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49 Cards in this Set

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Outline risk factors for high risk pregnancy
Add 1 pt for each if > 4 pts = growth restricted
Previous LBW baby
Previous stillborn or neonatal death in 1st week
Maternal disease: e.g., BP > 140/90; Renal disease, Hx of UTI, present UTI
Bleeding
Wt gain > 0.5kg in 1 wk after 20 wks
Decrease or no increase in girth
Smoking (2 pts)
Decrease or no increase in fundal height (3 pts)
What details on history are important when assessing a fetus which may be small for gestational age or have restricted uterine growth?
Fetal movement
PV loss
Previous history of GR baby
Maternal illnesses incl. HT --> oligohydramnios and GR; IBD and renal failure --> GR
Drugs, smoking, alcohol (cocaine and cigs --> decreased placental perfusion)
Low SES
What are you going to examine in a woman with a suspected restricted uterine growth?
Symphysis-fundus height measurements: most accurate from 20-33 wks - plot on reference chart
CTG
If mother at high risk OR SFH lags > 2cm behind GA -->
Anatomy US - assess biparietal diameter (gives an estimate of fetal weight), head and abdomen circumference, femur length, and fetal weight, amniotic fluid volume
Doppler fetal blood flow velocity - if compromised (hypoxia), fetal blood flow is directed to the brain and decreased peripherally - look for reversed diastolic flow = poor outlook
Cordocentesis (fetal blood sampling) - not justified > 1500g due to risk of fetal death
What are non-reassuring and abnormal fetal measurements on a CTG?
HR
Non-reassuring 100-109 or 161-180; abnormal < 100 or > 180
Variability
< 5 for 40-90 mins - non-reassuring
< 5 for > 90 mins - abnormal
Decels
Non-reassuring - early, variable
abnormal - late, atypical
Definition of macrosomia
infant weight > 90th percentil for a particular GA or > 4000g
Causes of IUGR
Fetal causes:
Genetic; Chromosomal abnormalities; TORCH infections; multiple pregnancy
Maternal causes:
Smoking, ETOH, Drugs, stress, malnutrition
Maternal medical hx: DM, SLE, pulmonary insuffieiency
Maternal-fetal
Any disease causing placental insufficiency (DM, gestational HTN, chronic HTN, chronic renal insufficeicny, placental morphological abnormalities (infarction, haemangiomas)
Describe the 2 types of IUGR
Symmetric/ type I (20%)
early in pregnancy, inadequate growth of head and body
head: abdomen ratio may be normal
usually associated with congenital anomalies or TORCH infections
Asymmetric/type II (80%)
Occurs late in pregnancy
brain is spared, therefore head: abdomen ratio increased
usually associated with placental insuffieicny
more favourable prognosis than type 1
What investigations should be done to determine the cause of IUGR
FBC
EUC, LFT, urate - pre-eclampsia
TORCH screen - viral studies on swab/serology
Karyotyping if early IUGR, severe < 3rd centile, structural anomaly identified, IUGR in the presence of polyhydramnios
How should IUGR be managed?
Prevention
Induce labour if close to term
< 34 weeks: US?AFI and CTG twice weekly, steroids if expect premature delivery
Birth should NOT be > 40 wks
What complications are neonates with IUGR prone to?
meconium aspiration, asphyxia, polycythemia, hypoclycaemia, mental retardation
Greater risk of perinatal morbidity and mortality
Causes of macrosomia
maternal obesity
gestational DM
past hx of macrosomic infant
prolonged gestation
multiparity
Birth risks of macrosomia
birth trauma for baby and mother
birth asphyxia
shoulder dystocia
Erbs palsy - stretching of brachial plexus results in neuropathy: limb atony with shorter arm, internally rotated shoulder and flexed wrist
Investgiations to diagnose macrosomia
serial SFH
US predictors
polyhydramnios
third trimester abdominal circumference > 1.5cm/week
head circumference/AC ratio < 10th percentile
femur length/AC ratio < 20th percentile
Macrosomia - NVB or CS?
There is no evidence that prophylactic C/S improves outcomes BUT C/S reasonable option if estimated fetal weight > 5000g in nondiabetic women and > 4500 g in diabetic women
Early induction of labour is not recommended for non-diabetic moethers
Define polyhydramnios
amniotic fluid volume > 2000 cc at any stage in pregnancy
US criteria: > 8 x 8cm (3.1 x 3.1 in) pocked of amniotic fluid
Causes of polyhydramnios
Idiopathic (most common)
maternal - type 1 DM (causes abnormalities of transchorionic flow)
maternal-fetal - chorioangiomas, multiple gestation, fetal hydrops
fetal - chromosome anomaly, cystic adenomatoid malformed lung, anencephaly, hydrocephalus, meningocele, tracheoesophageal fistula, duodenal atresia, facial clefts (interfere with swallowing)
Clinical features of polyhydramnios in the mohter
pressure sx from overdistended uterus (dyspnoea, oedema, hydronephrosis)
uterus large for dates, difficulty palpating fetal parts and hearing fetal heart tones
Complications of polyhydramnios
cord prolapse, placental abruption, malpresentation, preterm labour, uterine dysfunction and PPH
Management of polyhydraminos
Determine underlying cause (maternal disease/infection; US)
mild-moderate - no Rx
severe - hospitalise and consider therapeutic amniocentesis
Define oligohydramnios
Amniotic fluid index of 5cm (2 in) or less
Causes of oligohydramnios
Early onset
Decreased production: renal agenesis or dysplasia, urinary obstruction, posterior urethral valves (male), chronic hypoxemia leading to IUGR resulting in shunting away from the kidneys to ensure profusion of the brain
Increased loss: prolonged amniotic fluid leak (most often labour ensues)
Late onset
Amniotic fluid normally decreases after 35 weeks; common in post-term pregnancies; US doppler studies
Clinical features of oligohydramnios
Cord compression
increased risk of adverse fetal outcomes
early onset - fetal anomalies, amniotic fluid bands can lead to Potter's facies, limb deformities, abdominal wall defects
Late onset: pulmonary hypoplasia
Management of oligohydramnios
maternal hydration with oral or IV fluids to help increase amniotic fluid
vesicoamniotic shunt: if aetiology is related to fetal obstrcutvei uropathy
injection of fluid via amniocentesis (improves condition for 1 week)
consider delivery if at term
What is chorioamnionitis
Infection of the chorion, amnion and amniotic fluid typically due to ascending infection by organisms of normal vaginal flora
What are the common organisms in chorioamnionitis
GBS
Bacteroides
Prevotella
E coli
Strep
RF for chorioamnionitis
Prolonged ROM
long labour
Multiple vaginal exams during labour
internal monitoring
bacterial vaginosis and other vaginal infections
Clinical features of chorioamnionitis
Maternal fever
Maternal or fetal tachycardia
uterine tenderness
foul and purulen cervical discharge
Raised maternal WCC
Investigations in chorioamnionitis
FBC
blood and amniotic fluid - leukocytes or bacteria in amniotic fluid
Management of chorioamnionitis
IV antibiotics
expedient delivery regardless of gestational age
Complications of chorioamnionitis
Bacteraemia of mother or fetus
wound infection if CS
pelvic absecess
infant meningitis
Which type of twin gives you a lambda sign on US
Monozygotic
Dichorionic
Diamniotic
Which type of twin gives you the C sign on US
Monozygotic
monochoroionic
Diamniotic
Fetal complications with twins
prematurity (multiple gestation is more common cause of prematurity)
IUGR
malpresentation
congenital anomalies
twin-twin transufion
twin interlocking (twin A breech, twin B vertex)
single fetal demise
Maternal complications with twins
hyperemesis gravidarum
GDM - jump straight to GTT 75mg
gestational HTN
anaemia
Cholestasis, acute fatty liver, PUPPS
Thromboembolism
increased physiological stress on all systems
increased compressive symptoms
C/S
Utero-placental complications of twins
increased PROM
polyhydramnios
placenta praevia
placental abruption
PPH (uterine atony)
umbilical cord prolapse
cord anomalies (velementous insertion, 2 vessel cord)
How do you diagnose multiple gestations?
Usually via US
but also seen with rapid maternal weight gain, rapid uterine growth, increased beta-HCG, HPL(human placental lactogen), MSAFP (maternal serum alpha fetoprotein) for GA
What is twin twin transfusion syndrome?
Unequal flow within vascular communications between twins in a shared placenta --> one anaemia, hypovolaemic, IUGR twin and one large, plethoric, polycythemic, hypervolaemic, CHF, oedema, polyhydramnios, kernicterus
How do you diagnose twin twin transfusion syndrome
US screening
Doppler flow analysis
How do you treat twin twin transfusion syndrome?
therapeutic serial amniocentesis to decompress polydyramnios of recipient twin and decrease pressure in cavity and on placenta
intrauterine blood transfusion of donor twin if necessary
Laser ablation of placental anastomoses
Delivery of twins
If twin A presents as vertex + no maternal complications, and not MAMC - vaginal
Otherwise C/S - MAMC - done elective at 37 weeks
Must have electronic monitoring and scalp monitoring, must have epidural or regional analesia
What is a complication of mo-mo twins
They circulate in the same amnion (fluid sac) and so can get entangled
high rates of intrauterine foetal demise
What are the 2 different mechanisms for twinning?
Monozygotic - both fetuses arise from a single fertilised ova
- both fetuses share placenta and chorion
- 98% of MZ twins have their own amnion (fluid sac) 2% share amnion (risk of cord entanglement)

Dizygotic - result of multiple ovulation with fertilisation by separate sperm
Each fetus has own placenta, amnion, chorion
RF for dizygotic twins
IVF
increased maternal age
newly discontinued OCP
Ethnicity (e.g., certain African regions)
Family hx
Previous DZ twins
What are the 4 types of monozygotic twins?
Di-Di - split before day 3
Mo-Di (monochorionic (one placenta), diamniotic) - split on day 3-8
Mo-Mo - split day 8-13
Conjoined - split day 13-15
What type of twin is at risk of twin twin transfusion?
What % develop it?
10% of monochorionic twins
What is the incidence of twins?
1: 80 twins (2/3 are dizygotic) 69% DZ, 31% MZ
1: 7000 triplets
Multiple gestation seen in 30-50% of IVF pregnancies
Describe the pathophysiology of rhesus iso-immunisation?
If a mother is rhesus negative and a baby is rhesus positive, she can become sensitiesd to Rh antigen and develop antibodies against this. These are a problem with the second pregnancy.
IgG antibodies against Rh antigen can cross the placenta and cause foetal hydrops (foetal haemolysis and anaemia with extramedullary production of RBCs)
NB: Risk in pregnancy is 1.5% but Rx reduces this to 0.2%
When is anti-D given?
To Rhesus negative woman at:
28 weeks and 34 weeks and postpartum is neonate is Rh positive within 72 h of birth
If fetal cells are present in maternal blood via Kleihauer test, then additional injection is needed
OR
fater CVS or amniocentesis
ectopic preg, threatened miscarriage, APH or abdo trauma, abortion
What are mother's who've just given birth to twins particularly at risk of?
PPH
Distended uterus - atonic + larger placental mass
MUST give syntocinon with twins
NB: also at big risk of PND