Current development in prenatal care - Hassan Nasrat

Current
Development of
Prenatal Care
Professor Hassan Nasrat FRCS, FRCOG
The Fetal Medicine Clinic
The First Clinic
Tuesday, June 18, 13

oMost
complications
occur
toward
the
end
of
pregnancy.
oAdverse
outcomes
cannot
be
predicted
Ministry of Health Report, 1929- UK

Major Complications
•Hemorrhagic complications
•Abnormal presentation and
•Abnormal Lie
•-----
•--

•Changes Of The Nature Of Obstetric
Complications
•Current Obstetric Challenges
❖ Fetal Anueploidy and other fetal Anomalies
❖ Pre-eclampsia
❖ Fetal Growth Restriction
❖ Preterm Labor
❖ Fetal Macrosomia
❖ Gestational Diabetes
❖ Others.....

How Can We Predict Complications ?

Background Risk (PRIORI RISK)
Age
Race
Previous PTL
Previous PET
Previous Anomalies
Underlying Medial Disorders
Other Maternal Characteristics
The First Ante-NatalVisit
+

LOW RISK PATIENT HIGH RISK PATIENT

LOW RISK PATIENT HIGH RISK PATIENT
❖ Most OfThose Complications Develop Late
❖ Same Standard Of Care Regardless Of Potential
Risks
❖ Complications Occur More Among Women Who
Has No Historical Risk Factors
❖ The Importance Of Rationalizing Prenatal Care

Deﬁne Patient Speciﬁc Risk
How Can We Predict Complications ?
Individualized Patient Care

DATA FROM ULTRASOUND SCANNING
+

FINDINGS OF BIOPHYSICALAND BIOCHEMICALTESTS
+
+

FINDINGS OF BIOPHYSICALAND BIOCHEMICALTESTS
+
+
➧
Patient Speciﬁc Risk

 For
Every
Disorder
There
is
background
risk

(Priori

Risk)

Calculation
of
Patient
Speciﬁc
RISK

 The
risk
may
increase
or
decrease
based
on
the
presence

(or
absence)
of
certain
marker
(s)
E.g.
❖Maternal Age > 35 Predict 20-30 % of DS
❖Maternal Characteristics can Predict 30% of PET

Screening
for
Risk
Factors
Important
proper+es
of
a
screening
test
are
its
sensi+vity,

speciﬁcity,
and
predic+ve
values
nega+ve
and
posi+ve.

Screening
for
Risk
Factors
Important
proper+es
of
a
screening
test
are
its
sensi+vity,

speciﬁcity,
and
predic+ve
values
nega+ve
and
posi+ve.
The
sensi(vity
and
speciﬁcity
cannot
be
used
to
es+mate

the
probability
of
the
disease
in
an
individual.

Screening
for
Risk
Factors
Important
proper+es
of
a
screening
test
are
its
sensi+vity,

speciﬁcity,
and
predic+ve
values
nega+ve
and
posi+ve.
The
sensi(vity
and
speciﬁcity
cannot
be
used
to
es+mate

the
probability
of
the
disease
in
an
individual.
Posi(ve
and
nega(ve
predic(ve
are
dependent
on
the

prevalence
of
the
disease

Screening
for
Risk
Factors
Important
proper+es
of
a
screening
test
are
its
sensi+vity,

specificity,
and
predic+ve
values
nega+ve
and
posi+ve.
The
sensi(vity
and
specificity
cannot
be
used
to
es+mate

the
probability
of
the
disease
in
an
individual.
Posi(ve
and
nega(ve
predic(ve
are
dependent
on
the

prevalence
of
the
disease
The
likelihood
ra(o
are
independent
of
disease
prevalence

and
integrate
the
sensi+vity
and
specificity
of
screening

tests


The
likelihood
ra(o

Indicate by how much a given test result
increases or decreases the probability of
developinga condition.

Calculation
of
Patient
Speciﬁc
RISK

“Using
Positive
&
Negative
Likelihood
Ratio”
The
Background
“Priori
Risk”

Calculation
of
Patient
Speciﬁc
RISK

“Using
Positive
&
Negative
Likelihood
Ratio”
×
The
Background
“Priori
Risk”

Calculation
of
Patient
Speciﬁc
RISK

“Using
Positive
&
Negative
Likelihood
Ratio”
×The
Likelihood
ratio
as

Calculated
from
a

given
marker
The
Background
“Priori
Risk”

Calculation
of
Patient
Speciﬁc
RISK

“Using
Positive
&
Negative
Likelihood
Ratio”
×The
Likelihood
ratio
as

Calculated
from
a

given
marker
a
new
priori

Posterior

Risk

For
the
next
test

The
Background
“Priori
Risk”

0.6 0.4 2.0
LR=1.7 LR=10.6 LR=2.0
AFP(MOM) UE3(MOM) hCG(MOM)
Age Risk
30 years
1:900
Likelihood Ratio
AFP UE3 hCG
1.7 × 10.4 × 2.0
× =
Adjusted
Risk
1:25
Normal
DS
Calculations
of
LRs
for
three
analytes.

At
a
MSAFP
level
of
0.6
MoM,
approximately
twice
as
many
fetuses
with
Down

syndrome
are
at
this
level
than
chromosomally
normal
fetuses.
Therefore,
the

LR
for
Down
syndrome
at
a
MSAFP
level
of
0.6
MoM
is
1.7.
Patients
Speciﬁc
Risk
for
DS

 Every woman has a background or a
priori risk for any given disorder/
complication.
 A new individual “patient-specific”
risk is calculated by multiplying the
priori risk with a series of likelihood
ratios obtained from screening tests.
Summary

Current
Development in
Prenatal Care

Prediction of Fetal Complications ?
What Is The Role of Feto-
Maternal Service

❖FetalAnueploidy and other fetalAnomalies
❖Pre-eclampsia
❖Fetal Growth Restriction
❖Preterm Labor
❖Fetal Macrosomia
❖Gestational Diabetes
❖ Others.....

The
11–13+6
weeks
Scan

Package
What Is The Role of
Feto-Maternal Service

Screening
Aneuploidy

Maternal Characteristics
“A Priori Risk”
Biophysical Markers
Biochemical Markers
Early Screening for PET
Adjusted Risk
+
+

cted
uE3
(MoM)
UnaffectedDown’s syndrome
Down’s syndromeUnaffectedfected
Down’s syndrome Unaffected
AFP (MoM) uE3
(MoM)
Nuchal translucency (MoM)
Down’s syndromeUnaffectedDown’s syndrome
PAPP-A (MoM)
Unaffected
AFP (MoM) uE3
(MoM)
Down’s syndromeUnaffectedDown’s syndrome
PAPP-A (MoM)
Unaffected
Nuchal tra
Unaffected
Unaffected
Inhibin-A (MoM)
Down’s syndrome
PAPP-A (MoM)
Unaffected
Unaffected Down’s
syndrome
free ß
9
Down's
syndrome
Unaffected
Inhibin-A (MoM)
Unaffected Down’s
syndrome
free ß-hCG (MoM)
AFP (MoM) uE3
(MoM)
Down’s syndromeUnaffected
Down's
syndrome
Unaffected
Down’s syndrome
PAPP-A (MoM)
Unaffected
Unaffected Down’s
syndrome
UnaffectedD Syndrome
UnaffectedD Syndrome
D SyndromeUnaffected
Unaffected Unaffected
Unaffected D Syndrome
D Syndrome D Syndrome

THREE SCREENING OPTIONS
2nd Trimester
Quad
1st Trimester
Combined Test
1st and 2nd Trimester
Fully Integrated Test
Serum Integrated
Stepwise Sequential Contingent
Sequential Screen

First Trimester Screening “The Combined Test”
Maternal Age NT+ + B-hCG
& PAPP-A

1...9 10 11 12 13 14 15 16 17 18 19 20......40
15 to 20wks
Blood Draw
Quad
AFP
hCG
Ue3
Inhibin
Second Trimester Screening “The QUAD Test”

THREE SCREENING OPTIONS
2nd Trimester
Quad
1st Trimester
Combined Test
1st and 2nd Trimester
Fully Integrated Test
Serum Integrated
Sequential Screen
Contingent Screen

First
Trimester
Second
Trimester
1st & 2nd
Trimester

0
25
50
75
100
First
Trimester
Second
Trimester
1st & 2nd
Trimester

0
25
50
75
100
75
First
Trimester
Second
Trimester
1st & 2nd
Trimester

0
25
50
75
100
75
85
NT NT
+
PAPP-A
&
β-hCG
First
Trimester
Second
Trimester
1st & 2nd
Trimester

0
25
50
75
100
75
85
75
NT
AFP
+
Ue3
&
β-hCG
NT
+
PAPP-A
&
β-hCG
First
Trimester
Second
Trimester
1st & 2nd
Trimester

0
25
50
75
100
75
85
75
NT
AFP
+
Ue3
&
β-hCG
NT
+
PAPP-A
&
β-hCG
85
AFP
+
Ue3
&
β-hCG
&
Inhibin
“QUAD“
First
Trimester
Second
Trimester
1st & 2nd
Trimester

0
25
50
75
100
75
85
NT NT
+
PAPP-A
&
β-hCG
85
AFP
+
Ue3
&
β-hCG
&
Inhibin
“QUAD“
First
Trimester
Second
Trimester
1st & 2nd
Trimester

0
25
50
75
100
75
85
NT NT
+
PAPP-A
&
β-hCG
85
AFP
+
Ue3
&
β-hCG
&
Inhibin
“QUAD“
95
NT
+
PAPP-A
&
β-hCG
“QUAD”
First
Trimester
Second
Trimester
1st & 2nd
Trimester

0
25
50
75
100
75
85
NT NT
+
PAPP-A
&
β-hCG
85
AFP
+
Ue3
&
β-hCG
&
Inhibin
“QUAD“
95
NT
+
PAPP-A
&
β-hCG
“QUAD”
What
if
NT

is
Not
Available?
First
Trimester
Second
Trimester
1st & 2nd
Trimester

0
25
50
75
100
75
85
NT NT
+
PAPP-A
&
β-hCG
85
AFP
+
Ue3
&
β-hCG
&
Inhibin
“QUAD“
95
85
NT
+
PAPP-A
&
β-hCG
“QUAD”
PAPP-A
&
β-hCGWhat
if
NT

is
Not
Available?
First
Trimester
Second
Trimester
1st & 2nd
Trimester
“QUAD”

Nasal Bone
Tricuspid Regurgitation
Ductus Venousus
Figure 3 Four-chamber view illustrating an endocardial cushion
defect in which a ventricular (VSD) and atrial (ASD) septal defect
are present. LA, left atrium; LV, left ventricle; RA, right atrium;
RV, right ventricle.
SUGGESTED USE OF FETAL
ECHOCARDIOGRAPHY AS PART OF THE
GENETIC SONOGRAM GIVEN CURRENT
SCREENING TECHNOLOGIES
At present, common screening tests for trisomy 21 may
include any of the following: (1) first-trimester combined
NT and serum screening, (2) first-trimester combined
NT and serum screening plus second-trimester QUAD
screening, (3) first-trimester serum and second-trimester
Genetic sonography as an adjunct to first-trimester NT
and serum and/or second-trimester serum screening
When genetic sonography was first introduced in the
early 1990s it was an option for screening for trisomy
21 in women less than 35 years of age for two reasons:
(1) the detection rate was similar to or higher than that
using MSAFP screening, and (2) the ultrasound exam only
required measurements of the biparietal diameter, femur
length and nuchal skin fold (Table 1). However, as more
analytes were added, second-trimester maternal serum
(triple and QUAD) screening increased the detection
rate for trisomy 21, was easier to use, and did not
require the specialized ultrasound skills needed to keep
the genetic sonogram comparable in terms of detection
rates (Table 2).
Investigators have reported the use of genetic sono-
graphy as an adjunct to other screening protocols.
In 2001, Roberto Romero and I11
reported offer-
ing genetic sonography to women considered to be
at moderate risk (1 : 190–1 : 1000) for trisomy 21
Figure 4 Four-chamber view illustrating a ventricular septal defect (VSD) at the level of the inflow tracts. (a) B-mode image; (b) power
Doppler image confirming flow at the level of the VSD. LV, left ventricle; RV, right ventricle.

Screening

Pre-‐eclampsia

Pathophysiology of PET
Impaired Trophoblastic Invasion of
Maternal Spiral Arteries
Placental hypoxia
Release of Inﬂammatory cytokines
Platelets and endothelial cell
activation and damage
Clinical symptoms of preeclampsia
Figure 1. Trophoblasts are the first cells to differentiate from the fe
becoming the outer layer of a blastocyst. They further differentiate
phoblast and the outer syncytiotrophoblast. Trophoblast cells prot
immune system.
clear sugar from the blood and is often a precursor to
demonstrated in active PE, and women with insulin re
of developing PE during pregnancy.[66] It is also sugg
ments of insulin resistance based on a single determin
glucose could predict pre-eclampsia at least as well as
for prediction of pre-eclampsia, uterine artery Dopple
Sibai have proposed that pregnancies complicated wit
metabolic syndrome (e.g. adiposity, increased insulin r
excess thrombin generation) and inflammatory signals
developing pre-eclampsia.[99]

782 Section VI Pregnancy and Coexisting Disease
hypertension and approaches 50% wh
tension develops before 32 weeks’
these cases result in preterm deliver
Therefore, such women require close
detection of preeclampsia (frequen
serial evaluation of platelets and live
growth (serial ultrasound).
Preeclampsia should also be con
tional hypertension is severe becau
preterm delivery.11,20
Preeclampsia is clearly a heteroge-
neous condition for which the pathogenesis could be
different in women with various risk factors.11,20,21
The
pathogenesis of preeclampsia in nulliparous women may
be different than that in women with preexisting vascular
disease, multifetal gestation, diabetes mellitus, or previous
FIGURE 35-2. Various clinical and laboratory ﬁndings in women with
preeclampsia or atypical preeclampsia. CNS, Central nervous system;
DIC, disseminated intravascular coagulopathy; HELLP, hemolysis,
elevated liver enzymes, and low platelets.
Excessive
weight gain
Capillary
leak
Blood
pressure
Symptoms
Fibrinolysis
Hemolysis
DIC
Low platelets
↑ Liver enzymes
Nausea/vomiting
Bleeding
CNS
Epigastric
pain
Severe
Mild
Normal
Proteinuria
Facial edema
Pulmonary
edema
Ascites
Pleural
effusions
HELLP
Renal
failure
• Gestational hypertension plus o
following:
• Symptoms of preeclampsia
• Hemolysis
• Thrombocytopenia (<100,000/mm
• Elevated liver enzymes: two tim
the normal value for aspartate
and alanine transaminase (ALT)
• Gestational proteinuria plus on
following:
• Symptoms of preeclampsia
• Hemolysis
• Thrombocytopenia
• Elevated liver enzymes
• Early signs and symptoms of pree
at <20 weeks
• Late postpartum preeclampsia-ec
postpartum)
CRITERIA FOR ATYPICAL PR

Figure 1. Trophoblasts are the first cells to differentiate from the fertilized egg in early pregnancy,
becoming the outer layer of a blastocyst. They further differentiate into two layers, the inner cytotro-
phoblast and the outer syncytiotrophoblast. Trophoblast cells protect the fetus against the maternal
immune system.
Syncytiotrophoblast
Cytotrophoblast
Uterine epithelium
of developing PE during pregnancy.[66] It is also suggested that simple assess-
ments of insulin resistance based on a single determination of fasting insulin and
glucose could predict pre-eclampsia at least as well as the current gold standard
for prediction of pre-eclampsia, uterine artery Doppler velocimetry.[103] Ness and
Sibai have proposed that pregnancies complicated with IUGR lack the maternal
metabolic syndrome (e.g. adiposity, increased insulin resistance, hyperlipidemia,
excess thrombin generation) and inflammatory signals which prevent patients from
developing pre-eclampsia.[99]
Syncytrop
hoblast
Cytotrop
hoblast
Uterine
epithelium
•Maternal syndrome:
BP with or without
system dysfunction
•Fetal syndrome:
(FGR, reduced amniotic
ﬂuid, and abnormal
oxygenation).
Clinically can manifest as either a:
The pathophysiology of early- onset PE may be
different than that of PE developing at term

Decidual
Areteriolopathy
Placental Pathology, Fetal, Neonatal and Maternal
Complications in early and late onset PE
FGR
Perinatal
Death
Maternal Death

Candidate screening tests for preeclampsia and IUGR
5. Markers of insulin resistance
•Tumor necrosis factor
•Sex hormone–binding globulin (SHBG) Adiponectin
•Leptin
1. Maternal Characteristics “Clinical risk factors screening”
2. Placenta perfusion dysfunction–related tests
• Uterine artery Doppler ultrasonography
• Two-dimensional (2D) placenta imaging Three-dimensional (3D) placenta imaging
• Placental volume
• Placenta quotient
• Placenta vascular indices
3. Maternal serum analytes
•Down syndrome markers
•a-Fetoprotein (AFP)
•Human chorionic gonadotropin (hCG) Estriol
•Inhibin A
•disintegrin and metalloproteases (ADAM) Placental protein 13
4. Endothelial dysfunction–related tests “Circulated angiogenic factors”
•Placental growth factor (PlGF)
•Soluble fms-like tyrosine kinase 1
•Vascular endothelial growth factor (VEGF) Soluble endoglin (sEng)
•Entholial cell adhesion molecules
•Selectin
6. Genomics and proteomics

Independent
Variable Adjusted OR (95% CI)Adjusted OR (95% CI)Adjusted OR (95% CI)Adjusted OR (95% CI)Adjusted OR (95% CI)
Early PEEarly PE Late-PELate-PELate-PE
Maternal Age -- 1.04 (1.00-1.07)1.04 (1.00-1.07)1.04 (1.00-1.07)
BMI -- 1.10 (1.07-1.13)1.10 (1.07-1.13)1.10 (1.07-1.13)
Racial Origin
•White
•Black
•Indian or Pakistani
•White
•Black
3.64(1.84-7.21)3.64(1.84-7.21) 2.97(1.98-4.46)2.97(1.98-4.46)2.97(1.98-4.46)
•White
•Black
•Indian or Pakistani -- 2.66 (1.29-5.48)2.66 (1.29-5.48)2.66 (1.29-5.48)
ParousParous
•No Previous PE
•Previous PE
•Maternal History
of PE
0.31(0.14-0.71)0.31(0.14-0.71) 0.24(0.15-0.38)0.24(0.15-0.38)0.24(0.15-0.38)•No Previous PE
•Previous PE
•Maternal History
of PE
4.02(1.58-10.24)4.02(1.58-10.24) 2.18(1.24-3.83)2.18(1.24-3.83)2.18(1.24-3.83)
•No Previous PE
•Previous PE
•Maternal History
of PE
8.70(2.77-27.33)8.70(2.77-27.33) ---
Ovulation drugs 4.75(1.55-14.53)4.75(1.55-14.53) ---
0
10
20
30
40
50
60
70
80
90
100
Early-PE Late-PE
28.00
34.00
Detection Rate for FPR 5%
9149 Pregnancies; Early-PE 0.5% Late-PE 1.5% GH 1.7%
Maternal Characteristics
“Priori Risk”
Race

32
history, uterine artery pulsatility index (UAPI), maternal mean arterial pressure
(MAP), maternal serum pregnancy-associated plasma protein-A levels (PAPP-A),
and maternal serum placental growth factor levels (PlGF) in screening for pre-ec-
lampsia in the first trimester.[39, 107, 108, 110] The specific maternal factors that
appear to play the most significant role in adjusting the risk of pre-eclampsia are
maternal BMI, age, ethnicity, smoking and parity. In a study, which included 7,797
patients, the combination of these parameters predicted early severe pre-eclamp-
sia in 93% cases, late pre-eclampsia in 36% of the cases, and 18% of the cases
of gestational hypertension with a 5% false positive rate.
In comparison, using maternal history alone predicts only 30% of early severe pre-
eclampsia and 20% of late pre-eclampsia for a 5% false positive rate.
Measuring uterine artery PI using Doppler at 11-13+6 weeks’ gestation
Identification of the uterine arteries begins by obtaining a sagittal view of the lower
uterine segment and the cervix. The cervical canal is visualized and the endocervix
is identified at the
junction of the canal
and the lower uterine
segment. The uterine
artery is generally found
in the paracervical tissue
at the level of the endo-
cervix. Therefore, the
transducer is directed to
this region and the uter-
ine artery may be found
there with the aid of
color Doppler.
Figure 4. Color Doppler of
uterine arteries (upper) and
uterine artery waveform
(lower) obtained using the
conditions described in the
text. Images courtesy of
Cathy Downing, Fetal Medi-
cine Foundation, USA.
32
centation is less advanced, the chance of any future preventative steps succeeding
is increased.
The Fetal Medicine Foundation has evaluated the utility of combining maternal
color Doppler.
Uterine Artery 11-13 weeks

Blood Pressure at 11-13 weeks
Mean Arterial Blood Pressure =
Diastolic BP+ (Systolic BP- Diastolic BP)/3
34
In clinical practice MAP measurement in the first trimester may not make a clinical
impact in isolation but could be suitable for use with other markers, including ma-
ternal serum markers, to improve the accuracy for estimating risk of pre-eclampsia.
Already it has been shown following a large prospective study that maternal vari-
ables such as ethnic origin, body mass index, and personal history of PE, combined
with MAP at 11+0 to 13+6 weeks is able to identify a group at high risk for pre-
eclampsia.[105]
How MAP is measured
The Fetal Medicine Foundation recommends the following protocol for the
measurement of blood pressure (see also the FMF’s automatic calculator on
https://courses.fetalmedicine.com/calculator/map?locale=en). The measurement
should be made when the gestational age is between 11 and 13+6 weeks and
when the crown rump length is between 45 and 84 mm.
Figure 5. Measurement of
mean arterial pressure (MAP).

History
Maternal Age
BMI (Kg/m2)
Racial Origin
•White
•Black
Parous
•No Previous PE
•Previous PE
•Maternal History of PE
History of BP
Ovulation drugs
32
Moving screening for pre-eclampsia to the first trimester appears to improve the
detection rate. Furthermore, since this is done at a time when the process of pla-
is increased.
color Doppler.
Maternal
Priori Risk + UaD mBP+

Impaired
Trophoblastic
Invasion
Pre-eclampsia
Placental Growth Factor,PAPP-A,PP13 at 11-13 wks

Cell-free Fetal DNA in Maternal Blood
Release of necrotic
placental fragments
Impaired
Trophoblastic
Invasion
Placental Hypoxia
Endothelial cell
activation

UaD mBP
32
is increased.
In comparison, using maternal history alone predicts only 30 % of early severe pre-
eclampsia and 20 % of late pre-eclampsia for a 5% false positive rate.
color Doppler.
+ PLGP
+

History
Maternal Age
BMI (Kg/m2)
Racial Origin
•White
•Black
Parous
•No Previous PE
•Previous PE
•Maternal History of
PE
History of BP
Ovulation drugs
10,000 pregnancies
600 pregnancies
Late-PE
75/150
Early-PE
45/50
20%
Screen +ve
6%
32
In comparison, using maternal history alone predicts only 30 % of early severe pre-
eclampsia and 20 % of late pre-eclampsia for a 5% false positive rate.
color Doppler.

Objective: to develop algorithms based on a
combination of maternal factors, uterine
artery PI, MAP and serum biomarkers to
estimate patient-specific risks for PE at:
➡Early (< 34Weeks),
➡Intermediate (34-37Weeks)And
➡Late (>37Weeks)

Maternal
age
years

Maternal
weight
kg

Maternal
height
cm

Racial
origin

Past
Obstetric
and
Medical
History:

Pre-‐existing
diabetes
mellitus
type
I

Chronic
hypertension

Cigarette
smoker
in
this
pregnancy

Systemic
lupus
erythematosus

Family
history
of
preeclampsia

Current
Obstetric
History

Method
of
conception
Spontaneous

IVF

Ovulation
drugs
without
IVF

Obstetric
history
Parity
&
Previous
history
of
PE

U/S
Data
Fetal
crown-‐rump
length
mm

Uterine
artery
PI
MoM

Mean
arterial
pressure
MoM

Maternal
serum
PAPP-‐A
MoM

Maternal
serum
PlGF
MoM
(placental
growth
factor
)

Biochemical
Data
Maternal
serum
PAPP-‐A
MoM

Maternal
serum
PlGF
MoM
(placental
growth
factor
)


Receiver
operating
characteristic
(ROC)
curves
in
the
prediction
of
early
(left),

intermediate
(middle)
and
late
pre-‐eclampsia
(PE)
(right)
by
maternal
factors

only
(
.
.
.
.
.
.
.)
and
by
a
combination
of
maternal
factors,
biochemical
and

biophysical
markers
(____)
Early
PE

(<
34
wks)
Intermediate
(PE
34-‐37
wks) Late
(PE
>37
wks)
Detectionrat(%)
33.0%
24.5%
27.8%
80%
91.0%
60.0%

PREECLAMPSIA
In PET the incidence of adverse fetal and maternal short-
term and long-term consequences are inversely related to
the gestational age at the onset of the disease.
Algorithms which combine maternal characteristics,
mean arterial pressure, uterine artery Doppler and
biochemical tests at 11 to 13 weeks could potentially
identify about 90, 80 and 60% of pregnancies that
subsequently develop early (before 34 weeks), intermediate
(34–37 weeks) and late (after 37 weeks) preeclampsia, for a
false positive rate of 5% (Akolekar et al., 2011b).

Kozer et al., First Trimester aspirin = 2.37 Odds
ratio for Gastroschisis
AJOG 2002

❖FetalAnueploidy and other fetalAnomalies
❖Pre-eclampsia
❖Fetal Growth Restriction
❖Preterm Labor
❖Fetal Macrosomia
❖Gestational Diabetes

SMALL FOR GESTATIONAL
AGE FETUSES
 GA include constitutionally small and growth restricted
 FGR due to impaired placentation, genetic disease or
environmental damage is associated with increased perinatal
death and handicap
 Algorithms which combine maternal characteristics, mean
arterial pressure, uterine artery Doppler and the
measurement of various placental products in maternal
blood at 11 to 13 weeks could potentially identify, at a false
positive rate of 10%, about 75% of pregnancies without
preeclampsia delivering SGA neonates before 37 weeks and
45% of those delivering at term
(Karagiannis et al., 2011)

PRETERM DELIVERY
The patient-speciﬁc risk for spontaneous
delivery before 34 weeks can be determined
by an algorithm combining maternal
characteristics and obstetric history (Beta et al.,
2011).
sonographic measurement of cervical length at
11 to 13 weeks can modiﬁes the priori risk of
spontaneous early delivery (Greco et al., 2011).

GESTATIONAL DIABETES
MELLITUS
 Traditional screening at the end of the second trimester by a
series of independent maternal characteristics is poor with a
detection rate of about 60%, at a false positive rate of 30 to 40%
(Waugh et al., 2007).
 Algorithms which combine maternal characteristics and maternal
serum levels of adiponectin, an adipocyte-derived polypeptide, and sex
hormone binding globulin, a liver-derived glycoprotein, at 11 to 13
weeks could potentially identify about 75% of pregnancies that
subsequently develop GDM, for a false positive rate of 20% (Nanda et
al., 2011).
 Additionally, the diagnosis of GDM can be made in the ﬁrst trimester by
appropriate adjustments to the traditional criteria of the oral glucose
tolerance test (Plasencia et al., 2011).

FETAL MACROSOMIA
Screening for macrosomia (birth weight above
the 90th centile for gestational age at delivery)
by a combination of maternal characteristics
and obstetric history with fetal NT and
maternal serum- free ß-hCG and PAPP-A at 11
to 13 weeks could potentially identify, at a false
positive rate of 10%, about 35% of women who
deliver macrosomic neonates (Poon et al., 2011).

What Is The Role of Feto-
Maternal Service

An integrated first first trimester scan (11 – 13 weeks)
combining data from maternal characteristics and
historywithfindingsof biophysicalandbiochemicaltests
candefinethepatient-specificriskforawidespectrumof
pregnancycomplications.

THE NEW PYRAMID OF
PRENATAL
CARE

oMost
complications
occur
toward
the
end
of
pregnancy.
oAdverse
outcomes
cannot
be
predicted

o Early estimation of patient-speciﬁc complications risks
o Individualized patient and disease-speciﬁc approach

“we should learn the past and
research the present to predict the
future”
Hippocrates

Thanks
The studies and some of the slides are found on FMF web
page (k Nicholides)

Current development in prenatal care - Hassan Nasrat

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