2. DEFINITION
• Pre eclampsia when complicated with
convulsion and/or coma is called eclampsia
• It may occur abruptly without any warning
manifestation but in majority (over 80%) ,
however , the disease is preceded by features
of severe pre eclampsia
3. INCIDENCE
• It occurs in 0.2% to 0.5% of all deliveries.
• Varies widely from 1 in 100 to 1 in 2000
pregnancies.
• Varies widely from country to country.
• Varies in different zones of the same country.
• It is more in developing countries than
developed countries.
4. INCIDENCE
• Its incidence is much common in the
developing countries particularly in the rural
areas and contribute a major cause of
maternal mortality.
• It is common in PGR (about 75% of cases ) and
in twin pregnancies.
5. RISK FACTORS
• Primigravida
• Previous history of pre-eclampsia
• Family history of pre-eclampsia in mother or sister
(increases risk 3 fold)
• Insulin resistant states (e.g. hypertension, obesity,
and overt type 1 diabetes)
• Thyroid disorders
• Hyper prolactinemia
• Chronic hypertension – super imposed by pre-
eclampsia
6. Continued…..(RISK FACTORS)
• Presence of Anti-phospholipid Antibodies
• Factor V Leiden Mutations
• Stress (working women have 2-3 times more risk)
• Pregnancy associated risk factor (e.g. twins, triplets,
polyhydramnios)
• Fetal abnormalities like hydrops fetalis, trisomy 13 or
triploidy, and H mole
• Nutritional factor (low calcium intake)
• Low socio economic status
7. CAUSE OF CONVULSION
It may be caused by:-
• 1) ANOXIA:-Spasm of the cerebral vessel
----Increased cerebral vascular resistance
----fall in cerebral oxygen consumption
---anoxia
• 2) CEREBRAL EDEMA :- may contribute to
irritation.
• 3) CEREBRAL DYSRYTHMIA:- Increases following
anoxia or edema
8. PATHOPHYSIOLOGY
• The actual physiological changes that lead to
convulsions in pre-eclampsia are still unclear.
Normally the cerebral perfusion is maintained
at the level of
55 ml/ 100 grams/ per minute
despite variations in M.A.P. With worsening of
hypertension the M.A.P. exceeds the upper
limit of cerebral auto regulation.
9. So, high blood pressure auto-regulation fails leading to
Cerebral vasodilatation Reactive vasospasm
Increased cerebral perfusion Local ischemia
Segmental dilatation of blood
vessels
Fibrinoid changes and
arteriolar necrosis
Over distension of dilated
segments resulting in necrosis of
medial muscle fibers
Disruption of
endothelial lining
Plasma/ RBC’s leak out into
extra vascular space
Peri-capillary hemorrhage
Foci of abnormal electric discharge
SEIZURES
10. ONSET OF FITS
• It occur most commonly in 3rd trimester(>50%
cases). On rare occasion convulsion may occur
early as in H.mole or in twin pregnancy.
• ANTEPARTUM(50%) --fits occurs before the onset
of labor.
• INTRAPARTUM(30%)– fits occur for the 1st time
during labor.
• POSTPARTUM(20%)—fits occur for the first time
in puerperium, usually within 48 hrs of delivery.
• Fits occurring beyond 7 days of delivery,
reasonably rules out eclampsia.
11. CLINICAL FEATURES
• Clinical features are combination of severe pre
eclampsia and convulsion.
1) Severe pre eclampsia : persistent systolic B.P. of
>160mm of Hg and diastolic B.P>110mm of Hg.
2) Persistent severe epigastric pain.
3) Cerebral or visual disturbances
4) Oliguria (<400ml/day) , Proteinuria>5gm/day
5) Platelets count < 1 lakh/ml
6) IUGR
7) 7) Pulmonary edema
12. CLINICAL FEATURES cont….
• ECLAMPTIC CONVULSIONS: consist of 4 stages:
1) Premonitory stage:-last for 30 sec..
Pt. become unconscious---there is twitching of
face,tongue and limbs---eyeballs roll or are
turned to one side and become fixed.
2) Tonic stage: last for 30 sec
The whole body goes into tonic spasm--- the
trunk opisthotonus,limbs are fixed and hands
clenched---respiration ceases and tongue
protrudes b/w the teeth--- cyanosis appear---
eyeball are fixed.
13. 3) Clonic stage:- All voluntary muscles undergo alternate
contraction and relaxation.
• Twitching start in face—involve one side—whole body
is involved in convulsion.
• Biting of tongue occurs
4) stage of coma: it may last for brief period or in other
deep coma persist till another convulsion.
• Patient appear to be in confused state and fail to
remember happenings.
• When fits occur in quick succession it is called status
eclampticus.
15. ORGAN DYSFUNCTION IN PRE-
ECLAMPSIA AND ECLAMPSIA
• CARDIOVASCULAR:
Generalized vasospasm
Increased peripheral vascular resistance
Decrease in CVP
Decrease in pulmonary wedge pressure
19. MATERNAL COMPLICATIONS
• INJURIES:- Tongue bite, injuries due to fall
from bed, bed sore.
• PULMONARY COMPLICATIONS:-
EDEMA:- due to leaky capillaries
PNEUMONIA:-Due to aspiration, infections
ADULT RESPIRATORY SYNDROME
EMBOLISM
20. COMPLICATIONS (contd.)
• HYPERPYREXIA
• CARDIAC: Acute left ventricular failure
• RENAL FAILURE
• HEPATIC:--- Necrosis, sub-capsular hematoma
• CEREBRAL:--- edema, hemorrhage
• DISTURBED VISION: due to retinal
detachment or optic lobe ischemia.
• HAEMATOLOGICAL: Thrombocytopenia & DIC
21. PROGNOSIS
• MATERNAL:-
Immediate : uncertain
Prognosis depends on various factors and
ominous features are:-
1) Long interval between onset of fits and
commencement of treatment.
2) Ante-partum eclampsia specially with long
delivery interval.
3) Number of fits > 10
4) Coma in b/w fits
5) Temp>102 with pulse rate>120/minute
22. 6) systolic B.P > 200mm of Hg
7) Oliguria with proteinuria > 5gm/24hr
8) Jaundice
9) Non responsive to treatment
23. MATERNAL MORTALITY
• It is very high in India and varies from 2-30%
with more mortality in rural based hospitals.
CAUSES:- 1.Cardiac failure
• 2.Pulmonary edema
• 3.Aspiration or septic pneumonia
• 4.cerebral hemorrhage
• 5.Pulmonary embolism
• 6.Puerperal sepsis
• 7. Renal failure
24. FETAL MORTALITY
• It is very high to an extent of about 30-50%.
• CAUSES:-
• 1. Prematurity
• 2. Intra uterine asphyxia due to placental
insufficiency.
• 3. Effect of drugs used to control convulsions
• 4. Trauma during operative delivery
25. PREVENTION
• In majority of cases, eclampsia is preceded by
severe pre-eclampsia.
• Prevention of eclampsia is based on early
detection & treatment along with termination of
pregnancy during pre-eclampsia.
• Eclampsia is not always a preventable condition
because it can bypass the pre-eclamptic state.
• Adequate sedation,anti-hypertensive therapy
and /or prophylactic anticonvulsant help to
prevent POSTPARTUM ECLAMPSIA.
26. MANAGEMENT
• HOSPITAL--- PRINCIPLES OF MANAGEMENT:-
Maintain airway
Oxygen administration
Ventilator support (if needed)
Hemo-dynamic stabilization
Organize investigation
Deliver by 12 hrs
Postpartum care
27. GENERAL MANAGEMENT
• The patient should be placed in an isolated
room protected from noxious stimuli.
• Detailed history should be taken relevant to
diagnosis of eclampsia, duration of pregnancy,
no. of fits, nature of medication administered
outside.
• Only when the patient Is stabilized a thorough
but quick general, abdominal & vaginal
examination are done.
28. • Half hour pulse, RR, B.P to be recorded
• Hourly urinary output is to be noted
• Immediately after the convulsion ,fetal
bradycardia is common probably due to
maternal acidosis & hypoxia induced by a fit.
• Fluids –RESTRICTED
total fluid should not exceed previous 24 hr.
urinary output+1000ml.
• Antibiotics-to prevent the infection
29. SPECIFIC TREATMENT
• Anticonvulsant regime:-aim is to control the fits
& prevent recurrence.
• MgSO4 is the drug of choice because:
It reduces motor endplate sensitivity to Ach
.thereby reducing the NM irritability
Mg blocks neuronal ca influx also.
It induces vasodilation, dilates uterine arteries,
increase the endothelial prostacyclin synthesis.
It has no adverse effect on neonates within
therapeutic value.
30. Regimes of MgSO4
REGIMEN LOADING DOSE MAINTENANCE DOSE
Pritchard et al 4g over 3-5 min i/v 10g
i/m
5g, 4 hourly i/m
Zuspan 4g over 5-10 min 1-2g/h i/v
Sibai 6g over 20 min i/v 2 g/h i/v/
Dhaka Regimen 4gm MgSO4 i.v. & 6gm
i/m (3gm on each
buttock )
2.5gm i/m 4 hrly for
31. OTHER REGIMENS
• LYTIC COCKTAIL REGIME: chlorpromazine,
pethidine & promethazine. OBSOLETE
• DIAZEPAM THERAPY:- Not used now because of
complication. OBSOLETE
• PHENYTOIN THERAPY:- initial dose is 10mg/kg
followed by 5mg/kg 2hr later. Thereafter 200mg is
given orally after 12 hrs.
32. ANTIHYPERTENSIVE & DIURETICS
• If B.P remain above 160/90mm of Hg even
after using anticonvulsants and sedatives,
antihypertensive drugs are to be administered
.
• Drugs commonly used are Hydralazine,
Labetalol, Calcium Channel Blocker or
Nitroglycerine
• If pulmonary edema is present furosemide to
be used
33. MANAGEMENT DURING FITS
A) in the premonitory stage: a mouth gag is
placed to prevent tongue bite and should be
removed after the clonic phase is over.
B) the air passage is to be cleared of mucus with
mucus sucker
C) oxygen is given until cyanosis disappear
34. STATUS ECLAMPTICUS
• Thiopentone sodium 0.5mg dissolved in 20ml
of 5% dextrose is given i.v slowly.
• Expert anesthetist must be present during
procedure.
• In unresponsive pt. C.S is a life saving attempt.
35. ECLAMPSIA OVERVIEW
• Eclampsia , a life-threatening complication of pregnancy,
results when a pregnant woman previously diagnosed
with preeclampsia develops seizures or coma.
• In some cases, seizures or coma may be the first
recognizable sign that a pregnant woman has
preeclampsia.
• Key warning signs of eclampsia in a woman diagnosed
with preeclampsia may be severe headaches, blurred or
double vision, or seeing spots.
• Toxemia is a common name used to describe
preeclampsia and eclampsia.
