PREECLAMPSIA

AND ECLAMPSIA
 Preeclampsia is a multisystem disorder of
unknown aetiology and unique to pregnant
women after 20 weeks gestation.
 It is a progressive disease with a very
variable mode of presentation and rate of
progression.
 It is pregnancy specific with reduced organ
perfusion secondary to vasospasm and
endothelial classification. 
 Preeclampsia is said to complicate 5% of all
deliveries.
It is said to affect 5.8% of primigravidas and
0.4% of secundagravidas.
The incidence is influenced by parity, race,
multiple gestations, environmental
factors,maternal age, maternal size and history
of chronic hypertension
 Classification of hypertensive
disorders of pregnancy

1. Gestational hypertension
(formerly pregnancy-induced
hypertension or transient
hypertension). 
 2. Preeclampsia 

 3. Eclampsia

 4. Preeclampsia superimposed on
chronic hypertension 
 5. Chronic hypertension
 Definition and Diagnosis
 Preeclampsia can not be accurately
defined until its cause is known. It is
described as a syndrome comprising of
hypertension, oedema and proteinuria
occurring after 20 weeks gestation.
 Hypertension -140/90 mm of Hg or
more on at least two occasions four
hours or more apart after the 20th week
of pregnancy in a woman known to be
normotensive and in whom blood
pressure has returned to normal by the
sixth postpartum week. 
 Proteinuria is defined as the excretion of
0.3 g protein or more within 24 Hr or a
measurement of 1+ or more using
 Classification
 This is classified as mild or
severe forms as the latter
is associated with
increased maternal and
fetal morbidity.
 

 Severe form is said to occur

if one or more of the
conditions in this table is
 Definition of severe pre-eclampsia
  1. Arterial pressure > 160mmHg systolic or
> 110mmHg diastolic on two occasions
at least 6 hrs apart
 2. Proteinuria > 5g in 24 hour > 3 + un
dipstick
 3. Oliguria < 400 mm in 24 h
 4. Cerebral signs – headache, blurred vision
or altered consciousness
 5. Pulmonary oedema or cyanosis
 6. Epigastric or right upper quadrant pain
 7. Impaired liver function
 8. Hepatic rupture
 9. Thrombocytopenia
 Hypertensive Disorders During Pregnancy: Indications of
Severity

Abnormality Mild Severe

Diastolic blood pressure < 100 mg Hg 110mmHg or higher

Proteinuria Trace to 1 + Persistent 2 + or more

Headache Absent Present

Visual disturbances Absent Present

Upper abdominal pain Absent Present

Oliguria Absent Present

Convulsion Absent Present

(eclampsia)

Serum creatinine Normal Elevated

Thrombocytopenia Absent Present

Liver enzyme elevation Minimal Marked

Fetal growth restriction Absent Obvious

Pulmonary edema Absent Present

 Material Faculty Excessive
Vascular Placentation Trophoblast
Disease

Genetic
Immunologic or
Inflammatory
Factors

Reduced Uteroplacental
Perfusion

Vasoactive Agents: Noxious Agents:

Prostaglandins Cytokines
Nitric Oxide Lipid Peroxidases
Endothelins

Endothelial
Activation

Capillary Leak

Vasospasm Activation of
Coagulation

Edema Proteinuria

Hemo- Thrombo
concentration cytopenia

Hyper Oliguria Liver

tension Ischemia

Seizures Abruption
 Pathophysiology
  
 The summary is that as a result of
the damage of the endothelial
cells, it
 looses its functions and in addition
also produces proagulants,
vasoconstrictions and mitogens.
The increased pressor sensitivity of
the maternal vessels leads to
profound vasospasm and reduced
organ perfusion which are
arious Changes

etus  IUGR Preterm delivery Abruptio placental

aternal

idneys - Proteinuria, ↓ GFR, ↑ Plasma Creatinine

- Glomerular endothehosis  Renal failure (ATN, Cortical

necrosis)
Cardiovascular - ↓ Plasma Volume, ↓ CVP, AP ↑ & SVR
  Contractility usually unchanged.

Brain HT encephatopathy, ischaemia and infarction, vasospasm, Haemorrhage Oedema Eclampsia

Liver Altered LFT, Periportal hepatic necrosis, Subcapsulaar haemorrhage, FDP, HELLP.

Lungs Leaking Capillaries  pulmonary Oedema

ARDS

Coagulation - Thrombocytopenia (↑ Platelet activation and

consumption)
Platelet Production ↑ Less often Erythrocyte destruction
 Prediction and Prevention
  No ideal predictive tests that fulfils all
described criteria.Two most important
predictive factors:
  1. Nulliparity - Preeclampsia in 5.8%
primigravida, 0.4% Secundagravida.
  2. Family History - Considerable evidence
support significant genetic contribution
  Aetiology & pathophysiology are still not
understood fully and this has hindered
development of effective premature measures.
 . Anti-platelet therapy - Low dose
Aspirin
  
 . Calcium Supplementation
 TREATMENT
 Delivery is the cure for Preeclampsia.
The prime objective is to prevent
convulsion.
 The management ideally should be
multidisciplinary. It is based on the
severity of the disease and also
influenced by gestational age.
 Management should include
  
 1. Treatment of hypertension
  
 The risk of cerebral haemorrhage is a major
cause of maternal deaths (60%)
 Significant risk of CVA occurs when MAP >
 140mmHg (180/120).
  
 The aim of treatment is to prevent intracerebral
haemorrhage while not
 affecting uteroplacental blood flow and
maternal renal functions.
  
 Prolonged treatment of HT is advisable
when the fetus is immature in an attempt
to delay delivery.
 However, this can only be undertaken
provided the mother is not placed at risk
and that strict monitoring of both the
mother and the fetus is carried out at
frequent regular intervals, hospitalization
and bed rest may be all that is required in
some patients.
 Antihypertensive
therapies
 Acute therapy-hydrallazine, labetalol

 Prolonged therapy-methyldopa
nifedipine, atenolol

 ACE inhibitors not recommended

 For Severe Preeclampsia
  Anticonvulsant

Antihypertensive
- Follow by Delivery
  Conservative management in
severe cases – Need to be
cautious.
 Think of maternal safety.
MANAGEMENT IN HOSPITAL
1.Detailed examination followed by daily scrutiny
for clinical findings such as headache, visual
disturbances, epigastric pain, and rapid weight
gain.
2. 2.Weight on admittance and every day
thereafter
3 3.Analysis for proteinuria on admittance and at
least every 2 days thereafter
 4.4Blood pressure readings in sitting position
with an appropriate-size cuff every 4 hours,
except between midnight and morning.
5.Measurement of plasma or serum
creatinine,uric acid, hematocrit, platelets, and
serum liver enzymes, the frequency to be
 ECLAMPSIA
 Eclampsia is defined as the new onset of
convulsions, before or during pregnancy
or post partum, unrelated to other
cerebral pathologic conditions in a woman
with preeclampsia. Incidence Reported
rate 1:2000 to 1:3000 deliveries. The
incidence is signficiantly higher in non
industrialized nations. Estimates in
developing countries varies from 1 in 100
to 1 in 1700.
  Worldwide of estimated 500,000,
maternal deaths every year – 10 – 15% are
associated with HDP.
  Reported maternal mortality rates varies
 Management Aim
  
 1. Stop Convulsions and prevent
recurrence
  
 2. Control the blood pressure
  
 3. Avoidance of diuretics and
limitation of fluid administration
  
 4. Correct fluid and electrolyte
imbalance
  
 5. Deliver the patient
 Anticonvulsants
  - Valium
 - Phenytoin
  - Chlomethiazole
  - Magnesium sulphate
  
 The anticonvulsant therapy
should protect the woman and
her fetus from deleterious
effects of convulsion but
should not expose either to
additional risks from the
therapy.
 Supportive Management
  
 - Airways
  - Nasogatric tube
  - Oxygen
  - Catheterization / Urinary output
monitoring
  - Tepid sponge / Expose to fan
 - Management of an unconscious
patients.
  
 Complications
  
 - Pulmonary Oedema
 - Renal and hepatic failiure
  - Hemiplegia
 - Altered Consciousnes/Coma
  - Some degree by Blindness
  - Psychoses