Neuro-Emergency

Update

Status Epilepticus in
Children
Adult
Pregnancy
Childbearing

1
 Status Epilepticus (SE)
The term status epilepticus may be used to describe any
continuing type of seizure.

Status epilepticus is a common, life-threatening

neurologic disorder. It is essentially an acute, prolonged
epileptic crisis.

In early studies, SE was defined by its duration, that is,

as continuous seizures occurring for longer than 1 hour.
Clinical and animal experiences later showed that
pathologic changes and prognostic implications occurred
when SE persisted for 30 minutes. Therefore, the time
for the definition was shortened.

EFNS guideline on the management of status epilepticus in adults

European Journal of Neurology 2010, 17: 348355 2
 Status Epilepticus (SE)-cont
More than 30 minutes of continuous seizure
activity or two or more sequential seizures
without full recovery of consciousness between
seizures.
More recently, SE be defined as any seizure
lasting longer than 5 minutes based on natural
history data that show typical generalized
convulsive seizures that resolve spontaneously
after 3-5 minutes.

3
 Causes of SE
Diagnosis Children (%) Adults (%)
Stroke 3 25
Drug change/noncompliance 20 20
Alcohol/other drugs 2 15
CNS infection 5 10
Hypoxia 5 10
Metabolic 10 10
Tumor <1 5
Trauma 3.5 5
Fever/infection 35 2
Congenital 10 <1
4
 Causes of SE

o Low blood concentrations of AED (34%)

o Remote symptomatic causes (24%)
o Cerebrovascular accidents (22%)
o Anoxia or hypoxia (10%)
o Metabolic causes (10%)
o Alcohol and drug withdrawal (10%)

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 SE Classification

Generalized convulsive SE (GCSE)

Subtle SE
Non-Convulsive SE (NCSE)
Absence SE
Complex partial SE
Simple Partial SE

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 Non Colvulsive
Status Epilepticus
NCSE refers to continuous seizure activity
without predominant motor activity.

This should not be confused with subtle

status epileptics which refers to GCSE in
which the motor findings have diminished
either through high doses of administered
medications or from muscular fatigue due
to prolonged seizure activity

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 Patomekanisme Status
Epilepticus
Proses dasar dari munculnya SE adalah
gagalnya mekanisme normal untuk mengakhiri
serangan.
Inhibisi yang menurun dan excitasi yang
persisten menimbulkan aktifitas serangan yang
berlangsung terus menerus.
Selama aktifitas serangan yang berkepanjangan,
terjadi perubahan dinamika pada fungsi reseptor
GABAA dan fungsi reseptor NMDA yang dikenal
dengan receptor traficking.
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 Patomekanisme Status
Epilepticus cont.
Aktifitas serangan yang berlangsung terus akan
mengurangi secara bertahap reseptor2 GABAA
pada synaptic membrane diikuti dengan
internalisasi reseptor ke dalam vesikel2
endositotik dan degradasi berikutnya.
Proses ini berakibat pada erosi endogen GABA
ergic inhibisi yang akan meningkatkann aktifitas
epileptic berkepanjangan.

9
 Patomekanisme Status
Epilepticus cont.
Hilangnya reseptor GABAA post sinaptik
merupakan factor patofisiologik yg relevan
sehingga terjadi farmakoresisten terhadap obat2
seperti benzodiazepine, barbiturate dan propofol.
Sebaliknya, selama aktifitas epileptic berlangsung,
reseptor NMDA secara progresif berpindah ke
synaptic membrane, sehingga menambah
reseptor NMDA exitatorik presynaps. Proses ini
memudahkan exitabilitas neuron dan berikutnya
memperpanjang SE.

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 Patomekanisme Status
Epilepticus cont.

Namun sebaliknya, meningkatnya expressi

reseptor Glutamat dapat merupakan target yang
dipakai pada farmakological management dari
SE advanced stage.
Absance SE with 3-Hz spike wave discharge
akan menginduksi dengan excessive inhibition.
Bentuk SE spt ini tdk menyebabkan neuronal
injury dengan excitasi yang excessive.

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 Seizures produce a number of
physiologic consequences.

During a generalized convulsion transient

apnea and hypoxia.
Initially, brain compensatory mechanisms may
prevent neuronal injury from seizures
hypertension with increased cerebral blood flow.
Normal physiological response includes an
increase in body temperature with up to 43%
Temperature >100 F

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 Seizures produce a number of
physiologic consequences. Cont.

Glucose levels also increase, and lactic acidosis

(occurs within 60 seconds of a convulsive event and
normalizes within one hour after ictus).

A rise in the peripheral white blood cell count without

an increase in bands is often seen.

If the seizure persists, at approximately 30 minutes

the homeostatic mechanisms begin to deteriorate.
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 Seizures produce a number of
physiologic consequences. Cont.
Animal models suggest that, even if systemic factors,
such as acidosis and hypoxia are controlled,
prolonged status epilepticus results in direct neuronal
damage from neurotoxic amino acids and calcium
influx.

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 Differential Diagnosis
of Status Epilepticus
A number of conditions mimic seizures. These
include convulsive syncope (with or without cardiac
dysrhythmias), decerebrate posturing, psychogenic
events, dystonia, and migraine headaches.
Patients with strychnine poisoning may develop
seizure-like activity yet demonstrate normal mental
status.

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 Management of
Status Epilepticus

oPrehospital Concerns
oEmergency Departement
oICU

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Prehospital Concerns

Managing the airway

Maintaining oxygenation
Obtaining Intra Venous access
Protecting the patient from injury.
(The use of a padded tongue blade
is contraindicated since it may induce
emesis or break a tooth )

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 Prehospital Concerns cont..
In most cases, pre-hospital personnel will arrive at
least 5 minutes after the onset of seizure activity,
such that patients who are still seizing should be
managed as presumed status epilepticus.

If a patient is found convulsing or remains confused

or unresponsive, paramedics should immediately
measure the patients blood sugar or, if this test is
not available, they can empirically administer
dextrose (D50).

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 Prehospital Concerns cont..
When IV access is not immediately available, rectal
diazepam is an option.
One prospective study reported that there were no
significant differences between rectal and
intravenous diazepam therapy with regard to SE
duration, intubation, or recurrent seizures in the
emergency department (ED).
These data suggest that prehospital administration
of diazepam may shorten the duration of SE in
children and simplify the subsequent management.

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 Prehospital Concerns cont..
In a retrospective study on prehospital seizure
management in children, rectal diazepam (5 mg/kg),
was compared to IM midazolam(15 mg /kg).
Over the 4 year study period,
2566 children presented with seizures and
107 children were eligible for entry into the study.
Of these 107 patients received diazepam
and 45 received midazolam.

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 Prehospital Concerns cont..
Both drugs were effective in stopping seizures within
5 minutes of drug administration; however, fewer
patients in the midazolam group suffered apnea.

In a study comparing IV diazepam to IM midazolam,

Chamberlain et al concluded that IM midazolam is
an effective anticonvulsant for children with motor
seizures and an important alternative when IV
access is not easily available.

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Prehospital Concerns cont..
Vilke et al compared IM to IV midazolam and
reported that IV delivery was more effective:
47/49 in the IV group vs 20/25 with IM
administration (p less than 0.05).
Four patients (three treated IM and one IV) had
respiratory compromise necessitating field airway
management. In light of the Chamberlain and Vilke
studies, some experts recommend IV midazolam as
the agent of choice in the prehospital management
of seizures.

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Diagnostic Testing
Laboratory
Tests include a determination of :
serum glucose
electrolytes
urea nitrogen, creatinine
magnesium, phosphate, calcium
complete blood count
pregnancy tests
anti-epileptic drug levels
liver function tests
drugs of abuse screening.
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 Status Epilepticus
Clinical manifestations
Convulsive SE
Related to acutely elevated serum
catecholamine levels
Respiratory interference
Cardiovascular system adversely affected
Acidosis and rhabdomyolysis
Hyperkalemia
Myoglobinuria

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 Status Epilepticus
Clinical manifestations
Nonconvulsive SE (10-15%)
Obtundation
underlying systemic or neurological disorder
sedating or paralyzing medication
Alterations in behavior
Slow mentation
Confusion
Stupor coma
Unexplained, prolonged coma

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 Subtle clinical and physiological
changes in Nonconvulsive Seizures
Clinical changes Physiological changes
Early Hyperglycemia
Tachycardia Acidosis respiratory and
Hypertension metabolic
Eye deviation Increased prolactin
Facial twitch
Rapid and deep
respiration
Salivation
Pupillary dilation
Desaturation EEG should be considered if any
Late of these symptoms detected in a
Hypotension patient with unexplained coma
Hypo- or hyperthermia

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 Protocol for Convulsive SE
Minutes 0-5
100% O2 by mask or canula
Head position for airway patency
Assist ventilation if necessary
Cardiac monitoring
Record vital signs: BP, temperature, etc.
Check glucose
Establish IV
Draw blood for glucose, chemistry, CBC, toxicology,
antiseizure medication level, etc.

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 Protocol for Convulsive SE
Minutes 5-15
Thiamine 100 mg IV and 50 ml D50W if indicated
Sedatives
Lorazepam (ativan) 0.1 mg/kg IV, 2 mg/min, OR
Diazepam (valium) 0.2 mg/kg IV, 5 mg/min, OR
Diazepam (valium) 0.5 mg/kg per rectum (if no IV)
Anticonvulsant
Fosphenytoin 15-20 mg/kg IV, 150 mg/min, OR
Phenytoin (dilantin) 15-20 mg/kg IV, 50 mg/min, OR
Valproic acid (depakin) 800 mg IV
Monitor BP and cardiac rhythm
Do not infuse phenytoin through a line containing
glucose
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 Protocol for Convulsive SE
Minutes 15-30
Repeat lorazepam or diazepam if seizure continues
Additional fosphenytoin or phenyoin in increments dose of
5 mg/kg to total 30 mg/kg
Minutes 30-60
Monitor respirations because patient may require assisted
ventilation (intubation). Monitor EEG.
If status persists, give phenobarbital 20 mg/kg, 100 mg/min
Midazolam (dormicum) IV infusion (0.2 mg/kg slow bolus;
0.1-2.0 mg/kg/hr)
Propofol 1-5 mg/kg bolus over 5 min, then 2-4 mg/kg/hr
Minutes 60 or more
If status remains refractory, consider pentobarbital 5 mg/kg
load, then 1-4 mg/kg/h infusion
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 Treatment of Nonconvulsive SE
Treatment
IV diazepam (5-10 mg), or
IV lorazepam (1-2 mg)
Disappearance of epileptiform EEG
abnormality and improvement of mental state
Long-term seizure control
IV phenytoin, phenobarbital, valproic acid
Oral gabapentin (Neurontin) or levetiracetam
(Keppra)

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 Seizures continuing stage of
Refractory Status Epilepticus
General anesthesia should be induced
Propofol : 2mg/kg IV bolus, Repeat if necessary, followed by
infusion (5mg/kg/hr)
Thiopental : 100-250mg IV bolus over 20 sec. with further
50mg bolus every 2-3 min.until seizure control followed by IV
infusion(3-5mg/kg/hr)
Midazolam : 0.1-0.3mg/kg IV bolus dose at the rate of 4mg/min
followed by infusion(0.05-0.4mg/kg/hr)
If seizures have been controlled for 12hrs., reduce the dose
over further 12hrs.
If seizure recurs again GA agent should be given
Lancet Neurol 2006; 5: 252
Differential Diagnosis Of Altered
Mental Status In The Patient
Who Has Seized

Post-ictal state
NCSE or subtle convulsive status
Hypoglycemia
CNS infection
CNS vascular event
Drug toxicity
Psychiatric disorder
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 Nonconvulsive
Status Epilepticus (NCSE)
NCSE, like convulsive status epilepticus, is a state of
continuous or intermittent seizure activity lasting more
than thirty minutes without a return to baseline function.

NCSE can be either a primary generalized process

(absence status) or secondary generalized (complex
partial status).

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 NCSE
Though the distinction is not clear in the
literature, NCSE in general should be
distinguished from subtle GCSE, which is the
end stage of GCSE, associated with anoxic
brain injury, and has a very poor prognosis.

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 Treatment of NCSE

When presented with a patient thought to be in NCSE, EEG

confirmation is indicated.
Benzodiazepines are generally effective in terminating the
seizure, though they do not provide long term control.
The literature is unclear as to the urgency of controlling
NCSE, although there is evidence that ongoing neuronal
firing does result in neuronal injury.
A neurology consultation should be obtained to determine
long-term therapy.

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 Special Situations
Alcohol Withdrawal Seizures (AWS)

Of special concern to any emergency physician is the relation

of alcohol to seizures. Twenty to 40% of seizure patients
presenting to an ED will have their seizures related to
alcohol abuse, and alcohol is reported as a causative factor
in 15 to 24% of patients with status epilepticus.
Diagnostic yield for CT after first alcohol related seizure is high,
mainly because patients who overuse alcohol have a high
incidence of structural intracranial lesions, such as subdural
hematomas or other intracranial hemorrhages.
 Eclampsia
Eclampsia is the major consideration in pregnant
patients of more than 20-week gestation and up to
23 days postpartum who present with new onset
seizures. Magnesium has been demonstrated to
be the therapy of choice in the treatment of acute
eclamptic seizures and for prevention of recurrent
eclamptic seizures. A systematic review of four
good quality trials involving 823 women found
magnesium sulfate to be substantially more
effective than phenytoin with regards to recurrence
of convulsions and maternal death.

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 Eclampsia
Complications, such as respiratory depression
and pneumonia, were also less for magnesium
than for phenytoin.
Magnesium showed a trend towards increased
incidence of renal failure when compared to
phenytoin; however, this was not statistically
significant. Magnesium sulfate was also
associated with benefits for the baby, including
fewer admissions to the NICU.

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 Eclampsia
In the eclamptic patient, give 4 grams of
intravenous magnesium sulfate followed by a
2 gm/h drip (some centers use intramuscular
regimens).
Control the patients blood pressure if very high
(SBP greater than 160 and/or DBP greater than
110)

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 Febrile Seizures

The major challenge of an emergency physician

when presented with a febrile seizure idifferentiating
simple from complex febrile seizure. By definition,
a simple febrile seizure lasts less than 15 minutes,
is non-focal, does not have a prolonged postictal
period and occurs in a child between six months
and five years of age.

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 Febrile Seizures
Ten to 50% of cases of status epilepticus in children
are associated with febrile seizures; status in this
group is a consistent predictor of increased risk for
subsequent seizures.
Simple febrile seizures are a benign process.
When they occur in children older than 18 months
who have not been on antibiotics, they do not
require any particular diagnostic work-up, even for a
first time event. Management focuses on a careful
history and physical, and on parental education.

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 Febrile Seizures
Two to four percent of all children will have a simple
febrile seizure. Children who have had a febrile seizure
have a 25 to 50% chance of having a second event,
usually within a year. Children at highest risk for
recurrence are those with a first degree relative who has
had a febrile seizure, complex first febrile seizure, or age
younger that one year when the first event occurred.
There is an increased incidence of developing epilepsy in
children who have had a simple febrile seizure (2.4%
versus a .4% incidence in the general population).

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 Febrile Seizures
Patients with simple febrile seizures require no special
workup or treatment. Reassuring the parents is often the
most Herculean task. Nearly half of parents think that
their child is dying during the seizure. Such concerns
need to be addressed; simply suggesting the child be
discharged on acetaminophen is not appropriate.

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 Non-Febrile Seizures
The evaluation of non-febrile seizures, complex seizures, and
febrile seizure outside of the usual age group, in essence, parallels
the discussion presented on adults in the preceding sections. If the
seizure was exertional, consider the possibility of convulsive
syncope secondary to a cardiac arrhythmia. In children, this could
be due to a prolonged QT syndrome or hypertrophic
cardiomyopathy. During the evaluation, be attentive to the
stigmata of the phakomatoses (hereditary disease characterized by
tumors in multiple tissues) such caf au lait spots (tuberous
sclerosis) or fleshy bumps (neurofibromatosis). Both of these may
result in seizures secondary to CNS tumors.

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 Status Epilepticus
In Children
The treatment of status seizures in children is similar to
that of adults. Interosseous access is an alternative when
intravenous access is not secured. While rectal diazepam
has long been used as an alternative to parenteral
administration in children, buccal midazolam may be
equally effective (and more palatable).
Intranasal midazolam (0.2 mg/kg) has been reported to
have equal efficacy with IV diazepam (0.3 mg/kg) for
prolonged febrile seizures.
.

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 Status Epilepticus
in Children
Both phenytoin and phenobarbital are often effective in
pediatric status if a bolus administration of a benzodiazepine
fails. However, as in adults, continuous infusion of
benzodiazepines have been reported as successful. Infection
has been reported as a more common cause of status in
children than in adults. Therefore, many physicians will
empirically cover such children with broad-spectrum
antibiotics, usually ceftriaxone (or the combination of
ceftriaxone and amoxicillin in neonates). The routine use of
empiric acyclovir to treat presumed herpes encephalitis in the
neonate remains unstudied.

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 Status Epilepticus
in Children
Status epilepticus (SE) presents in a
multitude of forms, dependent on
etiology and patient age (myoclonic,
tonic, subtle, tonic-clonic, absence,
complex partial etc.)
Generalized, tonic-clonic SE is the most
common form of SE

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 Causes

Fever 36%
Medication change. 20%
Unknown.. 9%
Metabolic. 8%
Congenital 7%
5%
Anoxic...
Other (trauma, vascular, infection,
tumor, drugs)... 15%

DeLorenzo RJ. Epilepsia 1992;33 Suppl 4:S15-25

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Drugs which can cause seizures

Antibiotics Psychopharmaceuticals
Penicillins Antihistamines
Isoniazid Antidepressants
Metronidazole Antipsychotics
Anesthetics, narcotics Phencyclidine
Halothane, enflurane Tricyclic antidepressants
Cocaine, fentanyl
Ketamine

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 Mortality

Adults 15 to 22%
Children 3 to 15%

Reviewed in: Fountain NB, Epilepsia 2000; 41 Suppl 2:S 23-30

51
 Prolonged seizures

Temporary Life threatening Death

Systemic changes systemic changes

Duration of seizure

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 Respiratory
Hypoxia and hypercarbia

ventilation (chest rigidity from muscle spasm)

Hypermetabolism ( O2 consumption, CO2 production)
Poor handling of secretions
- Neurogenic pulmonary edema?

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 Hypoxia
Hypoxia/anoxia markedly increase the risk
of mortality in SE
Seizures (without hypoxia) are much less
dangerous than seizures and hypoxia

Towne AR. Epilepsia 1994; 35(1): 27-34

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 Neurogenic pulmonary edema

Rare complication
Likely occurs as
consequence of marked
increase of pulmonary
vascular pressure

Johnston SC. Postictal pulmonary edema requires pulmonary vascular

pressure increases. Epilepsia 1996; 37(5):428-32
55
 Acidosis

Respiratory

Lactic
Impaired tissue oxygenation
Increased energy expenditure

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 Hemodynamics

Sympathetic overdrive
Massive catecholamine /
autonomic discharge
Hypertension
Tachycardia
High CVP Exhaustion
Hypotension
hypoperfusion

0 min 60 min

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Cerebral blood flow
Cerebral O2 requirement

Hyperdynamic phase
CBF meets CMRO2
O2 requirement Exhaustion phase
CBF drops as
Hypotension sets in
Autoregulation
exhausted
Blood flow
Neuronal demage
ensue
Blood pressure

Seizure duration

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Glucose Glucose

SE

30 min
SE + hypoxia

Seizure duration

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 Hyperpyrexia

Hyperpyrexia may develop during protracted

SE, and aggravate possible mismatch of
cerebral metabolic requirement and substrate
delivery

Treat hyperpyrexia aggressively

Antipyretics, external cooling
Consider intubation, relaxation, ventilation

60
 Other alterations
Blood leukocytosis (50% of children)
Spinal fluid leukocytosis (15% of children)
K+
Creatine kinase
Myoglobinuria

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 Oxygen, oral airway. Avoid
A hypoxia!

B Consider bag-valve mask

ventilation. Consider intubation

C IV/IO access. Treat hypotension, but

NOT hypertension

62
 Treatment
Arterial blood gas?
All children in SE have acidosis. It often resolves
rapidly with termination of SE
Intubate?
It may be difficult to intubate the actively seizing
child
Stop or slow seizures first, give O2, consider BVM
ventilation
If using paralytic agent to intubate, assume that SE
continues

63
Initial investigations

Labs
Na, Ca, Mg, PO4 , glucose
CBC
Liver function tests, ammonia
Anticonvulsant level
Toxicology

64
 Initial investigations
Lumbar puncture
Always defer LP in unstable patient, but never
delay antibiotic/antiviral rx if indicated
CT scan
Indicated for focal seizures or deficit, history of
trauma or bleeding d/o

65
 Treatment
give Glucose (2-4 ml/kg D25%, infants 5 ml/kg D10%),
unless normo- or hyperglycemic

Hyperglycemia has no negative effect in SE

(as long as significant hyperosmolality is being avoided)

66
 Treatment
Hyponatremia:
Give 5 cc/kg of 3% (hypertonic saline)

Hypocalcemia:
Give 20-25 mg/kg of Calcium Chloride

67
 Treatment

The longer you wait with anticonvulsant, the

more anticonvulsant you will need to stop SE

Most common mistake is ineffective dose

68
Anticonvulsants

Rapid acting

plus

Long acting

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Anticonvulsants - Rapid acting
Benzodiazepines
Lorazepam 0.1 mg/kg i.v. over 1-2 minutes
Diazepam 0.2 mg/kg i.v. over 1-2 minutes

If SE persists, repeat every 5-10 minutes

70
 Benzodiazepines

Lorazepam
Low lipid solubility
Action delayed 2 minutes
Anticonvulsant effect 6-12 hrs
Less respiratory depression than
diazepam
Midazolam
May be given i.m.
Diazepam
High lipid solubility
Thus very rapid onset
Redistributes rapidly
Thus rapid loss of
anticonvulsant effect
Adverse effects are
persistent:
Hypotension
Respir depression

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Anticonvulsants - Long acting

Phenytoin Fosphenytoin
20 mg/kg i.v. over 20 min 20 mg PE/kg i.v. over 5-7
min PE = phenytoin equivalent
pH 12 pH 8.6
Extravasation causes Extravasation well
severe tissue injury tolerated
Onset 10-30 min Onset 5-10 min
May cause hypotension, May cause hypotension
dysrhythmia
Cheap Expensive

72
Anticonvulsants - Long acting

Phenobarbital
20 mg/k g i.v. over 10 - 15 min
Onset 15-30 min
May cause hypotension, respiratory depression

73
 Initial choice of long acting
anticonvulsants in SE

Is patient an infant?
Is patient already receiving phenytoin?

No Yes

At high risk for extravasation Phenobarbital

?
(small vein, difficult access etc.)?

No Yes

Phenytoin Fosphenytoin
74
 If SE persists

Midazolam infusion 1 - 10 mcg/kg/min

after bolus 0.15 mg/kg

Pentobarbital infusion 1-3 mg/kg/hr

after bolus 10 mg/kg

75
 NCSE?
Neurologic signs after termination
of SE are common:
Pupillary changes
Abnormal tone
Babinski
Posturing
Clonus
May be asymmetrical

76
 NCSE?

Up to 20% of children with SE have

NCSE after GCSE

77
 NCSE?

If child does not begin to respond to

painful stimuli within 20 - 30 minutes
after tonic-clonic SE
suspect non-convulsive SE
Urgent EEG

78
 Management of a pregnant
patient in status epilepticus
Establish the ABCs, and check vital signs, including
oxygenation.
Assess the fetal heart rate or fetal status.
Rule out eclampsia.
Administer a bolus of lorazepam (0.1 mg/kg, ie, 5-10 mg) at
no faster than 2 mg/min.
Load phenytoin (20 mg/kg, ie, 1-2 g) at no faster than 50
mg/min, with cardiac monitoring.
If this is not successful, load phenobarbital
(20 mg/kg, ie, 1-2 g) at no faster than 100 mg/min.
Check laboratory findings, including electrolytes, AED levels,
glucose, and toxicology screen.
If fetal testing results are nonreassuring, move to emergent
delivery.
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80
 Management of WWE
upon labor and delivery
Check levels of antiepileptic drugs (AEDs).
Inform all care providers, including nurses,
anesthesiologists, and pediatricians, that the patient has
epilepsy.
Consider seizure prophylaxis with intravenous
benzodiazepines or phenytoin.
Manage seizures acutely with intravenous benzodiazepines
(1-2 mg of diazepam), then load phenytoin (1 g loaded over
1 h).
Labor management should be based on routine standards
of care.
Start administration of vitamin K for the infant, and send
the cord blood for clotting studies.

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Semoga bermanfaat

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