Case Report

INFARCTION STROKE

By:
Ary Anggi Kristiana

1408465581

Supervisor:
dr. Riki Sukiandra, Sp.S

DEPARTMENT OF NEUROLOGY
MEDICAL SCHOOL UNIVERSITY OF RIAU
ARIFIN ACHMAD GENERAL HOSPITAL
PEKANBARU

2015
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
PE K AN B AR U

I. PATIENTS IDENTITY
Name

Mrs. B

Age

74 years 6 months

Gender

Female

Address

Jalan Hangtuah Gang Hangtuah No. 44 Pekanbaru

Religion

Moslem

Marital Status

Married

Occupation

Housewife

Date of Admission

November, 24th 2015

Medical Record

90 81 xx

II. ANAMNESIS
Alloanamnesis (November, 25th 2015)
Chief Complaint
The weakness on the right arm and leg
Present Illness History
Since a day before admission, the patient has complained the weakness on
her right arm and leg. At first, the patient has complained the numbness
and then weakened suddenly when she woke up on the morning. She never
complained the numbness before.
Furthermore, the patients speech became slurred and nonfluent. The patient
also cant control her urination and defecation.

 No history of headache, vomiting, losing of vision and decreasing of

consciousness. No history of trauma.
Past Illness History

Unknown history of Hypertension, Diabetes mellitus and Cardiovascular

disease

No history of obesity

Family Illness History

No history of Hypertension

No history of Diabetes mellitus

No history of Cardiovascular disease

Socioeconomic History

Menopause on 52 years old.

No history of oral contraception used

THE SUMMARY OF ANAMNESIS

Mrs. B, 74 years old admitted to the hospital on November, 24th 2015. The
patient has complained the sudden weakness on the right arm and leg since a day
before admission. The patients speech became slurred and nonfluent and she
also cant control her urination and defecation. There were unknown history of
hypertension, diabetes mellitus and cardiovascular disease.
III. PHYSICAL EXAMINATION
A. General status
Blood Pressure : 170/80 mmHg
Heart Rate

: 98 bpm

Respiratory Rate
Temperature

: 20 times per minute

: 37.8C

B. Neurological status
1) Consciousness

: Alertness

2) Cognitive Function

: Cognitive Impairment

GCS : E4M6Vaphasia

3) Neck Stiffness

: Negative

4) Cranial Nerves
1. Cranial nerve I (Olfactory)
Right
Sense of Smell
Cant be assessed

Left
Cant be assessed

Interpretation
Cant be assessed

2. Cranial nerve II (Optic)

Visual Acuity
Visual Fields
Colour Recognition

Right
Cant be
assessed
Cant be
assessed
Cant be
assessed

Left
Cant be
assessed
Cant be
assessed
Cant be
assessed

3. Cranial nerve III (Oculomotor)

Right
Ptosis
(-)
Pupil
Shape
Round
Size
3 mm
Extraocular movements
Normal
Pupillary reactions to light
Direct
(+)
Indirect
(+)

Left
(-)
Round
3 mm
Normal

Interpretation

Cant be assessed

Interpretation

Normal

(+)
(+)

4. Cranial nerve IV (Trochlear)

Extraocular movements

Right
Normal

5. Cranial nerve V (Trigeminal)

Right
Left
Motor
Normal
Normal
Sensory
Cant be
Cant be
assessed
assessed
Corneal
(+)
(+)
reflex

Left
Normal

Interpretation
Normal

Interpretation
Motor and reflex examination is
normal, sensory examination cant
be assessed

6. Cranial nerve VI (Abducens)

Extraocular movements
Strabismus
Deviation

Right
Normal
(-)
(-)

Left
Normal
(-)
(-)

Interpretation
Normal

7. Cranial nerve VII (Facial)

Right
Tic
(-)
Motor
Normal
Sense of Taste
Cant be
assessed
Chvostek Sign
(-)

Left
(-)
Normal
Cant be
assessed
(-)

8. Cranial nerve VIII (Acoustic)

Right
Sense of Hearing Cant be assessed

Interpretation
Motor
examination is
normal,
sensory
examination
cant be
assessed

Left
Cant be assessed

9. Cranial nerve IX (Glossopharyngeal)

Right
Left
Pharyngeal
Normal
Normal
Arch
Cant be
Cant be
Sense of
assessed
assessed
Taste
(+)
(+)
Gag Reflex

Interpretation
Cant be assessed

Interpretation
Pharyngeal Arch and gag reflex is
normal, sense of tase cant be
assessed

10. Cranial nerve X (Vagus)

Pharyngeal Arch
Dysphonia

Right

Left

Interpretation

Normal
(-)

Normal
(-)

Normal

11. Cranial nerve XI (Accessory)

Right
Motor
Normal
Trophy
Eutrophy
12. Cranial nerve XII (Hypoglossal)
Right
Motor
Normal
Trophy
Eutrophy
Tremor
(-)
Dysarthria
(+)

Left
Normal
Eutrophy

Left
Normal
Eutrophy
(-)
(+)

Interpretation
Normal

Interpretation
Dysarthria

IV. MOTOR SYSTEM

Upper Extremity
Strength
Distal
Proximal
Tone
Trophy
Involuntary movements
Clonus
Lower Extremity
Strength
Distal
Proximal
Tone
Trophy
Involuntary movements
Clonus
Body
Trophy
Involuntary movements
Abdominal Reflex

Right

Left

Interpretation

1
1
Normal
Eutrophy
(-)
(-)

5
5
Normal
Eutrophy
(-)
(-)

1
1

5
5

Eutrophy
(-)
(-)

Eutrophy
(-)
(-)

Eutrophy
(-)
(-)

Eutrophy
(-)
(-)

Hemiparesis
(UMN Type)

Hemiparesis
(UMN Type)

Normal

V. SENSORY SYSTEM
Right
Light Touch
Pain
Temperature
Proprioceptive
Position
Two point discrimination
Stereognosis
Graphestesia
Vibration

Left

Cant be
assessed

Not Tested

Not Tested

VI. REFLEX

Physiologic
Biceps
Triceps
Knee
Ankle
Pathologic

Interpretation

Right

Left

(+)
(+)
(+)
(+)

(+)
(+)
(+)
(+)

Interpretation
Physiologic reflex
(+)

Babinsky
Chaddock
Hoffman Tromer
Openheim
Schaefer
Primitive Reflex
Palmomental
Snout

(-)
(-)
(-)
(-)
(-)

(-)
(-)
(-)
(-)
(-)

(-)
(-)

(-)
(-)

Pathologic reflex (-)

No Primitive Reflex

VII. COORDINATION

Point to point movements

Walk heel to toe
Gait
Tandem
Romberg

Right
Cant be
assessed
Not Tested
Not Tested
Not Tested
Not Tested

Left
Cant be
assessed
Not Tested
Not Tested
Not Tested
Not Tested

VIII. AUTONOMY SYSTEM

Urination

: bladder incontinence

Defecation

: bowel incontinence

IX. Others Examination

a. Laseque

: Unlimited

b. Kernig

: Unlimited

c. Patrick

: -/-

d. Kontrapatrick

: -/-

e. Valsava test

: -

f. Brudzinski

: -

X. THE SUMMARY OF EXAMINATION

General Status

: Hypertension (170/80 mmHg)

Cognitive Function : Cognitive Impairment

Neck Stiffness

: Negative

Cranial Nerves

: Dysarthria

Motoric

: Hemiparesis (UMN Type)

Interpretation
Cant be assessed

Sensory

: Cant be assessed

Coordination

: Cant be assessed

Autonomy

: Abnormal urination and defecation

Reflex

: Normal

Gajah Mada Algorithm: Infarction stroke

Siriraj Score

: Infarction stroke

XI. WORKING DIAGNOSIS

CLINICAL DIAGNOSIS : Stroke
TOPICAL DIAGNOSIS : Carotid system
ETIOLOGICAL DIAGNOSIS: Infarction stroke
DIFFERENTIAL DIAGNOSIS : Hemorrhagic stroke
XII. SUGGESTION EXAMINATION

Blood routine

Blood chemistry

Electrocardiography

Chest X-ray

Head CT Scan

XIII. SUGGESTION FOR MANAGEMENT THERAPY

General
-

Immobilization and head up 30

Monitoring of vital sign

Medical rehabilitation

IVFD (30ml/kgBB/day) Ringer Lactate 20 dpm

Special
-

Neuroprotector

: Citicoline 2 x 500 mg per IV

Antiplatelets

: Aspilet 3 x 500 mg per oral

XIV. LABORATORY AND RADIOLOGY FINDINGS

1. Blood Routine (November, 24th 2015)
-

Hemoglobin

: 12.2 g/dL

Hematocrit

: 34 %

Leukocyte

: 6.600/mm3

Thrombocyte

: 247.000/mm3

Interpretation: Normal
2. Blood Chemistry
(November, 24th 2015)
-

Glucose

: 155 mg/dL

Ureum

: 38.4 mg/dL

Creatinin

: 0.96 mg/dL

AST

: 19.6 U/L

ALT

: 12 U/L

Electrolite:
-

Sodium

: 144.8 mmol/L

Potassium

: 2.89 mmol/L

Chloride

: 115.9 mmol/L

(November, 25th 2015)

-

Chor

: 165 mg/dL

HDL

: 46.0 mg/dL

Triglyceride

: 75 mg/dL

Uric acid

: 6.3 mg/dL

LDL Cholesterol

: 104 mg/dL

LDP

: 144 U/L

3. Electrocardiography

Interpretation : synus rithm, no abnormal morphology waves.

4. Chest X-ray (November, 24th 2015)

Interpretation: normal

5. Head CT Scan without contrast

Interpretation: infarction on the left hemisphere cerebri

XV. FINAL DIAGNOSIS

-

Infarction stroke

FOLLOW UP
November, 26th 2015
S

: lethargic, weakness of the right extremity, aphasia, fever.

:
GCS E4M6Vaphasia
Blood Pressure 160/90 mmHg
Heart Rate 92 bpm
Respiratory Rate 22 tpm
Temperature 38.1C
Cognitive Function

: Cognitive Impairment

Neck Stiffness

: Negative

Cranial Nerves

: Dysarthria

Motoric

: right extremity hemiparesis

Sensory

: Cant be assessed

Coordination : Cant be assessed

Autonomy

: Abnormal urination and defecation

Reflex

: normal limit

: Infarction stroke

IVFD RL 20 dpm

Citicolin 3 x 500 mg per IV

Aspilet 2 x 80 mg per oral

Folic acid 2 x 400 g per oral

November, 27st 2015

S

: lethargic, weakness of the right extremity, aphasia, fever.

:
GCS E4M6Vaphasia

Blood Pressure 160/90 mmHg

Heart Rate 80 bpm
Respiratory Rate 22 tpm
Temperature 38.0C
Cognitive Function: Cognitive Impairment
Neck Stiffness

: Negative

Cranial Nerves

: Dysarthria

Motoric

: Hemiparesis

Sensory

: Cant be assessed

Coordination

: Cant be assessed

Autonomy

: Abnormal urination and defecation

Reflex

: Normal

: Infarction stroke

IVFD RL 20 dpm

Citicolin 3 x 500 mg per IV

Aspilet 2 x 80 mg tab per oral

Folic acid 2 x 400 g tab per oral

November, 28th 2015

S

: lethargic, weakness of the right extremity, aphasia, fever (-)

:
GCS E4M6Vaphasia
Blood Pressure 150/90 mmHg
Heart Rate 88 bpm
Respiratory Rate 20 tpm
Temperature 37.6C
Cognitive Function : Cognitive Impairment
Neck Stiffness

: Negative

Cranial Nerves

: Dysarthria

Motoric

: Hemiparesis

Sensory

: Cant be assessed

Coordination

: Cant be assessed

Autonomy

: Abnormal urination and defecation

Reflex

: Normal

: Infarction stroke

IVFD RL 20 dpm

Citicolin 3 x 500 mg per IV

Aspilet 2 x 80 mg per oral

Folic acid 2 x 400 g per oral

Discussion
INFARCTION STROKE
1. Definition
Stroke is applied to a sudden focal neurologic syndrome, specifically the
type due to cerebrovascular disease. The term cerebrovascular disease designates
any abnormality of the brain resulting from a pathologic process of the blood
vessels. Pathologic process is given an inclusive meaning namely, occlusion of
the lumen by embolus or thrombus, rupture of a vessel, an altered permeability of
the vessel wall, or increased viscosity or other change in the quality of the blood
flowing through the cerebral vessels. The vascular pathologic process may be
considered not only in its grosser aspects embolism, thrombosis, dissection, or
rupture of a vessel but also in terms of the more basic or primary disorder, i.e.,
atherosclerosis, hypertensive arteriosclerotic change, arteritis, aneurysmal
dilation, and developmental malformation. Equal importance attaches to the

secondary parenchymal changes in the brain resulting from the vascular lesion.
These are of two main types ischemia, with or without infarction, and hemorrhage
and unless one or the other occurs, the vascular lesion usually remains silent. The
only exceptions to this statement are the local pressure effects of an aneurysm,
vascular headache (migraine, hypertension, temporal arteritis), multiple small
vessel disease with progressive encephalopathy (as in malignant hypertension or
cerebral arteritis), and increased intracranial pressure (as occurs in hypertensive
encephalopathy and venous sinus thrombosis). Also, persistent acute hypotension
may cause ischemic necrosis in regions of brain between the vascular territories of
cortical vessels, even without vascular occlusion.1
More than any other organ, the brain depends from moment to moment on
an adequate supply of oxygenated blood. Constancy of the cerebral circulation is
assured by a series of baroreceptors and vasomotor reflexes under the control of
centers in the lower brainstem. Obstruction of an artery by thrombus or embolus is
the usual cause of focal ischemic damage, but failure of the circulation and
hypotension from cardiac decompensation or shock, if severe and prolonged
enough, can produce focal as well as diffuse ischemic changes.1
Focal cerebral ischemia differs fundamentally from global ischemia. In the
latter state, if absolute, there is no cerebral blood flow of the entire brain and
irreversible destruction of neurons occurs within 4 to 8 min at normal body
temperature. In focal ischemia, there is nearly always some degree of circulation
(via collateral vessels), permitting to a varying extent the delivery of oxygenated
blood and glucose.
The effects of a focal arterial occlusion on brain tissue also vary depending
on the location of the occlusion in relation to available collateral and anastomotic
channels. If the obstruction lies proximal to the circle of Willis (toward the heart),
the anterior and posterior communicating arteries of the circle are often adequate
to prevent infarction. In occlusion of the internal carotid artery in the neck, there
may be anastomotic flow from the external carotid artery through the ophthalmic
artery or via other smaller externalinternal connections. With blockage of the
vertebral artery, the anastomotic flow may be via the deep cervical, thyrocervical,
or occipital arteries or retrograde from the other vertebral artery. If the occlusion

is in the stem portion of one of the cerebral arteries, i.e., distal to the circle of
Willis, a series of meningeal interarterial anastomoses may carry sufficient blood
into the compromised territory to lessen (rarely to prevent) ischemic damage.
There is also a capillary anastomotic system between adjacent arterial branches,
and although it may reduce the size of the ischemic field, particularly of the
penetrating arteries, it is usually not significant in preventing infarction. Thus,
in the event of occlusion of a major arterial trunk, the extent of infarction ranges
from none at all to the entire vascular territory of that vessel. Between these two
extremes are all degrees of variation in the extent of infarction and its degree of
completeness.1
Additional ischemia-modifying factors determine the extent of necrosis.
The speed of occlusion assumes importance; gradual narrowing of a vessel allows
time for collateral channels to open. The level of blood pressure may influence the
result; hypotension at a critical moment may render anastomotic channels
ineffective. Hypoxia and hypercapnia are presumed to have deleterious effects.
Altered viscosity and osmolality of the blood and hyperglycemia are potentially
important factors but difficult to evaluate. Finally, anomalies of vascular
arrangement (of neck vessels, circle of Willis, and surface arteries) and the
existence of previous vascular occlusions must influence the outcome.1
The specific neurologic deficit obviously relates to the location and size of
the infarct or focus of ischemia. The territory of any artery, large or small, deep or
superficial, may be involved. When an infarct lies in the territory of a carotid
artery, as would be expected, unilateral signs predominate: hemiplegia,
hemianesthesia, hemianopia, aphasia, and agnosias are the usual consequences. In
the territory of the basilar artery, the signs of infarction are frequently bilateral and
occur in conjunction with cranial nerve palsies and other segmental brainstem and
cerebellar signs; quadriparesis, hemiparesis, and/or unilateral or bilateral sensory
impairment are typical, coupled with diplopia, dysarthria, and vertigo in various
combinations.1
2. Risk factor
According to the American Heart Association (AHA), the risk factors of
stroke are divided into two, that are not modifiable risks factors and modifiable

risk factors. Not modifable risk factors include: age, sex, low birth weight, race or
ethnicity, and genetic factors. Modifiable risk factors include: hypertension,
smoking, diabetes, nutritional imbalance, lack of physical activity, alcohol
consumption, and drug abuse. Incidence of stroke can occur with one or more risk
factors (multifactor).1-3
Table 3. Stroke risk factors1-3
Not Modifable
1 Age
2 Gender
3 Genetic
4 Ethnic

Modifable
1 Stroke history
2 Hypertension
3 Heart disease
4 Diabetes melitus
5 Carotid stenosis
6 TIA
7 Hypercholesterolemia
8 Oral contraception
9 Obesity

10. Smoking
11. Alcohol
12. Drug abuse
13. Hyperhomosisteinemia
14. Antibody anti fosfolipid
15. Hyperurisemia
16. Elevation of hematocrit
17. Elevation of fibrinogen

3. Clinical Manifestation
The specific neurologic deficit obviously relates to the location and size of
the infarct or focus of ischemia. The territory of any artery, large or small, deep or
superficial, may be involved. When an infarct lies in the territory of a carotid
artery, as would be expected, unilateral signs predominate: hemiplegia,
hemianesthesia, hemianopia, aphasia, and agnosias are the usual consequences. In
the territory of the basilar artery, the signs of infarction are frequently bilateral and
occur in conjunction with cranial nerve palsies and other segmental brainstem and
cerebellar signs; quadriparesis, hemiparesis, and/or unilateral or bilateral sensory
impairment are typical, coupled with diplopia, dysarthria, and vertigo in various
combinations.1,2
4.

Management
Stroke patients should be handled by a multidisciplinary team.

Management stroke be done by improving the general state of the patient, treat the
risk factors, and prevent complications.3-6
4.1 Hyperacute stadium
Action at this stadium is done at the Emergency Room, the aim is to
prevent the widespread of brain tissue damaging. At this stage, patients were

given oxygen 2 L / min and crystalloid/colloid fluid, avoid administration of

dextrose. Brain CT scan examination, electrocardiography, chest X-ray, complete
peripheral blood and platelet count, prothrombin time / INR, APTT, blood
glucose, blood chemistry (including electrolytes), and if hypoxia, do the blood gas
analysis. Other actions in the Emergency Room are providing mental support to
patients and provide an explanation to the family to remain calm.3-6
4.2 Acute stadium
4.2.1 General treatment
Place the patients head in 30o positions, head an chest in a field, change
the sleep position every 2 hours. Mobilization began gradually when
hemodynamically stable. Furthermore, free the airway, give oxygen 1-2 liters /
min. If necessary, intubation. Fever overcome with compresses and antipyretic,
then look for the cause, when the bladder is full, emptied (preferably with
intermittent catheters).3-6
Fluid nutrition with 1500-2000 isotonic cristalloid or colloid and
electrolyte as needed, avoid fluids containing glucose or isotonic saline. Nutrition
orally only if swallowing function well, if there is swallowing disorders or
decreased consciousness, nasogastric tube is recommended. 3-6
Blood glucose levels > 150 mg% should be corrected with continuous
intravenous drip insulin during 2-3 days. Hipoglikemia (blood glucose < 60 mg%
or < 80mg% with symptoms) should be corrected immediatelywith dextrose 40%
iv until return to normal and the cause must be sought. 3-6
Headache, nausea, and vomiting treated according to the symptoms. Blood
preassure doesnt need taken down immediately, except when the systolic pressure
220 mmHg and diastolic pressure 120 mmHg, Mean Arterial Blood Pressure
(MAP) 130 mmHg (the two measurements with an interval of 30 minutes), or
obtained acute myocardial infarction, congestive heart failure as well as kidney
failure. Maximal blood pressure reduction was 20%, and the recommended drugs
are sodium nitroprusside, alpha-beta receptor blockers, ACE blockers, or
antagonists calsium. 3-6
If hypotension occurs, the systolic pressure 90 mmHg, diastolic 70 mm
Hg, the patient should be given 250 mL of 0.9% NaCl for 1 hour, followed by 500

mL for 4 hours and 500 mL for 8 hours or until hypotension treated. If not
corrected, that is systolic blood pressure still <90 mmHg, dopamine 2-20 mcg / kg
/ minute can be given until the systolic blood pressure 110 mmHg. 3-6
If there is seizure, give diazepam 5-20 mg iv slowly for 3 minutes, the
maximum dosage is 100 mg per day, followed by oral administration of
anticonvulsants such as phenytoin, carbamazepine. If the seizure appeared after 2
weeks, given orally long-term anticonvulsant. 3-6
If there is an increased of intracranial pressure, bolus mannitol were given
an of 0.25 to 1 g / kg per 30 minutes intravenously, and if rebound phenomenon
suspected, or general condition deteriorated, followed by 0,25g / kg per 30
minutes every 6 hours for 3-5 days. Monitoring of the osmolarity should be
performed (<320 mmol), alternatively can be administered hypertonic solutions
(NaCl 3%) or furosemid. 3-6
4.2.2

Special treatment
The goal is to reperfusion by administration of antiplatelet agent such as
aspirin and anticoagulant, or with trombolytic

rt-PA (combinant tissue

Plasminogen Activator), and neuroprotective agent, such as citicoline or

piracetam. 3-6
4.3 Subacute Stadium
Medical measures may include cognitive therapy, behavior, swallowing,
speech therapy, and bladder training (including physical therapy). Given the long
course of the disease, it takes a special intensive treatment of post-stroke in the
hospital with the goal of independence of the patient, understand, comprehend and
implement primary and secondary prevention programs.6
Subacute phase treatment:6
-

Continuing the appropriate treatment of acute conditions before

The management of complications
Restoration / rehabilitation (as needed of patients), which is
physiotherapy, speech therapy, cognitive therapy, and occupational

therapy
Secondary Prevention
Family education and discharge planning

THE BASIC OF DIAGNOSIS

1. Basic clinical diagnosis
From the history taking, a 74 years old woman had a sudden weakness on
the right arm and leg (Hemiparesis). And her speech became slurred and
nonfluent. She also cant control her urination and defecation. No history of
trauma. It is consistent with the WHOs definition that clinical symptoms of
stroke is cerebral disorders, either focal or global attack in 24 hours or more, no
illness is found other than vascular disorders. And elderly is a risk factor of stroke.
2. Basic topical diagnosis
Carotid system had been considered in this patient because there is
hemiparesis and aphasia. Hemiparesis and aphasia is symptoms of middle cerebral
artery occlusion. Middle cerebral artery is the greatest branch of internal carotid
artery. From the physical examination there is right hemiparesis, so the lesion is
on the left hemisphere because a lesion in one side of carotid system will lead to
contralateral neurological deficit.
3. Basic etiological diagnosis
Basic etiological diagnosis of this patient has been leaded to infarction
stroke, because on this patient there are no losing of consciousness, no projectil
vomiting, no headache, no increasing of diastolic blood pressure and hemiparesis.
It is also supported by Siriraj score and Gajah Mada Algorithm that give the
impression of the infarction stroke.
4. Basic differential diagnosis

The gold standard examination for diagnosing the non hemorrhagic or

hemorrhagic stroke is CT Scan. The consideration of the hemorrhagic stroke
because of it almost has the same manifestation, like the immediate onset, the
patient was not in severe activity, and there is neurological deficit.
5. Basic secondary diagnosis
From the physical examination the blood pressure is 170/80 mmHg. This
is appropriated with JNC 8 criteria that for patients >60 years old the diagnosis of
hypertension is when the sistolic blood pressure 150 mmHg or the diastolic
blood pressure 90 mmHg.
6. Basic final diagnosis
The final diagnosis of this patient is infarction stroke. This diagnosis is
based on history taking, physical examination and supporting examination.
7. Basic treatment
a. The aim of Bed rest with head position elevated 20-300 is to maintain the
adequate circulation to the brain.
b. The aim of IVFD (30ml/kgbb/day) Ringer Lactate 20 dpm is to
maintain the euvolemic condition and glucose level needed.
c. The aim of Inj aspilet 2 x 80 mg is to prevent from recurrent stroke attack
d. The aim of Inj citicoline 2 x 500 mg is as the neuroprotector

REFFERENCE
1

Ropper AH, Brown RH. Adams and Victors Principles of Neurology. 8th Ed.
New York: McGraw-Hill Companies, Inc. 2005. Chapter 34, Cerebrovascular
Disease; p.660-770.

Rumantir CU. Gangguan Peredaran Darah Otak. Pekanbaru: SMF Saraf

RSUD Arifin Achmad/FK UNRI. Pekanbaru. 2007.

Warlow C, van Gijn J, Dennis M, Wardlaw J, Bamford J, Hankey G. Stroke

Practical Management. 3th Ed. 2008. Blackwell Publishing. p.39-40.

Guideline Stroke Tahun 2011. Pokdi Stroke. Perhimpunan Dokter Spesialis

Saraf Indonesia (PERDOSSI). Jakarta. 2011.

Powers WJ. AHA/ASA Guideline 2015 AHA/ASA Focused Update of the

2013 Guidelines for the Early Management of Patients With Acute Ischemic
Stroke Regarding Endovascular Treatment. AHA journals. 2015;46:000-000.

Setyopranoto I. Stroke: Gejala dan Penatalaksanaan. CDK 185/Vol.38

no.4/Mei-Juni 2011; hal.247-250.