acute stroke

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ACUTE STROKE

SyahrulDepartment of NeurologyFaculty of Medicine, Syiah Kuala UniversityBanda Aceh, March 29, 2011

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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. (20% of all stroke)

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KLASIFIKASI Patologi Anatomi

Stroke Iskemik Trombosis Serebri Emboli Serebri

Stroke Hemoragik Perdarahan Intra Serebral Perdarahan Sub-Arakhnoid

Perjalanan Klinis Transient Ischemic Attack Reversible Ischemic Neurological Defisit Stroke In-evolution Komplit Stroke

Sirkulasi Serebral Stroke Sirkulasi Serebral Anterior Stroke Sirkulasi Serebral Posterior

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STROKE

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Hemorragic Stroke Ischemic Stroke

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Ischemic Stroke

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Ischemic Stroke

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ISCHEMIC STROKE

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RECENT MANGEMENTOF 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

Kematian sel saraf< 10 – 20 cc

Aktifitas listrikotak terhenti

20 – 35 cc

Kehilangan fungsi35 – 40 cc

Daya cadangserebrovaskuler

50.9 cc/100 gr otak/menit

CBF

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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

I SCHEMI C CORE AND I SCHEMI C PENUMBRA(Friedlander 2003)

(caspase apoptosis: programmed cell death)

(necrosis)

(necrotic cell death)

(apoptosis :programmed cell death) Caspase

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Cellular Injury During IschemiaConsequences of Calcium Overload

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Cellular Injury During IschemiaCellular Changes During Ischemia

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Thrombus Formation Role of Platelets

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EDEMA FORMATION3/4/2011

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Clinical Signs & Symptoms

Anatomy of Stroke

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CLINICAL SIGNS & SYMPTOMS


Trombosis Serebri Emboli Serebri

Onset Akut, saat istirahat, pagi hari

Akut, saat aktifitas

Nyeri Kepala Tidak ada Nyeri kepala hebat, akutKesadaran Menurun Tidak ada 1-2 jam

Defisit fokal neurologi Ringan BeratTekanan darah Normal, sedikit meningkat Sering normal,

meningkatReflek patologi

(babinsky)Tidak dijumpai Sering positif

Sumber trombus/emboli

Trombus : arteriosklerosis, platelet, hiperkoagulasi,

hiperviskositas

Emboli : penyakit jantung,

pembuluh darah besarCT Scan/MRI otak Lakunar, small vessel

oclusive Teritorial, large vessel

oclusivePemeriksaan Penunjang

Darah rutin, agregasi trombosit, INR, fibrinogen, GD, Lipid profile, fs ginjal, as urat, EKG, Foto torak,

TCD

Echokardiografi, TCD, Angiografie;

Darah rutin, agregasi trombosit, INR, fibrinogen, GD, Lipid profile, fs ginjal, as urat, EKG, Foto torak

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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.

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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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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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ECHOCARDIOGRAMExamines 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 ManagementHospital Management

Emergency Medical ServiceFacilities 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-PAIntravenous 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 TherapyAfter 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?

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 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. Rapid onset of action2. Predictable dose response3. Titratable to desired BP4. Minimal dosage adjustment5. Minimal adverse effects6. Easy conversion to oral agents7. Acceptable cost-to-benefit ratio8. Does not impair blood flow to vital organs (No

sudden dips in BP; Does not decrease cardiac output)

9. Does not increase ICP10. 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 ClomethiazoleFree 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 & SYMPTOMSClinical Signs & Symptoms

Perdarahan Intraserebral

Perdarahan Sub-arakhnoid

Onset Akut, saat aktifitas Akut, aktifitasNyeri Kepala ++++ +++

Kesadaran Menurun ++++ +Defisit fokal neurologi hebat KK +

Tekanan darah Tinggi sekali N (sedikit meningkat)Reflek patologi

(babinsky)+ KK +

Sumber perdarahan Ruptur mikroaneurisma berry, sakular

Ruptur AV-M

CT Scan/MRI otak Perdarahan intraserebral

Perdarahan sub arakhnoid

Pemeriksaan Penunjang CT scan, MRI, Angiografie;EKG, hematologi

CT scan, MRI, Angiografie;EKG, hematologi

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MANAGEMENTManagement Perdarahan

IntraserebralPerdarahan Sub-arakhnoid

Kesadaran Menurun Perawatan Intensive Perawatan IntensiveTekanan Darah Regulasi cepat 1-2 jam Pemberian antiserebral

vasospasmePemeriksaan Neuro-

DiagnostikCT scan, MRI kepala,

Angiografi; HematologiCT scan, MRI kepala,

Angiografi; HematologiMedikamentosa/

OperatifKomprehensif Komprehensif

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BRAIN CT SCAN

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BRAIN CT SCAN

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acute stroke