Status Epilepticus in Children Toni Petrillo

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Status Epilepticus in Children Toni Petrillo Pediatric Critical Care Children’s Healthcare of Atlanta

Transcript of Status Epilepticus in Children Toni Petrillo

Page 1: Status Epilepticus in Children Toni Petrillo

Status Epilepticus in Children

Toni Petrillo

Pediatric Critical Care

Children’s Healthcare of Atlanta

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Status epilepticus 2

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

Generalized, tonic-clonic SE is the most common form of SE

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Definition Conventional definition:

Single seizure > 30 minutes

Series of seizures > 30 minutes without full recovery

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Definition

“If appropriate therapy is delayed, SE can cause permanent neurologic sequelae or death …”

thus

“ … any child who presents actively convulsing should be assumed to have SE.”

Haafiz A. Pediatr Emerg Care 1999;15(2):119-29

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The longer SE persists,the lower is the likelihood of spontaneous cessationthe harder is it to controlthe higher is the risk of morbidity and mortality

Treatment for most seizures needs to be instituted after > 5 minutes of seizure activity

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

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Causes Fever Medication change Unknown Metabolic Congenital Anoxic Other (trauma, vascular,

infection, tumor, drugs)

36%

20%

9%

8%

7%

5%

15%

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

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Drugs which can cause seizures Antibiotics

Penicillins Isoniazid Metronidazole

Anesthetics, narcotics Halothane, enflurane Cocaine, fentanyl Ketamine

Psychopharmaceuticals Antihistamines Antidepressants Antipsychotics Phencyclidine Tricyclic antidepressants

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Mortality

Adults Children

15 to 22%

3 to 15%

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

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Prolonged seizures

Duration of seizureDuration of seizure

Life Life threateningthreatening

systemicsystemicchangeschanges

DeathDeathTemporaryTemporary

systemicsystemicchangeschanges

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Respiratory Hypoxia and hypercarbia

- ventilation (chest rigidity from muscle spasm)- Hypermetabolism ( O2 consumption, CO2

production)- Poor handling of secretions- Neurogenic pulmonary edema?

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Hypoxia Hypoxia/anoxia markedly increase (triple?) the

risk of mortality in SE Seizures (without hypoxia) are much less

dangerous than seizures and hypoxia

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

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Neurogenic pulmonary edema

Rare complication Likely occurs as consequence of marked increase of pulmonary vascular pressure

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

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Acidosis Respiratory Lactic

Impaired tissue oxygenation Increased energy expenditure

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Hemodynamics

Sympathetic overdrive Massive catecholamine /

autonomic discharge Hypertension Tachycardia High CVP

Exhaustion Hypotension Hypoperfusion

Exhaustion Hypotension Hypoperfusion

0 min0 min 60 min60 min

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Cerebral blood flow - Cerebral O2 requirement

Blood pressure

Blood flow

O2 requirement

Seizure duration

Hyperdynamic phase CBF meets CMRO2

Exhaustion phase CBF drops as

hypotension sets in Autoregulation

exhausted Neuronal damage

ensues

Hyperdynamic phase CBF meets CMRO2

Exhaustion phase CBF drops as

hypotension sets in Autoregulation

exhausted Neuronal damage

ensues

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GlucoseG

luco

se

Seizure duration

30 min

SE

SE + hypoxia

Hyperdynamic phase Hyperglycemia

Exhaustion phase Hypoglycemia

develops Hypoglycemia

appears earlier in presence of hypoxia

Neuronal damage ensues

Hyperdynamic phase Hyperglycemia

Exhaustion phase Hypoglycemia

develops Hypoglycemia

appears earlier in presence of hypoxia

Neuronal damage ensues

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Hyperpyrexia Hyperpyrexia may develop during protracted SE,

and aggravate possible mismatch of cerebral metabolic requirement and substrate delivery

Treat hyperpyrexia aggressively Antipyretics, external cooling Consider intubation, relaxation, ventilation

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Other alterations Blood leukocytosis (50% of children) Spinal fluid leukocytosis (15% of children) K+

creatine kinase Myoglobinuria

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Oxygen, oral airway. Avoid hypoxia!

Consider bag-valve mask ventilation. Consider intubation

IV/IO access. Treat hypotension, but NOT hypertension

AA

BB

CC

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Treatment Arterial blood gas?

All children in SE have acidosis. It often resolves rapidly with termination of SE

Intubate? It may be difficult to intubate the actively seizing child Stop or slow seizures first, give O2, consider BVM

ventilation If using paralytic agent to intubate, assume that SE

continues

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Initial investigations

Labs Na, Ca, Mg, PO4 , glucose CBC Liver function tests, ammonia Anticonvulsant level Toxicology

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Initial investigations Lumbar puncture

Always defer LP in unstable patient, but never delay antibiotic/antiviral rx if indicated

CT scan Indicated for focal seizures or deficit, history of trauma

or bleeding d/o

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Treatment Give glucose (2-4 ml/kg D25%, infants 5 ml/kg D10%),

unless normo- or hyperglycemic

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

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Treatment Hyponatremia:

Give 5 cc/kg of 3% (hypertonic saline)

Hypocalcemia: Give 20-25 mg/kg of Calcium Chloride

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Treatment The longer you wait with anticonvulsant, the more

anticonvulsant you will need to stop SE Most common mistake is ineffective dose

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Anticonvulsants Rapid acting

plus

Long acting

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Anticonvulsants - Rapid acting Benzodiazepines

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

If SE persists, repeat every 5-10 minutes

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Benzodiazepines

Diazepam High lipid solubility Thus very rapid onset Redistributes rapidly Thus rapid loss of

anticonvulsant effect Adverse effects are

persistent: Hypotension Respir depression

Lorazepam Low lipid solubility Action delayed 2 minutes Anticonvulsant effect 6-12 hrs Less respiratory depression than

diazepam

Midazolam May be given i.m.

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Anticonvulsants - Long acting Phenytoin

20 mg/kg i.v. over 20 min

pH 12

Extravasation causes severe tissue injury

Onset 10-30 min May cause hypotension,

dysrhythmia Cheap

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

min PE = phenytoin equivalent

pH 8.6

Extravasation well tolerated Onset 5-10 min May cause hypotension

Expensive

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Anticonvulsants - Long acting Phenobarbital

20 mg/k g i.v. over 10 - 15 min Onset 15-30 min May cause hypotension, respiratory depression

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Initial choice of long acting anticonvulsants in SE

Is patient an infant?Is patient already receiving phenytoin?

Is patient an infant?Is patient already receiving phenytoin?

YesNo

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

Phenobarbital

YesYesNoNo

Phenytoin Fosphenytoin

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If SE persists

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

Pentobarbital infusion 1-3 mg/kg/hr after bolus 10 mg/kg

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Non - convulsive status epilepticus

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

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Non - convulsive SE ? Neurologic signs after termination of SE are

common: Pupillary changes Abnormal tone Babinski Posturing Clonus May be asymmetrical

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Non - convulsive SE ?

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

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Non - convulsive SE ?

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

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References Haafiz A, Kissoon N. Status epilepticus: current concepts. Pediatr Emerg

Care 1999;15(2):119-29. Bleck TP. Management approaches to prolonged seizures and status

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