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Case Report

HEMORRHAGIC STROKE

By :
Wilda Arfiana
NIM : 1608437610

Supervisor :
dr. Riki Sukiandra, Sp.S

MEDICAL CLERKSHIP
NEUROLOGY DEPARTEMENT
FACULTY OF MEDICINE RIAU UNIVERSITY
ARIFIN ACHMAD GENERAL HOSPITAL
PEKANBARU
2018
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. S
Age 57 years old
Gender Female
Address Kuantan Singingi
Religion Moeslim
Marital’s Status Married
Occupation Housewife
Entry Hospital Jul, 30th 2018
Medical Record 9926XX

II. ANAMNESIS :
Alloanamnesis with patient’s son (Jul, 31th2018 on 15.00 PM)
Chief complain
Muscle weakness on the right side of her body.
Present illness history
 Patient presented with muscle weakness on the right side of her body when
she was waking up since 6 days before admitted to Arifin Achmad’s General
Hospital. The weakness equally intense in both upper and lower limbs. Few
hours after present the muscle weakness, patient directly bring by her family
to AB Hospital and treated for 5 days. Apart from that, the patient also
complained of speech difficulties and headache. The patient did not present
any other complaint, including nause, vomits, loss of consciousness or
seizures.

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Past illness history
 Uncontrolled Hypertension, diagnosed 10 years ago
 History of seizure (+) 4 years ago
 History of diabetes mellitus (-)
 History of stroke (-)
 History of heart disease (-)

The family disease history


 There is history of hypertension from patient’s mother
 There is no history of diabetes mellitus
 There is no history of stroke
 There is no history of heart disease

Socioeconomic history
 History of smoking (-)
 History of alcohol consumption (-)
 Dietary habit is regular

Occupation
Housewife

SUMMARY
Patient Mrs. S, 59 years old, was admitted to Arifin Achmad’s General
Hospital with her main complaint being muscle weakness in the right side of
her whole body since 5 days ago, speech difficulties and headache were
present. No history of seizure and loss of consciousness. There is history of
uncontrolled hypertension since 10 years ago and seizure since 4 years ago.

III. Physical examination


A. Generalized condition (Jul,31th2018 on 15.00 pm)
Blood Pressure : 180/100 mmHg
Heart Rate : 88 bpm

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Respiratory rate : 20 cpm
Temperature : 37,0°C
Weight : 50 kg Height : 151 cm BMI : 21,9 (Normoweight)

B. NEUROLOGICAL STATUS
1) Consciousness : Composmentis non cooperative
GCS : E(4)V(afasia)M(6)
2) Cognitive Function : Difficult to assess
3) Meningeal Sign : Neck stiffnes (-)
Brudzinki I, II (-)
4) Cranial Nerves
1. Cranial nerve I (Olfactory)
Right Left Interpretation
Non-
Sense of Smell NT NT
Interpretable

2. Cranial nerve II (Optic)


Right Left Interpretation
Visual Acuity NT NT
Non-
Visual Fields NT NT
Interpretable
Colour Recognition NT NT

3. Cranial nerve III (Oculomotor)


Right Left Interpretation
Ptosis (-) (-)
Pupil
Shape Isochoric Isochoric
Size Φ3mm Φ3mm
Normal
Pupillary reactions to light
Direct (+) (+)
Indirect (+) (+)

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4. Cranial nerve IV (Trochlear)
Right Left Interpretation
Doll eyes movement
Extraocular movements (+) (+)
(+)

5. Cranial nerve V (Trigeminal)


Right Left Interpretation
Motor NT NT
Sensory NT NT Normal
Corneal reflex (+) (+)

6. Cranial nerve VI (Abducens)


Right Left Interpretation
Eyes movement (+) (+)
Strabismus (-) (-) Normal
Deviation (-) (-)

7. Cranial nerve VII (Facial)


Right Left Interpretation
Tic (-) (-)
Motor:
- Frowning NT NT
Paresis of the
- Raised eye NT NT
right inferior
brow
side of the
- Closed eyes Normal Normal
face –
- Corners of Flatter Normal
Central
the mouth
lesion of the
- Nasolabial Flatter Normal
left VII
fold
nerve
Sense of Taste NT NT
Chvostek Sign (-) (-)

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8. Cranial nerve VIII (Acoustic)
Right Left Interpretation
Hearing sense Normal Normal Normal

9. Cranial nerve IX (Glossopharyngeal)


Right Left Interpretation
Pharyngeal Arch NT NT
Non-
Sense of Taste NT NT
interpretable
Gag Reflex + +

10. Cranial nerve X (Vagus)


Right Left Interpretation
Pharyngeal Arch NT NT
Non- interpretable
Dysphonia - -

11. Cranial nerve XI (Accessory)


Right Left Interpretation
Motoric Normal Normal
Non- interpretable
Trophy Eutrophy Eutrophy

12. Cranial nerve XII (Hypoglossal)


Right Left Interpretation
Motoric Paresis NT
Trophy Eutrophy Eutrophy Paresis of N. XII
Tremor - - dextra, central lesion
Disartria + +

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IV. MOTOR SYSTEM
Right Left Interpretation
Upper Extremity
Strength
Distal 1 5
Proximal 1 5
Tone Normal Normal
Trophy Eutrophy Eutrophy
Involuntary movements - - Hemiparesis of the
right upper and lower
Clonus - - extremities – central
Lower Extremity lesion of the motor
pathway (Upper
Strength Motor Neuron)
Distal 1 5
Proximal 1 5
Tone Normal Normal
Trophy Eutrophy Eutrophy
Involuntary movements - -
Clonus - -
Body
Trophy Eutrophy Eutrophy
Involuntary movements - - Normal
Abdominal Reflex + +

V. SENSORY SYSTEM
Right Left Interpretation
Touch Normal Normal
Pain NT NT
Non-
Temperature NT NT
interpretable
Propioseptive NT NT

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VI. REFLEX
Right Left Interpretation
Physiologic
Biceps (+) (+)
Triceps (+) (+) Physiologic reflex (+)
Knee (+) (+)
Ankle (+) (+)

Pathologic
Babinsky (-) (-)
Chaddock (-) (-) Pathological reflex(-)
HoffmanTromer (-) (-)
Openheim (-) (-)
Schaefer (-) (-)

VII. COORDINATION
Right Left Interpretation
Point to point movement NT NT
Walk heel to toe NT NT
Gait NT NT Non-Interpretable
Tandem NT NT
Romberg NT NT

VIII. AUTONOM
Urination : Urine catheterized (+)
Defecation : No defecate

IX. OTHERS EXAMINATION


a. Laseque : Not limited (>70)
b. Kernig : Not limited (>130)
c. Patrick : -/-

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d. Kontrapatrick : -/-
e. Valsava test : NT
f. Brudzinski : -

GADJAH MADA STROKE ALGORITHM


Loss of consciousness (-), headache (+), pathology reflex (-) Hemorrhagic
stroke.
SIRIRAJ STROKE SCORE (SSS)

Consciousness(C) : Alert (0)


Vomitting(V) : No (0)
Headache within 2 hours(H) : Yes (1)
Diastolic blood pressure(DBP) : 100 mmHg (100)
Atheroma (A) : No (0)

SSS = 2.5 C + 2 V + 2 H + 0.1 DBP – 3A – 12

Blood pressure at emergency room 130/80mmHg


SSS = 2,5 (0) + 2 (0) + 2 (1) + 0,1 (100) - 3 (0) – 12
=0
Interpretation : -1until 1= Confuse  Suggested to CT- Scan

X. EXAMINATION RESUME
Generalized condition
Consciousness : Composmentis non cooperative (E(4)V(afasia)M(5))
Blood Pressure :180/100 mmHg
Heart Rate : 88 bpm
Respiratory Rate : 20 bpm
Temperature : 37,0°C
Cognitive Function : Difficult to assess
Meningeal sign : Neck stiffness (-), Brudzinski I-IV (-)

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Cranial Nerves : N. VII – Right inferior paresis (UMN lesion)
N. XII – Right paresis (UMN lesion)
Motoric :Right hemiparesis, Central lesion of Upper Motor Neuron
Sensory : Non - interpretable
Coordination : Non - interpretable
Autonomy : Urine catheterized
Reflex : Physiology (+), Pathology (-)
Gajah Mada Score : Hemorrhagic stroke
Siriraj score : Confuse

XI. WORKING DIAGNOSIS :


CLINIC DIAGNOSIS : Stroke
TOPIC DIAGNOSIS : Left Carotid system
ETIOLOGIC DIAGNOSIS : Hemorrhagic stroke
DIFFERENTIAL DIAGNOSIS: Stroke infarction, Stroke trombus

SUGGESTION EXAMINATION :
o Blood routine Hb, Ht, leucocyte, platelets
o Blood chemistryBlood glucose, ureum, creatinin, SGOT, SGPT, total
cholesterol, HDL, LDL, Trygliseride
o Electrolyte
o Coagulation studies ( PT, aPTT, INR )
o Head CT Scan without contrast
o Chest X-Ray AP
o ECG
MANAGEMENT :
o General
 Bed rest with head elevation at 300
 Vital signs’ monitoring
 Intracranial pressure signs’ monitoring
 Oxygen FiO2 21% 2-3 L/minute (Nasal Cannula)
 IVFD Ringer Lactate (30cc/kgBW/day)  20 dpm

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 Calorie needs 25-30 kkal/kgBW/day: Carbohydrate 30-40% of total
calories, fat 20-35% of total calories, protein 20-30% of total calories
 Consult the patient to physical medicine and rehabilitation (PM&R)

o Special
- Anti-edema : Manitol 125 cc/8 h
- Antifibrinolytic : Tranexamic acid 3x500 mg iv
- Neuroprotector : Citicolin 3x500 mg iv
- Gastric protector : Ranitidin 2x50 mg iv

LABORATORIUM FINDING :
1. Blood Routine (Jul, 31th 2018)
Hemoglobin : 12,8 gr/dl
Hematocrit : 38 %
Leucocytes : 8.630 /mm3
Platelets : 192.000/mm3
2. Blood Chemistry (Jul, 31th 2018)

Glucose : 140 mg/dl (<200 mg/dl)

Urea : 28 mg/dl (15 – 41)

Creatinin : 0.69 mg/dl ( 0,55 – 1,30)

SGOT : 16 U/L (15 – 37)

SGPT : 16 U/L (12 – 78)

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3. Thorax X- Ray

Interpretation:
- Cardio : Normal, CTR <50%
- Pulmo : Infiltrat in both of lungs

4. CT SCAN

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Interpretation :
Hyper dens lesion filling right lateral ventricle, III and IVIntravesicular
hemorrhage right lateral ventricle, III and IV
Intracerebral hemorrhage at region frontal dextra

FINAL DIAGNOSE
- Hemorrhagic stroke
- Intraventricullar hemorrhage

FOLLOW UP
1. August, 1st 2018
S : right extremities felt heavy, speech difficulties
O : GCS E4M6Vafasia motorik
Blood Pressure :160/90 mmHg
Heart Rate : 84 bpm, reguler
Respiratory Rate : 20 tpm
Temperature : 37,5°C
Cognitive Function : NT
Neck Stiffness : Negative
Cranial Nerves : parese CN VII central dextra, parese CN XII
dextra
Motoric : Hemiparese dekstra
Motoric strength :
1 5
1 5

Sensory : NT
Coordination : NT
Autonomy : Normal
Reflex : Normal

A : Haemorrhagic stroke

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P :
 IVFD RL 20 dpm
 Manitol 125 cc/12 h
 Tranexamic acid 3 x 500 mg iv
 Citicoline 3 x 500 mg iv
 Ranitidine 2 x 50 mg iv
 Suggested to do physiotherapy
 Suggested to consult with nutritionist

2. August, 2nd 2018


S : right extremities felt heavy, speech difficulties
O : GCS E4M6Vafasia motorik
Blood Pressure :160/80 mmHg
Heart Rate : 80 bpm
Respiratory Rate : 20 tpm
Temperature : 36,8°C
Cognitive Function : NT
Neck Stiffness : Negative
Cranial Nerves : parese CN VII central dextra, parese CN XII
central dextra
Motoric : Hemiparese dekstra
Motoric strength :
1 5
1 5

Sensory : NT
Coordination : NT
Autonomy : Normal
Reflex : Normal

A : Haemorrhagic stroke

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P :
 IVFD RL 20 dpm
 Manitol 125 cc/12 h
 Tranexamic acid 3 x 500 mg iv
 Citicoline 3 x 500 mg iv
 Ranitidine 2 x 50 mg iv

3. August, 3nd 2018


S : right extremities felt heavy, speech difficulties
O : GCS E4M6Vafasia motorik
Blood Pressure :150/70 mmHg
Heart Rate : 84 bpm
Respiratory Rate : 20 tpm
Temperature : 36,8°C
Cognitive Function : NT
Neck Stiffness : Negative
Cranial Nerves : parese CN VII central dextra, parese CN XII
central dextra
Motoric : Hemiparese dekstra
Motoric strength :
3 5
3 5

Sensory : NT
Coordination : NT
Autonomy : Normal
Reflex : Normal

A : Haemorrhagic stroke

P :

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 IVFD RL 20 dpm
 Manitol 125 cc/12 h
 Tranexamic acid 3 x 500 mg iv
 Citicoline 3 x 500 mg iv
 Ranitidine 2 x 50 mg iv

4. August, 4nd 2018


S : right extremities felt heavy, speech difficulties
O : GCS E4M6Vafasia motorik
Blood Pressure :150/80 mmHg
Heart Rate : 90 bpm
Respiratory Rate : 20 tpm
Temperature : 36,8°C
Cognitive Function : NT
Neck Stiffness : Negative
Cranial Nerves : parese CN VII central dextra, parese CN XII
central dextra
Motoric : Hemiparese dekstra
Motoric strength :
3 5
3 5

Sensory : NT
Coordination : NT
Autonomy : Normal
Reflex : Normal

A : Haemorrhagic stroke

P :
 IVFD RL 20 dpm
 Manitol 125 cc/12 h

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 Tranexamic acid 3 x 500 mg iv
 Citicoline 3 x 500 mg iv
 Ranitidine 2 x 50 mg iv

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DISCUSSION

1. Stroke
1.1. Definition
Stroke is a collection of symptoms characterized by the development of
clinical manifestations of cerebral function disorders either focal or global (for the
patient in a coma), which happens quickly and more than 24 hours or ended up
with death without being discovered other causes than vascular disorders. This
definition includes stroke due to cerebral infarction (ischemic stroke), non
traumatic intracerebral hemorrhage, intraventricular hemorrhage and some cases
of subarachnoid hemorrhage.1

1.2. Epidemiology
The increasing age of life expectancy will tend to increase the risk of
vascular disease (coronary heart disease, stroke and peripheral artery disease).
Data in Indonesia showed the tendency of an increase in stroke cases both in
terms of mortality, incidence, and disability. The mortality rate based on age is:
15.9% (age 45-55 years) and 26.8% (age 55-64 years) and 23.5% (age 65 years).
The incidence of stroke amounted to 51.6 / 100,000 population. Sufferers are men
more than women and age profile under 45 years of 11.8%, 54.2% aged 45-64
years, and age over 65 years amounted to 33.5%. Stroke attacking reproductive
age and the elderly that could potentially give rise to new problems in health
development nationally at a later date.2

1.3 Etiology and classification


Stroke can occur because of some pathological circumstance, such as
emboli, thrombus, ruptur of blood vessels, change in the blood vessels
permeability, increasing the viscocity, or because there is a change in the quality
of blood flow to the brain blood vessels. That pathological condition assosiated
with stroke classification. Stroke is classified into two types of major categories,
non hemorrhagic stroke and hemorrhagic stroke. Non hemorrhagic stroke more

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commonly known as ischemic stroke, which is a common occurrence of all types
of stroke. From the overall incidence of stroke, 80% to 85% is the incidence of
ischemic stroke. Ischemic cerebrovascular disease is basically due to the
occlusion of blood vessels of the brain that cause the cessation of the oxygen and
glucose supply. This stroke is categorized into two groups, namely thrombus
occlusion and embolic occlusion.3,4,5
Hemorrhagic stroke occurs due to intracranial hemorrhage. The incidence
reaches 15% to 20% of the overall incidence of stroke. Most hemorrhage occurs
due to hypertensive. However, other causes may occur such as saccular aneurysm
(Berry) or arteriovenous malformations (MAV) .4,5 The major classifications of
stroke are listed in Table 1.
Table 1. Major classification of stroke5
Ischemia-infarct cerebrum (80-85%) Intracranial hemorrhage (15-20%)

Thrombus occlusion Intraserebrum hemorrhage


Lakunar Subaraknoid hemorrhage
Embolic occlusion Intraventrikuler hemorrhage
Kardiogenik
Arteri to arteri

1. Ischemic stroke
Ischemic stroke can occur with or without infarct. It is the most common
stroke. Stroke is caused by obstruction in one or more arteries located in the
cerebrum, which led to the cessation of the supply of oxygen and glucose.4,5 The
obstruction that occur can be a clot (thrombus) that are present in the brain blood
vessels as wll as inherited from the distal organ blood vessels (embolism) which
causes blockage in the brain vascularization. The most common cause of
thrombosis in the form of atherosclerosis that is cause stenosis or narrowing of the
blood vessels. While the most common of embolic stroke is an embolus coming
from large blood vessels or heart.5
The brain gets blood from the heart, blood containing oxygen and
nutrients to the brain. The amount of blood flow to the brain in normal

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circumstances usually about 50-60 ml / 100 g of brain tissue / min, mean the brain
needs 20% of the blood pumped from the heart. If the clogged arteries, brain cells
(neurons) can not generate enough energy and the brain stops working.7,8 When
the blood flow to the brain stops within 6 seconds will occur neuron metabolic
disorders, if more than 30 seconds EEG picture will be horizontally, within 2
minutes there will be termination of brain activity, within 5 minutes began to
brain damage and more than 9 minutes, humans will die. Ischemic brain occurs
when blood flow to the brain is reduced to 25-30 ml/100 grams of brain tissue
perminutes.1

2. Hemorrhagic stroke
Hemorrhagic stroke is a stroke that occurs due to intracerebral
hemorrhage. This can happen if intraserebrum vascular lesions rupture, causing
bleeding in the subarachnoid space and in brain tissue. Cerebral hemorrhage can
cause rapid neurological manifestations in the brain due to the presence of the
pressure on the nerve structure in the brain. If bleeding occurs slowly, most likely
symptoms is a severe headache.5 Some of the etiology that can cause
intraserebrum hemorrhage showed in Table 2 :
Table 2. Intracerebrum hemorrhages etiology2
Some intracerebrum hemorrhages etiology

Hypertensif intracerebrum hemorrhage


Subarakhnoid hemorrhage
Ruptura of the aneurisma sakular (Berry)
Ruptura of the malformasi arteriovena (MAV)
Trauma
Cocain and amfetamin abuse
Brain tumor
Hemorrage infarct
Systemic bleeding diseases including anticoagulant therapy

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1.4 Risk factors
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).3,6
Table 3. Stroke risk factors3,6
Not Modifable Modifable

1. Age 1. Stroke history 10. Smoking


2. Gender 2. Hypertension 11. Alcohol
3. Genetik 3. Heart disease 12. Drug abuse
4. Ras 4. Diabetes melitus 13. Hyperhomosisteinemia
5. Carotic stenosis 14. Antibody anti fosfolipid
6. TIA 15. Hyperurisemia
7. Hypercholesterolemia 16. Elevation of hematocrit
8. Oral contraception 17. Elevation of fibrinogen
9. Obesity

1.5 Clinical manifestation


The differences in clinical manifestation between infarction stroke and
hemorrhage stroke showed in Table 4.
Tabel 4. Difference of clinical manifestation between infarction and haemorrhage
stroke5,7
Symptom or Infarction Intracerebral haemorrhage
examination

Prodormal sign TIA (+) 50% TIA (-)

Doing activity/resting Rest, right after Often while doing physical

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wake activity
Up

Headache and vomit Rarely Often or severe

Lost of consciousness at Rarely Often


Onset

Hypertension moderate/ Moderate-severe


normotension

Meningeal sign No Yes

High intracranial pressure Rarely Subhialiod bleeding


symptom

Bloody LCS No Yes

Head CT Scan Hypodensity area Intracranial mass with


hyperdensity area

Angiography Stricture aneurism, AVM, massa


appearance
intrahemisfer or vasospasme

1. Gajah Mada Stroke Algorhytm7


Acute stroke 1. Lost of consciousness
2. Headache
3. Pathology reflex

All criteria or two of the three


Lost of consciousness (+),headache (-), pathology reflex (-) hemorrhagic stroke
Lost of consciousness (-),headache(+),pathology reflex (-) hemorrhagic stroke
Lost of consciousness (-), headache(-),pathology reflex (+) infarction
Lost of consciousness (-), headache (-),pathology reflex (-) infarction

2. Siriraj Stroke Score (SSS)7

SSS = 2.5 C + 2 V + 2 H + 0.1 DBP - 3A – 12

C = Consciousness (composmentis = 0, somnolen = 1, sopor/koma = 2)

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V = Vomit (none = 0, yes = 1)
H = Headache (none = 0, yes = 1)
DBP = Diastolic blood pressure
A = Ateroma (none = 0, one or more: DM, Angina, vaskular disease = 1)

SSS DIAGNOSE
>1 Hemorrhagic stroke

<-1 Infarction stroke

-1 to 1 Uncertain

1.6 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.2,4,9

1.6.1 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.10

1.6.2 Acute stadium


1. Ischemic stroke
General treatment:
Place the patient’s head in 300positions, 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

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antipyretic, then look for the cause, when the bladder is full, emptied (preferably
with intermittent catheters).10
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.10
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.10
Headache, nausea, and vomiting treated according to the symptoms.
Blood preassure doesn’t 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 kalsium.10
If hypotension occurs, the systolic pressure ≤ 90 mmHg, diastolic ≤70
mmHg, 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.10
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.10
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

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performed (<320 mmol), alternatively can be administered hypertonic solutions
(NaCl 3%) or furosemid.10
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.10

2. Hemorrhage stroke
General treatment:
Patients with hemorrhagic stroke should be treated in the ICU if the
hematoma volume> 30 mL, intraventricular hemorrhage with hydrocephalus, and
clinical situation tends to be worsen. Blood pressure should be reduced until
premorbid blood pressure or 15-20% when the systolic pressure> 180 mmHg,
diastolic> 120 mmHg, MAP> 130 mmHg, and hematoma volume increases.
When there is heart failure, blood pressure should be reduced immediately with
10 mg iv labetalol (administration within 2 minutes) to 20 mg (administration
within 10 minutes) maximum dosage is 300 mg, enalapril iv 0,625-1.25 mg per 6
hours, captopril given three times of 6.25 to 25 mg orally. If there are signs of
increased the intracranial pressure, head position elevated 300, the position of the
head and chest in one area, mannitol (see treatment of ischemic stroke), and
hyperventilation (pCO220-35 mmHg). General management same with ischemic
stroke, stomach ulcers resolved with parenteral H2 antagonists, sucralfate, or
proton pump inhibitors; airway complications prevented with physiotherapy and
treated with broad spectrum antibiotics.10
Special treatment:
Neuroprotective drug can be administered except vasodilator. The
surgery considering with age and location of the bleeding is in patients whose
condition worsened with hemorrhage cerebellar diameter >3 cm, acute
hydrocephalus due to intraventricular hemorrhage or cerebellum, conducted VP-
shunting and hemorrhage lobar> 60 mL with signs of increased the intracranial
pressure and acute threat herniation.10

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At subarachnoid hemorrhage, calcium antagonists (nifedipin) can be used
or surgery (ligation, embolization, extirpation, or gamma knife) if the cause is an
aneurysm or arteriovenous malformation.10

1.6.3 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.10
Subacute phase treatment:10
- 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 pevention
- Family education and discharge planning

1.7 Complication
Some complications can occure and need to be monitored.
a. Neurological complication:4
- Cerebral edema
- Hemorrhagic transformation
- Seizures
- Recurrent stroke
b. Non neurological complication:4
- Increased the blood pressure
- Hiperglikemia
- Cardio-respiratory disorder
- Stress ulcer
- Depression
- Decubitus ulcer, etc

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1.8 Prognosis
Stroke can cause a variety of morbidity, mortality, and recurrence in the
future. Deaths due to stroke was 41.4% from 100,000 population. A third of
patients who have had a stroke, 5-14% will suffer recurrent stroke within a span
of five years.Statistical stroke data by the Stroke Association UK shows that 42%
disability caused by stroke is permanent. In 2010, stroke accounted for 7% of all
causes of mortality in men and 10% of all causes of death among women.
Recurrence of stroke increases with the time. The possibility of recurrent stroke
within five years was 26.4% and in ten years was 39.2%.3,6,11

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THE BASIC OF DIAGNOSIS

1. Basic Clinical Diagnose


According to anamnesis, a 57 year-2-months-old female patient had a
sudden muscle weakness on rhe right side of her body when she was waking
up since 6 days before admitted to Arifin Achmad’s General Hospital. The
weakness equally intense in both upper and lower limbs. The patient also
complained of speech difficulties and headache. No history of nausea,
vomits, loss of consciousness. She had history of seizure 4 years ago and
uncontrolled hypertension since 10 years ago. From physical examination
we’re found paresis of Cranial nerve VII Central dextra, paresis of Cranial
nerve XII Central dextra and hemiparesis on both right extremities. It
consistent with the WHO definition that clinical symptoms of stroke is
cerebral disorders, either focal or global attack in 24 hours.

2. Basic topic Diagnose


Carotid system had been considered in this patient because there are right
central CN VII and XII paresis and hemiparese dextra. Hemiparese caused by
lesion on the brain. The lesion come from obstruction in cerebral arteries, in this
case; sinistra cerebral media artery. From the physical examination there is right
hemiparese, so the lesion is on the left hemisphere because a lesion in one side of
carotid system will lead to contralateral neurological deficit.
In the head CT Scan we can also find intraventricular hemorrhage which
means there is a breakdown of artery in the ventricle. Choroid artery branch of
internal carotid artery has greater contribution in supplying blood to the ventricle.

3. Basic etiological diagnose


Basic etiological diagnose of this patient is leads to hemorrhagic stroke,
because on this patient there is sudden weakness of right extremities and
headache. It is also supported by Gajah Mada Algorithm that give the impression
of the hemorrhagic stroke.

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4. Basic differential diagnosis
The gold standard examination for diagnosing the hemorrhagic or non
hemorrhagic stroke is CT Scan. The consideration of the non hemorrhagic
stroke because of it almost has the same manifestation, like the immediate
onset, the patient was not in severe activity and there is neuroogical deficit.

5. Basic Workup
a. Hematology : to find the risk factor for stroke, exclude other cause of
symptoms, assess condition of patient, and consideration therapy.
b. Head CT-scan : to know the final pathology diagnose from the location
and the wide of the lesion.
c. ECG and chest x-ray : to find the heart abnormality which is the risk
factor of the stroke attack

6. Basic final diagnose


The final diagnose of this patient is hemorrhagic stroke with
intraventricular hemorrhage. This diagnosed is considered by anamnesis, physical
examination and workup examination. From anamnesis we found sudden
weakness of the right extremity that occured when she wake up, speech
difficulties and headache. No history of vomits, seizure, trauma or loss of
conciousness. From physical examination we’re found paresis of Cranial nerve
VII and cranial nerve XII central dextra and hemiparesis on both right extremities.
From head CT-Scan we can see there is intraventricular hemorrhage and
intracerebral hemorrhage.

7. Basic treatment
a. The aim of bed rest is saving energy and lowering metabolisme to
maintain the adequate circulation to the brain.
a. The aim of IVFD (30ml/kgBW/day) Ringer Lactate 20 dpm is to
maintain the euvolemic condition
b. The aim of injection citicoline 3x500 mg iv is as the neuroprotector.

28
c. The aim of manitol infusion125 mg/8 hours is to maintain intra cranial
pressure.
d. The aim of tranexamid acid 3x100mg/ml iv is to prevent the bleeding.
e. The aim of ranitidine injection 50 mg/12 hours is to prevent peptic ulcer.

29
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1. Warlow C, van Gijn J, Dennis M, Wardlaw J, Bamford J, Hankey G. Stroke


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

2. Guideline Stroke Tahun 2011. Pokdi Stroke. Perhimpunan Dokter Spesialis


Saraf Indonesia (PERDOSSI). Jakarta. 2011.

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

4. Martono H, Kuswardani RAT. Buku Ajar Ilmu Penyakit Dalam: Stroke dan
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Alwi I, Sidrabimata M, Setiati S, editor. Jakarta: InternaPublishing; 2009.
BAB 138, Stroke dan Penatalaksanaannya oleh Internis; hal.892-897.

5. Price SA, Wilson LM. Patofisiologi: Konsep Klinis Proses-Proses Penyakit.


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6. Stroke Association. Stroke Statistics. London. 2013.

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


RSUD Arifin Achmad/FK UNRI. Pekanbaru. 2007.

8. deGroot J. Neuroanatomi Korelatif. Edisi ke-21. Jakarta: EGC. 1997.

9. World Health Organization. WHO Step Stroke Manual: The WHO STEPwise
Approach to Stroke Surveillance. 2011.

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10. Setyopranoto I. Stroke: Gejala dan Penatalaksanaan. CDK 185/Vol.38
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11. Hoyert DL, Xu J: NVSS. Deaths: Preliminary Data for 2011. National Vital
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12. James PA, Oparil S, Carter BL, Cushman WC, Dennison C, Handler J, dkk.
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Committee (JNC 8). JAMA. 2014.

13. Benardini GL, Yavagar DL. Management of Ischemic stroke: currentconcepts


and treatment options. Hospital Physician. 2006. p. 13-23

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