Pre eclampsia

Criteria of sever preeclampsia:

• Severe hypertension (systolic BP ≥160 mm Hg or diastolic
BP ≥110 mm Hg).
• Renal insufficiency
• Cerebral or visual disturbances
• Pulmonary edema
• Epigastric or right upper quadrant pain
• Elevated liver enzymes
Treatments of sever PE:
• Intravenous infusion of hydralazine or labetalol can be used
in sever cases.
• Magnesium sulphate should also be used in women with
severe pre-eclampsia to prevent the onset of convulsions
(eclampsia).
Screening for PE
• There is currently no screening test for preeclampsia.
• Doppler ultrasound uterine artery waveform may be used
to identify women at risk of PE, a characteristic ‘notch’ can
often be seen in the waveform pattern. Uterine artery
Doppler may have a role in screening the women with high
risk for PE, However, it is not of value in screening low risk
women.
Prevention of PE
Established preventative interventions include:
• low-dose aspirin (typically 75 mg daily), which modestly
reduces the risk of pre-eclampsia in highrisk women
• calcium supplementation may also reduce risk, but only in
women with deficient dietary intake.
• vitamins C and E do not lower the risk of preeclampsia,
despite encouraging preliminary studies.
Other variants of hypertension in pregnancy
1. Chronic hypertension in pregnancy: (with or without
renal disease) existing prior to pregnancy can predispose
to the later development of superimposed pre-eclampsia.
Even in the absence of superimposed pre-eclampsia, chronic
hypertension is associated with increased maternal and fetal
morbidity and pregnancies complicated by chronic
hypertension should regarded as high risk.
2. Non-proteinuric gestational
hypertension: it’s a hypertension arising for the first time in the
second half of pregnancy and in the absence of proteinuria, is not
associated with adverse pregnancy outcome.
Fetal growth restriction (FGR)
definition: is failure of a fetus to reach its full growth potential,
which associated with a significant increased risk of perinatal
morbidity and mortality.
Small for gestational age (SGA) means that the weight of the fetus is
less than the tenth centile for its gestation.
The terms SGA and FGR are not the same. It is important to
remember that not all fetuses with SGA are growthy restricted, most
SGA fetuses are constitutionally small and are not compromised.
Intrauterine growth restriction (IUGR) indicates that there is a
pathological process operating to restrict the growth rate of the
fetus. Consequently, some FGR fetuses may not actually be SGA, but
nevertheless will have failed to fulfil their growth potential.
Aetiology of FGR
1. Internal influences: factors that directly affect the intrinsic
growth of the fetus which include:
• Chromosome abnormalities, e.g. trisomy 18
• structural abnormality e.g. renal agenesis
• Intrauterine infections, e.g. cytomegalovirus, toxoplasmosis
2. External influences: of the fetal growth, can be subdivided
into:(maternal and placental)
• maternal systemic factors:
 Under-nutrition, e.g. poverty, eating disorders
 Maternal hypoxia, e.g. living at altitude,
 Drugs, e.g. alcohol, cigarettes, cocaine
 Women with underlying medical disorders such as
hypertension, diabetes, renal disease, cyanotic heart
disease and antiphospholipid syndrome
•placental factors
 Reduced uteroplacental perfusion, e.g. inadequate
trophoblast invasion, sickle cell disease, multiple gestation
 Reduced fetoplacental perfusion, e.g. single umbilical
artery, twin–twin transfusion syndrome
Pathophysiology and classification
the sonographically determined head-to abdomen
circumference ratio (HC/AC) are used to classify growth
restricted fetuses into two types:
1. symmetrical FGR: were proportionately small, an early
insult could result in a relative decrease in cell number and
size. symmetrical FGR associated with factors that directly
impair fetal growth, such as chromosomal disorders and fetal
infections.
2. Asymmetrical FGR:
• had disproportionately lagging abdominal growth compare to
head growth.
• it might follow a late pregnancy insult such as placental
insufficiency which leads to reduced oxygen transfer to the fetus
and impaired excretion of carbon dioxide by the placenta.
• A fall in PO2 and a rise in pCO2 in the fetal blood induces a
chemoreceptor response in the fetal carotid bodies with resulting
vasodilatation in the fetal brain, myocardium and adrenal glands,
and vasoconstriction in the kidneys, splanchnic vessels, limbs and
subcutaneous tissues.
• The result of all these circulatory changes is an asymmetrical
fetus with relative brain sparing, reduced abdominal girth and
skin thickness.
• The vasoconstriction in the fetal kidneys results in impaired
urine production and oligohydramnios.
detection of FGR:
1. Uterine Fundal Height
• serial fundal height measurements are recommended as a
simple, safe, inexpensive, and reasonably accurate screening
method to detect growth-restricted fetuses.
• from 22 week, the uterine fundal height in centimeters
coincides within 2 weeks of gestational age.
• Thus, if the measurement is more than 2 to 3 cm from the
expected height, inappropriate fetal growth is suspected.
2. Sonography assessment of:
• biometric measurements: including femur length, Biparietal
diameter, head circumference and abdominal circumference
measurements. these measurements performed at 2-weekly
intervals.
• Amniotic Fluid Volume Measurement: An association
between pathological fetal-growth restriction and
oligohydramnios has long been recognized.
3. Doppler Velocimetry
• the umbilical artery Doppler: abnormal umbilical artery
Doppler velocimetry findings characterized by absent or
reversed end-diastolic flow have been uniquely linked
with fetal-growth restriction
• Middle cerebral artery Dopplers: in the presence of fetal
hypoxemia, blood flow is redistributed to the brain,
known as the brain-sparing effect. blood flow increases in
the middle cerebral artery (increasing diastolic flow).
4. Fetal cardiotocography
Management
• the detection of an SGA infant contains two elements:
first, the accurate assessment of gestational age and
second, the recognition of fetal smallness.
• When a diagnosis of SGA has been made, the next step is
to clarify whether the baby is normal and simply
constitutionally small or whether it is FGR.
• ultrasound examination of the fetal anatomy should be
made looking for fetal abnormalities that may explain the
size. Even if the anatomy appears normal, the presence of
symmetrical growth restriction in the presence of a
normal amniotic fluid volume raises the suspicion of a
fetal genetic defect.
• Features suspicious of uteroplacental insufficiency are an
asymmetrically growth restricted fetus with a relatively
small abdominal circumference, oligohydramnios and a
high umbilical artery resistance
• At present, there are no widely accepted treatments
available for FGR related to uteroplacental insufficiency.
Obvious contributing factors, such as smoking, alcohol
and drug abuse, should be stopped and the health of the
women should be optimized.
• delivery of a suspected growth-restricted fetus with normal
umbilical artery Doppler velocimetry, normal amniotic fluid
volume, and reassuring fetal heart rate testing can likely be
deferred until 38 weeks’ gestation.
• Consider immediate delivery if there is absent or reverse
end diastolic flow in umbilical artery.
• Most clinicians, however, recommend delivery at 34 weeks
or beyond if there is clinically significant oligohydramnios.
• With a reassuring fetal heart rate pattern, vaginal delivery
is planned. However, some of these fetuses do not tolerate
labor, necessitating cesarean delivery.
• When growth restriction is severe and the fetus is too
immature to be delivered safely, bed rest in hospital is
usually advised in an effort to maximize placental blood flow.
Prognosis
• The prognosis of FGR is highly dependent upon the
cause, severity and the gestation at delivery.
• When FGR is related to a congenital infection or
chromosomal abnormality, subsequent development of the
child will be determined by the precise abnormality.
• babies with FGR secondary due to uteroplacental
insufficiency, some babies will suffer morbidity or mortality
as a result of prematurity. For the survivors, the long-term
prognosis is good with low incidences of mental and
physical disability and most infants demonstrate ‘catch-up
growth’ after delivery when feeding is established.
• There is a link between FGR and the adult onset of
hypertension and diabetes has been established.