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acute stroke Syahrul Department of Neurology

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1 acute stroke Syahrul Department of Neurology
Faculty of Medicine, Syiah Kuala University Banda Aceh, March 29, 2011 acute stroke

2 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 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

3 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)

4 Klasifikasi Patologi Anatomi Perjalanan Klinis Sirkulasi Serebral
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


6 Hemorragic Stroke Ischemic Stroke

7 Ischemic Stroke

8 Ischemic Stroke

9 ischemic Stroke

10 Recent Mangement of acute ischemic stroke
Approach : Pathophysiology Clinical Signs & Symptoms Diagnostic Supports Neuro-Pharmacology Intervention

11 Pathophysiology

12 Pathophysiology : The Ischemic Penumbra

13 Ischemic core and penumbra in human stroke (Stroke. 1999;30:93-99)

14 Ischemic core and penumbra in human stroke (Stroke. 1999;30:93-99)

15 Pathophysiology : The Ischemic Penumbra

16 Cellular Injury During Ischemia Consequences of Calcium Overload

17 Cellular Injury During Ischemia Cellular Changes During Ischemia

18 Thrombus Formation Role of Platelets


20 Clinical Signs & Symptoms
Anatomy of Stroke

21 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 1-2 jam Defisit fokal neurologi Ringan Berat Tekanan darah Normal, sedikit meningkat Sering normal, meningkat Reflek patologi (babinsky) Tidak dijumpai Sering positif Sumber trombus/emboli Trombus : arteriosklerosis, platelet, hiperkoagulasi, hiperviskositas Emboli : penyakit jantung, pembuluh darah besar CT Scan/MRI otak Lakunar, small vessel oclusive Teritorial, large vessel oclusive Pemeriksaan 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

22 Clinical Signs & Symptoms

23 Diagnostic Supports

24 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.

25 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.

26 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.

27 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.

28 Ischemia, Infarction (Size, Location) Edematous (Midline Shift)
CT scan : Brain CT scan Gold Standard Ischemia, Infarction (Size, Location) Edematous (Midline Shift)

29 Carotid Ultrasound (Carotid Doppler, Carotid Duplex)

30 Cerebral Angiography (Cerebral Angiogram, Cerebral Arteriogram, Digital Subtraction Angiography [DSA])

31 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)

32 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

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

34 Neuro-Pharmacology Intervention

35 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

36 “Time is brain” Prehospital Management Hospital Management
Emergency Medical Service Facilities for Emergency Stroke Care

37 “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)

38 Trombolysis rt-PA The ‘’engine for emergency stroke”
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, 20104 hours

39 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)

40 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.

41 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: )

42 Loss of CBF Regulation During Acute Ischemic Stroke Hypertension 2009;54;702-703

43 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)


45 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.

46 Recent Advances in the Treatment of Hypertensive Emergencies
Crit Care Nurse 2010;30: 24-30

47 The Ideal Acute Antihypertensive Agent
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

48 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

49 Hemorragic Stroke

50 Hemorragic stroke

51 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) 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

52 Management Management Perdarahan Intraserebral
Perdarahan Sub-arakhnoid Kesadaran Menurun Perawatan Intensive Tekanan Darah Regulasi cepat 1-2 jam Pemberian antiserebral vasospasme Pemeriksaan Neuro-Diagnostik CT scan, MRI kepala, Angiografi; Hematologi Medikamentosa/Operatif Komprehensif

53 Brain CT Scan

54 Brain CT Scan


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