Neonatal seizures by Dr. David Maher
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This document discusses neonatal seizures including their classification, causes, clinical presentation, evaluation, and treatment. It notes that neonatal seizures are a sign of neurological dysfunction in newborns and outlines their main etiologies such as hypoxic ischemic encephalopathy, intracranial hemorrhage, and metabolic disturbances. The document also describes different seizure types including subtle, tonic, clonic, and myoclonic seizures. Evaluation involves history, examination, laboratory and imaging workup. Treatment focuses on identifying and correcting the underlying cause as well as using antiepileptic medications to stop seizure activity.
Neonatal seizures by Dr. David Maher
- 2. Paroxysmal alteration in neurological function (i.e., behavioral, motor, or autonomic function). A signal of neurological disease: Most distinctive indicator of neurological problem in newborn period
- 3. 1.PathophysiologicaL. 2.Etiological. 3. Classification acc. to age of onset 4. Clinical.
- 4. 1.Epileptic seizures: originates from cortical neurons and are associated with corresponding EEG seizure activity. 2.Non-epileptic seizures: initiated in the sub- cortical area and are not usually associated with EEG changes.
- 5. Common causes: 1. Hypoxic ischemic encephalopathy: the most common cause represent 25-40% of neonatal seizures. 2. Focal ischemic injury:2nd most common cause esp. in FT it’s cause still unclear. 3. Intracranial Hge:10% of causes of seizures it may be subarachnoid, subdural, periventricular or intraventricular hge.
- 6. 4.Transient metabolic disturbance:5% of seizures Hypoglycemia.(<40 mg/dl in 1st 24 hr and <50 after 24 hr) Hypocalcemia. Hypo or hypernatremia. Pyridoxine dependence. Hypomagnesemia 5.CNS infection:5% of seizures Meningitis Sepsis TORCH
- 7. 1.Inborn error of metabolism: Aminoacidopathies Organic aciduria Peroxisomal disorders Disorder of glucose transport (GLUT-1 deficiency) 2.Congenital brain anomalies: Cerebral dysgenesis Neurological disorders (Sterge –Weber syndrome -tuberous sclerosis) 3.Epileptic syndromes 4.Maternal drug withdrawal: Herion, barbiturates, cocaine. 5.Kernictrus. 6.Drug toxicity. 7.CNS trauma. 8.Polythythemia. 9.Hydrocephalus 10.Folinic acid responsive seizures
- 8. Benign Familial Neonatal Convulsions (BFNC): 1. Occur in otherwise well infants on day 2 or 3 of life, family history usually unreported 2. Seizures may be focal clonic or tonic usually asymmetrical ,resolve after variable period within 6 months 3. Developmental outcome is normal, but 5- 10% may have later non febrile convulsions
- 9. Benign Idiopathic Neonatal Seizures (BINS or Fifth-day fits): Suddenly appear on day 4-6 of life Often with frequent seizures leading to status epilepticus Seizures are initially focal clonic often with apnea .tonic seizures are not expected in this disorder Seizures often cease within 2 weeks The etiology is not known
- 10. Early myoclonic encephalopathy (EME): Usually present in the first few days of life Focal motor seizures and myoclonus, which may be subtle and erratic and usually affect the face and limbs. tonic convulsions appear late in this disease Seizures are very refractory to ttt EEG ccc by brust-supression pattern may be seen during sleep It is often associated with underlying metabolic disorder Development is severely affected and may infant die ,often within their first year
- 11. Early infantile epileptic encephalopathy (Ohtahara syndrome): Usually associated with very refractory epilepsy. It is ccc by early onset of tonic spasms along with focal motor seizures. Myoclonus is rare in the early stages EEG show a burst suppression pattern Usually associated with structural lesions Developmental prognosis is very poor Accompanied by infantile spasms
- 12. In the first 24 hr HIE Sepsismeningitis Metabolic Pyridoxine dep(min-3days) Drug withdrawal. Intracranial Hge. local anesthetic intoxication Intrauterine infection. Cerebral trauma. Cerebral infection. Within 24-72 hr: Sepsismeningitis. In PT :IVH In FT: infarction, venous thrombosis. Metabolic problems late onset. Cerebral dysgenesis. Inborn metabolic errors. Maternal substance abuse Subdural Hge
- 13. 1. Subtle 2. Tonic 3. Clonic 4. Myoclonic 5. Autonomic
- 14. They are not clearly tonic ,clonic,or myoclonic More common in PT than in FT EEG changes in PT > FT They consist of : 1.Tonic horizontal deviation of the eyes with or without jerking: eyelid blinking or fluttering 2.Sucking ,smacking or drooling 3.swimming,rowing or pedaling movement 4.Apneic spells: must be accompanied with
- 15. EEG changes to be differentiated from non- convulsive apneas (due to sepsis ,lung disease, or metabolic abnormality). N.B. convulsive apnea is usually preceded or accompanied by other subtle manifestations. In PT apnea is less likely to be a manifestation of seizures
- 16. More common in FT>PT Commonly associated with EEG changes 2 types: Focal clonic: well localized ,rhythmic, biphasic with a fast contraction and slow relaxation movement involving the face and upper or lower extremities on one side of the body or the neck or trunk on one side of the body, infants are usually not unconscious during or after the seizures. Multi focal: several body parts in a sequential fashion(LT arm followed by RT leg jerking)
- 17. Occur 1ry in PT Focal seizures: sustained posturing of a limb, asymmetric posturing of the trunk or neck ,or both, this usually associated with EEG changes Generalized seizures: most commonly ,these occur with tonic extension of both upper and lower extremities (as in decerebrate posturing) but may occur with tonic flexion of the upper extremities (as in decorticate posturing. It is uncommon to see EEG seizure disorder
- 18. Seen both in FT and PT CCC by single or multiple synchronous jerks Focal seizures: involves the flexor muscles of UL and not commonly associated with EEG activity Multifocal: exhibit asynchronous twitching of several parts of the body and are not commonly associated with EEG activity Generalized: present with bilateral jerks of flexion of UL and sometimes LL .they are commonly associated with EEG activity
- 19. Such as apnea, often associated with tachycardia rather than bradycardia (particularly in term
- 20. 1.Jitterness: Symmetrical rapid fine movements of the hands and feet not jerky. Stimulus sensitive: it can be initiated by sudden movement or noise. Contain movements with low amplitude & high frequency No abnormal eye movements No autonomic changes Movements cease with passive flexion or when grasped EEG is normal
- 21. 2.Benign myoclonic activity: Benign isolated jerky non-repetitive movements of an extremity or other part of the body occur mainly during sleep.
- 23. Family history: Positive family history of neonatal seizures is usually obtained in cases of metabolic errors and benign familial neonatal convulsions. Maternal drug history :in cases of narcotic withdrawal syndrome. Delivery: 1. regarding maternal anesthesia 2. the mode and nature of delivery 3. the fetal intrapartum status 4. the resuscitative measures used ,Apgar score 5. Information regarding maternal infections during pregnancy
- 24. 1.A thorough general examination: Gestational age. Vital signs: temp, BP, HR, RR. Presence of skin lesions. Presence of HSM. 2.Neurological examination: Level of consciousness, AF level, HC Cranial nerves Motor functions Primary neonatal reflexes
- 25. Sensory functions Eye exam :pupillary size, reaction to light, extraoccular movement, Fundus exam for retinal Hge, chorioretinitis. Changes in muscle tone 3.Seizure pattern: The site of onset Spread Nature Duration Level of consciousness.
- 26. Initial Work-Up Blood gas and check blood glucose Basic metabolic panel (serum glucose ,serum electrolytes; sodium, potassium, calcium total and ionized, magnesium, BUN, creatinine) CBC with differential, (blood,urine,and CSF culture and sensitivity), TORCH screen LP Coagulation studies Urine drug screen Studies for inborn error : ammonia ,lactate, AA in urine
- 27. Cranial ultrasound: detect perventricular and intraventricular Hge Cranial CT: diagnose subarachnoid or subdural Hge,congenital malformation and cerebral infarction MRI: diagnose cerebral infarction Routine EEG: normal in 1/3 of cases video EEG better
- 28. The first step in treatment is to identify and treat the underlying cause ABC to ensure oxygenation and ventilation and correct any metabolic acidosis and check RBS. Hypoglycemia: (D10W) 2-4 ml/kg IV bolus followed by continuous IV infusion If no hypoglycemia start Phenobarbital: 20 mg/kg IV loading dose given slowly over 10-15 min consider additional dose : 5-10 mg /kg IV to a max of 40 mg / kg Maintenance dose :3-5 mg/kg/day/12hr Side effects: sedation, respiratory depression
- 29. If baby still convulsing Start phenytoin loading 15-20 mg/kg IV slowly over 10-15 min then maintenance 4-8mg /kg /day /12-8hrs IV (up to 8 mg/kg/dose/8 to 12 hr after one week of age) flush IV with saline before and after administration It is highly unstable in any iv solution, and avoid using in central lines because of risk of precipitation Side effects: cardiac arrhythmias, hypotension
- 30. If still convulsing: Midazolam (dormicum): loading dose 0.15mg /kg IV over at least 5 min then 0.06-0.4 mg/kg/hr infusion. Side effects: respiratory depression ,respiratory arrest, (severe hypotension and seizures if given rapidly). Diazepam(valium): 0.1- 0.3 mg/kg IV an infusion rate of 0.3mg/kg/hr Lorazepam:0.05-0.1 mg /kg /ds/8-12hr IV slow push can be repeated 4-6 times over 24 hr
- 31. If the baby still convulsing High dose phenobarbital (>30mg/kg to achieve serum level >60mic/ml) Pentobarbital:10 mg/kg IV then 1mg/kg/hr Thiopental:10mg/kg then 2-4mg/kg/hr Midazolam: 0.2 mg/kg, then 0.1 to 0.4 mg/kg per hour Clonazepam: 0.1 mg/kg Lidocaine: 2 mg/kg, then 6 mg/kg per hour Paraldehde:200-400mg/kg IV over 2hrs in D5 then 16mg/kg/hr
- 32. Newer drugs: Oral carbamazepine(10mg/kg initially then followed by 15-20 mg/kg/day) Valproic acid :10-25mg/kg, then 20mg/kg/ day/8hr Vigabatrin:50mg/kg/day/12hr up to 200mg /kg/day Lamotrigin :12.5mg in 2doses Toprimate:3mg/kg/day Levetiracetam:10mg/kg/day/12hr
- 33. Hypocalcemia: Calcium gluconate 10%, 1- 2ml/kg IV bolus (slow) (dilute 1:1 D 5%) Dose :100-200mg/kg of 10% IV over 1-3 minutes, followed by maintenance(50 mg/kg/6h) Hypomagnesemia: Magnesium sulfate 50%, 0.25 ml/kg IV bolus (slow) Dose : 25-250mg/kg/dose. HIE: usually in 1st 6-8 hrs after birth 1. Careful observation for seizures +supportive ttt 2. Prophylactic phenobarbital within 6 hrs 3. Fluid restriction to 60 ml/kg fup UOP and electrolytes 4. If seizures occurred ttt started
- 34. Pyridoxine(B6): 50-100mg IV with EEG monitoring seizures will subside within min then oral form is given as maintenance 50- 100mg/day every 24 hr TTT with folinic acid in refractory cases to anticonvulsants and pyridoxine start with 2.5mg /12hr for 24-48hr up to 8mg/kg/day TTT of hypo or hypernatremia TTT of infection: start with empiric broad spectrum anti- biotic till cultures results. Increase fluids or partial exchange in TTT of polythycemia
- 36. Critical determinant factors: Neonatal neurological examination Cause of the neonatal seizures EEG pattern
- 38. The major predictors: 1. Underlying etiology 2. EEG finding 3. Neurological exam finding 4. Neuroimaging finding The best prognosis in: 1. Hypocalcaemia 2. Pyridoxine dependency 3. Subarachnoid hge
- 39. The worst prognosis: 1. Brain malformation 2. Severe IVH 3. Prolonged or persistant hypoglycemia 4. Hypoxia Sequelae can include : 1. Chronic seizures 2. MR 3. CP