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8/6/2019 The Seizing Child (2)
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Pediatric Seizures
Muhammad Waseem, MDMuhammad Waseem, MD
Emergency MedicineEmergency MedicineLincoln HospitalLincoln Hospital
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Few things are more frightening to
parents than to witness their childhaving a seizure
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Objectives Wide spectrum of Pediatric seizure
Etiologies specific to children Treatment modalities in children
Quality of life issues
Legal implications
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Seizure Common neurologic disorder
3 - 5% of children 1/2 classified as febrile seizures
Epilepsy (0.5 - 1%)
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Seizure 10% ambulance calls for children
1.5% of total ED visit Most resolve in the pre-hospital setting
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Seizure - ED visits Febrile seizure 53%
Established epilepsy 31% New-onset seizure 10%
Status epilepticus 5%
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Causes Idiopathic 76%
Developmental 13% Infection 5%
Head trauma 3%
Other 2%
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Seizure Fit
Spell Attack
Convulsion
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What is Seizure?
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Seizure Paroxysmal, time-limited event that
results from abnormal neuronal activityin the brain
Paroxysmal alteration in neurologicfunction (i.e, behavioral, motor, or
autonomic function, or all three - volpe1989.
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Convulsion A seizure with prominent motor
manifestation
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Epilepsy Disorder of CNS whose symptoms are
seizures
Recurrent seizures
Unprovoked
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Seizure Most seizures are not epileptic
Non-epileptic seizures are physiologic Hypoxia
Fever
Toxins
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Seizure Seizure is a symptom of a disorder that
need further investigations
Does not constitute a diagnosis
May occur in both normal & abnormaltissue
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Non-epileptic Events
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Mimic Seizures Breath-holding spells
Syncope Migraine
Tics
Night terror Pseudo-seizures
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Non-epileptic Events Inaccurate diagnoses
Inappropriate use of AED
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Non-epileptic Events
Careful history
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Breath-holding spells Frightening
6 months - 4 years Inciting event-Shrill cry-Breath holding-
Cyanosis
Disappear spontaneously before schoolage
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Night Terrors 5 - 7 years
Between midnight and 2 AM Slow wave sleep stage 3 or 4
Frightened and screaming
Increased autonomic activity Sleep follows in few minutes
No recall
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Pseudo-seizure Diagnosis of exclusion
10 - 18 years Bizarre, unusual postures
Verbalization
Uncharacteristic movements Can be persuaded to have an attack on
request
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Pseudo-seizure Lack of cyanosis
Talking during seizure Normal reaction to pupil
No loss of sphincter control
Normal plantar responses Lack of post-ictal drowsiness
Poor response to AED
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Why Should I know type of
Seizure?
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Seizure Clue to cause
Appropriate treatment Prognosis
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Epileptic Seizures Partial (40%)
Generalized
Unclassified
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Partial Seizure Simple Partial
Complex Partial
Partial with secondary generalization
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Generalized Convulsive
Non convulsive
Absence Seizure
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Generalized- Convulsive Myoclonic
Clonic
Tonic
Tonic-clonic
Atonic
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Simple Partial Seizures (SPS) Consciousness not altered
Aura
Motor activity (face, neck or extremity)
Feeling funny or something crawlinginside me
No post-ictal phenomenon
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Complex Partial Seizures (CPS) Impairment of consciousness
Aura
Brief blank stare or sudden cessation orpause in activity
Automatism (lip smacking, chewing,swallowing and excessive salivation)
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Complex Partial Seizures (CPS) Dystonic posturing, tonic or clonic
movement
Postictal phase
Duration 1 - 2 minutes
Usually during waking hours
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Absence Seizure Sudden cessation of motor activity or
speech
Blank facial expression
Flickering of eye lids
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Absence Seizure Uncommon before age 5 year
Girls
No Aura
No postictal state
Rarely persist longer than 30 sec
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Absence Seizure Hyperventilation induces an absence
seizure
3/sec spike on EEG
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Myoclonic Quick muscle jerks
Loss of body tone
Consciousness usually unimpaired
Specific epilepsy syndromes
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Tonic Tonic spasms of truncal & facial
muscles
Flexion of upper extremities
Extension of lower extremities
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Clonic Resembles myoclonus
Loss of consciousness
Slower
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Tonic-clonic Extremely common
Begins suddenly without warning
Tonic contraction of the trunk
Rhythmic clonic contraction alternatingwith relaxation of all muscle groups
Marked increase in HR and BP
incontinence
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Tonic-clonic Seizure last 1 to 2 minutes
Post-ictal 30 minutes to 2 hours
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Atonic Seizures Suddenly dropping to the floor
Lanox-Gastaut syndrome
Can occur without LOC
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Case 1
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Case 1 9-year-old boy
Parents were aroused one night bynoise from his bed room
Noted bed sheets awry & breathingdeeply
bitten his tongue
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Case 1 Confused
Afebrile
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First Non-Febrile Seizure
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History Was this a true seizure or a non-
epileptic event?
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History Circumstances
Normal activity vs. provoked
Upon awakening
Duration
Aura
Abnormal motor movements
Abnormal eye movements/automatism
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History Post-ictal period
Urinary or fecal incontinence
Fever, trauma or drug
Birth history
Delayed milestones Family history of seizures
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Physical Examination Vital signs
Level of consciousness
Head circumference (percentile)
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Café-au-lait spot Uniformly hyper-pigmented
sharply demarcated macules
Normal children (1-3 spots)
10% of normal children
May be present at birth or develop later
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Neurofibromatosis (NF-1) Six or more, >5 mm in prepubertal
Six or more, >15 mm in postpubertal
Crowe sign
freckled appearnace in axilla
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Neurofibromatosis (NF-1) Present in 100% of patients
present at birth
Increase in size, number &pigmentation
Predilection for trunk & extremities
Spare face
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Lisch nodules Pigmented hamartomas of the iris
NF-1
Prevalence increases with age
5% (<3 years)
42% (3-4 years)
100% (21 years)
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Lisch nodules Asymptomatic
Do not correlate with the extent &severity
Do not occur in normal individuals
Best identified with slit lamp
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Adenoma Sebaceum Erythematous papules over nose &
malar areas
Develop between 4 and 6 years of age
coalesce & assume fleshy appearance
Tuberous sclerosis
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Ash-leaf spots Hypo-pigmented
Irregular borders
May be present at birth
Detectable by 2 years in 50%
Woods ultraviolet lamp
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Shagreen patch Roughened raised lesion
Orange-peel consistency
Primarily lumbo-sacral area
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Tuberous Sclerosis Infantile spasm
Hypsarrhythmic EEG pattern
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CT Scan Periventricular calcifications
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MRI Multiple cortical tubers
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Port-wine stain Macular cutaneous nevus
Present at birth
Always involves upper face & eye lids
unilateral
Sturge-Weber Disease
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Port-wine stain Tonic clonic seizure contralateral to the
side of facial nevus
Refractory to anticonvulsant
hemiparesis
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CT Scan Normal at birth
Gyriform contrast enhancement
Hemispheric atrophy
Parenchymal calcification
Railroad track
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Physical Examination Café-au-lait spots (NF)
Adenoma sebaceum (TS)
Facial hemangioma (Sturge-Weber)
Petechiae (meningitis)
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Physical Examination Hematoma or skull fractures
Signs of raised ICP
Retinal hemorrhages (Child abuse)
Signs of meningeal irritation
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Diagnostic Evaluation Bedside glucose
Serum Ca & Mg (< 3 months old)
Urine drug screen
CT head
Outpatient EEG
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Rolandic Epilepsy
Benign Partial Epilepsy withCentrotemporal Spikes (BPEC)
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Rolandic Epilepsy Common in childhood
2 - 14 years
Peak age 9 -10 years
Normal children
Unremarkable past history
Normal neurologic examination
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Rolandic Epilepsy Simple partial seizure
3-13 years (peak 9-10 years)
Almost always at night (75% sleep)
EEG (centrotemporal spike)
Carbamazepine
Excellent prognosis
Spontaneous remission by age 15 year
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Infantile Spasm (Wests synd) Sudden jerks of group of muscles
4-12 months
Characteristic EEG (hypsarrhythmia)
Poor prognosis
ACTH/Steroid
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Case 2
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Case 2 7-month-old boy with runny nose and
fever. His pediatrician saw him &
diagnosed URI. He received tylenol. Onthe same afternoon while sitting on hismothers lap he began to stare and had
a generalized tonic-clonic seizure. Theentire episode lasted approx 5 minutes
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Case 2 He fell asleep after the seizure.
Normal development
T 102 F, HR 124, R 30 BP 90/50
Wt 7.9 Kg (50%)
Ht 66.5 cm (50%)
HC 44 cm (50%)
No NC lesions
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Febrile Seizures
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Febrile seizures Most common type of seizures in the
pediatric age
usually benign
Can cause considerable parental anxiety
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Febrile seizures Seizures that occur in infancy or
childhood usually occurring between 3
months and five years, associated withfever, but without evidence of intracranial infection or defined cause
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Febrile Seizures Age dependent
Rare before 9 months & after 5 years
Peak age 9-20 months
Incidence 3 - 4%
Family history
Diagnosis of exclusion
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Febrile Seizures Risk factors
Height of temperature
Male sex
Family history of febrile seizure
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Febrile Seizures A family history of epilepsy has not been shown to be a risk factor for first
febrile seizures
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Febrile Seizures Risk factors for recurrence
Young age at onset
Febrile seizures in first degree relative
Lower degree of fever
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Febrile Seizures Generalized tonic-clonic
Duration few seconds to 10 minutes
Excellent prognosis
20% are complex
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Febrile Seizures Complex febrile seizure
> 15 minutes
More than once in 24 hours
Focal neurologic features
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Febrile Seizures Risk of recurrence 34%
Most recurrences within 6-12 months
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Lumbar Puncture < 12 months
Strongly recommend
12 - 18 months Should consider
> 18 months
If history & physical examination suggest intracranial infection
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Red flags Focal seizure
Suspicious physical examination
findings (eg, rash, petechiae) cyanosis,hypotension, or grunting
Abnormal neurologic examination
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Febrile Seizures Determine and treat the cause of fever
IV benzodiazepine
Rectal diazepam
No routine AED prophylaxis
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Febrile Seizures Incidence of epilepsy
1% (No other risk factor)
9% (Other risk factors)
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Epilepsy Family history of later epilepsy
Preexisting neurologic abnormality
Complex febrile seizure
> 15 minutes duration
> 1 febrile seizure per 24 hour
Focal febrile seizure
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Neonatal Seizures
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Neonatal Seizures Seizures during first 28 days
0.5% of all live births
Do not indicate epilepsy
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Jitteriness Vs Seizure Movements are stimulus sensitive
Appear during active state (crying)
Disappear on passive flexion
Not jerky
No abnormal eye movements
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Neonatal Seizures Neonates are at particular risk
Metabolic
Toxic Structural
Infectious
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Neonatal Seizures
Not generalized tonic-clonic
incomplete myelination
Can be very subtle
Minimal physical findings
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Neonatal Seizures
Subtle
Tonic
Clonic
Myoclonic
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Subtle Seizure More common in premature infants
Eye deviation + jerking
eyelid blinking
fluttering
smacking or drooling
Apneic spells
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Causes
Perinatal asphyxia
Intracranial hemorrhage
Metabolic - hypoglycemia, hypocalcemia
Infections
Drug withdrawl
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Lab
Head sonogram
IVH/periventricular
CT head Hemorrhage
Calcifications
Malformations EEG
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Management
The method of treatment depends onthe cause
Anticonvulsant Phenobarbital
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Status Epilepticus
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Status Epilepticus Seizure >30 minutes
Intermittent seizures longer than 30
minutes from which the patient doesnot regain consciousness
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Status Epilepticus (SE) Any type of seizure
Generalized (most common)
Absence or partial (10%)
Febrile SE (25%)
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Life-threatening causes
Bacterial meningitis
Hypoglycemia
Increased intra-cranial pressure
Hypoxemia
Toxins
TCA, Cocaine, Theophylline, insulin
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Management
Rapid stabilization of cardio-respiratoryfunctions
Termination of both clinical & electricalseizures
Diagnosis & treatment of life
threatening precipitant
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Status Epilepticus The child is often given too much IVbenzodiazepine.Blood gases are
measured and perhaps the values arefound to be slightly decreased. Thechild is then paralyzed, intubated, andsent to the intensive care unit torecover from the iatrogenic morbidity.
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Status Epilepticus Freeman JM: Status epilepticus: Its not
what weve thought or taught.
Pediatrics 1989;83:444-445
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Status Epilepticus Primary goal is to stop the seizure
First line (benzodiazepine)
Second line (phenytoin or fosphenytoin)
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Diazepam Rapid onset (3 - 5 minutes)
Orally, IV, IM, IO or Rectal
Duration of action 20 - 30 minutes
Respiratory depression, sedation,hypotension
Diastat (rectal gel)
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Diazepam IV 0.1 - 0.5 mg/kg
Rectal 0.2 - 2 mg/kg
(maximum 10 mg)
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Lorazepam Slower onset
Longer duration (12 - 24 hours)
Orally & IV
Inappropriate for rectal administration
0.05 - 0.2 mg/kg
Must be refrigerated
Tachyphylaxis
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Phenobarbital Long duration (24 hours)
IV 10-20 mg/kg bolus
rate 1-2 mg/kg/min Intubation (>30-40 mg/kg)
Respiratory depression, hypotension &
bradycardia
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Phenytoin 1950 - Massachusetts General Hospital
pH 12, limited solubility in water
Propylene glycol & ethanol 1956 - Parenteral formulation approved
1962 - pediatric dose recommendation
1986 - Revised Pediatric dose(15-20 mg/kg, 1-3 mg/kg/min)
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Phenytoin High pH
Burning & cutaneous reactions
Purple glove syndrome
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Phenytoin Propylene glycol
Seizures
Arrhythmia Asystole
Hepatic & renal damage
Hemolysis Hyperosmolality
Lactic acidosis
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Phenytoin The amount of propylene glycol in a
typical loading dose of phenytoin
administered to a 1 kg prematureneonate is about seven times greaterthan WHO standard
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Fosphenytoin 1996 Pro-drug of phenytoin
pH 8
Far more soluble in water
No organic solvent
Both IV & IM
Rapid & complete conversion tophenytoin
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Sports Participation
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Sports Participation Unnecessary restrictions
Successful athelete with epilepsy
Gary Howatt (hockey player)
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Sports Participation Which sport
Common sense
Significant metabolic imbalance Scuba diving
Potential for serious in jury
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AMA Committee for Sports Patients with epilepsy will not be
affected by indulging in any sport,
including foot ball, provided the normalsafegaurds for sports participation arefollowed, including adequate headprotection
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Reasonable precautions Bicycling
Diving
Foot ball
Skating
Swimming
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Prohibited Sports Boxing
Bungee jumping
Polo
Scuba diving
Skydiving
Waterskiing
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Driving & Regulatory Issues
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Driver Licensing Each state has its own regulations
Seizure free period
1 Year (NY)
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Reporting responsibility Patient responsibility (most states)
Physician responsibility (Six states)
CA, DE, NE NJ, OR, PA
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Employment
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Employment Average intelligence
Good health
Unpredictable loss of consciousness
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Employment No hard-and-fast rules
Should avoid workplaces in which a
sudden loss of consciousness mayexpose them or their coworkers to riskor in jury
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Employment Interstate truck
Forklift
Working in heights
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Pregnancy & Epilepsy
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Pregnancy & Epilepsy 20,000 births women with epilepsy
Lower seizure threshold
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Offspring & AED
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Offspring & AED Pheytoin
fetal hydantoin syndrome
Valproate neural tube defect
Carbamazepine
spina bifida
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Labor & Delivery
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Labor & Delivery Bleeding tendency in neonate
induction of hepatic enzymes
overcome by Vitamin K
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Breast feeding & AED
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Breast feeding & AED Nearly all epileptic drugs are transferred
in breast milk
Phenytoin 18% Phenobarbital 36%
Carbamazepine 41%
Valproate 5% Breast feeding is not contraindicated
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Oral contraceptives & AED
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Oral contraceptives & AED
Increase the dose of Oralcontraceptives
(AED induces hepatic metabolism of hormones)
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Dont forget child abuse
Discrepancy between history &in jury
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You are mandated by law toprotect these children
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Its not optional
New York State Law (Social ServicesLaw Section 413) requires that any
health professional who suspects that achild is being endangered or maltreatedmust report his/her suspicion to NY City, to the local child protectionservices
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New AEDs
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New AEDs
Gabapentin (Neurontin)
Lamotrigine (Lamictal)
Vigabatrin (Sabril) Felbamate (Felbatol)
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Take home message
Wide range of presentation
Efficiently obtain information
Always undress & examine Establish underlying etiology
Suspect abuse with inconsistent history
Recommended