O&G Flashcards
What are the two types of multiple pregnancies, which is most common and explain how each occurs
- Monozygotic (Genetically Identical)
- Result of division of the fertilized oocyte into two embryonic layers
- 1/3 of all twins
- Dizygotic (Genetically Different)
- Result of fertilization of two oocytes with two spermatozoa
- 2/3rds of twins
What are the different ways in which the amniotic sac and placenta can be arranged in multiple pregnancies?
For Dizygotic Pregnancies
- Always Dichorionic-Diamniotic (DCDA)
For Monozygotic Pregnancies:
- Dichorionic-Diamniotic (DCDA) (20-30%) - each twin has own individual placenta and amniotic sac. Embryo seperates before 4 days.
- Monochorionic-Diamniotic (70%). Embryo seperates between 4-8 days
- Monochorionic-Monoamniotic (1-5%). Embryo seperates between 8-12 days.
- Monochorionic-Monoamniotic (Conjoined). Embryo seperates >12 days
Complications of multiple pregnancies to the fetus
Fetal
- Spontaneous Reduction or Vanishing Twin Syndrome
- Twin-Twin transfusion Syndrome
Occurs in Monochorionic Twin Pregnancies (Monozygotic). Blood flowing in a fixed direction from from one twin results in the transfer of blood from the donor twin to the recipient twin. Risk to both fetuses:
i) Recipient Twin –> Polycythemia, polyhydramnios in diamniotic pregnancies
ii) Donor Twin –> anaemia, dehydration, growth retardation, oligohydramnios in diamniotic pregnanies - Growth Restrictions
- Congenital Abnormalities
Complications of multiple pregnancies for the mother
- hyperemesis gravidarum
- gestational diabetes
- gestational hypertension, pre-eclampsia, eclampsia
- pervical incompitence, premature birth, preterm labour, PROM
- placenta previa
- miscarriage or loss of one fetus in first trimester
- birth complications - placental abruption, prolonged first stage of labour
- Uterine atony and PPH
Describe the anatomy of the cervix, including Endocervix, ectocervix, transformation zone and cercival ectropion
- Cervical canal communicates with the corpus by the internal os and the vagina by the external os
- Ectocervix – exposed to vagina (stratified squamous epithelium)
- Endocervix – within cervical canal between external and internal cervical os (Columnar epithelium)
- Squamocolumnar junction – meeting point of ecto and endocervical mucosa
- Transformation zone – area of squamous metaplasia between originally squamous and originally columnar epithelium, the area at most risk of cervical neoplasia
- Cervical ectropion – is when columnar epithelial cells are exposed to the vagina
What are the four degrees of perineum laceration during childbirth
- First degree laceration – involves the perineal skin or vaginal mucosa
- Second degree laceration – includes muscles of perineal body, including superficial transverse perineal, bulbovcavernosus and ischiocavernosus. If the laceration is deep it may also include the levator ani muscles (pubococcygeus and ileococcygeus.
- Third degree lacerations – in addition to the muscles of the perineum, will also involve disruption of the anal sphincter. There are three degrees
- Less than 50% of external sphincter thickness torn
- More than 50% of external sphincter thickness torn
- Internal anal sphincter torn
- Fourth degree laceration – extends into the anal epithelium
What is Endometriosis, endometrioma, chocolate cyst and adenomyosis
Endometriosis – the lining of the uterus (endometrium) developing outside the uterus
Endometrioma – area of endometriosis large enough to be considered a lump
Chocolate cyst – entometrioma filled with old blood, usually an ovarian cyst
Adenomyosis – presence of endometrial tissue in the uterine muscle
Symptoms of Endometriosis
Up to 1/3 of patients are asymptomatic
- Chronic pelvic pain that worsens before the onset of menses
- Dysmenorrhoea
- Pre- or post-menstrual bleeding – premenstrual spotting, heavy periods, mid cycle bleeding
- Dyspareunia – pain during or after sex
- Infertility/ subfertility
- Dyschezia – difficult or painful defecation (usually due to hard stools or constipation)
- Urinary symptoms – blood, dysuria, Bowel symptoms – pain opening bowels
- Tiredness
*Intensity of symptoms does not correlate with severity or amount of endometriosis
Examination findings for endometriosis
- Rectovaginal tenderness
- Adnexal masses
- Fixed retroflexed uterus
- Immobility of the pelvis
Investigations for endometriosis
- Transvaginal U/S - make pick up ovarian cysts, not too likely to pick up endometriosis
- Laparoscopy - Gold Standard
Treatment for endometriosis
Medical therapy
- Analgesia - NSAIDs, paracetamol, tramadol
- Induce no periods - COCP, Mirena, Depot Provera, GnRH agonist
Surgical
- Laparoscopic excision and ablation
- Hysterectomy +/- bilateral salpingo-oopherectomy
Definitions of premenopause, menopause and postmenopause
- Premenopause – period from first occurrence of climacteric irregular menstruation cycles to the last menstrual period. Characterized by increasingly infrequent menstruation
- Menopause – time at which menstruation ceases permanently. Confirmed after 12 months of amenorrhoea. Average age at menopause is 49-52 years.
- Postmenopause – the time period beginning 12 months after LMP
Treatment options for menopause
Lifestyle
- Atrophic vaginal symptoms –> Vaginal oestrogen cream (vagifem)
- Impaired sleep –> exercise, relaxation, treating hot flushes
- Preventing osteoporosis –> vitamine D, exercise, stop smoking
Hormone Replacement Therapy
- Oestrogen therapy –> for women who have a hysterectomy
- Oestrogen plus progesteron –> for women with uterus (unopposed oestrogen could lead to endometiral cancer)
Can give transdermally, or oral.
Can give sequentially (If still having irregular periods/ first year of menopause - have bleeding) OR Continuous
If still having any periods, even if irregular, consider adding a mirena for contraception
Risks of HRT –> DVT/ PE, breast cancer, endometrial cancer
Advantages of HRT –> CVD benefit?, increase bone mineral density
Non-hormonal
- Selective oestrogen receptor modulator - tamoxifen (treats dyspareunia), Raloxifene (osteoporosis)
- For hot flushes and mood - venlafaxine
- For hot flushes and slightly high BP - clonidine
- For hot flushes - gabapentin
Symptoms of menopause
- Irregular menses –> complete amenorrhoea
- Autonomic symptoms
- Increased sweating, hot flushes, heat intolerance
- Vertigo
- Headache
- Mental symptoms
- Impaired sleep (insomnia and/or night sweats)
- Depressed mood or mood swings
- Anxiety/ irritability
- Loss of libido
- Atrophic features
- Breast tenderness and reduced breast size
- Vulvovaginal atrophy
- Atrophy of vulva, cervix, vagina
- May present with features that mimic a uti
Causes of preterm labour
Maternal factors
- Infection and Inflammation - UTI, BV, Systemic Infections (malaria, listeria)
- Cervical Trauma such a iatrogenic dilation or previous cervical intra-epithelial neoplasm
- Short cervical legnth
- Uterine anomalies - fibroids
- Placental abruption, Placenta previa
- Medical conditions - pre-eclampsia, diabetes
- premature rupture of membranes
Fetal factors
- multiple pregnancies
- fetal abnormalities and polyhydramnios
What is the difference between labour and threatened premature labour
Labour is diagnosed by regular cervical contractions resulting in cervical change or dilation. However, once these changes have occurred the opportunity to intervene is limited. Management may therefore be investigated before confirmation of labour. Threatened premature labour refers to those women who present with preterm uterine contractions but without cervical effacement or dilation.
Differences between Braxton Hicks Contractions and Labour Contractions
Braxton Hicks Contractions
- Usually last 30 seconds
- Can be uncomfortable but usually aren’t painful
- Come are irregular times
- Usually occur no more than once or twice an hour (until late in pregnancy)
- Usually stop if you change position or activity
Might start to feel them at 16 weeks. These contractions help prepare uterus for birth.
Labour contractions
- Get closer together
- Last longer as time goes by
- Get stronger or come more often when you walk
- Get stronger over time
Investigations for possible Preterm Labour
- Cardiotocogram
* Detection of fetal heartbeat - Tocography
* Frequency of contractions - Transvaginal U/S of cervix
* Indicates likelihood of imminent delivery, as cervical length under 2cm are associated with much higher risk of delivery - Cervico-vaginal swab for fetal fibronectin
* 20% of those with positive fibronectin test deliver within 1 week, compared with only 1% with a negative test - FBC
* Threatened preterm labour should have FBC to look for elevated WBC indicative of infection and check haemoglobin levels in cases of suspected antepartum haemorrhage - CRP
* Infection screen - Urine dipstick
* Proteinuria in pre-eclampsia, leukocytes and nitrites in infection - High vaginal/ rectal swab
* Test for group B streptococcus
Diagnosis of premature labour involves establishing the likelihood of delivery, determining fetal well-being with a non-stress cardiotocogram (CTG), and looking for an underlying cause such as placental abruption or infection. One third of women who deliver preterm will present with preterm premature rupture of membranes (PPROM). Making a diagnosis of labour on a single examination is unreliable. However, frequent uterine contraction, a positive fetal fibronectin test, cervical dilation to >3 cm, and ruptured membranes all increase the likelihood that labour has started.
Management for a women with with high risk of imminent delivery without PPROM (Labour Contractions, with cervical changes)
- Maternal evaluation and assessment of fetal viability
- Corticosteroid
- 11.4g betamethasone IM repeated after 24 hours – halves the rate of respiratory distress syndrome and death. Given from 23+ to 34 weeks. Repeated courses highly controversial and may affect brain development.
- Transfer to neonatal unit
- Intravenous antibiotics
- Benzylpenicillin sodium: 3g IV initially, followed by 1.5g every 4 hours
- Clindamycin: 900mg IV every 8 hours
- Used as GBS prophylaxis
- Tocolytic agent
- Nifedipine 30mg orally, followed by 10-20mg every 4-6 hours
- Tocolytic agents do not prevent preterm birth, but may delay birth for 48 hours to enable transfer to a tertiary centre and give corticosteroids for lung maturation
How do you Diagnose PPROM
- Sterile speculum examination
- Positive pool - amniotic fluid exiting the cervix and pooling in the vaginal fornix
- Detection of amniotic fluid
- Litmus test – turns blue
- Positive fern test
- Positive IGF1 (present in amniotic fluid)
- U/S – oligohydramnios
Management of PPROM
Stable patients
- < 23 weeks
Expect management
Bed rest, antenatal corticosteroids (to avoid fetal lung hypoplasia or immaturity), antibiotic prophylaxis (GBS) and planned delivery > 34 weeks
Outcome is usually poor and termination may be considered - 23-33 weeks
Same as above
+ Tocolysis may be used to delay delivery up to 48 hours (Contraindicated in advanced labour), chorioamniotis, nonreassuring fetal signs, abrupto placentae, risk of cord prolapse - > 34 weeks
Delivery of fetus is usually recommended
risk of prematurity are diminished compared to the risk of infection
Unstable
- Prompt delivery of fetus
- Due to - abruptio placentae, cord prolapse, chorioamniotis, nonreasuring heart rate
The 7 Things used to prevent preterm delivery
- Measurement of the length of the cervix at all mid-pregnancy scans
- Natural vaginal progesterone 200mg each evening if cervix < 25mm
- If cervix < 10mm, consider cerclage or progesterone
- Vaginal progesterone if prior history of spontaneous preterm birth
- No pregnancy to be ended until at least 39 weeks unless there is obstetric or medical justification
- Women who smoke should be identifies and offered quit line support
- A new preterm birth prevention clinic
Causes of Malpresentation and malposition
Uterus
- Uterine abnormalities e.g. fibroids
- Laxity of muscular layer in the walls of the uterus
- Abnormally increased or decreased amniotic fluid
- plecenta previa
- multiple pregnancy
Outside Uterus
- Abnormal shape pelvis
- Masses e.g. ovarian cysts, tumours
Previous Breech Delivery
Hydrocephaly
Consequences of Malpresentation
- PROM and premature labour
- Uncoordinate, pain ful contractions
- Prolonged and obstructed labour –> Ruptured uterus
- PPH
- fetal and maternal distress
- Cord prolapse
- Placental Abruption
- Birthing Injury
Causes of obstructed labour
Fetal
- Malpresentation
- malposition
- Macrosomia
- Congneital anomalies
Maternal
- Bony or soft tissue masses in maternal pelvis
- small pelvis
Clinical features of obstructed labour
Maternal
- Oedematous vulva
- High temperature
- Frequent uterine contractions
Fetus
- high presenting part, not engaged; ruptured membranes
- moulding (extent of overlap of the foetal skull bones; excessive during obstructed labour)
- Caput succedaneum - scalp swelling
Risk factors for breast cancer
- Gender, Age
- Previous Breast carcinoma and other benign proliferative breast disease
- Family Hx
- Radiation
- Dense Breasts
- Oestrogen exposure
- Early menarche, late menopause
- Nulliparity, did not breastfeed
- HRT, COCP
- obesity
Which Breast Lesions have no increased risk have no risk for breast cancer
- Inflammatory conditions
- fibrocystic change
- fibroadenoma
- PASH (Pseudoangiomatous stromal hyperplasia)
- Sclerosing Adenosis
Which proliferative breast conditions increase the risk of breast cancer
- Epithelial hyperplasia
- Columnar cell change
- Complex Sclerosing Lesion/ radial scar
- Intraductal papilloma
Note: the magnitude of risk is related to degree of histological atypia
Explain the screening for breast cancer in Australia
- Target group 50-74yo women
- involves 2 yearly mammograms
If 2000 women are offered mammography over 10 years
- 1 woman would have her life prolonged
- 10 women would be treated unnecessarily (biopsy)
- 200 women would undergo psychological distress of additional testing (false positive)
What is the triple assessment of a breast lump
- Medical History and Clinical Breast Examination
- Imaging
> 35 –> Mammogram +/- U/S
<35 –> U/S - FNA biopsy or core biopsy
What are the two types of breast carcinoma in situ (Pre-malignant)
- Ductal CIS
BC cells confined to ductal space. Management is surgical Excision with clear margins +/- radiotherapy. - Lobular CIS
BC cells confined within lobular space. RISK OF SUBSEQUENT BC IS BILATERAL. Management involves surgical excision + INCREASED SURVEILLANCE, consider anti-oestrogen medication.
Clinical features of invasive breast cancer
- Discrete mass/ lumpiness
- Pain
- Nipple changes (inversion)/ discharge
- Skin changes (tethering, peau d-orange, ulceration etc.)
Biomarkers for breast cancer
Hormone receptor status (Oestrogen and Progesteroen Receptors)
- 80% of BC are ER +ve
- 65% of BC are PR +ve
- ER+/PR+ have 80% response rate, compared to 10% for ER-/PR-
- Assessed by immunohistochemistry
HER2
- Assessed by immunohistochemistry or silver in situ hybridisation
- Prognostically HER2 + BC has poorer survival than HER2 -ve BC
Treatments for breast cancer
- Surgical excision with clear margins – mastectomy or wide local excision (WLE)
- +/- axillary surgery – SLN biopsy, with axillary clearance if SLN positive
- +/- radiotherapy
- to the chest wall – if WLE, locally advanced disease or positive margins on mastecotomy
- to the axilla or supraclavicular nodes – if nodal burden > 4
- +/- chemotherapy – if high risk clinopathological features
Adjuct therapy
- Selective Estrogen Receptor Modulators (SERMs) for ER+ve BC
- Compounds that exhibit tissue-specific ER agonists or antagonist activity: molecularly diverse, non-steroidal (except fulvestrant), varying effects in different tissue but often anti-oestrogenic effect on breast epithelium, oestrogenic effect on bone
- Tamofixen – antagonistic effect on E2
- Used in prevention and treating ER+ve BC in premenopausal women
1. Aromatase Inhibitors (Anastrozole, letrozole, exemastane) For ER+ve BC - Blocks conversion of androgen to oestrogen
- Used to treate ER positive invasice BC
- Post-menopausal women (contraindicated in premenopausal women)
- Survival benefit > tamoxifen
- Side effects include:
- Hot flushes
- Arthralgia
- Accelerated OP
- But no increase in DVT or EC
- Herceptin (Trastusumab) for HER2 +ve BC
A monoclonal antibody that fits the shape of the HER2 binding site to prevent gorwth factor molecules from binding and causing unwanted cell growth
Treatment for Mastitis
- Frequent breast feeding with both breasts (every 2-3 hours)
- Analgesia (ibuprofen)
- Cold compresses
- Antibiotics (Pathogen usually Staphylococcus aureus) –> flucloxacillin or dicloxacillin
May need drainage of abscess if no response to initial treatment
Primary Dysmenorrhoea Treatment
Primary dysmenorrhoea is a diagnosis of exclusion, must rule out secondary causes.
Treatment
- NSAIDs, topical application of heat
- hormonal contraceptives (COCP, IUD)
Secondary dysmenorrhoea causes
- Endometriosis
- PID
- Intrauterine device
- Uterine leiomyoma
- Adenomyosis
- Psychological
Causes of primary amenorrhoea
- Patients with normal puberty
- Anatomic anomalies: hymenal atresia, vaginal septum, Mayer-Rokitansky-Kuster-Hauser syndrome
- Competitive athlete
- Patients with growth delay and developmental retardation
* Hypogonadism
- Hypergonadotropic hypogonadism (primary hypogonadism)
Insufficiency sex steroid production in the gonads - Primary gonadal insufficiency – Turner syndrome, androgen insensitivity syndrome, anorchia
- Secondary gonadal insufficiency – chemotherapy, pelvic irradiation, trauma/ surgery, autoimmune disease, infections (mumps, TB)
- Hypogonadotropic hypogonadism
Insufficient GnRH from HPA axis - Genetic – Kallmann syndrome, Prader-Willi syndrome
- Hypothalamic/ pituitary lesion – tumour, trauma, surgery, infection
- Easting disorders
- Patients with virilisation (male secondary characteristics)
- Congenital adrenal hyperplasia
- Polycystic ovary syndrome
Causes of Secondary amenorrhoea
- Pregnancy - most common cause of secondary amenorrhoea
- Ovarian disorders (e.g. polycystic ovary syndrome)
- Hypogonadism
- Hypergonadotropic hypogonadism
- Hypogonatotropic hypogonadism e.g. functional hypothalamic amenorrhoea
- Excessive exercise, reduced calorie intake, stess
- Treat with lifestyle changes e.g. improve nutrition, increase BMI or offer pulsatile GnRH therapy
iv. Hypothyroidism (Decrease T3/4, Increase TRH à increase prolastin - decrease GnRH - decrease oestrogens)
PMS (Premenstrual Syndrome) Clinical featues
- Onset of symptoms 5 days before menstruation; symptoms end within 4 days of start of menstruation
- Pain - dyspareunia, breast tenderness, headache, back pain, abdominal pain
- GI - Nausea, diarrhoea, changes in appetite
- Tendency to oedema formation
- Neurological - migraine, increased sensitivity to stimuli
- Psychiatric - mood swings, drowsiness, lethargy, exhaustion, depression, anxiety, aggressiveness
*Premenstrual dysphoric disorder (PMDD) - severe form of affective symptoms that interferes with daily life, including abnormal disagreements with family and friends
Treatment of PMS
- Lifestyle changes e.g. exercise, healthy diet, avoiding triggers like alcohol and smoking
- NSAIDs
- Oral Contraceptive
- If PMDD à SSRIs (Fluoxetine)
What is gravidity and parity?
Gravidity - the number of times a woman has been pregnant
Parity - number of times a women has given birth
Common clinical symptoms of pregnancy
- Amenorrhoea
- Nausea and vomiting
- Breast enlargement and tenderness
- Hyperpigmentation or the areola and formation of linea nigra
- Increased urinary frequency
- Fatigue
- Cravings or aversions for certain foods
- Abdominal bloating and constipation
Confirmatory tests for pregnancy
- Pregnancy test
- Urine beta-hCG (home pregnancy test) - beta-hCG may be detected in urine 14 days after fertilization
- Serum beta-hCG (higher sensitivity) - detectable 6-9 days after fertilization. Beta-hCG doubles every 2.5 days in early pregnancy, peaks at 10 weeks gestation and then declines
- Low value may indicate ectopic pregnancy or abortion, high value may indicated beta-hCG secreting tumour or twins
- U/S (abdominal or transvaginal)
- At 5-6 weeks - detection of embryo
- 10-12 weeks - detection of fetal heart beat with Doppler U/S
- 18-20 weeks - fetal movements
What are the 5 ways you can determine gestational age and date of delivery?
- Gestational age à the age (in weeks and days) of the fetus calculated from the first day of the last menstrual period
- Embryonic age à the age of the fetus calculated from the day of conception (fertilization)
- Naegele’s rule à used to calculate the delivery date
- First day of the last menstrual period + 7days + 1 year – 3 months
- Inaccurate if:
- The date of the last menstrual period is uncertain or unknown
- The patient has irregular menstrual cycles
- The patient conceived while taking contraceptive pills
- Ultrasound à more accurate than Naegele’s rule
- Measurement of the crown-rump length in the first trimester
- Measurement of biparietal diameter, femur length, and abdominal circumference (starting at 14 weeks)
- Fundal height during pregnancy à correlated with gestational age
What physiological changes take place in pregnancy?
- Cardiovascular - progesterone decreases peripheral vascular resistance –> Increases CO, SV, CO
- Resp - Increase oxygen consumption, diaphragm displaced up so decreased TLC, RV
- Renal - Increased GFR so decreased creatinine, increase glucose in urine
- Endocrine - increase insulin, triglycerides and cholesterol
- Haem - haematocrit decreases (dilutional anaemia), increase RBC, platelets and WBC
- GI - constipation, increase salivation
- Skin - hyperpigmentation, striae gravidarum, palmar erythema, spider angioma
Investigations for Nausea and vomiting; hyperemesis gravidarum
Occurs in 90% of pregnancies, onset at 5-6 weeks gestation, peaking at 9 weeks, usually abating by 16-20 weeks. Caused by surge in b-hCG
Clinical diagnosis
- Urinalysis – look for ketonuria or signs of infection
- Blood glucose
- Blood tests: FBC, UEC’s, LFTs, TFTs
- U/S scan – arrange if this has not already been performed to exclude molar pregnancies which precipitate hyperemesis
- In sever vomiting or electrolyte abnormality:
- Serum magnesium, phosphate and calcium
- Bicarbonate level
- Blood gases if required
*Women with diabetes should be monitored carefully as dehydration increases risk of diabetic ketoacidosis
Treatment for Nausea and vomiting; Hyperemesis gravidarum
- Diet and lifestyle changes
- Stay hydrated and try have small meals regularly
- Avoid fatty and spicy foods
- Referral to dietitian if severe
- IV Fluid therapy
- 0.9% sodium chloride 1000mL
- IV multivitamins if needed
- First line pharmacotherapy
- Ginger – 250mg orally four times per day to reduce nausea
- Pyridoxine (Vitamin B6) - 25mg OD at night to reduce nausea
- Doxylamine 25mg OD night (start with 12.5mg) – Sedating antihistamine
- Second line pharmacotherapy
If nausea and vomiting persists then a second sedating antihistamine should be added. H1 antagonists safe in pregnancy - Promethazine (H1 antagonist and weak dopamine agonist effect) 10-25mg tabled TD
- Third line therapy
- Metoclopramide 5-10mg orally TD (dopamine agonist)
- Prochloroperazine (sedating antihistamine for short term use only) 5-10mg TD
- Fourth line therapy
- Odansetron (5HT3 antagonist) 4-8mg tablet orally (max 16mg in 24 hours)
- Fifth line
If all else fails… - Hydrocortisone 100mg IV BD or prednisolone 50mg orally faily for 3 days with ranitidine 300mg
Causes of oligohydramnios
Definition: amount of amniotic fluid < 500mL in the third trimester
Aetiology:
- Fetal anomalies
- Urethral obstruction
- Bilateral renal agenesis
- Autosomal recessive polycystic kidney disease
- Chromosomal aberrations e.g. trisomy 18
- Intrauterine infections e.g. TORCH
- Maternal conditions
- Late or post-term pregnancies (>42 weeks)
- Placental insufficiency
- Preeclampsia
- Premature rupture of membranes
Treatment
- Amnioinfusion: infusion of fluid into the amniotic cavity through amniocentesis
- Treat underlying cause
- Delivery is advised if fetus is close to term
What is the definition of labour
Labour is the process by which regular, painful contractions bring about effacement and dilation of the cervix and descent of the presenting part ultimately leading to expulsion of the foetus and the placenta from the mother.
- Cervical effacement refers to the gradual inclusion of the cervix into the lower uterine segment. The muscle fibres surrounding the internal os are drawn upwards and the cervix merges into the lower segment.
- Cervical dilatation is the opening of the cervix from closed to full dilatation. Cervical dilatation is measured in cm from 1-10cm
Causes of polyhydramnios
Definition: excessive amniotic fluid (>2000mL in the third trimester) that results in uterine distention and is associated with an increased risk of fetal complications
Aetiology:
- Fetal anomalies
- Gastrointestinal anomalies (Tracheo-oesophageal fistula, oesophageal atresia, duodenal atresia and stenosis)
- CNS anomalies e.g. anencephaly, meningomyelocele
- Chromosomal aberrations
- Intrauterine infections e.g. TORCH
- Maternal conditions
- Diabetes mellitus
- Rhesus incompatibility
Treatment
- Amnioreduction – drain excess amniotic fluid
- Treat underlying cause
What are the three stages of labour and their duration
-
First Stage
* Time of onset of labour - full dilatation of the cervix (10cm) -
Latent Labour – is the time between the onset of labour to 4cm dilatation
* No time frame -
Active labour – describes the time from 4cm to 10cm dilatation (full dilatation).
* 1cm/hour
* Average duration – 12-14hours in a nullipara and 8 hours in a multipara (6 hours active) - Second Stage
- Full dilatation of the cervix until expulsion of the foetus from the birth canal (delivery of the baby)
- Average duration – 1-2 hours in nulliparae and < 1 hour in multipara
- Third Stage
- Begins after the delivery of the foetus and ends expulsion of the placenta and membranes
- Average duration – no more than 50 minutes, often 5 minutes depending on management employed
What hormonal changes occur to induce labour
Glucocorticoids produced by foetus
- –> Decreases progesterone –> Increase uterine stretching
- –> Increases oestrogen –> increasing uterine contractions, softening the cervix and increased uterine sensitivity to oxytocin
What are the three P’s of labour
- Pelvis - size and shape of maternal pelvis
- Passanger - size and position of infant
- Lie - long axis of fetus to long axis of mother
- Presentation - cephalic or breech
- Attitude of head - should be flexed
- Station - relationship of bony presenting part to maternal ischial spines (if passed ischial spines by 2 cms –> +2)
- Power - stregnth and frequency of contractions
Management in the 3 stages of labour
First stage
- Analgesia as requested
- Epidural, heat backs, hypnotherapy. nitrous oxide and oxygen administration
- Fetal heart rate monitoring
- Determine fetal position with abdominal and pelvic examination
- Regular assessment of cervical dilation and descent of the fetal head
- Amniotomy may be performed during the active phase if the fetal head is well applied
Second stage
- Warm compresses and perineal massage
- Assist the mother to find any comfortable and safe position
- Episiotomy
- Usually a midline incision of the perineum to enlarge the vaginal opening during delivery
- Indications - shoulder dystocia, forceps or vacuum-assisted delivery, or vaginal breech delivery
- Delay cord clamping for 1 minute
Third stage
- Oxytocin – administered after cutting the umbilical cord (reduces blood loss by inducing stronger uterine contractions)
- Controlled traction while allowing the placenta to separate spontaneously (Brandt-Andrews manouvre)
- Examine the placenta to confirm completeness (regular surface with complete cotyledons), which should consist of the umbilical, complete amniotic membranes, and 3 blood vessels (one vein, two arteries)
8 Stages of delivery - the cardinal movements
- Before engagement
- Engagement, flexion, descent
- Further descent, internal rotation
- Complete rotation, beginning extension
- Complete extension
- Restitution/ external rotation
- Delivery of anterior shoulder
- Delivery of posterior shoulder
Indications for induction of labour
- Post-term pregnancy (>= 42 weeks)
- Preterm premature rupture of membranes after 34 weeks
- Repature rupture of membranes at term
- Hypertension during prengnancy, pre-eclampsia, eclampsia, HELLP syndrome
- Maternal diabetes to avoid post-term pregnancy
- Maternat request at term
- Intrauterine death
- Reduced fetal movements, changes in heart rate, not growing well
- Multiple pregnancies
What is a bishop score and what is its use
- Used to assess the cervix and the likelihood of a successful induction
- Interpretation
- Bishop score >= 8 - favourable cervix for vaginal delivery
- Bishop score <= 6 - unripe or unfavourable cervix; not ready for vaginal delivery
Approach to inducing labour
- Artificial rupture of membranes (shortens time to onset of labour)
* Amniotomy hook - If the cervix is still unfavourable: cervical ripening with prostaglandin E1 or E2 (e.g. misoprostol)
- Cervidil (Dinoprostone PGE2 10mg) continuous release vaginal pessary
- Foleys Catheter (balloon catheter)
- Prostin (PGE2) vaginal gel
- Membrane sweeping (stretch and sweep) - best used in multipara. Examining finger passes through cervix to rotate against the wall of the uterus, to separate the chorionic membrane from the decidua. Placenta previa is absolute contraindication, not recommended if GBS carriage.
- Maternal oxytocin infusion (syntocinin)
* Exogenous oxytocin can be used to induce labor, strengthen uterine contractions during labor, contract uterine muscle after delivery of the placenta, and control postpartum hemorrhage. - Consider amniotomy (only if cervix is partially dilated and completely affaced, and the fetal head is well applied)
- Administer under fetal heart rate monitoring
What are two options for assisted delivery
- Obstetric forceps delivery
- A forcep is a metal device that enables gentle rotation and/ or traction of the fetal head during vaginal delivery
- Instrument of choice when: can effect more rapid delivery, can be used in malpresentations, can be used for rotation
- Vacuum extractor
- A vacuum extractor is a metal or plastic cup, attached to the fetal head with a suction device, that enables traction of the fetal head during vaginal delivery
- Instrument of choice: easier to apply, follows pelvic curve automatically, less force applied to fetal head, fewer cervical and vaginal lacerations
Indications for assisted delivery
Maternal
- Maternal exhaustion
- Drug-induced analgesia
- Soft tissue resistance with failure to descend
- Maternal illness – haemorrhage
Materno-fetal indications
- Relative cephalopelvic disproportion
- Melposition – e.g. occiput posterior
- Malpresentation – e.g. presentation
- Non-reassuring FHR tracing
Complications of vaccum and forceps delivery
Vacuum
- Scalp emphysema
- Caput formation, cephalohaematoma
- Hyperbilirubinaemia
- Subgleal haematoma
Forceps
- Fractured clavicle
- Caphalohaematoma
- Lacerations – abrasions
- Facial nerve palsy
- Forceps marks normal and benign
What complications can occur with the umbilical cord in labour
-
Umbilical cord compression
* Part of the umbilical cord lies between the antecendent part of the fetus and the pelvic wall; the amniotic sac is intact -
Umbilical cord prolapse
* Acute, life-threatening emergency for the fetus, in which a part of the umbilical cord lies between the antecendent part of the fetus and the pelvic wall, causing rupture of membranes
iii. Knotting of umbilical cord
What perineal injuries can be sustained in labour
- First degree - cutaneous and subcutaneous skin tear
- Second degree –> + perineal muscles
- Third degree –> + involvement of external anal sphincter
- fourth degree –> + anterior wall of anal canal
Indications of C/S
What are the hypertensive disorders that can occur in pregnancy?
Gestational hypertension: pregnancy-induced hypertension with onset after 20 weeks’ gestations. Defined as a SBP >= 140mmHg or DBP >=90 on 2 separate measurements at least 4 hours apart
Chronic hypertension: Diagnosed < 20 weeks’ gestation or before pregnancy
Pre-eclampsia: Gestational hypertension with proteinuria, renal insufficiency, thrombocytopenia, evidence of liver damage (e.g. elevated liver enzymes, epigastric pain), pulmonary oedema, and/ or cerebral oedema (headache, visual blurring, vomiting, an altered mental status)
- Superimposed pre-eclampsia: pre-eclampsia that occurs in a patient with chronic hypertension
- HELLP syndrome: a life-threatening form of pre-eclampsia
- (H = haemolysis, EL = elevated liver enzymes, LP = low platelets)
Eclampsia: Severe form of pre-eclampsia with convulsive seizures and/ or coma
Risk factors for developing pre-eclampsia
Moderate risk
- Age 40 years or more
- First pregnancy
- Multiple pregnancy
- Interval since last pregnancy of more than 10 years
- BMI > 35
- Family history of pre-eclampsia
High risk
- Chronic hypertension
- Chronic kidney disease
- Hypertensive disease during a previous pregnancy
- Diabetes
- Autoimmune disease
Clinical features of pre-eclampsia
90% occur after 34 weeks’ gestation
- Without severe features
- Usually asymptomatic
- Non-specific symptoms – headaches, visual disturbances, RUQ/ epigastric pain, rapid development of oedema
- Hypertension
- Proteinuria
- With severe symptoms
- Severe hypertension (Systolic >=160mmHg or Diastolic >=110mmHg)
- Proteinuria, oliguria
- Headache
- Visual disturbances (e.g. blurred vision, scotoma)
- RUQ or epigastric pain
- Cerebral symptoms (altered mental state, nausea, vomiting, hyperreflexia, clonus)
Clinical features of Eclampsia
- Onset - the majority of cases occur in the intrapartum and postpartum period
- Most often associated with severe preeclampsia (but can be associated with mild preeclampsia)
- Eclampsia seizure - generalized tonic-clonic seizure
Investigations for a women presenting with hypertenion after 20 weeks gestation
Maternal Investigations
- Assess for signs and symptoms of pre-eclampsia - sever hypertension, headache, epigastric pain, oliguria, N+V, oedema
- FBC
- UEC
- LFTs
- Urinalysis - proteinuria
- IF evidence of thrombocytopenia or falling haemoglobin
- Peripheral smear (haemolysis)
- Coagulation studies (HELLP syndrome)
Fetal investigaitons
- U/S + AFI
- Doppler U/S
- CTG
Management of Hypertension in Pregnancy
Gestational hypertension and pre-eclampsia without severe symptoms
- Delivery if > 37 weeks
- Maternal monitoring (1-2x week BP, urine dipstick, blood tests)
- Fetal monitoring (U/S 3 weekly)
- Educate patients about symptoms (vaginal bleeding, RFM)
- Antihypertensives
- Labetalol 20-80mg
- Hydralazine 5-10mg
- Nifedipine 10mg
Severe Pre-eclampsia
- Delivery if > 34 weeks
- If before 34 weeks need to stabilise and give corticosteroids
- Oral Antihypertensives - Labetalol, Hydralazine, Nifedipine
- Magnesium Sulfate for prophylaxis of eclampsia
Only use diuretics if have pulmonary oedema
Eclampsia
- Stabilise - Airway management, supplemental oxygen
- Midazolam (0.1-0.2mg/kg IV or IM if long seizure)
- Magnesium sulfate to prevent further seizures
- Deliver once stable
HELLP syndrom
- IV fluids
- Blood trnasfusion
- Antihypertensive agents
- Magnesium sulfate
- Delivery if > 34 weeks
What are the 6 types of misscarriage (Pregnancy loss before 20 weeks)
- Complete miscarriage - all tissue passed
- Incomplete miscarriage - confirmed non-viable pregnancy on U/S with some product of conception passes, some remain in uterus
- Missed miscarriage - confirmed non-viable pregnancy on U/S with intact gestational sac. the cervix is closed an no products of conception have been passed
- Recurrent miscarriage - 3 or more successive pregnancies ended in spontaneous miscarriage
- Threatened miscarriage - the continuation of pregnancy is in doubt (vaginal bleeding with mild abdominal cramps and closed cervix)
- Inevitable miscarriage - it is inevitable that this pregnancy will end before viability (Vaginal bleeding, cervical dilation)
- septic miscarriage - products of conception become infected
What is a still birth
Absence of fetal movement and cardiac activity at greater than 20 weeks gestation
Causes of Miscarriage
Maternal
- Uterine abnormalities - fibroids, uterine adhesions, septate uterus, cervical incompitence
- systemic disease - DM, hyperthyroidism, infections, hypercoaguability
Feto-placental
- Chromosomal abrnoamlaities (account for 50%)
- congenital anomalites
Misc
- Trauma
- iatrogenic (amniocentesis or chorionic villus sampling)
- Environmental - alcohol, smoking, drugs
Causes of stillbirth
Maternal
- Fetal-maternal haemorrhage
- Diabtes mellitus
- Hypertensive pregnancy disorders
- Uterine rupture
- Advanced age
- Heavy smoking
Feto-placental
- Intrauterine growth restriction
- Placental abruption
- Infection
- Chromosomal abnormalities
- Congenital malformations
- Umbilical cord complications
- Placental abnormalities
- Fetal hydrops
Investigations if suspected miscarriage
- Dooppler U/S - abscence of fetal cardiac activity
- Pelvic examination - visualisation that bleeding from cervix
- Transvaginal U/S - do if cant find heart of transabdominal scan
- Downtrending b-hCG
Treatment for threatened miscarriages + inevitable, incomplete, missed miscarriage + Stillbirth
Threatened miscarriage
- Avoid strong physical activity
- weekly pelvic U/S
- rule out tratable causes for vaginal bleeding
- Rh(D) negative women need Rh9D) immunoglobulin
Inevitable, incomplete, missed misscariage
- Conservative - allow nature to take its course and review in 7-14 days
- Medical - misoprostol 800mg PV, review in 14 days
- Surgical - Dilation and Curretage
Stillbirth
- do not such delivery unless maternal health risk
- spontaneous labour usually begins within 2 weeks of intrauterine fetal death
- vaginal delivery is safer than C/S but most opt for C/S
- patients should be offered a fetal autopsy
What is Pelvic Inflammatory Disease and what organisms cause is?
PID is bacterial infection that spreads beyond the cervix to infect the upper female reproductive tract, including the uterus, fallopian tubes, ovaries and surrounding tissue
Pathogens
- Chlamydia trachomatis
- Neisseria gonorrhoea
- E.coli, ureaplasma and other anaerobes
Clinical features of PID
- Lower abdominal pain, which may progress to acute abdomen
- Nausea and vomiting
- fever
- dysuria, urinary urgency
- menorrhagia and metorrhagia
- dyspareunia
- abnormal vaginal discharge
Examination features and investigations of PID
Abdominal Palpation
- rebound tenderness if peritoneal irritation
Pelvic Examination
- cervical motion tenderness
- uterine and/ or adnexal tendesness
- purulent, blood cervical and/or vaginal discharge
Investigations
- FBC - leukocytosis
- CRP - elevated
- Pregnancy test - rule out ectopic
- cervical, rectal and urethral swab –> gonococcal and chalmydial DNA (PCR) and culture
- U/S –> free fluid, abscess, pyosalpinx/ hydrosalpinx
- exloratory laparoscopy
Treatment for PID
- One single dose of IM ceftriaxone 250mg and oral therapy with doxycycline 100mg orally BD for 14 days
- If signs of vaginitis or recent gynaecological instrumentation - add oral metronidazole 500mg orally BD for 14 days
- Treatment of sexual contacts and avoid intercourse until treatment finished
- Consider removing IUD if symptoms have not resolved in 72 hours
Complications from PID
Short term
- Pelvic peritonitis
- Fitz-Hugh-Curtis syndrome
- Rare complication of PID involving liver capsule inflammation leading to the creation of adhesions.
Long term
- Tubo-ovarian abscess
- Infertility: cause by adnexitis, adhesion of the fallopian tubes and ovaries, and tubal scarring (resulting in loss of ciliary action and tubal occlusion)
- Ectopic pregnancy
- Chronic salpingitis and hydrosalpinx
Causes of Vulvovaginosis
- Bacterial Vaginosis (45%)
- Candidiasis
- Trichomoniasis
- Gonorrhoea
- Chlamydia
and more
Cause and clinical features of bacterial vaginosis
Lower concentrations of Lactobacilli in vagina leads to overgrowth of anaerobes such as Gardnerella Vaginalis
Clinical features
- Increased vaginal discharge, usually grey or milky with fishy odour
- pruritis and pain uncommon
What is Amsels Crieteria
Criteria to diagnose bacterial vaginosis
3 of 4 must apply to confirm diagnosis
- Whiff test: add 1-2 drops of 10% KOH to vaginal fluid - intensification of the fishy odour
- Vaginal pH > 4.5
- No leukocytes visible on microscopy
- Clue cells; vaginal epithelial cells covered with bacteria identifies on wet mount preparation
treatment for bacterial vaginosis
Metronidazole 500mg orally BD for 7 days
Clinical features of candidiasis
- White, crumbly and sticky vaginal discharge that may appear like cottage cheese and is odourless
- Erythematous vulva and vagina
- vaginal burning sensation, strong pruritis, dysuria, dyspareunia
Risk factors
- immunodeficiency
- pregnancy
- topical corticosteroids
- systemic antibiotic treatments
Diagnostic features from investigations for candidiasis and treatment
- pseudohyphae on wet mount with KOH
- vaginal pH between 4-4.8
treat with topical azole (miconazole 2% cream insert 5g)
Clinical features, diagnostics and treatment of trichomoniasis
Clinical features
- foul smelling, frothy, yellow-green, purulent discharge
- vulvovaginal pruritis, burning sensation, dyspareunia, dysuria, straberry cervix
Diagnosis
- saline wet mount –> protozoa with multiple flagella
- culture if wet mount inconclusive
- pH of vaginal discharge > 4.5
treatment with oral metronidazole
clinical features of PCOS
- Typical onset during adolescence
- menstrual irregularities - primary or secondary amenorrhoea, oligomenorrhoea
- Obesity and possibly other signs of metabolic syndrome
- Hirtuism
- Androgenic alopecia
- acne vulgaris and oily skin
- Acanthosis nigricans
- Subfertility
What is included in the Rotterdam criteia to diagnose PCOS
Two of the following 3 must be present, and other disorders must be excluded:
- Hyper-androgenism and/ or hyper-androgenaemia
* Increased testosterone 9total and free), increased LH (LH:FH ratio > 2:1). Oestrogen is normal or slightly elevated. - Oligo- or anovulation
- Polycystic ovaries on U/S
Also evaluation for metabolic disease
- test for hypertension
- monitor BMI
- assess for insulin resistance or T2DM
- assess for hyperlipidaemia
Treatment of PCOS
If treatment for infertility is not sought:
Therapy is aimed at controlling menstrual, metabolic and hormonal irregularities
- First line: if BMI >25 - Weight loss
- Second line: Combined oral contraceptive therapy
If seeking treatment for infertility
- Weight loss
- Metformin 500mg orally (immediate release) TD or 850-1000mg orally (immediate release) BD, or 1500-200mg orally (extended release) OD
- Metformin can restore ovulation/ menses to the point where conception is possible
- 6-9 months may be needed to take full effect
- meta-analysis shows that continuing metformin throughout pregnancy may decrease rates of early pregnancy loss and premature birth
- Clomifene
- First-line in normal-weight women with PCOS. It is a non-steroidal anti-oestrogen that inhibits oestrogen negative feedback on the hypothalamus/ pituitary, which in turn leads to increasing FSH secretion that may allow follicular maturation and ovulation
- If three treatments of clomifene have failed it is reasonable to add metformin
- When clomifene fails to result n pregnancy, adding dexamethasone may be considered if patient has evidence of adrenal androgen excess
Definition and cause of Post-partum Haemorrhage
Postpartum haemorrhage is an obstetric emergency and is defined as a blood loss > 500mL following vaginal birth or > 1000mL after caesarean section delivery at any time, either before, during, or after placental delivery.
Causes
- Tone (most common)
- Uterine tone (uterine atony) à soft, spongy, boggy uterus results in slow and steady loss of blood
- Trauma
- Incision from caesarean
- Medical instruments à forceps, vacuum extraction, episiotomy
- From baby coming through vaginal canal
- Tissue
- Abnormal placental separation (e.g. retention or incomplete placental detachment)
- Thrombin
- Bleeding diathesis – often due to hypocoaguability à can lead to DIC
- Genetic – Von Willebrand Disease
- Obstetric – Eclampsia, Placental abruption
What are the types of abnormal placental attachment
- Placenta accrete (80%)
- Chorionic villi attach to the myometrium (but do not invade or penetrate the myometrium) rather than decidua baalis
- Leads to uterine atony
- Placenta increta (15%)
* Chorionic villi invade or penetrate into the myometrium - Placenta percreta (5%)
* Chorionic villi penetrate through the myometrium, penetrate the serosa, and in some cases, adjacent organs
Antepartum haemorrhage in the third trimester common causes:
- bloody show associated with labour
- stillbirth
- placental previa
- placental abruption
- uterine rupture
- cervical trauma
What is placental abruption and its clinical features
The partial or complete seperation of the placenta from the uterus prior to delivery.
Clinical features
- Continuous, dark, vaginal bleeding
- In 20% of cases, the haemorrhage is mainly retro-placental, vaginal bleeding does not occur
- Abdominal pain or back pain, uterine tenderness
- As the uterus tenses up to reduce bleeding
- Hypertonic contractions, premature labour
- Fetal distress - decelerations
investigations for placental abruption
*Vaginal exam contraindicated à may worsen bleeding
- U/S – rule out placenta previa, U/S can show retroplacental collection of blood
- Fetal heart rate monitoring
- Lab tests – FBC, coagulation factors
What is placenta previa and its clinical features
Presence of the placenta in lower uterine segment, which might lead to partial or full obstruction of the neck of the uterus with high risk of haemorrhage (rupture of placental vessels) and birth complications
Clinical features
- Sudden, painless, bright red vaginal bleeding
- Usually occurs during the 3rd trimester, stops spontaneously after 1-2 hours, and recurs during birth
- Often causes preterm delivery (45%)
- Soft, non-tender uterus
- Usually no fetal distress
NOTE: digital vaginal examination CONTRAINDICATED
Risk factors for ectopic pregnancy
Anatomic alteration of the fallopian tubes is the main cause, may be due to:
- History of PID
- Previous ectopic pregnancy
- Past surgeries involving the fallopian tubes
- Endometriosis
- Bicornate uterus
Non-anatomical risk factors
- IUD
- History of infertility
- Hormone therapy
Clinical features of ectopic pregnancy
Patients usually present with signs and symptoms 4-6 weeks after their last menstrual period
- Lower abdominal pain and guarding
- Vaginal bleeding
- Signs of pregnancy - amenorrhoea, nausea, breast tenderness, frequent urination
- Tenderness in the area of the ectopic pregnancy
- Cervical motion tenderness (extreme pain on bimanual examination), closed cervix
- Enlarged uterus
- Intestinal pregnancies tend to present late, at 7-12 weeks of gestation
Tubal rupture
- Acute course with sudden and severe lower abdominal pain (acute abdomen)
- Signs of haemorrhagic shock e.g. tachycardia, hypotension, syncope
- More common in intestinal pregnancy
Investigations in ectopic pregnancy ?
- Positive pregnancy test: Increased beta-hcG
* Follow up measurements are required to monitor the increase of beta-hCG over time (usually stay constant and don’t rise) - Transvaginal U/S
- Best initial imaging test for determining the localization of the pregnancy and finding a heartbeat
- U/S findings in an ectopic pregnancy
- Empty uterine cavity in combination with a thickened endometrial lining
- Tubal ring sign: echogenic ring that surrounds an unreuptured ectopic pregnancy
- Possibly free fluid in the pouch of douglas
- Endometrial biopsy
* Shows decidualization of the endometrium with chorionic villi or fetal parts
Management of ectopic pregnancy
- Methotrexate - should have a decrease in bhCG in a week
- Surgery - salpingostomy (tube conserving), salpingectomy (if does not desire future pregnancies
+ Anti D immunoglobulin for Rh(D) negative mothers
What are the two high risk HPV types and where is epithelium where most cervical cancers arise
HPV 16, 18
Oncogenic HPV infection of the metaplastic epithelium at the transformation zone - most commonly Squamous Cell Carcinoma (80%), also adenocarcinoma (80%)
Risk factors for cervical cancer
- Early onset of sexual activity; multiple sexual partners
- High parity
- Immunosuppression
- History of STIs
- Cigarette smoking and/ or exposure to second-hand smoke
- Oral contraceptives
- Low SES
- Lack of regular screening
- Age
- Previous abnormality of cancer of cervix
- Having many children
- Diethylstilboestrol - if exposed in mother’s womb then at risk of clear cell carcinoma
Clinical features of cervical cancer
- Abnormal vaginal bleeding
- Post-coital spotting, menometorrhagia, irregular vaginal bleeding
- Abnormal vaginal discharge
- Blood-stained or purulent malodorous discharge
- Cervical ulceration
- Dyspareunia
Late symptoms include:
- Hydronephrosis – obstructive nephropathy caused by compression of the ureters
- Compression of veins or lymphatic vessels in the pelvic area, leading to swelling of the lower extremities
- Features of disseminated disease: lymphadenopathy, or, rarely abdominal, bone or chest abnormalities (pain)
What is the primary prevention for cervical screening
HPV immunization preferably before first sexual intercourse
- Women 9-26 years of age
- Men 9-21 years of age
- Tetravalent vaccine (Gardasil) protection against high-risk HPV types 16 and 18, as well as against low risk types 6 and 11 (most common cause of genital warts)
- 9-valent vaccine (Gardasil9): protection against high-risk HPV types 16,18,31,33,45,52,58 as well as against low risk types 6 and 11
Explain the difference between the pap smear and cervical screening test
Cervical cancer has recognised precursor lesions which if treated, can prevent the development of cervical cancer. Organised screening programs are estimated to be able to prevent 90% of cancers.
The old screening test – The pap smear.
Was a 2 yearly screen for women 18-69 which looked at cell changes (cytology).
The new screening test – Cervical Screening (Introduced December 2017)
5 yearly cervical screening for ages 25-69, with exit testing at ages 70-74. Apart of a new national registry used to send invitations and reminders to women of appropriate age. It is more effective at preventing cervical cancers than the pap smear test. 99% of cervical cancers lesions contain HPV DNA.
What are the 4 outcomes that can come from the cervical screening test?
- HPV negative à don’t need another cervical screening test for another 5 years. Sent a reminder from the National cervical screening program.
- HPV infection positive (not 16 or 18) à 1/3rd of women will have HPV. 50-80% of sexually active women will be infected with HPV at some stage in their life. 95% of women clear the infection. body will probably get rid of the HPV itself. If positive for HPV - sent for LBC.
- If liquid based cytology is negative or LSIL à you will need another cervical screening test in 12 months. This assesses if you have cleared the infection. It takes 10-15 years for cervical cancer to develop, so waiting 12 months won’t be a problem. If the second test is clear, you won’t need another test for 5 years. If you still have the HPV infection after 12 months, you may need to see a specialist and have a colposcopy.
- If LBC shows HSIL à refer for colposcopy and specialist input
- Certain type of HPV – 16 or 18 à refer to specialist and do colposcopy
- You have an unsatisfactory test result à need a repeat test in 6-12 weeks
Investigations for cervical cancer
- Cervical screening test
- Liquid based cytology
- Colposcopy - special microscope used to examine surface of cervix for abnormalities (cervical leukoplasia)
- Conization - excision of a cone of cervical tissue that contains parts of the ectocervix and endocervix
Treatment of cervical cancer
Non invasive
CIN I
Preceded by LSIL
- Follow up HPV and LBC after 12 months. If positive go for colposcopy. if negative go routine screening
Preceded by HSIL
- Can manage observationally or treat
CIN II, III
Prefer to treat - through excision or ablation, women can opt for observation if seeking pregnancy or pregnant
Invasive Disease
- Micro-invasive - cone biopsy or hysterectomy
- Advanced disease - radical hysterectomy + Chemo + radiation
Also address fertility concerns and risk factors
Vulvar cancer risk factors
- Infection with HPV 16, 18, 31 and 33 (16 and 33 account for 55% of HPV-related cases of vulvar cancer)
- Immunosuppression
- Vulvar dystrophy and vulvar or cervical intraepithelial neoplasia (VIN/ CIN)
- First VIN pathway à HPV related
- Second VIN pathway à Lichen Sclerosus – differentiated VIN (older women, itchy)
- Smoking
- Smoking impaired HPV clearance along with immunosuppression
- Precancerous lesions – Lichen sclerosus
Clinical features of vulvar cancer
- May initially be asymptomatic
- Local pruritis, possibly with bruising sensation and pain
- Reddish, blackish and or whitish patches of discoloration
- Lumps or growth of various shapes, often wart-like lesions or ulcers
- Dysuria, dyspareunia
- Lymphadenopathy in the groin area
Clinical features of vaginal cancer
- Vaginal bleeding, vaginal ulceration with contact bleeding
- Malodorous discharge
- Possible urinary frequency
- Leukoplakia, vaginal ulceration with contract bleeding
Classification of vulva cancer
- Squamous cell carcinoma (>80%)
- Basal cell carcinoma
- Melanoma
- Adenocarcinoma
classification of vaginal cancer
- Squamous cell carcinoma (most common)
- Clear cell adenocarcinoma à seen in daughters of women who received diethylstilbestrol during pregnancy
- Sarcoma botryoides – rare, highly malignant
Classification of endometrial cancers
- Type I endometrial cancer: endometriod adenocarcinomas derived from atypical endometrial hyperplasia
- Type II endometrial cancer: tumours of nonendometrial histology
- Serous, clear cell, carcinosarcoma, mucinous
- sarcomas - endometial stromal sarcoma, leiomyosarcoma
Risk factors for endometrial cancer
The development of type I endometrial cancers has been shown to be directly related to long-term exposure to increased oestrogen levels. Type II endometrial cancer is mostly oestrogen-independent and is strongly associated with a genetic predisposition.
Risk factors for oestrogen-dependent tumours
Broken down to Exogenous and Endogenous Oestrogen and other
- Nulliparity
- Early menarche and late menopause
- PCOS
- Obesity
- Unopposed oestrogen replacement therapy
- Breast cancer - history of BC, tamoxifen treatment
- Metabolic syndrome (obesity and T2DM)
- Lynch syndrome (HNPCC) - 30% chance of endometrial cancer. Recommended to have hysterectomy after family completed.
Clinical features of endometrial cancer
Tumour-related
- Abnormal uterine bleeding is the main symptom
- Postmenopausal – any amount of vaginal bleeding, including spotting or staining
- Perimenopausal/ premenopausal: metorrhagia, menometorrhagia
- Vaginal bleeding usually does not occur in type II cancer
- Later stages may present with pelvic pain, palpable abdominal mass, and/ or weight loss
- Pelvic exam often normal; possible findings include an abnormal cervix, enlarged uterus, or evidence of local metastases
Metastasis
- Localised - spread to cervix, vagina, fallopian tubes, ovaries
- Lymphogenic metastasis - seen in late stage cases – pelvic or para-aortic lymph nodes
- Haematogenic metastasis - rare; occurs at a very late stage and usually in the lungs
Investigations for endometrial cancer
- Endometrial biopsy with histology
- Imaging
- U/S transvaginal
- U/S transabdominal and perhaps CXR, MRI, CT to exclude metastasis
- Lab tests
- FBC
- Coagulation studies
- b-hCG
- TFTs
Management of endometrial cancer
Surgical management
- Indication - women with endometrial cancer who are postmenopausal, perimenopausal or do not intend to become pregnanct
- Procedure - total hysterectomy with bilateral salpingo-oopherectomy with or without lymph node withdrawal
Medical management
- Progestins: indicated for women with early stage endometrial carcinoma (well-differentiated and progesterone and oestrogen receptor positive) who want to preserve fertility or as adjuvant
- Radiotherapy and/ or chemotherapy (adjuvant or palliative)
Causes of endometrial hyperplasia
increased oestrogen stimulation leads to excessive proliferation of the endometrium
- Follicle persistence
- PCOS
- Oestrogen producing ovarian tumours
- Hormone replacement therapy
Investigations for endometrial hyperplasia
- U/S – endometrial thickening
- Hysteroscopy with fractional curettage
Classification of endometrial hyperplasia and their prognosis
- Simple endometrial hyperplasia
* Risk of carcinoma – 1% without atypica, 10% with atypia - Complex endometrial hyperplasia
* Risk of carcinoma 3-10% without atypia, 30% with atypia
Treatment for endometrial hyperplasia
- Endometrial hyperplasia without atypia
- Progestin therapy - COCP
- Endometrial hyperplasia with atypia
- total abdominal hysterectomy with/ without bilateral salpingo-oophorectomy
- In women trying to conceive can go on progestin and close surveillence
Classification of Uterine leiomyomas (Fibroids)
- Intramural leiomyoma (most common)
- Subserosal leiomyoma
- Submucosal leiomyoma
- Diffuse uterine leiomyomatosis
Clinical features of uterine leiomyoma (fibroids)
- Abnormal menstruation
- Hypermenorrhoea, menorrhagia, metorrhagia (anaemia?)
- Dysmenorrhoea
- Features of mass effect
- Enlarged, firm and irregular uterus during bimanual pelvic examination
- Back or pelvic pain syndrome
- Urinary tract or bowel symptoms (urinary frequency/ retention, constipation, features of hydronephrosis)
- Reproductive abnormalities
- Infertility
- Dyspareunia
Treatment for uterine leiomyoma (fibroids)
Symptomatic fibroids
Medical therapy
Preoperative medical therapy may help reduce tumour size and decrease tumour vasculization
- Hormone therapy
- GnRH agonist e.g. goserelin, leuprolide
- Exogenous progestins
- NSAIDs – for pain
- Antifibrinolytics (tranexamic acid) à reduce bleeding
- Androgenic agonist e.g. danazol à suppress growth of fibroids (may have side effects of acne, hair loss, oedema etc.)
Surgical therapy
Indicated for rapidly growing fibroid, recurrent refractory bleeding secondary to medical therapy, severe symptoms
- Myomectomy
- Hysterectomy
What is adenomyosis and its clinical features
Benign disease characterised by the occurence of endometrial tissue within the uterine wall
- dysmenorrhoea
- menorrhagia
- chronic pelvic pain, aggravated during menses
- uniformly enlarged uterus, tender on palpation
Treatment fo Adenomyosis
Conservative
- Combined oral contraceptives
- Progestin-only contraceptives
+ NSAIDs for pain relief
Surgical
- Hysterectomy
Classification of ovarian cancer
Epithelial tumours (70%)
- Cystadenoma/ cystadenocarcinoma
- Endometriod carcinoma
- Clear cell carcinoma
Germ Cell Tumours
- Teratoma - mature or immature
- Dysgerminoma
- Yolk sac tumour of ovary
- Non-gestational choriocarcinoma
Sex cord-stromal tumour of the ovary
- Granulosa cell tumours, theca cell tumours (secrete oestrogen)
- Sertoli-Leydig cell tumour
- ovarian fibroma
clinical features of ovarian cancer
General Symptoms
- Abdominal pain
- Ascites/ bloating
- Cancer cachexia/ satiety
- Abdominal or pelvic mass
- Urinary symptoms
Granulosa cell tumours
- Express aromatase (oestrogen synthesis occurs in 25%)
- Menstrual irregularities such as postmenopausal bleeding or metorrhagia
- Precocious puberty
Sertoli-Leydig cell tumours - Can produce oestrogen or testosterone
Struma ovarri - Symptoms of hyperthyroidism
investigations for ovarian cancer
- Tumour markers
- Epithelial ovarian tumour: CA-125
- Yolk sac tumour: alpha-fetoprotein
- Non-gestational choriocarcinoma: beta-hCG
- Granulosa cell tumour: inhibin B
- Imaging
* Transvaginal U/S is the gold standard, but abdominal or rectal U/S may also be conducted - Histology
- Granulosa cell tumour: call-Exner bodies (granulosa cells arranged in clusters surrounding a central cavity with eosinophilic secretions, resembling primordial follicles)
- Sertoli-Leydig cell tumour
- Ovarian fibroma: clusters of spindle-shaped cells
What is gestational trophoblastic disease
GTD includes:
- Hydatiform moles (both complete and partial)
- Benign
- Invasive moles
- Malignant
- choriocarcinoma
- Malignant
They typically arise from the abnormal fertilization of the ovum.
Patients with GTD present with vaginal bleeding and pelvic tenderness
What is the cause of complete and partial moles (Hydatiform moles)
Complete mole
- Does not contain any fetal or embryonic parts
- Caused by fertilization of an empty egg that does not carry any chromosomes - the physiological haploid chromosome set contributed by the sperm is subsequently duplicated.
- Fetal karyotypes - 46XX, 46XY
Partial mole
- Contains fetal or embryonic parts in addition to trophoblastic tissue
- Caused by fertilization of an egg containing a haploid set of chromosomes with two sperm (each containing a haploid set of chromosomes as well)
- Fetal karyotypes: 69XXX, 69XXY, 69XYY
Clinical features of hydatiform moles (Complete and partial)
Complete mole
- Vaginal bleeding during the first trimester
- Uterus size greater than normal for gestational age
- Passage of vesicles that may resemble a bunch of grapes through the vagina
- Endocrine symptoms
- Pre-eclampsia
- Hyperemesis gravidarum
- Ovarian theca lutein cysts: bilateral, large, cystic, adnexal masses that are tender to the touch
- Hyperthyroidism
Partial mole
- Less severe symptoms due to b-hCG levels that are lower than in complete moles
- Vaginal bleeding
- Pelvic tenderness
Treatment for hydatiform moles
- Dilation and suction curettage
* Complete moles have a 20% risk of becoming invasive and a 25 risk of developing into choriocarcinoma - Monitor beta-hCG levels until roughly 12 weeks
- Chemotherapy (usually methotrexate) if unresolved, as indicated by any of the following:
- Beta-hCG values do not decrease
- Histological features of malignant GTD are present
- If metastases are present on CXR
What are the causes of choriocarcinoma
Choriocarcinoma is a highly aggressive, malignant tumour which only develops after fertilization and implantation of an egg. Most cases of choriocarcinoma preceded by a hydatidiform mole:
- 50% hydatidiform mole
- 25% miscarriage or ectopic
- 25% normal pregnancy
Investigations and treatment of choriocarcinoma
Diagnostics
- Very high b-HCG
- Pelvic ultrasound – mass of varying appearance
- Uterine D&C
- Staging – CXR, CT
Treatment
- Chemotherapy
- Surgical treatment – hysterectomy – indicated maybe to stop bleeding
- Monitor B-hCG for 12 months
Causes of endometritis
The cervix usually keeps bacteria out of the uterus. However, when the cervix is open, bacteria can get into the womb. Both bacteria normally found in the vagina and abnormal bacteria can be the cause of endometritis.
Possible risk factors for endometritis include:
- Childbirth or miscarriage
- Caesarean delivery
- STIs and other bacteria
- Pelvic procedures – D&C, endometrial biopsy, hysteroscopy, IUD insertion
- PID (oftenassociated with, or the cause of endometritis)
Investigations for endometritis
- FBC, CRP
- Cervical culture - chlamydia or gonorrhoea
- Wet mount - discharge from cervix under microscope
- Endometrial biopsy
- Laparoscopy or hysteroscopy
Treatment for endometritis
- Antibiotics – if bacteria causing the uterus lining inflammation
- Removing retained products on conception if this is causing it
- Drainage of any abscess’
Clinical features of endometriosis
Up to 1/3 of patients are asymptomatic
- Chronic pelvic pain that worsens before the onset of menses
- Dysmenorrhoea
- Pre- or post-menstrual bleeding – premenstrual spotting, heavy periods, mid cycle bleeding
- Dyspareunia – pain during or after sex
- Infertility/ subfertility
- Dyschezia – difficult or painful defecation (usually due to hard stools or constipation)
- Urinary symptoms – blood, dysuria, Bowel symptoms – pain opening bowels
- Tiredness
*Intensity of symptoms does not correlate with severity or amount of endometriosis
Diagnostics for endometriosis
- Examination
- Rectovaginal tenderness
- Adnexal masses
- Fixed retroflexed uterus
- Immobility of the pelvis
- Transvaginal U/S
- The uterus is generally not enlarged
- Evidence of ovarian cysts, most do not detect endometriosis
- Nodules in bladder or rectovaginal septum
- Laparoscopy (confirmatory test) and biopsy of lesion
* General anaesthesia, small incision at naval, telescope inserted at naval after abdomen inflated with CO2 - MRI, colposcopy, cystoscopy, or other interventions
Treatment for endometriosis
Medical therapy – Analgesia and Aim to Induce No periods
- Mild to moderate pelvic pain without complications
- Analgesia - NSAIDs, paracetamol
- Inducing no periods
- Continuous hormonal contraceptives (COCP)
- Progestin’s – Depot Provera, Mirena, oral
- However – significant side effects, not as effective in advanced disease, not useful in ovarian endometriomas, not useful for fertility, high rate of recurrence after therapy
- NSAIDs alone if pregnancy desired
- Severe symptoms
- GnRH agonists (goserelin) and oestrogen-progestin OCPs (to avoid hypooestrogenic effects)
Surgical therapy
- First line - laparoscopic excision and ablation of endometrial implants
- Confirms diagnosis and excludes malignancy
- If there is a lack of response to medical therapy
- Treat expanding endometriomas and complications, improves fertility in mild cases
- Second line - open surgery with hysterectomy with or without bilateral salpingo-oophorectomy
- Treatment-resistant symptoms
- No desire to bear additional children
- Least recurrence of symptoms but higher injury rate
Chronic pain management
- Pain specialist
- Psychiatry
- Stay at work, loose weight, yoga etc.
What are the definitions of IUGR and macrosomia
IUGR – fetus with birth weight < 10th percentile for gestational age due to pathological process. Cuttoff at term is < 2500g. Can be symmetric or asymmetric.
- Symmetric (primary) growth restriction is characterized by all internal organs being reduced in size.
* Due to intrinsic factors – chromosomal abnormalities, congenital anomalies, intrauterine infection - Asymmetric (secondary) growth restriction is characterized by the head and brain being normal in size, but the abdomen is smaller. Typically, this is not evident until the third trimester.
* Due to extrinsic factors – utero-placental insufficiency, hypertension, multiple gestations, placental disease
Macrosomia - Fetal weight of more than 4500g at term or fetal birth weight > 90th percentile
Causes of IUGR
Maternal factors
- Hypertension
- CKD, CVD
- Malnutrition, severe anaemia
- Infection
- Substance abuse (alcohol, drugs)
- Cigarette smoking
Factors involving the uterus and placenta
- Decreased blood flow in the uterus and placenta
- Placental abruption (placenta detaches from the uterus)
- Placenta previa
- Infection in the tissue around the fetus
- Chorioangioma
Factors related to the developing fetus
- Multiple pregnancy
- Infection
- CMV, Rubella, toxoplasma gondii
- Syphilis, Tuberculosis, Malaria, listeriosis
- Herpes simplex, chicken pox
- Congenital anomalies
- Congenital Heart diseases
- Anencephaly
- Chromosomal abnormality
- Trisomy 18, 13, 21, turner Syndrome
Causes of macrosomia
- Diabetes
- Obesity, excessive weight gain in pregnance
- Hydrops fetalis
- Post-term pregnancy
- Multiparity
Complications of IUGR
- Hypoxia
- Low Apgar score
- meconium aspiration
- hypoglycaemia
- difficulty maintaining body temperature
- polycythaemia
Causes of error in fundal height
- Inter-observer variations
- Obese patients
- Transverse lie
- Multiple gestation
- Polyhydramnios/ oligohydramnios
- Uterine fibroids
Investigations to determine if IUGR or Macrosomic baby
- Physical examination - fundal Height
- U/S + AFI
- Doppler flow
- Mothers weight gain
- Non-stress testing
- Foetal movement counting
Complications of macrosomia
Maternal complications
- Genital tract lacerations
- PPH
- Uterine rupture
Fetal complications
- meconium aspiration
- obstructed labour
- shoulder dystocia
Newborn complications
- hypoglycaemia
- childhood obesity
- metabolic syndrome
What are the TORCH Infections
Pathogens transmitted from mother to child during pregnancy.
Toxoplasmosis gondii
Other - Syphillis, Listeriosis, varicella, Parvovirus B19
Rubella
CMV
Herpes simplex Virus
Toxoplasmosis:
- worst time to get it
- clinical features
- investigations
- treatment and prevention
- First trimester
- Increased risk of premature birth and miscarriage
Newborn –> chorioretinitis, intracranial calfiications, hydrocephalus
Mother –> asymptomatic, fever, malaise - Maternal - Serology (IgM, IgG)
Fetus - PCR for T.gondii DNA in amniotic fluid - Mother - spiramycin
Newborn - Pyrimethamine, sulfadiazine and folinic acid
Syphillis (Treponema pallidum)
- Worse time to get it
- Clinical features
- Investigation
- Treatment
- Any time - if syphillis is transmitted transplacentally
- Early congenital syphilis (<2yo)
- Hepatomegaly and jaundice
- Rhinorrhoea
- Maculopapular rash on palms and soles
- Skeletal abnormalities – metaphyseal dystrophy, periostitis
- Late congenital syphilis (onset after 2 years of age)
- Facial features – saddle nose, frontal bossing, short maxilla
- Hutchinson teeth (notched, widely spaced)
- Sensorineural hearing loss
- Maternal screening in early pregnancy - RPR or VDRL
Fetus –> U/S - hepatomegaly, ascites, hydrops fetalis
Newborn - RPR or VDRL then confirm with darkfield microscopy of lesion - Treat with IV penicillin
Listeriosis
- When is worse to get it
- Clinical features
- Investigation
- treatment
- 2nd or 3rd trimester - mortality is 40-50% for fetus
- Fetus - Increase chance of miscarriage/ preterm birth, meningitis, respiratory distress syndrome
Maternal - Diarrhoea, fever, myalgia - Blood culture of CSF culture (if meningitis)
- Treat - IV ampicillin
Varicella
- first and second trimester [5-24 weeks] –> congenital varicella syndrome
- clinical
- Congenital varicella syndrome - hypertrophic scars, limb defects, cataracts, chorioretinitis, CNS defects (seizure, intellectual disability)
- Neonatal varicella
- > 5 days before birth - mild infection
- < 5 days before birth - haemorrhagic exanthema. encephalitis, pneumonia, congenital varicella syndrome
- investigations - Serology, PCR of fluid collected/ amniotic fluid
- treatment
- acyclovir for infected women of newborns
- IgG antibodies if mother has symptoms < 5 days before delivery
Parvovirus
- When is it dangeous to get
- clinical features
- investigations
- treatment
- 1st or 2nd trimester –> sever anaemia and hydrops fetalis –> miscarriage/ stillbirth
- Clinical
- mother - rash and arthralgia
- fetus - severe anaemia and hydrops fetalis
- Investigations
- Mother - Serology for IgG and IgM against parvovirus
- fetus
- PCR amniotic fluid
- Doppler U/S
- fetal blood sampling can confirm anaemia
- Treatment - Intrauterine fetal blood transfusion
Congenital Rubella
- when is it worse
- clinical features
- investigation
- treatment
- First trimester
- clinical
- Fetal - congenital rubella syndrome
- cataracts
- cochlear defects - sensorineural hearing loss
- cardiac defects - PDA, pulmonary artery stenosis
- Mother - mild - macropapular rash, lymphadenopathy, arthralgia
- Fetal - congenital rubella syndrome
- Investigations
- PCR (throat swab, CSF, urine)
- serology
- Treatment - termination if < 16weeks, otherwise reassurance
Congenital CMV
- When is it worse to get
- clinical features
- investigations
- treatment
- Most commonly gotten in third trimester, but can get whenever
- clinical
- 90% subclinical - most commonly get hearling loss
- fetal - IUGR, periventricular calcifications, oligohydramnios, polyhydramnios
- Newborn - periventricular calcification, chorioretinitis, sensorineural hearing loss, SGA, vision impairment
- Investigations
- Newborns, fetus and women
- CMV IgM antibodies
- Viral culture or PCR
- Newborns, fetus and women
- Treatment
- mother/ newborn - antivirals - ganciclovir and valganciclovir
- fetus - intrauterine blood ant platelet transfusion
HSV in newborns
- when is it worse
- clinical features
- investigations
- treatment
- Usually transmitted during vaginal birth
- clinical features
- skin, eye, mouth disease vesicular skin lesions, cataracts, chorioretinitis, meningoencephalitis
- Investigations - clinical
- treatment - acyclovir
Explain GBS screening in pregnant women
- Self-obtained lower vaginal and rectal swab between 35 and 37 weeks gestation and sent off for culture
Prophylactic antibiotics - Penicillin 5 million units IV initial dose, 2.5 mill every four hours OR ampicillin 2g IV initial dose
- gestational age < 37
- temperature > 38 degs
- rupture of amniotic membranes > 18 hours
- intrapartum NAAT positive for GBS
- gbs bacteriuria in current pregnancy
- delivery of an infant with early onset GBS disease in previous pregnancy
What is neonatal abstinence syndrome and what are the features
A new baby is no longer exposed to the medications and drugs taken by the mother during pregnancy and can result in the baby developing signs of withdrawal.
features
- CNS – terrors, irritability, sleep disturbances, seizures
- Respiratory – tachypnoea, nasal flaring, chest recession
- ANS – sneezing, yawning, fever, sweating
- GI system – poor feeding, vomiting, diarrhoea
Treatment for neonates from neonatal abstinence syndrome
- Morphine – drug of choice for opiate withdrawal
- Phenobarbitone – for benzodiazepine and/ or alcohol withdrawal and as an adjunct to morphine
Often need to be taken for months i.e. infants are being discharged home on morphine once stable and dose small enough
Risk factors for gestational diabetes mellitus
- Previous hyperglycaemia in pregnancy
- Previously elevated BGL
- Ethnicity: South and south-east Asian, aboriginal, Pacific Islander, Maori, Middle Eatern
- Age > 40
- Family history of diabetes mellitus
- Obesity – BMI > 35
- Hypertension prior to 20 weeks
- PCOS
- Medications: corticosteroids, antipsychotics
- Recurrent pregnancy loss
- At least one birth of a child diagnosed with fetal macrosomia (>4500g or > 90th percentile)
Screening for GDM
Third trimester screening at 24-28 weeks recommended in all pregnancies
Aim is to test as close to 28 weeks as possible as testing at 24-26 weeks may miss some women who develop abnormal glucose tolerance.
One-step test option; 75g Oral Glucose Tolerance Test (OGTT)
The OGTT should be performed in the morning after an overnight fast of at least 8 hours.
- Glucose level: >/ 5.1 mmol/L fasting
- >=10.0 mmol/L at 1 hour
- >=8.5 mmol/L at 2 hours
Treatment for GDM
General management
- weight loss and exercise (50% controlled this way)
- Diabetes educator and dietician
- bloog glucose monitoring and dietary intake
Anti-hyperglycaemic medications
- insulin - pre-prandial bolus and basal insulin at night may be required
- metformin
Other management consideration
- Elevated BP - monitor
- Psychosocial concerns
- Obstetric considerations
- Deliver at due date if well controlled on diet alone and no complications
- Deliver at 39 weeks if on anti-hyperglycaemic drugs and no complications
- 36-38 weeks if elevated BP/ sub-optimal control, failing insulin, macrosomia or IUGR
complications of GDM
Antenatal
- Maternal - hypertension, pre-eclampsia, UTI, insulin related hypoglycaemia
- Fetal - macrosomia, polyhydramnios (fetal hyperglycaemia –> fetal polyuria)
Perinatal
- maternal - increase risk of C/S
- neonate - jaundice, polycythemia, hypoglycaemia, hypocalcaemia, shoulder dystocia, at risk of clavicle fracture
Post-partum
- Mother - 50% risk over 10 years of developing T2DM, 50% risk of GDM in subsequent pregnancies
- Baby - increased risk of being overweight and devloping diabetes
Complications of pre-existing diabetes in pregnancy
all the same as GDM
+ fetal embryopathy (first trimester)
Hyperglycaemia – inhibition of myoinositol uptake – abnormalities in the arachidonic acid-prostaglandin pathway – birth defects and spontaneous abortion
- Effects:
- Congenital heart disease – transposition of great vessels, VSD, PDA, dextrocardia, truncus arteriosis, tricuspid atresia
- Neural tube defects
- Duodenal atresia
- Cleft palate, Flexion contracture of limbs
- Renal agenesis
Explain the concept of rhesus disease
In a Rh-negative mother and Rh-positive child: Maternal exposure to fetal blood –> production of maternal IgM antibodies against the Rh antigen –> over time, seroconversion to Rh-IgG (able to cross the placenta)
In a subsequent pregnancy with an Rh-positive child: rapid production of maternal IgG anti-D antibodies to fetal RhD antigens –> Rh-IgG agglutination of fetal RBCs with haemolytic anaemia –> risk of of haemolytic disease of the fetus and newborn with possible hydrops fetalis.
Treatment for Rh-D negative mothers
Give Anti-D immunoglobulin
- Is administered at 28 weeks, and following the delivery of a Rh-positive infant or at 40 weeks (whichever occurs first)
- If massive haemorrhage or vaginal bleeding
- After amniocentesis or after chorionic villuc sampling
Complications from rhesus disease
Short term
- Hyperbilirubinaemia and kernicterus
- Fetal and neonatal hydrops
- Neonatal aneamia
What are the types of ovarian cysts
Functional cysts
- Follicular cyst
* Cysts lined with follicular epithelium; the most common form of ovarian cysts - Corpus luteum cyst
* Corpus luteum cysts developed physiologically during the menstrual cycle or during pregnancy (corpus luteum gradiditatis). They produce progesterone, which may delay menses.
Benign pathological cysts
Larger, complex symptomatic, do not resolve
- E.g. dermoid, cystadenoma, endometrioma, fibroma
- Chocolate cysts
- Related to endometriosis
Neoplastic cysts
- U/S, CA125, Menopausal status
If multiply all of these and > 200 –> refer to gynaecological oncologist
Work-up of an ovarian cyst
- Pelvic U/S
* Functional à Smooth lining on all sides, single or multiple, hypoechoic to anechoic, fluid-level - Ca125
- Laparotomy
Complications of ovarian cysts
- Ovarian torsion
- Ruptured ovarian cyst
Both present with unilateral lower abdominal pain
Contraindications to VBAC
- Classical C/S
- Previous Uterine rupture
- Some types of previous uterine surgery, such as removal of fibroids
- Woman needs induction of labour and has unfavourable cervix
- Woman has an anusual pelvic shape
- Baby is in transvers position
- Macrosomic baby
- Any other contraindications to labour e.g. placenta previa
Factors in favour of a successful VBAC
- Younger age
- Normal BMI
- Previous successful vaginal birth
- OA position
- > 24 months since C/S
- Spontaneous labour
Common pathogens that cause neonatal sepsis
- Group B streptococcus
- E.coli
- Listeria monocytogenes
- Staph aureus
Risk factors for neonatal sepsis
- Premature Rupture of Membranes, clinical chorioamnionitis and/or discoloured liquor
- Prolonged rupture of membranes > 18 hours
- Pre-term labour or birth
- Multiple gestation
- Maternal peri-partum pyrexia (>38)
- Maternal GBS, UTI
- Resuscitation required at birth
- Invasive procedures – cannula, catheter, endotracheal tubes
- Inadequate hand-washing
- Parenteral nutrition
- Ongoing respiratory disease
Investigations for suspicion of neonatal sepsis
- Blood culture
- FBC
- CRP
- CXR
- gastric aspirate and ear swab
May include LP
*If late onset - add urine sample
Treatment of neonatal sepsis
- Antimicrobial therapy
- EOS: Penicillin/ amoxicillin plus gentamicin
- LOS: Vancomycin plus gentamicin
- Always narrow therapy according to sensitivity
- Supportive
- pink (respiratory support)
- warm (temperature)
- Sweet (watch for hypoglycaemia, provide glucose either through milk if able or IV)
- BP, minimal handling
Cause of respiratory distress in neonates
- Transient tachypnoea of the newborn
- Sepsis/ Pneumonia
- Aspiration (meconeum)
- Hyaline membrane disease (Most common in preterm)
- Pneumonthorax
Pathophysiology of hyaline membrane disease (Respiratory distress Syndrome)
RDs is primarily a function of surfactant deficiency. Spontaneous or mechanical ventilation of the surfactant-deficient lung causes epithelial injury, protein leakage and pulmonary oedema which is prevented with exogenous surfactant treatment.
Lack of surfactant results in collapse of alveoli and hence decreased lung compliance, increased resistance and decreased lung volume. Decreased alveolar ventilation impairs effective gas exchange. An increased mean airway pressure is required to open up the lung and to establish effective tidal volumes.
Investigations for respiratory distress in neonate
- Blood culture
- FBC
- CRP
- CXR
- Oxygen saturation, ABG
Treatment of respiratory distress in neonates
- Pink
- Oxygen
- CPAP
- Invasive mechanisal ventilation
- Chest drain (ICC) – pneumothorax
- Antibiotics – pneumonia
- Surfactant if hyaline membrane disease
- Warm - euthermia, prone position
- Sweet – monitor for hypoglycaemia - withhold neteran feeds, consider IV fluids
causes of neonatal jaundice
if jaundice presents before 24 hours —> its pathological
If jaundice is present for > 14 days –> its pathological
causes of early jaundice:
- physiological jaundice
- haemolysis - rhesus iso-immunisation, ABO incompatability
- sepsis
- polycythaemia (diabetes?)
- bruising (birth trauma)
- Rarer - G6PD def., red cell membrane defects (Hereditary spherocytosis)
*also breast milk jaundice
complication of neonatal jaundice
Acute bilirubin encephalopathy - hypotonia, poor feeding, high pitched cry, lethargy, siezures
and very seriously…
KERNICTERUS (Chronic bilirubin Encephalopathy)
- developmetal delay
- cerebral palsy
- oculomotor dysfunction
- sensori-neural deafness
Investigations of neonatal jaundice
- Serum bilirubin level
- FBC
- Direct anitbody test and blood group (haemolysis detection)
- Septic screen? culture, cxr, fbc, crp?
treatment for neonatal jaundice
- Phototherapy is indicated in unconjugated hyperbilirubinaemia to prevent acute bilirubin encephalopathy and kernicterus arising as a consequence of bilirubin deposition in the basal ganglia and certain brainstem nuclei.
- Phototherapy lowers the concentration of circulating unconjugated bilirubin to a level at which the risk of CNS deposition is minimised
- The native form of unconjugated bilirubin is photo-reactive to photons with a wavelength of 450nm-510nm
- Perform SBR day after cessating phototherapy
- Intravenous Immunoglobulin and exchange transfusion
- Used for aggressive haemolysis, most frequently occurring in response to Rhesus isoimmunisation
- IVIG is unlikely to prevent the need for a first exchange transfusion, however the need for repeated transfusion is decreased
triad of features in obstetric cholestasis and any extra investigations you would order
- pruritis without rash
- increased serum bile acids
- abnormal LFTs
+ Bilirubin, FBC, coagulation profile
Treat with Vit K (liver disease can increase risk of haemorrhage) and Urseodeoxycholic acid (protects hepatocytes from toxic effects of bile salts)
Classification of pelvic organ prolapses
Anterior vaginal wall prolapses
- Cystocele (descent of the bladder)
- Urethrocele (descent of the urethra)
Posterior vaginal wall prolapses
- Rectocele (descent of the rectum)
- Enterocele (herniated section of the intestines)
Uterine prolapse – descent of the uterus
Vaginal vault prolapse – descent of the apex of the vagina
Uterine procidentia – protrusion of all vaginal walls or cervix beyond the vaginal introitus
Treatment for VTE in pregnancy
Women with VTE should not get warfarin as crosses the placenta
- LMWH (clexane 1mg/kg twice daily)
- Proximal DVT or PE for at least 6 weeks postpartum
- Distal DVT 6-8 weeks
Complications of post-term pregnancy (>42 weeks gestation)
- fetal macrosomia
- placental insufficiency
- meconeum aspiration
treatment of pelvic organ prolapse
Conservative
- Insertion of a vaginal pessary (not long term and can lead to pressure ulcers)
- Reduction of modifiable risk factors (smoking to prevent cough, weight loss, prevent constipation)
- Kegel exercises – pelvic floor muscle training
Surgery
- Obliterative surgery – vagina is closed off or narrowed to provide more support for pelvic organs
- Reconstructive surgery – restore original position of descended pelvic organs
what can be examined on abdominal examination
- lie
- presentation
- position
- engagement
- fundal-height
- liquor volume
- fetal heart rate
What is being assessed on vaginal examination
- cervical position
- cervical consistency
- cervical effacement
- cervical dilation
- application
- membranes
- presentation
- position
- attitude
- station
- caput
- moulding
APGAR score
