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Status Epilepticus
Status Epilepticus
Preface
Clinical Recognition
Neuroimaging and Laboratory Tests
First Steps in Management
Deterioration: Causes and Management
Outcome
Conclusion
Preface
Two intravenous peripheral catheters must be placed in large arm veins for
administration of antiepileptic drugs and possibly a peripherally inserted
central catheter for vasopressors.
In patients with multiple seizures, hydration with 0.9% saline (200 mL/hr)
is started immediately to reduce the risk of renal failure from
rhabdomyolysis, particularly if the admission serum creatine kinase is
considerably increased.
Metabolic acidosis is frequently found but should not be corrected with
bicarbonate until the pH has declined to 7.0.
Acute non-oliguric renal failure from rhabdomyolysis (acutely rising serum
creatinine, hyperkalemia, and hyper phosphatemia). Initial treatment is to
change iv fluids from normal saline to D5W with 3 ampules of bicarbonate
at 200 mL/ hr to maintain urinary output of more than 100 mL/ hr.
Phosphate binders (calcium acetate) are needed until laboratory values
normalize.
First Steps in Management
(3)
The enthusiasm for propofol has diminished after an early initially unexplained report of
fourfold higher mortality. There have been many reports of a propofol infusion
syndrome (PRIS), an unexplained sudden cardiovascular collapse in patients treated
with high doses (more than 10 mg/kg/hr) and for more than 3 days, although PRIS may
occur hours after infusion of propofol and in much lower doses. Propofol is currently ill-
advised in the treatment of status epilepticus when often high doses or prolonged
treatment is anticipated.
Pentobarbital can be strongly considered if prior drugs fail. Iv Pentobarbital with initial
bolus of 10-15 mg/kg over 1~2 hours followed by infusion of 1-3 mg/ kg/ hr until
seizures stop clinically and on EEG. Pentobarbital has a marked cardio depressant
effect, and many patients need vasopressors for blood pressure support. Aiming f0r an
EEG without seizure activity may considerably reduce the side effects of pentobarbital.
However, in daily practice, the EEG may fluctuate from burst suppression to bilateral
PLEDS without appreciable bursts of seizures. This EEG recording may be a satisfactory
end point.
Major management problem arises when generalized tonic-clonic seizures are not
controlled/continue to recur after discontinuation of barbiturate therapy. Failure to
control seizures with barbiturate anesthesia seems very uncommon, but if it happens,
the chance of effectively controlling seizures is low and morbidity is high in these
Deterioration: Causes and
Management (4)
lsoflurane is an attractive option and highly effective. In a series of 11 patients with
treatment-refractory status epilepticus, morbidity and mortality remained high despite
seizure control. Isoflurane is used in concentrations of minimum alveolar concentration
(MAC of 1.15%) but progressively higher concentrations are often needed to control
seizures.
Lidocaine has shown efficacy in therapy; refractory status epilepticus. Lidocaine is
injected in a bolus of 1.5-2 mg/ kg in several minutes, fOIlOWed by an infusion of 3
mg/kg/ hr. The infusion should not be continued for more than 12 hours. Its use is limited
in patients with a history of cardiac arrhythmias or ecg evidence of any type of heart
block and poor ejection fraction on echocardiography, Use in patients with liver failure is
also contraindicated due to decreased hepatic clearance, and a high level of lidocaine,
which itself can lead to seizures, may result.
New alternative agents are ketarnine and valproate. Experience is very limited and only
successful cases have been published. Physician must exercise great caution in their use
as a treatment for status epilepticus. A short-acting anticonvulsant, an N-methyl-D-
aspartate receptor antagonist, ketarnine, surprisingly controlled status epilepticus in one
patient refractory to phenytoin, phenobarbital, midazolam, propofol, valproate, and
lidocaine infusion. This unconfirmed experience is valuable. Ketamine was used in a bolus
of 2 mg/kg over 2 min followed by an infusion of 10-50 mg/kg/ min, a dose that does not
cause respiratory depression The infusion dose is then tapered to 7.5 mg/ kg/ hr for 7-14
days.
Deterioration: Causes and
Management (5)
Valproate iv has been recently introduced, but its efficacy is unknown, control of seizures
is only 30%. Major advantage may be that it does not reduce blood pressure and may be a
good alternative in patients who have become cardiovascularly unstable with midazolam
and propofol. It also has virtually no respiratory depression. Iv loading doses of valproate
can be 25-30 mg/ kg, with infusion rate of 20 mg / min to attain a steady-state serum
concentration of 75 mg/ L. It is highly bound to albumin, and toxicity may rapidly arise in
patients with poor nutritional intake and it has been implicated in abnormal hemostasis.
When all else fails, it makes common sense to try to treat seizures with a radically
different approach. Levetiracetam, Nimodipine, resection of an (identifiable) epileptic
focus, vagus nerve stimulation, high-dose phenobarbital (100-300 mg/mL plasma levels),
or electroconvulsive therapy have all been considered with variable success.
Weaning from intravenous antiepileptic drugs has not been carefully studied. We prefer to
treat patients aggressively (burst-suppression or mostly suppressed EEG pattern) for at
least 24 hours, aiming for a seizure-free period of another 24 hours. Then we reduce the
dose 10% every hour, while monitoring with video EEG for recurrence and then either stop
weaning or increase the dose.
An aggressive approach with prolonged use of anesthetic drugs for several months may be
justified only in young patients with traumatic brain injury, in encephalitis, and in patients
with NIRI findings that do not suggest widespread cortical damage.
Outcome (1)