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P2 > Fetal medicine > Flashcards

Fetal medicine Flashcards

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
Q

Barts hydrops fetalis

A

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

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26
Q

TAPS

A

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

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27
Q

Who to refer to fetal medicine- re RC alloimmunisation

A

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

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28
Q

Identifying fetus with fetal anaemia

A

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

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29
Q

Process of intrauterine transfusion

A

US guided percutaneous needle (2-22G)
via umbilical vein
Intraperitoneal fetal transfusion

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30
Q

Medical treatment fetal anaemia

A

IvIG - blocks transprt of alloantibodies across the placenta

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31
Q

Neonatal Outcomes assoc with fetal anaemia

A

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)

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32
Q

Hydrops fetalis -

A

excess fluid in more than one body cavity - subcutaneous oedema, pleural effusion, pericardial effusion, ascites

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33
Q

Maternal risk factors for hydrops

A

Racial background
Prev pregnancy
Genetic FHx
Consanguity
Illness or contact with illness during pregnancy

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34
Q

Causes of hydrops

A

Isoimmunisation
Chromosomal - trisomies, turners
Anaemia - alpha thalassaemia, chronic FMH
Genetic
CVS - structural, tachyarrythmias
Pulmonary - diaphragmatic hernia
Cystic hygroma
Infections - parvo/ CMV/ syphilis/ coxI

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35
Q

Investigations in hydrops

A

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

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36
Q

Rh sensitizing events

A

Delivery
ERPC
CVS
Amnio
ECV
Miscarriage >12/40
APH

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37
Q

Treatment hydrops

A

IU transfusions for isoimmunisation and parve
Syphilis - hugh dose penicillin
Cox - resolve spontaneously
CMV - poor outcome
Tachyarrhthmia - antiarrhythmics
Termination - karyotyping

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38
Q

Incidence gastroschisis

A

1-6 per 10000

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39
Q

Incidence omphalocoele

A

1 in 4000-7000

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40
Q

Risk factors for omphalocoele

A

AMA>40
Obesity
Smokng
ETOH
SSRIs

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41
Q

What is an omphalocoele

A

Abdominal wall defect - bowel +/- other abdominal organs protrude within a thin layered sac, near the base of the umbilical cord
Defect usually 4-12cm

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42
Q

Differentials for omphalocoele

A

Gastroschisis
Cloacal extrophy
physiological gut herniation
Hernia of the cord

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43
Q

Aetiology of omphalocoele

A

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

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44
Q

Defects associated with omphalocoele

A

Abdo, Cardiac, neuro, gu

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45
Q

Chromosomal abnormalities associated with omphalocoele

A

Trisomy 13, 18, 21
45XO
Klinefelter
Triploidy
Brockwith-Wiedeman syndrome
Pentology of Cantrell
OEIS complex

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46
Q

Types of omphalocoele

A

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

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47
Q

Diagnosing omphalocoele

A

Increased AFP in T1
USS + growth surveillance
Amnio/ NIPT
Fetal echo/ MRI

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48
Q

What is a Schuster procedure

A

Staged surgical repair for large omphalocoele

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49
Q

Risk factors for gastroschisis

A

Mat age <20
Smoking
Env exposures- nitrosamines
Maternal COX inhibitors (aspirin/ ibuprofen)

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50
Q

Definition of gastroschisis

A

Full thickness abdominal wall defect with no protective membrane. Direct intestinal exposure to amniotic fluid –> chemical reactions –> thick inflammatory film covering

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51
Q

Aetiology of gastroschisis

A

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

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52
Q

Differentials for gastroschisis

A

Omphalocoele
Cloacal extrophy
physiological gut herniation

53
Q

Features of gastroschisis

A

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
Q

Diagnosing gastroschisis

A

IncreasedAFP in T1
Free floating bowel on USS and growth scans

55
Q

Incidence of isolated single umbilical artery (SUA)

A

1% singleton/5% twin pregnancy
Usually left artery absent

56
Q

Relevant prev pregnancy hx in SUA

A

Congenital anomalies
Any teratogens in pregnancy (nb phenytoin)
Medical hx-hyperglycaemia

57
Q

Incidence of SUA with other anomalies

A

9%

58
Q

Anomalies assoc with SUA

A

Renal/CVS/ GI/ CNS
NB to do fetal echo and karyotyping if non-isolated/ abnormal screening or IUGR

59
Q

Genetic syndromes assoc w SUA

A

VATER complexx/ VACTERL
Meckel-Gruber
Zellweger

60
Q

Pathophysiology diaphragmatic hernia

A

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
Q

Congenital anomalies/ syndromes assoc with Bochdalek hernia

A

1/3 cases assoc w other congenital anomalies
Donnal-Barrow syndrome
Fryns syndrome
Pallister-Killian mosaic syndrome

62
Q

Clinical features of diaphragmatic hernia

A

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
Q

Incidence of double bubble sign

A

1 in 5000

64
Q

Causes of double bubble sign

A

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
Q

Anomalies associated with double bubble sign

A

Chromosomal
- T21:in 30%
Other defects- cardiac, renal, vertebral in 10-20%

66
Q

USS interpretation of double bubble sign

A

Represents dilatation or swelling or the duodenum and stomach
seen at >24/40
Polyhydramnios noted in 50% cases

67
Q

Investigations in light of double bubble sign

A

Detailed USS and ECHO
Aneuploidy testing
Growth and AFI scans every 2-3 weeks

68
Q

Delivery if double bubble sign present

A

IOL at 38/40
NICU + paeds

68
Q

Incidence cystic hygroma

A

1 in 8000

69
Q

Symptoms of cystic hygroma

A

Ingestion issues
Airway obstruction

70
Q

Genetic associations of cystic hygroma

A

Turners
Downs
Noonan

70
Q

Investigations when cystic hygroma noted

A

Prenatal: CVS, amnio
Postnatal: CXR, CT, MRI

70
Q

Complications of cystic hygroma

A

Airway
Facial deformity
Cellulitis
Surgical complications - nerve damage, heavy bleeding
Recurrence

71
Q

Features of parvovirus

A

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
Q

Symptoms of parvovirus infection

A

Asymptomatic 20-25%
Flu-like
Fever
Rash
Arthralgia
Rare sx: anaemia, myocarditis, aplastic crisis

73
Q

Diagnosis parvovirus

A

B19 IgG+ andIgM neg

74
Q

Things to do if confirmed parvovirus infection

A

Inform public health
IgM and DNA
IgM repeated if negative= outside incubation -repeat 2/52
Placental passage rates 17-33%

75
Q

Fetal effects of parvovirus

A

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
Q

USS features noted in parvovirus

A

Ascites
Skin oedema
Pleural and pericardial effusions
Placental oedema

77
Q

Longterm complications parvovirus infection

A

Hepatic insufficiency
Myocarditis
Anaemia
CNS effects

78
Q

Monitoring in known parvovirus infection

A

Serial fetal med USS weekly x 8-1/52 (incl MCA dopplers to monitor ?anaemia)
Mat med referral

79
Q

Interpretation of maternal immunity in parvovirus infection

A

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
Q

How to confirm fetal parvovirus infections

A

Amnio PCR
- IgM only made after 22/40, so amnio only useful in viraemic phase

81
Q

IgM -ve, IgG-ve and recent exposure to or sx of parvovirus

A

Bloods show no previous infection
If very recent exposure, re-check in 2-4 weeks
If remains negative, no current infection

82
Q

IgM -ve and IgG+ve and recent exposure to or sx of parvovirus

A

Past infection/ immune - reassure

83
Q

IgM +ve and IgG -ve/+ve and recent exposure to or sx of parvovirus

A

<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
Q

Management of HSV if first episode in1st or 2nd trimester

A

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
Q

Management first episode HSV in third trimester

A

Rx aciclovir 400mg tds x 5/7, then cont prophylactic doses
CS delivery recommended if first episode within 6/52 of EDD

86
Q

Managing recurrent episode HSV in pregnancy

A

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
Q

Intrapartum/ MOD in HSV

A

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
Q

Management of labour in primary HSV infection

A

IV aciclovir
No ARM/ FBS
Neonatal care

89
Q

Risk of NN HSV infection in recurrent HSV

A

0-3%, even if lesions present at delivery

90
Q

NB points in history when VZV exposure

A

Immunity?
Timing of exposure
Proximity-significant exposure:
- same room: >15min
-face to face:>5min
Type of varicella:
- high risk: disseminated, opthalmic, immunocompromised

91
Q

Duration of infectiousness in VZV

A

48hours before rash appears –> lesions crusted over. (+/- 5 days)

92
Q

Use of VZIG

A

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
Q

Management of active VZV disease

A

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
Q

Maternal complications of VZV infection

A

Pneumonia (10-14%). Worse at increased GA, morbidity 14%
Hepatitis
Encephalopathy
Resp recurrence
Fever
Painful skin lesions -GAS superinfection
Delivery may precipitate haemorrhage

95
Q

Fetal complications VZV infection

A

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
Q

Neonatal complications VZV infection

A

Mat infection w/in 4/52 delivery - 50% babies affected
- severe if infection <1/52
Aim for delivery 7/7 after rash

97
Q

Epidemiology VZV

A

Seasonal: Jan - April
Incubation period: 8-21days
Spread: vesicles, droplet, airborne
Infective 2/7 before rash develops –> lesions crusted over (+/- 7/7)

98
Q

VZV igG levels - cut off

A

<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
Q

Associations with GBS

A

Maternal:
- endometritis
- chorioamnionitis
Fetal:
- >500000 PTB
- 100000 NNDs
- 46000 stillbirths/ IUD
- longterm neurodevelopmental delay

100
Q

Risk factors for EOGBS

A

Increased perinatal transmission
ROM > 18 hours
PROM
Prematurity
Intrapartum fever

101
Q

EOGBS

A

D0-6
Sepsis/ pneumonia
Late - D7-90 : meningitis

102
Q

Incidence of GBS

A

10-30% women colonised
36% babies born to GBS+ women become colonised
1-3% babies develop EOGBS bacteraemia

103
Q

Three strategies for GBS screening

A

Risk based
Intrapartum/ real-time testing
Routine screening at 35-37/40

104
Q

Who to offer intrapartum antibiotic prophylaxis to (re GBS)

A

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
Q

Protocol for intrapartum antibiotic prophylaxis. (GBS)

A

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
Q

Increased risks assoc w twin pregnancy

A

PET
Obs chole
PPH

107
Q

When should chorionicity be determined

A

<14/40

108
Q

When should twin pregnancy be referred to tertiary unit

A

Monochorionicity
TTTS
Growth discordance >18%
Higher order multiples
Single fetal demise + monochorionicity
- risk: 18% neuro defect, 12% death in remaining twin

109
Q

Monitoring in twin pregnancies

A

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
Q

Delivery of twin pregnancies

A

DCDA: 37 - 37+6/40
MCDA: 36 -36+6/40
MCMA: 32-34/40
SVD success: 77%
Twin 2- r/o CS 4%

111
Q

What is selective growth restriction

A

Growth discordance, w normal/ reverse/ absent/ cyclical UAD

112
Q

Incidence of growth discordance in twin pregnancy

A

15-25%

113
Q

How to calculate growth discordance

A

[(larger twin EFW- smaller twin EFW) x100]

114
Q

Causes of growth discordance

A

Mostly placental cause
? chromosomal cause

115
Q

Monitoring in growth discordant twins

A

> 18%: increased monitoring
20% : increased perinatal risk
2/52 UAD+ EFW
Check dopplers and DVP

116
Q

Delivery in growth discordant twins

A

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
Q

TTTS donor vs recipient

A

Donor: oligo, abnormal UAD, empty bladder, cardiac signs
Recipient: poly, abnormal UVD, cardiac signs

118
Q

Incidence of TTTS in MC twins

A

15%

119
Q

Parameters used in staging TTTS

A

UAD
MCA PSV
Ductus venosus doppler

120
Q

When is laser ablation recommended

A

TTTS detected < 26/40

121
Q

Monitoring in TTTS

A

Weekly USS: UAPI, MCA PSV, DV

122
Q

Delivery timing in TTTS

A

Post-treatment: 34-36/40

123
Q

Staging system used in TTTS

A

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
Q

What is TAPS

A

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
Q

Dx TAPS

A

Using MCA PSV
Donor: anaemia MCA >1.5
Recipient: polycythaemia MCA <1

126
Q
A

P2 (11 decks)

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