Obs 4 Flashcards
Define large for gestational age (LGA)
A neonate who, at birth, weighs at or above the 90th percentile for gestational age
Define foetal macrosomia
Babies with birth weight >4,000 g
What are the tools to diagnose LGA prenatally?
- SFH: Greater than 90th centile for gestational age (top of fundus to top of symphysis pubis)
- AC: >95th centile for gestational age
- EFW: >90th centile on customised growth chart or over 4000g on USS
What are the RFs for LGA?
- High BMI
- Foetal macrosomia (>4kg in a term infant)
- Gestational or DM
- Syndromes: Beckwith-Wiedemann, Simpson-Golabi-Behemel, Soto’s syndrome
- Molar pregnancy
- Polyhydramnios
- Multiparity
- Advanced maternal age
What are the S/S of LGA?
- On inspection > excessive distension for gestational age
- Abdomen > increased SFH, increased abdominal circumference
What are the investigations for LGA?
- OGTT – for gestational diabetes
- Bloods – serum βHCG
- USS – liquor volume, biometry
- Genetic testing
What is the management for LGA?
At every antenatal appointment after 26 weeks, measure SFH:
If greater than expected on two or more occasions, or there is a significant increase in growth on one occasion, offer a growth scan at the hospital (check baby’s growth, AF volume and blood flow through the placenta)
Serial SFH plots show linear growth pattern >90th centile with no other concerns:
- Reassure this is normal, arrange another routine scan
- Refer to ANC by 37wks if EFW projects to be >4000g at 40wks
Serial SFH plots show accelerated growth at <36wks:
- Refer for USS
- If EFW >90th centile, refer for OGTT
- If normal OGTT, organise 1 week of BM testing
- If not diabetic, refer to consultant ANC by 37wks
- Offer IOL between 37-40wks if predicted to be >4000g at 40wks
Serial SFH plots show accelerated growth at >36wks:
- Refer for USS
- If EFW >90th centile, offer home BM monitoring for 1wk
- If not diabetic, refer to consultant ANC by 37wks
- Offer IOL between 37-40wks if predicted to be >4000g at 40wks
What are the complications of LGA?
Baby:
- Shoulder dystocia - Brachial plexus injury
- Fractures
- Stillbirth
- HIE
- Hypoglycaemia in GDM
- Increased mortality
Mother:
- 3rd/4th degree tears
- Prolonged labour
- PPH
Prognosis > early planning/care > no difference in outcomes for LGA compared to normal
Define small for gestational age (SGA)
Babies with a birth weight below the 10th percentile for their GA
Define IUGR
Derived from growth rate:
Describes a baby with a reduced growth rate (baby becomes SGA)
All IUGR babies are SGA but not all SGA babies are IUGR
What are the RFs for SGA?
Maternal:
- Previous SGA baby
- Previous stillbirth
- Maternal disease - CKD , chronic HTN, APLS
- Placental insufficiency (asymmetrical IUGR)
Foetal:
- Chromosomal abnormalities (symmetrical IUGR)
- Infection (CMV, rubella)
- Multiple pregnancy
What are the investigations for SGA?
1st: SFH or risk status determined
- At booking or any antenatal appointment
- ≥1 major RF or ≥3 minor RFs
- Reassess at 20 weeks
2nd: confirm SGA with foetal biometry (20w)
- Biparietal diameter, HC, AC, FL
3rd: uterine artery doppler (20-24w)
- Normal = repeat scans every 2 weeks (from 20-24w onwards)
- Abnormal = Serial USS growth scans every week (from 26-28w onwards), Doppler USS can be performed twice a week (umbilical artery flow)
+Screen for congenital infections
What is the management of SGA?
General:
- Smoking, alcohol and drugs should be stopped
- Low-dose aspirin may have some role in preventing (not reversing) IUGR in high-risk pregnancies
Delivery:
Indications for IMMEDIATE DELIVERY:
- Abnormal CTG (and reduced foetal movements)
- Reversal of end-diastolic flow
Delivery by 37 weeks is usually necessary > dependent on severity and gestation:
- Steroids should be given <36 weeks
- Consultant-led clinics and decision-making
What are the complications of SGA?
- Stillbirth
- PTL
- Intrapartum foetal distress
- Birth asphyxia
- Meconium aspiration
- Postnatal hypoglycaemia
- Neurodevelopmental delay
- Risk T2DM and HTN in adult life
Prognosis > increased perinatal morbidity and mortality, increased neurodevelopmental delay if onset <26/40
What is obstetric cholestasis?
Pruritus in pregnancy, resolves on delivery, associated with abnormal liver function in the absence of other identifiable pathology
What is the aetiology of obstetric cholestasis?
Likely genetic (defect in membrane phospholipid) and hormonal (oestrogen impairing sulphation) factors
What are the RFs for obstetric cholestasis?
- Previous OC
- FHx
- ethnicity (South Asia, Chilean, Bolivian)
- multiple pregnancy
- pruritis on COCP
- Affects ~1% of pregnancies in the 2nd half of pregnancy
What are the S/S of obstetric cholestasis?
- Pruritus with excoriations (palms and soles; worst at night)
- Raised bilirubin (and jaundice in 20%)
- No rash
What are the investigations for obstetric cholestasis?
- Bile acids (raised)
- LFTs (raised bilirubin / liver enzymes) - repeat weekly
Consider:
- Coagulation screen (may be high if vitamin K deficient)
- FBC
- Hepatitis C serology (increased risk of OC in hepatitis C)
What is the management of obstetric cholestasis?
Symptomatic relief:
- Ursodeoxycholic Acid – reduces itching and improves LFTs
- Vitamin K supplementation (if clotting impaired)
- Sedating antihistamines (chlorphenamine or promethazine)
- Topical emollient and wear loose cotton clothes (may help reduce itching)
Antenatal Monitoring:
- Weekly LFTs until delivery
- Twice-weekly Doppler and CTG until delivery
- Consultant-led care
Delivery:
- Offer induction of labour at 37 weeks
Postnatally (with GP):
- Arrange follow-up, after delivery, to ensure that LFTs have returned to normal
What are the complications of obstetric cholestasis?
Baby:
- Stillbirth
- Premature birth
- Meconium aspiration
- Foetal distress
Mother:
- PPH (due to low vitamin K)
- Severe liver impairment
What is acute fatty liver of pregnancy?
Rare pregnancy associated disorder characterised by fatty infiltration of the liver
- Accumulation of microvesicular fat in hepatocytes, periportal sparing, small yellow liver on gross examination
- Likely mitochondrial disorder affecting fatty acid oxidation