Overview of Status Epilepticus
Kassandra Barkley, ANP-BC
Department of Neurology
Vanderbilt Medical Center
Definition of Status Epilepticus(Lowenstein DH. 1999)
• Traditionally defined as continuous, unremitting
seizure lasting longer than 30 minutes, or recurrent
seizures without regaining consciousness between
seizures for greater than 30 minutes.
• Newer literature and common neurology practice
usually accepts 5 minutes or longer as definition for
status epilepticus.
Epidemiology (Alldredge et al 2001)
• In the United States, the incidence is around 18-41 per
100,000 people per year
• Mortality rate can be around 20%, especially if treatment is
not initiated quickly
– Highest mortality occurs with anoxic and cerebrovascular
causes
– Seizure duration is greatest predictor of mortality. SE
lasting > 1 hour has significantly higher mortality
*Better prognosis: AED withdrawal in patients w/ epilepsy
and ETOH related etiologies
Epidemiology
• Most common in ages > 60 & < 12 months
• Approximately 10% to 15% of patients with
chronic epilepsy will experience an episode of
SE at some point of their clinical course.
• Approximately 7% to 10% of patients with
chronic epilepsy initially present with an
episode of SE.
Epidemiology
• At a health economics level, SE costs
approximately $4 billion per year in the United
States .
Epidemiology
• In Neuro Intensive Care Units, up to 1/3 of
patients will have nonconvulsive seizures and
most of these will be in nonconvulsive status
epilepticus (Jordon KG 1994)
• In Medical Intensive Care Units, up to 10% of
patients undergoing continuous EEG
monitoring have nonconvulsive seizures (Towne
AR et al 2000)
ETIOLOGIES OF STATUS
Antiepileptic drug (AED)
noncompliance/insufficient
dosing 20%
CNS infection 5%
Old brain injury 15%
Cerebral tumor 5%
Acute vascular injury 15%
Acute Trauma 5%
Alcohol related 10%
Drug toxicity < 5%
Metabolic/electrolyte
disturbances 10%
Global hypoxic injury < 5%
Unknown/cryptogenic 10%
Idiopathic epilepsy < 5%
TIME IS BRAIN!!
TIME IS BRAIN
• Status should always be treated as
an emergency and be treated
promptly!
Physiologic Changes in Status Epilepticus
• Phase 1: Compensation (First 30 mins)
– During this phase, cerebral metabolism is greatly
increased because of seizure activity, but
physiological mechanisms are sufficient to meet
the metabolic demands, and cerebral tissue is
protected from hypoxia or metabolic damage.
The major physiological changes are related to
the greatly increased cerebral blood flow and
metabolism, massive autonomic activity, and
cardiovascular changes
Phase 1: Compensation Physiologic Changes
Increased brain
metabolism w/ increased
use of oxygen & glucose
Elevated systemic and
pulmonary artery
pressures
Increased cardiac output
Hypertension
Tachycardia
Cardiac arrythmias
Hypercalcemia
Lactic acidosis
Massive catecholamine
release
Hyperthermia
Incontinence
Vomiting
Physiologic Changes in Status Epilepticus
• Phase 2: Decompensation (After 60mins)
– During this phase, the greatly increased cerebral
metabolic demands cannot be fully met,
resulting in hypoxia and altered cerebral and
systemic metabolic patterns. Autonomic changes
persist and cardiorespiratory functions may
progressively fail to maintain homeostasis
Phase 2: Decompensation Physiologic Changes
Failure of cerebral auto-regulation.
Cerebral blood flow dependent on
systemic BP
Respiratory and cardiac
impairments (pulmonary edema,
PE, cardiac failure, respiratory
collapse)
Hypoglycemia
Systemic hypoxia
Hypotension
Falling cardiac output
Hepatic & Renal dysfunction
Metabolic & Respiratory Acidosis
Hypokalemia; Hyperkalemia
Consumptive coagulopathies
Falling lactate lvls
Rhabdomyolysis
Multi-organ failure
Hyperthermia
Leukocytosis
Increased intracranial pressure (ICP)
Types of Seizures
• Seizures can manifest as motor, sensory, or cognitive dysfunction
• Classification of seizures
– Partial – seizures localized to an area of the brain resulting in a
corresponding localized dysfunction. Often described by
presence of absence of automatisms (ie lip smacking, jaw
mvmts, swallowing, fumbling with nearby objects) or repeated
subconscious or involuntary movements .
• Simple (w/o impairment of consciousness)
• Complex (w/ impairment of consciousness)
**Please note partial seizures can develop into secondarily
generalized seizures as abnormal electrical activity spreads
through the brain
Classification of Seizures
- Generalized seizures are characterized by the resulting
dysfunction
-Absence (loss of consciousness with no motor dysfunction)
-Myoclonic (bilaterally synchronous, arrythmic jerking)
-Clonic (repetitive and rhythmic motor movement)
-Tonic (extension of the arms, legs, & trunk)
-Tonic-clonic (extension of the arms, legs, & trunk followed
by repetitive, rhythmic movement)
-Atonic (aka drop-attack, absence of motor movement)
[Parillo & Dellinger, 2008]
Frontal Seizure with vocalizations, and
hypermotor activity
Partial seizure w/ secondary generalization
Types of Status Epilepticus
• CONVULSIVE
– Generalized (Most common presentation of SE)
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Myoclonic
Clonic
Tonic
Tonic-Clonic
– Partial
• Simple
• Complex
• Secondarily Generalized
Types of Status Epilepticus
• SUBTLE CONVULSIVE
– About 30% SE population
– Longer duration & more difficult to treat
– Clinical features:
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•
•
Continuous rhythmic subtle motor phenomena
Facial twitching, nystagmoid eye jerks
Subtle twitching of trunk or extremities
Cognitive impairment (altered awareness)
Head or eye deviation
Automatisms
Types of Status Epilepticus
• NON-CONVULSIVE
– Generalized
• Absence
• Atonic
– Partial
• Simple
• Complex
• Secondarily Generalized
Possible Findings in Convulsive Status
• Generalized convulsions w/ bilaterally
symmetric myoclonic, tonic, clonic, or tonicclonic movements
• Convulsions on 1 side of body (not symmetric)
with repetitive involuntary movements
Possible findings in Non-convulsive Status
Behavioral, cognitive, or sensory findings:
– Agitation, aggression, amnesia, aphasia muteness,
catatonia, coma, confusion, delerium, delusions,
hallucinations, laughter, perseveration, singing, psychosis
Autonomic:
• Abdominal sensation, apnea, hyperventilation, brady or
tachyarrythmia, flushing, miosis, mydriasis, hiccups,
nausea, vomiting
Motor:
– Automatisms, dystonic posturing, eye blinking, eye
deviation, facial twitching, finger twitching, nystagmus,
tremulousness
Responsiveness of Treatment of SE
• Treatment with 1st line therapy within 30
minutes of onset stopped status in 80% of
patients
• Treatment with first line therapy started >/= 2
hrs after onset stopped status in 40% of
patients
Monitoring For Status in the ICU……
• Continuous EEG [cEEG] (continuous EEG 24 hr order
in WIZ) is ideal for capturing seizure activity
• Using cEEG captures 56% of seizures in first hour and
88% of seizures in first 24 hrs (Sutter et al 2013)
• Note: some factors which may limit obtaining and/or
interpreting EEG include head bandages, delerium w/
mvmts, sweating, and aritifact from electrical
interference of mechanical devices ie vent, ECT,
dialysis. Also availability of EEGs in the hospital plays
a role
INITIAL MEDICAL MANAGEMENT
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ABCS (airway, breathing, circulation)
Obtain IV access (2 sites preferably)
Check finger stick glucose
Give thiamine 100mg IV prior to Dextrose D50W 50ml IV
if low or unknown glucose
• Continuous monitoring (ECG, BP, HR, oxygen)
• Send stat labs (CBC, BMP, LFTs, Ca, Mg, PO4, troponins,
ABGs, AED lvls if on seizure meds, tox screen (urine,
blood), Hcg if pregnancy possible
• Continuous EEG, stat neurology consult
Obtain history & exam
• History of epilepsy & AED use, structural brain lesion
(stroke, intracranial hemorrhage, tumor), head
trauma, meningitis, social history (illegal drug or
ETOH use), pregnancy
• Medical History including medications
• Seizure onset & duration, description of seizure
• Full neurologic exam including mental status, cranial
nerves, motor exam, sensory exam, reflexes,
cerebellar testing
Treatment of Convulsive SE
First Line Agents:
•▪Lorazepam Load IV 0.1mg/kg up to 4mg (2mg/min)
•▪Midazolam Load IM 0.2mg/kg up to 10mg IM
•▪Diazepam Load 0.2mg/kg (20mg rectally or 10mg IV)
Second-Line Agents
•▪Fosphenytoin 20mg/kg infused at a rate of 150mg/min
•▪Valproate 20-40mg/kg infused at a rate of 6mg/kg/min
•▪Levetiracetam 1500-4000mg infuse 500mg/min
•▪Lacosamide 400mg IV infuse over 5 mins
•▪Phenobarbital 20mg/kg IV infuse 60mg/min
Treatment of Convulsive SE
Third Line Agents
• ▪Midazolam infusion (Hypotension, withdrawl seizures)
• ▪Propofol infusion (Hypotension, propofol infusion syndrome)
• ▪Pentobarbital (Ileus, metabolic acidosis, thrombocytopenia,
immunosuppression)
• ▪Ketamine infusion (Hypertension, possible rise in ICP)
• ▪Etomidate infusion (Adrenal insufficiency, non-epileptic
myoclonus)
• ▪Lidocaine administration every 5 minutes (cardiac
arrhythmia)
Treatment of SE
Oral Agents
•▪Topiramate 400-800mg/day (metabolic
acidosis
•▪Pregabalin 150-600mg per day
•▪Vigabatrin 0.5-1gr q8h (no short term side
effects)
Summary
• Status is an emergency & requires immediate
treatment
• Remember sometimes status seizures are not
obvious, symptoms can be very subtle or may
only present as altered mental status
• If you are concerned about seizures, consult
neurology right away for continuous EEG
monitoring
References
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Lowenstein DH. Status epilepticus: an overview of the clinical problem. Epilepsia
1999; 40(Suppl 1); discussion S21-22
Jordan KG. Status epilepticus. A perspective from the neuroscience intensive care
unit. Neurosurg Clin N Am. 1994;5:671-686
DeLorenzo RJ, Pellock JM, Towne AR, Boggs JG. Epidemiology of status epilepticus.
J Clin Neurophys 1995 Jul; 12(4) 316-25
Allredge BK, Gelb AM, Isaacs SM, et al. A comparison of lorazepam, diazepam, and
placebo fo the treatment of out of hospital status epilepticus. N Engl J Med 2001;
345(9):631-637.
Towne AR, Waterhouse EJ, Boggs JG, Garnett LK, Brown AJ, Smith JR Jr, DeLorenzo
RJ. Presence of nonconvulsive status epilepticus in comatose patients. Neurology
2000;54:340-345
Parillo JE & Dellinger RP. (2008). Critical Care Medicine: Principles of Diagnosis and
Management in the Adult. St Louis, MO: Mosby Elsevier
Sutter, R, Stevens R, and Kaplan P. Continuous Electroencephalographic Monitoring
in Critically Ill Patients: Indications, Limitations, and Strategies. CCM Journal. 2013,
41(4) 1124-1132