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Posterior Circulation StrokeJessica Heckenberger BSN RN

St. Luke’s University Health Network

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

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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 – 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 20-50% 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 – 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”– 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)

• 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• Ipsilateral tongue weakness and later hemiatrophy of the tongue

• Contralateral hemiparesis of the arm and leg

• Hemisensory loss—touch and proprioception

Pons• 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.

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Effects of tPA

Fibrin strand Fibrin Strands

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Activase (Alteplase)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

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

– 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

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90th

Percentile

SLA/B SLRA SLM SLQ SLWFY 14 FY 15

YTDFY 14 FY 15

YTDFY 14 FY 15

YTDFY 14 FY 15

YTDFY 14 FY 15

YTD

VTE Prophylaxis 98.65 98.7 100 100 100 100 100 100 100 100 100Discharge 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 ---- ---- ----- 100 ----

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 66.7Rehab 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 ---- ----- ----- 0 0

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Thank youAnd please always remember...

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References

http://brainfoundation.org.au/medical-info/205-locked-in-syndrome-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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