Download - Seizures
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Seizures
Mark WahbaAugust 7, 2003
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Statistics• 10% of population will have 1 seizure in
their lifetime• 6% of population will have at least 1
afebrile seizure in their lifetime• Incidence of epilepsy in the population
is <1%• 1% of ED visits is for seizures
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Sub-presentations
• Status epilepticus• Febrile Seizures• Medical
management acute and chronic
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Outline• Definitions• Classification of seizures• Pathophysiology• Clinical Features• Postictal state• Emergency Department Management• Summary
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Definitions
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Seizure• “clinical manifestation of excessive,
abnormal cortical neuron activity” Rosen’s p.1445
• Not a diagnosis but a series of signs and symptoms
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Epilepsy• “recurring seizures without consistent
provocation” Rosen’s p1445
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Ictal• “pertaining to, marked by, or due to a
stroke or an acute epileptic seizure” Dorland’s Pocket Medical Dictionary 25th Ed. 1995 W.B. Saunders Company
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Classification of Seizures
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Primary and Secondary• Primary seizure• Idiopathic/Genetic• Epilepsy
• Secondary seizure• aka reactive seizure• Response to certain
toxic, pathophysiologic, or environmental stress
• Not epilepsy
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Generalized and Partial• Generalized• Electrical activity
simultaneously involves both cerebral hemispheres
• Loss of consciousness
• Partial (Focal )• Electrical activity
limited to part of one cerebral hemisphere
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Partial Seizure
• Partial with secondary Generalization• Starts partial then becomes generalized
• Complex Partial• Consciousness is
impaired
• Simple Partial• Consciousness is
maintained
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Cryptogenic Seizure• Thought to be secondary but identifiable
cause found
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Febrile Seizure• Most common pediatric seizure• 2-5% of children between 6mo -5years• 20-30% have at least 1 recurrence• Impt. to differentiate febrile seizure from
seizure with fever
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Pathophysiology
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Pathophysiology• Not completely
understood• Knowledge is from
animal studies• Electrical or
pharmacologic stimulation applied to the brain cortex
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Recruitment• Generalized:• “when the initiating neurons’ abnormal,
increased electrical activity activates adjacent neurons and propagates until the thalamus and other subcortical structures are recruited” Rosen’s p.1446
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Recruitment• Partial:• Less recruitment and ictal activity does not
cross the midline
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Why?• Unclear• Disruption of normal structure:
congenital, maturational, acquired• Disruption of local metabolic or
biochemical function
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Neurotransmitters• acetylcholine-excitatory to cortical
neurons• gamma-aminobutyric acid (GABA)-
inhibitory to cortical neurons• changes in concentration of these NTs
may produce membrane depolarization, then hyperpolarization, then recruitment
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Why is consciousness altered?• Ictal discharge reaches below the
cortex• Enters brainstem and effects the
reticular activating system
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Why does the seizure stop?• hyperpolarization subsides• electrical discharges terminate• “Due to reflex inhibition, loss of
synchrony, neuronal exhaustion, alteration of the local balance of ACH and GABA in favor of inhibition” Rosen’s p. 1446
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How are seizures confirmed?• Electroencephalography (EEG)
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Clinical Features
Primary Seizures
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Simple Partial• Specific function of initiating neurons
determines the clinical manifestation of the ictal event
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Features• motor
• somato-sensory• special sensory
• autonomic• psychic
• focal clonic movements
• paresthesias• visual, auditory,
olfactory, gustatory• sweating, flushing• sense of déjà vu,
fear
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Complex Partial• Impairment but not loss of
consciousness• Amnesia, but may be responsive during
seizure• Automatisms: lip smacking, swallowing• Aura: taste, smell, visual • Maintain high cortical functioning
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Generalized Seizures• Loss of consciousness• No aura• May have a vague prodrome or
dysphoric state prior• Convulsive or Non-Convulsive
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Convulsive Generalized Seizures• ‘Grand-Mal’• generalized hypertonus• “rhythmic, violent contractions of
multiple, bilateral, symmetric muscle groups”
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• posterior shoulder dislocation, # thoracic spine vertebral bodies
• transient apnea• incontinence: urinary > fecal• followed by postictal state, headache,
drowsiness that may last for hours
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Nonconvulsive Generalized Seizures• Absence or ‘Petit mal’• Myoclonic• Tonic• Atonic
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Absence Seizures• Begin in childhood• Sudden cessation of normal, conscious
activity• dissociative state lasting secs to min• sudden termination of such state• No postictal state
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Myoclonic and Tonic Seizures• Sudden, brief muscle group
contractions• If entire body involved: ‘drop attack’• No postictal state
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Atonic Seizure• Loss of muscle tone• May cause ‘drop attack’
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Clinical Features
Secondary seizures
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Caused by Metabolic Derangements
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Hypoglycemia• Most common metabolic cause of
seizure activity• Plasma glucose level <45mg/dL or
2.5mmol/L• Extremes of age particularly susceptible
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Ketotic Hypoglycemia• Most common cause of childhood
hypoglycemia• Small for age kids• “Episodes of symptomatic hypoglycemia
during periods of caloric deprivation or under provocation by a ketogenic diet” Rosen’s p.1448
• Hypoglycemia and ketonuria• Dietary management
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Osmolar Disorders• Hyponatremia Na<120mmol/l• Rate of decline is factor• Treat slowly: increase Na by 0.5mmol/h• Treat with 3% NaCl only if seizing
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Osmolar Disorders• Hypernatremia Na>160mmol/l• Usually due to dehydrating illness• Correct slowly
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others• Hypocalcemia, Hypoparathyroidism• Hypomagnesemia• Nonketotic Hyperosmolar Hyperglycemia• Uremic Encephalopathy in renal failure• Hypothyroidism• Thyrotoxicosis• High anion gap acidosis• Hypertensive Encephalopathy• Acute Intermittent Porphyria
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Infectious Causes
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Infectious Causes• Independent of febrile mechanism• Usually CNS infections
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Meningitis• 15-40% of pts will seize• More common at extremes of age• Partial seizures > general
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Meningoencephalitides• Usually partial motor• Postictal paralysis common esp. with
herpetic infections• Presenting sign in 1/3 of cerebral
abscesses
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Other• Neurocysticercosis: parasite in
immigrants from Latin America• Latent syphilis• Primary HIV disease and its infections
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Drugs and Toxins
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Drugs and Toxins• Antimicrobials• Neuroleptics• Sympathomimetics• Anticholinergics:
tricyclics, antihistamines
• cocaine• amphetamines• PCP
• Withdrawal:alcohol, BZD
• Overdose: ASA,theophylline, INH, Li, phenytoin
• Insecticides• Rodenticides• hydrocarbons
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Cocaine induced Seizures• Fever• Rhabdomyolysis• Arrhythmias• Rx: BZD
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EtOH Associated seizures• Overdose• Withdrawal• Must r/o other causes• Rx: BZD• “substitute for the GABA enhancing
effect of ethanol in the CNS” Rosen’s p.1449
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Trauma Associated Seizures
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Early• <1 week post injury• Epi + Sub dural hematomas• Intracerebral Hemorrhage• SAH
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Late• >1week post injury• 1 year after significant head trauma,
incidence of seizures is increased 12 x• Severity of head injury is directly
proportional to likelihood of seizures• 10-15% will develop post traumatic
epilepsy
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Malignancy Associated Seizures
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Malignancy Associated Seizures• Primary tumors or metastases• Usually partial with secondary
generalization
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Vasculitic Associated Seizures
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Vasculitic Associated Seizures• Systemic Lupus Erythematosus• Polyarteritis Nodosa• Complex partial
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Other Neurologic Causes
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• Stroke: incidence of seizures 4-15%• Incidence of epilepsy post stroke is 4-
9%• Aneurysm and AVM• Migrainous activation of an epileptic
focus• MS - 5% of patients
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• Neurofibromatosis: café au lait, axillary freckling
• Tuberous Sclerosis: ash leaf spots, adenoma sebaceum
• Sturge-Weber syndrome: facial port wine nevus
• Alzheimer’s Dementia
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Gestational Seizures
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Gestational Seizures• Gestational epilepsy• Hormonal and metabolic changes
unmask underlying epilepsy• Eclampsia• Seizures, hypertension, proteinuria,
edema, coma
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Pseudoseizures
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Pseudoseizures• Functional• Not the result of abnormal CNS
electrical activity• “lower intelligence and have an
underlying anxiety or hysterical personality disorder” Rosen’s P.1450
• ED evaluation is difficult• Can co-exist with seizures
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Post ictal state
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Postictal State• Decreased level of arousal and
consciousness• Amnesia• Headache• Minutes to hours
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• Must monitor and investigate altered mental status after a seizure
• Airway, pulse oximetry, blood glucose, cardiac monitoring
• Monitor until recovery
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Postictal Paralysis• “Todd’s Paralysis”• May follow generalized or complex
partial• Focal motor deficit • Lasts up to 24h• High likelihood of an underlying
structural cause
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Neurogenic Pulmonary Edema• Common, but often subclinical feature of any
CNS insult• “centrally mediated sympathetic discharge
and generalized vasoconstriction, coupled with increased pulmonary capillary membrane permeability” Rosen’s p.1451
• May appear like aspiration pneumonia• Ventilatory support if necessary
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Emergency Department Management
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http://www.seizurerobots.com/
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Diagnosis• Hx of ictal event, known or potential
precipitants and exposures and PMHx• Thorough Physical Examination
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History taking• 1. Hx of seizures?• 2. If no, was the event witnessed?
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Differential Diagnosis• Syncope• Hyperventilation• Breath holding• Toxic state: DTs• Metabolic state:
hypoglycemia
• TIA• Narcolepsy• Movement disorders• Psychogenic illness
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COLD• Character-type of seizure• Onset-when, what was pt doing• Location-where• Duration-how long
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seizure• Abrupt onset-no aura• Brief duration-usually <120s• Altered mental status• Purposeless activity• Unprovoked• Postictal state
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Previous Seizures• Focus on:• Anticonvusant level, med
noncompliance, med change• Drugs, etoh• Drug-drug interactions• Change in ictal pattern• Cause for lowered seizure threshold
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Physical Examination• Medic alert• Hypertension,
tachycardia, tachypnea• Tongue biting• Shoulder dislocation• Back pain• Urinary or fecal
incontinence• Neurocutaneous signs
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Lab• Stat glucose is vital• in neurologically N, healthy pt: little
value• Medically ill: labs• Anticonvulsant levels• Tox screen if suspicion of abuse• BHCG if eclampsia suspected• Meningitis or SAH: LP if no inc. ICP
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Lab abnormalities• Hypoglycemia- cause/effect?• Lactic Acidosis• Rhabdomyolysis
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First time seizure• Never assume it is idiopathic• 46% will need admission• Focus on medical, toxicologic,
neurologic cause
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First time seizure:CT scan in the department?
• if you suspect a ‘serious structural lesion’
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Suspect a ‘serious structural lesion’?• New focal deficit• Persistent altered
metal status• Fever• Trauma• Persistent headache
• History of cancer• Anticoagulant use• Suspicion or known
AIDS• Age > 40• Partial onset seizure• Increased ICP
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First time Seizure• Scan as an outpatient if:• Complete recovery and no apparent
cause of seizure found• If follow up questionable: scan in ED
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Recurrent Seizures• Initial stabilization same• Most common cause is med noncompliance• Must measure anticonvulsant levels• Supratherapeutic levels of phenytoin and
carbamazepine may cause seizures• Be careful about giving loading dose before
checking a serum level• Hx and PE
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Known or Recurrent Epilepsy:CT scan in dept?• Same considerations as with first time
seizure• Also: • Change in seizure pattern• Prolonged post-ictal state
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Management
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Stabilization• Monitored bed• Oxygen• Pulse oximetry• Heart rate monitor, BP cuff• IV access
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Airway• Anticipatory• Gag reflex suppressed• +/- vomiting• Left lateral decubitus• ?Bite block to prevent tongue biting and
to allow suctioning• +/- nasopharyngeal airway
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Apneic or airway threat• If O2 sat<90% or inability to protect
airway• Endotracheally intubate• BZD for induction• If trismus, may need neuromuscular
blockade
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Think:• If seizure lasts longer than 5 minutes it
is unlikely to stop• should start thinking about status
epilepticus• Treat ASAP
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stolen from Dr. S. Bernbaum
Drug Rx of SE
• Starting Rx ASAP has been correlated with a better response rate to drug Rx, and lower morbidity– Lowenstein DH, Alldredge BK
Neurology 1993 (43): 483-8• < 30 min - 80% stopped• > 120 min - < 40% stopped
but - retrospective review; • ? groups comparable
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Reversible causes• Hypoglycemia• Isoniazid• Eclampsia
• Dextrose• Pyridoxine• Magnesium
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Medications• First Line: Benzodiazepines IV• Directly enhance GABA-mediated neuronal
inhibition• affect both clinical and electrical
manifestations of seizures • Terminate seizure activity in 75-90% of pts• May cause hypotension and respiratory
depression
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Lorazepam (Ativan)• 0.1mg/kg/IV• 1-2mg/min• Up to 10mg• Peds: 0.05mg to 0.1mg/kg IV• Longer duration of seizure suppression
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Diazepam (Valium)• 0.2mg/kg IV• at 2mg/min• up to 20mg• Peds: 0.2-0.5mg/kg IV/IO/ET or 0.5-
1.0mg PR• Works well rectally, endotracheally,
interosseously
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Midazolam (Versed)• 2.5-5.0mg IV• 0.2mg/kg IM• Peds: 0.15mg/kg IV then 2-10ug/kg/min• Works well IM
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Second line• anticonvulsants
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Phenytoin (Dilantin)• suppresses neuronal recruitment • does not suppress electrical activity at
the ictogenic focus• No sedation or resp depression• May cause hypotension if given rapid IV• Takes 30min to infuse
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Phenytoin• 20mg/kg IV at <50mg/min• Peds: 20mg/kg IV at 1mg/kg/min
• If pt subtherapeutic:• May give loading dose IV or PO to
boost serum levels
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Fosphenytoin• Phenytoin prodrug• Water soluble• May be administered quickly• Better tolerated, more safe, more stable
than phenytoin• More difficult to monitor, delayed
hypotension
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Fosphenytoin• 15-20 PE/kg at 100-150mg PE/min• PE: phenytoin sodium equivalent• Peds: not established
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Phenobarbital• third-line• in pediatrics is second-line therapy• CNS depressant decreases both ictal
and physiologic cortical electrical activity
• anticipate: sedation and depression of respiratory drive and BP
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Phenobarbital• 20mg/kg IV at 60-100mg/min• Ped: same• May give as IM loading dose
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Eclampsia• Magnesium is not an anticonvulsant• 4-6g IV followed by 1-2g/h infusion with
hydralazine• Unexplained efficacy• BZD effective short term• Phenytoin may be efficacious-teratogenic• Should consult Obs/Gyn or have established
protocol
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stolen from Dr. S. Bernbuam
Status Epilepticus• continuous or rapidly repeating seizures• no consensus on exact definition - “abn prolonged”
– “no recovery between attacks”– “20-30 min” --> injury to CNS neurons– more practical definition: since isolated tonic -
clonic seizures rarely last > few minutes ... consider Status if sz > 5 min or 2 discrete sz with no regaining of consciousness between
• vs. serial sz - close together - regained consciousness in between
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stolen from Dr. S. Bernbaum
CNS damage can occur• uncontrolled neuronal firing• excess glutamate (exitatory NT)• this sustained high influx of calcium ions
into neurons leads to cell death (“excitotoxicity”)
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Management of ‘Status’• Valproate: PR, increases GABA conc.• Valproate IV 25mg/kg in future• Barbiturate Coma
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Barbiturate coma• works well but suppresses all brainstem function• Neuro, ICU consults recommended: resp arrest,
myocardial depression, hypotension, dec ICP, dec cerebral perfusion
• phenobarbital 20mg/kg IV at 60mg/min• pentobarbital 10-15mg/kg IV load then 0.5-
1.0mg/kg/hr infusion• Need intubation and ventilatory support, cardiac
monitoring, invasive hemodynamic monitoring, +/- pressors = ICU
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Midazolam and Propofol• midazolam 0.2mg/kg bolus then
0.045mg/kg/h infusion• propofol 1mg/kg bolus then 2mg/kg/h
infusion• Hypotension• Intubation and ICU
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Isoflurane Anaesthesia• Final alternative in refractory status• Anaesthesia involved• BZD induction agent + lidocaine
pretreatment• ICU
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Not moving = Not seizing?• NO• Visual manifestations of convulsive
ictus are extinguished by neuromuscular blockade.
• Need electroencephalographic monitoring arranged
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Disposition• Individualized for pt.• Home, home with GP follow, neuro
consult in ED, neuro follow up• Shouldn’t drive for 6 months• Law varies from province to province
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Summary• Several types of and many causes for
seizures• History is important• First seizure likely needs imaging• Treat immediately• If seizure lasts >5min think status
epilepticus• “Sub” areas to consider: febrile seizures,
status epilepticus
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References• Dorland’s Pocket Medical Dictionary 25th Ed. 1995 W.B.
Saunders Company• Neuroimaging in the emergency department patient presenting
with seizures, Neurology 47:26, 1996.• Rosen’s Emergency Medicine 5th edition, Marx et al. Mosby,
Toronto, 2002• Emergency Medicine Secrets 3rd Ed. Markovchick et al. Hanley
& Belfus, Philadelphia 2003• Seizures in the Emergency Department, Nicholl J.S. et al
http://www.emedicine.com/neuro/topic694.htm• Status Epilepticus, Stan Bernbaum MD CCFP-EM, May 31,
2001, http://www.calgaryhealthregion.ca/em/