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Mohebullah Faqiri, MD
E-mail: mohabfaqiri@gmail.com
September 8, 2016
Ataturk National Children
Hospital
Children’s Healthcare of Afghanistan
 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
Status epilepticus 2
Definition
 Conventional definition:
 Single seizure > 30 minutes
 Series of seizures > 30 minutes without full recovery
Status epilepticus 3
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
Status epilepticus 4
The longer SE persists,
the lower is the likelihood of spontaneous cessation
the harder is it to control
the 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
Status epilepticus 5
Causes
Fever
Medication change
Unknown
Metabolic
Congenital
Anoxic
Other (trauma, vascular,
infection, tumor, drugs)
36%
20%
9%
8%
7%
5%
15%
Status epilepticus 6
DeLorenzo RJ. Epilepsia 1992;33 Suppl 4:S15-25
Drugs which can cause seizures
 Antibiotics
 Penicillins
 Isoniazid
 Metronidazole
 Anesthetics, narcotics
 Halothane, enflurane
 Cocaine, fentanyl
 Ketamine
 Psychopharmaceuticals
 Antihistamines
 Antidepressants
 Antipsychotics
 Phencyclidine
 Tricyclic antidepressants
Status epilepticus 7
Mortality
 Adults
 Children
15 to 22%
3 to 15%
Status epilepticus 8
Reviewed in: Fountain NB. Epilepsia 2000;41 Suppl 2:S23-30
Prolonged seizures
Status epilepticus 9
Duration of seizure
Life
threatening
systemic
changes
Death
Temporary
systemic
changes
Respiratory
 Hypoxia and hypercarbia
-  ventilation (chest rigidity from muscle spasm)
- Hypermetabolism ( O2 consumption,  CO2 production)
- Poor handling of secretions
- Neurogenic pulmonary edema?
Status epilepticus 10
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
Status epilepticus 11
Neurogenic pulmonary edema
Rare complication
Likely occurs as consequence
of marked increase of
pulmonary vascular pressure
Status epilepticus 12
Johnston SC. Postictal pulmonary edema requires pulmonary vascular pressure increases.
Epilepsia 1996;37(5):428-32
Acidosis
 Respiratory
 Lactic
 Impaired tissue oxygenation
 Increased energy expenditure
Status epilepticus 13
Hemodynamics
 Sympathetic overdrive
 Massive catecholamine /
autonomic discharge
 Hypertension
 Tachycardia
 High CVP
Status epilepticus 14
 Exhaustion
 Hypotension
 Hypoperfusion
0 min 60 min
Cerebral blood flow - Cerebral O2 requirement
 Hyperdynamic
phase
 CBF meets CMRO2
 Exhaustion phase
 CBF drops as
hypotension sets in
 Autoregulation
exhausted
 Neuronal damage
ensues
Status epilepticus 15
Blood pressure
Blood flow
O2 requirement
Seizure duration
Glucose
Hyperdynamic
phase
 Hyperglycemia
Exhaustion
phase
 Hypoglycemia
develops
 Hypoglycemia appears
earlier in presence of
hypoxia
 Neuronal damage
ensues
Status epilepticus 16
Glucose
Seizure duration
30 min
SE
SE + hypoxia
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
Status epilepticus 17
Other alterations
 Blood leukocytosis (50% of children)
 Spinal fluid leukocytosis (15% of children)
  K+
  creatine kinase
 Myoglobinuria
Status epilepticus 18
Oxygen, oral airway. Avoid hypoxia!
Consider bag-valve mask ventilation. Consider
intubation
IV/IO access. Treat hypotension, but NOT
hypertension
Status epilepticus 19
A
B
C
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
Status epilepticus 20
Initial investigations
 Labs
 Na, Ca, Mg, PO4 , glucose
 CBC
 Liver function tests, ammonia
 Anticonvulsant level
 Toxicology
Status epilepticus 21
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
Status epilepticus 22
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)
Status epilepticus 23
Treatment
 Hyponatremia:
 Give 5 cc/kg of 3% (hypertonic saline)
 Hypocalcemia:
 Give 20-25 mg/kg of Calcium Chloride
Status epilepticus 24
Treatment
 The longer you wait with anticonvulsant, the more
anticonvulsant you will need to stop SE
 Most common mistake is ineffective dose
Status epilepticus 25
Anticonvulsants
 Rapid acting
plus
 Long acting
Status epilepticus 26
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
Status epilepticus 27
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.
Status epilepticus 28
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
Status epilepticus 29
Anticonvulsants - Long acting
 Phenobarbital
 20 mg/k g i.v. over 10 - 15 min
 Onset 15-30 min
 May cause hypotension, respiratory depression
Status epilepticus 30
Initial choice of long acting anticonvulsants in
SE
Status epilepticus 31
Is patient an infant?
Is patient already receiving phenytoin?
YesNo
At high risk for extravasation ?
(small vein, difficult access etc.)?
Phenobarbital
YesNo
Phenytoin Fosphenytoin
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
Status epilepticus 32
Non - convulsive status epilepticus
 How do you tell that patient’s seizures have stopped?
Status epilepticus 33
Non - convulsive SE ?
 Neurologic signs after termination of SE are common:
 Pupillary changes
 Abnormal tone
 Babinski
 Posturing
 Clonus
 May be asymmetrical
Status epilepticus 34
Non - convulsive SE ?
 Up to 20% of children with SE have non - convulsive SE
after tonic - clonic SE
Status epilepticus 35
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
Status epilepticus 36
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.
Status epilepticus 37
Thank You
38

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Seizures epileptics in children

  • 1. Mohebullah Faqiri, MD E-mail: mohabfaqiri@gmail.com September 8, 2016 Ataturk National Children Hospital Children’s Healthcare of Afghanistan
  • 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 Status epilepticus 2
  • 3. Definition  Conventional definition:  Single seizure > 30 minutes  Series of seizures > 30 minutes without full recovery Status epilepticus 3
  • 4. 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 Status epilepticus 4
  • 5. The longer SE persists, the lower is the likelihood of spontaneous cessation the harder is it to control the 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 Status epilepticus 5
  • 6. Causes Fever Medication change Unknown Metabolic Congenital Anoxic Other (trauma, vascular, infection, tumor, drugs) 36% 20% 9% 8% 7% 5% 15% Status epilepticus 6 DeLorenzo RJ. Epilepsia 1992;33 Suppl 4:S15-25
  • 7. Drugs which can cause seizures  Antibiotics  Penicillins  Isoniazid  Metronidazole  Anesthetics, narcotics  Halothane, enflurane  Cocaine, fentanyl  Ketamine  Psychopharmaceuticals  Antihistamines  Antidepressants  Antipsychotics  Phencyclidine  Tricyclic antidepressants Status epilepticus 7
  • 8. Mortality  Adults  Children 15 to 22% 3 to 15% Status epilepticus 8 Reviewed in: Fountain NB. Epilepsia 2000;41 Suppl 2:S23-30
  • 9. Prolonged seizures Status epilepticus 9 Duration of seizure Life threatening systemic changes Death Temporary systemic changes
  • 10. Respiratory  Hypoxia and hypercarbia -  ventilation (chest rigidity from muscle spasm) - Hypermetabolism ( O2 consumption,  CO2 production) - Poor handling of secretions - Neurogenic pulmonary edema? Status epilepticus 10
  • 11. 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 Status epilepticus 11
  • 12. Neurogenic pulmonary edema Rare complication Likely occurs as consequence of marked increase of pulmonary vascular pressure Status epilepticus 12 Johnston SC. Postictal pulmonary edema requires pulmonary vascular pressure increases. Epilepsia 1996;37(5):428-32
  • 13. Acidosis  Respiratory  Lactic  Impaired tissue oxygenation  Increased energy expenditure Status epilepticus 13
  • 14. Hemodynamics  Sympathetic overdrive  Massive catecholamine / autonomic discharge  Hypertension  Tachycardia  High CVP Status epilepticus 14  Exhaustion  Hypotension  Hypoperfusion 0 min 60 min
  • 15. Cerebral blood flow - Cerebral O2 requirement  Hyperdynamic phase  CBF meets CMRO2  Exhaustion phase  CBF drops as hypotension sets in  Autoregulation exhausted  Neuronal damage ensues Status epilepticus 15 Blood pressure Blood flow O2 requirement Seizure duration
  • 16. Glucose Hyperdynamic phase  Hyperglycemia Exhaustion phase  Hypoglycemia develops  Hypoglycemia appears earlier in presence of hypoxia  Neuronal damage ensues Status epilepticus 16 Glucose Seizure duration 30 min SE SE + hypoxia
  • 17. 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 Status epilepticus 17
  • 18. Other alterations  Blood leukocytosis (50% of children)  Spinal fluid leukocytosis (15% of children)   K+   creatine kinase  Myoglobinuria Status epilepticus 18
  • 19. Oxygen, oral airway. Avoid hypoxia! Consider bag-valve mask ventilation. Consider intubation IV/IO access. Treat hypotension, but NOT hypertension Status epilepticus 19 A B C
  • 20. 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 Status epilepticus 20
  • 21. Initial investigations  Labs  Na, Ca, Mg, PO4 , glucose  CBC  Liver function tests, ammonia  Anticonvulsant level  Toxicology Status epilepticus 21
  • 22. 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 Status epilepticus 22
  • 23. 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) Status epilepticus 23
  • 24. Treatment  Hyponatremia:  Give 5 cc/kg of 3% (hypertonic saline)  Hypocalcemia:  Give 20-25 mg/kg of Calcium Chloride Status epilepticus 24
  • 25. Treatment  The longer you wait with anticonvulsant, the more anticonvulsant you will need to stop SE  Most common mistake is ineffective dose Status epilepticus 25
  • 26. Anticonvulsants  Rapid acting plus  Long acting Status epilepticus 26
  • 27. 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 Status epilepticus 27
  • 28. 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. Status epilepticus 28
  • 29. 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 Status epilepticus 29
  • 30. Anticonvulsants - Long acting  Phenobarbital  20 mg/k g i.v. over 10 - 15 min  Onset 15-30 min  May cause hypotension, respiratory depression Status epilepticus 30
  • 31. Initial choice of long acting anticonvulsants in SE Status epilepticus 31 Is patient an infant? Is patient already receiving phenytoin? YesNo At high risk for extravasation ? (small vein, difficult access etc.)? Phenobarbital YesNo Phenytoin Fosphenytoin
  • 32. 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 Status epilepticus 32
  • 33. Non - convulsive status epilepticus  How do you tell that patient’s seizures have stopped? Status epilepticus 33
  • 34. Non - convulsive SE ?  Neurologic signs after termination of SE are common:  Pupillary changes  Abnormal tone  Babinski  Posturing  Clonus  May be asymmetrical Status epilepticus 34
  • 35. Non - convulsive SE ?  Up to 20% of children with SE have non - convulsive SE after tonic - clonic SE Status epilepticus 35
  • 36. 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 Status epilepticus 36
  • 37. 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. Status epilepticus 37