Posterior Circulation Stroke

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Transcript Posterior Circulation Stroke

Posterior Circulation Stroke
Jessica Heckenberger BSN RN
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Stroke Statistics
 Stroke is the 5th leading cause of death in the U.S.
 Stroke kills almost 130,000 Americans each year—that’s
1 out of every 19 deaths.
 On average, one American dies from stroke every 4
minutes.
 Stroke costs the United States an estimated $38.6 billion
each year. This total includes the cost of health care
services, medications to treat stroke, and missed days of
work.
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F.A.S.T.
F-Face Drooping – Does one side of the face droop or is it numb? Ask
the person to smile. Is the person's smile uneven?
A- Arm-Is one arm weak or numb? Ask the person to raise both arms.
Does one arm drift downward?
S-Speech Difficulty – Is speech slurred? Is the person unable to speak
or hard to understand? Ask the person to repeat a simple sentence, like "The
sky is blue." Is the sentence repeated correctly?
T-Time-What was the time the person was last known well?
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Beyond Fast: B.E. F.A.S.T
B-Balance-Sudden trouble walking, dizziness, loss of balance or
coordination
E-Eyes-Sudden trouble seeing in one or both eyes
Vision
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St. Luke’s Primary Stroke Center’s
St. Luke’s Allentown Campus
St. Luke’s Anderson Campus
St. Luke’s Bethlehem Campus
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Posterior Circulation Stroke
 Posterior circulation stroke accounts for 20-25% of
ischemic strokes
 Specialist assessment and administration of intravenous
tissue plasminogen activator are delayed in posterior
circulation stroke compared with anterior circulation
stroke
 Basilar occlusion is associated with high mortality or
severe disability, especially if blood flow is not restored in
the vessel; if symptoms such as acute coma, dysarthria,
dysphagia, quadriparesis, pupillary and oculomotor
abnormalities are detected, urgently seek the input of a
stroke specialist
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The Posterior Circulation
 Vertebral arteries
 The basilar artery
 The posterior cerebral arteries and their
branches
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PCA Supply
 Posterior Circulation Brain Structures
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Brainstem (medulla, pons, and midbrain)
Cerebellum
Thalamus
Hippocampus
Areas of temporal and occipital cortex
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Etiology
 Arterial atherosclerosis (large artery disease) and
penetrating artery disease (lacunes).
 Cardiogenic embolization is more common than
previously suspected and is responsible for 2050% of posterior circulation strokes
 Vascular obstruction or occlusion is the
fundamental disorder leading to hypoperfusion
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Time is Brain
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Risk Factors
 Uncontrollable Risk Factors
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Age
Gender
Race
Family history of stroke or TIA
Personal history of diabetes
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Risk Factors
 Medical Risk Factors
– Hypertension
– Heart disease (such as atrial fibrillation or left ventricular
hypertrophy)
– Previous stroke or TIA
– Previous heart surgery
– Carotid artery disease
– Peripheral vascular disease
– Smoking
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Signs and Symptoms
 “5 D’s”
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Dizziness
Diplopia
Dysarthria
Dysphagia
Dystaxia
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Signs and Symptoms
 Changes in eye movement–
Visual field loss in one or both
eyes.
– Ptosis
– Diplopia
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Signs and Symptoms
 Dizziness/Vertigo
– Symptoms ranging from near-syncope, lightheadedness or
faintness to a sensation of movement or disequilibrium,
unsteadiness, or imbalance
– Vertigo with or without nausea and vomiting
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Signs and Symptoms
 Dysphagia or dysarthria
 “Crossed” syndromes, consisting of ipsilateral cranial nerve dysfunction
and contralateral long motor or sensory tract dysfunction are highly
characteristic of posterior circulation stroke
 Sensory deficits (numbness, including loss of sensation or par aesthesia in
any combination of extremities, sometimes including all four limbs or both
sides of the face or mouth)
 Isolated reduced level of consciousness is not a typical stroke symptom but
can result from bilateral thalamic or brainstem ischemia
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Posterior Circulation Infarction According to
Anatomical Location and Vascular Territory Affected
 Lateral medulla (intracranial vertebral artery infarct, also known
as Wallenberg syndrome)
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Nystagmus, vertigo, ipsilateral Horner’s syndrome, ipsilateral facial sensory loss, dysarthria,
hoarseness, and dysphagia
Contralateral hemisensory loss in the trunk and limb—pain and temperature
 Medial medulla
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Ipsilateral tongue weakness and later hemiatrophy of the tongue
Contralateral hemiparesis of the arm and leg
Hemisensory loss—touch and proprioception
 Pons
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Hemiparesis or hemisensory loss, ataxic hemiparesis, dysarthria, horizontal gaze palsy
Complete infarction causes “locked-in syndrome” with quadriparesis, loss of speech, but
preserved awareness and cognition, and sometimes preserved eye movements
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Locked-in Syndrome
 Locked-in Syndrome (LIS) results from a lesion to the brainstem,
most frequently an ischemic pontine lesion. It results in severe
impairments due to the complete disruption of the motor pathways
controlling eyes, face, trunk and limb movements, including
breathing, swallowing and phonation. However consciousness and
cortical functions are preserved.
 LIS is defined as a syndrome characterized by preserved
awareness, relatively intact cognitive functions, and by the ability to
communicate while being paralyzed and voiceless.
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Locked-in Syndrome
 Locked-in syndrome affects around 1% of people who
have as stroke
 Individuals with LIS have the highest level of disability
among stroke survivors
 It is a condition for which there is no treatment or cure,
and it is extremely rare for patients to recover any
significant motor functions.
 90% die within four months of its onset
– Initial stroke primary cause of death (25% of cases)
• Voluntary cough is often impossible, and sometimes there is no reflex cough
• Aspiration pneumonias are more common during the acute phase
– Secondarily to infections such as pneumonia (40% of cases)
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Locked-in Syndrome
 Acute Phase
– Respiratory tract monitoring and cardiovascular support
– Thrombolysis or the prescription of blood thinners based on the
type of vascular impairment
– Peg tube feeding
– Tracheostomy
– VTE prophylaxis
– Skin care management
– PT
• ROM
• Bracing
• Proper posturing in bed
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Locked-In Syndrome
 Rehabilitation Phase
– Individuals use eye movements to communicate
– Communication devices (as computer with synthetic voice)
– Some individuals may be suitable for weaning from their
tracheostomy as their condition improves during the first months
– Exercises to maintain range of motion, as well as breathing,
eyes, head, trunk and limb control exercises are performed
throughout the rehabilitation process.
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Diagnosing
 History and physical exam
– Horner’s syndrome- ptosis, small pupil, and anhydrosis on the
same side, bilateral small or fixed pupils, and ataxia may aid
early diagnosis.
 Non-contrast CT of head
 CT angiography- identify basilar artery occlusion
 MRI
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Management
 Thrombolysis
 Intra-arterial thrombolytic therapy
 Heparin Therapy
 Neurosurgery
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tPA (Activase)
 Tissue plasminogen activator.
 Activase is indicated for the management of
acute ischemic stroke in adults for improving
neurological recovery and reducing the incidence
of disability
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Rationale for Use
 Limit size of infarct by dissolving clot & restoring
blood flow to ischemic brain.
 Prompt treatment with (t-PA) may promote
reperfusion and improve functional outcomes for
patient.
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Time Frame
 Given intravenously within 3 hours of acute
ischemic stroke (FDA)
 The window can be extended to 4.5 hours if
patient meets additional criteria
 Goal Door to Needle Time:
Administer (t-PA) within 1 hour of arrival to hospital
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Effects of tPA
 Binds to fibrin in a thrombus and converts
plasminogen to plasmin which initiates local
fibrinolysis…Tips the scale in the other direction.
 Fibrinolysis: the breakdown of a blood clot.
Clot/
Fibrin
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t-PA
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Effects of tPA
Fibrin strand
Fibrin Strands
Activase (Alteplase)
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Contraindication 0-3hr Window
 Evidence of intracranial hemorrhage
 Suspicion of subarachnoid hemorrhage on pretreatment evaluation
 Recent intracranial or intraspinal surgery, serious head trauma, or previous stroke
 Major surgery / serious trauma
 History of intracranial hemorrhage
 Uncontrolled hypertension at time of treatment (eg, > 185 mm Hg systolic or > 110 mm
Hg diastolic)
 Allergy to t-PA
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Seizure at the onset of stroke (unless neuroimaging confirms ischemia)
Active internal bleeding
Glucose < 50 or > 400
Known bleeding diathesis including but not limited to:
Current use of oral anticoagulants (eg, warfarin sodium) or an International Normalized
Ratio (INR) > 1.7or a prothrombin time (PT) > 15 seconds
 Administration of heparin within 48 hours preceding the onset of stroke and have
an elevated activated partial thromboplastin time (aPTT) at presentation
 Platelet count < 100,000/mm3
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Contraindications 0 to 4.5 Hour Window
 CONTRAINDICATIONS - IN ADDITION TO THE
0 TO 3 HOUR WINDOW
 Patient age
 Patient taking oral anticoagulation despite INR
level
 History of both stroke and diabetes
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Risk Factors
 Largest risk factors is bleeding
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Benefits of tPA
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Neurosurgical
 External ventricular drainage or decompression may be
lifesaving in large volume cerebellar infarction with falling
level of consciousness attributable to raised intracranial
pressure or acute hydrocephalus.
 Emergency posterior fossa decompression with partial
removal of the infarcted tissue may be lifesaving.
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Diagnostic Work-up
 Diagnostic work-up done to:
– Determine etiology of stroke
– Identify risk factors
– Determine most appropriate secondary stroke prophylaxis
• Anticoagulation
• Antiplatelet
• Statins
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Cardiac Diagnostics
 Electrocardiogram
– Look for arrhythmias, conduction problems
 Transthoracic echocardiogram (TTE)
– screen for cardioembolic conditions
 Transesophageal echocardiogram (TEE)
– Screen for cardioembolic conditions
– Invasive test
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Other Diagnostic Studies
 Carotid Doppler
 EEG
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Inpatient Rehabilitation
 Speech Therapy
 Physical Therapy
 Occupational Therapy
 Dietary Consultation
– Multidisciplinary Rounds
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Patient/ Family Education
 On going education from all disciplines
 Stroke Patient Education Binder
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Diagnosis
Risk Factors
Risk Factor Modification
Family Risk
Teach S/S of stroke
Importance of taking medications
Importance of regular medical follow-up
 Stroke Club
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Stroke Prevention
 Hypertension
– BP < 120/80 (after acute phase of stroke)
– Dietary changes, exercise, medications
 Smoking
– Cessation counseling
– Treatment (meds, hypnosis, etc..)
 Diabetes
– HgbA1C goal < 7.0%
– Meds, diet, exercise
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Prevention Cont….
 Dyslipidemia
– Lipid Profile (goals)
• Total Cholesterol < 200
• LDL < 100 (<70)
• HDL > 35
• Triglycerides < 200
– Meds, diet, exercise
 Obesity
– BMI > 25
– Exercise for 30 minutes on most days
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Stroke Data
90th
SLA/B
SLRA
SLM
SLQ
SLW
Percentile
FY 14
FY 15
YTD
FY 14
FY 15
YTD
FY 14
FY 15
YTD
FY 14
FY 15
YTD
FY 14
FY 15
YTD
VTE Prophylaxis
98.65
98.7
100
100
100
100
100
100
100
100
100
Discharge
Antithrombotics
98.92
100
100
100
100
100
100
100
100
100
100
Discharge
Anticoagulation A.
Fib.
94.12
100
100
100
100
100
100
100
100
100
100
Thrombolytic
Therapy
89.47
85.7
90
66.7
50
50
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100
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Antithrombotic by
Day 2
98.53
98.7
100
100
94.7
100
100
100
100
100
100
Discharge Statin
98.15
99.6 99.1
100
100
100
100
95.7 95.7 96.2 96.2
Stroke Education
97.5
99.5 95.9
92
100
77.8 77.8
100
88.9
75
66.7
Rehab Assessment
98.8
100
100
100
100
100
100
100
100
100
100
Door to tPA 60 min
50
68.2
80
50
33.3
0
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0
0
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Thank you
And please always remember...
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References
 http://brainfoundation.org.au/medical-info/205-locked-insyndrome-lis
 http://cirrie.buffalo.edu/encyclopedia/en/article/303/
 http://www.bmj.com/content/348/bmj.g3175
 Lewandowski, C., & Santhakumar, S., Posterior
Circulation Stroke, Foundation for Education and
Research in Neurological Emergencies. 2012.
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