logging in or signing up Cerebrovascular diseases 2 neurology1 Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 127 Category: Science & Tech.. License: All Rights Reserved Like it (0) Dislike it (0) Added: February 27, 2011 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript Treatment of Ischemic Stroke : Treatment of Ischemic Stroke Dr Rahul Chakor MD., DM Assoc Prof Dept of Neurology T. N. Medical College B. Y. L. Nair Hospital MumbaiSlide 2: Interruption of nutrient blood flow Cellular metabolic events Duration, severity & location of ischemia Severity of stroke .Slide 3: Loss of (ATP) Na/K pump failure Membrane depolarization ↑Na, ↑Ca Cell loses potassium Anaerobic glycotic pathways -damaging by-products, lactic acid and hydrogen ions Stimulates the massive release of the amino acids glutamate and aspartate, excitatory neurotransmitters in the brain. Calcium channels is the N-methyl-D aspartate (NMDA) channel. Na & Ca ions rapidly accumulate within the cells, inflow of water, cytotoxic edema of neurons and glia.Slide 4: ↑Ca Activation of Phospholipases Proteases Lipases Nucleases NOS Arachidonic acid metabolites Oxygen free radicals, Damage cell membranes, Genetic material, Structural proteins Leading to cell death. Excitotoxicity NMDA receptors Non NMDA receptors Glutamate binds to the receptor Excites” the cells Depolarizes Moves positive ions into the cellSlide 6: Core - Infarct Penumbra – ischemic but viable Continuation of Ischemia converts penumbra to infarct Ischemic PenumbraTreatment: TreatmentTreatment: Treatment Tests for the Emergent Evaluation of the Patient with Acute Ischemic Stroke CT of the brain without contrast Electrocardiogram Chest x-ray Hematologic studies (complete blood count, platelet count, prothrombin time, partial thromboplastin time) Serum electrolytes Blood glucose Renal and hepatic chemical analyses National Institutes of Health Scale (NIHSS) scoreThrombolysis: Thrombolysis IV rt-PA for acute stroke thrombolysis is based on the NINDS rt-PA study, a two-part randomized, double blind, placebo-controlled trial.IV rt – PA (alteplase, actylise): IV rt – PA (alteplase, actylise) Inclusion Criteria Clearly defined time of onset <3 h Measurable stroke-related deficit No intracranial hemorrhage on CT Dose Total dose 0.9mg/kg (max 90mg) 10% of the total dose as bolus over 1min 90% of the remaining over 60 min Exclusion Criteria Stroke or head trauma within 3 months Major surgery within 14 days History of intracranial hemorrhage SBP > 185 mm Hg or DBP >110 mm Hg Rapidly improving or minor symptoms Symptoms suggestive of subarachnoid hemorrhage Gastrointestinal hemorrhage or urinary tract hemorrhage within the previous 21 days Arterial puncture at a noncompressible site within the previous 7 days Seizure at stroke onset Anticoagulant or heparin use <48 h before onset with elevated partial-thromboplastin time Prothrombin time >15 s Platelet count <100,000/mm3 Glucose concentration <50 mg/dL or >400 mg/dL 1995 NINDS rt-PA studyIntra-arterial Thrombolysis: Intra-arterial Thrombolysis Microcatheter techniques Smaller dose of fibrinolytic agent More complete recanalization Complications reduced treatment window can be extended beyond the typical IV window of 3 hours Combined with mechanical manipulation of the clot,Endovascular treatment: Endovascular treatment Mechanical manipulation of the clot MERCI clot retrieval device Thrombectomy Thromboaspiration –Penumbra stroke systemPrevention: Prevention Avoidance of risk factors Treatment of specific risk factors (HT,DM) Treatment to reduce coagulability Antiplatelet therapy Anticoagulation Carotid stenosisSlide 15: Primary prevention DM, HT, AF, Hypercholesterolemia, Lifestyle modification Secondary prevention ThrombosisSlide 16: HT Target 120/80 Depends on associated diseases DM As carefully as possible Cholesterol LDL <100 mg/dl, Ch <135mg/dl StatinsAntiplatelet: Antiplatelet Aspirin – 50 to 325mg/day Clopidogrel 75mg/day CombinationAnticoagulation: Anticoagulation Cardioembolism Major vessel occlusion – ICA, BA Arterial dissection – ICA, extra cranial VA Prothrombotic states Severe carotid stenosis Anti platelet failure Cerebral venous thrombosisSlide 19: Carotid artery endarterectomy Symptomatic > 70% Symptoms within 6 months Fit for surgery Expertise available Carotid artery stenting Selected patientsThank You: Thank You You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.
Cerebrovascular diseases 2 neurology1 Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 127 Category: Science & Tech.. License: All Rights Reserved Like it (0) Dislike it (0) Added: February 27, 2011 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript Treatment of Ischemic Stroke : Treatment of Ischemic Stroke Dr Rahul Chakor MD., DM Assoc Prof Dept of Neurology T. N. Medical College B. Y. L. Nair Hospital MumbaiSlide 2: Interruption of nutrient blood flow Cellular metabolic events Duration, severity & location of ischemia Severity of stroke .Slide 3: Loss of (ATP) Na/K pump failure Membrane depolarization ↑Na, ↑Ca Cell loses potassium Anaerobic glycotic pathways -damaging by-products, lactic acid and hydrogen ions Stimulates the massive release of the amino acids glutamate and aspartate, excitatory neurotransmitters in the brain. Calcium channels is the N-methyl-D aspartate (NMDA) channel. Na & Ca ions rapidly accumulate within the cells, inflow of water, cytotoxic edema of neurons and glia.Slide 4: ↑Ca Activation of Phospholipases Proteases Lipases Nucleases NOS Arachidonic acid metabolites Oxygen free radicals, Damage cell membranes, Genetic material, Structural proteins Leading to cell death. Excitotoxicity NMDA receptors Non NMDA receptors Glutamate binds to the receptor Excites” the cells Depolarizes Moves positive ions into the cellSlide 6: Core - Infarct Penumbra – ischemic but viable Continuation of Ischemia converts penumbra to infarct Ischemic PenumbraTreatment: TreatmentTreatment: Treatment Tests for the Emergent Evaluation of the Patient with Acute Ischemic Stroke CT of the brain without contrast Electrocardiogram Chest x-ray Hematologic studies (complete blood count, platelet count, prothrombin time, partial thromboplastin time) Serum electrolytes Blood glucose Renal and hepatic chemical analyses National Institutes of Health Scale (NIHSS) scoreThrombolysis: Thrombolysis IV rt-PA for acute stroke thrombolysis is based on the NINDS rt-PA study, a two-part randomized, double blind, placebo-controlled trial.IV rt – PA (alteplase, actylise): IV rt – PA (alteplase, actylise) Inclusion Criteria Clearly defined time of onset <3 h Measurable stroke-related deficit No intracranial hemorrhage on CT Dose Total dose 0.9mg/kg (max 90mg) 10% of the total dose as bolus over 1min 90% of the remaining over 60 min Exclusion Criteria Stroke or head trauma within 3 months Major surgery within 14 days History of intracranial hemorrhage SBP > 185 mm Hg or DBP >110 mm Hg Rapidly improving or minor symptoms Symptoms suggestive of subarachnoid hemorrhage Gastrointestinal hemorrhage or urinary tract hemorrhage within the previous 21 days Arterial puncture at a noncompressible site within the previous 7 days Seizure at stroke onset Anticoagulant or heparin use <48 h before onset with elevated partial-thromboplastin time Prothrombin time >15 s Platelet count <100,000/mm3 Glucose concentration <50 mg/dL or >400 mg/dL 1995 NINDS rt-PA studyIntra-arterial Thrombolysis: Intra-arterial Thrombolysis Microcatheter techniques Smaller dose of fibrinolytic agent More complete recanalization Complications reduced treatment window can be extended beyond the typical IV window of 3 hours Combined with mechanical manipulation of the clot,Endovascular treatment: Endovascular treatment Mechanical manipulation of the clot MERCI clot retrieval device Thrombectomy Thromboaspiration –Penumbra stroke systemPrevention: Prevention Avoidance of risk factors Treatment of specific risk factors (HT,DM) Treatment to reduce coagulability Antiplatelet therapy Anticoagulation Carotid stenosisSlide 15: Primary prevention DM, HT, AF, Hypercholesterolemia, Lifestyle modification Secondary prevention ThrombosisSlide 16: HT Target 120/80 Depends on associated diseases DM As carefully as possible Cholesterol LDL <100 mg/dl, Ch <135mg/dl StatinsAntiplatelet: Antiplatelet Aspirin – 50 to 325mg/day Clopidogrel 75mg/day CombinationAnticoagulation: Anticoagulation Cardioembolism Major vessel occlusion – ICA, BA Arterial dissection – ICA, extra cranial VA Prothrombotic states Severe carotid stenosis Anti platelet failure Cerebral venous thrombosisSlide 19: Carotid artery endarterectomy Symptomatic > 70% Symptoms within 6 months Fit for surgery Expertise available Carotid artery stenting Selected patientsThank You: Thank You