fetal wellbeing Flashcards
IUGR hydrops dopplers
Small for gestational age definition
- infant with birthweight less than the 10th birth weight centile
- a fetus with an estimated fetal weight (EFW) less than the 10th customised centile for gestation.
Fetal growth restriction
- SGA + abnormal dopplers OR EFW <3rd
* EFW or AC crossing centiles / major discrepancy between HC and AC
What are the major risk factors that recommend serial growth scans identified at booking
• a history of a previous SGA or stillborn infant
• maternal age >40
• maternal or paternal history of being SGA at birth
• smoking >10 cigarettes daily
• using cocaine
• Maternal diseases associated with increased risk (e.g. chronic hypertension,
renal disease, diabetes with vascular disease, anti-phospholipid syndrome)
What complications in the current pregnancy are recommended to have a plan for serial growth scans in the third trimester
- heavy early pregnancy bleeding
- fetal echogenic bowel
- Preeclampsia
- Severe pregnancy-induced hypertension
- Unexplained ante-partum haemorrhage or abruption
- Low gestational weight gain
- Low PAPP-A
Who should get an Uterine artery Doppler studies at 20-24 weeks to help diagnose severe SGA?
- previous early SGA with delivery <34 weeks
- anti-phospholipid syndrome
- severe chronic hypertension
- Maternal renal disease
- autoimmune condition
What is the significance of raised uterine artery doppler at 20-24 weeks?
Woman with very abnormal uterine artery Doppler studies have an approximately 60% risk of developing SGA or preeclampsia requiring delivery <34 weeks should have regular scans and maternal surveillance
Prevention of SGA
≤ 16 weeks’ gestation low dose aspirin (100 mg per day) may be considered as this reduces the risk of SGA, especially in women who also have risk factors for preeclampsia, such as those with underlying medical disorders
Smoking cessation
If no risk factors, who gets growth scans?
- A growth scan is recommended if SFH is reducing centiles (e.g. >30%) or is < 10th %
- A growth scan is not recommended in women where SFH is tracking along or above the 90th centile if GDM has been excluded and there is no clinical concern re polyhydramnios.
what is the risk of SGA infant if previous SGA
three-fold increase in risk of SGA
Underlying Medical Conditions if associated with SGA require additional monitoring eg
Serial growth scans (3-4 weekly) are recommended with more frequent growth scans (2-3
weekly) if sup-optimal growth is suspected.
Consequence of smoking on SGA
Women who become smoke-free by 15 weeks have no increase in risk of SGA compared with nonsmokers
Obese Women
how to perform SGA monitoring
plan for growth scans is recommended with a
BMI of >35 is not possible to assess fetal growth clinically, growth scans may be considered at 30-32
weeks’ and at 36-38 weeks’ to enable serial assessment of fetal growth If a single scan is performed – better at 36-38 weeks (not allow trends)
More frequent / earlier scans are indicated if additional risk factors are present.
how does PAPP A affect SGA
Low PAPP-A is associate with increased SGA and PET - Low dose aspirin if low PAPP-A (<0.2 MoM) if less then 20 weeks
Management of SGA
- advice about fetal movements.
- Monitor for PET / HTN as can be the initial presenting complaint (In nulliparous women about 25% of SGA babies are born to women with hypertensive complications (preeclampsia, gestational hypertension, chronic hypertension)
- regular monitoring of BP and urinalysis performed at each clinical visit
Management of SGA with abnormal UA Doppler -
Plan for twice-weekly fetal and maternal surveillance as an outpatient, Association with maternal hypertension (PET) is common
SGA with normal UA Doppler –
2/3 SGA have normal dopplers
¾ of these pregnancies with have histological evidence of abnormal uteroplacental perfusion
Increased risk if morbidity if also growth restricted – if SGA and growth restricted they should be delivered by 38 weeks
SGA with abnormal MCA/ CRP –
Twice weekly surveillance, including
• clinical review
• CTG
• least weekly umbilical artery and MCA Doppler studies
• amniotic fluid volume (single deepest vertical pool of amniotic fluid)
• Scans for growth every two to three weeks
• Document the management plan in the clinical record.
• Deliver by 38 weeks
What are the investigations for early onset IUGR
If severe SGA is identified at the anatomy scan then referral to fetal medicine and uterine artery dopplers is indicated
Karyotyping is offered if SGA identified before 23 weeks or is there are associated structural abnormalities
CMV and toxoplasmosis is indicated
Syphilis and Malaria should be tested in at risk populations
Delivery based on MCA?
What does the MCA represent?
Preterm - do not deliver based on MCA
Term (37 weeks) deliver if abn MCA
bn MCA is a sign of brain sparing affect of chronic hypoxia - it is an early sign of fetal hypoxia
Moderative predictive value for acidaemia at birth (increased EMLSCDS and neonatal admission) in term infants
What is the DV?
When to measure?
When to deliver?
Used as a surveillance in preterm infants with abnormal umbilical artery doppler to time delivery
Moderate predictive value for acidosis and adverse outcomes
DV flow velocity reflects atrial pressure volume changes over the cardiac cycle
Retrograde a wave signifies overt fetal cardiac compromise
How to diagnose hydrops
+ what are the USS associations
2 of the following 4
- Ascites
- Pleural effusion
- Pericardial effusion more then 2mm - increasing is a bad sign
- Skin oedema (chest / scalp more then 5mm)
Associated with polyhydramnios (SDP over 8 or AFI > 24)
Placental thickening due to intravillous oedema - more then 4cm in T2 or 6cm in T3
Note if poly can obscure thickening of placenta
What are the maternal effects of having a hydropic baby?
Large for dates
Theca lutein cysts (increased hcg – unclear pathology - ? increase villous oedema)
PET (mirror syndrome)
Generalised maternal oedema often with pulmonary involvement
Can occur at any time – presenting with rapid weight gain, increasing peripheral oedema, SOB
Maternal haematocrit is low (in contrast to PET)
Rate IUD 50%
Severe polyhydramnios – maternal respiratory symptoms
What are theca lutein cysts?
Theca lutein cysts (increased hcg – unclear pathology - ? increase villous oedema)
Functional ovarian cysts, typically bilateral and multiple
Highest in GTD , also GDM pregnancies and hydropic babies
More likely in PCOS woman
Ovaries can be 10-15cm, pressure symptoms, 30% of woman with these will be hirsute or virilized
They are thought to originate due to excessive amounts of circulating gonadotrophins such as beta-hCG. Hyperplasia of the theca interna cells is the predominant characteristic on histology. The ovarian parenchyma is often markedly edematous and frequently contains foci of luteinized stromal cells.
Causes of fetal anaemia
Infection - parvovirus B12
Red cell alloimmunisation
Fetal maternal haemorrhage
hematological disorder eg thalassaemia
rarely red cell production disorders Enzymopathies structural red cell abnormalities (hereditary spherocytosis) myeloproliferative disorders (leukaemia)
Work up for hydrops
MFM referral
Indirect coombs test for alloimmunisation
Detailed anatomy
Fetal ECHO
Maternal Hb - if low genetic screen thalassaemias
MCA doppler velocimetry for anaemia
Amnio for karyotype and for infection screen, chromosomal microarray
Kleihauer
Ddx hydrops
Alloimmunisation Aneuploidy T1 50% T2 20% turners post common Cardiovascular 20% - structural - arrhythmia - cardiomyopathy Hematological 10% - haemoglobinopathies - enzyme or membrane disorders, erythrocyte aplasia FHM Infection - parvovirus B19, syph, CMV, EBV, Toxo, rubella, enterovirus varicella, Thoracic abnormalities 6% - pulmonary sequestration, cystic adenomatoid malformation, diaphragmatic hernia Lymphatic abnormalities Placenta/ twin complications Kidney and urinary tract abnormalties Syndromic Weird and wonderful
Mortality rate of hydrops
chance of live birth after prenatal dx 40%
Neonatal survival 50%
What is mirror syndrome
How is it different to PET
What tests can be done
associated with fetal hydrops and maternal oedema
associated with Rh D alloimmunisation, TTTS, Placental chorioangioma, fetal cystic hygroma, infections, cardiac anomalies, renal / bladder anomalies
90% oedema, 60% HTN, 40% proteinuria,
Similar to PET but haemodilution (not concentration like PET)
Elevated sfms-like kinase 1
Decreased placental growth factor
elevated vascular endothelial growth factor receptor 1
Generally prompt delivery indicated
what doppler detects anaemia
MCA peak systolic volume PSV
not just PI
why is alloimmunisation actually pretty uncommon
1%
- low prevalence of incompatible antigens
- Insufficient transplacental passage
- Maternal fetal ABO incompatability so rapidly clearance of antigens before an immune response
- variable antigenicity
- variable immune response to the antigen
What antibodies cause severe HDFN
Anti D,
Anti c
Level >7.5 but <20 correlates with a moderate risk of HDFN – referral once >7.5
If Anti E is also present then referral at lower titres maybe indicated
Anti K
Referral once detected as severe fetal anaemia can occur at 1:8
Antibodies that do NOT cause alloimmunisation
Lewis antibodies Le (a) Le (b) and I antibodies – mainly IgM and not expressed on fetal red cells
Also Duffy group B – fy(b)
What is the indirect coombs test
Indirect coombs test
Patients plasma + Red cells with known antigens + coombs reagent (antibodies againt human antigens)
Agglutination = positive test
Use Indirect coombs test for pretransfusion testing and blood type cross matching
What to consider with kell antibodies
Anti Kell antibodies cause hemolysis AND suppress erythropoieses by destroying the RBC progenitor cells in the BM
Severe anaemia can occur at low titres
Not for titre measurement – does have MCA PSV from 16 weeks
Anti D What gene Complication rate How much blood results is needed for sensitisation What si the ethnic variation
D is the most immunogenic
Complicates 0.5-0.9% pregnancies
0.1mls of Rh postive blood can cause sensitization
Responsible genes chromosome 1 RHD and RHCE
A single transion of + blood to a negative person have a 50% of forning anti D IgG
Ethnic variation in prevalence
85% Americas Rh +, 90% native americas, 93% African Americans, 99% Asians
Maternal alloimmunisation by exposure to anti D by incompatible blood transion or needle sharing
How to prevent anti D sensitisation
Recognise and treat sensitizing events
Within 72 hours but can give up to 9-10 days
6 weekly
Management
Blood group antibody screen at blooking and 28 weeks
Antenatal prophylaxis 28 + 34 weeks 625 IUI
Indicated prophylaxis
First trimester
CVS
Miscarriage
Termiantion
Ectopc
Not enough evidence for threatened miscarriage before 12 weeks
Second and third trimester
APH
Amniocentesis. Cordocentesis
ECV (successful ir not)
Abdo trauma or other suspective intrauterine bleeding
Directed prophylaxis in the Rh + neonate
Can assess volume after sensitising event
Kleihauer, flow cytometry
Give additional anti D if needed
Approach to a sensitised pregnancy
Maternal antibody titres and quantification
Anti D, c, K monthly until 28 weeks then every 2 weeks
If other antibodies consider paternal testing
Assess fetal risk
- paternal testing
Fathers blood phenotype and genotype
If father is Rh + but hereozygous 50% of children with be RH neg
NIPT
Assess fetal genotype – if doesnt have Antigen then not as risk
Indicated if father is heterozygous
Amniocentesis and PCR of amniocytes
CVS is not used may worsen alloimmunisation and increased FMH
Maternal hx
Monitoring antibody
Quantitation is more reliable then titre
Referral 1:16/32 = 4-6 quant
Refer to MFM Hx of haemolytic disease High titres, abnormal USS Critical titre reached MCA PSV approaching / 1.5 MoM
Management of an at risk pregnancy
- high titres
- anti Kell
Fetal monitoring
MCA PSV (peak systolic velocity)
Increased velocity due to creased cardiac output, vasodilation of the brain, decreased blood viscosity
Technique
Resting fetus, Circle of Willis imaged in axial image using colour doppler, Entire length of MCA, Close to origin of internal carotid artery
Gestation dependent Measure from 18-20 weeks, to 36 weeks Not as efficacious after 36 weeks Levels <1.5Mom = 100% not anaemic Measure 2 weekly Levels >1.5 Mom = 65% anaemic 12% false + Repeat in 24 hours – if the same then FBS +/- transfuse After IUT MCA maybe unreliable Liver length is a helpful adjunct Assess for signs of hydrops
incidence and definition of polyhydramnios
1-2% o pregnancy
SDP > or=8
AFI >24
Ddx for polyhydramnios
Causes - Likelihood of finding a cause is related to severity of polyhydramnios
Idiopathic 40%
Fetal structural anomaly/anomalies
Most commonly when swallow was affected
GI obstruction – duodenal, esophageal, intestinal
Neuromuscular disorders – anencephaly
Secondary obstruction eg massive unilateral dysplastic kidneys
Fetal chromosomal abnormality (eg, Trisomy 18)
IUGR + Poly think T18
10-20% of severe poly has a chromosomal condition
High fetal cardiac output state (eg, any condition resulting in anemia)
Anaemia from alloimmunization, haemolysis
Twin-twin transfusion syndrome
Maternal diabetes mellitus // lithium use / substance us
Fetal neuromuscular disorders
Fetal infection (eg, parvovirus)
Fetal Bartter syndrome
Rare autosomal renal tubular disorder
What does having poly increase the risk of ?
maternal respiratory compromise PTB PPROM PTL Malposition Macrosomia Umbilical cord prolapse abruption (with ROM) Longer second stage POst partum atony
perinatal mortality 5.5X higher
Idiopathic - increases the risk of low 5 min apgar, TTN, needing resus, NICU, hypoglycemia, structural abnormalities, jaundice
Long tern neurological disorders , developmental delay,
What is the management only poly diagnosed?
Detailed family hx
Genetic testing for severe polyhydramions
GTT
TORCH if other signs of fetal infection
Review blood group and antibody status
Anatomy - (with a normal anatoym scan and severe poly risk of a major malformation 11%)
Are there any treatments for polyhydramnios
The aim is to relieve maternal symptoms and to reduce the risk of preterm labour, by reducing uterine stretch.
Amnioreduction
Studies have shown that this can prolong gestation and improve perinatal survival. However, it may need to be repeated and can result in stimulation of preterm labour, or abruption due to the rapid reduction in intrauterine pressure.
Indomethacin
This may work by enhancing fetal renal reabsorption of water and sodium and, hence, reducing the amount of urine produced by the fetal kidneys.
Indomethacin has been reported to be associated with premature closure of the ductus arteriosus, cerebral vasoconstriction, and impaired renal function in the neonatal period. For these reasons, its use is usually discontinued at 32 weeks of gestation. The use of indomethacin is contraindicated in twin-to-twin transfusion syndrome as it may have adverse effects on the oliguric donor twin.
