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Syahrul

Department of Neurology Faculty of Medicine, Syiah Kuala University Banda Aceh, March 29, 2011

ACUTE STROKE
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STROKE

The third leading cause of death The leading cause of serious, long-term disability Indonesia : Riskesdas Depkes RI, 2007 Prevalence of stroke 8,3 per 1.000 people Mortality : stroke 15,4%, hypertensive 6,8% & ischemic heart disease 5,1% Stroke Statistics,U.S. Statistics, 2010 143,579 people die each year from stroke Each year, about 795,000 people suffer a stroke About 600,000 of these are first attacks, and 185,000 are recurrent attacks
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STROKE
A major economic burden on healthcare system Incidence is expected to increase 25% by 2050 Ischemic stroke, when arteries are blocked by blood clots (emboli) or by the gradual build-up of plaque other fatty deposits. (Approximately 80% of stroke are ischemic) Hemorrhagic stroke, occur when a blood brain breaks leaking blood into the bain.

KLASIFIKASI

Patologi Anatomi

Stroke Iskemik

Trombosis Serebri Emboli Serebri Perdarahan Intra Serebral Perdarahan Sub-Arakhnoid

Stroke Hemoragik

Perjalanan Klinis

Transient Ischemic Attack Reversible Ischemic Neurological Defisit Stroke In-evolution Komplit Stroke Stroke Sirkulasi Serebral Anterior Stroke Sirkulasi Serebral Posterior
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Sirkulasi Serebral

STROKE

Hemorragic Stroke

Ischemic Stroke

Ischemic Stroke

Ischemic Stroke

ISCHEMIC STROKE

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/ 100 gr otak/menit Daya cadang serebrovaskuler Kehilangan fungsi Aktifitas listrik otak terhenti Kematian sel saraf

CBF

35 40 cc 20 35 cc < 10 20 cc

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Ischemic core and penumbra in human stroke


(Stroke. 1999;30:93-99)

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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

ISCHEMIC CORE AND ISCHEMIC PENUMBRA


(Friedlander 2003)

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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

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CLINICAL SIGNS & SYMPTOMS


Clinical Signs & Symptoms Onset Nyeri Kepala Kesadaran Menurun Defisit fokal neurologi Trombosis Serebri Akut, saat istirahat, pagi hari Tidak ada Tidak ada Ringan Emboli Serebri Akut, saat aktifitas Nyeri kepala hebat, akut 1-2 jam Berat

Tekanan darah
Reflek patologi (babinsky) Sumber trombus/emboli CT Scan/MRI otak Pemeriksaan Penunjang

Normal, sedikit meningkat


Tidak dijumpai Trombus : arteriosklerosis, platelet, hiperkoagulasi, hiperviskositas Darah rutin, agregasi trombosit, INR, fibrinogen, GD, Lipid profile, fs ginjal, as urat, EKG, Foto torak, TCD

Sering normal, meningkat


Sering positif Emboli : penyakit jantung, pembuluh darah besar

Lakunar, small vessel oclusive Teritorial, large vessel oclusive


Echokardiografi, TCD, Angiografie; Darah rutin, agregasi trombosit, INR, fibrinogen, GD, Lipid 21

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

Left: diffusion-weighted MRI in acute ischemic stroke performed 35 minutes after symptom onset. Right: apparent diffusion coefficient (adc) map obtained from the same patient at the same time. 25

MRI in Acute Ischemic Stroke

Diffusion-perfusion mismatch in acute ischemic stroke. The perfusion abnormality (right) is larger than the diffusion abnormality (left), indicating the ischemic penumbra, which is at risk of infarction.
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MRI in Acute Ischemic Stroke

Left: Perfusion-weighted MRI of a patient who presented 1 hour after onset of stroke symptoms. Right: Mean transfer time (MTT) map of the same patient.
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CT SCAN : BRAIN
CT scan Gold Standard
Ischemia, Infarction (Size, Location) Edematous (Midline Shift)

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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

Blood routine, Glucose, Lipid Profile, Uric Acid Fibrinogen, Agregation of Trombocyte,INR Protein C, S; Anticardiolipin Antibody (ACA)

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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
Medical emergency, early hospital management Time depedent therapy

Rapid confirmation (CT scan or MRI) Urgent investigation (cause of stroke)

Acute therapy Comprehensive risk factor management (antihypertensive therapy, early rehabilitation, discharge planning)

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TROMBOLYSIS rt-PA
Intravenous Recombinant Tissue Plasminogen Activator

The engine for emergency stroke Beneficial within 3 hours of stroke onset
(NINDS 1995, PROACT II study 1999, National Stroke Foundation 2007, AHA/ASA 2007)

World Stroke Congress, Seoul Korea, 20104 hours


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Antithrombotic & Anticoagulant 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): 2629.

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When & How To Treat Hypertension ?


When and how to treat hypertension in acute ischemic stroke? The effect of BP modification during the acute phase of ischemic stroke on functional outcome is strongly dependent on age.
(Hypertension 2009; 54:769-774)
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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 43 cause edema and hemorrhagic transformation. 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. 2. 3. 4. 5. 6. 7. 8.

9. 10.

Rapid onset of action Predictable dose response Titratable to desired BP Minimal dosage adjustment Minimal adverse effects Easy conversion to oral agents Acceptable cost-to-benefit ratio Does not impair blood flow to vital organs (No sudden dips in BP; Does not decrease cardiac output) Does not increase ICP 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


Clinical Signs & Symptoms Onset Nyeri Kepala Kesadaran Menurun Defisit fokal neurologi Tekanan darah Reflek patologi (babinsky) Sumber perdarahan CT Scan/MRI otak Perdarahan Intraserebral Akut, saat aktifitas ++++ ++++ hebat Tinggi sekali + Ruptur mikroaneurisma berry, sakular Perdarahan intraserebral Perdarahan Subarakhnoid Akut, aktifitas +++ + KK + N (sedikit meningkat) KK + Ruptur AV-M Perdarahan sub arakhnoid

Pemeriksaan Penunjang

CT scan, MRI, Angiografie; EKG, hematologi

CT scan, MRI, Angiografie; EKG, hematologi

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MANAGEMENT
Management Kesadaran Menurun Perdarahan Intraserebral Perdarahan Subarakhnoid Perawatan Intensive Perawatan Intensive

Tekanan Darah
Pemeriksaan NeuroDiagnostik Medikamentosa/Operatif

Regulasi cepat 1-2 jam


CT scan, MRI kepala, Angiografi; Hematologi Komprehensif

Pemberian antiserebral vasospasme


CT scan, MRI kepala, Angiografi; Hematologi 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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