Disclosures Case Study

10/11/2019

40th Annual Neurorehabilitation Conference on Traumatic Brain Injury, Stroke and Other Neurological Disorders Saturday & Sunday, November 16 & 17, 2019 Hyatt Regency Cambridge 575 Memorial Drive Cambridge, MA encompasshealth.com/braintreerehab Neuro Assessment For Nurses Vincent M. Vacca, Jr., MSN, RN

Disclosures • None

Case Study • The case study is fictional and used only for instructional purposes • References are cited throughout and at the end of the presentation • Nothing presented will be off label

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Objectives • At the conclusion of this presentation the participant will be able to: 1. Discuss 3 assessments of normal neurological function. 2. Describe 3 assessments of abnormal neurologic function using validated stroke measurement scale. 3. List 3 evidence based nursing care interventions for individuals with neurologic abnormalities from stroke.

What are we “Normally” doing at this moment? • Maintaining posture • Looking • Listening • Thinking • Processing information – Visual/Auditory/Emotional • Learning • Creating memories • Feeling thirsty/hungry • Planning dinner

• Other………….. 5

? Are you able to……. • See and eat food from the left side of your plate? • Dress the left side of your body? • Understand why people cheer at sporting event? • Or why people experience pain from an injury? • Recall these numbers (5438693) in 2 minutes? • Recognize the face of someone you previously met?

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Frontal Lobe Functions

• Hypothalamus and limbic systems send large number of projections to the frontal lobes. • Mediate biological drives (thirst, hunger) and emotions (fear, anger) • Frontal lobe networks fuse biological drives and impulses with knowledge to satisfy them. – Fusion = goal-oriented behavior. • Frontal lobes project to motor systems enabling motivational states to initiate overt behavior.

Frontal Lobe Intact - Injury/Damage • Intact frontal lobes – Resist biological drives to satisfy long-term goals • Injured/damaged frontal lobes – Regulation of drives is dysfunctional/lost – Poor Planning, – Lack of Insight, – Impulsivity, – Loss of Flexibility, – Poor Social Judgment.

Knowledge: The convergence of language, perception, and memory

• Now imagine the impact of a brain injury on your studies, profession, goals, life. • What it would be like for family members to live with you? • What were those numbers? 5 4 3 8 6 9 3

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Human Brain • Consists of 100 billion neurons & around 100,000 miles of blood vessels. • There are more than 100,000 chemical reactions happening in the human brain every second. • In each minute of ischemia, 1.9 million neurons, 14 billion synapses, and 12 km (7.5 miles) of myelinated fibers are destroyed. Stroke. 2006; Proc Natl Acad Sci U S A. 2012

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Despite increase in global burden of stroke • advances are being made. • Stroke is the fifth leading cause of death if considered separately from other cardiovascular diseases. • In the United States (US), an estimated 795,000 strokes occur annually, and the prevalence of stroke increases with age. • The lifetime risk of all strokes is higher in women; attributed to longer life-expectancy. • An estimated 6.8 million (2.8%) of people in the US are living after a stroke, including 3.8 million women and 3 million men. 13

Stroke in women

• The lifetime risk of stroke and mortality due to stroke is higher in women than men. • Some factors that contribute to an increased risk of stroke in women include: – pregnancy, – oral contraceptive use (especially when combined with smoking), – preeclampsia/eclampsia, – gestational diabetes, – migraine with aura, – increased risk of atrial fibrillation, – hormonal replacement therapy.

Nearly half of stroke survivors in the US • have residual deficits, including weakness or cognitive dysfunction, 6 months after stroke, which translates into ≈200 000 more disabled women than men. • Globally, at least 5 million people die from strokes and millions other remain disabled. • Stroke is the leading cause of adult disability worldwide.

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RFI…..

• Fewer than half of 9-1-1 calls for stroke events were made within 1 hour of symptom onset, and fewer than half of those callers thought stroke was the cause of their symptoms. (~795K strokes/yr) Stroke. published online February 6, 2014 • The brain is exquisitely sensitive to ischemia and other physiologic imbalances; & once injured, the

adult brain heals very poorly. (Emerg Med Clin N Am 30 (2012). • And when it doesn’t = – neurological dysfunction, – abnormalities, – deficits 16

BE-FAST#’s (balance, eyes, face, arm, speech, time/911) • One or more of face weakness, arm weakness, and speech difficulty symptoms are present in 88% of all

strokes and TIAs. Stroke. published online February 6, 2014

General examination is important

• Trauma • Seizures • Carotid bruits • Congestive heart failure. • Cardiac murmurs, arrhythmias • Pneumonia/pulmonary infiltrates • Evidence of coagulopathies, platelet disorders

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The goal of neuro-critical care for the patient • is to optimize long-term functional outcomes and quality of life by minimizing the amount of brain tissue that is lost. • optimize brain perfusion, limit secondary brain injury, and compensate for dysfunction in other organ systems. • Given data indicating that acute stroke patients might spend an average of 5 hours in the emergency department (ED), it is clear that optimal neurocritical care should begin in the ED and not be delayed until the patient arrives in the intensive care unit (ICU). (Emerg Med Clin N Am 30 (2012) 19

Recommended Not Recommended • Manage ABC’s • Excessive IV fluids • Cardiac Monitoring • Dextrose-containing fluids • O2 Sats > 94% in non-hypoglycemic • Establish IV access patients • • Determine blood glucose Medications by mouth and treat accordingly (maintain NPO until passes dysphagia screen) • Perform Dysphagia Screen Stroke 2013 before anything by mouth • Determine time of symptom onset or last known normal, and obtain family contact information,

preferably a cell phone 20

• The use of a stroke rating scale, preferably the NIHSS is recommended (Class I; Level of Evidence B). Stroke 2013 • NIHSS <5 most strongly associated with D/C home • NIHSS 6-13 most strongly associated with D/C to rehab • NIHSS >13 most strongly associated with D/C to nursing facility Schlegel, et al. 2003 Stroke 2011 Modified NIHSS: 1abc, 4, 5, 9. 21

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NIHSS: stroke-specific quantitative (0-42) scale assesses: – level of consciousness, (Brainstem, either/both hemisphere) – language function, (Left hemisphere) – neglect, (Right hemisphere) – visual field, (Either hemisphere, occipital lobe) – eye movements, (Brainstem, both hemispheres) – facial palsy, (Either hemisphere) – motor strength, (Either hemisphere, basal ganglia, brainstem) – sensory function, (Thalamus, basal ganglia) – coordination (Cerebellum) • Although most patients with potentially disabling symptoms will have NIHSS scores ≥4, certain patients, such as those with gait disturbance, isolated aphasia, or isolated hemianopia, may have potentially disabling symptoms although their NIHSS score is just 2. Ther Clin Risk Manag. 2012; 8: 87–93 22

NIHSS Scores/Severity

Neuro Assessment especially for Suspected Stroke Patients • Levels of consciousness Assessment & descriptors : – Alert – Drowsy – Stuporous – requires repeated stimulation, but will speak briefly and could be accurate – Obtunded – requires repeated noxious stimulation for one word or grunt response – Comatose – reflex response/movements only AANN Core Curriculum 6th edition

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Neuro Assessment especially for Suspected Stroke Patients • Level of consciousness questions: – Name – Date – Place – Hospital (Which one) – Situation – Why are you here? – City – State – Season • Typically we expect all to be correct; but the fewer correct the more concerned we are. • Compare w/ baseline. • Can possibly R/O or R/I signs of delirium

Neuro Assessment especially for Suspected Stroke Patients • Visual Acuity: • Test 4 quadrants (RUQ/RLQ/LUQ/LLQ) – For awake alert cooperative patients – test peripheral vision by: “tell me when you see my fingers wiggling” OR “how many fingers do you see”? – Keep them looking at your nose & bring the fingers for each quadrant in slowly. – This tests CNs II,III,IV,VI,VIII • Corneal reflex or do they blink to threat? – From all 4 quadrants? • This tests CN II, CN V, CN VII corneal/blink reflex

6 Cardinal Fields of Gaze – Cranial Nerves III, IV, & VI

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Neuro Assessment for (Anyone) but especially for Suspected Stroke Patients • If there's a problem with speech, ask the patient to repeat: • 'pa pa pa‘ • 'la la la‘ • 'ta ta ta‘ • 'ka ka ka‘ • You could combine all this into one and have them say Pawtucket 3 times listening for ability to make the sounds clearly Emerg Med Clin N Am 27 (2009) 1–16 Goldstein & Greer • This will reveal if the problem is with the – lip movements (CN VII), (Pa/Paw) – tongue movements (CN XII) (Ta/Tu ) – pharyngeal (CN’s IX or X) (Ka/Cut ).

Neuro Assessment especially for Suspected Stroke Patients • Level of consciousness commands: – Open eyes – Close eyes – Make fist – Relax fist • These maneuvers test: comprehension; CN III (Oculomotor) eyelid muscles & VII (Facial) & motor pathways to extremities • Shrug shoulders/turn head side to side evaluates CN XI (spinal accessory)

Upper Motor Neuron disorder (Stroke) the nerve is dysfunctional in the cortex; however the forehead has DUAL innveration - the forehead will be spared with a “central” or upper motor neuron disorder

Lower Motor Neuron disorder (Bells’) the ENTIRE face will be hypo-reflexic (Not Stroke)

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Neuro Assessment especially for Suspected Stroke Patients

• Motor Upper Extremities: • Observe for slow pronation • Pronator Drift – patient must of the wrist, flexion of fingers be able to comply. and/or elbow and a • Have them raise both arms downward and lateral drift of like holding a tray – elbows the hand. extended. • This is a very sensitive test • Palms up, eyes closed & for hemiparesis (mild) and hold it for 20 -30 seconds. can be suggestive that much worse weakness is • Look for weakness or drift – developing. note which extremity is affected. • Will be Contra-lateral to area of damage in the cerebral • Testing for pronator drift is motor strip/pathways. the best screen for muscle weakness of central origin.

Assessment - Localize lesions: Cortex or Brainstem • Lesions in the cerebral • Pontine Lesions result in cortex result in contralateral hemiplegia contralateral deficits of and ipsilateral deficits of the face and body. CN’s V, VI, VII, VIII. • Midbrain Lesions result • Medullary Lesions result in contralateral in contralateral hemiplegia and hemiplegia and ipsilateral peripheral ipsilateral deficits of paralysis of CN’s III & IV. CN’s IX, X, XI, XII.

Brainstem reflexes Reflex Technique Cranial Nerves Tested Shine light in eye and Pupillary light observe II/III response direct and consensual pupillary constriction Squirt water on cornea V1/VII Corneal reflex observe for blink

Nasal tickle Tickle nasal passage with V2/VII cotton swab and observe for symmetric grimace

Stimulate posterior pharynx IX/X Cough/Gag and observe for palatal reflex elevation

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A consensus panel convened by the National Institutes of Neurological Disorders and Stroke (NINDS) Established goals for time frames in the evaluation of

suspected stroke patients in the ED Stroke 2013 ED-Based Care Action Time Door to physician (AND NURSE) ≤10 minutes Door to stroke team ≤15 minutes Door to CT initiation ≤25 minutes Door to CT interpretation ≤45 minutes Door to drug ≤60 minutes (≥80% compliance) Door to stroke unit admission ≤3 hours

Features of Clinical Situations Mimicking Stroke or why you need a Stroke Neurologist Psychogenic Lack of objective cranial nerve findings, neurological findings in a nonvascular distribution, inconsistent examination Seizures History of seizures, witnessed seizure activity, postictal period Hypoglycemia History of diabetes, low serum glucose, decreased level of consciousness Migraine with aura (complicated migraine) History of similar events, preceding aura, headache Hypertensive encephalopathy Headache, delirium, significant hypertension, cortical blindness, cerebral edema, seizure Wernicke’s encephalopathy History of alcohol abuse, ataxia, ophthalmoplegia, confusion CNS abscess History of drug abuse, endocarditis, medical device implant with fever CNS tumor Gradual progression of symptoms, other primary malignancy, seizure at onset Drug toxicity Lithium, phenytoin, carbamazepine 35

Immediate Diagnostic Studies: Evaluation of a Patient With Suspected Acute Ischemic Stroke All patients Selected patients Noncontrast brain CT or brain MRI TT and/or ECT if it is suspected the patient Blood glucose is taking direct thrombin inhibitors or Oxygen saturation direct factor Xa inhibitors Serum electrolytes/renal function tests* Hepatic function tests Complete blood count, including platelet Toxicology screen count* Blood alcohol level Markers of cardiac ischemia* Pregnancy test Prothrombin time/INR* Arterial blood gas tests (if hypoxia is Activated partial thromboplastin time* suspected) ECG* Chest radiography (if lung disease is *Although it is desirable to know the results of these tests suspected) before giving intravenous recombinant tissue-type plasminogen activator, fibrinolytic therapy should not be Lumbar puncture (if subarachnoid delayed while awaiting the results unless hemorrhage is suspected and CT scan is (1) there is clinical suspicion of a bleeding abnormality or thrombocytopenia, negative for blood) (2) the patient has received heparin or warfarin, or Electroencephalogram (if seizures are (3) the patient has received other anticoagulants (direct suspected) thrombin inhibitors or direct factor Xa inhibitors). Stroke 2013 36

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Tissue Plasminogen Activator FDA Approvals

The major risk of IV TPA treatment remains sICH. • In the NINDS rtPA Stroke Trial, early minimal neurological symptoms or neurological deterioration temporally associated with any intracranial hemorrhage occurred in 6.4% of patients treated with intravenous rtPA and 0.6% of patients given placebo. • However, mortality in the 2 treatment groups was similar at 3 months (17% versus 20%) and 1 year

(24% versus 28%). Stroke 2013

Patients with mild to moderate strokes (NIHSS score <20) • and people <75 years of age had the greatest potential for an excellent outcome with treatment. • Around one in three patients treated with alteplase within 3 h of symptom onset, and one in six treated within 4·5 h, achieves significant benefit.

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Time Zero – Recognition by member of Sudden Weakness healthcare provider team of onset of Sudden Speech difficulty – Content &/or Articulation suspected acute evolving stroke Sudden Visual loss Sudden Dizziness Sudden severe headache with or without nausea and vomiting NOTE: Determine time of “Last known well” or at baseline 0-5 minutes of onset of suspected acute Stabilize patient, promote safety. evolving stroke; RRS/SART/ESAT/Code Blue Now up to 5 minutes of recognition/interventions for suspected acute as indicated, and covering LIP paged. evolving stroke

5 - 10 minutes following recognition & Now up to 15 minutes from onset of suspected acute evolving stroke assessment of suspected acute evolving Stroke Neurologist response by telephone within 10 minutes from page to stroke an evaluation by RRS & covering LIP patient evaluation for suspected acute evolving stroke completed and Stroke Neurologist notified of suspected acute evolving stroke. 15 minutes following page by RRS or Now up to 20 minutes from onset of suspected acute evolving stroke designee; evaluation performed by Stroke Neurologist. Stroke neurologist activates “Code Stroke” Now up to 25 minutes from onset of suspected acute evolving stroke. group beeper. Radiology clears and performs Non-contrast Now up to 45 minutes from onset of suspected acute evolving stroke head CT scan. Following completion of Non- Contrast Head CT scan; stroke neurologist determines eligibility for intravenous fibrinolysis (IVrtPA). 15 minutes or less following activation of Now up to 60 minutes from onset of suspected acute evolving stroke Stroke Team group pager: IV-tPA administered to eligible patient.

Social Work Clergy/Chaplaincy page as Patient & Family Support 40 needed.

Treatment of Acute Ischemic Stroke: IV TPA • Measure blood pressure and • Infuse 0.9 mg/kg (maximum perform neurological assessments dose 90 mg) over 60 minutes, every 15 minutes during and after with 10% of the dose given as a IV rtPA infusion for 2 hours, then every 30 minutes for 6 hours, then bolus over 1 minute. hourly until 24 hours after IV rtPA • If the patient develops severe treatment. headache, acute hypertension, • Delay placement of nasogastric tubes, indwelling bladder nausea, or vomiting or has a catheters, or intraarterial pressure worsening neurological catheters if the patient can be examination, discontinue the safely managed without them. • Obtain a follow-up CT or MRI scan infusion (if IV rtPA is being at 24 hours after IV rtPA before administered) and obtain starting anticoagulants or emergent CT scan. antiplatelet agents. Stroke 2013

IV TPA • (0.9 mg/kg, maximum dose 90 mg) is recommended for administration to eligible patients who can be treated in the time period of 3 to 4.5 hours after stroke onset (Class I; Level of Evidence B). • The eligibility criteria for treatment in this time period are similar to those for people treated at earlier time periods within 3 hours, with the following additional exclusion criteria: – patients >80 years old, – those taking oral anticoagulants regardless of INR, – those with a baseline NIHSS score >25, – those with imaging evidence of ischemic injury involving more than one third of the MCA territory, – those with a history of both stroke and diabetes mellitus.

(Revised from the 2009 intravenous rtPA Science Advisory)42

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The use of IV TPA • in patients taking direct thrombin inhibitors or direct factor Xa inhibitors may be harmful and is not recommended. • Similar consideration should be given to patients being considered for intra-arterial rtPA (Class III; Level of Evidence C). (New recommendation) Further study is required. Stroke 2013

For patients who are / have received IV TPA: • If clinical suspicion of intracerebral hemorrhage deterioration, new headache, acute hypertension, nausea or vomiting), discontinue IV rt-PA infusion and notify Stroke Team immediately. • Obtain STAT CT scan for any neurological deterioration. • STAT labs: INR, PTT, platelet count, fibrinogen, type & cross. • Prepare for administration of 6-8 units cryoprecipitated fibrinogen (Cryo) & factor VIII. • Riastap is a solution containing 1 g human fibrinogen per vial. • Prepare for administration of 6-8 units platelets. 44

Cortical Stroke – Assessment Findings

RIGHT BRAIN LEFT BRAIN Right gaze Left gaze preference preference Neglect Aphasia Paresis Paresis If present, think LARGE VESSEL stroke

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Case Study – 75 y/o Female w/ Left MCA Large-vessel occlusion typically causes severe stroke independently predicts poor neurological outcome. • Assessments: aphasia, dense right hemiparesis, and right hemianopia within 3 hours of symptom onset. Hyperdense LMCA Left MCA dot sign • The CT scan shows a hyperdensity of an M2 branch in the sylvian fissure (MCA dot sign) • It is associated with loss of 4 hours 32 hours gray-white differentiation and parenchymal hypodensity in the temporal and parietal

lobes. 46

LMCA Occlusion & Manifestations • results in Middle cerebral artery syndrome, potentially showing the following defects: • Paralysis (-plegia) or weakness (-paresis) of the contralateral face and arm (faciobrachial) • Sensory loss of the contralateral face and arm. • Damage to the dominant hemisphere (usually the left hemisphere) results in aphasia i.e. Broca's or Wernicke's

• Our LMCA patient NIHSS Eval (pre IVrtPA) 1a. 1 – alert/responsive 1b. 1 – one correct 1c. 1 – both correct 2. 1 – left gaze palsy 3. 1 – partial hemianopsia 4. 3 – facial palsy 5. 3 – right arm 6. 2 – right leg 7. 1 (+) ataxia 8. 1 – hemisensory 9. 2 – severe aphasia 10. 2 – severe dysarthria 11. 1 (+) neglect Total – 20 c/w mod to

severe stroke 48

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TPA Inclusion/Exclusion Criteria Inclusion criteria are a diagnosis of ischemic stroke with “measurable neurological deficit,” symptom onset within 3 hours before treatment, and age 18 years or older.

IV TPA • (0.9 mg/kg, maximum dose 90 mg) is recommended for selected patients who may be treated within 3 hours of onset of ischemic stroke (Class I; Level of Evidence A). • The door-to-needle time (time of bolus administration) should be within 60 minutes from

hospital arrival (Class I; Level of Evidence A). Stroke 2013 • Our patient weighs 65 kg’s (Verified) • 65 X 0.9 = 58.5 • 10% of 58.5 = 5.85 (bolus administered over 1 minute) • 52.65 administered over next hour by pump 50

The rich anastomotic connections • between the carotid and vertebral arteries provide a powerful collateral system which is able to compensate for the occlusion of up to three of these arteries. • The good collateral system results in lesser ischemic area than is a territory supplied by occluded artery • The bad collateral system results in ischemic area equal to a territory supplied by occluded artery.

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In AIS higher blood pressures are better than lower blood pressures

• Two pathophysiologic issues underlie this approach. • First, to reach the ischemic penumbra, blood must either flow through the significant stenosis in the native circulation that is causing the stroke or travel through probably higher resistance collateral routes in the case of occlusion of the native artery. • Second, autoregulation in ischemic brain is impaired, thus making flow (and therefore oxygen delivery) entirely dependent on perfusion pressure. • (Emerg Med Clin N Am 30 (2012) 52

Decreased systemic BP & blood flow • "End arteries" most at risk for ischemia. • Arteries start out close together so nourishment via diffusion is sufficient, but as we age, arteries separate and renders the Watershed Areas/Border Zones at risk for loss of arterial supply. • Pump/Thrombosis – Fix pump/Give TPA can dissolve ‘clot’ on ‘plaque’

Effects of Hypoxia • “normal” cerebral tissue perfusion in normotensive adults, is maintained at BFR ~50 mL/100 gm/min, provided CPP is in the range of ~60 to 160 mmHg. • Remember significant brain injury occurs when autoregulatory mechanisms are lost. • Supplemental oxygen should be provided to maintain oxygen saturation >94% (Class I; Level of Evidence C). (Revised from the previous guideline) Stroke 2013

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Ischemic brain edema has two phases:

• Initially main mechanism damage of cells: • cytotoxic component - disturbances of cell volume regulation w/ intracellular edema • Later on: vasogenic component: - disruption of the blood - brain barrier to circulating macromolecules significant extracellular edema • What further damage does edema cause?

• Once intracranial compensatory mechanisms are exhausted, small increases in intracranial volume can cause large increases in ICP • June 2012; Volume 18(3) Critical Care Neurology; p 532–546 • How can you know where your patient is on the Brain Pressure Compliance curve? • Normal ICP

Consider ICP monitoring and/or EVD for patients based on poor neurological status:

• Glasgow Coma Scale (GCS) score <8 or neurological deterioration with hydrocephalus or any concern for ICP elevation. • If EVD placed, ICP goal < 20 • If rapid edema formation is suspected or observed consult Neurosurgery Service for initial evaluation for emergency decompressive craniectomy should it become a therapeutic option.

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Glasgow Coma Scale Assessment Tool

Hypothermia (Not OHCA?) • There is insufficient data to support therapeutic hypothermia in acute ischemic strokes currently. • A retrospective study recently demonstrated an association between a peak temperature in the first 24 hours of greater than 39 C and increased risk of in-hospital mortality.

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Hypoglycemia • It is reasonable to follow the current American Diabetes Association recommendation to maintain the blood glucose in a range of 140 to 180 mg/dL. (Regardless of HbgA1c). • Hypoglycemic patients less than 60 mg/dL should be treated to achieve normoglycemia.

For all patients during the acute phase after ischemic stroke or TIA, and independent of thrombolytic therapy: • Keep Cerebral Perfusion Pressure (CPP) > 70 and Mean Arterial Pressure (MAP) 80-110. • Avoid Hypo/Hyper-glycemia. • Observe for & prevent hyponatremia. • Maintain normothermia. • Maintain euvolemia. • Early enteric feeding should be encouraged. – For patients with dysphagia, use a nasogastric tube to promote enteric feeding. 62

Post AIS management • Bed rest for 24 hours, then increase activity as tolerated to promote active exercise, strength training, and gait training. • Dysphagia screening to be completed and documented prior to anything by mouth using the Bedside Nurse Administered Swallow Screen.

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Quality Metrics/Standards/Core Measures • Identify patient and family education needs and provide appropriate information and resources found in the stroke education packet. • This should include identification of personal modifiable risk factors, such as  smoking cessation,  nutrition,  exercise,  blood pressure regulation,  warning signs for stroke,  activation of EMS,  need for follow-up after discharge,  medications prescribed. • Document education provided in the Patient Education section of the electronic medical record.

What about IA therapies? • Perform a CT angiogram first to understand vessels. • If a large vessel lesion discovered and patient has a ‘double digit’ NIHSS meaning significant deficits. • Can get to “the lesion” within/by 6 hours from onset is best. • If however it’s a Basilar artery & especially if the signs/symptoms are ‘fluctuating’ can go 12 hours. • Balloon angioplasty is Not Commonly performed. • Stents are: Trevo/Solitaire – once stent deployed flow is again antegrade and clot(s) can be retrieved. • IV rtPA for large vessel – can still go to interventional for catheter based interventions.

Mechanical Thrombectomy • The use of mechanical thrombectomy should be considered in all patients, even in those who received fibrinolytic therapy. • The AHA/ASA guidelines do not recommend observation for a response after IV alteplase in patients who are being considered for mechanical thrombectomy. • Multiple stroke trials in 2015 showed that Endovascular thrombectomy in the first six hours is much better than standard medical care in patients with large vessel occlusion in the arteries of the proximal anterior circulation. • These benefits sustained irrespective of geographical location and patient characteristics.

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Again in 2018, a significant paradigm shift happened in stroke care. • DAWN trial showed significant benefits of Endovascular thrombectomy in patients with large vessel occlusion in the arteries of the proximal anterior circulation. • This trial extended stroke window up to 24 hours in selected patients using perfusion imaging. • Due to this, we can treat more patients even up to 24 hours.

The current recommendation in selected patients • with large vessel occlusion with acute ischemic stroke in the anterior circulation and meet other DAWN and DEFUSE 3 criteria, mechanical thrombectomy is recommended within the time frame of 6 to 16 hours of last known normal. • In selected patients who meet the DAWN criteria, mechanical thrombectomy is reasonable within 24 hours of last known normal.

Our patient Post IV-TPA & IA Therapy - NIHSS • 1a. 0 • 1b. 0 • 1c. 0 • 2. 1 partial gaze palsy • 3. 1 partial visual deficit • 4. 1 minor facial palsy • 5. 1 drift of RUE • 6. 1 drift of RLE • 7. 0 • 8. 0 • 9. 1 mild aphasia • 10. 1 mild dysarthria • 11. 0 • Total = 7 • Disposition to rehab facility for short term treatment, then hopefully back home. 69

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MODIFIED RANKIN SCALE (MRS) • Patient Name: Our Patient • Rater Name: Us • (MRS) Date: Today • Score Description – 0 No symptoms at all – 1 No significant disability despite symptoms; able to carry out all usual duties and activities – 2 Slight disability; unable to carry out all previous activities, but able to look after own affairs without assistance – 3 Moderate disability; requiring some help, but able to walk without assistance – 4 Moderately severe disability; unable to walk without assistance and unable to attend to own bodily needs without assistance – 5 Severe disability; bedridden, incontinent and requiring constant nursing care and attention – 6 Dead 70

Prognosis for CVA is highly dependent

• on the extent of: • involved cerebral structures, • cerebral area involved, • time to identification and diagnosis, • time to treatment, • length and intensity of physical and occupational therapy, • and prior baseline functioning.

References

• Stroke. 2018;49:eXXX–eXXX. DOI: 10.1161/STR.0000000000000158. • Hui C, Tadi P, Patti L. Ischemic Stroke. [Updated 2019 May 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499997/ • Sabih A, Tadi P, Kumar A. Stroke Prevention. [Updated 2019 Mar 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470234/ • Khaku AS, Hegazy M, Tadi P. Cerebrovascular Disease (Stroke) [Updated 2019 Aug 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430927/ • AANN Core Curriculum 6th edition • Emerg Med Clin N Am 27 (2009) 1–16 Goldstein & Greer