PRE-ECLAMPSIA /

ECLAMPSIA

Hypertensive disorders
Pre-eclampsia
Eclampsia
Chronic hypertension
Pregnancy induced hypertension
Chronic hypertension with superimposed preeclampsia

PRE-ECLAMPSIA
Is a disease of pregnancy
...hypertension of at least 140/90mmHg
recorded on 2 separate occasions at least
4 hrs apart and in the presence of at least
300mg protein in a 24hr collection of
urine, arising de novo after the 20th week
of gestation in a previously normotensive
woman and resolving completely by the
6th postpartum week.

PRE-ECLAMPSIA
Mild

Pre-eclampsia:

Mild/Mod

HTN (systolic < 160 and Diastolic <

110) with 1+ Proteinuria with no symptoms of
severe PE or imminent Eclampsia

Severe

Pre-eclampsia:

Severe

HTN + Sig. Proteinuria +/- clinical

features of severe pre-eclampsia.
Diastolic 110 or systolic 160 measured on

two occasions 6 hours apart.

Proteinuria of at least 1g/L or 2+ on dipstick.

ECLAMPSIA
Eclampsia is the development of
epileptiform convulsions of the grand-mal
tonic clonic type in pregnancy.
Is also defined as seizure activity or coma
unrelated to other cerebral conditions in
an obstetrical patient.
20% of eclamptic convulsions occur with no
prodromal symptoms, while the rest show
symptoms and signs of impending
eclampsia.

ECLAMPSIA

Respiration Ceases during the seizure.

The seizure may be divided into 2

phases:
Phase 1 :generalized muscular contractions.
Phase 2 : muscles begin alternating between
contracting and relaxing in rapid sequence.
A coma or a period of unconsciousness follows
phase 2.

IMMINENT ECLAMPSIA

A transitional condition characterized by

increasing symptoms and signs

INCIDENCE
PRE-ECLAMPSIA

occurs

in 6-8% of all pregnancies and accounting for 12-18%

of pregnancy-related maternal deaths in the US
The global incidence of preeclampsia has been estimated at
5-14% of all pregnancies.
ECLAMPSIA

Eclampsia

Occurs in 1 in 3000 pregnancies in the Caribbean.

0.2 0.5% of all deliveries affected.
60 % of seizures occur before delivery
50% of post-partum seizures occur within 48 hrs, but they
may occur as late as 6 weeks
U.H.W.I.

(2007)

118 Total Cases of Pre-eclampsia / Eclampsia

43 mild / 67 severe / 8 Eclampsia

RISK FACTORS
PRE-ECLAMPSIA
Past Hx of pre-eclampsia (esp. Same partner)
Family Hx of pre-eclampsia
<16 or >35 yrs
Nulliparity
Change of consort in subsequent pregnancy
Chronic HTN and renal disease
Sickle cell anaemia (SS/SC disease)
Obesity
Hyperplacentosis (a condition of heightened trophoblastic
activity characterized by increased placental weight and
circulating hCG levels higher than those associated with
normal pregnancy.)
Poor antenatal care
Smoking

RISK FACTORS
CHRONIC HTN W/ SUPERIMPOSED PREECLAMPSIA
Renal disease

Maternal age >40 yrs

Diabetes
Connective tissue disease
Coarctation of the aorta
Blood pressure >160/100mmHg in early
pregnancy

AETIOLOGY OF PRE-ECLAMPSIA
Aetiology

is unknown but there are several

theories
1. Genetics
2. Immunological
3. Renin-angiotensin aldosterone pathway
abnormalities
4. Altered prostacyclin-thromboxane ratio
5. Endothelial dysfunction

Physiology Review

Normal Placentation
Functional unit is the fetal cotyledon.
Primary villus which secondary and tertiary
stems terminal villi.
Cotyledons develop around entries of
maternal spiral arteries.
Maternal blood flow increases progressively
from 50 ml/min to 600 ml/min at term.
Conversion of maternal spiral arteries from
narrow tortuous vessels wide-bored flaccid
vessels.

Spiral Arteries

Physiology Review

The first phase of invasion:

During the initial 12 weeks the decidual
segments of spiral arteries are invaded.
At the end, trophoblast plugs that have
occupied the lumen of spiral arteries are
released
Sudden increase in blood flow to intervillous
space.

Physiology Review

The second phase of invasion

After 12 weeks, invasion of the
intramyometrial segment of spiral arteries
occurs.
Further reduces resistance to blood flow.
Creates a mid-trimester fall in maternal blood
pressure

The new flaccid spiral arteries not only

permit increased perfusion but because
they lack smooth muscle are less likely to
respond to vaso-active compounds.

AETIOLOGY

Pre-eclampsia is a clinical manifestation

of total or patchy failure of trophoblastic
invasion of the myometrial segment of
the spiral arteries.
Spiral arteries retain their muscular walls
Under perfusion of placenta and release
of factor(s) into the maternal circulation
targeting vascular endothelium

AETIOLOGY contd

The hypo-perfused placenta has reduced

synthesis of vasodilatatory factors such
as NO and prostacyclin (PGI2). The
ischaemia also causes endothelial
damage.

These substances are known to oppose

the effects of the maternal renin
angiotensin system and endothelial
damage is known cause vasospasm; all
accounting for the HTN

AETIOLOGY
GENETIC PREDISPOSITION
ABNORMAL IMMUNOLOGICAL RESPONSE
DEFICIENT TROPHOBLAST INVASION
HYPOPERFUSED PLACENTA
CIRCULATING FACTOR(S)
VASCULAR ENDOTHELIAL CELL ACTIVATION
CLINICAL MANIFESTATIONS OF DISEASE

PATHOPHYSIOLOGY

KIDNEY

Glomerulo-capillary endotheliosis :
renal flow
GFR
proteinuria =
acute renal failure.

BRAIN
Vasospasm+oedema = incr. Neural activity
and convulsions
Central effects= headache, visual
disturbances, nausea + vomiting,
hyperreflexia
Cerebrovascular haemorrhage

PATHOPHYSIOLOGY

LIVER
Periportal heamorrhages; hepatocellular
necrosis; epigastric/rt hypochondrial pain ;
hepatic rupture(rare);

transaminases from subendothelial fibrin

deposition
HELLP syndrome (2-4%)

CARDIO-RESPIRATORY

Peripheral resistance + vasospasm = HTN,

cardiac failure, pulmonary oedema
ARDS

PATHOPHYSIOLOGY
HEAMATOLOGY

plasma volume=
perfusion = hypovoleamic shock
Microangiopathic haemolytic anaemia =
thrombocytopenia
Altered thromboxane/prostacyclin ratio = platelet
aggregation

EYES

Optic

nerve is an extension of white matter thus

hypoxia inc. excitability in Retina visual
disturbance
Serous retinal detachment
Cortical blindness

PATHOPHYSIOLOGY

UTERUS & PLACENTA

Utero-placental perfusion
= IUGR

trophoblastic invasion = abruptio placentae

DIC

Loss of endothelial cell integrity results

in an increase in vascular permeability
and generalized oedema

CLINICAL FEATURES OF PREECLAMPSIA

Findings are dependent on the severity of the
disease.

SIGNS:
Elevated BP and proteinuria on dipstick
Fundal height small for dates
Papilloedema
Hyperreflexia and ankle clonus
Petechiae and bruising
Generalized oedema with dyspnoea

CLINICLA FEATURES OF PREECLAMPSIA

SYMPTOMS:
Asymptomatic
Headache
Visual disturbances
Epigastric and right upper quadrant pain

MANAGEMENT

AIMS
Early recognition of symptomless syndrome
Control BP
Prevent development of eclampsia
Detect IUGR, prevent intra-uterine demise, assess
foetal well being
Deliver foetus by the safest and fastest means when
the risk to mother and/or foetus if pregnancy is
continued outweighs the risk of delivery and
prematurity.

CURE = DELIVERY OF FOETUS AND

PLACENTA

EARLY RECOGNITION
Booking and antenatal visits
History note risk factors

Examination

Evaluation of mother
Full systemic evaluation of the mother for signs
BP measurements
Presentation is extremely variable and may be

antepartum, intrapartum or postpartum

Evaluation of fetus
Symphysio fundal height
Leopolds maneuvers
Fetal Heart Rate

Investigation

Urine dipstick

MANAGEMENT OF PREECLAMPSIA

Pts w/ HTN & proteinuria, ADMIT

Bed rest, in Left lateral position
Investigations
Anti-hypertensives if severe:
Bp160/110mmHg or diastolic
>100mmHg
Dexamethsone for foetal lung maturity
depending on gestational age
Anticonvulsant therapy dependent on
severity
Plan delivery

INVESTIGATIONS OF PRE-ECLAMPSIA
1.

Urinalysis and 24hr Urine Collection:

to confirm proteinuria and to rule out other causes of
proteinuria

2.

MSU

3.

To rule out an infective cause of a proteinuria e.g. UTI

Complete Blood count:

4.

Caused of Proteinuria Preeclampsia, eclampsia, UTI, Vaginal

discharge, blood, mucous & meconium, Renal disease e.g.
glomerulonephritis / pyelonephritis, Collagen Vascular Disorder,
HbSS/SC, Orthostatic proteinuria of pregnancy

Assess haemoglobin, white cells and platelet count.

Urea+Electrolytes:

INVESTIGATIONS contd
5. Uric Acid:
glomerular filtration rate and creatinine clearance
decreases resulting in elevated uric acid levels.

6. Liver Function Tests:

Elevated transaminase levels result from hepatocellular
necrosis

7. Clotting Indices:
Screening for DIC

8. Non-Stress Test
Assessment of fetal well-being

9. Ultrasound Examination of foetus

Detects IUGR and Oligohydramnios. Monitors Foetal growth

MANAGEMENT OF MILD PREECLAMPSIA

Vitals done regularly, at least 4hrly

Urinalysis twice daily
Monitor Mother for symptoms and signs of
impending Pre-Eclampsia
Monitor foetal well-being with Kick Charts, daily
Non-Stress tests and Weekly Biophysical Profiles.
Monitor Foetal Growth with serial SFH
measurements and U/S scans
Plan the time of delivery to ensure best neonatal
and maternal outcome.

MANAGEMENT OF
SEVERE PRE-ECLAMPSIA

Severe Pre-Eclampsia management involves

Antihypertensive management and
antepartum surveillance as stated before as
well as seizure prophylaxis with MgSO4.

Controlling Blood Pressure

Acute Control

Options Available:
Labetalol: I.V.
Hydralazine: IV or IM
Nifedipine: P.O. (not sublingually)

Maintenance Therapy
Oral aldomet / nifedipine / labetalol

Controlling Blood
Pressure
Hydralazine

5mg

boluses q20mins are given IV slowly until diastolic

BP ranges 90-100mmHg
Then an infusion 10mg in 100mls N/S is titrated
against BP readings
Side-effects include reflex tachycardia, palpitations
and headache

Nifedipine

(Calcium Channel Blocker)

10 mg p.o. tid.
increase to maximum dose of 120 mg/day
May cause profound hypotension

Controlling Blood
Pressure

Labetalol
200mg in 200mls N/S starting at 20mg/hr and

doubling every 30mins until diastolic BP falls below

100mmHg.
Max dose is 160mg/hr.
Contraindicated in Asthmatics

Aldomet
Central acting alpha-adrenergic stimulant which

produces vasodilatation by reducing sympathetic

outflow.
Drug of choice for chronic HTN in pregnancy
Dose: 250mg-500mg q6hrly
Side Effects include postural hypotension and
depression

Fluid Management

Pulmonary oedema has been a significant cause

of maternal death in PE and has often been
associated with inappropriate fluid
management
Fluid restriction is advisable
Total fluids should be limited to 80 ml/hr or 1
ml/Kg/hr
Close fluid balance with charting of input and
output is essential.
Catheterization for hourly urine output
assessment is important.

Preventing Convulsions

Magnesium Sulphate is the drug

of choice and has been proven
to reduce the risk of eclamptic
seizure. (MAGPIE study)

MgSO4

Mg Compete with Calcium for neuronal impulse

transmission and hence inhibits excessive neuronal
discharge and muscular activity.

MgSO4 Therapy Must be Monitored for signs of Toxicity.

Pulse Rate, Respiration, Reflexes, Urine Output and

Serum Mg Levels should be Monitored.

Ensure
PR > 60
RR > 12
Deep tendon Reflexes Normal
Hourly Urine Output > 30ml/hr
Serum Mg is 4-7mg/dl

MgSO4
MAGNESIUM TOXICITY
1.5-3
4-7

Normal
Therapeutic levels

5-10

ECG changes

8-12

Loss of patellar reflex. Flushing

10-12

Somnolence. Slurred Speech

15-17

Muscle paralysis. Respiratory difficulty

30

Cardiac arrest

Calcium gluconate -10ml of 10% over 10 minutes if concern over resp.

depression.

MgSO4

The Parkland IM protocol is as follows:

Loading dose: MgSO4 4 g IV over 5-10 min
Maintenance: MgSO4 10 g deep IM divided in
both buttocks and mixed with 1 mL 2%
lidocaine.
Magnesium sulfate 5 g IM q4h is then given,
starting 4 h later.

The Zuspan IV Regimen:

4g IV over 15 mins followed by a maintenance

dose of 1-2g per hour.

DELIVERY

INDICATIONS

Maternal:
Persistent increase in BP to severe level

(160/110mmHg or Higher)
Rapid weight gain and generalized swelling
Development of persistent cerebral symptoms e.g.
visual disturbances headache, hyperreflexia.
Persistent Thrombocytopaenia
HELLP Syndrome

Foetal:

Severe Growth retardation by U/S

Non reactive Non-Stress Test
Abnormal Biophysical Profile
Foetal Maturity greater than 37 weeks

DELIVERY

Decision made after woman is stable

If GA > 34/40 immediate delivery is

recommended.

If GA < 34/40 and the pregnancy can be

prolonged in excess of 24 hours
corticosteroids should be administered.

Prolonging the pregnancy at very early

GA can only be considered if the mother
remains stable.

Corticosteriods

Given between 24 and 34 weeks

gestation

BETAMETHASONE:

2 doses IM 12mg each, 24hrs apart

DEXAMETHASONE

4 doses IM 6mg each, 12 hrs apart

DELIVERY

The preferred mode of delivery is vaginal.

Induction of Labour is done by hospital

protocol

Caesarean Section is done for Obstetric

indications

Adequate analgaesia in the form of epidural

anaesthesia should be considered because
labour pain may significantly elevate
pressures.

MgSO4 seizure prophylaxis is done during and

at 24 hrs after labour.

MANAGEMENT OF ECLAMPSIA

History
Examination

to rule out other causes of seizures.

Investigations
As for Pre-eclampsia
Blood Glucose
Calcium and Magnesium
CSF if indicated
MRI if indicated

MANAGEMENT OF ECLAMPSIA

Initial Treatment

Arrest of Convulsions

Seizure Prophylaxis

Stabilization

Expeditious Delivery

MANAGEMENT OF ECLAMPSIA

Initial Treatment
ABCs.
Put Patient in Left lateral Position
Give O2 Via nasal cannula
Gently restrain patient to prevent injury

Arrest of Convulsions
When safe to do so, establish IV access
4g MgSO4 bolus is given IV over 3-5mins
2g bolus may be given after initial 4g bolus after
15 mins.
Status Epilepticus requires ICU admission for
muscle relaxation, intubation and ventilation
because severe hypoxaemia may ensue.

MANAGEMENT OF ECLAMPSIA

Arrest of Convulsions

Seizure Prophylaxis

Diazepam 10mg IV boluses up to 40mg or

Lorazepam 0.5mg/kg IV may also be used.

Done as described for pre-eclamptics by

Parkland IM or Zuspan IV protocol with MgSO4.

Stabilization
BP controlled as in pre-eclamptics with
emergency antihypertensives
Urine Output monitoring by Urinary Catheter
and Fluid is restricted
Foetal Assessments Conducted by NST and
Biophysical profile.

MANAGEMENT OF ECLAMPSIA

Expeditious Delivery
Delivery should be done within 12 hrs of
admission
Vaginal Delivery is the aim with induction of
labour, if necessary, and Syntocin
augmentation of labour.
Caesarean Section is done for Obstetric
Indications
General Anaesthesia is preferred for
abdominal delivery.

Close monitoring of the Mother is

necessary post-delivery and seizure
prophylaxis continues at least 24 hrs

Post-delivery

44% of Eclampsia postpartum.

Continuous assessment prior to

discharge.

Incidence of severe pre-eclampsia and

eclampsia falls after the fourth
postpartum day.

Post-delivery

Continue anti-hypertensive meds as

dictated by blood pressure.

Alpha methyldopa - drug of choice

In breastfeeding women, labetalol,

atenolol, nifedipine and enalapril are
used either singly or in combination.

Follow-up

Assess BP and proteinuria at 6 week visit

If still present further investigation is

recommended.

Pre-conceptional counseling should be

offered where any risk factors and
preventive therapy can be discussed.

PROGNOSIS
Approximately 25% of women with eclampsia have
hypertension in subsequent pregnancies.
Only 5% of patients with hypertension develop severe preeclampsia.
Approximately 2% of women with eclampsia develop
eclampsia with future pregnancies.
Multiparous women with eclampsia may be at higher risk
for development of essential hypertension.
Multiparous women with eclampsia have a higher mortality
rate in subsequent pregnancies than primiparous women.

Outcomes:
Perinatal Death
SGA
Prematurity

SUMMARY

Pre-eclampsia is a hypertensive state of

pregnancy that is either mild or severe.
High risk patients require vigilant antenatal
care.
Pathophysiology is related to abnormal
placentation and multiorgan involvement
The only cure is Delivery.
Mother comes first at all times.
MgSO4 is the drug of choice in prophylaxis
and treatment of seizures and knowledge of
its use, therapeutic and toxic levels is a must.
After delivery Pre-eclampsia and Eclampsia
can still occur.

REFERENCES
Rhoopnarinesinghs

Textbook of Gynaecology,3 rd
ed.Eniaths Printing Company Limited;2003:66-81.
Monga et al, Gynaecology by Ten Teachers, 18 th
ed.,BookPower; 2006:gggg
Hyperplacentosis: A Novel Cause of Hyperthyroidism

J. Ginsberg, R.Z. Lewanczuk, L.H. Honore. Thyroid. April

2001, 11(4): 393-396. doi:10.1089/10507250152039154.
Published in Volume: 11 Issue 4: July 9, 2004
www.rcog.org.uk/resources/public/pdf/management_pre_
eclampsia_mar06.pdf
Current Obstetrics and Gyanecology