Prof Mohammad Salah Abduljabbar

Objectives

Define cerebrovascular accident and associated terminology

Discuss related pathophysiology and presentation of various types of stroke

Discuss etiology, risk factors, diagnostics, management, and outcomes of stroke

Review case studies and nursing diagnoses, interventions, and goals

Definition

Stroke or “brain attack” is an acute CNS injury that results in neurologic Symptoms and signs brought on by a reduction or absence of perfusion to a territory of the brain. The disruption in flow is from either an occlusion (ischemic) or rupture (hemorrhagic) of the blood vessel.

Incidence & Prevalence

Third leading cause of death in the USA 750,000+ people/year 175,000 die within one year (25%)

Leading cause of long-term disabilities 5.5 million survivors (USA) 15 to 30 % live with permanent disability

Stroke Statistics

15% of adults > age 50 cannot name a single symptom of stroke

13 hours after onset of symptoms is the median time to presentation

58% of stroke patients don’t present during the first 24 hours after onset

52% of stroke patients in the ED are unaware that they are experiencing a stroke

Classification

Cerebrovascular Accident Ischemic Stroke

Thrombotic Embolic Lacunar infarct TIA

Hemorrhagic Stroke ICH SAH

Stroke Knowledge

MYTHS

Can’t prevent stroke Can’t treat stroke Stroke affects the heart Stroke affects the

elderly Recovery happens for a

few months after stroke

FACTS

Stroke is preventable Stroke is treatable Stroke is a brain attack Stroke affects anyone Stroke recovery occurs

throughout life

Stroke: Emergency Care

Stroke Symptoms

Sudden numbness or weakness of face, arm or leg, especially on one side of the body

Sudden confusion, trouble understanding or speaking

Sudden trouble seeing in one or both eyes

Sudden trouble walking, dizziness, loss of balance or coordination

Sudden severe headache with no known cause

Other Symptoms

Sudden nausea, fever and vomiting, distinguished from a viral illness by rapid onset (minutes or hours vs. days)

Brief loss of consciousness or period of decreased consciousness (fainting, confusion, convulsions or coma)

Cerebral Ischemia

Embolism

Abrupt onset Small vascular area Focal deficit

Pure aphasia Pure hemianopia

Acute CT normal High recurrence risk

Thrombosis

Preceded by TIAs Abrupt onset Large vascular area More complex

symptoms Acute CT normal

Thrombotic Stroke

Occlusion of large cerebral vessel

Older population Sleeping/resting Rapid event, but slow

progression (usually reach max deficit in 3 days)

Embolic Stroke

Embolus becomes lodged in vessel and causes occlusion

Bifurcations are most common site

Sudden onset with immediate deficits

Hemorrhagic Transformation

Lacunar Strokes - 20% of all stokes

Minor deficits Paralysis and sensory loss

Lacune Small, deep penetrating

arteries High incidence:

Chronic hypertension Elderly DIC

Lacunar Strokes

15 – 20% of ischemic strokes Small penetrating branches of circle of

Willis, MCA, or vertebrobasilar artery Atherothrombotic or lipohyalinotic

occlusion Infarct of deep brain structures

Basal ganglia, cerebral white matter, thalamus, pons, and cerebellum

From 3 mm to 2 cm

Lacunar Stroke Syndromes

Well-defined syndromes Pure motor hemiparesis (with dysarthria) Pure sensory stroke (loss or

paresthesias) Dysarthria-clumsy hand (with

contralateral face and tongue weakness) Ataxia-hemiparesis (contralateral face

and leg weakness) Isolated motor-sensory stroke

Risk factors Diabetes Hypertension Polycythemia

Variable course progressing over days Fluctuating; progressing in steps; or

remitting Preceded by TIAs in 25% Without headache or vomiting

Remember Lacunar Strokes

Transient Ischemic Attack

“Sudden, focal neurologic deficit lasting less than 24 hours, confined to an area of the brain or eye perfused by a specific artery.”

Based on assumption that TIAs do not cause infarction or other permanent brain injury.

Time criterion is arbitrary.

Transient Ischemic Attack

Warning sign for stroke Brief localized ischemia Common

manifestations: Contralateral numbness/

weakness of hand, forearm, corner of mouth

Aphasia Visual disturbances-

blurring

Deficits last less than 24 hours (usually less than 1 or 2 hrs)

Can occur due to: Inflammatory artery

disorders Sickle cell anemia Atherosclerotic

changes

TIA - Differential Diagnosis

Anxiety (panic attack)

Hyperventilation Neuropathy (focal) Neuropathy

(ischemic) Vertigo Disequilibrium

Migraine Orthostatic

hypotension Syncope Arrhythmias

(ischemia) Seizures Conversion disorder

Hemorrhagic Stroke Definitions

Intracerebral hemorrhage Intracranial hemorrhage Parenchymal hemorrhage Intraparenchymal hematoma Contusion Subarachnoid hemorrhage

Cerebral Hemorrhage

Epidural hemorrhage Smooth onset Arterial origin Mass effect causes

coma over hours Similar (but slower

in evolution) to hemorrhage in basal ganglia

Subdural hemorrhage

Smooth onset Venous origin May be recurrent Fluctuating, falsely

localizing signs

Hemorrhagic Stroke

Rupture of vessel Sudden Active Fatal HTN Trauma Varied

manifestations

Hemorrhagic Stroke

Intracerebral Hemorrhage

Subarachnoid Hemorrhage

PathophysiologyHemorrhagic Stroke

Changes in vasculature Tear or rupture Hemorrhage Decreased perfusion Clotting Edema Increased intracranial pressure Cortical irritation

Hearing/association & Smell & taste Short term Memory

Voluntary Motor

Sensations Pain & Touch Taste

Balance, Coordination of each muscle group

Arms

Head

LegsMom: Bowel/bladder Reasoning/judgment Long term memory

Vision & visual memory

CN 5,6,7,8 P,R, B/P CN 9,10,11,12

Tracks cross over Coordinate movement, HR,B/P

Vessels of the Brain

Vessels of the Brain

Right Side

Circle of Willis

PhysiologyNormal Cerebral Blood Flow

Oxygen Glucose 20% of Cardiac Output / oxygen Arterial supply to the brain:

Internal carotid (anteriorly) Vertebral arteries (posteriorly)

Venous drainage 2 sets of veins - venous plexuses

Dural sinuses to internal jugular veins Sagittal sinus to vertebral veins

No valves, depend on gravity and venous pressure gradient for flow

Risk Factors

NON-MODIFIABLE MODIFIABLE

Age 2/3 over 65

Gender M=F Female>fatality

Race AA > hispanics, NA Asians > hem

Heredity Family history Previous TIA/CVA

Hypertension Diabetes mellitus Heart disease A-fib Asymptomatic carotid stenosis Hyperlipidemia Obesity Oral contraceptive use Heavy alcohol use Physical inactivity Sickle cell disease Smoking Procedure precautions

EtiologyIschemic Stroke

Embolism Prothrombotic states Atrial fib Sinoatrial Disease Recent MI Endocarditis Cardiac tumors Valvular heart disease Patent foramen ovale Carotid/basilar artery

stenosis Atherosclerotic lesions Vasculitis

Hemostatic regulatory protein abnormalities

Antiphospholipid antibodies

Hep cofactor II

Etiology Hemorrhagic Stroke

Chronic HTN** Cerebral Amyloid Angiopathy* Anticoagulation* AVM Ruptured aneurysm (usually subarachnoid) Tumor Sympathomimetics Infection Trauma Transformation of ischemic stroke Physical exertion, Pregnancy Post-operative

Aneurysm

Localized dilation of arterial lumen Degenerative vascular disease Bifurcations of circle of Willis

85% anterior 15% posterior

AneurysmSubarachnoid Hemorrhage

SAH Mortality 70% 97% HA Nuchal rigidity Fever Photophobia Lethargy Nausea Vomiting

Aneurysm/SAH

Complications HCP Vasospasm

Triple H Therapy HTN Hemodilution Hypervolemia

Surgical treatment Clip Coil INR

Nursing Management

Assessment Monitoring

BP TCDs CBC

Preventing complications Bowel program DVT prophylaxis Seizure prophylaxis Psychological support Discharge planning

Arteriovenous Malformations AVM

Tangled mass of arteries and veins Seizure or ICH

Presentation

Sudden onset Focal neurological deficit Progresses over minutes to hours HA, N/V, <<LOC, HTN Depends on location

Treatment of AVM

Endovascular Neurosurgery Radiosurgery

Manifestationsby Vessel

Vertebral Artery Pain in face, nose, or eye Numbness and weakness of face (involved

side) Gait disturbances Dysphagia Dysarthria (motor speech)

Manifestationsby Vessel

Internal carotid artery Contralateral paralysis (arm, leg, face) Contralateral sensory deficits Aphasia (dominant hemisphere

involvement) Apraxia (motor task), Agnosia (obj. recognition), Unilateral neglect (non-dominant

hemisphere involvement) Homonymous hemianopia

Initial Stroke Assessment/Interventions

Neurological assessment & NIH assessment Call “Stroke Alert” Code Ensure patient airway VS IV access Maintain BP within parameters Position head midline HOB 30 (if no shock/injury) CT, blood work, data collection/NIH Stroke

Scale Anticipate thrombolytic therapy for ischemic

stroke

NIH Stroke Scale Score

Standardized method measures degree of stroke r/t impairment and change in a patient over time.

Helps determine if degree of disability merits treatment with tPA. As of 2008 stroke patients scoring greater than 4 points can be treated with

tPA.

Standardized research tool to compare efficacy stroke treatments and rehabilitation interventions.

Measures several aspects of brain function, including consciousness, vision, sensation, movement, speech, and language not measured by Glasgow coma scale.

Current NIH Stroke Score guidelines for measuring stroke severity: Points are given for each impairment.

0= no stroke 1-4= minor stroke 5-15= moderate stroke 15-20= moderate/severe stroke 21-42= severe stroke A maximal score of 42 represents the most severe and devastating stroke.

Comic Relief

Question

The neurologic functions that are affected by a stroke are primarily related to A. the amount of tissue area involved. B. the rapidity of the onset of symptoms. C. the brain area perfused by the

affected artery. D. the presence or absence of collateral

circulation.

Question

A patient is admitted to the hospital with a left hemiplegia. To determine the size and location and to ascertain whether a stroke is ischemic or hemorrhagic, the nurse anticipated that the health care provider will request a A. CT scan. B. lumbar puncture. C. cerebral angiogram. D. PET scan.

Diagnosis

Tests for the Emergent Evaluation of the Patient with Acute Ischemic Stroke

CT head (-) 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 Institute of Health Scale (NIHSS) score

Diagnosis

Ischemic Stroke Hemorrhagic Stoke

Medical Management

BP MAP CPP

Factor VII, Vit K, FFP ICP

HOB Sedation Osmotherapy Hyperventilation Paralytics

Fluid management euvolemia

Seizure prophylaxis Keppra Dilantin

Sedation Body temperature PT/OT/ST DVT prophylaxis

Treatment

Ischemic Hemorrhagic

Medical management TPA Endovascular

Carotid endarectomy Merci clot removal

http://youtu.be/P2TNz-TniIA

Medical management Decompression

Craniotomy Craniectomy

PT/OT/STREHABILITATION

Medications

Anti-coagulants – A fib & TIA Antithrombotics Calcium channel blockers – Nimotop

(nimodipine) Corticosteroids ??? Diuretics – Mannitol, Lasix (Furosemide) Anticonvulsants – Dilantin (phenytoin) or

Cerebyx (Fosphenytoin Sodium Injection) Thrombolytics - tPA (recombinant tissue

plasminogen activator)

Medications

Thrombolytics Recombinant Alteplase (rtPA) Activase, Tissue plasminogen activator Treatment must be initiated promptly after CT to

R/O bleed Systemic within 3 hours of onset of symptoms Intra-arterial within 6 hours of symptoms

Some exclusions: Seizure at onset Subarachnoid hemorrhage Trauma within 3 months History of prior intracranial hemorrhage AV malformation or aneurysm Surgery 14 days, pregnancy, Cardiac cath. 7 days

Neurosurgical Management

Craniotomy Craniectomy EVD placement ICP monitor placement

Recommendations for Surgical Treatment of ICH

Nonsurgical candidates Small hemorrhage Minimal deficit GCS </= 4 (unless

brain stem compression)

Loss of brainstem reflexes

Severe coagulopathy Basal ganglion or

thalamic

Surgical candidates >3cm

Neuro deficit Brain stem

compression MLS, HCP

Aneurysm, AVM, cavernous hemangioma

Young c mod/large lobar hemorrhage c clinical deterioration

Reducing Primary Risk

Obstructive sleep apnea Homocysteine folate, B6, B12 Hypertension – morning BP surge Smoking 50% risk reduction in 1

yr Hyperlipidemia statins Migraine triptans Drugs – cocaine, ephedra, PPA

Reducing Primary Risk

Asymptomatic carotid stenosis Endarterectomy for > 60% stenosis Risk reduction for 3% to 1% per year Benefit related to surgical risk

Nonvalvular atrial fibrillation Aspirin for patients < 65 years, healthy Warfarin for patients > 65 years or

having other stroke risk factors

Reducing Secondary Risk

Reducing risk of recurrence TIA with ipsilateral carotid stenosis

endarterectomy for > 70% stenosis

Cardiogenic embolism warfarin

Lacunar infarcts aspirin, dipyridamole

Cryptogenic infarcts (40% embolic) anticoagulation?

Reducing Risk in Children Sickle cell disease

Screen with transcranial doppler q 6 mo Transfusion therapy for 2 abnormal

studies Congenital heart disease Arterial dissections (trauma) Prothrombotic disorders Mitochondria disorders (MELAS)

Using Statins

Pooled results after 5 years Pravastatin or Simvastatin 40

mg/day Changes in cholesterol levels

Total cholesterol decreased 20% LDL cholesterol decreased 28% HDL cholesterol increased 5% Triglycerides decreased 13%

Using Statins

Reducing LDL cholesterol by 1 mmol/L 22% stroke reduction in patients with

known vascular disease 6% stroke reduction in patients without

known vascular disease 28% reduction in thromboembolic stroke

Complications

Increased intracranial pressure Rebleeding Vasospasm HCP Death

Outcomes

Age Size, volume Location HCP, IVH Deficit, LOC, MAP Duration Co-morbidities

44% mortality

References

AANN Core Curriculum for Neuroscience Louis, MO. Nursing, 4th Ed. 2004. Saunders. St.

Broderick, J., et. al. (1999) Guidelines for the management of spontaneous intracerebral hemorrhage. AHA.

El-Mitwali, A., Malkoff, M. (2001) Intracerebral hemorrhage. The Internet Journal of Neurosurgery. 1.1.

Greenberg, Mark. (2006). Handbook of Neurosurgery. Greenberg Graphics,

Tampa, Florida.