Escolar Documentos
Profissional Documentos
Cultura Documentos
Syahrul
Department of Neurology
Faculty of Medicine, Syiah Kuala University
Banda Aceh, March 29, 2011
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STROKE
• The third leading cause of death
• The leading cause of serious, long-term disability
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Stroke
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Ischemic Stroke
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Ischemic Stroke
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ischemic Stroke
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Recent Mangement
of acute ischemic stroke
• Approach :
–Pathophysiology
–Clinical Signs & Symptoms
–Diagnostic Supports
–Neuro-Pharmacology Intervention
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Pathophysiology
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Pathophysiology : The Ischemic Penumbra
CBF
50.9 cc/ Daya cadang
100 gr otak/menit serebrovaskuler
35 – 40 cc Kehilangan fungsi
CBF
20 – 35 cc Aktifitas listrik
otak terhenti
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Ischemic core and penumbra in
human stroke
(Stroke. 1999;30:93-99)
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Pathophysiology : The Ischemic
Penumbra
(caspase apoptosis: programmed cell death)
(necrosis)
(necrotic
cell death)
(apoptosis :programmed
cell death) Caspase
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Cellular Injury During Ischemia
Consequences of Calcium Overload
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Cellular Injury During Ischemia
Cellular Changes During Ischemia
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Thrombus Formation Role of Platelets
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3/4/2011
EDEMA FORMATION
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Clinical Signs & Symptoms
Anatomy of Stroke 18
Clinical Signs & Symptoms
stroke iskemik
Clinical Signs & Symptoms Trombosis Serebri Emboli Serebri
Onset Akut, saat istirahat, pagi hari Akut, saat aktifitas
Nyeri Kepala Tidak ada Nyeri kepala hebat, akut
Kesadaran Menurun Tidak ada 1-2 jam
Defisit fokal neurologi Ringan Berat
Tekanan darah Normal, sedikit meningkat Sering normal, meningkat
Reflek patologi (babinsky) Tidak dijumpai Sering positif
Trombus : arteriosklerosis, Emboli : penyakit jantung,
Sumber trombus/emboli platelet, hiperkoagulasi, pembuluh darah besar
hiperviskositas
CT Scan/MRI otak Lakunar, small vessel oclusive Teritorial, large vessel oclusive
Pemeriksaan Penunjang Darah rutin, agregasi trombosit, Echokardiografi, TCD, Angiografie;
INR, fibrinogen, GD, Lipid profile, Darah rutin, agregasi trombosit,
fs ginjal, as urat, EKG, Foto torak, INR, fibrinogen, GD, Lipid profile,
fs ginjal, as urat, EKG, Foto torak
TCD
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Clinical Signs & Symptoms
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Diagnostic Supports
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MRI : Brain Gold Standard
Coronal orientation: in a slice dividing the head into front and back halves.
Sagittal orientation: in a slice dividing the head into left and right halves.
Axial orientation: in a slice dividing the head into upper and lower halves.
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MRI in Acute Ischemic Stroke
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Carotid Ultrasound
(Carotid Doppler, Carotid Duplex)
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Cerebral Angiography
(Cerebral Angiogram, Cerebral Arteriogram, Digital Subtraction Angiography [DSA])
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Echocardiogram
Examines the heart through the chest (called transthoracic echocardiogram, or
TTE), and one that examines the heart through the throat (called
transesophageal echocardiogram, or TEE)
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Electrocardiogram
(EKG, ECG)
• Atrial fibrilation
• CAD, Ischemic heart disease
• Infarct myocard (acute, acute)
• RBB, LBB
• LVH, RVH
T inversion; Q pathology;
ST depretson; ST elevation
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Laboratory test
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Neuro-Pharmacology
Intervention
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Neurocritical Care Intervention
Optimization of medical treatment is key in
the care of the stroke patient and we
should be cautious when prognosticating
early in the setting of acute stroke and be
aware of the potential effect ‘do not
resuscitate’ status may have on patient
outcome
J NeuroIntervent Surg 2011;3:34-37
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“Time is brain”
Prehospital Management
Hospital Management
Emergency Medical Service
Facilities for Emergency Stroke Care
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“Time is brain”
• Acute therapy
• Comprehensive risk factor management
(antihypertensive therapy, early rehabilitation,
discharge planning)
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Trombolysis
rt-PA
Intravenous
Recombinant Tissue Plasminogen Activator
Antithrombotic Therapy
After the onset of stroke (>3 hours)
aspirin 325 mg
Anticoagulant Therapy
After the onset of stroke (emboli )(3 – 8 hours)
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Aspirin and Clopidogrel in the
Acute Treatment of Ischemic Stroke
• The acute treatment window for ischemic stroke is
the loading of aspirin and clopidogrel within 36
hours of symptom onset of stroke
• Treated with 325 mg of aspirin and 375 mg of
clopidogrel within 36 hours of symptom onset
• Loading with 375 mg of clopidogrel and 325 mg of
aspirin appears to be safe when administered up to
36 hours after stroke and transient ischemic attack
onset in this pilot study. Neurologic deterioration
may be decreased and warrants further study .
J Stroke Cerebrovasc Dis. 2008; 17(1): 26–29.
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When & How To Treat Hypertension ?
When and how to treat hypertension in
acute ischemic stroke?
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Loss of CBF Regulation During Acute Ischemic Stroke
Hypertension 2009;54;702-703
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Autoregulation of cerebral blood flow in a normal brain and in the ischemic
penumbra (the tissues surrounding the ischemic core after a stroke)
In the normal brain, cerebral blood flow is kept at 50 mL/100 g per minute, despite continuous
fluctuations of mean blood pressure between 70 and 120 mm Hg (continuous line). Any increase in
pressure leads to vasoconstriction and any decrease to vasodilation, which prevents the risk of cerebral
hyper- and hypoperfusion, respectively. Above and below the limits of cerebral blood flow
autoregulation, cerebral perfusion passively follows the perfusion pressure. In the ischemic penumbra,
tissue perfusion follows perfusion pressure (dashed line): any fall in blood pressure may precipitate
ischemia, while an increase in blood pressure may cause edema and hemorrhagic transformation.
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CMAJ, March 1, 2005; 172 (5)
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Anti-hypertensive Medications
in the Acute Ischemic Stroke
• Mostly as mono-therapy was common among a
history of hypertension
• Angiotensin-converting enzyme inhibitors (ACEI)
65 (45.6%)
• Diuretics 41 (34.5%)
• ACEI were used in combination with diuretics in 29
(23.4%)
• In Cochrane review found no evidence that giving
calcium antagonists after an ischemic stroke saves
lives or prevents disabilities.
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Recent Advances in the Treatment of Hypertensive Emergencies
Crit Care Nurse 2010;30: 24-30
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The Ideal Acute Antihypertensive
Agent
1. Rapid onset of action
2. Predictable dose response
3. Titratable to desired BP
4. Minimal dosage adjustment
5. Minimal adverse effects
6. Easy conversion to oral agents
7. Acceptable cost-to-benefit ratio
8. Does not impair blood flow to vital organs (No sudden
dips in BP; Does not decrease cardiac output)
9. Does not increase ICP
10. Normalizes CBF autoregulatory curve
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Neuroprotective Agents in Stroke
• Prevention of Early Ischemic Injury
– N-Methyl-D-Aspartate Receptor Antagonists
– Modulation of Non-NMDA Receptors
• Nalmefene
• Lubeluzole
• Clomethiazole
Free Radical Scavengers and Trapping Agents
NXY-059
• Prevention of Reperfusion Injury
– Antiadhesion Antibodies
– Membrane Stabilization
– Neuronal Healing
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Hemorragic Stroke
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Hemorragic stroke
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Clinical Signs & Symptoms
stroke hemorragic
Clinical Signs & Symptoms Perdarahan Intraserebral Perdarahan Sub-arakhnoid
Onset Akut, saat aktifitas Akut, aktifitas
Nyeri Kepala ++++ +++
Kesadaran Menurun ++++ +
Defisit fokal neurologi hebat KK +
Tekanan darah Tinggi sekali N (sedikit meningkat)
Reflek patologi (babinsky) + KK +
Sumber perdarahan Ruptur mikroaneurisma berry, Ruptur AV-M
sakular
CT Scan/MRI otak Perdarahan intraserebral Perdarahan sub arakhnoid
Pemeriksaan Penunjang CT scan, MRI, Angiografie; CT scan, MRI, Angiografie;
EKG, hematologi EKG, hematologi
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Management
Management Perdarahan Intraserebral Perdarahan Sub-arakhnoid
Kesadaran Menurun Perawatan Intensive Perawatan Intensive
Tekanan Darah Regulasi cepat 1-2 jam Pemberian antiserebral
vasospasme
Pemeriksaan Neuro- CT scan, MRI kepala, CT scan, MRI kepala,
Diagnostik Angiografi; Hematologi Angiografi; Hematologi
Medikamentosa/Operatif Komprehensif Komprehensif
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Brain CT Scan
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Brain CT Scan
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Terimong geunaseh...
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