1. PERIPARTUM
CONVULSIONS
DR. RAJEEV SOOD
Dept of OBG
IGMC, SHIMLA

2. CONVULSIVE DISORDERS
 Are episodic neurological dysfunction &
leading to sensory or motor
manifestations in the form of sensory,
cognitive, emotional or abnormal motor
movements
 Always originate from central nervous
system
 May be confined to one area of brain or
involve whole brain
 So can be focal, partial or generalized

3. In obstetrics & gynecology
4.Obstetric causes- 98%
7.Non obstetric causes- 2%

4. Obstetric cause 
Eclampsia

5. ECLAMPSIA
Is a disease complex confined
to pregnancy where patient
has
2.High blood pressure
3.Convulsions
4.Proteinuria

6. Non obstetric causes In pregnant constitute 2%
of the patients
t Epilepsy 0.5-1% (idiopathic)
h Focal lesions in the brain
Tumours  primary or metastatic
s Tuberculoma
s Other infective lesions e.g
cystecercosis
l Tetanus
l Cerebral malaria

7. NON OBSTETRIC CAUSES CONT..
Vascular causes
o Cerebral venous thrombosis
o Thrombosis of cavernous
sinuses or other venous
sinuses in brain
o Thromboembolism
o Vascular malformations

8. NON OBSTETRIC CAUSES CONT…
Metabolic causes
o Uremia
o Hepatic failure
o Hypo or hyperglycemia

9. NON OBSTETRIC CAUSES CONT…
o Electrolyte
abnormality
Hyponatremia
Hypernatremia
Hypocalcemia
Hypercalcemia
Pyridoxine deficiency
Hypomagnesemia

10. NON OBSTETRIC CAUSES CONT…
Others
oFebrile convulsions
oTrauma
oPoisoning
oAlcohol

11. OBSTETRIC CAUSES 98%
ECLAMPSIA:
o Obstetric patient with
seizure should be treated
as eclampsia until proven
otherwise
o Eclampsia is occurrence of seizures
or coma not attributable to any
cause other than pregnancy

12. ECLAMPSIA
o Incidence varies from 1 in 30 to 500
pregnancy
o Eclampsia can start without any
prior symptoms or can have warning
symptoms like
 High blood pressure
 Excessive weight gain >1 kg/week in
last trimester
 Significant proteinuria >2+ on
dipstick

13. ECLAMPSIA
Mostly a disease of
Primigravidae- 75%
Multiple pregnancy
In low socio economic
group

14. TYPES OF ECLAMPSIA
 Antepartum 50%
 Intrapartum 30%
 Postpartum 20% usually within 48
hrs & fits beyond 7 days reasonably
rule out eclampsia, but has been
reported as long as 23 days after
delivery

15. ATYPICAL ECLAMPSIA
 Before 20 weeks of gestation or
48 hrs after delivery
 Any patient presents with
hypertension & proteinuria &
additional feature of blindness
without convulsions should be
treated as eclampsia
 About 10% of the eclamptic
patients can be normotensive

16. Presentation can be
 Antepartum 50%
 Peripartum 30%
 Postpartum 20%
 Majority have hypertension but 10%
of patients never have high BP
 Headache 80%
 Visual disturbances 40-50%
 Pain epigastrium before seizure 30%
 Hyperactive deep tendon reflexes
30%

19. ECLAMPTIC CONVULSION OR FIT
S Premonitary stage(30 sec): twitching of face,
tongue, limbs, eye balls turn to one side
y Tonic stage opisthotonus (30 sec): limbs flexed
& hands clenched, respiration caeses, tongue
protrude in between teeth, cyanosis appear
e Clonic stage (1-4 min): alternate contraction &
relaxation of voluntary muscles
l Stage of coma: for brief period in some or
continue to next convulsion
Status eclampticus: in quick succession

20. ECLAMPSIA
20-35% of patients have signs
& symptoms of pre
eclampsia.
40% patients have no
symptoms & present first
time with convulsions

21. CAUSES OF CONVULSIONS
• Hypoxia or anoxia  spasm of cerebral
vasculature
• Cerebral oedema
• Cerebral dysrhythmia  due to hypoxia &
oedema
• Disseminated intravascular coagulation in
cerebral microcirculation

22. ECLAMPSIA
 The convulsions are not related with
level of hypertension as they are not
as a result of hypertensive
encephalopathy, as they are not
associated with retinal hemorrhage,
exudates & may not be associated
with even papillodema

23. INVESTIGATIONS
LAB FINDINGS:
2. Complete hemogram which include
platelet count
3. Coagulation profile
 Bedside BT, CT, CRT
 Lab findings
 prothrombin time
 partial thromboplastin time

24. LAB FINDINGS (CONTD)
 Haemoconcentration leads to
 Increased Hb
 Increased urea
 Increased serum creatinine level once raised
reflects deranged glomerular function
o Serum uric acid level  increased & reflects
deranged tubular function
o Tubular functions are knocked out about 4-6
weeks prior to the glomerular function
o Liver function are affected more in patients who
have pain epigastrium & is reflected by
 Increased serum transaminases (increased
SGOT, SGPT) more so in HELLP SYNDROME

25. LAB FINDINGS (CONTD)
 Lactatedehydrogenase are reflection of
endothelial damage
 HELLP syndrome One form of eclampsia
showing
 Hemolysis
 Elevated liver enzymes 10% of eclamptic
 Low platelet count patients
 Urinary protein estimation in clean catch sample
and 24 hr urinary protein estimation

26. CT SCAN (OPTIONAL)
 Cerebral oedema
 Diffuse white matter low density area
 Patchy areas of low density
 Occipital white matter oedema
 Loss of normal cortical sulci
 Reduced ventricular size
 Acute hydrocephalus
o Cerebral haemorrhage
 Intraventricular haemorrhage
 Parenchymal haemorrhage (high density)
o Cerebral infarction
 Low attenuation areas
 Basal ganglia infarction
Similar findings are observed in MRI

27. FUNDUS EXAMINATION
To differentiate between the chronic
hypertensive patient and eclamptic
patient

28.  Doppler studies shows vasoconstriction
 Angiography
 EEG: findings are non specific apart form
eclampsia seen in
 Polycythemia
 Hypoxia
 Renal disease
 Hypocalcemia
 Hypercalcemia
 Water intoxication

29. MANAGEMENT

30. MANAGEMENT
• PRINCIPLES are
• To keep the patient in quiet environment
• Keep the airway clear & put patient in left
lateral position with head end slightly low
on the bed with the rails
• Secure the I/V line
• Maintain vitals
• Avoid injury  bed side rails, mouth gag
if patient is unconscious
• Control convulsions by anti convulsives
(Magsulph)
• Treat hypertension (anti- hypertensives)

31. MANAGEMENT

32. MANAGEMENT (CONTD.)
• Monitor hypoxia & fluid balance(SpO2 &
CVP monitor)
• Organize investigation
• Prevent recurrence of convulsion
• Delivery of the woman safely as soon as
possible
• Postpartum care
• Catheterize the bladder for monitoring
hourly urine output

33. MANAGEMENT DURING FIT
In premonitary stage:
2.Place mouth gag between
teeth
3.Air passage cleaned
4.Patient head turned to one
side to prevent aspiration

34.  DON’T DO VIGOROUS TREATMENT
DURING THE FIT
 AS USUALLY TENDENCY IS TO RUSH
THE DRUGS IN THE FIT TO CONTROL
IMMEDIATELY
 IT MAY PROVE
COUNTERPRODUCTIVE DUE TO
RAPID INFUSION OF DRUG (diazepam
& magsulf) WHICH MAY
DANGEROUSLY INCREASE THE
BLOOD LEVEL OF DRUG LEADING TO
CARDIAC ARREST

35.  First aid treatment outside hospital
 Patient should be transferred to
tertiary hospital as soon as possible
 Control of convulsion: zero hour
treatment
 Magnesium sulphate
 Phenytoin
 Diazepam
Magnesium sulphate should be given
zero hour dose at peripheral
institution

36. PRITCHARD REGIMEN
• (50% magsulph ) 2ml  1 gram
• 4 gram 20% I/V slowly in 3-4 minutes
• 4 ampoules (8ml) to be diluted to make it 20 ml
• 5 gram (5%) in each buttock
• Total dose 14 grams
• Monitored by
7. Tendon reflexes
8. Urine output >100ml in 4 hrs
9. Respiratory rate > 16/ minute

37. ZUSPAN REGIMEN:
Loading dose 4 gm I/V (20%)
Followed by 1 gm/ hr I/V
infusion
SEBAI REGIMEN:
Loading dose 6 gm I/V
Followed by 2gm/ hr infusion

38. DHAKA REGIMEN:(Begam R etal)
 Loading dose 4 gm I/V & 3 gm IM
in each buttock(10 gm total)
 Followed by 2.5 gm I/M every 4 hrly
 Magnesium sulphate prophylaxis
has to be continued 24 hours after
delivery
A combination of magsulf with
nifedipine should be avoided  it
decreases the blood pressure
dangerously low as both act on
calcium channels

39. MAGNESIUM SULPHATE LEVELS
CLINICAL FINDINGS SERUM LEVEL
Loss of patellar reflex 8-10 µg/dl
Feeling of warmth, flushing 9-12 µg/dl
Double vision & slurred speech & 10-12 µg/dl
oliguria
Muscular paralysis 15-17 µg/dl
Respiratory difficulty 15-17 µg/dl
Cardiac arrest 30-35 µg/dl

40. MANAGEMENT OF MAGNESIUM
SULPHATE TOXICITY
• Discontinue magsulf
administration
• Begin oxygen administration
• Administer 1gm calcium
gluconate (10cc of 10% calcium
gluconate)
• If respiratory arrest occurs then
cardio pulmonary resuscitation

41. ANTI HYPERTENSIVES
STARTING DOSE MAXIMUM DOSE
HYDRALAZINE 5-10 MG I/V every 20 30 mg
min
LABETALOL 20-40 mg I/V every 220 mg
10-15 min
NIFEDIPINE 10-20 mg per orally 120 mg/d
every 30 min
DILTIAZEM 120-180 mg QID 540 mg/d
ATENELOL 50 mg QID 100 mg/d
AIM is to lower the B P between 95-100 mm Hg diastolic &
mean arterial pressure between 105-115 mm Hg

42. PHENYTOIN:
 Loading dose 15-25 mg/kg I/V in 2
hrs
 Under ECG tracing 100 mg 6 hrly
SIDE EFFECTS:
5. Cardiac toxicity
6. Nystagmus
7. Hypotension
8. Ataxia
9. Lethargy

43. DIAZEPAM:
Lean regimen :10mg I/V
every 2 minutes to
maximum 40 mg
followed by 40 mg in 500
ml normal saline in 24 hrs

44. Definitive treatment is termination of
Pregnancy
After stabilisation of the patient
 P/V examination done
 Ripening agent put & delivery conducted
in next 8-12 hrs
 Labour managed partographically

45. OMINOUS FEATURES OF
ECLAMPSIA
1. Long interval between the onset of fits
and commencement of treatment
2. Antepartum eclampsia early in
pregnancy
3. Number of seizures more than ten
4. Systolic BP > 200 mm Hg
5. Temperature > 102º F
6. Oliguria
7. Non response to treatment
8. Jaundice

46. INDICATION OF
LSCS
1. Uncontrolled fits inspite vigorous
therapy
2. General condition of the patient
deteriorating very fast
3. Patient not responding to ripening
agent & induced labour
4. Other obstetric indications

47. CARRY HOME
MESSAGE
 Identification of high risk patient in the antinatal
period
 Early referral of high risk patients to experts
 Administration of anti hypertensives to the
subjects & regular anti natal care in the indoors
 Procurement & Administration of magsulph to
the severely pre-eclamptic and emplamptic
patiets in zero hour before referral
 Management of the severely pre-eplamptic and
eplamptic patients in the tertiary institutes
under team of experts