Seizure/Status Epilepticus Flashcards

1
Q

Provoked seizures

A

intoxication
withdrawal (benzo, alcohol)
trauma
meningitis
psychiatric
metabolic derangements

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2
Q

Unprovoked seizures

A

may or may not need treatment
first time unprovoked does not require medication

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3
Q

Seizure physiology

A

mismatch of normal inhibitory mechanisms which are responsible for preventing/terminating seizures
GABA (inhibitory)
Glutamate, aspartate, ach (exitatory_

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4
Q

Seizure Epidemiology

A

most are self limited
30 day mortality of generalized convulsive status epilepticus is 20%
rapid control of seizures fundamental to tx

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5
Q

Status epilepticus definition

A

old: >30 min
new: > 5 min

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6
Q

Seizure pharm goals

A

rapid/safe termination of seizure
prevent reoccurence
Avoid CV or respiratory ADRs

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7
Q

Drugs to stop seizure

A

Benzodiazepines (MLD)
Lorazepam
Diazepam
Midazolam

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8
Q

Drugs to prevent seizure

A

Phenytoin
Fosphenytoin
levetiracetam
valproic acid

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9
Q

Stage 1 seizure

A

airway, circulation, lab test, IV thiamine, then dextrose

IV lorazepam or midazolam repeat if needed

0 to 10 min

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10
Q

Stage 2 seizure

A

Phenytoin or fosphenytoin

Alt:
VPA, phenobarbital, levetiracetam

10 to 30 min

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11
Q

Stage 3 seizure

A

Midazolam or Propofol
IV infusion
* if intubated = paralyzed, get LTM via EEG

30 min to 90 min

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12
Q

Stage 4 seizure

A

Pentobarbital

90 min to hours/days

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13
Q

Benzodiazepines first line choice

A

IV lorazepam 0.1-0.2 mg/kg
(4mg)

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14
Q

Benzodiazepines second line choices

A

Diazepam IV
0.15mg/kg (5-20mg)
Midazolam IM
0.15-0.20 mg/kg (10mg)

diazepam PR for outpatient

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15
Q

Benzodiazepines ADR

A

impaired consciousness (20-60%)
Respiratory depression (3-10%)
hypotension (<2%)

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16
Q

Benzodiazepines MOA

A

bind GABA = increase gaba-ergic transmission

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17
Q

Fos(Phenytoin) MOA

A

stabilizes neuronal membrane
increase efflux Na
Decrease influx Na

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18
Q

Fos(Phenytoin) Dosing

A

LD: 20mg/kg (max 50mg/min)
MD: 4-6 mg/kg/day divided 2-3 doses

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19
Q

Fos(Phenytoin) PK

A

highly protein bound (90%)
uremia increases [free]
Peak [brain] = 6 min after infusion completed
Liver: hydroxylation (primary)
MM kinetics: saturable PK

20
Q

Fos(Phenytoin) ADR

A

CV: Na blocker (arrythmia, hypotension, bradycardia, QTc prolongation)
Extravasation (poor IV access)
Rashes/fever/SJS
Neutropenia/ thrombocytopenia

PHENYTOIN mneumonic

21
Q

PHENYTOIN ADR Mneumonic

A

P-450
Hirsutism/hypertrichosis
Enlarged gums
Nystagmus
Yellow-browning skin (hepatitis)
Teratogenicity
Osteomalacia (D deficiency)
Interfere folate metabolism (anemia)
Neuropathies (ataxia, headache, vertigo)

22
Q

Phenytoin CV ADR cause

A

Incidence correlated to infusion rate
Attributable to diluent: propylene glycol

23
Q

Fos(Phenytoin) monitoring

A

Goal 10-20 mcg/dL total
if seizing: higher goal 15-25
level >30 = seizures
Correct for low albumin (<3.5) & CrCL<30

24
Q

Levetiracetam MOA

A

binds to SV2A (synaptic vessel protein)
involvement in NT release

NT = neurotransmitter

25
Q

Levetiracetam Dosing

A

Status epilepticus: 60 mg/kg IV bolus (max 1000mg IV BID)

CKD AKU adjust, except active SE

26
Q

Levetiracetam monitoring

A

Don’t get level - doesnt correlate with efficacy
only get level to verify compliance

27
Q

Levetiracetam ADR

A

Agitation
Drowsiness

28
Q

VPA MOA

A

MORE GABA
Less exitatory AA
Less NMDA excitation
Blocks voltage dependent NA channels = inhibit excitable membranes

29
Q

VPA dosing

A

LD: 40mg/kg (max 3000 mg)
MD: 5mg/kg IV Q8H

increase MD based on levels

30
Q

VPA PK and DDI

A

Highly protein bound
VPA will displace phenytoin = more free phenytoin = toxicity

31
Q

VPA ADR

A

drowsiness, headache
thrombocytopenia
pancreatitis (peds)
hyperammonemia

32
Q

Lacosamide MOA

A

stabilize neuronal membrane
inhibit repetitive neuronal firing
Enhances slow inactivation of Na channels

33
Q

Lacosamide dosing

A

100 - 200 mg IV BID

34
Q

Lacosamide ADR

A

well tolerated
dizziness, abnormal vision, diplopia, ataxia

bradycardic arrythmias, avoid if hx

35
Q

Refractory status epilepticus definition

A

no repsonse to initial anticonvulsants
1. seizure >2 hrs
OR
2. rate of 2+ seizure/hr w/o recovery to baseline despite AED tx

respiratory/cv compromise + systemic complications

36
Q

Refractory status epilepticus Tx

A
  1. High dose BZD
    * Midazolam bolus + cont infusion
    * 2mg IV bolus + 2mg/kg/hr, double infusion prn up to 64 mg/kg/hr
  2. Propofol IV infusion - watch LTM
  3. Last line: phenobarbital/pentobarbital coma
36
Q

Post intubation SE tx

A
  1. start IV antiepileptic (propofol/midazolam)
  2. long term EEG monitoring
    Unable to tell if seizing due to paralytic use for intubation

pt usually on 2-3 IV AED + 1≥ cont IV infusion

37
Q

Phenobarbital/Pentobarbital Coma MOA

A

sensory cortex supression (sedative hypnotic)
shuts brain down

38
Q

Phenobarbital dosing

A

LD: 20mg/kg IV x 1
MD: 1-2 mg/kg IV twice daily

39
Q

Pentobarbital dosing

A

5-15 mg/kg IV x 1
0.5-5mg/kg/hr IV infusion

40
Q

Phenobarbital/Pentobarbital Coma ADR

A

IV - respiratory depression
Hypotension - pressors
lethargy
nystagmus
thrombocytopenia
decreased GI motility
supress immune system (watch for infection labs, pt won’t spike fever)

41
Q

SE Tx goal

A

attain burst supression on LTM for 24-48 hours
slowly titrate off IV infusion while monitoring LTM for reoccurrence

42
Q

SUPER refractory SE Tx

pt in barb induced coma and still seizing

A

Ketamine infusion (NMDA antagonist)
LD: 1.5 - 3 mg/kg IV x 1
MD: 0.1-4mg/kg/hr (max 15 mg/kg/hr)

43
Q

How to wean drugs after attaing burst supression

A

Wean ADR causing drugs first
- barbituates, propofol (results in need for pressors)
- Midazolam (accumulates in fat)

44
Q

SE outcomes

A

Post ictal - repeat neuro exam, investigate cause of seizure

45
Q

Mortality of SE

A

non-convulsive: 51%
refractory: 19-60%