Thromolytic; lyse (break
down) existing clots i.e.
Streptokinase, t-PA, rTpa
tPA
Must be administered within 3
to 4.5 hours of the onset of
clinical signs of ischemic
stroke (Lewis et al., 2011).
Administered IV to re-establish
blood flow through a blocked
artery to prevent cell death
(Lewis et al., 2011).
The door-to-needle time for tPA remains less than
60 mins or 1 hour after onset of clinical signs.
Thrombolytics given in this time frame reduce
disability, but at the expense of an increase in
deaths within 7 to 10 days and an increase in
intracranial hemorrhage (Lewis et al., 2011).
Anticoagulants;
Inhibit platelet
aggregation,
prevent platelet
plugs e.g. ASA,
Plavix
No anticoagulant or
antiplatelet drugs are given for
24 hours after tPA treatment
(Lewis et al., 2011).
Not recommended in the
emergency phase because of
the risk for intracranial
hemorrhage (Lewis et al., 2011).
Aspirin at a dose of 325 mg may be initiated
within 24 to 48 hours after the onset of an
ischemic stroke
Complications of aspirin: GI bleeding.
Therefore used cautiously in those
who have a history of peptic ulcer
disease (Lewis et al., 2011).
Antiplatelets
Used only after patient’s condition
has been stabilized and to prevent
further clot formation (Lewis et al.,
2011).
Vasodilators (Lewis et al., 2011).
Anti-hyperlipidemics (Lewis
et al., 2011).
Anti-hypertensives
e.g. metoprolol
Hypertension may be a protective response
to maintain cerebral perfusion
Use of drugs to lower BP is recommended
only if BP is markedly increased (MAP>130
mm Hg or systolic BP>220 mm Hg) (Lewis et
al., 2011).
Signs and Symptoms
Cognitive
(Ignatavicius
& Workman,
2013).
Denial of illness
Spatial and proprioveptive dysfunction
Impairment of memory, judgment,
problem solving, and decision making
Decreased concentration
Motor
(Ignatavicius &
Workman, 2013).
Hemiplegia (paralysis) or hemiparesis
(weakness) contralateral to which part
of the brain is affected
Quadriparesis if the brainstem is
involved
Ataxia (gait) if the cerebellum is
affected
Hypotonia or flaccid
paralysis
Hypertonia or spastic
paralysis
Agnosia: unable to use objects
correctly
Apraxia: unable to carryout purposeful
motor activity or speech
Bladder and bowel incontinence from
the loss of neurological control in the
cerebral cortex
Sensory (Ignatavicius &
Workman, 2013).
Decreased sensation of touch
and pain contralateral to where
the stroke is in the brain
Unilateral body neglect
syndrome
Amaurosis fugax: brief episode of
blindness in one eye
Hemiaopsia: blindness in half the
visual field
Homonymous hemianopsia
blindness in the same side of both
eyes
Nystagmus: or other involuntary
eye movements caused from
brainstem and cerebellar
damage
Embolic strokes are associated
with heart murmurs,
dysrhythmias (atrial fibrillation is
the most common, and HTN.
Left vs. Right Hemisphere
(Ignatavicius & Workman,
2013).
What is an ischemic stroke?
Ischemic stroke is caused by
occlusion of cerebral artery by
either a thrombus or embolus
(Lewis et al., 2010).
Brain stores no oxygen or
glucose and thus needs
constant blood flow for normal
function and waste removal
(Lewis et al., 2010).
Stroke ranks third for mortality
rates in developed countries
(Kearney, 2014).
Pathophysiology
Thrombic
Stokes
Consists of more than
half of all strokes
(Ignatavicius &
Workman, 2013).
Caused by the development of
atherosclerosis (Ignatavicius &
Workman, 2013).
A rupture of one of these plaques
exposes cells to clot promoting
elements (Ignatavicius &
Workman, 2013).
End result is a formation of a blood clot in an
artery supplying blood to the brain. This blood
clot is large enough to interrupt blood flow to
cerebral tissue (Ignatavicius & Workman, 2013).
Thrombic strokes are
characterized by a slow onset,
taking minutes to hours
(Ignatavicius & Workman, 2013).
Embolic
Strokes
Caused by thrombus or thrombi breaking
off an artery anywhere in the body and
traveling to cerebral arteries (Ignatavicius
& Workman, 2013).
Thrombus formation can be caused from
heart disease, MI, heart valve
prosthetics, non valvular atrial
fibrillation, and plaque (Ignatavicius &
Workman, 2013).
Embolic strokes are characterized by a
sudden development, rapid
neurological deficits (Ignatavicius &
Workman, 2013).
Can lead to hemorrghaic stroke because
arterial vessel wall is vulnerable to ischemic
damage (Ignatavicius & Workman, 2013).
Diagnostic
Tests
Laboratory Values
Elevated hematocrit and hemoglobin with severe or major stroke because
body is compensating for decreased oxygen to the brain (Ignatavicius &
Workman, 2013).
PT, PTT, and INR: used to establish baseline
information for anticoagulation therapy
(Ignatavicius & Workman, 2013).
Elevated WBC: can indicate presence of
infection (Ignatavicius & Workman, 2013).
Lumbar puncture: used to rule out meningitis
and subarachnoid hemmorhage (Ignatavicius &
Workman, 2013).
Imaging Studies
MRI: to determine the extent
of brain injury and has
greater specificity in
determining the location of
vascular lesions and
blockages than CT (Jauch,
2016).
CT scan: indicates the size
and location of the lesion
and helps to differentiate
between ischemic and
hemorrhagic stroke (Jauch,
2016).
Ultrasonography and
echocardiography: help
determine additional
cardiovascular risks (Jauch,
2016).
Risk Factors
Modifiable (Choudhury et al.,
2015; Ignatavicius &
Workman, 2013).
Blood clotting disorders (high risk for thrombotic
stroke and require preventive anticoagulants)
TIA patients (should seek anticoagulation
therapy)
Non modifiable (Choudhury et
al., 2015; Ignatavicius &
Workman, 2013).
Age; increased risk as age
increases
Gender; men 30% higher
incidence, post menopausal
women
Race or ethnicity; American
Indian, Alaskan Natives, Blacks,
Hispanics have a higher chance
Heredity
Myocardial
Infarction
Sickle Cell
Disease
Collaborative Care
Nursing
Managing circulation, airway, breathing → Patients may have
difficulty keeping an open and clear airway because of a
decreased LOC or decreased or absent gag and swallowing
reflexes (Lewis et al., 2011).
Oxygenation
Maintaining oxygenation is important - Both hypoxia
and hypercarbia are to be prevented because they can
contribute to secondary neuronal injury (Lewis et al.,
2011).
Oxygen administration, artificial airway insertion,
intubation, and mechanical ventilation may be required
(Lewis et al., 2011).
Neurological
Assessment
Glasgow Coma Scale to address LOC, orientation,
motor, pupils, speech.language, vital signs, and
blood glucose (RNAO, 2005).
Fluid and
electrolytes
keep the patient adequately hydrated to
promote perfusion and decrease further
brain injury (Lewis et al., 2011).
Adequate fluid intake during acute care via oral,
IV, or tube feedings should be 1500 to 2000
mL/day (Lewis et al., 2011).
IV solutions and water ware avoided because
they are hypotonic and may further increase
cerebral edema and ICP(Lewis et al., 2011).
Hyperglycemia may be
associated with further brain
damage and should be treated
(Lewis et al., 2011).
Management of Increased
ICP
Improve venous drainage (i.e.
elevate HOB)
Maintain head and neck in alignment
(Lewis et al., 2011).
Quiet environments will reduce headaches and
reduce aggravation of increased ICP
(Ignatavicius & Workman, 2013).
Avoid extreme hip and neck flexions that increase
intrathoracic pressure making ICP more difficult to
control. Extreme neck flextion interferes with venous
drainage as well (Lewis et al., 2011).
Avoid clustering nursing procedures all at
once because the effect of ICP elevation is
more dramatic (Ignatavicius & Workman,
2013).
CSF drainage (Ignatavicius &
Workman, 2013).
Diuretic drugs (e.g. mannitol,
furosemide) (Lewis et al., 2011).
Removal of bone flap to allow for cerebral
edema without increases in ICP (Lewis et al.,
2011).
Management of Constipation
Constipation can be caused
from decreased mobility
(Kasaeaneni & Hayes, 2014).
High fiber food such as fruits or vegetables can be
added to the diet to help increase the volume present
and cause bowel movement by distension (Kasaeaneni
& Hayes, 2014).
Fiber supplements such as bran, psyllium, or
methylcellulose can be added to help increase the
fiber consumed by the patient (Kasaeaneni & Hayes,
2014).
Contributes to increased cerebral metabolism. A
temperature elevation of even one degree increases
brain metabolism by 10% and contribute to further brain
damage (Lewis et al., 2011).
Treatment: Aspirin Acetaminophen Cool
blankets (Lewis et al., 2011).
Education
Teach patients to recognize the symptoms
of a stroke by using the acronym FAST
Return demonstrations assist in
evaluating family' ability to perform
patient care tasks; provide verbal and
oral instruction Ignatavicius &
Workman, 2013).
Teach family about depression that
can occur within 3 months of a
stroke. Post stroke depression is
associated with increased morbidity
(Ignatavicius & Workman, 2013).
Health teaching for the patient
includes drug therapy, ambulation
skills, nutritional management, and self
management skills (Ignatavicius &
Workman, 2013).
Health Care Resources
(Ignatavicius & Workman, 2013)
Available online resources to share with patients
and family include American Heart Association,
National Stroke Association, Agency of Health care
Research and Quality
SLP (Speech
Language
Pathologist)
Appointments for
outpatients speech may be
arranged to help the
patient relearn to talk
(Ignatavicius & Workman,
2013).
Collaborate with the SLP to
conduct a bedside swallowing
screening and evaluation. Patient
may remain NPO until SLP
determines the patient can
tolerate fluids without aspirating
(Ignatavicius & Workman, 2013).
Home
Collaborate with case manager
to plan patient's discharge;
coordinate with rehabilitation
therapist to identify need of
assistive devices (Ignatavicius &
Workman, 2013).
PT
(Physiotherapist)
To restore movement, balance,
and coordination
Climb stairs, transfer in and out of bed and chair,
transfer to and from car, mobility aids (Ignatavicius
& Workman, 2013).
OT (Occupational
Therapist)
To relearn basic skills such as
bathing and dressing
Community
Care
Patients with stroke may be discharged
to a rehabilitation centre or skilled
nursing fac.ility depending on the extent
of their disability and the availability of
caregiver/family support (Ignatavicius &
Workman, 2013).
Complications
Increase ICP
Occurs in response to cerebral
edema (American Heart
Association, 2015).
Pneumonia
Due to decreased mobility after a
stroke (American Heart
Association, 2015).
Aspiration
pneumonia
Can be caused by impaired tongue
movement, decreased swallowing,
or absent gag reflex (American
Heart Association, 2015).
Urinary Tract Infection
Caused by foley catheter being placed
due to bladder incontinence (American
Heart Association, 2015).
Seizure
Abnormal electrical activity in the brain
causing convulsions from cerebral damage
(American Heart Association, 2015).
Clinical
depression
Causes unwanted emotional and physical
reactions to changes and losses
(American Heart Association, 2015).
Pressure ulcers
Results from decreased ability to move and
pressure on areas of the body because of
immobility (American Heart Association, 2015).
Limb contractures
Shortened muscles in an arm or leg from
reduced ability to move the affected limb
or lack of exercise (American Heart
Association, 2015).
Deep Vein
Thrombosis
Blood clots form in veins of the legs
because of immobility from stroke.
(American Heart Association, 2015).