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Fetal and Maternal MedicineRCOG Part 2 MRCOG Course
Dr Janet R Ashworth
Consultant in Fetal and Maternal Medicine
Royal Derby HospitalConflicting interests: none.
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Aim of session
• To cover some of the current and some poorly but commonly-managed areas of high risk pregnancy.
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Subjects
• Complex multiple pregnancy• Pre-term labour and delivery• Red cell antibodies.
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Complex Multiple Pregnancy
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Complex Multiple Pregnancy
• Monochorionic Twins
• Higher multiples
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General points for all multiple pregnancies
-NICE guidance, 2011-11-14 weeks, dating, Down’s screen (prn), determine chorionicity and determine identifiers for fetuses.-Core teamRisks: -Miscarriage -Stillbirth(1 -0.5%; 2-1.2%; 3-3.1%)
-Anaemia -Maternal mortality x2.5-Hypertensive disorders-APH/PPH -Congenital anomaly x5-Operative delivery -IUGR (aspirin)-Preterm delivery (60%; 10%<32/40)
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Monozygotic Twins; additional risks
• DCDA (1/3 of MZ twins. Will be same sex!)• MCDA: Discordant growth; TTTS; TAPS; Demise of co-twin effects.• MCMA: Cord entanglement; TRAP syndrome.• Conjoined Twins: Co-dependence risk; separation risk.
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Fetal Medicine Centre Role
• Triplet pregnancies with one or more monochorionic element• Monoamniotic twinning• Discordant growth or death• Fetal anomaly• TTTS/TAPS.
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Delivery in Uncomplicated Multiple Pregnancies
• DCDA 37-38 weeks• MCDA 36-37 weeks, with steroids• Triplets 35-36 weeks, with steroids• MCMA by 34 weeks, with steroids.
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Red Cell Alloimmunisation
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Problems with red cell antibodies
• Fetal anaemia, haemolytic disease of the newborn (HDN), crossmatching problems
• HDN and x-matching problems• X-matching only.
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Red Cell Alloimmunisation
• Fetal anaemia
• Rhesus D• Rhesus c• Kell• Anti-G• (Duffy a)
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Rhesus (D) Disease
• Anti-D antibodies (Rhesus negative mother)- Now less common problem since prophylactic anti-D.- Rhesus disease typically increases in severity with serial Rhesus positive
fetuses.- Next fetus may be affected up to 10 weeks earlier in gestation than last.- Anti-D titres above 4 iu/ml suggest risk.- Low titres only reassuring in 1st affected pregnancy.
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The Other Red Cell Antibodies Causing FetalAnaemia
• Anti-c, Anti-Kell- May cause fetal anaemia in first pregnancy where alloimmunisation
identified.- Anti-Kell causes profound early-onset fetal anaemia by affecting red cell
progenitors. - Kell alloimmunisation usually transfusion-acquired. Shouldn’t occur any more!
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The Changing Role of Ultrasound in Managing Rhesus Disease …..• The development of non-invasive monitoring for fetal anaemia. • Mari et al Ultrasound Obstet Gynecol 1995; 5: 400-5. N Eng J Med
2000; 342: 9-14.1.
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Middle Cerebral Artery on USS
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Measuring MCA PSV
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Using MCA PSV in Rhesus Disease
• Has been shown to better predict fetal anaemia than serial amniocentesis and delta OD 450. Oepkes et al N Eng J Med 2006; 355: 156-64.
• High sensitivity and low false positive rate• Now used in monitoring post-intrauterine transfusion.
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Monitoring Fetuses at Risk of Fetal Anaemia due to Rhesus Disease.
• Significant maternal anti-D levels (>4iu/ml) or previously affected fetus.• Fetal genotype• If fetus Rhesus D positive, monitor MCA PSV from 10 weeks prior to
previous gestation at which affected.• If first pregnancy with alloimmunisation, monitor MCA PSV weekly from
16 weeks. Increase surveillance if rising anti-D titres.• Severely affected previous fetus – consider IVIg to delay serial
transfusion.
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Monitoring in c/Kell Alloimmunisation
Fetal genotyping (most people are Kell-negative!).• Weekly monitoring from 16-18 weeks (or when anti-c titre > 7.5
iu/ml).• Management as for anti-D alloimmunisation once anaemia suspected.• May need intra-peritoneal transfusion or to consider ivIg infusions.
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• Fetal blood sampling and intravascular transfusion
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Outcome of IUT in Rhesus Disease
• 95% survival with intravascular IUT.• 70-80% if hydropic.• Median number of transfusions 3.• Mean Hb at transfusion 7.7g/dl.• Mean gestation at delivery 34 weeks.• Managed by caesarean delivery 34-36 weeks.• Serial IUT inhibits fetal haematopoiesis; top-up neonatal transfusions
likely.
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Red Cell Alloimmunisation• Haemolytic Disease of the Newborn (anaemia with jaundice, risk of
kernicterus)Rhesus C, E, e
Duffy (Fya)
Kidd (Jka (Jkb)M, S, s
• Neonatal liaison. Cord bloods (DAT, group and bilirubin)
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Pre-term Delivery
• Prophylaxis• Diagnosing PPROM• Diagnosis and treatment of PTL• Steroids• Magnesium sulphate• Delivery
NICE guidance 2015
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Preventing Preterm delivery
Vaginal progestogen OR elective cerclage-Previous delivery 16-34 weeks + cervical length 16-24wk <25mm
Vaginal progestogen-no Hx prematurity but cervix <25mm 16-24wk
Cerclage-previous PPROM or cervical trauma and <25mm 16-24wk
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Pre-term premature rupture of membranes
• Diagnosis:
• Liquor seen on speculum• No liquor seen but positive specific test (ILGF binding pr-1 or
placental alpha-macroglobulin-1. NOT nitrazine); if history supportive then treat as PPROM. Diagnostic test not indicated if in established labour.
• Diagnosis of infection requires CRP, WBC, fetal HR. Single marker unreliable.
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Diagnosing Pre-term Labour
• Clinical history• Speculum with digital VE if cervix not clearly seen• If <30 weeks, treat as pre-term labour• If>30 weeks use TV USS <15mm or fFN>50ng/ml if available to
confirm high risk of delivery in <48 hours. Negative tests allow reassurance.
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Management of Pre-term Labour
• Rescue cerclage considered if 16-27wk, dilated cervix and no PPROM, no infection, no bleeding and no contractions.
• Consider tocolysis (nifedipine if not contra-indicated, oxytocin receptor antagonist otherwise) if 24-26 weeks and suspected PTL, or >26 weeks and diagnosed PTL.
• + considering in-utero transfer• - bleeding, infection.
• Steroids prior to 36 weeks
• MgSO4 for fetal neuroprotection if 24-30wks(consider up to 34wk).
• Consider caesarean for breech 26-37 weeks. Otherwise no advantage just for prematurity.
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Maternal Medicine – Recent Information
• MBRACE• UKOSS• National Perinatal Cardiology Review• Green-top guidelines:• Thalassaemia• Thrombosis• AIP (abnormally invasive placenta) pathways; praevia guideline.
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Questions?
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