INTENSIVE MANAGEMENT OF STATUS EPILEPTICUS

dr. Johana Herlin, Sp.S

SMF ILMU PENYAKIT SARAF
RSUD PROF. W. Z. JOHANNES KUPANG
2017
OBJECTIVES

 Current definition of status epilepticus

 Classification
 Epidemology
 Etiology
 Types of status epilepticus
 Clinical manefestations-convulsive/nonconvulsive
 Diagnosis
 Therapy

Current guidelines for the management of status epilepticus-Neurocritical care society guide lines-2013
DEFINITION STATUS EPILEPTICUS
 Conventional “textbook” definition of status epilepticus:
 Single seizure > 30 minutes
 Series of seizures > 30 minutes without full recovery

 Operational definition Generalized, convulsive status epilepticus in children

and adults refers to > 5 minutes of continuous seizure or >2 discrete seizures with
incomplete recovery of consciousness
STATUS EPILEPTICUS-EPIDEMIOLOGY

 US-20-40/100 000
 Bimodal-< 1 year & >60 years
 25% have history of pre existing Epilepsy
 Status epilepticus with 14% mortality rate – 86/100,000 in elderly , with
38% mortality rate
Classification framework

Axis 1:Semiology Axis 2 : Etiology of status epilepticus

the clinical presentation of SE : Known (i.e., symptomatic)
Acute (stroke, intoxication, malaria, encephalitis, etc.)
1.The presence or absence of prominent motor Remote (posttraumatic, postencephalitic, poststroke,
symptoms Progressive (e.g., brain tumor, Lafora’s disease and
2 The degree (qualitative or quantitative) of other PMEs, dementias)
SE in defined electroclinical syndromes
impaired con- sciousness
Unknown (i.e., cryptogenic)

Axis 3:Electroencephalographic Axis 4:Age

1Location:generalized,lateralized,bilateral independent,multifocal. 1 Neonatal (0 to 30 days).
2 Name of the pattern 2 Infancy (1 month to 2 years).
3Morphology:sharpness,number of,absolute and relative amplitude, 3 Childhood (> 2 to 12 years).
polarity. 4 Adolescence and adulthood (> 12 to 59 years). 5
4 Time-related features
Elderly
5 Modulation: stimulus-induced vs.spontaneous.
6 Effectofintervention(medication)onEEG. (≥ 60 years).
 STATUS EPILEPTICUS ETIOLOGY
 stroke,including haemorrhagic 20%
 low AED levels 35%
 alcohol withdrawal 15%
 anoxic brain injury 15%
 Metabolic disturbances 15%
 remote brain injury/congenital malformations 20%
 infections 5%
 brain neoplasms 5%
 Idiopathic 5%
 ETIOLOGICAL CLASSIFICATION OF SE:

• CRYPTOGENIC: SE in absence of an acute precipitating CNS insult or metabolic

dysfunction in a patient without a pre-existing neurologic abnormality.
• REMOTE SYMPTOMATIC: SE in a patient with a known history of a neurologic insult
asociated with an increased risk of seizures(Stroke,TBI,static encephalopathy).
• FEBRILE:THE MOST COMMON TYPE IN CHILDREN.SE provoked solely by fever
in a patient without a history of afebrile seizures.
• ACUTE SYMPTOMATIC: SE during an acute illness involving a known neurologic
insult or metabolic dysfunction.
• PROGRESSIVE ENCEPHALOPATHY: SE in a pt. with aprogressive neurologic
disease.
PATHOPHYSIOLOGY
POSTICTAL CELL CHANGES
SPROUTING / CHANGES OF THE NEURONAL FEEDBACK MECHANISM
Susceptibility to
seizures
Neuro-
g e n e sis
Neuronal
cell death
Glial
a c tiv a t i o n

S p r o u t in g

Protein
expression
Act i v at i o n of k i n a s e s

Early
g e n e activation

C a l c i u m ion influx

1 sec. 1 min. 1 h 1 day 1 wk 1 month 1 yeTaimr e (logarithmic)

modified after ColeA.J.(2000) Epilepsia 41(S2):13-22

 ASTROCYTES CHANGE THEIR MORPHOLOGY AND PROTEIN
EXPRESSION IN A PROCESS TERMED REACTIVE ASTROGLIOSIS
 As a consequence of SE and subsequent
inflammation, “Became hypertrophic,
increase expression of intermediate
filament proteins (for example, GFAP),
and develop longer and thicker
processes”

 A number of molecules and signaling

pathways are known to trigger reactive
Astrogliosis, such as ATP and glutamate,
inflammatory cytokines such as TNF-α
and Il1-β.
MICROGLIA MORPHOLOGICAL AND MOLECULAR
ACTIVATION AT DIFFERENT STAGES AFTER SEIZURES.
STATUS EPILEPTICUS : SYSTEMICAND BRAIN METABOLISM

From Hirsch LJ,Gaspard N.Status epilepticus.Continuum 2013;19(3):767

Neuronal destruction occurs when cerebral metabolic requirements cannot be met by the
available oxygen, glucose and metabolic substrates.
Cerebral
Hypoxic/metabolic cerebral damage
Excitotoxic cerebral damage (seizure related) Cerebral oedema and raised intracranial pressure
Cerebral venous thrombosis
Cerebral haemorrhage and infarction
Cardiorespiratory and autonomic
Hypo- or hypertension
Cardiac failure
Tachy or bradyarrhythmias
Respiratory failure, Pulmonary oedema, hypertension, aspiration, pneumonia Hyperpyrexia ,
Hypersecretion, tracheobronchial obstruction
Metabolic and systemic
Dehydration, Electrolyte disturbances (especially hypoglycaemia, hyponatraemia and
hypokalaemia) Acute renal failure (acute tubular necrosis)
Acute hepatic failure, Acute
pancreatitis Disseminated 13
intravascular coagulation
Multiorgan failure, Rhabdomyolysis, Fractures or joint
dislocations
 APPROACH : DIAGNOSTICWORKUP

All patients
• Obtain IV access
• Monitor vital signs (ABC).
• Head CT (appropriate for most cases)
• Labs: blood glucose, CBC, renal function tests, Calcium, Magnesium, electrolytes, AED
levels.
• cEEG monitoring (preferably)
Consider based on clinical presentation
• Brain MRI
• Lumbar puncture
• Toxicology panel (i.e. isoniazid, TCAs, theophylline, cocaine, sympathomimetics,
organophosphates, cyclosporine)
• Other relevant investigations as per the need Brophy G, Bell . Guidelines for the evaluation and managem ent
of status epilepticus. Neurocritical care society. 2012;17:3- 3
 CONTINUOUS EEG MONITORING

 Continuous EEG monitoring should be initiated within 1 hour of SE onset if ongoing

seizures are suspected. The duration of cEEG monitoring should be at least 48 hours
in comatose patients to evaluate for non-convulsive seizures.
• Indication :
• Recent clinical seizure or SE without return to baseline > 10 min, Coma,
including post-cardiac arrest, Epileptiform activity or periodic discharges on
initial 30 min EEG, Suspected non-convulsive seizures in patients with
altered mental status
• End point : Cessation of non-convulsive seizures, Diffuse beta activity, Burst
suppression 8 – 20 seconds intervals, Complete suppression of EEG

Brophy G,Bell R,Claassen J,Alldredge B,BleckT,GlauserT,et al.Guidelines for the evaluation and management of status
epilepticus. Neurocritical care society. 2012;17:3-23
 MANAGEMENT STATUS EPILEPTICUS :
THINKTIME
 Time to treatment needs to be shorter.
 Response to treatment is time dependent.
 Morbidity and mortality are related to etiology and duration (time) of
status epilepticus.
 Prolonged seizures predict future prolonged seizures.
1. Termination of Status Epilepticus
2. Prevention of Seizure Recurrence
3. Management of Precipitating cause
Brophy G, Bell R, Claassen J,Alldredge B, Bleck T, Glauser T, et al.
4. Management of complications Guidelines for the evaluation and management of status epilepticus.
Neurocritical care society. 2012;17:3-23
ALGORITHM STATUS EPILEPTICUS
PROPOSED ALGORITHM FOR STATUS EPILEPTICUS
NONPHARMACOLOGICALTREATMENTS
IN STATUS EPILEPTICUS.

 Hypothermia-decrease brain metabolism which is neuroprotective,

 Resective surgery.
 Ketogenic diet.
 Vagal nerve stimulation.
 Resective surgery.1
 Electroconvulsive therapy (ECT)
 STEROIDS AND IMMUNOTHERAPY

 Rationale that refractory SE may be due to antibodies directed against neural

elements.
 Increasing recognition the role of inflammation in epileptogenesis.
 SE may be the initial presenting feature of some immune mediated encephalopathies.

Shorvon S, Ferlisi M.The treatment of super-refractory status epilepticus: a critical review of available therapies and a clinical treatment
protocol. Brain:a journal of neurology. 2011;134:2802-18
STEROIDS AND IMMUNOTHERAPY (IVIG )
KETOGENIC DIET

Diet high in fat and low in

carbohydrates

Induces ketosis in body and

thought to suppress seizures
by release of Leptin.

Exact mechanism remains

unknown.
SURGERY IN REFRACTORY SE
 Procedures based on
standard epilepsy surgery
 Success has been reported
with focal resections,subpial
transections,corpus
callosotomy,hemispherecto
my
ELECTROCONVULSIVE THERAPY (ECT)

 dose-1 session daily for 3-8 days.

PROGNOSIS
 NEURONAL INJURY CORRELATED WITH STATUS DURATION
ELEVATION OF NSE FOLLOWING STATUS EPILEPTICUS
ipsilateral injury (score)

= Status duration
= NSE in serum
Seizure duration in min.
DeGiorgio et al. Neurology1999;52:746–749
Gruenthal,M.,Epilepsy Res.,29 (1998) 221-232.
OUT COME

 Depends on age,etiology,degree of impairment of

consciousness
 Refractory & super refractory>>worse prognosis
 No irreversible brain damage>>Good recovery is possible even
after weeks of Status epilepticus
 SUMMARY
 Status epilepticus (SE) is a relatively common medical emergency with high morbidity
and mortality.
 Stroke, hypoxic injury, low antiepileptic drug level, metabolic disorders, alcohol, trauma
and brain tumor are the most commonly reported underlying etiologies of SE.
 SE duration,age,level of consciousness and EEG patterns have also been found to
impact the outcomes of SE.
 Phenobarbital,valproic acid,levetiracetam,lacosamide and topiramate can serve as the
third line of treatment.
 General anesthesia is used commonly to treat refractory SE; however, specifics of
treatment (i.e.,the anesthetic agent choice and dose,duration of treatment and EEG goal)
are yet to be determined.
 Aggressive treatment is necessary and appropriate for all presentations of SE in order to
maximize the probability of a successful outcome, even when the etiology suggests a
poor prognosis
THANK YOU THANK YOU 