AHA/ASA Guidelines

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

Assess patient’s ABC Physical Examination

Los Angeles Prehospital Stroke ScreenLast time patient known to be symptom free, Date _____ Time _____Screening criteriaAge 45 y Yes Unknown NoNo history of seizures or epilepsy Yes Unknown NoSymptoms present 24 h Yes Unknown NoNot previously bedridden or wheelchair bound Yes Unknown NoIf unknown or yesBlood glucose 60 to 400 mg/dL Yes NoExaminationFacial smile grimace Normal Right droop Left droopGrip Normal Right weak Left weak

No grip No gripArm strength Normal Right drift Left drift

Right falls Left fallsBased on examination, patient has unilateral weakness Yes

NoIf items are yes or unknown, meets criteria for stroke

Cincinnati Prehospital Stroke ScaleFacial droop

Normal—both sides of face move equally

Abnormal—one side of face does not move as well as the otherArm 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 otherSpeech

Normal—says correct words with no slurring

Abnormal—slurs words, says the wrong words, or is unable to speak

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

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

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

ABC’s Head & neck (signs of trauma or seizure) Cardiac examination Skin and extremities

◦ Hepatic dysfunction, coagulopathies, platelet disorder)

National Institutes of Health Stroke ScaleTested Item Title Responses and Scores1A Level of consciousness 0—alert 1—drowsy

2—obtunded 3—coma/unresponsive1B Orientation questions (2) 0—answers both correctly 1—answers one correctly 2—answers neither correctly1C Response to commands (2) 0—performs both tasks correctly 1—performs one task correctly 2—performs neither2 Gaze 0—normal horizontal movements 1—partial gaze palsy

2—complete gaze palsy3 Visual fields 0—no visual field defect 1—partial hemianopia

2—complete hemianopia 3—bilateral hemianopia4 Facial movement 0—normal 1—minor facial weakness

2—partial facial weakness 3—complete unilateral palsy5 Motor function (arm) 0—no drifta. Left 1—drift before 5 secondsb. Right 2—falls before 10 seconds

3—no effort against gravity4—no movement

6 Motor function (leg) 0—no drifta. Left 1—drift before 5 secondsb. Right 2—falls before 5

seconds3—no effort against gravity4—no movement

7 Limb ataxia 0—no ataxia1—ataxia in 1 limb2—ataxia in 2 limbs

8 Sensory 0—no sensory loss1—mild sensory loss2—severe sensory loss

9 Language 0—normal1—mild aphasia2—severe aphasia3—mute or global aphasia

10 Articulation 0—normal1—mild dysarthria2—severe dysarthria

11 Extinction or inattention 0—absent1—mild (loss 1 sensory

modality)2—severe (loss 2 modalities)

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

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)

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

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

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

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

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)

MRI ◦ Better at distinguishing acute, small cortical,

small deep, and posterior fossa infarcts◦ Distinguishing acute from chronic ischemia◦ Identifying subclinical satellite lesion that provide

information on stroke mechanism Limitation:

◦ Cost, limited availability, claustrophobia, cardiac pacemakers, metal implants

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

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

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

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

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 renal failure, acute pulmonary edema, or acute myocardial infarction

There are some studies that noted an unfavorbale outcome with the decline or blood pressure

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

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

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

Hypovolemia should be corrected with normal saline

If these measures are ineffective, vasopressor agents such as dopamine may be used

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

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

Recombinant Tissue Plasminogen Activator 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

Characteristics of Patients With Ischemic StrokeWho Could Be Treated With rtPA

Diagnosis of ischemic stroke causing measurable neurological deficitThe 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 treatmentNo head trauma or prior stroke in previous 3 monthsNo myocardial infarction in the previous 3 monthsNo gastrointestinal or urinary tract hemorrhage in previous 21 daysNo major surgery in the previous 14 daysNo arterial puncture at a noncompressible site in the previous 7 daysNo history of previous intracranial hemorrhageBlood pressure not elevated (systolic 185 mm Hg and diastolic 110

mm Hg)No evidence of active bleeding or acute trauma (fracture) on

examinationNot taking an oral anticoagulant or, if anticoagulant being taken, INR

1.7If receiving heparin in previous 48 hours, aPTT must be in normal

range.Platelet count 100 000 mm3Blood glucose concentration 50 mg/dL (2.7 mmol/L)No seizure with postictal residual neurological impairmentsCT does not show a multilobar infarction (hypodensity 1/3 cerebral

hemisphere).The patient or family members understand the potential risks and

benefits from treatment.

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

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

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.

glycoprotein IIb/IIIa inhibitors They may increase the rate of spontaneous

recanalization and improve microvascular patency

Ongoing research is testing the usefulness of intravenously administered antiplatelet agents (glycoprotein IIb/IIIa receptor blockers) when given alone or in combination with other Interventions

when used alone, have an acceptable safety profile

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

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 withrapid opening of the artery◦ FDA has approved the use of the MERCI device for

reopening intracranial arteries extraction of the thrombus

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.

(1) swelling of the ischemic tissue causing mass effect◦ hyperventilation, osmotic diuretics, drainage of

cerebral fluid, or decompressive surgery◦ Mannitol is typically used at 0.25 to

0.5 g/kg IV administered over 20 minutes

(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.