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FETAL MEDICINE
INTROTO EMBRYOLOGY
Implantation and Placental Developmento Implantation occurs ~day 6: blastocyst emerges from zona
pelucida and begins to adhere to uterine wall (mechanistic
details unknown)
Inner cell mass is nearest to attachment site
o Trophoblast development of 2 cell types:
1) Syncytiotrophoblast: very invasive, eats into
uterine wall
2) Cytotrophoblast
o Blastocyst sinks entirely into uterine wall and begins to
receive all nourishment from maternal tissue rapid growth
Abnormal Implantationo Normal implantation: occurs at anterior/posterior wall of uterus
o Placenta previa : results from implantation at internal os
o Extrauterine/Ectopic
Tubal Ectopic Pregnancy 95% of ectopics
Most common site: fallopian tube 95% Cause: fertilized ovum stopped for unknown reasons in the tubal lumen
o No cause found for many ectopics Problem: unsatisfactory site for implantation b/c thin walled tube unable to
sustain trophoblastic invasion bleeding and/or rupture
o Embryo cannot survive
Risk factor: pelvic inflammatory disease Peritoneal cavity: rectouterine pouch
Within ovary
Placental Developmento Components which will develop into placenta
1) Endometrium in secretory phase: maximum thickness following ovulation
Glands: corkscrew shape & producing glycogen and lipids, which are the mainsource of nutrients later
Under influence of estrogen and progesterone from corpus luteum and
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trophoblast
2) Trophoblast
3) Fetal tissue forms chorionic villi which grow into maternal blood sinuses
o Stages of Development
Double layered trophoblast invades endometrium and erodes capillaries
Lakes of maternal blood form: lacunae
Chorionic villi surround lacunae and have following endocrine functions:
Secretion of HCG Secretion of HCS: stimulates lactogenesis Secretes estrogens and progesterone
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Early Stages: Villi surround the chorion
Later 2 sides form:
Chorion frondosum : fetal side
Chorion leave : maternal side
o 2 Circulations: do NOT mix
Endothelial barrier w/ trophoblast outside, which gets very thin as fetus develops
Villi rupture Rh incompatablity
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Decidua = functional layer of endometriumo Deciduas basalis : covers chorion frondosum
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o Deciduas capsularis : anembryonic pole and degenerated as anembrionic pole joins opposite
uterine wall
o Decidua parietalis : lines anembrionic uterine wall
o Amnion and chorion fuse membrane which eventually ruptures during pregnancy
Fetal Developmento Inner cell mass differentiates into 2 cell layers
Hypoblast : inner layer, primitive endoderm
Epiblast : outer layer, primitive ectoderm
o Cells develop fluid filled cavities divided by blilaminar disk = embryonic disk
Cells above disk form amniotic membrane and space
o Development of body axis and gastrulation
Primitive streak: appears in epiblast 13-14 days post-fertilization
Gastrilation : cells in epiblast migrate into groove, detach and drop off to lie between the
epiblast and hypoblast layers trilamenar disk
Mesoderm : new middle layer formed during gastrulation
Visceral mesoderm = splanchnico Neural tube
Begins formation around day 17-18
Ectoderm along the axis begins to thicken to form neural plate
Plate begins to fold & the folds on either side come into contact with each other and fuse
neural tube.
Closure begins in the middle of the embryos back & then extends cranially and caudally
until zipped up around day 28
Developmental Problemso Spina bifida: failure of complete closure of neural tube
o Lung agenesis - lung buds fail to form right or left bronchi - unilateral or bilateral - rare
o Respiratory distress syndrome - in premature babies, surfactantproduction may be
inadequate.
The lungs may collapse & endoderm surfaces damaged.
About 6000 premature babies in the UK suffer from this and 33% die.
Surfactant either from human or animal sources also synthetically produced improves
survival rate.
o Tracheo-oesophageal fistula - an abnormal connection between the oesophagus and trachea
(1;100,000 births)
This is commonly associated with oesophageal atresia - blind ending of the oesophagus
(1;3000 for the combined condition).
Baby gags as the milk enters lungs, respiratory distress
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THE PLACENTA
Anatomyo Fetal surface: 2 membranes inner amnion and outer chorion
o Umbilical cord: 2 arteries and 1 vein surrounded in Whartons jelly and covered by connective
tissue
Arteries divide over the surface of the placenta as chorionic vessels which then divide
into the placental tissue and supply the placental villio Villi bathed in maternal blood that flow from spiral arteries into intervillous space and out
through uterine veins
o Hemomonochorial membrane : consists of fetal epithelium, connective tissue and
syncytiotrophoblast and functions to separate fetal and maternal blood
o Maternal surface: made of 15-20 lobules = cotyledons
Cotyledon : hundreds of frond-like structures called villi that are richly supplied by
capillaries that drain back into chorionic veins to the umbilical vein
o Abnormal Anatomy
Velamentous insertion of the cord: cord inserts at the margin rather the center of placenta
Seccenturiate lobe : an extra lobe of placenta which is separate from the main organ Usually a communicating vessel runs in membranes btw placenta and lobe Vasa previa : communicating vessel runs across cervix, can bleeding in labor
or w/ AROM rapid fetal death
Physiologyo Gas exchange across hemomonochorial membrane
o Fetal Blood flow
Arteries carry deoxy-blood and vein carries oxygenated from mother to fetus
Low resistance to blood flow in the placenta gives umbilical arteries characteristic
waveform with good flow of blood during diastole
Wave can be seen in umbilical artery dopplers inearly pregnancy Abnormal wave: may indicate impaired placental
invasion/function and may be early predictor of IUGR or pre-eclampsia
Powerful constriction of umbilical vessels occurs post partum to cease circulation
between the fetus and the placenta
Cord blood: can be used just after delivery to determine fetal blood group and acid base
status
pH: 7.28 0.15 pO2: 1510 kPa
pCO2: 4515kPa Base excess: 74 mmol/L Fetal blood compared to maternal blood
Larger RBCs (MCV) Higher [Hb]: 18 vs 12g/100mL Higher oxygen saturation: 80% vs 40% Lower oxygen partial pressure (compensated for by high affinity HbF)
Maternal Blood flow
Maternal flow to uterus is 100-150mL/kg/min w/ 80-85% going to the placenta inlate pregnancy
Q = 1000mL/min by end of pregnancy Affected by posture: Pressure of the uterus on the IVC in the supine positionobstructs venous return from the uterus
Completely obstructed during peak of strong contractions: Venules in the
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myometrium are completely occluded by surrounding muscle fibers
in pre-eclampsia: important component in the pathophysiology of PETo Endocrine Functions
-HCG: stimulates corpus luteum in early pregnancy and may control progesteronemetabolism in later pregnancy
Estrogens : stimulate growth of maternal tissues including breasts and uterus
Progesterone : dampens down intrinsic uterine activity produced by corpus luteum until
8-10w then by placenta
Human placental lactogen (HPL): influences glc metabolism and insulin resistance andmay initiate lactation
o Filtration
Involved in water and ion transfer which contributes to volume of amniotic fluid
Pathologyo Abruption : sudden bleed behind the placenta causing it to separate from the uterine wall
Complications: fetal hypoxia and/or death, severe maternal bleeding
o Placenta previa : placenta covering cervix
Diagnosed after 32w in most cases
o Placental accreta/percreta : placenta invaded into/through myometrium into another organ Complications: massive hemorrhage requiring hysterectomy
Risk factors: any condition interfering w/ the decidua (infection, previous curettage,
previous section), chronic endometritis
A/w placenta previa and Ashermans syndrome (intrauterine adhesions)
o Small placenta : may cause w/ intrauterine growth restriction and pre-eclampsia, trophoblast
invasion has been inefficient smaller more resistant spiral arteries less efficient nutrient
and oxygen exchange fetal growth May be detectable early via umbilical artery Doppler abnormal wave form
o Oligohydramnios : may be caused by placental failure amniotic fluid productiono Molar pregnancy : abnormal placental development grape-like mass, may be complete or
incomplete
Snowstorm appearance on US
Complications: severe hyperemesis, thyrotoxicosis, early onset pre-eclampsia,
haemorrhage, persistent trophoblastic disease, choriocarcinoma
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FETAL ABNORMALITIES
Goal: to identify from a large population a smaller group of patients that have an increased risk of adisorder and to offer that smaller group a more specific diagnostic test
Screening vs diagnosiso Screening test: estimates risk of disease presence, usually simple and w/o major risk
o Diagnostic test: confirms presence/absence of disease, often more invasive w/ significant
risks/complications
Advantages of Prenatal Diagnosiso Patient reassurance when normal
o Allows time for preparation when abnormal
o Avail of subspecialty consultation
o Avail of pregnancy termination
o Delivery at tertiary-care facility
o Optimise mode of delivery
o In-utero therapy
Should NOT be assumed that all patients undergoing prenatal diagnosis will request a
termination of pregnancy if they receive an abnormal result
What is screened for antenatally: major birth defects present in 2-3% of all birthso Mendelian defects
o Polygenic/multifactorial conditions
o Teratogenic conditions
o Chromosomal disorders 1:160 , most either autosomal trisomy or sex chr abnormalities
Specific conditions screened for:o Chr abnormalities
Trisomy 21 (Downs) Trisomy 18 (Edwards)
Trisomy 13 (Pataus)
Triploidy
Sex Chromosome Abnormalities 45X: Turner Syndrome, XXY: Klinefelters, XYY,
XXX
Balanced Translocations
o Familial genetic disorders: CF, DMD, Huntingtons
o Disease in high risk populations:
Tay Sachs in Ashkenazi Jews
-thal in SE Asians -thal in Mediteranians Sickle cell
o Structural fetal anomalies
Congenital heart disease
Neural tube defects
Abdominal Wall defects
Genitourinary defects
Lung Disorders
o Congenital infection
Toxoplasma CMV
Rubella
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Chickenpox
Parvovirus B19
Syphillis
Listeria
Pretest counseling addresses following issues:o Risk of affected fetus
o Nature and consequences of problem
o Risks and limitations of procedures to diagnose problem
o Time limitation of reporting
o Failed or inconclusive reporting
Types of Screening Testso Serum screening
o Ultrasound
o Chorionic Villus Sampling
Performed at 11 to 14 weeks results available in 2 days
Risk of loss 1/100 (1%)
Transabdominal / transcervical approach with ultrasound guidance
Sample of placental cells removed to test for karyotype, FISH or PCR
o Amniocenteis
Performed after 15 weeks gestation
Risk of loss (miscarriage rate) 0.1% to 0.5%
Continuous US guidance used to ensure needle doesnt hit fetus
Sample of amniotic fluid removed for karyotype, FISH or PCR (results in 2d)
Screening for Chr Abnormalities common cause of morbidity and mortalityo Involves combo of biochem and US markers
o Performed in 1st and 2nd trimesters now more emphasis on Downs screening in 1st
o Should be voluntary and only provided after pre-test counseling of benefits and limitations
o Downs is most common serious abnormality 1:660 live births
Increased risk with advancing maternal age
o 1 in 1,000 risk at 20 yrs, increases to 1 in 20 at 45 yrs
o Limiting screening to just those older than 35 years will only detect 30% of
Down Syndrome so screening should be made available to all patients who want
it, irrespective of age
o 50% have major cardiac or GI abnormalities and most have IQ
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o US screening
o Nuchal translucency : normal space seen on US btw back of fetal neck and
overlying skin
o NT space chance of Downso Combined screening
o Combining maternal age and NT and serum screening in 1st trimester
identifications of 87% of affected fetuses w/ a 5% false positive rate
2nd Trimester: US 30% of DS have major structural defect visible by mid-trimester
o Atrial septal defect/Ventricular septal defect 40-50%
o Duodenal atresia 4%
o Omphalocele
o Ventriculomegaly
o Cystic hygroma
o Other soft markers, aka red flags for DS
o Nuchal fold thickness
o Short femur
o Renal dilatation
o Hypoplasia of middle phalanx 5th finger (Clinodactyly)
o Sandal gap between toes of feet
o Echogenic bowel (?)
o Edwards Syndrome: trisomy 18
Prevalence = 1:3000
Lifespan: hours days
US features: single umbilical artery, IUGR, strawberry
head, choroid plexus cysts, hyrocephalus, micrognathia,
nuchal edema, CHD, NTD Amniocentesis: confirms prenatal dx
o Patau Syndrome: trisomy 13
Prevalence = 1:5000
Prognosis: poor 50% die in hours-days, most my 6mo
US features: holoprosencephaly, facial abnormalities, microcephaly, CHD, omphalocele,
polydactyly
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Amniocentesis: confirms prenatal dx
o Turner Syndrome: 45XO
Prevalence = 1:3000, not related to maternal age
US features: cystic hygroma, generalized edema, cardiac defects
Neonatal features: short stature, coarctation of aorta, streak/rudimentary ovaries, usuallyhave normal IQ
o Kleinfelters Syndrome: 47XXY
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Prevalence = 1:2000
Phenotype: tall male w/ sparse facial hair, gynecomastia, azoospermia, occasionally IQ Commonest cause of male hypogonadism and usually diagnosed during infertility Ix
Structural Abnormalitieso Congenital Heart Disease
Prevalence 8/1,000 live births Most common congenital abnormality
Overall prevalence likely higher as many cases of CHD are not apparent until later in life
33% are associated with abnormal karyotype
45% also have extracardiac malformations
CHD responsible for 20% -35% infant deaths
90% CHD cases occur without identifiable risk factor in the general population, and are
therefore mostly unpredictable
Only 10% CHD cases occur in a high risk group:
o Family history of CHD
o Maternal medical disease (e.g. Diabetes)
o Teratogen exposure (e.g. Lithium)
o Genetic syndromes (e.g. DiGeorge)
o Fetuses with chromosomal abnormalities
o Fetuses with extracardiac abnormalities
Best screening test: 4 chamber heart view at 18-22w
o 90% detection rate in high risk population
o 50% detection rate in low risk population
o Allows Dx of: AV defects, VSD, hypoplastic LR ventricle, Ebsteins anomaly,
pericardial effusions, cardiac tumors
o Limitations:
o Performance can depend on the gestational age, maternal body habitus,
fetal position, amniotic fluid volume, and experience of the sonographer.
o Certain malformations can be present with a normal appearing 4-chamberview, such as transposition, tetralogy of Fallot, double outlet right
ventricle, coarctation.
o Most experts now add views of the right and left cardiac outflow tracts to
the routine exam to maximise detection of these abnormalities
Management of CHD
o Detailed Ix for extracardiac malformations: present in up to 50%, impact Px
o Fetal karyotyping offered: 1/3 will have chr abnormality
o Pre-natal counseling w/ sub-specialists and expert medical team for delivery
o Early dx may help optomize either delivery timing or location (tertiary vs comm.)
o Neural Tube Defects
Incidence: 3:1000 (USA is 1:1000)
Cause: failure of closure of neural fold at 26-28d
Risk factors: none in 90%, others include folate, antiepileptic drugs Dx: 90% detectable by US at 16-20 weeks (midtrimester)
Recurrence risk: 2-3%
Types: spina bifida, anencephaly, encephalocele
o Anencephaly : skull vault and cerebral cortex absent
o Dx on midtrimester US in 100%
o Open spina bifidao 1/3 neonatal death
o 2/3 Survive w/ long term disability: LL paralysis, bladder/bowel
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dysfunction, hydrocephalus, clubfoot, scoliosis, meningitis, mental
retardation
o Dx:
Midterm (18-20W) US in 90%: lemon sign (frontal bone
scalloping), banana sign (cerebellum pulled down)
Maternal serum: FP levels from 15-20w onwardo Management
Sonographic surveillance indicated to confirm appropriate fetal
growth and to rule out development of polyhydramnios(complicates over 50% of cases and is associated with preterm
delivery)
Karyotyping: rule out trisomy via amniocentesis
Prenatal consult w/ sub-specialist to prepare for delivery and care
Eg: perinatologist, neonatologist, pediatric neurologist andpossibly also a pediatric neurosurgeon
NTD dx shouldnt affect timing of delivery
In severe NTD elective c-section should be offered
o Prevention
0.4mg Folic acid 3mo before and continuing 12w after conceptionto risk by 70%
4.0mg recommended is previous NTD
o Screening:
1) Elevated msAFP a/w NTD and abdominal wall defects
Detects 80% of all open NTDs: 80% of SB and 90%anencephaly
2) US amniocentesis
o Abdominal Wall Defects
Omphalocele : incomplete return of abd contents to abd cavity inearly pregnancy herneation of bowel or liver through base of
umbilical cord (hernia contained in membrane)
o Incidence: 0.1% - w/ maternal ageo A/w chr and cardiac abnormalities: amniocentesis usually
recommended
o W/o other abnormalities outcome is good
Gastroschisis : herniation of abd contents to R of umbilical cord, w/ free-floating bowel
not contained by membrane
o No associated chr abnormalities amniocentesis not
indicatedo Early transfer to pediatric surgeon after birth for closure
o Prognosis: 10% neonatal mortality from bowel ischemia,
complications of IV feeding
o GUT Abnormalitites
Renal Dysplasia
Cystic Kidney Disease
Hydronephrosis /Pyelectasis: unilateral (80%) or bilateral renal
pelvic dilation
o A/w postnatal UTI and reflux nephropathy
o All started on ABics after dx and followed up w/ renal US
nostnatally
Posterior Urethral Valves : mucosal folds obstructing bladder neck
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o M>F
o Causes anhydramnios renal damage and poor often fatal prognosis
Potters Syndrome : pulmonary hypoplasia, limb deformity
o Pathogenesis: bilateral renal agenesis extrememe oligohydramnios Potters
sequence
o Amniotic fluid important for alveolar maturation, esp 16-22w absence
hypoplasia death
o Diaphragmatic Hernia:
Defect allows stomach, bowel liver to enter thoracic cavity
pulmonary hypoplasia
15-30% a/w chr abnormality, often w/ other structural abn
Survival: 50% - determining factor is presence of liver in chest
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US AND FETAL WELL BEING
1st Trimester USo Confirm viability and location of pregnancy exclusion of Ectopic
o Confirm dates by measuring crown-rump length (CRL)
o Exclude multiple gestation
o CRL: Incomplete Miscarraige Irreg Uterine Sac: missed MC
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2nd Trimester: 18-22weekso Detailed fetal anatomical survey to exclude malformation
o Confirm pregnancy dating by measuring biparietal diameter (BPD), head
circumference (HC) and femur length (FL)
o Placental location , esp in women w/ vaginal bleeding to exclude placenta
previa, or in women w/ previous section to exclude abnormal placentation
(eg accreta)
3rd Trimestero Estimation of fetal weight (EFW): biparietal diameter (BPD), HC, FL and abdominal
circumference (AC)
o Also for fetal well being, confirmation of presentation and placental location
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Antepartum Fetal Surveillanceo Methods available:
Maternal perception of fetal activity: kick counts/charts
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Cardiotocography (CTG) = non-stress test (NST) in N America
Biophysical profile (BPP)
Doppler studies
o Who to test: examples
Postdates pregnancy: >40 0/7 weeks
Chronic HT
IDDM
IUGR
Decreased fetal activity
Maternal disease, eg chronic renal disease, SLE, etc
o Maternal Perception of Fetal Activity
Should be recommended routinely from 28 weeks in all pregnancies
Inexpensive and sensitive
3rd trimester: normoxic, healthy fetus spends 10% of its time making gross bodymovement
Use of a fetal kick counting chart (e.g. Cardiff count-to-ten chart) can reduceperinatal mortality (PNM) from 8 to 2 per 1,000
In high risk patients who report diminished fetal movement, up to 60% of fetuseswill be compromised
o CTG/NST
Top line: FHR, Bottom line: pressure transducer tracing of uterine activity
Accelerations of fetal heart rate (FHR) are associated with fetal normoxia (wellbeing)
90% of fetal movements (FM) are associated with in fetal heart rate (FHR) Criteria for a reassuring CTG: 2 accelerations of 15bpm for 15sec twice in 20 min
o Called Reactive CTG
o No accelerations = Nonreactive CTG v suspicious for fetal hypoxia
o Reactivity is gestational age dependent, typically only expected after 28weeks gestation
Should be significant beat-to-beat variability in the heart rate tracing (shouldnot be flat line!)
Late accelerations are non-reassuring Any abnormality in CTG should be reviewed promptly, and a decision needs to be taken
as to whether it is safe to leave the fetus in utero.
If a non-reassuring tracing: confirmatory test to exclude significant hypoxia must be
done promptly (such as a fetal scalp sampling), or delivery must be expedited
Normal CTG:
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Abnormal/Non-reassuring CTG: no accelerations present sign of fetal hypoxia
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Early decelerations and variability (first not worrying, second sign is)
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Non-reassuring: Late decelerations, sign of hypoxia 2 to uteroplacental insufficiency
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Abnormal CTG: variable decelerations indicating cord compression not worrying
unless repetitive and deep
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o Biophysical Profile/Score (BPP/BPS)
Fetal hypoxia decreased CNS-regulated activities, altered heart rate patterns,
decreased fetal breathing movement, decreased body movement and poor fetal tone.
These can be quantified by ultrasound Four parameters: 2 points each 2 if present and 0 if absent (never give 1)
Fetal tone Fetal gross body movement Fetal breathing movement Amniotic fluid volume (CTG: modified profile gives additional 2pts for reactive CTG for total of 10)
Scores less than 6/8 are suspicious for fetal hypoxia and must be promptly evaluated for
a decision on delivery versus continued in utero management
On average only 8 minutes required to complete the scan and score 8/8
Test valid from 28 weeks onwards
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Normal BPP score is very reassuring - false negative rate of only 0.7 / 1,000
i.e. less than 1 patient in every 1,000 who are given a score of 8/8 will have afetus that is hypoxic
False positive rate: 40-100% (3% were abnormal) Specific schedule / frequency of BPP is dictated by particular clinical need
e.g. IDDM or postdates testing - twice weekly BPP
o Contraction Stress Testing (CST)
Rarely used now
Based on the observation that late decelerations were associated with stillbirth and low
Apgars
Method: oxytocin infusion, fetal heart response to induced contractions is studied
If late decelerations are noted, this is a positive CST and implies high likelihoodof fetal hypoxia requiring delivery
Used as a second-line test to further evaluate an abnormal CTG Mostly replaced now by BPP
o Doppler US
Should be performed for IUGR , not required in normal fetal growth, routine anomaly USscan, 1st/2nd/3rd trimester US screening
Umbilical artery blood flow : towards the placenta, with peak velocity during fetal cardiac
systole, and slower velocity during fetal cardiac diastole
Ratio of systolic to diastolic flow (S/D ratio) is used to quantify how well blood is
flowing to the placenta
Diastolic flow (leading to a larger S/D ratio) is reflective of increased placentalresistance due to placental pathology (e.g. abruption, chronic hypertension, etc)
Absent end diastolic flow (AEDF) or reversal of end diastolic flow (REDF) inumbilical artery is a strong marker for significant hypoxia in the fetus
Normal waveform: reassuring of fetal well being, esp in IUGR fetus
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AEDF: can occur in IUGR, may require close monitoring
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REDF: sign of fetal compromise, most cases suggests need for prompt delivery
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ABNORMAL FETAL GROWTH
Small for Gestational Age (SGA)o Definition: fetus has failed to achieve a specific biometric or estimated fetal weight by a specific
gestational age
o Two Types:
1. Fetal growth restriction (FGR) or intrauterine growth restriction (IUGR)
Definition: fetuses that have failed to achieve their growth potential.
Better to use term FGR or IUGR rather than SGA prenatally, as it is difficult toknow for sure that a fetus in utero is simply constitutionally small
2. Fetuses that are constitutionally small
o Quantification:
SGA cut-off is 10th percentile so 10% of population are SGA, 2/3 of which have FGR
Low birth weight:
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o Oligohydramnios
o Fetal hypoxia
Neonatalo Hyperbilirubinemia
o Hypoglycemia
o Meconium aspiration
o Polycythemia
o Pulmonary hemorrhage
o Pneumothorax
o 6xPerinatal mortality Infant:
o Physically small
o Delayed neuro development
Adult: risk of cardiovascular disease and DM Management
Assess for chr defects: 20% w/ both AC and EFW 20 if there are other structural abnormalities, normal amniotc
fluid and normal umbilical artery doppler
Surveillance of fetal well beingo Umbilical artery Doppler in high risk fetuses
o If abnormal US scan but normal Doppler fetus is likely normally small
Monitor as OP w/ US for growth every 2 weeks, w/ aim to deliver
at 37w or earlier if distress
o If abnormal Doppler admit w/ close monitoring via CTG and biophysical
profile
A/REDF a/w perinatal morbidity and mortality Give steroids if 4000g = macrosomia
o Risk Factors:
DM
Post term pregnancy
Maternal obesity
Multiparity
Excessive weight gaino Diagnosis
Serial clinical exams
US EFW >90th centle or AC>90th centile for gestational age
o Morbidity
Prolonged labor
Risk of c-section Shoulder dystocia
o Management: controversial
Screen for gestational DM
Aim to minimize maternal and fetal trauma at delivery
Non-DM mother: no evidence for prophylactic induction of labour
Doesnt reduce the risk of caesarean section or shoulder dystocia
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DM mother: no evidence to support elective caesarean section of infants whose EFW >
4.25Kg
o Management of Shoulder Dystocia
50% of shoulder dystocia occurs in fetuses of normal weight so difficult to prevent
In certain diabetic patients with EFW > 4,500g planned c-section may be appropriate b/c
distribution of truncal obesity in the fetus of a diabetic mother increases the risk of
shoulder dystocia
PRETERM LABORAND PREMATURE RUPTUREOF MEMBRANES
Preterm Labor (PTL) = labor occurring before 37w from the 1st day of the LMPo Labor 20-24weeks referred to as threatened miscarriage
o Diagnosis: regular contractions + cervical change + cervical dilation
o PTL which ends in preterm delivery accounts for majority of perinatal morbidity in normally-
formed infants
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o Incidence: 11% of all live births
1/3 are due to spontaneous PPROM
1/3 are iatrogenic (i.e. deliberate medical decision to deliver early)
1/3 are idiopathic (i.e. no cause found)
o Causes of Prematurity
Iatrogenic:
Pre-eclampsia IUGR Maternal disease necessitating delivery
Spontaneous Preterm Delivery
PTL PPROM Cervical incompetence
o Risk Factory for PTL
Non-pregnancy related
o Low socio-economic group
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o Extremes of age
o Poor nutritional status (as reflected by either maternal weight
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2. Tocolysis: controversial role may temporarily delay delivery until steroids complete
or patient transferred to tertiary level facility with appropriate NICU some units do not
use this
Limited role: prolong gestation for administration of corticosteroids and transferto a tertiary care centre
Has not been shown to improve overall perinatal outcome: role is controversial Examples: atosiban (oxytocin receptor antagonist), nifedipine (Ca channel
blocker), ritodrine or terbutaline ( -adrenergic agonist), magnesium sulphate(competitive antagonist to calcium), indomethacin (interferes with PG synthesis)
3. Transfer to tertiary level facility with NICU
Delivery in PTL if preferable vaginal 4. Role of antibiotics
Infection plays an aetiolgoic role in preterm labour in at least 15 -20% of caseso Organisms: GBS, listeria, mycoplasma, bacteroides, ureaplasma
Only role for antibiotics is when PPROM occurs: no benefit of antibiotics inprevention of PTL when membranes are still intact
o Some evidence that the treatment of bacterial vaginosis in 2nd trimester
may decrease the likelihood of PTL/PPROM in high-risk women
Main role in PTL is penicillin for GBS prophylaxis 5. Role of Cervical Cerlage: Prophylactic or therapeutic suturing of cervix
Multiple trials have failed to show benefit There "may" be a role for cerclage in select high-risk cases in which a short
cervix is found on transvaginal ultrasound
o e.g. may be a benefit of cervical cerclage in women with cervical length
less than 25mm if patient has a history of previous preterm delivery or
other high risk factors
o Neonatal Complications of PTL
Respiratory distress syndrome (RDS) Necrotising enterocolitis (NEC)
Intraventricular haemorrhage (IVH)
Periventricular leukomalacia (PVLM)
Sepsis
Patent ductus arteriosus (PDA)
Preterm Premature Rupture of Membraneso Terminology:
Preterm Premature ROM: rupture of the chorioamniotic membranes before 37w
Incidence: 1-3% of all pregnancies Premature ROM: rupture of the membranes prior to the onset of labor, may occur at term
Prolonged ROM: membrane rupture >24h before delivery
o Diagnosis of PPROM
History: gush of fluid, constantly wet
Physical exam: sterile speculum exam, pooling of fluid in posterior vaginal fornix
Confirmatory tests:
Ferning : cervical mucous shows a broad fern pattern on microscopy vs narrowfern pattern of amniotic fluid
Vaginal swab pH: Nitrazine sticks turn blue in presence of amniotic fluid Cervico-vaginal fetal fibronectin positive in presence of amniotic fluid Intraamniotic instillation of indigo carmine dye with demonstration of blue dye
on a vaginal tampon confirms PPROM (only use in very special situations as
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needs invasive test i.e. amniocentesis)
o Causes of PPROM
Spontaneous / Idiopathic (most cases)
Infection: Chlamydia, GBS, Bacteroides
Smoking
Placental abruption
PPROM in prior pregnancy
Incompetent Cervix
Multiple Pregnancy (twins / triplets etc)
Iatrogenic (after amniocentesis)
o Management of PPROM
Must balance risk of prolonging pregnancy to fetal maturity vs risk of fetal infection &sepsis w/ continued pregnancy (later gestation: the benefit of 1stwhile risk of 2nd)
Intrauterine infection (20% - 60% of PPROM cases) Placental abruption (5% - 15% of PPROM cases) Cord compression leading to fetal compromise
Fetal demise (1% - 2% of PPROM cases) Prolong gestation for as long as it is safe to do so
Monitor for signs of intrauterine infection
Maternal signs of infectiono Pyrexia
o Tachycardia
o Uterine tenderness
o Preterm labour
o Foul smelling vaginal fluid
Fetal signs of infectiono Fetal tachycardia
o Non-reactivity / reduced variability on CTG / variable decelerations
o Alteration in biophysical profile
Loss of breathing movements
Decrease in gross body movements
Serum markers of infection Ultrasound markers of fetal compromise & Altered biophysical profile (BPP) CTG abnormalities Amniotic fluid tests
o Glucose low
o WCC high
o Gram stain/culture positive
o C-reactive protein >20mg/L
Promote lung maturity by administering antenatal corticosteroids
Optimize the time and mode of delivery
All cases of PPROM should be delivered by 37 weeks , as there is no benefit tocontinuing pregnancy beyond this time, while there is considerable risk
Some centres deliver all cases of PPROM by 34 weeks, but this is not universallyaccepted (timing of delivery of PPROM between 34 and 36 weeks is therefore
individualized between centres)
Delivery should be arranged immediately in the setting of PPROM if fetal lungmaturity has been documented
Delivery should be arranged immediately in the setting of PPROM if there is any
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evidence of fetal compromise or infection, even without evidence of fetal lung
maturity
Role of Antibiotics
When PPROM occurs at 24 to 32 weeks gestation, 7 day course of Ampicillinplus Erythromycin significantly prolongs pregnancy and is associated with
improved perinatal outcome
OPD Management: most doctors manage PPROM as an inpatient because of risks of
sudden preterm delivery or deterioration in fetal status
o Mi-trimester PPROM: 16-25w
Rare occurrence, but associated with poor overall perinatal outcome
In absence of infection overall survival is 50-75%
Stillbirth rate 3.8 - 21.7% (compared with 0-2% at 30-36 weeks)
Incidence of infection with earlier gestation at time of occurrence of PPROM 50% deliver within a week, 20% continue for over a month after occurrence of PPROM
Pulmonary hypoplasia is a major complication when PPROM occurs at
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Maternal
Hemorrhage Placenta accreta (15%) Hysterectomy Death
Fetal
Preterm birth IUGR: rare b/c placental function usually normal Death
o Management
1) Focused history
2) Initial exam: maternal and fetal
3) Immediate management if presenting bleeding previa
IV Line (14G x 2) FBC/Coag/X-match 4 units IV Fluids O Negative blood (be prepared to use O negative blood for transfusion if life
threatening haemorrhage and cross-matched blood not available yet)
Call for senior help (obstetric and anaesthesia) and notify NICU 4) Immediate delivery indicated if:
Severe life-threatening maternal haemorrhage regardless of gestational age Evidence of non-reassuring fetal testing regardless of gestational age Advanced gestational age 34-36 weeks.
o If patient has already received antenatal corticosteroids and has recurrent
significant bleeds, 34 weeks is a reasonable threshold for delivery.
If only minor bleed, and is not recurrent and steroids have not been completedyet, it may be reasonable to hold off on delivery until 36-37 weeks
5) Expectant management depends on:
Ongoing risk of placenta praevia: sudden unpredictable major / life-threateninghaemorrhage
Gestational age at delivery: directly related to perinatal mortalityo If < 35 weeks, steroids should be given
o Inpatient hospital admission from viability (24 - 26 weeks)
Outpatient management is acceptable only in very exceptional / stablecircumstances in women who have never had significant vaginal bleeding and
live close to the hospital with good immediate family supports
Repeat ultrasound at 36 weeks to confirm if still praevia Aim for delivery at 37w or before if start substantial / recurrent vaginal bleeding Delaying c-section until 39-40 weeks is risky, with minimal perinatal benefit
Morbidly Adherent Placentao Placenta accreta: abnormal attachment of the placenta to the uterine
wall (decidua) such that the chorionic villi invade beyond the
endometrium and directly into the myometrium.
Possible Cause: primary deficiency of or secondary loss of
decidual elements (decidua basalis).
Classification: 3 grades based on pathologic assessment ofmyometrial invasion by the chorionic villi:
Accreta - chorionic villi in contact with myometrium(80% of cases)
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Increta - chorionic villi invade into myometrium (15% of cases) Percreta - chorionic villi invade into serosa or beyond (5% of cases)
Associations: history of prior cesarean section, uterine instrumentation, fibroid surgery,
or prior placenta praevia.
Rarely, abnormal attachment is seen in the absence of prior surgery and in theabsence of placenta praevia
Prior to C-section: patient w/ suspected should be consented for possibility of
hysterectomy, massive hemorrhage intrapartum and need for blood transfusion
Pre-op assessment may require MRI
Placental Abruption: premature separation of a normal sited placentao Incidence: 1/150 deliveries
o Recurrence risk: 5-15 %
o Classification
Revealed hemorrhage : blood tracks down between membranes and uterine wall and
results in obvious vaginal bleeding
Conceled hemorrhage : blood remains inside uterine cavity
o Risk factors
Chronic hypertension / preeclampsia Abdominal trauma
Cocaine use
Smoking
Prolonged PROM
High parity
Abruption in prior pregnancy
o Symptoms: severe abdominal pain, backache PV bleeding
o Classical signs:
Shock fainting
Woody uterus: firm, tender and does not relax Fetus difficult to palpate inaudible fetal heart
Irritable uterus
o Diagnosis
Clinical: must exclude previa and other causes of hemorrhage
Confirmed by demonstration post-delivery of retro-placental clot indenting placental
substance
US: small role in dx, more for fetal assessment and to out rule previa
ALWAYS rule out previa 1st
o Management Early delivery is vital
Mother must be stabilised
IV Line: FBC, Group and x match 4 units, Coagulation screen
Continuous CTG
If baby is alive and gestation is not too early as to make fetal survival unlikely, delivery
should be by emergency caesarean section
If fetus already dead usually better to aim for a vaginal delivery & amniotomy should be
performed to hasten this
o Complication: coagulopathy
Coagulopathy = decreased fibrinogen level, decreased platelets & raised fibrindegradation products
Occurs in 30% of cases with placental abruption
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Cause: Release of thromboplastins from the damaged placenta DIC
Hypovolaemia can result in multisystem failure
Expert haematological opinion is advised
Increased risk of postpartum haemorrhage and haemorrhage at time of caesarean section
when coagulopathy present
Local causes of APHo Cervical pathology: cancer, ectropion cervicitis, foreign body
o Check date of last smear and take new smear if indicated
Vasa previao Definition: vessels of the umbilical cord run in the fetal
membranes and cross the internal cervical os
Coexists with velamentous insertion of the cord in
which veins traverse the membranes before they come
together into the umbilical cord
Incidence: 0.1% or less
o Presentation: intrapartum hemorrhage in early labor w/ ROM
Fetus: rapid fetal haemorrhage, fetal bradycardia and fetaldeath if delivery is not accomplished immediately
In contrast to placenta praevia, it is fetal blood that is
being lost and therefore will not take much blood loss before fetus is compromised or
dies
Kleihauer test or an Apt test can be performed to confirm that the blood is in factfetal blood, though rarely done b/c baby is usually delivered by emergency
caesarean section due to life-threatening fetal compromise
o Diagnosis: confirmed post-natally on placental and membrane exam
Rhesus Isoimmunizationo All rhesus negative women should receive anti-D injection if they have an APH, or an event thatmight cause a concealed abruption (? trauma)
o A kleihauer test estimates the volume of fetomaternal haemorrhage and allows the appropriate
dose of anti D to be calculated
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MULTIPLE GESTATION
Incidence:o Twins: 1 in 30 births
o Higher order multiples: 1 in 500 births
Approx 7,000 triplet births per year in US
o Increasing in last 10years
Advancing maternal age effect: higher likelihood of spontaneous multiple ovulation
More widespread use of assisted reproduction techniques for infertility (ART)
8% - 15% risk of multiples with ovulation induction 25% - 50% risk with IVF (depending on how many embryos replaced)
Types of Twinningo 2/3 twins are dizygotic:
Non-identical / fraternal twins
Variable incidence depending on age,
race, parity, medications
3/1,000 < 20 years old
14/1,000 > 35 years oldo 1/3 twins are monozygotic :
Identical twins
Incidence constant (4/1,000)
o Zygosity is an embryological term, which
clinicians in general do not use, as it is difficult
to be certain of zygosity based on ultrasound
information alone.
o Chorionicity and amnionicity are terms more
commonly used by clinicians in practice
Twin Placentationo All dizygotic twins must be dichorionic
o All dichorionic twins must, by definition be also
diamniotic.
o Similarly, all monoamniotic twins must, by
definition, be also monochorionic
o Monozygotic twins:
30% are dichorionic: Embryo divides within 2-3 days fertilization
70% are monochorionic / diamniotic: Embryo divides between days 3 and 8
1% are monochorionic / monoamniotic: Embryo divides between days 8 and 13 1/50,000 are conjoined twins: Embryo divides after days 13 15
o Importance of Chorionicity: Certain complications are seen only in monochorionic twins
o Optimal time to determine chorionicity: 8-11weeks, hard to see placentas and membranes later
Dichorionicity
Can be confirmed by twins of different sex If same gender look for separate placentas (one anteriorly and one posteriorly in
uterus) or a thick dividing membrane between the two sacs
Twin Peak Sign : placental tissue visible in base of dividing membrane
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Role of USo Diagnosis of multiple gestation
100% of multiple gestations should be correctly diagnosed antenatally with a policy of
routine ultrasound
Up to 10%-15% multiples will not be diagnosed until in labor if ultrasound not routinely
performed in all pregnancies
o Vital for determining chorionicity
o Detection of fetal anomalies: 80%-90% anomaly detection rate with routine ultrasound in twins
o Evaluation of fetal growth
Always compare fetal sizes in multiple gestations, and if > 20% growth discordance, this
may be abnormal
o Confirmation of fetal well-being
BPP and Doppler (umbilical and middle cerebral artery) studies allow confirmation of
adequate oxygenation of each fetus
Antepartum Managemento Very high risk for preterm labour and preterm delivery
o No role for elective cervical cerclage, inpatient bed rest, or prophylactic tocolysis
o Cervical length (using trans-vaginal scan) is a useful tool for predicting preterm delivery:
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BPP / Dopplers only required if IUGR or significant growth discordance
Intrapartum Managemento Deliver all twins by 38 to 39 weeks
Probably safer to deliver monochorionic twins by 34-36 weeks
o Deliver all triplets by 36 to 37 weeks
o Most standard labour management interventions are also applicable in twins
Can utilize prostaglandins for induction, and oxytocin for augmentation
Vaginal birth after cesarean section {VBAC} also safe in carefully selected cases
o IV access is mandatory / epidural recommended for all twins undergoing vaginal delivery
o Electronic fetal monitoring mandatory for both fetuses (CTG)
o Deliver in (or near) operating theatre, with anaesthetist back-up
o Availability of intrapartum ultrasound useful to determine the position and presentation of the
second twin)
o Vertex-Vertex Twins:
Most common presentation: 40% - 45% of all twins will be vertex-vertex when in labour
Vaginal delivery possible for most such cases
No evidence that routine cesarean delivery for all such twins is beneficial
Following vaginal delivery of twin A, should rapidly confirm presentation of second twin
(either by vaginal exam or scan)
Management of twin (B) delivery is then based on heart rate tracing, but in general
should expedite delivery
o Vertex-Nonvertex Twins
Vertex-breech / vertex-transverse presentations when in labour, occurs in 35%-40%
Twin A can be delivered vaginally, while mode of delivery of twin B depends on:
Size of B / concordance in size with A / presence of staff skilled in breechextraction
Standard singleton breech criteria also apply (e.g. flexed head)
Options for delivery of twin B are vaginal breech delivery / external cephalicversion (ECV) from breech to vertex / cesarean section
Breech extraction of second twin (twin B) after vaginal delivery of twin A is likely safe
for fetuses that are >1,500g. However, there are insufficient data to confirm safety of this
if < 1,500g
Assisted breech / total breech extraction OK
o Nonvertex First Twin
Breech-vertex / breech-breech presentations occur in 15%-20% of twins
Fear of interlocking chins if breech-vertex twins delivered vaginally
Almost all such cases are therefore delivered by elective cesarean
o Higher Order Multiples Safe vaginal delivery of triplets possible but practical difficulty of 3 or more fetal hearts
to monitor c-section delivery in most cases
Problems of Monochorionic twinso Twin-Twin Transfusion Syndrome (TTTS)
Definition: unequal sharing of blood-flow across the single shared placenta between both
fetuses
Incidence: 10-20% of monochorionic gestations
Pathogenesis uncertain: presence of AV shunt?
Donor fetus : sends much of its blood supply to its co-twin
failure to thrive
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Smaller size / growth restricted / hypovolemic Oligohydramnios / stuck Small bladder
Recipient Fetus : receives a large amount of blood from its co-twin fluid
overload
Plethoric, hyper-perfused Larger size / hypervolemic Polyhydramnios Heart failure / tricuspid regurgitation
Diagnosis
Confirm monochorionic twin pregnancy: Same sex / single placenta Discordant fluid: Oligohydramnios / polyhydramnios sequence Discordant growth: 20% discrepancy in size, measure HC, AC and CRL Abnormal umbilical arterial Dopplers: AEDF more common in donor twin
Treatment
Reduction Amniocentesis: US-guided needle drainage of as much amniotic fluidas possible from around the recipient fetus
o Repeat the procedure, possibly every few days, or as often as needed, to
maintain normal amniotic fluid volume
o Unclear how this therapy helps:
Reduce pressure from recipient sac on stuck twin
May allow increase in perfusion of stuck twin
Probably reduces uterine overdistension, thereby reducing chances
of preterm delivery
o Does not prevent neurologic sequelae if one twin dies
10% - 20% incidence severe brain injury in this situation
Likely occurs because of sudden flow of blood from remaining
live fetus, across the placenta, into the dead fetus, at the moment
of death of one fetus. This sudden flow of blood may be enough to cause death of the
remaining fetus, or may be sufficient to transiently drain blood
from brain of surviving fetus
Laser Ablationo Percutaneous / ultrasound guided 2 mm fetoscope
Laser fiber placed in recipient sac
Placental surface near dividing membrane examined
AV shunt vessels near membrane visualized
Selective photocoagulation of these communicating vessels
o Amniotic fluid reduction performed at same timeo More invasive than amniocentesis, but results in definitive treatment of
underlying pathology
o Recent randomized trial suggests laser is better treatment option than
amniocentesis
Mortality Rate of TTTF: 60% to 100% for both fetuses if untreated
o Monoamniotic Twins
Only 1% of monochorionic gestations are also monoamniotic (i.e. both fetuses sharing
the same amniotic sac) Prenatal diagnosis confirmed by ultrasound with failure to visualize dividing membrane
and also clearly entangled umbilical cords
> 50% perinatal mortality rate
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Mortality unpredictable due to sudden cord compression or occlusion
Intensive fetal surveillance required from time of viability (24 26 weeks)
Hospitalization and daily fetal monitoring (CTG) If variable decelerations present, continuous fetal heart rate monitoring required
Deliver if testing is non-reassuring
Elective delivery, after steroids, at 34 weeks Vaginal delivery possible, but cesarean likely