Transcript 674_File_6 - Bermuda Hospitals Board

SEIZURES
Jean B. Fahey MSN, RN,
ACNS-BC, CCRN, CNRN
Neuroscience Clinical Nurse
Specialist
Massachusetts General Hospital
Boston, MA
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Nature of seizures & epilepsy
Incidence, risk factors
Brain anatomy and pathophysiology
Classification of seizure types
Signs and symptoms of seizures
Diagnosis & monitoring
Treatment, first aid, medications, surgery, other
Status epilepticus
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PRINCIPLES OF STAFF EDUCATION
Fluent with seizure first aid and
assessment
Awareness of what constitutes
a neurological emergency, and
the ensuing treatment /
antiepileptic medication use
Documentation
Recognize the various
manifestations of seizures
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STARRY STARRY NIGHT
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JAPAN, 1997, POKEMON
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EPILEPSY FACTS
Prevalence of epilepsy in the United States is 0.5% to
1% (2.3 million). 1.4 million (15 to 64 years), 550,000
(>65), 300,000 (<14 years)
Approximately 2% to 5% of children have febrile seizures
with an age range of 3 months to 5 years.
Most persons have one type of seizure
80% Occur before age 20
From Epilepsy: A Report to the Nation. Published in 1999 by the
Epilepsy Foundation
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PATHOGENESIS
Seizure : Behavior
change associated with
an  electrical discharge
in cortex. Neurons recruit
other neurons to fire, thus
clinical manifestations are
related to the number of
neurons affected &
correlate with the focus &
path of spread.
Status epilepticus :
recurring seizures with
incomplete recovery
between attacks.
Epilepsy : Two or more
unprovoked seizures.
Convulsion : a seizure in
which motor manifestations
predominate.
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ETIOLOGY
80
70
60
50
symptomatic
idiopathic
40
30
20
10
0
seizures
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Metabolic - drugs:
amphetamines, cocaine,
theophylline drug
withdrawal: alcohol,
sedatives, antiepileptic
medications, electrolyte:
hyponatremia, acidosis,
Magnesium/Calcium /Amino
acid disturbances
Genetic / birth or
development abnormalities
Infections/poisoning
Lesions /trauma
Toxemia of pregnancy
Precipitating factors /
triggers: alcohol,
hyperventilation, menses,
flashing lights, fever,
exhaustion, nutrition,
sounds, psych factors
Seizure Mimics /behavior
disorders, breath holding,
cardiac dysrhythmias,
hyperventilation, migraine
syndromes, movement
disorders, psuedo seizures,
sleep disturbances,
syncope, transient ischemic
attack, panic attack,
psychogenic, toxic/metabolic
abnormalities
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CLASSIFICATION OF SEIZURES
GENERALIZED
(Bilateral hemisphere)
PARTIAL
(Local onset, aura)
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GENERALIZED (Bilateral hemisphere)
Primary generalized seizures. Bilateral & symmetric
without focal onset & usually idiopathic. Sign of “4”
exception.
Absence (petit mal). 2 -10 second lapse of consciousness.
Onset 4-12 y/o & decreased frequency in adolescence.
Manifested by staring, eye blinking, lip smacking.
Myoclonic. Quick contractions of partial, whole, or groups
of muscles. Single or intermittent jerk in the same or
different body parts. Note: not all myoclonus is epileptic.
Clonic (flexion), tonic (extension), and tonic-clonic (grand
mal). Abrupt loss of consciousness with tonic, clonic, or
tonic-clonic convulsion, followed by postictal confusion.
The most common, also the most dangerous
Atonic, loss of motor tone
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PARTIAL (Local onset, aura)
Simple. Partial (focal) seizures. Consciousness is not
impaired. Subjectively, patients are likely to experience
déjà vu and sensory, motor, or autonomic symptoms.
For example, patients may note vague abdominal or
thoracic sensations. With motor involvement, patients
are likely to exhibit hemifacial or hemibody twitching.
Complex: Consciousness is impaired. May have
automatic behaviors such as lip smacking, fumbling with
clothes, or even walking. Patients are amnesic for part or
the entire episode.
Partial seizures that secondarily generalize
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SEIZURE OBSERVATION
Motor movement observation predominate
seizure documentation, but emphasis should be
placed on key observational details such as
responsiveness.
Videotaped seizures & periodic retraining retain
quality of assessment skills.
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FOCAL SYMPTOMS
Lateralizing signs assist to classify partial seizures with
secondary generalization: head turning, neck extension,
mouth or eye deviation.
The same type of seizure may manifest in different
symptoms between patients
Seizures are unpredictable, they may startle the
observer and the observer may not see the actual
beginning of the seizure until it progresses, the details
may be incomplete.
The need to provide first aid may shift attention away
from the observation task.
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POSSIBLE ICTAL MANIFSTATIONS
Emotions: disassociated affects, negative affects, panic
attacks, rage, transient psychosis
Gustatory affects: metallic or foul taste, burning,
decaying, ammonia, overpowering perfume
Visual: patterns, shaped, flashing lights, fully formed
complex images, sudden distortions (metmorphosia),
micropsia, macropsia
Auditory: ringing or buzzing, repetitive stereotyped
phrases, music, distortion, illusions of echo, alteration of
volume
Somatosensory: headache, discomfort, pain, tingling,
numbness, vertigo
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POSSIBLE ICTAL MANIFSTATIONS
Motor: automatisms (simple or complex), abnormal eye
movements, nystagmus, jerking, staring, twitching,
repetative speech, lurring of speech, speech arrest
Autonomic: flushing, piloerection, perspiration, shortness
of breath, chest pain, palpitations, sinus tachycardia,
nausea, epigastric rising or sinking, incontinence,
salivation, belching, coughing
Experiential Phenomena: Intrusive memory flashbacks,
illusions of familiarity (déjà vu), or unfamiliarity (jamais
vu), feeling of clairvoyance or of an observing presence,
mind body disassociation, derealization,
depersonalization, confusion, disorientation, sense of
profundity, illusion of possession
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SPECIALIZED LOBULAR FUNCTION AND
ASSOCIATED SYMPTOMS
Frontal: primary motor, expressive language, executive
functions, attention, social & sexual behaviors, olfactory
Parietal: primary somatosensory cortex, integration of sensory
output, spatial location of sensory input, guidance of
proximal limb movement, body image, graphic construction
Temporal / Limbic: primary auditory cortex, language
comprehension, memory, emotion
Occipital: primary visual, perception of form, color, depth, &
mvmt.
Right hemisphere: visuospatial functions, construction, spatial
attention, affective speech
Left hemisphere: language, fine motor control, manipulation of
numbers., linear thinking, detail oriented
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EEG RECORDING
Temporal
Lobe
Partial
Seizures
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PARTIAL COMPLEX SEIZURES
Hippocampus
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DIAGNOSTIC EVALUATION
History & Examination
Laboratory investigation
Computerized
tomography & Magnetic
resonance imaging
Electro encephalographic
tests - Surface
electrodes,
Nasopharyngeal or
sphenoid leads, Cortical
strip electrodes or depth
electrodes
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INTRACRANIAL DEPTH
ELECTRODES
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SUBDURAL GRID
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TREATMENT
Management of a
convulsion
Idiopathic (Seizure control)
Symptomatic (Treat cause)
Anticonvulsants
Surgical resection,
disconnection, or
augmentation
Other
DRUG THERAPY
Anticonvulsants
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INTRAVENOUS PHENYTOIN
Vesicant, (pH- 14), necrosis at site if infiltration occurs.
Do not use in hand, wrist, or foot lines. Forearm
suggested. Always affirm vein patency.
Rate per institution, 25mg/minute suggested. Possible
50mg/ minute maximum.
Only compatible with normal saline –precipitates with
glucose contaminated line.
Cardiovascular side effects, hypotension, bradycardia.
Limited stability once placed in solution.
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Vesicant Infiltration, Purple Glove
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MANAGEMENT OF A CONVULSION: (preictal
state)
Note time of onset and duration
Note any precipitating factors
Note presence of an aura
Stay in attendance, remain calm
Guide person to a safe place and remove
harmful objects from surroundings
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MANAGEMENT OF A CONVULSION:
(ictal state)
Note seizure activity: body parts, sequence,
character of movement
Autonomic signs
Level of consciousness
Protect from secondary injury, do not place
anything in the mouth during a seizure
Do not restrain
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MANAGEMENT OF A
CONVULSION: (postictal state)
Assess level of consciousness & maintain airway protection
Suction and oral airway as required, remove pillows
Nothing by mouth until fully awake, position patient on side to
prevent silent aspiration
Remain in attendance with patient until stable
Reassure & reorient: assess for Todd’s Paralysis.
Note associated injuries
Consider need for oxygen face mask
Continue neurological assessment
Maintain bed rest until back to baseline
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STATUS EPILEPTICUS
Recurring seizures with
incomplete recovery
between attacks
Etiology:
-known seizure disorder:
withdrawal or subtherapuetic
antiepileptic medications,
superimposed illness.
-without seizure history:
encephalitis, intracranial bleed,
hypoglycemia, alcohol
withdrawal, cerebral trauma
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MANAGEMENT: STATUS
EPILEPTICUS- (initial 10-12 minutes)
(MGH 2007, Status Epilepticus Protocol, Epilepsy Service)
Initial rapid assessment: airway, vital signs
Monitor: oxygen saturation, electrocardiogram
Establish intravenous access & obtain laboratory tests:
Complete blood count, electrolytes, Blood urea
nitrogen/Creatinine, Glucose, Calcium, Magnesium,
Phosphorous, liver function tests, antiepileptic
medication levels, Toxicology screen, arterial blood gas
Administer intravenous Thiamine -100mg & 50%
Dextrose - 50 cc
Lorazepam, 0.1 mg/kg IV (<2 mg/min)
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MANAGEMENT : STATUS
EPILEPTICUS (within 40 minutes)
Phenytoin, 20mg/kg IV @ 50 mg/min. or
Fosphenytoin 20mg/kg IV @ 150mg/min.
monitor electrocardiogram, assess for
hypotension- blood pressures every 2 minutes
Phenytoin 10mg/kg IV @ 50/min. or
Fosphenytoin 10mg/kg IV @ 150/min. Send
repeat Dilantin level 20 minutes after load.
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MANAGEMENT : STATUS
EPILEPTICUS (within 40 minutes)
As alternative: Valproic Acid 30mg/kg IV
@150mcg/min. or Levetiracetam 50mg/kg IV @
100mg/min
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MANAGEMENT : STATUS
EPILEPTICUS (within 60 minutes)
Phenobarbital 20mg/kg
@ 75 mg/min
Intubate, if not already
done
Initiate
electroencephalographic
monitoring
Contact Neurologist/
Epilepsy specialists
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MANAGEMENT : STATUS EPILEPTICUS
Load and titrate to stop clinical and
electroencephalographic seizures, or maintain burst
suppression on electroencephalogam. Use fluid to
support blood pressure, add vasopressors if fluids fail.
Pentobarbital 5mg/kg IV load, then titrate (0.3-9
mg/kg/hr, avg..= 4mg/kg/hr), or
Midazolam 0.2 mg/kg IV, load preferred if BP is
unstable, then titrate 0.1-0.4mg/kg/hr, or
Propofol 1-2 mg/kg IV load/hr, then titrate 2-10mg/kg/hr
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MANAGEMENT : STATUS
EPILEPTICUS (ideally within 48 hours)
Obtain CT scan (if clinically
indicated)
Correct underlying cause of status
epilepticus
Adjust the principal anticonvulsants
to therapeutic effect
Taper Midazolam, PentobarbitaL,
or Propofol after above is complete
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MANAGEMENT : STATUS EPILEPTICUS
Care of the patient on
paralytics, or in
barbiturate coma.
Associated hazards of
immobility - pulmonary,
skin, GI, positioning &
splinting, eye care,
hemodynamic support &
assessment
Consider antibiotics,
antiviral agents, or lumbar
puncture, cool patient if
febrile, frequent lab
assessments
Family support &
education
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PRINCIPLES OF LONG TERM
MONITORING
Wean from antiepileptic medications
Capture and collect electric, visual, & auditory
data on seizure events in a controlled situation.
Maintain safety at all times
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DOCUMENTATION
Inherent in good seizure observation is good
documentation. Accurate documentation can lead to a
more definitive and expedited diagnosis. Note time of
onset and duration, precipitating factors, presence of an
aura, note seizure activity- body parts involved,
sequence and character of movement, autonomic signs,
level of consciousness and content of consciousness,
neurological exam and presence of postictal deficits, or
secondary injury related to seizure activity
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DOCUMENTATION
1.
2.
3.
4.
5.
Describe the beginning
Describe responsiveness
Describe movement, mobility, and tone
Describe sensation and perception
Describe post ictal responses
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DOCUMENTATION-1
Describe the beginning
Describe circumstances.
Describe precipitating factors.
Was the seizure onset observed?
Was there an aura?
Did the person continue, stop, or slow down their
activity?
What happened first and how did it proceed?
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DOCUMENTATION-2
Describe responsiveness
Describe responses to you, self & environment.
Describe responses, automatic or complex?
Assess response to touch.
Assess response to auditory stimuli.
Assess response to visual stimuli, check pupils.
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DOCUMENTATION-3
Describe movement, mobility, and tone
Was there movement or posture change?
Was there movement of the head or eyes?
Was it unilateral or bilateral, was it symmetrical if
bilateral?
Assess whether tone is increased (rigid) or
decreased (limp)?
Were there any automatisms (repetitive
purposeless movements), or purposeful
movements?
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DOCUMENTATION-4
Describe sensation and perception
What does the person describe or say? Ask
them for a description.
Are there any automatic signs (skin temperature
change, change in color, sweating)?
Did they say or do anything unusual (cursing,
swearing, mumbling, wandering, combative)?
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DOCUMENTATION-5
Describe post ictal responses
What were they like after the seizure?
How long before they were back to baseline?
Could thy recall the event or what happened at
the beginning of the seizure?
Were there any temporary deficits?
Was there any confusion or disorientation?
Was there any bowel or bladder incontinence?
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Non-epileptic seizures (NES)
Events that may present similar to epileptic seizures,
however there is no electrographic correlate on EEG
May be unable to determine type of seizures based on
clinical presentation alone
Of patients admitted to inpatient epilepsy monitoring
units, up to 40% are diagnosed with NES
More common in females in their 30’s
Can also have concurrent epilepsy
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NES – Clinical features
Most episodes occur with a witness present
NES tend NOT to occur during sleep
Episodes are often frequent
– Most report at least daily episodes
Often have an incomplete loss of consciousness
Are rarely less than 1 minute, usually much longer
May have forced eye closure
– During true ictal events, eyes are usually open
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Criteria to distinguish epileptic versus
psuedo seizures
Description
Epileptic
Psuedoseizure
Apparent
cause
absent
Emotional disturbance
warning
Varies: commonly unilateral or
epigastric
Palpitations, malaise, choking, bilateral foot aura
onset
Common sudden
Often gradual
scream
At onset
During course
convulsion
Rigidity followed by jerking,
rarely rigid alone
Rigidity or struggling, throwing limbs and head
about
biting
tongue
Lips, hands, or other people or things
micturation
frequent
never
defecation
occasional
never
duration
A few minutes
Often > 30 minutes
termination
spontaneous
Spontaneous or artificially induced (water etc)
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Psychiatric conditions with NES
- Depression
–
–
–
–
–
Anxiety
Somatoform/conversion disorder
Post Traumatic Stress Disorder
Dissociative disorder
Personality disorders (borderline personality,
Obsessive Compulsive Disorder, narcissistic,
histrionic and antisocial personalities)
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Diagnosis of NES
Routine Electroencephalogram
– Often not very useful
Video Electroencephalogram
– Gold standard for diagnosis
Serum testing
Neuropsychological testing
Neuroimaging
– Magnetic resonance imaging – often normal in true
epileptics
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Presenting the diagnosis of NES
Often is a challenge to present the diagnosis to the
patient
Should emphasize that the patient is not “making it up”,
the episodes are real, however they are not epilepsy
Stress the importance of psychiatric follow-up
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Treatment and Prognosis of NES
Treatment:
– Traditional psychotherapy
– Cognitive behavioral therapy
Prognosis:
– A minority achieve seizure-freedom (25 – 33%)
– Children do better than adults do
– Risk factors for worse prognosis include older age at
onset, lower educational level, longer duration of
symptoms, more limited family support, male gender,
anger at diagnosis
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REFERENCES:
American Association of Neuroscience Nurses, Clinical guideline series,
Seizure Assessment, 1997.
DB Hoch MD, Partners neurology service, Epilepsy service- MGH
Epilepsy Foundation of Massachusetts and Rhode Island. (888) 576-9996
MGH,Up to Date. Psychogenic Non-Epileptic Seizures, 2008.
Misra UK, Kalita J, Patel R. Sodium valproate vs phenytoin in status
epilepticus: a pilot study. Neurology 2006 Jul 25: 67(2): 340-2.
Reuters, Abnormal Brain Response Caused Pokemon- Induced Seizures,
Nature Neuroscience, 2000,3:259-263.
Rowe,R. Celebrating Who We Are: Famous People with Epilepsy, Epilepsy
Association, Metro Toronto, 1998:.9.
Uges JW, van Huizen MD, Engelsman J., Wilms EB, Touv DJ, Peters E,
Vecht CJ. Safety and pharmacokinetics of intravenous levetiracetuam
infusion as add-on in status epilepticus. Epilepsia, 2009. Mar. 50(3):415-21.
Epub 2008
Wulf, J. Evaluation of Seizure Observation and Documentation, Journal of
Neuroscience Nursing, 2000, 32, 27-36.
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