Fetal medicine Flashcards
Definition of FGR vs SGA vs IUGR
FGR = EFW <10%
SGA (isolated FGR) = physiologically small
IUGR = EFW <10%, abnormal dopplers/ AFI, poor growth velocity
Antenatal monitoring for those with known IUGR risk factors
Growth
AF
UAD from 26/40 every 2-4/52
Consider aspirin if risk factors present
Incidence and outcome of IUGR
Affects 10% pregnancies
Recurrence 25%
70% normal outcome
if EFW <3%, significant increase in adverse perinatal outcomes
Monitoring diagnosed IUGR
Growth scan every 2/52
If raised dopplers (PI > 95%) = increase monitoring to weekly, UAD every second week
AEDF <34/40 - admit, daily CTG, twice weekly AFI + UAD
REDF <30/40 - admit, daily CTG, AFI/ UAD 3x/week, +/- fetal med opinion
MCA and DV can be measured - not used for delivery timing
Delivery in IUGR
Consider timed steroids - 24-34/40 and up to 38/40 in some situations
AEDF - delivery </= 34/40 or sooner if poor growth/ dec AFI
Isolated FGR w normal LV/ UAD - deliver 37/40 or up to 38-39/40
If <32/40, consider MgSO4
Continuous CTG in labour w abnormal UAD, low threshold for CS
Cord gases and placenta for histology
MOD - individual basis decision. CS advised if AEDF or very PT
PN counselling if <34/40 - review of placenta and thrombophilia screen, future pregnancy plan
Women at high risk for pre-eclampsia
Hypertensive disease in prev pregnancy
Chronic kidney disease
Autoimmune disase
T1 or T2 diabetes
Chronic hypertension
Moderate risk factors for pre-eclampsia
First pregnancy
Age 40+
Pregnancy interval of >10 years
BMI >35
FH PET
Multi-fetal pregnancy
Definition of dopplers, absent end and reverse
Doppler: uses sound waves to determine flor and velocity of blood flow in a vessel, shift in observed frequency of a wave due to motion
AEDF - no flow towards fetus in diastole
REDF - blood flow away from fetus during diastole
Causes of abnormal dopplers
Maternal:
- medical dx
- prev SGA
- poor weight gain/ excessive exercise
- uterine anomalies
- ERT
Paternal:
- low birthweight
Fetal:
- female
- chromosomal
- malformations
- infections
- multiple fetuses
Placental:
- developmental abnormalities
- cord coil
- infarction
- villisitis
Risks to baby in the neonatal period with detected abnormal dopplers
increased risk CS
Low BSL after delivery
Hypoxia during delivery
Admission to SCBU
Meconium aspiration
Increased risk of motor and neurological abnormalities
Feeding difficulties
NEC
Sepsis
Fetal anaemia - definition
Normal fetal Hb shoudl increase throughout GA - 150g/L at 40/40
Anaemia: > 70g/L below mean for gestation
Hydrops zone - gestation dependent. Ranges from fHb <40g/L at 18/40 to fHb 80g/L at 40/40
Implications of fetal anaemia
Reduced tissue perfusion –> brain injury, cardiac failure, IUFD
Causes of fetal anaemia
MC: alloimmune red cell destruction
MC non-immune infectious red cell destruction - parvovirus
Others:
disorders of fetal red cell production
fetal haemorrhage
fetal tumours
complications of monochorionicity
Definition and incidence of red cell alloimmunisation
Haemolytic disease of the fetus and newborn (HDFN) - occurs after a woman is exposed to a mismatch of paternally derived RBC antigens from fetus
Affects 1 in 300-600 live births
RBC alloantibodies present in 1 in 80 pregnant women
Causes of red cell alloimmunisation
Sensitizing events
Blood transfusion
Types of rhesus antibodies
D, c, E K
D - antiD reduced D-alloimmunisation to 2%
Anti-E most prevalent
Rare - K (Kepp group) - can cause severe, early onset anaemia –> suppresses erythropoesis and RC destruction
If incompatibility with Rh D, c and E –> severe HDFN
Why does Rh affect second pregnancy and not the first
First responmse IgM can’t cross the placenta
Second response IgG - can cross, therefore affecting subsequent pregnancies
Antenatal screening for RC alloimmunisation
Booking and 28/40 G&H for antibody status
+/- fetal genotyping depending on unit
cffDNA - diagnostic for RC antibodies
Monitoring in cases with RC alloimmunisation
Blood test 4 weekly up to 28/40, then 2 weekly until delivery
Levels and titre measured
Kell AB - low threshold for referral
Prevention of alloimmunisation
RAADP prophylactic doses - 28/40, postnatally
AntiD within 72 hours of sensitizing event
1 500iu dose anti-D sufficient to cover 4ml of fetal RBCs
Kleihauer-Betke test confirms fetal-maternal haemorrhage (FMH)
Sensitization can occur with silent FMH, failure to administer antiD or if too small a dose given
Large FMH - needs 125u/ml
Max dose 10000units/day
Parvovirus spread and consequences
ssDNA virus
Spread via resp droplets
More than 1/2 population immune
Infection in first 1/2 pregnancy - fetal anaemia and hydrops - d/t viral destruction of fetal erythroid progenitor cells
Fetal loss: <20/40 - 13%, > 20/40 0.5%
CMV testing
Avidity testing - tests strength of IgG and antigen complex
Gradually increasing with time after primary infection –> latency of infection
Low acidity = recent infection
2% associated with reactivation after previous primary infection
USS signs of congenital infection
Echogenic bowel
Hepatic calcifications
Organomegaly
Dysplastic kidneys
Ventriculomegaly
FGR
Disorders of fetal erythropoeisis
Aplastic anaemia
Thalassaemia
Genetic disorders - porphyria, fanconi anaemia, G6PD
Vascular tumours
Fetomaternal haemorrhage
Vasa praevia
Monochorionicity - twin anaemia polycythaemia sequence
Barts hydrops fetalis
Complication seen in fetus born to two parents with alpha thalassaemia trait (1 in 4 major)
Occurs in the absence of any normal Hb
Classic US sign: thickened placenta
Fetal features:
- severe pallor, generalised oedema and massive HSM
- signs of fetal distress usually evident by third trimester
TAPS
Twin anaemia polycythaemia sequence
- occurs in monochorionic twins
- similar to TTTS but placental connections smaller
- small caliber AV anastomoses occur, typically near the edge of the placenta, <1mm in diameter
- normal AFI, unlike TTTS
Who to refer to fetal medicine- re RC alloimmunisation
Rising antibody titres/ above specific threshold
USS features
Unexplained severe neonatal jaundice/ anaemia with HDFN excluded
Ab other than anti-D, anti-C, anti-K
Hx prev significant HDFN/ OUT/ titre >/=32
Anti-D >4iu but <15 = moderate reisk/ >15iu = severe HDFN
ANti-c >7.5iu/ml but <30 = moderate risk/ >30 = high risk
Identifying fetus with fetal anaemia
High risk - booking hx, G&H, screening, USS
Diagnosis: direct fetal blood sampling
Doppler MCA-PSV - >1.5MoM = action
Hydrops: effusions, ascites, oedema, poly
MRI to estimate fetal haematocrit
CTG - sinusoidal pattern
Process of intrauterine transfusion
US guided percutaneous needle (2-22G)
via umbilical vein
Intraperitoneal fetal transfusion
Medical treatment fetal anaemia
IvIG - blocks transprt of alloantibodies across the placenta
Neonatal Outcomes assoc with fetal anaemia
cord bloods of at risk neonates - direct antiglobuylin test, Hb, bilirubin
Antibodies remain for 6 months - continuing RC destruction –> chronic unconjugated hyperbilirubinaemia and brain injury (kernicterus)
Early neonatal anaemia in HDFN (w/in 7/7)
Hydrops fetalis -
excess fluid in more than one body cavity - subcutaneous oedema, pleural effusion, pericardial effusion, ascites
Maternal risk factors for hydrops
Racial background
Prev pregnancy
Genetic FHx
Consanguity
Illness or contact with illness during pregnancy
Causes of hydrops
Isoimmunisation
Chromosomal - trisomies, turners
Anaemia - alpha thalassaemia, chronic FMH
Genetic
CVS - structural, tachyarrythmias
Pulmonary - diaphragmatic hernia
Cystic hygroma
Infections - parvo/ CMV/ syphilis/ coxI
Investigations in hydrops
Blood group and ab screen
Haemoglobinopathy screen
TORCH and parvo screen
Syphilis serologyu
Coxsackie
Kleihauer
US - other abnormalities, MCA doppler, amnio for karyotype and virology
Rh sensitizing events
Delivery
ERPC
CVS
Amnio
ECV
Miscarriage >12/40
APH
Treatment hydrops
IU transfusions for isoimmunisation and parve
Syphilis - hugh dose penicillin
Cox - resolve spontaneously
CMV - poor outcome
Tachyarrhthmia - antiarrhythmics
Termination - karyotyping
Incidence gastroschisis
1-6 per 10000
Incidence omphalocoele
1 in 4000-7000
Risk factors for omphalocoele
AMA>40
Obesity
Smokng
ETOH
SSRIs
What is an omphalocoele
Abdominal wall defect - bowel +/- other abdominal organs protrude within a thin layered sac, near the base of the umbilical cord
Defect usually 4-12cm
Differentials for omphalocoele
Gastroschisis
Cloacal extrophy
physiological gut herniation
Hernia of the cord
Aetiology of omphalocoele
in early pregnancy- organs form outside the body and return to the abdominal cavity by 11/40- failure–> omphalocoele
Not genetic; appears sporadic
Can be a part of a genetic syndrome
Defects associated with omphalocoele
Abdo, Cardiac, neuro, gu
Chromosomal abnormalities associated with omphalocoele
Trisomy 13, 18, 21
45XO
Klinefelter
Triploidy
Brockwith-Wiedeman syndrome
Pentology of Cantrell
OEIS complex
Types of omphalocoele
Small: bowel only
- associated with genetic syndromes - T18, T13, T21, Turners, aneuploidy
Large: includes other organs
- more likely associated with pulm hypoplasia, 1/3 also have cardiac anomalies
Diagnosing omphalocoele
Increased AFP in T1
USS + growth surveillance
Amnio/ NIPT
Fetal echo/ MRI
What is a Schuster procedure
Staged surgical repair for large omphalocoele
Risk factors for gastroschisis
Mat age <20
Smoking
Env exposures- nitrosamines
Maternal COX inhibitors (aspirin/ ibuprofen)
Definition of gastroschisis
Full thickness abdominal wall defect with no protective membrane. Direct intestinal exposure to amniotic fluid –> chemical reactions –> thick inflammatory film covering
Aetiology of gastroschisis
Exact mechanism unknown
- ?compromise vascular supply to anterior wall
- ?defect in the primordial umbilical ring
- ? abnormal involution of the right umbilical vein–> weakened point at risk of rupture
Differentials for gastroschisis
Omphalocoele
Cloacal extrophy
physiological gut herniation
Features of gastroschisis
Visible at birth and on USS at 20/40
Often to the right of the UC
Involves intestines, liver, stomach
Swollen, inflamed, thickened tissue
Thick fibrous peel
Abdo cavity smaller than expected
Assoc w intestinal malrotation
10-15% intestinal atresia due to small size of abdo defect
Extra-structural anomalies not commonly associated
Diagnosing gastroschisis
IncreasedAFP in T1
Free floating bowel on USS and growth scans
Incidence of isolated single umbilical artery (SUA)
1% singleton/5% twin pregnancy
Usually left artery absent
Relevant prev pregnancy hx in SUA
Congenital anomalies
Any teratogens in pregnancy (nb phenytoin)
Medical hx-hyperglycaemia
Incidence of SUA with other anomalies
9%
Anomalies assoc with SUA
Renal/CVS/ GI/ CNS
NB to do fetal echo and karyotyping if non-isolated/ abnormal screening or IUGR
Genetic syndromes assoc w SUA
VATER complexx/ VACTERL
Meckel-Gruber
Zellweger
Pathophysiology diaphragmatic hernia
Either Bochdalek or Morgagni
Bochdalek more common - 1 in 5000
- defect in posterior attachmen
- left-sided
Morgagni
- herniation at foramen of Morgagni
- anterior and rightsided
Congenital anomalies/ syndromes assoc with Bochdalek hernia
1/3 cases assoc w other congenital anomalies
Donnal-Barrow syndrome
Fryns syndrome
Pallister-Killian mosaic syndrome
Clinical features of diaphragmatic hernia
Congenital - asymptomatic
May present in the perinatal period
In utero:
- pulmonary hypoplasia
- respiratory compromise
At birth:
- dyspnoea
- chest pain
- bowel obstruction
Bochdalek: most are small
Incidence of double bubble sign
1 in 5000
Causes of double bubble sign
Congenital obstruction:
- duodenal web
- duodenal atresia
- duodenal stenosis
- angular pancreas
Volvulus
External compression:
- choledochal cyst
- mesenteric duplication cyst
- intramural duodenal haematoma
-preduodenal portal vein
- retroperitoneal tumour
- SMA syndrome
Anomalies associated with double bubble sign
Chromosomal
- T21:in 30%
Other defects- cardiac, renal, vertebral in 10-20%
USS interpretation of double bubble sign
Represents dilatation or swelling or the duodenum and stomach
seen at >24/40
Polyhydramnios noted in 50% cases
Investigations in light of double bubble sign
Detailed USS and ECHO
Aneuploidy testing
Growth and AFI scans every 2-3 weeks
Delivery if double bubble sign present
IOL at 38/40
NICU + paeds
Incidence cystic hygroma
1 in 8000
Symptoms of cystic hygroma
Ingestion issues
Airway obstruction
Genetic associations of cystic hygroma
Turners
Downs
Noonan
Investigations when cystic hygroma noted
Prenatal: CVS, amnio
Postnatal: CXR, CT, MRI
Complications of cystic hygroma
Airway
Facial deformity
Cellulitis
Surgical complications - nerve damage, heavy bleeding
Recurrence
Features of parvovirus
Causes slapped cheek syndrome/ fifth disease/ erythema infectiosum
ssDNA virus
Incubation: 4-20 days
50-65% population immune
Spread via droplets/ hand-to-hand
Symptoms of parvovirus infection
Asymptomatic 20-25%
Flu-like
Fever
Rash
Arthralgia
Rare sx: anaemia, myocarditis, aplastic crisis
Diagnosis parvovirus
B19 IgG+ andIgM neg
Things to do if confirmed parvovirus infection
Inform public health
IgM and DNA
IgM repeated if negative= outside incubation -repeat 2/52
Placental passage rates 17-33%
Fetal effects of parvovirus
Affects 10%
Fetal sx occur 6/52 post infection
Most vulnerable in 2nd trimester (17-24/40)
Spontaneous abortion (10% above baseline)
Hydrops fetalis (accounts for 8-10% of non-immune hydrops)
- severe anaemia, hypoxia, high output cardiac failure
- impaired hepatic function, direct damage to hepatocytes and indirect via haemosiderin deposits
USS features noted in parvovirus
Ascites
Skin oedema
Pleural and pericardial effusions
Placental oedema
Longterm complications parvovirus infection
Hepatic insufficiency
Myocarditis
Anaemia
CNS effects
Monitoring in known parvovirus infection
Serial fetal med USS weekly x 8-1/52 (incl MCA dopplers to monitor ?anaemia)
Mat med referral
Interpretation of maternal immunity in parvovirus infection
IgG +ve, IgM -ve = immunity
IgG -ve, IgM +ve= very recent infection; retest in 1-2/52
IgG and IgM-ve = susceptible
IgGand IgM +ve = recent infection
How to confirm fetal parvovirus infections
Amnio PCR
- IgM only made after 22/40, so amnio only useful in viraemic phase
IgM -ve, IgG-ve and recent exposure to or sx of parvovirus
Bloods show no previous infection
If very recent exposure, re-check in 2-4 weeks
If remains negative, no current infection
IgM -ve and IgG+ve and recent exposure to or sx of parvovirus
Past infection/ immune - reassure
IgM +ve and IgG -ve/+ve and recent exposure to or sx of parvovirus
<20/40: check booking bloods as IgM + may represent IgM persistance. If positive, likely pre-pregnancy infection. Repeat serology to confirm seroconversion
>20/40: suggests recent infection
- refer to FM specialist
- serial ultrasound for MCA dopplers and signs of hydrops for 8-12/52
- If anaemia occurs, in utero resolution may occur spontaneously OR hydrops may develop
- Assess for intrauterine transfusion
Management of HSV if first episode in1st or 2nd trimester
No evidence for incr risk spontaneous miscarriage
Should be seen by GUM
Rx: aciclovir 400mg tds x 5/7
- decreases duration and severity of disease, decreases duration of viral shedding
- paracetamol and topical lidocaine for sx relief
- Suppression rx from 36/40 - prophylactic aciclovir 400mg bd in 3rd trimester
- can have SVD, avoid invasive procedures
- augment delivery to minimise risk
Management first episode HSV in third trimester
Rx aciclovir 400mg tds x 5/7, then cont prophylactic doses
CS delivery recommended if first episode within 6/52 of EDD
Managing recurrent episode HSV in pregnancy
Rx episodes and give prophylactic rx in T3
Delivery by CS if presents. in T3
If infection w/in 6/40, risk of transmission 40%
Doesn’t require additional monitoring in pregnancy
Intrapartum/ MOD in HSV
SVD if:
- recurrent HSV
- first episode in T1/2 or at least >6/52 since episode and no visible lesions
Offer CS if:
- visible lesions
Recommended CS:
- first episode within 6/52 of EDD
Management of labour in primary HSV infection
IV aciclovir
No ARM/ FBS
Neonatal care
Risk of NN HSV infection in recurrent HSV
0-3%, even if lesions present at delivery
NB points in history when VZV exposure
Immunity?
Timing of exposure
Proximity-significant exposure:
- same room: >15min
-face to face:>5min
Type of varicella:
- high risk: disseminated, opthalmic, immunocompromised
Duration of infectiousness in VZV
48hours before rash appears –> lesions crusted over. (+/- 5 days)
Use of VZIG
Ideally w/in 96 hours, but can be within 10/7
Adverse reactions: pain/ erythema at IV site, anaphylaxis, subclinical infection
Second dose required if re-exposed 3/5 post last exposure
Management of active VZV disease
W/in 24hours of rash - aciclovir 800mg x5/day x 7/7
- Caution <20/40- not licenced
>24 hours post exposure - don’t give
Fet med referral for detailed USS 5/52 post infection
Maternal complications of VZV infection
Pneumonia (10-14%). Worse at increased GA, morbidity 14%
Hepatitis
Encephalopathy
Resp recurrence
Fever
Painful skin lesions -GAS superinfection
Delivery may precipitate haemorrhage
Fetal complications VZV infection
In first 28/40 => fetal varicella syndrome
- scarring
- microcephaly
- cortical atrophy
- mental retardation
- bowel/ bladder dysfx
FVS not seen >28/40
- caused by in utero reactivation, not initial infection
No increased risk of miscarriage
Amnio - diagnostic of fetal infection
**time lag NB - FM review 5/52 post infection
Neonatal complications VZV infection
Mat infection w/in 4/52 delivery - 50% babies affected
- severe if infection <1/52
Aim for delivery 7/7 after rash
Epidemiology VZV
Seasonal: Jan - April
Incubation period: 8-21days
Spread: vesicles, droplet, airborne
Infective 2/7 before rash develops –> lesions crusted over (+/- 7/7)
VZV igG levels - cut off
<100mlU/mL- administer PEP
- first line, aciclovir 800mgQDS from D7-D14 post exposure. IVIG for specific pts, on advice from microbio
>100mlU/mL - no need for PEP
Associations with GBS
Maternal:
- endometritis
- chorioamnionitis
Fetal:
- >500000 PTB
- 100000 NNDs
- 46000 stillbirths/ IUD
- longterm neurodevelopmental delay
Risk factors for EOGBS
Increased perinatal transmission
ROM > 18 hours
PROM
Prematurity
Intrapartum fever
EOGBS
D0-6
Sepsis/ pneumonia
Late - D7-90 : meningitis
Incidence of GBS
10-30% women colonised
36% babies born to GBS+ women become colonised
1-3% babies develop EOGBS bacteraemia
Three strategies for GBS screening
Risk based
Intrapartum/ real-time testing
Routine screening at 35-37/40
Who to offer intrapartum antibiotic prophylaxis to (re GBS)
SVD + prev baby with invasive GBS
Preterm labour <37/40
GBS detected in current pregnancy
Hx GBS prior to pregnancy * offer IAP or repeat testing
ROM > 18 hours
Protocol for intrapartum antibiotic prophylaxis. (GBS)
3g benzylpenicillin IV stat
Then 1.5-1.8g IV 4hourly
Non-immed hypersensitivity: cefuroxime 1.5g IV 4 hourly
Immed allergy- clindamycin 900mg IV TDS OR vanc 15mg/kg BD (max 2g)
Increased risks assoc w twin pregnancy
PET
Obs chole
PPH
When should chorionicity be determined
<14/40
When should twin pregnancy be referred to tertiary unit
Monochorionicity
TTTS
Growth discordance >18%
Higher order multiples
Single fetal demise + monochorionicity
- risk: 18% neuro defect, 12% death in remaining twin
Monitoring in twin pregnancies
MC:
- USS 2/52 from 16/40 -growth and screening for TTTS
- TTTS < 26/40 - consider laser ablation
DC:
- USS 4/52 from 24/40
Cx length if prev risk factors
Delivery of twin pregnancies
DCDA: 37 - 37+6/40
MCDA: 36 -36+6/40
MCMA: 32-34/40
SVD success: 77%
Twin 2- r/o CS 4%
What is selective growth restriction
Growth discordance, w normal/ reverse/ absent/ cyclical UAD
Incidence of growth discordance in twin pregnancy
15-25%
How to calculate growth discordance
[(larger twin EFW- smaller twin EFW) x100]
Causes of growth discordance
Mostly placental cause
? chromosomal cause
Monitoring in growth discordant twins
> 18%: increased monitoring
20% : increased perinatal risk
2/52 UAD+ EFW
Check dopplers and DVP
Delivery in growth discordant twins
Discordance, normal dopplers x 2 = deliver 34-36/40
Discordance, AREDF x 1 or 2 = deliver by 32/40
Discordance, intermittent AREDF =deliver by 32/40
TTTS donor vs recipient
Donor: oligo, abnormal UAD, empty bladder, cardiac signs
Recipient: poly, abnormal UVD, cardiac signs
Incidence of TTTS in MC twins
15%
Parameters used in staging TTTS
UAD
MCA PSV
Ductus venosus doppler
When is laser ablation recommended
TTTS detected < 26/40
Monitoring in TTTS
Weekly USS: UAPI, MCA PSV, DV
Delivery timing in TTTS
Post-treatment: 34-36/40
Staging system used in TTTS
Quintero staging:
I. Significant discordance in amniotic fluid volumes
II. Bladder of donor twin not visible + severe oligo
III. Doppler critically abnormal in donor or recipient; typically abN UAD in donor and abN DV in recipient
IV. Ascites, pericardial or pleural effusions, scalp oedema or overt hydrops in recipient
V. One or both babies demised
What is TAPS
Twin anaemia (donor) polycythaemia (recipient) syndrome
Form of TTTS
Unequal Hbs between twins
Can happen post ablation
Cause= small AVM in placenta
Differs from TTTS as LV remains the same
Dx TAPS
Using MCA PSV
Donor: anaemia MCA >1.5
Recipient: polycythaemia MCA <1
