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neonatal seizures IAP.pps.pptx presentation
- 1. NEONATAL SEIZURES Dr TSunitha reddy Associate Professor Pediatrics GMC, Suryapet
- 2. INTRODUCTION seizures are themost distinctive manifestation of neurologic dysfunction in the newborn infant. the decreased seizure threshold in the newborn is because of the over development of the excitatory systems compared to the inhibitory systems.
- 3. Neonatal Seizures: ASignal 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
- 4. INCIDENCE 3 / 1000full term infants 60 / 1000 preterm infants seizures are more common in the newborn period than at any other time in life
- 5. Pathogenesis OF NEONATALSEIZURES • 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.
- 6. Etiology of neonatalseizures 1)hypoxic ischemic encephalopathy 2)Focal ischemic injury -neonatal arterial stroke -cerebral vein thrombosis 3)intracranial hemorrhage- sub arachnoid hemorrhage 4)CNS infections 5)metabolic disturbance a)transient metabolic disturbances: hypoglycemia, hypocalcemia, hyponatremia b)inborn errors of metabolism: pyridoxin, folinic acid responsive seizures. 6)cerebral dysgenesis 7)epileptic syndromes a)benign familial neonatal seizures b)benign idiopathic neonatal seizures c)neonatal myoclonic encephalopathy d)ohtahara syndrome e)migrating partial seizures of infancy
- 7. CORRELATION OF TIMEOF 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
- 8. Types of NeonatalSeizures 1) SUBTLE SEIZURES • Eyes : sudden Sustained eye Opening with visual fixation, Ocular Movements, Blinking, Tonic eye Deviation • Oral : Chewing, Sucking, lip smacking movements associated with drooling • Apnea : Full Term ? Premature • Motor : Boxing, Hooking, Rotary Pedalling, Stepping movements of the Extremities • Autonomic : change in skin colour, Elevated Blood Pressure & Heart Rate In Premature Infants
- 9. CLINICAL SEIZURES -Contd.. 2) Clonic Seizures stereotypic and repetitive biphasic movements with fast contractions and slower relaxation phase • Focal : Involve face upper + /- lower extremities on one side “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.
- 10. CLINICAL SEIZURES -Contd.. 3) 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 infants are lethargic and obtunded in between seizures.
- 11. 4) Myoclonic seizuresCharacterised brief repeated extension and flexion movements and non rhythmic character. irregular and erratic • Multifocal :Asynchronous twitching of several parts of body. • Generalized :Bilateral jerks of upper and some times lower limbs associated with diffuse and serious brain damage associated with poor long term outcome.
- 12. NORMAL NEONATAL MOTORACTIVITY 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
- 13. CLINICAL CHARACTERISTICS WHICHDISTINGUISH 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 heart rate normal or bradycardia tachycardia
- 14. 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 in dianosis - neurosonogram, CT and MRI of brain
- 15. MANAGEMENT OF NEONATALSEIZURES DURING ACUTE PHASE GENERAL MEASURES : optimise: Ventilation, Circulation, Electrolytes,Acid-Base Balance exclusion or treatment of rapidly correctable conditions establishing the diagnosis of seizures by the clinical or EEG criteria specific therapies for treatable conditions like meningitis should be started but should not delay the start if anticonvulsant therapy.
- 16. MANAGEMENT – Contd.. step1 stabilisation of vital functions step2: correct transient metabolic disturbance HYPOGLYCEMIA(RBS<70mg/dl) I.V. 10% DEXTROSE 2ml/kg followed by continuous infusion at 8mg/kg/min HYPOCALCIMIA 5%calcium gluconate IV at 4ml/kg HYPOMAGNESEMIA: 50% MGSO4 IM at 0.2ml/kg
- 17. step 2 Ifthe 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. MANAGEMENT – Contd..
- 18. MANAGEMENT – Contd.. Ifthere 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..)
- 19. 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
- 20. DIAGNOSIS & MANAGEMENTOF PDE • Failure of conventional AEDs • Pyridoxine 50-100 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
- 21. DURATION OF ANTICONVULSANTTHERAPY 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
- 22. 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
- 23. EEG BACKGROUND SCORES •Normal • Mildly abnormal • Moderately Abnormal • Low – Voltage Undifferentiated • Suppression – Burst Pattern • Electrocerebral Inactivity Better Worse
- 24. PROGNOSIS OF NEONATALSEIZURES 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
- 25. CONCLUSION • Neonates withseizures 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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