Post on 13-Feb-2020
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