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What Every Stroke Patient Wants
Their Nurse to Know…
Presented by:
Mary Kay Bader
RN, MSN, CCNS, CCRN, CNRN, FAHA
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Disclosures
• Bader– American Association Neuroscience Nurses
• President
– Honorarium
• Bard
– Medical Advisory Board
• Neurooptics and Brain Trauma Foundation
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Objectives
• Identify the cerebrovascular anatomy of the brain
and differentiate between strokes in the various
cerebral vessels
• Describe the pathophysiology of occlusion and the
importance of collateral blood flow and BP
• Differentiate between the management of BP in
patients receiving tPA and those who do not
receive tPA
• Describe the major nursing priorities in caring for
the acute stroke patient.
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What is a stroke?
• Sudden development of a focal neurologic deficit
caused by blockage in an artery feeding the
brain or a rupture of the artery in the brain
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Introduction• Statistics
– 795,000 new strokes each year
• 610,000 1st stroke
• 6.4 million stroke survivors in US
• 130,000 deaths each year (decrease of 18.4% between 1996 and 2006) with 25% reduction by 2008
• 20% survivors institutional care after 3 months
• 25-30% permanently disabled
– 4th leading cause of death in US
CDC Prevalence of Stroke in United States 2006-2010. MMWR. 2012. 61 (20): 379-382.
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Circulation of Brain
• Anterior circulation
– Carotid arteries
• Posterior circulation
– Vertebral arteries
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What kinds of Stroke?
• Ischemic
• Hemorrhagic
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Ischemic Stroke
• 87%
– Thrombotic/atherosclerotic disease
• 20%
– Embolic
• 20%
– Lacunar or subcortical stroke
• 20-25%
• Small vessel disease
– Cryptogenic: cause unknown
• 30%
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Hemorrhagic Stroke
• 13%
– Intracerebral
– Subarachnoid Hemorrhage
• Aneurysm
–8 to 10 per 100,000 population
»1-5% of population
–10-12 million
–50-80% don’t rupture over lifetime• Vascular Malformations
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The Anatomy of Stroke
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Right vs Left Brain
• If clockwise, then you use more
of the right side of the brain
• If counterclockwise, then you
use more of the left side of the
brain
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Cerebrum
• Left Hemisphere
– rational/logical reasoning, intellectual
deductive/analytical thinking, science, math,
language, reading, writing, sequential ordering,
and the ability to perform fine motor learned acts
• Right Hemisphere
– imagination, inductive reasoning, spatial, art,
music, nonverbal ideation, spiritual, visual images,
shape, recognizing faces, & facial expressions
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Anatomy of Cerebral
Vasculature
• Anterior circulation
• Posterior circulation
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Anatomical
Assessment
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Arterial Syndromes
• Carotid System– Contralateral hemiparesis with facial asymmetry and
sensory changes
– HH, horner’s syndrome, & amourosis fugax
– Dominant hemisphere- aphasia, dyslexia, agraphia,
acalculia
– Non-dominant hemisphere-loss of spatial
relationships, dressing/constructional apraxia
– Headache over ipsilateral eye
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Arterial Syndromes
• ACA:
– Contralateral sensorimotor deficit > foot than arm or
face; urinary incontinence;& rigidity
– Abulia-slowness of all reactions
– Distractibility, perseveration, cognitive impairment,
personality changes
– Expressive aphasia
– Apraxia
– Contralateral grasping reflex & sucking reflex
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Arterial Syndromes
• MCA– Contralateral paralysis & sensory loss > arm than leg
& homonymous hemianopia
– Dominant hemisphere- aphasia, dyslexia, agraphia, acalculia
– Non-dominant hemisphere-loss of spatial relationships, dressing/constructional apraxia
– Decrease in LOC with massive infarct
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Arterial Syndromes
• Vertebrobasilar Artery Syndrome
– Ataxia, vertigo, nausea, transient global amnesia, dysarthria, dysphagia, dysmetria
– Visual disturbances, HH, diplopia, nystagmus, conjugate gaze paralysis
– Facial weakness, tinnitus, deafness
– Altering hemiparesis
– Drop attacks and syncope
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Arterial Syndromes
• Posterior cerebral arteries
– Visual changes: field cuts, possible 3rd
nerve palsy, visual perception, inability to
recognize objects, faces, pictures, colors,
or symbols
– Paralysis of contralateral side if pyramidal
tract is affected
– Some hemi-sensory changes
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Arterial Syndromes
• PICA-Wallenburg’s syndrome
– Ipsilateral numbness of face & horner’s syndrome (miosis, ptosis, & anhydrosis)
– Contralateral loss of pain & temperature over half of the body
– Dysphagia, dysphonia, decreased gag reflex, & paralysis of soft palate/larynx
– Nystagmus, diplopia, vertigo, nausea & vomiting, hiccoughs
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Stroke Signs/Symptoms
• Key Stroke Syndromes
– Left Vessels (dominant hemisphere)
• Left gaze preference
• Right visual field deficit
• Right hemiparesis
• Right hemisensory loss
– Right Vessels (non-dominant hemisphere)
• Right gaze preference
• Left visual field deficit
• Left hemiparesis
• Left hemisensory loss
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Stroke Signs/Symptoms
• Key Stroke Syndromes– Brainstem (basilar-vertebral arteries)
• Nausea and/or vomiting
• Diplopia, dysconjugate gaze, gaze palsy
• Dysarthria, dysphagia
• Vertigo, tinnitus
• Hemiparesis or quadriplegia
• Sensory loss in hemibody or all 4 limbs
• Decreased level of consciousness
• Hiccups, abnormal respirations
– Cerebellum
• Truncal/gait ataxia
• Limb ataxia/neck stiffness
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Pathophysiology
of Ischemic Stroke
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Pathophysiology of Ischemic
Stroke
• Dense core of dead tissue
• Penumbra
• Interruption of blood flow
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Pathology of Occlusion
• Once vessel is occluded
– Systemic arterial BP influences CPP and
collateral blood flow during ischemia
– Permanent ischemic cell death ensues
after 30 minutes
• Continued ischemia (< 50% of baseline
CBF) will kill the rest of the vessel
territory
• What can save this area around core?
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Collateral Flow
• Example MCA occlusion
– Leptomeningeal arteries
– Cross perfusion from internal system
• Opposite side
• Posterior circulation
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Pathophysiology of
Ischemic Stroke
• Cellular Responses to reduced Flow
• Disturbances in calcium homeostasis
• Buildup of lactic acidosis
• Oxygen free radical production
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Pathophysiology of
Ischemic Stroke
• Three Factors Affecting
Outcome
– Time dependent
– Degree of ischemia
– Collateral circulation
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Pathophysiological Issues
Related to Stroke
• Edema and Increased ICP
– Occurs as natural evolution of insult
– Minimized if restore perfusion
– Assess for change in neurologic
status
• Do not medicate with sedation
agents unless monitoring for
increased ICP
• Prepare for CT
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Pathophysiological Issues
Related to Stroke
• Blood Pressure
• Blood Glucose
• Temperature
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Pathophysiology:
BP & Stroke
• Alteration in cerebral blood flow
• Brain perfusion dependent on
MAP
• Increases in BP
– may be normal homeostatic
response
– usually falls spontaneously within
24 hours to several days
• Do Not treat BP unless…...
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Pathophysiology:
BP & Stroke
• Treat BP in acute ischemic stroke
– No thrombolytics
• Systolic > 220 mm Hg
• Diastolic > 120 mm Hg
• MAP > 130 mm Hg
– Thrombolytics
• Systolic >185 mm Hg – After tPA 180 mm Hg
• Diastolic >110 mm Hg – After tPA 105 mm Hg
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Pathophysiology:
Blood Glucose & Stroke
• Maintain blood glucose <
180
– When blood glucose level
exceeds 180 begin
strategies to lower serum
glucose
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Pathophysiology:
Body Temperature & Stroke
• Temperature control
–Avoid hyperthermia
•Stroke – normothermia
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Don’t Forget the 5 Fs of Stroke
Care
• Flow – (reestablish flow)
• Flat – (head of bed if no edema)
• Fluids – (euvolemia)
• Fever – (normothermia)
• Finger sticks – (control glucose)
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Diagnostic Tests in
Stroke Diagnosis
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• All Patients
– Non-contrast CT/MRI
– Blood glucose
– Oxygen saturation
– Serum electrolytes/
renal function tests
– CBC / platelets
– Markers of cardiac
ischemia (if needed)
– PT/INR/aPTT
– ECG
• Selected Patients
– TT or ECT
– Hepatic function
– Tox screen
– Blood alcohol
– Pregnancy
– ABG
– Chest Xray
– LP
– EEG
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Diagnostic Tests
• Non Contrast CT
• CT angiogram
• CT Perfusion
• Cerebral Angiogram
• MRI
• MRA
• Diffusion Weighted MRI
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Computerized Tomography
• CT – Technique: x-ray beam projected thru narrow section of
brain or spine; detectors at opposite side measure attenuation of radiation as it passes through tissues
– Produce a series of thin slices of adjacent anatomy
– Hyperdense tissue (bone) absorbs more x-rays and appears whiter on image. Hypodense (air,fluid) absorb fewer xrays and appear darker
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Computerized Tomography
Angiography
• CT
– Technique: Post contrast CT scan
reconstructed to outline cerebral
vasculature.
– Useful in screening for vascular lesions
such as aneurysms or AVMs.
– Enhance tissue where there is
disruption of blood-brain barrier (i.e.
tumors)
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Computerized Tomography: Perfusion
• Perfusion CT
– Technique: Ct scan performed during IV bolus
administration of iodinated contrast material.
– Computer calculations provide measures of
regional CBV, MTT, and RCBF
– Used in acute stroke to determine marginally
perfused areas/vulnerable potentially
salvageable areas, and infarcted tissue
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Diagnostic Tests
• MTT Mean Transit Time
– How long does it take blood to get to the capillaries
– Delay in arrival of blood ---- increase MTT
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CT Perfusion
• CBV=Cerebral Blood Volume
– Think of the brain as a sponge filled with blood
• If ischemic but not dead—blood still be present
in the tissue (picture normal)
• If completed stroke and tissue irreversible—
lack of flow is visible
• CBF=Cerebral Blood Flow
– Flow map cc/gram/cm3
– See Defect in flow
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Magnetic Resonance Imaging
• Technique: magnetic fields and radiofrequency waves create signals that generate an image
• Gadolinium can be added as a contrast agent
• Useful for brain (tissue contrast is better than CT) and spine (better for soft tissues and defining lesions such as cysts, vascular lesions, contusions, tumors, edema, hemorrhage or ischemia)
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Cerebral Angiography
• Technique: contrast material is injected into
the vertebral and carotid arteries to enable
radiographic visualization of intracranial and
extracranial vessels
• Requires trained interventional team
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Focus on
Ischemic Stroke
Care
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Two Effective Therapies for
Stroke
• Thrombolysis
–Reduces death and
disability
• Comprehensive Stroke
Care
–Multidisciplinary teamwork
reduces mortality by more
than 25%
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Nursing Priorities
• Approach through Case Studies
– Airway and Breathing
– Circulation: telemetry, BP, DVT prophylaxis
– Deficit: neuro monitoring
• Cerebral edema/ICP
– Temperature control
– System support
• Mobility
• GI/GU
• Skin
• Education
• Emotional support
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Case 31 yr old Male
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Entry of Stroke Patient
• Hospitals must have an
organized Stroke Intervention
Program
– rapid identification and triage
– organized stroke response team
– protocols for emergent work-up
– nursing protocols for preparing,
administering, and monitoring drug
therapy
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Arrival of Stroke Patient in
the Emergency Department
• Rapid identification and work-up
– Key symptoms
• Triage to acute area
– Classify as emergent
• Time of symptom onset is crucial
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Initial Management
• Primary & secondary survey
– Neurologic assessment with NIHSS
• Start IV and draw labs
• Check Blood glucose
• Monitor: ECG, SpO2, and serial manual BP assessments
• CT scan of brain without contrast STAT
• 12 Lead EKG and chest x-ray
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NIH Stroke Scale
� LOC
� LOC Questions
� LOC Commands
� Gaze Abnormalities
� Visual Loss
� Facial Weakness
� Motor Weakness in
Arms
� Motor Weakness in
Legs
� Limb ataxia
� Sensory Loss
� Language
� Dysarthria
� Extinction and
Inattention
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Abbreviated NIHSS
• Level of Consciousness
• Level of Consciousness Questions
• Level of Consciousness Commands
• Motor Weakness in Arms
• Motor Weakness in Legs
• Language
• Cardinal Sign-dependent of patient
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Time is Brain �
• 911
• Door to ED Physician exam 10 minutes
• Door to Stroke expertise 15 minutes
• Door to CT scan of brain 25 minutes
• Door to CT interpretation 45 minutes
• Door to drug (tPA) 60 minutes
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Anatomy of the Lesion
http://www.google.com/imgres?imgurl
This Case - Signs and Symptoms consistent with
Superior Division:
Brachiofacial paralysis
Sensorimotor deficit involving face and arm, leg to a
lesser extent. Foot is spared.
Ipsilateral deviation of head/eyes.
With Left lesion may have initial global aphasia ->
motor aphasia.
No impairment of alertness.
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Medical Management
• Goal: reestablish perfusion
• Rule out stroke mimics
• Interventions:
– Traditional interventions
– Thrombolytics
• IV tPA
• Combination IV/IA
• Intraarterial thrombolytics
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Intravenous tPA
• Results of NINDS trial
– patients receiving tPA within 3 hours of symptoms
onset had better outcomes at 3 months than those
treated with placebo
– increase risk of intracerebral hemorrhage in
patients treated with tPA
• NIH stroke score > 201
• Brain edema or mass effect on CT1
1NINDS Study Group. Stroke 1997. 28: 2109-2118.
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Treatment Decisions
• Treatment Options Ischemic
– Acute
• Within 180-270 minutes tPA unless
contraindicated
–IV (typical dose 60-90 mg total) given
in ED then admit to ICU
• Within 6 hours of presentation
–IA tPA with typical dose 5-8 mg
–Merci retrieval
device/penumbra/solitaire
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Intravenous tPATime Window
was < 3 hours
� �It has now moved to 4 ½
hours
Intravenous tPA
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Intravenous tPA: Indications
• Patient symptoms < 4.5 hours from symptom onset– CT scan excludes hemorrhage
– NIH stroke scale > 4
– Isolated aphasia
– Age > 18
• Note exclusions for 3-4.5 hour IV tPA– Age > 80 years
– Taking oral anticoagulants
– NIHSS > 25
– Combination of history of prior stroke and diabetes
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IV tPA:
Nursing Management
• Start 2nd IV for thrombolytics
• Reassess neuro status using NIHSS q 15 min
• Weigh patient or assess likely weight
• Avoid invasive tubes: foley/NG
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Infusion Guidelines tPA
• Preparation of IV tPA drip
– 0.9 mg/kg
– 10% IV bolus over 1-2 minutes
– 90% IV over 60 minutes
• Administration of tPA
– Monitor VS: Q 15 min x 2 hrs, Q 30 min x 6
hrs, then Q 1 hour x 16 hours
– Treat BP accordingly
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Team Priorities
• Goal: preserve life and prevent further
neurologic deterioration
• Airway
• Breathing
• Circulation
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Team Priorities
• BP Management
– Do not drop BP rapidly
– Decision to treat is based on treatment options
• Thrombolytics:
–Systolic > 185 or diastolic > 110
After bolus > 180/105
• No thrombolytics
–Systolic > 220 mm Hg
–Diastolic > 130 mm Hg
–Mean > 130 mm Hg
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Team Priorities
• BP Medications
– Labetalol
– Nicaridipine
• Never give sublingual nifedipine
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Team Priorities
• Fluid Management
• Recheck Blood Glucose
• Start 2nd IV for thrombolytics
• Reassess neuro status using NIHSS q 15 min
• Weigh patient or assess likely weight
• Avoid invasive tubes: foley/NG
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Post Infusion Guidelines tPA
• Admit to ICU
• Vigilant monitoring of VS and neuro checks
• Avoid NG/central lines for 24 hours
• If neuro condition worsens, notify MD, and prepare
for stat CT of brain
• Do not administer heparin, warfarin, or ticlopidine for
24 hours after tPA
• Keep patient NPO until swallow assessment
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Case 86 year oldAcute onset of stroke signs and symptoms
911 called
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Pre-Hospital Care Providers
• EMT and/or Paramedic key role– Stabilization of airway, breathing, circulation
– Recognize signs/symptoms of stroke
• Rapid assessment using pre-hospital stroke scale
– Place IV/ cardiac monitor
– Establishing verification of last seen normal
• Patient history from reliable witness
– Provision of supplemental O2 if hypoxic
– Checking blood glucose level
– Avoiding fluids with dextrose
– Load and GO
• Rapid transport to a facility capable of caring for stroke patients
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Hyperacute Ischemic Stroke
Onset 1641
• 86 year old at home when developed acute onset of aphasia, left gaze, and right facial droop/arm hemiparesis (5/5 arm/ 5/5 leg)
– NIHSS 16
• Arrives in ED 1716: Code Stroke
• History– Prior stroke minor
– New onset Atrial fibrillation
– Hypothyroidism and chronic thrombocytopenia (platelets 48,000)
• Medications– Dabigatran x 1 dose
– Levothyroxine
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ED Priorities
• Airway and Breathing adequate with
99% pulse oximetry
• Circulation: BP 162/87 Afib
• NIHSS 16 and GCS 11
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Anatomy of the Lesion
• Left middle cerebral artery M2 branch
Sylvian (M2) Segment
Middle Cerebral Artery Segment divides
into superior and inferior divisions which
can be a site for an embolus to lodge.
Branches supply:
Temporal Lobe and Insular Cortex (sensory
language area of Wernicke)
Parietal Lobe
(Sensory cortical areas)
Inferolateral frontal lobe.
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Anatomy of the
Lesion
This Case - Signs and Symptoms
consistent with Superior Division:
Brachiofacial paralysis
Sensorimotor deficit involving
face and arm, leg to a lesser
extent. Foot is spared.
Ipsilateral deviation of head/eyes.
With Left lesion may have initial
global aphasia -> motor aphasia.
No impairment of alertness.
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Treatment Options
• IV tPA 0.9 mg/kg– 10% IV bolus
– 90% over one hour
• To Interventional– IA tPA
– Solitaire retrieval
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Diagnostic Pictures
• Occlusion of MCA
• Reopening of vessel with
complete reperfusion
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Post Procedural Abbreviated NIHSS
• Taken to SICU at 2300: VS and NC q 15
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14 hours Post onset• Improvement in Abbreviated NIHSS
• BP within correct parameters post tPA
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Nursing Priorities
in Care
• Neuro assessment
and vital signs
• Parameters to call MD
• O2 saturation> 92%
• Monitor for major
bleeding complications
• ECG monitoring for
72h or more
• I/O
• IV fluids 75-100 ml/h
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36 hours Post Intervention
• NIHSS improving to 2
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NIHSS Full Score
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Pupillometer Assessment
• Minimal cerebral edema
• NPI 4.8/4.9
• Constriction velocity normal
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NIHSS Full Score
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Patient Education
Hypertension
Diabetes
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Patient Education
Cholesterol
Smoking
Alcohol
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Patient Education
Obesity
Activity
Other recommendations related to: Interventional
approaches (Extracranial carotid disease/vertebro-
basilar disease), and Cardioembolic (AFib,
cardiomyopathy, valvular disease)
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Preparing for DC/Transfer
• Make a connection with Patient and their Care Partner– Involve family in decision making
– Family and team meetings to discuss progress
– Encourage care partner to participate in educational and training sessions
– Conduct a pre-discharge needs assessment of the home before D/C (OT or PT)
– Caregiver training if aphasic, positioning, handling shoulder care, how to promote independence, and mobility
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Preparing for DC/Transfer
• Make a connection with Patient and their Care
Partner
– Provide education for patient’s family/Care Partner on
stroke pathology, prevention, stroke s/s, actions to
take, follow-up appointments, treatment plan, and
community resources
– Liaison with community providers
– Review individual patient and care partner
psychosocial needs and support needs
– Provide information on discharge plans and post
discharge management to primary care MD/community
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ARU Stay Patient transferred to acute rehab on Day 5 -
Progress by Day 10
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Outcome
• Discharged home after 13 day stay in ARU
– Supervised transfer to bed mobilty
– Ambulating 150 feet with contact guard assist only
– Cognition – minimal assist with problem solving
– Speech clear and able to communicate
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Outcome
• Discharged home after 13 day stay in ARU
– Supervised transfer to bed mobilty
– Ambulating 150 feet with contact guard assist only
– Cognition – minimal assist with problem solving
– Speech clear and able to communicate
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Conclusion