Download A transient ischemic attack

NEUROVASCULAR
EMERGENCIES
Dana Bartlett, BSN, MSN, MA, CSPI
Dana Bartlett is a professional nurse
and author. His clinical experience
includes 16 years of ICU and ER
experience and over 20 years of as a
poison
control
center
information
specialist.
Dana
has
published
numerous CE and journal articles,
written NCLEX material and textbook
chapters,
and
done
editing
and
reviewing for publishers such as Elsevier, Lippincott, and Thieme. He has
written widely on the subject of toxicology and was recently named a
contributing editor, toxicology section, for Critical Care Nurse journal. He is
currently employed at the Connecticut Poison Control Center and is actively
involved in lecturing and mentoring nurses, emergency medical residents and
pharmacy students.
ABSTRACT
The diagnosis of a neurovascular accident is multifactorial. It involves
recognition of associated risk factors as well as signs and symptoms,
which does not always guarantee a correct diagnosis. Depending on
the neurovascular event, some injuries become more apparent after
the actual neurovascular event occurs. Some signs are acutely severe
and immediate while others can be subtle, making neurological injury
diagnosis difficult and possibly delayed. Treatment with anticoagulants
or thrombolytic agents is discussed, including inclusion and exclusion
criteria for administration. The complications of a neurovascular
accident are reviewed.
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Policy Statement
This activity has been planned and implemented in accordance with
the policies of NurseCe4Less.com and the continuing nursing education
requirements of the American Nurses Credentialing Center's
Commission on Accreditation for registered nurses. It is the policy of
NurseCe4Less.com to ensure objectivity, transparency, and best
practice in clinical education for all continuing nursing education (CNE)
activities.
Credit Designation
This educational activity is credited for 4 hours. Nurses may only claim
credit commensurate with the credit awarded for completion of this
course activity.
Statement of Learning Need
The early identification and treatment of a neurovascular accident is
critical to prevent further brain damage. The clinical signs and
symptoms of a neurovascular accident may vary. Much depends on the
ability of the clinician to act swiftly to physically assess and initiate
recommended imaging and laboratory testing to diagnose an acute
condition. Importantly, lifestyle prevention is an essential aspect of
clinical care to identify risk factors related to a neurovascular accident.
Course Purpose
To provide clinicians with needed skills to promote health prevention
and to treat neurovascular accidents in all healthcare settings.
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Target Audience
Advanced Practice Registered Nurses and Registered Nurses
(Interdisciplinary Health Team Members, including Vocational Nurses
and Medical Assistants may obtain a Certificate of Completion)
Course Author & Director Disclosures
Dana Bartlett, BSN, MA, MSN, CSPI, William S. Cook, PhD,
Douglas Lawrence, MA, Susan DePasquale, MSN, FPMHNP-BC - all
have no disclosures.
Acknowledgement of Commercial Support
There is no commercial support for this course.
Please take time to complete a self-assessment of knowledge,
on page 4, sample questions before reading the article.
Opportunity to complete a self-assessment of knowledge
learned will be provided at the end of the course.
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1.
A transient ischemic attack:
a. causes temporary neurological dysfunction.
b. is typically caused by a coagulation disorder.
c. causes permanent neurological dysfunction.
d. is very common in children and young adults.
2.
A transient ischemic attack:
a. is caused by bleeding into the subarachnoid space.
b. is considered to be a significant risk factor for stroke.
c. is characterized by persistent neurological deficits.
d. does not require the use of neuroimaging.
3.
Treatment priorities for transient ischemic attack includes:
a. the use of rtPA and ICP monitoring.
b. withdrawal of anticoagulants and antihypertensives.
c. induced hypothermia and maintaining euvolemia.
d. anticoagulation and antiplatelet therapy.
4.
An ischemic stroke is characterized by:
a. bleeding into the subarachnoid space.
b. temporary neurological dysfunction caused by a thrombus or
embolism.
c. cerebral infarction caused by decreased blood flow.
d. rupture of small arteries and bleeding into the brain
parenchyma.
5.
True or False: Evidence for an increased risk for stroke is
strongest for atrial fibrillation, cigarette smoking,
dyslipidemia, hypertension, physical inactivity, and sickle
cell disease.
a. True
b. False
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Introduction
Neurovascular emergencies require timely and accurate assessments
and treatments to ensure the best clinical outcomes. This course will
give a brief overview of the anatomy of the neurovascular system,
describe some of the common neurovascular emergencies, and explore
the immediate assessment and treatment recommendations for each
type of emergency as well as some of the potential complications
clinicians may encounter while caring for patients.
Neurovascular Anatomy
The neurovascular system consists of the brain, spinal cord and
associated vasculature. This course will focus mainly on issues of the
brain. The anatomy of the brain is complex due its intricate structure
and function. This amazing organ acts as a control center by receiving,
interpreting, and directing sensory information throughout the body.
The brain is made up of many specialized areas that work together.
The cortex is the outermost layer of brain cells. Thinking and voluntary
movements begin in the cortex. The basal ganglia are a cluster of
structures in the center of the brain. The basal ganglia coordinate
messages between multiple other brain areas. The limbic system is a
group of structures that controls emotions, emotional responses,
hormonal secretions, mood, motivation, as well as pain and pleasure
sensations. The limbic system consists of the amygdala, cingulate
gyrus, fornix, hippocampus, hypothalamus, olfactory cortex, and the
thalamus. The brain is composed of the frontal, occipital, temporal,
and parietal lobes as well as the cerebellum and the brain stem.
Several layers of tissue including the meninges and the dura surround
the brain. The skull (cranium) helps protect the brain from injury.
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Frontal Lobe
The frontal lobe is located in the anterior part of the brain. It is
involved in planning, organizing, problem solving, selective attention,
personality and a variety of higher cognitive functions including
behavior and emotions. The most anterior portion of the frontal lobe is
called the prefrontal cortex. It is very important for the higher
cognitive functions and the determination of the personality. The
posterior portion of the frontal lobe consists of the premotor and motor
areas. Nerve cells that produce movement are located in the motor
areas. The premotor areas serve to modify movements.
Occipital Lobe
The occipital lobe is in the back of the brain and processes visual
information. Not only is the occipital lobe mainly responsible for visual
reception, it also contains association areas that help in the visual
recognition of shapes and colors. Damage to the occipital lobe can
cause visual deficits.
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Temporal Lobe
The temporal lobes are located on each side of the brain at about the
level of the ears. These lobes allow one to differentiate sounds and
smells. They also help in sorting new information and are believed to
be responsible for short-term memory. The right temporal lobe is
mainly involved in visual memory (i.e., memory for pictures and faces)
while the left temporal lobe is mainly involved in verbal memory (i.e.,
memory for words and names).
Parietal Lobe
The parietal lobes are located on each side of the brain behind the
frontal lobe at the top of the brain. The parietal lobes contain the
primary sensory cortex, which controls sensation (touch, pressure).
Behind the primary sensory cortex is a large association area that
controls fine sensation (judgment of texture, weight, size, shape).
Damage to the right parietal lobe can cause visuospatial deficits (i.e.,
the patient may have difficulty finding his or her way around new, or
even familiar, places), while damage to the left parietal lobe may
disrupt a patient's ability to understand spoken and/or written
language.
Cerebellum
The cerebellum is the portion of the brain (located at the back) that
helps coordinate movement (balance and muscle coordination).
Damage to this area may result in ataxia, which is a problem of muscle
coordination. This can interfere with a person's ability to walk, talk,
eat, and to perform other self-care tasks.
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Brainstem
The brainstem is the lower extension of the brain where it connects to
the spinal cord. Neurological functions located in the brainstem include
those necessary for survival (breathing, digestion, heart rate, blood
pressure) and for arousal (being awake and alert).
Most of the cranial nerves come from the brainstem. The brainstem is
the pathway for all fiber tracts passing up and down from peripheral
nerves and spinal cord to the highest parts of the brain. The brainstem
is further divided into the midbrain, medulla oblongata, and the pons.
Cerebral Vasculature
The cerebral vascular system is also complex and intricate. The brain
receives blood from two sources; the internal carotid arteries (ICAs),
which arise at the point in the neck where the common carotid arteries
bifurcate, and the vertebral arteries. The internal carotid arteries
branch to form two major cerebral arteries, the anterior cerebral
artery (ACA) and middle cerebral artery (MCA). The right and left
vertebral arteries come together at the level of the pons on the ventral
surface of the brainstem to form the midline basilar artery.
The basilar artery joins the blood supply from the internal carotids in
an arterial ring at the base of the brain called the circle of Willis. The
posterior cerebral arteries (PCAs) arise at this confluence, as do two
small bridging arteries, the anterior and posterior communicating
arteries. Conjoining the two major sources of cerebral vascular supply
via the circle of Willis presumably improves the chances of any region
of the brain continuing to receive blood if one of the major arteries
becomes occluded.
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The major branches that arise from the internal carotid artery - the
anterior and middle cerebral arteries - form the anterior circulation
that supplies the front part of the brain. These arteries also originate
from the circle of Willis. Each gives rise to branches that supply the
cortex and branches that penetrate the basal surface of the brain,
supplying deep structures such as the basal ganglia and thalamus.
Especially prominent are the lenticulostriate arteries that branch from
the middle cerebral artery. These arteries also supply the basal ganglia
and thalamus. The posterior circulation of the brain supplies the
posterior cortex, the middle part of the brain and the brainstem. It
comprises arterial branches arising from the posterior cerebral, basilar
and vertebral arteries.
The pattern of arterial distribution is similar for all the subdivisions of
the brainstem. Midline arteries supply medial structures, lateral
arteries supply the lateral brainstem and dorsal-lateral arteries supply
dorsal-lateral brainstem structures and the cerebellum. Among the
most important dorsal-lateral arteries are the posterior inferior
cerebella artery (PICA) and the anterior inferior cerebella artery
(AICA), which supply specific areas of the medulla and pons. These
arteries, as well as branches of the basilar artery that penetrate the
brainstem from its ventral and lateral surfaces are especially common
sites of occlusion and result in specific functional deficits of cranial
nerve, somatic sensory and motor function.
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Transient Ischemic Attack
A transient ischemic attack (TIA) was first formally defined (1975) as
“ ... episodes of temporary and focal cerebral dysfunction of vascular
origin, rapid in onset ... variable in duration, commonly lasting from 2
to 15 minutes but occasionally lasting as long as a day (24 hours). The
resolution or disappearance of each episode is swift (ordinarily a few
minutes at most). Each attack leaves no persistent neurological
deficit.”1 This definition, however, has proved to be incorrect and
inadequate.
The 24-hour time limit for symptoms was chosen arbitrarily and the
duration of signs or symptoms should not be used to identify a TIA.
The definition implied that compared to a stroke a TIA was a less
serious event, and advances in imaging techniques clearly showed that
TIAs can, and often do, cause permanent CNS tissue damage; and for
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some patients a TIA is not transient in its consequences.2-4 The
current definition of TIA, as endorsed by the American Heart
Association and the American Stroke Association is: a transient episode
of neurologic dysfunction caused by focal brain, spinal cord, or retinal
ischemia, without acute infarction.5
The word transient would seem to indicate that the effects of a TIA are
temporary and that a TIA can be distinguished from more serious
neurological events by the duration of signs and symptoms. Neither of
these is true. A TIA that causes signs and symptoms for a few minutes
may cause an infarction and the duration of symptoms is unlikely to be
a reliable indicator for the risk of infarction.3,6,7
Epidemiology
It is not known exactly how many individuals each year have a TIA but
recent (2015) information indicates that in the United States the
prevalence of TIA is 2.3% with an incidence of 0.7-0.8 per 1000
people.8 Other important epidemiological facts about TIA are outlined
below.8-16
Men, African Americans, and Mexican Americans have a higher incidence
of TIA than women.
The incidence of TIA increases with age.
A TIA in a young adult is rare but the incidence of TIA in this population
has been increasing.
TIA is rare in children and the risk profile for TIA and subsequent stroke
are different for children than they are for adults.
Most people who are having signs and symptoms of a TIA do not seek
medical help or delay seeking help.
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Etiology and Pathophysiology
Transient ischemic attack is caused by focal brain, spinal cord, or
retinal ischemia. This temporary decrease or cessation of blood flow to
a specific area is the result of a pathologic process; a TIA is not a
disease in and of itself. TIA etiology is often divided into three
categories that refer to the underlying basic pathologic process of the
TIA.9,17
These pathologies (listed below) overlap to some degree and a TIA
caused by any of the three has the same end results: focal hypoperfusion, and reduced blood volume, impaired glucose metabolism,
and oxygenation in the affected area.9 They are all listed as: 1) Large
blood flow occlusion, 2) Small vessel occlusion, and 3) Cardioembolic.
Given the general nature of these categories it is obvious that there
are many medical conditions that can cause TIA. Some of the more
common causes of TIA are listed in Table 1. Undetermined is included
as a category because in a significant number of patients a cause for
TIA cannot be identified.18 Most TIAs are caused by cardioembolic
diseases.9
Table 1: Common Causes of TIA
Atherosclerosis
Atrial fibrillation
Diabetes
Hypercoagulable states
Hypertension
Undetermined
Valvular disease
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Risk Factors
Risk factors for TIA are non-modifiable and modifiable/preventable.
There is also a multitude of potential risk factors in which the
association between the condition or disease and TIA is speculative
and unproven; these will not be discussed.

Non-modifiable:
Age, male gender, ethnicity, family history of stroke.

Modifiable/preventable:
Atrial fibrillation, cigarette smoking, diabetes, high-risk alcohol
use, hypertension, obesity, and physical inactivity.
Signs and Symptoms
Some of the signs and symptoms that are common in patients that are
having a TIA are listed in Table 2.
Table 2: Common Signs and Symptoms of TIA
Aphasia
Ataxia
Blurred vision
Dizziness
Hemiparesis
Numbness
Localized weakness
The table above clearly shows that the patient’s complaints and the
findings of the physical examination will be nonspecific. However, a
TIA is a distinct and unique neurologic event and there are aspects of
its clinical presentation that distinguish it from stroke, TIA mimics, and
other neurologic diseases. TIA is a diagnosis of exclusion and its
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presence is strongly indicated if a patient has some of the signs and
symptoms in Table 2, including:2,9,17

He/she has focal neurological deficits.

The patient’s signs and symptoms have resolved; the episode
was transient.

He/she has negative neurological signs/symptoms, i.e., signs
and symptoms of a loss of a function such as sensation,
speech, or vision.

The signs and symptoms occurred suddenly. There was no
prodromal period.

There was no obvious precipitating event.

The duration of the episode was brief; most TIAs last less
than one hour.
The signs and symptoms are often focal
because the ischemia is caused by
FOCAL SIGN =
decreased perfusion to a specific area and a
COMPROMISED
specific blood vessel or vessels. A focal sign,
BRAIN FUNCTION
often called a focal deficit, is a neurological
finding that indicates compromised function
OR DAMAGE
or damage to a specific area of the brain. This compromised function
or damage then causes a decreased function in a specific
part of the body. Examples of focal deficits are aphasia, blurred vision,
facial droop, or weakness in one arm or leg. An example of a global
sign or deficit would be loss of consciousness.
Transient Ischemic Attack and Stroke
Transient ischemic attack and stroke have many similarities. Key
differences between the two are highlighted below.2,9
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Table 3: TIA versus Stroke








A stroke can cause global and focal deficits.
Negative symptoms, i.e., a loss of function such as hearing,
sensation, or vision, are more often seen in TIA.
Stroke may be accompanied by severe and/or life-threatening
clinical conditions.
Imaging studies of patient who had a stroke show cerebral
necrosis or bleeding.
The duration of stroke signs and symptoms is usually, but not
always, longer than that of a TIA.
A TIA usually occurs suddenly, without prodromal signs and
symptoms.
Irreversible tissue death is relatively common in stroke.
Treatment of a stroke often requires the use of specific therapy
to preserve tissue and function.
The risk for stroke after a TIA was once considered to be relatively
high, in the range of 10-20%. Recent (2016) research however has
produced more cheerful news. Amarenco, et al., found that the
incidence of stroke one year after a TIA was 5.1%, and 1.5% of people
who had a TIA developed a stroke within 48 hours.23
Conditions That Mimic TIA
Transient ischemic attack is a clinical diagnosis24 and it can be a
difficult one to make. There is no confirmatory test, and the patients
are often examined after the event when they are asymptomatic.25
Research has shown that clinicians, including experienced neurologists,
will often disagree as to whether or not a patient is having a TIA,24,26,27
and that TIA is often misdiagnosed.28,29
Diagnosis of TIA is made more difficult by common medical conditions
that mimic TIA, conditions that can be, and often are misdiagnosed as
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TIA.25 The most common of these mimics are migraine aura,
psychiatric disorders, seizures, and syncope.25,30 Table 4 provides
more examples of TIA mimics. 2,9,25,30 This list is not all-inclusive;
many of these are seldom encountered, very complex, or both, and it
is beyond the scope of this module to explain each one. Interested
readers are recommended to pursue further readings found in the list
of footnotes at the end of this study.
Table 4: Transient Ischemic Attack Mimics
Brain tumors
Central nervous system infections
Cerebral amyloid angiopathy
Compressive myelopathy
Conversion disorder
Drug toxicity
Encephalopathies of hepatic, pulmonary, or renal origin
Functional disorder
Hypertensive encephalopathy
Hypoglycemia
Intracerebral hemorrhage
Migraine aura
Multiple sclerosis
Paroxysmal symptoms associated with multiple sclerosis
Peripheral vestibular disorder
Pressure or position-related nerve compression
Psychiatric disorders
Seizures
Spinal dural arteriovenous fistulas
Structural brain lesions
Subdural hematoma
Syncope
Transient global amnesia
Characteristics of the TIA mimics that can be used to distinguish
between these conditions and a TIA are listed below.2,25
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
Age: A TIA is unusual in children and young adults.

Previous medical history: History of stroke, diabetes, seizure
disorder, drug or alcohol use.

Characteristics of the event: Loss of consciousness, tonic-clonic
activity, incontinence, fever, drug/alcohol withdrawal, postictal
state, a migraine aura, and a slow, progressive development of
signs and symptoms - if any of these are present a TIA is highly
unlikely.

Negative symptoms: Negative symptoms are less often seen in
TIA mimics.

Onset: The onset of a TIA is very sudden. For many of the TIA
mimics the onset is gradual.

Progression: A TIA starts and progresses quickly and then the
signs and symptoms gradually decrease in intensity. This slope
of progression is not seen for many of the TIA mimics.

Duration: TIAs usually have duration of an hour or less. A
seizure will typically last about five minutes, syncope for a few
seconds, and a migraine aura may last for hours.
Evaluation and Treatment
A TIA should be considered a medical emergency. Patients who are
having a TIA are at risk for developing a stroke, having another TIA, or
having a serious cardiovascular event such as myocardial
infarction,9,31,32 and a TIA precedes 14-23% of strokes.33 Timely
diagnosis and treatment has been shown to significantly improve
outcome after a TIA.34
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Evaluation of the patient who is having or is suspected to have had a
TIA should include the following tests and procedures.9,35,36 Some of
these are important for the immediate evaluation, and others pertain
to the evaluation of risk factors and for making decisions about
preventative therapies.

A comprehensive physical, neurological, and cardiovascular
examination.

A diffusion weighted MRI scan if possible.5,33,35 This type of
imaging is much more sensitive than a CT scan. Imaging studies
should be done within 24 hours of symptom onset or as soon as
possible if there is a delayed presentation.9

Vascular imaging techniques involve current recommendations to
perform intracranial and extracranial vasculature imaging as part
of the evaluation of TIA33,37 and noninvasive (ultrasound) and
invasive modes (angiography) can be used. In most patients,
transthoracic echocardiography (TTE) is the recommended
method for detecting an aortic or cardiac source of an
embolism.35

A 12-lead electrocardiogram and 24 hours of continuous cardiac
monitoring.9

Cardiac enzymes, complete blood count, serum glucose,
hemoglobin A1c, or an oral glucose tolerance test, serum
electrolytes and creatinine, erythrocyte sedimentation rate, pulse
oximetry, lipid profile, and coagulation studies; keeping in mind
that laboratory tests cannot confirm the presence of TIA and are
used to detect conditions/diseases that have similar
presentation.
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
Screening tests for the unusual causes of TIA or TIA mimics
should be done on a case-by-case basis.

Screening for obesity and sleep apnea.
Risk assessment tool scores like the ABCDD scale (age, blood
pressure, clinical factors, duration of symptoms, and diabetes) have
been used to evaluate the risk for subsequent stroke in patients who
are having or had a TIA, but they have limited predictive value and
their use is not recommended.9,33,35
A patient who is having or recently had a TIA should be admitted if
any of criteria in Table 5 are present.33 If the patient is clinically stable
and he/she has the ability and willingness to comply with follow-up
care, evaluation in a TIA clinic is an option; this will be discussed later
in the learning module.
Table 5: TIA Admission Criteria






Atrial fibrillation
Crescendo or continued neurologic symptoms
Inability or unwillingness to follow-up.
Ischemic areas seen on imaging studies
Multiple risk factors
Vascular disease seen on imaging studies
The goals of treatment are stroke prevention, treating the etiology of
the TIA, and reduction of risk factors. Specific treatments include
anticoagulant therapy, antiplatelet therapy, and revascularization.
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Anticoagulant therapy with a vitamin K antagonist or one of the new
oral anticoagulants should be started if the patient with a TIA is found
to have nonvalvular atrial fibrillation or if the patient had an ischemic
TIA but the cause cannot be ascertained.35,36 If the patient cannot
tolerate anticoagulation with a vitamin K antagonist or the new
anticoagulants, aspirin can be used and a combination of aspirin and
clopidogrel should be considered.36
There are specific recommendations for anticoagulation when a TIA
has been caused by arterial dissection, aortic arch atherosclerosis,
hyperhomocysteinemia (a hypercoaguable condition), patent foramen
ovale, or sickle cell disease, or if the patient has antiphospholipid
antibody or antiphospholipid body syndrome and a TIA. These
recommendations are in the American Heart Association and American
Stroke Association 2014 guidelines for the prevention of stroke in
patients with stroke and transient ischemic attack.36 It should be noted
that homocysteine is an amino acid and elevated homocysteine levels
have been observed in patients who have had a stroke.
Antiphospholipid syndrome is an autoimmune disorder that causes
peripheral thrombus formation.
Antiplatelet therapy should be started if the patient had a noncardioembolic TIA.35,36 Aspirin, clopidogrel, ticlodipine, or aspirin and
dipyridamole are Food and Drug Administration (FDA)-approved
therapies for stroke prevention in this patient population; aspirin and
clopidogrel has been used, as well.35,36
Revascularization with carotid endarterectomy is indicated if the TIA
was caused by carotid artery stenosis and (in most cases) the blood
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vessel narrowing is >50%.35,36 Carotid angioplasty and stenting can
also be used.36
Risk factor reduction is an important part of TIA treatment.
Dyslipidemia, diabetes, heavy alcohol consumption, hypertension,
obstructive sleep apnea, obesity, physical inactivity, smoking, and
possibly diet all contribute to the risk for TIA and stroke. Specific
treatment goals for reduction of these risk factors can be found in the
2014 American Heart Association/American Stroke Association
guidelines for the prevention of stroke in patients with stroke and
transient ischemic attack.36 Several abbreviated examples from these
guidelines are highlighted below.

Hypertension:
Antihypertensive therapy should be started if the patient who had a
TIA has a systolic blood pressure ≥140 mm Hg or a diastolic blood
pressure ≥90 mm Hg.

Dyslipidemia:
Patients who have had a TIA should be started on statin therapy if
the TIA is presumed to be caused by atherosclerosis, the lowdensity lipoprotein cholesterol (LDL-C) level is ≥100 mg/dL, with or
without evidence for other atherosclerotic cardiovascular disease
(ASCVD), or the TIA is presumed to be caused by atherosclerosis,
and the LDL-C level is <100 mg/dL, and there is no evidence of
ASCVD.
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
Diabetes:
Use of existing guidelines from the ADA (American Diabetic
Association) for glycemic control and cardiovascular risk factor
management is recommended if the patient had an ischemic TIA
and he/she has diabetes mellitus or pre-diabetes.
Transient Ischemic Attack: Alternatives to Admission
The risk of stroke is greatest in the first few hours and days after a
TIA,38 and emergency evaluation by a neurologist and treating risk
factors are essential for stroke prevention. For some patients, the
specialist evaluation and initiation of therapies should be done on an
in-patient basis and the admission criteria for TIA were previously
discussed. But this is a very resource intense approach; it is clear in
retrospect that every patient who has had a TIA does not need
admission, and many patients who are admitted for a suspected TIA
will not have a TIA.38
In response to these issues, models for outpatient management of
suspected TIA have been developed. Examples of these approaches
include TIA clinics that evaluate patients within 24 hours and
telephone triage services that can be used by primary care physicians.
When compared to hospital admission these nontraditional methods of
care have produced good results and they have been shown to be
safe.9,38
Stroke
A stroke is a disease process that interrupts blood flow to the brain
and causes CNS tissue death by infarction, and a CNS infarction is
defined as: “... brain, spinal cord, or retinal cell death attributable to
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ischemia ...” and the ischemia is documented by pathological
examination, imaging studies, or other objective evidence, or it is
documented by clinical evidence of infarction, i.e., symptoms that
persist ≥24 hours or until death, and other causes have been
excluded.4
A significant decrease in blood supply deprives organs and tissues of
the two compounds they need to survive, oxygen and glucose.
Neurons are very metabolically active. Normal cerebral blood flow is
approximately 50-60mL/100 grams of brain tissue every minute. If the
flow decreases to 20-40 mL/100 grams, neurological dysfunction will
be observed and if the flow decreases to 10-15 mL/100 grams there
will be irreversible tissue damage to CNS tissues.39
Stroke Epidemiology
Stroke is a significant public health problem. Each year in the United
States approximately 795,000 people have a stroke or a recurrent
stroke, and stroke is the leading cause of long-term disability and the
fourth leading cause of death.8 Other important statistical or
epidemiological facts about stroke are:8,36,40

Eighty-seven percent of strokes are ischemic, 10% are
hemorrhagic, and 3% are subarachnoid.

The incidence of stroke is higher in women than in men and
higher in African Americans than in White Americans.

Of the 795,000 people who have a stroke approximately 610,000
will have their first stroke and 185,000 will have had a prior
stroke
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
Each year, approximately one of every 20 deaths in the United
States is caused by stroke.

The number of deaths caused by stroke has been slowly
decreasing, probably due to greater use of stains and improved
detection/treatment of atrial fibrillation and hypertension.

Stroke in children is much less common than in adults and there
are stroke etiologies that are specific to this population.

Stroke is a significant cause of cognitive deficits and functional
impairment in people who are ≥65 years of age.
Stroke Classification
Stroke is typically divided into three categories: ischemic stroke,
hemorrhagic stroke, and silent stroke. The definitions given here are
from the American Heart Association/American Stroke Association.4

Ischemic stroke: “An episode of neurological dysfunction caused
by focal cerebral, spinal, or retinal infarction.”

Hemorrhagic stroke: “Rapidly developing clinical signs of
neurological dysfunction attributable to a focal collection of blood
within the brain parenchyma or ventricular system that is not
caused by trauma.”

Silent stroke: “Imaging or neuropathological evidence of CNS
infarction, without a history of acute neurological dysfunction
attributable to the lesion.”
A reasonable way to view strokes is that an ischemic stroke is caused
by decreased blood flow; intracerebral bleeding in the brain itself or in
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the subarachnoid space causes a hemorrhagic stroke. The majority of
ischemic and hemorrhagic strokes have easily identifiable and common
etiologies such as atherosclerosis, atrial fibrillation, or hypertension.
Some stroke etiologies however are unusual and seldom seen; i.e.,
strokes caused by hypercoagulability disorders; and, for some
patients, the cause of the stroke cannot be determined, or there may
be several reasons the stroke has occurred. Strokes with no
identifiable cause are called cryptogenic strokes.
Determining the cause of stroke is crucially important in order to
initiate the proper treatment, and there are stroke classification
systems that use clinical and diagnostic information and patient risk
factors to determine stroke etiology.41 The TOAST system determines
if a stroke was caused by larger artery atherosclerosis, cardioembolic
source, small vessel occlusion, stroke of other determined cause, and
stroke of undetermined cause. The TOAST system has been widely
accepted and used, but some researchers feel that the ASCO and CSS
systems are more accurate in identifying the causes of ischemic
stroke.18,42
Stroke Classification Systems43-45
ASCO: Atherosclerosis, Small vessel disease, Cardioembolic, Other.
CCS: Causative Classification of Stroke.
TOAST: Trial of Org 10712 in Acute Stroke Treatment.
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Ischemic Stroke
An ischemic stroke is caused by decreased blood flow, and the
decreased blood flow is the result of a thrombus, an embolism, or
hypoperfusion.46,47 Thrombotic causes of ischemic stroke include:
1) Atherosclerosis, 2) Vasculitis, 3) Arterial dissection, 4) Dehydration,
4) Polycythemia, 5) Hypercoaguable states, and 6) Infections such as
HIV and tuberculosis.46-48
Embolic causes of ischemic stroke include: 1) Valvular vegetation
2) Mural thrombi 3) Atrial fibrillation 4) Cardiac tumors 5) Paradoxical
embolism from a patent foramen ovale or other malformation 6) Fat
emboli 7) Particulate emboli from intravenous amphetamine or cocaine
8) Septic emboli, and 9) Arterial-arterial emboli, myocardial infarction,
and cardiomyopathy.46,48 Hypoperfusion from cardiac failure or
hypotension can cause ischemic stroke.46,48,49 If the decrease in
cerebral blood decrease is complete and persists for 4-10 minutes
there will be irreversible damage. Brain tissue that is not perfused
does not receive oxygen and glucose, it cannot make ATP and without
ATP neurons will die. The decrease in blood flow that occurs during an
ischemic stroke also causes cell death by secondary mechanisms of
injury, i.e., apoptosis, inflammation, and oxidative stress; these are
collectively called reperfusion injury.50-52
Risk Factors for Ischemic Stroke
Risk factors for ischemic stroke are modifiable and non-modifiable, and
common risk factors for ischemic stroke are listed in Table 6.8,53 Some
are clearly contributing causes of the etiology of ischemic stroke. The
evidence for an increased risk for stroke is strongest for atrial
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fibrillation, cigarette smoking, dyslipidemia, hypertension, physical
inactivity, and sickle cell disease,53 and for these risk factors, control
and modification significantly lowers the risk of ischemic stroke. For
others, there is an association with stroke but their contribution to the
disease is not clearly outlined. An example of a significant risk factor
for stroke is hypertension. Lackland, et al., (2014) stated:
“Epidemiological studies have shown that elevated blood pressure is
the most important determinant of the risk of stroke. The risk is
almost linear, beginning at relatively low levels of systolic blood
pressure (SBP) and diastolic blood pressure (DBP) … The evidence for
the benefits of lower blood pressures and reduced stroke risks is
strong, continuous, graded, consistent, independent, predictive, and
pathogenically significant for those with and without coronary heart
disease.”40
Table 6: Common Risk Factors for Ischemic Stroke
Age
Alcohol and Drug abuse
Atrial fibrillation
Cardiovascular disease
Chronic kidney disease
Diabetes mellitus
Dietary factors
Early menopause (Before age 42)
Ethnicity
Dyslipidemia
Family history of ischemic stroke
Hypercoaguable states
Hyperhomocysteinemia
Hypertension
Low birth weight
Metabolic syndrome
Migraine
Obesity
Obstructive sleep apnea
Sedentary life style
Sickle cell disease
Smoking
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Stroke is uncommon in adults under age 55. In this population nonmodifiable and modifiable risk factors are certainly common, but if a
young adult has a stroke uncommon causes of stroke should be part of
the differential diagnosis list. For example, hypercoaguable states that
can cause stroke are more common in younger adults and these
include antiphospholipid syndrome, antithrombin III deficiency,
essential thrombocytosis, Factor V Leiden (resistance to activated
protein C) heparin-induced thrombocytopenia, protein C or S
deficiency, acquired or congenital, hyperhomocysteinemia,
polycythemia vera, prothrombin gene mutation, and sickle cell
anemia.47
The factors that increase risk for stroke have been identified, but using
these for assessing a patient’s risk for having a stroke is an inexact
science. The 2014 American Heart Association/American Stroke
Association review on stroke prevention states that, although the
effect of individual factors on stroke risk is clearly outlined, the
interaction between individual risk factors and how that interaction
affects stroke risk is less well understood. Additionally, the
effectiveness of risk assessment tools for primary stroke prevention
has not been well studied and the existing assessment tools do not
include all possible risk factors such as age, gender, and race.58
There is no ideal stroke risk
assessment tool, but the 2014
American Heart Association/American
Stroke Association guidelines for the
primary prevention of stroke notes
that the American Heart
AHA/ACC CV
RISK CALCULATOR
A quick online resource for
health professionals,
available online at:
http://www.cvriskcalculator.com/.
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Association/American College of Cardiology (AHA/ACC) CV Risk
calculator can help identify patients who may benefit from therapeutic
interventions that can prevent stroke.53 The AHA/ACC CV Risk
calculator uses age, race, total cholesterol, HDL cholesterol, systolic
and diastolic blood pressure, presence of diabetes, smoking, and
treatment for hypertension to determine the 10 year risk for stroke.
Ischemic Stroke Signs and Symptoms
The clinical presentation of an ischemic stroke is highly variable and it
will depend on the patient’s age, comorbidities, and the size and
location of the affected area. Commonly seen signs and symptoms are
outlined in Table 7.46,48
Table 7: Signs and Symptoms of Ischemic Stroke
Aphasia
Ataxia
Confusion
Decreased or altered consciousness
Dizziness
Diplopia
Dysarthria
Facial droop
Focal or global deficits
Numbness/Weakness
Hemiparesis
Visual defects
Hemorrhagic Stroke
Hemorrhagic stroke is cause by an intracerebral bleed or a
subarachnoid hemorrhage. This section of the learning module will
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discuss intracerebral bleeding and stroke; stroke caused by
subarachnoid hemorrhage will be discussed separately.
Hemorrhagic strokes, either intracerebral or subarachnoid, are much
less common than ischemic strokes but they are much more serious.
These strokes are typically severe, they have a high short-term and
long-term mortality rate, and they are more disabling than ischemic
strokes.
The clinical presentation of a hemorrhagic stroke is quite similar to
that of an ischemic stroke but there are some differences. The onset of
symptoms is sudden. Intracranial bleeding causes increased
intracranial pressure so that alterations in consciousness, headache,
nausea, and vomiting are typically prominent in a patient having a
hemorrhagic stroke, and hypertension and seizures are common.54,55
However, signs and symptoms alone cannot be used to distinguish a
hemorrhagic stroke from an ischemic stroke.55
Epidemiology of Hemorrhagic Stroke
Intracranial hemorrhage and stroke are less common than ischemic
stroke but hemorrhagic strokes are usually more severe. The fatality
rate at one month post-stroke has been reported to be from 3552%.54 Most deaths caused by hemorrhagic stroke happen within two
days of the stroke.54 Hemorrhagic stroke is associated with a high rate
of disabilities and an increased risk for death.55,56 Most people who
have had a hemorrhagic stroke will have a deficit or disability.55
Prognosis after a hemorrhagic stroke depends on the size and location
of the bleeding and the patient’s age and pre-existing medical
conditions. Prior use of anticoagulants or antiplatelet agents may
contribute to a worse outcome.55
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Pathophysiology of Hemorrhagic Stroke
An intracerebral hemorrhage is caused by the rupture of blood vessels
and bleeding into the brain parenchyma.55,57 The duration of active
bleeding is typically brief, but the hematoma, the subsequent edema,
and the pressure on adjacent brain tissue disrupt perfusion and causes
cell death.57 Because the skull is a closed space, the bleeding causes
increased intracranial pressure and secondary mechanisms of injury,
which are similar to those caused by an ischemic stroke, and will occur
after the initial hemorrhage.55
Hypertension is the most common cause of hemorrhagic stroke,
cerebral amyloid angiopathy is the most common cause of nontraumatic lobar intracranial hemorrhage in the elderly, and vascular
malformations are the most common cause of intracranial hemorrhage
in children.54 Causes of hemorrhagic stroke are listed in Table 8.54,55,57
Table 8: Causes of Hemorrhagic Stroke
Amphetamine, appetite suppressants, cocaine
Anticoagulant therapy
Bleeding disorders
Brain tumor
Central nervous system infections
Cerebral amyloid angiopathy
Coagulopathies
Hypertension
Liver disease
Moyamoya disease
Septic embolism
Sympathomimetic drug abuse
Thrombolytic therapy for myocardial infarction or stroke
Vascular malformations
Vasculitis
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Some of these are common, and some are rare. A complete discussion
of them all would be very lengthy and this module will instead cover
three: one that nurses may not be familiar with, cerebral amyloid
angiopathy; and two that many nurses are very familiar with, oral
anticoagulant therapy and thrombolytic therapy.
Risk Factors for Hemorrhagic Stroke
The risk factors for and causes of, hemorrhagic stroke overlap: a
condition such as hypertension can be a risk factor and a cause of
stroke. Also, risk factors can interact and be synergistic.65 Risk factors
for hemorrhagic stroke include the following:54,55

Advanced age.

High intake of alcohol: High intake of alcohol has been clearly
and consistently associated with an increased risk for hemorrhagic
stroke.66-68 People who drink heavily often have hypertension, and
hypertension and changes in platelet aggregation and fibrinolysis
may explain why heavy alcohol consumption increases the risk for
hemorrhagic stroke.68

Hypertension.

Low serum cholesterol, low serum triglycerides: Low serum
cholesterol and low serum triglycerides are inversely related to the
risk for, and mortality from, hemorrhagic stroke.69-72 Lipid levels
may contribute to the risk for and mortality of, hemorrhagic stroke
and mortality by causing necrosis of the arterial walls, they may
reflect poor nutritional status, and/or the presence of chronic
disease.69

Previous stroke: A previous stroke increases the risk for
intracerebral hemorrhage.73
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
Ethnic status: Blacks and Asians have a higher risk for
hemorrhagic stroke than Caucasians.54,55
Signs and Symptoms of Hemorrhagic Stroke
The clinical presentation of hemorrhagic stroke was previously
discussed. It is important to emphasize that signs and symptoms alone
are not specific enough to distinguish ischemic from hemorrhagic
stroke, but that indications of increased intracranial pressure such
nausea, vomiting, and headache, as well as an altered level of
consciousness, and seizures are more common with hemorrhagic
strokes and large ischemic strokes.
Cerebral Amyloid Angiopathy
Cerebral amyloid angiopathy (CAA) is a disease that is characterized
by the accumulation of amyloid beta peptide deposits in small and
medium-sized blood vessels in the brain.59 The disease is relatively
common in the elderly, both in people with normal neurological
functioning and those with dementia. It causes progressive fibrosis and
necrosis of the vasculature, and CAA causes approximately 20% of all
cases of intracranial hemorrhage.55
Anticoagulant Therapy
Anticoagulation therapy is very effective at preventing TIA and stroke,
but the use of warfarin and the newer oral anticoagulants carries a
significant risk of intracerebral hemorrhage. The risk has been
estimated at 0.67% per year60 but it may be lower or higher61,62 and it
is associated with clinical factors such as age and medical conditions.
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The risk of intracerebral hemorrhage caused by anticoagulation
therapy has been reported to be higher for Asians, Blacks, and the
elderly. Additionally, people who have had a stroke or a TIA, have an
elevated diastolic blood pressure, or a reduced baseline serum albumin
or platelet count are reported to be at higher risk of intracerebral
hemorrhage from anticoagulation therapy.62 The newer oral
anticoagulants do not appear to be more likely than warfarin to cause
intracerebral bleeding.63
Thrombolytic Therapy
Thrombolytic therapy with recombinant tissue plasminogen activator
(r-tPA) is a highly effective therapy for treating ischemic stroke.
Recombinant tissue plasminogen activator can cause bleeding, and the
rate of symptomatic intracranial hemorrhage caused by r-tPA given to
patients having an ischemic stroke has been reported to be 4.97.7%.64
Evaluation Of The Stroke Patient
This section discusses the evaluation process for a patient suspected of
having a stroke.54,55,64,74
Stabilization of ABCs
The patient should be on continuous cardiac monitoring. The blood
pressure and temperature should be closely monitored.
History and Physical Examination
A complete neurological exam and a detailed history should be
obtained. Particular attention should be paid to the possibility of stroke
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mimics; refer to the TIA section of the module as many of the TIA and
stroke mimics are the same. The single most important piece of
historical information is the time of symptom onset. Stroke scales such
as the NIHSS (shown in the chart below), the Stroke Impairment
Assessment Set, or the Canadian Neurological Scale can be used to
determine the severity of the stroke.74,75
NIHSS Scale
Instructions
1a. Level of consciousness:
The investigator must choose a
response if a full evaluation is
prevented by such obstacles as an
endotracheal tube, language
barrier, orotracheal
trauma/bandages.
A 3 is scored only if the patient
makes no movement (other than
reflexive posturing) in response to
noxious stimulation.
1b. LOC questions: The patient is
asked the month and his/her age.
The answer must be correct - there
is no partial credit for being close.
Aphasic and stuporous patients who
do not comprehend the questions
will score
2. Patients unable to speak because
of endotracheal intubation,
orotracheal trauma, severe
dysarthria from any cause,
language barrier, or any other
problem not secondary to aphasia
are given a 1. It is important that
only the initial answer be graded
and that the examiner not "help"
the patient with verbal or nonverbal cues.
Scale definition
0 = Alert; keenly responsive.
1 = Not alert; but arousable by
minor stimulation to obey, answer,
or respond.
2 = Not alert; requires repeated
stimulation to attend, or is
obtunded and requires strong or
painful stimulation to make
movements (not stereotyped).
3 = Responds only with reflex
motor or autonomic effects or
totally unresponsive, flaccid, and
areflexic.
Score
____
0 = Answers both questions
correctly.
1 = Answers one question correctly.
2 = Answers neither question
correctly.
____
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1c. LOC commands: The patient is
asked to open and close the eyes
and then to grip and release the
non-paretic hand. Substitute
another one step command if the
hands cannot be used.
0 = Performs both tasks correctly.
1 = Performs one task correctly.
2 = Performs neither task correctly.
Credit is given if an unequivocal
attempt is made but not completed
due to weakness.
____
If the patient does not respond to
command, the task should be
demonstrated to him or her
(pantomime), and the result scored
(i.e., follows none, one or two
commands). Patients with trauma,
amputation, or other physical
impediments should be given
suitable one-step commands. Only
the first attempt is scored.
2. Best gaze: Only horizontal eye
movements will be tested.
Voluntary/reflexive (oculocephalic)
eye movements will be scored, but
caloric testing is not done. If the
patient has a conjugate deviation of
the eyes that can be overcome by
voluntary or reflexive activity, the
score will be 1.
0 = Normal.
1 = Partial gaze palsy; gaze is
abnormal in one or both eyes, but
forced deviation or total gaze
paresis is not present.
2 = Forced deviation, or total gaze
paresis not overcome by the
oculocephalic maneuver.
If a patient has an isolated
peripheral nerve paresis (CN III, IV
or VI), score a 1.
Gaze is testable in all aphasic
patients. Patients with ocular
trauma, bandages, pre-existing
blindness, or other disorder of
visual acuity or fields should be
tested with reflexive movements,
and a choice made by the
investigator.
____
Establishing eye contact and then
moving about the patient from side
to side will occasionally clarify the
presence of a partial gaze palsy.
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3. Visual: Visual fields (upper and
lower quadrants) are tested by
confrontation, using finger counting
or visual threat, as appropriate.
Patients may be encouraged, but if
they look at the side of the moving
fingers appropriately, this can be
scored as normal.
0 = No visual loss.
1 = Partial hemianopia.
2 = Complete hemianopia.
3 = Bilateral hemianopia (blind
including cortical blindness).
If there is unilateral blindness or
enucleation, visual fields in the
remaining eye are scored. Score 1
only if a clear-cut asymmetry,
including quadrantanopia, is found.
If patient is blind from any cause,
score 3. Double simultaneous
stimulation is performed at this
point. If there is extinction, patient
receives a 1, and the results are
used to respond to item 11.
4. Facial palsy: Ask - or use
pantomime to encourage - the
patient to show teeth or raise
eyebrows and close eyes. Score
symmetry of grimace in response to
noxious stimuli in the poorly
responsive or non-comprehending
patient.
If facial trauma/bandages,
orotracheal tube, tape or other
physical barriers obscure the face,
these should be removed to the
extent possible.
5. Motor arm: The limb is placed in
the appropriate position: extend
the arms (palms down) 90 degrees
(if sitting) or 45 degrees (if supine).
Drift is scored if the arm falls
before 10 seconds.
The aphasic patient is encouraged
using urgency in the voice and
pantomime, but not noxious
stimulation.
Each limb is tested in turn,
beginning with the non-paretic arm.
____
0 = Normal symmetrical
movements.
1 = Minor paralysis (flattened
nasolabial fold, asymmetry on
smiling).
2 = Partial paralysis (total or neartotal paralysis of lower face).
3 = Complete paralysis of one or
both sides (absence of facial
movement in the upper and lower
face).
0 = No drift; limb holds 90 (or 45)
degrees for full 10 seconds.
1 = Drift; limb holds 90 (or 45)
degrees, but drifts down before full
10 seconds; does not hit bed or
other support.
2 = Some effort against gravity;
limb cannot get to or maintain (if
cued) 90 (or 45) degrees, drifts
down to bed, but has some effort
against gravity.
3 = No effort against gravity; limb
falls.
4 = No movement.
____
____
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Only in the case of amputation or
joint fusion at the shoulder, the
examiner should record the score
as untestable (UN), and clearly
write the explanation for this
choice.
UN = Amputation or joint fusion,
explain:________________
5a. Left arm
5b. Right arm
6. Motor leg: The limb is placed in
the appropriate position: hold the
leg at 30 degrees (always tested
supine). Drift is scored if the leg
falls before 5 seconds.
0 = No drift; leg holds 30-degree
position for full 5 seconds.
1 = Drift; leg falls by the end of the
5-second period but does not hit
bed.
2 = Some effort against gravity; leg
falls to bed by 5 seconds, but has
some effort against gravity.
Each limb is tested in turn,
beginning with the non-paretic leg.
____
Only in the case of amputation or
joint fusion at the hip, the examiner
should record the score as
untestable (UN), and clearly write
the explanation for this choice.
3 = No effort against gravity; leg
falls to bed immediately.
4 = No movement.
UN = Amputation or joint fusion,
explain:________________
6a. Left leg
6b. Right leg
7. Limb ataxia: This item is aimed
at finding evidence of a unilateral
cerebellar lesion. Test with eyes
open. In case of visual defect,
ensure testing is done in intact
visual field.
0 = Absent.
1 = Present in one limb.
2 = Present in two limbs.
UN = Amputation or joint fusion,
explain:________________
The finger-nose-finger and heelshin tests are performed on both
sides, and ataxia is scored only if
present out of proportion to
weakness. Ataxia is absent in the
patient who cannot understand or is
paralyzed. Only in the case of
amputation or joint fusion, the
examiner should record the score
as untestable (UN), and clearly
write the explanation for this
choice. In case of blindness, test by
having the patient touch nose from
extended arm position.
8. Sensory: Sensation or grimace
to pinprick when tested, or
withdrawal from noxious stimulus in
the obtunded or aphasic patient.
____
0 = Normal; no sensory loss.
1 = Mild-to-moderate sensory loss;
patient feels pinprick is less sharp
or is dull on the affected side; or
____
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Only sensory loss attributed to
stroke is scored as abnormal and
the examiner should test as many
body areas (arms [not hands], legs,
trunk, face) as needed to
accurately check for hemisensory
loss. A score of 2, "severe or total
sensory loss," should only be given
when a severe or total loss of
sensation can be clearly
demonstrated. Stuporous and
aphasic patients will, therefore,
probably score 1 or 0.
there is a loss of superficial pain
with pinprick, but patient is aware
of being touched.
2 = Severe to total sensory loss;
patient is not aware of being
touched in the face, arm, and leg.
The patient with brainstem stroke
who has bilateral loss of sensation
is scored 2. If the patient does not
respond and is quadriplegic, score
2. Patients in a coma (item 1a=3)
are automatically given a 2 on this
item.
9. Best language: A great deal of
information about comprehension
will be obtained during the
preceding sections of the
examination. For this scale item,
the patient is asked to describe
what is happening in the attached
picture, to name the items on the
attached naming sheet and to read
from the attached list of sentences.
Comprehension is judged from
responses here, as well as to all of
the commands in the preceding
general neurological exam. If visual
loss interferes with the tests, ask
the patient to identify objects
placed in the hand, repeat, and
produce speech.
The intubated patient should be
asked to write. The patient in a
coma (item 1a=3) will
automatically score 3 on this item.
The examiner must choose a score
for the patient with stupor or
limited cooperation, but a score of
3 should be used only if the patient
is mute and follows no one-step
commands.
0 = No aphasia; normal.
1 = Mild-to-moderate aphasia;
some obvious loss of fluency or
facility of comprehension, without
significant limitation on ideas
expressed or form of expression.
Reduction of speech and/or
comprehension, however, makes
conversation about provided
materials difficult or impossible. For
example, in conversation about
provided materials, examiner can
identify picture or naming card
content from patient's response.
2 = Severe aphasia; all
communication is through
fragmentary expression; great need
for inference, questioning, and
guessing by the listener. Range of
information that can be exchanged
is limited; listener carries burden of
communication. Examiner cannot
identify materials provided from
patient response.
3 = Mute, global aphasia; no usable
speech or auditory comprehension.
____
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10. Dysarthria: If patient is thought
to be normal, an adequate sample
of speech must be obtained by
asking patient to read or repeat
words from the attached list. If the
patient has severe aphasia, the
clarity of articulation of
spontaneous speech can be rated.
Only if the patient is intubated or
has other physical barriers to
producing speech, the examiner
should record the score as
untestable (UN), and clearly write
an explanation for this choice. Do
not tell the patient why he or she is
being tested.
11. Extinction and inattention
(formerly neglect): Sufficient
information to identify neglect may
be obtained during the prior
testing.
If the patient has a severe visual
loss preventing visual double
simultaneous stimulation, and the
cutaneous stimuli are normal, the
score is normal. If the patient has
aphasia but does appear to attend
to both sides, the score is normal.
0 = Normal.
1 = Mild-to-moderate dysarthria;
patient slurs at least some words
and, at worst, can be understood
with some difficulty.
2 = Severe dysarthria; patient's
speech is so slurred as to be
unintelligible in the absence of or
out of proportion to any dysphasia,
or is mute/anarthric.
UN = Intubated or other physical
barrier,
explain:________________
0 = No abnormality.
1 = Visual, tactile, auditory, spatial,
or personal inattention or extinction
to bilateral simultaneous
stimulation in one of the sensory
modalities.
2 = Profound hemi-inattention or
extinction to more than one
modality; does not recognize own
hand or orients to only one side of
space.
____
____
The presence of visual spatial
neglect or anosognosia may also be
taken as evidence of abnormality.
Since the abnormality is scored
only if present, the item is never
untestable.
____
The following diagnostic tests should be performed on all stroke
patients during the evaluation process.54,55,64,74,76
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Table 12: Diagnostic Tests for Stroke Evaluation
Activate partial thromboplastin time (aPTT)
Blood glucose
Complete blood count
INR
ECG
Markers of cardiac ischemia
Non-contrast brain CT or brain MRI
Oxygen saturation
Prothrombin time
Platelet count
Renal function tests
Serum electrolytesrenal function tests
Fibrinolytic therapy should not be delayed for these test results unless: 1)
there is clinical suspicion of a bleeding abnormality or thrombocytopenia;
2) the patient has received heparin or warfarin, or; 3) the patient has
received other anticoagulants.
The diagnostic tests listed in the table below should be performed for
selected patients during the evaluation of a stroke.76,77
Table 13: Diagnostic tests for Stroke Evaluation/Selected Patients
Arterial blood gas
Blood alcohol level
Chest x-ray
Eletroencephalogram
Hepatic function tests
Lumbar puncture
Pregnancy test
Thrombin time (TT) and/or ecarin clotting time (ECT)
Toxicology screen
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Brain and Vascular Imaging
Emergency imaging of the brain by CT scan or MRI scan should be
done, and it should be done before any specific therapy is started.
Non-invasive vascular imaging of the intracranial blood supply is
strongly recommended in order to detect large vessel occlusion that
may need fibrinolytic therapy or thrombectomy. This procedure should
not be done if it would delay the use of rtPA. CT angiography,
conventional angiography, MRI-angiography, and Doppler ultrasound
can all be used. Assessment of the carotid blood supply can be done,
as well.
Subarachnoid Hemorrhage And Stroke
Subarachnoid hemorrhage (SAH) is a bleed into the subarachnoid
cavity, the space between the arachnoid membrane and the pia mater.
Each year approximately 30,000 people suffer a SAH and it is an
infrequent cause of stroke but it is often a devastating event.78 The
30-day mortality rate of SAH caused by rupture of an aneurysm is
approximately 30-45% and 30% of the patients who survive have
significant disabilities.78,79
The most common cause of SAH is trauma. The majority of nontraumatic SAH are caused by rupture of an aneurysm;78 amyloid
angiopathy, moyamoya disease, arteriovenous malformations, and
vasculitis can also cause SAH. Risk factors for SAH are listed in Table
14.78,80
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Table 14: Risk Factors for SAH
Alcohol (especially binge drinking)
Caffeine
Cocaine
Hypertension
Smoking
Family history
Female gender
Alpha-1 antitrypsin deficiency
Polycystic kidney disease
Sickle cell disease
The most common symptoms of a SAH are dizziness, nausea,
vomiting, and a sudden onset of a severe headache;78 patients often
describe the headache as the worst pain they have ever had. If the
area of bleeding is small and stops the headache pain may not last
long, and these are called sentinel headaches. Sentinel headaches are
relatively common, and they can happen days and weeks before the
SAH.78,81 Rebleeding has been reported to occur in 8-23% of
patients.82 This will usually happens in the first 24 hours and the risk is
especially high in the first six hours.83 The risk for rebleeding can be
predicted by: 1) the Hunt and Hess grade; 2) the size of the
aneurysm; 3) blood pressure; 4) the presence of a sentinel headache,
and; 5) a longer interval between the onset and when medical care is
sought.83
There are assessment scales that have been developed for grading the
severity of SAH: the Hunt and Hess scale, World Federation of
Neurological Surgeons (WFNS) scale, Fisher scale, Claasen grading
system, and the Ogilvy and Carter scale. There is no evidence that one
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is better than another,83 but the Hunt and Hess is the most widely
accepted and used.
Hunt and Hess Grading system for subarachnoid hemorrhage.
Grade
Neurologic status
1
Asymptomatic or mild headache and slight nuchal rigidity
2
Severe headache, stiff neck, no neurologic deficit except cranial nerve
palsy
3
Drowsy or confused, mild focal neurologic deficit
4
Stuporous, moderate or severe hemiparesis
5
Coma, decerebrate posturing
Evaluation of suspected SAH is done in
essentially the same way as for other
types of stroke but there are important
Reasons for misdiagnosis of
subarachnoid hemorrhage

failure to understand
differences. Headache is often the only
the signs and symptoms
presenting symptom of a SAH, but
associated with
subarachnoid
headache is a very common complaint
and only a small percentage of people
hemorrhage

not performing a CT
who have a headache have a SAH.85
scan or not
Because the morbidity and mortality of
understanding the
SAH are quite high, and re-bleeding
limitations of the
relatively common, it is important to
rule in/rule out SAH quickly and
procedure

not performing a lumbar
puncture
accurately.
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If there is a suspicion that the patient is having a SAH, a non-contrast
CT scan of the head should be performed immediately and a lumbar
puncture should be done.78 The non-contrast CT scan is very sensitive
at detecting SAH if the hemorrhage occurred less than 24 hours prior
to the exam,78 but the sensitivity of the CT scan for this purpose
decreases with time, and with other factors, as well.78 If the CT scan of
the head is negative a lumber puncture must be performed.78
Some clinicians feel that if the patient has an acute headache and the
CT scan of the head is negative, a lumbar puncture (LP) is not
needed.78 However, there is not insignificant number of patients of this
description who will have a SAH, and recent literature (i.e., Abraham,
Chang, 2016; Singer, Ogilvy, Rordorf, 2013) recommends a lumbar
puncture. Abraham and Chang note that although “… the LP continues
to have benefit in the diagnostic work-up of SAH, the utility is greatly
debated. With a low diagnostic yield, a serious discussion with the
patient about the risks and benefits of the procedure needs to
occur…”78
Misdiagnosing a SAH can be potentially catastrophic. The reasons for
misdiagnosis are: 1) failure to understand the signs and symptoms
associated with SAH; 2) not performing a CT scan or not
understanding the limitations of the procedure; and, 3) not performing
a lumbar puncture.83
Treatment Of Ischemic Stroke
Patients should be admitted to the ICU and have continuous
hemodynamic and neurologic monitoring. The following
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recommendations are from the 2013 guidelines from the American
Heart Association and the American Stroke Association (AHA/ASA).76
Stabilization of ABCs
Patient Positioning
If the patient is hypoxic or may become so, or if he/she is at risk for
airway obstruction, aspiration, or increased intracranial pressure, the
head of the bed should be elevated at a 15-30 degree angle. If not, a
neutral position (0-15 degrees elevation) should be maintained.64,76,77
Oxygen
Many patients who have had a stroke are hypoxic. Supplemental
oxygen should be used to maintain an oxygen saturation of greater
than 94%.64 Supplemental oxygen should not be used if the patient is
not hypoxic.76
Hyperthermia
Hyperthermia is common after a stroke and it has been associated
with a poor outcome.77 If the temperature is greater than 38°C the
source should be identified and treated. Patients who are hyperthermic
should have their body temperature lowered.76,77
Blood Pressure Monitoring
Hypertension is common in patients who have had a stroke;
hypotension is uncommon. Maintaining adequate perfusion is
important as is avoiding dangerous elevations of blood pressure, but
the ideal level of blood pressure for patients who have had an ischemic
stroke is not known. The consensus is that if the patient will not be
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receiving thrombolytic therapy, hypertension should not be treated
unless the blood pressure is >220 mm Hg systolic or >120 mm Hg
diastolic, or unless there is a pre-existing medical condition for which
blood pressure control is needed.64,76,77
The recommendations for managing blood pressure that are in Table
15 are from the 2013 AHA/ASA 2013 guidelines for managing ischemic
stroke.76
Table 15: Blood Pressure Management in Patients with Ischemic Stroke
Patients who are otherwise eligible for reperfusion therapy
but the BP is >185/110 mm Hg:
Labetalol 10–20 mg IV over 1–2 minutes, may repeat 1 time; or
Nicardipine 5 mg/hr IV, titrate up by 2.5 mg/hr every 5–15 minutes,
maximum 15 mg/hr; when desired BP reached, adjust to maintain proper
BP limits; or other drugs may be used when needed.
If BP is not maintained at or below 185/110 mm Hg, do not administer rtPA
Management of BP during and after rtPA or other acute reperfusion therapy
to maintain BP at or below 180/105 mm Hg:
Check BP every 15 minutes for 2 hours from the start of rtPA therapy, then
every 30 minutes for 6 hours, and then every hour for 16 hours
If systolic BP >180–230 mm Hg or diastolic BP >105–120 mm Hg:
Labetalol 10 mg IV followed by continuous IV infusion 2–8 mg/min; or
Nicardipine 5 mg/h IV, titrate up to desired effect by 2.5 mg/h every 5–15
minutes, maximum 15 mg/hr
If BP not controlled or diastolic BP >140 mm Hg,
IV Sodium Nitroprusside can be used
Intravenous Hydration
Most patients who have had an ischemic stroke are dehydrated or
euvolemic and euvolemia is recommended.76 Hypovolemia decreases
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perfusion to the organs and hypervolemia can increase cerebral edema
and is stressful for the myocardium. Fluid replacement is best done
using an isotonic, glucose-free solutions such as 0.9% normal
saline.76,77 Using these fluids helps with glucose control and prevents
free water from entering the CNS tissues.
Serum Glucose
Hyperglycemia has been noted in more than 40% of patients who have
had an ischemic stroke
86,87
and it is consistently associated with a
worse outcome.88,89 The elevated serum glucose in the acute phase of
stroke may be related to uncontrolled or undetected diabetes mellitus
or stress-induced hyperglycemia caused by cortisol and norepinephrine
release at the time of insult. The 2013 AHA/ASA guidelines recommend
that “… it is prudent to treat hyperglycemia during acute stroke in a
manner that avoids excessive resources, labor, and risk,”76 and that
the ADA recommendation of maintaining serum glucose between 140180 mg/dL in all hospitalized patients should be observed.76 A serum
glucose <60 mg/dL should be treated.76 Rapid assessment, evaluation,
and treatment of ischemic stroke is essential. Table 16 provides an
outline of the desired time sequence from the time of arrival until, if
needed, the use of a thrombolytic.77
Table 16: Optimal Stroke Care Time Limits
Evaluation by physician ≤10 minutes
Stroke team/neurologist contacted ≤15 minutes
Imaging study ≤25 minutes
Imaging interpretation ≤45 minutes
Use of thrombolytic ≤60 minutes
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Thrombolytic Therapy
Thrombolytic therapy with recombinant tissue plasminogen activator
(rtPA) is the only Food and Drug Administration (FDA) approved
thrombolytic therapy for the treatment of ischemic stroke. The use of
rtPA has been shown to improve functional outcomes in patients who
have had an ischemic stroke if the drug can be given 4.5 hours or less
from the onset of symptoms.76,90
Recombinant tissue plasminogen activator promotes clot dissolution,
aka fibrinolysis, by binding to fibrin in a clot and converting
plasminogen to plasmin. These drugs, i.e., alteplase (Activase) are
enzymes that increase the conversion of plasminogen to plasmin;
plasminogen is the inactive precursor to plasmin, and plasmin is an
enzyme that breaks down fibrin clots. Recombinant tissue plasminogen
activators must be given carefully and correctly. The inclusion and
exclusion criteria for thrombolytic therapy with rtPa in tables 17 and
18 are from the 2013 AHA/ASS guidelines.76
It should be noted that the newer anticoagulants are becoming
popular. Using rtPA in patients who are have been taking one of these
drugs that act by inhibiting factor Xa or thrombin is not recommended
unless laboratory tests such as aPTT, ECT, INR, factor Xa activity
assay, platelet count, and TT time can be measured and are normal or
if the patient has not had a dose in greater than 48 hours and his/her
renal function is normal.76
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Table 17: rtPA Inclusion Criteria
Ischemic stroke and measurable neurological deficit
Onset of symptoms <3 hours before beginning treatment
Aged ≥18 years
Table 18: rtPA Absolute Exclusion Criteria
Active internal bleeding
Arterial puncture at non-compressible site in previous 7 days
Blood glucose <50 mg/dL
CT shows multilobar infarction (hypodensity >1/3 cerebral hemisphere)
History of intracranial hemorrhage
Intracranial neoplasm, arteriovenous malformation, or aneurysm
Recent intracranial or intraspinal surgery
Significant head trauma or a stroke in previous 3 months
Symptoms suggest subarachnoid hemorrhage
Systolic BP >185 mm Hg or diastolic >110 mm Hg
Acute bleeding diathesis, including but not limited to:
a. Platelet count <100 000/mm3
b. Heparin received within 48 hours, resulting in abnormally elevated aPTT
greater than the upper limit of normal
c. Current use of anticoagulant with INR >1.7 or PT >15 seconds
d. Current use of direct thrombin inhibitors or direct factor Xa inhibitors
with elevations of laboratory tests such as aPTT, ECR, factor Xa assay, INR,
platelet count, and thrombin time
The AHA/ASS also has relative inclusion and exclusion criteria for
thrombolytic therapy with rtPA.76 These are listed in Tables 19 and 20,
and the 2013 guidelines state: “Recent experience suggests that under
some circumstances — with careful consideration and weighting of risk
to benefit — patients may receive fibrinolytic therapy despite one or
more relative contraindications. Consider risk to benefit of IV rtPA
administration carefully if any of these relative contraindications are
present.”76
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Table 19: rtPA Relative Exclusion Criteria
Acute myocardial infarction (within 3 months)
Age >80 years
Gastrointestinal or urinary tract hemorrhage within 21 days
History of diabetes and prior ischemic stroke
Major surgery or serious trauma within 14 days
Minor or rapidly improving stroke symptoms
Pregnancy
Seizure and postictal residual neurological impairments
Severe stroke (NIHSS score >25)
Use of an oral anticoagulant, regardless of INR
Table 20: Inclusion Criteria: Symptom Onset between 3 - 4.5 Hours
Ischemic stroke causing measurable neurological deficit
Symptoms onset within 3 to 4.5 hours before beginning treatment
Table 21: Administration of rtPA76
1.
2.
3.
4.
5.
6.
7.
Infuse 0.9 mg/kg (maximum dose 90 mg) over 60 minutes: give 10%
of the dose as a bolus over 1 minute.
Admit the patient to an intensive care or stroke unit for monitoring.
If the patient develops severe headache, hypertension, nausea,
vomiting, or neurologic deterioration, discontinue the rtPA infusion
obtain an emergent CT scan.
Measure blood pressure and perform neurological assessments every
15 minutes during and after IV rtPA infusion for 2 hours, then every
30 minutes for 6 hours, then hourly until 24 hours after rtPA
treatment.
Increase the frequency of blood pressure measurements if systolic
blood pressure is >180 mm Hg or if diastolic blood pressure is >105
mm Hg; administer antihypertensive medications as described in Table
15. to maintain blood pressure below these levels.
Do not place nasogastric tubes, indwelling bladder catheters, or intraarterial pressure catheters if the patient can be safely managed
without them.
Obtain a follow-up CT or MRI scan at 24 hours after IV rtPA before
starting anticoagulants or antiplatelet agents.
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Thrombolysis is an effective treatment for ischemic stroke but it has
significant limitations. It can only be given within 4.5 hours (3 hours is
considered preferable) after the onset of symptoms and many patients
with ischemic stroke present to the hospital well outside of that time
frame. Thrombolysis has serious adverse effects and although it has
what could be described as a good success rate, there are certainly
people who do not respond.
Endovascular therapies such as stenting, intra-arterial fibrinolysis,
mechanical thrombectomy, clot aspiration can be used alone for
patients who are not eligible for rtPA treatment or used with rtPA if the
patient is likely to respond poorly to rtPA, i.e., if the patient has a
severe stroke caused by a large occlusion and several clots.91-93 At this
point the evidence for the effectiveness of these techniques has been
described as equivocal,94 and there are no trials that directly compare
one to another.76
Aspects of Stroke Care: 2013 AHA/ASS Guidelines
Other aspects of stroke care are outlined below according to the
recommendations in the 2013 AHA/ASS guidelines.76
Anticoagulation
Urgent anticoagulation with heparin or a low molecular weight heparin
does not decrease the risk of early neurological deterioration or
recurrent stroke and is not recommended.
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Platelet Inhibition
Administering aspirin 24-48 hours after the onset of the stroke is
recommended.
Statins
If the patient was taking a statin it is reasonable to continue use of the
drug.
Induced Hypothermia
There is no evidence that induced hypothermia is effective.
Carotid Endarterectomy
The use of carotid endarterectomy is not well established.
Stroke Centers
The use of specialized stroke centers is recommended.
Antibiotics
Prophylactic antibiotics are not recommended. Pneumonia is a serious
complication occurring in the first 48 to 72 hours after acute ischemic
stroke and accounts for approximately 15% to 25% of deaths
associated with stroke. Stroke-associated pneumonia increases length
of stay, mortality, and hospital costs. The most common cause of
pneumonia is aspiration due to dysphagia.
Urinary tract infections (UTIs) are also common, occurring in
approximately 15% to 60% of stroke patients, and independently
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predict poor outcome. If the patient has pneumonia or a UTI he/she
should be treated with the appropriate antibiotics.
Deep Vein Thrombosis Prevention
Subcutaneous heparin is recommended to prevent deep vein
thrombosis (DVT) in patients who are immobilized. Aspirin can be used
if the use of subcutaneous heparin is contraindicated. External
compression devices are another alternative.
Swallowing Assessment
A swallowing assessment should be done before liquids, solids, or oral
medications are allowed. Nasogastric tubes, PEG tubes, or other
devices can be used to provide hydration, medications and nutrition if
needed.
Mobilization
Early mobilization is recommended. Early mobilization reduces risk of
atelectasis, pneumonia, DVT, and pulmonary embolism. Complications
from immobility have been found to account for up to 51% of deaths
in the first 30 days after ischemic stroke. Immobility can also lead to
contractures, orthopedic complications, atrophy, and nerve pressure
palsies.
Indwelling Urinary Catheter
The most common urinary complication is incontinence, which occurs
30% to 60% of the time in the early recovery period. An indwelling
urinary catheter should not be used because of the risk for urinary
tract infection.
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Stroke Prevention Measures
Stroke prevention measures should be started as soon as possible.
Treatment Of Hemorrhagic Stroke
Many of the treatment concern and goals for hemorrhagic stroke are
identical to those of ischemic stroke, i.e., blood glucose, body
temperature, and fluid status must be closely monitored, the patient
closely observed for complications such as aspiration, DVT,
pneumonia, and UTI.95 Patients should be admitted to the ICU and
have continuous hemodynamic and neurologic monitoring. Specific
concerns in the management of these patients include those outlined
below.

DVT prevention: Intermittent pneumatic compression should be
used to prevent DVT.95

Intravenous Hydration: Normal saline should be used for IV
hydration. Isotonic fluids should not be used as they can worsen
cerebral edema and elevate intracranial pressure. Hypervolemia
should be avoided as it can worsen cerebral edema.95

Blood Pressure Control: Hypertension is common in patients who
have had a hemorrhagic stroke,95 and an elevated blood pressure is
associated with a poor outcome.96 A 2013 study found that
intensive lowering of blood pressure in patients who had a
hemorrhagic stroke did not change rates of mortality or severe
disability but did significantly improve functional outcomes, and was
not associated with an increase in death or serious adverse
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effects.97 Guidelines for managing blood pressure in patients who
have had an intracerebral hemorrhage are in Table 22.95
Table 15: Blood Pressure Management in Patients with Hemorrhagic Stroke
Systolic BP >200 mmHg or MAP >150 mmHg, consider
aggressive reduction of blood pressure
Systolic blood pressure >180 mmHg or MAP >130 mmHg and
evidence or suspicion of elevated ICP, consider lowering
blood pressure to maintain the cerebral perfusion pressure
between 61 to 80 mmHg
Systolic BP >180 mmHg or MAP >130 mmHg but no evidence
or suspicion of elevated ICP, use intermittent or continuous
IV infusion of an antihypertensive to
lower the MAP to 110 mm HG. Examine patient every 15 min.

Intracranial Pressure: Increased intracranial pressure (ICP)
caused by intracranial hemorrhage can cause further brain
injury. In order to avoid an increase in ICP the head of the
bed should be elevated 30 degrees and the patient should
receive appropriate analgesia and sedation.95
Glucocorticoids such as dexamethasone should not be used
to lower ICP.95
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Invasive ICP monitoring allows direct measurement of ICP
and it appears to be more sensitive to changes in ICP and
more effective at preventing complications, i.e.,
enlargement of a hematoma, than neurological examination
and brain scanning.98 If ICP needs to be lowered, IV
infusions of mannitol, barbiturate coma, hyperventilation,
ventriculostomy, and surgical evacuation of the hematoma
are considered reasonable options.95,100

Seizures: Seizures, both clinical and noted on
electroencephalography monitoring are common after
intracranial hemorrhage.95,100 There is no clear evidence
about how seizures affect patient outcome, whether seizures
should be treated, or what medications should use to treat
them.100 A 2014 review noted that “ ... clinically significant
seizures should be treated with anticonvulsants …”100 and
prophylaxis with anticonvulsants is not recommended.

55,101
Patients receiving anticoagulants: Warfarin should be
discontinued if the INR is elevated, IV vitamin K should be
administered, and specific vitamin K-dependent factors
should be given.101 If there is severe bleeding vitamin K,
fresh frozen plasma, and prothrombin complex
concentrates, recombinant factor VIIa, or idarucizumab can
be given.101-105
Treatment Of Subarachnoid Hemorrhage
Many of the treatment concern and goals for subarachnoid
hemorrhagic are identical to those of ischemic stroke, i.e., blood
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glucose, body temperature, and fluid status must be closely
monitored, and the patient closely observed for complications such as
aspiration, DVT, pneumonia, and UTI.78,95 Patients should be admitted
to the ICU and have continuous hemodynamic and neurologic
monitoring. Specific concerns in the management of these patients
include the following conditions.

Hyponatremia:
Hyponatremia occurs in approximately one-third of all patients who
have had a subarachnoid hemorrhage and it is associated with a
poor outcome.106 Hyponatremia is treated by restricting free water
consumptions and administering 1.5% or 2% sodium chloride
solutions.106 Fludrocortisone or hydrocortisone may help promote
diuresis and correct the hyponatremia.106

Re-bleeding:
Re-bleeding is managed by using antifibrinolytic drugs such as
tranexamic acid, aminocaproic acid, or surgical clipping and
endovascular coiling.95,106

Hydrocephalus:
Hydrocephalus is defined as an excess of fluid in the ventricles of
the brain and it is a relatively common complication of
subarachnoid hemorrhage. Symptomatic hydrocephalus is treated
making a burr hole in the skull and placing a ventricular drain.95,106

Seizures:
Prophylactic anticonvulsants should be considered if the patient has
a large hemorrhage that has not yet been surgically corrected.95
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
Vasospasm and delayed cerebral ischemia:
Some patients who have had a subarachnoid hemorrhage will have
neurologic deterioration after the initial event. This neurologic
deterioration is thought to be caused by arterial vasospasm that
reduces cerebral blood flow and in the setting of a subarachnoid
hemorrhage it is called delayed cerebral ischemia (DCI).106
Delayed cerebral ischemia (DCI) is defined as neurologic
deterioration that is not due to other causes or a new infarction that
is documented by CT scan more than 72 hours after the
hemorrhage.160
Prophylactic treatment of DCI includes nimodipine (Nimotop®), a
calcium channel blocker, maintaining euvolemia, and lumbar
drainage.106 If the patient is symptomatic the treatments include
induced hypertension, inotropic drugs such as dobutamine and
milrinone, transfusions to maintain a hemoglobin level between 810 mg/dL, angioplasty, and intra-arterial dilators such as milrinone,
nimodipine, nicardipine, and verapamil.106

Blood pressure management:
The best treatment for hypertension in a patient who has a
subarachnoid hemorrhage is not known. Clevidipine, enalapril,
labetalol, or nicardipine are the recommended
antihypertensives.78,95
Summary
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Transient ischemic attack and stroke are very common neurologic
emergencies. A TIA by definition does not cause serious impairment
but it is a significant neurological event. Strokes, caused by ischemia
or hemorrhage, can be devastating and cause permanent and severe
disabilities. Transient ischemic attack and ischemic stroke are caused
by thrombus, emboli, or hypoperfusion. Hemorrhagic stroke is caused
by rupture of small cerebral arteries, and bleeding into the
subarachnoid space causes subarachnoid hemorrhage. Advanced age,
ethnic background, and family history are some of the non-modifiable
risk factors for TIA and stroke; atrial fibrillation, cigarette smoking,
and hypertension are some of the common modifiable risk factors.
Treatment of TIA is primarily supportive, but the patient should
receive anticoagulation and antiplatelet therapy to prevent future TIAs
or a stroke. Treatment of an ischemic stroke primarily focuses on clot
dissolution using rtPA. Treatment of hemorrhagic stroke focuses
primarily on monitoring ICP and preventing cerebral edema, while
treatment of subarachnoid hemorrhage focuses on monitoring for
elevations in ICP and for the development of DCI. In all of these, TIA,
ischemic stroke, hemorrhagic stroke, and stroke caused by
subarachnoid hemorrhage, it should be remembered that the brain is
exquisitely sensitive to lack of blood and oxygen and rapid assessment
and treatment is essential to prevent permanent neurological damage.
Please take time to help NurseCe4Less.com course planners
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article, and providing feedback in the online course evaluation.
Completing the study questions is optional and is NOT a course
requirement.
1.
A transient ischemic attack:
a. causes a transient neurological dysfunction without acute
infarction.
b. is typically caused by a coagulation disorder.
c. causes permanent neurological dysfunction.
d. is very common in children and young adults.
2.
A transient ischemic attack:
a.
b.
c.
d.
3.
Treatment priorities for transient ischemic attack includes:
a.
b.
c.
d.
4.
is caused by bleeding into the subarachnoid space.
is considered to be a risk factor for stroke.
is characterized by persistent neurological deficits.
does not require the use of neuroimaging.
the use of rtPA and ICP monitoring.
withdrawal of anticoagulants and antihypertensives.
induced hypothermia and maintaining euvolemia.
anticoagulation and antiplatelet therapy.
An ischemic stroke is characterized by:
a. bleeding into the subarachnoid space.
b. temporary neurological dysfunction caused by a thrombus
or embolism.
c. cerebral infarction caused by decreased blood flow.
d. rupture of small arteries and bleeding into the brain
parenchyma.
5.
True or False: Evidence for an increased risk for stroke is
strongest for atrial fibrillation, cigarette smoking,
dyslipidemia, hypertension, physical inactivity, and sickle
cell disease.
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a. True
b. False
6.
A hemorrhagic stroke is characterized by:
a. decreased blood flow caused by a thrombus or embolism.
b. rupture of small arteries and bleeding into the brain
parenchyma.
c. bleeding into the subarachnoid space.
d. hypoperfusion caused by a coagulopathy.
7.
Subarachnoid hemorrhage is characterized by:
a.
b.
c.
d.
8.
A treatment priority in subarachnoid hemorrhage is
______________, reported to occur in 8-23% of patients
and will usually happen in the first 24 hours with the risk
especially high in the first six hours.
a.
b.
c.
d.
9.
temporary neurologic dysfunction.
cerebral ischemia that causes an infarct.
bleeding into the subarachnoid cavity.
hypercoaguability that causes decreed brain perfusion.
rebleeding
blindness
sudden sharp pain
None of the above
True or False: Epidemiological studies have shown that
elevated blood pressure is the most important determinant
of the risk of stroke.
a. True
b.False
10. Patients who have had a TIA should be started on _______
if: the TIA is presumed to be caused by atherosclerosis, the
low-density lipoprotein cholesterol (LDL-C) level is ≥ 100
mg/dL, with or without evidence for other atherosclerotic
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cardiovascular disease (ASCVD), or the TIA is presumed to
be caused by atherosclerosis, and the LDL-C level is < 100
mg/dL, and there is no evidence of ASCVD.
a. aspirin
b. statin therapy
c. plavix
d. warfarin
11. Which of the following is described as “An episode of
neurological dysfunction caused by focal cerebral, spinal,
or retinal infarction”?
a.
b.
c.
d.
Silent stroke
Transient ischemic attack
Ischemic stroke
Elevated INR
12. True or False: Hypertension and changes in platelet
aggregation and fibrinolysis may explain why heavy
alcohol consumption increases the risk for hemorrhagic
stroke.
a. True
b. False
13. A transient ischemic attack (TIA) includes the description
“transient” because
a. the effects of a TIA are temporary.
b. a TIA is distinguishable from more serious neurological
events.
c. the event is transient but not necessarily its consequences.
d. the duration of symptoms is a reliable indicator for the risk
of infarction.
14. Cerebral amyloid angiopathy (CAA) causes approximately
20% of all cases of
a.
b.
c.
d.
dementia.
hypertension.
intracranial hemorrhage.
strokes.
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15. Which of the following is a recommended antihypertensive
for hypertension in a patient who has a subarachnoid
hemorrhage?
a. There is no recommended treatment
b. Milrinone
c. Verapamil
d. Nicardipine
16. __________________ is treated making a burr hole in the
skull and placing a ventricular drain.
a.
b.
c.
d.
Cerebral amyloid angiopathy
Hyponatremia
Symptomatic hydrocephalus
Re-bleeding
17. True or False: Cerebral amyloid angiopathy (CAA) is a
disease in people with dementia; it is not present in those
with normal neurological functioning.
a. True
b. False
18. For patients receiving anti-coagulants, if the INR is
elevated,
a.
b.
c.
d.
warfarin should be administered.
idarucizumab should not be given.
IV vitamin K should be administered.
no anti-coagulant should be administered if there is
bleeding.
19. Pneumonia is a serious complication occurring in the first
48 to 72 hours after acute ischemic stroke and
a. so prophylactic antibiotics are recommended.
b. its most commonly caused by aspiration due to dysphagia.
c. so antibiotics are recommended unless there is a
concomitant UTI.
d. All of the above
20. After a hemorrhage, delayed cerebral ischemia (DCI) is
defined as neurologic deterioration that is due to
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a.
b.
c.
d.
other causes.
a new infarction less than 72 hours after the hemorrhage.
an unknown cause.
due to a new infarction more than one week later.
21. In order to avoid an increase in ICP (increased intracranial
pressure),
a.
b.
c.
d.
dexamethasone should be used to lower ICP.
the patient should not be sedated.
the head of the bed should be elevated 30 degrees.
an analgesia is not recommended.
22. True or False: If the patient is hypoxic, or may become so,
the head of the bed should be elevated at a 15-30 degree
angle.
a. True
b. False
23. Assessment scales that have been developed for grading
the severity of subarachnoid hemorrhage include all
EXCEPT:
a.
b.
c.
d.
Hunt and Hess scale.
World Federation of Neurological Surgeons (WFNS) scale.
Glasgow coma scale.
Fisher scale.
24. In patients who are otherwise eligible for reperfusion
therapy but the BP is >185/110 mm Hg, the following
agents may be used:
a. Labetalol 10–20 mg IV over 1–2 minutes, may repeat 1
time.
b. Nicardipine 5 mg/hr IV, titrate up by 2.5 mg/hr every 5–15
minutes.
c. Lidocaine 100 mg IV over 2 minutes.
d. Both a., and b., above
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25. In patients with an ischemic stroke, hyperglycemia has
been noted in more than _____ of patients and is
consistently associated with a ________ outcome.
a.
b.
c.
d.
40%;
24%;
50%;
50%;
worse
worse
static
worse
26. True or False: With diagnostic testing for stroke evaluation,
fibrinolytic therapy should NEVER be delayed for the
results of this diagnostic testing.
a. True
b. False
27. Administration of rtPA is an infusion of:
a.
b.
c.
d.
0.9 mg/kg (maximum dose 90 mg) over 60 minutes.
10% of the dose as a bolus over 1 minute.
20% of the dose as a bolus over 30 seconds.
Both a., and b., above
28. rtPA relative exclusion criteria may include all EXCEPT:
a.
b.
c.
d.
Acute myocardial infarction (within 5 months).
Age > 80 years.
History of diabetes and prior ischemic stroke.
Seizure and postictal residual neurological impairments.
29. Thrombolysis is an effective treatment for ischemic stroke
but it has significant limitations. It can only be given
within
a.
b.
c.
d.
2 hours after the onset of symptoms.
4.5 hours after the onset of symptoms
2 hours irregardless of symptom onset.
5 hours after the onset of symptoms.
30. _________________________ are common, occurring in
approximately 15% to 60% of stroke patients.
a. Pulmonary complications
b. Urinary tract infections
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c. Gastrointestinal infarctions
d. Cardiac infarctions
31. When the INR is elevate,
a. Warfarin should be discontinued.
b. IV vitamin K should be administered.
c. Specific vitamin K-dependent factors should be given.
d. All of the above
32. True or False: The incidence of stroke is higher in women
than in men and higher in African Americans than in White
Americans.
a. True
b. False
33. In order to avoid an increase in intracranial pressure, the
head of the bed should be elevated 30 degrees and
a. the patient should quietly rest in a supine position.
b. the patient should receive appropriate analgesia and
sedation.
c. sedation should be avoided, as it is disinhibiting.
d. Propofol infusion should be initiated for 24-48 hours.
34. Fibrinolytic therapy should be delayed for the following
reasons:
a. clinical suspicion of a bleeding abnormality or
thrombocytopenia.
b. the patient has received heparin or warfarin.
c. the patient has received other anticoagulants.
d. All of the above
35. If the patient develops severe headache, hypertension,
nausea, vomiting, or neurologic deterioration,
____________________ and obtain an emergent CT scan.
a.
b.
c.
d.
continue the rtPA infusion but monitor every 15 minutes
continue the rtPA infusion
discontinue the rtPA infusion
perform neurological assessments every 15 minutes.
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36. True or False: A common and oft seen cause of stroke is
hypercoagulability disorders.
a. True
b. False
37. At 24 hours after IV rtPA, obtain a follow-up CT or MRI
scan
a.
b.
c.
d.
as a routine follow-up procedure.
before discontinuing the rtPA infusion.
before starting anticoagulants or antiplatelet agents.
after starting anticoagulants or antiplatelet agents.
38. A silent stroke is defined by imaging or neuropathological
evidence of CNS infarction, without a history of
____________________ attributable to the lesion.
a.
b.
c.
d.
intracranial pressure
dementia
elevated INR
acute neurological dysfunction
39. A distinction between ischemic stroke and hemorrhagic
stroke is that ischemic stroke
a.
b.
c.
d.
is caused by decreased blood flow.
has hypertension as its unique etiology.
is caused by intracerebral bleeding.
is caused by bleeding in the subarachnoid space.
40. True or False: Subarachnoid hemorrhage (SAH) is a bleed
into the space between the arachnoid membrane and the
pia mater.
a. True
b. False
41. Strokes with no identifiable cause are called
a. silent strokes.
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b. delayed cerebral strokes.
c. cryptogenic strokes.
d. CAAs (cerebral amyloid angiopathy).
42. TOAST is a classification system that attempts to identify
the
a.
b.
c.
d.
cause of strokes.
risk of stroke in a patient.
epidemiology of stroke patients.
type of transient ischemic attack.
43. True or False: A majority of subarachnoid hemorrhage
(SAH) cases are caused by rupture of an aneurysm.
a. True
b. False
44. If there is a suspicion that the patient is having a SAH, a
non-contrast CT scan of the head should be performed
immediately and a lumbar puncture should be done
a.
b.
c.
d.
only if the CT scan is positive.
to relieve lumbar pressure.
even if the CT scan is negative.
if there is an elevated INR.
45. The majority of non-traumatic SAH cases are caused by
a.
b.
c.
d.
amyloid angiopathy.
vasculitis.
moyamoya disease.
rupture of an aneurysm.
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Correct Answers:
1.
A transient ischemic attack:
a. causes transient neurological dysfunction without acute
infarction.
“The current definition of TIA, as endorsed by the American
Heart Association and the American Stroke Association is: a
transient episode of neurologic dysfunction caused by focal
brain, spinal cord, or retinal ischemia, without acute
infarction.”
2.
A transient ischemic attack:
b. is considered to be a risk factor for stroke.
“The risk for stroke after a TIA was once considered to be
relatively high, 10-20%.... however … Amarenco, et al., found
that the incidence of stroke one year after a TIA was 5.1%,
and 1.5% of people who had a TIA developed a stroke within
48 hours.”
3.
Treatment priorities for transient ischemic attack includes:
d. anticoagulation and antiplatelet therapy.
“Antiplatelet therapy should be started if the patient had a
non cardioembolic TIA. Aspirin, clopidogrel, ticlodipine, or
aspirin and dipyridamole are FDA-approved therapies for
stroke prevention in this patient population; aspirin and
clopidogrel has been used, as well.”
4.
An ischemic stroke is characterized by:
c. cerebral infarction caused by decreased blood flow.
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“… an ischemic stroke is caused by decreased blood flow…”
5.
True or False: Evidence for an increased risk for stroke is
strongest for atrial fibrillation, cigarette smoking,
dyslipidemia, hypertension, physical inactivity, and sickle
cell disease.
a. True
“The evidence for an increased risk for stroke is strongest for
atrial fibrillation, cigarette smoking, dyslipidemia,
hypertension, physical inactivity, and sickle cell disease…”
6.
A hemorrhagic stroke is characterized by:
b. rupture of small arteries and bleeding into the brain
parenchyma.
“An intracerebral hemorrhage is caused by the rupture of
small arteries and bleeding into the brain parenchyma.”
7.
Subarachnoid hemorrhage (SAH) is characterized by:
c. bleeding into the subarachnoid cavity.
“Subarachnoid hemorrhage (SAH) is a bleed into the
subarachnoid cavity...”
8.
A treatment priority in subarachnoid hemorrhage is
______________, reported to occur in 8-23% of patients
and will usually happen in the first 24 hours with the risk
especially high in the first six hours.
a.
b.
c.
d.
rebleeding
blindness
sudden sharp pain
None of the above
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“Rebleeding has been reported to occur in 8-23% of patients.
This will usually happens in the first 24 hours and the risk is
especially high in the first six hours.”
9.
True or False: Epidemiological studies have shown that
elevated blood pressure is the most important determinant
of the risk of stroke.
a. True
“Epidemiological studies have shown that elevated blood
pressure is the most important determinant of the risk of
stroke.”
10. Patients who have had a TIA should be started on _______
if: the TIA is presumed to be caused by atherosclerosis, the
low-density lipoprotein cholesterol (LDL-C) level is ≥ 100
mg/dL, with or without evidence for other atherosclerotic
cardiovascular disease (ASCVD), or the TIA is presumed to
be caused by atherosclerosis, and the LDL-C level is < 100
mg/dL, and there is no evidence of ASCVD.
b. statin therapy
“Patients who have had a TIA should be started on statin
therapy if: the TIA is presumed to be caused by
atherosclerosis, the low-density lipoprotein cholesterol (LDLC) level is ≥ 100 mg/dL, with or without evidence for other
atherosclerotic cardiovascular disease (ASCVD), or the TIA is
presumed to be caused by atherosclerosis, and the LDL-C
11. Which of the following is described as “An episode of
neurological dysfunction caused by focal cerebral, spinal,
or retinal infarction”?
c. Ischemic stroke
“Ischemic stroke: ‘An episode of neurological dysfunction
caused by focal cerebral, spinal, or retinal infarction.’”
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12. True or False: Hypertension and changes in platelet
aggregation and fibrinolysis may explain why heavy
alcohol consumption increases the risk for hemorrhagic
stroke.
a. True
“People who drink heavily often have hypertension, and
hypertension and changes in platelet aggregation and
fibrinolysis may explain why heavy alcohol consumption
increases the risk for hemorrhagic stroke.”
13. A transient ischemic attack (TIA) includes the description
“transient” because
c. the event is transient but not necessarily its consequences.
“… for some patients a TIA is not transient in its
consequences. The current definition of TIA, … is: a transient
episode of neurologic dysfunction caused by focal brain, spinal
cord, or retinal ischemia, without acute infarction. The word
transient would seem to indicate that the effects of a TIA are
temporary and that a TIA can be distinguished from more
serious neurological events by the duration of signs and
symptoms. Neither of these is true. A TIA that causes signs
and symptoms for a few minutes may cause an infarction and
the duration of symptoms is unlikely to be a reliable indicator
for the risk of infarction.”
14. Cerebral amyloid angiopathy (CAA) causes approximately
20% of all cases of
c. intracranial hemorrhage
“CAA causes approximately 20% of all cases of intracranial
hemorrhage.”
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15. Which of the following is a recommended antihypertensive
for hypertension in a patient who has a subarachnoid
hemorrhage?
d. Nicardipine
“Blood pressure management: The best treatment for
hypertension in a patient who has a subarachnoid
hemorrhage is not known. Clevidipine, enalapril, labetalol,
or nicardipine are the recommended antihypertensives.”
16. __________________ is treated making a burr hole in the
skull and placing a ventricular drain.
c. Symptomatic hydrocephalus
“Symptomatic hydrocephalus is treated making a burr hole in
the skull and placing a ventricular drain.”
17. True or False: Cerebral amyloid angiopathy (CAA) is a
disease in people with dementia; it is not present in those
with normal neurological functioning.
b. False
The disease is relatively common in the elderly, both in
people with normal neurological functioning and those with
dementia.”
18. For patients receiving anti-coagulants, if the INR is
elevated,
c. IV vitamin K should be administered.
“Patients receiving anti-coagulants: Warfarin should be
discontinued if the INR is elevated, IV vitamin K should be
administered, and specific vitamin K-dependent factors should
be given.101 If there is severe bleeding vitamin K, fresh frozen
plasma, and prothrombin complex concentrates, recombinant
factor VIIa, or idarucizumab can be given.”
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19. Pneumonia is a serious complication occurring in the first
48 to 72 hours after acute ischemic stroke and
b. its most commonly caused by aspiration due to dysphagia.
“Prophylactic antibiotics are not recommended. Pneumonia is
a serious complication occurring in the first 48 to 72 hours
after acute ischemic stroke …. The most common cause of
pneumonia is aspiration due to dysphagia. Urinary tract
infections (UTIs) are also common, occurring in
approximately 15% to 60% of stroke patients, and
independently predict poor outcome. If the patient has
pneumonia or a UTI she/he should be treated with the
appropriate antibiotics.”
20. After a hemorrhage, delayed cerebral ischemia (DCI) is
defined as neurologic deterioration that is due to
b. a new infarction less than 72 hours after the hemorrhage.
“Delayed cerebral ischemia (DCI) is defined as neurologic
deterioration that is not due to other causes or a new
infarction that is documented by CT scan more than 72 hours
after the hemorrhage.”
21. In order to avoid an increase in ICP (increased intracranial
pressure),
c. the head of the bed should be elevated 30 degrees.
“In order to avoid an increase in ICP the head of the bed
should be elevated 30 degrees and the patient should receive
appropriate analgesia and sedation.”
22. True or False: If the patient is hypoxic, or may become so,
the head of the bed should be elevated at a 15-30 degree
angle.
a. True
“If the patient is hypoxic or may become so, or if he/she is at
risk for airway obstruction, aspiration, or increased
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intracranial pressure, the head of the bed should be elevated
at a 15-30 degree angle. If not, a neutral position (0-15
degrees elevation) should be maintained.”
23. Assessment scales that have been developed for grading
the severity of subarachnoid hemorrhage include all
EXCEPT:
c. Glasgow coma scale.
“There are assessment scales that have been developed for
grading the severity of SAH: the Hunt and Hess scale, World
Federation of Neurological Surgeons (WFNS) scale, Fisher
scale, Claasen grading system, and the Ogilvy and Carter
scale.”
24. In patients who are otherwise eligible for reperfusion
therapy but the BP is >185/110 mm Hg, the following
agents may be used:
a. Labetalol 10–20 mg IV over 1–2 minutes, may repeat 1
time.
b. Nicardipine 5 mg/hr IV, titrate up by 2.5 mg/hr every 5–15
minutes.
c. Lidocaine 100 mg IV over 2 minutes.
d. Both a., and b., above [correct answer]
“Patients who are otherwise eligible for reperfusion therapy
but the BP is >185/110 mm Hg: Labetalol 10–20 mg IV over
1–2 minutes, may repeat 1 time; or Nicardipine 5 mg/hr IV,
titrate up by 2.5 mg/hr every 5–15 minutes, maximum 15
mg/hr; when desired BP reached, adjust to maintain proper
BP limits; or other drugs may be used when needed.”
25. In patients with an ischemic stroke, hyperglycemia has
been noted in more than _____ of patients and is
consistently associated with a ________ outcome.
a. 40%; worse
“Hyperglycemia has been noted in more than 40% of patients
who have had an ischemic stroke and it is consistently
associated with a worse outcome.”
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26. True or False: With diagnostic testing for stroke evaluation,
Fibrinolytic therapy should NEVER be delayed for the
results of this diagnostic testing.
b. False
Fibrinolytic therapy should not be delayed for these
[diagnostic] test results unless: 1) there is clinical suspicion
of a bleeding abnormality or thrombocytopenia; 2) the patient
has received heparin or warfarin, or; 3) the patient has
received other anticoagulants.”
27. Administration of rtPA is an infusion of:
a.
b.
c.
d.
0.9 mg/kg (maximum dose 90 mg) over 60 minutes.
10% of the dose as a bolus over 1 minute.
20% of the dose as a bolus over 30 seconds.
Both a., and b., above [correct answer]
“Administration of rtPA: Infuse 0.9 mg/kg (maximum dose 90
mg) over 60 minutes: give 10% of the dose as a bolus over 1
minute.”
28. rtPA relative exclusion criteria may include all EXCEPT:
a. Acute myocardial infarction (within 5 months).
“rtPA relative exclusion criteria may include: Acute myocardial
infarction (within 3 months); Age > 80 years; Gastrointestinal
or urinary tract hemorrhage within 21 days; History of
diabetes and prior ischemic stroke; Major surgery or serious
trauma within 14 days; Minor or rapidly improving stroke
symptoms; Pregnancy; Seizure and postictal residual
neurological impairments; Severe stroke (NIHSS score > 25);
Use of an oral anticoagulant, regardless of INR.”
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29. Thrombolysis is an effective treatment for ischemic stroke
but it has significant limitations. It can only be given
within
b. 4.5 hours after the onset of symptoms.
“Thrombolysis is an effective treatment for ischemic stroke
but it has significant limitations. It can only be given within
4.5 hours (3 hours is considered preferable) after the onset of
symptoms and many patients with ischemic stroke present to
the hospital well outside of that time frame. Thrombolysis has
serious adverse effects and although it has what could be
described as a good success rate, there are certainly people
who do not respond.”
30. _________________________ are common, occurring in
approximately 15% to 60% of stroke patients.
b. Urinary tract infections
“Prophylactic antibiotics are not recommended. Pneumonia is
a serious complication occurring in the first 48 to 72 hours
after acute ischemic stroke …. The most common cause of
pneumonia is aspiration due to dysphagia. Urinary tract
infections (UTIs) are also common, occurring in
approximately 15% to 60% of stroke patients, and
independently predict poor outcome. If the patient has
pneumonia or a UTI she/he should be treated with the
appropriate antibiotics.”
31. When the INR is elevate,
a.
b.
c.
d.
Warfarin should be discontinued.
IV vitamin K should be administered.
Specific vitamin K-dependent factors should be given.
All of the above [correct answer]
“Patients receiving anti-coagulants: Warfarin should be
discontinued if the INR is elevated, IV vitamin K should be
administered, and specific vitamin K-dependent factors should
be given.”
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32. True or False: The incidence of stroke is higher in women
than in men and higher in African Americans than in White
Americans.
a. True
“The incidence of stroke is higher in women than in men and
higher in African Americans than in White Americans.”
33. In order to avoid an increase in intracranial pressure, the
head of the bed should be elevated 30 degrees and
b. the patient should receive appropriate analgesia and
sedation.
“In order to avoid an increase in ICP the head of the bed
should be elevated 30 degrees and the patient should receive
appropriate analgesia and sedation.”
34. Fibrinolytic therapy should be delayed for the following
reasons:
a. clinical suspicion of a bleeding abnormality or
thrombocytopenia.
b. the patient has received heparin or warfarin.
c. the patient has received other anticoagulants.
d. All of the above [correct answer]
“Fibrinolytic therapy should not be delayed for these
[diagnostic] test results unless: 1) there is clinical suspicion
of a bleeding abnormality or thrombocytopenia; 2) the patient
has received heparin or warfarin, or; 3) the patient has
received other anticoagulants.”
35. If the patient develops severe headache, hypertension,
nausea, vomiting, or neurologic deterioration,
____________________ and obtain an emergent CT scan.
c. discontinue the rtPA infusion
“If the patient develops severe headache, hypertension,
nausea, vomiting, or neurologic deterioration, discontinue the
rtPA infusion obtain an emergent CT scan.”
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36. True or False: A common and oft seen cause of stroke is
hypercoagulability disorders.
b. False
“Some stroke etiologies however are unusual and seldom
seen, i.e., strokes caused by hypercoagulability disorders.”
37. At 24 hours after IV rtPA, obtain a follow-up CT or MRI
scan
c. before starting anticoagulants or antiplatelet agents.
“Obtain a follow-up CT or MRI scan at 24 hours after IV rtPA
before starting anticoagulants or antiplatelet agents.”
38. A silent stroke is defined by imaging or neuropathological
evidence of CNS infarction, without a history of
____________________ attributable to the lesion.”
d. acute neurological dysfunction
“Silent stroke: ‘Imaging or neuropathological evidence of CNS
infarction, without a history of acute neurological dysfunction
attributable to the lesion.’”
39. A distinction between ischemic stroke and hemorrhagic
stroke is that ischemic stroke
a. is caused by decreased blood flow.
“A reasonable way to view strokes is that an ischemic stroke
is caused by decreased blood flow; intracerebral bleeding in
the brain or in the subarachnoid space causes a hemorrhagic
stroke. The majority of ischemic and hemorrhagic strokes
have easily identifiable and common etiologies such as
atherosclerosis, atrial fibrillation, or hypertension.”
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40. True or False: Subarachnoid hemorrhage (SAH) is a bleed
into the space between the arachnoid membrane and the
pia mater.
a. True
“Subarachnoid hemorrhage (SAH) is a bleed into the
subarachnoid cavity, the space between the arachnoid
membrane and the pia mater.”
41. Strokes with no identifiable cause are called
c. cryptogenic strokes.
“Strokes with no identifiable cause are called cryptogenic
strokes.”
42. TOAST is a classification system that attempts to identify
the
c. cause of strokes.
“Determining the cause of stroke is crucially important in
order to initiate the proper treatment, and there are stroke
classification systems that use clinical and diagnostic
information and patient risk factors to determine stroke
etiology. The TOAST system determines if a stroke was
caused by larger artery atherosclerosis, cardioembolic source,
small vessel occlusion, stroke of other determined cause, and
stroke of undetermined cause. The TOAST system has been
widely accepted and used, but some researchers feel that the
ASCO and CSS systems are more accurate in identifying the
causes of ischemic stroke.”
43. True or False: A majority of subarachnoid hemorrhage
(SAH) cases are caused by rupture of an aneurysm.
b. False
“The most common cause of SAH is trauma. The majority of
non-traumatic SAH are caused by rupture of an aneurysm.”
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44. If there is a suspicion that the patient is having a SAH, a
non-contrast CT scan of the head should be performed
immediately and a lumbar puncture should be done.
c. even if the CT scan is negative.
“If there is a suspicion that the patient is having a SAH, a
non-contrast CT scan of the head should be performed
immediately and a lumbar puncture should be done…. Some
clinicians feel that if the patient has an acute headache and
the CT scan of the head is negative, a lumbar puncture (LP) is
not needed. However, there is not insignificant number of
patients of this description who will have a SAH,…”
45. The majority of non-traumatic SAH cases are caused by
d. rupture of an aneurysm.
“The most common cause of SAH is trauma. The majority of
non-traumatic SAH are caused by rupture of an aneurysm;
amyloid angiopathy, moyamoya disease, arteriovenous
malformations, and vasculitis can also cause SAH.”
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References Section
The References below include published works and in-text citations of
published works that are intended as helpful material for your further
reading.
1.
2.
3.
4.
5.
6.
7.
8.
Advisory Council for the National Institute of Neurological and
Communicative Disorders and Stroke. A classification and outline
of cerebrovascular diseases, II. Stroke. 1975;6:564-616.
Caplan LR. Differential diagnosis of transient ischemic attack and
stroke. UpToDate. March 22, 2016.
http://www.uptodate.com/contents/differential-diagnosis-oftransient-ischemic-attack-andstroke?source=search_result&search=Differential+diagnosis+of
+transient+ischemic+attack+and+stroke.&selectedTitle=1%7E1
50. Accessed November 22, 2016.
Furie KL, Ay H. Definition of transient ischemic attack. UpToDate.
January 12, 2015.
http://www.uptodate.com/contents/search?search=Definition+of
+transient+ischemic+attack.+&x=15&y=9. Accessed November
22, 2016.
Sacco RL, Kasner SE, Broderick JP, et al. An updated definition of
stroke for the 21st century: a statement for healthcare
professionals from the American Heart Association/American
Stroke Association. Stroke. 2013;44(7):2064-2689.
Easton JD, Saver JL, Albers GW, et al. Definition and evaluation
of transient ischemic attack: a scientific statement for healthcare
professionals from the American Heart Association/American
Stroke Association Stroke Council; Council on Cardiovascular
Surgery and Anesthesia; Council on Cardiovascular Radiology
and Intervention; Council on Cardiovascular Nursing; and the
Interdisciplinary Council on Peripheral Vascular Disease. Stroke.
2009; 40(6):2276-2293.
Ay H, Koroshetz WJ, Benner T, et al. Transient ischemic attack
with infarction: a unique syndrome? Ann Neurol.
2005;57(5):679-686.
Tanaka K, Uehara T, Kimura K, et al. Differences in clinical
characteristics between patients with transient ischemic attack
whose symptoms do and do not persist on arrival. J Stroke
Cerebrovasc Dis. 2016;25(9):2237-2242.
Mozaffarian D, Benjamin EJ, Go AS, et al. American Heart
Association Statistics Committee and Stroke Statistics
nursece4less.com nursece4less.com nursece4less.com nursece4less.com 83
9.
10.
11.
12.
13.
14.
15.
16.
17.
Subcommittee. Heart disease and stroke statistics – 2015
update: A report from the American Heart Association.
Circulation. 2015;131(4):e29-e322.
Duca A, Jagoda A. Transient ischemic attacks: Advances in
diagnosis and management in the emergency department.
Emerg Med Clin North Am. 2016;34(4):811-835.
Kokubo Y. Epidemiology of transient ischemic attack. Front
Neurol Neurosci. 2014;33:69-81.
Wilson AD, Coleby D, Taub NA, Weston C, Robinson TG. Delay
between symptom onset and clinic attendance following TIA and
minor stroke: the BEATS study. Age Ageing. 2014;43(2):253256.
Johnston SC, Fayad PB, Gorelick PB, et al. Prevalence and
knowledge of transient ischemic attack among US adults.
Neurology. 2003;60(9):1429-1434
Tibæk M, Dehlendorff C, Jørgensen HS, Forchhammer HB,
Johnsen SP, Kammersgaard LP. Increasing incidence of
hospitalization for stroke and transient ischemic attack in young
adults: A registry-based study. J Am Heart Assoc. 2016 May
11;5(5). pii: e003158. doi: 10.1161/JAHA.115.003158.
Ramirez L, Kim-Tenser MA, Sanossian N, et al. Trends in
transient ischemic attack hospitalizations in the united States. J
Am Heart Assoc. 2016 Sep 24;5(9). pii: e004026.
Adil MM, Qureshi AI, Beslow LA, Jordan LC. Transient ischemic
attack requiring hospitalization of children in the United States:
kids' inpatient database 2003 to 2009. Stroke. 2014;45(3):887888.
Lehman LL, Watson CG, Kapur K, Danehy AR, Rivkin MJ.
Predictors of stroke after transient ischemic attack in children.
Stroke. 2016;47(1):88-93.
Furie KL, Ay H. Etiology and clinical manifestations of transient
ischemic attack. UpToDate. January 10, 2014.
http://www.uptodate.com/contents/etiology-and-clinicalmanifestations-of-transient-ischemicattack?source=search_result&search=Furie+KL%2C+Ay+H.+Eti
ology+and+clinical+manifestations+of+transient+ischemic+atta
ck.&selectedTitle=1%7E150. Accessed December 1, 2016.
nursece4less.com nursece4less.com nursece4less.com nursece4less.com 84
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
Desai JA, Abuzinadah AR, Imoukhuede O, et al. Etiologic
classification of TIA and minor stroke by A-S-C-O and causative
classification system as compared to TOAST reduces the
proportion of patients categorized as cause undetermined.
Cerebrovasc Dis. 2014;38(2):121-126.
Ström JO, Tavosian A, Appelros P. Cardiovascular risk factors
and TIA characteristics in 19,872 Swedish TIA patients. Acta
Neurol Scand. 2016;134(6):427-433.
Simmons BB, Gadegbeku AB, Cirignano B. Transient ischemic
attack: Part II. Risk factor modification and treatment. Am Fam
Physician. 2012;86(6):527-532
Fonville S, Zandbergen AA, Koudstaal PJ, den Hertog HM.
Prediabetes in patients with stroke or transient ischemic attack:
prevalence, risk and clinical management. Cerebrovasc Dis.
2014;37(6):393-400.
von Sarnowski B, Putaala J, Grittner U, et al. Lifestyle risk
factors for ischemic stroke and transient ischemic attack in
young adults in the Stroke in Young Fabry Patients study.
Stroke. 2013;44(1):119-125.
Amarenco P, Lavallée PC, Labreuche J, et al. One-year risk of
stroke after transient ischemic attack or minor stroke. N Engl J
Med. 2016;374(16):1533-1542.
Cereda CW, George PM, Inoue M, et al. Inter-rater agreement
analysis of the Precise Diagnostic Score for suspected transient
ischemic attack. Int J Stroke. 2016;11(1):85-92.
Nadarajan V, Perry RJ, Johnson J, Werring DJ. Transient
ischaemic attacks: mimics and chameleons. Pract Neurol.
2014;14(1):23-31.
Castle J, Mlynash M, Lee K, Caulfield AF, Wolford C, Kemp S.
Agreement regarding diagnosis of transient ischemic attack fairly
low among stroke-trained neurologists. Stroke.
2010;41(7):1367-1370.
Schrock JW, Glasenapp M, Victor A, Losey T, Cydulka RK.
Variables associated with discordance between emergency
physician and neurologist diagnoses of transient ischemic attacks
in the emergency department. Ann Emerg Med. 2012;59(1):1926.
Skinner TR, Scott IA, Martin JH. Diagnostic errors in older
patients: a systematic review of incidence and potential causes
in seven prevalent diseases. Int J Gen Med. 2016;9:137-146.
Prabhakaran S, Silver AJ, Warrior L, McClenathan B, Lee VH.
Misdiagnosis of transient ischemic attacks in the emergency
room. Cerebrovasc Dis. 2008;26(6):630-635.
nursece4less.com nursece4less.com nursece4less.com nursece4less.com 85
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
Noureddine A, Ghandehari K, Taghi Shakeri M. Differentiation of
true transient ischemic attack versus transient ischemic attack
mimics. Iran J Neurol. 2014;13(3):127-130.
Correia M, Fonseca AC, Canhão P. Short-term outcome of
patients with possible transient ischemic attacks: a prospective
study. BMC Neurol. 2015 May 13;15:78. doi: 10.1186/s12883015-0333-1.
Burns JD, Rabinstein AA, Roger VL, et al. Incidence and
predictors of myocardial infarction after transient ischemic
attack: a population-based study. Stroke. 2011;42(4):935-940.
Long B, Koyfman A. Best clinical practice: Controversies in
transient ischemic attack evaluation and disposition in the
emergency department. J Emerg Med. 2016 Nov 19. pii: S07364679(16)30904-0. doi: 10.1016/j.jemermed.2016.10.024. [Epub
ahead of print]
Rothwell PM, Algra A, Chen Z, Diener HC, Norrving B, Mehta Z.
Effects of aspirin on risk and severity of early recurrent stroke
after transient ischaemic attack and ischaemic stroke: timecourse analysis of randomised trials. Lancet.
2016;388(10042):365-375.
Furie KL, Ay H. Initial evaluation and management of transient
ischemic attack and minor ischemic stroke. UpToDate. October
27, 2016. https://www.uptodate.com/contents/initial-evaluationand-management-of-transient-ischemic-attack-and-minorischemic-stroke. Accessed December 2, 2016.
Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the
prevention of stroke in patients with stroke and transient
ischemic attack: a guideline for healthcare professionals from
the American Heart Association/American Stroke Association.
Stroke. 2014;45(7):2160-2236.
American College of Emergency Physicians Clinical Policies
Subcommittee (Writing Committee) on Suspected Transient
Ischemic Attack:, Lo BM, Carpenter CR, Hatten BW, Wright BJ,
Brown MD. Clinical Policy: Critical Issues in the Evaluation of
Adult Patients With Suspected Transient Ischemic Attack in the
Emergency Department. Ann Emerg Med. 2016;68(3):354370.e29. doi: 10.1016/j.annemergmed.2016.06.048.
Ranta A, Barber PA. Transient ischemic attack service provision:
a review of available service models. Neurology.
2016;86(10):947-953.
Flemming KD, Brown RD Jr, Petty GW, Huston J 3rd, Kallmes DF,
Piepgras DG. Evaluation and management of transient ischemic
attack and minor cerebral infarction. Mayo Clin Proc.
2004;79(8):1071-1086
nursece4less.com nursece4less.com nursece4less.com nursece4less.com 86
40.
41.
42.
43.
44.
45.
46.
47.
48.
Lackland DT, Rocella EJ, Deutsch AF, et al. Factors influencing
the decline in stroke mortality: a statement from the American
Heart Association/American Stroke Association. Stroke.
2014;45(1):315-353.
Chen PH, Gao S, Wang YJ, Xu AD, Li YS, Wang D. Classifying
Ischemic Stroke, from TOAST to CISS. CNS Neurosci Ther.
2012;18(6):452-456.
Montero MV, Pastor AG, Cano BC, et al. The A-S-C-O
classification identifies cardioembolic phenotypes in a high
proportion of embolic stroke of undetermined source (ESUS). J
Neurol Sci. 2016 15;367:32-3.
Amarenco P, Bogousslavsky J, Caplan LR, Donnan GA, Hennerici
MG: New approach to stroke subtyping: the A-S-C-O
(phenotypic) classification of stroke. Cerebrovasc Dis.
2009;27(5):502-508.
Ay H, Benner T, Arsava EM, et al: A computerized algorithm for
etiologic classification of ischemic stroke: the causative
classification of stroke system. Stroke. 2007;38(11):2979-2984
Adams HP Jr, Bendixen BH, Kappelle LJ, et al. Classification of
subtype of acute ischemic stroke. Definitions for use in a
multicenter clinical trial. TOAST. Trial of Org 10172 in Acute
Stroke Treatment. Stroke. 1993;24(1):35-41.
Go S, Worman DJ. Stroke, transient ischemic attack, and cervical
artery dissection. In: Tintinalli, JE, Stapczynski JS, Ma OJ, Cline
DM, Cydulka RK, Meckler, GD, The American College of
Emergency Physicians. Tintinalli's Emergency Medicine: A
Comprehensive Study Guide, 7th ed. New York, NY: McGraw-Hill;
2011. On line edition, retrieved December 8, 2014 from
www.UCHC.edu.
Caplan LR. Etiology, classification, and epidemiology of stroke.
UpToDate. February 2, 2016.
http://www.uptodate.com/contents/etiology-classification-andepidemiology-ofstroke?source=search_result&search=Stroke&selectedTitle=3%7
E150. Accessed December 5, 2016.
Kasper DL, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo
J, eds. Stroke. Harrison’s Principles of Internal Medicine, 19th ed.
New York, NY: McGraw-Hill; 2016. Online edition, retrieved
December 5, 2016 from www.UCHC.edu.
nursece4less.com nursece4less.com nursece4less.com nursece4less.com 87
49.
50.
51.
52.
53.
54.
55.
56.
57.
58.
59.
Vasivej T, Sathirapanya P, Kongkamol C. Incidence and risk
factors of perioperative stroke in noncardiac, and nonaortic and
its major branches surgery. J Stroke Cerebrovasc Dis.
2016;25(5):1172-1176
Ahmad M, Dar NJ, Bhat ZS, et al. Inflammation in ischemic
stroke: mechanisms, consequences and possible drug targets.
CNS Neurol Disord Drug Targets. 2014;13(8):1378-1396.
Yadollahikhales G, Borhani-Haghighi A, Torabi-Nami M, Edgell R,
Cruz-Flores S. Flow augmentation in acute ischemic stroke. Clin
Appl Thromb Hemost. 2016;22(1):42-51.
Nour M, Scalzo F, Liebeskind DS. Ischemia-reperfusion injury in
stroke. Interv Neurol. 2013;1(3-4):185-199.
Meschia JF, Bushnell C, Boden-Albala B, et al. Guidelines for the
primary prevention of stroke. A statement for healthcare
professionals from the American Heart Association/American
Stroke Association. Stroke. 2014;45(12):3754-3832.
Rordorf G, McDonald C. Spontaneous intracerebral hemorrhage:
Pathogenesis, clinical features, and diagnosis. UpToDate.
December 4, 2013.
http://www.uptodate.com/contents/spontaneous-intracerebralhemorrhage-pathogenesis-clinical-features-and-diagnosis.
Accessed December 5, 2016.
Morotti A, Goldstein JN. Diagnosis and management of acute
intracerebral hemorrhage. Emerg Med Clin N AM.
2106;34(4):883-889.
González-Pérez A, Gaist D, Wallander MA, et al. Mortality after
hemorrhagic stroke: data from general practice (The Health
Improvement Network). Neurology 2013; 81(6):559-565.
Greenberg, DA, Aminof MJ, Simon RP. Stroke. In: Greenberg,
DA, Aminof MJ, Simon RP. Clinical Neurology, 9th ed. New York,
NY: McGraw-Hill Education; 2015. Online edition. Accessed
December 5, 2016 from www.UCHC.edu
Marsh EB, Gottesman RF, Hillis AE, Maygers J, Lawrence E,
Llinas RH. Predicting symptomatic intracerebral hemorrhage
versus lacunar disease in patients with longstanding
hypertension. Stroke. 2014;45(6):1679-1683.
Greenberg SM. Cerebral amyloid angiopathy. UpToDate. October
31, 2103. http://www.uptodate.com/contents/cerebral-amyloidangiopathy. Accessed December 5, 2016.
nursece4less.com nursece4less.com nursece4less.com nursece4less.com 88
60.
61.
62.
63.
64.
65.
66.
67.
68.
69.
Fontaine GV, Mathews KD, Woller SC, Stevens SM, Lloyd JF,
Evans RS. Major bleeding with dabigatran and rivaroxaban in
patients with atrial fibrillation: a real-world setting. Clin Appl
Thromb Hemost. 2014;20(7):665-672.
Sanmartín-Fernández M, Marzal-Martín D. Safety of non-vitamin
K antagonist oral anticoagulants in clinical practice: Focus on
rivaroxaban in stroke prevention in patients with atrial
fibrillation. Clin Appl Thromb Hemost. 2016 Sep 13. pii:
1076029616668404. [Epub ahead of print]
Hankey GJ, Stevens SR, Piccini JP, et al. Intracranial hemorrhage
among patients with atrial fibrillation anticoagulated with
warfarin or rivaroxaban: the rivaroxaban once daily, oral, direct
factor Xa inhibition compared with vitamin K antagonism for
prevention of stroke and embolism trial in atrial fibrillation.
Stroke. 2014;45(5):1304-1312.
Alonso A, Bengtson LG, MacLehose RF, Lutsey PL, Chen LY,
Lakshminarayan K. Intracranial hemorrhage mortality in atrial
fibrillation patients treated with dabigatran or warfarin. Stroke.
2014;45(8):2286-2291.
Siket MS. Treatment of acute ischemic stroke. Emer Clin N Am.
2016;34(4):861-882.
Nordahl H, Osler M, Frederiksen BL, et al. Combined effects of
socioeconomic position, smoking, and hypertension on risk of
ischemic and hemorrhagic stroke. Stroke. 2014;45(9):25822587.
Larsson SC, Akesson A, Wolk A. Healthy diet and lifestyle and
risk of stroke in a prospective cohort of women. Neurology.
2014;83(19):1699-1704
O'Keefe JH, Bhatti SK, Bajwa A, DiNicolantonio JJ, Lavie CJ.
Alcohol and cardiovascular health: the dose makes the
poison…or the remedy. Mayo Clin Proc. 2014;89(3):382-393.
Zhang C, Qin YY, Chen Q, et al. Alcohol intake and risk of stroke:
a dose-response meta-analysis of prospective studies. Int J
Cardiol. 2014;174(3):669-677.
Wang X, Dong Y, Qi X, Huang C, Hou L. Cholesterol levels and
risk of hemorrhagic stroke: a systematic review and metaanalysis. Stroke. 2013;44(7):1833-1839.
nursece4less.com nursece4less.com nursece4less.com nursece4less.com 89
70.
71.
72.
73.
74.
75.
76.
77.
78.
79.
80.
Mustanoja S, Strbian D, Putaala J, et al. Association of prestroke statin use and lipid levels with outcome of intracerebral
hemorrhage. Stroke. 2013;44(8):2330-2332.
Roquer J, Cuadrado-Godia E, Rodríguez-Campello A, et al.
Serum cholesterol levels and survival after rtPA treatment in
acute stroke. Eur J Neurol. 2012;19(4):648-654.
Wieberdink RG, Poels MM, Vernooij MW, et al. Serum lipid levels
and the risk of intracerebral hemorrhage: the Rotterdam Study.
Arterioscler Thromb Vasc Biol. 2011;31(12):2982-2989.
Huhtakangas J, Löppönen P, Tetri S, et al. Predictors for
recurrent primary intracerebral hemorrhage: a retrospective
population-based study. Stroke. 2013;44(3):585-590.
Nentwich LM. Diagnosis of acute ischemic stroke. Emer Med Clin
N Am. 2016;34(4):837-859.
Seki M, Hase K, Takahashi H, Liu M. Comparison of three
instruments to assess changes of motor impairment in acute
hemispheric stroke: the Stroke Impairment Assessment Set
(SIAS), the National Institute of Health Stroke Scale (NIHSS)
and the Canadian Neurological Scale (CNS). Disabil Rehabil.
2014;36(18):1549-1554.
Jauch EC, Saver JL, Adams HP Jr, et al; American Heart
Association Stroke Council.; Council on Cardiovascular Nursing.;
Council on Peripheral Vascular Disease.; Council on Clinical
Cardiology. Guidelines for the early management of patients with
acute ischemic stroke: a guideline for healthcare professionals
from the American Heart Association/American Stroke
Association. Stroke. 2013;44(3):870-947.
Oliveira-Filho J, Mullen MT. Initial assessment and management
of acute stroke. UpToDate. August 15, 2016.
http://www.uptodate.com/contents/initial-assessment-andmanagement-of-acute-stroke. Accessed December 6, 2016.
Abraham MK, Chang W-T W. Subarachnoid hemorrhage. Emer
Med Clin N Am. 2016;34(4):901-916
Udy AA, Vladic C, Saxby ER, et al. Subarachnoid hemorrhage
patients admitted to intensive care in Australia and New
Zealand: A multicenter cohort analysis of in-hospital mortality
over 15 Years. Crit Care Med. 2016 Oct 3. [Epub ahead of print]
Andreasen TH, Bartek J Jr, Andresen M, Springborg JB, Romner
B. Modifiable risk factors for aneurysmal subarachnoid
hemorrhage. Stroke. 2013;44(12):3607-3612.
nursece4less.com nursece4less.com nursece4less.com nursece4less.com 90
81.
82.
83.
84.
85.
86.
87.
88.
89.
90.
91.
92.
Joswig H, Fournier JY, Hildebrandt G, Stienen MN. Sentinel
headache: A warning sign preceding every fourth aneurysmal
subarachnoid hemorrhage. AJNR Am J Neuroradiol.
2015;36(9):E62-E63.
Larsen CC, Astrup J. Rebleeding after aneurysmal subarachnoid
hemorrhage: a literature review. World Neurosurg.
2013;79(2):307-312.
Singer RJ, Ogilvy CS, Rordorf G. Clinical manifestations and
diagnosis of aneurismal subarachnoid hemorrhage. UpToDate.
September 26, 2013.
https://www.uptodate.com/contents/clinical-manifestations-anddiagnosis-of-aneurysmal-subarachnoid-hemorrhage. Accessed
December 6, 2016.
Tetsuka S, Matsumoto E. Diagnosis of a subarachnoid
hemorrhage with only mild symptoms using computed
tomography in Japan. BMC Neurol. 2016 Oct 18;16(1):196.
Backes D, Rinkel GJ, Kemperman H, Linn FH, Vergouwen MD.
Time-dependent test characteristics of head computed
tomography in patients suspected of nontraumatic subarachnoid
hemorrhage. Stroke. 2012;43(8):2115-2119.
Gentile NT, Seftchick MW, Huynh T, Kruus LK, Gaughan J.
Decreased mortality by normalizing blood glucose after acute
ischemic stroke. Acad Emerg Med. 2006;13(2):174-180.
Williams LS, Rotich J, Qi R, et al. Effects of admission
hyperglycemia on mortality and costs in acute ischemic stroke.
Neurology. 2002;59(1):67-71.
Luitse MJ, Velthuis BK, Kappelle LJ, et al. Chronic hyperglycemia
is related to poor functional outcome after acute ischemic stroke.
Int J Stroke. 2016 Oct 26. pii: 1747493016676619. [Epub ahead
of print]
Jauch-Chara K, Oltmanns KM. Glycemic control after brain
injury: Boon and bane for the brain. Neuroscience.
2014;283C:202-209.
Oliveira-Filho J, Samuels OB. Reperfusion therapy for acute
ischemic stroke. UpToDate. October 6, 2016.
http://www.uptodate.com/contents/reperfusion-therapy-foracute-ischemic-stroke. Accessed December 6, 2016.
Gill HL, Siracuse JJ, Parrack IK, Huang ZS, Meltzer AJ.
Complications of the endovascular management of acute
ischemic stroke. Vasc Health Risk Manag. 2014 Nov
28;10:675-681. eCollection 2014.
Hassan AE, Chaudhry SA, Grigoryan M, Tekle WG, Qureshi AI.
National trends in utilization and outcomes of endovascular
nursece4less.com nursece4less.com nursece4less.com nursece4less.com 91
93.
94.
95.
96.
97.
98.
99.
100.
101.
102.
103.
treatment of acute ischemic stroke patients in the mechanical
thrombectomy era. Stroke. 2012;43(11):3012-3017.
Lin MP, Sanossian N. Reperfusion therapy in the acute
management of ischemic stroke. Cardiol Clin. 2015;33(1):99109.
Asadi H, Dowling R, Yan B, Wong S, Mitchell P. Advances in
endovascular treatment of acute ischemic stroke. Intern Med J.
2015;45(8):798-805.
Rordorf G, McDonald C. Spontaneous intracerebral hemorrhage:
Treatment and prognosis. UpToDate. May 21, 2014.
http://www.uptodate.com/contents/spontaneous-intracerebralhemorrhage-treatment-and-prognosis. Accessed December 7,
2016.
Jusufovic M, Sandset EC, Bath PM, Berge E; Scandinavian
Candesartan Acute Stroke Trial Study Group. Blood pressurelowering treatment with candesartan in patients with acute
hemorrhagic stroke. Stroke. 2014 Nov;45(11):3440-2.
doi:10.1161/STROKEAHA.114.006433. Epub 2014 Sep 25.
Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure
lowering in patients with acute intracerebral hemorrhage. N Engl
J Med. 2013;368(25):2355-2365.
Zeng J, Zheng P, Tong W, Fang W. Decreased risk of secondary
brain herniation with intracranial pressure monitoring in patients
with haemorrhagic stroke. BMC Anesthesiol. 2014 Mar 21;14:19.
doi: 10.1186/1471-2253-14-19.
Kim MY, Park JH, Kang NR, et al. Increased risk of acute kidney
injury associated with higher infusion rate of mannitol in patients
with intracranial hemorrhage. J Neurosurg. 2014
Jun;120(6):1340-1348. doi: 10.3171/2013.12.JNS13888. Epub
2014 Jan 31.
Chan S, Hemphill JC 3rd. Critical care management of
intracerebral hemorrhage. Crit Care Clin. 2014;30(4):699-717.
Morgenstern LB, Hemphill JC 3rd, Anderson C, et al. Guidelines
for the management of spontaneous intracerebral hemorrhage: a
guideline for healthcare professionals from the American Heart
Association/American Stroke Association. Stroke.
2010;41(9):2108-2129.
Frontera JA, Gordon E, Zach V, et al. Reversal of coagulopathy
using prothrombin complex concentrates is associated with
improved outcome compared to fresh frozen plasma in warfarinassociated intracranial hemorrhage. Neurocrit Care.
2014;21(3):397-406
Cabral KP, Fraser GL, Duprey J, et al. Prothrombin complex
concentrates to reverse warfarin-induced coagulopathy in
nursece4less.com nursece4less.com nursece4less.com nursece4less.com 92
patients with intracranial bleeding. Clin Neurol Neurosurg.
2013;115(6):770-774.
104. Woo CH, Patel N, Conell C, et al. Rapid warfarin reversal in the
setting of intracranial hemorrhage: a comparison of plasma,
recombinant activated factor VII, and prothrombin complex
concentrate. World Neurosurg. 2014;81(1):110-115.
105. Raimondi P, Hylek EM, Aronis KN. Reversal agents for oral
antiplatelet and anticoagulant treatment during bleeding events:
current strategies. Curr Pharm Des. 2016 Dec 5. [Epub ahead of
print]
106. Raya AK, Diringer MN. Treatment of subarachnoid hemorrhage.
Crit Care Clin. 2014;30(4):719-733.
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