this ppt will help you alot in managing a child with status epilepticus

1. STATUS EPILEPTICUS

2. Outline
 Introduction
 Epidemiology
 Etiology
 Risk factors
 Pathophysiology
 Complications
 Treatment
 Prognosis
 In nutshell
 Reference
2

3. Introduction
Definition proposed by the ILAE task force on classification of SE
in 2015:
 The ILAE has refined the definition of SE to reflect the time at
which treatment should be initiated (t1 ) and time at which
continuous seizure activity leads to long-term sequelae (t2 )
 In the past, the cutoff time was 30 min based on animal
studies that showed evidence of neuronal damage after this
time point
 But this has been reduced to emphasize the risks involved
with the longer durations and the need for early and
aggressive pharmacologic intervention.
3

4. Introduction conti…
 Generalized tonic-clonic seizures, SE is defined as continuous
convulsive activity or recurrent generalized convulsive seizure
activity without regaining of consciousness
 (t1 = 5 min, t2 ≥ 30 min)
 SE consisting of focal seizures with impaired awareness
(t1 = 10 min, t2 = 30 min)
 Absence SE
 (t1 = 10-15 min, t2 = unknown )
4

5. Introduction conti…
 The most common type of SE is convulsive status epilepticus
(generalized tonic, clonic, or tonic-clonic)
 But other types do occur, including
Nonconvulsive status (focal with impaired awareness,
absence)
 Myoclonic status
Epilepsia partialis continua
Neonatal status epilepticus.
5

6. Introduction conti…
Nonconvulsive status epilepticus
 Continious or repeated episodes of focal motor, sensory or
cognitive symptoms with impaires conciousness
Manifests as a confusional state, dementia,
Hyperactivity with behavioral problems,
Fluctuating impairment of consciousness
Confusional state, hallucinations, paranoia, aggressiveness
catatonia, and or psychotic symptoms.
Considered in unresponsive and encephalopathic child
6

7. Introduction conti…
Epilepsia partialis continua - can be caused by
 tumor
 vascular etiologies
 mitochondrial disease (mitochondrial myopathy,
encephalopathy, lactic acidosis, and stroke-like episodes
[MELAS])
 Rasmussen encephalitis
7

8. Introduction conti…
Refractory status epilepticus
 That has failed to respond to therapy, usually with at least two
medications (such as benzodiazepine and another
medication).
 The trend is not to assign a minimum duration
 The past a minimum duration of 30 min, 60 min, or even 2 hr
was cited
Superrefractory status epilepticus
 That has failed to resolve, or recurs, within 24 hr or more
despite therapy that includes a continuous infusion such as
midazolam and/or pentobarbital.
8

9. Introduction conti…
New-onset refractory status epilepticus (NORSE)
 Caused by almost any of the causes of SE in a patient without
prior epilepsy.
 Is often of unknown etiology, presumed to be encephalitic or
postencephalitic
 Can last several weeks or longer
 Has a poor prognosis
9

10. Introduction conti…
Fever-induced refractory epileptic encephalopathy in school age
children (FIRES)
 Is associated with acute febrile infections, appears to be para
infectious in nature
 Appears to be highly drug resistant but is often responsive to
the ketogenic diet.
Electrical (subclinical ) seizure
 Recognized only on EEG and can continue after clinical activity
has been stopped by anticonvulsant
 Controversy exists about type of EEG pattern that should be
considered ictal without clinical manifestations
10

11. Epidemiology
 The estimated incidence of childhood SE is between 17 to 23
episodes per 100,000 per year.
 SE can be a complication of acute illness such as encephalitis,
or can occur as a manifestation of epilepsy.
 Incidence rates, causes, and prognosis vary substantially by
age.
 The highest incidence is in the first year of life.
 Approximately 60 percent of children are neurologically
healthy prior to the first episode of SE.
11

12. Epidemiology
 30% of patients with SE are having their first seizure
 40% of these later develop epilepsy
 Febrile status epilepticus is the most common type of SE in
children
 mortality rate of 4–5% is observed
 14% risk of new neurologic deficits, most of them 12.5%
secondary to the underlying pathology.
12

13. Etiology
 Drug intoxication
 Drug withdrawal or overdose in patients taking AEDs
 Metabolic ( Hypoglycemia ,hypocalcemia, hyponatremia,
hypomagnesemia)
 Acute head trauma
 Encephalitis ;meningitis
 Autoimmune encephalitis
 Ischemic (arterial or venous) stroke
13

14. Etiology
 Intracranial hemorrhage
 Folinic acid and pyridoxine and pyridoxal-phosphate
dependency
 Inborn errors of metabolism
 Ion channel–related epilepsies
 Hypoxic -ischemic injury
 Systemic conditions (such as hypertensive encephalopathy,
renal or hepatic encephalopathy)
 Brain tumors
 Brain malformations
 Neurodegenerative disorders
14

15. Risk factors
 Have been defined in a setting of established epilepsy
 10-20% of epilepsy patients have at least 1 SE
Seizures that tend to occurs in clusters (2-3 in 24 hrs )
Focal seizures with secondary generalization
SE as a first seizure
Generalized abnormalities on neuro imaging
History of prior SE
Young age at onset (<1year )
Symptomatic etiology of epilepsy
Focal background EEG abnormalities
15

16. PATHOPHYSIOLOGY
 SE occurs because of failure of the normal mechanisms that
limit the spread and recurrence of isolated seizures.
 Failure occurs because excitation is excessive and/or inhibition
is ineffective.
 Multiple mechanisms probably are involved.
 Glutamate is the major amino acid excitatory
neurotransmitter in the brain.
 Some affected individuals had prolonged seizures thought to
be caused by excessive activation of excitatory amino acid
receptors.
 Other excitatory neurotransmitters that contribute to SE
include aspartate and acetylcholine
16

17. PATHOPHYSIOLOGY
 Gamma-aminobutyric acid (GABA) is the main inhibitory
neurotransmitter in the brain, and antagonists to its effects or
alterations in its metabolism in the substantia nigra may
contribute to SE.
 Reduction of GABA-mediated inhibition as a result of
intracellular internalization of GABAA receptors
This explains why
 Less likely to stop in the next specific period of time the
longer the seizure has lasted
 why benzodiazepines appear to be decreasingly effective the
longer seizure activity lasts.
17

18. PATHOPHYSIOLOGY
 Other inhibitory mechanisms include the calcium ion
dependent potassium ion current and blockage of N-methyl-
D-aspartate (NMDA) channels by magnesium.
 SE increases cerebral metabolic rate
 Compensatory increase in cerebral blood flow that
 After approximately 30 min, is not able to keep up with the
increases in cerebral metabolic rate
 when NAMDA channels are depolarized Ca enters and
causes injury or death
 Focal radiologic changes after focal SE is not uncommon
 Increased serum level of neuron specific enolase
18

19. PATHOPHYSIOLOGY
Some of the changes are
 Mild edema
 Decreased attenuation with effacement of sulci
 Loss of grey white differentiation
 Acute changes are followed by regional brain atrophy
19

20. CLASSIFICATION
The usual classification of SE is similar to that used for individual
seizures and includes four major types:
 Focal SE without impairment of consciousness or awareness
(simple partial SE)
 Focal SE with impairment of consciousness or awareness
(complex partial SE)
 Generalized convulsive SE including tonic-clonic, tonic, and
clonic
 Absence SE
20

21. COMPLICATIONS
 Hypoxemia
 Lactic and respiratory acidosis
 Early hyperglycemia(SNS and cathecolamine discharge)
followed by hypoglycemia
 Elevated WBC (60%) demargination of WBC related to
stress,13% CSF pleocytosis without infection
 Elevated body temperature and rhabdomyolysis (inc muscle
contraction)
21

22. COMPLICATIONS
 Myoglobinuria
 Increased intracranial pressure (MA, hypoxemia,CO2 retention
with compensatory vasodialation and increased cerebral flow)
 BP disturbance-initially BP, HR increases (cathecolamine )to
increase cerebral blood flow to compensate metabolic needs
,later hypotension
22

23. URGENT FOCUSED EVALUATION
During the course of resuscitation, the clinician or designee
should obtain a focused history from a parent or caregiver to
determine:
 Prehospital administration of benzodiazepines and any other
ant seizure medications
 Patient history of epilepsy
 Precipitating factors prior to seizure (eg, febrile illness,
possible toxic exposure, trauma, change in ant seizure
medications)
 Current medications, including prior or current use of ant
seizure medications
23

24. URGENT FOCUSED EVALUATION
 For patients with prior SE, history of treatment response
 Other active medical diagnoses, especially those associated
with hypoglycemia, hyponatremia , or hypocalcemia
 Allergies to any medications
24

25. URGENT FOCUSED EVALUATION
 In patients with SE, the initial physical examination is limited.
 In addition to assessing vital signs, airway, breathing, and
circulation, the clinician should identify:
Signs of head trauma (eg, swelling, ecchymosis, or
lacerations)
Signs of sepsis or meningitis (eg, fever, poor perfusion, or
rash [eg, petechiae, erythroderma, or cellulitis])
Seizure characteristics (eg, focal or generalized
25

26. IMMEDIATE SUPPORTIVE CARE
The main goals of treatment are:
 Establish and maintain adequate airway, breathing, and
circulation
 Identify and treat hypoglycemia
 Stop the seizure and thereby prevent brain injury
 Identify and treat life-threatening causes of SE such as
trauma, sepsis, meningitis, encephalitis, or structural brain
lesion
26

27. IMMEDIATE SUPPORTIVE CARE
Airway
 Ensure a patent airway .
 Put the child in the recovery position .
 If the airway is not patent, use an airway manoeuvre or
airway adjunct .
 Airway compromise is an indication for intubation
27

28. IMMEDIATE SUPPORTIVE CARE
Breathing
 Assess breathing – signs of respiratory distress, respiratory
rate, oxygen saturations, clinical examination of the chest .
 Give high flow oxygen via a non-rebreathe face mask to all
children.
 Hypoventilation should be supported with oxygen via a bag-
valve-mask
28

29. IMMEDIATE SUPPORTIVE CARE
 Indications for rapid sequence endotracheal intubation (RSI)
and mechanical ventilation:
Unprotected or unmaintainable airway
Apnea or inadequate ventilation
Hypoxemia
SE lasting 30 minutes
29

30. IMMEDIATE SUPPORTIVE CARE
Circulation
 Assess circulation – pulse rate, blood pressure, capillary refill
time, cardiovascular examination
 Malignant hypertension may require treatment.
 Intravenous, or intraosseous , access must be established
 Blood tests: CBC, calcium, magnesium , sodium, serum
glucose, blood gas and blood cultures for suspected
meningitis .
 Hypoglycemia? Give 5 ml/kg of 10% dextros
30

31. IMMEDIATE SUPPORTIVE CARE
Disability
 Assess conscious level , pupil size and reaction, and posture.
 Look for signs of meningitis
Exposure
 Temperature
 Look for a petechial or purpuric rash .
 Look for signs of trauma.
31

32. LABORATORY INVESTIGATIONS
 Plasma glucose and a rapid "finger-stick" or point- of-care
glucose
 Serum electrolytes and calcium
 Serum ant seizure medication levels, if applicable
 If substance use or poisoning is suspected, urine and blood
toxicology
 In postmenarchal females, qualitative pregnancy test (urine or
blood)
 Sepsis work up
 Meningitis work up
32

33. LABORATORY INVESTIGATIONS
Electroencephalogram (EEG)
 When there is uncertainty regarding the presence of SE, an
urgent portable EEG should be obtained.
Neuroimaging
 Neuroimaging is generally deferred until the patient is
stabilized.
33

34. EMERGENCY ANTISEIZURE TREATMENT
 Initial emergent therapy should be started for convulsive
seizures lasting for >5min and involves use of benzodiazepines
 American epilepsy society recommends intravenous
lorazepam, intravenous diazepam, or intramuscular
midazolam as a first-line agent.
 Neurocritical Care Society SE Guidelines recommend
intravenous lorazepam as a first-line agent
34

35. BENZODIAZEPINES
 First-line agents for SE
 Includes lorazepam, midazolam, diazepam
 Stimulates GABA receptors
 Benzodiazepine-sensitive GABA receptors are internalized as
SE continues; 20-fold decrease in potency of benzodiazepines
after 30 minutes in SE
 IV is preferred route for all benzodiazepines.
 Midazolam can also be given via intramuscular, intranasal
and buccal routes.
 Diazepam can be given via rectum (gel or IV formulation).
35

36. BENZODIAZEPINES
 Recommendations to increase efficacy and reduce side effects
are
Use IV lorazepam preferentially if IV access available.
Use intranasal midazolam if no IV available.
Use rectal diazepam if IV and midazolam are not available.
 Need to wait 4-5 minutes between doses
 If there is no response after 2-3 doses, this class is unlikely to
work.
 Side effects include sedation and respiratory depression;
cumulative with dosing
36

37. FIRST LINE TREATMENT
Benzodiazepine:
IV or IO access achieved within 3 minutes:
 Lorazepam -0.1 mg/kg IV or IO, maximum 4 mg OR
 Diazepam -0.2 mg/kg IV or IO, maximum 10 mg
IV or IO access not achieved within 3 minutes:
 Buccal midazolam 0.3 to 0.5 mg/kg, maximum 10 mg
 IM midazolam 0.1 to 0.2 mg/kg, maximum 10 mg
 Rectal diazepam 0.5 mg/kg, maximum 20mg
37
If seizures persist 5 min after the initial
benzodiazepine dose, give second dose

38. FIRST LINE TREATMENT
Lorazepam Diazepam
Low lipid solubility High lipid solubility
Actions delayed 2minutes Thus very rapid onset
1minutes
Anticonvulsant effect 4-
6hrs
Rapid loss of
anticonvulsant effect
20minutes
Less respiratory depression S/E
 Hypotension
 respiratory depression
Refrigeration is
recommended
Not required
38

39. Early Benzodiazepine Treatment
 Retrospective study of 38 children with generalized convulsive
SE, use of prehospital diazepam (0.6 mg/kg rectally) was
associated with a shorter seizure duration (32 vs. 60 minutes)
and a reduced likelihood of seizure recurrence in the
emergency department (58% vs. 85%)
39

40. Lorazepam vs Diazepam for Pediatric Status Epilepticus
A Randomized Clinical Trial
40
 MAIN OUTCOMES AND MEASURES The primary efficacy out come was cessation of status
epilepticus by 10 minutes without recurrence within 30 minutes. The primary safety outcome
was the performance of assisted ventilation. Secondary outcomes included rates of seizure
recurrence and sedation and times to cessation of status epilepticus and return to baseline
mental status. Outcomes were measured 4 hours after study medication administration.
 RESULTS Cessation of status epilepticus for 10 minutes without recurrence within 30 minutes
occurred in 101 of 140 (72.1%) in the diazepam group and 97 of 133 (72.9%) in the
lorazepam group, with an absolute efficacy difference of 0.8%(95%CI, −11.4%to 9.8%).
Twenty-six patients in each group required assisted ventilation (16.0%given diazepam and
17.6%given lorazepam; absolute risk difference, 1.6%; 95%CI, −9.9%to 6.8%). There were no
statistically significant differences in secondary outcomes except that lorazepam patients
were more likely to be sedated (66.9%vs 50%, respectively; absolute risk difference, 16.9%;
95%CI, 6.1% to 27.7%).
 CONCLUSIONS AND RELEVANCE Among pediatric patients with convulsive status epilepticus,
treatment with lorazepam did not result in improved efficacy or safety compared with
diazepam. These findings do not support the preferential use of lorazepam for this condition

41. SECOND LINE TREATMENT
 If seizures continue for 10 minutes after at least two injections
of lorazepam or diazepam
 A second therapy with a long-acting antiseizure medication is
indicated. Levetiracetam, phenytoin/fosphenytoin, and
valproate are reasonable choices in this setting.
 The onset of action is delayed with these drugs. Therefore, it
may be helpful to give an additional dose of a benzodiazepine
as the ant seizure medication is being administered.
41

42. SECOND LINE TREATMENT
 Intravenous phenobarbital is an alternative option if
valproate, fosphenytoin, or levetiracetam is not available but
is not recommended as a first-line urgent therapy
 Definitive seizure control should be within 60 min of seizure
onset
 After the second or third medication is given, and sometimes
before that, the patient might need to be intubated.
 Emergent and urgent therapies should have been received
within less than 30 min
42

43. SECOND LINE TREATMENT
When IV or IO access is available
 Levetiracetam 60 mg/kg IV or IO, maximum single dose 4500
mg OR
 Fosphenytoin 20 mg PE per kg IV or IO, maximum single dose
1500 mg OR
 Valproate 20 to 40 mg/kg IV or IO
 Phenobarbital 20 mg/kg IV or IO, maximum 1 g
When IV and IO access are not available
 Fosphenytoin can be given by intramuscular injection.
43

44. SECOND LINE TREATMENT
Fosphenytoin
 Second-line agent for SE
 Slows the recovery of voltage gated sodium channels
 Dosage is a 20 mgPE/kg IV bolus over ~7 minutes (3
mg/kg/min with a maximum of 150 mg PE/minute).
 Can re-dose with another 10 mg/kg
 Side effects
Thrombophlebitis
Hypotension
Cardiac arrhythmias
 Fosphenytoin converted to phenytoin in serum
44

45. SECOND LINE TREATMENT
fosphenytoin phenytoin
Can be given IV or IM Can not be given IM
Less cardiac toxicity more cardiac toxicity
Dextrose containing fluids can be used Can not be used
Can be infused in faster rate Slower infusion
45

46. SECOND LINE TREATMENT
Levetiracetam
 Commonly regarded as a new second-line agent
 Multiple mechanisms of action, SV2A inhibitor
 Dosed at 40 mg/kg IV over ~10 minutes
 Published recommendations range from 20-50 mg/kg for
loading dose.
 Can re-dose with another 20 mg/kg.
 Side effects include sedation at high doses.
 Fewer complications than many other antiepileptic drugs but
must adjust dosing with decreased renal function
46

47. SECOND LINE TREATMENT
Phenobarbital
 Third-line agent, but commonly used in neonatal seizures
 Enhances GABA activity
 Dosed at 20 mg/kg IV bolus over ~20 min
 Can re-dose with another 10mg/kg
 High incidence of respiratory suppression and sedation
47

48. SECOND LINE TREATMENT
Valproic acid
 Second-line agent
 Enhances GABA and modulates sodium/calcium channels
 Dosed at 20 mg/kg IV bolus over ~5-10 minutes
 Rare side effects of
Hyperammonemia
Hepatotoxicity
Encephalopathy
48

49. SECOND LINE TREATMENT
Oral vs IV loads
 Phenobarbital PO: peak concentration after 2-4 hours
 Phenytoin PO: peak concentration after 4-8 hours
 Valproic Acid PO: peak concentration after ~2 hours
49

50. Levetiracetam versus phenytoin for second-line treatment
of paediatric convulsive status epilepticus (EcLiPSE):
a multicentre, open-label, randomised trial
 Methods This open-label, randomised clinical trial was undertaken at 30 UK emergency departments at secondary and
tertiary care centres. Participants aged 6 months to under 18 years, with convulsive status epilepticus requiring second-line
treatment, were randomly assigned (1:1) using a computer-generated randomisation schedule to receive levetiracetam (40
mg/kg over 5 min) or phenytoin (20 mg/kg over at least 20 min), stratified by centre. The primary outcome was time from
randomisation to cessation of convulsive status epilepticus, analysed in the modified intention-to-treat population
(excluding those who did not require second-line treatment after randomisation and those who did not provide consent).
This trial is registered with ISRCTN, number ISRCTN22567894.
 Findings Between July 17, 2015, and April 7, 2018, 1432 patients were assessed for eligibility. After exclusion of ineligible
patients, 404 patients were randomly assigned. After exclusion of those who did not require second-line treatment and
those who did not consent, 286 randomised participants were treated and had available data: 152 allocated to
levetiracetam, and 134 to phenytoin. Convulsive status epilepticus was terminated in 106 (70%) children in the
levetiracetam group and in 86 (64%) in the phenytoin group. Median time from randomisation to cessation of convulsive
statu epilepticus was 35 min (IQR 20 to not assessable) in the levetiracetam group and 45 min (24 to not assessable) in the
phenytoin group (hazard ratio 1·20, 95% CI 0·91–1·60; p=0·20). One participant who received levetiracetam followed by
phenytoin died as a result of catastrophic cerebral oedema unrelated to either treatment. One participant who received
phenytoin had serious adverse reactions related to study treatment (hypotension considered to be immediately life-
threatening [a serious adverse reaction] and increased focal seizures and decreased consciousness considered to be
medically significant [a suspected unexpected serious adverse reaction]).
 Interpretation Although levetiracetam was not significantly superior to phenytoin, the results, together with previously
reported safety profiles and comparative ease of administration of levetiracetam, suggest it could be an appropriate
alternative to phenytoin as the first-choice, second-line anticonvulsant in the treatment of paediatric convulsive status
epilepticus.
50

51. THRID LINE
Refractory status epilepticus treatment
 An intravenous bolus followed by continuous infusion of
midazolam, propofol, pentobarbital, or thiopental is used.
Superrefractory status epilepticus (SRSE)
• Have persistent seizure activity or seizure recurrence despite
24 hr of general anesthesia with medications such as
midazolam, pentobarbital, and/or propofol
• In addition to these continuous infusions, polytherapy with
other AEDs is usually initiated,
51

52. RSE TREATMENT
Midazolam continuous infusion
 Start with 0.2 mg/kg bolus then begin 0.05 to 2 mg/kg/hr infusion.
 May repeat boluses and increase infusion to max 2 mg/kg/hr.
 Half life 1-4 hours
Thiopental (barbiturate coma)
 Anesthetic
 Thiopental metabolized to pentobarbital
 5 mg/kg IV bolus followed by 3-5 mg/kg/hr infusion
 Serious side effects
Hypotension
Respiratory depression
Decreased cardiac contractility
52

53. RSE TREATMENT
53

54. Midazolam vs Pentobarbital
 Multicenter study of 111 pediatric patients with RSE found
that midazolam was the first-line anesthetic agent in 78%
 Pentobarbital was used in 82% of midazolam refractory
cases.
 RSE treatment was achieved in 94% of patients with these two
therapies
54
Tasker RC, Goodkin HP, Sánchez Fernández I, et al. Refractory status
epilepticus in children. Pediatr Crit Care Med. 2016

55. RSE TREATMENT
Propofol
 Anesthetic
 GABA receptor activity, different than benzodiazepines and
barbiturates
 Side effects
Respiratory suppression
Hypotension
Rhabdomyolysis
Cardiac failure
Renal failure
Propofol infusion syndrome: metabolic acidosis
55

56. Treatment
Superrefractory status epilepticus (SRSE)
 Commonly used drugs are fosphenytoin, valproate,
phenobarbital, levetiracetam, topiramate, and lacosamide.
 Ketamine infusion is becoming a better-recognized treatment
option. It is an NMDA receptor antagonist
 Ketogenic diet has also been found to be effective in children,
although the response may take up to a week following diet
56

57. KETOGENIC DIET THERAPY
 The classic ketogenic diet is a high-fat, adequate-protein (1
gram/kg) low carbohydrate diet that produces metabolic
changes associated with the starvation state.
 KDT is associated with increased
Mitochondrial biogenesis
Oxidative phosphorylation enhanced gamma amino
butyric acid (GABA) levels
Reduced neuronal excitability and firing, and stabilized
synaptic function
57

58. KETOGENIC DIET THERAPY
INDICATIONS KDT
 Drug-resistant epilepsy
 Super-refractory status epilepticus
 Doose syndrome
 Dravet syndrome
 GLUT-1 deficiency
 Infantile spasms
 Pyruvate dehydrogenase deficiency
 Tuberous sclerosis complex
 Gastrostomy- or formula-fed children
58

59. Treatment
Superrefractory status epilepticus (SRSE)
59

60. Treatment
 ketosis may be more difficult to achieve if the patient is
receiving pentobarbital, which has a carbohydrate-rich carrier
fluid.
 Other options for SRSE
Inhaled anesthetics such as isoflurane
Induced hypothermia
Pyridoxine trial in infants
60

61. Treatment
 Lesional SRSE, emergent neurosurgery may be an option.
 Performing hemispherectomy for Rasmussen encephalitis
Focal resection if the seizures are secondary to an area of
cortical dysplasia.
 Immunotherapy with intravenous steroids, immunoglobulin's ,
and/or plasma exchange is often used in
Cases of SRSE of unclear etiology
 In specific situations such as anti-NMDA receptor
encephalitis or CNS vasculitis
61

62. Clinical Profile and Short-term Outcome of Pediatric Status Epilepticus at
a Tertiary-care Center in Northern India
 Objective: To assess clinical profile and short term treatment outcomes of pediatric
status epilepticus (SE) at a tertiary-care center in northern India.
 Methods: Prospective cohort study enrolled children aged 1 month to 18 years
presenting with SE to the emergency department. Enrolled children (109) were
treated as per hospital protocols. Clinical features during hospitalization were
noted. Pediatric overall performance category (POPC) scale was used for
classification of outcome at the time of discharge.
 Results: Acute symptomatic etiology was identified in 66 (60.6%) cases (CNS
infections were predominant). Previous diagnosis of epilepsy was found in 32
(29.4%) children; and benzodiazepine responsive SE were seen in 65 (59.6%)
children. Predictors of unfavorable outcome were acute symptomatic etiology
(adjusted OR 4.50; 95% CI 1.49, 13.62) and no treatment administered prior to
hospital (adjusted OR 3.97; 95% CI 1.06, 14.81).
 Conclusions: Acute symptomatic etiology, mainly acute CNS infections, is the
leading cause of SE in this region. Early and prehospital management with
benzodiazepines may improve SE outcome.
62

63. Treatment
63

64. POSTICTAL RECOVERY AND FURTHER
EVALUATION
 Most children begin to recover responsiveness within 20 to 30
minutes after generalized convulsions
 Close monitoring during the immediate postictal phase is
critical, particularly for respiratory status.
 The two most common reasons for delayed postictal recovery
are sedation from medications and ongoing nonconvulsive
seizures
 All children who do not return to a normal level of
consciousness within a few hours after initial treatment of SE
should therefore undergo an emergency EEG
64

65. POSTICTAL RECOVERY AND FURTHER
EVALUATION
 During the postictal recovery period.
 It is important to perform a detailed history, physical
examination, and a full neurologic examination that looks for
asymmetric or focal findings or signs of increased intracranial
pressure that may suggest clues to the underlying etiology.
 Neuroimaging — A neuroimaging study is essential when SE is
the first presentation of epilepsy as well as in children whose
recovery from SE does not follow the expected course.
65

66. OUTCOME
 SE can be fatal or associated with long-term morbidity,
including seizure recurrence and neurologic problems.
 The outcome depends upon the underlying cause, the
duration of the seizure, and age of the child
 Mortality — Mortality associated with SE can result from the
underlying condition
 From respiratory failure
Cardiovascular failure
Metabolic complications of SE .
 Morbidity — Neurologic sequelae of SE include focal motor
deficits, intellectual disability, behavioral disorders, and
chronic epilepsy
66

67. Prognosis
 Mortality varies from 3-9%
 Focal deficit is usually due to the underlying condition rather
than the seizure
 Those with cryptogenic and febrile SE don’t have increased
sequel
 Encephalopathy 6-15%
 Neurologic deficit 9-11%
 In refractory SE 17-32%mortality,recurrent seizure in 31-97%,
new neuro deficit in 71-100%
67

68. Prognosis
Risk factors for recurrence
 Abnormal EEG
 Seizure during sleep
 History of prior febrile seizure
 Remote symptomatic etiology
 Focal post ictal deficit incliding todds paralysis
 Presentation with SE
68

69. IN NUTSHELL
 Note T1, T2
 First line therapy: benzodiazepines
 Second line therapy: Anti-seizure medicines
 Third line therapy
Midazolam, Pentobarbital, Propofol, Ketamine
 Fourth Line Therapy
Additional ASMs, Ketogenic Diet, Immune-modulating
therapy
 Most high risk etiologies have ~10-20% incidence of non-
convulsive seizures, and even higher in HIE
 Giving the correct doses of the correct medicines at the
correct time will significantly improve your patient’s prognosis
69

70. References
 Nelson text book of pediatrics 21st edition
 UP TO DATE 2023
 American epilepsy society guideline 2018
 International league against epilepsy guideline
70

71. THANK YOU!!!