (PID from chlamydia or gonorrhoea) Asherman's syndrome (adhesions in uterus and cervix) Deformity of uterus Fibroids Cervical mucus Endometriosis
What drugs can lead to sub/infertility?
Phenothiazines (antipsychotics) Metoclopramide NSAIDs Immunosuppressants Spironolactone Chemotherapy Neuroleptic drugs
Causes of infertility - male
Structural or hormonal
- Genetic (Klinefelters XXY), Kallman syndrome (hypogonatrophic hypogonadism)
- Androgen insensitivity
- Cryptorchidism (testicular dysgenesis)
- Varicocoele
- Pituitary causes (tumours)
- Testicular tumours
- Severe hyperprolactinaemia
- Obstruction
- Erectile dysfunction
- Hypospadias
- Retrograde ejaculation
Advice for couple trying to conceive
Regular sexual intercourse (2-3x per week)
Preparation for pregnancy (folic acid, rubella check, cervical screening)
Decrease stresses
Smoking and alcohol cessation
BMI between 19 and 25
Investigations for sub/infertility
Start if not conceived in 1 year
FEMALE
- Measure mid-luteal progesterone day 21 of 28 (7 days before period
- If irregular cycles measure FH and LSH
- Test thyroid function
- Measure prolactin
- Screen for chlamydia and other STIs
MALE
- Semen analysis
- Screen for STIs
Semen sample should be collected after at least 2 days but less than 7 from sexual abstinence
After referral
- Tubal patency (hysterosalpinography or contrast ultrasonography) HSG
- If co-morbidities the lap and dye testing
- Ovarian reserve testing - on day 3 to predict response to stimulation in IVF
Males - further sperm assessment - microbiology, culture
Imaging of tracts
When should sub/infertility be referred
Follow local guidelines
- Under 36 refer after 1 year
Consider early referral if
- over 36 (6 months)
- known cause for infertility
- history of factors that predispose to infertility
- treatment planned that may result in infertility (chemotherapy)
Management of subfertility/infertility
Treat underlying problem
- Ovulation induction with Clomifene
- Gonadatrophins if clomifene resistant (pulsatile)
- If male obstruction, correct surgically
- Surgical correction of tubes
Different types of assisted conception
Intrauterine insemination In vitro fertilisation Intracytoplasmic sperm injection (ICSI) Donor insemination Oocyte donation
Describe intrauterine insemination
15% success in under 35s
Prepared sperm placed into uterine cavity at ovulation (induced or spontaneous)
Used when
- difficult to have intercourse (unable, disability, psychological)
- HIV+ male (sperm washing)
- Same sex relationships
Describe IVF
33% success in under 35s
25% of treatments result in live births
Offered after 2 years
- Ovarian stimulation prior to IVF with US measured response
- Embyro inserted into uterus
- Progesterone given after embryo for luteal phase support
- transfer single embryo
Under 40s up to 3 cycles - stop once reach 40
Over 40s, 1 cycle if never had IVG, no evidence of low ovarian reserve
Some CCGs in addition
- No previous children, or partner with any children, healthy weight, non-smoker
Describe Intracytoplasmic sperm injection (ICSI)
Single sperm injected into oocyte
Used when severe deficits in sperm or after failed IVF
When can donor insemination be used
Azoospermia
Severe deficits in sperm quality and don’t want ICSI
High risk of transmitting genetic disorder
High risk of transmitting infectious disease to child/partner
Complications of assisted conception
OVARIAN HYPERSTIMULATION SYNDROME (OHSS)
Symptoms of ovarian Hyperstimulation syndrome
lower abdo discomfort nausea and vomiting diarrhoea abdo distension ascites rapid weight gain tachycardia hypotension oliguria
What factors should be considered when prescribing contraception?
Womens preference and choice Education - must be fully informed Co-morbidities Medications Age and parity Smoking history Weight Family plans (long vs short term) Protection from STIs Exclude pregnancy
MOA of COCP
Prevents conception by acting on hypothalamic-pituitary-ovarian axis to suppress synthesis and secretion of FSH and LH
Inhibits development of ovarian follicles and ovulation
Cervical mucus to prevent sperm penetration
Endometrium to inhibit blastocyst secretion of LH and LSH
Advantages and disadvantages of COCP
Advantages:
Non invasive
Regular and lighter periods, decrease pain
Control time of periods
Can improve acne
Decreases ovarian, endometrial and colorectal cancer
Decrease PMS symptoms
Disadvantages: User dependent Less effective than long acting Side effects VTE risk No protection from STIs Breakthrough bleeding in first few months Increased breast and cervical cancer
When prescribing contraception - what criteria should be checked?
UKMEC - UK Medical Eligibility Criteria 1 - no restriction for use 2 - advantages > disadvantages 3 - risks outweigh advantage - not recommended 4 - use is unacceptable
What questions must be asked before prescribing COCP
Advice to give
Migraine Smoker HTN Thrombophilia Previous VTE FHx of VTE Hyperlipidaemia BP BMI Exclude pregnancy
Start on first day of bleeding (or within 5 days)
Drug interactions
D&V advice - use alterative protection
Need alternative protection for first 7 days
MOA of progestogen only pill POP
Ovulation is inhibited by varying degrees depending on the drug
Delays transport of ovum
Cervical mucus thickens
Endometrium becomes unsuitable for implantation
Advantages and disadvantages of POP
A Non invasive Easily reversible Avoids CV risk of COCP Less restriction Can be used up to 55 and while breastfeeding
D
- Amennorhoea and breakthrough bleeds
- narrower window
- increase risk of cysts
- increased risk of ectopic pregnancy if become pregnant
- Irregular periods
Describe depot progesterone injections and MOA
Every 12 weeks
Long acting reversible progesterone only
Failure rate 2 in 1000
Thickens mucus
Endometrium unsuitable for implantation
Can be used 4 weeks post partum
Advantages and disadvantages of POP
A
- Reliable
- Infrequent
- Low risk
- Low failure rate
- Decreases bleeding
- Used in breast feeding
D
- not quickly reversible
- Decrease bone mineral density
- irregular periods
- weight gain (up to 3kg)
Describe Implanon/implants
Etonogestrel subdermal slow release in upper arm
Failure rate < 1 in 1000
Inhibits ovulation , thickens mucus, thins endometrium
Inserted with local anaesthetic
Can be given 21 days post partum
Can be given straight after termination
Advantages and disadvantages of Implants
A
- No large initial dose or fluctuations
- Low failure rate
- Reversible after 4 days
- Decreased menstrual problems
- Safe
D
- irregular bleeding
- weight, mood and libido changes
- Changes with bleeding DO NOT SETTLE WITH TIME
- Increases risk of congenital malformation
Describe IUD
Copper containing
Long acting
Reversible
T shape, sits in fundus of uterus
Cytotoxic - inflammatory reaction and is spermicidal
Very low failure rate
5-10 years lifespan
Advantages and disadvantages of IUD
A
- Effective, reversible
- Long acting (up to 10 years)
- Can be used as emergency contraception
- No hormones
D
- Spotting
- Increased bleeding and pain in first few cycles
- Perforation 0.2%
- Increased ectopic pregnancy
- Uncomfortable insertion
Describe IUS
Progesterone releasing
Decreased endometrial growth, thickens mucus
Advantages and disadvantages of IUS
A
- effective, convenient
- reversible
- decreased blood loss and dysmenorrhoea
- decrease risk of PID
- local action only
D
- common - irregular periods
- increase ovarian cysts
- increased ectopic pregnancy
- expulsion or perforation
Side effects of progesterone
acne
breast tenderness
headache
mood changes
Describe caps and diaphragms
Rarely used
High failure rate
Diaphragms - thin dome 55-100mm. Lie between posterior fornix and pubic bone
Caps are smaller and fit over cervix, held by suction
Only used if problem with diaphragm
Often used with spermicide
Effectiveness of female barrier contraception
Percentage to conceive
16% - diaphragm
32% parous with cap
16% cap in nulliparous
21% female condom
Describe natural planning and A&D
Calendar methods/temperature/mucus thickness/palpating cervix
A - no side effects. complies with religious beliefs
D - commitment. unreliable. not effective
Steps in fertilisation
12-24 hours after ovulation
Sperm enter vagina and swim to uterus
Prostaglandin in semen stimulate uterine contractility
CAPACITATION (increase speed of sperm tail wiggle, removal of proteins/coatings)
Acrosomal enzymes aid penetration of corona radiata and zona pellucida
ZP3 in zona pellucida acts as sperm receptor and depolarises cell once in contact to prevent polyspermy
Procedure of termination
Offer antibiotic prophylaxis as 10% get genital tract infection (metronidazole +/- doxycycline or arythromycin)
Surgical
- Less than 14 weeks, vacuum aspiration + vaginal misoprostol 3 hours prior
- 14-24 weeks, dilation and evacuation
- Under sedation, local or general
Medical
- 200mg oral mifepristone followed by misoprostol
- NSAID for pain relief
Complications of termination
Infection (10%) Cervical trauma - surgical only Failed termination <1% Haemorrhage Perforation - surgical Long term psychological consequences
What is cryopreservation?
Freezing of gametes to preserve fertility
Availability if undergoing treatment that may affect fertility like chemotherapy
If
- will not worsen their condition
- enough time is available before the start of treatment
what is PCOS
polcystic ovarian syndrome
syndrome of polcystic ovaries AND systemic symptoms causing reproductive, metabolic and psychological disturbance
infertility, amenorrhoea, acne and hirsuitism
epidemiology of PCOS
33% of women have polcystic ovaries but not the syndrome
affects 5-10% of reproductive age women
pre menopausal women
onset at age of menarche
pathophysiology of PCOS
unknown but is multifactorial
excess androgen so by theca cells of ovary
insulin resistance
raised LH due to increased production
raised oestrogen
genetic link but no gene found
symptoms of PCOS
oligomenorrhoea infertility or subjectivity acne hirsuitism alopecia obesity psychological- mood swings, depression, anxiety sleep apnoea
signs of PCOS
hirsuitism
alopecia
central obesity
acanthosis nigricans (hyperpigmented skin in folds)
rarely - increased muscle mass, deep voice
what are the diagnostic criteria for PCOS
2 out of 3
- polcystic ovaries on US. 12+ peripheral follicles or increased ovarian volume >10cm3
- oligo ovulation or anovulation
- clinical and/or biochemical signs of hyperandrogenism
investigations for PCOS
total testosterone - normal or slightly raised
free testosterone- may be raised
Sex hormone binding globulin - normal or low
free androgen index- normal or raised
LH - typically raised
LH: FSH >2 with normal FSH
ultrasound. cysts. raised volume
also consider: TFTs, prolactin, cortisol
fasting glucose and lipids
management of PCOS
advice on weight control
if not planning pregnancy
- co-cyprinolol for hirsuitism and acne. induces regular bleeds to decrease endometrial cancer
- COCP: for menstrual irregularity
- metformin
- eflornithine for hirsuitism
- orlistat for weight loss
if planning pregnancy - clomifene - metformin one of both - laparoscopic ovarian drilling or gonadotrophins (if clomifene resistant)
complications of PCOS
infertility amenorrhoea increased CV risk sleep apnoea increased type 2 or gestational diabetes increased pre term birth or pre eclampsia
In Down’s screening what is tested in a quadruple test?
Beta-hcg
AFP (alpha fetoprotein)
Inhibin A
UE3 (unconjugated estriol)
What are the results of serum markers if a baby has Down’s?
PAPP-A - lower in Down's beta-hcg - raised in Down's AFP - lower in Down's UE3 - lower in Down's Inhibin A - raised in Down's
What factors can affect Down’s screening?
Weight Race IVF Diabetes Smokers Twins
Describe nuchal scanning in Downs
- Performed between 11 and 14 weeks
- Measure nuchal pad at nape of neck
- Increased nuchal translucency = higher change of chromosomal abnormality
- 20% false positive rate
Describe amniocentesis
- Sample of amniotic fluid to examine foetal cells
- Done between 12-18 weeks
- Chromosomal, genetic and biochemical analysis
- Management of rhesus disease
- Estimation of maturity
Indicated if:
- Mother over 35
- Previous child with chromosomal abnormality
- antenatal screening
Procedure
- give rhesus prophylaxis where needed
- US guided, 22 gauge spinal needle through abdo wall into uterus
10-20ml aspirated
7% loss of pregnancy is done 12-14 weeks
Describe chorionic villus sampling
Sampling of developing plancenta late in the first trimester to allow examination of foetal karyotype/genotype
- Done transabdominally
Indicated if:
- advanced maternal age
- PHx of chromosomal/genetic abnormality
Procedure
- between 11 and 13 weeks
- US guided needle aspiration
First trimester, 2% miscarry, 2nd trimester 3%
What information should be provided during antenatal care?
FIRST CONTACT
- folic acid supplementation
- lifestyle advice - smoking, drugs, alcohol
- food hygiene
- information on all antenatal screening
AT BOOKING
- nutrition and diet
- place of birth
- exercises
- pregnancy care pathway
- discuss mental health issues
BEFORE or AT 36 weeks
- breastfeeding information
- preparation for labour and birth
- recognising active labour
- care of the new baby
- vitamin K prophylaxis
Lifestyle advice to be given in pregnancy
Folic acid 400 micrograms/day ideally before conception
Avoid vitamin A (teratogenic)
Vitamin D supplementation if darker skin or low
Avoid unpasteurised milk, soft cheese, pate (listeriosis)
Avoid salmonella risk - no raw or partially cooked eggs
Seatbelt placed above and below bump
What screening is done Antenatally?
Anaemia - booking, 28 weeks
Blood grouping - blood group and rhesus D status
Haemoglobinopathies
Foetal anomalies - 18-20 weeks US scan
Infection - MSU early pregnancy, BV, chlamydia, hep B, HIV, syphilis, rubella
Placenta praevia
How is foetal growth monitored?
Symphysis-fundal height from 24 weeks
Management of breech baby at 36 weeks?
external cephalic version
Management of pregnancy over 41 weeks
- Vaginal exam plus membrane sweeping
- Induction offered after 41 weeks
- if declined, twice weekly cardiotocography
At what weeks are antenatal appointments offered?
10 weeks 16 weeks 18-20 weeks - US scan NP - 25 weeks (start symphysis-fundal height) 28 weeks - antiD NP - 31 weeks 34 weeks - 2nd dose antiD 36 weeks 38 weeks NP - 40 weeks 41 weeks - for induction
All appointments - BP and proteinuria
Definition of miscarriage
Loss of pregnancy before 24 weeks of gestation.
Types of miscarriage
Threatened - mild bleeding, little or no pain. Cervical os closed. Ongoing pregnancy
Inevitable - heavy bleeding + clots and pain. Cervical os is open. Pregnancy will not continue
Incomplete - products of conception partially expelled
Missed/silent - foetus is dead but retained. uterus small for dates.
Habitual/recurrent - 3+ consecutive miscarriages
Septic - complication of incomplete or therapeutic abortion when intrauterine infection occurs
Epidemiology and risk factors for miscarriage
Increases with age
10-15% of pregnancies
85% in the first trimester
RFs
- increased number of births (parity)
- Smoking
- Excess alcohol
- Illicit drug use
- Uterine surgery or abnormalities e.g. incomplete cervix
- Connective tissue disorders (SLE, APLS)
- uncontrolled diabetes
Aetiology of miscarriage
Often no cause found
- Abnormal foetal development - abnormal chromosomes
- Genetically balanced parental translocation
- Placenta failure
- uterine abnormality - bicornuate, fibroids
- Incompetent cervix (2nd trimester)
- Multiple pregnancy
- Autoimmune - SLE, APLS
- PCOS
50% unexplained
Presentation of miscarriage
Vaginal bleeding (heavier bleeding = increased risk)
Abdominal pain
Passed products of conception/clots
50% with threatened miscarriage will later miscarry
- Open cervical os
- Uterine size not appropriate for dates
- Products of conception in cervical canal
Investigations for miscarriage
US - TV, if there is no visible heart beat, a 2nd scan should be done in 7-14 days depending on size of sac
Serum hcg - levels below 1000 in pregnancy of unknown location or complete miscarriage
Management of miscarriage
Support, follow up and counselling
Anti-D to all rhesus negative
CONSERVATIVE
- Expectant, should resolve naturally 7-14 days
- Consider other management if: risk of haemorrhage, late in first trimester, previous adverse miscarriage outcome, infection, coagulopathies
- Pregnancy test 3 weeks after - if still positive, medical or surgical management
MEDICAL
- Vaginal misoprostol, analgesia and anti-emetics
- Causes more pain and bleeding than surgical
- Pregnancy test 3 weeks after
SURGICAL
- If persistent bleeding, haemodynamic instability, retained tissue, gestationaltrophoblastic disease
- Manual vacuum aspiration under local or surgical under GA
- Complications: perforation, cervical tears, adhesions, haemorrhages
- Screen for chlamydia
Types of gestational trophoblastic disease
Can be pre-malignant or malignant - due to abnormal proliferation of trophoblastic tissue.
Pre-malignant
- Complete hydratiform mole
- Partial hydratiform mole
Malignant
- Invasive mole
- Choriocarcinoma
- Placental site trophoblastic disease
- Epitheliod trophoblastic disease
Describe complete molar pregnancies
All genetic material comes from the father when an empty oocyte is fertilised
- No foetal tissue
- 46 XX karyotype
- Placental tissue has marked hyperplasia and gross swelling of villi
- “bunch of grapes” appearance
- 10-15% become malignant, very sensitive to chemo
- No embryo
Describe partial molar pregnancy
- 3 sets of chromosomes
- 2 sperm fertilise at the same time
- 69 chromosomes, 46 paternal, 23 maternal
- embryo visible on early US
- usually diagnosed on histology after miscarriage
- <1% malignancy
Describe complete mole
- Develops form a complete molar pregnancy
- Invades into myometrium
- Uterine mass with elevated hCG
- Responds well to chemo
Describe choriocarcinoma
Synctiotrophoblasts
- Often follows a molar pregnancy but can be post normal pregnancy, ectopic or abortion
- continued vaginal bleeding post-pregnancy
- Often metastasises - lung, brain, GI, liver, kidney
- Can occur up to 20 years post pregnancy
Epidemiology and risk factors for gestational trophoblastic disease
GTD - 1 in 714 births
Complete molar pregnancy - 1-3 per 1000 pregnancies
Partial - 1 per 1000
GTN - 1 in 50,000 live births
RFs
- over 45 or under 16
- previous molar pregnancy
- multiple pregnancy
- menarche over 12, light menstruation
- COCP of history of use
- Asian
Presentation of GTD
Vaginal bleeding in first trimester
Hyperemesis
Rare
- abnormal uterine enlargement
- hyperthyroidism
- anaemia
- respiratory distress
- pre-eclampsia
Investigations for GTD
- hCG (best for follow up)
- Histology for definitive diagnosis (should be done for all products of conception
- US: snowstorm appearance in 2nd trimester, heterogenous mass, no foetal development
- CT if staging for metastatic disease
Management of GTD
Refer for follow up at a trophoblastic screening centre
- Suction curettage
- Uterine pregnancy test at 3 weeks
- Anti D prophylaxis
- SENIOR SURGEON
Follow up
- 2 weekly until hCG normal
- monthly for 6 months after
Chemotherapy
- if choriocarcinoma, mets, heavy bleeding, plateaued or rising hCG
- LOW risk: methotrexate & calcium folinate
- HIGH risk: EMA/CO chemotherapy combination
Epidemiology and RF for ectopic pregnancy
1.1 per 1000 pregnancies
97% in fallopian tubes
2-3% interstitial (not extrauterine part of the tube)
RF
- IVF
- Hx of pelvic infection
- Adhesions from inflammation, infection or endometriosis
- tubal surgery
- IUD/IUD
Symptoms of ectopic pregnancy
Abdominal or pelvic pain Amenorrhoea or missed period Vaginal bleeding (with or without clots)
Dizziness, fainting or syncope Breast tenderness Shoulder tip pain Urinary symptoms Passage of tissue Rectal pain or tenesmus Diarrhoea and vomiting
Signs of ectopic pregnancy
Pelvic or abdominal tenderness Adnexal tenderness Rebound tenderness Cervical tenderness Pallor Abdominal distension Enlarged uterus Tachycardia and/or hypotension Shock or collapse
Investigations of ectopic pregnancy
Pregnancy test in all women of child bearing age and lower abdominal pain
- Transvaginal US most accurate
- Need to identify: location of pregnancy, foetal pole, heartbeat
- Serial hCG, 48 hours apart
Management of ectopic pregnancy
- Admit as emergency
- Anti-D prophylaxis in all rhesus negative women
- Conservative if hCG declining and patient clinically well
MEDICAL
- single dose methotrexate
- First line if can return for follow up with no significant pain, unruptured, no intrauterine pregnancy on US and hCG <1500
- Contraception for 3-6 months due to methotrexate teratogenicitiy
SURGICAL
- If can’t come for follow up OR
- significant pain
- adnexal mass >35mm
- Foetal heartbeat visible
- Serum hCG>5000
- Laparoscopic approach preferable
- Salpingectomy
- Complications: bleeding, infection, damage to surrounding organs
Describe BP in pregnancy
Falls slightly in 1st trimester due to decreased vascular resistance
- Falls in 2nd to lowest point at 22-24 weeks
- Increases in 3rd trimester to pre-pregnancy levels
- Falls immediately after birth
Risks of hypertension in pregnancy
Abruptio placentae
Cerebrovascular accident
Disseminated Intravascular Coagulopathy
Intrauterine growth restriction
Prematurity
Intrauterine death
Management of hypertension of pregnancy
Education on symptoms of pre-eclampsia
- US at 34 weeks for foetal growth and amniotic fluid volume
- High risk of pre-eclampsia then 75mg aspirin daily
PRE-EXISTING
- Review medication
- Stop ACEi and ARBs
- Keep BP <150/110
- Test for proteinuria regularly
- US for foetal growth restriction, amniotic fluid volume
MILD - 140/90
- Measure BP twice weekly and urine for protein at each visit
MODERATE - 150-159/100-110
- Measure BP twice weekly
- Start labetalol (alternatives: methyldopa, nifedipine)
- Bloods
SEVERE >160/110
- Admit, discharge when <150
- Measure BP at least 4 times per day
When should aspirin be given in pregnancy?
- Hypertension or pre-eclampsia in past pregnancy
- CKD
- Autoimmune disease
- Diabetes mellitus
- Chronic hypertension
OR 2 of the following
- first pregnancy
- aged over 40
- previous pregnancy over 10 years ago
- BMI > 35
- FHx of pre-eclampsia
- multiple pregnancy
Definition of antepartum haemorrhage
Vaginal bleeding after week 24 of gestation and before 2nd stage of labour
Epidemiology and risk factors for antepartum haemorrhage
3-5% of pregnancies
20% of very preterm babies are associated with APH
RFs depends on causes
- Smoking
- Cocaine use
- Increasing maternal age
- Increased parity
- Pre-eclampsia
- polyhydramnios
Aetiology of APH
No definitive cause found in 50%
- Placenta praevia (insertion of placenta, partially or fully, in lower segment of the uterus)
- Placental abruption (premature separation of normally placed placenta)
- Local causes (vulval, cervical infection, trauma or tumours)
- Domestic violence
- Vasa praevia (bleeding from foetal vessels in foetal membranes, high risk of foetal haemorrhage)
- Uterine rupture
- Inherited bleeding problems
Presentation of APH
Bleeding With pain - abruption Without pain - praevia Uterine contractions Malpresentation or failure of head to engage Signs of foetal distress If severe - hypovolaemic shock
Investigations of APH
FBC
Group and save
Clotting studies
ADMIT
Urgent US for placenta praevia
Foetal monitoring
Rhesus negative women should have Kleihauer test - give anti-D after each bleed
Management of APH
Admit, even if only small amount of bleeding
Estimate blood loss - Minor <50ml, Major 50-1000ml, massive>1000ml
If foetal distress - urgent delivery regardless of gestation
If severe bleeding - mother’s life takes priority
Give corticosteroids if gestation between 24 and 36 weeks
Definition of placenta praevia
Placenta inserted wholly or partially into the lower segment of the uterus
MAJOR - placenta covers internal os of cervix
MINOR - leading edge is in lower segment but not covering the os
Epidemiology and risk factors for placenta praevia
1/200 births
1/1000 are major
Incidence is increasing
RFs
- Previous history of placenta praevia
- Previous C-section
- Increased maternal age
- Increased parity
- Smoking
- Cocaine use during pregnancy
- Previous spontaneous or induced abortion
- Deficient endometrium due to past history of endometritis, manual removal of placenta, curettage
- Assisted conception
Presentation of placenta praevia
Painless bleeding after 28th week - sudden, profuse, does not last long
- 25% have spontaneous labour in the next few days
- Can just have bleeding in labour or membrane rupture
- High presenting part or abnormal lie
- No foetal distress unless complications
- Bleeding provoked by sexual intercourse
Diagnosis/ investigations of placenta praevia
Should have high index of suspicion in bleeding after 20 weeks.
Diagnosis relies on US
- Leading edge may be low on a 20 week scan
- Apparent migration occurs during 2nd and 3rd trimester with development of lower uterine segment
- Cannot exclude placental abruption (this is a clinical diagnosis)
- TV US for all women whose placenta reaches or overlaps cervical os at anomaly scan
- Minor - scan again at 36 weeks
- major - scan again at 32 weeks
Assists in planning and delivery
Management of placenta praevia
MINOR - may be able to deliver vaginally.
Placental edge <2cm from the os = caesarean section
If anterior, reaching os with history of C-section then treat as placenta accrete
MAJOR
- Deliver by C-section
- No penetrative intercourse
- Should admit to hospital from 34 weeks
- Defer C-section to 38 weeks if possible
Placenta accrete and management
Morbidly adherent placenta
- high risk if placenta praevia with history of C-section
- Requires consultant obstetrician and anaesthetist
- Blood products on site
- MDT pre-op planning
- Deliver baby without disturbing placenta
- DO NOT PERFORM VAGINAL EXAM
Describe implantation bleeding
Light spotting or bleeding
Occurs 10-14 days after conception
NORMAL
Occurs when fertilised egg attaches to lining of uterus
Describe normal placenta at term
Blue-red colour, discoid shape
450g in weight
Maternal surface - divided into lobules or cotyledons with irregular grooves or clefts
Foetal surface - smooth, shiny and translucent, choronic plane covered in amniotic membrane
Describe normal umbilical cord
50-60cm long
Abundant Wharton’s jelly, no true knots
2 umbilical arteries, 1 umbilical vein
Abnormalities of placental shape, size or surfaces
Circumvallate - foetal membranes double back on foetal side around edge of placenta, small central chorioic area inside a paler ring of membranes on foetal side
Succenturiate lobe - accessory lobes, associated with retained placenta and increased infection
Bipartate placenta - bilobed (uncommon)
Placenta membranacea - failure of chorion to atrophy during development, placental cotyledons form envelope around greater part of uterine wall
Describe placenta accreta and levels
PLACENTA ACCRETA
Placenta morbidly attached to uterine wall - chorionic villi penetrate the decidua basalis to attach to myometrium
PLACENTA INCRETA
villi penetrate deeply into myometrium
PLACENTA PERCRETA
villi breech myometrium into perioteum
Epidemiology of placenta accreta
1/2500 deliveries
40% deliver before 38 weeks
C-section planned at 36-37 weeks
RFs
- Previous C-section
- Placenta praevia
- Increased age
Management of placenta accreta
Placenta is left in place with therapeutic uterine artery embolization, surgical internal iliac artery ligation or methotrexate therapy
Elective hysterectomy later has less blood
Describe placental abruption
Premature separation of a normally placed placenta before delivery of the foetus with blood collecting between placenta and uterus
- 30% of all APH
- 6 per 1000 births
Concealed (20%) - haemorrhage confined within uterine cavity, more severe as blood loss usually underestimated
Revealed (80%) - blood drains through cervix
Risk factors for placental abruption
Previous abruption Pre-eclampsia Multiple pregnancy Threatened miscarriage Hypertension Multiparity Past C-section Smoking Non-vertex presentation Cocaine/amphetamines Thrombophilia Intrauterine infections Polyhydramnios Trauma - RTA, domestic violence, iatrogenic
Presentation of placental abruption
Vaginal bleeding Continuous abdominal pain Uterine contractions Shock Foetal distress
CLINICAL DIAGNOSIS
- Tense, tender uterus with woody feel
- Foetal hypoxia with HR abnormality on CTG
- Low platelet count
- Large level of compensation
Management of placental abruption
Mothers life takes priority ABCD Crossmatch 4 units Kleihauer test for anti-D Left lateral position
Delivery -
If foetus alive, C-section or artificial rupture of amniotic membranes
If foetus dead - vaginal delivery
Determining gestational age
Physical exam/US
History - LMP
Naegele’s rule - EDD = -3months + 7 days from LMP
Uterine size - 6-8weeks = small pear, 8-10 weeks = orange, 10-12weeks = grapefruit
16 weeks = midway pubic symphysis and umbilicus
20 weeks = umbilicus
US
- gestational sac diameter (until embryo visible)
- Crown rump length
- After 10 weeks - biparietal diameter and head circumference
Foetal biometry
- Biparietal diameter
- Head circumference
- Femur length
- Abdominal circumference
Symptoms of pregnancy
Amenorrhoea Nausea and vomiting Breast enlargement and tenderness Increased urinary frequency Fatigue
Uterine cramping Abdominal bloating Constipation heartburn SOB Mood changes Food cravings/aversions
Diagnosis of pregnancy
hCG
- first secreted 6-8 days post ovulation
- doubles every 30-50 hours during the first 30 days
- slower rise in abnormal pregnancy
- urine requires high levels to detect
US
- gestational sac at 4-5 weeks
- yolk sac from 5 weeks to 10 weeks
- foetal pole and cardiac activity 5-6 weeks
Reasons for pregnancy false positives
operator error (home kits)
pregnancy loss soon after implantation
interference from hCG from infertility treatment
hCG from tumour
Pituitary hCG secretion in perimenopausal women
Describe pre-eclampsia
Pregnancy induced hypertension in association with proteinuria +/- oedema
Characterised by
- Maternal hypertension
- Proteinuria
- Oedema
- Foetal IUGR
- premature birth
Severe SBP > 160, diastolic >110
Foetus may have neurological damage post-hypoxia
Epidemiology and RF for pre-eclampsia
2nd leading cause of direct maternal death
- 5 per 1000
- Death rate 0.4 per 100,000
- 20% stillbirths without congenital abnormality is caused by pre-eclampsia
- 50% with severe will deliver by 36 weeks
RFs HIGH - past pre-eclampsia, eclampsia, hypertension in a previous pregnancy - pre-existing hypertension - Pre-existing CKD - Pre-existing diabetes - SLE or APLS
MODERATE
- 10+ years since last pregnancy
- first pregnancy
- aged over 40
- BMI>35
- FHx of pre-eclampsia
- multiple pregnancy
Pathophysiology of pre-eclampsia
Suboptimal uteroplacental perfusion associated with maternal inflammatory response and maternal vascular endothelial dysfunction
Phase 1 - Abnormal placentation
NORMAL
- During 6-18 weeks placentation occurs
- Alterations in spiral arteries occur to increase blood supply
- Trophoblasts invade spiral arteries to 5x diameter
- Coverts low flow, high pressure to low resistance, high flow
PRE-ECLAMPSIA
- inadequate trophoblast invasion, inadequate placental perfusion
- Causes IUGR and pre-eclampsia
Phase 2 - endothelial dysfunction
- Platelet adhesion and thrombosis
- Exaggerated maternal systemic inflammatory response
- Decreased organ perfusion - HELLP
Presentation of pre-eclampsia
Systolic BP>140, diastolic >90 in 2nd half of pregnancy with >1+ of proteinuria
- New hypertension
- New proteinuria
SEVERE
- Severe frontal headache
- Sudden swelling (oedema)
- Liver tenderness
- Visual disturbance
- Epigastric pain
- Vomiting
- Low platelet count
- Raised ALT and AST
- Clonus
- HELLP syndrome
- Papilloedema
- Foetal distress
Monitoring of pre-eclampsia
If patient has any risk factors - increasing frequency of BP and urine measurements
Admit if they have:
- BP>140/90, >1+ proteinuria
- Systolic BP >160
- Diastolic >100
- Any symptoms or signs
Investigations of pre-eclampsia
- Urinanalysis - microscopy, culture
- Frequent monitoring of FBC, LFTs, renal function, electrolytes & urate
- Look for HELLP syndrome
- Clotting if severe or thrombocytopaenia
- 24 hour urine for protein and creatinine
- Assessment of foetus - US and amniotic fluid
HELLP
Haemolysis
Elevated Liver enzymes
Low Platelets
Management of pre-eclampsia
Conservatively until at least 34 weeks where possible (no HELLP)
Delivery of the placenta is the ONLY cure
SEVERE
- Antihypertensives (labetolol) if BP>160/110
Can also use nifedipine or hydralazine
- Magnesium sulphate to prevent seizures
- Fluid restruction - to minimise fluid overload which can result in pulmonary oedema
- Delivery
- If under 34 weeks, give corticosteroids
- Method of delivery depends on presentation of foetus, foetal condition and chance of success
- IM syntocinon to prevent haemorrhage
- Prophylaxis against VTE
Management of eclampsia
Resuscitation Magnesium sulphate as anticonvulsant Intubation may be required if repeated seizures IV labetalol or hydralazine Continuous foetal monitoring Monitor fluid intake, and urine output Attempts to prolong pregnancy not of use
- it is unsafe to deliver a baby from an unstable mother
- Control seizures, reduce HTN and correct hypoxia
- c-section
Complications of pre-eclampsia
Haemolysis HELLP AKI DIC Adult respiratory distress syndrome Cerebrovascular haemorrhage
Prevention of pre-eclampsia
75mg aspirin from 12 weeks if high risk
Maternal issues associated with substance misuse in pregnancy
Low nutrition Risk of anaemia Oral hygiene issues Infection from needles Increased risk of mental health problems Increased obstetric complications Increased premature delivery
Foetal issues associated with substance misuse in pregnancy
IUGR Pre-term delivery Increase perinatal mortality Increased miscarriage Increased placental abruption
Management of opioid addiction in pregnancy
Maintenance with methadone to stop/minimise illicit use
Detox in first trimester has high miscarriage risk
Can detox in 2nd or 3rd trimester, small frequent reductions
Withdrawal will increase foetal distress and still birth
Management of a cocaine use in pregnancy
STOP - no safe prescribed alternative
Risks of cocaine in pregnancy
Increased miscarriage, still birth
PROM
Placental abruption
Preterm labour
For baby
- stroke
- poor growth
- deformed limbs
- feedbing problems
- brain damage
- SIDS
NO BREAST FEEDING
Risks of opiates in pregnancy
Increased pre term delivery
Still born
IUGR
Increased neonatal death
Neonatal withdrawal syndrome - high pitch cry, poor feeding, tremors, irritability, D&V, sweating, seizures
Heroin = NO BREAST FEEDING Opiates = OK to breastfeed
Induction of labour
60-80% success rate
Starting labour by uterine stimulation. Approximately 20% of births.
Offer to women in healthy pregnancy over 41 weeks to decrease risk of still birth
Offer to diabetic women before term
Offer if PROM after 37 weeks
- Membrane sweep
- Prostaglandin gel or pessary (PV)
- Oxytocin +/- artificial rupture of membranes
Monitor with CTG for myometrial over-reaction
Contraindications for induction of labour
Severe placenta praevia Transverse foetal lie Severe cephalopelvic disproportion Cervix <4 on Bishop's score Active primary genital herpes infection High and floating foetal head (risk of prolapsed cord)
Complications of induction of labour
Uterine Hyperstimulation - foetal distress, hypoxic damage
Uterine rupture
Intrauterine infection with prolonged membrane rupture
Prolapsed cord if presenting part not engaged
Amniotic fluid embolization
Atonic PPH
Prevention for instrumental delivery
Presence of supporting person with the woman at all times
Mother labouring in upright or left lateral position
Avoidance of epidurals
What is Bishop’s system?
Score for ripeness of cervix
>8 = successful delivery
Classification of forceps deliveries
OUTLET - foetal scalp visible, labia separated
Foetal skull has reached pelvic floor
Rotation required > 45 degrees
LOW - leading point (not caput) is at +2, rotation required
MIDCAVITY - head 1/5 palpable per abdomen, leading point >2+ but not above ischial spines
HIGH = not recommeded
Indications for instrumental delivery
Presumed or diagnosed foetal compromise
Protect head during breech delivery
MATERNAL Avoid Valsalva manourvre Hypertensive crisis CV disease Myasthenia gravis Spinal cord injury
Inadequate progress
- Active stage > 2 hours in nulliparous, >1 hour in multiparous
- Maternal fatigue
Contraindications for instrumental delivery
Predisposition to fractures in foetus
Bleeding tendency or active bleeding in foetus
Face presentation
Vacuum extractor should not be used under 34 weeks
Requirements for an instrumental delivery
Fully dilated cervix Occipital-anterior position Ruptured membranes Cephalic presentation Engaged presenting part Pain relief adequate Sphincter (bladder) empty
Mediolateral episiotomy before instrumental delivery to reduce tears
If unsuccessful with 3 pulls - c-section
Indications for episiotomy
Rigid perineum preventing delivery Large tear imminent Instrumetnal delivery Shoulder dystocia Vaginal breech delivery
What is an episiotomy
Right mediolateral incision with local anaesthetic
Degrees of tears
1st - injury to vaginal epithelium and vulval skin only
2nd - injury to perineal muscles but not anal sphincter
3rd - injury to perineum, involving anal sphincter
4th - injury to perineum, anal sphincter complex and anal or rectal mucosa
Indications for induction of labour
uteroplacental insufficiency prolonged pregnancy > 41 weeks IUGR Oligo or anhydramnios Abnormal uterine or umbilical artery Doppler Non-reassuring CTG PROM Severe pre-eclampsia, eclampsia Intrauterine death of foetus APH Chorioamnitis
Severe hypertension
Uncontrolled diabetes
Deteriorating renal function
Malignancy
Methods for induction of labour
Cervical ripening
- Separation of membranes from the cervix - stretch and sweep
Amniotomy
- Artificial rupture of membranes
Prostaglandins - DINOPROSTONE
- Intravaginally as tablets or gel
- VE after 6 hours
- CTG before and after
- Only 2 doses as risk of Hyperstimulation
Oxytocin infusion
- best after rupture of membranes
- wait 6 hours after prostaglandins
- continuous CTG and want 3-4 contractions in 10 minutes
First stage of labour
Begins with regular contractions when the foetal presenting part has reached true pelvis
End when the cervix is fully dilated (10 cm)
Latent phase
- 2-24 hours
- Cotnractions not painful, 5-10 minute intervals
- Cervix dilating slowily
ACTIVE PHASE
- Primi - 12-14 hours, multi 6-10 hours
- Start when cervix 3-4 cm dilated
- Rapid dilation 0.5-1cm per hour
- Foetal head descends into maternal pelvis and foetal neck flexes
Management of first stage of labour
Hourly temp and HR
4 hourly BP
30 minute monitoring frequency of contractions
Foetal HR auscultated for 1 minute immediately after a contraction every 15 minutes
Should be 100-160
VE every 4 hours
Discuss need for pain relief
Second stage of labour
Starts when cervix is fully dilated
Ends with birth of baby
Contractions are stronger, 2-5 minute intervals lasting 60-90 seconds
Primigravida 60 minutes, multi 30 minutes
Feotal head descends and rotates anteriorly
Wants to push
After head through, shoulders rotate to allow shoulders through
Midwife/doctor present throughout
Monitor contractions, and foetal HR ever 5 minutes
Push during contractions, relax between
If >2 hours nulliparous or > 1 hour multiparous then consider instrumental delivery or c-section
Third stage of labour
Starts with birth of baby
Ends with delivery of placenta and membranes
Separation of placenta occurs immediately after birth
20-30 minutes or 5-15 with active management
Haemorrhaging prevented by contraction of uterine muscle fibres
Separation noted by gush of blood, prominence of fundus in abdomen and lengthening of umbilical cord
Management of 3rd stage of labour
Expectant - uterus rubbed up to produce contraction, uterus pushed to vagina to aid expulsion
Active - IM oxytocin after birth
Controlled traction of umbilical cord to aid expulsion
Examine placenta and membranes for completeness
Braxton Hicks contraction
Mild
Irregular
Non-progressive
can occur from 30 weeks, more common after 36 weeks
Poor progress in 1st stage of labour
- Criteria
- Causes
Criteria
<2cm progression in 4 hours
- Slowing in progress in parous woman
Insufficient uterine activity (power) Malpositions, malpresentation, large baby (passenger) Inadequate pelvis (passage)
Management of poor progress in 1st stage of labour
Amniotomy and reassess in 2 hours
Amniotomy + oxytocin infusion
C-section if foetal distress
Benefits of active management of 3rd stage of labour
Decreased PPH Decreased length of time in 3rd stage Decrease blood loss Decreased post-natal anaemia Decreased transfusions
Definition of premature labour
Contractions of sufficient strength and frequency to effect progressive effacement and dilation of cervix before 37 weeks
Very premature is before 32 weeks
Risk factors for premature labour
Multiple pregnancy Genital tract infection P-PROM Antepartum haemorrhage Cervical incompetence Congenital uterine abnormality APLS Diabetes Past pre-term delivery
30% are unexplained and spontaneous
Investigations for pre-term labour
If under 30 weeks with in tact membranes, no investigations
If over 30 weeks
- TV US to estimate cervical length
- Foetal fibronectin: if less than 50 then unlikely to be pre-term labour
No VE if ruptured membranes unless confirmed labour
Vaginal swabs
Management of pre-term labour
Tocolytic drugs - not if P-PROM
- Nifedipine
- Can delay delivery for up to 7 days
Corticosteroids if between 24 and 36 weeks
Magnesium sulphate to reduce risk of CP
Emergency cervical cerclage if between 16 and 34 weeks with dilated cervix and exposed unruptured membranes
Delivery vaginally if cephalic
Breech under 32 weeks = C-section
Most over 30 weeks survive without lasting abnormality
Non-pharmacological methods of pain relief in labour
Maternal support
Environment - light diet, keep mobile, soothing music, comfortable position
Birthing pool - not within 2 hours of opioids due to drowsiness
Drugs used as analgesia in labour
Entonox
- Inhaled
- Patient controlled, works in seconds, wears off quickly, minimal side effects
IM opiate
- SE nausea, vomiting, drowsiness
- Pethidine
- Short term respiratory depression and drowsiness
- Drowsy neonate
Epidural
- Central nerve block with local anaesthetic
- Most effective, avoids further analgesia for instrumental delivery.
- Increases length of 2nd stage, rate of operative delivery
- Can cause transient hypotension, dizziness
- Severe headache if dural tap
- need CTG
Local anaesthesia
- if tear, episiotomy or instrumental delivery
Differences between epidural and spinal
Epidural
- extradural catheter placement
- cannula allows top up
- patchy analgesia
Spinal
- subarachnoid injection
- 1 off injection, can last 2-4 hours
- dense, reliable block
Causes of cerebral palsy
Unknown Complication of prematurity Peripartum asphyxia Postnatal (encephalitis, accidents) Perinatal infection (CMV, rubella) Multiple pregnancy Chromosomal abnormality
Types of multiple pregnancy
Dizygotic - non identical twins
- Foetus has it’s own placenta, own amnion and chorion
Monozygotic
Depends on when the embryo splits
- 3 days: 2 chorion, 2 amnion
- 4-7 days, 1 placenta, 1 chorion, 2 amnion
- 8-12 days: 1 placenta, 1 chorion, 1 amnion
- 13 days - conjoined twins
Risk factors for multiple pregnancy
RFs at only for dizygotic twins - monozygotic has no RFs
- Past multiple pregnancy FHx on maternal side Increased maternal age West African Assisted conception
Antenatal care in multiple pregnancy
Refer to obstetrics
US as normal at 11-13 wees and 18-20 for abnormality
Monitor carefully for IUGR and feto-feto transfusion syndrome
Scan
Dichorionic - 20, 24, 28, 32 and 26 weeks
Monochorionic - 18, 20, 22, 24, 26, 28, 30, 32 and 34 weeks
Inform
- increased risk of Down’s and increased risk of false positive on screening
- Twins use combined test
- Triplets use nuchal translucency
Take 75mg aspirin OD from 12 weeks if 1st pregnancy, over 40, pregnancy interval over 10 years, BMI > 35or FHx of pre-eclapmsia
Delivery of multiple pregnancy
Offer elective birth at 36 weeks (mono-chorionic) after course of steroids
Dichorionic - 37 weeks
Triplets - 35 weeks
If 1st twin is cephalic presentation then trial vaginal delivery, if breech or transverse then C-section
- May need IV oxytocin after first child as contractions can decrease
- 2nd should be born within 45 minutes
Maternal complications of multiple prengnacy
Increased miscarriage anaemia pre-eclampsia APH PPH C-section symptoms of pregnancy Polyhydramnios Hyperemesis gravidarum Post natal illness death
Foetal complications of multiple prengancy
Increased Still birth pre-term birth neonatal mortality morbidity FFTS Umbilical entanglement IUGR congenital abnormality
Physiological changes in prengnacy
Increased blood volume Decreased Hct (due to dilution) - anaemia of pregnancy is physiological Increased RBC Increased stroke volume, cardiac output Decreased peripheral vascular resistance BP stable or decreased
Increased tidal volume
Decreased functional residual capacity from gravid uterus
Decreased total lung capacity
Increased clotting
Increased renal function
increased uterine blood flow
Increased uterine weight
No autoregularion of uterine blood flow - hypotension can cause foetal distress
Why is left lateral an important position in pregnancy
Otherwise can have overt caval compression- IVC compression
- Hypotension
- Sweating
- Bradycardia
- Pallor
- Nausea and vomiting
Spinal anaesthesia
L3/L4
Pierce the ligamentum flavum before dura
Use heavy LA to prevent upwards movement
Uterus supply at T10 - block up to nipple line (T4)
Phenyepherine - alpha blocker to counteract hypotension
Inject bupropripcaine
- 20x safer than GA
GA in prengancy
Avoid at all costs Need to neutralise stomach acid with ranitidine and metoclopramide No strong opioids prior to delivery Difficult airway Give +++ oxygen before anaesthesia
Only if spinal or epidural contraindicated e.g. raised ICP, coagulopathy, patient refusal or infection
Reasons for CTG
MATERNAL Past C-section cardiac problems pre-eclampsia prolonged pregnancy >42 weeks PROM induction of labour Diabetes APH
FOETAL IUGR prematurity oligohydramnios abnormal Doppler multiple pregnancy meconium stained liquor breech position
INTRAPARTUM oxytocin augmentation epidural anaesthesia intrapartum PV bleed pyrexia > 37.5 fresh meconium bleeding abnormal foetal HR prolonged labour
Normal baseline foetal HR
110-160
Bradycardia <110
Tachycardia > 160
Normal baseline variability on CTG
Normal 5-25bpm
Reduced 0-5
Saltatory >25
Define acceleration and deceleration on CTG
Transient rise in FHR > 15 bpm for >15 seconds
Transient decrease as above
Early decelerations - peaks co-incides with contraction and is due to head compression - 2nd stage of labour
Late decelerations - acidosis, if shallow with decrease baseline variability very concerning
Maternal factors that can cause abnormal CTG
Position - not left lateral Hypotension VE Emptying bladder or bowels Vomiting Vasovagal episodes Topping up anaesthesia
Foetal blood sampling
Taken from scalp via needle and speculum
Obtain if pathological CTG
Woman in L lateral
Normal ph>7.25 then repeat in 1 hour if CTG still abnormal
Borderline 7.21-7.24, repeat in 30 mins
Abnormal <7.20 IMMEDIATE DELIVERY
RF for pre term premature rupture of membranes P-PROM
Smoking
Previous pre-term delivery
Vaginal bleeding
Lower genital tract infection
Investigations for PROM
No VE Visualise amniotic fluid draining through cervix Sterile speculum exam US to determine liquor volume 12 hourly temperatures Foetal monitoring
Management of PROM
Refer to hospital, admit for first 48 hours
Prophylactic antibiotics
Antenatal steroids if between 24 and 35 weeks
Consider delivery post-34 weeks
Complications of PROM
prematurity Sepsis Pulmonary hypoplasia Umbilical cord prolapse Placental abruption Oligohydramnios Increased retained placenta and PPH
Epidemiology and RF for post-natal depression
As common as depression
Most common in first few weeks post-natally
10-15%
MAJOR RF Previous history of MH problems Psychological disturbance in pregnancy Poor social support Poor relationship with partner Baby blues Recent major life events
Other RF Unplanned pregnancy Not breast feeding Unemployment Antenatal parental stress Depression in father 2+ children Neonatal illness/death/SIDS Substance misuse Low family outcome History of abuse
Presentation of post-natal depression
Low mood Anhedonia Anxiety Disturbed sleep Decreased appetite Poor concentration Decreased self-esteem Decreased energy Decreased libido Suicidal thoughts
Assessment of post-natal depression
Questions to be asked in history
Hx or FHx or MH problem Physical wellbeing Alcohol and drug misuse Mother-baby relationship Relationships, social networks, isolation Domestic violence, abuse, sexual abuse, trauma Housing Employment Economic and migration status
Management of post-natal depression
Mild-moderate = consider self-help strategies
Mild + history of severe depression = consider antidepressant
Moderate-severe = CBT, antidepressants or combination
Psychological therapies are first line
Women can breastfeed unless taking = lithium, sodium valproate, carbamazepine, clozapine
Higher threshold for pharmacological therapy due to risk
Complications in post natal depression
Adverse effects in the children
Poorer cognitive, emotional, social and behavioural development
Post-partum psychosis 1/1000
- first few weeks
- psychiatric emergency
- paranoia, delusions, hallucinations, loss of inhibition
Most resolves in 3-6 months
Course of illness widely variable
Incidence and factors that increase breast feeding
81% of mothers, increasing
1/3 are still breast feeding at 6 months
Only 1% are exclusive breast feeding at 6 months
More likely to breast feed if…
- From ethnic minority group (Chinese, black)
- managerial and professional occupation
- aged over 30
- Live in England (vs. rest of GB)
- First time mother
- Left full time education over 18
Advantages of breast feeding
Free No preparation Immunity Infection protection (decreased LRTI, otitis media, gastroenteritis) May protect against asthma and eczema Decrease SIDS Protection from future Type 2 diabetes (in mother and child) Decrease breast and ovarian cancer Contraception - lactational amenorrhoea
Disadvantages of breast feeding
issues with feeding in public
low in vitamin D (may need supplements)
transmission of HIV and hep C
Can transmit maternal infection - N. gonorrhoea, H. influenza, group B strep, staph
cracked/sore nipples
blocked ducts and breast engorgement
mastitis
thrush
Causes of cracked and sore nipples (breast feeding)
Nipple soreness is very common in the first few weeks
Caused by
- improper positioning of baby - alter
- improper feeding technique - incomplete suction release
- improper nipple care - excessively dry or moist
Blocked ducts and breast engorgement (breast feeding)
caused by poor drainage of the breast
swollen, hard, painful, redness
nipples can protrude to allow baby to latch
causes by pressure on breast and prolonged gaps between feeds
nurse 8+ times in 24 hours for 15+ minutes
can develop in mastitis if persists
Mastitis (breast feeding)
occurs in 20%
Increased if: nipple damage, over supply of milk, S.aureus
Engorgement can lead to mastitis which can lead to abscess
Treat with flucloxacillin
Advice for breast feeding mothers
Should begin within an hour of birth
It should be on demand - when baby wants it
Avoid pacifiers or bottles
Baby head and body in line
Hold baby close
Place baby nipple to nose - baby will tip head back
Milk released by oxytocin
Define neonatal abstinence syndrome
Infant born to mother addicted to opioids at the risk of withdrawal.
- Heroin
- Methadone
Presentation of neonatal abstinence syndrome
CNS
- tremors
- irritability
- increased wakefulness
- high pitched cry
- hypertonicity
- hyperactive reflexes
- seziurs
- yawning, sneezing
GI TRACT
- poor feeding
- uncoordinated, constant sucking
- vomiting
- regurgitation
- loose, watery stools
- dehydration
AUTONOMIC
- increased sweating
- nasal stuffiness
- fever
- temperature instability
- tachypnoea
- mottling of skin
Starts within 24 hours if heroin or 24-72 days if methadone
Management of neonatal abstinence syndrome
Decrease sensory stimulation
Small frequent feeding
Increased calorie dense formula
MONITOR
Pharmacology if seizures, poor feeding, fever, significant D&V
Opioid therapy - morphine/methadone/buprenorphine
Adjunct therapy if multiple drug exposure = phenobarbital
Information required for post-partum contraception advice
Normally discussed at 6 week GP check
Contraceptive needs Future child plans Any periods Breastfeeding Any medical conditions
Contraception for non-breast feeding mother under 21 days post partum
Barrier methods
POP
Progesterone only injectable and implants
Contraception for non-breast feeding mother over 21 days post partum
COCP
Barrier methods
POP
Progesterone only injectable and implant
IUS over 6 weeks
Contraception for breast feeding mother under 6 weeks post partum
Lactational amenorrhoea methods
POP
Progesterone only implants
Barrier methods
Contraception for breast feeding mother over 6 weeks post partum
LAM POP Progesterone injectable and implant IUS - from 6 weeks IUD Barrier methods Sterilisation
No COCP until after 6 months
Criteria for lactational amenorrhoea methods
Under 6 months post partum
Amennorhoeic
Full daily breast feeding
Define 3rd stage of labour
From the time of birth to expulsion of placenta
Define prolonged 3rd stage of labour
Prolonged if not completed in:
30 minutes - active
60 minutes - physiological
Describe management of 3rd stage of labour
Active management
- routine use of uterogenic drugs - oxytocin IM with birth of anterior shoulder
- deferred clamping and cutting of cord (between 1 minutes to 5 minutes)
- controlled cord traction
Physiological
- delivery of placenta by maternal effort
Care of newborn immediately post-partum
Apgar score at 1 minute and 5 minutes
Record time from birth to regular respirations
Skin to skin contact
Avoid separation of mother and baby for 1 hours
Encourage breast feeding within 1st hour
Record head circumference, body temp and weight
Care of mother immediately post-partum
Assess uterine contraction and lochia Examine placenta and membranes Assess emotional and physical condition Successful voiding of bladder Assess for genital trauma If genital trauma then rectal exam If required perineal repair
Define post-partum haemorrhage
Excessive bleeding post-delivery
Primary - loss of blood >500ml within 24 hours of delivery
MINOR - 500-1000ml
MAJOR - over 1000ml
Secondary - abnormal bleeding between 24 hours and 6 weeks
Aetiology of PPH
Tone - uterine atony (most common), distended bladder
Trauma - lacerations of uterus, cervix or vagina
Tissue - retained placenta, clots
Thrombin - pre-existing or acquired coagulopathy
Epidemiology and RF for PPH
5-10%
Severe less than 1%
Increased in Asians
Increased in over 40s
Antenatal RF
- APH
- Placenta praevia (x12)
- Placental abruption
- Multiple pregnancy (x5)
- Uterine over-distension (polyhydramnios, macrosomia)
- pre-eclampsia
- multi parity > 4
- previous PPH or retained placenta
- increased if BMI > 35
Delivery RFs
- emergency section (x4)
- elective seciont (x2)
- Retained placenta (x5)
- episiotomy (x5)
- induction of labour
- instrumented delivery
- labour > 12 hours
- Baby > 4kg
- Maternal pyrexia in labour
Clotting disorders
Management of PPH
Resusciattion
- Minor = 14G cannula and crystalloid infusion
- Major = ABCs, high flow O2, 2x14G cannula, transfuse bloods ASAP and Hartmanns until blood available
Monitor and investigate
- Minor = blood group, coag screen
- Major = FBC, coag, U&E, LFTs, crossmatch 4 units. Consider arterial line and ITU transfer, MEOWS charts
Stop bleeding
- If uterine atony:
- bimanual uterine compression
- empty bladder
- oxytocin infusion
- ergometrine
- carboprost or misoprostol
- balloon tamponade
- haemostatic brace suturing
- bilateral ligation of uterine or internal iliac arteries
- selective arterial embolization
Hysterectomy - should be a 2 consultant decision
Complications from primary PPH
Hypovolaemic shock DIC AKI Liver failure Acute respiratory distress syndrome Death in 1 in 100,000 deliveries
Aetiology of secondary PPH
Infection - endometritis
Retained products of conception
RF for secondary PPH
1-3% of vaginal deliveries
C-section prolonged rupture of membranes severe meconium staining in liquor long labour with multiple examinations manual removal of placenta extremes of maternal age decreased socio economic status maternal anaemia prolonged surgery
symptoms of secondary PPH
fever abdominal pain offensive smelling lochia abnormal vaginal bleeding abnormal vaginal discharge dyspareunia dysuria malaise
signs of secondary PPH
fever rigors tachycardia tenderness of suprapubic area and adnexa elevated boggy uterus if retained products of conception
Investigations for secondary PPH
FBC Blood cultures MSU High vaginal swab - gonorrhoea, chlamydia US if ?RPOC
Management of secondary PPH
Urgent referral if any red flags (sepsis)
- pyrexia >38
- sustained tachycardia»_space;90
- RR >20
- abdominal and chest pain
- D+V
- uterine or renal angle pain
- IV antibiotics (for endometriits) - piperacilin/taxobactam (tazocin)
Epidemiology of cervical cancer
Increased in developing countries 30% detected through screening 13th most common cancer in females 1 per 10,000 Peak age 25-29
RF
- HPV 16 and 18
- Heterosexual
- multiple sexual partner
- Smoking
- Lower social class
- Immunosuppression
- COCP
Pathogenesis of cervical cancer
70% squamous carcinoma
15% adenocarcinoma
15% mixed
CIN
- CIN1 - disease confined to lower 1/3 epithelium
- CIN2 - confined to lower and middle 1/3 of epithelium
- CIN3 - full thickness of epithelium
Symptoms of cervical cancer
Abnormal vaginal bleeding vaginal discharge bleeding - post coital, on micturition or defaecation Vaginal discomfort Urinary symptoms
Late symptoms
- painless haematuria
- chronic urinary frequency
- painless fresh rectal bleeding
- altered bowel habit
- leg oedema, pain, hydronephrosis
If any suspicion refer on 2 week wait, do not do a smear
Signs of cervical cancer
White patches on cervix Abnormal cervical appearance - erosion, ulcer, tumour Mass on rectal exam Pelvic bulkiness or mass peripheral oedema Hepatic/pulmonary mets
Investigations for cervical cancer
Pre-menopausal - STI screen
Post-menopausal - urgent gynae referral
Colposcopy - cleaned with acetic acid - Insepction +/- biopsy +/- treatment Cone biopsy FBC, U&Es, LFTs
Staging of cervical cancer
FIGO staging Based on tumour size Vaginal or parametrial involvement Bladder or rectum involvement Mets
Most are diagnosed in early stages
Management of cervical cancer
Surgery, radiotherapy, chemotherapy or combination
Fertility sparing treatment may be important
If pregnant may delay for a few weeks or abort
Surgery
- If fertility sparing, removal with margins
- Or hysterectomy
- Radical: Wertheim’s hysterectomy: tumour + main lymph nodes + upper 1/3 vagina
Radiotherapy
- external beam or internal brachytherapy
Chemo - cisplatin
Prognosis of cervical cancer
1 = 90% survival at 5 years 2 = 60-90% 3 = 30-50% 4 = <20%
Prevention of cervical cancer
HPV vaccine 16 and 18
or 16, 8, 6 and 11 (includes for warts)
- Given in females aged 11 to 13
2 doses
Screening for cervical cancer
From 25
Every 3 years until 50
After 50 every 5 years until 65
Pathophysiology of endometrial cancer
Mainly adenocarcinoma from lining of uterus
OESTROGEN DEPENDENT
Epidemiology of endometrial cancer
90% are over 50
Increased with age
Most common in Western societies
3% of total cancer cases
RF
- prolonged periods of unopposed oestrogen
- Nulliparous
- Post menopausal
- Obesity
- Endometrial hyperplasia
- PCOS
- HNPCC
- Diabetes
- Tamoxifen
Presentation of endometrial cancer
POST MENOPAUSAL BLEEDING IS endometrial cancer unless proven otherwise
Investigations for endometrial cancer
TV US
- 3mm cut off for endometrial cancer
Endometrial biopsy
- pipelle
- done as outpatient and offers definitive diagnosis
- hysteroscopy and biopsy
Management of endometrial cancer
TAH and BSO for all
If stage 2 - TAHBSO and systematic pelvic node clearance
If stage 3/4 - debulking surgery
- surgery/radio/chemotherapy
Types of ovarian cancer
Epithelial (85-90%)
- In over 50s
- Serous is most common subtype (40-60 years)
- Endometroid
- Clear cell tumour
- Mucinous tumour
Germ cell (2-10%)
- derived from germ cells of embryonic gonad
- <35
- Curable
- Rapid enlarging, bloating, pain, rupture, torsion
- Dysgerminoma, endodermal sinus tumours, teratoma, embryonal carcinoma, choriocarcinoma
Sex cord stromal tumour (<5%)
- derived from connective tissue cells
Borderline (10-15%)
- Not benign or malignant
- Do not respond well to chemotherapy
Epidemiology of ovarian cancer
2% lifetime risk
17 per 100,000
Peaks in 70-80s
RF
- Increasing age
- Smoking
- Obesity
- Decreased exercise
- Talcum powder use pre 1975 (asbestos)
- Hx of infertility or treatment
- Nulliparous
- FHx
- BRCA1 or 2
- Endometriosis
- HRT
Protective factors - COCP, child bearing, breastfeeding, early menopause
Presentation of ovarian cancer
58% present with stage 3 or 4 Insidious onset - Abdominal discomfort Distension Bloating Urinary frequency Dyspepsia Pelvic or abdominal mass associated with pain Abnormal uterine bleeding Ascites Pleural effusion
Investigations for ovarian cancer
Refer with any mass or ascites
Test over 50s if symptomatic with multiple attendances
Test over 50s with new IBS
CA125
If raised then US and refer
CT pelvis and abdo for staging
If aged under 40, alpha fetoprotein (endodermal sinus tumours)
- beta hCG for dysgerminomas, embryonal carcinoma, choriocarcinoma
Biopsy prior to chemotherapy
Staging of ovarian cancer
1 limited to ovaries
2 one or both ovaries with pelvic extension
3 microscopically confirmed peritoneal deposits outside pelvic
4 distant mets
Management of ovarian cancer
Explorative laparotomy for staging and tumour debulking
TAH and BSO
Conservative if fertility sparing
Chemo post surgery
- Paclitaxel and carboplatin
Relapses are treated with chemotherapy
CA125 useful for monitoring
Complications of ovarian cancer
Torsion Rupture Infection Malnutrition Electrolyte imbalance Bowel obstruction Ascites Pleural effusion
10 year survival 35%
Better outcome if under 40
Define metorrhagia
Irregular and frequent periods
Aetiology of post-coital bleeding
Infection Cervical ectropion Cervical or endometrial polyps Vaginal cancer Cervical cancer Trauma
No specific cause is found in 50%
Aetiology of intermenstrual bleeding
Pregnancy related - ectopic, GTD Physiological - 1-2% spot around ovulation Vaginal - adenosis, vaginitis, tumour STI Cervical cancer Cervical/endometrial polyps Ectropion Fibroids Endometrial cancer Adenomyosis Enodmetritis Oestrogen secreting ovarian cancers
Tamoxifen
Missed oral contraceptive
Drugs altering clotting - anticoagulants, SSRIs, steroids
Dysfunctional uterine bleeding
History features for vaginal bleeding
LMP Usual cycle length and regularity Duration of abnormal bleeding Menorrhagia? Associated symptoms - abdo pain, fever, vaginal discharge, dyspareunia, aggravating factors
Previous pregnancies and deliveries
Risk of current pregnancy
RF for ectopic - PID, IVF, IUCD, POCP
Current contraception
Smear history
Past gynae investigations or surgery
Sexual history - STIs
Medical history - diabetes, bleeding disorders
Current medications
Cervical ectropion
red ring around external os due to extension of endocervical columnar epithelium over ectocervix
More common in young people on COCP
Cervicitis
red, congested oedematous cervix
May have purulent discharge with tender cervix on palpation
Chlamydia or gonorrhoea
Strawberry cervix
Trichomonas vaginalis infection
Cervix is friable
Prominent papillae
Punctate haemorrhages
When to refer a woman with PV bleeding
Women with abnormal looking cervix
Suspicious looking cervical polyp
Pelvic mass
High risk of endometrial cancer (Fhx, prolonged or irregular cycles, on tamoxifen
Over 45 + IMB
Under 45 with persistent symptoms or RFs for endometrial cancer
Investigations for PV bleeding
Always exclude pregnancy Exclude STI Smears only if due FBC, clotting, TFT, FSH/LH TV US is investigation of choice (best to do immediately post-menstrually as thinnest and cysts and polyps most obvious) Endometrial biopsy using Pipelle Colposcopy
Define polymenorrhoea
Bleeding at intervals <21 days
Dysfunctional uterine bleeding
Abnormal uterine bleeding without any structural or systemic pathology
Usually menorrhagia
Diagnosis of exclusion
Aetiology of menorrhagia
40-60% have no pathology 20% anovulatory cycles Fibroids Endometrial polyps Endometriosis Adenomyosis PID Endometritis Endometrial hyperplasia/carcinoma Systemic disease - hypothyroid, liver or kidney disease, obesity, bleeding disorder IUCD Anticoagulants
Investigations for menorrhagia
FBC Haemotinics (iron deficiency) TFTs Assessment of bleeding disorders US to assess underlying pathology
Management of menorrhagia
Pharmacological
- Mirena IUS
- Tranexamic acid, NSAIDs (mefamic acid), COCP
- Progestogens - POP or depot
- 3-4 months of gonadotrophin releasing hormone (GnRH)
- Hysterectomy/myomectomy
Surgical
- Endometrial ablation if not enlarged utuerus (not if large fibroids)
- Radiofrequency/microwave etc.
- Uterine artery embolization (if wish to keep uterus)
- Hysteroscopic myomectomy
- Hysterectomy
Complications of endometrial ablation
Vaginal discharge Increased period pain Need for additional surgery Infection Perforation
Fibroid
Bengin monoclonal tumours of smooth muscle cells of uterine myometrium with disordered collagen
Growth is stimulated by oestrogens and progesterone
Classification of fibroids
Intramural (most )
Submucosal (growing into uterine cavity)
Subserosal - growing outwards from uterus
Epidemiology of fibroids
77% of women
Increased in Africans
30-40 years old
FHx (x2.5 if first degree relative)
RF
- Obesity
- Early menarche
Protective factors: increased parity, smoking and exercise
Presentation of fibroids
50% are asymptomatic
30-50 years old
Excessive or prolonged heavy periods
IMB
Pelvic pain (especially in pregnancy due to pressure and resultant fibroid degeneration)
Constipation/ urinary symptoms from pressure
Recurrent miscarriage or infertility (only if submucosal)
Palpable mass
Enlarged irregular firm non-tender uterus
Iron deficiency anaemia
Investigations for fibroids
Pregnancy test FBC and haematinics TV US MRI if US not definitive Endometrial sampling with pipelle for other causes Hysteroscopy and biopsy
Management of fibroids
- NSAIDs to reduce blood loss
- Transexamic acid
- COCP
- Mirena coil
- GnRH agonists decrease size but will regrow when stopped
- Surgery: if pressure symptoms, increased uterine size, medical treatment insufficient or fertility affected
- Myomectomy (recurrence rate 3%)
- Hysteroscopic endometrial ablation
- Laparoscopic hysterectomy
Complications of fibroids
Iron deficiency anaemia Bladder frequency Constipation Infertility Problems in pregnancy - miscarriage, premature labour and PPH, IUGR.
Define endometriosis
Chronic oestrogen dependent condition characterised by growth of endometrial tissues in sites other than the uterine cavity
Most common sites for endometriosis
Pelvic cavity including ovaries Uterosacral ligaments Pouch of Douglas Rectosigmoid colon Bladder and distal ureter Rare sites - umbilicus, scar sites, pleura, pericardium, CNS
Define adenomyosis
Invasion of myometrium by endometrial tissue
Epidemiology of endometriosis
10-15% of women of reproductive age
Exclusive to reproductive age
Diagnosed in 30s
RFs - Infertile - Early menarche - Delayed child bearing - Long duration of menstrual flow - Obstruction to vaginal flow (hydrocolpos) - FHx (6x with first degree relative) Chromosomes 7 and 10
Protective; multiparity and use of oral contraceptives
Symptoms of endometriosis
Dysmenorrhoea (painful periods) Dyspareunia Cyclical or chronic pelvic pain Subfertility Bloating Lethargy Constipation Lower back pain
Less common: cyclical rectal bleeding menorrhagia diarrhoea haematuria
Severity of symptoms increase with age
Worsening of symptoms at the time of menstruation or just prior to it
Signs of endometriosis
Examination often normal Posterior fornix or adenexal tenderness Palpable nodules Bluish haemorrhagic nodules in posterior fornix Chocolate cysts on ovaries
Investigations for endometriosis
Lapararoscopy is gold standard
Symptoms and laparoscopic findings do not always correlate
TV US to exclude ovarian pathology
FBC, Urinalysis Cervical swabs beta hCG MRI may be useful
Management of endometriosis
Medical treatment may decrease symptoms in 80-90%
- Try suppressing ovarian function for 6 months
- COCP, danazol, oral or depot progesterone, IUS
- NSAIDs for pain
- or GnRH analogues with add back therapy
Surgery
- Laparoscopic excision or ablalation
- Endomeriomata (large cysts from endometriosis) need stripping out
- Hysterectomy as last resort
Complications of endometriosis
Increased breast and ovarian cancers
Infertility due to tubal damage
Adhesions post-op
Increased IBD
Pathophysiology of atrophic vaginitis
Decreased oestrogen
Vaginal mucosa thins, drier, decreased elasticity
Can become inflamed and lead to urinary symptoms
Changes in vaginal pH and flora can predispose to UTIs
Aetiology of atrophic vaginitis
Natural menopause or oophorectomy Anti-oestrogen treatments: tamoxifen. aromatase inhibitors Radiotherapy Chemotherapy Post partum Breastfeeding
Presentation of atrophic vaginitis
Vaginal dryness Burning/itching of vagina or vulva Dyspareuunia Vaginal discharge (white/yellow) Vaginal bleeding Post coital bleeding Urinary symptoms: frequency, nocturia, dysuria, recurrent UTI, stress incontinence
Decreased pubic hair Narrow introitus Thin mucosa Diffuse erythema Dryness Lack of vaginal folds
Investigations for atrophic vaginitis
Exclude other causes of PCB/infection/UTI
Vaginal pH testing - alkaline
Vaginal cytology - lack of maturation of vaginal epithelium
Often a clinical diagnosis
Management of atrophic vaginitis
Lubricants - short term relief
Water or silicone based
Moisturisers - regular use
Hormonal treatments:
- HRT topical
Restores pH, thickens epithelium, improves lubrication
Very effective in long term, minimal side effects
Define menopause
12 months of spontaneous amenorrhoea
Early menopause is between 40-45
Symptoms of menopause
Menstrual irregularity Hot flushes - head, face, neck, chest Sweats Urogenital symptoms - dyspareunia, vaginal discomfort, dryness, recurrent UTI, incontinence Sleep disturbance Mood changes - anxiety, nervousness, irritability Loss of libido Brittle nails, thinning skin, hair loss
Investigations for menopause
Generally clinical
Lab requirements only if under 45
Raised FSH
Check
TFTs
Blood glucose
cholesterol
Check up to date with cervical and breast screening
Define premature ovarian failure
Amennorhoea
Raised gonadatrophins
Oestrogen deficienct
Women under 40
Aetiology for ovarian failure
Decreased ovarian follicles at birth, accelerated follicle atresia or follicular dysfunction
Mutations in FSH receptor
Iatrogenic - surgery, radio or chemotherapy
X linked chromosomal abnormality - Turners
Autoimmune lymphocytic oophritis
Infections - mumps, TB, malaria, chicken pox, CMV
Investigations for premature ovarian failure
Raised FSH - on 2 occasions, 4 weeks apart
Decreased oestrodiol
TFTs and prolactin
DEXA scan
Anti-Mullerian hormone as a measure of decreased ovarian reserve
Test - adrenal antibodies, autoimmune, hypothyroid, diabetes, addison’s
Management of premature ovarian failure
Manage depression and anxiety
Lifestyle advice to decrease CV risk
Adequate vitamin D and calcium
HRT until 51 (no risks of HRT as under 50s)
Benefits of HRT
Decreased vasomotor symptoms in 4 weeks Increased quality of life Increased sleep Increased mood Decreased vaginal atrophy Decreased osteoporosis risk Decreased CV disease (doesn't increase if started under 60) Decreased colorectal risk Decreased aging
Risks of HRT
VTE PE Stroke Breast and endometrial cancer (If BMI normal) Gallbladder disease
Side effects of HRT
Breast tenderness Leg cramps Bloating Nausea Headache PMS Backache Depression Pelvic pain
Prescribing HRT
Check personal and FHx of VTE Confirm no sinister pathology No maximal duration Transdermal has fewer risks Continuous combined Erratic bleeding common for first 3-6 months
Ovarian cycles of menstruation
Follicular phase - follicles are stimulated due to rise of FSH
Ovulation - ovarian follicles mature, egg released, rise in oestrogen causes rise of LH. LH surge causes release of egg
Luteal phase - corpus luteum forms and produces progesterone which causes decrease in FSH and LH. When corpus luteum dies, decrease in progesterone which causes menstruation
Describe changes of LH and FSH in menstruation
LH remains at baseline until day 12-14 where there is very large LH surge
There is a corresponding increase in FSH during this period but much lower than LH
Describe levels of oestrogen and progesterone in menstruation
oestrogen peaks just before ovulation
progesterone is low until after ovulation at which is steadily rises before dropping just before mensturation
Pathogenesis of dysmenorrhoea
Thought to be due to excess or imbalance of prostaglandins and leukotrienes in the menstrual fluid
Causes vasoconstriction in uterine vessels
Causes uterine contractions and pain
Define dysmenorrhoea
Low anterior pelvic pain which occurs in association with menstruation
Types of dysmenorrhoea
Primary
- Occurs in young females with no pelvic pathology
- Often begins 6-12 months after menarche
- Pain begins with onset of period and lasts for 24-72 hours
Secondary
- Occurs in association of pelvic pathology
- Can precede period by several days and last for the whole period
- May be associated with dyspareunia
Aetiology of dysmenorrhoea
Endometriosis Adenomyosis PID Fibroids Adhesions Developmental abnormalities IUD
Adenomyosis
Invasion of myometrium with endometrial tissue
Causes inflammation, pain and adhesions
Chronic pelvic pain, dyspareunia and infertility
Epidemiology of dysmenorrhoea
Very common, incidence unknown
RFs
- Longer duration of periods
- Early menarche
- Smoking
- Alcohol
- Obesity
- Depression
Severity decreases with age
Incidence decreases with childbirth
Presentation of dysmenorrhoea
Pain is usually suprapubic, but may be felt in the lower back/ back of legs
May have pathological features: discharge, IMB or PCB, dyspareunia
Dyschezia/rectal pain - endometriosis
Hx features - age at menarche, cycle length, regularity, duration of period, timing of pain, smoking, sexual activity, obstetric and contraceptive history
Investigations for dysmenorrhoea
Speculum High vaginal swab/chlamydia screen Smear (if due) Pelvic US/TV US MRI Laparoscopy
Management of dysmenorrhoea
Lifestyle - smoking cessation TENS and locally applied heat NSAIDs - all are equally effective COCP POP Depo-medroxyprogesterone The above only if not trying to conceive
If trying to conceive then Danazol (only under specialist)
Surgery - laparoscopic uterine nerve ablation or hysterectomy (only in refractory)
Aetiology of acute pelvic pain
UTI Miscarriage Ectopic pregnancy Torsion or rupture of ovarian cysts PID In late pregnancy - premature labour, placental abruption, uterine rupture Ovulation Dysmenorrhoea Degeneration of fibroid Pelvic tumour Pelvic vein thrombosis
Appendicitis, IBS, adhesions, prostatitis, strangulated hernia
Pelvic vein thrombosis
Associated post partum or in malignancy
Pelvic pain
Fever
Abdominal mass
Investigations in acute pelvic pain
Urinalysis MSU High vaginal swab and endocervical swab Pregnancy test FBC Urgent US - if ?ectopic or miscarriage Laparoscopy (if severe)
Define chronic pelvic pain
Intermittent or constant pain in lower abdomen for >6 months.
Does not occur exclusively with menstruation or sex
Not associated with pregnancy
Aetiology of chronic pelvic pain
Endometriosis Adhesions IBS Interstitial cystitis MSK Pelvic organ prolapse Nerve entrapment Psychological and social issues - depression, physical or sexual abuse as children
Red flags for chronic pelvic pain
Rectal bleeding New bowel symptoms in over 50s New pain after menopause Pelvic mass Suicidal ideation Excessive weight loss Irregular vaginal bleeding in over 40s PCB
Investigations for chronic pelvic pain
STI screen] FBC, CRP CA125 if ?ovarian Ca (new IBS >50 is suspicious) Urinalysis and MSU TV US MRI if ?adenomyosis Diagnostic laparoscopy is gold standard
Management of chronic pelvic pain
Treat cause and psychological causes
Challenging as pain often continues after treatment without diagnosis
Treat underlying disorder
Most managed in primary care
If cyclical pain can use COCP or GnRH agonists or mirena
Types of benign ovarian tumours
Functional (24%)
Benign (70%)
Malignant (6%)
Benign epithelial neoplastic cysts (60%)
- Serous cystadenoma (40-50 years, papillary growths can appear solid, 20% malignant)
- Mucinous cystadenoma (20-40 years - filled with mucinous material, become enormous, 5% malignant)
Benign neoplastic cystic tumours of germ cell origin
- Benign cystic teratoma (rarely malignancy, may contain well differentiated tissue, common in young women)
Benign neoplastic solid tumours
- Fibroma (<1% malignant, small solid, benign fibrous tumours - associated with Meig’s syndrome and ascitets)
- Thecoma
- Adenofibroma
- Brenner’s tumour
Epidemiology of benign ovarian tumours
30% of females with regular periods
50% of females with irregular periods
Occur in premenopausal women
Uncommon pre-menarche and post-menopausal
RF
- Obesity
- Tamoxifen
- Early menarche
- Infertility
- Dermoid can run in families
Presentation of benign ovarian tumours
Asymptomatic
Dull ache or pain in lower abdomen/back
If rupture/torsion - severe abdominal pain and fever
Dyspareunia
Swollen abdomen, palpable mass
Pressure effects - urinary frequent, peripheral oedema
Torsion - severe pain, can be intermittent
Rupture - peritonitis, shock, mucinous cystadeomas can continue to secrete mucin causing build up and death (psudomyxoma peritonei)
Ascites
Meig’s syndrome
Ascites
Pleural effusion
Benign ovarian tumour
(fibroma, fibrothecoma, Brenner tumour)
Investigations for benign ovarian tumour
Pregnancy test FBC - infection, haemorrhage Urinalysis TV US CT or MIR if US inconclusive Diagnostic laparoscopy CA125 (do not do if premenopausal with cyst on US) - it is not reliable in distinguishing malignant/benign in fertile women LDH, AFP, beta - HCG for germ cell tumours
Risk of malignancy index
For suspected ovarian cancer
Not to be used pre-menopausally
Uses CA125, menopausal status and US score
RMI = U x M x Ca125
US - 1 point each for: multilocular cysts, solid area, mets, ascites, bilateral lesions
RMI > 200 = CT abdo pelvis
Management of benign ovarian tumours
<50mm, expectant management
50-70mm = yearly US follow up
>70mm = MRI/surgery
Do not use COCP
Laparoscopic removal
If torsion may need oophorectomy and uncoiling
Immediate surgery if haemorrhagic - more common in R ovary
Epidemiology of dyspareunia
More common in women
9% of all women
Increase in 20s-30s and over 60s
RFs
- Sexually inexperienced
- peri or post-menopausal
Presentation of dyspareunia
Superficial (felt at introits) OR deep (felt with thrusting and deep in pelvis)
tightening of vaginal muscles on penetration - vaginismus
When/where/duration
Is intercourse possible? Desired?
Any evidence of sexual abuse, rape or trauma
Any FGM
STI risk
Aetiology of dyspareunia
Pain with arousal
- Hymenal ring bands
- Swelling of Bartholin’s gland cyst
Sensitive external genetalia
- Vulvodynia
- Chronic vulvitis - allergy, candida, herpes, trichomonas
- Lichen planus/sclerosis
Pain at introitus on penetration
- Painful episiotomy scar
- rigidity of hymenal ring
- Inadequate lubrication
- atrophic vaginitis
- vaginitis
- vaginismus
- insufficient foreplay
- congenital abnormality
Mid vaginal pain
- Acute/chronic cystitis
- Urethritis
- Shortened vagina
Deep pain
- PID
- Vaginiits
- Cervicitis
- Malposition of IUS/IUD
- Endometrisosis/adenomysosis
- Fibroids
- Fixed retroverted uterus
- IBS
- IBD
- Pelvic mass
- Interstitial cystitis
Investigations for dyspareunia
Swab for STIs
Urine dip &; MSU
US
Types of incontinence
Functional Stress Urge Mixed Overactive bladder syndrome Overflow True
Functional incontinence
Patient is unable to reach the toilet in time e.g. poor mobility or unfamiliar surroundings
Stress incontinence
Involuntary leakage of urine on effort or exertion e.g. sneezing or coughing.
Due to incompetent sphincter
May be associated with GU prolapse
Urge incontinence
Involuntary urine leakage accompanied or preceded by urgency of micturition
Detrusor instability or hyper-reflexia leading to involuntary detrusor contraction
Idiopathic or neurological
Mixed incontinence
Involuntary leakage associated with both urgency and exertion
Overactive bladder syndrome
Urgency that occurs with or without urge incontinence and usually with frequency and nocturia
Overflow incontinence
Usually due to chronic bladder outflow obstruction
e.g. prostatic disease
Can cause obstructive nephropathy
True incontinence
Fistulous track between vagina and ureter or bladder and urethra.
Continuous urine leakage
Epidemiology of incontinence
Very common ~ 8%, up to 40% Increase in females Most common = stress incontinence Increases with age Increased if in institution
RFs
- Pregnancy, vaginal delivery especially with forceps
- Diabetes
- Oral oestrogen therapy
- Raised BMI
- Hysterectomy (RF for stress)
- Increased parity (RF for stress)
- Frequent UTIs
- Neurological disease - stroke, dementia, Parkinson’s
- Cognitive impairment
History features of incontinence
Leakage on sneezing, coughing, exercise, standing
Urgency
LUTS - dribbling, frequency, dysuria, incomplete emptying
Sexual dysfunction
Full obstetric history
Bladder chart
Investigations for incontinence
Urine dipstick + MSU
Assessment of residual volume (bladder scan for post-void volume)
Urinary flow rates
Urodynamic studies
Refer
- any haematuria
- prolapse below introitus
- neurological disease
- persisting pain
- faecal incontinence
Management of incontinence
Temporary containment products only until specific diagnosis and management plan.
STRESS
- Pelvic floor exercises for 3 months, 8 contractions TDA
- Duloxetine
- Retopubic mid-urethral tape
- Colopsuspension
- Autologous rectal fascial sling
MIXED
- pelvic floor exercises and bladder taining
- Oxybutinin (anitmuscarinic)
- Annual review
OVERFLOW
- relieve obstruction
- intermittent self-catheterisation if persistent retention
- botulinum toxin A
- desmopressin if troublesome nocturia
Define overactive bladder
Urgency
Often with frequency
Nocturia
Sometimes urge incontinence
Often associated with detrusor muscle over activity
Epidemiology of overactive bladder
2nd most common cause of female urinary incontinence
Increases with age
Associated with Parkinson’s, spinal cord injury, diabetic neuropathy, MS, dementia, stroke
Presentation of overactive bladder
Sudden urge to urinate Hard to delay Frequency of micturition Nocturia Abdominal discomfort Urge incontinence
Management of overactive bladder
Lifestyle - decrease caffeine, increase fluid intake, lose weight if BMI > 30
Bladder tainting - 1st line, minimum of 6 weeks. Scheduled voiding, regular intervals, increasing time intervals
Drugs - anticholinergics (oxybutynin, propiverine)
Decreases involuntary contractions to increase bladder capacity
Intravaginal oestrogens in vaginal atrophy
Botulinum A toxin
Nerve stimulation - sacral nerve
Surgery - only for severe
Epidemiology of faecal incontinence
Increased in women
3 per 100,000
Increases with age
RFs diarrhoea anal problems - obstetric injury, rectal or pelvic organ prolapse, pelvic radiotherapy Urinary incontinence Frail elderly patients Neuro problems/spinal disease Vaginal delivery Severe cognitive impairment
Aetiology of faecal incontinence
Child birth Obstetric trauma Anal surgery Chronic anal fissure Degeneration of smooth muscle in internal anal sphincter Neurological disease Dementia Congenital disorders - Hirschprung's, spina bifida Constipation Rectal prolapse IBD
Management of faecal incontinence
Treat underlying cause Diet Encourage bowel opening after a meal Sitting or squatting to avoid straining Antidiarrhoeal medications - loperamide or codeine
Continence produces
Skin care
Odour control
If faecal loading - clear bowel
Pelvic floor training
Bowel retraining
Electrical stimulation
Rectal irrigation
Physiology of micturition
Pudendal nerve is under our control
- when activated causes contraction of external sphincter to contract
Hypogastric nerve (sympathetics) - NA causes contraction of external sphincter
Sympathetics cause urinary retention
Parasympathetic causes voiding
Parasympathetic pelvic nerve causes detrusor contraction
Empty bladder
- no stretching
- slow impulse along sensory pelvic nerve
- this activates hypogastric nerve
- causes relaxation of detrusor
Full bladder
- stretching
- increasing fast signals to sacral region
- bypass straight to pontine micturition centre
- inhibits sympathetics (hypogastric nerve)
- Relaxation of external sphincter - contracts detrusor
Where in brainstem is micturition centre?
pons
Aetiology of vaginal discharge
Physiological - New born infants - from maternal oestrogens - Reproductive age: normal Low oestrogen = mucus thick and sticky High oestrogen = mucus clearer, wetter - Cervical ectopy and polyps - Foreign bodies e.g. retained tampon - Vulval dermatitis - Erosive lichen planus - Genital tract malignancy - Fistulae
Infection
- BV
- Thrush. Candidiasis
- Chlamydia trachomatis
- Neisseria gonorrhoea
- Trichomonas vaginalis
Presentation of vaginal discharge
BV - thin, profuse, fishy smelling. No soreness, no itch.
Candidiasis - thick, curd like, white, non-offensive. Vulval itch, soreness. Mild dyspareunia and dysuria.
Chlamydia - copious purulent discharge. Asymptomatic in 80%
Trichomonas - offensive, yellow discharge. profuse and frothy. Vulval itch, soreness, dysuria, abdo pain, superficial dyspareunia
Gonorrhoea - purulent vaginal discharge. asymptomatic in 50%
Retained foreign body - foul smelling seroanguinous discharge
Fistulae - foul or faeculent discharge
Signs vaginal discharge is abnormal
Discharge heavier than normal Discharge thicker than normal Pus like discharge White and clumpy discharge Grey/green/yellow/blood tinged Foul smelling Accompanied by itching, burning, rash or soreness
Causes of vaginal discharge in pregnancy and consequences
BV - poor perinatal outcomes
Candida - No harm to foetus
Chlamydia - doesn’t affect pregnancy outcome but mother baby transmission can occur
- opthlamia neonatorum 15-25%
- pneumonitis 5-15%
Investigations for vaginal discharge
If typical BV or candidia, can be treated without testing
STI screening and swabs
- Vulvovaginal/ endocervical swabs
- Urine chlamydia testing
- Blood tests for HIV and syphilis
Vaginal pH testing
- BV pH>4.5
Epidemiology of bacterial vaginosis
5-12% of normal population
30% undergoing termination of pregnancy
Increased in sexually active women
RFs
- Sexual activity
- New sexual partner
- Other STIs
- Increased in Afro-Caribbean
- IUCD (copper)
- Vaginal douching
- Bubble baths
- Receptive oral sex
- Smoking
Protective
- COCP
- Condoms
- Circumcised partner
Aetiology of bacterial vaginosis
Overgrowth of anaerobic organisms
Most common - Gardnerella vaginalis, prevotella, mycoplasma hominis, mobiluncus
They replace the lactobacilli
Raised pH from 4.5 to 6 (becomes alkaline)
Presentation of bacterial vaginosis
Offensive, fishy smelly discharge
No soreness or irritation
50% are asymptomatic
Thin wall of white discharge on vaginal walls
Investigations for bacterial vaginosis
Amsel’s criteria (3+ of)
- Homogenous offensive discharge
- Microscopy - large numbers of bacilli “clue cells” on vaginal epithelial cells
- pH>4.5
- Fishy odour on adding 10% potassium hydroxide
- Cannot use isolation of G. vaginalis as it is normal flora in 40%
Often treated empirically
Examine and swab
Vaginal pH
management of bacterial vaginosis
Avoid vaginal douching
Avoid shower gel and bubble bath
Do not need treatment if asymptomatic
Oral metronidazole +/- clindamycin
Complications of bacterial vaginosis
Endometritis and PID
Increased risk of acquiring HIV and STIs
Late miscarriage, pre-term delivery, PROM, decreased birth weight
70% relapse in 3 months
Chlamydia
Small, obligate, intracellular
Gram negative
Infected columnar and transitional epithelium
Can cause
- Ocular infections
- GU infections
- Proctitis
- Sexually acquired reactive arthritis
- Lymphgranuloma venerum - STI tropical infection, genital ulcer and inguinal lymphadenopathy
Epidemiology of GU chlamydia
Most common STI in UK
Most common preventable cause of infertility worldwide
Prevalence dependent on age
Increased in under 25s
Decreasing numbers presenting to screening
RFs
- Age < 25
- Sexual partner chlamydia positive
- 2+ sexual partners in 1 year
- Recent change in sexual partner
- Non barrier contraception
- Infection with another STI
- decreased socio-economic status
Presentation of chlamydia infection
Most cases are asymptomatic
Female
- Vaginal discharge
- Dysuria (sterile pyuria)
- Lower abdominal pain
- Fever
- IMB, PCB
- Deep dyspareunia
Male
- Urethritis
- Dysuria
- Urthethral discharge
- Epididymo-orchiditis
- Fever
Reiter’s syndrome - urethritis, arthritis, conjunctivitis. Associated with HLAB27
Proctitis with mucopurulent discharge if anal chlamydia
Signs of chlamydia infection
Female
- Friable, inflamed cervix
- Mucopurulent discharge
- abdominal tenderness
- adnexal tenderness
- cervical excitation
Males
- epididymal tenderness
- mucopurulent discharge
- perineal fullness
Investigations for chlamydia
Samples for nucleic acid amplification tests (NAATs)
Vulvovaginal swabs
Can do endocervical swab or first catch urine
Opportunistic screening at GP
Test when
- Symptoms suggest infection
- Sexual partners of chlamydia positive patients
- All sexually active under 25 annually or with change of partner
- Termination of pregnancy
- At GUM clinic
Management of chlamydia
Antibiotics - doxyxyxline 100mg BD 7/7 or azithromycin 1g stat
Screen for other STIs
Partner notification
- If asymptomatic: back to 6m
- If symptomatic 4/52 before symptoms
No need to retest after treatment unless pregnant, persistent symptoms, non-compliant or re-exposed
Complications of chlamydia infection
PID Female infertility Ectopic pregnancy Perihepatitis (Fitz-Hugh and Curtis syndrome) Reactive arthritis (Reiter's syndrome)
Gonorrhoea
Gram negative diplococcus
Infects mucus membranes
Transmission via direct inoculation of infected secretions - sexually or perinatally
Epidemiology of gonorrhoea
Increasing prevalence
Most causes in homosexual men
Most diagnosed in GUM clinics
Increased in younger ages
RFs
- History of previous STI
- Co-existent STIs
- New or multiple sexual partners
- Recent sexual activity abroad
- Inconsistent condom use
- Anal intercourse and frequent insertive oral sex
- Drug use or commercial sex work
Presentation of gonorrhoea
Symptomatic in most men (90-95%)
Asymptomatic in 50% of women
Male
- urethral discharge
- dysuria
- rectal infection (anal discharge)
- pruritus
- urthethral discharge
Female
- discharge
- abdominal pain
- dysuria
- rare cause of IMB
- pelvic tenderness
- mucopurulent discharge
Investigations for gonorrhoea
Culture - for resistant strains
NAAT - urine or urthethral swabs
Vulvovaginal swab is superior in women
Management of gonorrhoea
Check for other STIs
Partner notification
Ceftriaxone 500mg IM stat + azithromycin 1g stat
Resistance is an ongoing issue
Complications of gonorrhoea
male - urethral scarring and stricture (BOO), acute epididymitis, prostatitis, peri-urethral abscess
Female PID Infetrilty Peri-hepatitis (Fitz-Hugh Curtis syndrome) Bartholin's abscess Ectopic pregnancy Premature labour miscarriage
Can have haematogenous dissemination <1%
Skin lesions, Reiter’s syndrome, arthralgia, meningitis, endocarditis
Trichomonas vaginalis
Flagellated protozoan Most curable STI worldwide Urethral infection in 90% Most are women Underdiagnosed and undertreated
Presentation of trichomonas vaginalis
FEMALE
- vaginal discharge, frothy and yellow
- Vulval itching
- dysuria
- offensive odour
- lower abdominal discomfort
- cervicitis
- 10-50% have no symptoms
- 5-15% have normal exam
MALE
- usually asymptomatic
- dysuria
- urethral discharge
- most have no signs
Investigations for trichomonas vaginalis
High vaginal swab Refer to GUM clinic Wet microscopy Test for other STIs Urethral culture or urine culture NAATs are being gold standard
Management of trichomonas vaginalis
Treat both partners at the same time
Avoid sex 7/7 post-treatment
Metronidazole 2g stat
Complications of trichomonas vaginalis
Pre term delivery Low birth weight Increased maternal post partum sepsis Prostatis in men Persistent and recurrent infections
Epidemiology of HIV
6000 new UK diagnoses per year Increased in males Increased in men who have sex with men (MSM) Increased in Blacks Increased if born abroad
Stages of HIV infection
Seroconversion illness Asymptomatic infection Persistent generalised lymphadenopathy Symptomatic infection AIDS
Seroconversion illness in HIV
1-6 weeks post infection 20-60% present at this time Glandular fever like illness Fever, malaise, myalgia, headaches, diarrhoea, lymphadenopathy, maculopapular rash Viral p24 antigen positive High HIV RNA levels Antibody tests negative
Persistent generalised lymphadenopathy in HIV
Nodes>1cm in diameter at 2 extra inguinal sites
Persists for longer than 3 months
Symptomatic HIV infection
Non specific constitutional symptoms - fever, night sweats, diarrhoea, weight loss
Minor opportunistic infections: oral candida, herpes zoster, recurrent herpes simplex, seborrheic dermatitis
- Prodrome to AIDS
Investigations for HIV
anti-HIV IgG antibody tests (not reliable in under 18m old)
HIV DNA PCR and virus culture
In acute infection will be p24 positive
IgG and IgM to HIV
4 weeks to get test results back
HIV counselling before and after testing
Staging of HIV
CD4 grade
- CD4 > 500 cells/mm3 or 29%
- CD4 200-499 cells/mm3 or 14-28%
- CD4<200 cells/mm3 or <14%
Clinical grade
A. Documented HIV infection. Asymptomatic or persistent lymphadenopathy
B.. Symptomatic but no category C conditions
C. AIDs indicator condition. Cannot move out of category C
Receive both clinical and CD4 grading
Clinical Grade
AIDS defining conditions
Candidiasis - lung/trachea/oesophagus Invasive cervical carcinoma Coccidiodomycosis. Crytococcosis. CMV (not liver or spleen) Encephalopathy Herpes simplex Histoplasmosis Kaposi's sarcoma Lymphoma - Burkitt's, primary brain or immunoblastic TB Pneumocystis jirovecci Recurrent pneumonia Progressive multifocal leukoencephalopathy Toxoplasmosis of brain Wasting syndrome due to HIV
Management of HIV
Support
Anti retroviral therapy for all patients
HAART - combination of 3 drugs to decrease resistance
Efaurenz + tenofovir + lamivudine
Chemoprophylaxis to prevent infection
Preventing spread of HIV
Promote lifelong safer sex Barrier contraception Decrease number of partners Condom program in brothels Warn heterosexuals the dangers of sex tourism Treat other STIs Don't share needle - needle exchange programs Decrease unnecessary blood transfusions Encourage HIV tests in pregnancy Pre-exposure prophylaxis in high risk
Karposi’s sarcoma
Multiple echhymotic skin nodules, macules or papules.
Skin or mucosal surfaces
Can have visceral disease e.g. lungs and GIT
HIV encephalopathy
Brain involved in most late HIV Decreased concentration and memory Gradual decrease in intellect Increased motor problems and weakness Hyper-reflexia Extensor plantars
Aetiology of anogenital warts
HPV infection
Sexually transmitted
60% transmission rate between partners
95% caused by HPV 6 or 11
Epidemiology of anogenital warts
Most common viral STI
Numbers should decrease with HPV vaccination
35% of those being screened for chlamydia
RF Smoking Multiple sexual partners Early age of first intercourse History of other STIs Anoreceptive intercourse Immunosuppression
Symptoms of anogenital warts
Painless lesions
Can be disfiguring or embarrassing
Can cause itching, bleeding or dyspareunia
Urethral lesions may distort urinary stream
Pelvic or scrotal pain
Signs of anogenital warts
Often multiple lesions Can become confluent (huge in immunocompromised) Can be keratinsed or non-keratinised May be broad based or pedunculated may be pigmented
In women on: labia, clitoris, urethral meaturs, introitus, vagina or cervix
Men - frenulum, corona, glans penis, shaft, scrotum, urethral meatus
both - perineum, groin, pubic, perianal area, anal canal
Investigations for anogenital warts
Biopsy and viral typing not usually required
Only biopsy if anything suspicious e.g. over 35 with minimal risk factors
Diseases associated with anogenital warts
cervical cancer
Vaginal, penile and vulval cancer
Anal cancer
Oral and oropharyngeal cancer
Management of anogenital wards
Explain long term latency - does not mean infidelity
Advise condom use until resolved
Advise HPV persists long after warts
20% have concurrent STIs = SCREEN
Assess current and past partners - last 6 months
Non-smokers have better response to treatment
No treatment, 1/3 regress spontaneously in 6 months
Podaphylotoxin cream or imiquimod 5%
Can use ablation. cryotherapy or excision if resistant
Treatments cause itching, burning, pain.
Recurrence occurs after all treatmetns.
Herpes Simplex
HSV Type 1- usual cause of cold sores. Now most common cause of genital herpes
HSV type 2 - causes genital infection.
transmission:
Contact with infected secretion
Close contact
Vaginal, anal and oral sex
Cause of genital herpes
Herpes simplex - type 1 and 2
Epidemiology of herpes simplex
7% of new STIs Numbers are increasing Highest in 15-24s Lifelong disease 80% are not aware they have it 20% of population
Rf Sexual promiscuity Previous history of STIs Early age of first intercourse MSM HIV infection Females
Presentation of herpes simplex
Primary infection Commonly asymptomatic Febrile flu like prodrome 5-7 days Myalgia. Fever Tingling neuropathic pain in genital area Extensive painful crops of blisters/ulcers in genital area Usually bilateral Tender inguinal lymph nodes Dysuria/ Vaginal or urethral discharge
Secondary infection After latency, reactivation Episodes are shorter e.g. 10 days Mild and self-limiting Lesions unilateral
HSV type 1 less recurrence (1/year) 2 = 4 per year
Investigations for herpes simplex
Viral culture
DNA detection using PCRR
Serology testing - takes 12 weeks
Management of herpes simplex
Refer to GUM clinic
Swab
Supportive management
Saline bathing
Oral analgesia
Topical lidocaine
Micturation sitting in bath to prevent urinary retention
Increase fluid intake to dilute urine to decrease pain
Antivirals not recommended unless within 5 days, aciclovir
Complications of herpes simplex infection
Autonomic neuropathy e.g. urinary retention aseptic meningitis Spread to extra-genital areas 2y infection with candida or strep Perinatal transmission psychological or psychosexual problems