Case Report

HEMORRHAGIC STROKE

Presented by :
Nurul Hasanah Surury
NIM : 1708435974

Supervisor :
dr. Enny Lestari, Sp.S

CLINICAL CLERKSHIP
NEUROLOGY DEPARTEMENT
MEDICAL FACULTY UNIVERSITY OF RIAU
ARIFIN ACHMAD GENERAL HOSPITAL
PEKANBARU
2019
 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. EM
Age 41 years old
Gender Female
Address Kandis
Religion Moeslim
Marital’s Status Married
Occupation Housewife
Date of admission Dec, 18th 2018
Medical Record 01003XXX

II. ANAMNESIS :
Alloanamnesis with patient’s husband (Dec, 19th 2018 on 03.00 PM)
Chief complain
Weakness on left extremities since two days before admission to hospital.
Present illness history
 Patient presented with weakness on left extremities two days before
admission to Arifin Achmad General Hospital. The weakness came in
sudden along with headache, vomit and lips deviation to the right side.
Family took the patient to the Emergency room Prima hospital as soon as
it happened. While in the Emergency room the patient unconscious around
30 minutes. The patient hospitalized for a day and referred to Arifin
Achmad General Hospital as the patient need High Care Unit. The patient

1
 got Mannitol therapy, antipyretic and antihypertensive drugs. There are no
history of seizures or trauma in this patient.

Past illness history

 Uncontrolled Hypertension, diagnosed since 6 years ago
 There is no history of trauma
 There is no history of diabetes mellitus
 There is no history of stroke
 There is no history of heart disease

The family disease history

 There is no history of hypertension in patient’s family
 There is no history of diabetes mellitus
 There is no history of stroke
 There is no history of heart disease

Socioeconomic and habit history

 Patient is a housewife
 Oral contraceptive consumption since 6 years ago until now
 Dietary high salt and fat habit
 There is no history of smoking
 There is no history of alcohol consumption

SUMMARY
Mrs. EM, 41 years old, was admitted to Arifin Achmad General Hospital
with weakness on left extremities since 2 days ago. The complain followed
by headache, vomit and lips deviation to the right side. There is history loss
of conscious, uncontrolled hypertension since 6 years ago and oral
contraceptive consumption since 6 years ago until now.

2
 III. Physical examination
Blood Pressure : 170/100 mmHg
Heart Rate : 88 bpm
Respiratory rate : 20 tpm
Temperature : 37,0°C
Weight : 78 kg Height : 160 cm BMI : 30,4 (Obesity 1)
A. NEUROLOGICAL STATUS (Dec, 19th 2018 on 03.00 pm)
1) Consciousness : Composmentis
GCS : E(4)V(5) M(6)
2) Cognitive Function : Normal
3) Meningeal Sign : Neck stiffness (-)
Brudzinki I, II, III, IV (-)
4) Cranial Nerves
1. Cranial nerve I (Olfactory)
Right Left Interpretation
Sense of Smell + + Normal

2. Cranial nerve II (Optic)

Right Left Interpretation
Visual Acuity >3/60 >3/60
Visual Fields Normal Normal Normal
Colour Recognition + +

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
Extraocular movements (+) (+) Normal

5. Cranial nerve V (Trigeminal)

Right Left Interpretation
Motoric Normal Normal

Normal
Sensory Normal 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 Normal Normal
- Raised eye Normal Normal
brow
Paresis of
- Closed eyes Normal Normal
left N. VII,
- Corners of Upward Flat (When
central type.
the mouth Patient Smile)
- Nasolabial Normal Flatter
fold
Sense of Taste Normal Normal
Chvostek Sign (-) (-)

4
8. Cranial nerve VIII (Acoustic)
Right Left Interpretation
Hearing sense Normal Normal Normal

9. Cranial nerve IX (Glossopharyngeal)

Right Left Interpretation
Pharyngeal Arch Normal Normal
Sense of Taste Normal Normal Normal
Gag Reflex + +

10. Cranial nerve X (Vagus)

Right Left Interpretation
Pharyngeal Arch Normal Normal
Normal
Dysphonia - -

11. Cranial nerve XI (Accessory)

Right Left Interpretation
Motoric Normal Normal
Normal
Trophy Eutrophy Eutrophy

12. Cranial nerve XII (Hypoglossal)

Right Left Interpretation
Motoric Normal Deviation to
left side
Trophy Eutrophy Eutrophy
Paresis of left N. XII,
central type

Tremor - -
Disartria - -

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IV. MOTORIC SYSTEM
Right Left Interpretation
Upper Extremity
Strength
5 1
Distal
5 1
Medial
5 1
Proximal
Normal Normal
Tone
Eutrophy Eutrophy
Trophy
- -
Involuntary movements
- -
Clonus
Lower Extremity Left hemiparesis
Strength 5 3
Distal 5 3
Medial 5 3
Proximal Normal Normal
Tone Eutrophy Eutrophy
Trophy - -
Involuntary movements - -
Clonus
Body
Trophy Eutrophy Eutrophy
Involuntary movements - - Normal

6
V. SENSORY SYSTEM
Right Left Interpretation

Touch Normal Decreased

Hypoesthesia
Pain Normal Decreased
on the left
Temperature NT NT
side of body

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

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

VII. COORDINATION
Right Left Interpretation
Point to point movement Normal Normal
Walk heel to toe
Difficult to
Gait Difficult to Difficult to
Interpretate
Tandem asses asses
Romberg

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VIII. AUTONOM
Urination : Normal
Defecation : Normal
IX. OTHERS EXAMINATION
a. Laseque : Unlimited (>70)
b. Kernig : Unlimited (>130)
c. Patrick : -/-
d. Kontrapatrick : -/-
e. Valsava test : -
f. Brudzinski : -

GADJAH MADA STROKE ALGORITHM

- Loss of consciousness (+), headache (+), pathology reflex (-)
Hemorrhagic stroke.

SIRIRAJ STROKE SCORE (SSS)

- Consciousness(C) : Alert (0)
- Vomitting(V) : Yes (1)
- 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 170/100 mmHg

SSS = 2,5 (0) + 2 (1) + 2 (1) + 0,1 (100) - 3 (0) – 12
=2
Interpretation : > 1 = Hemorrhagic Stroke

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X. EXAMINATION RESUME
Generalized condition
Consciousness : Composmentis cooperatif (GCS : E(4)V(5) M(6) )
Blood Pressure : 170/100 mmHg
Heart Rate : 88 bpm
Respiratory Rate : 20 tpm
Temperature : 37,0°C
Cognitive Function : Normal
Meningeal sign : Neck stiffness (-), Brudzinski I-IV (-)
Cranial Nerves : N.VII: Left paresis (Central type)
N. XII: Left paresis (Central type)
Motoric :Left hemiparesis
Sensory : Hypoesthesia on the left side of the body.
Coordination : Difficult to interpretable
Autonomy : Normal
Reflex : Physiology reflex (+), Pathology (-)
Gajah Mada Score : Hemorrhagic stroke
Siriraj score : Hemorrhagic stroke

XI. WORKING DIAGNOSIS :

CLINICAL DIAGNOSIS : Stroke
TOPICAL DIAGNOSIS : Right Carotid system
ETIOLOGIC DIAGNOSIS : Hemorrhagic stroke
DIFFERENTIAL DIAGNOSIS : Ischemic stroke

ADJUNCT EXAMINATION :
o Blood routine Hb, Ht, leucocyte, platelets
o Blood chemistry Blood glucose, ureum, creatinin, total cholesterol,
HDL, LDL, Trygliseride
o Electrolyte
o Head CT Scan without contrast

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MANAGEMENT :
o General
 Bed rest with head elevation at 300
 Vital sign monitoring
 Intracranial pressure sign monitoring
 Oxygen 2-3 L/minute (Nasal Cannula)
 IVFD Ringer Lactate (30cc/kgBW/day)  20 dpm
 Calories 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 Specific
- Osmotherapy : Manitol 125 cc/6 h IVFD
- Antifibrinolytic : Tranexamic acid 500 mg/8 h IV
- Neuroprotector : Citicolin 500 mg/8 h IV
- Gastric protector : Ranitidin 50 mg/12 h IV

LABORATORY FINDING :
1. Blood Routine (Dec, 19th 2018)
Hemoglobin : 14,4gr/dl
Hematocrit : 43,1 %
Leucocytes : 10.390 /mm3
Platelet : 308.000/uL
2. Blood Chemistry (Nov 19th 2018)

Glucose : 162 mg/dl (<200 mg/dl)

Urea : 28 mg/dl (15 – 41)
Creatinin : 0,90 mg/dl ( 0,55 – 1,30)
AST : 18 U/L (15 – 37)
ALT : 17 U/L (12 – 78)
3. Electrolyte (Dec, 17th 2018)
a. Cl : 109 mmol/L

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4. CT- Scan

- Hyperdens lesion at right basal ganglia

- Interpretation : Intracerebral hemorrhage at right basal ganglia

FINAL DIAGNOSE
- Hemorrhagic stroke caused by intracerebral hemorrhage at right basal
ganglia
- Hypertension Gr II

FOLLOW UP
1. December, 20th 2018
S : Headache, heaviness on left extremities, lips deviation to the right side
(+)
O : GCS E(4)V(5) M(6)
Blood Pressure : 170/110 mmHg

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Heart Rate : 88 bpm
Respiratory Rate : 18 tpm
Temperature : 36,8°C
Cognitive Function : Normal
Neck Stiffness : Negative
Cranial Nerves : Paresis of left N.VII Central type, Paresis of left N.XII
sinistra central type.
Motoric : Left hemiparesis
Motoric strength :
5 2
5 3

Sensory : Hypoesthesia on the left side of the body.

Coordination : NT
Autonom : Urination (Normal), Defecation (Normal)
Reflex : Normal

A : Hemorrhagic stroke + Hypertension grade II

P :
 IVFD RL 20 dpm
 IVFD Manitol 125 cc/6 h
 Tranexamic acid 500 mg/8 h IV
 Citicoline 500 mg/8 h IV
 Ranitidine 50 mg/12 h IV
 Suggested to do physiotherapy

2. December, 21st 2018

S : Headache minimal, heaviness on left extremities, lips deviation to the
right side (+)
O : GCS E(4)V(5) M(6)
Blood Pressure :170/100 mmHg
Heart Rate : 80 bpm, reguler

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 Respiratory Rate : 20 tpm
Temperature : 37,0°C
Cognitive Function : Normal
Neck Stiffness : Negative
Cranial Nerves : Parese of left N.VII Central type, Parese of left
N.XII central type.
Motoric : Left hemiparesis
Motoric strength :
5 2
5 3

Sensory : Hypoesthesia on the left side of the body.

Coordination : NT
Autonom : Urination (Normal), Defecation (Normal)
Reflex : Normal

A : Hemorrhagic stroke + Hypertension grade II

P :
 IVFD RL 20 dpm
 Tranexamic acid 500 mg/8 h IV
 Citicoline 500 mg/8 h IV
 Ranitidine 50 mg/12 h IV

3. December, 22nd 2018

S : Heaviness on left extremities (+), There is no headhache
O : GCS E(4)V(5) M(6)
Blood Pressure :160/90 mmHg
Heart Rate : 84 bpm, reguler
Respiratory Rate : 18 tpm
Temperature : 37,0°C
Cognitive Function : Normal
Neck Stiffness : Negative

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 Cranial Nerves : Parese of left N.VII Central type, Parese of left
N.XII central type.
Motoric : Left hemiparesis
Motoric strength :
5 2
5 4

Sensory : Hypoesthesia on the left side of the body.

Coordination : NT
Autonom : Urination (Normal), Defecation (Normal)
Reflex : Normal

A : Hemorrhagic stroke + Hypertension grade II

P :
 Citicoline tab 500 mg/8 h
 Amlodipine tab 10 mg/24 h

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DISCUSSION

1. Stroke
1.1. Definition
Definition of stroke from World Health Organization is: “rapidly
developing clinical signs of focal (or global) disturbance of cerebral function, with
symptoms lasting 24 hours or longer or leading to death, with no apparent cause
other than of vascular origin”. 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). In
Indonesia 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. Men suffer 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 attack at 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 occurred 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 quality change in the
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
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

15
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 (AVM) .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
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

16
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

17
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. Genetic 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

Clinical manifestation based on localization of the lesion :
- Cerebral cortex: A lesion involving the cerebral cortex causes weakness
of part of the body on the opposite side. Hemiparesis is seen in the face
and hand (brachiofacial weakness) more frequently than elsewhere,
because these parts of the body have a large cortical representation. The
typical clinical finding associated with a lesion in site a predominantly
distal paresis of the upper limb, most serious functional consequence of
which is an impairment of fine motor control. The weakness is incomplete

18
 (paresis rather than plegia), and it is flaccid, rather than spastic, because
the accessory (nonpyramidal) motor pathways are largely spared. An
irritative lesion at site can cause focal (jacksonian) seizures.5
- Basal ganglia: Clinical presentation of the stroke due to the basal ganglia
bleed; 1) change in body movement, 2) cognitive impairement, 3)
unconcioussness, vomiting, headache, 4) personality change.7
- Internal capsule : If the internal capsule is involved (e.g., by hemorrhage
or ischemia), there will be a contralateral spastic hemiplegia—lesions at
this level affect both pyramidal and nonpyramidal fibers, because fibers of
the two types are in close proximity here. The corticonuclear tract is
involved as well, so that a contralateral facial palsy results, perhaps
accompanied by a central hypoglossal nerve palsy. No other cranial nerve
deficits are seen, however, because because the remaining motor cranial
nerve nuclei are bilaterally innervated. The contralateral paresis is flaccid
at first (in the “shock phase”) but becomes spastic within hours or days
because of concomitant damage to nonpyramidal fibers. 5
- Cerebral peduncle : Lesions at the level of the cerebral peduncle such as
a vascular process, a hemorrhage, or a tumor, produce contralateral spastic
hemiparesis, possibly accompanied by an ipsilateral oculomotor nerve
palsy. 5
- Pons : Pontine lesions involving the pyramidal tract (e. g., a tumor,
brainstem ischemia, a hemorrhage) cause contralateral or possibly
bilateral hemiparesis. Typically, not all of the fibers of the pyramidal tract
are involved, because its fibers are spread over a wider cross-sectional area
at the pontine level than elsewhere (e. g., at the level of the internal
capsule). Fibers innervating the facial and hypoglossal nuclei have already
moved to a more dorsal position before reaching this level; thus, an
accompanying central facial or hypoglossal palsy is rare, though there may
be an accompanying ipsilateral trigeminal nerve deficit or abducens palsy.5
- Medula oblongata lesion : A lesion of the medullary pyramid can dam
age the pyramidal tract fibers in isolation, as the nonpyramidal fibers are
further dorsal at this level. Flaccid contralateral hemiparesis is a possible

19
 result. The weakness is less than total (i.e., paresis rather than plegia),
because the remaining descending pathways are preserved. 5
- Spinal cord : Lesions of the pyramidal tract in the spinal cord. A lesion
affecting the pyramidal tract at a cervical level causes ipsilateral spastic
hemiplegia: ipsilateral because the tract has already crossed at a higher
level, and spastic because it contains nonpyramidal as well as pyramida
fibers at this level. A bilateral lesion in the upper cervical spinal cord can
cause quadriparesis or quadriplegia. A lesion affecting the pyramidal tract
in the thoracic spinal cord causes spastic ipsilateral monoplegia of the
lower limb. Bilateral involvement causes paraplegia. 5

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
stroke5,8
Symptom or Infarction Intracerebral haemorrhage
examination

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

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

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

20
 hyperdensity area

Angiography Stricture aneurism, AVM, massa

appearance
intrahemisfer or vasospasme

1. Gajah Mada Stroke Algorhytm8

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)8

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

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

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

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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.2,4,10

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.11

1.6.2 Acute stadium

1. Ischemic stroke
General treatment:
Place the patient’s head in 300 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).11
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.11
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.11

22
 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.11
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.11
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.11
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.11
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.11

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2. Hemorrhagic 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.11
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.11
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.11

1.6.3 Subacute Stadium

Medical measures may include cognitive therapy, behavior, swallowing,
speech therapy, and bladder training (including physical therapy). Given the long

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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.11
Subacute phase treatment:11
- 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 plannin
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
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.

25
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%.3,6,12

THE BASIC OF DIAGNOSIS

1. Basic clinical diagnose

According from anamnesis, a 41 years-old female patient had a sudden
Weakness on left extremities since two days before admission to hospital. The
complain followed by headache, vomit and lips deviation to the left side. There is
history loss of conscious, uncontrolled hypertension since 6 year ago and oral
contraceptive pill since 6 years ago. There are no history of seizure and trauma.
From physical examination, there was hemiparesis on left extremities and paresis
of left VII cranial nerve with central type, and left XII cranial nerve with central
type. It is corresponded with stroke definition from WHO which is characterized
by the rapidly progress of clinical manifestations of cerebral function disorders
either focal or global, with symptom lasting for 24 hours or longer with no
apparent cause other than of vascular disorders. In this patients, are found
uncontroled hypertension which is the main risk factor for stroke.

2. Basic topic diagnose

Carotid system was considered for topical diagnose because lesion from
carotid system will lead to contralateral neurological deficit. This contralateral
neurological deficit caused by decuscation of corticospinal tract in
mesencephalon. In this patients we found left paresis of CN VII central lesion,
left paresis CN XII central lession and left hemiparesis UMN. It suggest that
lesion is upward from nucleus of nervus cranialis and motorneuron. Hemiparese
caused by lesion on the brain. The lesion come from obstruction in cerebral
arteries, in this case; cerebral posterior arteries and coroidal anterior arteries.
In the head CT Scan we can also find intracerebral haemorrage at right basal
ganglia dextra which means there is a breakdown of artery on that region.

26
3. Basic etiological diagnose
Basic etiological diagnose of this patient leads to hemorrhagic stroke,
because on this patient there is sudden weakness of left extremities, headache and
vomit. It also supported by Gajah Mada Algorithm and Siriraj Stroke Score and
the result of CT-Scan that gave the impression of hemorrhagic stroke.

4. Basic differential diagnosis

The consideration of the non hemorrhagic stroke because of it has almost
the same manifestation, like the immediate onset and there is neurological deficit.
This patient also has history of hypertension since 6 years ago which the gold
standard examination for diagnosing the hemorrhagic or non hemorrhagic stroke
is a Head CT Scan.

5. Basic Workup
a. Hematology: to find the risk factor for stroke, to 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.

6. Basic final diagnose

The final diagnose of this patient is hemorrhagic stroke caused by
intracerebral hemorrhage with hypertensive emergency. This diagnose is
considered by anamnesis, general and neurological examination and adjunct
examination. From anamnesis, we found sudden weakness on the left side of
extremities, headache and vomit. Patient also had history of uncontrolled
hypertension since 6 years ago. From physical examination there is hemiparesis
on left extremities and paresis of left VII cranial nerve with central type, and left
XII cranial nerve with central type. From head CT-Scan, it showed the
hemorrhage at right basal ganglia.

27
7. Basic treatment
a. The aim of bed rest is saving energy and lowering metabolism to maintain
the adequate circulation to the brain.
b. The aim of IVFD (30ml/kgBW/day) Ringer Lactate 20 dpm is to
maintain the euvolemic condition
c. The aim of citicoline injection 500 mg/12 h IV is as the neuroprotector.
d. The aim of manitol infusion 125 mg/6 hours is to maintain intra cranial
pressure.
e. The aim of tranexamid acid 500 mg/8 h IV is to prevent the bleeding
getting worse.
f. The aim of ranitidien 50 mg/12 hours is to prevent stress ulcer in patient
stomach.

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