neonatal seizures
DESCRIPTION
Neonatal SeizuresTRANSCRIPT
NEONATAL
SEIZURES
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INTRODUCTION Paroxysmal alteration in neonatal behavior and (or)
motor, autonomic function initiated by
hypersynchronous activity of neurons in the brain.
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Neonatal Seizures: A Signal of
Neurological Disease
Most distinctive indicator of neurological problem
in newborn period
Common problem in the neonatal ICU that
evokes urgent reaction
Therefore, it is critical to
RECOGINZE neonatal seizures
DETERMINE ETIOLOGY
TREAT
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CORRELATION OF TIME OF
ONSET OF SEIZURES AND
AETIOLOGY
Most Frequent Time Aetiology of Seizures
< 48 Hrs. Hypoxic - ischaemic encephalopathy
Intra cranial haemorrhage
Hypoglycemia, Hypoelectrolytemia
Congenital Viral infections
Drug induced
Pyridoxine dependency
Non-ketotic Hyperglycemia
Urea cycle disorder
48-72 Hrs. Cerebral dysgenesis, Early sepsis, Urea cycle
disorder
7 days Organic acidemias, Amino acidopathies,
Bacterial meningitis, BFNC and BINS www.similima.com 4
CAUSES OF NEONATAL SEIZURES
– Contd.. Developmental brain abnormalities Cerebral malformation and dysgenesis and
chromosomal disorders.
Anoxic-Ischaemic Encephalopathy Resulting from prenatal, intrapartum and postnatal
factors
Other causes explained The impairment of potassium dependent
repolarisation is likely to cause this age specific epileptic syndrome.
Receptors families of Excitatory Amino-Acids (EAA) are over expressed at the stage of brain ontogenesis. www.similima.com 5
CLINICAL FEATURES SUBTLE SEIZURES
Eyes : Sustained Opening, Ocular Movements, Blinking, Tonic Horizontal Deviation
Oral : Chewing, Drooling, Sucking, Laughing
Apnea : Full Term ? Premature
Motor : Boxing, Hooking, Rotary Pedalling, Stepping movements of the Extremities
Autonomic : Elevated Blood Pressure & Heart Rate
In Premature Infants www.similima.com 6
NORMAL NEONATAL MOTOR ACTIVITY
COMMONLY MISTAKEN FOR SEIZURES
AWAKE or DROWSY
Roving eye movements
Nystagmoid jerks
Unsustained, Sucking, Puckering
SLEEP
Fragmentary myoclonic jerks
Isolate, generalized myoclonic jerks on arousal
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CLINICAL CHARACTERISTICS WHICH
DISTINGUISH JITTERINESS FROM
SEIZURES
CLINICAL FEATURES JITTERINESS SEIZURES
Stimulus – Sensitive
Movements
+ 0
Movements Cease with
Restraint
+ 0
Associated Abnormal Eye
Movements
0 +
Quality of Movement Tremor Clonic
Jerking
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CLINICAL SEIZURES - Contd..
II Clonic Seizures Focal : Involve face upper + /- lower extremities on
one site “axial structures (neck / trunk) : Usually associated with neuropathology
(i.e. Cerebral infarction and intra cerebral haemorrhage)
Multi focal : Involve several body parts and often migrate in a non-jacksonian (random) manner may also involve the face.
: Consider the neonatal equivalent of generalized tonic – clonic seizures.
: Clonic movement are rhythmic and slow movements of limbs (about 1-3 jerks / sec.) at the onset and lateral declines. www.similima.com 9
CLINICAL SEIZURES - Contd.. III Tonic Seizures
Focal : Sustained posturing of a limb or asymmetric posturing of the trunk and / or neck
Generalised :Decerebrate posturing
Decorticate posturing
Usually associated with apnoea and upward gaze of eyes
Most common in preemies and usually
indicates structural brain damage and IVH
IV Myoclonic seizures
Involve flexor muscles of an Upper extremity www.similima.com 10
CLINICAL SEIZURES - Contd..
Multifocal :Asynchronous twitching of several parts of body.
Generalized :Bilateral jerks of upper and some times lower limps
:Rapid movements of distal flexors All 3 types
of may occur during sleep in the new born.
:Characterised brief repeated extension and
flexion movements of the arms, legs or all limbs.
:Presence suggests severe diffuse brain
damage
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INVESTIGATIONS - Complete Hemogram
- Blood : Sugar, Calcium, Magnesium, Na+, K+ & HCO3 Elevated Ammonia,
Lactate Levels Culture & Sensitivity
- CSF : Analysis, Biochemical & C/s.
- EEG : Plays an important role www.similima.com 12
MANAGEMENT OF NEONATAL SEIZURES
DURING ACUTE PHASE
GENERAL MEASURES :
OPTIMISE : Ventilation, Circulation,
Electrolytes,
Acid-Base Balance
NONEPILEPTIC
EVENTS : Associated with No EEG
Seizure Activity. These
Types of Neonatal
Seizures Should not be Treated.
EPILEPTIC
EVENTS : Associated with EEG Seizure
Activity
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MANAGEMENT – Contd.. SPECIFIC MEASURES
Identify the Cause & Treat
IF HYPOGLYCEMIA IS PRESENT
↓
ADMINISTER BY I.V. 2-4 ml of 25% DEXTROSE
↓
If There Is No Seizures
Stop Further Management
Monitor Vital Signs
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MANAGEMENT – Contd.. If the Convulsions Persist
↓
Inj. Phenobarbitone 20mg/kg by IV
Given over to 10 mints.
↓
Wait for 30 Mts. if the convulsion
Still Persists
↓
Inj. Phenobarbitone 10mg/kg is given
As IInd Dose.
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MANAGEMENT – Contd.. If there is further convulsion repeat inj. Phenobarbitone
10mg/kg by I.V. as third Dose (Cumulative dose of 40 mg/kg) consider omission of this additional phenobarbitol if the infant is severely Asphyxiated.
+
Administer Inj. Phenytoin sodium concomitantly 15-20 Mg/kg diluted in Normal Saline (1mg/kg/mt) followed by Maintenance Dose of Inj. Phenytoin & Phenobarbitone Alternatively
↓
Even then if the convulsions persists inj. Lorazepam 0.05 to 0.1 mg/kg/by I.V. is Administered.
(Contd..) www.similima.com 16
MANAGEMENT – Contd.. (or)
Inj. Clonzepam Loading dose of 0.25 mg/kg followed by 0.01 to 0.03 mg/kg/orally given
(or)
Inj. Midazolam 0.02 to 0.1 mg/kg - I.V. can be given
DIAZEPAM : Not safe in neonates as it interferes with vital functions its sedative effect half life exceeds 24 hours
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MANAGEMENT – Contd..
I.V. DIAZEPAM
↓
Ends you in trouble
↓
answerable for three generations
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MANAGEMENT – Contd..
OTHER MEDICATIONS
Calcium : 10% Cal. Gluconate 2 ml/kg mixed
with equal amount of 10% dextrose given by
slow I.V. over 3 mts.
Magnesium : Hypomagnesimia is treated with
50% magnesium sulphate 0.2 ml/kg
administered by IM route.
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DIAGNOSIS & MANAGEMENT OF
PDE
Failure of conventional AEDs
Pyridoxine 100 mg iv
Caution: May cause severe hypotonia, bradycardia,
apnea
Treat with daily B6, 200 mg/ day
B6 withdrawal challenge to confirm dx
Seizure recur in 7 days to 3 weeks
Restart B6
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PROGNOSIS OF NEONATAL SEIZURES
IN RELATION TO ETIOLOGY
Etiology Normal Development (%)
Hypoxic Ischemic Encephalopathy
16-50
Hemorrhage
a) Intraventricular
b) Sub Arachnoid
0-10
85-90
Bacterial Meningitis 25-65
Development Defect 0-5
Hypocalcemia
Early Onset
Late Onset
42-50
91-100
Hypoglycemia 25-50
Unknown 50-62
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EEG BACKGROUND SCORES
Normal
Mildly abnormal
Moderately Abnormal
Low – Voltage Undifferentiated
Suppression – Burst Pattern
Electrocerebral Inactivity
Better
Worse
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DURATION OF ANTICONVULSANT
THERAPY GUIDELINES
NEONATAL PERIOD
- If neonatal Neurologic examination becomes normal, discontinue therapy.
- If Neonatal Neurologic examination is persistently abnormal, consider etiology & obtain EEG.
- In most such cases. - Continue Phenobarbital - Discontinue phenytoin - Re-evaluate in 1 month.
1 Month After Discharge
- If neurologic examination has become normal, discontinue Phenobarbital If neurologic examination is persistently abnormal, obtain EEG. If no seizure activity on EEG, discontinue Phenobarbital
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EPILEPSY AFTER NEONATAL
SEIZURES
Overall, 15 – 30% develop seizures later in life
Again, depends on the cause of neonatal
seizures
Hypoxic – ischemic brain injury 30%
Cortical dysgenesis 100%
Hypocalcemia, late 0%
Other factors include neurologic examination and
neonatal EEG
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CONCLUSION Neonates with seizures require unique
Diagnostic & Perspective considerations compared with Older Infants and Children. Neurophysiologic evaluation preferably with EEG / Video polygraphic monitoring is required for accurate Detection & Classification
Fetal (or) Neonatal Disease states may contribute to seizure Occurrence in later years. Hence the main aim should be to control the seizure with Anti-convulsants at any cost apart from treating the underlying cause.
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Thank you
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