Guidelines for the Early Management of Adults with Ischemic Stroke

1. Guidelines for the Early Management of Adults with Ischemic Stroke AHA/ASA Guidelines

2. Prehospital Management • Patient’s history • Time of onset • Recent events • Stroke • MI • Trauma • Surgery • Bleeding • Relatives • Comorbid diseases • Hypertension • Diabetes Mellitus • Use of medications • Anticoagulants • Insulin • Antihypertensive

3. Assess patient’s ABC • Physical Examination

4. Los Angeles Prehospital Stroke Screen Last time patient known to be symptom free, Date _____ Time _____ Screening criteria Age 45 y Yes Unknown No No history of seizures or epilepsy Yes Unknown No Symptoms present 24 h Yes Unknown No Not previously bedridden or wheelchair bound Yes Unknown No If unknown or yes Blood glucose 60 to 400 mg/dL Yes No Examination Facial smile grimace Normal Right droop Left droop Grip Normal Right weak Left weak No grip No grip Arm strength Normal Right drift Left drift Right falls Left falls Based on examination, patient has unilateral weakness Yes No If items are yes or unknown, meets criteria for stroke

5. Cincinnati Prehospital Stroke Scale Facial droop Normal—both sides of face move equally Abnormal—one side of face does not move as well as the other Arm drift Normal—both arms move the same or both arms do not move at all Abnormal—one arm either does not move or drifts down compared to the other Speech Normal—says correct words with no slurring Abnormal—slurs words, says the wrong words, or is unable to speak

6. Management • Recommended • Manage ABC • Cardiac Monitoring • IV access • O2 ( O2 sat <92%) • Assess for hyperglycemia • NPO • Transfer patient to a hospital with proper facilities to manage patient with acute stroke

7. Emergency Evaluation and Diagnosis of Acute Ischemic Stroke • Stabilization of the ABC’s • Secondary assessment of neurological deficits and possible comorbidities • Exclude stroke mimics • Identify other conditions requiring immediate intervention • Determine potential causes of stroke

8. History • Time of symptoms onset • Potential cause of the symptoms • Conversion disorder, hypertensive encephalopathy, hypoglycemia, complicated migraine, seizures • Risk factors for arterioscelrosis and cardiac disease • HX of drug abuse, seizures, infection, trauma, pregnancy, heparin or warfarin use, bleeding problems

9. Physical Examination • ABC’s • Head & neck (signs of trauma or seizure) • Cardiac examination • Skin and extremities • Hepatic dysfunction, coagulopathies, platelet disorder)

10. Neuro Exam National Institutes of Health Stroke Scale Tested Item Title Responses and Scores 1A Level of consciousness 0—alert 1—drowsy 2—obtunded 3—coma/unresponsive 1B Orientation questions (2) 0—answers both correctly 1—answers one correctly 2—answers neither correctly 1C Response to commands (2) 0—performs both tasks correctly 1—performs one task correctly 2—performs neither 2 Gaze 0—normal horizontal movements 1—partial gaze palsy 2—complete gaze palsy 3 Visual fields 0—no visual field defect 1—partial hemianopia 2—complete hemianopia 3—bilateral hemianopia 4 Facial movement 0—normal 1—minor facial weakness 2—partial facial weakness 3—complete unilateral palsy 5 Motor function (arm) 0—no drift a. Left 1—drift before 5 seconds b. Right 2—falls before 10 seconds 3—no effort against gravity 4—no movement

11. 6 Motor function (leg) 0—no drift a. Left 1—drift before 5 seconds b. Right 2—falls before 5 seconds 3—no effort against gravity 4—no movement 7 Limb ataxia 0—no ataxia 1—ataxia in 1 limb 2—ataxia in 2 limbs 8 Sensory 0—no sensory loss 1—mild sensory loss 2—severe sensory loss 9 Language 0—normal 1—mild aphasia 2—severe aphasia 3—mute or global aphasia 10 Articulation 0—normal 1—mild dysarthria 2—severe dysarthria 11 Extinction or inattention 0—absent 1—mild (loss 1 sensory modality) 2—severe (loss 2 modalities)

12. Diagnostic Test • Noncontast brain CT or brain MRI • Blood glucose • Serum electrolytes/renal function test • ECG • Markers for cardiac ischemia • CBC w/ PLT • PT/INR • aPTT • Oxygen saturation

13. Selected patients • Hepatic function test • Toxicology screen • Blood alcohol level • Pregnancy test • ABG (hypoxia) • Chest Radiograph ( lung disease) • Lumbar Puncture ( subarachnoid hemorrhage suspect and CT negative for blood) • Electroencephalogram (seizure)

14. Early Diagnosis: Brain and Vascular Imaging • Size, location, and vascular distribution of the infarction, presence of bleeding and short-term and long term decisions. • Degree of reversibility of ischemic injury, intracranial vessel status, and cerebral hemodynamic status

15. Non-contrast Enhanced CT Scan • Insensitive in detecting acute and small cortical or subcortical infarction (posterior fossa) • Identify subtle, early signs of ischemic brain injury or arterial occlusion- treatment • Loss of gray-white differentiation in cortical ribbon, lentiform nucleus, and sulcal effacement detected within 6 hours- poorer outcomes • Widespread signs of early infarction are correlated with a higher risk of hemorrhagic transformation after thrombolytic agents

16. Multimodal CT • Noncontrast CT • Perfusion CT • Whole brain perfusion CT • Map of cerebral blood volume • Region of hypoattenuation represent ischemic core • Advantage of providing whole-brain coverage • Inability to provide measures of cerebral blood flow • Dynamic perfusion CT • Potential provide absolute measures of cerebral blood flow, mean transit time, and cerebral blood volume • Limited to 2 to 4 brain slices- incomplete visualization of all pertinent vascular territories

17. CT angiography • Rapid and noninvasive method to evaluate intracranial and extracranial vasculature • Advantage of relatively rapid data acquisition and can be performed with conventional CT • Disadvantage iodine contrast and additional radiation exposure

18. MRI • Acute stroke evaluation • Diffusion-weighted imaging (DWI) • Visualization of ischemic regions w/in minutes of symptoms onset • Detect lesion size, site, age and small cortical or subcortical lesion in brain stem or cerebellum poorly visualized with standard CT scan • Perfusion weighted imaging (PWI) • Measure cerebral hemodynamic status • MR angiography • Gradient echo • Fluid-attenuated inversion recovery (T2 weighted)

19. MRI Over CT • MRI • Better at distinguishing acute, small cortical, small deep, and posterior fossainfarcts • Distinguishing acute from chronic ischemia • Identifying subclinical satellite lesion that provide information on stroke mechanism • Limitation: • Cost, limited availability, claustrophobia, cardiac pacemakers, metal implants

20. General Supportive Care and Treatment of Acute Complications • Airway, Ventilatory Support, and Supplemental Oxygen • Prevent hypoxia • Most common cause partial airway obstruction, hypoventilation, aspiration pneumonia, and atelectasis • Prognosis- require endotracheal intubation is poorer- 50% dead within 30 days after stroke • Pneumonia- leading complication of stroke and important cause of death

21. Temperature • Fever • Poor neurological outcome • Increased metabolic demands • Enhanced release of neurotransmitters • Increase free radicals production • Hypothermia • Neuroprotective in experimental and focal hypoxic brain injury models • May delay depletion of energy reserves • Lessen intracellular acidosis • Slow influx of calcium into ischemic cells • Suppress production of oxygen free radicals • Lessen the impact of excitatory amino acids

22. Cardiac monitoring • Patient with infarction of right hemisphere (Insula)- increased risk of cardiac complications • Sec disturbance in autonomic nervous system function • ECG changes • ST segment depression • QT dispersion • Inverted T waves • Prominent U waves • Atrial fibrillation- most common arrhythmia

23. Arterial Hypertension • For every 10-mm HG increase >180mm Hg • neurologic deterioration increased by 40% • Risk of poor outcome increased by 23% • Elevated blood pressure – secondary to stress of cerebrovascular event. Full bladder, nausea. Pain. Pre-existing hypertension, physiological response to hypoxia

24. Reasoning for lowering blood pressure • reducing the formation of infarction • Preventing further vascular damage • and forestalling early recurrent stroke. • urgent antihypertensive therapy may be • needed to treat patients with stroke who also have hypertensive encephalopathy, aortic dissection, acute renalfailure, acute pulmonary edema, or acute myocardial infarction • There are some studies that noted an unfavorbale outcome with the decline or blood pressure

25. agreed that patients with markedly elevated blood pressure may have their blood pressure lowered. A reasonable goal would be to lower blood pressure by 15% during the first 24 hours after onset of stroke • medications should be withheld unless the systolic blood pressure is >220 mm Hg or the diastolic blood pressure is >120 mm Hg

26. Patients who have elevated blood pressure and are otherwise eligible for treatment of rtPA may have their blood pressure lowered so that their systolic blood pressure is <185 mm Hg and their diastolic blood pressure is <110 mm Hg before lytic therapy is started

27. Arterial hypotension • potential causes are aortic dissection, volume depletion, blood loss, and decreased cardiac output secondary to myocardial ischemia or cardiac arrhythmias, that might be reducing cardiac output should be corrected • Hypovolemiashould be corrected with normal saline • If these measures are ineffective, vasopressor agents such as dopamine may be used

28. Hypoglycemia • may produce neurological signs that mimic ischemic stroke and because hypoglycemia itself may lead to brain injury • should be treated in patients with acute ischemic stroke. • The goal is to achieve normoglycemia

29. Hyperglycemia • one third of patients with stroke • presence of hyperglycemia is associated with poor outcomes after ischemic stroke, including among patients treated with thrombolytic agents • desired level of blood glucose has been in the range of 80 to 140 mg/dL

30. Intravenous Thrombolysis • Recombinant Tissue PlasminogenActivator • associated with improved outcomes for a broad spectrum of patients who can be treated within 3 hours of stroke onset • Earlier treatment (ie, within 90 minutes) may be more likely to result in a favorable outcome. Later treatment, at 90 to 180 minutes, also is beneficial • major risk of treatment was symptomatic brain hemorrhage( 6.4% of patients treated with rtPA) • death rate was similar at 3 months and 1 year compared with placebo

31. Characteristics of Patients With Ischemic Stroke Who Could Be Treated With rtPA Diagnosis of ischemic stroke causing measurable neurological deficit The neurological signs should not be clearing spontaneously. The neurological signs should not be minor and isolated. Caution should be exercised in treating a patient with major deficits. The symptoms of stroke should not be suggestive of subarachnoid hemorrhage. Onset of symptoms 3 hours before beginning treatment No head trauma or prior stroke in previous 3 months No myocardial infarction in the previous 3 months No gastrointestinal or urinary tract hemorrhage in previous 21 days No major surgery in the previous 14 days No arterial puncture at a noncompressible site in the previous 7 days No history of previous intracranial hemorrhage Blood pressure not elevated (systolic 185 mm Hg and diastolic 110 mm Hg) No evidence of active bleeding or acute trauma (fracture) on examination Not taking an oral anticoagulant or, if anticoagulant being taken, INR 1.7 If receiving heparin in previous 48 hours, aPTT must be in normal range. Platelet count 100 000 mm3 Blood glucose concentration 50 mg/dL (2.7 mmol/L) No seizure with postictal residual neurological impairments CT does not show a multilobar infarction (hypodensity 1/3 cerebral hemisphere). The patient or family members understand the potential risks and benefits from treatment.

32. Other Thrombolytic Agents • Clinical trials of streptokinase were halted prematurely because of unacceptably high rates of hemorrhage • reteplase, urokinase, anistreplase, and staphylokinase, might have been considered • for treatment of patients with acute ischemic stroke. None of these agents has been tested extensively • Tenecteplase and Desmoteplase has been tested in a • pilot study; results appear promising

33. Anticoagulants • Urgent anticoagulation with the goal of preventing • early recurrent stroke, halting neurological worsening, • or improving outcomes after acute ischemic stroke is • not recommended for treatment of patients with acute • ischemic stroke • early administration of either heparin or a LMW heparin/danaparoid is associated with an increased risk of bleeding complications. • increase the risk of symptomatic hemorrhagic • transformation of ischemic strokes

34. AntiplateletAgents • Aspirin is the only oral antiplatelet agent that has been evaluated for the treatment of acute ischemic stroke. • nonsignificant trend in reduction in death or disability when treatment with aspirin was initiated within 48 hours of stroke • ticlopidine, clopidogrel, or dipyridamole in the setting of acute ischemic stroke has not been evaluated.

35. Intravenous Antiplatelet Agents • glycoprotein IIb/IIIa inhibitors • They may increase the rate of spontaneous recanalizationand improve microvascular patency • Ongoing research is testing the usefulness of intravenously administered antiplatelet agents (glycoprotein IIb/IIIareceptor blockers) when given alone or in combination with other Interventions • when used alone, have an acceptable safety profile

36. Surgical Intervention • Little information exists about the effectiveness of surgical treatment of patients with acute ischemic stroke • Emergency carotid • endarterectomy generally is not performed in other settings of acute ischemic stroke because the risks of the procedure are perceived to be high. • sudden restoration of blood flow might increase the development of brain edema or lead to hemorrhagic transformation

37. Endovascular Interventions • emergency angioplasty • Angioplasty and stenting have been used to treat patients with acute stroke secondary to carotid artery dissection • stenting • mechanical disruption of the clot • Mechanical Embolus Removal in Cerebral Embolism (MERCI) • was associated withrapidopening of the artery • FDA has approved the use of the MERCI device for reopening intracranial arteries • extraction of the thrombus

38. Combination Reperfusion Therapyin Acute Stroke • The standard treatment in many ACS patients includes antiplatelet therapy with aspirin, clopidogrel, glycoprotein IIb/IIIa blockers, antithrombotic therapy with heparin or LMW heparin, and direct percutaneous coronary intervention.

39. Treatment of AcuteNeurological Complications • (1) swelling of the ischemic tissue causing mass effect • hyperventilation, osmotic diuretics, drainage of cerebral fluid, or decompressivesurgery • Mannitol is typically used at 0.25 to • 0.5 g/kg IV administered over 20 minutes

40. (2) hemorrhagic transformation of the infarction withor without mass effect; and, less commonly • depends • on the amount of bleeding and its symptoms and may include clot evacuation in deteriorating patients • (3) seizures. • more likely to • occur within 24 hours of stroke and are usually partial • Few data are available on the efficacy of anticonvulsants in the treatment of stroke patients who have experienced seizures.