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Fetal medicine Flashcards

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1
Q

Definition of FGR vs SGA vs IUGR

A

FGR = EFW <10%
SGA (isolated FGR) = physiologically small
IUGR = EFW <10%, abnormal dopplers/ AFI, poor growth velocity

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2
Q

Antenatal monitoring for those with known IUGR risk factors

A

Growth
AF
UAD from 26/40 every 2-4/52
Consider aspirin if risk factors present

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3
Q

Incidence and outcome of IUGR

A

Affects 10% pregnancies
Recurrence 25%
70% normal outcome
if EFW <3%, significant increase in adverse perinatal outcomes

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4
Q

Monitoring diagnosed IUGR

A

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

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5
Q

Delivery in IUGR

A

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

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6
Q

Women at high risk for pre-eclampsia

A

Hypertensive disease in prev pregnancy
Chronic kidney disease
Autoimmune disase
T1 or T2 diabetes
Chronic hypertension

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7
Q

Moderate risk factors for pre-eclampsia

A

First pregnancy
Age 40+
Pregnancy interval of >10 years
BMI >35
FH PET
Multi-fetal pregnancy

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8
Q

Definition of dopplers, absent end and reverse

A

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

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9
Q

Causes of abnormal dopplers

A

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

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10
Q

Risks to baby in the neonatal period with detected abnormal dopplers

A

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

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11
Q

Fetal anaemia - definition

A

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

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12
Q

Implications of fetal anaemia

A

Reduced tissue perfusion –> brain injury, cardiac failure, IUFD

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13
Q

Causes of fetal anaemia

A

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

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14
Q

Definition and incidence of red cell alloimmunisation

A

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

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15
Q

Causes of red cell alloimmunisation

A

Sensitizing events
Blood transfusion

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16
Q

Types of rhesus antibodies

A

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

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17
Q

Why does Rh affect second pregnancy and not the first

A

First responmse IgM can’t cross the placenta
Second response IgG - can cross, therefore affecting subsequent pregnancies

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18
Q

Antenatal screening for RC alloimmunisation

A

Booking and 28/40 G&H for antibody status
+/- fetal genotyping depending on unit
cffDNA - diagnostic for RC antibodies

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19
Q

Monitoring in cases with RC alloimmunisation

A

Blood test 4 weekly up to 28/40, then 2 weekly until delivery
Levels and titre measured
Kell AB - low threshold for referral

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20
Q

Prevention of alloimmunisation

A

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

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21
Q

Parvovirus spread and consequences

A

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%

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22
Q

CMV testing

A

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

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23
Q

USS signs of congenital infection

A

Echogenic bowel
Hepatic calcifications
Organomegaly
Dysplastic kidneys
Ventriculomegaly
FGR

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24
Q

Disorders of fetal erythropoeisis

A

Aplastic anaemia
Thalassaemia
Genetic disorders - porphyria, fanconi anaemia, G6PD
Vascular tumours
Fetomaternal haemorrhage
Vasa praevia
Monochorionicity - twin anaemia polycythaemia sequence

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25
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
26
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
27
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
28
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
29
Process of intrauterine transfusion
US guided percutaneous needle (2-22G) via umbilical vein Intraperitoneal fetal transfusion
30
Medical treatment fetal anaemia
IvIG - blocks transprt of alloantibodies across the placenta
31
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)
32
Hydrops fetalis -
excess fluid in more than one body cavity - subcutaneous oedema, pleural effusion, pericardial effusion, ascites
33
Maternal risk factors for hydrops
Racial background Prev pregnancy Genetic FHx Consanguity Illness or contact with illness during pregnancy
34
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
35
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
36
Rh sensitizing events
Delivery ERPC CVS Amnio ECV Miscarriage >12/40 APH
37
Treatment hydrops
IU transfusions for isoimmunisation and parve Syphilis - hugh dose penicillin Cox - resolve spontaneously CMV - poor outcome Tachyarrhthmia - antiarrhythmics Termination - karyotyping
38
Incidence gastroschisis
1-6 per 10000
39
Incidence omphalocoele
1 in 4000-7000
40
Risk factors for omphalocoele
AMA>40 Obesity Smokng ETOH SSRIs
41
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
42
Differentials for omphalocoele
Gastroschisis Cloacal extrophy physiological gut herniation Hernia of the cord
43
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
44
Defects associated with omphalocoele
Abdo, Cardiac, neuro, gu
45
Chromosomal abnormalities associated with omphalocoele
Trisomy 13, 18, 21 45XO Klinefelter Triploidy Brockwith-Wiedeman syndrome Pentology of Cantrell OEIS complex
46
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
47
Diagnosing omphalocoele
Increased AFP in T1 USS + growth surveillance Amnio/ NIPT Fetal echo/ MRI
48
What is a Schuster procedure
Staged surgical repair for large omphalocoele
49
Risk factors for gastroschisis
Mat age <20 Smoking Env exposures- nitrosamines Maternal COX inhibitors (aspirin/ ibuprofen)
50
Definition of gastroschisis
Full thickness abdominal wall defect with no protective membrane. Direct intestinal exposure to amniotic fluid --> chemical reactions --> thick inflammatory film covering
51
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
52
Differentials for gastroschisis
Omphalocoele Cloacal extrophy physiological gut herniation
53
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
54
Diagnosing gastroschisis
IncreasedAFP in T1 Free floating bowel on USS and growth scans
55
Incidence of isolated single umbilical artery (SUA)
1% singleton/5% twin pregnancy Usually left artery absent
56
Relevant prev pregnancy hx in SUA
Congenital anomalies Any teratogens in pregnancy (nb phenytoin) Medical hx-hyperglycaemia
57
Incidence of SUA with other anomalies
9%
58
Anomalies assoc with SUA
Renal/CVS/ GI/ CNS NB to do fetal echo and karyotyping if non-isolated/ abnormal screening or IUGR
59
Genetic syndromes assoc w SUA
VATER complexx/ VACTERL Meckel-Gruber Zellweger
60
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
61
Congenital anomalies/ syndromes assoc with Bochdalek hernia
1/3 cases assoc w other congenital anomalies Donnal-Barrow syndrome Fryns syndrome Pallister-Killian mosaic syndrome
62
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
63
Incidence of double bubble sign
1 in 5000
64
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
65
Anomalies associated with double bubble sign
Chromosomal - T21:in 30% Other defects- cardiac, renal, vertebral in 10-20%
66
USS interpretation of double bubble sign
Represents dilatation or swelling or the duodenum and stomach seen at >24/40 Polyhydramnios noted in 50% cases
67
Investigations in light of double bubble sign
Detailed USS and ECHO Aneuploidy testing Growth and AFI scans every 2-3 weeks
68
Delivery if double bubble sign present
IOL at 38/40 NICU + paeds
68
Incidence cystic hygroma
1 in 8000
69
Symptoms of cystic hygroma
Ingestion issues Airway obstruction
70
Genetic associations of cystic hygroma
Turners Downs Noonan
70
Investigations when cystic hygroma noted
Prenatal: CVS, amnio Postnatal: CXR, CT, MRI
70
Complications of cystic hygroma
Airway Facial deformity Cellulitis Surgical complications - nerve damage, heavy bleeding Recurrence
71
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
72
Symptoms of parvovirus infection
Asymptomatic 20-25% Flu-like Fever Rash Arthralgia Rare sx: anaemia, myocarditis, aplastic crisis
73
Diagnosis parvovirus
B19 IgG+ andIgM neg
74
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%
75
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
76
USS features noted in parvovirus
Ascites Skin oedema Pleural and pericardial effusions Placental oedema
77
Longterm complications parvovirus infection
Hepatic insufficiency Myocarditis Anaemia CNS effects
78
Monitoring in known parvovirus infection
Serial fetal med USS weekly x 8-1/52 (incl MCA dopplers to monitor ?anaemia) Mat med referral
79
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
80
How to confirm fetal parvovirus infections
Amnio PCR - IgM only made after 22/40, so amnio only useful in viraemic phase
81
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
82
IgM -ve and IgG+ve and recent exposure to or sx of parvovirus
Past infection/ immune - reassure
83
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
84
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
85
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
86
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
87
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
88
Management of labour in primary HSV infection
IV aciclovir No ARM/ FBS Neonatal care
89
Risk of NN HSV infection in recurrent HSV
0-3%, even if lesions present at delivery
90
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
91
Duration of infectiousness in VZV
48hours before rash appears --> lesions crusted over. (+/- 5 days)
92
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
93
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
94
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
95
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
96
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
97
Epidemiology VZV
Seasonal: Jan - April Incubation period: 8-21days Spread: vesicles, droplet, airborne Infective 2/7 before rash develops --> lesions crusted over (+/- 7/7)
98
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
99
Associations with GBS
Maternal: - endometritis - chorioamnionitis Fetal: - >500000 PTB - 100000 NNDs - 46000 stillbirths/ IUD - longterm neurodevelopmental delay
100
Risk factors for EOGBS
Increased perinatal transmission ROM > 18 hours PROM Prematurity Intrapartum fever
101
EOGBS
D0-6 Sepsis/ pneumonia Late - D7-90 : meningitis
102
Incidence of GBS
10-30% women colonised 36% babies born to GBS+ women become colonised 1-3% babies develop EOGBS bacteraemia
103
Three strategies for GBS screening
Risk based Intrapartum/ real-time testing Routine screening at 35-37/40
104
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
105
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)
106
Increased risks assoc w twin pregnancy
PET Obs chole PPH
107
When should chorionicity be determined
<14/40
108
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
109
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
110
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%
111
What is selective growth restriction
Growth discordance, w normal/ reverse/ absent/ cyclical UAD
112
Incidence of growth discordance in twin pregnancy
15-25%
113
How to calculate growth discordance
[(larger twin EFW- smaller twin EFW) x100]
114
Causes of growth discordance
Mostly placental cause ? chromosomal cause
115
Monitoring in growth discordant twins
>18%: increased monitoring >20% : increased perinatal risk 2/52 UAD+ EFW Check dopplers and DVP
116
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
117
TTTS donor vs recipient
Donor: oligo, abnormal UAD, empty bladder, cardiac signs Recipient: poly, abnormal UVD, cardiac signs
118
Incidence of TTTS in MC twins
15%
119
Parameters used in staging TTTS
UAD MCA PSV Ductus venosus doppler
120
When is laser ablation recommended
TTTS detected < 26/40
121
Monitoring in TTTS
Weekly USS: UAPI, MCA PSV, DV
122
Delivery timing in TTTS
Post-treatment: 34-36/40
123
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
124
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
125
Dx TAPS
Using MCA PSV Donor: anaemia MCA >1.5 Recipient: polycythaemia MCA <1
126

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