1

Case Report

STATUS EPILEPTICUS

By:
Puji Yunisyah Rahayu
1608437723

Supervisor:
dr.Riki Sukiandra, Sp.S

DEPARTMENT OF NEUROLOGY
MEDICAL FACULTY OF RIAU UNIVERSITY
ARIFIN ACHMAD GENERAL HOSPITAL
PEKANBARU
2018
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KEMENTRIAN PENDIDIKAN DAN KEBUDAYAAN

FAKULTAS KEDOKTERAN UNIVERSITAS RIAU
SMF/ BAGIAN SARAF
Sekretariat : Gedung Kelas 03, RSUD Arifin Achmad Lantai 04
Jl. Mustika, Telp. 0761-7894000
E-mail : saraffkur@gmail.com
PEKANBARU

I. Patient’s Identity

Name Mrs.Bo
Age 43 years
Gender Female
Address Tampan District, Pekanbaru City
Religion Moslem
Marital’s Status Married
Occupation Housewife
Entry Hospital April,15th2018
Medical Record 9839xx

II ANAMNESIS :
Alloanamnesis with patient’s family (April, 16th 2018)
A. Chief Complain
Generalized Seizures since 1 day before admitted to the hospital.
B. Present illness history
 1 day before admitted to the hospital, the patient’s family complained that
the patient had seizure. The seizure occured5-10 times, the duration both
of them had 5-10 minutes and the space time between of them were 10
minutes with unconsciousness condition.Her seizures were described as
generalized tonic-clonic seizures,stiffness all over his body,the eyes aim to
the top, foam on the mouth (-), bitten tounge (-). After awake from her
unconciousness, she looks confused,very sleepy and no general weakness
is reported.
 She had non productive cough and subfebril fever for 3 days prior to the
onset of seizures. This symptoms was relieved by paracetamol.
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 Then the patient went to Awal Bros Hospital and reffered immediately to
Arifin Achmad General Hospital because of no room available in Awal
Bros Hospital.

C. Past Illness history

 1987, Her first seizure were occured when she was 12 years old, and no
medication that given to her.
 2016, The patient has complained the same seizure complaints as the
patients now.She routinely recieved antiepileptic drugs (Phenytoin 100 mg
1x1, Fluoxetine 10 mg 1x1/2, Clobazam 10 mg 1x1) from Tampan Mental
Hospital since 2 years ago. But, antiepileptic drugs were discontinue 1
month ago because she felt fully recovered.
 History of febrile seizures (-)
 Trauma history (-)
 History of central nervous system infection and tumor (-)
 Stroke (-)
 Hipertension (-)

D. Family Illness History

 No family has the same complaint
 History of seizures (-)
 History of hipertension (-)
 History of cancer or tumors in family (-)

RESUME
A 43 years old woman admitted to the hospital with generalized seizures 1 day
before admission. The seizure occurred 5-10 times, the duration both of them had
5-10 minutes and the space time between of them were 10 minutes with
unconsciousness condition.While seizure occur, the patient felt unconsciousness,
stiffness all over her body, the eyes aim to the top. This complaint were felt first
time when she was 12 years old, her last episode was 2 years ago with the same
characteristized as recent complaint. She routinely recieved antiepileptic drugs
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from Tampan Mental Hospital since 2 years ago. But, antiepileptic drugs were
discontinue 1 month ago because she felt fully recovered.

III. PHYSICAL EXAMINATION (Examined on April, 16th 2018)

A. Generalized Condition
Blood Presure : 110/70 mmHg
Heart Rate : 86 bpm
Respiratory rate : 20 tpm
Temperature : 36,8°C
Weight : 50 kg
Height : 150cm
IMT : 22,2 (normoweight)

B. Neurological status
1) Consciousness : Somnolen GCS : 10 (E3M5V4)
2) Cognitive Function : Difficult to assess
3) Neck Rigidity : Negative

C. Cranial Nerves
1. N. I (Olfactorius )
Right Left Interpretation
Sense of Smell Normal Normal Difficult to assess

2. N.II (Opticus)
Right Left Interpretation
Visual Acuity
Visual Fields Difficult Difficult
Difficult to assess
to assess to assess
Colour Recognition
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3. N.III (Oculomotorius)
Right Left Interpretation
Ptosis (-) (-)
Pupil
Shape Round Round
Side Φ3mm Φ3mm Normal
Extraocular movement Normal Normal
Pupillary reaction to light
Direct + +
Indirect + +

4. N. IV (Trokhlearis)
Right Left Interpretation

Extraocular movement Difficult Difficult

to assess to assess
Doll’s eye phenomen (+) (+) Normal

5. N. V (Trigeminus)
Right Left Interpretation
Motoric
Difficult Difficult
Sensory to to
assess assess

Corneal reflex (+) (+) Normal

6. N. VI (Abduscens)
Right Left Interpretation
Extraocular movement Difficult
Difficult
to
to assess
assess
Strabismus (-) (-)
Deviation (-) (-)

Doll’s eye phenomen (+) (+) Normal

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7. N. VII (Facialis)
Right Left Interpretation
Tic (-) (-)
Motoric Difficult Difficult
to assess to assess Difficult to assess
Chvostek sign
Flavour Sense (-) (-)

8. N. VIII (Acusticus)
Right Left Interpretation

Hearing sense Normal Normal Normal

9. N. IX (Glossopharyngeus)
Right Left Interpretation
Pharyngeal arches Normal Normal
Flavour sense Normal Normal Normal
Gag Reflex (+) (+)

10. N. X (Vagus)
Right Left Interpretation
Pharyngeal arches Normal Normal
Dysfonia (-) (-) Normal
Gag Reflex (+) (+)

11. N. XI (Accesorius)
Right Left Interpretation
Motoric Difficult Difficult
to assess to assess Difficult to assess

Trophy Eutrofi Eutrofi

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12. N. XII (Hypoglossus)

Right Left Interpretation
Motoric
Difficult Difficult
Trophy Difficult to assess
to assess to assess
Tremor
Disartria

D. Motoric
Right Left Interpretation
Upper Extremity
Strength
Distal Difficult Difficult
Proximal to assess to assess
Difficult to assess
Tone Normal Normal
Trophy Eutrophy Eutrophy
Involuntary movements (-) (-)
Clonus (-) (-)
Lower Extremity
Strength
Distal Difficult Difficult
Proximal to assess to assess
Difficult to assess
Tone Normal Normal
Trophy Eutrophy Eutrophy
Involuntary movements (-) (-)
Clonus (-) (-)
Body
Trophy Eutrophy Eutrophy
Involuntary movements (-) (-) Normal
Abdominal Reflex (-) (-)

E. Sensory
Right Left Interpretation
Light Touch
Pain
Temperature
Proprioceptive
 Position Normal
 Two point discrimination
 Stereognosis
 Graphestesia
 Vibration Not Tested Not Tested
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F. Reflex
Right Left Interpretation
Physiologic
Biceps (+) (+)
Triceps (+) (+) Normal
Knee (+) (+)
Ankle (+) (+)
Pathologic
Babinsky (-) (-)
Chaddock (-) (-)
HoffmanTromer (-) (-)
Openheim (-) (-) Normal
Schaefer (-) (-)
Gordon (-) (-)
Primitive Reflex
Palmomental (-) (-) No Primitive Reflex
Snout (-) (-)

G. Coordination
Right Left Interpretation
Point to point movements Normal Normal
Walk heel to toe Not Tested Not Tested
Difficult to assess
Gait Not Tested Not Tested
Tandem Not Tested Not Tested
Romberg Not Tested Not Tested

H. Autonom system
Urination : Urine Catheterized
Defecation : Normal
I. Others Examination
a. Laseque : >700
b. Kernig : >1300
c. Patrick : -/-
d. Kontrapatrick : -/-
e. Valsava test : -
f. Brudzinski : -
g. Spurling test : -
h. Head Traction : -
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EXAMINATION RESUME
General Status :
 Blood Pressure 110/70 mmHg
 Heart Rate 86 bpm
 Respiratory Rate 20 times per minute
 Temperature 36,8°C

Noble Function :Difficult to assess

Neck Stiffness :Negative
Cranial Nerves :Limitation of examination
Motoric :Difficult to assess
Sensory :Difficult to assess
Coordination :Difficult to assess
Autonomy :Normal
Reflex :Physiologic reflex (+) Patologic reflex (-)

IV. WORKING DIAGNOSIS

CLINICAL DIAGNOSIS : Status Epilepticus
TOPICAL DIAGNOSIS : Intracranial
ETIOLOGICAL DIAGNOSIS : Stopping medication in idiopathic epilepsy
DIFFERENTIAL DIAGNOSIS: Symptomatic

V. SUGGESTED EXAMINATION :
1. EEG 4. Blood chemistry
2. Head CT-Scan with contrast 5. Electrolyte
3. Routine blood 6. Chest X-Ray

VI. MANAGEMENT
 Airway management
 Nasal canule O2 2-4 liter/minute
 IVFD NaCl 0,9% 20 dpm
 Injection diazepam 10 mg per IV
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 Phenitoin 3 x 100 mg per IV bolus on Syringe 20 cc

 InjectionCiticolin 2 x 500 mg per IV
 Injection Ranitidin 2 x 50 mg per IV

VII. LABORATORY AND RADIOLOGY FINDINGS

(April, 14th 2018)
1. Blood Routine
- Hb : 13,3 g/dL - WBC : 10.900/uL
- Ht : 39,7 % - PLT : 292.000/uL

2. Blood Chemistry 3. Electrolyte

- Glucose : 119 mg/dL - Na : 141 mmol/L
- Ureum : 37 mg/dL -K : 3.7 mmol/L
- Creatinin : 0,88 mg/dL - Cl : 116 mmol/L
- AST : 24 U/L Interpretation : within normal limit
- ALT : 16 U/L

4. Chest X-Ray

Cor :
showed no abnormalities

Pulmo :
Showed infiltrates in both
lungs
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5. Head CT-Scan without contrast

Result :
Within normal limit
There is no mass on this
CT-Scan

VII. FINAL DIAGNOSIS : Status Epilepticus

Follow up (April, 17th 2018)

Subjective :
Disoriented (+) Agitated (+) Seizure (-) Headache (-) Fever (-) Cough (-)
Objective :
GCS : 13 (E4M5V4)
Blood Pressure : 120/80 mmHg
Heart Rate : 86 bpm
Respiratory rate : 22 tpm
Temperature : 36.5°C
Cognitive function : Difficult to assess
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Neck Stiffness : Negative

Cranial Nerves : Normal
Motoric : Difficult to assess
Sensory : Normal
Coordination : Difficult to assess
Autonomy : Normal
Reflex : Physiologic reflex (+)
Pathologic reflex (-)
Assessment :
Status Epilepticus
Plan :
 Nasal canule O2 2-4 liter/minute
 IVFD NaCl 0,9%20 dpm
 Phenitoin 3 x 100 mg per IV bolus on Syringe 20 cc
 Injection Citicolin 2 x 500 mg per IV
 Injection Ranitidin 2 x 50 mg per IV
 Injection Ceftriaxone 2 x 1 gr per IV
 Consultation plan with pulmonologist
 Consultation plan with psychiatrist

Follow up (April, 18th 2018)

Subjective :
Disoriented (+) Agitated (+) Seizure (-) Headache (-) Fever (-) Cough (-)
Objective :
GCS : 13 (E4M5V4)
Blood Pressure : 110/70 mmHg
Heart Rate : 76 bpm
Respiratory rate : 20 tpm
Temperature : 36.5°C
Cognitive function : Difficult to assess
Neck Stiffness : Negative
Cranial Nerves : Normal
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Motoric : Difficult to assess

Sensory : Normal
Coordination : Difficult to assess
Autonomy : Normal
Reflex : Physiologic reflex (+)
Pathologic reflex (-)
Assessment :
Idiophatic epilepsy
Plan :
 Nasal canule O2 2-4 liter/minute
 IV NaCl 0,9%20 dpm
 Phenitoin 3 x 100 mg per IV
 Injection Citicolin 2 x 500 mg per IV
 Injection Ranitidin 2 x 50 mg per IV
 Injection Ceftriaxone 2 x 1 gr per IV
 Consultation with pulmonologist : Pneumonia
o Ambroxol syrup 2x1
 Consultation with psychiatrist : Hyperactive Delirium
o Haloperidole 1 x 0,5 mg (night)

Follow up (April, 19th 2018)

Subjective :
Disoriented (+) with improvement of clinical symptoms, Agitated (-) Seizure (-)
Headache (-) Fever (-) Cough (-)
Objective :
GCS : 14 (E4M6V4)
Blood Pressure : 120/80 mmHg
Heart Rate : 78 bpm
Respiratory rate : 20 tpm
Temperature : 36.6°C
Cognitive function :Normal
Neck Stiffness : Negative
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Cranial Nerves : Normal

Motoric : Normal
5 5
5 5
Sensory : Normal
Coordination : Difficult to assess
Autonomy : Normal
Reflex : Physiologic reflex (+)
Pathologic reflex (-)
Assessment :
Idiophatic epilepsy + Hyperactive delirium + Pneumonia
Plan :
 Nasal canule O2 2-4 liter/minute
 IV plug
 Phenitoin 3 x 100 mg per oral
 Citicolin 2 x 500 mg per oral
 Injection Ranitidin 2 x 50 mg per IV
 Injection Ceftriaxone 2 x 1 gr per IV
 Haloperidole 1 x 0,5 mg (night)
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DISCUSSION

1. Definition of Status Epilepticus

Status Epilepticus (SE) is defined as continuous seizure activity of at least
30 minutes duration or intemittent seizure activity during which consciousness is
not regained with the last intermittent seizure less than 24 hours.1

2. Etiology
The Etilogy of status epilepticusare :2
1. Idiopathic: there are no structural lesions in the brain or neurological
deficits. The cause is unknown, thought to have a genetic predisposition.
2. Cryptogenic: Sympomatic, but the cause is unknown, including here the
western syndrome, lennox-gastaut syndrome, and myoclonic epilepsy. The
clinical presentation corresponds to diffuse encephalopathy.
3. Symptomatic: caused by abnormalities or lesions of the central nervous
system such as head trauma, nervous system infection (CNS), congenital
abnormalities, splitting lesions, cerebral circulatory disturbances, toxic
(alcohol, drug), metabolic, or neurodegenerative disorders.

The trigger factor of status epilepticusare :3

1. Patients with epilepsy without treatment or inadequate treatment dose.
2. Treatment abruptly terminated or impaired GIT absorption.
3. Decreased general condition due to lack of sleep, psychic stress, or
physical stress.
4. Use or withdrawal of alcohol, drug abuse, or antidepressants

3. Epidemiology
Epidemiological studies Hauser et al estimated that at the last census about
1,770,000 individuals in the United States suffered from epilepsy and about 44
new cases per 100,000 populations appear each year. It is also estimated that 1
percent of the population in the United States will get epilepsy around the age of
20 years. More than two-thirds of cases of epilepsy occur in childhood (especially
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in the first year of life) . In one-third of cases, epileptic status is a symptom that
occurs in patients with recurrent epilepsy. One third of cases occur in patients
diagnosed with epilepsy, usually due to irregularities in eating anticonvulsant
drugs.4

4. Classification
The classification of epileptic status is important for proper treatment,
since effective treatment depends on the type of epileptic status. Many clinical
approaches are applied to classify the status of epilepticus. One version
categorizes the status of epilepticus according to general epileptic status (tonic-
clonic, myoclonic, absent, atonic, akinetic) and partial epileptic status (simple or
complex). Other versions divide by status of general epilepticus (convulsion) and
non-convulsional epileptic status (simple partial, complex partial, absent). The
third version is based on the duration, ie: the status of early epilepticus (5-30
minutes), permanent epileptic status (> 30 minutes), stages of epilepticus reflux
(the resurrection persists after two or three initial anticonvulsants with adequate
doses). The status of epilepticus convulsions is defined as a seizure associated
with a rhythmic.5
The findings of general characteristics of epileptic status of convulsions
are general tonic-clonic movements of the legs and hands, mental state disorders
(coma, lethargy, confusion), have focal neurological deficits after the iktal period
(eg, Todd paralysis, is temporary neurologic deficits lasting several hours to the
next day after seizures). The non-convulsive epileptic status is defined as seizure
activity seen in the electroencephalogram (EEG) in the presence of a conventional
seizure associated with a generalized epilepticus status of the convulsions.
Patients will appear to be confused or symptoms of prolonged mental status
changes due to ongoing awakening activities. The status of undiagnosed epilepsy
is not diagnosed, often regarded as a psychiatric disorder. Patients with acute pain
with a status status are highly disturbed, with or without a smooth motor vehicle
(eg, or rhythmic, or cerebral cirrhosis commonly occurring in the cerebral cortex).
This term has also been referred to as the subtle status.5
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5. Pathophysiology
SEIZURE INITIATION AND PROLONGATION

Why seizures start and stop is unknown, although it is likely that seizure
initiation is caused by an imbalance between excitatory and inhibitory
neurotransmission, leading to the initiation of abnormal neural impulses. The
seizure threshold in the immature brain appears to be lower than in the mature
brain, but the mechanisms that underlie this susceptibility remain unclear.
Excitatory synapses mature earlier than inhibitory synapses and this coupled with
an increase in the susceptibility of excitatory neurotransmitter receptors,
6
increases the likelihood that an excitation– inhibition imbalance may occur.
There are other important differences between the immature and adult
brain. Stimulation of Gamma- Aminobutyric acid (GABA) a receptors in the
immaturebrain results in depolarisation rather than hyperpolarisation, as occurs in
the adult brain. The immature cerebral cortex has a high synaptic density at
around 2 months of age and this may contribute to the development of
6
hypersynchrony of neural groups.
The excitatory amino acid neurotransmitter glutamate increases at the site
of the seizure focus at the beginning of seizure activity in adults with temporal
lobe epilepsy when measured by in vivo intracerebral microdialysis It is believed
that the same may happen at the onset of generalised seizures. Inhibitory
neurotransmitters such as GABA later increase at the seizure focus and redress
the balance between excitation and inhibition. GABA also increases in the
substantia nigra pars reticulata, an area that can modulate a cortical inhibitory
response in adult rats, but not in immature rats. Other mechanisms of inhibitory
receptor modulation, such as adenosine receptor agonism, may also contribute to
seizure termination. Thus the increased incidence of convulsive status
epilepticusis (CSE) probably caused by a combination of increased seizure
6
susceptibility and decreased ability to mount an adequate inhibitory response.

SYSTEMIC AND CENTRAL PATHOPHYSIOLOGY

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The systemic effects of CSE are initially dominated by the body’s attempt
to maintain homeostasis. Blood pressure and central venous pressure increase,
blood glucose in- creases, and the patient becomes tachycardic. CSE may also
result in electrolyte imbalance and hyperthermia. Cerebral blood flow, blood
glucose, and oxygen utilisation increase in the initial phases of a seizure to
maintain cerebral homeostasis. After 30 minutes homeostatic failure begins and
the patient may need systemic support. Cerebral blood flow, brain glucose, and
parenchymal oxygenation all decrease and potentially play a part in the cell
damage associated with CSE. Respiratory and metabolic acidosis, electrolyte
imbalance (for example, hyperkalaemia), hyperthermia, and rhabdomyolysis
may all occur. Treatment with drugs with depressant cardiorespiratory side
effects (for example, benzodiazepines and barbiturates) may worsen the
6
systemic complications of CSE.

ELECTROPHYSIOLOGY

About 70-80% of cases of CSE throughout all age groups will have a
focal onset but be secondarily generalised. A predictable sequence of changes in
the electroencephalogram (EEG) has been shown in adult humans and in at least
six animal models. CSE starts with localised epileptic activity followed by
isolated general- ised bursts of seizure activity with a normal EEG in between. If
the patient does not regain consciousness between these episodes, then they meet
the clinical criteria for CSE. The isolated ictal discharges merge and become a
continuous discharge after about 30 minutes. Discharges then fragment and are
interspersed with flat periods. Ultimately, periodic epilepti- form discharges,
which may reflect underlying metabolic failure, will occur.6

The motor phenomena associated with CSE follow a similar pattern to the
EEG changes. Recurrent seizures will merge into continuous motor activity,
followed by fragmentation of the motor activity and myoclonus. If the seizure
persists, then electromechanical dissociation will ensue. The prognosis for a
good neurological outcome decreases the further the patient moves through this
6
continuum.
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MECHANISMS BY WHICH GLUTAMATE CAUSES CELL DEATH

Excess extracellular glutamate may result in cell death by causing

necrosis, gene determined cell death, or both. The primary receptor involved in
cytotoxicity related to glutamate is the NMDA receptor, although other glutamate
receptors may be involved. The NMDA receptor is an ionotropic receptor.
Binding of glutamate and glycine or D-serine to appropriate sites on the receptor
results in an influx of calcium through the ionophore. High intracellular
calcium concentrations result in the activation of a large number of calcium
6
dependent processes such as those described in the following.

 Activation of protein kinase C. This enzyme is moved from the cytosol to

the cell wall, resulting in destruction of the wall.
 Nitric oxide and free radical formation. Calcium stimulates constitutive
nitric oxide synthase, causing an increase in intracellular nitric oxide.
Nitric oxide can inhibit mitochondrial respiration directly or indirectly by
forming peroxynitrite free radicals, which are cytotoxic.
 Activation of phospholipase A2. This en- zyme breaks down membrane
lipids with the release of arachidonic acid and other fatty acids. One
consequence of this membrane destruction can be cell death.
 Activation of protease calpain I. The mechanism by which this enzyme
causes cell death is unclear, but calpain I inhibitors are partially
neuroprotective.

6. Clinical manifestation
the introduction of epileptic status is important at the start of the staging to
prevent delayed treatment. Generalized tonic-clonic status is the most common
form of epileptic status, the results of the survey are found to be about 44 to 74
percent, but other forms may also occur.7

General Epilepticus Epilepticus Status (Generalized tonic-clonic Status

Epilepticus)
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This is the form of the most commonly encountered and potentially

damaging Epilepticus Status. It is preceded by general tonic-clonic or partial
seizures that quickly turn into generalized tonic clones. In general tonic-clonic
status, attacks begin with general tonic-clonic seizures series without awareness
recovery between attacks and increased frequency. 7
Each seizure lasts two to three minutes, with a tonic phase involving axial
muscles and intermittent breathing movements. Patients become cyanosed during
this phase, followed by hyperpnea CO2 retention. Among the tachycardia and
increased blood pressure, hyperpireksia may develop.Hyperglikemia and serum
lactate elevation occurs resulting in decreased serum pH and respiratory and
metabolic acidosis. Seizure activity up to five times in the first hour in unresolved
cases. 7
Clonic-Tonic-Clonic Epilepticus Status (Clonic-Tonic-Clonic Status
Epilepticus)
Sometimes the status of epilepticus is encountered with general clonic
activity preceding the tonic phase and followed by clonical activity in the second
period.7
Status Epilepticus Tonic (Tonic Status Epilepticus)
The status of epilepsy of tonic occurs in children and adolescents with loss
of consciousness without clonal phase. This occurs in chronic encephalopathy and
is a feature of Lenox-Gestaut Syndrome. 7
Status of Myoclonic Epilepticus.
Usually seen in patients who have enselofati.Sentakan mioklonus is
thorough but often asymmetric and worsening level of consciousness.Tipe of
epilepticus status is not usually in severe anoksia enselofati with poor prognosis,
but can occur in the state of toxicity, metabolic, infection or degenerative
conditions. 7

Status of Epilepticus Absens

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Form of epileptic status is rare and is usually found at the age of puberty
or adult. There is a change in the level of consciousness and the status of the
presen as a dreamy state with a slow response that resembles a "slow motion
movie" and may persist for long periods of time. There may be a history of
generalized primary seizures or absent seizures in childhood. In EEG, there is a 3
Hz monotonous (monotonous 3 Hz spike) peak activity in all sites. There is a
response from an intravenous benzodiazepine to epileptic status. 7
Non-Convulsive Epileptic Status
This condition is difficult to distinguish clinically with the absence or
partial status of the complex, because the symptoms can be the same. Patients
with non-convulsive epileptic status are characterized by stupor or usually coma.
When conscious, there is a change of personality with paranodia, delusional,
irritability, hallucinations, impulsive behavior, psychomotor retardation and
psychosis in some cases. The EEG shows generalized spike wave discharges,
unlike 3 Hz spike wave discharges from absence status. 7
Somatomotor Status
Seizures begin with a myoclonic twitch from the corners of the mouth,
thumb and fingers in one hand or involve the toes and feet on one side and
develop into a jacksonian march on one side of the body. Seizures may persist
unilaterally and uninterrupted consciousness. In EEGs often but not necessarily
indicate periodic lateralized epileptiform discharges in opposing hemispheres
(PLEDs), which are often associated with major destructive processes in the brain.
Variations of somatomotor status are characterized by intermittent aphasia or
language disorder (affabel status). 7
Somatosensory Status
It is rare but resembles somatomotoric status with prolonged unilateral
sensory symptoms or a sensory jacksonian march. 7
Status of Complex Partial Epilepticus
Can be regarded as a serial of partial complex seizures of frequencies
sufficient to prevent recovery between episodes. There may be automatism,
speech impairment, and prolonged confusion. EEG is seen in focal activity in the
temporal or frontal lobes on one side, but epileptic seizures are often This
 22

condition can be distinguished from absence status by EEG, but it may be difficult
to separate the status of complex partial epilepticus and non-convulsive epileptic
status in some cases. 7

7. Diagnosis and Adjunct Examination

Diagnosis is done quickly within 5-10 minutes. The first thing we do is:8,9
Anamnesis
History of epilepsy, history of tumor, seizure history of drugs, alcohol,
other cerebrovascular diseases, and metabolite disorders. Notice the duration of
seizures, seizures (focal, general, tonic / clonic), level of consciousness between
seizures, previous seizure history, family history of seizures, fever, birth history,
growth, and illness.
Physical examination
Complete neurological examination includes the level of vision and
hearing awareness, physiological reflexes and pathology, lateralization, papillary
edema due to increased intracranial effects of tumors, bleeding, etc. The motor
system is paresthesias, hypesthesia, anesthesia.
Adjunct examination
Laboratory examination of blood, electrolytes, glucose, renal function with
urine analysis and culture, if there is an alleged infection, then performed blood
culture. Imaging of CT Scan and MRI to evaluate structural lesions in the brain.
EEG to know the electrical activity of the brain and done as quickly as possible if
the patient has mental disorders. Lumbar puncture, we may do if there is a
suspected CNS infection or subarachnoid hemorrhage.
8. Therapy
therapy should be given in conjunction with emergency therapy. The
choice of medication depends on previous therapy, the type of epilepsy, and
clinical. Whatever OAE was used before, should be continued at full dose. When
phenytoin or phenobarbital has been administered in emergency therapy,
maintenance doses may be administered orally or intravenously by monitoring
serum levels of the drug. Another maintenance OAE may be administered at an
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oral loading dose. If the patient is free to awaken for 12-24 hours and proved
adequate plasma drug levels, then the anesthetic agent can be slowly lowered.9
Examination of blood gases, glucose, liver function, kidney function,
calcium, magnesium, complete blood, hemostasis phyla, antiepileptic drug level.
When toxicology is required if the cause of epileptic status is unclear. Chest X-
rays are needed for the evaluation of possible aspirations. Other examinations
depend on clinical conditions, may include brain imaging and lumbar puncture
Supervision. 9
Observation of neurological status, vital signs, ECG, biochemistry, blood
gas, blood clotting, and OAE levels. Patients require full ICU facilities and are
treated by an anesthesiologist with a neurologist.EEG monitors need to be on the
status of refractory epilepticus. Consider the possibility of nonconvulsive epilepsy
status. In the status of refractory convulsive epilepticus, the primary goal is the
suppression of epileptic activity on the EEG, with the secondary aim being the
burst suppression pattern. 9

Manegement of Status Epilepticus1

Stadium Management
Stadium I (0-10 minutes) Maintain cardio-respiratory function.
Maintain airway pathway, give Oxygen,
resuscitation.
Stadium II (0-30 minutes) Examine neurologic stats
Examine vital sign.
Monitoring metabolic stats, Blood gas and
hematology stats.
Examine ECG.
Install an IV.
Take 50-100 cc blood for laboratorium
examination.
Give anti-epileptic drug : Diazepam 0,2 mg/kg
weightbody IV (speed of administration : 5
mg/minute, can be repeated in 15 minutes)
 24

Give 50 cc glucose 40% on hypoglicemic

condition.
give thiamin 250 mg IV on alcoholism.
Manage asidosis with bicarbonat.
Stadium III (0-60 minutes) Determine etiology.
If the seizure continues more than 30 minutes
after first diazepam, give phenytoin 15-20 mg/kg
weight body IV with speed of administration 50
mg/minute. And/or give Phenobarbital 20 mg/kg
weight body IV with speed administration 50-75
mg/minute (can be repeated with 5-10 mg/kg
weight body)
Stadium IV (30-90 minutes) If the seizure continues, transfer the patient to
ICU, Install EEG
give propofol (2 mg/kg weight body, IV, can be
repeated if necessary till SE controlled)
or Thiopentone(100-250 mg IV bolus, can be
repeated in 20 minutes, continues with bolus 50
mg every 2-3 minutes)
or Midazolam (0,1 mg/kg weight body IV bolus,
with speed of administration : 4 mg/minute)
continued until 12-24 hours after the last seizure,
then tappering-off.
Monitoring seizure, EEG, intracranial pressure,
and start giving maintanance dose of anti-
epileptic drugs.
 25

9. Prognosis
The prognosis of epilepticus status is dependent on the underlying cause of
epileptic status.Prognosis of treatment in new cases is generally good, in 70-80%
of cases the seizure will stop within the first few years. The prognosis of epilepsy
will be worse if there are any of the following:10
1. There are structural lesions in the brain
2. The rise of partial epilepsy
3. Severe epilepsy syndrome
4. History of epilepsy in the family
5. High frequency of tonic-clonic rise prior to treatment initiation
6. There are neurological and psychiatric abnormalities
 26

THE BASIC OF DIAGNOSIS

1. Clinical diagnosis:Status Epilepticus

According to anamnesis and physical examination, we have found:
 The seizure occurred 5-10 times
 The duration both of them had 5-10 minutes
 The space time between of them were 10 minutes with unconsciousness
condition.
 While seizure occur, the patient felt unconsciousness
 Stiffness all over her body
 The eyes aim to the top

This is in accordance with the status of epilepticus defined as the condition

in which the occurrence of two or more seizure sequences without any recovery of
consciousness between seizures, or continuous attacks for 30 minutes or more.
Continuous attacks of more than 5 minutes or whose consciousness has not
recovered after 5 minutes should be considered SE.

2. Topical diagnosis : Intracranial

From anamnesis, the patient had generalized seizures, characterized by

recurrent epileptic seizures due to intermittent brain function disorder that occurs
due to partial abnormal discharge of paradoxical neurons due to various
etiologies.

3. Basic etiological diagnosis : Stopping medication in idiopathic epilepsy

This etiological case is sudden drug withdrawal in idhiopathic epilepsy.
From anamnesis, since 2016 patient has routinely recieved antiepileptic drugs
(Phenytoin 100 mg 1x1, Fluoxetine 10 mg 1x1/2, Clobazam 10 mg 1x1) from
Tampan Mental Hospital. But, antiepileptic drugs were discontinue 1 month ago
because she felt fully recovered.Which mean there are big possibility that
clinical’s view of this patient comes from the sudden stopping medicine without
the supervision of a doctor. The trigger factor of status epilepticus are patients
 27

with epilepsy without treatment, inadequate treatment dose, treatment abruptly

terminated and impaired GIT absorption.

4. Differential diagnose : Simptomatic

From anamnensis patients get seizures, seizure occured 5-10 times with
duration both of them had 5-10 minutes. Seizures occur on the whole body, eyes
looking upwards. After the patient's seizure is unconscious. First we have to know
this etiological case is symptomatic, caused by central nervous system
abnormalities (CNS). This case shows that the patient had status epilepticus. In
patients with recurrent and severe seizures, it can cause damage to the brain and
may lead to new lesions, which is the lesions can trigger re-seizures in patients.
Head ct scan and another advanced imaging is important to find abnormality in
brain.

5. Basic supporting examination

a. EEG : to show the type and location of the activity in the brain during a
seizure for the evaluation of brain disorders.
b. Laboratory : to knowing risk factors whether infection exists, and knowing
the general condition of the patient
c. Head CT-Scan : to find abnormality in brain
d. Thoracax X-ray : to find abnormality at thorax

6. Basic treatment
 Airway management : to maintain the airway path, especially this patient
occurred seizure
 Nasal canule O2 2-4 liter/minute : to maintain oxigenation to tissue
 IVFD NaCl 0,9% 20 dpm : to maintain the euvolemic condition.
 Injection diazepam 10 mg per IV: to manage seizure
 Phenitoin 3 x 100 mg per IV bolus on Syringe 20 cc : to prevent next
seizure
 Injection Citicolin 2x500 mg per IV : to reduce brain tissue damage
 Injection Ceftriaxone 2 x 1 gr per IV : to prevent infection
 28

 Injection Ranitidin 2 x 50 mg per IV : as preventing side effects from use

of phenitoin in the stomach in the form of peptic ulcer.
 29

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