Status Epilepticus - Block 1 Flashcards

1
Q
A
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2
Q

What is SE?

A

continuous seizure activity (≥ 5 minutes) + risk of long-term consequences (≥ 30 minutes)

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3
Q

What is the most common form of SE?

A

generalized convulsive status epilepticus (GCSE)

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4
Q

What is characterized as epileptic twilight with altered consciousness?

A

nonconvulsive status epilepticus (NCSE)

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5
Q

What is the tx for nonconvulsive status epilepticus (NCSE)?

A

Benzodiazepines remain drugs of choice
* 2nd line: IV phenytoin, valproate, levetiracetam
* Lacosamide or topiramate can be tried in nonresponders

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6
Q

What are the phases of GCSE?

A
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7
Q

What are the causes of SE?

A

Neonates: drug withdrawl, pyroxidine def
1 YO: Acute encephalopathy and metabolic disorders
Young children: Fever/viral illness
Adult: Cerebrovascular dx, rapid antiseizure med withdrawl, low antiseizure med levels

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8
Q

What causes GCSE?

l[\

A
  1. Imbalance between excitatory and inhibitoiry neurotransmission
  2. is largely caused by glutamate acting on postsynaptic N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-isoxazole-4-propionate (AMPA)/kainate receptors
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9
Q

What are the clincal implications of GCSE?

A

A prolonged seizure can destroy neurons:
* (First 30 min): Hypertension, tachycardia, and cardiac arrhythmias
* Hyperglycemic initially and then serum glucose begins to fall
* Muscle contractions  rhabdomyolysis with secondary hyperkalemia and acute tubular necrosis
* Airway obstruction  cyanotic or hypoxic
* Increase in salivation and tracheal and pulmonary secretions  aspiration pneumonia

Severe complications begin to arise (hypotension, hypoglycemia, hypoxia, severe metabolic disturbances)
Convulsive SE (CSE) lasting 1 hour or more increases morbidity by 10-fold

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10
Q

Lab test for SE?

A
  1. CBC
  2. Serum
  3. Urinalysis
  4. Blood cultrue
  5. ABG
  6. Serum drug
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11
Q

Non pharm to stabilize patients?

A
  1. Time of seizure onset
  2. Vital signs
  3. Adequate and protected airway
  4. IV access
  5. Tx for hyperthermia (cooling blanket)
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12
Q

Pharm for SE?

A

Initial-therapy phase (5-20 minutes) - impending
Second-therapy phase (20-40 minutes) - established
Third-therapy phase (40-60 minutes) - refractory

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13
Q

What occurs in the initial tx phase?

A

BENZOS
Initial toc: IM midazolam, IV lorazepam, or IV diazepam
* Patients chronically on a benzodiazepine (eg, clobazam and clonazepam) might have developed tolerance and could require large doses

Alt: IV phenobarbital

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14
Q

What benzo is typically the drug of choice for most clinicians?

A

Lorazepam

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15
Q

What is the consideration when using diazepam?

A

Lipophilic and redistribution: efficacy is about 30 min and thus a longer-acting anticonvulsant should be administered afterwards

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16
Q

What is the consideration when using midazolam?

A

Maintenance doses must be given by continuous infusion due to short half-life

17
Q

What is given to patient once discharged?

A

IM midazolam
Intranasal (IN) and buccal midazolam
Per rectum (PR) and IN diazepam

18
Q

What are the second therapy agents?

A
  1. Hdantoin (Phenytoin or fosphenytoin)
  2. Valproate
  3. Phenobarbital
  4. Levetiracetam
  5. Lacosamide
19
Q

When should phenobarbital be used?

A

Paatients have failed other second therapy phase agents

20
Q

Third phase tx?

A

Anesthetic doses of midazolam, pentobarbital, or propofol may be used:
* If the patient is not already intubated and mechanically ventilated, this is required prior to administration of anesthetics – along with contin EEG

21
Q

Considerations of midazolam?

A
  1. If used, it should always be combined with another drug that acts at a different site and ideally initiated within 30 min
  2. No specific protocol for tapering of midazolam; some suggest a seizure-free period of 24 to 48 hours followed by decreasing by 1 to 2 mcg/kg/min every 15 minutes
  3. Return to consciousness more rapidly due to short half-life
22
Q

Considerations of Pentobarbital or thiopental (short-acting barbiturates)

A
  1. Although no controlled trials to support this practice, overall response rates were found to be significantly greater in those treated with pentobarbital compared to midazolam or propofol
  2. Potent hepatic enzyme inducer -> doses of most concurrent anticonvulsants will need to be larger than usual maintenance doses
23
Q

Proprafol considerations?

A
  1. Extremely lipid soluble, has a large volume of distribution, has a very rapid onset of action and its extremely short half-life
  2. Prolonged infusions greater than 4 mg/kg/hr have been associated with propofol-related infusion syndrome (PRIS)
24
Q

What to use in super refractory GCSE?

A
  1. Ketamine
  2. Lidocaine
  3. Inhaled anesthetics
  4. Immunomodulating tx
  5. Controlled mild hypothermia
25
Q

Ketamine

MOA, ADR

A

MOA: Noncompetitive antagonist of glutamatergic N-methyl-D-aspartate (NMDA) receptors
ADR: hallucinations upon awakening, increased salivation, and increased intraocular and intracranial pressure

26
Q

Lidocaine consdieration?

A

Serum concentrations and ECG should be monitored to avoid drug accumulation and toxicity

27
Q

Monitoring of SE?

A
  1. EEG
  2. Vital signs
  3. Infusion site
28
Q

Algorithm for convulsive SE?

A