Peripartum convulsions
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Transcript of Peripartum convulsions
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