Arstya Dewantara, MD, SE, Sp.S.

CEREBRO VASCULAR DISEASES

STROKE
Definition:
Stroke is a clinical syndrome characterized by RAPIDLY
developing symptom and/or sign of focal and at times
global loss of cerebral functions, with symptoms lasting
more than 24 hours or leading to death, with no
apparent cause other than that of vascular origin.
 Stroke subtypes
85% of strokes are ischemic. Of these,
• small artery 25%
• large artery 20%
• cardioembolic 20%
• other 5%
• cryptogenic 30%

15% of strokes hemorrhagic. Of these,

• intracerebral hemorrhage accounts for 2/3
• subarachnoid hemorrhage accounts for 1/3
 Clinical Features Of Non Hemorrhage Versus Hemorrhage Stroke

Non Hemorrhage Stroke Hemorrhage Stroke

Often history of transient ischemic attack No history of transient ischemic attack

Often onset at rest Onset during activity

Minimal cranial discomfort (often none) Headache(Often severe)

Focal neurologic deficit increasing in stepwise Rapidly advancing neurologic (1 to 5 hours),

fashion, consciousness intact early State of consciousness declining to coma

Moderately high blood pressure (ocassionaly Severe high blood pressure (ocassionaly
normotensive) moderately high blood pressure)

Clear cerebrospinal fluid Blood in cerebrospinal fluid

CT scan show infarction (often normal) CT scan shows hemorrhage

Causes of Stroke
 STROKE
RISK FACTOR
Risk Factor for Stroke

Non modifiable Modifiable

 Arterial hypertension
 Age
 Hypercholesterolemia
 Gender  Cigarette smoking
 Ras  Diabetes Mellitus
 Herediter  Hyperhomocysteinemia
 Alcohol abuse
 Oral contraceptive
 Menopause
 Physical inactivity
 Obesity
 Atrial Fibrillation
 Hipercoagulability
Risk Factors for First Ischemic Stroke

Well-documented risk factors

Modifiable, value established

Hypertension

Cardiac disease

Atrial fibrillation

Infective endocarditis

Mitral stenosis

Recent large myocardial infarction

Cigarette smoking

Sickle cell disease

Transient ischemic attacks

Asymptomatic carotid stenosis

 PICA,AICA,SCA :
~ Cerebellum

Posterior
Cerebellar artery
Superior
Cerebellar artery

Anterior and Posterior

Inferior Cerebellar artery
11
LENTICULOSTRIATE ARTERIES

12
PART OF BRAIN
CONTROL CENTER OF BRAIN
Anterior Cerebral
Artery

•Much rarer
•The classic presentation is
proximal arm/leg weakness
with present of distal
strength, the so-called
“man in a barrel”
 •Characterized by
Middle Cerebral weakness of the
Artery contralateral face with
hemianopsia and a
preference of the eyes and
head toward the side of the
involved hemispere
•Aphasia in dominant
hemisphere injury
•Hemineglect
•Involvement restricted to
branches of the MCA may
produces fragment of this
syndrome sparing of leg
strength
 •Involves the brainstem,
Posterior Cerebral cerebellum, thalamus &
occipital lobes
Artery •Present with bilateral limb
weakness or sensory
disturbances, cranial nerve
defisit, ataxia, nausea, and
vomiting or coma
•occlusion of the basilar
artery trunk : Present with
hemianopia, memory
disturbance, mild
personality disturbance
•Rarely; bilateral thalamus
: a state of decreased
responsiveness and apathy
without motor, sensory or
visual impairment
 Stroke Syndromes
Middle cerebral artery - complete

 Weakness - upper and lower extremity (C)

 Weakness - face - lower half (C)
 Hemisensory loss - upper and lower extremity (C)
 Sensory loss - face - all modalities (C)
 Aphasia – receptive (D)
 Aphasia – expressive (D)
 Hemineglect (ND)
 Lateral gaze weakness (C)
 Gaze preference (C)
 Visual loss - homonymous hemianopia (C)

(AHA Stroke Center, 2004)

Stroke Syndromes
Middle cerebral artery – superior division

 Weakness - upper and lower extremity (C)

 Weakness - face - lower half (C)
 Hemisensory loss - upper and lower extremity (C)
 Sensory loss - face - all modalities (C)
 Hemineglect (ND)
 Aphasia – expressive (D)

(AHA Stroke Center, 2004)

Stroke Syndromes
Middle cerebral artery – inferior division

 Visual loss - homonymous hemianopia (C)

 Visual loss - upper quadrant anopsia (C)
 Constructional apraxia (ND)
 Aphasia – receptive (D)

(AHA Stroke Center, 2004)

CBF Disturbances

 Normal : CBF 50 – 60ml/100 gr per mnts

 Ischemia : CBF < 30 ml/ 100 gr per mnts
 Penumbra : CBF 15 – 30 ml/100 gr per mnts
 Neuron death :CBF < 10 ml/100 gr per mnts
Clinical Categories:

 Global Ischemia.
 Hypoxemic encephalopathy
 Hypotension, hypoxemia, anemia.
 Focal Ischemia.
 Obstruction to blood supply to focal area.
 Thrombosis, embolism or hemorrhage.
Global Ischemia:

 Etiology:
 Impaired O2 supply – Lung dis.
 Impaired O2 carrying capacity – Blood dis.
 Impaired Blood supply – Heart, BP
 Morphology:
 Border zone infarcts – “Watershed”
 Sickle shaped band of necrosis on cortex.
 Clinical Features:
 Mild transient confusion state to
 Severe irreversible brain death.
Focal Ischemia:

 Thrombosis:
 Progressive, recurrent,
 Pale or ischemic infarct.
 Eg. Lacunar infarct
 Embolism / Hemorrhage:
 Sudden.
 Red or hemorrhagic infarct.
 Atherosclerosis – rupture/embolism
Aetiology Stroke :

 Atherosclerosis
 Risk Factors: Hypertension, Diabetes, Smoking.
 Vasculitis – Infective, Autoimmune.
 Embolism:
 Major artery Atherosclerosis.
 Heart Disease – MI, Valve disease & Atrial
fibrillation.
 Tumor embolism, septicemia, Fat etc.
Infarct Pathogenesis:

 Immediate – 6 hours
 No Change both gross & micro
 Acute stage – 2 days
 Oedema, loss of grey/white matter border.
 Inflammation, Red neurons, neutrophils
 Intermediate stage – 2 weeks.
 Demarcation, soft friable tissue, cysts
 Macrophages, liquifactive necrosis
 Late stage – After 4 weeks.
 Fluid filled cysts with dark grey margin
 Removal of tissue by macrophages
 Gliosis – proliferation of glia, loss of architecture.
 ISCHEMIC STROKE

• Almost 80% of strokes are from an emboli or a thrombus

• embolic & thrombotic strokes are ischemic
• < 15% of strokes are from hemorrhage, with an even smaller
percentage caused by hypoperfusion
Ischemic Stroke
Infarct
 When a stroke occurs, it
kills brain cells in that
immediate area
 This area of dead cells is
called an infarct
 These cells usually die
within minutes to a few
hours after the stroke
starts
< 20 : aktifitas listrik hilang
< 10 : Gangguan homeostasis
Konsep penumbra

31 CONFIDENTIAL
 (necrosis)

ISCHEMIC CORE AND ISCHEMIC PENUMBRA

(Friedlander
32
2003)
 Ischemic
Injury
Apoptotic
Cell Death
Necrotic
Cell Death

Dr.J.Husada 11-2003 33
ISCHEMIA


34 CONFIDENTIAL
CELULAR CHANGES DURING ISCHAEMIC

35 CONFIDENTIAL
Thrombotic

 A thrombotic stroke is
when a blood clot forms in
one of the arteries in the
brain, or supplying the
brain, and grows and
grows until it is large
enough to block blood
flow.
Embolic

 Once in your brain, the

embolus eventually
travels to a blood vessel
small enough to block its
passage
 The embolus lodges
there, blocking the blood
vessel and causing a
stroke
Stroke: Symptoms

 Onset of stroke symptoms varies as per type of stroke:

 Thrombotic stroke: Develop more gradually
 Embolic stroke: Hits suddenly
 Hemorrhagic stroke: Hits suddenly and
continues to worsen
Transient Ischemic Attack (TIA)

 “Mini stroke”
 Stroke symptoms last for less than 24 hours (usually 10
to 15 mins)
 Result as a brief interruption in blood flow to brain
 Every TIA is an emergency
 TIA may be a warning sign of a larger stroke
 Patients with possible TIA should be evaluated by a
physician
 Diagnosis of acute ischemic stroke

 Physical examination: For carotid bruits

 Brain imaging (cranial CT and/or MRI): Detect small vessel
disease. Helps to effectively discriminate between
ischemic and hemorrhagic stroke, and stroke from brain
tumours
 Doppler ultrasonography/Angiography: Detect large vessel
atherosclerosis
 ECG/Echocardiography: Detect cardiac embolism
 Exclusion of conditions mimicking stroke (hypoglycemia,
migraine, seizure)
 Ischemic stroke diagnostic algorithm

Acute focal brain deficit Excluded hypoglycemia, migraine

with aura, post-seizure deficit

< 1 hour TIA (if CT/MR brain imaging

Head CT without ischemic lesion)

Ischemic Stroke

Lacunar syndrome
Cortical
syndrome
Doppler MRI Vasculopathy CRYPTOGENIC
MRA CT Coagulopathy STROKE
ECG Angiogram
Echo

CARDIAC LARGE ARTERY SMALL OTHER DETERMINED

EMBOLISM ATHEROSCLEROSIS VESSEL DISEASE CAUSE
Diagnose Stroke Without CT
- ASGM
- Shiriraj score
 Gadjah Mada Stroke Algorithm
Patient admitted with sudden onset of stroke
with
Decreasing consciousness +, headache +, Babinski’s reflex + yes HS
No
Decreasing consciousness +, headache +, Babinski’s reflex - yes HS
No
Decreasing consciousness +, headache -, Babinski’s reflex - yes HS
No
Decreasing consciousness +, headache -, Babinski’s reflex + yes HS
No
Decreasing consciousness -, headache +, Babinski’s reflex + yes HS
No
Decreasing consciousness -, headache +, Babinski’s reflex - yes HS
No
Decreasing consciousness -, headache -, Babinski’s reflex + yes AIS
No
Decreasing consciousness -, headache43 -, Babinski’s reflex CONFIDENTIAL
- yes AIS
MANAGEMENT THERAPY
 Acute stroke care-
General management
 The mainstay of acute treatment (A,B,C)
 Treatment and stabilisation of general condition
 Specific therapy
 Recanalisation of a vessel occlusion
 Preventive of mecanism leading to neuronal death in the ischhemic
brain
 Early secondary prevention
 Early rehabilitation
 Prophylaxis and treatment of complications

(Lamsudin, 2004)
 Emergency Medical Care for Neurologic
Emergencies
• Provide reassurance.
• Ensure proper airway and breathing.
• Place the patient in a position of comfort.
• If you suspect stroke, transport immediately and
notify hospital.
• Assess and care for any injuries if you suspect any
type of trauma.
 Management of acute ischemic stroke

 Systemic thrombolysis: Intravenous

recombinant tissue plasminogen activator
(rt-PA): Within 3 hrs of onset of stroke. Dose
0.9 mg/kg, max 90 mg.
 Antiplatelet agents: Aspirin 160-300 mg
within 24- 48 hrs (not during first 24 hrs
following thrombolytic therapy). Clopidogrel
a potential alternative. Combination of
clopidogrel and aspirin currently being
evaluated
Management of acute ischemic stroke
(contd.)
 Anticoagulants: Heparin/LMWH are not
recommended in acute treatment of
ischemic stroke. Recommended in
setting of atrial fibrillation, acute MI
risk, prosthetic valves, coagulopathies
and for prevention of DVT.
 Intra-arterial thrombolytics: An option
for treatment of selected patients with
major stroke of < 6 hrs duration due to
large vessel occlusion.
Management of acute ischemic stroke
(contd.)
 BP management: Should be kept within higher normal limits
since low BP could precipitate perfusion failure. Markedly
elevated BP (>220/110mmHg) managed with nitroglycerin,
clonidine, labetalol, sodium nitroprusside. More aggressive
approach is taken if thrombolytic therapy is instituted
 Blood glucose management: Should be kept within
physiological levels using oral or IV glucose (in case of
hypoglycemia)/insulin (in case of hyperglycemia)
 Elevated body temperature management: Antipyretics and
use of cooling device can improve the prognosis
 Management of Acute hemorrhagic
stroke
 Analgesics/Antianxiety agents: To relieve headache.
Analgesics having sedative properties are beneficial for
patients having sustained trauma (e.g. morphine
sulphate)
 Antihypertensives:(e.g. sodium nitroprusside, labetolol)
 Hyperosmotic agents (e.g. mannitol, glycerol,
furosemide): To reduce cerebral edema, and raised
intracranial pressure.
 Adequate hydration is necessary
 Surgical intervention may occasionally be life saving
Management of TIA

 Evaluation within hours after onset of

symptoms
 CT scan is necessary in all patients
 Antiplatelet therapy with aspirin (50-325
mg/d), consider use of clopidogrel,
ticlopidine, or aspirin-dipyridamole in
patients who are intolerant to aspirin or
those who experience TIA despite aspirin use
 National Clinical Guideline for Stroke, 2nd ed., 2004

 Recommendation:
 All patients with ischemic stroke ot TIA who are not on
anticoagulation should be taking an antiplatelet agent, ie
aspirin (50-300 mg) daily, or copidrogel, or a combination
of low dose aspirin and dipyridamole modified release
(MR). Where patients are aspirin intolerant an alternative
antiplatelet agent (eg clopidrogel 75 mg daily or
dipyridamole MR 200 mg twice daily) should be used

(National Clinical Guideline for Stroke, 2nd ed., 2004)

 National Clinical Guideline for Stroke, 2nd ed., 2004

• Recommendation (cont):
– Anticoagulation should be started in every patient with
persisten or paroxysmal atrial fibrillation (valvular or
non-valvular) unless contraindicated
– Anticoagulants should not be used for patients in sinus
rhythm, unless there is a major source of cardiac
embolism.
– Anticoagulants should not be started until brain
imaging has excluded haemorrhage, and usually not
until 14 days have passed from the onset of an
ischaemic stroke

(National Clinical Guideline for Stroke, 2nd ed., 2004)

THERAPY
MECHANISM OF ACTION OF ANTITHROMBOTICS

Aspirin : Cyclooxygenase Inhibitors

Dipyridamole : Phosphodiesterase Inhibitor
Ticlopidine : ADP Receptor Antagonist
Clopidogrel : ADP Reseptor Antagonist
Cilostazol : Phosphodiesterase 3 Inhibitor
Heparin : Inhibition of Thrombin
Coumarin : Inhibition of Vit - K Dependent
Coagulation Factor (Prothrombin
Factors VII, IX, X)
Low Molecular Weight Heparin : Inhibition of Factor Xa
 INDICATION OF ANTITHROMBOTIC

• Acute Ischemic Stroke

• Secondary Prevention of Stroke Recurrence/ TIA

 ANTICOAGULANTS

• Less and more selectively used than antiplatelet

• Indication
1. Stroke - in- Evolution
2. Crescendo TIAS
3. Vertebro - Basilar Thrombosis
4. Cardioembolic Stroke
5. Carotid and Extracranial vertebral arteries dissection
6. Prophylaxis of deep vein thrombosis /
pulmonary embolism
 Effects of Aspirin

1. Antithrombotic effect
 Inhibition of COX by the irreversible acetylation of a specific serine
moiety
 Aspirin is 170-fold more potent in inhibiting COX-1 than COX-2
2. Antioxidant effect
 Decrease the progression of atherosclerosis
 Improves endothelial dysfunction in atherosclerotic vessel
3. Antiinflammatory effect   hs CRP (ASH 2003)
 Dipyridamol

 A phosphodiesterase inhibitor with vasodilatator effect

 mechanism of action may include increasing cyclic AMP
 indirectly increasing the plasma level of adenosine
 CURRENTLY AVAILABLE
ANTITHROMBOTIC DRUGS

ANTIPLATELET AGENTS ANTICOAGULANTS THROMBOLYTIC

AGENTS

ORAL PARENTERAL ORAL PARENTERAL -PARENTERAL

GPIIb/IIIa -STREPTOKINASE
Aspirin Coumarin
antagonists Heparin -UROKINASE
Dipyridamol LMWH -tPA
Ticlopidin melagatran
Hirudin
Clopidogrel Argatroban
Cilostazol Fondaparinux
 Pengaruh Platelet pada trombosis

1. Adhesi Platelet
Platelet

GP Ib 2. Aktivasi Platelet

Plaque rupture Activated Platelet

GP IIb/IIIa 3. Agregasi Platelet
TxA2
ASA,
Clopidogrel

GP IIb/IIIa Inhibitors

ASA, acetylsalicyclic acid. Fibrinogen

Cannon and Braunwald, Heart Disease. 2001.
PRINCIPLES THERAPY OF THROMBOSIS
BASED ON PATHOGENESIS

PATHOGENESIS THERAPY

RISK FACTORS PREVENTION

- PLATELET ADHESION

ANTIPLATELET

-PLATELET AGGREGATION

-BLOOD COAGULATION ANTICOAGULANT

-THROMBOSIS 63 THROMBOLYTIC
CONFIDENTIAL
ANTIPLATELET
 Antiplatelet Agents

 Thromboxane A2 inhibitor
 Acetylsalicylic acid (ASA)
 Phosphodiesterase inhibitor
 Dipyridamole
 Glycoprotein (GP) IIb/IIIa blockers
 Parenteral: abciximab, eptifibatide, tirofiban
 ADP-receptor antagonists
 Clopidogrel
 Ticlopidine
Mode of Action of
Antiplatelet Agents

CLOPIDOGREL C

ADP

ADP

GPllb/llla Collagen thrombin

(Fibrinogen receptor)
Activation TXA
2

ASA COX
TXA2

COX (cyclo-oxygenase)
ADP (adenosine diphosphate)
TXA2 (thromboxane A2)
Activated Clopidogrel
Platelet Ticlopidine

To neighboring
platelet

Gp IIb/IIIa
Aspirin
fibrinogen
receptor
IV Gp
IIb/IIIa Thrombin
Inhibitors Serotonin
COX Epinephrine
Activation Collagen

Adhesive proteins  
thrombospondin Degranulation
fibrinogen
p-selectin Platelet agonists
vWF
ADP
ATP
Inflammatory factors
Coagulation factors serotonin
platelet factor 4
factor V
CD 154 (CD 40 ligand)
calcium
factor XI
PDGF magnesium
PAI-1

67
TXA, thromboxane; PDGF, platelet-derived growth factor.
 Aspirin
 Ireversibel inhibits COX and prevent thromboxane A2 synthesis
 Influence on platelet after + 7-10 days..
 Inhibit agregagation induced by adenosine diphosphate (ADP).

CLOPIDOGREL C

ADP

ADP

GPllb/llla Collagen thrombin

(Fibrinogen receptor) Activation TXA2

COX (cyclo-oxygenase) ASA COX

ADP (adenosine diphosphate)
TXA2 (thromboxane A2)
TX 2

A
68 CONFIDENTIAL
 Aspirin

 Very cheap, Widely available

 Usual dose 50-200 mg/day  80-100 mg
most often used. FDA: 50-325 mg/day.
 Hart et al: effect of aspirin for high risk
patients: small benefit for those with
manifest vascular disease.
 Associated with an increase in ICH.
 Cast-study, 1997. Hart-et al, 2000.
 Clopidogrel
 Merupakan Platelet adenosine diphosphate (ADP) receptor antagonist.
 Mengurangi ikatan ADP shg menghambat agregasi platelet.
 Juga menghambat agregasi yg distimulasi trombin, platelet activating factor, dan kolagen.
 Berpengaruh pd platelet setelah ~7-10 hari.

CLOPIDOGREL C

ADP
ADP

GPllb/llla Collagen thrombin

(Fibrinogen receptor)
Activation TXA2

ASA COX

TXA2

70 CONFIDENTIAL
NEUROPROTEKTAN
 Citicholine

 Mechanism (neuronal)
 Increase choline formation and alter degradation phosphatydilcholine
 Increase glucose uptake, asetilkholine, prevention lipid radical
 Increase glutation
 Decrease lipid peroxida
 Na/K ATPase modulation
 Mechanism (vascular)
 Increase CBF
 Increase O2 consumption
 Decrease vasculer resistance

Dose: 150-250 mg in Hemorrhage Stroke, 2-3 times daily, 2-14 days

250-1000 mg in Ischemic Stroke,2-3 times daily, 2-14 days
(Perdossi, 2007)
 Piracetam
 Mechanism (neuronal)
 Repair cell membran fluidity
 Repair neurotransmission
 Stimulation adenylate kinase
 Mechanism (vascular)
 Increase eritrocyte deformability
 Decrease platelet hyperagregation
 Repair microcirculation

Dose : 12 g in infusion in first 20 minutes, followed by 3 gr iv/ 6 hour in

ischemic or hemorrhage stroke

(Perdossi, 2007)
 Ischemic Stroke

Indications for Thrombolysis:

 Reliable time of onset < 3hrs
 Stable deficit
 Clinically significant deficit
 No spontaneous resolution
 CT: No hemorrhage, no acute/ subacute
infarcts > 3 hrs
Ischemic Stroke

Contraindications to Thrombolysis
 Major surgery < 2 weeks
 Puncture of non-compressible site/artery within 7 days
 Known source of recent bleeding eg. GI
 MI in previous 3 weeks
 SBP > 185, DBP > 110
 Serious co-morbidity that would increase bleeding risk or limit
effectiveness of outcome
 Coma
 INR > 1.4, Platelets < 100
 Glucose <3 or >22
 Rapidly resolving neurologic signs
Ischemic Stroke

 Intra-arterial thrombolysis
 Acute Basilar Artery Stroke: fatal in 70-80%
 Window up to 24 hrs
 Hemorrhage not as big a problem
 MCA Stroke
Indications for Anticoagulation

 Basilar Artery Occlusion

 Stuttering stroke
 Cardiac source of emboli
Non Neurological:
Infection : Respiratory, Urinary, Septicaemia
Metabolic : Dehydration, Electrolyte Disturbance,
Hypoglycaemia
Drugs : Major and Minor Tranquillizers, Baclofen,
Lithium Toxicity, Antiemetics
Hypoxia : Pulmonary Embolism, Chronic Pulmonary
Disease, Pulmonary Oedema
Hypercapnoea: Chronic Pulmonary Disease
Others : Limb or Bowel Ischaemia in Patients with a
Cardiac or Aortic Arch Source of Embolism
 GOAL OF SECONDARY STROKE PREVENTION

 PREVENT RECURRENT STROKE

 CONTROL OF RISK-FACTORS TO PREVENT OTHER TARGET-
ORGAN FAILURE
 PREVENTION OF VASCULAR DEMENTIA
The traditional approach to stroke prevention: identification of
risk factors.
A risk-based approach to stroke: use of absolute risk to determine
treatment.

82 CONFIDENTIAL
 Antiplatelet:site of
action

83 CONFIDENTIAL
Neurological:
 Progression/completion of the stroke
 Extension/early recurrence
 Hemorrhagic transformation of an infarct
 Development of oedema around the infarct or hemorrhage
 Obstructive hydrocephalus in patients with stroke in the posterior fossa,
or after subarachnoid hemorrhage
 Epileptic seizures
 Delayed ischaemia (in subarachnoid hemorrhage)
 Incorrect diagnosis :
 Cerebral Tumor - Cerebral abscess
 Encephalitis - Chronic Subdural Haematoma
 Subdural empyema
HEMORRHAGE STROKE

85
Definition:
 Intracerebral
hemorrhage (ICH)
results from the
rupture of an
intracerebral vessel
leading to the
development of a
hematoma in the
substance of the brain.
Epidemiology

Incidence
 USA
 ICH represents 10-15 percent of all strokes (approximately 70,000
new cases each year)1.
 Internationally
 Asian countries >> incidence of ICH (30%) 2
 It is twice as common as subarachnoid hemorrhage and carries an
equally poor prognosis 3

1 Stroke. 1999; 30: 2523-2528.

2 Stroke. 2003;34:2091-2096

3 J Neurosurg. 1993; 78: 188-191.

Epidemiology

Mortality
 At 7 days: >20%
 At 1 month: >40%
 At 1 year: 53%
 Correlated with volume of ICH (>30 cc)

Functionally indipendence
 At 1 month: 10%
 At 6 months: 20%

Clev Clin J Med 2005;4:341-344

 Primary and Secondary
Causes of Intracerebral Hemorrhage

Primary Secondary
•Hypertension •Aneurysms
•Amyloid angiopathy •Arteriovenous
malformations
•Neoplasms
•Trauma
•Anticoagulation
•Use of thrombolytics
•Hemorrhagic conversion of
ischemic stroke
 Haemorrhage
Effects of blood Release
Increase Vasoconstrictor agen
toxic Intracranial press Serotonin, Prostaglandin,

Global ischemic
Influks Ca+

Influks Ca+ Vasospasme

Necrosis
Focal Ischemic
Neuron
 Vasospasme Process on
Haemorrhage
vasoconstrictor agens & blood componen release

Vasospasme

Influks Ca+ smooth muscle

vasculer

Lumen stronge
vasculer Vasospasme

Ischemic + deficit neurologic

 Effects of Vasospasme

 Insuffisiensi brain function which suplaied by

vasospasm artery
 Local vasospasm around hematome at intact
arteri (unrupture)
 Probable local vasospasm around central of
haemorrhage change into diffuse vasospasm
 Hasil optimal terapi Stroke perdarahan sampai 96
jam setelah onset
 Puncak vasospasme antara hari ke 5-10)
Clinical

 History
 Onset:
 usually during daytime activity, with progressive (ie,
minute to hours) development:
 Alteration in level of consciousness (appr 50%)
 Nausea and vomiting (appr 40-50%)
 Headache (appr 40%
 Seizure (appr 6-7%)
 Focal neurological deficit
Clinical

 Physical: Clinical manifestations of ICH are determined

by the size and location of hemorrhage, but may include
the following:
 Hypertension, fever, or cardiac arrhythmia
 Nuchal rigidity
 Subhyaloid retinal hemorrhages
 Altered level of consciousness
 Anisocoria
 Focal neurological deficits
Imaging studies

 CT scan
 Hyperdense signal intensity
 Hematoma volume (cc)
 Perihematomal edema and displacement of tissue
with herniation
 MRI
 Vessel imaging
 CT angiography: AVMs, vasculitis, and other
arteriopathies
 MR angiography
Management

 Medical Management
 Surgical Management
Management

 In emergency Room
 ABC rules
 BP continuous monitoring
 Continuous ECG monitoring
 O2 pulse oxymetry
 2 IV lines (norma saline only)
 Blood (CBC, SMAC, RBS, PTT, INR)
 Save 6 ml of blood
 Facilitate transfer to the operating room or ICU
HAEMORRHAGIC STROKE (CT)
 INTRACEREBRAL HAEMORRHAGE
 Hyperdense lesion (55-90 HU)
 Homogenous, sharply delineated, round/oval focus
(The absorption value ( ↓ density)  correlated 
Hm & Hb
In anemic Px, hyperdensity may be of weak condition,
could be < normal brain tissue
iso-or hypodense)
 SUBARACHNOID & INTRAVENTICULAR HS
(CT)
Blood  Subarach spaces 
Interhemisph. Cistern, 
Ventricles 
Basal cisterns
 Could be seen symmetrical hyperdensity in
occipital horns in supine position