DRANZCOG/Obstetrics Flashcards
Risk factors for shoulder dystocia
At least 50% of shoulder dystocias have no identifiable risk factors!
Antenatal (5):
- previous shoulder dystocia
- macrosomia
- maternal DM
- maternal obesity
- post-term pregnancy
Intrapartum (5)
- prolonged 1st stage
- prolonged 2nd stage
- labour augmentation
- instrumental delivery
- post-term pregnancy
Consequences of a shoulder dystocia
Neonatal (4)
- brachial plexus injury (Erb’s palsy)
- fractures (humeral and clavicular)
- hypoxia
- stillbirth
Maternal (6)
- PPH
- severe vaginal and perineal trauma (3rd and 4th degree tears)
- cervical tears
- uterine rupture
- bladder rupture
- psychological distress
When to suspect shoulder dystocia
- prolonged birth of face and chin
- head emerges and retracts against the perineum (turtle sign)
- fetus fails to undergo external rotation
- the anterior shoulder does not emerge with routine axial traction
Reassuring features on intrapartum CTG
Baseline FHR 110-160 bpm
Baselines variability of 5-25 bpm
No decels OR early decles OR variable decelerations with NO concerning features for less than 90 minutes
Non-reassuring features on intrapartum CTG
Baseline FHR 100-109 OR 161-180
Variability <5 for 30-50 minutes OR >252 for 15-25 minutes
Variable decels WITHOUT concerning characteristics for 90 minutes +
OR
variable decels with any concerning characteristics in <50% of contractions for 30 minutes +
OR
variable decels with any concerning characteristics in OVER 50% of contractions for LESS than 30 minutes
OR
Late decels in >50% of contractions for <30 minutes with no maternal or fetal clinical risk (e.g. signficicant mec, PV bleeding etc. )
ABNORMAL features of an intrapartum CTG
Baseline FHR <100 or >180
Variability <5 for more than 50 minutes OR >25 for more than 25 minutes OR Sinusoidal
Variable decels with any concerning characteristics in >50% of contractions for 30 minutes (or less if maternal of fetal clinical risk factors)
OR
Late decels for 30 minutes
OR
Acute bradycardia, or single prolonged deceleration lasting 3 minutes or more
Concerning characteristics of variable decelerations
>60 seconds duration Reduced baseline variability within the deceleration Failure to return to baseline Biphasic (W) shape No shouldering
Interpretation of normal v suspicious etc. intrapartum CTG
Normal = all reassuring features
Suspicious = 1 non-reassuring feature + 2 reassuring features
Pathological - 1 ABNORMAL feature OR 2 non-reassuring features
Urgent intervention required: acute bradycardia, or single prolonged deceleration 3+ minutes
Features to assess when describing decelerations on CTG
- timing related to peak of contractions
- duration of individual decels
- if FHR returns to baseline
- how long have decelerations been present
- do they occur with >50% of contractions
- presence of a biphasic (W) shape)
- presence or absence of shouldering
- normal or reduced variability WITHIN the deceleration
Definition of antepartum haemorrhage
Bleeding from the genital tract after the 20th week of pregnancy, and before the onset of labour
Epidemiology of antepartum haemorrhage
Occurs in 2-5% of all pregnancies
Up to 20% of preterm babies are born in association with APH
Causes of antepartum haemorrhage
- (non-vaginal e.g. PR bleed)
- Distal genital tract/gynae causes
- cervical (ectropion, polyp, cervicitis, cervical dilatation, cervical incompetence)
- Placental (praevia, abruption, abnormal placentation, abnormal shape, marginal bleed)
- Uterine (rupture)
- Foetal (vasa praevia)
Relevant history to obtain in woman presenting with antepartum haemorrhage
Gestation
Location of placenta
Bleeding: time of first bleed, pattern, previous APH (this pregnancy or previous)
- Potential causes (postcoital, trauma, exertion)
- CST results
- Pain (site, commencement, frequency, strength, duration)
Maternal assessment in antepartum haemorrhage
ABCs
Abdominal palpation (gently) for SFH, lie, presentation, tenderness
USS: placental location if not known
Blood loss (amount, colour, consistency)
Uterine activity and consistency
Bloods (CBE, Group and save +/- crossmatch if heavy bleeding, coagulation profile, Kleihauer if Rh negative)
Speculum examination - swabs (STI, LVS, HVS) and consider CST if not performed in the last 3 months + clear cervical bleeding
(CTG for fetal assessment)
Epidemiology of placental abruption
1% of births
- 20-35% of these are concealed, rest are revealed
Perinatal mortality rate of 11.9%
Risk factors for placental abruption
Maternal:
- hypertension
- thrombophilias
- increased parity
- poor nutrition
- previous abruption (~10% risk of recurrent)
- cigarette smoking
- substance abuse (esp. cocaine)
Uterine factors:
- Prolonged ROM (especially if PPROM)
- chorioamnionitis
- severe IUGR
- polyhydramnios (sudden decrease in uterine volume post SROM)
- Multiple pregnancy (sudden decrease in uterine volume following delivery of twin 1)
- abdominal trauma
- ECV
Presentation in placental abruption
Vaginal bleeding associated with PAIN, usually very distressed (out of proportion to amount of bleeding)
Usually dark, non-clotting b lood
Abdominal pain Or uterine contractions/tenderness/irritability
Can be associated with faint/collapse or haemorrhagic shock
Complications/associations of placental abruption (9)
- preterm labour
- foetal compromise
- uterine irritability (>5:10 contractions)
- coagulopathy
- disseminated intravascular coagulopathy
- postpartum haemorrhage
- renal failure
- Acute tubular necrosis (from hypovolaemia and DIC)
- perinatal mortality
What is the most common OBSTETRIC cause of coagulopathy
Placental abruption
Management in placental abruption
- IV access
- IDC and fluid balance
- Close maternal obs + CTG
- Resuscitation as indicated
- Urgent Group and cross-match, CBE, Coagulation studies, D-dimer, fibrinogen levels, EUC, LFT
- Anti-D prophylaxis for Rh neg (+ Kleihauer)
- delivery (LSCS if acute fetal compromise or other indication - be prepared for precipitous labour)
- prepare for increased risk of PPH
- examine placenta and send for histopathology
Perineal injury classifications
1st deg: injury to skin only
Second degree: injury to perineal muscles but NOT the anal sphincter
3rd degree: injury involving anal sphincter complex
3a: <50% external anal sphincter thickness torn
3b: >50% external anal sphincter rotn
3c: Internal anal sphincter town
4th degree: injury involving anal sphincter complex AND anal epithelium
Appropriate analgesia to use for perineal repair
1% lignocaine +/- adrenaline (or equiv)
Without adrenaline is preferred for labial tears to reduce risk of tissue ischaemia
Preferred suturing technique for vaginal wall and muscle layer
Continuous, non-locked
Approximate epidemiology of perineal injury
25% of NVD: intact perineum
12% episiotomy
40% tear requiring repair
Other minor tears that don’t require repair
Women with epidural higher risk of instrumental delivery and associated perineal morbidities
Antenatal methods to protect against perineal morbidity
- Perineal massage 1-2x/week from 35/40
- Pelvic floor muscle training for women (Continence Foundation of Australia)
Insufficient evidence to recommend raspberry leaf tea
Intrapartum care to protect from perineal morbidity
No specific position or pushing technique recommended
Warm compresses and perineal massage: lowers risk of 3rd and 4th degree tears
During crowning:
- minimise active pushing following crowning to ensure slower descent of head. - If rapid, consider counter pressure on foetal head if appropriate
- maximise flexion to help reduce presenting diameter
When to use episiotomy
Imminent perineal tear
OR
High risk of severe laceration:
1. Soft tissue dystocia
2. Foetal compromise indicating expedited delivery
3. Instrumental delivery (not always required for vacuum)
4. History of female genital mutilation
5. Past history of pelvic floor repair or third-degree tear
Anatomy involved in episiotomy
Vaginal mucosa
Perineal skin
Bulbocavernosus muscle
Transverse perineal muscle
Technique to perform episiotomy
Appropriate analgesia (e.g. 1% lignocaine) Incision 3-5cm length from the fourchette ad 60-80 degree angle from midline (will become 45 degrees following delivery, loss of distension)
Immediate postpartum perineal care
Repair if indicated
Rectal NSAID unless PPH if torn
If tear within close proximity of urethra, consider indwelling catheter
Postpartum perineal care recommendations
Cold packs (10-20 minute intervals) first 1-3 days
PRN PO paracetamol and NSAID
Urinary alkalinisers
Avoid opioids
Fibre rich, balance diet, adequate hydration
Support perineal wound when coughing or defecating Correct toileting position Avoid constipation Wash and pat dry post toileting Shower at least daily Check wound daily with hand mirror
Pelvic floor muscle training for women
Avoid sitting/propped positions (dependent perineal oedema)
Avoid increased intra-abdominal pressure for 6-12 weeks (e.g. straining, lifting etc.)
Postpartum perineal care methods that lack evidence currently
Sitz baths
Perineal ultrasound for perineal pain or dyspareunia
Topical anaesthetics
Ray lamps
Donut cushions (may lead to more dependent oedema)
Herbal remedies e.g. arnica
Anatomy of the Bartholin glands
Paired glands located in labia minor at 4 and 8 o’clock positions
Approx 5mm in diameter
Secrete mucus into 2.5cm ducts which emerge either side of vagina, inferior to the hymen
Pathophysiology of Bartholin gland cyst
Nonspecific inflammation or trauma -> obstruction of opening of duct -> distension of gland or duct
Pathophysiology of bartholin gland abscess
Either secondary to infected cyst, or a primary gland infection
Usually polymicrobial
Rarely caused by STIs
Epidemiology of Bartholin gland disease
2% of women of reproductive age will experience swelling of at least one Bartholin gland
Typically in women 20-30y
Rare in women >40y (malignancy should be considered)
Clinical presentation of Bartholins cyst
Painless (unless very large) labial swelling, usually unilateral
No signs of surrounding cellulitis
Discharge if has spontaneously ruptured will be non-purulent
Clinical presentation of Bartholin’s Gland Abscess
Acute painful unilateral labial swelling
Dyspareunia
Pain with walking and sitting
Sudden relief of pain followed by discharge (suggests spontaneous rupture)
Can occur spontaneously or on history of a painless cyst
Very tender with surrounding erythema and oedema
may have surrounding cellulitis
Purulent discharge if spontaneously ruptured
Management of Bartholin Gland Disease
Asymptomatic uncomplicated cyst:
- Sitz baths 3x per day for several days (may induce resolution +/- rupture)
Abscess:
Incision and drainage +/- marsupialisation
Antibiotics only required if significant surrounding cellulitis
Definitions of postpartum haemorrhage:
Traditionally primary postpartum haemorrhage = blood loss >500mL in first 24h
Minor: 500-1000mL
major: >1000mL (moderate 1000-2000mL, severe >2000mL)
note that some centres consider PPH as >600mL following NVD or >750mL following LSCS
Risk factors for PPH
2/3 of women who have PPH have no risk factors identified
Background risk:
- PPH in previous pregnancy
- grand multiparity (4+)
- Nulliparity
- Advanced maternal age (>35y)
- known coagulopathies or liver disease
- obesity
- previous LSCS
Antenatal complications:
- multiple pregnancy
- antepartum haemorrhage (esp placental abruption or previa)
- known placenta accreta
- anaemia
- pre-eclampsia
- macrosomia
Intrapartum: - need for/use of oxytocics - prolonged labour (especially 2nd stage) Pyrexia in labour operative delivery Episiotomy Placental retention Shoulder dystocia
Causes of PPH (general groups and %)
Tone (70%)
Trauma (20%)
Tissue (10%)
Thrombin (<1%)
Atonic causes o PPH
Uterine atony (e.g. physiological or prolonged 3rd stage)
Over-distended uterus (polyhydramnios, multiple gestation, macrosomia)
Uterine muscle exhaustion (rapid labour, prolonged labour, high parity, augmentation with oxytocin)
Intra-amniotic infection (PROM >24h)
Drug-induced (magnesium, nifedipine, salbutamol, GA)
Functional or anatomical distortion of the uterus (fibroids, placenta praevia, uterine abnormalities, bladder distention)
Tissue causes of PPH
Retained products
Abnormal or adherent placenta
Retained cotyledon or succenturiate lobe
Trauma causes of PPH
Lacerations to cervix, vagina, perineum (precipitous labour, operative delivery) Uterine rupture (high parity, fundal placenta) Extensions/lacerations at LSCS (malposition, deep engagement)
Thrombin causes of PPH
Non-obstetric abnormalities (Haemophilia, vWd, hereditary coagulopathies, liver disease)
Acquired in pregnancy (ITP, PET, DIC, IUFD, severe infection, abruption, AFE)
Therapeutic anti-coagulation (e.g. clexane for VTE)
Blood loss and signs of Class I hypovolaemic shock in late pregnancy
15% (1000mL) RR: normal HR: <100 BP: Normal Mental state: anxious Urine output: normal
Blood loss and signs of Class II hypovolaemic shock in late pregnancy
15-30% (1300mL) RR: 20-30 HR: >100 BP: Normal/increased diastolic Mental status: anxious/confused
Blood loss and signs of Class III hypovolaemic shock in late pregnancy
30-40% (2000mL) RR: 30-40 HR: >120 BP: reduced systolic and diastolic Mental state: confused/agitated
Blood loss and signs of Class IV hypovolaemic shock in late pregnancy
>40% (2700mL) RR: >40 HR: >140 BP: decreased systolic and diastolic Mental state: lethargic Negligible urine output
Indications for intrapartum antibiotics (general)
- prevention of early onset GBS infection
- women at risk of chorioamnionitis, or where infection is suspected (temp >38 on one occasion or >38.5 on two occasions)
- women with cardiac lesions susceptible to infective endocarditis
Relative contraindications to amniotomy
- Maternal HBV, HCV, HIV, HSV infection - minimise risk of vertical transmission to foetus
- high and mobile presenting part
Factors to assess progress in the second stage of labour
Flexion
Rotation
Descent of head
Risk factors for pre-eclampsia (11)
Antiphospholipid syndrome Previous history of PET Pre-existing diabetes Nulliparity Multiple pregnancy Family history of PET Obesity (BMI >30) Systolic BP >130 <20/40 Diastolic BP >80 <20 weeks Age >40y Overweight (BMI 25-29.9) Underlying renal disease Chronic autoimmune disease Inter-pregnancy interval >10y
Early onset pre-eclampsia definition (i.e. gestation)
Onset <32 weeks
Systems which can be involved in pre-eclapmsia
Neurological Pulmonary Haematological Hepatic Renal Uteroplacental
Requirements for renal dysfunction in diagnosis of PET
Proteinuria >300mg/24h PR PCR >30
Creatinin >90
Oliguria <80mL/4h
Criteria for hameatological end organ dysfunction in diagnosis of PET
Platelets <100
Haemolysis (shistocytes or red cell fragments on film, raised bilirubin, raised LDH >600, reduced haptoglobin)
Disseminated intravascular coagulopathy
Criteria for hepatic end organ dysfunction in diagnosis of PET
Increased transaminases
Severe epigastric and/or RUQ pain
Criteria for neurological end organ dysfunction in diagnosis of PET
Convulsions (=eclampsia) Hyperreflexia with sustained clonus Persistent, new headache Persistent visual disturbances (photopsia, scotomata, cortical blindness, posterior reversible encephalopathy syndrome, retinal vasospasm) Stroke
Criteria for pulmonary end organ dysfunction in diagnosis of PET
Pulmonary oedema
Criteria for uteroplacental end organ dysfunction in diagnosis of PET
Fetal growth restriction
Prophylaxis for women at risk of hypertensive disorders of pregnancy
Aspirin 50-150mg daily from diagnosis of pregnancy (aim for <16 weeks - 37 weeks) Calcium supplementation (esp if high risk and low calcium intake diet) 1.5g/day from <20/40 until delivery
Investigations in assessment for hypertensive disorders of pregnancy
Urine PCR
CBE (Hb, PLT)
EUC
Urate (not actually in diagnostic criteria)
LFTs
Coagulation studies (depending on severity of presentation)
USS: foetal growth, AFI, umbilical artery doppler assessment
Definition of SEVERE pre-eclampsia
BP >/= 160/110 with proteinuria
OR BP 140/90-159/109 with at least ONE of the following - severe headache - visual disturbances - severe pain below ribs OR vomiting - papilloedema - clonus (3+ beats) - liver tenderness - HELLP syndrome - PLT <100 - abnormal liver enzymes
Antihypertensives that can be considered during pregnancy
Methyldopa Labetalol Nifedipine XR Nifedipine IR Hydralazine
Antihypertensives for use in acutely lowering severe hypertension of pregnancy (and dose)
Nifedipine IR 10-20 mg repeated in 30 minutes if BP still above threshold
Labetalol 200mg PO repeated in 30 minutes if not below threshold OR 20mg IV with repeat doses 40-80mg every 10 minutes until BP controlled (max 4 dose)
Hydralazine f not controlled by nifedipine - 5mg IV bolus/5 minutes, repeated every 20 minutes until BP controlled (max 30mg)
Antihypertensives and doses for sustained BP control in pregnancy
Methyldopa 250-750mg every 8 hours
Labetalol 100-400mg every 8 hours
Nifedipine XR 30-60mg BD
Side effects of antihypertensives in pregnancy
Methyldopa:
- depression
- dry mouth
- sedation
- blurred vision
Labetalol:
- bradycardia (maternal and fetal)
- bronchospasm
- headache
- nausea
- scalp tingling
Nifedipine: - constipation - severe headache in first 24h - peripheral oedema tachycardia - flushing
Hydralazine:
- flushing
- headache
- nausea
- tachycardia
Onset of action of antihypertensives used to acutely lower blood pressure in pregnancy
Labetalol: peak effect within 5 minutes of each dose
Nifedpine IR: onset 30-45 minutes
Hydralazine: onset of action 20 minutes
(Methyldopa only used for sustained BP control, has slow onset over 24 hours)
Contraindications to specific antihypertensives used in pregnancy
Methyldopa: depression
Labetalol: Asthma/COAD
Nifedipine: Aortic stenosis
Hydralazine:
Treatment of severe pre-eclampsia
- Stabilise
- control BP (labetalol, nifedipine IR or hydralazine)
- MgSO4 loading + maintenance dose) - Monitor
- vital signs
- urine output/strict fluid balance
- neurological status
- clotting factors
- fetal conditions (CTG) - Plan for labour/birth
Indications for birth in women with pre-eclampsia (13)
Maternal:
- > 37/40 gestation
- falling PLT count
- intravascular haemolysis
- HELLP syndrome
- deteriorating LFTs
- deterioration renal function
- persistent neurological symptoms
- persistent epigastric pain, nausea or vomiting with abnormal liver function
- pulmonary oedema
Fetal:
- placental abruption
- severe fetal growth restriction
- non-reassuring fetal status
Additional considerations of management of PET
Thromboprophylaxis
Monitoring of PLT at least daily (peripartum bleeding complications nor significantly increased until PLT <50)
AND monitoring for intravascular haemolysis (CBE, blood film, LDH, haptoglobins)
Pregnancy complications associated with bipolar affective disorder (i.e. more likely in BPAD than in general population)
Pre-eclampsia Gestational diabetes Gestational hypertension Antepartum haemorrhage Severe fetal growth restriction Neonatal morbidity
Pregnancy complications associated with schizophrenia (i.e. more likely in pregnant schizophrenics than in general population)
Pre-eclampsia
Gestational hypertension
Pregnancy complications with a higher risk in borderline personality disorder
Gestational diabetes PPROM Chorioamnionitis VTE Caesarean section Preterm birth
High rates of substance abuse, referral to child protective services, anticipation of traumatic delivery and frequent request of early delivery
Optimising use of nitrous oxide
Start inhalation 30-50 seconds prior to contraction
Dosages of nitrous oxide
Start at 30% N2O, max of 70% N2O to prevent hypoxia
Adverse effects of nitrous oxide
If used with oxygen (as always should be in labour):
- nausea
- vertigo
- megaloblastic anaemia
N2O alone:
- increased maternal heart rate
- respiratory depression
Contraindications to nitrous oxide use
Inability to hold mouthpiece
Impaired consciousness
Impaired oxygenation (e.g. respiratory disease)
Women who have received excessive amounts of other sedating medications
Vitamin B12 deficiency (can cause megaloblastic anaemia)
Recent ear surgery
Hypersensitivity to N2O
Any condition where air is trapped within a cavity and expansion may be dangerous (e.g. occluded middle ear, cysts, gross abdominal distension, maxillofacial injuries)
Use >24h
Preconception management
(full history of woman and partner if possible - optimise any medical conditions)
Imms: MMR, VZV, HBV
Weight: reduce obesity BMI <30 ideal
Nutrition: ?vegan/vego, assess and manage for nutritional deficiencies (B12, iron, VitD)
Avoid excess caffeine (3-4 cup/day)
CARD: cease all prior to conception. Aim for paternal smoking cessation pre-conception also
Travel: avoid to areas particularly affected by Zika. mosquito and sexual protection if cannot avoid.
Supplements:
- Folic acid from 1/12 prior. 400mcg/day if low risk, 5mg/day if high risk (NTD hx, DM, AEDs, BMI >35, haemolytic anaemia)
- Vit D if high risk group
- B12 6mcg/day if vego/vegan or bariatric surgery
- Calcium 1200mg/day if low dietary intake
Iodine 150microg/day
- iron if deficient, vego/vegan
Genetic counselling:
If high risk refer to geneticist, iff low risk, offer carrier screening e.g. Eugene (out of pocket currently)
Folic acid supplement dose in pregnancy/pre-conception
400 microg/day if low risk 5mg/day if high risk: - DM - personal or FHx of NTD - BMI >35 - AEDs - multiple pregnancy - haemolytic anaemia
Vitamin B12 in pregnancy
6mcg/day if vegetarian/vegan/bariatric surgery
Immunisations to consider pre-conception
MMR
VZV
HBV
Risks of smoking in pregnancy
Pre-conception:
- delayed conception by 2 months
- 60% increased risk of female infertility
- male infertility
Obstetric:
- Miscarriage
- Preterm labour (2x)
- placenta praevia (2x)
- placental abruption (1.5x)
- stillbirth (3x)
- Ectopic (2.5x)
- PPROM (2x)
Fetal:
- low birth weight (<2500g) (2x)
- SGA (3x)
- Birth defects (limbs, clubfoot, cleft palate, eye defects, GI defects)
Postpartum:
- less breastmilk production
Child/adult:
- SIDS (2.5x)
- Behavioural issues (ADHD, CD, antisocial)
- Respiratory disease (asthma, recurrent infection, reduced lung function)
- Cognition (reduced academic performance)
- T2DM
- Obesity
- HTN
- Dyslipidaemia
- Pyschiatric disorders early adulthood
- Nicotine deopendence
Management of smoking in pregnancy
- Counselling and QuitLine referral
- NRT (1st line is intermittent short acting forms, if patches required make sure are removed at bedtime 16h patches)
Champix and Bupropion not evidenced to be safe or effective in pregnancy
Risks of heroin use during pregnancy
IUGR Pre-term labour Placental abruption intrauterine passage of meconium Neonatal abstinence syndrome Foetal and neonatal death
Other associations:
- inadequate antenatal care
- poor nutrition
- BBV exposure
- overdose
- financial hardship
- unstable accommodation
- pyschological instability
Opioid substitution therapy in pregnancy
Methadone and buprenorphine both cross the placenta
Methadone has been used for longer, more experience with it. >50% of exposed neonates will show signs of NAS
Buprenorphine - only the mono therapy (without naloxone) is offered to pregnant women. Evidence suggests associated with fewer neonatal complications than methadone (less frequency, less severe NAS and less medication and admission durations)
Concentrations in breastmilk are low, breastfeeding should be encouraged while on OST if no other contraindications
Features of neonatal abstinence syndrome
Develops within first 48-72 hours of birth
- lasts from 1-several weeks depending on type of opioid use
- difficulty feeding
- central and autonomic hyperactivity
- poor suckling
- irritability
- hyperactivity
- sleep disturbances
- high-pitched cry
- seizures (in 5%)
Management of neonatal abstinence syndrome
Close monitoring in special care nursery for prolonged period Observation with standardised NAS scoring Oral morphine (dose and duration based on NAS scoring)
Complications of alcohol in pregnancy
Miscarriage Stillbirth Low birth weight Premature birth Brain damage Birth defects Foetal alcohol spectrum disorders
Common impact on child(and then adult) from alcohol used in pregnancy
Hyperactivity/inattention/impulsivity Aggression Impaired social interactions Antisocial personality traits Disrupted schooling Substance use disorders Mental health issues Employment/financial/independent living issues Criminal system contact
Advice for alcohol and breastfeeding
Safest not to use alcohol at all while breastfeeding
Definitely no alcohol in first month postpartum and until BF established
If chooses to drink after than, limit consumption as much as possible
Avoid drinking immediately prior to breastfeeding
Option to express prior to alcohol consumption
Diagnostic features of foetal alcohol syndrome
- evidence of prenatal alcohol exposure
- Growth deficiency (pre or post natal <10th centile)
- Facial features (** = sentinel)
- epicanthal folds
- flat nasal bridge
- short palpebral fissures**
- upturned nose
- smooth/flat philtrum**
- thin upper lip ** - Neurological dysfunction
- Structural:
- -HC <10%
- -structural brain abnormality on imaging
- Neurological
- -any neurological issues NOT due to postnatal event
- Functional
- -performance below expected for age
Foods to recommend avoiding during pregnancy
Risk of listeriosis:
- pre-prepared salad vegies (e.g. salad bars)
- raw, undercooked, chilled pre-cooked meats, pate and meat spreads
- unpasteurised dairy, soft, semi-soft and surface-ripened cheeses
Risk of salmonella
- raw eggs/foods containing raw eggs
Risk of mercury
- shark/flake, marlin, broadbill/swordfish, catfish
Risk of hepatitis A
- frozen berries
- bean sprouts
Foods containing saturated fats, added salts and sugars
Recommended maximum daily caffeine intake per day during pregnancy
300g (3-6 cups coffee/tea per day)
Recommended water intake during pregnancy
750-1000mL above daily pre-pregnancy needs
Vitamin supplements that can be associated with harm if taken antenatally
Vitamin C (preterm birth, perinatal death, PPROM) Vitamin E (PPROM) Vitamin A (congenital malformation)
Physical activity advice in pregnancy
- Specifically designed programs can prevent pelvic girdle pain and reduce severity of back pain
- Yoga associated with less stress, enhanced relationships, reduced back pain and less reported pain in labour
- can prevent urinary incontinence
- low-moderate intensity exercise is safe throughout pregnancy
Impacts of pregnancy on oral health
Reduced immune system (increased risk of periodontal infections)
Vomiting/reflux in pregnancy increases acidity -> enamel damage -> decay
Frequent snacks/soft drinks and other cravings (often sweet) can increase risk of tooth decay
Recommendations to reduce impact of pregnancy induced vomiting on oral health:
Rinse mouth with bicarb soda after vomiting
Avoid tooth brushing directly after vomiting
Use fluoridated mouthwash and toothpaste
Small protein-rich non-cariogenic foods throughout the day
Chew sugar-free gum (esp ones containing xylitol or CPP-ACP) after meals/sugar/acidic drinks
Women in whom you should screen for haemoglobinopathies (pre-natal or antenatally)
- family history of anaemia or haemoglobinopathy
- MCV <80 OR MCH <27
Following ethnic backgrounds: - Southern European
- African
- Middle Eastern
- Chinese
- Indian subcontinent
- Central and SE asian
- Pacific Islander/Maori
- South American
- Caribbean
- Northern WA/NT ATSI communities
What to include in a haemoglobinopathy screen
FBE (for MCV+MCH)
Ferritin (exclude Fe def)
Hb electrophoresis
DNA testing if indicated (microcytosis with normal iron and Hb electrophoresis and risk of disease)
Hb electrophoresis results in beta-thalassaemia
High HbA2 (>3.5%)
Normal HbA2 with low MCV and normal ferritin may be alpha thalassaemia
Diagnosing alpha-thalassaemia
Requires DNA analysis for definitive diagnosis. Suggested with low MCV and normal Hb eletrophoresis + ferritin level
Hormones involved in the onset of labour
Progesterone
- suppresses uterine contractility
- systemic or functional withdrawal (due to reduced responsiveness due to inc. PR-A:PR-B intrauterine expression) leads to increased uterotonin production
Prostaglandins:
- stimulate contractions, cervical softening and rupture of membranes
- synthesis is catalysed by COX-2
- increase the intrauterine PR-A:PR-B ratio-> feed forward mechanism
Benefits of water immersion in labour
- more tolerable labour pains
- lower use of pharmacological analgesia
- lower augmentation rates
- lower bleeding, reduced risk of PPH
- shorter labour
Definition of the puerperium
the 6 weeks following delivery during which woman’s physiology returns to pre-pregnancy state
Expected course on uterine involution postpartum
Fundus at level of umbilicus immediately post delivery
By day 5-7 halfway between umbilicus and pubic symphysis
By 2 weeks not palpable
By 6 weeks almost back to pre-pregnancy state
Cause of involution and lochia
Contractions and reduction of size of myometrial muscle (Cause of after pains)
Thrombosis and hyalinisation of blood vessels -> decidual shedding
Normal progress of lochia
Until day 5-6: lochia rubra
Until day 10-12: lochia serosa (darker brown)
Then becomes lochia alba (yellowish/white)
Timing of return of ovarian function post partum
In non-lactating women usually by 10 weeks, can be as early as 4-6 weeks
In lactating women highly variable
Make sure to offer contraception from 4 weeks if sexually active
Healing time of perineal injury
Most 1st/2nd and episiotomies will heal within 3 weeks
Care of perineal injuries
Keep dry and clean, clean from front to back
Warm sitz baths
Avoid constipation
Advise to watch for excessive pain/PV discharge or malodourous discharge
Abstinence for 6 weeks, advise may be some discomfort when resumes
When to resume sexual activity postpartum
Advise abstinence for 6 weeks if any tears
If no tears, as soon as desired/comfortable
Lactating women can have vaginal atrophy and may require topical oestrogen (after BF established) or lubrication
Diet and exercise recommendations postpartum
Regular diet ASAP
Full ambulation ASAP
Abdominal strength exercises after delivery pains have subsided (usually 1 day post NVD, 6 weeks post LSCS) - curl-ups while lying in bed (flexing knees and hips)
Bladder changes postpartum
Massive diuresis can occur immediately post-partum due to withdrawal of oxytocin
Cathartics use postpartum
Psyllium husk
Docusate or
Bisacodyl
Should be given to all women with OASI injury postpartum, and to other women if BNO day 3 (or if otherwise desired)
Managing breast engorgement postpartum
If plans to BF:Hand expression in warm shower or pump between feeds, regular feed schedule, wear comfy nursing bra
If not wanting to BF: Supportive bra (avoid gravity), avoid nipple stimulation or manual expression, tight binding of breasts (e.g. with tight sports bra), cold packs and analgesia PRN
Post partum mental health changes
Transient depression is common in the first week - mood swings - irritability - anxiety - poor concentration - insomnia - crying spells Typically only mild and subsides by day 7-10
When to advise women to see their GP re: ?postpartum depression
- If depressive symptoms last >2 weeks post partum
- if symptoms interfering with daily life
- ANY suicidal or homicidal thoughts
Family planning recommendations post partum
Obstetric outcomes are improved by delaying conception until 18 months post delivery
MUST delay conception at least 4 weeks post live vaccines
Avoid combined oestrogen/progesterone contraceptives while lactation is being established
Vulnerable groups who are statistically less likely to breastfeed (thus require more support)
Aboriginal and Torres Strait Islander Women Younger women (especially <20y) Less educated women Obese women Lower socioeconomic status
Benefits of breastfeeding for the infant
- nutrients in perfect composition, bioavailability and readily absorbable state
- active and passive immunity
- improved visual acuity
- improved psychomotor and cognitive development (higher IQ with longer durations of breastfeeding)
Reduced risks of:
- malocclusion
- physiological reflux
- pyloric stenosis
- GI infections
- respiratory illness
- otitis media
- urinary tract infections
- meningitis
- SIDS
- NEC (in Prem babies)
- Atopy (breastfeeding during time of antigen introduction facilitates development of tolerance)
- Some childhood cancers
- T1DM/T2DM
- Coeliac diseae (if breastfeeding at time that gluten is introduced)
- IBD
- HTN, dyslipidaemia
- obesity
Maternal benefits of breastfeeding
- reduced risk of breast Ca
- reduced risk of ovarian Ca
- reduced risk of GDM women developing T2DM
- Promotes uterine involution (less bleeding -> preservation of iron stores)
- ?maybe helps return to pre-pregnancy weight
What to discuss around breastfeeding antenatally
- importance of exclusive breastfeeding to 6 months and recommend breastfeeding to at least 12 months for nutritional and protective benefits
- basic breastfeeding management
- anticipatory guidance for coping with minor problems
Factors that delay the initiation of lactation
- stressful delivery (due to reduced oxytocin release)
- Caesarean delivery
- Maternal T1DM (can delay lactation by 24h)
- retained placental fragment (persistent progesterone release)
- maternal obesity (higher levels of progesterone + attachment issues)
Correct technique for breastfeeding
- Mum upright/semi-reclined with good back/feet/arm support
- “C-hold” - if nipple erect, support outer area of breast, if flat/inverted should hold well behind areola from the bottom to shapebreast between thumb and index finger
- Support infant behind shoulders, body flexed around mum, nose at level of nipple
- Tease infant with underside of areola to encourage wide gape, then quickly bring INFANT to the BREAST
- should be no clicking or sucking in of infants cheeks, slow even rhythm with deep jaw movements, pauses are normal
- come off breast spontaneously
Number of breastfeeds per day
8-12 typically
Typically will establish pattern within first week
Absolute contraindications to breastfeeding
HIV infection (but discuss with specialist)
Active TB
Breast Ca treatment
Breast syphilis
Brucellosis
Infant metabolic conditions requiring special formula (e.g. galactosaemia)
Advice around smoking and breastfeeding
Ideally quit smoking during pregnancy and breastfeeding
If unable to quit, reduced as much as possible
COMPLETELY avoid smoking 60 minutes prior to feed (and during feed)
Never smoke in same room as infant
Champix and Zyban are not safe during pregnancy or lactation
Signs to monitor if breastfeeding has established
- Content neonate after feed (though may cluster feed at certain period of each day)
- time remaining on breast (should never be >60 mins)
- passing urine at least 1x/day first few days (6+ times/day as volume increases)
- transitional stools by 24-48h-> breastfed stools by day 3-4
- appropriate weight gain (averaged over 4 week period)
What is lactogenesis stage I
After maturation of alveoli of breasts due to prolactin, progesterone and human placental lactogen -> breast able to secrete small amounts of specific milk components (e.g. lactose)
- complete by mid pregnancy
Milk production is inhibited in late pregnancy by high progesterone levels
What is lactogenesis stage II
Rapid increase in milk production in the first 30-40h following delivery of placenta (due to progesterone withdrawal)
Average breast milk production per day
800mL/day AVERAGE
Milk ejection reflex
Sucking -> pulse of oxytocin from posterior pituitary -> contraction of myoepithelial cells surrounding alveoli -> milk ejected into ducts and lactiferous sinuses
Symptoms women may get due to milk-ejection reflex
- No symptoms at all
- tingling/prickling/pins and needles sensation
- sudden feeling of fullness
- increase in skin temperature
- feeling of wellbeing/relaxation
- pain or nausea
- dripping/leaking from other breast
- intense thirst
- uterine contractions + gush of lochia
- slow sucking of infant (approx 1/sec)
Recommended nutrition for lactating women
- overall increased energy requirements
- intake affects micronutrient composition of breastmilk only
Vitamin D and iodine (150 microg/day supplementary) is recommended
Advice to give vegan mothers who choose to raise infant on vegan diet
Breastfeed as long as possible (ideally 2+ years)
If not, then soy-based formula for the first 2 years AND dietary advice
Likely will require supplements especially for iron and B12
Schedule of solids introduction in infants
From AROUND 6 months (4-6mo depending on infant signs)
First introduce IRON-RICH foods (iron-enriched cereals, pureed meat/poultry/fish, cooked tofu and legumes)
6-8 mo: purees -> mashed -> minced -> chopped foods
Ensure lumpy foods <9mo
8mo: finger foods
12mo: same foods as rest of family, continue iron-rich foods, small frequent servings of nutrient-dense foods
Recommended drinks to offer infants/children
NOTHING other than breastmilk/formula first 6 months
Cows milk: only with cereals etc <12mo, >24mo max of 500mL/day
Water (after 12mo)
Fruit juice, soft drinks, cordial should be avoided
Tea, coffee, caffeinated drinks are unsuitable
Foods to avoid in infancy
Honey - do not give <12months due to risk of botulism
Animal milks
- FSCM ONLY with cereals/custards etc. in first 12 months
- goat’s milk NEVER GIVE TO A CHILD
- unpasteurised milk NEVER GIVE
- plant based milks (only acceptable is soy follow-on formula)
- nutrient poor, high fat/salt/suagr foods (e.g cakes, biscuits, chips, lollies etc)
Definition of subgaleal haemorrhage
Bleeding into the space between the epicranial aponeurosis and the periosteum
Cause of subgaleal haemorrhage
Rupture of emissary veins (which connect dural sinusess to scalp veins)
Most commonly after vacuum delivery
Potential consequence of subgaleal haemorrhage
Life threatening haemorrhage
- up to 250mL (50-75% of neonatal blood volume) can bleed into subgaleal space, with only a 1cm increase in scalp thickness
Mortality associated with subgaleal haemorrhage
12-25% in infants admitted to NICU
Risk factors for subgaleal haemorrhage
- Instrumental delivery (esp vacuum)
- nulliparous
- 5 min apgar 7 or less
- cup marks on sagittal suture
- leadingedge of cup <3cm from anterior fontanelle
- failed vacuum extraction (requiring forceps/LSCS)
- high number of pulls/cup detachments/prolonged time from cup attachment to delivery
Clinical features of subgaleal haemorrhage
Insidious onset
Localised signs:
- vague generalised scalp swelling
- laxity of scalp - then becomes fluctuant
- ballotable lesion crossing suture lines
- pitting oedema over scalp/preauricular/periorbital
Generalised signs:
- 5 minute apgar 7 or less without asphyxia
- irritable cry or evidence of pain with handling
- haemodynamic instability (later sign) (tachycardia, tachypnoea, poor activity, pallor, anaemia, coagulopathy, acidosis, death)
Clinical features of caput succadaneum
Can cross suture lines and midline
Size and firmness starts to reduce 1h post delivery
Clinical features of cephalohaematoma
(bleeding between periosteum and underlying skull)
more common after instrumental delivery
Soft, fluctuant, localised swelling with well-defined outline
Does NOT cross suturelines
Canincrease in size over 12-24 hours
Prevention of subgaleal haematoma
Promote neonatal IM vitamin K after instrumental delivery +++
Avoid vacuum when contraindicated
Ensure correct placement of cup, correct traction, and abandonment if too many pulls/detachments/prolonged
Early diagnosis guidelines for subgaleal haematoma
Surveillance of different levels for all infants post instrumental delivery
If higher risk (ie lots of pulls/detachments etc, more difficult extraction, incorrect cup placement) should have regular formal observations for 12 h, and cord gas + Hb and platelets at delivery
Management of possible subgaleal haemorrhage
Immediately discuss with neonatologist
Prompt evaluation, resuscitation and supportive treatment
- restore circulating blood volume (IVT, blood products)
- circulatory support
- correct acidosis or coagulopathy
Transfer to NICU
Definition of neonatal hypoglycaemia
Low BGL <2.6mmol/L
(note that intervention thresholds may differ according to clinical situation e.g. preterm deliveries or at risk babies intervention threshold is lower at 2.0 due to expected drop in BGL)
Risk factors for neonatal hypoglycaemia (14)
- nil by mouth
- preterm birth
- respiratory distress/TTN
- LGA/macrosomia
- IUGR
- hypoxic-ischaemic events
- systemic conditions e.g. infection
- hypothermia (<36C)
- inborn errors of metabolism
- maternal medications (esp. beta blockers or valproate)
- hyperinsulinaemia
- maternal diabetes
- congenital hyperinsulinaemic hypoglycaemia
- iatrogenic hypoglycaemia
Reasons- to check BGL in an infant not considered “at risk”
- disinterest in feeding for 8h or more from birth/last feed
- hypothermia <36
- jitteriness
Recommendations for neonatal hypoglycaemia screening
Screen all at risk neonates at 1 and 4h (SA PPG)
Symptoms of neonatal hypoglycaemia
Mild- moderate:
Neuro: irritability, jitters, tremors, hypotonia, lethargy, temperature instability, high-pitched cry
Respiratory: tachypnoea
CVS:
tachycardia, diaphoresis
Gastrointestinal: poor-feeding, vomiting
SEVERE:
Neuro: eye roll, seizures, altered conscious state
Resp: hypoventilation, apnoea, cyanosis
CVS: pallor
Investigations to consider in neonatal hypoglycaemia
Serum glucose insulin Growth hormone Cortisol Ketone level (via UA or glucometer)
Basic nursing management of neonatal hypoglycaemia
Check temp and manage as indicated
Offer breastfeed/EBM or formula as soon as practical
Alert medical team
Recheck BGL in 30-60 min
Management of neonatal hypoglycaemia
BGL 1.5-2.5 (or 2.0):
- offer feed
- consider 10% glucose infusion at 60mL/day esp if respriatory distress
- repeat in 30-60 min aiming for >2.5 if enteral or >3.5 in IV replacement
<1.5 at any time (or baby with major illness <2.5)
URGENT MANAGEMENT REQUIRED
- IV 10% glucose bolus 2ml/kg + infusion 90mL/day
- IM glucagon if IV access delayed
- repeat BGL in 30 min
- Aim for >3.5mmol by 30-60 min
Advice from paediatric team
Risk factors for neonatal jaundice
Set up for haemolysis
- previous child with antibody mediated HDN
- FHx G6PD deficiency or inherited red cell membrane/metabolic defects (hereditary spherocytosis, PKD etc.)
- +ve maternal blood group antibody screen and +ve cord DAT to antibodies associated with HDN
- visible jaundice of any degree within first 24h
Weight loss >10%/poor feeding
Gestation 35-38 weeks
Unwell infant
OR
Confirmed/likely haemolysis
- in utero haemolysis on basis of fetal anaemia + pos maternal antibody screen
- rate of rise of SBR >5 without PTx or continued rise despite PTx
- baby with bilirubin above exchange level
Maternal blood group antibodies associated with haemolytic diseaese of the newborn
Anti-D
Anti-C
Anti-kell
Others including Anti-A or -B are less likely to cause haemolysis
Recommended monitoring for neonatal jaundice
Daily clinical assessment for low risk babies prior to discharge
- blanching of skin with finger tip in appropriate light
OR
- transcutaneous POC light reflectance meter
higher risk babies requireblood bilirubin measurements
Clinical assessment of neonatal jaundice
Extending below nipple line has high sensitivity for plasma levels >75th centile
- therefore should be checked with bilimeter and/or SBR
Clinical assessment is limited in dark skinned babies, therefore should be checked with bilimeter or blood level
Bilimeter use and efficacy
Unaffected by gestation, postnatal age or skin pigmentation
Underestimates total bilirubin level, especially at higher blood levels
- therefore blood bilirubin should be checked if bilimeter result >75th%ile
Use of hour-specific bilirubin charts in neonates
Only validated in well babies without haemolysis
Therefore should only be used in well babies >38 weeks chart, and well babies 35-37+6 weeks
Indications of exchange transfusion
- Rising bilirubin despite intensive PTx, approaching exchange line
- anaemia with Hb <100, cardiac failure, or hydrops
- Suspected kernicterus regardless of bilirubin level
Definition of prolonged neonatal jaundice
> 2 weeks in >35/40 gestation
OR
3 weeks in <35/40 gestation
Requires investigation, advise parents to present for medical review if any visible jaundice after 2 weeks, or if pale stools at any time
Standard investigations for prolonged neonatal jaundice
- Review NNST results
- Total and conjugated bilirubin
- Free T4
- Urine culture
If above all normal and healthy breast fed baby, reassure that breast milk jaundice, and will resolve over 2-3 months
Follow up of jaundiced babies
HEARING: AABR for neonatal screening rather than usual test if:
- jaundice due to haemolytic disease
- bili >350 in term baby
- bili >250 in sick term, of a preterm >32/40
- all babies <32/40 or 1500g BW
Should be performed as close to discharge from hospital as possible. If passes, no routine audiology f/up required
ANAEMIA:
- if confirmed haemolysis, close f/up over 4-6 weeks to watch for late anaemia
- Most likely with Rh isoimmunisation - weekly CBE and reticulocyte
- folic acid supp where continued haemolysis suspected
- if unusual haemolysis, haem advice
ENCEPHALOPATHY
- if any symptoms/signs or who have been unwell with jaundice require long-term follow-up with paediatrician
10 significant viral infections in pregnancy:
- CMV
- Parvovirus
- Rubella
- Measles
- Mumps
- Varicella
- HIV
- Hepatitis A
- Hepatitis B
- Hepatitis C
Most common manifestations of congenital cytomegalovirus infection
Deafness Mental disability Hepatitis Pneumonitis Blindness
Transmission of cytomegalovirus
Transmitted through infectedblood, saliva, urine, breastmilk or through vertical transmission (in utero or intrapartum) or sexual contact
Risk of CMV infection in pregnancy transmitting to neonate
In primary infection - 50%
In reactivated disease: only 1% transmission rate
Features associated with symptomatic fetal infection (11)
Microcephaly Ascites Hydrops fetalis Oligo or polyhydraminos Hepatomegaly Pseudomeconium ileus hydrocephalus IUGR pleural or pericardial effusion Intracranial calcification Abdominal calcification
Rate of symptomatic congenital CMV in babies to mothers who develop infection in pregnancy
50% transmission in PRIMARY infection
- 10% of infants will be born symptomatic
90% of these infants will develop sequelae
(10-30% mortality rate, 18% hearing loss, neurological conditions - microcephaly, intellectual impairment, seizures, chorioretinitis)
Diagnosis of CMV in pregnancy
Maternal: CMV serology and repeat 2-4 weeks (if IgG -ve to positive OR rising then primary infection)
Management of CMV in pregnancy
Supportive management of mother
Check for fetal infection (amniocentesis for PCR/viral culture and serial USS)
Counsel mother re: option to continue pregnancy v terminate
Counsel re: risk of congenital CMV up to 4y following seroconversion (1% risk in 4th year)
Management of newborn with known congenital syphilis
Paeds at delivery for detailed examination
Test:
- ophthal examination
- cranial USS ?hydrocephaly
- CT brain - intracranial calcification, verntriculomegaly, cerebral atrophy
Labs <3weeks:
- CMV IgM serology
- PCR for viral detection +/- viral culture (blood, urine, NPA)
Consider ID input ?antivirals
Paeds review every 3-6 months if asymptomatic, likely more if symptomatic depending on presentation
Main pathophysiology behind congenital CMV
Fetal infection causes cytolysis leading to areas of focal necrosis and healing by fibrosis and calcification
Transmission of parvovirus
Direct contact with respiratory secretions and hand-mouth contact
Vertical transmission
Most infectious from 1 week after exposure to before rash onset (likely not infectious after that)
Clinical features of parvovirus
30-40% subclinica
Fever, myalgias and malaise which settle prior to rash onset (slapped cheek/reticular macular rash)
Arthralgia or arthritis common adults, can develop few weeks after infeciton
Can cause aplastic crisis in people with thalassaemia or sickle cell anaemia
Advice to pregnant women to avoid parvovirus
Standard precautions
Susceptible pregnant HCW avoid caring for women with known parvovirus
Routine screening not recommended
Complications of fetal parvovirus infection
Spontaenous miscarriage/stillbirth - 13% risk <20/40 - 0.5% risk >20/40 Hydrops fetalis - 3% risk if maternal infection 9-20/40 - on average 5 weeks after maternal infection
No evidence of congenital anomalies or long term sequelae for infant
USS findings of hydrops
Ascites
Skin oedema
Pleural and pericardial effusions
Placental oedema
Management of pregnant women exposed to parvovirus
Check IgG and IgM
- if IgG positive = immune, no further management
- if IgG negative monitor in 2-4 weeks ?seroconversion
If infection confirmed, serial USS every 1-2 weeks to assess for hydrops, if any signs, refer to MFM
Epidemiology of varicella in pregnancy
up to 4% of pregnant women NOT immune
VZV in pregnancy is complicated by pneumonia in 10% of cases
20-30% risk of transmission to neonate
Transmission of varicella
- through airborne/respiratory droplets and direct contact with vesicle fluid
- contagious from 2d before rash until all lesions crusted over (approx 1 week after onset)
Risk of foetal varicella syndrome in maternal varicella infection
0.5% risk in 1st trimester
1.4% risk in 2nd trimester
Nil in 3rd trimester (but may be at risk of neonatal disease if around time of delivery)
Consequences of foetal varicella syndrome
Skin scarring Eye and limb abnormalities IUGR/LBW Prematurity Cortical atrophy, intellectual disability Decreased sphincter control Early death
Risk of severe neonatal varicella infection secondary to maternal infection
If primary CHICKENPOX disease onset in mother >7 days before delivery, neonatal infection is mild (as maternal IgG is protective)
If <7days before or 2 days after, risk of severe infection
No risk if shingles infection - shingles in otherwise healthy pregnancy is not associated with intrauterine infection
Definition of significant varicella exposure for pregnant woman
Same household as someone with active varicella
Direct face-to-face contact with a person with varicella for at least 5 minutes
Same room for at least 1 hour
Prevention of foetal varicella syndrome
Preconceptual varicella serology+/- immunisation
If <96h post exposure and seronegative, give zoster immunoglobulin and seek medical care immediately if develop chicken pox
If >96h post exposure consider oral antivirals if >20 weeks, lung disease, immunocompromised or active smoker
Management of maternal varicella infection in pregnancy
Isolate
If <24h since appearance of rash- oral antivirals
If >24h since onset of rash:
- no antivirals
- monitor at home unless underlying lung disease, ISS, or active smoker (in which case monitor in hospital)
Complicated varicella infection (respiratory, haemorrhagic o neurological symptoms, fever >6 days, newpox developing after 6 days) - 7-10 days aciclovir 10mg/kg for 7-10 days (iV then oral)
Management of neonates exposed to varicella
Maternal chickenpox >7 days before delivery:
No interventions unless <28/40 or <1000g then IV aciclovir
Maternal chickenpox <7 days before to 2 days after delivery:
ZIG 200IU <24h after birth ideally (up to 72h)
no isolation req, still breastfeed
Maternal chicken pox 2-28 days after delivery (or other exposure when mumw as seronegative): Consider ZIG <96h
Maternal shingles - no risk
Varicella zoster immunoglobulin doses
Neonates: 200iu IM (1x vial)
Adults: 600IU I (3 vials)
Risk of vertical transmission of herpes simplex
40-50% risk in women with primary infection + active lesions at time of vaginal delivery/ROM
1-3% risk if lesions associated with recurrent infection (thought HSV1 higher at 15%, HSV2 <0.01%)
Risk factors for intrapartum neonatal infection with herpes simplex
Maternal PRIMARY infection
Multiple lesions
Premature delivery
Premature rupture of membranes
Management of HSV in pregnancy
If pre-existing:
- consider suppressive antiviral therapy from 36/40 if multiple recurrent lesions or sooner if frequent symptomatic recurrences
- careful speculum in early labour to check no active lesions
If first episode in pregnancy:
- obtain type specific HSV serology and PCR/culture from swab (if both positive for same type then likely recurrent infection)
- if confirmed new primary <28 weeks, counsel as per pre-gestaional
- if diagnosis >28/40, consider suppressive therapy from 36 weeks + caesarean delivery regardless of active lesions
If first episode diagnosed during labour:
- LSCS
- HSV type specific PCR on genital swab
Neonatal management of HSV exposure
Asymptomatic low risk neonate (e.g. maternal seroconversion >6 weeks before birth)
- normal postnatal care
- at 24h post birth collect surface swabs (eye, throat, umbilicus and rectum) for HSV1/2 PCR
- collect urine for HSV1/2 PCR
- observe for signs of infection
Asymptomatic high risk infant (i.e. maternal HSV close to birth or born through active HSV disease and no previous history of genital HSV)
- paeds at birth, complete exam for signs of HSV
- neonatal care unit
- urine for HSV 1/2 PCR
- CBE (?low PLT)
- LFT
- coags
- HSV PCR on bloods
- LP
- commence IV aciclovir
- surface swabs 24h after birth
Symptomatic infant
- Above tests
- IV aciclovir 14-21 days
- repeat LP after 7h if initially negative with signs of CNS disease
- repeat LP near end of treatment completion to confirm clearance
Clinical signs of neonatal HSV (9)
Vesicular skin lesions, atypical pustular or bullous lesions (especially on presenting part)
- ulcers involving buccal mucosa
- corneal ulcer, conjunctivitis, keratitis
- seizures
- unexplained fever or sepsis with negative blood cultures, not responding to antibiotics
- low PLT
- elevated LFTs
- DIC
- respiratory distress 24h after birth
Clinical features of rubella infection
Asymptomatic in 25-50%
May have:
- low grade fever
- transient erythematous rash - cephalocaudal spread with caudocephalic resolution within 3 days
- arthritis and arthralgia (most commonly in women of child-bearing age)
- neuro disorders, thrombocytopaenia (rare)
Infectious period of rubella
1 week before until 4 days after onset of rash
Incubation period of rubella
14-23 days
Potential (general) outcomes of a maternal rubella infection
No effect on fetus Placental infection only Placental/fetal asymptomatic infection, but can affect organs IUFD/miscarriage Congenital rubella syndrome
Risk of congenital rubella complications by gestation
- 90% of fetuses <8 weeks will be affected
- 50-80% fetuses 8-12 weeks will be infected, half of these will have fetal defects
- 12-16 weeks 30% fetuses infected, 10%overall risk of fetal defect (sensorineural deafness most likely)
- > 16 weeks fetal manifestations rare
Maternal reinfection in immune women very low risk of fetal damage
Potential features of congenital rubella syndrome
Sensorineural deafness
CNS dysfunction (intellectual impairment, developmental delay, microcephaly)
Eye abnormalities (cataracts, retinopathy, glaucoma, strabismus, micropthalmos)
Cardaic abnormalities (PDA, PA stenosis)
IUGR, short stature
Inflammatory lesions of brain, liver, lungs and bone marrow
Women who require post natal MMR vaccination
Anyone with Rubella IgG <10
OR
10-20 if born in Australia or the Western world
Should receive a second dose of MMR 4 weeks after the first
**ensure to inform NOT to get pregnant within 28 days of vaccination
Diagnosis of maternal rubella
Test rubella specific IgG and IgM for any pregnany woman with contact with OR clinical features of rubella
If both positive - possible recent infection, repeat test to confirm (4-fold increase in IgG titre is indicative of recent infection)
If both negative
- susceptible
- repeat serology if <3 weeks since contact or <7 days since onset of illness
- if no seroconversion, requires postnatal immunisation
- if seroconversion occurs, then consistent with maternal infection
IgG negative, IgM positive
- possible recent infection
- repeat - if no IgG seroconversion occurs may be false positive IgM (occurs especially in presence of rheumatoid factor)
IgG positive, IgM negative
- past infection or immunisation
Counselling women re: seroconversion that indicates maternal rubella infection
Counsel regarding risks relevant to gestation
- termination should be offered if infection occurs in first trimester
- consider fetal testing if maternal infection in 2nd trimester (CVS may be appropriate in 1st trimester if couple are uncomfortable about termination based solely on risk of fetal infection)
i. e. rubella PCR, culture and fetal IgM through CVS, amniocentesis or fetal blood sampling
Pre-pregnancy management of woman with HIV
Refer to HIV physician, sexual health physician and high risk obstetric consultant for discussion and screening
Ensure CST up to date (within last 12 months)
Management of HIV positive woman in pregnancy
Routine antenatal bloods+ serology for CMV, VZV, HSV, toxoplasmosis, cryptococcus, candida
- CBE, CD4 count, lymphotcyte subsets
- HIV viral load and resistance testing (unless already known)
- baselineLFT, EUC, amylase, lactate, HLA B5701
Refer to tertiary centre for MDT management with HIV specialist, ID specialist and High risk/MFM obstetrician
Intrapartum management of HIV positive woman
If SROM, consider augmentation
If PPROM 34-37 weeks, immediate delivery (with antibiotic and steroid cover)
If <34 week PPROM- MDT discussion and planning
If viral load undetectable at or after 36 weeks, can have vaginal delivery without intrapartum zidovudine
If viral load <400 - intrapartum zidovudine and consider LSCS
If viral load >400 intrapartum zidovudine and plan LSCS
Factors which increase risk of maternal to child transmission of HIV
> 70% occurs in labour
Risk increased by:
- advanced maternal illness
- high viral load
- poor maternal immune status (e.g. low CD4 count)
- ROM >4h before birth
- Preterm birth
- breastfeeding
- procedures that may damage integrity of natural barriers (e.g. FSE, vigorous suctioning, injections through unwashed skin, invasive testing such as CVS)
Tests performed in HIV screening
Screening test with ELISA for HIV antibody -if positive, then confirmed with Western Blot (if indeterminate, discuss with reference lab + virologist)
Risk of perinatal hepatitis B transmission
If mother is HBeAg positive risk is 70-90% of developing HBV infection by 6 months (if does not have HBIG and postpartum Hep B immunisation)
Risk with administering HBIG and Hep B reduces to 5-10%
If acute HBV in 1st or 2nd trimester, risk of transmission to newborn 10%, if in 3rd trimester, risk approx 75%
Recommended antenatal screening for hepatitis B
HBsAg to ALL pregnant women - positive = infection with Hep B
Can have false negatives though due to mutation in HBsAg therefore all women in HIGH RISK groups should also be screened with HBcAB
Further tests recommended if pregnant woman found to be HBsAg or HBcAb positive
HBeAg (positivity indicates high infective status)
HBeAb (positivity indicates lower risk of spreading HBV infection)
HBcAb
LFTs (and repeat at 28 weeks)
CBE
HBV viral load (repeat before 32 week gestation)
Management of HBV in pregnancy
Refer to ID specialist and high risk obstetric unit. If high viral loads may be considered from approx 32 weeks (or 28) to reduced risk of perinatal transmission(not indicated if very low viral laod)
Postpartum management of neonate born toHBV positive mother
HBIG 100 units AND HBV vaccine given within 12 hours - skin should be cleaned prior to injection - continue with normal childhood HBV schedule
Follow up at 8-12 months (2 months post completion of primary schedule) for HBsAg, HBsAb - if antigen positive, refer to paeds gastro or ID
Breastfeeding encouraged
Risk of perinatal transmission in HCV RNA positive women
approximately 5% - transmission is 3-4 x more likely in event of co-infection with HIV
Postpartum management of neonate born to HCV positive mother
Clean skin with soap and water if visible blood OR with alcohol wipe prior to injections
HBV vaccination within 12 hours of birth
If co-infection with HBV, also requires 100IU of HBIG
Test for HCV Ab at 18 months of age
Risk of fetal transmission and congenital abnormalities of toxoplasmosis
Depends on gestation at maternal seroconversion
1st trimester - low risk of vertical transmission (5-15%) but high risk of abnormalities (60-80%)
2nd trimester - moderate risk vertical transmission (25-40%), low risk of congenital abnormalities (15-25%)
3rd trimester - 30-75% risk of vertical transmission (higher rates closer to term), 2-10% risk of abnormalities
Abnormalities associated with congenital toxoplasmosis (9)
- Chorioretinitis/retinal scarring
- Hydrocephalus
- Intracranial calcification
- Mental retardation
- Hepatosplenomegaly
- Pneumonia
- Thrombocytopaenia
- Lymphadenopathy
- Myocarditis
Clinical features of toxoplasmosis
Most patients will be completely asymptomatic Potential symptoms in mild illness: - flu-like symptoms - malaise - myalgias - Swollen lymph glands
Severe disease (more likely in immunocompormised) - ocular toxoplasmosis (blurred vision, photophobia, red eye, tearing)
Diagnosis of toxoplasmosis
Consider testing toxoplasmosis serology in pregnant women with acute symptoms (e.g. malaise, fever, lymphadenopathy)
If IgG and IgM positive indicates POSSIBLE recent infection
- IgM can remain positive for years
- IgA, rising AigG and/or low IgG avidity are more specific for recent infection
- if both are positive, repeat serology for IgM, IgA and/or IgG titre and avidity
- if on repeat, High IgM, positive IgA and low IgG avidity consistent with recent toxoplasmos infection
transmission of toxoplasmosis
Faecal-oral route
- undercooked, contaminated meat (esp. pork, lamb or venison) or shellfish
- contaminated water
- accidental ingestion through contact with cat faeces (e.g. cleaning cat’s litterbox, touching or ingesting anything that has come into contact with cat faeces, accidentally ingesting contaminated soil)
Management of toxoplasmosis in pregnancy
Further investigations to determine risk to fetus:
- USS to detect abnormalities
- amniocentesis for PCR/culture at 18-20 weeks or >4 weeks after maternal infection
If both above are negative, consider pharmacological treatment if maternal infection is fairly certain
In 1st trimester: counsel woman/partner re: termination if amniocentesis PCR is positive
2nd trimester: Counsel re: termination if USS abnormal
Spiramycin, atavaquone or azithromycin if medication indicated (unknown efficacy)
3rd trimester (as above medical treatment, termination not advised)
Intra-/Postpartum management of toxoplasmosis in pregnancy
Paeds at delivery
Newborn assessment for congenital toxoplasmosis
- ophthal examination and cerebral ultrasound required
- placenta for histo/PCR
- infant whole blood for PCR, serology for specific IgM and/or IgA, persistent IgG
- infant CSF for PCR
Majority of infected babies will be asymptomatic
Manage with spiramycin oral syrup for first 12 months
- repeat IgG at 6 months
- regular paeds/ID review
Presentation of listeriosis in pregnancy
*always obtain a dietary history from pregnant women with febrile, flu-like ilness, myalgia, headache or diarrhoea
Often asymptmatic
Can mimic pyelonephritis due to loin pain
Risks of listeria in pregnanct
In early pregnancy: fetal infection can cause miscarriage
In 2nd and 3rd trimesters, if untreated maternal infection, associated with 40-50% fetal mortality (septicaemia, multi end organ damage, still birth, neonatal death)
Neonatal infection: pneumonia, sepsis or meningitis
Mortality rate 3-50%
Management of maternal listeriosis infection in pregnancy
Mild: PO amoxicillin
Severe: IV amoxicillin + gentamicin
(if penicillin allergy, consider bactrim PO or IV if >12/40)
Presentation of neonatal listeriosis
Variable, but most commonly:
- respiratory distress
- rash
- fever
- jaundice
- lethargy
Suspicious findings include:
- placental, cord, or post-pharyngeal granulomas
- multiple small skin granulomas, papular or pustular skin rash
- Meconium stained liquor <34 weeks
- purulent conjunctivitis
Pathophysiology of UTIs in pregnancy
- Obstructed urinary flow -> stasis -> increased risk of asymptomatic bacteriuria becoming pyelo
- Smooth muscle relaxation secondary progesterone -> reduced bladder and ureteral tone, dilatation of renal pelvices and ureters -> increased bladder volume, urinary stasis, residual volume and VUR
- pregnancy-induced changes in urine pH, osmolality, glycosuria and aminoaciduria may facilitate bacterial growth
Asymptomatic bacteriuria in pregnancy statistics
occurs in 5-10% of pregnancies
30% will develop acute pyelonephritis if untreated
Associated with preterm birth, LBW
Antibiotics associated with reduced preterm delivery and LBW infants
Pathogens involved in asymptomatic bacteriuria in pregnancy
E coli >80%
second most common is staphylococcus saprophyticus
Indications for antenatal MSSU
Routine MSSU at booking
Repeat after contaminated specimen
History of recurrent infections outside of pregnancy
Structural abnormality of the urinary tract
Gestation of highest risk of UTI in pregnancy
Risk begins at 6/40 and peaks 22-24/40
Risk factors for UTI in pregnancy
Low SES Sickle cell trait DM Neurogenic bladder retention History of previous UTIs Structural abnormality of urinary tract Renal stones
Diagnosis of asymptomatic bacteriuria/UTI in pregnancy
> 100,000 bacteria/mL
- <20 white cells (in AB)
- if 2+ organisms usually contamination and should be repeated
+ clinical findings in acute cystitis
General considerations for management of acute cystitis or asymptomatic bacteriuria in pregnancy
- 5 day course antibiotics (10-14 days for pyelo)
- at least 48h IV if bacteraemia
- increase fluid intake +/- IVT
- monitor urine output
- urinary alkalinisers are safe, but DO NOT USE WITH NITROFURANTOIN (will reduce efficacy)
- only commence antibiotics for asymptomatic bacteriuria AFTER culture and sensitivities (not empirical based on UA)
Antibiotics for uncomplicated UTI (empirical) in pregnancy
Cephalexin 500mg BD for 5 days
OR
Nitrofurantoin 100mgBD for 5 days
OR
Augmentin DF BD for 5 days (only if <20/40)
OR
Trimethoprim 300mg daily for 5 days (only if>12/40)
Antibiotic options for asymptomatic E coli bacteriuria
- cephalexin 500mg BD 5 days
- nitrofurantoin 100mg BD 5 days (but don’t use Ural)
- trimethoprim 300mg daily for 5 days
- ADF BD for 5 days
Augmentin duo forte use in pregnancy
Only use if <20 weeks
Associated with increased risk of necrotising enterocolitis, functional impairment and cerebral palsy, therefore only use inf no alternative
Antibiotics options for staph saprophyticus asymptomatic bacteriuria in pregnancy
- Cephalexin 500mg BD 5 days
OR - Amoxicillin 500mg TDS for 5 days
Antibiotics for pseudomonas asymptomatic bacteriuria in pregnancy
Norfloxacin 400mg BD 5 days
Repeat MSSU 48h after treatment completed
Management of GBS asymptomatic bacteriuria in pregnancy
Penicillin V 500mg BD 5 days OR cephalexin 500mg BD 5 days OR clindamycin 450mg TDS 5 days
(dependent on allergies)
THESE WOMEN NEED GBS PROPHYLAXIS IN LABOUR
Management of acute pyelonephritis in pregnancy
48h minimum IV antibiotics
IVT+ monitor urine output
Antipyretics PRN
Monitor for preterm labour
Amoxicillin 2g 6 hourly IV+ gentamicin 5mg/kg daily
OR
ceftriaxone 1g IV daily
Step down to oral antibiotics after >24h apyrexia, clinically improving. Base on susceptibilities.
(doses same as for UTI except cephalexin 500mg QID) and continue for 10 days
Indications for antibiotic prophylaxis for UTIs in pregnancy
2+ documented separate episodes of CYSTITIS (not asymptomatic bacteriuria)
OR
Single episode pyelonephritis
UTI prophylaxis options in pregnancy
Nitrofurantoin 50mg nocte (be careful using close to term)
OR
cephalexin 250mg nocte
OR
trimethoprim 150mg nocte (avoid 1st trimester or in women concerned about folate)
Indications for tuberculosis screening in pregnancy
HIV positive mothers
OR
recent contact with infectious TB (e.g. household)
Not otherwise performed as usually treatment would be deferred until 2-3 months postpartum in latent infection
Amphetamine effects on pregnancy
Amphetamines: - cardiac malformations - ?other malformations such as cleft palate - IUGR (impaired placental function) Methamphetamines(ice/speed): - preterm labour - placental abruption
MDMA/Ecstasy:
- little evidence of obstetric complications or teratogenicity, but likely confounding effect as multi-drug users
Risk of neonatal abstinence syndrome with all, lower than risk with opioids. 50% will have some withdrawal but only 5% of infants will require treatment
Effects of marijuana in pregnancy
Crosses the placenta - may cause withdrawal syndrome in neonates of heavy users
Some evidence of association with IUGR
Definition of polyhydramnios
AFI >20cm (used to be 24cm)
OR Maximal vertical pool >8cm
Amniotic fluid production
Mostly produced by amniotic membrane covering placenta and cord
>20 weeks also contribution by fetal kidneys
Composition of amniotic fluid
Same composition as maternal plasma for first half of pregnancy
Then hypotonic compared to fetal and maternal plasma, with more urea and creatinine than plasma
Prevalence of polyhydramnios
Affects 1% of pregnancies
Causes of polyhydramnios
- Impaired swallowing
- anencephaly
- CNS abnormalities
- myotonic dystrophy
- oesophageal atresia
- tetralogy of fallot - Reduced absorption
- gut atresias - increased production from fetal membranes
- spina bifida
- anencephaly - Excessive urination
- cardiac overload (high output cardiac failure, fetal anaemia) - Increased placental area
- multiple pregnancy
- diabetes
- placental tumour (rare)
Complications associated with polyhydramnios
Maternal:
- overdistention -> PROM
- pain
- unstable lie
- cord prolapse
- abruption
- PPH
Fetal/neonatal:
- associated fetal anomalies
- asphyxia from cord prolapse
- prematurity
Clinical features of polyhydramnios
- SFH large for dates
- tense abdomen
- difficulty palpating fetal parts
- reduced fetal movements
Investigations to consider in polyhydramnios
USS (to confirm)
- detect fetal structural anomalies
Diagnostic amniocentesis
Exclude treatable causes (fetal anaemia, cardiac failure)
Oligohydramnios definition
Varies with gestational age, but generally:
AFI <5cm
Deepest pool (MVP) <2cm
Causes of oligohydramnios
MATERNAL:
- PROM
- poor placental diffusion
- drug effect
FETAL:
- hypoxia
- fetal anomalies (renal agenesis, renal dysplasia, urethral valve anomalies)
Complications associated with oligohydramnios
High risk pregnancy
Fetal anomalies
IUGR
Fetal hypoxia (related to poor placental function)
Early severe oligohydramnios associated with pulmonary hypoplasia and fixed deformities of flexion
Risks associated with poor glycaemic control in pregnancy
- congenital malformations
- pregnancy complications
(macrosomia, IUGR, preterm birth, PET, shoulder dystocia, IUFD) - operative delivery or LSCS
- Neonatal complications (hypoglycaemia, jaundice, respiratory distress)
Hypoglycamic agents safe in pregnancy
Metformin
Insulin
All else have limited evidence and should be discontinued prior to pregnancy
Pre-conception counselling for pre-existing diabetes
- Discuss risks of poor glycaemic control in pregnancy
- plan reviews with woman’s GP, endocrinologist/physician, DNE
- delay attempts of conception until BGL optimised (HbA1c <75, ideally <6.5%
- change to pregnancy safe hypoglycaemics (metformin, insulin)
- If T1DM, consider change to continuous subcut pump (refer to diabetes service)
- folate 5mg daily for 6 weeks prior to conception
Antenatal care specific for women with pre-existing diabetes
- refer to high risk clinic + DNE
- aspiring 100mg nocte
- weekly DNE monitoringofBGL
- 2-4 weekly specialist appointments
ADDIT investigations:
- booking: HbA1c, TFTs, early morning spot urine ACR
- UA for protein every visit
- confirm dates with dating scan
- consider early 16/40 morphology if appropriate
- If HbA1c >10%, fetal echo at 20-22 weeks
- Consider growth scans in third trimester
BGL MONITORING:
- change monitoring to include fasting+ 2h post-prandial measurements
REFER:
- ophthal
- high risk clinic, obs med, endo, DNE
Timing of birth for women with T1DMor T2DM
Should always occur <40+6
(but only if BGL within target, normal growth and AFI and otherwise uncomplicated pregnancy)
Induction at 38+6 if: abnormal AFI, difficulty maintaining target BGL at 38/40, macrosomia or IUGR, HTN/PET developing
IF birth likely <37+0, consider steroids for fetal lung maturity, admitfor additional glucose monitoring and increased insulin at direction of obs med/endocrine
Method of birth for women with pre-existing diabetes
Vaginal birth is safe if EFW <4kg - discuss risks of IOL and potential shoulder dystocia
Intrapartum care for women with T1DM
CTG
Consul with physician
Avoid prolonged labour and water overload
If ordered, give oxytocin with NORMAL SALINE (not Hartmann’s) to prevent hyponatraemia
Insulin infusion as per protocol, with hourly BGL monitoring
Intrapartum care for women with T2DM
Continue pre-existing insulin regimen until labour is established, or no later than midnight on day of admission for IOL
Continue metformin until labour established
Hourly BGL (if >8 over 2h period and birth not imminent, to commence insulin infusion)
Continuous CTG
If giving oxytocin, give with normal saline
Beware of risk of shoulder dystocia
Cease dextrose/insulininfusionimmediately after birth
Management of neonates born to women with T1/T2DM
Paediatrician aware of birth
Feed within 60 minutes (ideally BF)
First BGL <1h of age
Most babies need close observation in nursery for hypoglycaemia, polycythaemia, jaundice, hypocalcaemia, RDS
Postpartum care for women with non-gestational diabetes
Send placenta for histopath
Review hypoglycaemic therapy early (risk of hypos)
Appropriate contraception
Encourage breastfeeding for minimum 2 months
Ensure appropriate hypoglycaemic agents for breastfeeding
Hypoglycaemics safe in breastfeeding
Insulin (all forms)
Metformin
Glibenclamide and glipizide (NOT gliclazide or glimeprimide)
NOT SAFE:
- glitazones, acarbose, DDP-4 inhibitors (-gliptins), GLP1 antagonists and SGLT-2 inhibitors
Target BGLs in pregnancy
Fasting <5
Postprandial (2h) <6.7
If 2 or more of the same reading is elevated in one week, step up in management
How to administer OGTT in pregnancy
75g glucose load Fast from food for at least 8h Drink glucose over 10-15 minutes Remain seated and non-smoking for duration of test Blood at fasting, 1h, and 2h
Contraindications to OGTT
Gastric bypass surgery
gastric banding usually okay
When to perform an early OGTT in pregnancy (8)
In women who are at risk for OVERT diabetes in pregnancy (FBG >7 or 2h BGL >11)
- previous hyperglycaemia (including in pregnancy)
- maternal age >40y
- ethnicity: Asian, Indian subcontinent, ATSI, Pacific islander, Maori, Middle eastern, non-white African
- Family history of DM (1st degree relative with DM OR sister who had GDM)
- pre-pregnancy or booking BMI >30
- Previous macrosomic baby (>4.5kg or >90th centile)
- PCOS
- Medicated with steroids or antipsychotics
Statistics of DVT in pregnancy
90& occur in LEFT leg
>70% are iliofemoral (higher risk of embolisation than calf DVT)
Management of VTE in pregnancy
LMWH 1mg/kg BD
3 months if uncomplicated distal DVT OR 6 months for PE or proximal DVT
If therapy finished before end of pregnancy, prophylactic dose should continue until 6 weeks postpartum
Postpartum options for pharmacological treatment or prevention of VTE
LMWH - safe in breastfeeding
Warfarin - safe in breastfeeding NOT SAFE IN PREGNANCY
NOACs unsafe in pregnancy AND breastfeeding
Management of uncomplicated superficial thrombophlebitis in pregnancy
Aspirin 100mg for 5-7 days + TEDS + analgesia
If not resolved, for enoxaparin 40mg for 7-10 days, if not resolved for ultrasound
Features which complicate superficial thrombophlebitis in pregnancy (and indicate management with enoxaparin from outset)
Previous episodes in current pregnancy
Length >20cm
Previous personal or family history (1st degree) of DVT
Incidence of VTE in pregnancy
- 5-2/1,000 pregnancies affected
- 25% are PE
- 1 in 40 PE in pregnancy is fatal
Increased risk of VTE in pregnancy and postpartum period
5-10 fold increased risk antenatally
Further 15-25-fold increased risk postpartum
Factors in assessing women with history of VTE for antenatal prophylaxis
If on previous long-term anticoagulation (therapeutic dose LMWH)
2 or more previous VTE (prophylactic or intermediate dose LMWH)
1 previous unprovoked or oestrogen related VTE (prophylactic dose)
1 previous VTE provoked by non-oestrogen transient risk factor (surveillance)
Consideration of antenatal VTE prophylaxis in women with family history of VTE
If 1st degree relative with VTE NOT in setting of active malignancy - clinical vigilance or prophylactic LMWH if significant clinical risk factors
Antenatal VTE prophylaxis for women with known thrombophilias
Protein C or S deficiency OR FVL heterozygote: clinical vigilance
FVL homozygotes, prohrombin gene mutation homozygotes, double heterozygote FVL/PGM or antithrombin deficiency: clinical vigilance may be appropriate if no family history of VTE, if family history prophylactic LMWH at least
Side effects of long term LMWH
Bruising and pain at injection site Allergic skin reaction (rare) Thrombocytopaenia (HIT uncommon) Reversible osteoporosis Rise in ALT
Contraindicationsto LMWH use in pregnancy
History of HIT
Actively bleeding
High risk (e.g. placenta praevia)
Delivery expected within 24h
Intracranial haemorrhage or ischaemic stroke within past 4 weeks
Uncontrolled hypertension (SBP>200 or DBP>120)
Precautions:
CrCl <30
PLT <80
Coagulopathy
Peripartum LMWH considerations
Therapeutic LMWH - no regional analgesia for 24h
Prophylactic LMWH- no regional analgesia for 12h
No LMWH within 4h of spinal or removal of epidural
Causes of thrombophilias
Inherited: PROGOACULANT factor abnormalities - FVL mutation (causes activated protein C resistance) - prothrombin gene mutation - plasminogen activator inhibitor
DEFICIENCIES of endogenous proteins in coagulation cascade:
- Protein C deficiency
- Protein S deficiency
- Antithrombin deficiency
ACQUIRED:
- lupus anticoagulant
- antiphospholipid antibodies
- anticardiolipin antibodies
MIXED inherited/acquired:
- hyperhomocystinaemia
epidemiology of thrombophilias in pregnancy
15% of Western populations are affected with inherited thrombophilia
Inherited disposition can be identified in 60-70% of women presenting with DVT
Indications for investigating a woman for thrombophilia
- Strong family history of VTE in 1st and 2nd degree relatives (only check for inherited conditions)
- recurrent (3+) first trimester miscarriages
- Second trimester fetal loss
- any previous history of VTE
- stillbirth
- Early onset PET <34 weeks
- IUGR delivered <34 weeks
Investigations to consider in thrombophilia screen
Lupus anticoagulant Protein C and S (Protein S should not be measured in pregnancy) Activated protein C resistance (APCR) Factor V leiden Prothrombin gene MTHFR homocysteine Anticardiolipin antibody
Antenatal management of women with thrombophilias
Refer to obs med/physician/obstetrician with expertise
Arrange ongoing care in level 2-3 hospital
Antenatal aspirin
Increased feto-placental surveillance antenatally
Consider if LMWH heparin necessary
Factor V Leiden statistics
Heterozygosity present in 20-40% of non-pregnancy people with VTE
Homozygosity carries 80-fold increased risk for VTE
Occurs in 5-15% of European populations (rare in Asian or African populations)
Risk of VTE in pregnancy for FVL carriers is 0.2% (due to low prevalence in pregnancy overall)
Obstetric risks associated with factor v Leiden disease
Second and third trimester fetal loss Severe IUGR Abruption Severe early onset PET Preterm delivery Increased risk of pathological Doppler measurements
how to screen for factor V leiden disease
Screen with abnormal phenotype (Activated protein C resistance/APCR)
Prevalence of Prothrombin gene mutation
2-5% prevalence
More prevalent in Caucasian women
Obstetric risks associated with prothrombin gene mutation
3-fold increased risk VTE
?PET (controversial association)
IUGR
Placental abruption
Which thrombophilia screens are altered in pregnancy
Protein S - there is a marked physiological decrease in pregnancy, therefore should not take until at least 8 weeks postpartum
Prevalence of protein C and S deficiency
PC: 0.3%
PS: 0.1%
Obstetric risks associated with protein C and S deficiency
VTE Stillbirth Fetal loss (PS deficiency associated with recurrent loss) PET Abruption IUGR
Epidemiology of antithrombin deficiency
Rarest of inherited thrombophilias but MOST thrombogenic- only thrombophilia that will ALWAYS require thromboprophylaxis in antenatal and postnatal period
Prevalence 1 in 1,000-5,000
Definition of antiphospholipid syndrome
Autoimmune disorder defined by associated of vascular thrombosis and/or pregnancy morbidity with specified levels of antiphospholipid antibodies (either Lupus anticoagulant or anticardiolipin antibody)
Epidemiology of antiphospholipid syndrome
Most common acquired thrombophilia in pregnancy
Predominantly affects young women
Prevalence in pregnancy approx 2%
Who to screen for antiphospholipid syndrome and how
ANF and ACA in women with history of:
- early onset(<32w) PET and/or IUGR
- fetal death
- placental abruption
Obstetric risks associated with antiphospholipid syndrome
Recurrent early pregnancy loss (<10 weeks) PET Thrombosis Abruption IUGR preterm birth
Diagnosis of antiphospholipid syndrome
Lupus anticoagulant detected on 2 or more occasions at least 6 weeks apart
Anticardiolipin antibodies with moderate-high IgG or or IgM antibodies on 2 occasions at least 6 weeks apart
Antenatal management of women with antiphospholipid syndrome
Aspirin 100mg/day - if history of late fetal loss or IUGR
- early dating scan
- close BP and UA surveillance
- uterine artery dopplers at 20 and 24 weeks(if abnormal, consider 2-3 weekly scans)
- 4 weekly scans to assess growth and AFI if uterine arteries normal
- consider heparin
Contributors to hyperhomocystinaemia
Deficiencies in Vit B12, folate, B6 GI malabsorption Renal disease Thyroid deficiency Smoking Coffee and alcohol consumption
Risks associated with hyperhomocystinaemia
- early onset PET
- placental abruption
- neural tube defects
- stillbirth
- IUGR
- Vascular disease
- recurrent VTE (if severe)
- fetal loss
most common gene mutation causing hyperhomocystinaemia
MTHFR
Antenatal management of women with hyperhomocystinaemia
Avoidsmoking, alcohol, coffee Well balanced diet Folic acid Early dating scan + 12 weeks scan for neural tube defect Close PET surveillance Regular growth and wellbeing ultrasound
Prevalence of hyperthyroidism in pregnancy
0.2%
95% of these cases are due to Graves’ disease
Management of Graves’ disease in pregnancy
Refer to endocrinologist + obstetrician
Anti-thyroid therapy (propothiouracil likely as less fetal effects) - on lowest maintenance dose to keep free T4 in high normal range
- check T4 and TSH 6-weekly
- monitor for fetal tachycardia
Propanolol 40mg TDS if symptomatic
Obstetric complications of untreated hyperthyroidism
Preterm birth
Perinatal mortality
Fetal and neonatal thyrotoxicosis
Risk of thyroid storm triggered by stressof infection, labour, or operative delivery (high risk of maternal and fetal morbidity and mortality)
Antenatal management of hypothyroidism
Optimise T4 and TSH pre-conceptually
Increase thyroxine by 30% immediately in first trimester (2 extra doses per week)
Check TFT 4 weekly in T2, then 6-8 weekly
Aim for TSH 0.5-2.5
Postpartum, return to pre-pregnancy dose and re-check 6-8 weeks postnatally
Timing of prophylacitc anti-D in Rh negative pregnant women
28 and 34 weeks
Sensitising events which indicate prophylactic anti-D in pregnancy Rhesus negative women
First trimester:
- miscarriage
- termination of pregnancy
- ectopic pregnancy
- Chorionic villus sampling
Second & Third trimester:
- Amniocentesis/cordocentesis
- Fetal death
- Abdominal trauma significant enough to cause fetomaternal haemorrhage
- Antepartum haemorrhage
- External cephalic version
Antii-D dose
Multiple pregnancy: 625IU
Sensitising event <12 weeks: 250IU
Sensitising event >12 weeks (or routine prophylaxis): 625IU
How much Rh positive fetal RBCs will anti-D dose neutralise
250IU:2.5mL fetal RBC
625IU: 6mL fetal RBC
Rationale for routine anti-D prophylaxis
Silent transplacental haemorrhages will lead to very small amounts (0.1mL) of fetal RBC accessing maternal circulation, this usually occurs after 28 weeks and especially around time of delivery
Management of pregnant women with preformed anti-D antibodies
Discuss with MFM specialist
Assess monthly until 28 weeks, then every 2weeks in 3rd trimester
Non-invasive fetal genotyping (cell-free DNA)
If significant rise, maternal anti-D titre >1/16, or history of Rh disease in previous pregnancy fetal monitoring with MCA PSV
Requirements of RBCs use in fetal intrauterine transfusion
- O group (or ABO identical with fetus)
- leucodepleted
- CMV negative
- irradiated (to prevent graft v host disease)
- Plasma reduced
- <5 days old
- Rh and Kell negative
- Indirect antiglobulin test crossmatch compatible with mother’s plasma
Physiological changes to the renal system during pregnancy
Increased renal blood flow (due to increased cardiac output), increasing GFR by up to 50%
- fall in serum creatinine, urea, calcium and bicarbonate
- tubular capacity to resorb glucose and protein is exceeded -> proteinuria + glycosuria
Size of kidney increases due to increased blood flow (R>L due to dextrorotation of uterus)
Dilatation of pelvicalyceal system R>L, up to 15-20mm, due to progesterone activity on relaxing smooth muscle
Increased renin and aldosterone secretion -> sodium and water retention, fall in serum albumin and osmolality
Increased EPO and vit D secretion
Diagnostic criteria for GDM
OGTT results:
Fasting BGL 5.1-7
1h BGL 10-11
2h BGL 8.5- 11
(any one of these results = diagnosis)
Below this range is normal
Above this range is OVERT diabetes
Epidemiology of PROM and PPROM
PROM occurs in 10% of all pregnancies
PPROM occurs in 2-3% of pregnancies, but is associated with 40% of preterm deliveries
Risk factorsfor PPROM
- Past history of PPROM/preterm delivery
- urogenital tract infection/colonisation
- APH
- cigarette smoking
- past history of cervical surgery
- amniocentesis in current pregnancy (PPROM in this setting associated with more favourable outcomes)
- cervical length <25mm
- positive fetal fibronectin
- nutritional deficiencies
- lean maternal body mass
- multiple pregnancy
- polyhydramnios
Risks associated with PPROM
Maternal:
- infection (chorio, endometritis, septicaemia)
- increased risk of operative delivery and associated risks
Fetal:
- preterm delivery (most deliver within 1 week of PPROM)
- associated neonatalmorbidities (HMD, IVH, periventricular leukomalacia, neurological sequelae, infection - sepsis, pneumonia, meningitis, NEC, retinopathy)
- pulmonary hypoplasia
- MSK/facial deformities
- malpresentation
- cord events incl. prolapse
- placental abruption
- perinatal mortality
Investigations to perform in PPROM
HVS MCS LVS MCS GBS PCR \+/- STI screen MSSU
USS: fetal growth, +/- dopplers,
CRP + CBE daily for 3 days (then twice weekly if expectant management)
If expectant management, weekly HVS MCS
Management of PPROM (general principles regardless of gestation)
Antibiotics:
- prophylactic: IV benzylpenicillin 3g loading then 1.2g 4 hourly for 48 hours PLUS PO erythromycin 250mg QID for 10 days
- if signs of chorio: amox 2g IV 6 hourly, gentamicin 5mg/kg IV daily, metronidazole 500mg IV BD (total 5 days treatment - can change to PO postnatal if afebrile)
Tocolytics;
- NEVER GIVE if signs of chorio
- if contractions present but not in established labour, nifedipine can be given to prolong pregnancy for 4h while obtain steroid cover
Corticosteroids
- 11.4mg IM betamethasone in 2 doses 24h apart
Magnesium sulphate:
- if delivery anticipated within 24h, 24-30/40 gestation
Aim to deliver >34/40 if GBS positive OR >36/40 if GBS negative
However if any contraindicationsto expectant management (APH, fetal compromise, signs of chorioamnionitis, established labour), delivery when indicated
Surveillance required in expectant management of PPROM
- CTG daily for first 3-6 days then twice per week unless indicated
- CBE + CRP daily for 3 days then twice weekly
- HVS swab weekly
Statistics of preterm labour
- > 50% of women who present in preterm labour will continue their pregnancy
- occurs in 5-10% of all deliveries
- prematurity is the cause for 75% perinatal deaths
Risk factors associated with spontaneous preterm labour (12)
- previous preterm birth
- multiple pregnancy
- polyhydramnios
- urogenital tract infection
- previous cervical surgery
- uterine anomalies
- periodontal disease
- bleeding in 2nd trimester
- extremes of age
- smoking
- low pre-pregnancy weight
- pregnancies achieved through ART
Strategies for prevention of preterm labour
No population based interventions, but following may be suitable in at risk women:
- cervical length assessment at 20/40 (mean is 42mm, intervention considered if <25mm)
- supplemental progesterone (Cxlength10-20mm)
- Cervical cerclage (history of cervical incompetence, length <25mm at <24/40)
Factors to consider when using fetal fibronectin
Should be undetectable from 22-35 weeks (>35 weeks less valuable)
Must use STERILE water as lubricant - as intravaginal lubricants or disinfectants may interfere with antibody reaction and cause false negatives
False positive can occur with blood or semen
Management of pre-term labour:
Antibiotics- IV benzylpenicillin 3g loading, 1.2g 4hrly (only if active preterm labour, reduces maternal infection rate, no benefit to fetus)
Tocolytics - if need to transfer to another unit/give time to cover with steroids
Corticosteroids: if gestation age 23-34+6 and risk of imminent preterm birth or planned/expected within next 7 days
Mode of Magnesium sulphate: 24-30/40 gestation for neuroprotection where birth is anticipated within 24h
Mode of delivery:
If breech and viable -> caesarean
If cephalic, aim for vaginal
If <26/40 multiple, caesarean
Attendance of paeds/neonatologist at delivery. Dual vessel cord blood gas, sent placenta for histopath + swab
Definition of small for gestational age, IUGR, or low birthweight
SGA: weight OR abdo circumference <10th percentile for GA
IUGR: Evidence of growth restriction or arrest with EFW or birthweight<10th centile
Low birthweight: <2500g
Very low BW: <1500g
Extremely low BW <1000g
Normal growth velocity of the fetus
5g/day 14-15/40
10g/day 20/40
30-35g/day 32-34/40
Growth rate decreases >34 weeks
(growth rate lower in multiples than singletons)
Factors commonly associated with SGA (not IUGR)
Race Maternal size Female fetus Nulliparity History of baby with SGA Matrilineal tendency
Common factors assocaited with fetal growth restriction
MATERNAL:
- multiple pregnancy
- smoking, alcohol, amphetamines, cocaine
- Low SES
- DV
- PET
- previous stillbirth
- obesity
- Chronic HTN
- Connective tissue disorders
- Thrombophilias
- diabetes
- cardiac disorders
- hypotension (<60mmHg diastolic)
- respiratory disease e.g. severe asthma
- anaemia
- renal disease
- medications (narcotics, chemo)
- poor nutrition
FETAL FACTORS:
- fetal infection
- malformations
- chromosomal defects
PLACENTAL FACTORS:
- abruption
- praevia
- placentitis/vasculitis
- chorioamnionitis
- Placental cysts
- decreased uteroplacental blood flow
UTERINE FACTORS:
- fibroids
- morphological abnormalities (especially uterine septum)
Causes of SGA/IUGR
CCPP acronym
Constitutional
Chromosomal
Perinatal infections
Placental insufficiency
Aetiology of asymmetric v symmetric IUGR
Symmetric (20-30%)
- all organs decreased proportionally
- due to impairment of early fetal cellular hyperplasia
Asymmetric (70-80%)
- Relatively greater decrease in abdominal size (liver and subcut fat) than HC
- due to fetal adaptation to hostile environment, redistribution of blood flow in favour of vital organs
Percentage of SGA babies who are constitutionally small
70%
Healthy fetuses with no long term morbidity
Risks associated with babies who have IUGR
Still birth Birth hypoxia Neonatal complications Impaired neurodevelopment T2DM and hypertension in long term
Chromosomal causes of IUGR
(20% of IUGR/SGA)
Usually EARLY and SYMMETRICAL <5th%ile
- aneuploidy
- multiple deletions
- gene mutations
- placental mosaicism
Perinatal infections which can cause IUGR
(5% of IUGR due to infection)
- CMV most common
- rubella
- toxoplasmosis
- varicella
- syphilis
Placental insufficiency causes of IUGR
Many causes, often recurrent
e.g. PET, abruption etc. manifestaitions
“Other” causes of IUGR
Non-genetic congenital abnormalities (2%)
- hypoxaemia (e.g. cyanotic heart disease, severe anaemia)
Multiple gestation
- nutritional
- complications e.g. twin-twin, PET
Maternal factors
- reduced placental blood flow (HTN, DM, collagen disease, lupus, obstetric causes)
- smoking
- toxins e.g. warfarin, AEDs
Prevention strategies for SGA/IUGR
Smoking cessation Nutritional advice - well balanced - severe dietary restriction associated with LBW - low fasting BGL associated with LBW
Most sensitive measurements for detecting SGA/IUGR
AC is most sensitive SINGLE measurement (EFW also good)
Serial RELATIONSHIP between HC and AC, along with AFI interpretation is most useful for identifying growth pattern
- i.e. reduced AC growth with maintained HC growth, associated with oligohydramnios = IUGR
** oligohydramnios without an obvious cause is associated with high perinatal mortality
Investigations to perform in a fetus thought to be IUGR
Bloods (if early <32/40): - Hb - ?thrombocytopaenia - TORCH screen If severe early IUGR, consider: - thrombophilia screen - karyotype
USS:
- AC/HC/AFI
- UA Doppler surveillance (if increased resistance, repeat in 2 weeks, if absent or reversed diastolic flow, admit and steroid load, usually needs delivery within days)
Management of late onset growth restriction (>32 weeks)
Usually reflects mild-moderate uteroplacental dysfunction
Serial growth and AFI every 2 weeks
Delivery planning for growth restricted fetuses
Depends on aetiology, severity and gestation
If moderate:
- consider IOL if cervix favourable >36/40
- delay until >37/40 if normal surveillance
If significant:
- Aim to delivery 34-36 weeks
- if very preterm, delay until imminent signs of fetal compromise
- delivery if>34/40 and AREDF
- If IUGR and oligohydramnios >36 weeks, deliver
**If associated with AREDF, almost always requires LSCS delivery
Neonatal recommendations for low birthweight babies on discharge
Routine iron supplement for all babies <2500g
- 2mg/kg/day from approx 8 weeks to 12 months of age
Procedure for instrumental delivery
A: abdo palp (No fetal head palpable), address woman, analgesia, assistants
B: bladder empty
C: cervix check (fully, membranes ruptured)
D: determine position, station and pelvic adequacy
E: equipment- inspect vacuum cup, pump and tubing, check pressure. OR check correct forceps, blades match and lock
F: FLEXION POINT- position cup 3cm anterior to posterior fontanelle and using Finger to clear maternal tissue
FORCEPS: apply blades (left first)
G: Gentle traction
H: HALT - stop vacuum if no progress with 3 pulls, 3 pull offs or no significant progress after 20 minutes
HANDLE ELEVATED: elevate forceps handles in axis of birth canal
I: Incision - consider episiotomy
J: Jaw - remove cup/forceps when jaw is reachable or delivery assured
Indications for operative vaginal delivery
Maternal:
- inability to push
- Prolonged 2nd stage (3h with epidural, 2h without)
- Cardio or vascular conditions
- neurological or muscular disease
- significant vaginal bleeding
Fetal:
- suspected compromise
- malposition with relative dystocia (e.g. OP/OT)
Contraindications to operative vaginal delivery
- operator inexperience
- incompletely dilated cervix
- unknown fetal position
- unengaged head
- malpresentation (e.g. face or brow)
- suspected CPD
- GA <36/40 (for vacuum only)
(Relative:)
- fetal predisposition to fracture e.g. OI
- fetal bleeding disorder (e.g. haemophilia)
- Maternal bloodborne virus
Postpartum care following caesarean
- analgesia
- early removal of IDC (within 24h)
- early mobilisation and hydration
- deep breathing and coughing exercises +/- physio
- diet as tolerated
- debrief on birth and impact on future pregnancies
- observe for postop complications (ileus, UTI, URTI, DVT, wound infection)
Criteria for confirmed miscarriage
- evidence of intrauterine fetal pole (CRL) >6mm on TV scan with absent heartbeat
- Gestation sac >15mm without fetal pole
- successive scans of gestation sac <15mm fail to show change in size over 10-14 days
- substantial tissue within uterus >15mm with a history of blood loss and possible passage of tissue (incomplete miscarriage)
- Small fetal pole seen and bHCG is falling
Expectant management of miscarraige
- 70% will resolve spontaneously
- contents <15mm likely to resolve spontaneously
- 20% will need subsequent D&C especially if contents >15mm
- Complete resolution may take weeks
- less likely to be successful if there is an intact non-viable fetus and gestation sac
Need review 7-10 days after diagnosis, consider repeat ultrasound if there were previously contents noted
Risks of D&C when managing miscarriage
Bleeding
Infection
Perforation (1 in 300)
Asherman’s syndrome (1:1000) - less likely with suction curette
GA risks
Small risk of repeat procedure in presence of ongoing
bleeding
Most common sites for ectopic pregnancy
Tubal (95%) - Ampullary (55%) - Isthmic (25%) - fimbrial (17%) - Interstitial (2%) Other (5%) - Cervical - ovarian - peritoneal - C-section scar
Epidemiology of ectopic pregnancy
in developed countries:
Approx 1% of pregnancies are ectopic
(1% of ART pregnancies are heterotopic, 1 in 30,000 spontaneous conceptions are heterotopic)
- most common in 25-34yo
- mortality rate in developed countries 0.2%
- 10% recurrence risk after a single ectopic
Risk factors for ectopic pregnancy
- PID (7-fold increased incidence)
- smoking (impairs tubal motility)
- tubal surgery
- previous ectopic pregnancy
- POP, emergency pill, IUD (lower risk than those NOT on contraception, but higher risk than COCP users as progesterone reduces tubal mobility)
- ART
- endometriosis
- Abnormal embryo
Investigations to confirm ectopic pregnancy
- inappropriately rising quant serum bHCG (though up to 1% will have hCG levels <25 therefore neg on UPT_
- no intrauterine sac seen with HCG levels suggestive that should be visible ultrasonographically (PUL, not confirmed ectopic)
- fluid in pouch of douglas if ruptured, may have adnexal mass
Laparoscopy - gold standard for diagnosis
At what hCG level should an intrauterine pregnancy be visible on USS
TV scan: 1000-1500
TA: 1800-2000
Indications for surgical management of ectopic pregnancy
- Significant pain
- Adnexal mass >35mm
- fetal activity on USS
- hCG 5000IU or higher
- no availability for follow up of medical management
- maternal preference or seeking permanent contraception
- subsequent ectopic pregnancy in ipsilateral tube after previous medical management
Options for surgical management of ectopic pregnancy
- Salpingectomy (ideally laparoscopic, especially if haemodynamic compromise
Salpingotomy
- if other risk factors for infertility (i.e. already had other tube removed)
- 5% risk of persistent ectopic, 20% risk of further treatment, higher rates of recurrent ectopic
Local injection of MTX, KCl or prostaglandins
- high risk of persisting
Contraindications for medical management of ectopic pregnancy
- haemodynamic instability
- fetal cardiac activity
- hCG >5000
- mass >35mm
- no access to emergency facilities within 30 minutes of home
- heterotopic pregnancy
- immunodeficiency
- free fluid in pelvis
- sensitivity to MTX
pre-existing liver, haematological, pulmonary or peptic ulcer disease
Method of medical management of ectopic pregnancy
- Cease folate supplements
- 50mg/m2 TBSA methotrexate single dose IM
- Avoid UV light and high FODMAP foods to avoid side effects
- paracetamol (+/- NSAIDs if safe)- can get separation pain approx day 3-4
- quant hCG on day 0(+baseline bloods), 4 and 7
- if fails to fall more than 15% between days 4 and 7, will need second dose
- avoid pregnancy for 3 months
Consider if anti-d required (all Rh negative women)
Predictors that medical management of ectopic pregnancy will be successful
- lower serum hCG
- slow-risking plateau or falling hCG prior to treatment
- falling hCG by day 4
Presentation of a female with Kallmann syndrome
Delayed or absent puberty with an impaired sense of smell +/- colour blindness
(Autosomal dominant condition, causing GnRH deficiency (hypothalamic hypogonadotrophic hypogonadism)
Further defining the cause of hypogonadotrophic hypogonadism
GnRH test
- administer GnRH, if LH response is appropriate = hypothalamic failure
- if absence of LH response = pituitary failure
Causes of abnormal UTERINE bleeding
PALM COEI N
PALM = visually objective structural
COEI = unrelated to structural anomalies
N = not yet classified (e.g. AV malformations etc. )
Polyps
Adenomyosis
Leiomyoma (i.e. fibroids)
Malignancy
Coagulopathy
Ovulatory disorders
Endometrial
Iatrogenic
keep in mind women may have NON-uterine causes of vaginal bleeding (urethral, vulvar, vesical, vaginal, cervical and recto-anal)
Clinically significant maternal red cell antibodies
Anti-D
Anti-c
Anti-kell
Anti-S Anti-s Anti-u Anti-dia Anti-Coa
Acceptable antibody titres for clinically significant maternal red cell antibodies
Levels <1:32 are reasonable UNLESS
- >2-fold increase in titre
OR
- Anti-kell antibodies (even low titres are at risk for HDFN)
Mechanism for significant fetal/neonatal disease with maternal anti-kell antibodies
Suppressed erythropoiesis PLUS haemolysis PLUS peripheral sequestration of red cells
Monitoring pregnancies with clinically significant red cell antibodies
4 weekly titres until 28 weeks, then every 2 weeks
If titre >1:32 then needs weekly MCA PSV (through MFM department)
Causes for maternal collapse (12)
Vasovagal syncope
Postural hypotension
Haemorrhage (PPH, APH, Splenic artery aneurysm rupture, hepatic rupture)
Thromboembolism
Amniotic fluid embolism
Epilepsy
Eclampsia
Intracranial haemorrhage
Cardiac disease (MI, aortic dissection, cardiomyopathy, arrhythmia)
Drug toxicity/overdose (MgSO4, Local anaesthetic, illicit drugs)
Anaphylaxis
When should perimortem caesarean section be performed?
If there is no response after 4 minutes of correctly performed CPR in a woman >20 weeks
Amniotic fluid embolism “cause”
Can occur in any trimester
Caused by changes in the normal relationship between the membranes, placenta and uterine wall -> disruption of the integrity of the uterine blood vessels
amniotic fluid/debris is deposited in maternal lungs -> pulmonary vasoconstriction (?anaphylactic-type reaction)
Clinical presentation of amniotic fluid embolism
Sudden collapse during labour/delivery or immediate postpartum associated with:
- dyspnoea
- pink frothy sputum
- cyanosis
- Cardiorespiratory failure
- convulsions (10-20% of cases)
HYPOTENSION
HYPOXIA with respiratory failure
DIC
COMA OR SEIZURES
Presentation of regional anaesthesia toxicity
Onset almost immediately (within up to 20 mins max) of administering local anaesthetic
- complain of metallic taste, tinnitus, confusion and disorientation
- respiratory muscle paralysis and cardiac arrest may occur
