STATUS EPILEPTICUS.docx - Fiji National University


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STATUS EPILEPTICUS.docx - Fiji National University

  1. 1. 1 STATUS EPILEPTICUS May be definedasseizureactivitythatlastslongerthan30 minutesorrepeatedseizures between which the child does not return to the baseline level of consciousness. 2 categories Convulsive Non-convulsive Had prolong, generalizedtonic-clonicseizure or repetition of such seizure without a return o full consciousness between episodes Prolong twilight or semi-coma state  Epilepsiapartialiscontinua  Generalizedmyoclonus  Complex partial statusepilepticus –involveda small areaof the brain,normallythe temporal lobe  Absence statusepilepticus –generalizeseizure affectingwhole brain andresultinlonglasting stupor,staringand unresponse History In the initial presentationof statusepilepticus,adirected historysuffices.Obtainamore detailedhistoryafter stabilization,includingthe followingdetails:  The course of current seizure activity o Time and nature of onsetof seizure activity o Involvementof extremitiesorotherbodyparts o Nature of movements(eg,eye movements,flexion, extension,stiffeningof extremities),includingany focal movementsanddetailsof postictal neurologic deficit o Incontinence o Cyanosis(perioral orfacial) o Durationof seizure activitypriortomedical attention o Mental status aftercessationof seizure activity  Feveror intercurrentillnesses  Priorhistoryof seizures - If present,specify medications,anticonvulsantuse,andcompliance.  Headinjury(recentandremote)  Central nervoussystem(CNS)infectionordisease(eg, meningitis, neurocutaneous syndrome)  Intoxication or toxic exposure (see Causes for examples)  Other CNS abnormality (eg, ventricular-peritoneal shunt, prior CNS trauma)  Birth history and developmental delay (eg, anoxic encephalopathy, cerebral palsy)  Other medical history (eg, acquired immunodeficiency syndrome, systemic lupus erythematosus, type 1 diabetes mellitus) Physical Perform a rapid, directed physical and neurologic examination during status epilepticus, followed by a detailed examination when the child is stabilized.  Signs of sepsis or meningitis o Temperature more than 38.5°C; in patients younger than 2-3 months, more than 38.0°C o Respiratory distress o Cyanosis o Poor peripheral perfusion o Bulging fontanelles in infant o Meningismus (in children >12-18 mo) o Presence of petechiae or purpura, herpetic vesicles  Evidence of head or other CNS injury o Bradycardia, tachypnea, and hypertension (Cushing triad for signs of increased intracranial pressure) o Poor pupillary response o Asymmetry on neurologic examination o Abnormal posturing o Gross deformity or soft tissue injury to head  Hallmarks of neurocutaneous syndromes (eg, port wine stain)
  2. 2. 2 Causes  Neonates (first month of life) o Birth injury (eg, anoxia, hemorrhage) and congenital abnormalities o Metabolic disorders (eg, hypoglycemia, hypocalcemia, hyponatremia) and inborn errors of metabolism (eg, lipidoses, amino acidurias) o Infection (eg, meningitis)  Early childhood (<6 y) o Birth injury o Febrile convulsions (3 mo to 6 y) o Infection o Metabolic disorders o Trauma o Neurocutaneous syndromes o Cerebral degenerative diseases o Tumors o Idiopathic  Children and adolescents (>6 y) o Birth injury o Trauma o Infection o Epilepsy with inadequate drug levels o Cerebral degenerative disease o Tumor o Toxins o Idiopathic  Toxins and medications o Topical anesthetics (eg, lidocaine) o Anticonvulsant overdose o Camphor o Hypoglycemic agents (eg, insulin, ethanol) o Carbon monoxide o Cyanide o Heavy metals (eg, lead) o Pesticides (eg, organophosphate) o Cocaine o Phencyclidine o Belladonna alkaloids o Nicotine o Sympathomimetics (eg, amphetamines, phenylpropanolamine [recalled from US market]) o Tricyclic antidepressants Pathophysiology 1. ↑ majoraminoacidsexcitatoryneurotransmitters – glutamate,aspartate andacetylcholine 2. ↓majorinhibitoryneurotransmitterssuchasGamma aminobutyricacid(GABA),↓inhibitorof calciumion dependentpotassiumioncurrentand blockage of N- methyl-d-aspartate(NMDA) bymagnesium. Neuronsdepolarized Ca entercellsthruNMDA channels 3. Neuronal loss-occurineveryepisodes,especially prolong episodes Hypoxia, ↑variousproteinsthatcausesapoptosis Systemic complications 1. Hypoxemia– due to impairedventilation; ↑ oxygen consumption,excessivesalivationor tracheobronchial secretion;metabolicdisturbance (↓brainglucose,lacticacidosis,depletionof brain ATP);impairedmyocardial function,andhypotension 2. Acidemia- ↓pH<7.0 –lactic acidosisandrespiratory acidosis 3. Glucose alteration Release of catecholamine &sympatheticdischarge (RCSD) ---->↑bloodglucose Prolongseizures ---->↓bloodglucose 4. Blood Pressure ↑BP, ↑HR, ↑central venous pressure release of catecholamine & sympatheticdischarge Increase cerebral bloodflow (compensate forbrains↑metabolicneed) Prolongor persistseizure ↓BP, ↓CBTbut normal levels
  3. 3. 3 5. ↑intracranial pressure ↑ICP --->↓perfusion,metabolicacidosis,hyposemia,CO₂ retentionwithcompensatingcerebral vasodilation,and ↑CBT --->cerebral oedema 6. ↑peripheral white bloodcells 7. Generalisedmuscle contraction – increasedbody temperature 8. Rhabdomyolysis- Hyperkalemia;increaserelease of muscle enzymesandmyoglobinuria 9. Hypothension----->myoglobinuria---->acute renal faiture Investigations Initial investigations: Glucose,urea& creatinine,sodium,potassium, calcium Anti-epilepticdruglevels Complete bloodcount Oximetryorarterial bloodgases Urinalysis Furtherinvestigationsafterstabilization: 1. Liverfunctiontests 2. Magnesium 3. Toxicologyscreen 4. CT scan 5. Lumbar puncture 6. EEG  not all of the investigationsneedbe performedin everypatient;  selectiondependsonboththe patient'shistoryand presentation.MostpatientswithSEshouldhave aCT scan performedatsome stage butpatientswith establishedepilepsywhohave alreadyhada CT scan do notusuallyrequire anotherscan.  CNSinfection mustbe seriouslyconsideredinall patients,especiallyyoungchildrenwithafever. Lumbar puncture isindicatedinpatientswithfitsnot controlledwithabenzodiazepineandphenytoin,or evidence of craniofacialinfection(egotitis, mastoiditis),ornuchal rigidity.Itiscontraindicatedin those inwhoman intracranial space occupyinglesion issuspected.AlthoughCTscanningpriortolumbar puncture isnot considered,bysome,tobe mandatory,itshouldbe bourne inmindthat inadults CNStumoursare a more commoncause of epilepsy than CNSinfectionandthatlumbarpuncture isnever a life-savingprocedure.Ithasbeensuggestedthat, eveninsuspectedmeningitis,lumbarpuncture be delayedfor30 minutesaftera fitbecause of the transientcerebral oedemathataccompaniesafit. AlthoughCSFleucocytosisoccursin20% of patients withSE, patientswithCSFleucocytosisshouldbe treatedforsuspectedmeningitisuntil the diagnosisis excludedbymicrobiological culture orantibody assays. Management Prehospital Care  Secure the airway.  Administersupplemental 100% oxygen.  Infuse isotonicintravenousfluidsandglucose.  Immobilize the cervical spine inpatientswith possible trauma.  Consider rectally administered diazepam (0.5 mg/kg/dose) or intramuscularly administered midazolam (0.1-0.2 mg/kg/dose; not to exceed a cumulative dose of 10 mg).2 EmergencyDepartment Care The principles of treatment are to terminate the seizure while resuscitating the patient, treating complications, and preventing recurrence.  Assessment and stabilization of ABCs concurrent with management of the seizure is imperative. o Administer 100% oxygen by facemask, assist ventilation, and use artificial airways (eg, endotracheal intubation) as needed. Suction secretions and decompress the stomach with a nasogastric tube. o Immobilize the cervical spine if trauma is suspected. o Closely monitor vital signs, cardiorespiratory function, and oxygen saturation. o Perform rapid blood glucose assay (eg, Dextrostix) at bedside.  Establish intravenous access. Use intraosseous (IO) infusion if intravenous access is not immediately available in the child younger than 6 years. Most available anticonvulsants may be administered intravenously or intraosseously. o Infuse isotonic intravenous fluids 20 mL/kg with glucose (eg, 200 mL dextrose 5% in normal saline [D5NS] intravenously over 1 h for a 10-kg child). o Consider treatment with the following agents:
  4. 4. 4  Dextrose - 0.25-0.5 g/kg/dose (1-2 mL of 25% dextrose) intravenously for hypoglycemia; not to exceed 25 g/dose  Naloxone - 0.1 mg/kg/dose intravenously preferably (if needed may administer intramuscularly/subcutaneously) for narcotic overdose  Thiamine - 100 mg intramuscularly for possible deficiency  Pyridoxine - 50-100 mg intravenously/intramuscularly for possible deficiency  Antibiotics - If meningitis is strongly suspected, initiate treatment with antibiotics prior to cerebrospinal fluid (CSF) analysis or CNS imaging.  Administer anticonvulsant medication. The optimal protocol for management of status epilepticus begins with a benzodiazepine. In the United States, lorazepam is the first drug of choice in patients with intravenous or intraosseous access. For patients without parenteral access, intramuscular midazolam is best. If the seizures cease, no further drugs are immediately necessary, and the etiology of status epilepticus should be investigated. If seizures continue, administer intravenous phenytoin or parenteral fosphenytoin. If these are not effective, administer intravenous phenobarbital titrated to induce barbiturate coma. Finally, consider general anesthesia with pentobarbital or midazolam. o The goal is prompt cessation of seizure activity. Patiently allow infused anticonvulsants to act before using additional anticonvulsants. Proceed to the next drug if seizure activity continues. o Lorazepam (0.05-0.1 mg/kg intravenously/IO slowly infused over 2-5 min) has rapid onset and long duration of anticonvulsant action. It is preferred over diazepam. o Phenytoin (18-20 mg/kg intravenously/IO) or fosphenytoin (15-20 mg/kg intravenously/IO) loading doses: These long-acting anticonvulsants usually are infused if benzodiazepines do not stop the seizures. Phenytoin and fosphenytoin are effective for most idiopathic generalized seizures and for posttraumatic, focal, or psychomotor status epilepticus. Use a slow rate of infusion (<1 mg/kg/min or <50 mg/min) to avoid hypotension or cardiac arrhythmias. A full loading dose should be delivered unless the patient is known to have a current therapeutic level. o Midazolam (0.1-0.2 mg/kg intramuscularly) is most effective when intravenous or intraosseous access is not immediately available. Midazolam is the only benzodiazepine that can be administered safely intramuscularly with equivalent rapid onset and moderate duration of action. o Phenobarbital (20-25 mg/kg intravenously/IO) is effective for febrile and neonatal status epilepticus and may be infused after lorazepam or other benzodiazepines if the child is likely to have these types of seizures. Phenobarbital's major disadvantages are that it significantly depresses mental status and causes respiratory difficulty. Obtain serum anticonvulsant levels prior to administering additional long-acting anticonvulsants such as phenytoin or fosphenytoin.  General anesthesia o Pentobarbital (5-10 mg/kg intravenously/IO loading dose followed by 0.5-3 mg/kg/h) or midazolam (0.2 mg/kg intravenously/IO loading dose followed by 0.75- 10 mcg/kg/min) o All children must be intubated and paralyzed, have continuous cardiorespiratory and EEG monitoring, and be in a pediatric critical care setting. Consultations After initial emergency stabilization, consider consultation with the following specialists:  Pediatric emergency or critical care specialist or general pediatrician  Pediatric neurologist  Pediatric neurosurgeon if needed