Pemicu 1A

Kenapa Anakku?
JESLY CHARLIES 405100171
Kelompok 11 Blok Sistem Saraf dan Kejiwaan FK UNTAR
Learning Objectives:
1. Menjelaskan mengenai Kejang.
Definisi
Faktor risiko
Manifestasi klinis
Klasifikasi
Patofisiologi
Etiologi
Diagnosa
DD
Komplikasi
Tatalaksana
Kejang pada anak
Definisi
Manifestasi klinis khas yang berlangsung secara intermitten,
dapat berupa gangguan kesadaran, tingkah laku, emosi, motorik,
sensorik, dan atau otonom yang disebabkan oleh lepasnya
muatan listrik yang berlebihan di neuron otak.
Etiologi
Patofisiologi
Peningkatan aktifitas listrik yg berlebihan pd neuron-
neuron dan mampu secara berurutan merangsang sel
neuron lain secara bersama-sama melepaskan muatan
listriknya :
1. Kemampuan membran sel sebagai pacemaker neuron untuk
melepaskan muatan listrik yang berlebihan
2. Berkurangnya inhibisi oleh neurotransmitter asam gama amino
butirat (GABA)
3. Meningkatnya eksitasi sinaptik oleh transmiter asam glutamat
dan aspartat melalui jalur eksitasi berulang
KLASIFIKASI
Manifestasi Klinis
ANAMNESIS
Sangat penting untuk menentukan diagnosis
Harus dilakukan seteliti mungkin untuk mendapatkan gambaran
jenis kejang, faktor presipitasi dan resiko
Pada anak-anak riwayat perkembangan harus ditanyakan
ANAMNESIS
* Faktor resiko (Hauser WA, 1990)
Trauma kepala (luka dlm peperangan)
Stroke
Ensefalitis virus
Alkohol
Penyakit Alzheimer
Cedera kepala sedang
PEMERIKSAAN FISIK
Biasanya tidak dijumpai kelainan
Bila dijumpai defisit fokal neurologis menunjukan adanya
proses patologis di otak
Asimetris wajah atau ekstremitas dapat menunjukan atrofi
serebri pada kontra lateral
PEMERIKSAAN LABORATORIUM
Untuk mencari faktor-faktor yang berkontribusi sbg
penyebab kejang
Pemeriksaan serum elektrolit, glukosa, fungsi ginjal dan
hati
Elektolit, cbc dan lft sebagai base line sblm tx
Pemeriksaan toksikologi urine dan darah
LP bila ada tanda-tanda infeksi
EEG
Merupakan pemeriksaan yg paling penting untuk
menegakkan diagnosis
Membantu menegakkan diagnosis dan karakteristik
spesifik sindroma epilepsi
Menentukan manajemen dan prognosis
Discharge epileptiform : gelombang tajam dan runcing
NEUROIMAGING
MRI harus dikerjakan pada pasien-pasien dengan epilepsi
simptomatik, usia >18 tahun, perkembangan yg abnormal
serta bila defisit fokal neurologis +
CT scan < sensitif utk lesi-lesi ttt
CT scan > sensitif utk lesi kalsifikasi
PENGOBATAN
# Pada kejang parsial dan secondarily generalized
Karbamazepine
Valproate
Phenytoin
Lamotrigine
Phenobarbital pada negara sedang berkembang
PENGOBATAN
# Pada kejang umum tonik-klonik
Valproate
Karbamazepine
Lamotrigine
Phenytoin
Phenobarbital (negara sedang berkembang)
PENGOBATAN
# Pada kejang mioklonus
Valproate
Klonazepam
Lamotrigine

# Pada kejang absans

Valproate
Ethosuximide
PENGOBATAN
Efek samping hrs dimonitor
Efek samping yg berhubungan dengan dosis
Efek samping idiosinkrasi
OPERASI
Dilakukan pada kasus-kasus yg kejangnya tidak dapat
dikontrol dengan obat-obatan anti epilepsi yg optimal
serta telah mengganggu kualitas hidup
Epilepsi and other seizure
disorder
 Convulsion
an intense paroxysm of involuntary repetitive muscular contractions,
inappropriate for a disorder that may consist only of an alteration of
sensation or consciousness.
Seizure
as a generic term
it embraces all paroxysmal electrical discharges of the brain
Motor or convulsive seizure,
sensory seizure or psychic seizure.
Epilepsy
Greek words= "to seize upon" or a "taking hold of."
"falling sickness" or the "falling evil."
recurrent seizures
Status epilepticus
Convulsive seizures by their nature, if prolonged or repeated every few
minutes
may threaten life.
Seizures require three conditions:
(1) a population of pathologically excitable neurons;
(2) an increase in excitatory glutaminergic activity through
recurrent connections in order to spread the discharge
(3) a reduction in the activity of the normally inhibitory
gabanergic projections.
International Classification of Epileptic Seizures
Generalized Tonic-Clonic Seizures
(Grand Mal)
Primary type
convulsion starts with little or no warning.
patient senses the several subjective phenomena (prodrome).
some hours= apathetic, depressed, irritable, or, rarely, the
oppositeecstatic.
myoclonic jerks of the trunk or limbs
 initial motor signs
-mouth and eyelids open
-brief flexion of the trunk
-upward deviation of the
eyes
-arms =elevated and
abducted
-elbows =semiflexed
-hands =pronated
tonic phase
(10 to 20 s)
-piercing cry
-skin and lips cyanotic
-bladder empty
-dilated pupils -unreactive
to light
deep inspiration terminal phase
end of the clonic phase movements
have ended
Autonomic signs
-the pulse is rapid
-blood pressure is elevated pupils begin
-pupils are dilated, to contract
-salivation and sweating to light
-bladder pressure increase
Breathing quiet
-Violaceous face
or stertorous
-Grimaces
-tongue is bitten
opens eyesconfused
violent flexor spasms -
rhythmic - agitate
drowsy and falls
mild generalized tremor asleep pulsatile
headache
clonic phase
(30 s) no memory
 DD/:
vasodepressor syncope or a Stokes-Adams hypotensive attack.
clonic jerking of the extended limbs
brain waves are slow and flat
basilar artery occlusion.
"limb-shaking TIAs"
clonic movements of one limb or one side episode of cerebral
ischemia.
Infants
a breath-holding spell tonic phase of a generalized seizure.
Absence, Petit Mal Seizures
moment of absentmindedness or daydreaming.
coming without warning
sudden interruption of consciousness
stares and briefly stops talking or ceases to respond.
Childhood>>
=adults with frontal lobe epilepsy
begin or end with a generalized tonic-clonic seizure
Postural tone may be slightly decreased or increased
 EEG abnormality,
generalized 3-per-second spike-and-wave pattern
Minor automatisms
lip-smacking, chewing, and fumbling movements of the
fingers.
After 2 to 10 s
reestablishes full contact with the environment and resumes
his preseizure activity.
inducing
voluntary hyperventilation for 2 to 3 min
absence or petit mal status
attacks last for hours with no interval of normal mental
activity between them
children with absence attacks

1/3 1/2
display some time
symmetrical or have major
asymmetrical generalized
myoclonic jerks (tonic-clonic)
without loss of convulsions.
consciousness,
Absence Variants
Atypical petit mal
long runs of slow spike-and-wave activity,
no apparent loss of consciousness.
External stimuli asking the patient to answer a question or
to count interrupt the run of abnormal EEG activity.
 Lennox-Gastaut Syndrome
symptomatic generalized epilepsy 2 - 6 years of age
characterized by
atonic, or astatic,
seizures (i.e., falling attacks),
succeeded by various combinations of minor motor, tonic-clonic, partial
seizures
progressive intellectual impairment
distinctive, slow (1- to 2-Hz) spike-and-wave EEG pattern.
preceded in earlier life by infantile spasms
characteristic high-amplitude chaotic EEG picture ("hypsarrhythmia"),
arrest in mental development,
~ West syndrome
underlying conditions:
Prematurity
perinatal injury
metabolic diseases of infancy
persist into adult life
one of the most difficult forms of epilepsy to treat.
Myoclonic Seizures
Characterized by
brusque, brief, muscular contraction,
small
only one muscle or part of a muscle
large
displace a limb on one or both sides of the body
or the entire trunk musculature.
lasting 50 to 100 ms
intermittently and unpredictably
Uremia any age myoclonus, twitching, and
sometimes seizures.
 disseminated Suspect:
myoclonus Childhood -myoclonus-opsoclonus-ataxia syndrome,
(polymyoclonus) -lithium or other drug toxicity,
-subacute sclerosing
panencephalitis.(lasting a few weeks)
Chronic
progressive
polymyoclonus +
dementia disseminated -Creutzfeldt-
middle and
myoclonus + late adult Jakob disease -
dementia years Alzheimer
-juvenile lipidosis, disease

-certain mitochondrial
disorders,
Intraneuronal cortical inclusions
-chronic familial of amyloid (+muscle, liver, and
degenerative diseases of skin)
undefined type
triad =
-Lafora-type familial autosomal
-progressive dementia,
myoclonic epilepsy, recessive in
-myoclonus,
transmission
-episodes of generalized seizures
Juvenile Myoclonic Epilepsy
begins in adolescence(15 years)
a generalized seizure
often upon awakening
myoclonic jerks in the morning that involve the entire body;
absence seizures
EEG shows characteristic
bursts of 4- to 6-Hz irregular polyspike activity.
linkage chromosome 6 no clear mendelian pattern of
inheritance has been established.
not impair intelligence and tends not to be progressive
Th/= Valproic acid + anticonvulsants
Partial or Focal Seizures
Frontal Lobe Partial Seizures (Focal
Motor and Jacksonian Seizures)
turning movement of the head and eyes to the side
opposite the irritative focus, + tonic extension of
limbs, also on the side contralateral to the affected
hemisphere.
jacksonian motor seizure
begins with a tonic contraction of the fingers of one hand,
the face on one side, or the muscles of one foot. clonic
movements
localized or spread ("march") from the part first affected to
other muscles on the same side of the body.
20 to 30 s.
Consciousness is not lost
 transient paralysis of the affected limbs"Todd
paralysis"
persists for minutes or at times for hours after the seizure
focal motor epilepsy
process or focus of excitation in or near the rolandic
(motor) cortex, i.e., area 4 of Brodmann
Lesions confined to the motor cortex form of clonic
contractions,
confined to the premotor cortex (area 6) tonic
contractions of the contralateral arm, face, neck, or all of
one side of the body.
high medial frontal lesions (area 8 and supplementary motor
cortex)
Tonic elevation and extension of the contralateral arm ("fencing
posture") and choreoathetotic and dystonic postures
bizarre, and flailing movements of a contralateral limb
 from the cortical language areas brief aphasic
disturbance (ictal aphasia) , ejaculation of a word, a
vocal arrest.
Ictal aphasia
In focal or generalized seizure activity ,
in isolation,
without loss of consciousness,
Postictal aphasia
Verbalization no such significance
associated with an origin in the nondominant hemisphere.
Somatosensory, Visual, and Other
Types of Sensory Seizures
Somatosensory seizures,
in or near the postrolandic convolution of the opposite
cerebral hemisphere.
numbness, tingling, or a "pins-and-needles" feeling and
occasionally as a sensation of crawling (formication),
electricity, or movement of the part.
onset of the sensory seizure is in the lips, fingers, or toes,
and the spread to adjacent parts of the body follows a
pattern determined by sensory arrangements in the
postcentral (postrolandic) convolution of the parietal lobe.
 Visual seizures
Lesions in or near the striate cortex of the occipital lobe
produce elemental visual sensations of darkness or sparks and
flashes of light, which may be stationary or moving and
colorless or colored.
lesions on the lateral surface of the occipital lobe (Brodmann
areas 18 and 19) sensation of twinkling or pulsating lights.
focus in the posterior part of the temporal lobe, near its
junction with the occipital lobe visual hallucinations (+
auditory hallucinations).
 Auditory hallucinations
focus in one superior temporal convolution
buzzing or roaring in the ears.
more posterior part of one temporal lobe.
A human voice, sometimes repeating unrecognizable words, or the sound of
music

Vertiginous sensations
vestibular origin in the superoposterior temporal region or the
junction between parietal and temporal lobes.

Olfactory hallucinations
disease of the inferior and medial parts of the temporal lobe region of
the parahippocampal convolution or the uncus
perceived odor is exteriorized,
 Gustatory hallucinations
temporal lobe disease and less often with lesions of the insula and
parietal operculum;
salivation and a sensation of thirst may be associated.
Electrical stimulation in the depths of the sylvian fissure, extending into
the insular region, has produced peculiar sensations of taste.

Vague and often indefinable visceral sensations arising in the thorax,

epigastrium, and abdomen
Auras
temporal lobe origin, localized to the upper bank of the sylvian
fissure, in the upper or middle frontal gyrus, or in the medial frontal area
near the cingulate gyrus.
Palpitation and acceleration of the pulse at the beginning of the attack
Complex Partial Seizures (Psychomotor
Seizures, Temporal Lobe Seizures)
(1) the aura (i.e., the initial event in the seizure) may
be either a focal seizure of simple type or a
hallucination or perceptual illusion, indicating (usually)
a temporal lobe origin
(2) instead of a complete loss of control of thought
and action, there is a period of altered behavior and
consciousness, for which the patient is later found to
be amnesic.
 Benign Childhood Epilepsy with
Centrotemporal Spikes (Rolandic Epilepsy,
Sylvian Epilepsy) and Epilepsy with Occipital
Spikes
self-limited disorders transmitted
autosomal dominant
5 and 9 years of age
nocturnal tonic-clonic seizure with focal
onset.
interictal EEG = high-voltage spikes in the
contralateral lower rolandic or
centrotemporal area.
 Infantile Spasms (West Syndrome)
infancy and early childhood.
characterized by
recurrent,
single or brief episodes of gross flexion movements of the trunk and limbs
extension movements (hence the alternative terms infantile spasms or salaam
or jackknife seizures).
major EEG abnormalities
continuous multifocal spikes and slow waves of large amplitude.
diminish and usually disappear by the fourth to fifth year.
MRI and CT scans abnormal =cortical dysgeneses.
treatment
=ACTH, corticosteroids, or the benzodiazepine drugs (clonazepam)
tuberous sclerosis gamma-aminobutyric acid (GABA)-inhibiting drugs
Later=
left mentally impaired.
Infantile spasms Lennox-Gastaut syndrome
 Febrile Seizures
infants and children (6 months - 5 years of age )
inherited
single, generalized motor seizure occurring as the patient's
core temperature rises or reaches its peak.
>38C (100.4F).
precipitant of the fever= viral (herpesvirus 6) or bacterial
illness,an immunization,
risk factor
Bacterial meningitis
head and birth trauma
complex febrile convulsions (focal, prolonged, or repeated
episodes of febrile seizures) complicating features.
 Reflex Epilepsies
seizures can be evoked in certain individuals by a discrete physiologic or
psychologic stimulus.
visual -flickering light, myoclonic
-visual patterns, generalized
-specific colors (especially red), triggered by
-leading to rapid blinking or eye closure -the photic stimulation of television
-an EEG examination
-photic or pattern stimulation of
video games.
auditory -sudden unexpected noise (startle), induced by music myoclonic,
-specific sounds, simple, or complex partial.
-musical themes,
-voices
somatosensory -a brisk unexpected tap focal or generalized
-sudden movement after sitting or lying one or a series of myoclonic jerks /
still, absence / tonic-clonic
-a prolonged tactile
-thermal stimulus
writing or reading complex partial type;
of words or
numbers
eating
 caused by focal cerebral disease occipital lesions.
Treatment=
Clonazepam, valproate, carbamazepine, and phenytoin
learn to avert the seizure by undertaking a mental task,
thinking about some distracting subject,
counting,
initiating some type of physical activity.
 Epilepsia Partialis Continua
focal motor epilepsy
characterized by
persistent rhythmic clonic movements of one muscle group (face, arm, or leg)
repeated at fairly regular intervals every few seconds
continue for hours, days, weeks, or months
without spreading to other parts of the body
persistent focal motor status epilepticus
induced by a variety of acute or chronic cerebral lesions
the underlying cause is not found
focal EEG abnormalities
either repetitive slow-wave abnormalities
sharp waves
spikes over the central areas of the contralateral hemisphere.
part of a spectrum that includes stimulus-sensitive myoclonus, focal
motor seizures, and grand mal seizures.
common in patients with Rasmussen encephalitis (an autoimmune disorder. )
 Psychogenic, Nonepileptic Seizures (Pseudoseizures)
convulsive or nonconvulsive seizures,
not the result of an abnormal neuronal discharge.
a symptom of
hysteria female
compensation neurosis and malingering males and females.
unconventional motor display
completely asynchronous thrashing of the limbs
repeated side-to-side movements of the head;
striking out at a person who is trying to restrain the patient;
hand-biting, kicking, trembling, and quivering;
pelvic thrusting
opisthotonic arching postures;
screaming or talking during the ictus.
the eyes are kept quietly or forcefully closed
precipitated by emotional factors,
prolonged for many minutes or hours;
Lack of =tongue-biting, incontinence, hurtful falls, postictal confusion
The serum creatine kinase levels normal
Neonatal Seizures
first days of postnatal life.
fragmentaryan abrupt movement or posturing of a limb, stiffening of the
body, rolling up of the eyes, a pause in respirations, lip-smacking, chewing, or
bicycling movements of the legs.
focal or multifocal cortical discharges;
The EEG is nonetheless helpful in diagnosis.
Periods of EEG suppression sharp or slow waves / discontinuous theta
activity.
Neonatal seizures occurring within 24 to 48 h of a difficult birth
severe cerebral damage, usually anoxic, either antenatal or parturitional.
Seizures having their onset several days or weeks after birth
acquired or hereditary metabolic disease
pyridoxine deficiency.
Biotinidase deficiency
Nonketotic hyperglycemia,
maple syrup urine disease,
hypoglycemia
hypocalcemia with tetany,
Infantile Seizures (Occurring in the First
Months, Up to 2 Years)
characteristic pattern
massive sudden myoclonic jerk of head and arms leading to
flexion or, less often, to extension of the body (infantile
spasms, salaam spasms).
West syndrome most threatening
metabolic encephalopathy of unknown type
cortical dysgenesis (Jellinger)
tuberous sclerosis (diagnosed in infancy by dermal white spots),
phenylketonuria,
Sturge-Weber angiomatosis,
developmental delay.
myoclonus begins in infancy with fever
unilateral or bilateral clonic seizures
partial seizures followed by focal neurologic abnormalities
 Phenytoin, carbamazepine
blocking sodium channels
Valproate
complex partial seizures effectiveness<<
Lamotrigine
is emerging alternative for partial seizures
Carbamazepine initial drug
Carbamazepine and valproate epileptic children
not coarsen facial features
not produce gum hypertrophy or breast enlargement.
myoclonic epilepsy in adolescence
valproate first drug
SE= Weight gain, menstrual irregularities , teratogenic effects
decrease in bone density increased risk of fracture from
osteoporosis in older patients(women).
calcium supplements or one of the bisphosphonates
 Phenytoin
PO, IM, IV
Idiosyncratic side phenytoin hypersensitivity
effects -Rash, fever, lymphadenopathy, eosinophilia and other
blood dyscrasias, and polyarteritis

Choreoathetosis
Overdose ataxia, diplopia, and stupor.
prolonged use hirsutism (mainly in young girls), hypertrophy of gums, and
coarsening of facial features in children.
Chronic use peripheral neuropathy , cerebellar degeneration
An antifolate effect pregnant women = + folate supplementation and vitamin K
on blood and before delivery
interference with the newborn infant = + vitamin K
vitamin K
metabolism
Interaction disulfiram (Antabuse), chloramphenicol, sulfamethizole,
phenylbutazone, or cyclophosphamide, warfarin
(Coumadin)
Carbamazepine
idiosyncratic reactions
Mild leukopenia
pancytopenia,
hyponatremia (inappropriate antidiuretic hormone [ADH]),
diabetes insipidus
before treatment complete blood count
checked regularly white cell counts
Valproate
Adverse effect=
Hepatotoxic
weight gain first months of therapy.
menstrual irregularities and polycystic ovarian syndrome
young women
Pancreatitis rare
An intravenous form of valproate is available.
The maximum recommended rate of administration is 3
mg/kg per min.
Phenobarbital
highly effective
toxic effects
drowsiness
mental dullness,
nystagmus,
staggering,
may provoke behavioral problems in retarded
children.
still used to
adjunctive anticonvulsant
primary therapy in infantile seizures.
The adverse effects of primidone are much the same.
Lamotrigine
selectively blocking the slow sodium channel,
preventing the release of the excitatory transmitters glutamate
and aspartate.
Indications=
generalized and focal seizures
first-line
adjunctive drug
young women
alternative does not provoke weight gain and
ovarian problems.
Levetiracetam
uncertain mechanism
The agent affects the SV2A synaptic vesicle protein
useful in the treatment of partial and generalized seizures
initiated slowly well tolerated
SE=
sleepiness and dizziness
no important interactions with other antiepileptic drugs.
Other Antiepileptic Drugs
Felbamate,
an adjunctive generalized seizures, complex partial seizures, and Lennox-Gastaut
syndrome,
bone marrow suppression and liver failure.
gabapentin and vigabatrin,
enhance the intrinsic inhibitory system of GABA in the brain.
moderately effective in partial and secondary generalized seizures
not being metabolized by the liver.
few toxic effects and few known adverse drug interactions.
Topiramate,
serious dermatologic , induce renal stones , Angle-closure glaucoma , hyperchloremic
metabolic acidosis.
Ethosuximide and valproate
absence seizures, children older than 4 years of age.
single dose of 250 mg of ethosuximide per day and to increase it every week until the
optimum therapeutic effect is achieved.
Methsuximide (Celontin)
in individual cases where ethosuximide and valproate have failed.
Treatment of Seizures in the Neonate
and Young Child
phenobarbital seizure control in infancy.
Lennox-Gastaut syndrome.
Valproic acid (900 to 2,400 mg/d) reduce the frequency of
spells
newer drugslamotrigine, topiramate, vigabatrin
Clonazepam limited success.
infantile spasms
ACTH or adrenal corticosteroids
+ tuberous sclerosis vigabatrin
Pharmacologic treatment of generalized tonic-clonic status epilepticus in adults.
Surgical Treatment of Epilepsy
careful analysis of clinical and EEG findings
The most favorable candidates for surgery
complex partial seizures and a unilateral temporal lobe focus,
still required some anticonvulsant medication.
Excision of cortical tissue outside of the temporal lobe 50 %.
sectioning of the corpus callosum and hemispherectomy.
callosotomy control of intractable partial and secondarily generalized
seizures
Removal of the entire cortex of one hemisphere, +++ amygdala and
hippocampus,
severe and extensive unilateral cerebral disease and intractable
contralateral motor seizures and hemiplegia.
Rasmussen encephalitis, Sturge-Weber disease, and large
porencephalic cysts
Surgical, focused radiation, or endovascular reduction of arteriovenous
malformations reduce the frequency of seizures
Ketogenic Diet
ages of 1 and 10 years.
hospitalization starvation 1-2 days - to induce
ketosis diet in which 80 to 90 percent of the
calories are derived from fat (Vining).
effective in
refractory cases of epilepsy in childhood,
reducing seizure frequency in 2/3 of children
reduction in the amount of anticonvulsant medication
some benefit persists after the diet has been stopped.
Complication= Nephrolithiasis.
 ketogenic diet

1. child fasts in the hospital for 24 to 72 hours until a 4+ ketonuria is produced

2. stop antiepileptic drugs

ketosis

the "traditional" approach the medium-chain triglyceride

(MCT)-based approach

Caloric intake (kcal) replaces the long-chain fats of the

fat :protein/carbohydrate = 4:1 traditional diet with MCT
75% kilocalories fat. MCT oil
Protein odorless, colorless, tasteless oil
about I g/kg/day
nonketogenic foods can be allowed
Carbohydrates ketosis - MCT more readily
A multiple vitamin/mineral and extra achieved
calcium supplement fruits
provided in a sugar-free form.
vegetables
Mild dehydration small amounts of bread and other
Fluids not to exceed 2 L/dav starches
Fluids are not limited.
Regulation of Physical and Mental
Activity
A moderate amount of physical exercise is allowable
potentially more dangerous sports +proper safeguards,
incompletely controlled epilepsy not be allowed to=
drive an automobile,
operate unguarded machinery,
climb ladders,
take tub baths behind locked doors;
Psychosocial difficulties must be identified and addressed early.
feelings of inferiority
allowed to live as normal a life as possible.
keep children in school, and adults should be encouraged to
work.
communities
Partial (Focal) Seizures
Generalized Seizures
Kejang demam
Kejang demam
Bangkitan kejang yang terjadi pada kenaikan suhu tubuh
(suhu rektal >38C) yang disebabkan oleh suatu proses
ekstrakranial.
terjadi pada 2-5% anak antara usia 6 bulan sampai 5 tahun
Kejang disertai demam pada bayi berumur kurang dari 1
bulan tidak termasuk dalam kejang demam
Pada usia 6bulan 5 tahun, demam > 38
EEG : normal tapi berpotensi jadi epilepsi di kemudian
hari
ETIOLOGI
Intrakranial
Asfiksia : Ensefolopati hipoksik iskemik
Trauma (perdarahan) : perdarahan subaraknoid, subdural, atau
intra ventrikular
Infeksi : Bakteri, virus, parasit
Kelainan bawaan : disgenesis korteks serebri, sindrom zelluarge,
Sindrom Smith Lemli Opitz.
Ekstra kranial
Gangguan metabolik : Hipoglikemia, hipokalsemia,
hipomognesemia, gangguan elektrolit (Na dan K)
Toksik : Intoksikasi anestesi lokal, sindrom putus obat.
Kelainan yang diturunkan : gangguan metabolisme asam amino,
ketergantungan dan kekurangan produksi kernikterus.
Idiopatik
Kejang neonatus fanciliel benigna, kejang hari ke-5 (the fifth day
fits)
Faktor resiko kejang demam pertama
Riwayat KD dalam keluarga
Pemulangan neonatus >28 hari
Perkembangan terlambat
Anak dengan pengawasan
Kadar natrium rendah
Temperatur tinggi
FAKTOR RESIKO BERULANGNYA
KEJANG
Riwayat KD dlm keluarga
Usia < 12 bulan
Cepatnya timbul kejang setelah demam
Temperatur yang rendah saat kejang (<38oC)
Riwayat keluarga epilepsi
FAKTOR RESIKO MENJADI EPILEPSI
1. KELAINAN NEUROLOGIS
2. KEJANG DEMAM KOMPLEKS
3. RIWAYAT EPILEPSI DLM KELUARGA.
KLASIFIKASI

Sederhana

Kejang
demam
Kompleks
KEJANG DEMAM SEDERHANA
Kejang bersifat umum
Lama kejang < 15 menit
Usia waktu KD pertama < 6 tahun
Frekwensi serangan 1-4 x dlm 1 th
EEG normal.
KEJANG DEMAM KOMPLEKS
( ILAE 1993)
Adalah KD dg salah satu gejala sbb:
Kejang berlangsung lama, 15 menit.
Kejang fokal atau parsial satu sisi, atau kejang umum
didahului kejang parsial.
Kejang berulang 2 kali atau lebih dlm 24 jm
KRITERIA DIAGNOSA
Kriteria diagnosis kejang demam:
Kejang didahului oleh demam.
Pasca-kejang anak sadar kecuali kejang lebih dari 15 menit.
Pemeriksaan cairan serebrospinalis dalam batas normal.
DIAGNOSIS
Anamnesis
Adanya kejang, jenis kejang, kesadaran, lama kejang, suhu
sebelum/saat kejang, frekuensi, interval, pasca kejang,
penyebab kejang di luar SSP.
Tidak ada riwayat kejang tanpa demam sebelumnya.
Riwayat kelahiran, perkembangan, kejang demam dalam
keluarga, epilepsi dalam keluarga (kakak-adik, orangtua).
Singkirkan dengan anamnesis penyebab kejang yang lain.
DIAGNOSIS
Pemeriksaan fisik dan neurologis
Kesadaran, suhu tubuh, tanda rangsang meningeal, tanda
peningkatan tekanan intrakranial, dan tanda infeksi di luar SSP.
Pada umumnya tidak dijumpai adanya kelainan neurologis,
termasuk tidak ada kelumpuhan nervi kranialis.
DIAGNOSIS
Pemeriksaan penunjang
Darah tepi lengkap penyebab demam
Elektrolit, glukosa darah diare, muntah, hal lain yg dpt
mengganggu kesimbangan elektrolit atau gula darah.
L P curiga meningitis, umur 12 bl sangat dianjurkan, 12-18 bl
dianjurkan.
EEG tdk dpt memprediksi berulangnya kejang/ menjadi
epilepsi tidak perlu.
DIAGNOSIS
Pemeriksaan penunjang
PCR HHV-6, HHV-7 dan virus influenza
Kadar TNF alfa, IL-1 alfa & IL-6 pada CSS meningkat
Ensefalitis akut / Ensefalopati.
CTscan atau MRI tidak dilakukan pd KDS
Vaksinasi bukan merupakan kontra indikasi
 PENGOBATAN pd saat DEMAM
ANTI PIRETIK tidak mengurangi resiko berulangnya kejang, tapi
dianjurkan untuk menurunkan demam
asetaminofen 1015 mg/kg/hari setiap 46 jam

ibuprofen 510 mg/kg/hari tiap 46 jam.

ANTI KONVULSAN INTERMITEN DIAZEPAM

Oral: 0,3mg/kgBB/kali 3-4X

Rektal: 0,3-0,5mg/kgBB/kali tiap 8 jam

PENGOBATAN dlm kead. KEJANG
DIAZEPAM*
REKTAL ( 5 mg BB < 10 kg , 10 mg BB > 10 kg ) , atau
PARENTERAL ( 0,3 0,5 mg/ kgBB/ kali ).
Pemberian dpt diulangi setelah 5 menit 2 kali I.V / 2 kali Rektal + 1
kali I.V.
MASIH KEJANG FENITOIN ( 10-14 mg/ kgBB 50 mg/ mnt )
BELUM TERATASI I C U

*dosis maksimal 20mg

OBAT YG DIGUNAKAN
PHENOBARBITAL 4-6 mg/kgBB/hr 2X
Efek samping:
Gangguan perilaku
Kesulitan belajar
ASAM VALPROAT 20-40 mg/ kgBB/ Hr
diberikan 2 3 kali
Efek samping: gangguan fungsi hati
LAMA PEMBERIAN 1 tahun
TIDAK EFEKTIF MENCEGAH EPILEPSI
PROGNOSIS
Kejang demam sederhana tidak berbahaya.
Tidak ada bukti bahwa mereka menyebabkan
kematian, kerusakan otak, epilepsi, keterbelakangan
mental, penurunan iq, atau kesulitan belajar.
Sekitar sepertiga anak yang pernah kejang demam
akan mengalami kejang demam ke dua.
Dari orang-orang yang memiliki serangan kedua,
sekitar setengah akan memiliki kejang ketiga.
KOMPLIKASI
Menggigit diri
Masuknya cairan ke paru-paru melalui pernapasan
Meningitis
Luka dari jatuh atau menabrak benda
Luka dari kejang yang lama
kejang yang tidak disebabkan oleh demam