Critical Care: Seizure Flashcards
the thing you get when you read all the typos
inhibitory neurotransmitte4r
gaba
exctatory neurotransmitters
- glutamte
- asparate
- acetylcholine
how long must a seizure last to be considered status epilepticus
5 min
at what point does a pt warrantt an antiepileptic
after 2nd seizew
goals of treatment of seizure
- rapid and safe termination
- prevent recurrence
- avoid CV and resp complicaations
initial treatment of seizure
- benzosssss - the stop the seizure
- first line: lorazepam and diazepam IV
- second line: diazepam PR and midazolam IM - anti-epileptics - prevent recurrence
- fos/phenytoi
- keppra
- VPA
lacosamide can be used as an add on anti-epileptic
fos/phenytoin MOA
affect movement of Na across cell membranes -> stabilize neuronal membranes and decrease seizure activity
fos/phenytoin dose in treatment of seizure
- loading dose: 20mg/kg IV (max 50 mg/min)
- maintenance: 4-6 mg/kg/day divded BID or TD
fos/phenytoin monitoring
- goal total phenytoin 10-20 mcg/dL
- if pt actively seizing, can increase goal to 15-25
- levels above 30 can cause seizures
fos/phenytoin PK
- highly protein bound - correct phenytoin level if albumin < 3.5
- liver metabolis
- Michaelis-Menten saturable kinetics: once saturated, a small change in dose can lead to a big change in steady state level
fos/phenytoin ADR
- CV: hypotension, bradycardia, QT prlongation (reduce indicince rate with lower infusion rate)
- extravasation
- rash -> SJS
- neutropenia/thrombocytopenia
- ==========
- P - cyp450
- H - hirsutism/hypertrichosis
- E - enlarged gums
- N - nystagmus
- Y - yellow (hepattis)
- T - teratogenicity
- O - osteomalcia (vit D deficiency)
- I - interferene with folate metabolism (anemia)
- N - neuropathies (vertigo, ataxia, HA)
keppra MOA in treatment of seizures
unclear, but it is involved in neurotransmitter release
keppra dose in treatment of seizure
- loading: 60 mg/kg IV (max 4500 mg)
- maintenacne: 1000 mg IV BID
do NOT need to djust for AKI in pts with status epilepticus
keppra adr
- drowsiness
- agitation (aggression, agitatio, emotional lability)
VPA MOA
- increase GABA synthesis and release
- decrease excitatory amino acids and attenuate neuronal excitation mediated by NMDA receptors
- block voltage dependent Na channels -> inhibit excitable membranes
VPA dose in treatment of seizures
- loading: 40 mg/kg (max 3000mg)
- maintenance: 5mg/kg IV q8h
VPA monitoring
goal 50-100 mcg/mL
VPA ADR
- drowsiness
- HA
- thrombocytopenia
- pancreatisi in peds
- hyperammonia
important VPA/phenytoin DDI
both are strong protein binders but VPA displaces phenytoin -> icreased serum phenytoin -> higher potential ofr phenytoin tox
lacosamide MOA
enhance slow inactivtion of Na cchannels -> stabolize hyperexcitable neuronal membranes and inhibit repititve neuronal firing
lacosamide dose in treatment of seizure
100-200mg iV BID
refractory status epilepticus
- seizure > 2 hrs long
- 2+ seizures/hr with no recovery to baseline despite treatment
these pts often need to be intubated
intubating refractory status epilepticus pts
- start a continuous anti-epileptic infusion: propofol or midazolam (or both if needed)
- paralytic will be needed -> hard to tell if pt is actively seizing -> need an EEG or LTM to monitor seizure activity
IV midazolam dose for treatment of refractory status epilepticus
2 mg bolus follwoed by 2mg/hr
- doubled prn if pt still seizign
when to do a phenobarb or pentobarb induced coma in a status epilepticus pt?
- when nothing else works lol
- pt is s/p several doses of benzos and at least 2-3 anti-epileptics with one of them being continouous
phenobarb and pentobarb are sedative hypnotics that suppress sensory cortex
phenobarb and pentobarb ADR
- resp depresion - pt MUST be intubated
- hypotension - may need vasopressors
- decreased GI mobility
- suppressed immune system - monitor for s/s of infection, pt likely won’t develop a fever even if infected
- thromocytopenia
when to treat a status epilepticus pt with ketamine
when the phenobarb/pentobarb coma didn’t help
status epilepticus treatment goal
burst suppression on LTM
what to do when a status epilepticus pt achieves burst suppression is achieved on LTM (long term monitoring)/EEG
- maintain burst suppression for 24-48 hrs then slowly tirtrate off IV infusions
- start with agents with bad ADR: phenobarb, pentobarb, midazolm, propfol
- slap the agents back on if pts starts seizing again
post-ictal recovery care
frequent neuro exams to try and figure out cause of seizure/SE
