1. DR. SANKALP MOHAN SENIOR RESIDENT, NEUROLOGY

2. Etiology and classification Ischemic stroke 1. thrombosis 2. embolism 3. systemic hypoperfusion Hemorrhagic stoke 1 . intracerebral 2 . subarachnoid 3. THREE STROKE TYPES Intracerebral HemorrhageIschemic Stroke85%Clot occluding arterySubarachnoid Hemorrhage10%Bleeding into brain5%Bleeding around brain 4. ISCHEMIC STROKE PATHOPHYSIOLOGY The First Few Hours TIME IS BRAIN: SAVE THE PENUMBRACorePenumbra is zone of reversible ischemia around core of irreversible infarctionsalvageable in first few hours after ischemic stroke onset Penumbra damaged by: Hypoperfusion Hyperglycemia Fever SeizurePenumbraClot in Artery 5. INVESTIGATIONS ANDMANAGEMENT GUIDELINES 6. Emergency evaluation and diagnosis of acute ischemic stroke Data: ER Evaluation and Management Assessment Goal: in first 10 minutes Assess ABCs, vital signs Provide oxygen by nasal cannula Obtain IV access; obtain blood samples (CBC, lytes, coagulation studies) Obtain 12-lead ECG, check rhythm, place on monitor Check blood sugar; treat if indicated Alert Stroke Team: neurologist, radiologist, CT technician Perform general neurologic screening assessment 7. National Institutes of Health Stroke Scale 1a. Level of Consciousness (LOC): tests stimulation. Graded from 0-3. 1b. LOC Questions: tests the patient's ability to answer questions correctly. Graded from 0-2. 1c. LOC Commands: tests the patient's ability to perform tasks correctly. Graded from 0-2. 2. Best Gaze: tests horizontal eye movements. Graded from 0-2. 3. Visual: tests visual fields. Graded from 0-3. 4. Facial Palsy: tests the patient's ability to move facial muscles. Graded from 0 5. Motor Arm: tests motor abilities of the arms. Graded from 0-4. 6. Motor Leg: tests motor abilities of the legs. Graded from 0-4. 7. Limb Ataxia: tests coordination of muscle movements. Graded from 0-2. 8. Sensory: tests sensation of the face, arms, and legs. Graded from 0-2. 9. Best Language: tests the patient's comprehension and communication. Graded from 0-3. 10. Dysarthria: tests the patient's speech. Graded from 0-2. 11. Extinction and Inattention: tests patient's recognition of self. Graded from 0-2. 8. STROKE EMERGENCY BRAIN IMAGING: NONCONTRAST CT SCAN Acute (4 hours) InfarctionRLSubtle blurring of gray-white junction & sulcal effacementSubacute (4 days) Infarction L RObvious dark changes & mass effect (e.g., ventricle compression) 9. MRI BRAIN IN HYPERACUTE ISCHEMIC STROKE DWI & ADC: Early infarction visible FLAIR: No signal changes; possible sulcal effacement in area of infarction RLDWIRLADCRLFLAIR 10. MEDICAL MANAGEMENT 1. supportive management- airway, temperature, blood pressure, blood glucose, cardiac assessement2. thrombolysis intravenous / intra arterial3. antiplatelet drugs4. anticoagulant drugs5. hemodilution, vasodilators and induced hypertension 6. Neuroprotective agents 11. SURGICAL MANAGEMENT A) endovascular interventions 1) angioplasty and stenting 2) mechanical clot disruption 3) clot extraction B)carotid endartectomy 12. MANAGEMENT OF COMPLICATIONS 1.cerebral edema 2. hemorrhagic transformation 3. siezures 13. AIRWAY AND VENTILATION Patients with decreased consiousness AND or patients with brainstem stroke are at the greatest risk for airway compromise in stroke Seriously ill patients or those at risk for aspiration Elective intubation may help in the management of who have severely increases ICT 14. SUPPLEMENTAL OXYGEN adequate tissueoxygenation is important to prevent further brain injury Most common causes of hypoxia are partial airwayobstruction, hypoventilation. ,aspiration pneumonia,atelectasis.. Some patients develop cheynes stoke s respiration which is readily reversed by oxygen Hyperbaric oxygen studies done have been inconclusive or haveshown that it does not improve outcome 15. TEMPERATURE FEVER in the setting of acute stroke is associated withpoor outcome possibly due to 1. increased metabolic demands 2.enhanced release of neurotransmitters 3.increased free radical production Lowering acutely elevated body temperature mightimprove the prognosis in stroke pateints .. Antipyretic agents like acetaminophen and coolong devices might be used .. 16. HYPOTHERMIA Has been shown to be neuroprotective in experimentaland focal hypoxic brain injury models.. Inspite of expermimental and clinical evidence shows that hypothermia is neuroprotective data about induced hypothermia for the treatment of stroke are not available 17. BLOOD PRESSURE MANAGEMENT Reducing formation of brain edema lessening hemorrhagic transformation preventing early recurrent stroke 18. HOWEVER ,,, aggressive treatment of blood pressure may reduce the perfusion pressure to the ischemic areas of the brain In majority of patients decline in blood pressure occurs within the first few hours of stroke even without any treatment 19. When To Lower Blood pressure the hypertension is extreme (systolic blood pressure >220 mmHg or diastolic blood pressure >120 mmHg) ischemic coronary disease, heart failure, Aortic dissectionHypertensive encephalopathy Acute renal failure or pre-eclampsia/ Eclampsia 20. When treatment is indicated, cautious lowering ofblood pressure by approximately 15 percent during the first 24 hours after stroke onset is suggested Systolic blood pressure > 185 and diastolic > 110 is a contraindication for thrombolysis 21. BLOOD GLUCOSE LEVELS Hyperglycemia may augment brain injury by several mechanisms including increased tissue acidosis from anaerobic metabolism free radical generation increased blood brain barrier permeability. CONCLUSION evidence suggests that persistenthyperglycemia >140 mg/dl is associated with poor outcomes within the first 24 hrs of stroke .. The American Heart Association/American Stroke Association guidelines recommend treatment with insulin for patients who have serum glucose concentrations >140 to 185 mg/dL (>7.8 to 10.3 mmol/L) 22. HYPOGLYCEMIA- Hypoglycemia can cause focalneurologic deficits mimicking stroke, and severe hypoglycemia alone can cause neuronal injury Check the blood sugar and rapidly correct low serumglucose Normoglycemia is the desired goal while avoiding marked elevation of serum glucose. 23. Management of complications 24. INTRAVENOUS THROMBOLYSIS Results from the NINDS trial showed that intravenous alteplase (recombinant tissue-type plasminogen activator or tPA) improves functional outcome at three months, if given within 3 hours of symptom onset The ECASS 3 clinical trial found that intravenous alteplase is beneficial when given up to 4.5 hours after stroke onset 25. Despite recommendations, less than 1% of potentially eligible patients are currently being treated in India Principle behind the time dependency ofthrombolysis is that of penumbra the salvageable tissue which decreases every minute after stroke 26. CCrainCONTRAINDICATIONS The following contraindications apply in general: significant bleeding disorder at present or within the past 6 months, known haemorrhagic diathesis patients receiving oral anticoagulants, .g. warfarin sodium (INR> 1.7) any history of central nervous system damage (i.e. neoplasm, aneurysm, intracranial or spinal surgery) history or evidence or suspicion of intracranial haemorrhage including sub-arachnoid haemorrhage severe uncontrolled arterial hypertension major surgery or significant trauma in the past 15 days (this includes any trauma associated with the current acute myocardial infarction), recent trauma to head or cranium prolonged or traumatic cardiopulmonary resuscitation (> 2 minutes), obstetrical delivery, within the past 10 days, recent puncture of a non-compressible blood-vessel (e.g. subclavian or jugular vein puncture) severe hepatic dysfunction, including hepatic failure, cirrhosis, portal hypertension (oesophageal varices) and active hepatitis bacterial endocarditis, pericarditis acute pancreatitis documented ulcerative gastro-intestinal disease during the last 3 months arterial aneurysms, arterial/venous malformations hypersensitivity to the active substance alteplase or to any of the excipients 27. In the indication acute ischaemic stroke the following contraindications apply in addition: symptoms of ischaemic attack began more than 4.5 hours prior to infusion start or when time of symptom onset is unknown symptoms of acute ischaemic stroke that were either rapidly improving or only minor before start of infusion severe stroke as assessed clinically (e.g. NIHSS>25) and/or by appropriate imaging techniques seizure at the onset of stroke history of previous stroke or serious head-trauma within three months a combination of previous stroke and diabetes mellitus administration of heparin within 48 hours preceding the onset of stroke with an elevated activated partial thromboplastin time (aPTT) at presentation platelet count of less than 100,000 / mm3 systolic blood pressure > 185 or diastolic blood pressure > 110 mmHg, or aggressive management (IV medication) necessary to reduce blood pressure to these limits blood glucose < 50 or > 400 mg/dlACTILYSE is not indicated for the therapy of acute stroke in children and adolescents under 18 years or adults over 80 years of age. 28. HEMORRHAGE IN CLINICAL PRACTICE In clinical trials of IV alteplase, the rates of symptomaticintracerebral hemorrhage were 5 to 6 percent Early CT changes Brain edema or mass effect on the pretreatment CT scan was one of two major variables associated with an increased risk of intracerebral hemorrhage in patients treated with IV alteplase Stroke severity In addition to CT changes, the severity of neurologic deficit as measured on the NIHSS score) was the second major variable associated with intracerebral hemorrhage 29. Perform neurological assessments every 15 minutesduring the infusion and every 30 minutes thereafter for the next 6 hours, then hourly until 24 hours after treatment. If the patient develops severe headache, acutehypertension, nausea, vomiting, discontinue the infusion (if rtPA is being administered) and obtain an emergency CT scan. 30. INTRA ARTERIAL THROMBOLYSIS Intra-arterial thrombolysis The dose of thrombolytic drugs can be limited to that needed for recanalization, since the procedure is done under direct visualization. Intra arterial thrombolysis is an option of selected patients who have a major stroke < 6 hrs duration due to occlusion of MCA and who are not candidates for intravenous thrombolysis Treatment requires the patient to be at an experienced stroke center with immediate excess to cerebral angiography 31. Combined intravenous and intra-arterialthrombolysis The rationale for combined thrombolytic therapy is to unite the advantages of each: the wide availability of early rapid IV thrombolysis and potentially higher recanalization rates and therefore better outcomes of IA thrombolysis. 32. Mechanical/Endovascular methods Endovascular methods New catheter-based therapies are being developed for angioplasty, stenting, and mechanical clot disruption .Such approaches may decrease the risk of hemorrhage that is inherent with the use of thrombolytic drugs Mechanical clot disruption Endovascular embolectomy and clot disruption is undergoing study for acute treatment of ischemic stroke They offer the possibility of faster recanalization, higher recanalization rates, reduced total thrombolytic dose, and ultimately improved outcome 33. MERCI DeviceSource: St. Petersburg Times, October 2003 34. Conclusion Contraindications Early anticoagulation should be avoided when potential contraindications to anticoagulation are present, such as a large infarction It is recommended NOT using full-dose anticoagulation for treatment acute ischemic stroke because of limited efficacy an increased risk of bleeding complications. 35. ANTIPLATELET AGENTS 36. CONCLUSION Early aspirin therapy (initial dose 325 mg, thereafter 150 to 325 mg/day) be given to patients with ischemic stroke. The development of secondary hemorrhagic transformation of an ischemic infarct (ie, scattered and punctate). does not preclude the early use of aspirin, INTRAVENOUS ANTIPLATELET AGENTSGP II b III A INHIBITORS more research is needed to determine whether these agents have a role in stroke 37. VOLUME EXPANSION, INDUCED HYPERTENSION 38. Volume expansion and hemodilution were tried but it does not reduce case fatality or improve functional outcome in survivors VASODILATORS IN STROKE- methyl xanthine derivatives like pentoxyphylline have been tried but they do not have any role in acute stroke 39. NEUROPROTECTIVE AGENTS 40. SURGICAL INTERVENTIONS INDICATIONS Carotid endarterectomy (CEA) ismost commonly performed for symptomatic or asymptomatic high-grade (>60 or 70 percent) internal carotid artery stenosis HOWEVER , emergency carotid endartectomy efficacyis not established 41. GENERAL ACUTE TREATMENT FOR HOSPITALISED PATIENTS 42. INTRACEREBRAL HEMORRHAGE 43. ETIOLOGY Hypertensive vasculopathy is the most common etiology of spontaneous ICH. Hemorrhagic infarction (including venous sinus thrombosis) Cerebral amyloid angiopathy mycotic aneurysm Brain tumor Bleeding disorders, anticoagulants, thrombolytic therapy Central nervous system (CNS) infection (eg, herpes simplex encephalitis) Vasculitis Drugs (cocaine, amphetamines) Phenylpropanolamine in appetite suppressants, 44. INTRACEREBRAL HEMORRHAGE PROGNOSIS Initial ICH volume and level of consciousness The ICH volume on initial head CT scan and level of consciousness on admission may be particularly important prognostic indicators Hematoma growth Hematoma growth is also an independent predictor of mortality and poor outcome 45. Intraventricular extension Independent predictorof poor outcome in patients with spontaneous ICH Preceding antithrombotic use Preceding use of anticoagulants or antiplatelet agents might be expected to have larger initial hematoma volumes or greater hemorrhage enlargement Early neurologic deterioration Early neurologic deterioration within 48 hours after ICH is associated with a poor prognosis. 46. ICH score A simple six-point clinical grading scale called theICH score has been devised to predict mortality after ICH The ICH score is determined by adding the score from each component as follows: Glasgow Coma Scale (GCS) score 3 to 4 (= 2 points); GCS 5 to 12 (= 1 point) and GCS 13 to 15 (= 0 points) ICH volume 30 cm3 (= 1 point), ICH volume 130 mmHgand evidence or suspicion of elevated ICP, consider monitoring ICP and reducing blood pressure using intermittent or continuous intravenous medication to keep cerebral perfusion pressure in the range of 61 to 80 mmHg For patients with SBP >180 mmHg or MAP >130 mmHg and no evidence or suspicion of elevated ICP, consider a modest reduction of blood pressure (eg, target MAP of 110 mmHg or target blood pressure of 160/90 mmHg) using intermittent or continuous intravenous medication, and clinically reexamine the patient every 15 minutes 53. Seizure prophylaxis and treatment Appropriate intravenous antiepileptic drug (AED)treatment should be used to quickly control seizures for patients with ICH. Current guidelines suggest lorazepam or diazepam followed directly by intravenous fosphenytoin or phenytoin Guidelines recommend against prophylactic use of AEDs 54. TREATMENT OF ACUTE NEUROLOGIC COMPLICATIONS 55. SURGICAL TREATMENT Surgical removal of hemorrhage with cerebellardecompression should be performed for patients with cerebellar hemorrhages greater than 3 cm in diameter who are deteriorating, or who have brainstem compression and/or hydrocephalus due to ventricular obstruction For patients with supratentorial ICH, current guidelines suggest consideration of standard craniotomy only for those who have lobar clots >30 mL within 1 cm of the surface.. 56. Resumption of antiplatelet therapy -Timing anddose The AHA/ASA guidelines state that antiplatelets should be discontinued for at least one to two weeks Resumption of anticoagulation AHA/ASA guidelines conclude that intravenous heparin may be safer than oral anticoagulation 57. THANK YOU