A unique disease (syndrome) of pregnant woman in

the second half of pregnancy.

Carries significant maternal & fetal morbidity and

mortality.

Two criteria for diagnosing preeclampsia

hypertension & proteinuria, in eclampsia

tonic and clonic convulsions.

The definite cure of preeclamsia & eclampsia is

delivery.

The presence of hypertension of at least

140/90 mm Hg recorded on two separate

occasions at least 4-6 hours apart and in the

presence of at least 300 mg protein in a

24 hours collection of urine arrising de novo

after the 20th week gestation in a previously

normotensive women and resolving

completetly by the sixth postpartum week.

Preeclampsia / eclampsia

Chronic hypertension

Chronic hypertension with superimposed

preeclampsia

Gestational or transient hypertension

Hypertension after 20 weeks gestation

Proteinuria > than 300 mg/dl or +1 dipstick

Convulsions: eclampsia

Multiple theories: toxins, nephritis,

parasites, malnutrition, vitamin deficiency,

immunologic, inflammation, oxidation,

prostaglandin imbalance, angiogenic

factors,……..

(Genetic predisposition)

(Abnormal immunological response)

(Deficient trophoplast invasion)

(Hypoperfused placenta)

(Circulating factors)

(Vascular endothelial cell activation)

(Clinical manifestations of the disease)

In preeclampsia Incomplete trophoblastic invasion The magnitude of defective trophoblastic invasion of

the spiral arteries correlated with the severity of the hypertensive disorder

Using electron micorscopy Endothelial damage Insudation of plasma constituents into vessel walls Proliferation of myointimal cells Medial necrosis Lipid and macrophage accumulates in myointimal cells

9

Implantation

Rogers et al: Obst Gynecol Survey 54:189,1999

Endothelial cell injury

Generalized vasoconstriction

Possible mechanisms in Preeclampsia

Friedman and Lindheimer,1999

May be initiated by placental factors that enter the maternal circulation and cause endothelial dysfunction resulting in hypertension and proteinuria.

soluble fms-like tyrosine kinase 1 (sFlt-1) an antiangiogenic protein has been found to be increased in preeclampsia

+ PIGF

- sFlt1

+ VEGF

Endothelium

sFlt-1 acts by binding to placental growth

factor(PGF) and vascular endothelial

growth factor (VEGF), preventing the

interaction with endothelial receptors on

the cell surface and inducing endothelial

dysfuntion.

Exogenous administration of sFlt-1 in

pregnant rats induces hypertension,

proteinuria, and glomerular endotheliosis.

Increase sFlt-1

Increase Endoglin

Decrease PGIF

in patients that will develop clinical preeclampsia

Headache.

Blurring of vision.

Nausea and vomiting.

Epigastric pain (distension of the liver capsule)

Oliguria or anuria

In order to make the diagnosis, one of the following should be present:

Blood pressure of 160 mm Hg systolic or higher or 110 mm Hg diastolic or higher on two occasions at least 6 hours apart while the patient is on bed rest

Proteinuria of2g or higher in a 24-hour urine specimen or 2+ or

greater on two random urine samples collected at least 4 hours apart

Oliguria of less than 500 mL in 24 hours

Cerebral or visual disturbances

Pulmonary edema or cyanosis

Epigastric or right upper-quadrant pain

Impaired liver function

Thrombocytopenia

Fetal growth restriction

ACOG,Practice Bull.2002

Depends on severity of hypertension and gestational age!!!!

Observational Management Restricted activity

Close Maternal and Fetal Monitoring

BP Monitoring

S/S of preeclampsia

Fetal growth and well being (NST, and U/S)

Routine weekly or biweekly blood work

Severe Mild Abnormality

110 mm Hg or higher < 100 mg Hg Diastolic blood pressure

Persistent 2+ or more Trace to 1+ Proteinuria

Present

Absent Headache

Present Absent Visual disturbances

Present Absent Upper abdominal pain

Present Absent Oliguria

Present (eclampsia) Absent Convulsion

Elevated Normal Serum creatinine

Present Absent Thrombocytopenia

Marked Minimal Liver enzyme elevation

Obvious Absent Fetal growth restriction

Present Absent Pulmonary edema

< 37 weeks gestation

inpatient or outpatient management

worsening disease: delivery, magnesium sulfate

> 40 weeks gestation

delivery, magnesium sulfate

37 - 39 weeks gestation

inducible cervix: delivery, magnesium sulfate

cervix not inducible: inpatient or outpatient

management

Complications of preeclampsia ECLAMPSIA

Maternal

CVA

HEELP syndrome

Pulmonary edema

Adult RDS

Renal failure

Fetal

IUGR

IUFD

Placental Abruption

Prompt delivery is curative and avoids

possible bad consequences to mom and baby.

(abruption, seizures…)

Prompt delivery may cause significant

morbidity or mortality to baby due to

prematurity

Fetal risks Maternal risks

Gestational Age Course

More than 34 weeks Delivery

Less than 26 weeks Delivery

26 to 34 weeks Expectant

management v/s

Delivery

gestational age: not recommended for < 24

weeks or > 34 weeks gestation

hospitalization: tertiary care center

antenatal testing: daily

maternal indications

eclampsia, thrombocytopenia, pulmonary edema,

acute renal failure

persistent severe headache or visual changes

elevated liver enzymes with persistent severe

epigastric pain or right upper quadrant tenderness

labor or rupture of membranes

vaginal bleeding, placental abruption

fetal indications

repetitive severe variables or late decelerations

biophysical profile < 4 on two occasions 4 hours apart

amniotic fluid index < 2 cm

intrauterine growth restriction

fetal death

> 34 weeks gestation

admission to labor and delivery for 24 hours

magnesium sulfate IV for 24 hours

antihypertensives if diastolic blood pressure >

110 mmHg

meet guidelines for expedited delivery?

yes? delivery

Expedited delivery? no?

< 23 weeks: counseling for termination of pregnancy

23-32 weeks: steroids, antihypertensive medications,

daily maternal and fetal evaluation, delivery at 34

weeks

32-33 weeks: amniocentesis

immature fluid - steroids, delivery in 48 hours

comment Side effect dose action agent

Late onset 24hours

dpression 500-4000 mg

central Methyl dopa

Drug of emergency

Headache,

Flushing

palpitation

5mg…10mg

Direct vasodilator

hydralazine

Avoid in

h.Failure

b.asthma

Nausea

Vomiting

h.block

20mg…40mg every 10m

Beta&alpha blocker

labetalol

For

emergency

Severe

headache

5mg sub. Ca.channel

blocker

nifedipine

Eclampsia Is a life threatening complications of

preeclampsia,defined as tonic,clonic convulsions

in a pregnant woman in the absence of any other

neurological or metabolic causes.It is an

obstetric emergency.

It occurs antenatal,intrapartum,postpartum

(after delivery 24-48hs)

Management(carried out by a team)

1.Turn the patient on her side

2.Ensure clear airway(suction,mouth gag)

3.Maintain iv access

4.Stop fits(mag.sul,diazepam)

5.Control BP(hydralazine,labetalol)

6.Intake & output chart

7.Investigations(urine,FBC,RFT,LFT,

clotting profile,cross match)

8.Monitor patient and her fetus

9.After stabilization(BPcontrolled,no

convulsions,hypoxia controlled) deliver

Mag.sulphate Drug of choice in ecclampsia

Given iv,im(4-6gr bolus dose,1-2gr maintenance)

Acts as cerebral vasodilator and menbrane

stabilizer

Over dose lead to respiratory depression

and cardiac arrest

Monitor patient(reflexes,RR,urine output)

Antidote cal.gluconate 10ml 10%.

Delivery is the ultimate cure

•Vaginal.

•LSCS is done for obstetric reasons, or before 32 weeks of gestation. •Anesthesia – •General to be avoided, as it increases blood pressure during intubation and extubation. •Epidural is better than spinal.

IV access

Repeat haematological investigations

Fluid management

Seizure prophylaxis and anti hypertensives

Electronic fetal monitoring

Analgesia and Anaesthesia

No ergometrine