Downloaded 416 times
More Related Content
Similar to Neonatal seizures
Neonatal seizures
- 1. THE NICUPROTOCOLFOR NEONATAL SEIZURES Dr.C. Kannan Postgraduate Pediatrics MGMCRI
- 2. EPIDEMIOLOGY • Incidence • 10.3/1000(Term neonates) • 20.8/1000 (Preterm neonates) • 36.1/1000 (VLBW neonates • From NNPD; 2002-03
- 3. DEFINITIONS • Seizures • Paroxysmalalteration in neurological function • Motor/behavior/autonomic function • Epileptic seizures • Clinical seizures corresponding EEG seizure activity • Eg. Clonic seizures • Non epileptic seizures • Clinical seizures without EEG seizure activity • Eg. Subtle and generalised tonic seizures • EEG seizures • Abnormal EEG activity with no clinical correlation
- 4. ETIOLOGY Hypoxic-ischemic injury • Perinatalasphyxia Focal infarction • Arterial • Venous CNS infection • Escherichia coli/GBS/Listeria monocytogenes/HSV Intracranial hemorrhage • Intraventricular • Parenchymal • Subdural • Subarachnoid
- 5. Contd., Inborn errors ofmetabolism • Aminoacidopathies • Organic acidurias • Peroxisomal diseases • Mitochondrial disorders • Disorder of glucose transport (GLUT-1 deficiency) • Pyridoxine-dependent seizures • Folinic acid responsive seizures Acute metabolic disorders • Hypoglycemia • Hypocalcemia • Hypomagnesemia
- 6. Contd., Malformations and otherstructural lesions • Neuronal migration disorders • Cerebral dysgenesis • Neurocutaneous disorders, • E.g., Sturge-Weber syndrome, tuberous sclerosis Epilepsy syndromes • Benign familial syndromes • Severe neonatal epileptic encephalopathies • E.g., EIEE, Ohtahara syndrome, EME
- 7. NEUROTRANSMITTERS/RECEPTORS • GABA isa Inhibitory neurotransmitter • Glutamate is a excitatory neurotransmitter • GABA receptors • GABA-A/GABA-B(G-Protein coupled receptor)/GABA-C(Retina) • GABA-A is a part of GABA-A-BDZ-Cl channel complex • GABA binds to GABA-A receptors in brain • Increases duration of Cl channel opening • Causes CNS depression
- 8. PATHOPHYSIOLOGY • Excitatory andinhibitory processes in immature brain are • Unbalanced towards excitatory side • Glutaminergic synapses > GABA ergic synapses • GABA may temporarily act as an • Excitatory neurotransmitter via an • Alteration in chloride gradient and transportation • These developmental features are etiology for • High tendency of seizures in neonates • Reduced efficacy of GABA ergic drugs
- 9. TYPES OF SEIZURES •Subtle • Clonic • Tonic • myoclonic
- 10. SUBTLE SEIZURES Commonest type(50% of all seizures) Mild & often are missed Examples • Ocular • Tonic horizontal deviation of eyes • Sustained eye opening • Ocular fixation • Cycled fluttering • Oral-facial-lingual movements • Chewing/tongue-thrusting/lip smacking/etc.,
- 11. Contd., • Limb movements •Cycling/paddling/boxing-jabs/etc., • Autonomic phenomena – Tachycardia/bradycardia • Apnea • Rare manifestation of seizures • Apnea due to seizures may have normal or increased HR
- 12. CLONIC SEIZURES • Rhythmicmovements of muscle groups • Both slow and fast components • 1-3 jerks/second • Associated with EEG changes • Best prognosis
- 13. TONIC SEIZURES • Sustainedflexion /extension of • Axial or appendicular muscles • Focal or generalised • May resemble • Decerebrate (tonic extension of all limbs) • Decorticate posturing (flexion of UL/extension of LL) • No EEG changes
- 14. MYOCLONIC SEIZURES • Single/multiplelightening fast jerks of UL/LL • How to differentiate from clonic seizures • More rapid speed • Absence of slow return • Predilection for flexor groups • EEG changes • Burst suppression pattern • Focal sharp waves • Hypsarrhythmia • Worst prognosis (Neurodevelopmental outcome )
- 15. APPROACH TO SEIZURES •History • Examination • Investigations
- 16. HISTORY Seizure history • Completedescription of seizures from parents • Eye/limb movements/skin colour change • Autonomic phenomena/consciousness • Day of life Antenatal history • Intrauterine infection/maternal diabetes/narcotic addiction • Sudden increase in fetal movements
- 17. Perinatal history • Perinatalasphyxia • Fetal distress/reduced fetal movements/instrumental delivery • Need for resuscitation/Apgar/cord pH (<7), base deficit (>10) • Pudental block for mid cavity forceps Feeding history • Lethargy/poor activity/drowsiness/vomiting • After initiation of DBF • Indicates IEM • Late onset hypocalcaemia • Due to top feeding with cow’s milk
- 18. Family history of •Consanguinity /seizures / mental retardation • Fetal/neonatal deaths – IEM • Seizures of either parent or sibling indicates • Benign familial neonatal convulsions
- 19. EXAMINATION Vital signs General examination •Gestation / birth weight / weight for age • Eg., seizure in a term well baby – SAH • Eg., seizure in a LGA baby – Hypoglycemia • Malformations / dysmorphic features
- 20. CNS examination • Consciousness– Alert / drowsy / comatose • Tone – hypo/hypertonia • Bulging anterior fontanel – S/O meningitis / ICH Systemic examination • Hepatosplenomegaly / abnormal urine odour S/O IEM • Neurocutaneous markers
- 21. INVESTIGATIONS Essential investigations • Bloodsugar / sodium / Ca / CSF / Cranial USG / EEG • CSF • Must in all cases (seizure – may be first sign of meningitis) • Even though other etiology is present ( eg., Hypoglycemia) • Can withhold • Severe cardiovascular compromise • Severe birth asphyxia • Do all other investigations • Even 1 or 2 were positive - Multiple etiologies may coexist
- 22. Additional investigations • Whodo not respond to Phenobarbitone + phenytoin (or) • Earlier in neonates with specific features • Neuroimaging • Screen for congenital infections (TORCH) • Screen for IEM (ABG if strongly suspected) Imaging • Cranial USG • Detects - IVH / Parenchymal bleed • Unable to detect SAH / SDH
- 23. • CT scan •Where etiology is not available • After first line of investigations • Diagnostic in SAH / Developmental malformations • MRI • Seizures resistant to usual AEDs • Diagnostic in • Cerebral dysgenesis / lissencephaly / neuronal migration defects
- 24. EEG • Has bothdiagnostic and prognostic role • For all neonates requiring AED therapy • Preferably done within first week of seizure • Atleast for one hour • Ictal EEG – suspected seizures / SZ in mu. relaxed neonates • Inter - Ictal EEG - For long term prognosis
- 25. • Background abnormalities •Burst suppression pattern Indicates for high risk for • Low voltage invariant pattern Neurological sequelae • Electro- cerebral inactivity aEEG • New method provides continuous monitoring of • Cerebral electrical activity at bedside • In critically sick NB
- 26. Screen for Congenitalinfections • TORCH / VDRL • HSM / thrombocytopenia / IUGR / SGA / chorioretinitis Metabolic screen • Blood & urine ketones / urine reducing substances / sr. NH3 • Anion gap / urine & plasma AAs / • Sr & CSF lactate pyruvate ratio
- 27. MANAGEMENT OF SEIZURES Initialmedical management • Nurse the baby in thermoneutral environment • Ensure TABC • Oxygen support / IV access / sampling within 2-5 mins • Brief relevant history • Quick clinical examination
- 28. Contd., Correction of hypoglycemia/ hypocalcaemia • If you suspect hypoglycemia & unable to investigate • Give 2 ml/kg of 10% D as bolus F/B 6-8 mg/kg/min as infusion • If hypoglycemia is excluded • NB should receive 2ml/kg of 10 % Ca IV over 10 mins • If hypocalcemia + • 8 ml/kg/d for 3 days • If SZ persists despite hypocalcemia correction • 0.25 ml/kg of 50% MgSO4 IM
- 29. AED Therapy • Evenwith single clinical seizure • SZ after the correction of Ca & sugar • Phenobarbitone • DOC in NS - Max. dose – 40 mg/kg • Loading - 20 mg/kg IV over 20mins (not faster than 1 mg/kg/min) • Half loading – 10mg/kg IV over 10 mins • If SZ reoccur after completion of loading • 2nd Half loading – 10 mg/kg IV over 10 mins • If SZ reoccur after completion of 1st half loading
- 30. • Maintenance: • 3-5mg/kg/day– 2divided doses – 12 hrs after Ld dose MOA of Phenobarbitone • Acts by 2 ways • Directly binds and activates GABA-A receptors • GABA Mimetic • Increases binding of GABA to GABA-A receptors • GABA Facilitatory • Increases duration of Cl ion channels • Causes CNS depression
- 31. Phenytoin • SZ aftermaximum dose of Phenobarbitone is used • Due to adverse effects of Phenobarbitone • Loading - 20 mg/kg IV over 20 mins • Dilute with normal saline (incompatible with dextrose) • Not faster than 1 mg/kg/min • Under cardiac monitoring • Half loading – 10mg/kg IV over 10 mins • If SZ reoccur after completion of loading • Maintenance: • 3-5mg/kg/day – 2-4 divided doses – 12 hrs after Ld dose
- 32. MOA of phenytoin •Inhibit the sodium channels when they are open • Prolong the inactivated stage of sodium channels • Na channels are refractory to stimulation • Until they reach closed/resting phase • Similar action is seen in • Carbamazepine • Valproate • Topiamate • Lamotrigine • Lacosamide
- 33. Benzodiazepines • Lorazepam &midazolam • Diazepam is avoided in neonates • Short antiepileptic effect/prolonged sedation • Narrow therapeutic index/Na benzoate as preservative • Lorazepam (0.05 mg/kg IV bolus over 2-5 mins) • longer duration/less adverse effects • Midazolam (0.15 mg/kg – bolus F/B infusion 0.1- 0.4 mg/kg/hr) • Faster acting than lorazepam • More sedation & resp. depression • Needs continuous monitoring
- 34. MOA of benzodiazepine •Acts by • Binding to BZD receptor (GABA-A-BDZ-Cl channel complex) • Increases binding of GABA to GABA-A receptors • GABA Facilitatory • Increases frequency of Cl ion channels • Causes CNS depression
- 35. Other AEDs (veryrare) • Lidocaine • Paraldehyde • Sodium valproate • Vigabatrin • Topiramate Other therapies • Pyridoxine/Folinic acid • Exchange transfusion
- 36. • Neonate withseizure Identify/characterize seizure ABCT secure IV line/sample • R/O or treat hypoglycemia/hypocalcemia SZ persisting • Phenobarbitone 20 mg/kg IV over 20 mins SZ persisting • Repeat Phenobarbitone 10 mg/kg IV over 20 mins SZ persisting • Repeat Phenobarbitone 10 mg/kg IV over 20 mins SZ persisting • Phenytoin 20 mg/kg over 20 mins with cardiac monitoring SZ persisting • Repeat phenytoin 10 mg/kg/dose SZ persisting • Lorazepam bolus F/B midazolam infusion, if needed SZ persisting • Other AEDs/pyridoxine/exchange transfusion SZ controlled • Wean AED slowly to maintenance Phenobarbitone
- 37. WHEN TO DISCONTINUEAED New born on AED Wean all AED except Phenobarbitone, once seizures controlled Perform neurological examination prior to discharge Normal Abnormal Stop Phenobarbitone continue PBN for 1 month Repeat neurological examination at 1 month Normal Abnormal Taper drugs over 2 wks Evaluate EEG 1. Normal EEG – taper drugs over 2 wks 2. Abnormal EEG continue drug reassess at 3 months
- 38.