Status Epilepticus

54
Generalized, Tonic-Clonic Generalized, Tonic-Clonic Status Epilepticus in Status Epilepticus in Children Children Heinrich Werner, MD Heinrich Werner, MD Pediatric Critical Care Pediatric Critical Care University of Kentucky University of Kentucky Children’s Hospital Children’s Hospital

Transcript of Status Epilepticus

Page 1: Status Epilepticus

Generalized, Tonic-Clonic Generalized, Tonic-Clonic Status Epilepticus in ChildrenStatus Epilepticus in Children

Heinrich Werner, MDHeinrich Werner, MD

Pediatric Critical CarePediatric Critical CareUniversity of Kentucky Children’s HospitalUniversity of Kentucky Children’s Hospital

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Status epilepticus

ObjectivesObjectivesObjectivesObjectives The participant will increase her/hisThe participant will increase her/his

ability to define status epilepticus using a ability to define status epilepticus using a practical, mechanistic approachpractical, mechanistic approach

ability to list probable causes for status ability to list probable causes for status epilepticus in childrenepilepticus in children

understanding of the pathophysiologic understanding of the pathophysiologic eventsevents

knowledge of treatment strategies for knowledge of treatment strategies for pediatric status epilepticuspediatric status epilepticus

The participant will increase her/hisThe participant will increase her/his

ability to define status epilepticus using a ability to define status epilepticus using a practical, mechanistic approachpractical, mechanistic approach

ability to list probable causes for status ability to list probable causes for status epilepticus in childrenepilepticus in children

understanding of the pathophysiologic understanding of the pathophysiologic eventsevents

knowledge of treatment strategies for knowledge of treatment strategies for pediatric status epilepticuspediatric status epilepticus

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Status epilepticus

Status epilepticus (SE) presents in a Status epilepticus (SE) presents in a multitude of multitude of formsforms, dependent on etiology and patient age , dependent on etiology and patient age (myoclonic, tonic, subtle, tonic-clonic, absence, (myoclonic, tonic, subtle, tonic-clonic, absence, complex partial etc.)complex partial etc.)

Generalized, tonic-clonic SE (GCSE) is the most Generalized, tonic-clonic SE (GCSE) is the most common form of SEcommon form of SE

The following presentation refers to The following presentation refers to generalized, generalized, tonic-clonic SEtonic-clonic SE

Status epilepticus (SE) presents in a Status epilepticus (SE) presents in a multitude of multitude of formsforms, dependent on etiology and patient age , dependent on etiology and patient age (myoclonic, tonic, subtle, tonic-clonic, absence, (myoclonic, tonic, subtle, tonic-clonic, absence, complex partial etc.)complex partial etc.)

Generalized, tonic-clonic SE (GCSE) is the most Generalized, tonic-clonic SE (GCSE) is the most common form of SEcommon form of SE

The following presentation refers to The following presentation refers to generalized, generalized, tonic-clonic SEtonic-clonic SE

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Status epilepticus

DefinitionDefinitionDefinitionDefinition

Conventional “textbook” definition of status Conventional “textbook” definition of status epilepticus:epilepticus:

Single seizure > 30 minutesSingle seizure > 30 minutes

Series of seizures > 30 minutes without full Series of seizures > 30 minutes without full recoveryrecovery

Conventional “textbook” definition of status Conventional “textbook” definition of status epilepticus:epilepticus:

Single seizure > 30 minutesSingle seizure > 30 minutes

Series of seizures > 30 minutes without full Series of seizures > 30 minutes without full recoveryrecovery

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Why 30 minutes ?Why 30 minutes ?Why 30 minutes ?Why 30 minutes ?

Animal experiments in the 1970s and 1980s had Animal experiments in the 1970s and 1980s had shown that ...shown that ...

… … neuronal injury could be demonstrated after neuronal injury could be demonstrated after 30 min of seizure activity, even while 30 min of seizure activity, even while maintaining respiration and circulationmaintaining respiration and circulation

Nevander G. Ann Neurol 1985;18(3):281-90.Nevander G. Ann Neurol 1985;18(3):281-90.

Animal experiments in the 1970s and 1980s had Animal experiments in the 1970s and 1980s had shown that ...shown that ...

… … neuronal injury could be demonstrated after neuronal injury could be demonstrated after 30 min of seizure activity, even while 30 min of seizure activity, even while maintaining respiration and circulationmaintaining respiration and circulation

Nevander G. Ann Neurol 1985;18(3):281-90.Nevander G. Ann Neurol 1985;18(3):281-90.

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Status epilepticus

More practical: Mechanistic More practical: Mechanistic definitiondefinition

More practical: Mechanistic More practical: Mechanistic definitiondefinition

GCSE is a condition which most likely will not GCSE is a condition which most likely will not terminate rapidly and / or spontaneouslyterminate rapidly and / or spontaneously

GCSE is a condition which requires prompt GCSE is a condition which requires prompt interventionintervention

Lowenstein DH. Epilepsia 1999Lowenstein DH. Epilepsia 1999

GCSE is a condition which most likely will not GCSE is a condition which most likely will not terminate rapidly and / or spontaneouslyterminate rapidly and / or spontaneously

GCSE is a condition which requires prompt GCSE is a condition which requires prompt interventionintervention

Lowenstein DH. Epilepsia 1999Lowenstein DH. Epilepsia 1999

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Status epilepticus

The longer SE persists,The longer SE persists,

the lower is the likelihood of spontaneous cessationthe lower is the likelihood of spontaneous cessationthe harder it is to controlthe harder it is to controlthe higher is the risk of morbidity and mortality the higher is the risk of morbidity and mortality

Bleck TP. Epilepsia 1999;40(1):S64-6Bleck TP. Epilepsia 1999;40(1):S64-6

The Status Epilepticus Working Party. Arch Dis Child 2000;83(5):415-9.The Status Epilepticus Working Party. Arch Dis Child 2000;83(5):415-9.

The longer SE persists,The longer SE persists,

the lower is the likelihood of spontaneous cessationthe lower is the likelihood of spontaneous cessationthe harder it is to controlthe harder it is to controlthe higher is the risk of morbidity and mortality the higher is the risk of morbidity and mortality

Bleck TP. Epilepsia 1999;40(1):S64-6Bleck TP. Epilepsia 1999;40(1):S64-6

The Status Epilepticus Working Party. Arch Dis Child 2000;83(5):415-9.The Status Epilepticus Working Party. Arch Dis Child 2000;83(5):415-9.

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Status epilepticus

Typical seizure durationTypical seizure durationTypical seizure durationTypical seizure duration

Children > 5 years:Children > 5 years:

Typical, generalized tonic-clonic seizure lasts < 5 minutesTypical, generalized tonic-clonic seizure lasts < 5 minutes

Young children and infants:Young children and infants:

Paucity of data. Suggested time frame for typical tonic-Paucity of data. Suggested time frame for typical tonic-clonic seizure : < 10-15 minutesclonic seizure : < 10-15 minutes

Reviewed in: Lowenstein DH. It's time to revise the definition of status epilepticus. Epilepsia Reviewed in: Lowenstein DH. It's time to revise the definition of status epilepticus. Epilepsia 1999;40(1):120-2.1999;40(1):120-2.

Children > 5 years:Children > 5 years:

Typical, generalized tonic-clonic seizure lasts < 5 minutesTypical, generalized tonic-clonic seizure lasts < 5 minutes

Young children and infants:Young children and infants:

Paucity of data. Suggested time frame for typical tonic-Paucity of data. Suggested time frame for typical tonic-clonic seizure : < 10-15 minutesclonic seizure : < 10-15 minutes

Reviewed in: Lowenstein DH. It's time to revise the definition of status epilepticus. Epilepsia Reviewed in: Lowenstein DH. It's time to revise the definition of status epilepticus. Epilepsia 1999;40(1):120-2.1999;40(1):120-2.

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Status epilepticus

Revised DefinitionRevised DefinitionRevised DefinitionRevised Definition

Generalized, convulsive Generalized, convulsive status epilepticusstatus epilepticus in in older children (> 5 years) refers to older children (> 5 years) refers to > 5 minutes > 5 minutes of continuous seizureof continuous seizure or or >>2 discrete seizures 2 discrete seizures with incomplete recovery of consciousnesswith incomplete recovery of consciousness

Patients with generalized seizure activity at Patients with generalized seizure activity at arrival in the ER are treated promptly arrival in the ER are treated promptly regardless of prior durationregardless of prior durationLowenstein DH, Bleck T, Macdonald RL. It's time to revise the definition of status epilepticus. Lowenstein DH, Bleck T, Macdonald RL. It's time to revise the definition of status epilepticus. Epilepsia 1999;40(1):120-2.Epilepsia 1999;40(1):120-2.

Generalized, convulsive Generalized, convulsive status epilepticusstatus epilepticus in in older children (> 5 years) refers to older children (> 5 years) refers to > 5 minutes > 5 minutes of continuous seizureof continuous seizure or or >>2 discrete seizures 2 discrete seizures with incomplete recovery of consciousnesswith incomplete recovery of consciousness

Patients with generalized seizure activity at Patients with generalized seizure activity at arrival in the ER are treated promptly arrival in the ER are treated promptly regardless of prior durationregardless of prior durationLowenstein DH, Bleck T, Macdonald RL. It's time to revise the definition of status epilepticus. Lowenstein DH, Bleck T, Macdonald RL. It's time to revise the definition of status epilepticus. Epilepsia 1999;40(1):120-2.Epilepsia 1999;40(1):120-2.

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Status epilepticus

CausesCausesCausesCausesFeverFeverMedication changeMedication changeUnknownUnknownMetabolicMetabolicCongenitalCongenitalAnoxicAnoxicOther Other (trauma, vascular, infection, (trauma, vascular, infection,

tumor, drugs)tumor, drugs)

FeverFeverMedication changeMedication changeUnknownUnknownMetabolicMetabolicCongenitalCongenitalAnoxicAnoxicOther Other (trauma, vascular, infection, (trauma, vascular, infection,

tumor, drugs)tumor, drugs)

36%36%

20%20%

9%9%

8%8%

7%7%

5%5%

15%15%

36%36%

20%20%

9%9%

8%8%

7%7%

5%5%

15%15%

DeLorenzo RJ. Epilepsia 1992;33 Suppl 4:S15-25DeLorenzo RJ. Epilepsia 1992;33 Suppl 4:S15-25

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Status epilepticus

Drugs which can cause seizuresDrugs which can cause seizuresDrugs which can cause seizuresDrugs which can cause seizures

AntibioticsAntibiotics PenicillinsPenicillins IsoniazidIsoniazid MetronidazoleMetronidazole

Anesthetics, narcoticsAnesthetics, narcotics Halothane, enfluraneHalothane, enflurane Cocaine, fentanylCocaine, fentanyl KetamineKetamine

AntibioticsAntibiotics PenicillinsPenicillins IsoniazidIsoniazid MetronidazoleMetronidazole

Anesthetics, narcoticsAnesthetics, narcotics Halothane, enfluraneHalothane, enflurane Cocaine, fentanylCocaine, fentanyl KetamineKetamine

PsychopharmaceuticalsPsychopharmaceuticals AntihistaminesAntihistamines AntidepressantsAntidepressants AntipsychoticsAntipsychotics PhencyclidinePhencyclidine Tricyclic antidepressantsTricyclic antidepressants

PsychopharmaceuticalsPsychopharmaceuticals AntihistaminesAntihistamines AntidepressantsAntidepressants AntipsychoticsAntipsychotics PhencyclidinePhencyclidine Tricyclic antidepressantsTricyclic antidepressants

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MortalityMortalityMortalityMortality

AdultsAdultsChildrenChildren

AdultsAdultsChildrenChildren

15 to 22%15 to 22%

3 to 15%3 to 15%

15 to 22%15 to 22%

3 to 15%3 to 15%

Reviewed in: Fountain NB. Epilepsia 2000;41 Suppl 2:S23-30Reviewed in: Fountain NB. Epilepsia 2000;41 Suppl 2:S23-30Reviewed in: Fountain NB. Epilepsia 2000;41 Suppl 2:S23-30Reviewed in: Fountain NB. Epilepsia 2000;41 Suppl 2:S23-30

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MortalityMortalityMortalityMortality

The primary determinant of mortality and The primary determinant of mortality and morbidity of SE in children is its etiologymorbidity of SE in children is its etiology

The greatest mortality and highest rate of The greatest mortality and highest rate of neurological deficits occurs when SE is caused neurological deficits occurs when SE is caused by an acute neurological condition (infection, by an acute neurological condition (infection, trauma, stroke)trauma, stroke)

The primary determinant of mortality and The primary determinant of mortality and morbidity of SE in children is its etiologymorbidity of SE in children is its etiology

The greatest mortality and highest rate of The greatest mortality and highest rate of neurological deficits occurs when SE is caused neurological deficits occurs when SE is caused by an acute neurological condition (infection, by an acute neurological condition (infection, trauma, stroke)trauma, stroke)

Mitchell WG. J Child Neurol 2002;17 Suppl 1:S36-43.Mitchell WG. J Child Neurol 2002;17 Suppl 1:S36-43.

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Status epilepticus

Prolonged seizuresProlonged seizuresProlonged seizuresProlonged seizures

Duration of seizureDuration of seizure

Life Life threateningthreatening

systemicsystemicchangeschanges

DeathDeathTemporaryTemporary

systemicsystemicchangeschanges

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Status epilepticus

RespiratoryRespiratoryRespiratoryRespiratory

Hypoxia and hypercarbiaHypoxia and hypercarbia Ventilation Ventilation

• (chest rigidity from muscle spasm)(chest rigidity from muscle spasm) Hypermetabolism Hypermetabolism

• (( O O22 consumption, consumption, CO CO22 production) production)

Poor handling of secretionsPoor handling of secretions Neurogenic pulmonary edema?

Hypoxia and hypercarbiaHypoxia and hypercarbia Ventilation Ventilation

• (chest rigidity from muscle spasm)(chest rigidity from muscle spasm) Hypermetabolism Hypermetabolism

• (( O O22 consumption, consumption, CO CO22 production) production)

Poor handling of secretionsPoor handling of secretions Neurogenic pulmonary edema?

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HypoxiaHypoxiaHypoxiaHypoxia

Hypoxia/anoxia markedly increase (triple?) Hypoxia/anoxia markedly increase (triple?) the risk of mortality in SEthe risk of mortality in SE

Seizures (without hypoxia) are much less Seizures (without hypoxia) are much less dangerous than seizures and hypoxiadangerous than seizures and hypoxia

Towne AR. Epilepsia 1994;35(1):27-34Towne AR. Epilepsia 1994;35(1):27-34

Hypoxia/anoxia markedly increase (triple?) Hypoxia/anoxia markedly increase (triple?) the risk of mortality in SEthe risk of mortality in SE

Seizures (without hypoxia) are much less Seizures (without hypoxia) are much less dangerous than seizures and hypoxiadangerous than seizures and hypoxia

Towne AR. Epilepsia 1994;35(1):27-34Towne AR. Epilepsia 1994;35(1):27-34

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Neurogenic Pulmonary EdemaNeurogenic Pulmonary EdemaNeurogenic Pulmonary EdemaNeurogenic Pulmonary EdemaRare complication of SE Rare complication of SE

in childrenin childrenLikely occurs as Likely occurs as

consequence of marked consequence of marked increase of pulmonary increase of pulmonary vascular pressure vascular pressure during SEduring SE

Rare complication of SE Rare complication of SE in childrenin children

Likely occurs as Likely occurs as consequence of marked consequence of marked increase of pulmonary increase of pulmonary vascular pressure vascular pressure during SEduring SE

Johnston SC. Postictal pulmonary edema requires pulmonary vascular pressure increases. Johnston SC. Postictal pulmonary edema requires pulmonary vascular pressure increases. Epilepsia 1996;37(5):428-32Epilepsia 1996;37(5):428-32Johnston SC. Postictal pulmonary edema requires pulmonary vascular pressure increases. Johnston SC. Postictal pulmonary edema requires pulmonary vascular pressure increases. Epilepsia 1996;37(5):428-32Epilepsia 1996;37(5):428-32

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AcidosisAcidosisAcidosisAcidosis

RespiratoryRespiratoryLacticLactic

Impaired tissue oxygenationImpaired tissue oxygenation Increased energy expenditureIncreased energy expenditure

RespiratoryRespiratoryLacticLactic

Impaired tissue oxygenationImpaired tissue oxygenation Increased energy expenditureIncreased energy expenditure

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HemodynamicsHemodynamicsHemodynamicsHemodynamics

Sympathetic overdrive Sympathetic overdrive Massive catecholamine / Massive catecholamine /

autonomic dischargeautonomic discharge HypertensionHypertension TachycardiaTachycardia High CVPHigh CVP

Sympathetic overdrive Sympathetic overdrive Massive catecholamine / Massive catecholamine /

autonomic dischargeautonomic discharge HypertensionHypertension TachycardiaTachycardia High CVPHigh CVP

ExhaustionExhaustion HypotensionHypotension HypoperfusionHypoperfusion

ExhaustionExhaustion HypotensionHypotension HypoperfusionHypoperfusion

0 min0 min 60 min60 min

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Cerebral blood flow - Cerebral OCerebral blood flow - Cerebral O22 requirement requirementCerebral blood flow - Cerebral OCerebral blood flow - Cerebral O22 requirement requirement

Blood pressureBlood pressure

Blood flowBlood flow

OO22 requirement requirement

Seizure duration

Hyperdynamic Exhaustion

Lothman E. Neurology 1990;40(5 Suppl 2):13-23.Lothman E. Neurology 1990;40(5 Suppl 2):13-23.

HyperdynamicHyperdynamic phasephase CBF meets CMROCBF meets CMRO22

Exhaustion phaseExhaustion phase CBF drops as CBF drops as

hypotension sets inhypotension sets in Autoregulation Autoregulation

exhaustedexhausted Neuronal damage Neuronal damage

ensuesensues

HyperdynamicHyperdynamic phasephase CBF meets CMROCBF meets CMRO22

Exhaustion phaseExhaustion phase CBF drops as CBF drops as

hypotension sets inhypotension sets in Autoregulation Autoregulation

exhaustedexhausted Neuronal damage Neuronal damage

ensuesensues

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Status epilepticus

GlucoseGlucoseGlucoseGlucoseG

luco

se

Seizure duration

30 min

SESE

SE + hypoxiaSE + hypoxia

Lothman E. Neurology 1990;40(5 Suppl 2):13-23.Lothman E. Neurology 1990;40(5 Suppl 2):13-23.

HyperdynamicHyperdynamic phasephase HyperglycemiaHyperglycemia

Exhaustion phaseExhaustion phase Hypoglycemia developsHypoglycemia develops Hypoglycemia appears Hypoglycemia appears

earlier in presence of earlier in presence of hypoxiahypoxia

Neuronal damage Neuronal damage ensuesensues

HyperdynamicHyperdynamic phasephase HyperglycemiaHyperglycemia

Exhaustion phaseExhaustion phase Hypoglycemia developsHypoglycemia develops Hypoglycemia appears Hypoglycemia appears

earlier in presence of earlier in presence of hypoxiahypoxia

Neuronal damage Neuronal damage ensuesensues

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HyperpyrexiaHyperpyrexiaHyperpyrexiaHyperpyrexia

Hyperpyrexia may develop during protracted Hyperpyrexia may develop during protracted SE, and aggravate possible mismatch of SE, and aggravate possible mismatch of cerebral metabolic requirement and substrate cerebral metabolic requirement and substrate deliverydelivery

Treat hyperpyrexia aggressivelyTreat hyperpyrexia aggressively Antipyretics, external coolingAntipyretics, external cooling Consider intubation, relaxation, ventilationConsider intubation, relaxation, ventilation

Hyperpyrexia may develop during protracted Hyperpyrexia may develop during protracted SE, and aggravate possible mismatch of SE, and aggravate possible mismatch of cerebral metabolic requirement and substrate cerebral metabolic requirement and substrate deliverydelivery

Treat hyperpyrexia aggressivelyTreat hyperpyrexia aggressively Antipyretics, external coolingAntipyretics, external cooling Consider intubation, relaxation, ventilationConsider intubation, relaxation, ventilation

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Blood leukocytosis (50% of children)Blood leukocytosis (50% of children)Spinal fluid leukocytosis (15% of children)Spinal fluid leukocytosis (15% of children) KK++

creatine kinasecreatine kinaseMyoglobinuriaMyoglobinuria

Blood leukocytosis (50% of children)Blood leukocytosis (50% of children)Spinal fluid leukocytosis (15% of children)Spinal fluid leukocytosis (15% of children) KK++

creatine kinasecreatine kinaseMyoglobinuriaMyoglobinuria

Other alterationsOther alterationsOther alterationsOther alterations

Blood leukocytosis (50% of children)Blood leukocytosis (50% of children)Spinal fluid leukocytosis (15% of children)Spinal fluid leukocytosis (15% of children) KK++

creatine kinasecreatine kinaseMyoglobinuriaMyoglobinuria

Blood leukocytosis (50% of children)Blood leukocytosis (50% of children)Spinal fluid leukocytosis (15% of children)Spinal fluid leukocytosis (15% of children) KK++

creatine kinasecreatine kinaseMyoglobinuriaMyoglobinuria

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Oxygen, oral airway. Suction. Avoid Oxygen, oral airway. Suction. Avoid hypoxia!hypoxia!

Consider bag-valve mask ventilation. Consider bag-valve mask ventilation. Consider intubationConsider intubation

IV/IO access. Treat hypotension, but NOT IV/IO access. Treat hypotension, but NOT hypertensionhypertension

Oxygen, oral airway. Suction. Avoid Oxygen, oral airway. Suction. Avoid hypoxia!hypoxia!

Consider bag-valve mask ventilation. Consider bag-valve mask ventilation. Consider intubationConsider intubation

IV/IO access. Treat hypotension, but NOT IV/IO access. Treat hypotension, but NOT hypertensionhypertension

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BBBB

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TreatmentTreatmentTreatmentTreatment

Arterial blood gas?Arterial blood gas? All children in SE develop acidosis. It often resolves rapidly All children in SE develop acidosis. It often resolves rapidly

with termination of SEwith termination of SE

Intubate?Intubate? It may be difficult to intubate a child with active seizuresIt may be difficult to intubate a child with active seizures Stop or slow seizures first, give OStop or slow seizures first, give O22, consider BVM , consider BVM

ventilationventilation If using paralytic agent to intubate, assume that SE If using paralytic agent to intubate, assume that SE

continuescontinues

Arterial blood gas?Arterial blood gas? All children in SE develop acidosis. It often resolves rapidly All children in SE develop acidosis. It often resolves rapidly

with termination of SEwith termination of SE

Intubate?Intubate? It may be difficult to intubate a child with active seizuresIt may be difficult to intubate a child with active seizures Stop or slow seizures first, give OStop or slow seizures first, give O22, consider BVM , consider BVM

ventilationventilation If using paralytic agent to intubate, assume that SE If using paralytic agent to intubate, assume that SE

continuescontinues

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Status epilepticus

Initial investigationsInitial investigationsInitial investigationsInitial investigations

LabsLabs Na, Ca, Mg, PONa, Ca, Mg, PO4 4 , glucose, glucose CBCCBC Liver function tests, ammoniaLiver function tests, ammonia Anticonvulsant drug levelAnticonvulsant drug level ToxicologyToxicology

LabsLabs Na, Ca, Mg, PONa, Ca, Mg, PO4 4 , glucose, glucose CBCCBC Liver function tests, ammoniaLiver function tests, ammonia Anticonvulsant drug levelAnticonvulsant drug level ToxicologyToxicology

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Initial investigationsInitial investigationsInitial investigationsInitial investigations

Lumbar punctureLumbar puncture Always defer LP in unstable patients, but never Always defer LP in unstable patients, but never

delay antibiotic/antiviral treatment if indicateddelay antibiotic/antiviral treatment if indicated

CT scanCT scan Indicated for focal seizures or focal deficit or focal Indicated for focal seizures or focal deficit or focal

EEG, history of trauma or bleeding disorderEEG, history of trauma or bleeding disorder

Lumbar punctureLumbar puncture Always defer LP in unstable patients, but never Always defer LP in unstable patients, but never

delay antibiotic/antiviral treatment if indicateddelay antibiotic/antiviral treatment if indicated

CT scanCT scan Indicated for focal seizures or focal deficit or focal Indicated for focal seizures or focal deficit or focal

EEG, history of trauma or bleeding disorderEEG, history of trauma or bleeding disorder

Treatment of convulsive status epilepticus. Recommendations of the Epilepsy Foundation of Treatment of convulsive status epilepticus. Recommendations of the Epilepsy Foundation of America's Working Group on Status Epilepticus. JAMA 1993;270(7):854-9.America's Working Group on Status Epilepticus. JAMA 1993;270(7):854-9.

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TreatmentTreatmentTreatmentTreatment

Give glucose Give glucose (2-4 ml/kg D25%, infants 5 ml/kg D10%),(2-4 ml/kg D25%, infants 5 ml/kg D10%), unless normo- or hyperglycemicunless normo- or hyperglycemic

Hyperglycemia has no negative effect in SE Hyperglycemia has no negative effect in SE (as long as significant hyperosmolality is being avoided)(as long as significant hyperosmolality is being avoided)

Give glucose Give glucose (2-4 ml/kg D25%, infants 5 ml/kg D10%),(2-4 ml/kg D25%, infants 5 ml/kg D10%), unless normo- or hyperglycemicunless normo- or hyperglycemic

Hyperglycemia has no negative effect in SE Hyperglycemia has no negative effect in SE (as long as significant hyperosmolality is being avoided)(as long as significant hyperosmolality is being avoided)

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TreatmentTreatmentTreatmentTreatment

The longer you wait to administer The longer you wait to administer anticonvulsants, the more anticonvulsants anticonvulsants, the more anticonvulsants you will need to stop SEyou will need to stop SE

Most common mistake is ineffective doseMost common mistake is ineffective dose

The longer you wait to administer The longer you wait to administer anticonvulsants, the more anticonvulsants anticonvulsants, the more anticonvulsants you will need to stop SEyou will need to stop SE

Most common mistake is ineffective doseMost common mistake is ineffective dose

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AnticonvulsantsAnticonvulsantsAnticonvulsantsAnticonvulsants

Rapid actingRapid acting

plusplus

Long actingLong acting

Rapid actingRapid acting

plusplus

Long actingLong acting

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Anticonvulsants - Rapid actingAnticonvulsants - Rapid actingAnticonvulsants - Rapid actingAnticonvulsants - Rapid acting

BenzodiazepinesBenzodiazepines Lorazepam 0.1 mg/kg i.v. over 1-2 minutesLorazepam 0.1 mg/kg i.v. over 1-2 minutes Diazepam 0.2 mg/kg i.v. over 1-2 minutesDiazepam 0.2 mg/kg i.v. over 1-2 minutes

If SE persists, repeat every 5-10 minutesIf SE persists, repeat every 5-10 minutes

BenzodiazepinesBenzodiazepines Lorazepam 0.1 mg/kg i.v. over 1-2 minutesLorazepam 0.1 mg/kg i.v. over 1-2 minutes Diazepam 0.2 mg/kg i.v. over 1-2 minutesDiazepam 0.2 mg/kg i.v. over 1-2 minutes

If SE persists, repeat every 5-10 minutesIf SE persists, repeat every 5-10 minutes

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BenzodiazepinesBenzodiazepinesBenzodiazepinesBenzodiazepines

DiazepamDiazepam High lipid solubilityHigh lipid solubility Thus very rapid onset Thus very rapid onset Redistributes rapidlyRedistributes rapidly Thus rapid loss of Thus rapid loss of

anticonvulsant effectanticonvulsant effect Adverse effects are Adverse effects are

persistent:persistent:• HypotensionHypotension

• Respiratory depressionRespiratory depression

DiazepamDiazepam High lipid solubilityHigh lipid solubility Thus very rapid onset Thus very rapid onset Redistributes rapidlyRedistributes rapidly Thus rapid loss of Thus rapid loss of

anticonvulsant effectanticonvulsant effect Adverse effects are Adverse effects are

persistent:persistent:• HypotensionHypotension

• Respiratory depressionRespiratory depression

LorazepamLorazepam Low lipid solubilityLow lipid solubility Action delayed 2 minutesAction delayed 2 minutes Anticonvulsant effect 6-12 hrsAnticonvulsant effect 6-12 hrs Less respiratory depression Less respiratory depression

than diazepamthan diazepam

MidazolamMidazolam May be given i.m.May be given i.m.

LorazepamLorazepam Low lipid solubilityLow lipid solubility Action delayed 2 minutesAction delayed 2 minutes Anticonvulsant effect 6-12 hrsAnticonvulsant effect 6-12 hrs Less respiratory depression Less respiratory depression

than diazepamthan diazepam

MidazolamMidazolam May be given i.m.May be given i.m.

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Benzodiazepine - RectalBenzodiazepine - RectalBenzodiazepine - RectalBenzodiazepine - Rectal

Rectal diazepamRectal diazepam 0.3 to 0.5 mg/kg rectal gel, typically reaches 0.3 to 0.5 mg/kg rectal gel, typically reaches

anticonvulsant levels within 5-10 minutesanticonvulsant levels within 5-10 minutes Intravenous solution given rectally is equally effectiveIntravenous solution given rectally is equally effective (and much cheaper)(and much cheaper) Seigler RS. J Emerg Med1990;8(2):155-9.Seigler RS. J Emerg Med1990;8(2):155-9.

Cost : Cost : • 5 mg Diastat rectal gel 5 mg Diastat rectal gel $ 78.00$ 78.00• 5 mg diazepam intravenous solution5 mg diazepam intravenous solution $ 1.40$ 1.40

Rectal diazepamRectal diazepam 0.3 to 0.5 mg/kg rectal gel, typically reaches 0.3 to 0.5 mg/kg rectal gel, typically reaches

anticonvulsant levels within 5-10 minutesanticonvulsant levels within 5-10 minutes Intravenous solution given rectally is equally effectiveIntravenous solution given rectally is equally effective (and much cheaper)(and much cheaper) Seigler RS. J Emerg Med1990;8(2):155-9.Seigler RS. J Emerg Med1990;8(2):155-9.

Cost : Cost : • 5 mg Diastat rectal gel 5 mg Diastat rectal gel $ 78.00$ 78.00• 5 mg diazepam intravenous solution5 mg diazepam intravenous solution $ 1.40$ 1.40

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Benzodiazepine - IntramuscularBenzodiazepine - IntramuscularBenzodiazepine - IntramuscularBenzodiazepine - Intramuscular

Intramuscular midazolamIntramuscular midazolam 0.2 mg/kg i.m. 0.2 mg/kg i.m. Aqueous solution is rapidly absorbed, anticonvulsant Aqueous solution is rapidly absorbed, anticonvulsant

effect begins after 2 minuteseffect begins after 2 minutes

Intramuscular lorazepamIntramuscular lorazepam Can be given, but lacks water solubility, thus later Can be given, but lacks water solubility, thus later

onset than midazolam onset than midazolam

Chamberlain JM. Pediatr Emerg Care 1997;13(2):92-4.Chamberlain JM. Pediatr Emerg Care 1997;13(2):92-4.

Towne AR. J Emerg Med 1999;17(2):323-8.Towne AR. J Emerg Med 1999;17(2):323-8.

Intramuscular midazolamIntramuscular midazolam 0.2 mg/kg i.m. 0.2 mg/kg i.m. Aqueous solution is rapidly absorbed, anticonvulsant Aqueous solution is rapidly absorbed, anticonvulsant

effect begins after 2 minuteseffect begins after 2 minutes

Intramuscular lorazepamIntramuscular lorazepam Can be given, but lacks water solubility, thus later Can be given, but lacks water solubility, thus later

onset than midazolam onset than midazolam

Chamberlain JM. Pediatr Emerg Care 1997;13(2):92-4.Chamberlain JM. Pediatr Emerg Care 1997;13(2):92-4.

Towne AR. J Emerg Med 1999;17(2):323-8.Towne AR. J Emerg Med 1999;17(2):323-8.

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Anticonvulsants - Long actingAnticonvulsants - Long actingAnticonvulsants - Long actingAnticonvulsants - Long acting

PhenytoinPhenytoin 20 mg/kg i.v. over 20 min20 mg/kg i.v. over 20 min

pH 12pH 12

Extravasation causes Extravasation causes severe tissue injurysevere tissue injury

Onset 10-30 minOnset 10-30 min May cause hypotension, May cause hypotension,

dysrhythmiadysrhythmia CheapCheap

PhenytoinPhenytoin 20 mg/kg i.v. over 20 min20 mg/kg i.v. over 20 min

pH 12pH 12

Extravasation causes Extravasation causes severe tissue injurysevere tissue injury

Onset 10-30 minOnset 10-30 min May cause hypotension, May cause hypotension,

dysrhythmiadysrhythmia CheapCheap

FosphenytoinFosphenytoin 20 mg PE/kg i.v. over 5-7 min 20 mg PE/kg i.v. over 5-7 min

PE = phenytoin equivalentPE = phenytoin equivalent

pH 8.6pH 8.6

Extravasation well toleratedExtravasation well tolerated Onset 5-10 minOnset 5-10 min May cause hypotensionMay cause hypotension ExpensiveExpensive

FosphenytoinFosphenytoin 20 mg PE/kg i.v. over 5-7 min 20 mg PE/kg i.v. over 5-7 min

PE = phenytoin equivalentPE = phenytoin equivalent

pH 8.6pH 8.6

Extravasation well toleratedExtravasation well tolerated Onset 5-10 minOnset 5-10 min May cause hypotensionMay cause hypotension ExpensiveExpensive

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If in doubt, measure free phenytoin!If in doubt, measure free phenytoin!If in doubt, measure free phenytoin!If in doubt, measure free phenytoin!

Phenytoin is largely protein bound Phenytoin is largely protein bound (> 90%, varies with serum protein concentration)(> 90%, varies with serum protein concentration)

Free phenytoin = active phenytoin Free phenytoin = active phenytoin (anticonvulsant and toxic effects)(anticonvulsant and toxic effects)

Toxicity more likely with hypoalbuminemia Toxicity more likely with hypoalbuminemia (usually if < 2 g/dL)(usually if < 2 g/dL)

Therapeutic levels Therapeutic levels TotalTotal phenytoin: 10 - 20 mcg/ml phenytoin: 10 - 20 mcg/ml FreeFree phenytoin: 0.8 - 1.6 mcg/ml phenytoin: 0.8 - 1.6 mcg/ml

Phenytoin is largely protein bound Phenytoin is largely protein bound (> 90%, varies with serum protein concentration)(> 90%, varies with serum protein concentration)

Free phenytoin = active phenytoin Free phenytoin = active phenytoin (anticonvulsant and toxic effects)(anticonvulsant and toxic effects)

Toxicity more likely with hypoalbuminemia Toxicity more likely with hypoalbuminemia (usually if < 2 g/dL)(usually if < 2 g/dL)

Therapeutic levels Therapeutic levels TotalTotal phenytoin: 10 - 20 mcg/ml phenytoin: 10 - 20 mcg/ml FreeFree phenytoin: 0.8 - 1.6 mcg/ml phenytoin: 0.8 - 1.6 mcg/ml

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Anticonvulsants - Long actingAnticonvulsants - Long actingAnticonvulsants - Long actingAnticonvulsants - Long acting

PhenobarbitalPhenobarbital 20 mg/kg i.v. over 10 - 15 min20 mg/kg i.v. over 10 - 15 min Onset 15-30 minOnset 15-30 min May cause hypotension, respiratory depressionMay cause hypotension, respiratory depression

PhenobarbitalPhenobarbital 20 mg/kg i.v. over 10 - 15 min20 mg/kg i.v. over 10 - 15 min Onset 15-30 minOnset 15-30 min May cause hypotension, respiratory depressionMay cause hypotension, respiratory depression

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Initial choice of long acting Initial choice of long acting anticonvulsants in SEanticonvulsants in SE

Initial choice of long acting Initial choice of long acting anticonvulsants in SEanticonvulsants in SE

Is patient an infant?Is patient an infant?Is patient already receiving phenytoin?Is patient already receiving phenytoin?

Is patient an infant?Is patient an infant?Is patient already receiving phenytoin?Is patient already receiving phenytoin?

YesYesNoNo

At high risk for extravasation ?At high risk for extravasation ?(small vein, difficult access etc.)?(small vein, difficult access etc.)?

PhenobarbitalPhenobarbital

YesYesNoNo

PhenytoinPhenytoin FosphenytoinFosphenytoin

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If SE persistsIf SE persistsIf SE persistsIf SE persistsPropofolPropofol infusion 5-10 mg/kg/hr after bolus 2 infusion 5-10 mg/kg/hr after bolus 2

mg/kgmg/kgMidazolamMidazolam infusion 1 - 10 mcg/kg/min after infusion 1 - 10 mcg/kg/min after

bolus 0.15 mg/kgbolus 0.15 mg/kgPentobarbitalPentobarbital infusion 1-3 mg/kg/hr after bolus infusion 1-3 mg/kg/hr after bolus

10 mg/kg10 mg/kgParaldehyde: no longer allowed for human useParaldehyde: no longer allowed for human useIsofluraneIsoflurane

PropofolPropofol infusion 5-10 mg/kg/hr after bolus 2 infusion 5-10 mg/kg/hr after bolus 2 mg/kgmg/kg

MidazolamMidazolam infusion 1 - 10 mcg/kg/min after infusion 1 - 10 mcg/kg/min after bolus 0.15 mg/kgbolus 0.15 mg/kg

PentobarbitalPentobarbital infusion 1-3 mg/kg/hr after bolus infusion 1-3 mg/kg/hr after bolus 10 mg/kg10 mg/kg

Paraldehyde: no longer allowed for human useParaldehyde: no longer allowed for human useIsofluraneIsoflurane

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Non - convulsive status epilepticusNon - convulsive status epilepticusNon - convulsive status epilepticusNon - convulsive status epilepticus

How do you tell that patient’s seizures have How do you tell that patient’s seizures have stopped?stopped?

How do you tell that patient’s seizures have How do you tell that patient’s seizures have stopped?stopped?

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Non - convulsive SE ?Non - convulsive SE ?Non - convulsive SE ?Non - convulsive SE ?

Neurologic signs after termination of SE are Neurologic signs after termination of SE are common:common: Pupillary changesPupillary changes Abnormal toneAbnormal tone Abnormal Babinski reflexAbnormal Babinski reflex PosturingPosturing ClonusClonus May be asymmetricalMay be asymmetrical

Neurologic signs after termination of SE are Neurologic signs after termination of SE are common:common: Pupillary changesPupillary changes Abnormal toneAbnormal tone Abnormal Babinski reflexAbnormal Babinski reflex PosturingPosturing ClonusClonus May be asymmetricalMay be asymmetrical

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Non - convulsive SE ?Non - convulsive SE ?Non - convulsive SE ?Non - convulsive SE ?

Up to 20% of children with SE have non - Up to 20% of children with SE have non - convulsive SE after tonic - clonic SEconvulsive SE after tonic - clonic SE

Particularly common in infants < 2 monthsParticularly common in infants < 2 months

Up to 20% of children with SE have non - Up to 20% of children with SE have non - convulsive SE after tonic - clonic SEconvulsive SE after tonic - clonic SE

Particularly common in infants < 2 monthsParticularly common in infants < 2 months

Mitchell WG. J Child Neurol 2002;17 Suppl 1:S36-43.Mitchell WG. J Child Neurol 2002;17 Suppl 1:S36-43.

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Non - convulsive SE ?Non - convulsive SE ?Non - convulsive SE ?Non - convulsive SE ?

If child does not begin to respond to painful If child does not begin to respond to painful stimuli within 20 - 30 minutes after tonic - stimuli within 20 - 30 minutes after tonic - clonic SE stops, suspect non - convulsive SEclonic SE stops, suspect non - convulsive SE Urgent EEGUrgent EEG

If child does not begin to respond to painful If child does not begin to respond to painful stimuli within 20 - 30 minutes after tonic - stimuli within 20 - 30 minutes after tonic - clonic SE stops, suspect non - convulsive SEclonic SE stops, suspect non - convulsive SE Urgent EEGUrgent EEG

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Case Scenario (1a)Case Scenario (1a)Case Scenario (1a)Case Scenario (1a)

A 2 y.o. boy arrives in your ER via ambulance, A 2 y.o. boy arrives in your ER via ambulance, with active seizures. Parents had called 911, with active seizures. Parents had called 911, crew found pt having generalized, tonic-clonic crew found pt having generalized, tonic-clonic seizureseizure

No drugs given yetNo drugs given yetWhat are your priorities?What are your priorities?

A 2 y.o. boy arrives in your ER via ambulance, A 2 y.o. boy arrives in your ER via ambulance, with active seizures. Parents had called 911, with active seizures. Parents had called 911, crew found pt having generalized, tonic-clonic crew found pt having generalized, tonic-clonic seizureseizure

No drugs given yetNo drugs given yetWhat are your priorities?What are your priorities?

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Case Scenario (1b) Case Scenario (1b) Case Scenario (1b) Case Scenario (1b)

A,B,C. Stopping seizure.A,B,C. Stopping seizure.With supplemental OWith supplemental O22, saturation signal comes and , saturation signal comes and

goes, but reads 100% when plethysmographic tracing goes, but reads 100% when plethysmographic tracing looks acceptable. Lips are pink. Child is moving air looks acceptable. Lips are pink. Child is moving air with proper head positioning and jaw thrustwith proper head positioning and jaw thrust

HR 145/min, BP 130/85HR 145/min, BP 130/85Several unsuccessful i.v. attempts, still trying after 5 Several unsuccessful i.v. attempts, still trying after 5

minutes. Continued seizure activityminutes. Continued seizure activity

What next?What next?

A,B,C. Stopping seizure.A,B,C. Stopping seizure.With supplemental OWith supplemental O22, saturation signal comes and , saturation signal comes and

goes, but reads 100% when plethysmographic tracing goes, but reads 100% when plethysmographic tracing looks acceptable. Lips are pink. Child is moving air looks acceptable. Lips are pink. Child is moving air with proper head positioning and jaw thrustwith proper head positioning and jaw thrust

HR 145/min, BP 130/85HR 145/min, BP 130/85Several unsuccessful i.v. attempts, still trying after 5 Several unsuccessful i.v. attempts, still trying after 5

minutes. Continued seizure activityminutes. Continued seizure activity

What next?What next?

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Case Scenario (1c)Case Scenario (1c)Case Scenario (1c)Case Scenario (1c)

Use alternate route for initial dose of Use alternate route for initial dose of benzodiazepinebenzodiazepine

A few minutes after midazolam 7.5 mg im, A few minutes after midazolam 7.5 mg im, seizures stop, but then start again. There was seizures stop, but then start again. There was time enough for one of your best nurses to insert time enough for one of your best nurses to insert a 24g iv catheter into the pt’s hand.a 24g iv catheter into the pt’s hand.

Vital signs unchangedVital signs unchangedEverybody looks to you for new ordersEverybody looks to you for new orders

Use alternate route for initial dose of Use alternate route for initial dose of benzodiazepinebenzodiazepine

A few minutes after midazolam 7.5 mg im, A few minutes after midazolam 7.5 mg im, seizures stop, but then start again. There was seizures stop, but then start again. There was time enough for one of your best nurses to insert time enough for one of your best nurses to insert a 24g iv catheter into the pt’s hand.a 24g iv catheter into the pt’s hand.

Vital signs unchangedVital signs unchangedEverybody looks to you for new ordersEverybody looks to you for new orders

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Case Scenario (1d)Case Scenario (1d)Case Scenario (1d)Case Scenario (1d)After two doses of lorazepam and initiation of 20 After two doses of lorazepam and initiation of 20

mg/kg fosphenytoin, the child stops convulsingmg/kg fosphenytoin, the child stops convulsingHe currently is unresponsive, RR 12/min, OHe currently is unresponsive, RR 12/min, O22Sat 100% Sat 100%

in oxygen, HR 115/min, BP 105/60in oxygen, HR 115/min, BP 105/60ABG drawn earlier (sent by RN, you had not asked ABG drawn earlier (sent by RN, you had not asked

for it): pH 7.02 pCOfor it): pH 7.02 pCO22 76 pO 76 pO22 95 BE - 8 95 BE - 8

What will you do ? Intubate (mental state, What will you do ? Intubate (mental state, pCOpCO22)? Give bicarb? Repeat ABG?)? Give bicarb? Repeat ABG?

After two doses of lorazepam and initiation of 20 After two doses of lorazepam and initiation of 20 mg/kg fosphenytoin, the child stops convulsingmg/kg fosphenytoin, the child stops convulsing

He currently is unresponsive, RR 12/min, OHe currently is unresponsive, RR 12/min, O22Sat 100% Sat 100%

in oxygen, HR 115/min, BP 105/60in oxygen, HR 115/min, BP 105/60ABG drawn earlier (sent by RN, you had not asked ABG drawn earlier (sent by RN, you had not asked

for it): pH 7.02 pCOfor it): pH 7.02 pCO22 76 pO 76 pO22 95 BE - 8 95 BE - 8

What will you do ? Intubate (mental state, What will you do ? Intubate (mental state, pCOpCO22)? Give bicarb? Repeat ABG?)? Give bicarb? Repeat ABG?

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Case Scenario (1e)Case Scenario (1e)Case Scenario (1e)Case Scenario (1e)

Combined metabolic/respiratory acidosis to be Combined metabolic/respiratory acidosis to be expected during SE. Does not dictate intubation, does expected during SE. Does not dictate intubation, does not require HCOnot require HCO33

As long as pt is oxygenating well, can wait for post-As long as pt is oxygenating well, can wait for post-ictal state to resolve, without further ABGictal state to resolve, without further ABG

If pt remains completely unresponsive 30 minutes If pt remains completely unresponsive 30 minutes after cessation of GCSE, suspect non-convulsive SEafter cessation of GCSE, suspect non-convulsive SE

Combined metabolic/respiratory acidosis to be Combined metabolic/respiratory acidosis to be expected during SE. Does not dictate intubation, does expected during SE. Does not dictate intubation, does not require HCOnot require HCO33

As long as pt is oxygenating well, can wait for post-As long as pt is oxygenating well, can wait for post-ictal state to resolve, without further ABGictal state to resolve, without further ABG

If pt remains completely unresponsive 30 minutes If pt remains completely unresponsive 30 minutes after cessation of GCSE, suspect non-convulsive SEafter cessation of GCSE, suspect non-convulsive SE

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Case Scenario (2a)Case Scenario (2a)Case Scenario (2a)Case Scenario (2a)

3 month old infant with a 4 day history of vomiting 3 month old infant with a 4 day history of vomiting and diarrhea. Parents tried to maintain hydration and diarrhea. Parents tried to maintain hydration using diluted formula , soda and now rice waterusing diluted formula , soda and now rice water

Lethargic all day, then started convulsingLethargic all day, then started convulsingActive, generalized tonic-clonic seizure on arrival in Active, generalized tonic-clonic seizure on arrival in

ERER

Your initial actions?Your initial actions?Possible cause?Possible cause?

3 month old infant with a 4 day history of vomiting 3 month old infant with a 4 day history of vomiting and diarrhea. Parents tried to maintain hydration and diarrhea. Parents tried to maintain hydration using diluted formula , soda and now rice waterusing diluted formula , soda and now rice water

Lethargic all day, then started convulsingLethargic all day, then started convulsingActive, generalized tonic-clonic seizure on arrival in Active, generalized tonic-clonic seizure on arrival in

ERER

Your initial actions?Your initial actions?Possible cause?Possible cause?

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Case Scenario (2b)Case Scenario (2b)Case Scenario (2b)Case Scenario (2b)Meningo-encephalitis? Sepsis? Electrolyte Meningo-encephalitis? Sepsis? Electrolyte

disturbance?disturbance?After you start high flow oxygen via a partial After you start high flow oxygen via a partial

rebreather mask, suction the airway and position the rebreather mask, suction the airway and position the head in mild hyperextension with jaw thrust, Ohead in mild hyperextension with jaw thrust, O22

saturation reads around 60%, and the child looks saturation reads around 60%, and the child looks blue. He is still seizing . You see no chest rise and hear blue. He is still seizing . You see no chest rise and hear no air entry.no air entry.

What is your plan of action?What is your plan of action?

Meningo-encephalitis? Sepsis? Electrolyte Meningo-encephalitis? Sepsis? Electrolyte disturbance?disturbance?

After you start high flow oxygen via a partial After you start high flow oxygen via a partial rebreather mask, suction the airway and position the rebreather mask, suction the airway and position the head in mild hyperextension with jaw thrust, Ohead in mild hyperextension with jaw thrust, O22

saturation reads around 60%, and the child looks saturation reads around 60%, and the child looks blue. He is still seizing . You see no chest rise and hear blue. He is still seizing . You see no chest rise and hear no air entry.no air entry.

What is your plan of action?What is your plan of action?

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Case Scenario (2c)Case Scenario (2c)Case Scenario (2c)Case Scenario (2c)Saturation improves to about 85% with BVM ventilation, the pt Saturation improves to about 85% with BVM ventilation, the pt

looks less blue but not pink. Fairly violent seizure activity looks less blue but not pink. Fairly violent seizure activity continues.continues.

Per your order, the first dose of lorazepam is going into the IV, but Per your order, the first dose of lorazepam is going into the IV, but pt continues to seize and is cyanoticpt continues to seize and is cyanotic

You give rocuronium 1 mg/kg rapidly iv, and expertly intubate the You give rocuronium 1 mg/kg rapidly iv, and expertly intubate the child. He is now being ventilated, pink and not seizing any morechild. He is now being ventilated, pink and not seizing any more

Good job! Anything else to be done? What information Good job! Anything else to be done? What information are you eagerly waiting for?are you eagerly waiting for?

Saturation improves to about 85% with BVM ventilation, the pt Saturation improves to about 85% with BVM ventilation, the pt looks less blue but not pink. Fairly violent seizure activity looks less blue but not pink. Fairly violent seizure activity continues.continues.

Per your order, the first dose of lorazepam is going into the IV, but Per your order, the first dose of lorazepam is going into the IV, but pt continues to seize and is cyanoticpt continues to seize and is cyanotic

You give rocuronium 1 mg/kg rapidly iv, and expertly intubate the You give rocuronium 1 mg/kg rapidly iv, and expertly intubate the child. He is now being ventilated, pink and not seizing any morechild. He is now being ventilated, pink and not seizing any more

Good job! Anything else to be done? What information Good job! Anything else to be done? What information are you eagerly waiting for?are you eagerly waiting for?

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Case Scenario (2d)Case Scenario (2d)Case Scenario (2d)Case Scenario (2d)

Have to assume ongoing electrical seizures. What Have to assume ongoing electrical seizures. What is the sodium?is the sodium?

Blood sugar is 180 mg/dL, Na is 118 mEq/LBlood sugar is 180 mg/dL, Na is 118 mEq/LNeuromuscular blockade is beginning to wear off, Neuromuscular blockade is beginning to wear off,

there is still seizure activitythere is still seizure activity

What now?What now?

Have to assume ongoing electrical seizures. What Have to assume ongoing electrical seizures. What is the sodium?is the sodium?

Blood sugar is 180 mg/dL, Na is 118 mEq/LBlood sugar is 180 mg/dL, Na is 118 mEq/LNeuromuscular blockade is beginning to wear off, Neuromuscular blockade is beginning to wear off,

there is still seizure activitythere is still seizure activity

What now?What now?

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Case Scenario (2e)Case Scenario (2e)Case Scenario (2e)Case Scenario (2e)

After 20 mg/kg phenobarbital, and halfway After 20 mg/kg phenobarbital, and halfway into an infusion of 3% NaCl, seizure activity into an infusion of 3% NaCl, seizure activity slows, and then stopsslows, and then stops

You consider a CT, plan an LP, start You consider a CT, plan an LP, start antibiotics antibiotics

You have a high index of suspicion for ongoing You have a high index of suspicion for ongoing electrical seizures (non-convulsive SE) in this electrical seizures (non-convulsive SE) in this infantinfant

After 20 mg/kg phenobarbital, and halfway After 20 mg/kg phenobarbital, and halfway into an infusion of 3% NaCl, seizure activity into an infusion of 3% NaCl, seizure activity slows, and then stopsslows, and then stops

You consider a CT, plan an LP, start You consider a CT, plan an LP, start antibiotics antibiotics

You have a high index of suspicion for ongoing You have a high index of suspicion for ongoing electrical seizures (non-convulsive SE) in this electrical seizures (non-convulsive SE) in this infantinfant

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Suggested ReadingSuggested ReadingSuggested ReadingSuggested Reading1. Fountain NB. Status epilepticus: risk factors and complications. Epilepsia

2000;41 Suppl 2:S23-30.2. Treatment of convulsive status epilepticus. Recommendations of the Epilepsy

Foundation of America's Working Group on Status Epilepticus. JAMA 1993;270(7):854-9.

3. Bassin S, Smith TL, Bleck TP. Clinical review: status epilepticus. Crit Care 2002;6(2):137-42.

4. Bleck TP. Management approaches to prolonged seizures and status epilepticus. Epilepsia 1999;40(1):S64-6.

5. DeLorenzo RJ, Towne AR, Pellock JM, et al. Status epilepticus in children, adults, and the elderly. Epilepsia 1992;33 Suppl 4:S15-25.

6. Haafiz A, Kissoon N. Status epilepticus: current concepts. Pediatr Emerg Care 1999;15(2):119-29.

7. Lowenstein DH, Bleck T, Macdonald RL. It's time to revise the definition of status epilepticus. Epilepsia 1999;40(1):120-2.

8. Orlowski JP, Rothner DA. Diagnosis and treatment of status epilepticus. In: Fuhrman BP, Zimmerman JJ, editors. Pediatric Critical Care. St. Louis: Mosby; 1998. p. 625-35.