status epilepticus
DESCRIPTION
Status Epilepticus. by Robert S. Fisher, M.D., Ph.D. Department of Neurology Stanford, California USA. Definition of Status Epilepticus. A state of continuing seizures for greater than 30 minutes, or recurrent seizures for at least 30 minutes without intervening - PowerPoint PPT PresentationTRANSCRIPT
Status Epilepticus
by
Robert S. Fisher, M.D., Ph.D.
Department of Neurology
Stanford, California USA
Definition of Status Epilepticus
A state of continuing seizures for greater than 30 minutes, or recurrent seizures for at least 30 minutes without intervening return of consciousness.
TYPES OF STATUS
Simple partial motorComplex partialAbsenceMyoclonicTonic-clonic
Epilepsia partialis cont.
Non-convulsive
Tonic-clonic
*
*Petit mal, spike-wave, absence
About 30,000per year
Rochester Richmond
The longer you wait, the harder to treat
With delay of treatment, more diazepam is required to stop seizures in an experimental model of status.
Walton & Treiman Epilepsia 1995 S4:45
0
1
2
3
4
5
mg
Val
ium
1st sz
2nd sz
EARLY TREATMENT IS KEY
0 5 10 15 20 25 30 3560
70
80
90
100
110
DAYS
% SURVIVING
DeLorenzo, 1992 Epilepsia S4:15
rapid treatment
delayed treatment
<1hr
>1hr
Symptomatic
Idiopathic
140,00060,000
2,000,000
Epilepsy Status
CONCEPT OF - Overt status- Subtle status
Encephalopathy
Mild twitching
Unresponsiveness
EEG general ictal
CAUSES OF STATUS: ADULTS
0 5 10 15 20 25 30
Cerebrovascular
Med change
Anoxia
ETOH-drug
Metabolic
Unknown
Fever/infection
Trauma
Tumor
Congenital%
from DeLorenzo et al. Epilepsia 1992; 33 (Suppl. 4): S15-25
COMPLICATIONS OF STATUS
HyperthermiaShockRhabdomyolysisArrhythmiasAspirationPhysical Injuries
PsychosocialBrain cell lossDeath in 5-30%Iatrogenic injury
Walker MC, Howard RS, Smith SJ, Miller DH, Shorvon SD, Hirsch NP. Diagnosis and treatment of status epilepticus on a neurological intensive care unit. QJM 1996; 89: 913-20.
26 pts admitted to neuro-ICU as status epilepticus Only 14 (54%) were in status epilepticus Six were in drug-induced coma or were encephalopathic Six had pseudo-status epilepticus: 4 were intubated.
MISDIAGNOSIS
Discrete seizures
Waxing ictal
Continuous ictal
Continuous ictal with flat
PLEDs on flat background
SEQUENCE OF EEG CHANGESIN STATUS EPILEPTICUS
Discrete seizures
FP1-F7
F7-T3
T3-T5
T5-O1
FP2-F8
F8-T4
T4-T6
T6-O2
1 sec 100 µV
Continuous ictal discharges
FP1-F7
F7-T3
T3-T5
T5-O1
FP2-F8
F8-T4
T4-T6
T6-O2
1 sec 200 µV
Fp1-F7
F7-T3
T3-T5
T5-O1
Fp2-F8
F8-T4
T4-T6
T6-O2
Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4
C4-P4
P4-O21 sec100 µV
PLEDS
0
10
20
30
40
50
60
70
80
%
Discrete Waxing Continuous Cont with flat PLEDs
STAGE OF EEG & RESPONSE TO THERAPY
Treiman et al. from VA study 1996
% recovery
In 1685, King Charles II of England suffered from an illness
that caused him to have convulsions. The treatments he underwent included: "letting" of one pint of blood; an enema of antimony, sacred bitters, rock salt, marrow leaves, violets,
beetroot, chamomile flowers, fennel seeds, linseed, cinnamon, cardamon seeds, and aloe; and
having his head shaved and blistered. Needless to say, the
King died.
quoted in:http://www.epilepsynl.com/newsletters/NewsletterFall2004.pdf
Charles II of EnglandKing of Scots, King of England and King of Ireland
(and Ruler of the American Colony)Reign: 29 May 1660 – 6 February 1685
Born: 29 May 1630 Died: 6 February 1685
A 42 year old male known alcoholabuser was brought to the ER stiffand trembling. He was thought tobe exhibiting DT's (1), and was there-fore given diazepam by NG tube.This precipitated emesis and associatedaspiration (2). Then all 4 extremitiesbegan to jerk rhythmically.
HOW NOT TO TREAT STATUS
An iv was established, and routinebloods sent to the lab (3). Anticonvul-sants were withheld for 45 minutespending arrival of the medical record (4).Seizure activity was terminated with 10mg diazepam iv push, but tonic-clonicmovements recurred 15 minutes later(5). Phenytoin 300 mg was given intra-muscularly to no effect (6).
HOW NOT TO TREAT STATUS
Phenobarbital 500 mg iv was given as athird drug, resulting in apnea and hypo-tension (7). The patient resided in anICU for 24 hours, whereupon he awoke,exhibited no further seizures, and wasdischarged that day (8)
HOW NOT TO TREAT STATUS
1. Secure the correct diagnosis2. Stabilize patient first3. Treat the treatable4. Stop within 30 minutes5. Immediate + long-term control6. Proper routes and doses of meds7. Expect cardiorespiratory trouble8. Diagnosis and follow-up
PRINCIPLES FOR STATUS
STABILIZE
Airway Breathing Circulation Oxygen Dextrose ?
Breathing Pulse Blood Pressure EKG EEG
MONITOR
Ten Centers, 530 evaluable patients
Four iv regimens for initial Rx GTC status PHT 18 mg/kg DZP 0.15 mg/kg, then PHT 18 mg/kg PBB 15 mg/kg LOR 0.1 mg/kg
Endpoint: seizure-free from 20-60 minutes Clinical
EEG
VA COOP STATUS STUDY
Treiman et al. from VA study 1996
0
10
20
30
40
50
60
70
%
LOR PBB DZP+PHT PHT
CONTROL BY DRUG
You stop the visible seizures,but the patient doesn’t wake upfor an hour.
What should you do?
20% had EEG statuscontinuing after behavioralseizures had stopped.
80%
20%
Treiman et al. from VA study 1996
Rate of recurrence39 day outcomeAdverse events
No differences amongfour treatment group for :
Treiman et al. from VA study 1996
Outcome Overt Subtle
Improved, discharged 53% 9%Still in hospital 21% 25%Died 27% 65%
Treiman et al. 1996 VA Coop
But – is usual outcome really this poor?
100 consecutive ICU NCSE patients. 18 (18%) died: 14/52 (27%) in acute medical group 1/31 (3%) in the epilepsy group 3/17 (18%) in the cryptogenic group
Mental status impairment was severe in 33 Complications occurred in 39
Shneker BF, Fountain NB. Assessment of acute morbidity and mortality in nonconvulsive status epilepticus. Neurology 2003;61:1066-1073.
lorazepam (Ativan) phenytoin (Dilantin) phenobarbital
pentobarbitalpropofol (Diprivan)midazolam (Versed)
isofluoraneetomidatelidocaineparaldehydemagnesiumfurosemide
cooling ???
DRUG THERAPY
PENTOBARBITAL
CVP line or Swan Load: 5-15 mg/kg in 250 cc NS over 1 hr Orders for neosynephrine or pressors Continuous EEG monitoring Maintain 1-20 mg/kg per minute Aim for about 70-90% EEG suppression Taper after a few days over half a day
FP1-F7F7-T3T3-T5T5-O1FP2-F8F8-T4T4-T6T6-O2FP1-F3F3-C3C3-P3P3-O1FP2-F4F4-C4C4-P4P4-O2
1 sec 100 µV
PROPOFOL: USE IN STATUS
Quicker wake-up
Maybe less respiratory depression
Bolus of 2 mg/kg
Continuous infusion 1-10 mg/kg/hr (17-170 ug/kg/m)
EEG monitoring with titration to burst-suppression
Supportive care for comatose patients
Be aware of expense
PROPOFOL: ADVERSE EFFECTS
Respiratory depression with induction > 2.5 mg/kg
Hypotension in about 15%
Bradycardia in about 5%
< 0.2% of 25,981 pts needed hemodynamic support
Increases serum triglycerides
Lipid, egg, glycerol solvent may get infected
Propofol infusion syndrome (rare)
Sometimes paradoxical induction of seizures
6 y/o Boy with Shunt Failure
Elderly Man Post-Anoxia
36 y/o man with 10 Tonic-Clonic Seizures Today
Prior EEG: Half-Speed
Triphasics vs. Nonconvulsive Status
• Difficult EEG distinction, perhaps impossible• Both show periodic frontal 3-phase sharp potentials• Triphasics can have an after-going slow wave• Both wax and wane• Both can have an anterior-posterior gradient• Triphasics tend to decline with sleep (but variably)• Waxing-waning awareness in both• Involves BDZ receptors in both• What is metabolic encephalopathy anyway?
6 y/o Girl with Status Epilepticus
Elderly Woman with Renal Failure
1 sec
100 µV
FP1-F7F7-T3T3-T5T5-O1FP2-F8F8-T4T4-T6T6-O2FP1-F3F3-C3C3-P3P3-O1FP2-F4F4-C4C4-P4P4-O2
Triphasic waves
SPECIAL CIRCUMSTANCES
Need IV medication phenytoin
fosphenytoin phenobarbital
diazepam, lorazepam, midazolam Depacon (valproic acid)
paraldehyde (if obtainable) levetiracetam (Keppra) lacosamide (Vimpat)
SPECIAL CIRCUMSTANCES
Need to avoid sedation
Most except
phenobarbital
benzodiazepines
SPECIAL CIRCUMSTANCES
Need to avoid WBC depression
Most OK, Except
carbamazepine
oxcarbazepine
valproic acid
felbamate
SPECIAL CIRCUMSTANCES
Need to avoid low sodium
Most OK, Except carbamazepine
oxcarbazepine
COMMON MISTAKES
1. Fail to recognize status
2. Fail to deliver emergency support
3. Not treating reversible causesHypoglycemiaHypocalcemiaHypoxiaToxic ingestionHyperthermiaOther reversible causes
4. Too slow with meds
5. Partial polypharmacy
CONCLUSIONS
1. Status is common and lethal
2. Early/effective treatment makes a difference
3. Subtle status can be missed
4. First support the patient & treat the treatable
5. Lorazepam is the favored therapy
6. Several other drugs can be used later: e.g., propofol or pentobarbital coma
7. With best therapy, mortality remains high