Prof Mohammad Salah Abduljabbar. Objectives Define cerebrovascular accident and associated...
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Transcript of Prof Mohammad Salah Abduljabbar. Objectives Define cerebrovascular accident and associated...
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.