Complications in pregnancy Flashcards
complications/risks of intrahepatic cholestasis of pregnancy (ICP)/obstetric cholestasis (OS)?
- increased rate of stillbirth/intrauterine death-fetal death before or during birth, at 24 weeks or later gestation, and fetal distress-partly due to increased likelihood of meconium passage (baby opens bowels before being born causing green/brown discolouration of fluid)
- increased risk of premature birth (spontaneous and iatrogenic) (1 in 10 will deliver before 37wks).
- maternal morbidity due to intense pruritus and sleep lack
management of intrahepatic cholestasis of pregnancy?
- weekly monitoring of LFTs, if return to normal or soar then revise diagnosis, wait at least 10 days before re-checking after delivery as normal LFT fluctuations during this time in normal pregnancies
- ursodeoxycholic acid for symptomatic relief-GS dissolving agent which reduces cholesterol content in bile
- Vit K PO as may be vit K malabsorption, this will reduce haemorrhagic disease in both mother and baby
- induction from 37 weeks onwards to avoid late stillbirth, has been shown from this time that perinatal and maternal morbidity increases, offer continuous fetal monitoring during labour
definitive management of acute fatty liver of pregnancy?
delivery
RFs for obstetric cholestasis?
occurrence in previous pregnancy FH of condition multiple pregnancy gallstones Hep C
during what stage of pregnancy does obstetric cholestasis tend to present?
3rd trimester
presentation of obstetric cholestasis?
intense pruritus, particularly of palms of hands and soles of feet but can affect any part of body, may be excoriations, no rash
itching often worse at night, may affect sleep
itching can preceed raised LFTs by days or weeks, so important to rpt bloods poss. weekly
may be other symptoms of cholestasis e.g. pale stools, dark urine, jaundice
generalised malaise, fatigue
differentials important to rule out before diagnosing obstetric cholestasis?
other causes of liver disease and pruritus:
- viral hepatitis, including CMV, EBV
- AI hepatitis-anti-smooth muscle, ANA, anti-liver and kidney microsomal type 1 Abs
- drug induced hepatitis
- gallstones
must also exclude fatty liver of pregnancy, and pre-eclampsia-*HELLP-haemolysis, raised LFTs, low PLT-do FBC, BP+urine dip, ?clotting profile
also do liver USS
LFTs-ALT/AST, GGT raised, bilirubin usually raised
total bile acid level
outcome of obstetric cholestasis?
should settle spontaneously following delivery
f/u long enough to allow LFT normalisation, usually recheck at 6weeks
further specialist input needed if have not normalised by 6 months
a/v that significant risk of recurrence (45-90%)
causes of polyhydramnios?
anything which impairs amniotic fluid swallowing by the fetus, increases fetal urination, increases fetal production of fluid from lungs+oral+nasal cavities or interferes with intramembranous and transmembranous absorption-between fetal blood and placenta and across amnion and chorion:
-idiopathic
-congenital anomalies-upper GI atresia, CVS defects, micro or ancephaly, NTDs, renal defects e.g. bartters’s syndrome
-and genetic disorders-trisomy 21, 13, 18
maternal DM
-fetal anaemia-increases CO hence kidney perfusion and urination
-maternal diabetes
-multiple pregnancy
-congenital infections-toxoplasma, parvovirus, CMV, rubella
-hydrops fetalis-assoc. with rhesus haemolytic disease
-maternal substance abuse
-maternal metabolic abnormalities e.g. hypercalcaemia
the more severe the polyhydramnios, the more likely an underlying cause will be found
functions of amniotic fluid?
protect baby from trauma and infection
facilitate lung development
help with development and movement of limbs and other skeletal parts
presentation of polyhydramnios?
- large for dates uterus on antenatal examination-symphysis-fundal height, fetal parts may be difficult to palpate, may see on US examination
- mum-excessive breathlessness, early labour onset or PROM, cord prolapse, abnormal fetal presentation
- acute polyhydramnios-uterus enlarges rapidly, most commonly seen with twin pregnancies-twin to twin transfusion syndrome-unequal blood supply, 1 twin gets most (recipient) whereas other gets little (donor). recipient produces large amount of urine.
differentials for polyhydramnios?
multiple pregnancy
fetal macrosomia
placental abruption-uterine size may rapidly enlarge due to intrauterine haematoma development
chorioangioma-benign lesion of placenta due to excess capillary formation in absence of villus differentiation.
what methods are used via US to diagnose polyhydramnios?
amniotic fluid index-uterine cavity divided into 4 segments, total volume more than 24cm=polyhydramnios
single deepest pocket-deepest pocket measured vertically, more than 8cm.
lab tests that can help exclude associated diseases in polyhydramnios?
blood glucose and OGTT
maternal infection screen
if fetal anemia or hydrops fetalis suspected-maternal anitbodies,
genotyping
management of polyhydramnios?
secondary care
1st step-try to identify underlying cause, treat as appropriate e.g. intravascular transfusion for hydrops fetalis
aim to minimise preterm labour-regular antenatal checks, serial US
during labour require CTG-continuous monitoring
induce labour if fetal distress
corticosteroids if preterm labour suggested or iminent
PG synthetase inhibitors e.g. indometacin-reduce renal blood flow but risk of premature closure of DA, used for max 48hrs
amnioreduction-fluid drainage under US guidance, more commonly used in twin to twin transfusion syndrome, this may also benefit from connecting placental vessel ablation.
polyhydramnios complications?
prematurity, low birth weight, fetal death PROM placental abruption malpresentation PPH cord prolapse mother-UTIs, increased dyspnoea, HTN
what chromosomal abnormalities might be associated with a cystic hygroma?
also known as a macrocystic lymphatic malformation, this is a fluid filled sac, commonly found in neck, head, axilla or chest, that results from obstruction in the lymphatic system. assoc. with: downs syndrome turner's noonan
how is oligohydramnios defined from US?
amniotic fluid volume less than 500ml at 32-38wks
AFI less than 5 from late-mid trimester
max vertical pocket less than 2cm from late-mid trimester
why is oligohydramnios more common in pregnancies beyond term?
amniotic fluid volume normally decreases at term (to around 800ml)
also ?reduced placental function, and reduced fetal renal blood flow and urine production
fetal causes of oligohydramnios?
- congenital problems e.g. renal agenesis, ureteral atresia, obstructive uropathy
- chromosomal factors
- IUGR-chronic hypoxia causes blood shunting away from fetal kidneys towards the brain
- pre-labour rupture of membranes (PROM)
- post-term pregnancy
- fetal demise
placental causes of oligohydramnios?
- abruption
- twin to twin transfusion syndrome (monochorionic twins)
maternal causes of oligohydramnios?
- maternal dehydration
- uteroplacental insufficiency
- HTN, pre-eclampsia
- DM-villous oedema
- drugs-indometacin, ACEis
- chronic hypoxia
-may be idiopathic
3 main ways of amniotic fluid removal?
fetal swallowing-with GI tract absorption, then recirculating by the kidneys or transfer to mother via placental
fetal respiration
continuous bulk flow-hydrostatic and oncotic forces-at chorionic plate
causes of talipes equinovaris (clubfoot)?
idiopathic-most commonly spina bifida cerebral palsy oligohydramnios arthrogryposis edward's syndrome (trisomy 18)-overlapping of the fingers, rocker bottom feet, microcephaly and micrognathia, low set ears, cleft lip and plate, VSD, exomphalos (omphalocele).
who is most commonly affected by clubfoot?
males (twice as common)
usually bilateral
clubfoot features?
CAVE: cavus (high arched foot) forefoot adductiob varus heel hindfoot equinus (plantarflexed)
clubfoot management after birth?
early intervention: ponseti method of serial casting, usually corrected after 6-10 weeks, most also need achilles tenotomy-usually done under LA, and will need to wear night-time braces until 4 years of age.
investigations in cases of oligohydramnios?
- must assess for SLE-ANA, anti-dsDNA, as causes immune mediated placental infarcts and insufficiency, and also other maternal RFs-DM-?OGTT, HTN.
- US-can measure AFI (summation of largest vertical pocket depths in each quadrant) and maximum vertical pocket. look for IUGR-measurements of head+abdo circumference, and femur length. can look at kidneys and fetal bladder to rule out renal agenesis, cystic dysplasia and ureteral agenesis. can do fetal doppler if clinically indicated to look for placental insufficiency.
- sterile speculum examination to assess for PROM.
oligohydramnios management?
- if before term, usually expectant management. regular antepartum monitoring with US-assess fetal growth and f/u of AFV, ensure continuous fetal heart rate monitoring during labour.
- if at term, then deliver, may safely delay with reassuring fetal testing.
- post term-insufficient evidence to recommend induction.
if mum dehydrated, PO or IV rehydration can increase AFV by 30%.
oligohydramnios complications?
pulmonary hypoplasia
fetal compression syndrome
amniotic band syndrome
fetal infection
why are women at increased risk of renal stones in pregnancy?
increased renal excretion of calcium
why is there increased calcium absorption by mum in pregnancy?
increased production of calcitriol due to production of 1 alpha hydroxylase by the placenta which converts vit D into its active form
why is antepartum haemorrhage associated with cerebral palsy?
up to 1/5 of very preterm babies are born in associated with antepartum haemorrhage
define antepartum haemorrhgae
bleeding from or into the genital tract from 24+0 weeks gestation up until before birth of the baby.
causes of antepartum haemorrhage?
placenta praevia-abnormal placentation near or covering the internal cervical os
placental abruption-placenta separation from the uterus
local causes in gential tract-bleeding from the vulva, vagina or cervix
advice regarding induction of older patients in pregnancy?
women aged 40 or over advised induction on their due date if haven’t gone into spontaneous labour by this time to reduce the risk of stillbirth.
why is sensitisation in a pregnancy with a rhesus -ve mother and rhesus +ve fetus problematic for future pregnancies?
risk of sensitisation is greatest in the 1st pregnancy
usually no effect on pregnancy with which it occurs, but for future pregnancies there is a much greater and quicker immune response-production of anti-D Abs by mum which cross placenta and bind to RhD antigen on fetal rbc, causing their removal from the fetal circulation.
severe anaemia can result, which can cause fetal heart failure, fluid retention, fetal hydrops (fluid accumulation in compartments) and fetal death.
also unconjugated hyperbilirubinaemia after birth as bilirubin no longer cleared by placenta and neonatal liver not yet fully mature, which can cause brain damage (kernicterus)-can lead to cerebral palsy, deafness, motor and speech delay.
how can fetal hydrops be managed before birth?
intrauterine transfusions
but this carries a 2% risk of fetal loss
role of anti-D given after potentially sensitising events?
neutralise any RhD antigen on fetal rbc that have gone into the maternal circulation to stop maternal immune response
this is given in addition to routine antenatal anti-D prophylaxis at 28 wks (1500 IU)-may also be given as 2 doses at 28 and 34 weeks-both 500 or both 1000-1650.
usually given by community midwife or at routine antenatal clinic.
iron requirements in pregnancy?
3X that of a non-pregnant menstruating woman, and requirements increase as pregnancy advances
deficiency in pregnancy usually due to nutritional deficiency or low Fe stores from previous pregnancy or heavy menstrual blood loss.
RFs for group B strep infection in baby?
prematurity
prolonged rupture of membranes
maternal pyrexia e.g. secondary to chorioamnionitis
previous sibling GBS infection
management of normocytic or microcytic anaemia in pregnancy?
1st line-trial of oral iron tablets, further investigations only required if no improvement in Hb after 2 wks
indications for parenteral iron in treatment of anaemia in pregnancy?
if oral iron not tolerated, absorbed, patient not compliant, or patient near term and insufficient time for oral iron to be effective.
RFs for placental abruption?
- has happened in a previous pregnancy
- multiparity
- maternal HTN
- cocaine use
- trauma
- uterine overdistension
- smoking
- increasing maternal age
clinical features of placental abruption?
sudden onset severe abdo pain, constant tense, tender uterus shock out of keeping with visible loss PV bleeding normal lie and presentation fetal heart-distress/absent coagulation problems
RFs for placenta praevia?
- multiparity
- multiple gestation
- previous C sections-embryos more likely to implant on a lower segment scar
