Status epilepticus management treatment

Status epilepticus -- treatment
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1. Management of Status
Epilepticus
ZIKRULLAH

2. Status Epilepticus-Definition
Status epilepticusis defined as more than 30
minutes of continuous seizure activity
OR
recurrent seizure activity without an
intervening period of consciousness
more practical definition: since isolated tonic -
clonicseizures rarely last > few minutes ...
consider Status if sz> 5 min or 2 discrete szwith
no regaining of consciousness between

3. Types of status epilepticus
Generalized convulsive status epilepticus
-Most common form
Non-convulsive generalized status epilepticus
(subtle status epilepticus)
-requires electroencephalography for diagnosis
Refractory status epilepticus(>60 min )
-or is refractory to therapy with 2 or 3
anticonvulsant agents
Myoclonicstatus epilepticus
-characterized by irregular and repetitive
movements of the face and extremities

4. Etiology
infection (systemic / CNS)
structural: trauma, CVA, IC bleed
CNS malformations
metabolic -hypoxia, abnelectrolytes,
hypoglycemia
toxic -alcohol, other drugs
drug withdrawal -AED’s, benzos
congenital -inborn errors of metabolism

5. Physiological Changes in
GCSE-
Compensation
Cerebral changes
Increased blood
flow
Energy
requirements are
matched by
increased lactate,
increased glucose
Metabolic changes
Hyperglycemia
Lactic acidosis
Autonomic
changes
Hypertension
Increased CO
Increased CVP
Massive
Catecholamines
Tachycardia
Arrythmias
Hyperpyrexia
Vomiting

6. Physiological Changes in
GCSE-
Decompensation
Cerebral changes
Failure of
autoregulation
Hypoxia
Hypoglycemia
Decreased lactate
Increased ICP
Cerebral edema
Metabolic changes
Hypoglycemia
Hyponatremia
Hypo/Hyperkalemia
Acidosis
Hepatic/Renal
dysfunction
DIC
Rhabdomyolysis
Serum/CSF
leukocytosis
Autonomic
changes
Hypoxia
Decreased blood
pressure
Falling CO
Pulmonary edema
CHF
Arrythmias
Hyperpyrexia

7. Status epilepticus
It is a medical emergency –requires prompt and
aggressive treatment
Therapy should be aimed at:
Rapid termination of status epilepticus
Prevention of seizure recurrence
Treatment of underlying cause

8. Management of SE General
measures
ABC (Airway ,breathing, and circulation)is
the first priority
Protect airway, tongue, head
insert nasal airway or intubateif needed
Check blood pressure.
Begin nasal oxygen.
Monitor ECG and respiration.
Check temperature frequently.
Obtain history.
Perform neurologic examination.

9. Send blood for evaluation of electrolytes, BUN,
glucose level, CBC, toxic drug screen, and AED
level and ABG
Start EEG recording as soon as feasible.
Imaging with computed tomography is
recommended
If imaging is negative, lumbar puncture is
required to rule out infectious etiologies.

10. Start IV line containing isotonic saline at a
low infusion rate.
Inject 50 mLof 50 percent glucose IV and
100 mg of thiamine IV or IM.
Correct electrolyte imbalance -acidosis lowers
seizure threshold, treat with bicarbonate if pH<7.1
Treatment of underlying cause may proceed
concurrently with drug therapy, e.g., neurosurgical
decompression.

11. Pharmacological Management of SE
Anti -Epileptic Drugs:
Benzodiazepines
Phenytoin/ Fosphenytoin
Barbiturates
Propofol
others / new possibilities

12. Status Epilepticus-Definitive Treatment
Lorazepam
1st agent to use
Dose: Adults -0.1 mg/kg IV over 1 min
Peds.05 -.1 mg/kg (to 4 mg) IV
less lipid soluble than Diazepam --> smaller
volume of distribution / longer T1/2
effects last 12 -24 hr
S/E: respdepression, hypotension, confusion,
sedation (but less than diazepam)

13. Diazepam
Dose -0.2 mg/kg IV (max,10mg) over 1 min
repeat after 5 minsif no response
High lipid solubility
Fast redistribution: 15-20 minutes
Effect lasts for 15-30 min
Adverse effects:
respiratory depression
Hypotension

14. Second Stage-Established GCSE(20-
60 min)
Phenytoin: still the standard 2nd IV Rx after
Benzo
Dose:15 -20mg/kg (slow iv)
max rate 50mg/min
IV solution is highly alkaline -pH is 12
-give in large vein, dilute N/S, flush .
Do not add to dextrose drip as it preciptiates
onset of action: 10 -30 min
Duration of action:12-24hrs

15. Phenytoincontinued
S/E -(most avoided if slower administration)
hypotension
arrhythmias -(must monitor ECG )
respiratory depression
extravasation-->tissue injury / necrosis
C/I-in pt with second degree heart block
or severe hypotension

16. Fosphenytoin
a prodrugof Phenytoin
it has no anticonvulsant action itself, but is
rapidly converted to Phenytoin
Dosage: in “PhenytoinEquivalents” to
attempt to avoid confusion
15-18 phenytoinequivalent (PE)/kg iv/imat
max rate of 150 mg PE/min
Molecular wt = 1.5 x Phenytoin... so
1.5 mg Fosphen--> 1 mg Phenytoin
delivered

17. Fosphenytoin
Advantages over Phenytoin:
pH 8(vs Phenytoin pH 12)
does not require solvent (Phenytoin is dissolved
in propylene glycol)
can give IM when no IV access
IV: -less potential for irritation -can give faster
-no risk of tissue necrosis if goes interstitial
-does not precipitate in IV solutions
lower risk of hypotension and dysrhythmias

18. Alternative therapeutic option
Sodium Valproate: 25-35 mg/kg iv at max rate
of 6mg/kg/hr
S/E -Local irritation ,GI distress, Lethargy
Phenobarbitone:20 mg/kg iv at 60 mg/min
S/E: profound hypotension
respiratory depression
patient will likely need intubation & ventilation at
this point; (and will need ICU admission and
continuous EEG monitoring if SE persists)

19. Refractory Status Epilepticus
(>60min)
Admit the pt in ICU
Prepare to mechanically ventilate
If intubating/ ventilating -avoid long-acting n-m
blockers -masks szactivity
Obtain central venous acces
Continuous hemodynamic monitoring through
arterial line
Start EEG monitoring

20. Refractory SE T/t
Midazolam: 0.2 mg/kg iv (max 10 mg) bolus over
2 min followed by 0.1-0.4 mg/kg/h continuous iv
infusion
Continue pharmacologic coma for 12 hrs after
last seizures with EEG goal of burst suppression

21. Thiopental
Thiopental:10-20 mg/kg iv bolus followed by
0.5-1 mg/kg/h iv infusion
rapid onset: 30 -60 sec
short duration: 20 -30 min
Thiopental -negative aspects:
accumulates in fatty tissues
long recovery time after infusion
hemodynamic instability -CV depression,
hypotension, arrhythmias

22. Propofol
Dose: 2-5mg/kg iv bolus
Rate: 5-10 mg/kg/hr
Onset: 2-4 min
Half-life: 30-60 min
does not accumulate --> rapid recovery
Mechanism:
stimulates GABA receptors (like
Benzos/Bbts)
suppresses CNS metabolism

23. Weaning phase
Reduce infusion every 3 hrs with EEG
monitoring
If no clinical or electrographic seizures then
wean off
If seizures recur re-institute coma therapy

24. Status epilepticusmanagement
Lorazepamo.1mg/kg i.v. over1-2 min
(Repeat x1 if no response after 5 min)
Additional emergent drug may not be
required if seizures stop or etiology is rapidly
controlled.
Fosphenytoin20 mg/kg PE IV @ 150
mg/min or
Phenytoin20 mg/kg IV @ 50 mg/min

25. seizures continuing
Fosphenytoin7–10 mg/kg PE IV @ 150
mg/min
or Phenytoin7–10 mg/kg IV @ 50 mg/min
Consider valproate
25mg/kg IV
Consider admitting to ICU

26. Phenobarbital 20 mg/kg IV @ 60 mg/min
seizures continuing
Phenobarbital 10 mg/kg IV @ 60 mg/min
IV anesthesia with propofolor midazolamor
pentobarbital

27. Maintenance AED treatment
To prevent recurrence of seizures
In known case of epilepsy, usual AEDs
maintained and dose adjusted depending on
serum AED levels
In patients presenting for the first time drugs like
PHT or VPA used to control the status continued
as oral maintenance therapy

28. Possible new drugs for Status
Lidocaine-some positive trials
Gabapentin/ Vigabatrin/ Lamotrigine
Felbamate-blocks NMDA receptors
Ketamine-blocks NMDA receptors

29. Ketaminein SE
blocks NMDA receptors -this may protect
brain from effects of excitatory NT’s
may be neuroprotectiveas well as
antiepileptic
some animal studies have demonstrated
control of refractory SE with Ketamine:
more efffectivethan Phenobarbin LATE
SE (>60 min); not as effective in EARLY
SE

30. THANK YOU.