MFM and neonates Flashcards
DCDA twin delivery
Induce 37-38 weeks aiming for vaginal birth providing the following criteria are met:
- Twins diamniotic
- Twin 1 is cephalic
- Twin 2 is not >500g bigger than twin 1
- Neither twin has any evidence of fetal
compromise requiring c-section
Twin birth study (2013) RCT of planned c-section vs vaginal delivery for twin pregnancy.
c-section delivery after 32 weeks did not significantly decrease or increase the risk of neonatal or fetal death or serious morbidity as compared with planned vaginal birth.
Cochrane review (2015) With planned vaginal delivery 30-40% risk of emergency c-section. No evidence of lower maternal or fetal morbidity having c-section. C-section for 2nd twin occurs in 10% of cases.
Risks with DCDA twins
▪ Antenatal: growth scans, anatomy scan, GTT, PET screening, vigilance re: FM, sleep on side, 28/40 bloods, anaesthetic discussion
▪ Intrapartum: MOD depending on T1, deliver ~ 37/40, IVL, CEFM, hospital, personnel at delivery, early epidural delivery of T2
▪ Postpartum: PND, breastfeeding support, VTE prophylaxis
Complications in MC twins
Twin to Twin Transfusion (TTTS) 10-15%
One twin receives more blood supply than the other due to unidirectional flow along a large arterio-venous anastomoses deep in the placenta. This leads to oligohydramnios, poor growth and abnormal umPI in the donor and polyhydramnios progressing to cardiac dysfunction and cardiac failure in recipient
Twin Anaemia Polycythaemia Syndrome (TAPS) 5%
A small arterio-venous anastomoses on the placenta leads to unidirectional blood supply from one twin to the other but this is a very slow transfusion leading to one twin becoming anaemic and the other polycythaemic.
Twin reversal arterial perfusion sequence (TRAPS) <5% Presence of a live twin and an acardiac twin. The live twin pumps blood through both twins and this leads to high out-put heart failure.
Selective IUGR 10-15%
Due to unequal sharing of placental mass leading to growth restriction in one twin. Can be contributed by marginal/velamentous cord insertion of smaller twin .
Management in MC twins
Counsel woman regarding complications related to MCDA twins
· Inform woman with written and verbal information regarding model of care for MCDA twins.
· This should include what symptoms to be aware of e.g. sudden increase in abdominal girth and SOB could indicate polyhydramnios due to TTTS. PET symptoms.
Early anatomy scan ~ 18 weeks
Aneuploidy screening is less sensitive in twin pregnancy. MC twins have a higher rate of congenital abnormalities and an increase risks of congenital heart disease so a fetal ECHO may be required
Fortnightly growth scans from 16 weeks at a centre with sufficient experience to recognise these complications Scans should include
· growth -discordance >20% suggest sIUGR
· liquor volume, bladder and stomach filling- screening for TTTS
· umbilical artery doppler
Scan for MCA PSV from 20 weeks
To look for fetal anaemia (TAPS)
Refer for obstetrician care or multiple pregnancy clinic MC twins are high risks pregnancies. Should be managed by a MDT team including senior MW and obstetricians
Prompt referral to fetal medicine if any concerns regarding twin related complications
Prompt review to allow optimal treatment before onset of severe disease e.g. laser ablation for TTTS
Ambiguous Genitalia
Whether we develop into a male or female gender depends on the presence of our chromosomes, hormones, and hormone receptors. Chromosomes are the genetic building blocks that make up who we are. Male gender is typically associated with XY and female XX. However we also need the presence the corresponding male or female sex hormone, and the ability of our body to process and recognise this. Ambiguous genitalia can result from a range of conditions affecting our chromosomes, our production or sex hormones, or our ability to recognise these sex hormones.
history:
History - drugs in pregnancy, consanguinity, or family hx of ambiguous genitalia, IUD/NND, hyperandrogenism, congenital abnormalities
Exam”
vital signs, evidence of dehydration (fontanelles), head to toe examination, genital examination looking a urethral meatus / vagina / labial folds / clitoris / gonads / phallus / groin
CAUSES:
• CAH (AR),
• 5 alpha reductase deficiency (AR - conversion testosterone to DHT),
• tumours,
• maternal hormones in pregnancy,
• androgen insensitivity syndrome (AR)
Investigations:
FBC, UEC, LFT, karyotype, SRY gene (FISH specific probes), AMH, 17 OHP, testosterone, DHEAS, androstenedione, cortisol, dihydrotestosterone, FSH, LH, USS abdomen and pelvis
MDT approach:
paediatrician, psychologist, endocrinologist, paediatric surgeon, social work.
?genetic referral
Echogenic bowel
Echogenic bowel associated with CF, perinatal infections such as CMV and toxoplasmosis, and aneuploidy, as well as rarely intrauterine bleeding, bowel malformation, fetal alcohol syndrome and mesenteric ischaemia
Refer to MFM.
Investigations:
1. Detailed USS assessment of anatomy to check for markers of aneuploidy or infection
• Usually focal and mass-like in the lower abdomen – CF and aneuploidy tend towards multifocal, whereas CMV tends to be focal.
• Assess for amniotic fluid volume
• Detailed review of growth and placenta
• Check for markers of aneuploidy – nuchal thickening, hypoplastic/absent nasal bone, major structural anomalies, intracardiac echogenic foci, shortened femur
• Check for markers of fetal infection – microcephaly, ventriculomegaly, cerebral calcification, hydrops, SGA
2. Fetal genetic assessment
• Usually recommend amniocentesis for karyotype, virology PCR and DNA analysis (CF)
• Could also do CFDNA maternal bloods (but would then need diagnostic test if +ve)
3. Maternal virology screen for toxoplasma and CMV (TORCH).
4. Parental Cystic Fibrosis Carrier Status Screening (80% detection rate)
Follow up:
• Prognosis usually good, but will depend on above assessment
• Monthly growth scans should be initiated as there is an association with IUGR and death.
CMV in pregnancy
o Transmitted in body fluids/saliva
o Self limiting flu like illness or asymptomatic in mother
o Risk of transmission for primary infection is 30 to 40% in the first and second trimesters, and 40 to 70% in the third trimester.
10% risk of long term harm.
Risks:
o Fetal risks include neurological disability, hearing loss, chorioretinitis, stillbirth, seizures, microcephaly, cerebral palsy
o Amniocentesis tells us the baby has been exposed to infection but does not predict long term effects – most babies are normal. Decisions about termination are difficult because of this.
Plan:
o Referral to MFM
o Serial growth USS
o MRI brain
o If normal USS and MRI prognosis good
o Give hygiene advice to prevent future infections
Neonatal CMV
• Thorough physical exam at birth -90% are healthy at birth and have normal development
• Encourage breastfeeding
Investigations:
o Should be done <3 weeks old
o CMV IgM
o CMV PCR (urine, saliva, blood)
o FBC, LFTs
o Also do testing in those with abnormal hearing screen without known maternal history.
• If positive
o Do an ophthalmology and radiological exam
• Head USS –> Hydrocephalus
• MRI –> intracranial calcification, atrophy, ventriculomegaly, migrational or white matter abnormalities
Asymptomatic: 3-6monthly review including hearing and neurodevelopmental assessment
MUTANISM for MFM
M- MFM referral U - USS tertiary T - Torch A - Amnio N - Neonatal review T - TOP consider I - information S - Support M - Management specific to the condition
Omphalocele
Explain issues :
Congenital abdominal wall defect related to base of umbilicus, abdominal viscera contained within membranous sac. Thought due to failure of midgut to return to abdomen after 10 weeks gestation
Differential:
Amniotic band
Urachal cyst
Gastroschisis
Risks: Strong association with other anomaly 70% association with aneuploidy Mortality 40% IUGR/PTB
Plan :
Tertiary anatomy scan esp for cardiac defects and other GI abnormalities eg malrotation, atresia, volvulus
MFM
Amniocentesis for karyotype
Support groups/condolences
Offer termination vs conservative management with ongoing growth surveiullance
Involve paeds surg, deliver at tertiary centre, NVD except where defect super large prior to delivery, CFM in labour etc.
Parvovirus
IgG + IgM positive recent infection
High risk groups: Mother’s of children, teachers amd childcare workers
Risk to fetus only if infected within the first 20 weeks
- 10% excess fetal loss
- 3% hydrops (33% resolve, 33% need IUT & 33% IUFD)
Management: USS 1 - 2 weeks intervals for 12 weeks and MCA PSV
Listeria
Found in soil and water - wash all fruit and veg
Symptoms fever, malaise, N+V and diarrohoea
Transmission highest 3rd trimester
Overall mortality 50%
Risks: PTB, neonatal meningitis and IUFD
Treat: Ampicillin and Gentamicin IV 10-14 days
CMV
Frequent close contact with children who tend to shed virus from nasal secretions and salvia
IgM + IgG positive IgG avidity low recent primary infection
Trimester 1 - adverse outcome 10%
Amnio >20 weeks/ 6 weeks post infection if -ve reassure and if positive 1:4
Fetal MRI 28 + 32 weeks
Leading cause of non genetic sensorineural hearing loss.
Also causes IUGR and hydrops
CMV prevention
Do not share food, drinks or utensils used by children < 3 years old
Do not put a child’s dummy in your mouth
Attention to hand hygiene when in touch with your young child’s bodily fluids.
Toxoplasmosis
IgM can remain +ve for months/years check antenatal serum
Low avidity more specific for recent
Amnio 18 - 20 weeks or > 4 weeks after maternal infection
1st - Risk low 5-15% infection high risk fetal damage
2nd - Risks 25-45 infection with 20-30% risk of fetal damage
3rd - risk transmission 33-70% but risk fetal damage low 5-15%
Treatpyrimethamine sulfadiazene and folinic acid if +ve PCR
4 weekly USS for fetal infection
Baby needs bloods after delivery and full examination neurological, hearing and occular examinations
