Case Report

Non Hemorrhagic Stroke

Arranged by :
Nur Rahmat
1708436412

Supervisor :

dr. Riki Sukiandra, Sp.S

DEPARTMENT OF NEUROLOGY
MEDICAL FACULTY OF RIAU UNIVERSITY
ARIFIN ACHMAD RIAU PROVINCE GENERAL HOSPITAL
PEKANBARU
2019
 KEMENTERIAN 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 Ny. SM
Age 44 years old
Gender Female
Address Payung Sekaki – Pekanbaru
Religion Moeslem
Marital Status Married
Occupation Entrepreneur
Entry Hospital May, 6th 2019
Medical Record 010147xx

II. ANAMNESIS :
Allo anamnesis with her husband (May, 7th 2019)
Chief Complain
Feeling weakness half of the right body side since 2 hours before admitted to the
hospital.
A. Present Illness History
2 hours before admitted to the hospital, the patient complained about half of his
right body side from the head to the feet feeling weakness suddenly. It happened
when she still took a rest. The patient still could walk but by dragging his right foot.
Still able to speak without any difficulty to pronounce words and no complaints lips
stick to one side of the face and tongue deviation. She also felt numb half of the her
right body side.
2 days ago before admitted to the hospital, patients complained headache. Pain
was felt throughout the head and neck which was felt continuously. Pain did not

1
diminish even though the patient had taken self-purchased headache medicine.
Headache was felt more severe. Patients also complained nausea and sometimes
accompanied by vomiting. There were no complaining of seizures, urinate and
defecate problems.

Past Illness History

 Hypertension (-).
 Diabetes mellitus (+) since 2014 without consume any drugs of DM until
now.
 Trauma history (-).
 Seizure (-).

Socioeconomic History
 The patient is an entrepreneur.
 History of smoking (-), consume alcohol (-).

The Family Disease History

 No family history with the same complains.
 A history of hypertension (+) found from her mother.
 A history of DM (+) found from her father.
 A history of stroke (-).
 A history of epilepsy (-).

ANAMNESIS RESUME
 Feeling weakness half of his right body side from the head to the feet (hemiparese
dextra). Happened suddenly when she still took a rest. Felt numb half of her right
body side (paresthesia right upper and lower extremities).
 Still able to speak without any difficulty to pronounce words (dysarthria) and no
complaints lips stick to one side of the face.
 Patients complained headache. Pain was felt throughout the head and neck which
was felt continuously. Complained nausea and sometimes by vomiting.
 Patient have Diabetes Mellitus since 2014 and no drugs is consumed until now.

2
III. Physical Examination (May, 7th 2019)
A. Generalized Condition
Blood Presure : Dextra :160/90 mmHg, sinistra :160/90 mmHg
Heart Rate : Dextra : 72 bpm, sinistra : 90 bpm, regular
Respiratory rate : 20x/minute
Temperature : 36,8°C
Weight : 63 kg
Height : 140 cm
Body Mass Index (BMI) : 32,1 kg/m2 (obesity)

B. Neurological status
1) Consciousness : Composmentis, GCS : E4V5M6
2) Noble Function : Normal
3) Meningeal Sign : Nuchal rigidity (-)
Brudzinki I, II, III, IV (-)
4) Cranial Nerves
1. N. I (Olfactorius )
Right Left Interpretation
Sense of Smell Normal Normal Normal

2. N.II (Opticus)
Right Left Interpretation
Visual Acuity Normal Normal
Visual Fields Normal Normal Normal
Colour Recognition Normal Normal

3. N.III (Oculomotorius)
Right Left Interpretation
Ptosis - -

Pupil isokor isokor

Shape Round Round
Normal
Side Φ2mm Φ2mm
Pupillary reaction to light
direct + +
Indirect + +

3
4. N. IV (Trokhlearis)
Right Left Interpretation
Extraocular movement Normal Normal Normal

5. N. V (Trigeminus)
Right Left Interpretation
Motoric Normal Normal
Sensory Decrease Normal Normal
Corneal reflex + +

6. N. VI (Abduscens)
Right Left Interpretation
Extraocular
Normal Normal
movement
(-) (-) Normal
Strabismus
(-) (-)
Deviation

7. N. VII (Facialis)
Right Left Interpretation
Tic (-) (-)
Motoric
1. Frowning Normal Normal
2. Raised eye brow Normal Normal
3. Close eyes Normal Normal
4. Corners of the (-) (-)
mouth Normal
5. Nasolabial fold (-) (-)

Sense of Taste Normal Normal

(-)
Chvostek Sign (-)

8. N. VIII (Akustikus)
Right Left Interpretation
Hearing sense Normal Normal Normal

9. N. IX (Glossofaringeus)
Right Left Interpretation
Arcus farings Normal Normal
Normal
Flavour sense Normal Normal
4
 Gag Reflex Normal Normal

10.N. X (Vagus)
Right Left Interpretation
Arcus farings Normal Normal
Normal
Dysfonia - -

11.N. XI (Assesorius)
Right Left Interpretation
Motoric Normal Normal
Normal
Trophy Eutrophy Eutrophy

12.N. XII (Hipoglossus)

Right Left Interpretation
Motoric Normal Normal
Trophy Eutrophy Eutrophy Normal
Tremor - -
Disartria - -

5) MOTORIC
Right Left Interpretation
Upper Extremity
Strength
4 5
Distal
4 5
Medial
4 5 Hemiparese
Proximal
Normal Normal dextra
Tone
Eutrophy Eutrophy
Trophy
(-) (-)
Involuntary movements
(-) (-)
Clonus
Lower Extremity
Strength
4 5
Distal
4 5
Medial
4 5
Proximal
Normal Normal
Tone
Eutrophy Eutrophy
Trophy
(-) (-)
Involuntary movements
(-) (-)
Clonus
Body
Trophy Eutrophy Eutrophy
Involuntary movements (-) (-) Normal
Abdominal Reflex (+) (+)

5
 Cremaster Reflex (+) (+)

6) SENSORY
Right Left Interpretation
Touch Decrease Normal Neurological
Pain Decrease Normal Deficit in
Temperature Decrease Normal Right
Extremities.
Proprioceptive
All tests did
 Position Decrease Normal
except the
 Two point Decrease Normal vibration test
discrimination was difficult to
 Stereognosis Decrease Normal assess
 Graphestesia Decrease Normal
 Vibration No test No test

7) REFLEX
Right Left Interpretation
Physiologic
Biseps + + Physiologic reflex
Triseps + + (+)
Patella + +
Achilles + +
Pathologic
Babinsky (-) (-)
Chaddock (-) (-)
Pathological Reflex
HoffmanTromer (-) (-) (-)
Openheim (-) (-)
Schaefer (-) (-)
Primitive Reflex
Palmomental (-) (-) Primitive Reflex (-)
Snout (-) (-)

8) COORDINATION
Right Left Interpretation
Point to point movement ↓ NT Deficit in Right Test
Walk heel to toe NT NT
Gait NT NT
6
 Tandem NT NT
Romberg NT NT

9) AUTONOM
Urinate : Normal
Defecate : Normal
Erection : Normal

10) OTHERS EXAMINATION

a. Laseque : Negative
b. Kernig : Negative
c. Patrick : Negative
d. Kontrapatrick : Negative
e. Valsava test : None
C. GAJAH MADA STROKE ALGORITHM

GAJAH MADA STROKE ALGORYTHM (ASGM)

Loss of conciousness (-) Headache (-) Babinski reflex (-)

Non Hemorrhage stroke

D. SIRIRAJ STROKE SCORE

SSS = 2.5C + 2V + 2H + 0.1DBP – 3A – 12
SSS = 2.5(0) + 2(1) + 2(1) + 0,1(90) – 3(1) - 12
SSS = -2 (Infarction Stroke)
C = Consciousness (Composmentis = 0, Somnolen = 1, Sopour/Coma = 2)
V = Vomit (None = 0, Yes = 1)
H = Headache (None = 0, Yes = 1)
DBP = Diastole Blood Pressure
A = Aterome (None = 0, One or more = DM, Angina, Vaskular Disease = 1)
Interpretation :
 SSS > 1 = Hemorrhagic Stroke
 SSS < - 1 = Infarction Stroke
 SSS -1 to 1 = Uncertain

7
11). EXAMINATION RESUME (May, 7th 2019)
Generalized Condition
Consciousness : Composmentis GCS : E4M6V5
Blood Presure : 160/90 mmHg
Heart Rate : 90 bpm regular
Respiratory rate : 20 x/s ,
Temperature : 36,8°C
Weight : 63 kg
Height : 140 cm
Body Mass Index (BMI) : 32 (obesity class I)
Noble Function : No cognitive impairment
Meningeal Sign : (-)
Cranial Nerve : No sign disturbed
Motoric : Hemiparese dextra
Sensory : Disturbed in right side
Coordination : Normal
Autonom : Normal
Reflex : Physiology (+), Pathology (-)
Gajah Mada Stroke Algorithm : Non Haemorrhage stroke
Siriraj Stroke Score : Infarction Stroke

C. WORKING DIAGNOSE
CLINICAL DIAGNOSE : Hemiparese Dextra
TOPICAL DIAGNOSE : Carotid system
ETIOLOGICAL DIAGNOSE : Non Hemorrhage Stroke
DIFFERENTIAL DIAGNOSE : Hemorrhage Stroke
SECONDARY DIAGNOSE : DM type II

D. SUGGESTION EXAMINATION
 Routine Blood Test
 Blood Glucose Profile Test
 Cholesterol profile Test

8
  Electrolyte Test
 Chest X-Ray
 Head CT-Scan without contrast
 Electrocardiogram (EKG)

E. MANAGEMENT
1) Bed rest
2) Nasal Canule O2 2-4 L/minute
3) Pharmacology
 IVFD RL 500 mL 30 tpm
 Inj Citicolin 3 x 500 mg
 Aspilet 2 x 80 mg
 Inj novorapid 3 x 8 IU (for DM)
 Inj Ranitidin 2 x 50 mg

LABORATORIUM FINDING :
1. Blood routine (May, 6th 2019)
Hb : 13,7 g/dL
Leucosyte : 10.430/mm3
Trombocyte : 241.000/uL
Hematocryte : 40,1%
Interpretation : normal

2. Blood Glucose Profile Chemistry (May, 6th 2019)

- Glucose : 299 mg/dl

Interpretation : Hyperglycemia

3. Electrolyte (May, 6th 2019)

- Na : 145 mmol/L
- K : 2,3 mmol/L
Interpretation : Hypokalemia

4. Renal and liver function

AST : 21 U/L
ALT : 19 U/L
Ureum : 19 mg/dL

9
 Creatinin : 0,84 mg/dL
Interpretation: Normal

5. Chest Xray (May, 6th 2019)

Interpretation :

Cor and Pulmo are normal

5. Head CT Scan (May, 6th 2019)

- CT –scan in axial pieces non contrast

- Patient’s identity is appropriete (name, date of birth, medical record
number)
10
 - Markers accordingly
- Swelling (-)
- Ventrikulomegally (-), there is hipodens lession appearence in occipital
lobe sinistra hemisphere
- No mideline shift
- Edema cerebri (-)

Interpretation :
Hipodens lession appearence in occipital lobe sinistra hemisphere leads to
Infarction Stroke

FINAL DIAGNOSE :
DEXTRA HEMIPARESE EC NON HEMORRHAGE STROKE +
UNCONTROLLED DIABETES MELITUS TYPE II
FOLLOW UP
May 8th 2019
S : Numb in right upper and lower extremities (+) weak (+), difficult to
speech (-), nausea and vomitus (-), fever (-)
O : GCS E4M6V5
Blood Pressure :130/80 mmHg
Heart Rate : 70 bpm
Respiratory Rate : 20 tpm
Temperature : 37°C
Cognitive Function : Normal
Meningeal Sign : Negative
Cranial Nerves : Normal
Motoric : Hemiparese dextra
Motoric strength :
4 5
4 5
Sensory : 1. Touch : ↓/+
2. Pain : ↓/+

11
 3. Temperature : ↓/+
Coordination : Normal
Autonomy : Normal
Reflex : Normal

A : dextra hemiparese ec non hemorrhage stroke (RIND type) + uncontrolled

diabetes melitus type II day care 2

P :
 IVFD RL 500 mL 30 tpm
 Inj Citicolin 3 x 500 mg
 Aspilet 2 x 80 mg
 Inj novorapid 3 x 8 IU (for DM)
 Inj Ranitidin 2 x 50 mg
 Suggested to physiotherapist
 Sugessted to nutrisionist

May 9th 2019

S : Numb in right upper and lower extremities has diminished, weakness has
diminished, difficult to speech (-), nausea and vomitus (-), fever (-)
O : GCS E4M6V5
Blood Pressure :130/70 mmHg
Heart Rate : 88 bpm
Respiratory Rate : 20 tpm
Temperature : 37°C
Cognitive Function : Normal
Meningeal Sign : Negative
Cranial Nerves : Normal
Motoric : Hemiparese dextra
Motoric strength :
5 5

12
 5 5
Sensory : 1. Touch : ↓/+
2. Pain : ↓/+
3. Temperature : ↓/+
Coordination : Normal
Autonomy : Normal
Reflex : Normal

A : dextra hemiparese ec non hemorrhage stroke + uncontroled diabetes

melitus type III day care 2

P :
 IVFD RL 500 mL 30 tpm
 Inj Citicolin 3 x 500 mg
 Inj Ranitidin 2 x 50 mg
 Aspilet 2 x 80 mg
 Inj novorapid 3 x 8 IU (for DM)
 Suggested to outpatient care and control 1 weeks again
May 9th 2019
Patient has gone home

13
 DISCUSSION

A. Stroke
1.1 Definition of Stroke
According to the World Health Organization (WHO) stroke is the clinical
manifestations of disturbance of cerebral function, whether focal or global, which
progresses rapidly and more than 24 hours or end in death without the discovery of
diseases other than disorders vaskular.1

1.2 Classification of Stroke

Based on pathology, stroke can be divided into:2,3
a. Hemorrhagic stroke
Rupture of cerebral blood vessels cause bleeding into the brain
parenchyma tissue, cerebrospinal fluid space around the brain or both. The
bleeding causes disruption of brain nerve fibers through the suppression of
brain structure and also because of hematoma which causes ischemia of
the surrounding tissues. Increased intracranial pressure will cause
herniation of brain tissue and suppress the brain stem.
i. Intracerebral hemorrhage
ii. Extra cerebral hemorrhage (sub-arachnoid)
b. Non-hemorrhagic stroke (stroke infarction)
i. cerebral thrombosis
Thrombotic strokes are strokes caused by blockage of a brain blood
vessel lumen due to thrombus progressively thicken, so that blood
flow is not smooth. Decreased blood flow can cause ischemia.
Cerebral thrombosis is the obstruction of blood flow that occurs in the
process of blood vessel occlusion one or more local.
ii. cerebral embolism
Stroke can be caused by embolic infarction arising from ateromatous
lesions located at a more distal vessels. Small clumps can be detached
from a larger thrombus and taken to another place in the bloodstream.
If the embolus reached the arteries that are too narrow to pass and
become clogged, blood flow from the distal fragment is interrupted,
14
 causing brain tissue infarction distal due to lack of nutrients and
oxygen. Embolism is 32% of the causes infarction stroke.

Based on the timing of the stroke can be divided into:2,3

a. Transient ischemic attack (TIA), the symptoms of neurological deficit
lasted less than 24 hours.
b. Reversible ischemic neurologic deficit (Rind), symptoms of neurological
deficits disappeared in the time between more than 24 hours up to 3 weeks.
c. Stroke in evolution (progressive stroke), stroke clinical symptoms
gradually progressed from mild to more severe.
d. Stroke complete (completed stroke), stroke with persistent neurological
deficits and had not grown again and disappeared after 3 weeks or cause
disability.

Based on the location of vascular lesions, stroke can be divided into:2,3

a. carotid system
1. motor : hemiparesis contralateral, dysarthria
2. sensory : hemihipestesi contralateral, paresthesia
3. visual disturbances : hemianopsia contralateral homonymous,
amaurosisfugax
4. Malfunctioning of the sublime: aphasia, agnosia
b. vertebrobasilar system
1. motor : Hemiparesis alternans, dysarthria
2. sensory : hemihipestesi alternans, paresthesia
3. other Disorders : balance disorders, vertigo, diplopia.

15
1.3 Risk Factors Stroke4
Can not be Can be modified
modified
Age Smoke history of stroke
Gender consumption of alcohol Hypertension
genetic The use of narcotics Heart disease
Race hiperhomosisteinemia Diabetes mellitus
Anti-phospholipid antibodies carotid stenosis
hyperuricemia TIA
increased hematocrit hypercholesterolemia
Increased levels of fibrinogen PO contraceptive use
obesity

B. Hemorrhagic Stroke
Rupture of cerebral blood vessels cause bleeding into the brain parenchyma
tissue, cerebrospinal fluid space around the brain, or the keduanya.Perdarahan
causing disruption of nerve fibers of the brain with emphasis on brain structure and
also because of hematoma which causes ischemia of the surrounding tissues.
Increased intracranial pressure will cause herniation of brain tissue and the pressing
rod otak.3
C. Stroke Infarction
2.1 Definition
Infarction Stroke is a stroke caused by a blockage in the blood vessels of the
brain tissue hypoperfusion servikokranial or by various factors such as further
atherothrombotic, embolic or hemodynamic instability symptomatic focal cerebral,
occur suddenly and disappear within 24 hours or lebih.Pada macroscopic level,
stroke infarkbiasanya caused by emboli from the extracranial or intracranial
thrombosis, but can also be caused by reduced cerebral blood flow. At the cellular
level, any process that disrupts blood flow to the brain can trigger an ischemic
cascade, which will result in the death of brain cells and infarction otak.6,7
Stroke infarction occurs when occlusion or narrowing of blood flow to the
brain where the brain needs oxygen and glucose as an energy source to keep its

16
function well. Cerebral blood flow or cerebral Blood Flow (CBF) is maintained at a
constant speed between 50-150 mmHg. Blood flows to the brain is affected by: 6.7
a. The state of the blood vessels
When the narrowing due to stenosis, atheroma, thrombus or embolus of blood
flow to the brain is disrupted.
b. Blood circumstances
Increased blood viscosity, such as polycythemia causes blood flow to the brain
more slowly and anemiaberat which can lead to decreased brain oxygenation.
c. Systemic blood pressure
Cerebral autoregulation is the intrinsic ability of the brain to maintain blood flow
to the brain remains constant despite changes in cerebral perfusion pressure.
d. Abnormalities of the heart
Cardiac abnormalities such as atrial fibrillation, heart block causes decreased
cardiac output. Besides the release of an embolus also cause ischemia in the brain
due to vessel blood lumen.Jika okulsi CBF partially clogged, then the concerned
region directly suffered from a lack oxygen. Ischemic Area. Death area is called
neurons, glia and vascular caused by lack of oxygen and nutrients or disruption
of metabolism.
In ischemia wide, seemed region is not homogeneous due to differences steps
of ischemic, which consists of three layers (area) is different:7
a. The core layer very ischemia (ischemic core) look very pale because it has the
lowest CBF. Looks neuron degeneration, dilation of blood vessels without blood
flow. Lactic acid levels in this area are high with low PO2. This area will undergo
necrosis.
b. Penumbrayang ischemic regions also have a low CBF, but still more
tinggidaripada CBF in the ischemic core. Although not neuron cells to die,
selterhenti function and be functional paralysis. In this area a low PO2, PCO2
tinggidan lactic acid increases. There is damage to neurons in every steps, tissue
edema due to dams and a network of blood vessels to dilate pale. This area can
still be saved by resuscitation and proper management.

17
c. The area around the penumbra looked reddish and edema. Blood vessel
maximum dilated, PCO2 and PO2 high and collateral CBF maximally. In this
area is very high so-called area with perfusiberlebihan (luxury perfusion).
The concept of "ischemic penumbra" is the basis for the treatment of stroke,
because still have a cellular structure of neurons were still alive and reversible if
prompt treatment is done. Restoration program reperfusion penumbra done on time
so that the blood flow back to the area of ischemia not late. The component of this
time is called the therapeutic window (therapeutic window) that is a window of time
reversibility penumbra neurons.

Figure 1. Infarction Stroke8

2.2 Classification

2.2.1 Stroke Embolism Infarction

Nearly 90% of emboli originating from the heart ends up in the brain, and this
is because:6,7
 Blood flow to the brain is derived from the aortic arch that yanglepas
embolism from the left ventricle to be circulated through the bloodstream
kearteri and left common carotid artery brachiochepalic.
 Brain tissue is very sensitive to the obstruction of blood flow, so that the size
of 1 mm embolism can already severe neurological casue disturbance,

18
 embolism sizes same if entrance to another network may be no symptoms at
all.
Intracranial emboli primarily in cerebral hemister, it inidisebabkan because
of the amount of blood through the carotid artery (300ml / min) is much more than
that through the vertebral artery (100ml / min) .In addition it is also caused by the
meandering flow of the arteries subclavian to achieve vertebral system. Embolism
have a predilection for arterial bifurcation branch a.cerebri especially in the media,
the distal portion a.basilaris and a.cerebri
posterior.6,7
Most cerebral artery emboli found in the media because it is a direct
ramification of the internal carotid artery receive 80% of the blood into the carotid
artery embolism interna.Medula spinal rarely affected, but emboli from danaorta
abdomen can cause blockage of blood flow to the spinal cord and cause symptoms
of neurological deficits .Berbeda embolism in atherosclerosis, embolism of the heart
consists of a blood clot (clot) loose binding power of the blood vessel wall or heart,
these emboli can break and move to a more distal blood vessels so that when
performed angiography after 48 hours embolism usually has not looked. The amount
depends on the size of the infarct cardioembolism embolism, arterial blood vessels
are affected, the stability of emboli and collateral circulation.6
 Obstruction / blockage of an artery, usually there are in branching of arteries,
because the lumens are smaller than distal section and siasis tissue blood flow,
so akanmembentuk clot at both distal maupunproksimal stagnation region.
Neurological symptoms can arise immediately dalambeberapa seconds, when
a blood vessel collateral not function directly will soon arise irreversible
changes.
 Irritation will cause local vasospasm. Vasospasme which still can arise in
response to which small embolism, especially in young people which has not
happened atherosclerosis.

2.2.2 stroke infarction Thrombosis

Thrombus is platelet or fibrin clot formation in the blood that can clog veins
or arteries and cause ischemia and tissue necrosis lokal.Trombus it can be detached

19
from the vessel wall and called thromboembolism. Thrombosis and
thromboembolism plays an important role in the pathogenesis of stroke infarction.
Location thrombosis determine the type of interference caused, for example, arterial
thrombosis can lead to myocardial infarction, stroke, and intermittent claudication,
venous meanwhile trombosis can cause lung embolism. Trombosis the result of
changes of one or more major components of hemostasis include coagulation factors,
plasma proteins, stream blood, vascular surface, and cellular constituents, especially
platelets and endothelial cells. Arterial thrombosis is a complication of
atherosclerosis due to the presence of atherosclerotic plaque rupture.7,11
Thrombosis begins with endothelial damage, so it looks tissue of collagen
underneath. The process of thrombosis occurs due to the interaction between platelets
and blood vessel walls, as a result of damage to the vascular endothelium. Normal
vascular endothelium is antithrombotic, this is because the glycoproteins and
proteoglycans lining endothelial cells and their prostacyclin (PGI2) on endothelial
vasodilator nature and inhibition of platelet aggregation. In endothelial damage,
blood will be associated with the collagen fibers of blood vessels, then it will
stimulate platelet and platelet aggregation and stimulate platelets secrete substances
contained in granules in platelets and substances derived from macrophages
containing fat. Due to a receptor on platelets causes platelet adhesion to collagen
vascular tissues other darah.Penyebab thrombosis is polycythemia, sickle cell
anemia, defisiensiprotein C, fibromuscular dysplasia of the cerebral arteries, and
prolong vasoconstriction due to migraine attacks. Any process that causes cerebral
artery dissection can also cause trombous stroke.7,11
Thrombosis in atherosclerosis suspected because of the rupture or visura on
atherosclerotic plaque followed by vasoconstriction. Underlying factors that
allegedly played a role in this incident is the plasma cholesterol levels. Friction factor
in the local blood vessels, exposure of thrombogenic surface and
vasokontriksi.Trombogenesis effects occur at the site of endothelial damage resulting
intrinsic and extrinsic coagulation pathway, which ended with the formation of
thrombus fibrin.Penghancuran need of some enzymes, namely plasminogen
circulating in the blood, in tissue plasminogen activator (tissue-type plasminogen
activator / tPA) and inhibits plasmin. Tissue-type plasminogen activator is resulted

20
by local trauma and neurohumoral factors that lead to the destruction of fibrin to
fibrin degenaration product (FDP). The FDP will inhibit the conversion of fibrinogen
to fibrin. Plasmin jugamenghidrolisis prothrombin, factor V, VIII, and XII. Plasmin
activity is inhibited by anti-plasmin contained in darah.7,11
Thrombotic stroke can be divided into stroke on the large blood vessels
(carotid arterial system) and small vessels (the circle of Willis and the circle
posterior). Points thrombosis is the most frequent cerebral artery branch points,
especially in the area of distribution of interna. With carotid artery stenosis can cause
blood flow turbulence. The energy required to run the neuronal activity is derived
from the metabolism of glucose and is stored in the brain in the form of glucose or
glycogen to supply usage for 1 minute.9,10
When the blood flow stops the brain tissue oxygen and glucose that is
required for the formation of ATP decreases and the decrease of Na + K + ATPase,
thereby potentially decrease. Calium will move to the extracellular, while Na and Ca
will move to intra cell. This causes the cell surface becomes more negative, causing
membrane depolarization. When the initial cell membrane depolarization is still
reversible, but when settling a structural change room cause tissue of brain death.9,10
This occurs immediately when the perfusion decreases below the threshold
tissue death, which is when blood flow is reduced to less than 10 ml / 100 g / min.
As a result of lack of oxygen acidosis which causes malfunctioning of enzymes,
because of the high ion H. acidosis cause cerebral edema is characterized cell
swelling (especially glial cells) and result in an increase microcirculation. Therefore,
vascular resistance and decreased perfusion pressure, causing expansion of ischemic
area.9,10

Figure 2. Differences thrombotic strokes and Stroke Emboli.8

21
2.3 Clinical Stroke Infarction
Neurological symptoms that arise depend on the severity of vascular
disorders and it’s areas.9

Table 1. Comparison of embolic stroke and myocardial infarction trombus

stroke.9

Difference Embolic infarction Stroke Thrombotic stroke infarction

Age Younger age Old age (over 50 years)
The onset of - Sudden exertion - Suddenly at rest, preceded by
neurological - Awareness can be prodromal symptoms.
deficit decreased when a large - Awareness is usually good
embolus
Blood pressure Normal often hypertension
comorbid Heart valve disease, atrial Atherosclerotic heart disease
fibrillation, and others

2.4 Basic infarction Stroke Diagnosis

2.4.1 Score algorithm Gajah Mada
Acute Stroke PatientsThe three or two of the three.1

Impairment of consciousness (+), headache (-), pathological reflexes (-) hemorrhagic

stroke
Impairment of consciousness (-), headache (+), pathological reflexes (-)

Impairment of consciousness (-), headache (-), reflex pathology (+) stroke

infarction
Impairment of consciousness (-), headache (-), reflex pathology (-)

2.4.2 Siriraj Stroke Score (SSS).

C = Consciousness (Awareness)
- Alert 0
- Drowsy and stupor 1
- Semicoma & coma 2
V = vomitting (Vomiting)
- No. 0
- Yes 1
H = Headache within 2 hours (Headache)
- No. 0

22
 - Yes 1
A = atheroma (Diabetic history, angina, claudication)
- No. 0
- One or more 1
DBP = Diastolic Blood Pressure. 1

SSS DIAGNOSE
>1 cerebral haemorhage
<- 1 cerebral infarction
-1 to 1 Uncertained diagnosis, use probability curve and / or CT Scan

2.5 Stroke Management Infarction

1. Anticoagulation.4
a) Urgent anticoagulation with the goal of preventing recurrent stroke, stop
worsening neurologic deficits or improve output after acute ischemic stroke
is not recommended as a treatment for patients with acute ischemic stroke.
b) Urgent anticoagulation is not recommended in patients with moderate to
severe acute stroke due to increases in intracranial bleeding complications.
c) In general administration of heparin, LMWH or heparinoid after acute
ischemic stroke is not beneficial. But some experts still recommend full-
dose heparin in patients with acute ischemic stroke with a high risk of
reembolisasi, arterial dissection or severe stenosis of the carotid artery
before surgery. Contraindication to heparin also include large infarcts>
50%, uncontrolled hypertension and extensive brain microvascular
changes.
2. Giving antiplatelet.4
1. Giving aspirin with an initial dose of 325 mg in 24 to 48 hours after onset
of stroke is recommended for any acute ischemic stroke.
2. Aspirin should not be used as a substitute for acute stroke interventions,
such as intravenous rtPA administration.
3. If the planned administration of thrombolytics, aspirin should not be given.
4. The use of aspirin as adjunctive therapy within 24 hours after
administration of thrombolytic agents is not recommended.
5. Clopidogrel alone or in combination with aspirin in acute ischemic stroke
is not recommended, unless the patient is no specific indications, such as
23
 unstable angina pectoris, non-Q-wave MI, or recent stenting, treatment
should be given up to nine months after the incident.
6. Giving intravenous antiplatelet that inhibit receptor glycoprotein IIb / IIIa
inhibitors is not recommended. The combination of extended-
releasedipyridamol Aspilet + option accepted by the FDA as a secondary
prevention of ischemic stroke compared to only aspilet only.
Warfarin and other oral anticoagulants increase the risk of bleeding, so it is
not recommended.
3. Neuroprotektan.4
The use of drugs neuroprotektan yet to show effective results so far have not
dianjurkan.Namun, citicoline to date provide benefits in stroke akut.Penggunaan
citicoline in acute ischemic stroke with a dose of 2 x 1000 grams intravenously for 3
days followed by 2 x 1000 grams orally for 3 weeks. In addition, oral administration
of plasmin 3 x 500 mg in 66 patients at six major teaching hospital in Indonesia
showed a positive effect on patients with acute stroke in the improvement of the
motor, MRS score, and Barthel index.

24
 THE BASIC OF DIAGNOSE
1. Basic Clinical Diagnose
The history known to the patient felt weakness in the limbs to the right suddenly
while the patient is resting. Complaints are not accompanied by difficulty speaking
(pelo), lips twisted into one sis face, and tongue interested when extended. There is
no loss of consciousness, nausea, vomiting, headache, seizures started the attack.
Have a history of poorly controlled diabetes mellitus. No history of trauma.
Komposmentis awareness of physical examination (GCS 15), hemiparesis dekstra,
and found no disruptions in the cranial nerve examination. This is consistent with the
definition of stroke is cerebral disorders, both focal and global attacks and the sudden
onset of the clinical symptoms lasting 24 hours or more, without the discovery of a
disease other than vascular disorders.
In these patients also found that risk factors for diabetes mellitus who are not
controlled. Based Gadjah Mada Stroke Algorithm patients found no loss of
consciousness, headache, and Babinski reflex, thus summed up as stroke infarction.
Assessment using Siriraj stroke score showed -2 whose interpretation is non-
hemorrhagic stroke / Infarction Stroke.

2. Basic Topic Diagnose

Based on the history and physical examination, obtained dekstra hemiparesis,
and found no abnormality in the cranial nerve examination, so the diagnosis is a topic
in patients carotid system. Disturbances in the carotid system will provide neurologic
deficits that are contralateraland cranial nerve palsies sesisi central type with motor
paralysis of the arms and legs. So based on history and physical examination, motor
and sensory disorders are found on the right side, so that the lesion is estimated in
the left cerebral hemisphere.
3. Basic Etiology Diagnose
Comparison stroke infarction and hemorrhagic stroke in the case, namely:

Symptoms and Signs Stroke Infarction Hemorrhagic Case

Stroke
Symptoms that TIA (+) 50% TIA (-) (-)
precede
Activity / rest Rest Often during Rest
physical activity
25
 Headache and Rarely Very frequent and (+)
vomiting intense
Decreased Rarely Often (-)
consciousness onset
time
Symptoms and Signs Stroke Infarction Hemorrhagic Case
Stroke
Hypertension Medium / Weight, sometimes moderate
normotensive being
hemiparesis Often from scratch Often from scratch When the
initial
attack
speech disorders Often can there (-)
stimulation of No Yes No
meninges

Symptoms ICT / rarely papilledema Papilledema and Funduscop

papilledema bleeding subhialoid
y not be
tested
From the above comparison table of these patients tend to lead to stroke
infarction / non hemorraghic stroke. Therefore, the diagnosis of the etiology of these
patients suffered a stroke infarction / non hemorraghic stroke.

The cause of stroke is a process aterotrombotik infarction or embolism. The

cause of stroke infarction patients can be seen in the following table:

Criteria for Thrombosis Embolism Case

Diagnosis
Age Old age (50-70 Young age Old age (44
years) years)
onset Travel Often at rest It often happens During a
when on the move break
Awareness Usually a good Decreased Good
awareness consciousness when awareness
a large embolus
Risk factors
- Hypertension +/- - -
- Heart disease +/- RHD -
- DM ++ - +
- Hyperlipidemia ++ - -
There should be a
source of emboli
(rhythm disorders /
heart valves)

26
4. Basic Differential Diagnosis
In these patients the diagnosis of appeals is a hemorrhagic stroke. This is
because of the history and physical examination circuit that has been done, there are
direct results that these patients also have a tendency to suffer a hemorrhagic stroke.
Therefore, to get rid of the differential diagnosis, investigations submitted in the form
of gold standard CT scan Head of Non-Contrast.
From the results of a CT scan patients had their picture hypodense lesions that
cover the area of the occipital lobe of the left hemisphere. This then supports that
patients suffering from non-hemorrhagic stroke.
5. Basic and Additional Clinical Laboratory Tests
a. Routine blood tests are performed to detect risk factors that increase the
hematocrit.
b. Examination of blood sugar levels during fasting and 2-hour post-prandial
performed to detect stroke risk factors are diabetes mellitus. And in this case
the patient is suffering from diabetes mellitus who are not controlled since
2014.
c. Liver function and kidney function is done to get rid of the differential
diagnosis of toxic-metabolic disorders.
d. Serum electrolyte levels is done to rule out diagnosis of stroke is
hyponatremia. And in patients found a picture hiponakalemia.
e. AP electrocardiography and chest X-ray done to detect risk factors, namely
the treatment of heart failure and plan.
f. CT scans were performed to confirm the diagnosis, determine the type of
stroke and planning treatment of pathologies of the disease. In patients with
CT-Scan showed a picture of low-density lesion in the occipital lobe of the
left hemisphere infarcts leading to strokes.
6. Basic Final Diagnosis
The final diagnoses are stroke infarction patients. This diagnosis is made based
on history, physical examination and advanced examination. The history is known
that the symptoms experienced by patients is weak right arising limb suddenly while
having breakfast in the morning. Complaints are not accompanied by difficult to talk
(pelo), corners of the mouth are interested and the deviation of the tongue. From the

27
physical examination found composmentis (GCS E4V5M6), the patient's blood
pressure 170/90 mmHg, hemiparese dekstra without cranial nerve disorders, but there
is a neurological deficits in motor and sensory examination.

In follow-up trips, patient diagnosis turned into dextra hemiparese ec Rind +

uncontroled diabetes mellitus type III day care 2. This is because the inspection
findings there is a sign - a sign of improvement in the patient either on the sensory
and motor examination without any disturbance of the cranial nerves. These findings
are also in accordance with the definition of stroke time basis, ie Reversible ischemic
neurologic deficit (Rind), in the form of neurological deficit symptoms disappear in
the time between more than 24 hours up to 3 weeks.

In laboratory tests such as blood glucose tests showed that patients suffering
from hyperglycemia. This is in line with the conditions of the patients who had been
suffering from diabetes mellitus is not controlled since 2014. And as has been
described in the discussion, that diabetes mellitus is one of the causes of stroke
through atherosclerosis mechanism that causes damage to the large blood vessels and
peripheral.

7. Basic Treatment
a. RL 500 mL infusion to maintain the state euvolumik. Given 30 TPM is
based on the patient's fluid needs.
b. Giving citicoline as a neuroprotective agent. Citicoline serves as an
increase in the structural integrity of cell membranes. Citicoline provide
choline and cytidine to produce phospholipids it lowers free radicals in
ischemic conditions.
c. Giving Acetylsalicylic acid (aspirin) or aspillet as antiplatelet aggregation
aims to reduce platelet aggregation, platelet adhesion, thrombus
formation through suppression of thromboxane A2 in platelets.
d. Giving insulin aspart (Novorapid) for the treatment of diabetes mellitus
in these patients is to control the blood sugar levels of patients.
e. Injection of ranitidine for the prevention of the occurrence of stress ulcer
due to the influence of drugs.

28
 REFERENCES

1. Rumantir CU. Gangguan peredaran darah otak. Pekanbaru : SMF Saraf

RSUD Arifin Achmad/FK UNRI. Pekanbaru. 2007.
2. Hinkle, JL. Guanci, MM. Acute ischemic stroke review. J Neurosci Nurs.
2007; 39 (5): 285-293.
3. Maas, MB. Safdieh, JE. Ischemic stroke: pathophysiology and principles of
localization. Neurology Board Review Manual. Neurology. 2009; 13(1): 2-
16.
4. Guideline Stroke Tahun 2011. Pokdi Stroke. Perhimpunan Dokter Spesialis
Saraf Indonesia (PERDOSSI). Jakarta. 2011
5. Kementerian Kesehatan Republik Indonesia. 8 dari 1000 orang Indonesia
terkena stroke. 2011.
6. Misbach J. Stroke aspek diagnostik, patofisiologi, manajemen. Fakultas
Kedokteran Indonesia. Jakarta. 1999.
7. Japardi I. Patofisiologi stroke infark akibat tromboemboli. USU digital
library. Available from :http://repository.usu.ac.id.
8. Wijaya AK. Patofisiologi stroke non-hemoragik akibat trombus. Available
from: http://download.portalgaruda.org/article.php?article.
9. Kanyal N. The science of ischemic stroke: pathophysiology
&pharmacological treatment. International Journal of Pharma Research &
Review. 2015; 4(10):65-84.
10. Harsono. Kapita selekta neurologi. Edisi kedua. Gadjah Mada University
Press. Yogyakarta. 2009. Hlm. 79-100.
11. Mardjono M, Sudharta P. Neurologi klinis dasar. PT. Dian Rakyat. Jakarta.
2015. Hlm. 269-90.
12. Japardi I. Patofisiologi stroke infark aterotrombotik. USU digital library.
Available from :http://repository.usu.ac.id.
13. Carvalho M.V. De, Siqueira L.B., Luiza A., Sousa L., César P. and Veiga B.,
2013, The Influence of Hypertension on Quality of Life, Quality of life of
hypertensiive patients, 100 (2), 164–174.

29