PREECLAMPSIA

Preeclamsia is one of the leading cause of

maternal mortality and morbidity
throughout the world
It is also responsible for iatrogenic
preterm delivery leading to a lot of
neonatal morbidity and mortality
It is the most important and common
medical complication of pregnancy

Introduction
DEFINITION
Pregnancy-specific syndrome that reduce
organ perfusion due to vasospasm and
endothelial activation.
The diagnostic criteria for preeclampsia
are:
Hypertension
BP140/90 mmHg after 20 weeks gestation
Proteinuria
Proteinuria may not be a feature in some women
with the preeclampsia syndrome, so the Task
Force (2013) suggested other diagnostic criteria
 Chronic
Gestasional Preeclamsia
hypertension

Eclamsia Superimposed

Classification of hypertensive
disorder
Diagnosis
 Preeclamsia is not just significant
hypertension with proteinuria, instead
significant hypertension associated with
any organ damage should be called
preeclamsia
Indicators of Preeclampsia Severity
Indicators of Preeclampsia Severity
Headaches or visual disturbances such as
scotomata
can be premonitory symptoms of eclampsia.
Epigastric or right upper quadrant pain and
elevated serum hepatic transaminase levels
frequently accompanies hepatocellular necrosis,
ischemia, and edema that ostensibly stretches
Glisson capsule (impairment of the liver funcion)
Thrombocytopenia
Characteristic of worsening preeclampsia as it
signifies platelet activation and aggregation as well
as microangiopathic hemolysis.Thrombocytopenia
Progressive renal insufficiency (cr>1,1
mg/dl)
 Severe Preeclamsia
Eclamsia Deadly triad
Hellp syndrome

Deadly triad:
Preterm delivery
Renal failure
Placenta abrubtion
Fetal/maternal death
Hematoma liver
Recurrent preeclamsia
INCIDENCE AND RISK FACTORS
Maternal age (old women>40 yo)
Nulliparous
Multifetal gestation
Women with preeclampsia in the first pregnancy
Multipara, when pregnancy with new partner
Pregnancy distance >10 years
IDDM
Chronic HT
Kidney disease
Obesity
Hyperhomocysteinemia
Metabolic syndrome
PATHOPHYSIOLOGY
Vasospasm
Endothelial activation causes vascular
constriction with increased resistance and
subsequent hypertension.
Endothelial cell damage causes interstitial
leakage through which blood constituents,
including platelets and fibrinogen, are
deposited subendothelially.
Ischemia of the surrounding tissues can
lead to necrosis, hemorrhage, and other
end-organ disturbances characteristic of the
syndrome.
PATHOPHYSIOLOGY

Cardiovascular changes
Cardiac involvement in women with
preeclampsia is caused by
increased afterload due to increased peripheral
resistance
endothelial cell damage that cause intestitial
leakage, particularly in the lung
PATHOPHYSIOLOGY

Blood volume
Hemoconcentration has been a hallmark of
severe preeclampsia and eclampsia
Hemoconcentration results from generalized
vasoconstriction that follows endothelial
activation and leakage of plasma into the
interstitial space because of increased
permeability.
PATHOPHYSIOLOGY
Hematological changes
Thrombocytopenia
Defined by a platelet count < 100,000/L
Platelet are activated in the microcirculation of the
placenta, kidney, liver
Delivery is advisable because thrombocytopenia
usually continues to worsen
the platelet count usually increases progressively to
reach a normal level within 3 to 5 days after
delivery.
Some plasma clotting factors may be
decreased
Erythrocytes display abnormal morphology and
undergo rapid hemolysis.
PATHOPHYSIOLOGY
Kidney
During normal pregnancy, renal blood flow and
glomerular filtration rate are increased.
With development of preeclampsia, renal
perfusion and glomerular filtration are
reduced.
A small degree of decreased glomerular
filtration may result from reduced plasma
volume, causing increased serum creatinine
levels and can lead to AKF
PATHOPHYSIOLOGY
Placenta
Placenta vessel show atherosis because of
endothelial demage by mononuclear cell
infiltration, deposition of lipid & lipophage in
arterial walls. End result is placenta
hypoperfusion.
Complications : IUGR, Fetal demise, abruption
of placenta
PATHOPHYSIOLOGY
Liver
Regions of periportal hemorrhage in the liver
periphery elevate serum hepatic transaminase
levels
It typically manifests by moderate to severe
right-upper quadrant or midepigastric
pain and tenderness.
Hemorrhagic infarction may extend to form a
hepatic hematoma. These in turn may extend
to form a subcapsular hematoma that may
rupture.
PATHOPHYSIOLOGY
Brain
Headaches, mental confusion, dizziness, visual
symptoms, convultion are common with severe
preeclampsia. They arise from cerebrovascular
hyperperfusion that has a predilection for the occipital
lobes.
Headaches do not usually respond to analgesia, but
they improve after magnesium sulfate infusion is
initiated.
There are two theories to explain cerebral abnormalities
with preeclampsia:
Cerebrovascular overregulation in response to acute and
severe hypertension leads to vasospasm
Sudden elevations in systemic blood pressure exceed the
normal cerebrovascular autoregulatory that leads to
vasogenic edema
PREDICTION

Identification of early markers of faulty

placentation, impaired placental
perfusion, endothelial cell activation and
dysfunction, and activation of coagulation
have a poor sensitivity for preeclampsia
Currently, no screening tests are
predictably reliable, valid, and economical
Combinations of tests, some yet to be
adequately evaluated, that may be
promising
PREDICTION
PREVENTION
MANAGEMENT
In severe hypertension,
,recommend treatment
to lower systolic
pressure to or below
160 mmHg and
diastolic pressure to or
below 110 mmHg.
Nifedipine is calcium
channel blocking agent,
it has recommended a
10mg-initial oral dose
to be repeated in 30
minutes if necessary.
MANAGEMENT
The basic management objectives for any
pregnancy complicated by preeclampsia
are:
termination of pregnancy with the least
possible trauma to mother and fetus
birth of an infant who subsequently thrives
complete restoration of health to the mother.
In many women with preeclampsia,
especially those at or near term, all three
objectives are served equally well by
induction of labor.
MANAGEMENT
The treatment of severe preeclampsia is identical
to that described subsequently for eclampsia.
Mild cases can be managed conservatively until
labor commences spontaneously or until the
cervix becomes favorable for labor induction.
The prime objectives are to forestall convulsions,
to prevent intracranial hemorrhage and serious
damage to other vital organs, and to deliver a
healthy newborn.
MANAGEMENT

Early Diagnosis of Preeclampsia

Prenatal visits every 4 weeks until 28 weeks;
every 2 weeks until 36 weeks; every week
until delivery; to aids early detection of
preeclampsia.
 MANAGEMENT
Hospitalization
is considered at least initially for women with new-
onset hypertension, especially if there is persistent
worsening hypertension or development of
proteinuria.
A systematic evaluation is instituted to include the
following:
Detailed examination, observation for headache, visual
disturbances, epigastric pain, and rapid weight gain
Weight determined daily
Analysis for proteinuria or urine protein:creatinine ratio
on admittance and at least every 2 days thereafter
Blood pressure readings in the sitting position every 4
hours.
MANAGEMENT
A systematic evaluation is instituted to
include the following:
Measurements of plasma or serum creatinine,
hepatic aminotransferase levels and a
hemogram that includes platelet quantification.
Some recommend measurement of serum uric
acid and lactic acid dehydrogenase levels and
coagulation studies.
Evaluation of fetal size and amnionic fluid
volume, with either physical examination or
sonography
MANAGEMENT

Reduced physical activity throughout

much of the day is likely beneficial
Absolute bed rest is not desirable.
Sufficient protein and calories should be
included in the diet
sodium and fluid intake should not be
limited
MANAGEMENT

Delayed Delivery
Preterm severe preeclampsia are managed
with conservative management with the aim of
improving neonatal outcome without
compromising maternal safety.
Careful daily inpatient monitoring of the
mother and her fetus.
MANAGEMENT

Termination of pregnancy
It is the only cure for moderate or severe
preeclampsia that does not improve after
hospitalization
Labor induction is carried out, usually with
intravenous oxytocin or preinduction cervical
ripening from a prostaglandin or osmotic
dilator
If induction almost certainly will not succeed or
attempts have failed, then SC delivery is
indicated.
MANAGEMENT

Elective Cesarean Delivery

Unfavorable cervix, a perceived sense of
urgency because of preeclampsia severity, and
a need to coordinate neonatal intensive care,
have led some to advocate cesarean delivery.
 Magnesium sulphate is given as a loading dose
followed by a continuous infusion for 24
hours or until 24 hours after delivery -
whichever is the later.
The loading dose is bolus 4g magnesium
sulphate 20% in 80 cc RL i.v. Over 10
minutes.
The maintenance dose is 20% Magnesium sulphate
10 g in 500ml. This should be administered via a
volumetric pump at a rate of 25ml/hour (1g/hour of
magnesium sulphate) until 24 hours.
If seizure still exsist give 2-5 g magnesium
sulphate in 2-5cc aquabidest i.v (2 times)

PROTOCOL MAGNESIUM SULFATE

 Motor paralysis, absent tendon
reflexes, respiratory depression and
cardiac arrhythmia can occur but will be
at a minimum if magnesium
isadministered slowly and the woman is
closed monitored

SIDE EFFECTS
Hourly MEWS (Modified Early Warning
Score) should be recorded with the
following additional observations performed
:
1. Continuous pulse oximetry (alert
Anaesthetist if O2 sat<95%) and three lead
ECG monitoring if available
2. hourly urine output
3. Deep tendons reflexes (every 4 hours)

IMPORTANT OBSERVATIONS
reduction of the magnesium sulphate
infusion should be considered if:
i) The biceps reflex is not present.
ii) The respiratory rate is < 12/min.

The antidote is 10ml 10% calcium

gluconate given slowly intravenously.
ECLAMPSIA
 In woman with preeclampsia, a convulsion
that cannot be attributed to another cause
is termed eclampsia.

Depending on whether convulsion appear

before, during, or after labor, eclampsia is
designated as antepartum, intrapartum or
postpartum.

Eclampsia is most common in the last

trimester and become increasingly
frequent as term approaches.
 Preeclampsia complicated by generalized
tonic clonic convulsion appreciably
increase the risk to both mother and fetus

Almost without exception, but at times

unnoticed, preeclampsia precedes the
onset of eclamptic convulsions.
 Other diagnoses should be considered in
women with convulsions more than 48 hours
postpartum or in women with focal
neurological deficits, prolonged coma, or
atypical eclampsia.

In severe cases, coma persists from one

convulsion to another, and death may result.

Then can occur tacipneu, cyanosis,

proteinuria, oligouria till anuria, may be
hemoglobinuria.
In antepartum eclampsia, labor may begin
spontaneously shortly after convulsions
ensue and may progress rapidly. If the
convulsions occur during labor, contractions
may increase in frequency and intensity
and the duration of labor may be
shortened. Because of maternal hypoxemia
and lactic acidemia caused by convulsions,
it is not unusal for fetal bradycardia to
follow a seizure.
 Occasionally, sudden death occurs, which
result from a massive cerebral
hemorrhage. Blindness with eclampsia is
almost always due to occipital lobe
edema.
 Eclamptic seizures may be violent an the
woman must be protected, especially her
airway

Management eclampsia
In aggregate, magnesium sulfate therapy
associated with significantly lower incidence
of recurrent seizures compared given an
alternatife anticonvulsant. Importantly the
maternal death rate was signiicantly lower
than other regimen.

Magnesium sulate is not given to treat

hypertension, most likely exerts a specific
anticonvulsant action on the cerebral cortex
 Call appropriate personnel - including the resident
Anesthetist.
Remember ABC.
Give the loading dose of Magnesium Sulphate
4g over 5-10 minutes intravenously and start
an infusion of Magnesium Sulphate
Diazepam may be administered if the fitting
continues at the discretion of the Anesthetist 5-
10 mg intravenously.
Once stabilised the woman should be delivered.
Oximetry should be instituted if not already in
place.

Management eclampsia
Give a further bolus dose of Magnesium
of 2g and increase the rate of infusion
of Magnesium to 1.5g / hour. Continue
observations and consider the need for
ventilation. If two such boluses do not
control seizures, then other methods should
be instituted such as the
administration of conventional
anticonvulsants.

Management of Reccurent fits

Thank You