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

5. STROKE

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