PERIPARTUM CONVULSIONSDR. RAJEEV SOOD

Dept of OBGIGMC, SHIMLA

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

In obstetrics & gynecology

1.Obstetric causes- 98%

2.Non obstetric causes- 2%

Obstetric cause Eclampsia

ECLAMPSIA

Is a disease complex confined to pregnancy where patient has

1.High blood pressure2.Convulsions3.Proteinuria

Non obstetric causes In pregnant constitute 2% of the patients

1. Epilepsy 0.5-1% (idiopathic)2. Focal lesions in the braina) Tumours primary or metastaticb) Tuberculomac) Other infective lesions e.g

cystecercosisd) Tetanuse) Cerebral malaria

NON OBSTETRIC CAUSES CONT..

Vascular causesoCerebral venous thrombosisoThrombosis of cavernous sinuses or other venous sinuses in brain

oThromboembolism oVascular malformations

NON OBSTETRIC CAUSES CONT…

Metabolic causesoUremia oHepatic failureoHypo or hyperglycemia

NON OBSTETRIC CAUSES CONT…

oElectrolyte abnormalityHyponatremiaHypernatremia Hypocalcemia Hypercalcemia Pyridoxine deficiencyHypomagnesemia

NON OBSTETRIC CAUSES CONT…

OthersoFebrile convulsionsoTrauma oPoisoning oAlcohol

OBSTETRIC CAUSES 98%

ECLAMPSIA:

oObstetric 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

ECLAMPSIAo Incidence varies from 1 in 30 to

500 pregnancyo Eclampsia can start without any

prior symptoms or can have warning symptoms like

High blood pressureExcessive weight gain >1

kg/week in last trimesterSignificant proteinuria >2+ on

dipstick

ECLAMPSIA

Mostly a disease of Primigravidae- 75%Multiple pregnancyIn low socio economic group

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

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

Presentation can be

Antepartum 50%Peripartum 30%Postpartum 20%Majority have hypertension but 10%

of patients never have high BPHeadache 80%Visual disturbances 40-50%Pain epigastrium before seizure 30%Hyperactive deep tendon reflexes 30%

ECLAMPTIC CONVULSION OR FIT

1. Premonitary stage(30 sec): twitching of face, tongue, limbs, eye balls turn to one side

2. Tonic stage opisthotonus (30 sec): limbs flexed & hands clenched, respiration caeses, tongue protrude in between teeth, cyanosis appear

3. Clonic stage (1-4 min): alternate contraction & relaxation of voluntary muscles

4. Stage of coma: for brief period in some or continue to next convulsion

Status eclampticus: in quick succession

ECLAMPSIA20-35% of patients have signs & symptoms of pre eclampsia.

40% patients have no symptoms & present first time with convulsions

CAUSES OF CONVULSIONS

• Hypoxia or anoxia spasm of cerebral vasculature

• Cerebral oedema• Cerebral dysrhythmia due to

hypoxia & oedema• Disseminated intravascular

coagulation in cerebral microcirculation

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

INVESTIGATIONS

LAB FINDINGS:

1.Complete hemogram which include platelet count

2.Coagulation profileBedside BT, CT, CRTLab findingsprothrombin timepartial thromboplastin time

LAB FINDINGS (CONTD) Haemoconcentration leads to Increased Hb Increased urea Increased serum creatinine level once raised

reflects deranged glomerular functiono Serum uric acid level increased & reflects

deranged tubular functiono Tubular functions are knocked out about 4-6

weeks prior to the glomerular functiono 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

LAB FINDINGS (CONTD)

Lactate dehydrogenase 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

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 hydrocephaluso Cerebral haemorrhage Intraventricular haemorrhage Parenchymal haemorrhage (high density)o Cerebral infarction Low attenuation areas Basal ganglia infarction

Similar findings are observed in MRI

FUNDUS EXAMINATION

To differentiate between the chronic hypertensive patient and eclamptic patient

Doppler studies shows vasoconstriction Angiography EEG: findings are non specific apart form

eclampsia seen in Polycythemia Hypoxia Renal disease Hypocalcemia Hypercalcemia Water intoxication

MANAGEMENT

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)

MANAGEMENT

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

MANAGEMENT DURING FIT

In premonitary stage:1.Place mouth gag between teeth

2.Air passage cleaned3.Patient head turned to one side to prevent aspiration

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

First aid treatment outside hospitalPatient should be transferred to

tertiary hospital as soon as possibleControl of convulsion: zero hour

treatmentMagnesium sulphatePhenytoin Diazepam Magnesium sulphate should be

given zero hour dose at peripheral institution

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 1. Tendon reflexes2. Urine output >100ml in 4 hrs3. Respiratory rate > 16/ minute

ZUSPAN REGIMEN:Loading dose 4 gm I/V (20%)

Followed by 1 gm/ hr I/V infusion

SEBAI REGIMEN:Loading dose 6 gm I/VFollowed by 2gm/ hr infusion

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

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 & oliguria

10-12 µg/dl

Muscular paralysis 15-17 µg/dl

Respiratory difficulty 15-17 µg/dl

Cardiac arrest 30-35 µg/dl

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

ANTI HYPERTENSIVES

STARTING DOSE MAXIMUM DOSE

HYDRALAZINE 5-10 MG I/V every 20 min

30 mg

LABETALOL 20-40 mg I/V every 10-15 min

220 mg

NIFEDIPINE 10-20 mg per orally every 30 min

120 mg/d

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

PHENYTOIN:Loading dose 15-25 mg/kg I/V in 2 hrsUnder ECG tracing 100 mg 6 hrlySIDE EFFECTS:1.Cardiac toxicity2.Nystagmus 3.Hypotension 4.Ataxia 5.Lethargy

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

Definitive treatment is termination of Pregnancy

After stabilisation of the patientP/V examination doneRipening agent put & delivery conducted in next 8-12 hrs

Labour managed partographically

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 Hg5. Temperature > 102º F6. Oliguria 7. Non response to treatment8. Jaundice

INDICATION OF LSCS1. Uncontrolled fits inspite vigorous

therapy2. General condition of the patient

deteriorating very fast3. Patient not responding to

ripening agent & induced labour4. Other obstetric indications

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