2. Introduction
Eclampsia is defined by onset of convulsion in a case of pre-eclampsia
● It Lasts for 60-90 sec for most of the cases
● If it is repeated one after another then it is status eclampticus(very rare)
● Preeclampsia when complicated with GTCS ± coma is Eclampsia
● Incidence of eclampsia is 3.79% in Kolkata based report. Intrapartum eclampsia
accounted for almost 44.6% cases. C-section rate was 10.5% and maternal mortality
rate was 11.28% for PIH, of these 48.7% was due to eclampsia.
● Pre-monitory Phase
● Tonic phase: rigidity; messeter clenching
● Clonus: alternate contraction and relaxation of all voluntary muscle ; tongue bite ;
breathing stertorous; blood strained frothy secretion fillis mouth
● Coma / semiconsciousness
3. The fits consists of four stages
Pre-monitory Stage: Patients becomes irritable, rolls eye, taking long breathes
going to ophisthotonus position. This stage stays for 30sec
Tonic Stage: The whole body goes into a tonic spasm - the trunk ophisthotonus,
limbs are flexed, hands clentched. respiration ceases and the tongue protrudes
between the teeth. Cyanosis appears. Eyeballs becomes fixed. This stage lasts
about 30sec
5. Onset of fits
Fits occurs most commonly in 3rd trimester (more than 50%)on rare occasion fits may occur in early
months as in hydatidiform mole
Antepartum: (50%)
Fits occurs before onset of labour .more often labour starts soon after and at times it becomes difficult
to differentiate it from intrapartum. Most dangerous as placenta is still inside
Intrapartum (30%)
Fits occurs first time during labour
Postpartum (20%)
Fits occurs first time during puerperium usually within 48 hours of delivery
Fits occurs beyond 48 hr but within 4wk after delivery is accepted as late postpartum eclampsia
6. Associated with :
Abruption in 10 % cases
Neuromuscular deficit in 7 % cases
Aspiration in 7% cases
Pulmonary edema in 5% cases
1% risk of death
5-7% of preeclampsia pt develops eclampsia
7.
8. Pathophysiology
1. Theory of vasogenic edema
2. Loss of cerebral autoregulation > cerebral hyperperfision > cerebral edema >
endothelial damage > release of excitatory neurotransmitter > convulsion>
throbbing headache and blurring of vision
9.
10. Clinical feature:
● Generalised tonic clonic convulsion
● Post ictal phase
● Respiratory rate > 50 ( due to hypercarbia ; hypoxia ; lactic acidosis)
● Edema ; proteiniuria ; hypertension ( NOT IN ALL CASES)
● Usually after 20 wk of POG ( < 20WK is atypical presentation)
● Uterine contraction / abruption / labour
● Fetal bradycardia ( transient during convulsion ) ; If > 10 min : rule out
abruption
● Respiratory system : rule out PULMONARY EDEMA
● : Aspiration ( air entry may not be equal in both side)
11. Blindness: due to occipital lobe edema or retinal detachment . Prognosis is good
( reversible after Delivery of fetus)
Very rarely agitated ( psychosis)
14. Specific Management
● Definitive Management - Termination of Pregnancy
● Anticonvulsant and sedative therapy
● Antihypertensive and diuretic
● Management during fits
● Management of complications
15. Management
A)Stabilization with airway maintenance after convulsion.
● Call for HELP
● Prevent injuries ( mainly during clonic phase)
● Lateral decubitus ( left lateral position : secretion will drain out ; tongue will
not block glottis)
● Prevention of tongue bite ( spoon, syringe, tongue depressor, mouth gag)
● Suction out secretion
● O2 inhalation
● Monitor vitals; O2 monitoring by pulse oximeter
● Foleys catheterization ; IV line ; Blood investigation
16. B) anticonvulsant ( DOC: MgSO4 )
C) antihypertensive
D) definitive management: DELIVERY
18. MgSO4
● Excreted by urine
● Serum creatinine evaluation before mgso4 loading dose not required; it is
needed for maintenance dose only
● It acts on NMDA receptor( blocks it)
● Decrease presynaptic release of glutamate
● Not an antihypertensive drug
● Blocks ca2+ entry
● Decrease peripheral vascular resistance ( causes flushing and nausea : not
more than 15 min)
19. Effects on fetus
● Decreases beat to beat variability
● Few deceleration
● Mgso4 toxicity: neonatal depression
● Mgso4 is useful as neuroprotector for fetus ( cerebral palsy prevention).
Effects On Uterus
Tocolysis but for tocolysis it has to be in toxic range which we never allow so
not clinical use
20. Most common regimen used in INDIA
Pritchard regimen
Loading dose : 4gm iv in 20% dilution over 20 minutes. Not more than 1gm/min +
5gm I'm in 50% dilution in each buttock
Maintenance dose : 5gm Im in alternate buttock in 50%dilution
4hrly till 24hr post delivery or convulsion whichever is later
Monitoring:
● DTR : blunt or absent is C/I for maintenance dose
21. DTR:
++++ : CLONUS ( flexion extension alternatively ; pendulous; continuously(
+++ : BRISK
++ NORMAL
+ BLUNT
- ABSENT
BLUNT AND ABSENT: DONT GIVE Mgso4
22. Urine output: 30cc/hr ( 100 cc in 4hr atleast)
Respiratory rate ( < 16 is C/I for mgso4)
Therapeutic window:4-7 meq /L( 4.8-8.4 MG/dl)
>7 : CNS depression; DTR blunt or absent
>10 : respiratory depression
23. What if BREAK THROUGH CONVULSION:
2gm iv top-up dose in 20% dilution ( maximum 2 times)
STATUS ECLAMPTICUS:
Drugs used: sodium amobarbitol; thiopentone; GA drugs + ARTIFICIAL
VENTILATION required along with these drugs
24. Continuous IV Regimen ( SIBAI REGIMEN)
4-6 gm iv in 20% dilution + 1gm -2gm / hr iv ( maintenance dose)
( 5gm in 500 ml RL : 100 ml/hr infusion)
Strict monitoring required
25. Antidote:
10ml 10 % calcium gluconate iv slowly (1ml/min)
To be given only when RESPIRATORY DEPRESSION occurs
If abnormal DTR: only omit Mgso4
For thrombocytopenia ( platelet <1 lakh ) : preferred regimen is IV REGIMEN as there
is chance of bleeding on IM
if mgso4 is contraindicated; use midazolam or lorazepam
26. Antihypertensive:
Doc: LABETALOL
ACOG guideline
● A) LABETALOL ( alpha plus beta blocker ; IV; half life 5-8 hr)
● B)hydralazine ( vasodilator) IV
● C) NIFEDIPINE (Calcium channel blocker) oral
NITROGLYCERIN: for ICU USE ONLY
27. Definitive management
Delivery: not necessarily C-SECTION
IOL by 2 doses of prostaglandin gel 6hr apart and delivery (vaginal delivery)
Induction failure is indication for C-section
● Epidural anaesthesia
● Cut short 2nd stage of labour by Ventouse or Forceps
● Ergot derivatives are CONTRAINDICATED
● Deflate the catheter bulb before DELIVERY
28. Postpartum period:
● Monitor DTR; RR; U O. sameway
● If pt develops another convulsion: top-up dose of 2gm iv + 24 hr additional
coverage of maintenance dose
● Remove catheter only after stopping mgso4
● Anti hypertensive continued only if BP >160/110 ( in India we consider
150/100)
● Iv fluid with RL (75 ml/hr)
● Strict I/O CHART MONITORING is must
● Prevent PPH( Vasospasm cause less blood supply to uterus hampering it's
contraction leading to PPH or due to ABRUPTION )
30. Pulmonary edema
● Increased vascular permeability
● Decreased oncotic pressure
● Cardiogenic edema
● Excessive iv fluid
Breathlessness; O2 saturation<94 % on ABG
Management:
● No volume expander
● CV LINE IS must
● Diuretic + control of HTN; O2 + PROPPED UP POSTION
31. ICH
Leading cause of death in eclampsia
Clinical feature: coma ; convulsion; headache: stupor; neuromuscular deficit; unilateral pupil
dilatation
Diagnosis: lumbar puncture: BLOOD
CT: Hypodense areas
Poor prognosis.
Treatment:
● aggressive antiHTN
● Evacuation not useful (>60 cc hematoma poor prognosis)
● Osmotic agent if MIDLINE SHIFT
● hyperventilation
32. Renal involvement
● Oliguria ( Glomerulonephritis; acute tubular necrosis; renal failure)
● More in abruptio parents due to decreased blood flow ; deposition of
fibrinogen like material in glomeruli
● Anuria
● It may be PRERENAL AND RENAL
● In PRERENAL: urinary Na < 20 meq and osmolarity > 500
● In RENAL : urinary Na > 40 meq and osmolarity< 350
● Treatment:
CV line = IV fluid+ diuretic (20-40mg)
If poor BISHOP SCORE: C SECTION
33. CVS
Postpartum collapse
Shock : leads to ATN and seehans
Mechanism : electrolyte imbalance: severe hyponatremia; decreased K+ level ;
hypovolemia
Monitoring: within 1 hr of delivery upto 24 hr
● Hypotension
● Tachycardia
● Cold clammy extremity
● No urine output
● increased RR; Decreased O2 saturation
● Bilateral infiltrate in xray
Investigation: blood for CBC; ELECTROLYTES; BUN; CREATININE
35. PRES
● Posterior reversible encephalopathy syndrome
● Visual defect / disturbance / loss
● Seizures; headache; alter sensorium; confusion
● Vasospasm leads to vasogenic edema in OCCIPITAL region
● MRI : HYPERINTENSITY in posterior aspect of brain
● Reduction of BP should be slow in management
