Presentation on theme: "acute stroke Syahrul Department of Neurology"— Presentation transcript:
1 acute stroke Syahrul Department of Neurology Faculty of Medicine, Syiah Kuala UniversityBanda Aceh, March 29, 2011acute stroke
2 STROKE The third leading cause of death The leading cause of serious, long-term disabilityIndonesia : Riskesdas Depkes RI, 2007Prevalence of stroke 8,3 per peopleMortality : stroke 15,4%, hypertensive 6,8% & ischemic heart disease 5,1%Stroke Statistics,U.S. Statistics, 2010143,579 people die each year from strokeEach year, about 795,000 people suffer a strokeAbout 600,000 of these are first attacks, and185,000 are recurrent attacks
3 Stroke A major economic burden on healthcare system Incidence is expected to increase 25% by 2050Ischemic 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)
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.
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 outcomeJ NeuroIntervent Surg 2011;3:34-37
36 “Time is brain” Prehospital Management Hospital Management Emergency Medical ServiceFacilities for Emergency Stroke Care
37 “Time is brain” Medical emergency, early hospital management Time depedent therapyRapid confirmation (CT scan or MRI)Urgent investigation (cause of stroke)Acute therapyComprehensive risk factor management (antihypertensive therapy, early rehabilitation, discharge planning)
38 Trombolysis rt-PA The ‘’engine for emergency stroke” IntravenousRecombinant Tissue Plasminogen ActivatorThe ‘’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
39 Antithrombotic & Anticoagulant Antithrombotic TherapyAfter the onset of stroke (>3 hours)aspirin 325 mgAnticoagulant TherapyAfter 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 strokeTreated with 325 mg of aspirin and 375 mg of clopidogrel within 36 hours of symptom onsetLoading 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 inacute ischemic stroke?The effect of BP modification during the acutephase of ischemic stroke on functional outcomeis 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 hypertensionAngiotensin-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 actionPredictable dose responseTitratable to desired BPMinimal dosage adjustmentMinimal adverse effectsEasy conversion to oral agentsAcceptable cost-to-benefit ratioDoes not impair blood flow to vital organs (No sudden dips in BP; Does not decrease cardiac output)Does not increase ICPNormalizes CBF autoregulatory curve
48 Neuroprotective Agents in Stroke Prevention of Early Ischemic InjuryN-Methyl-D-Aspartate Receptor AntagonistsModulation of Non-NMDA ReceptorsNalmefeneLubeluzoleClomethiazoleFree Radical Scavengers and Trapping AgentsNXY-059Prevention of Reperfusion InjuryAntiadhesion AntibodiesMembrane StabilizationNeuronal Healing