Obstetric conditions Flashcards
Obstetric Cholestasis
In 0.7% of population
Clinical presentation = itch without rash (especially palms and soles of feet), abnormal LFTs +/- raised bile acids (does not need to be fasting), rarely pale stool/dark urine
Women with persistent pruritus and normal biochemistry should have LFTs repeated every 1–2 weeks.
Risk factors = personal or family Hx, hep C, gallstones, multiple pregnancy
Complications = preterm birth, FDIU, passage of meconium, caesarean section, PPH, fetal distress in labour, NICU admission
Treatment
= NO evidence that treatment improves fetal or neonatal outcomes
= Ursodeoxycholic acid (may improve itch and LFT, although recent RCT states it does not improve LFT, no data to state it reduces FDIU), warm showers, callomine lotion (improve itch)
Weekly LFTs until delivery, coags if abnormal LFTs, consider delivery >38 weeks if BA >40 or ALT >200; consider earlier if BA >100 (risk of stillbirth increased in women with intrahepatic cholestasis when serum bile acids >=100 as per systematic review), CEFM
Give vit K only if prolonged PT - dose 5-10mg PO daily (although oral Vit K may cause kernicterus, haemolytic anaemia, hyperbilirubinaemia in neonate). Can give vit K in normal PT but advise of above risks.
In more severe biochemical derangement, offer from 37wks but increased risk of maternal and perinatal morbidity
Active Mx 3rd stage due to increased risk of PPH
DDx = eczema, PUPPS (polymorphic eruption of pregnancy) or pemphigoid gestations (blisters), other causes of deranged LFTs (hepatitis, EBV, CMV, autoimmune disease, PET, acute fatty liver of pregnancy), liver US
Ultrasound and CTG are not reliable methods for preventing fetal death
Poor outcomes cannot be predicted based on biochemical results alone
Fetal death is usually sudden; there is no evidence of placental insufficiency and FGR/oligohydramnios are not features of the disease; UA Doppler assessment are no different from other pregnancies
Symptoms usually resolve postpartum
If very deranged LFTs, repeat 10days postpartum (not earlier as LFTs can increase in this time) and 6-8wks postpartum
Risk recurrence 40-90% future pregnancy
Family members should known increased risk of them having cholestasis in pregnancy
May get recurrence of symptoms if take COCP (oestrogen component) so best to avoid oestrogen containing contraception
For diagnosis of obstetric cholestasis levels must normalise by 6 weeks so need to be tested and if remain abnormal alternate diagnosis sought; symptoms must also have resolved
No long-term effects on mother or baby
Acute fatty liver of pregnancy
Most commonly in 3rd trimester, 20% postpartum
Aetiology poorly understood, thought to be due to defects in fatty acid metabolism in pregnancy
Risk factors: nulliparous, multiple pregnancy, PET, male fetus, BMI<20, fetal beta-fatty oxidation genetic disorders, previous acute fatty liver
Presentation: nausea, vomiting, anorexia, epigastric/RUQ pain, headache, jaundice, hypertension, ascites, encephalopathy
Ix: abnormal LFT, hypoglycaemia, coagulopathy, hyperbilirubinaemia, AKI, increased urate, increased ammonia, ascites on US
Treatment: maternal stabilisation, reverse coagulopathy, urgent delivery (CS or if VB can be expedited)
