Subhairline EEG Part II - Encephalopathy Teneille Gofton September 2013.
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Transcript of Subhairline EEG Part II - Encephalopathy Teneille Gofton September 2013.
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Subhairline EEG Part II - Encephalopathy
Teneille Gofton
September 2013
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Objectives To review the subhairline EEG changes
seen with encephalopathy To discuss specific EEG findings in
encephalopathy To outline basic EEG patterns associated
with HIE
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EEG and Encephalopathy Why use continuous EEG in
encephalopathy and coma? Evolution of coma pattern Assess for non-convulsive status
epilepticus Assist with prognosis
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EEG and Encephalopathy EEG is nonspecific in encephalopathy
and coma Some features may suggest etiology
e.g. generalised periodic epileptiform discharges
Similar EEG changes are seen with increasing depth of sedation or anaesthesia
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EEG recordings in Coma Quiet recording
To assess for spontaneous reactivity Should include external stimulus in
order to assess reactivity Auditory stimulus - clap, call name Painful stimulus - only if no response to
previous stimuli)
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EEG and Encephalopathy Spontaneous variability
Variety of different frequencies observed during the resting state
Changes in EEG seen with changes of state Awake vs asleep
Occurs due to normal oscillations in cerebral function
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EEG and Encephalopathy Reactivity to graded stimulus
Auditory Pain
Look for changes in voltage (height of the waveforms) or frequency (number of waveforms per second) May be brief or sustained
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EEG in Coma Usually get increased slowing with
decreased LOC
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Mild Encephalopathy Diffuse theta Occasionally delta Spontaneous variability present Reactivity present State changes present
e.g. clear difference in sleep and awake EEG
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Mild Encephalopathy
theta
delta
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Moderate Encephalopathy Some theta Diffuse delta Spontaneous variability present Reactivity present State changes present
e.g. clear difference in sleep and awake EEG
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Moderate Encephalopathy
delta
theta
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Severe Encephalopathy Predominantly delta May see periods of faster activity May alternate with periods of
suppression This is still spontaneous variability
May no longer see reactivity No clear state changes
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Severe Encephalopathy
delta
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Severe Encephalopathy
delta
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Severe Encephalopathy
suppression
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Severe Encephalopathy
suppression
EKG artifact
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Electrocerebral Inactivity No EEG activity >2 uV
Cannot make this distinction using subhairline EEG
Usually represents brain death May be seen in hypothermia, deep
anaesthesia
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Specific EEG Patterns When seen, these patterns are
suggestive of a particular etiology Triphasic waves Excess beta Alpha coma Burst-sppression
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Triphasic Waves Generalised, frontally predominant Brief negative phase (up) Larger positive phase (down)
Longer duration than 1st phase Followed by negative phase (up)
Longer duration than other 2 phases
May occur alone, periodically or in runs
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Triphasic Waves Seen in toxic, metabolic encephalopathy
Uremic, hepatic, septic Hypercalcemia, hyperosmolarity
Occasionally associated with seizures In this case, may be very difficult to
determine if seeing status epilepticus or periodic TWs
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Triphasic Waves
1
2 3
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Triphasic Waves
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Excess Beta Barbiturate or benzodiazepine overdose
Anaesthesia using propofol or midazolam
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Alpha Coma Nonreactive alpha pattern No spontaneous variability No reactivity Seen in hypoxic-ischemic
encephalopathy In this case, usually associated with poor
prognosis, but not always If posterior predominant think about
“locked-in” syndrome
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Burst Suppression High amplitude mixed frequencies
alternating with periods of suppression Duration of bursts and suppression is
variable Reversible if due to medication exposure
Associated with poor outcome in hypoxic-ischemic encephalopathy
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Burst Suppression
burst
suppression
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Hypoxic-Ischemic Encephalopathy (HIE) Associated with respiratory or cardiac arrest Prolonged recording is preferred because
EEG patterns change over time NB: EEG patterns are influenced by
medications used in the ICU
Most reliable EEG finding in HIE Myoclonic status epilepticus However, NOT absolute with respect to
prognosis after induced hypothermia
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HIE Status Epilepticus
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Hypoxic-Ischemic Encephalopathy (HIE) Other patterns that can be associated
with poor prognosis Complete suppression
But this may be due to medications Burst-suppression Generalised periodic epileptiform
discharges on a suppressed background
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Hypoxic-Ischemic Encephalopathy (HIE) Up to 35% of post-anoxic patients have
seizures often non-convulsive
Seizures may be focal multifocal Generalised
Background may be continuous, suppressed, burst suppression
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Hypoxic-Ischemic Encephalopathy (HIE) Subhairline EEG is inadequate for
prognostication in the setting of HIE Formal EEG is required