3 fetal medicine

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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



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



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:



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



Abnormal CTG: variable decelerations indicating cord compression not worrying

unless repetitive and deep



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



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

3 fetal medicine

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