Case Report

hemorrhagic stroke

Presented by:
Puja Iklima
NIM: 1708436413

supervisor:
dr. Yossi Maryanti, M.Biomed, Sp.S

CLINICAL clerkships
Neurology DEPARTMENT
FACULTY OF MEDICINE RIAU RIAU UNIVERSITYOF
Arifin Achmad GENERAL HOSPITAL
PEKANBARU
2019
 MINISTRY OF RESEARCH, TECHNOLOGY AND HIGHER
EDUCATION
RIAU UNIVERSITY
MEDICAL SCHOOL
THE NERVE
Secretariat: Classroom Building 03, Floor 04 Arifin Achmad
Jl. Mustika, Tel. 0761-7894000, Email:saraffkur@gmail.com

PATIENT STATUS

name koass Puja Iklima

NIM 1708436413

preceptor dr. Yossi Maryanti, M.Biomed, Sp.S

I. PATIENT IDENTITY

Name Ny. S

Age 53 years

Gender woman

Address Jl. Sudirman, gg Orchid

Religion Islam

Marital status marry

Work House wife

Date of admission 30 juni 2019

Medical records 9054xx

II. History •

1
Main complaint
Weak limbs since 1 day left SMRs

History of present illness

He was admitted with a chief complaint weak limbs since 1 day left SMRs.
Weakness is felt suddenly when the patient is an invitation. In addition the patients
also say severe headache that the patient almost fainted. Patients also experienced
vomiting> 5 times. Then the patient's family to bring the patient to the hospital in
the course of the patient's Syafira like gibberish and do not want to open my eyes
because her head hurt. RS syafira obtained until the patient's blood pressure
230/100, and doctors suggested a CT scan in Syafira suspected brain haemorrhage.
Ct scan after the results came out, the doctor said the patient had ruptured blood
vessels in the brain and needs to be treated at the Hospital HCU but it was full so
patients referred to Arifin Achmad.

Past medical history

o History of hypertension (+) but the patient claimed to regularly take medication
o A history of heart disease (-)
o History of DM (+) but the patient claimed to regularly take medication
o History of stroke (+) 2017 in the limbs left

Family history of disease

o A history of similar complaints in the family (-)
o Family history of stroke (-)

History habit
o A history of consumption of salty foods, fatty foods, smoking, alcohol (-)
o Sports history (-)

resume anamnesis

2
Patient S, aged 53 years attending with a weak limb since 1 day left SMRs. In
addition the patients also experienced vomiting and headache. Patients had a history
of hypertension and diabetes mellitus.

EXAMINATION
A. general state
Blood pressure : 222/100 mmHg
Pulse : right : 88 x / min, regular
left : 88x / minute, regular
Heart : HR : 88 x / minute, regular rhythm
lung : respiration : 22 x / min
Nutritional status : weight : 80 kg, height: 160 cm
BMI: 31; Impression = Obesity Type 1
Body temperature : 37.0oC

B. neurologic status
1) Awareness : Composmentis GCS E4V5 M5
2) noble function : well
3) stiff neck : not found
4) cranial nerve
1. N. I (Olfactorius)
Right Left Information

power smell Well Well Well

2. N. II (optic)
Right Left Information

eyesight normal normal

Field of view normal normal normal

The introduction of normal normal

color

3
 3. N. III (Oculomotorius)
Right Left Information

ptosis + + Normal

pupil Normal

Form Round Round

Size 4 mm 4 mm

Eye movement normal Parese N 3

pupillary

Directly (+) (+) Normal

Indirect (+) (+)

4. N. IV (Trokhlearis)
Right Left Information

Eye movement Normal Normal normal

5. N. V (trigeminal)
Right Left Information

motor normal normal Normal

sensibility normal disturbed Parese NV dextra

corneal reflex

6. N. VI (Abduscens)
Right Left Information

Eye movement

strabismus normal Normal Normal

Deviation

4
 7. N. VII (facial)
Right Left Information

Tic (-) (-)

motor

frowning normal normal

raised eyebrows normal normal

Close eyes normal normal

Normal

corners of the mouth Normal normal

nasolabial folds Normal normal

power flavorings Well well

Signs Chvostek Negative Negative

8. N. VIII (acoustic)
Right Left Information

Hearing normal Normal normal

9. N. IX (glossopharyngeal)
Right Left Information

pharyngeal arch normal normal

power flavorings normal normal normal

gag reflex normal normal

10. N. X (vagus)
Right Left Information

5
pharyngeal arch normal Normal
Normal
Dysfonia

11. N. XI (Assesorius)
Right Left Information

motor normal normal normal

trophy Eutrofi Eutrofi Normal

12. N. XII (Hipoglossus)

Right Left Information

motor Normal Normal

trophy normal normal

normal
tremor (-) (-)

dysarthria (-) (-)

III. MOTOR SYSTEM

Right Left Information

The upper limb

Power 5 1

distal 5 1

proximal
The left
tonus Normal spastic
hemiparese
trophy Eutrofi Eutrofi

Ger. involuntary (-) (-)

lower extremities

Power 5 2

6
 distal 5 2

proximal

tonus Normal Normal

trophy Eutrofi Eutrofi

Ger. involuntary (-) (-)

Body

trophy Eutrofi Eutrofi Normal

Ger. involuntary (-) (-)

IV. sensory system

Right Left Information

Raba -

painful Normal -
Hemihipestesia
Temperature -

proprioceptive -

V. REFLEX
Right Left Information

physiological reflex

biceps (+) (+) UMN

triceps (+) (-)

physiological reflex

KPR (+) (-) UMN

APR (+) (-)

pathological
reflexes Pathological
(-) (+)
reflex positive
Babinski
(-) (-)

7
 Chaddock (-) (-)

Hoffman-Tromer

primitive reflexes (-) (-)

Palmomental (-) (-)

snout

VI. FUNCTION OF COORDINATION

Right Left Information

Finger-nose test difficult to assess difficult to

assess
Heel-knee test difficult to assess
difficult to
gait difficult to assess assess difficult to assess

tandem difficult to assess difficult to

Romberg difficult to assess assess

difficult to
assess

difficult to
assess

VII. AUTONOMOUS SYSTEM

micturition : normal
defecation : normal

VIII. INVESTIGATION SPECIAL / OTHER

a. LASEQUE : Unlimited
b. Kernig : Unlimited
c. Patrick : (- / -)
d. Kontrapatrick : (- / -)
e. Valsalva test : (-)
f. Brudzinski : (- / -)

8
SCORE ELEPHANT MADA:
Impairment of consciousness (-), headache (+), pathological reflexes (+)
 hemorrhagic stroke
Siriraj SCORE:
(2.5 x 0) + (2 x 1) + (2 x 1) + (0.1 x 100) - (3 x 1) - 12
= 2 hemorrhagic stroke

IX. RESUME EXAMINATION

general state : Looks very ill
Awareness : composmentis GCS E4V5M5

Blood pressure : 222/100 mmHg

breathing : 22x / minute
noble function : well
excitatory meningeal : not found
cranial nerve : paresis N. V dextra and parese N III
motor : hemihipestesi
Coordination : difficult to assess
autonomous : normal
Reflex : Physiological : (+ / +)
pathological (- / +)

X. DIAGNOSIS OF WORK
clinical diagnosis : stroke
hypertension emergency
diagnosis topics : Carotid System dextra
etiologic diagnosis : hemorrhagic stroke
Differential diagnosis : stroke infarction

XI. PROPOSED Investigations

o routine blood
o When blood sugar levels

9
 o lipid profile
o Liver function (AST, ALT) and renal function (urea, creatinine)
o serum electrolytes
o PA chest X-ray, CT scan of the head without contrast
o Electrocardiography (ECG)

XII. RESULTS Investigations

Routine blood (30 June 2019)
o hb : 9.4 g / dl - WBC : 13940 / l𝜇
o Ht : 27.7 % - PLT : 239,000 / l𝜇

Blood chemistry (1 July 2019)

o Fasting blood sugar: 173 mg / dl
o AST : 17 mg / dl
o ALT : 14 mg / dl
o urea : 111 mg / dl
o creatinine : 7 mg / dl
o Uric acid: 8.3 mg / dl
o Total cholesterol: 230 mg / dl
o Trigleserida: 157 mg / dl

Serum electrolyte levels (January 20th 2019)

- Na+ : 139 mmol / l
- K+ : 5 mmol / l
- Cl : 144 mmol / l

10
Electrocardiography (June 29th 2019)

Sinus rhythm, HR 88x / minute, 0.08 seconds P wave, PR interval 0.20

seconds, 0.08 seconds QRS wave, ST segment and T wave normal 0.20
o Criteria sokolof-lyon S in V1 + R in V5 / V6 +> 35

11
 o 14 + 27 = 41

Impression: ECG LVH

Chest X-ray PA (June 29, 2019)

Cor : CTR> 50% (impression: cardiomegaly)
Pulmo : Diaphragm and normal sinus kostofrenikus

CT scan head (June 29th 2019)

12
Hiperdens lesion looked at
fronto parietal lobe dextra
Looks hiperden lesions in the left ventricle
Nothing seemed deviation of midline structures
Nothing seemed overview SOL
Impression: ich- ivh

XIII. DIAGNOSIS END

Hemorrhagic stroke + hypertension emergencies

XIV. TREATMENT PLAN

a. General
o Bed rest with the head elevated 30o
o Observation of vital signs and neurological status
o Oxygen 3 liters / minute with nasal canul

b. Special
o IVFD Rl 30 TPM

13
 o Osmotherapy: Mannitol 125 cc / 12 h
o Antifibrinolytic: tranexamic acid 3x500 mg iv
o Neuroprotector: Citicolin 2x250 mg iv
o Gastric protector: Ranitidine 2x50 mg iv
o Anty hypertensive: nicardipine drip until TD 130 mmHg

XV. FOLLOW-UP

FOLLOW UP
july, 1th2019
S :left extremities feels heavy
O : GCS E (4) V (5) M (6)
Blood Pressure: 222/100 mmHg
Heart Rate : 88 bpm
respiratory Rate : 22 bpm
temperature : 38.0 ° C
Cognitive Function: Normal
Neck stiffness: Negative
Cranial Nerves: parese N.III, parese NV dextra
Ptosis: + / +
Motoric: HemiparesisDextra
Motoric strength:
5 1
5 1

Sensory : Hemihipestesi on the left side of the body.

Coordination: NT
autonomic : Urine (Normal), defecation (Normal)
Reflex: Fisilogis + / +
Pathological + / +
A : Haemorrhagic stroke + hypertension emergencies

1
P :
 IVFD RL 30 bpm
 Tranexamic acid 3 x 500 mg IV
 Citicoline 2 x 250 mg IV
 Ranitidine 2 x 50 mg IV
 Nicardipin drip until TD 130 mmHg

DISCUSSION

1. stroke
1.1 Anatomy of the central nervous system
The brain consists of the cerebrum, cerebellum, and brainstem formed by
mesensefalon, pons, and medulla oblongata. When calvaria and dura mater
removed, under a layer of arachnoidmater cranial and cranial piamater seen gyrus,
sulcus and fissures of the cerebral cortex. Cerebral cortical sulci and fissures of the
cerebral hemispheres divide into smaller areas called lobus.1

13
 Figure 1. Parts otak1
1. Cerebrum1-3
a. The frontal lobe is a lobe section in the front part of the cerebrum. This lobe
includes all central sulcus anterior cortex. These lobes regulate emotional
functions, planning, creativity, judgment, cognition, movement and problem
solving. In this area there are areas of the motor to control the movement of
muscles, movement of the eyeball, Broca's area as the speech center, and
prefrontal areas (association areas) that control intellectual activity.
b. Lobe parietal lobe is located in the central part of the cerebrum. The parietal
lobe is limited by the front of the central sulcus and the back by a line drawn
14
 from parieto-occipital sulcus to the posterior end of the lateral sulcus (Sylvian).
This area serves to receive impulses from the thalamus sensory nerve fibers
associated with all forms of sensation and recognize all types of somatic
stimuli.
c. Temporal lobe is located at the bottom or side and separated from the occipital
lobe by a line drawn vertically downward from the upper end lateral sulcus.
Temporal lobe plays an important role in hearing, language function, emotional
processes, learning and language functions.
d. Occipital lobe berada behind the parietal lobe and temporal lobe. This lobe
associated with visual stimuli that allow human beings are capable of
interpretation to the object captured by the retina of the eye which then
interprets the signals as an image.

2. cerebellar 1.2
Cerebellum or cerebellum is the second largest component of the brain. The
cerebellum is located at the bottom of the back of the head, is behind the brainstem
and below the occipital lobe, near the tip of the upper neck. The cerebellum is the
central body in controlling the quality of movement. The cerebellum also controls
many automatic functions of the brain, such as: set the attitude or posture, balance
control, muscle coordination and body movement. In addition, the cerebellum
serves to store and carry out a series of automatic movements learned as driving
movement, hand gestures while writing, lock the door and forth motion.

4. Trunk otak1,2
The brain stem is located inside the skull or head cavity and extending to the
base of the spinal cord. The brain stem is responsible for controlling blood
pressure, heart rate, respiration, consciousness, as well as eating and sleeping
patterns. When there is a mass in the brain stem symptoms often present with
vomiting, weakness otat face either one or two sides, difficulty swallowing,
diplopia and headache when you wake up.

15
 The brain stem consists of three parts, namely:

a. Mesensefalon or midbrain (also called the midbrain) is the top of the brain
stem that connects the cerebrum and cerebellum. Cranial nerve III and IV
are associated with the midbrain. The middle brain function in response to
control sight, eye movement, enlarged pupils, regulate body movement and
hearing.
b. Pons is a part of the brain stem that lies between the midbrain and the
medulla oblongata. Pons is located in the posterior cranial fossa. Cranial
nerve (CN) V associated with ponssedangkan CN VI, VII and VIII are at the
nexus of the pons and medulla.
c. Medulla oblongata is the lowermost rear part of the brain stem that will
continue into the spinal cord. Medulla oblongata is also in the posterior
cranial fossa. CN IX, X, XI, and XII disosiasikan with medulla.

1.2 The brain vascularization

carotid system
Brain diperdarahi by two internal carotid arteries and two vertebral arteries,
the four arteries are located in the internal carotid subaraknoid.1,2Arteri space on
either side to give blood to the brain through its main branches namely cerebral
artery and anterior cerebral artery. The internal carotid artery is also called anterior
circulation because memperdarahi structure in the anterior cranial fossa and
media.4Carotid system mainly memperdarahi both hemispheres of the brain.
Carotid system also memperdarahi eye, the basal ganglia, the majority of the
hypothalamus, and frontal lobe, parietal lobe, temporal lobe and the majority of
serebrum.3
Both vertebral arteries unite in the midline at the caudal border of the pons to

16
form the basilar artery that delivers blood to the brain stem and cerebellum as well
as parts of the cerebral hemispheres through the posterior cerebral artery. Because
the vertebral artery and the posterior cranial fossa memperdarahai posterior cerebral
hemispheres then called the posterior circulation.2 Anterior and posterior circulation
associated with that circle of arterial anastomosis system Willisi.1
The internal carotid artery from the common carotid artery branching. The
rise in the neck arteries and penetrate the base of the skull through the carotid canal
of the temporal bone.1.2On the way to the carotid canal, this artery gives small
branches on the floor of the middle ear, the dura mater of klivus, semilunar ganglion
of the trigeminal nerve and gland hipofisis.2 then runs horizontally forward through
klinoideus prosessus anterior to penetrate the dura mater and into the subarachnoid
space and the spin substantia perforated back toward the brain in the medial end of
the lateral cerebral sulcus. Here branched out into the middle cerebral artery and
cerebral artery anterior.3,4

17
Figure 2. The arteries in the brain base 4

18
 Figure 3. Arterial circle Willisi4

1.3 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.5

1.4 classification stroke

A. Based on the pathological abnormalities in the brain
1. hemorrhagic stroke
 intracerebral hemorrhage
 Extracerebral hemorrhage (subarachnoid haemorrhage)
2. Non-hemorrhagic stroke (ischemic stroke, cerebral infarction, blockage)
Which is divided into subtypes:
 cerebral thrombosis
 cerebral embolism
 systemic hypoperfusion
B. Based on the assessment of the time it happened
1. Transient Ischemic Attack(TIA): neurological deficit in less than 24 hours
duration. 80% of all TIA disappear in less than 30 minutes.
2. Prolonged Reversible Ischemic Deficits Neurolagical (PRIND): neurologic
deficit that disappeared more than 24 hours to 3 weeks.
3. Stroke in Evolution (SIE) is a neurologic deficit that is gradually evolving
from mild to more severe within a few hours or days.
4. completed stroke, The neurological deficits that persist or have changed
little during the observation, and will disappear after more than 3 weeks or
cause kacacatan.

19
C. Based on the location of vascular lesions
1. carotid system
 Motor: hemiparese contralateral, dysarthria
 Sensory: hemihipestesia contralateral, paresthesias
 Visual disturbances: homonym hemianopsia contralateral, amourosis fugax
 Malfunctioning of the sublime: aphasia, agnosia
2. vertebrobasilar system
 Motor: hemiparese alternants, dysarthria
 Sensory: hemihipestesia alternants, paresthesias
 Other disorders: disorders of balance, vertigo, diplopia

1.5 pathophysiology stroke5,7,8

Stroke can be caused by one of several processes that include blood vessels in
the brain:
1. Intrinsic process of blood vessels, for example atherosclerosis, lipohialonosis,
inflammation, amyloid deposits, deseksi arterial malformations, dilatation of
the aneurysm or venous thrombosis.
2. The process that originated elsewhere cause embolus eg embolism from the
heart or extracranial circulation which causes intracranial vascular disorders.
3. The process arising from inadequate blood flow to the brain due to decreased
cerebral perfusion pressure or increased blood viscosity.
4. The process that occurs due to rupture of blood vessels in the subarachnoid
space or brain tissue / intracerebral.

1.6 Risk factors for stroke

20
 In general, risk factors for stroke can be divided into: 9.10
Table 1. Risk factors for stroke
Can not be
can be modified
modified
1. Age 1. history of stroke 10. Smoking
2. Gender 2. Hypertension 11. Alcoholics
3. genetic 3. Heart disease 12. The use of narcotics
4. Race 4. Diabetes mellitus 13. hiperhomosisteinemia
5. carotid stenosis 14. The anti-phospholipid antibodies
6. TIA 15. Hyperuricemia
7. hypercholesterolemia 16. The elevation of hematocrit
8. The use of oral contraceptives 17. Elevation fibrinogen
levels
9. obesity

1.7 Clinical features of stroke

Table 2. Differences Haemorrhagic Stroke and Non hemoragik7-10
Clinical PIS PSA Non
Haemorrhagic
focal deficits Weight Light The light weight
onset Minute / hour Minute / hour Slow (hours /
day)
headache Great Great Light
Vomiting at first Often Often Not unless the
lesions in the
brain stem
Hypertension Almost always Usually not Normal-being
Loss of There is There is There is no
consciousness
stiff neck Rarely There is There is no
hemiparesis From the Can from the Often from
beginning start scratch
speech disorders can there Rarely Often
cerebrospinal Blood may be Bloody Clear
liquor present when the
perk

21
Table 3. Different Clinical infarction and bleeding intraserebral7-10
Symptoms or Intracerebral
brain infarction
inspection hemorrhage
Symptoms that precede TIA (+) 50% TIA (-)
Activity / rest Rest, sleep or Often during physical
immediately upon waking activity
Headache and vomiting Could the presence / Very frequent and
intense
Decreased Rarely Often
consciousness onset
time
Hypertension usually nonnotensive Weight, sometimes
being
stimulation of meninges There is no There is
Symptoms of high Rarely papil udem Optic disc edema and
intracranial pressure / hemorrhage subhialoid
optic disc edema
Blood in the There is no There is
cerebrospinal fluid
Photos head Pinealis glands are
found shift
CT-Scan head There are areas Intracranial mass with
hipodensitas hiperdensitas area
angiography Overview can be found Can be found aneurysm,
clogging, narrowing and AVM, mass
vasculitis intrahemisfer or
vasospasm

Table 4. Difference stroke infarction because of thrombus and emboli7-10

stroke thrombus
Occurs at rest
More rarely at a young age
Slower and usually passed TIA
Not encountered source of embolism
or bleeding
Blockages due to the process of
thrombus formation in blood vessels
of the brain itself
embolic stroke
Occurred during the move
More often at a young age
Suddenly, can be accompanied by
headache a few hours earlier
There was found embolic source such
as the heart and a.carotis
Blockages from elsewhere eg
thrombus off of the heart or carotid
artery

22
 Is not accompanied by loss of Loss of consciousness can occur
consciousness
uneven distribution Often to the middle cerebral artery for
larger and straighter

1.8 scoring strokes

1. Gajah Mada algorithm score 5
Patients with acute stroke
The three or two of the three existing
- Impairment of consciousness (+), headache (-), pathological reflexes (-)hemorrhagic
- Impairment of consciousness (-), headache (+), pathological reflexes (-)stroke
- Impairment of consciousness (-), headache (-), pathological reflexes (+)
 stroke infarction
- Impairment of consciousness (-), headache (-), pathological reflexes (-)
 stroke infarction
2. Siriraj Stroke Score (SSS) 5
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
- Yes 1
A = atheroma (Diabetic history, angina, claudication)
- No. 0
- One or more 1
DBP = Diastolic Blood Pressure

scoring =

(Point C x 2.5) + (Point V x 2) + (Point H x 2) + (DBP x 10%) + (points A x (-3))

-12
23
 SSS DIAGNOSIS
>1 cerebral haemorhage
<- 1 cerebral infarction
-1 to 1 Uncertained diagnosis, use probability curve and / or CT Scan

1.9 Stadium Management of Acute Stroke

At this stage, do the handling of etiologic factors and complications. Also the action
of physical therapy, occupational, speech and psychological and social study to help
the recovery of the patient. Explanation and education to families of patients need,
with the impact of stroke on patients and families as well as procedures for the
treatment of patients who do keluarga.6
a. hemorrhagic stroke
General therapy:
Hemorrhagic stroke patients should be treated in the ICU if the hematoma volume>
30 mL, intraventricular hemorrhage with hydrocephalus and clinical situation tends
to worsen. Blood pressure should be lowered to premorbid blood pressure or 15-
20% when the systolic blood pressure> 180 mmHg, diastolic> 120 mmHg, MAP>
130 mmHg, and hematoma volume increases. When there is heart failure, blood
pressure should be lowered to 10 mg IV labetalol (administration within 2 minutes)
to 20 mg (giving 10 minutes) a maximum of 300 mg; iv enalapril 0,625-1.25 mg
per 6 hours; captopril three times from 6.25 to 25 mg orally. If found signs of
increased intracranial pressure, elevated head position 300, the position of the head
and chest in one area, mannitol (see handling strokeiskemik), and hyperventilation
(pCO2 20-35 mm Hg). General management together with ischemic stroke, gastric
ulcer parenteral coped with H2 antagonists, sucralfate, or proton pump inhibitors;
respiratory complications prevented with physiotherapy and treated with antibiotics
spectrum luas.6

Special treatment:

24
Neuroprotective may be granted unless that is a vasodilator. Surgical intervention
considering the age and location of the bleeding is in patients whose condition
worsened by hemorrhage cerebellar diameter> 3 cm 3, acute hydrocephalus due to
intraventricular hemorrhage or cerebellum, conducted VP-shunting, and bleeding
lobar> 60 mL with signs of increased intracranial pressure, acute and threats
herniation .6
In subarachnoid hemorrhage, can be used calcium antagonists (nimodipine) or
surgery (ligation, embolization, extirpation, or gamma knife) if the cause is
aneurysm or arteriovenous malformation (arteriovenous malformation, AVM) .6

Comparison of the treatment of haemorrhagic stroke by stroke in 2011 by

PERDOSSI guideline and guideline stroke by the European Stroke Organization
(ESO) 7.8
Criteria Guideline stroke 2011 Guideline ESO

Intracerebral hemorrhage (ICH)

Special care units There are no special Recommendations on the

stroke recommendations management of acute stroke
care units compared to a
regular room

A decrease in blood TD to 140 mmHg quickly In acute ICH within 6 hours

pressure (BP) still safe. of onset, decreased
Antihypertensive agents intensive TD (target
can be used: beta blockers systolic <140 mmHg in <1
(labetalol, esmolol), hour) is safe and may be
calcium channel blockers more beneficial than the
(nicardipin, diltiazem). target systolic <180 mmHg.
There is no specific agent
recommended.

Provision of Not recommended the use Not recommended the use

coagulation factors of recombinant factor of rFVIIa for adults with
VIIa (rFVIIa) for ICH spontaneous ICH were not
because of the increased associated with increased

25
 risk of thromboembolic risk of thromboembolic
and there is no real benefit events
for patients who are not
selected

Prevention of venous Intermittent pneumatic Use of short stockings or

thromboembolism compression is used in display is not
addition to the elastic recommended.
stockings Recommended use of
intermittent pneumatic
compression to improve
outcomes and reduce the
risk of DVT in immobile
patients with ICH.

Patients with elevated Should not be given There are no special

INR anticoagulant warfarin, a vitamin K- recommendations
drug related dependent gain factor,
corrects INR and receive
vitamin K

Patients with Given vitamin K 10 mg IV In patients who received

coagulation disorders with a speed of <1 mg / vitamin K antagonists with
min in an increase in INR the increase in INR,
anticoagulant medication is
FFP is given 2-6 unit for stopped, then given vitamin
correcting the coagulation K 5-10 mg IV, plus
factor deficiency transfusion of FFP (20 ml /
Protamine sulfate is given kg) or PCC (25-40 IU / kg)
10-50 mg IV in 1-3 Given protamine sulfate IV
minutes to the effects of to patients who received
heparin heparin

Anti-epilepsy drug When there is a seizure or There is no firm

administration status change of recommendations in the
consciousness with the administration of an
results of the EEG waves antiepileptic drug as a
epileptogenic then given prophylactic as well as the
antiepileptic drugs management of ICH

26
 No recommendation patients who had seizures
prophylactic antiepileptic beginning to lower the risk
of recurrent seizures.

operating procedure In most patients with There is no evidence to

intracranial hemorrhage, support the routine surgical
the usefulness of surgery intervention to improve
is still uncertain. outcome after
supratentorial ICH
Patients with a blood clot compared with
in the lobe of> 30 mm and conservative management,
are 1 cm from the surface, but immediate surgery may
the evacuation of be of value in patients with
intracranial bleeding GCS 9-12
supratetorial by standard
craniotomy can be
considered.

Blood pressure After the acute period of Recommended blood

control after ICH intracranial hemorrhage, pressure lowering for
TD can be considered to secondary prevention after
be <140/90 mm Hg or ICH incidence
<130/80 mmHg in
patients with diabetes or
chronic kidney disease.

Subarachnoid hemorrhage (SAH)

Observation Procedures beginning in Maintainability should be

the emergency room, then done in the ICU or
treatment is done in intermediate facilities
intensive care specialized stroke or
neurovascular unit.

Decreased blood Monitoring cerebral At SAH, TD maintained at

pressure perfusion pressure and <180 mmHg to do coiling
decrease in BP with a or clipping (can be achieved
target of 140-160 mmHg. by administration of
nimodipine and analgesic),
27
 For SAH can be MAP maintained> 90
administered nimodipine. mmHg.

antifibrinolytic Recommended in certain Tranexamic acid is given as

therapy clinical circumstances: early as possible after the
epsilon-aminocaproic acid diagnosis of SAH enforced,
4 mg IV loading followed given to occlusion of
by continuous infusion of aneurysms usually occur
1g / h or tranexamic acid after 72 hours.
loading of 1 g IV followed
1g / 6 hours for 72 hours But the therapy is said to
still deliver the end results
Contraindicated in are not very meaningful.
patients with
coagulopathy, acute
myocardial infarction,
ischemic stroke,
pulmonary embolism, or
DVT. It is recommended
in combination with
medications reducing
vasospasm

Operation of Do clipping or Do clipping or

aneurysm rupture endovascular coiling with endovascular coiling with
coiling action more coiling action more helpful.
helpful.

Management and Nimodipine given 1-2 mg Nimodipine 60 mg given

prevention of / hr IV on day 3 or 60 mg orally every 6 hours, if the
vasospasm orally every 6 hours for 21
patient can not swallow, it
days. is provided through NGT to
destroy the drug and
Another way: given the reconstituted with NaCl. If
3% NaCl 50 ml three not mungkinsecara oral,
times a day (beware of may be administered IV.
complications of central
pontine myelinosis).

In case of delayed
vasospasm, stop
28
 nimodipine,
antihypertensives and
diuretics. Give 5%
albumin 250 ml IV,
whenever possible pairs
swanganz and try to
wedge pressure of 12-14
mmHg, cardiac index case
about 4 L / min / sg.meter,
give dobutamine 2-15 ug /
kg / min

analgesics Asetominofen 0.5-1 g / 4- Acetaminophen 500 mg

6 hours up to 4 g / 4-6jam every 3-4 hours

30-60 mg of codeine For severe pain may be

phosphate oral or IM / 4-6 given tramadol (soups, or
hours IV) or codeine, or selection
piritramide terkhir (IM or
Tynanol with codeine IV) avoid giving aspirin
Avoid aspirin before occlusion of the
aneurysm

b. Stadium subacute
Medical measures may include cognitive therapy, behavior, swallowing, speech
therapy, and bladder training (including physical therapy). Given the long course
of the disease that requires special management of intensive post-strokedi hospital
with the goal of independence of the patient, understand, comprehend and
implement primary prevention programs and sekunder.6
Therapy subacute phase: 6
- Continuing therapy according akutsebelumnya conditions,
- Management of complications,
- Restoration / rehabilitation (according to the patient's needs), ie
physiotherapy, speech therapy, cognitive therapy, and occupational therapy,
- secondary prevention

29
- Family education and discharge Planning

2. basic diagnosis
2.1 Basic clinical diagnosis
Ny. U, age 60, came to the Arifin Achmad Hospital with complaints of loss
of consciousness 2 hours SMRs, the patient 10 hours SMRs experiencing right limb
weakness sudden, after which there is no headache, vomiting spraying, or blurred
vision. On physical examination found dekstra VII nerve paresis central type, and
the motion angggota obtained lateralized to the right. Based on the above data, the
clinical diagnosis in these patients is hemorrhagic stroke.±

2.2 Basic diagnosis topic

Abnormalities in the carotid system will provide clinical picture of
neurological deficits that are contralateral so that in these patients the diagnosis was
made on the topic of the left carotid system because it is based on history and
physical examination found lateralization limb to the right, and paresis N.VII
dekstra central type.

2.3 Basic etiologic diagnosis

Etiologic diagnosis of stroke in these patients is obtained based on history
and physical examination. The history is on the right limb weakness accompanied
by symptoms of increased intracranial pressure in the form of loss of consciousness.
On physical examination found dekstra VII nerve paresis central type, and
lateralization limb to dekstra.

30
Comparison stroke infarction and hemorrhagic stroke in the case
Symptoms or stroke hemorrhagic In patients
inspection infarction stroke
Symptoms that TIA (+) 50% TIA (-) TIA (-)
precede
Activity / rest Rest, sleep or Often during While on the
immediately physical move
upon waking activity
Headache and Could the Very frequent There is no
vomiting presence / and intense
Decreased Rarely Often Not
consciousness onset
time
Hypertension Normal-being Medium-weight Medium-weight
hemiparesis Often from Often from early attacks
scratch scratch
speech disorders Often can there Not known
stimulation of There is no There is There is no
meninges
Symptoms of high Optic disc edema Optic disc No assessment
intracranial pressure / are rare edema and funduskopi
papiludem hemorrhage
subhialoid

2.4 Basic diagnosis

Non-hemorrhagic stroke because of the presence of hemiparesis think that
could also occur in a stroke infarction. To get rid of the diagnosis carried out
investigations, in which the gold standard diagnosis of hemorrhagic and non-
hemorrhagic stroke would be used of CT Scan. A CT-Scan head on the stroke
infarction reveals a hipodensitas area, while in hemorrhagic stroke, it was shown
intracranial mass with hiperdensitas area.

2.5 A proposal made investigations

31
 o Routine blood tests (hemoglobin, hematocrit, leukocytes, platelets) was
performed to detect stroke risk factors, namely the increase in hematocrit.
o Examination of blood sugar levels when performed to detect stroke risk
factors, namely diabetes mellitus, and also to plan the management of
abnormalities detected if blood sugar levels.
o Liver function (AST, ALT) and renal function (urea, creatinine) were
conducted to rule out diagnosis of stroke, ie hepatic encephalopathy and
toxic-metabolic conditions.
o Lipid profile (total cholesterol, LDL, HDL, and triglycerides) were
conducted to detect stroke risk factors, namely dyslipidaemia, and also to
plan for the treatment of lipid profile if an abnormality is found
o Serum electrolyte levels is done to rule out diagnosis of stroke, namely
hyponatremia.
o Electrocardiography (ECG) and chest radiograph AP performed to detect
stroke risk factors, namely heart defects, and also to plan for the treatment
of cardiac abnormality if found.
o CT Scan performed to confirm the diagnosis of stroke, knowing the type of
pathology of stroke (hemorrhagic stroke infarction or stroke), get rid of
diagnosis (SOL intracranial), and plotting against the treatment of the
disease.

2.6 Basic final diagnosis

This diagnosis is made based on history, physical examination and investigation.
The history is known that occur limb weakness right of the sudden, accompanied
by loss of consciousness. Physical examination found awareness of somnolence,
GCS E3V1M4, blood pressure of 180/100 mmHg, on examination obtained
hemiparese dextra. Examination of head CT scan is the gold standard for
determining the cause of a stroke is happening. Results of head CT scans on patients
showed visible lesions hiperdens inhiperdens lesions in the lateral ventricles and

32
 the ventricles 4 which indicates that intra-ventricular hemorrhage, accompanied by
bleeding in the subarachnoid
2.7 Basic treatment plan
a. General
o Bed rest with head elevated position 30o done to maintain adequate blood
circulation to the brain
o Observation of vital signs and neurological status is done to monitor the
progress of the disease
o Oxygen 3 liters / minute with nasal canul, provision of oxygen at a higher
concentration to prevent the occurrence of hypoxemia and hypoxia will
result in cell death.
o NGT via the provision of a liquid diet, patients in a persistent decline in the
awareness that oral feeding is not possible. So that the needs of the food
provided through the NGT.

b. Special
o RL infusion of 20 drops / minute to maintain euvolaemic circumstances.
o Citicoline 2 x 250 mg IV given as neuroprotektan for citicoline provides
lucrative benefits in acute stroke conditions. Citicoline serves as an increase
in the structural integrity of cell membranes. Citicolin provide choline and
cytidine to produce phospholipids, it can reduce free radicals in ischemic
conditions.
- Tranexamic Acid 3 x 1000 mg IV given as an antifibrinolytic to prevent
rebleeding.
o Mannitol 4 x 25 g IV, hyperosmotic solution to reduce intracranial pressure
resulting from cytotoxic edema in hemorrhagic stroke
o 2 x 40 mg omeprazole as a proton pump inhibitor which serves to lower the
production of stomach acid in the long term.
o Paracetamol infusion of 3 x 1000 mg as an antipyretic therapy

33
 Ceftriaxone 2 x 1 g IV as antibiotic therapy because the patient is
suspected pneumonia or sepsis
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