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Status EpilepticusStatus Epilepticus
Dr. KalirattinameDr. Kalirattiname
DefinitionDefinition
Prolonged seizure activity lasting greaterProlonged seizure activity lasting greater
than 30 minutesthan 30 minutes
Or, recurrent seizures without the intervalOr, recurrent seizures without the interval
of recovery (consciousness) lastingof recovery (consciousness) lasting
greater than 30 minutesgreater than 30 minutes
RememberRemember
Most seizures are brief, lasting less than 5Most seizures are brief, lasting less than 5
minutesminutes
If a seizure is lasting greater than 10If a seizure is lasting greater than 10
minutes, are likely to be prolongedminutes, are likely to be prolonged
EpidemiologyEpidemiology
1/3 cases are due to acute insults to the1/3 cases are due to acute insults to the
brain, including meningitis, encephalitis,brain, including meningitis, encephalitis,
head trauma, hypoxia, hypoglycemia, drughead trauma, hypoxia, hypoglycemia, drug
intoxication or withdrawalintoxication or withdrawal
1/3 cases have a history of chronic1/3 cases have a history of chronic
epilepsy or febrile convulsionsepilepsy or febrile convulsions
1/3 of cases of new-onset epilepsy1/3 of cases of new-onset epilepsy
EtiologyEtiology
Idiopathic: no acute precipitating CNS orIdiopathic: no acute precipitating CNS or
metabolic insult– normal childmetabolic insult– normal child
Remote Symptomatic: no acuteRemote Symptomatic: no acute
precipitant, but prior CNS insult known toprecipitant, but prior CNS insult known to
increase seizure riskincrease seizure risk
Acute Symptomatic: an acute illness withAcute Symptomatic: an acute illness with
known CNS insult or metabolicknown CNS insult or metabolic
disturbancedisturbance
EtiologyEtiology
Progressive Encephalopathy: occurringProgressive Encephalopathy: occurring
with a known progressive neurologicalwith a known progressive neurological
disease- degenerativedisease- degenerative
Febrile: sole provocation is feverFebrile: sole provocation is fever
Precipitants of SE: stress, sleepPrecipitants of SE: stress, sleep
deprivation, fever, infections, misseddeprivation, fever, infections, missed
medications, medications that lower themedications, medications that lower the
seizure threshold, menstrual issues, andseizure threshold, menstrual issues, and
many othersmany others
PathophysiologyPathophysiology
Animal models with SE have shownAnimal models with SE have shown
irreversible neuronal damage occurs afterirreversible neuronal damage occurs after
30 minutes of continual convulsions30 minutes of continual convulsions
Neuronal damage occurs even whenNeuronal damage occurs even when
experimental animals are paralyzed andexperimental animals are paralyzed and
artificially ventilatedartificially ventilated
PathophysiologyPathophysiology
In these animals, in which adequateIn these animals, in which adequate
glucose levels have been maintained,glucose levels have been maintained,
these studies suggest although systemicthese studies suggest although systemic
complications such as hypoxia,complications such as hypoxia,
hypoglycemia, lactic acidosis, andhypoglycemia, lactic acidosis, and
especially hyperpyrexia may exacerbateespecially hyperpyrexia may exacerbate
the damage that results from sustainedthe damage that results from sustained
seizure activity, the seizure itself is aseizure activity, the seizure itself is a
substantial contributorsubstantial contributor
MortalityMortality
Determined largely by the underlyingDetermined largely by the underlying
etiology, but may be aggravated byetiology, but may be aggravated by
delayed or inadequate treatment whichdelayed or inadequate treatment which
prolongs the duration of the episodeprolongs the duration of the episode
In past, mortality rates in children haveIn past, mortality rates in children have
ranged from 6-18%ranged from 6-18%
More recent studies where patients haveMore recent studies where patients have
been treated aggressively, have mortalitybeen treated aggressively, have mortality
of 3-5%of 3-5%
MorbidityMorbidity
In one study, 9% of children suffered newIn one study, 9% of children suffered new
motor or cognitive deficits following SEmotor or cognitive deficits following SE
– However, only 1.5% of the patients withHowever, only 1.5% of the patients with
unprovoked (remote symptomatic orunprovoked (remote symptomatic or
idiopathic) or febrile status sustainedidiopathic) or febrile status sustained
neurologic sequellae attributable to the SEneurologic sequellae attributable to the SE
itselfitself
ClassificationClassification
Generalized Convulsive SE-Generalized Convulsive SE-
– 11°° or 2or 2°° GeneralizedGeneralized
– Bilateral tonic and clonic in some combination but notBilateral tonic and clonic in some combination but not
always symmetricalways symmetric
– Consciousness always impairedConsciousness always impaired
– Reasonable (but variable) post ictal periodReasonable (but variable) post ictal period
– Beware “burn out” - EEG can helpBeware “burn out” - EEG can help
– Most common and most dangerousMost common and most dangerous
Absence SE- nonconvulsiveAbsence SE- nonconvulsive
Complex Partial SE- nonconvulsiveComplex Partial SE- nonconvulsive
Simple Partial SESimple Partial SE
TreatmentTreatment
Step 1Step 1
ABCDEABCDE
– Maintain Airway- patient at risk for aspirationMaintain Airway- patient at risk for aspiration
– Breathing- place OBreathing- place O22, be ready for intubation, be ready for intubation
– Circulation- obtain IV accessCirculation- obtain IV access
– Dextrose: check glucose levelsDextrose: check glucose levels
– Electrolytes: check electrolytes (Na, Ca, Mg,Electrolytes: check electrolytes (Na, Ca, Mg,
POPO44), and anticonvulsent levels), and anticonvulsent levels
TreatmentTreatment
MedicationsMedications
Ideal drug for treating SEIdeal drug for treating SE
– Rapid entry into CNSRapid entry into CNS
– Rapid onset of actionRapid onset of action
– Long duration of actionLong duration of action
– SafetySafety
– Absence of sedationAbsence of sedation
– Useful as maintenance AEDUseful as maintenance AED
TreatmentTreatment
Step 2Step 2
Benzodiazepine TherapyBenzodiazepine Therapy
– DiazepamDiazepam
– LorazepamLorazepam
DiazepamDiazepam
Highly lipid solubleHighly lipid soluble
– Rapid CNS entry- stops seizures in 1-3 minutesRapid CNS entry- stops seizures in 1-3 minutes
Rapid redistribution in fatty tissuesRapid redistribution in fatty tissues
– Brain concentrations fall quicklyBrain concentrations fall quickly
– Duration of action is 15-30 minutesDuration of action is 15-30 minutes
– TT1/21/2= 30 hr= 30 hr
Dose: <3yrs, 0.5mg/kg, >3yrs, 0.3mg/kgDose: <3yrs, 0.5mg/kg, >3yrs, 0.3mg/kg
Side Effects: sedation, decreased respirationSide Effects: sedation, decreased respiration
and blood pressureand blood pressure
LorazepamLorazepam
Less lipid soluble than diazepamLess lipid soluble than diazepam
– Slower CNS, stops seizures in 6-10 minSlower CNS, stops seizures in 6-10 min
Not as rapidly redistributed to fat storesNot as rapidly redistributed to fat stores
– Longer duration of action 12-24 hrLonger duration of action 12-24 hr
– TT1/21/2 =14 hr=14 hr
Dose: 0.05—0.1mg/kgDose: 0.05—0.1mg/kg
Side Effects: decreased LOC, respiration andSide Effects: decreased LOC, respiration and
BPBP
TreatmentTreatment
Step 3Step 3
Phenytoin/FosphenytoinPhenytoin/Fosphenytoin
PhenytoinPhenytoin
IV dosing 20 mg/kg loadIV dosing 20 mg/kg load
Stops seizures in 10-30 minutesStops seizures in 10-30 minutes
Duration of action 24 hrs, T ½=24hrDuration of action 24 hrs, T ½=24hr
Max infusion rate of 1mg/kg/min, max- 50 mg/minMax infusion rate of 1mg/kg/min, max- 50 mg/min
Side Effects: arrhythmias, hypotension, wide QTSide Effects: arrhythmias, hypotension, wide QT
interval, phelibitisinterval, phelibitis
pH=11-12, may only give IV or popH=11-12, may only give IV or po
TreatmentTreatment
Step 3Step 3
Fosphenytoin- phenytoin prodrugFosphenytoin- phenytoin prodrug
IV dosing: 20 mg/kg loadIV dosing: 20 mg/kg load
Safer than phenytoinSafer than phenytoin
pH=8-9pH=8-9
May give IV or IMMay give IV or IM
May give faster than phenytoin(100-May give faster than phenytoin(100-
150mg/min)150mg/min)
Much more expensiveMuch more expensive
TreatmentTreatment
Step 4Step 4
PhenobarbitalPhenobarbital
– Lipid solubility < phenytoinLipid solubility < phenytoin
– Duration of action>48 hrs, TDuration of action>48 hrs, T1/2=1/2= 100 hours100 hours
– Dose 20 mg/kgDose 20 mg/kg
– Side Effects: sedation, decreased respirationSide Effects: sedation, decreased respiration
and BPand BP
– Be ready to intubate!!Be ready to intubate!!
TreatmentTreatment
Step 5Step 5
If you haven’t called Neurology, pleaseIf you haven’t called Neurology, please
call us!!!call us!!!
Consider IV Valproic Acid (Depacon)Consider IV Valproic Acid (Depacon)
– FDA approved only for replacement or oralFDA approved only for replacement or oral
dosingdosing
– Rapid loading dose appears safeRapid loading dose appears safe
– 25-30mg/kg rapidly infused25-30mg/kg rapidly infused
– Side Effects: dizziness, HA, nauseaSide Effects: dizziness, HA, nausea
Consider Keppra IV LoadConsider Keppra IV Load
– Off labelOff label
– I use 30mg /kg IV x1I use 30mg /kg IV x1
Refractory Status EpilepticusRefractory Status Epilepticus
Intubation, IV accessIntubation, IV access
Continuous EEG monitoringContinuous EEG monitoring
Medication ComaMedication Coma
– PentobarbitalPentobarbital
– MidazolamMidazolam
– PropofolPropofol
– Very high dose phenobarbVery high dose phenobarb
Consider the EtiologyConsider the Etiology
PE: focal – mass, traumaPE: focal – mass, trauma
Serum studies: electrolytes, LFTs, CBC,Serum studies: electrolytes, LFTs, CBC,
Cx, anticonvulsent levels, Tox screen,Cx, anticonvulsent levels, Tox screen,
follow u/a for possible rhabdomyolysisfollow u/a for possible rhabdomyolysis
Neuroimaging: plain CT of head (useNeuroimaging: plain CT of head (use
contrast if suspect brain tumor or AVM)contrast if suspect brain tumor or AVM)
Consider the EtiologyConsider the Etiology
LP: necessary for any febrile seizureLP: necessary for any febrile seizure
under the age of 18 monthsunder the age of 18 months
– Must strongly consider in comatose patient –Must strongly consider in comatose patient –
please check imaging firstplease check imaging first
– Remember SE can cause pleocytosis (usuallyRemember SE can cause pleocytosis (usually
< 20 cells)< 20 cells)
– Do not delay antimicrobial therapy if CNSDo not delay antimicrobial therapy if CNS
infection is suspectedinfection is suspected
– Consider acyclovirConsider acyclovir
SUMMARYSUMMARY
ABCDEABCDE
Lorazepam (0.1mg/kg) or DiazepamLorazepam (0.1mg/kg) or Diazepam
– Give 5 minute interval then may repeatGive 5 minute interval then may repeat
Fosphenytoin: 20mg/kg, may give additionalFosphenytoin: 20mg/kg, may give additional
10mg/kg after initial load10mg/kg after initial load
Phenobarb: 20mg/kg- be ready for intubationPhenobarb: 20mg/kg- be ready for intubation
If neurology not involved, call usIf neurology not involved, call us
Drug ComaDrug Coma

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Status epilepticus

  • 1. Status EpilepticusStatus Epilepticus Dr. KalirattinameDr. Kalirattiname
  • 2. DefinitionDefinition Prolonged seizure activity lasting greaterProlonged seizure activity lasting greater than 30 minutesthan 30 minutes Or, recurrent seizures without the intervalOr, recurrent seizures without the interval of recovery (consciousness) lastingof recovery (consciousness) lasting greater than 30 minutesgreater than 30 minutes
  • 3. RememberRemember Most seizures are brief, lasting less than 5Most seizures are brief, lasting less than 5 minutesminutes If a seizure is lasting greater than 10If a seizure is lasting greater than 10 minutes, are likely to be prolongedminutes, are likely to be prolonged
  • 4. EpidemiologyEpidemiology 1/3 cases are due to acute insults to the1/3 cases are due to acute insults to the brain, including meningitis, encephalitis,brain, including meningitis, encephalitis, head trauma, hypoxia, hypoglycemia, drughead trauma, hypoxia, hypoglycemia, drug intoxication or withdrawalintoxication or withdrawal 1/3 cases have a history of chronic1/3 cases have a history of chronic epilepsy or febrile convulsionsepilepsy or febrile convulsions 1/3 of cases of new-onset epilepsy1/3 of cases of new-onset epilepsy
  • 5. EtiologyEtiology Idiopathic: no acute precipitating CNS orIdiopathic: no acute precipitating CNS or metabolic insult– normal childmetabolic insult– normal child Remote Symptomatic: no acuteRemote Symptomatic: no acute precipitant, but prior CNS insult known toprecipitant, but prior CNS insult known to increase seizure riskincrease seizure risk Acute Symptomatic: an acute illness withAcute Symptomatic: an acute illness with known CNS insult or metabolicknown CNS insult or metabolic disturbancedisturbance
  • 6. EtiologyEtiology Progressive Encephalopathy: occurringProgressive Encephalopathy: occurring with a known progressive neurologicalwith a known progressive neurological disease- degenerativedisease- degenerative Febrile: sole provocation is feverFebrile: sole provocation is fever Precipitants of SE: stress, sleepPrecipitants of SE: stress, sleep deprivation, fever, infections, misseddeprivation, fever, infections, missed medications, medications that lower themedications, medications that lower the seizure threshold, menstrual issues, andseizure threshold, menstrual issues, and many othersmany others
  • 7. PathophysiologyPathophysiology Animal models with SE have shownAnimal models with SE have shown irreversible neuronal damage occurs afterirreversible neuronal damage occurs after 30 minutes of continual convulsions30 minutes of continual convulsions Neuronal damage occurs even whenNeuronal damage occurs even when experimental animals are paralyzed andexperimental animals are paralyzed and artificially ventilatedartificially ventilated
  • 8. PathophysiologyPathophysiology In these animals, in which adequateIn these animals, in which adequate glucose levels have been maintained,glucose levels have been maintained, these studies suggest although systemicthese studies suggest although systemic complications such as hypoxia,complications such as hypoxia, hypoglycemia, lactic acidosis, andhypoglycemia, lactic acidosis, and especially hyperpyrexia may exacerbateespecially hyperpyrexia may exacerbate the damage that results from sustainedthe damage that results from sustained seizure activity, the seizure itself is aseizure activity, the seizure itself is a substantial contributorsubstantial contributor
  • 9. MortalityMortality Determined largely by the underlyingDetermined largely by the underlying etiology, but may be aggravated byetiology, but may be aggravated by delayed or inadequate treatment whichdelayed or inadequate treatment which prolongs the duration of the episodeprolongs the duration of the episode In past, mortality rates in children haveIn past, mortality rates in children have ranged from 6-18%ranged from 6-18% More recent studies where patients haveMore recent studies where patients have been treated aggressively, have mortalitybeen treated aggressively, have mortality of 3-5%of 3-5%
  • 10. MorbidityMorbidity In one study, 9% of children suffered newIn one study, 9% of children suffered new motor or cognitive deficits following SEmotor or cognitive deficits following SE – However, only 1.5% of the patients withHowever, only 1.5% of the patients with unprovoked (remote symptomatic orunprovoked (remote symptomatic or idiopathic) or febrile status sustainedidiopathic) or febrile status sustained neurologic sequellae attributable to the SEneurologic sequellae attributable to the SE itselfitself
  • 11. ClassificationClassification Generalized Convulsive SE-Generalized Convulsive SE- – 11°° or 2or 2°° GeneralizedGeneralized – Bilateral tonic and clonic in some combination but notBilateral tonic and clonic in some combination but not always symmetricalways symmetric – Consciousness always impairedConsciousness always impaired – Reasonable (but variable) post ictal periodReasonable (but variable) post ictal period – Beware “burn out” - EEG can helpBeware “burn out” - EEG can help – Most common and most dangerousMost common and most dangerous Absence SE- nonconvulsiveAbsence SE- nonconvulsive Complex Partial SE- nonconvulsiveComplex Partial SE- nonconvulsive Simple Partial SESimple Partial SE
  • 12. TreatmentTreatment Step 1Step 1 ABCDEABCDE – Maintain Airway- patient at risk for aspirationMaintain Airway- patient at risk for aspiration – Breathing- place OBreathing- place O22, be ready for intubation, be ready for intubation – Circulation- obtain IV accessCirculation- obtain IV access – Dextrose: check glucose levelsDextrose: check glucose levels – Electrolytes: check electrolytes (Na, Ca, Mg,Electrolytes: check electrolytes (Na, Ca, Mg, POPO44), and anticonvulsent levels), and anticonvulsent levels
  • 13. TreatmentTreatment MedicationsMedications Ideal drug for treating SEIdeal drug for treating SE – Rapid entry into CNSRapid entry into CNS – Rapid onset of actionRapid onset of action – Long duration of actionLong duration of action – SafetySafety – Absence of sedationAbsence of sedation – Useful as maintenance AEDUseful as maintenance AED
  • 14. TreatmentTreatment Step 2Step 2 Benzodiazepine TherapyBenzodiazepine Therapy – DiazepamDiazepam – LorazepamLorazepam
  • 15. DiazepamDiazepam Highly lipid solubleHighly lipid soluble – Rapid CNS entry- stops seizures in 1-3 minutesRapid CNS entry- stops seizures in 1-3 minutes Rapid redistribution in fatty tissuesRapid redistribution in fatty tissues – Brain concentrations fall quicklyBrain concentrations fall quickly – Duration of action is 15-30 minutesDuration of action is 15-30 minutes – TT1/21/2= 30 hr= 30 hr Dose: <3yrs, 0.5mg/kg, >3yrs, 0.3mg/kgDose: <3yrs, 0.5mg/kg, >3yrs, 0.3mg/kg Side Effects: sedation, decreased respirationSide Effects: sedation, decreased respiration and blood pressureand blood pressure
  • 16. LorazepamLorazepam Less lipid soluble than diazepamLess lipid soluble than diazepam – Slower CNS, stops seizures in 6-10 minSlower CNS, stops seizures in 6-10 min Not as rapidly redistributed to fat storesNot as rapidly redistributed to fat stores – Longer duration of action 12-24 hrLonger duration of action 12-24 hr – TT1/21/2 =14 hr=14 hr Dose: 0.05—0.1mg/kgDose: 0.05—0.1mg/kg Side Effects: decreased LOC, respiration andSide Effects: decreased LOC, respiration and BPBP
  • 17. TreatmentTreatment Step 3Step 3 Phenytoin/FosphenytoinPhenytoin/Fosphenytoin PhenytoinPhenytoin IV dosing 20 mg/kg loadIV dosing 20 mg/kg load Stops seizures in 10-30 minutesStops seizures in 10-30 minutes Duration of action 24 hrs, T ½=24hrDuration of action 24 hrs, T ½=24hr Max infusion rate of 1mg/kg/min, max- 50 mg/minMax infusion rate of 1mg/kg/min, max- 50 mg/min Side Effects: arrhythmias, hypotension, wide QTSide Effects: arrhythmias, hypotension, wide QT interval, phelibitisinterval, phelibitis pH=11-12, may only give IV or popH=11-12, may only give IV or po
  • 18. TreatmentTreatment Step 3Step 3 Fosphenytoin- phenytoin prodrugFosphenytoin- phenytoin prodrug IV dosing: 20 mg/kg loadIV dosing: 20 mg/kg load Safer than phenytoinSafer than phenytoin pH=8-9pH=8-9 May give IV or IMMay give IV or IM May give faster than phenytoin(100-May give faster than phenytoin(100- 150mg/min)150mg/min) Much more expensiveMuch more expensive
  • 19. TreatmentTreatment Step 4Step 4 PhenobarbitalPhenobarbital – Lipid solubility < phenytoinLipid solubility < phenytoin – Duration of action>48 hrs, TDuration of action>48 hrs, T1/2=1/2= 100 hours100 hours – Dose 20 mg/kgDose 20 mg/kg – Side Effects: sedation, decreased respirationSide Effects: sedation, decreased respiration and BPand BP – Be ready to intubate!!Be ready to intubate!!
  • 20. TreatmentTreatment Step 5Step 5 If you haven’t called Neurology, pleaseIf you haven’t called Neurology, please call us!!!call us!!! Consider IV Valproic Acid (Depacon)Consider IV Valproic Acid (Depacon) – FDA approved only for replacement or oralFDA approved only for replacement or oral dosingdosing – Rapid loading dose appears safeRapid loading dose appears safe – 25-30mg/kg rapidly infused25-30mg/kg rapidly infused – Side Effects: dizziness, HA, nauseaSide Effects: dizziness, HA, nausea
  • 21. Consider Keppra IV LoadConsider Keppra IV Load – Off labelOff label – I use 30mg /kg IV x1I use 30mg /kg IV x1
  • 22. Refractory Status EpilepticusRefractory Status Epilepticus Intubation, IV accessIntubation, IV access Continuous EEG monitoringContinuous EEG monitoring Medication ComaMedication Coma – PentobarbitalPentobarbital – MidazolamMidazolam – PropofolPropofol – Very high dose phenobarbVery high dose phenobarb
  • 23. Consider the EtiologyConsider the Etiology PE: focal – mass, traumaPE: focal – mass, trauma Serum studies: electrolytes, LFTs, CBC,Serum studies: electrolytes, LFTs, CBC, Cx, anticonvulsent levels, Tox screen,Cx, anticonvulsent levels, Tox screen, follow u/a for possible rhabdomyolysisfollow u/a for possible rhabdomyolysis Neuroimaging: plain CT of head (useNeuroimaging: plain CT of head (use contrast if suspect brain tumor or AVM)contrast if suspect brain tumor or AVM)
  • 24. Consider the EtiologyConsider the Etiology LP: necessary for any febrile seizureLP: necessary for any febrile seizure under the age of 18 monthsunder the age of 18 months – Must strongly consider in comatose patient –Must strongly consider in comatose patient – please check imaging firstplease check imaging first – Remember SE can cause pleocytosis (usuallyRemember SE can cause pleocytosis (usually < 20 cells)< 20 cells) – Do not delay antimicrobial therapy if CNSDo not delay antimicrobial therapy if CNS infection is suspectedinfection is suspected – Consider acyclovirConsider acyclovir
  • 25. SUMMARYSUMMARY ABCDEABCDE Lorazepam (0.1mg/kg) or DiazepamLorazepam (0.1mg/kg) or Diazepam – Give 5 minute interval then may repeatGive 5 minute interval then may repeat Fosphenytoin: 20mg/kg, may give additionalFosphenytoin: 20mg/kg, may give additional 10mg/kg after initial load10mg/kg after initial load Phenobarb: 20mg/kg- be ready for intubationPhenobarb: 20mg/kg- be ready for intubation If neurology not involved, call usIf neurology not involved, call us Drug ComaDrug Coma