Download A transient ischemic attack

NEUROVASCULAR
EMERGENCIES
Dana Bartlett, RN, BSN, MSN, MA
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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Continuing Nursing Education Course Director & Planners:
William A. Cook, PhD, Director; Douglas Lawrence, MS, Webmaster;
Susan DePasquale, CGRN, MSN, FPMHNP-BC, Lead Nurse Planner
Accreditation 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.
Credit Designation:
This educational activity is credited for 5 hours. Nurses may only claim
credit commensurate with the credit awarded for completion of this
course activity.
Course Author & Planner Disclosure Policy Statements:
It is the policy of NurseCe4Less.com to ensure objectivity,
transparency, and best practice in clinical education for all continuing
nursing education (CNE) activities. All authors and course planners
participating in the planning or implementation of a CNE activity are
expected to disclose to course participants any relevant conflict of
interest that may arise.
Statement of Need:
The identification and treatment of a neurovascular accident is critical
to prevent further damage. Lifestyle prevention is an essential aspect
of nursing care of the patient with associated risk factors.
Course Purpose:
To provide nurses with the needed skills to promote health prevention
and to treat neurovascular accidents in all health care settings.
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Learning Objectives:
1. Define transient ischemic attack and stroke.
2. Identify treatment priorities for transient ischemic attack.
3. Identify treatment priorities for ischemic stroke.
4. Identify treatment priorities for hemorrhagic stroke.
5. Identify treatment priorities for subarachnoid hemorrhage
Target Audience:
Advanced Practice Registered Nurses, Registered Nurses, Licensed
Vocational Nurses, and Associates
Course Author & Director Disclosures:
Dana Bartlett, RN, BSN, MA, MSN, William S. Cook, PhD,
Douglas Lawrence, MS, Susan DePasquale, CGRN, MSN, FPMHNP-BC all have no disclosures.
Acknowledgement of Commercial Support: There is none.
Activity Review Information:
Reviewed by Susan DePasquale, CGRN, MSN, FPMHNP-BC.
Release Date: 1/23/2014
Termination Date: 1/23/2017
Please take time to complete the self-assessment Knowledge 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. Treatment priorities for ischemic stroke include
a. the use of rtPA and blood pressure management.
b. ICP monitoring and prophylactic antibiotics.
c. surgical evacuation of the hematoma and therapeutic
hyperglycemia.
d. monitoring for DCI and re-bleeding
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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. Treatment priorities for hemorrhagic stroke include:
a. administration of rtPA and emergent anti-coagulation.
b. therapeutic hypothermia and avoiding hyperglycemia.
c. prophylactic anti-convulsants and prophylactic antibiotics.
d. monitoring ICP and blood pressure control.
8. Subarachnoid hemorrhage is characterized by:
a. temporary neurologic dysfunction.
b. cerebral ischemia that causes an infarct.
c. bleeding into the subarachnoid space.
d. hypercoaguability that causes decreed brain perfusion.
9. Treatment priorities for subarachnoid hemorrhage include:
a. monitoring for rebleeding and DCI.
b. administration of rtPA and antiplatelet therapy.
c. the use of hypertonic glucose solutions and factor Xa inhibitors.
d. anticoagulation with warfarin and carotid endarterectomy.
10. Transient ischemic attacks and strokes are more likely to
occur in patients who:
a. are female, < age 45, and have a normal lipid profile.
b. are elderly and who have atrial fibrillation and/or hypertension.
c. are male, < age 50, and have insulin dependent diabetes.
d. do not smoke, have a normal BNP, and are black.
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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 care
providers for these patients may encounter.
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 this 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) is defined as “a transient episode of
neurological dysfunction caused by focal brain, spinal cord, or retinal
ischemia, without acute infarction.”1 A TIA had traditionally been
clinically defined by the temporary nature of the symptoms; a TIA was
considered to produce reversible neurologic effects that lasted < 24
hours.2 However, it has become clear that for many reasons this
definition was inadequate.
The 24-hour time limit in the clinical definition of a TIA was arbitrary.
The use of duration of symptoms as a dividing line that could be used
to distinguish between a stroke and a TIA was misleading. The
emphasis on time implied that a short duration of symptoms was
equivalent to a decreased risk for neurological damage, but a TIA that
lasts for only a few minutes can cause harm.
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A TIA can cause cerebral infarctions, albeit small in size.2 Ovbiagele, et
al., (2002) found that one-third of neurological episodes classified as a
TIA by the traditional definition would be considered to be an infarction
if a diffusion-weighted MRI scan had been done.3 Central nervous
system (CNS) infarction is defined as brain, spinal cord, or retinal cell
death caused by ischemia and confirmed by on pathologic, neuroimaging, and/or clinical evidence of permanent injury.4
Statistics
Transient ischemic attacks are acknowledged to be very common,2,5
but the exact incidence of TIAs is not known. Depending on the
source, each year anywhere from 200,000 to 5 million Americans each
year have a TIA,5,6 and it appears that because of under-reporting the
true number of TIAs is higher.7-9 Men have a higher risk of having a
TIA than do women, and the risk of having a TIA increases with
age.4,10
Transient ischemic attack is unusual in young adults age less than 50.
The risk profile for TIA in this age group is often quite similar to that of
older adults, i.e., atherosclerosis, hypertension, dyslipdemia, etc.11,12
However, young adults are more likely to have less common risk
factors for TIA such as a coagulation disorder.13
Transient ischemic attack in children is very unusual. Factors
associated with TIA in children include sickle cell disease, congenital
heart disease, moyamoya, recent stroke, and migraine.14
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TIA Etiology and Pathophysiology
A 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 end result of a pathologic process; a TIA is not a
disease in and of itself.15 There is a wide variety of diverse clinical
conditions that can cause a TIA.15,16 The processes by which they
cause ischemia can be usefully divided into three categories.6
Thrombosis or obstruction
Atherosclerosis is the most common cause of obstruction that leads to
a TIA; and, the carotid arteries, intracranial arteries, and vertebral
arteries (major arteries located in the neck) are common sites of
atherosclerosis that can cause a TIA. Hypertension is also a risk factor
for TIA but a pathologic process called lipohyalinosis (thickening of the
walls of the arterioles) causes the obstruction. Vascular obstruction
and TIA can also be caused by arteritis (inflammation of the blood
vessels), dissection of a vessel, and sympathomimetic drugs, such as
cocaine. Additionally, fibromuscular dysplasia, a non-atherosclerotic,
non-inflammatory condition that causes abnormal growth within the
wall of the affected artery, may lead to TIA.17
Embolism
An embolism causing TIA can be from a proximal area such as the
aorta, carotid arteries, or the heart; or, it may be from the peripheral
circulation. Cardiomyopathy, myocardial infarction, valvular heart
disease, or a prosthetic heart valve can be the source of an embolism.
Hypercoaguable states, which are typically caused by cancer, genetic
condition, or infections, may also cause TIAs.15,18
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Decreased systemic perfusion
Decreased systemic perfusion caused by hypotension or heart failure
can cause transient brain ischemia.6,19
TIA Risk Factors
Risk factors for a TIA may be non-modifiable or modifiable, and there
are other potential risk factors identified with TIA.

Non-modifiable risk factors:
Non-modifiable risk factors for TIA include age over 55, male
gender, African American ethnicity, low birth weight, and a
family history of stroke.6,7

Modifiable risk factors:
Atrial fibrillation, diabetes mellitus, dyslipidemia, high alcohol
intake, hypertension, obesity, patent foramen ovale, physical
inactivity, and smoking are considered to be modifiable risk
factors for TIA.6,20-25

Potential risk factors:

Acute respiratory and urinary infections, alcohol abstinence, drug
abuse, hyperhomocysteinemia, high lipoprotein levels,
hypercoaguability, infections with certain organisms, migraine
with aura, and sleep-disordered breathing.6
TIA Signs and Symptoms
The signs and symptoms of a TIA typically are seen in the patient’s
behavior, gait, memory, movement or muscle function, memory, and
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speech.6,15 Patients may present with or have a history of aphasia,
ataxia, diplopia, hemiparesis, sensory loss, muscle weakness, or vision
loss.6 The signs and symptoms are often focal because the ischemia is
caused by decreased perfusion to a specific area and a specific blood
vessel or vessels;26 and transient, usually last between 30 and 60
minutes.6,27 The signs and symptoms and their duration are not
accurate indicators of the absence of an infarction.27,28 In addition, the
patient who is having a TIA will have symptoms of rapid onset, no
prior history of similar symptoms, and he/she will not have nonspecific symptoms.6 These three factors are considered highly
suggestive for a TIA.6
A focal sign, often called a focal deficit, is a
neurological finding that indicates
compromised function 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
FOCAL SIGN =
COMPROMISED
BRAIN
FUNCTION OR
DAMAGE
one arm or leg. An example of a global sign or deficit would be loss of
consciousness.
Unfortunately most patients who have had a TIA are examined by a
health care professional after their symptoms have resolved.2 It has
been estimated that ≤ 7% of patients who have had a TIA are
examined when their symptoms are at the worst level.2 Approximately
one half of all patients who have a TIA do not know the signs and
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symptoms and do not tell their primary care provider about the
episode.29
Transient ischemic attack and stroke have many similarities, and
distinguishing between them requires a good knowledge base. Key
differences between the two include:

a stroke can cause global and focal deficits

the signs and symptoms can be severe and life-threatening

the duration of the signs and symptoms of stroke are typically
much longer than that of a TIA

irreversible tissue death is relatively common

a stroke can be caused by intracranial hemorrhage

treatment of a stroke often requires the use of specific therapy
to preserve tissue and function30,31
Conditions That Mimic TIA
Transient ischemic attack is a clinical diagnosis32 and it can be a
difficult one to make. There is no confirmatory test, and the patients
are often examined after the event and when they are asymptomatic.
Research has shown that experienced neurologists can often disagree
about whether or not a patient is having a TIA.33 There can be
significant differences of opinion between emergency room physicians
and neurologists when making the diagnosis of TIA,34 and that TIA is
often misdiagnosed.35
This difficulty is further increased by conditions that mimic TIA. There
are many medical conditions that can be and often are misdiagnosed
as TIA. The most common of these mimics are migraine aura,
seizures, and syncope:26 Table 1 provides more examples. Many of
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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 study found in the list of footnotes at
the end of this study.
Table 1: Transient Ischemic Attack Mimics,26,32,36
Cerebral amyloid angiopathy
Compressive myelopathy
Conversion disorder
Encephalopathies of hepatic, pulmonary or renal origin
Functional disorder
Hypoglycemia
Metastatic or primary tumor
Migraine aura
Paroxysmal symptoms associated with multiple sclerosis
Peripheral vestibular disorder
Pressure or position-related nerve compression
Seizures
Spinal dural arteriovenous fistulas
Structural brain lesions
Subdural hematoma
Syncope
Transient global amnesia
The number and complexity of conditions that mimic TIA makes the
task of diagnosing a TIA even more daunting. However, there are
characteristics of the TIA mimics that can be used to distinguish
between these conditions and a TIA.6,36
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
Age:
A TIA is unusual in children and young adults.

Negative symptoms:
Negative symptoms means that there is decreased function or
loss of a function, and negative symptoms are more common in
TIAs, less so in TIA mimics.

Onset:
The onset of a TIA is very sudden. In 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:
A seizure will typically last about five minutes, syncope for a few
seconds, and a migraine aura may last for hours.

Symptom characteristics:
Amnesia or confusion, bladder and/or bowel incontinence,
isolated sensory symptoms such as pins and needles, and tonicclonic motions are indicative of a TIA mimic.6
The ABCD2 clinical prediction rule can also be used to distinguish a TIA
from a mimic or a non-cerebrovascular cause of neurological signs and
symptoms. Several authors have found that the ABCD2 can be used to
accurately discriminate between a TIA from these other conditions.
The lower the ABCD2 score the less likely it is that the patient is
having or has had a TIA.37,38 The ABCD2 will be discussed in more
detail later in the study module.
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Evaluation and Treatment
A TIA should be considered a medical emergency. Between 10%-15%
of all patients who have had a TIA will eventually develop a stroke,39
usually within 90 days of the TIA.40 Approximately 50% of these
strokes happen within 48 hours of the occurrence of the TIA.6,40,41 In
addition, people who have had a TIA have an increased risk for
myocardial infarction, unstable angina, or a ventricular arrhythmia
within 90 days of a TIA.42-44 A timely diagnosis of TIA and starting
preventative treatments has been shown to significantly reduce the
early occurrence of stroke and the 90 day occurrence of stroke after a
TIA.16,45,46
Evaluation
Evaluation of the patient who is having or is suspected to have had a
TIA should include the following tests and procedures.6,15,16,40,47 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 neurological and cardiovascular examination.

An MRI scan if possible. An MRI scan is the preferred choice
because this mode of scanning can detect small areas of
ischemia that a CT scan cannot.6 Diffusion-weighted MRI is the
mode of choice.

Vascular imaging techniques, i.e., angiography,
echocardiography, and ultrasound can be used to detect lesions
and obstructions in the heart or the vasculature that may be the
cause of the TIA.
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
A 12-lead electrocardiogram and continuous cardiac monitoring.
Long-term portable cardiac monitoring should be considered for
the detection of atrial fibrillation.

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.

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.
Evaluation of the patient with the ABCD2 clinical prediction rule is
recommended.6 The ABCD2 uses five parameters to make an
estimation of the risk of stroke within 2, 7, 30, and 90 days of a TIA.
Table 2: The ABCD2 Scale
Age: > 60 years, 1 point
Blood pressure: > 140 mm Hg systolic or > 90 mm Hg diastolic, 1 point
Clinical factors: Unilateral weakness with
or without speech impairment, 2 points
(1 point for speech impairment without
weakness)
Duration of symptoms: > 60 minutes, 2 points. 1 minute to 59 minutes, 1 point
Diabetes: 1 point
The score can be from 0-7. A score of 0-3 is considered to represent a
1% risk for stroke within 48 hours; a score of 4-5 is considered to
represent a 4.1% risk for stroke within 48 hours; and, a score of 6-7 is
considered to represent a 8.1% risk for stroke within 48 hours. The
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ABCD2 has been evaluated and found to be a reliable tool,15 but it has
also been shown to have limits; the accuracy of the ABCD2 may
depend on the population it is applied to and the experience of the
clinician who uses it.16,48,49 Extensions of the ABCD2, the ABCD3 and
ABCD3-1, have been developed50 and, although they have shown
promise, they have not yet been validated for widespread use.51
Treatment
Assessment and stabilization of airway, breathing, and circulation (the
ABCs) are the first treatments. If these are stable then the diagnostic
work-up can proceed. The next step is to determine whether or not the
patient needs to be hospitalized. Clear and universally accepted
guidelines for making this decision are not available.16,52 The ABCD2
has been used for this purpose but it is not clear if it is effective.6
Treatment of a TIA is essentially concerned with stroke prevention and
treating the cause or causes of the TIA with the use of medication,
surgery, and life style modifications. The specific therapies used are
discussed below.
Anticoagulation:
If the embolism was caused by non-valvular atrial fibrillation the
patient should be anti-coagulated with warfarin, apixaban (Eliquis),
dabigatran (Pradaxa), or rivaroxaban (Xarelto) to prevent
embolism.6,47 The choice of which drug to use should be made on a
case-by-case basis. If the patient is unable to take one of these anticoagulants, she/he should be prescribed aspirin.6,47 Clopidogrel
(Plavix) can be used with aspirin or used alone if the use of aspirin is
contraindicated.6,47
47
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Aspirin and clopidogrel have been shown to be effective at preventing
stroke in patients who have atrial fibrillation, but not as effective as
warfarin.47 Combining warfarin and antiplatelet therapy does not
provide a decrease in the risk for stroke but does increase the risk for
bleeding.47 It is not clear when anticoagulation should be initiated in
this patient population.47
There are also specific guidelines for anti-coagulation when a TIA has
been caused by an aortic or mitral valve problem, cardiomyopathy,
myocardial infarction, patent foramen ovale, or a prosthetic heart
valve. These will not be discussed here in detail but in most cases
anticoagulation is recommended.47
Antiplatelet therapy:
Antiplatelet therapy is designed to prevent embolization or thrombus
caused atherosclerosis, and if the TIA was caused by large or small
vessel atherosclerosis the patient should be started on antiplatelet
therapy rather than anticoagulant therapy.6,47 Antiplatelet therapy has
been shown to be effective at preventing stroke after a TIA:47 aspirin,
aspirin with dipyridamole (Persantine), clopidogrel alone are the drugs
of choice.6,47 The choice of which drug to use should be made on a
case-by-case basis.
Antiplatelet therapy should be started within 24 hours of the
TIA.47Antiplatelet therapy is also recommended for patients who have
a significant degree of intracranial atherosclerosis, patent foramen
ovale, or aortic arch atheroma.47
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Hypertension:
Antihypertensive therapy should be started if the patient who has had
a TIA has an established systolic blood pressure ≥ 140 mm Hg or an
established diastolic blood pressure ≥ 90 mm Hg.47 Antihypertensive
therapy provides clear benefits.6 The target blood pressure is not clear
nor is the optimal drug regimen, but there is some evidence that the
angiotensin converting enzyme (ACE) inhibitors alone or with a
diuretic, or an angiotensin receptor blocker (ARB), are the best
choice.6,47
Life style modifications that can lower blood pressure such as limited
alcohol consumption, a diet low in fat and high in fruits and
vegetables, physical exercise, and salt restriction should also be
initiated.47
Carotid endarterectomy, carotid angioplasty and stenting:
Carotid endarterectomy and carotid angioplasty and stenting have
been successfully used in patients who have a significant degree of
carotid artery stenosis, and these procedures are often recommended
for secondary stroke prevention.6,47
Dyslipidemia:
Patients who have had a TIA that is thought to be caused by
atherosclerosis and have a low-density lipoprotein cholesterol (LDL-C)
level of ≥ 100 mg/dL should be started on statin therapy.47 This
recommendation applies to all patients who fit those criteria whether
or not there is evidence of other ASCVD. Lowering of LDL-C is
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considered to be an important part of preventing secondary
stroke.6,47,53
Diabetes:
There are no large-scale studies that have shown that secondary
prevention of stroke can be accomplished by treating either the prediabetes state or diabetes mellitus.47 However, there are many other
benefits to treating diabetes. The 2014 guidelines for the prevention of
stroke in patients with stroke and transient ischemic attack state:
“Use of existing guidelines from the ADA (American Diabetic
Association) for glycemic control and cardiovascular risk factor
management is recommended for patients with an ischemic stroke
or TIA who also have DM or pre-DM.”47
Life style factors:
Life style modifications such as limited alcohol consumption, a diet low
in fat and high in fruits and vegetables, physical exercise, salt
restriction, smoking cessation, and weight loss if appropriate should
also be initiated.47 The evidence for the effectiveness of these changes
in the prevention of secondary stroke is not vigorous but they have
obvious benefits aside from this.
There is a high prevalence of obstructive sleep apnea in people who
have had a TIA or stroke. Evaluation for obstructive sleep apnea
should be considered.
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Other screening tests:
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. However, routine screening for hyperhomocysteinemia and
antiphospholipid antibodies is not recommended.47
Screening for hypercoaguability disorders should be done on a caseby-case basis and should be considered if the patient is age 45 or
younger, has a TIA of undetermined origin, has a history of cancer or a
clotting disorder, has multiple arterial or venous occlusions, or a family
history of thrombosis.13,47
Stroke
A stroke is a disease process that interrupts blood flow to the brain
and causes cerebral infarction.54-56 Stroke and TIA are in many ways
the same. They are both caused by a decrease in blood flow. The
patient having a stroke or a TIA experiences neurological signs and
symptoms, and they are each caused by an underlying chronic,
pathological disease process. A stroke and a TIA are essentially similar
processes and they could be viewed as separate points on a continuum
and as symptoms of a disease rather than a disease.
Strokes, however, by definition involve tissue death - cerebral
infarction. Neurons are highly sensitive to hypoperfusion and the
resulting decrease and/or loss of oxygen and glucose. The normal
cerebral blood flow is approximately 50-50mL/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
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10-15 mL/100 grams there will be irreversible tissue damage.13 The
consequences of a stroke can be relatively mild. Unlike a TIA,
however, many people who have suffered a stroke have permanent
disabilities. In addition, intracranial bleeding causes some strokes
whereas TIAs are not.
Classification of Stroke
Strokes can be categorized in several ways and there are several
stroke classification schemes that have been developed that can be
used to optimize treatment and prevention. However, all strokes are
essentially ischemic or hemorrhagic and, as with a TIA, the
pathogenesis of a stroke is thrombotic, embolic, or hypoperfusion. A
reasonable way to view strokes is that an ischemic stroke is caused by
decreased blood flow; and, intracerebral bleeding in the brain itself 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. Some stroke etiologies however are unusual and seldom
seen, i.e., strokes caused by hypercoaguability disorders, and, for
some patients, the cause of the stroke cannot be determined or there
may be several reasons the stroke has occurred; these are usually
called cryptogenic strokes.
A commonly used classification scheme for
ischemic strokes is TOAST, which stands for
Trial of Org 10712 in Acute Stroke
Treatment. The TOAST scheme considers
the cause of the stroke, and the five TOAST
ischemic stroke categories are: 1) Large
TOAST:
Trial of
Org 10712 in
Acute
Stroke
Treatment
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artery atherosclerosis; 2) Cardiac embolism; 3) Small vessel occlusion;
4) Stroke of another undetermined cause, and; 5) Stroke of
undetermined cause.
The diagnosis and evaluation of ischemic and hemorrhagic stroke will
be discussed together. Treatment of ischemic and hemorrhagic stroke
will be discussed in separate sections.
Statistics
As with all major public health problems the statistics on stroke are
quite sobering. These are itemized below.
1. Approximately 795,000 people each year in the United States
have a stroke.57
2. Of those 795,000 approximately 610,000 will have their first
stroke and 185,000 will have had a prior stroke.57
3. Eighty-seven percent of strokes are ischemic, 10% are
hemorrhagic, and 3% are subarachnoid.57 The figures are
approximate.
4. The incidence of stroke is higher in women than in men and
higher in African Americans than in white Americans.57
5. Stroke is a significant cause cognitive deficits and functional
impairment in people who are ≥ 65 years of age.58
Although stroke is a significant cause of morbidity and mortality, the
death rate from stroke has been steadily decreasing.31,59 Stroke was
for many years the third leading cause of death in the Unite States,
but it is now the fourth leading cause of death.59 A recent (2014)
review noted that although there are many possible causes for this
decrease, i.e., the extensive use of statin drugs, more effective
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therapy for atrial fibrillation, better control of hypertension is probably
the primary reason why fewer people are dying from stroke.59
Pathophysiology and Causes of Ischemic Stroke
An ischemic stroke is caused by narrowing of a cerebral blood vessel,
the narrowing being the result of a thrombus, an embolism, or
hypoperfusion.60,61 The thrombotic causes of ischemic stroke are:60 1)
Atherosclerosis; 2) Vascultis; 2) Arterial dissection; 4) Polycythemia;
5) Hypercoaguable states, and; 6) Infections such as HIV and
tuberculosis.31,60
The embolic causes of ischemic stroke are:60 1) Valvular vegetation; 2)
Mural thrombi; 3) Cardiac tumors; 4) Paradoxical embolism from a
patent foramen ovale or other malformation; 5) Fat emboli; 6)
Particulate emboli from intravenous drug use; 7) Septic emboli, and;
8) arterial-arterial emboli. Hypoperfusion that causes a stroke is
usually the result of cardiac failure.60
If the decrease in cerebral blood decrease is complete and persists for
4-10 minutes there will be irreversible damage and tissue death. Brain
tissue that is not perfused does not receive oxygen and glucose.
Without oxygen and glucose the mitochondria cannot product
adenosine triphosphate (ATP), and if ATP is not produced the cells will
die.31 The decrease in blood flow that occurs during an ischemic stroke
also causes cell death by secondary mechanisms of injury, apoptosis,
inflammation, and oxidative stress; these are collectively called
reperfusion injury.61-64
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Risk Factors for Ischemic Stroke
Non-modifiable
Age, low birth weight, race, and family history of stroke increase the
risk for stroke.58 The risk for stroke increases significantly after age
55. Low birth weight (≤ 2500 grams) has clearly been associated with
an increased risk for stroke,65-66 but it is not know if low birth weight is
a cause for stroke.58
African Americans and to a lesser degree Hispanic Americans suffer
disproportionately from stroke and from morbidity and mortality
caused by stroke.58,67,68 These effects are primarily, but not
completely, explained by a higher incidence in these populations of
modifiable risk factors, i.e., diabetes, dyslipidemia, and
hypertension.58,68 A family history of stroke has been estimated to
increase the risk of stroke by approximately 30%.69,70
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.61
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Modifiable
Atrial fibrillation, cigarette smoking, diabetes mellitus, diet and
nutrition, dyslipidemia, hypertension, obesity and body fat distribution,
other cardiac conditions, physical inactivity, and sickle cell disease are
important risk factors for stroke.58 Of these, the evidence for an
increase risk for stroke is strongest for atrial fibrillation, cigarette
smoking, dyslipidemia, hypertension, physical inactivity, and sickle cell
disease.58 Atrial fibrillation is described as “ . . . a potent and treatable
risk for embolic stroke.”58 Atrial fibrillation confers a five-fold increase
in risk for stroke,58,71,72 and a stroke caused by atrial fibrillation is
typically more severe and disabling than a stroke not caused by atrial
fibrillation.72,73
Cigarette smoking doubles the risk for ischemic stroke,58 this level of
risk is almost identical for people exposed to second-hand smoke.74
During a four year period the number of strokes attributed to smoking
was estimated to average almost 160,000.75 Dyslipidemia is
considered to be a major risk factor for stroke57,76 and for recurrent
stroke.77 Hypertension is a significant risk factor for stroke. 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 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.”59
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Physical activity has long been considered to be a major risk factor for
stroke.57 Many studies have noted the inverse relationship between
level of physical activity and the risk for stroke.78-80 Stroke is a major
complication of sickle cell disease:81,82 Prengler et al., (2002) found
that 10% of all children who have sickle cell disease will have a
cerebrovascular event by the age of 20.83
The factors that increase risk for stroke have been identified, but using
these for assessing a single patient’s risk for having a stroke is an
inexact science. There are stroke risk assessment tools, however, 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 tools do not include all possible risk factors. They do not
completely account for age, gender, and race.58
There is no ideal stroke risk assessment
tool, but the 2104 review notes that the
AHA/ACC CV Risk calculator can help
identify patients who may benefit from
therapeutic interventions that can
prevent stroke.58 The AHA/ACC CV Risk
calculator uses age, race, total
AHA/ACC CV
RISK CALCULATOR
A quick online resource for
health professionals,
available online at:
http://www.cvriskcalculator.com/.
cholesterol, HDL cholesterol, systolic and
diastolic blood pressure, presence of diabetes, smoking, and treatment
for hypertension to determine the 10 year risk for stroke. The risk
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calculator can be viewed by using this link:
http://www.cvriskcalculator.com/.
Signs and Symptoms
The clinical presentation of an ischemic stroke is highly variable and it
will depend on the patient’s age, co-morbidities, and the size and
location of the affected area. Commonly seen signs and symptoms are
outlined in the table below.30
Table 3: Signs and Symptoms of Ischemic Stroke
Aphasia
Ataxia
Decreased or altered consciousness
Diplopia
Dysarthria
Facial droop
Focal or global deficits
Hemiparesis
Visual defects
Hemorrhagic Stroke
Hemorrhagic stroke is cause by an intracerebral bleed or a
subarachnoid hemorrhage. This section of the module will 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
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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 essentially the
same as that of an ischemic stroke but there are some differences.
Intracranial bleeding causes increased intracranial pressure so that
alterations in consciousness, headache, nausea, and vomiting are
more common in hemorrhagic strokes than in ischemic strokes.56
Seizures are also more common in hemorrhagic strokes.
56
Hypertension is also relatively common. Despite these differences
signs and symptoms alone cannot distinguish between a hemorrhagic
stroke and an ischemic stroke.
Statistics

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 35%85 to 50.3%86

Approximately 50% of these deaths happen within two days of
the stroke.87,88

Hemorrhagic stroke is associated with a higher mortality rate
and a higher rate of disabilities than ischemic stroke.89
Pathophysiology and Etiology of Hemorrhagic Stroke
An intracerebral hemorrhage is caused by the rupture of small arteries
and bleeding into the brain parenchyma.90,91 Disruption of blood supply
to the affected areas interrupts the delivery of oxygen and glucose,
and causes cell death. Because the skull is a closed space the bleeding
causes increased intracranial pressure and secondary mechanisms,
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which are similar to those caused by an ischemic stroke, will occur
after the initial hemorrhage.91
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. Vascular
malformations are the most common cause of intracranial hemorrhage
in children.91 The causes of hemorrhagic stroke are listed in the table
below.90,91
Table 4: Causes of Hemorrhagic Stroke
Anticoagulant therapy
Brain tumor
Central nervous system infections
Cerebral amyloid angiopathy
Coagulopathies
Hypertension
Moyamoya
Septic embolism
Sympathomimetic drug abuse
Thrombolytic therapy for myocardial infarction or stroke
Vascular malformations
A complete discussion of all the causes of hemorrhagic stroke would
not be practical here, and this module will focus on four of the most
common: hypertension, cerebral amyloidosis, anticoagulant therapy,
and thrombolytic therapy.
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Hypertension
Hypertension is the most common cause of hemorrhagic stroke, and it
is also the biggest risk factor for hemorrhagic stroke.90-92 Hypertension
has been associated with 60% of all cases of hemorrhagic stroke.56 It
has been suggested that hypertension doubles the risk for
intracerebral hemorrhage.93
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.94,95 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 is a common cause of
hemorrhagic stroke in the elderly.96,97
Anticoagulant therapy
Anticoagulation with warfarin or other drugs is a widely used therapy
for the prevention and treatment of thromboembolism. Anticoagulation therapy is very effective at preventing TIA and stroke, but
the use of warfarin carries a significant risk of intracerebral
hemorrhage. The risk has been estimated at 1% per year,98 however,
it may be higher,98,99 The mortality rate from intracranial hemorrhage
and stroke caused by anticoagulation with warfarin has been reported
to be 46% - 68%.98
The risk of intracerebral hemorrhage caused by anticoagulation
therapy has been reported to be higher for Asians, blacks, and the
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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 with anticoagulation therapy.100 The newer anticoagulants, i.e., dabigatran, rivaroxaban, do not appear to be more
likely than warfarin to cause intracerebral bleeding.101
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 3.3% 7.3%.102-105
Other causes of hemorrhagic stroke, such as moyamoya disease, are
much less common than hypertension or anticoagulant drug therapy;
or they are widespread, as with illicit sympathomimetic drug use.
However, determining the incidence of stroke is difficult.106-107
Risk Factors for Hemorrhagic Stroke
Risk factors for and causes of hemorrhagic stroke overlap. A condition
such as hypertension can be both a risk factor and cause of stroke.
Also, risk factors interact and are synergistic.108 Risk factors for
hemorrhagic stroke include the following:56,91

Advanced age.

High intake of alcohol: High intake of alcohol has been clearly
and consistently associated with an increased risk for
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hemorrhagic stroke.109-111. People who drink heavily often have
hypertension; this effect and changes in platelet aggregation and
fibrinolysis may explain why heavy alcohol consumption
increases the risk for hemorrhagic stroke.111

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.112-115 Lipid
levels may contribute to the risk for, and mortality of,
hemorrhagic stroke and mortality by causing necrosis of the
arterial walls; and, may reflect poor nutritional status and/or the
presence of chronic disease.112

Previous stroke: A previous stroke increases the risk for
intracerebral hemorrhage.116

Ethnic status: Blacks have a higher risk for hemorrhagic stroke
than Caucasions,117,118 and in some age groups this risk is five
times higher.118
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.
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Evaluation Of The Stroke Patient
This section discusses the evaluation process for a patient suspected of
having a stroke.56,119,120
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. 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) or the Canadian Neurological Scale can be used to
determine the severity of the stroke.121-122
NIHSS Scale
Instructions
Scale definition
1a. Level of consciousness: The
0 = Alert; keenly responsive.
investigator must choose a
1 = Not alert; but arousable by
response if a full evaluation is
minor stimulation to obey, answer,
prevented by such obstacles as an
or respond.
endotracheal tube, language
2 = Not alert; requires repeated
barrier, orotracheal
stimulation to attend, or is
trauma/bandages. A 3 is scored
obtunded and requires strong or
only if the patient makes no
painful stimulation to make
movement (other than reflexive
movements (not stereotyped).
posturing) in response to noxious
3 = Responds only with reflex
stimulation.
motor or autonomic effects or
Score
____
totally unresponsive, flaccid, and
areflexic.
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1b. LOC questions: The patient is
0 = Answers both questions
asked the month and his/her age.
correctly.
The answer must be correct - there
1 = Answers one question correctly.
is no partial credit for being close.
2 = Answers neither question
Aphasic and stuporous patients who
correctly.
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.
1c. LOC commands: The patient is
0 = Performs both tasks correctly.
asked to open and close the eyes
1 = Performs one task correctly.
and then to grip and release the
2 = Performs neither task correctly.
non-paretic hand. Substitute
another one step command if the
hands cannot be used. 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 (ie, follows none, one or two
commands). Patients with trauma,
amputation, or other physical
impediments should be given
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suitable one-step commands. Only
the first attempt is scored.
2. Best gaze: Only horizontal eye
0 = Normal.
movements will be tested.
1 = Partial gaze palsy; gaze is
Voluntary or reflexive
abnormal in one or both eyes, but
(oculocephalic) eye movements will
forced deviation or total gaze
be scored, but caloric testing is not
paresis is not present.
done. If the patient has a conjugate
2 = Forced deviation, or total gaze
deviation of the eyes that can be
paresis not overcome by the
overcome by voluntary or reflexive
oculocephalic maneuver.
activity, the score will be 1. 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, preexisting 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.
3. Visual: Visual fields (upper and
0 = No visual loss.
lower quadrants) are tested by
1 = Partial hemianopia.
confrontation, using finger counting
2 = Complete hemianopia.
or visual threat, as appropriate.
3 = Bilateral hemianopia (blind
Patients may be encouraged, but if
including cortical blindness).
____
they look at the side of the moving
fingers appropriately, this can be
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scored as normal. If there is
unilateral blindness or enucleation,
visual fields in the remaining eye
are scored. Score 1 only if a clearcut 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
0 = Normal symmetrical
pantomime to encourage - the
movements.
patient to show teeth or raise
1 = Minor paralysis (flattened
eyebrows and close eyes. Score
nasolabial fold, asymmetry on
symmetry of grimace in response to
smiling).
noxious stimuli in the poorly
2 = Partial paralysis (total or near-
responsive or non-comprehending
total paralysis of lower face).
patient. If facial trauma/bandages,
3 = Complete paralysis of one or
orotracheal tube, tape or other
both sides (absence of facial
physical barriers obscure the face,
movement in the upper and lower
these should be removed to the
face).
____
extent possible.
5. Motor arm: The limb is placed in
0 = No drift; limb holds 90 (or 45)
the appropriate position: extend
degrees for full 10 seconds.
the arms (palms down) 90 degrees
1 = Drift; limb holds 90 (or 45)
(if sitting) or 45 degrees (if supine).
degrees, but drifts down before full
Drift is scored if the arm falls
10 seconds; does not hit bed or
before 10 seconds. The aphasic
other support.
patient is encouraged using
2 = Some effort against gravity;
urgency in the voice and
limb cannot get to or maintain (if
____
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pantomime, but not noxious
cued) 90 (or 45) degrees, drifts
stimulation. Each limb is tested in
down to bed, but has some effort
turn, beginning with the non-
against gravity.
paretic arm. Only in the case of
3 = No effort against gravity; limb
amputation or joint fusion at the
falls.
shoulder, the examiner should
4 = No movement.
record the score as untestable
UN = Amputation or joint fusion,
(UN), and clearly write the
explain:________________
explanation for this choice.
5a. Left arm
5b. Right arm
6. Motor leg: The limb is placed in
0 = No drift; leg holds 30-degree
the appropriate position: hold the
position for full 5 seconds.
leg at 30 degrees (always tested
1 = Drift; leg falls by the end of the
supine). Drift is scored if the leg
5-second period but does not hit
falls before 5 seconds. The aphasic
bed.
patient is encouraged using
2 = Some effort against gravity; leg
urgency in the voice and
falls to bed by 5 seconds, but has
pantomime, but not noxious
some effort against gravity.
stimulation. Each limb is tested in
3 = No effort against gravity; leg
turn, beginning with the non-
falls to bed immediately.
paretic leg. Only in the case of
4 = No movement.
amputation or joint fusion at the
UN = Amputation or joint fusion,
hip, the examiner should record the
explain:________________
score as untestable (UN), and
6a. Left leg
clearly write the explanation for this
6b. Right leg
____
choice.
7. Limb ataxia: This item is aimed
0 = Absent.
at finding evidence of a unilateral
1 = Present in one limb.
cerebellar lesion. Test with eyes
2 = Present in two limbs.
open. In case of visual defect,
UN = Amputation or joint fusion,
ensure testing is done in intact
explain:________________
____
visual field. The finger-nose-finger
and heel-shin tests are performed
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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
0 = Normal; no sensory loss.
to pinprick when tested, or
1 = Mild-to-moderate sensory loss;
withdrawal from noxious stimulus in
patient feels pinprick is less sharp
the obtunded or aphasic patient.
or is dull on the affected side; or
Only sensory loss attributed to
there is a loss of superficial pain
stroke is scored as abnormal and
with pinprick, but patient is aware
the examiner should test as many
of being touched.
body areas (arms [not hands], legs,
2 = Severe to total sensory loss;
trunk, face) as needed to
patient is not aware of being
accurately check for hemisensory
touched in the face, arm, and leg.
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. 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.
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Patients in a coma (item 1a=3) are
automatically given a 2 on this
item.
9. Best language: A great deal of
0 = No aphasia; normal.
information about comprehension
1 = Mild-to-moderate aphasia;
will be obtained during the
some obvious loss of fluency or
preceding sections of the
facility of comprehension, without
examination. For this scale item,
significant limitation on ideas
the patient is asked to describe
expressed or form of expression.
what is happening in the attached
Reduction of speech and/or
picture, to name the items on the
comprehension, however, makes
attached naming sheet and to read
conversation about provided
from the attached list of sentences.
materials difficult or impossible. For
Comprehension is judged from
example, in conversation about
responses here, as well as to all of
provided materials, examiner can
the commands in the preceding
identify picture or naming card
general neurological exam.
content from patient's response.
If visual loss interferes with the
2 = Severe aphasia; all
tests, ask the patient to identify
communication is through
objects placed in the hand, repeat,
fragmentary expression; great need
and produce speech. The intubated
for inference, questioning, and
patient should be asked to write.
guessing by the listener. Range of
The patient in a coma (item 1a=3)
information that can be exchanged
will automatically score 3 on this
is limited; listener carries burden of
item. The examiner must choose a
communication. Examiner cannot
score for the patient with stupor or
identify materials provided from
limited cooperation, but a score of
patient response.
3 should be used only if the patient
3 = Mute, global aphasia; no usable
is mute and follows no one-step
speech or auditory comprehension.
____
commands.
10. Dysarthria: If patient is thought
0 = Normal.
to be normal, an adequate sample
1 = Mild-to-moderate dysarthria;
____
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of speech must be obtained by
patient slurs at least some words
asking patient to read or repeat
and, at worst, can be understood
words from the attached list. If the
with some difficulty.
patient has severe aphasia, the
2 = Severe dysarthria; patient's
clarity of articulation of
speech is so slurred as to be
spontaneous speech can be rated.
unintelligible in the absence of or
Only if the patient is intubated or
out of proportion to any dysphasia,
has other physical barriers to
or is mute/anarthric.
producing speech, the examiner
UN = Intubated or other physical
should record the score as
barrier,
untestable (UN), and clearly write
explain:________________
an explanation for this choice. Do
not tell the patient why he or she is
being tested.
11. Extinction and inattention
0 = No abnormality.
(formerly neglect): Sufficient
1 = Visual, tactile, auditory, spatial,
information to identify neglect may
or personal inattention or extinction
be obtained during the prior
to bilateral simultaneous
testing. If the patient has a severe
stimulation in one of the sensory
visual loss preventing visual double
modalities.
simultaneous stimulation, and the
2 = Profound hemi-inattention or
cutaneous stimuli are normal, the
extinction to more than one
score is normal. If the patient has
modality; does not recognize own
aphasia but does appear to attend
hand or orients to only one side of
to both sides, the score is normal.
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.
____
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The following diagnostic tests should be performed on all stroke
patients during the evaluation process.56,119,120
Table 5: 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 electrolytes*renal 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, page 45, should be
performed for selected patients during the evaluation of a
stroke.56,119,120
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Table 6: 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
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 is a bleed into the subarachnoid cavity, the
space between the arachnoid membrane and the pia mater. It is an
infrequent cause of stroke and most cases are caused by rupture of an
aneurysm. A subarachnoid hemorrhagic stroke is a potentially
devastating event.123 The mortality rate is approximately 50%124,125
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and, as with other types of hemorrhagic stroke, the 30 day mortality
rate is high.126
A stroke caused by a subarachnoid hemorrhage is characterized by the
sudden onset of a very severe headache. The headache is usually
localized on the same side of the head where the bleeding is occurring.
Dizziness, hyponatremia, nausea, and vomiting are often seen and a
“sentinel” headache that precedes the subarachanoid hemorrhage by
hours or a day is relatively common.127,128
Causes and Risk Factors

Alcohol use

Amyloid angiography

Aneurysms

Cigarette smoking

Coagulation disorders

Hypertension

Infection

Moyamoya disease

Neoplasms

Oral contraceptives,

Stimulants
129,130
There are assessment scales that have been developed for grading the
severity of subarachnoid hemorrhage. These are the Hunt and Hess
scale, World Federation of Neurological Surgeons (WFNS) scale, Fisher
scale, Claasen grading system, and the Ogilvy and Carter scale. The
Glasgow coma scale has been used for this purpose, as well. There is
no evidence that one is better than another.123 The Glasgow coma
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scale was not designed for assessment of subarachnoid hemorrhage.
The Hunt and Hess (outlined in the table on page 48) is widely used.
Re-bleeding has been reported to occur in 8%-23% of patients.131 This
will usually happened in the first 24 hours and the risk is especially
high in the first six hours.123 The risk for re-bleeding 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; 5) a longer interval
between the onset and when medical care is sought.123
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 subarachnoid hemorrhage is essentially the
same as for other types of stroke but there are important differences.
Headache is often the only presenting symptom of a subarachanoid
hemorrhage but headache is a very common complaint and only a
small percentage of people who have a headache have a
subarachanoid hemorrhage.132 Because the morbidity and mortality of
subarachanoid hemorrhage are quite high, and re-bleeding relatively
common, it is important to quickly and accurately make a diagnosis.
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If there is a suspicion that the patient
Reasons for misdiagnosis of
is having a subarachnoid hemorrhage,
subarachnoid hemorrhage
a non-contrast CT scan of the head

the signs and symptoms
should be performed immediately and
associated with
a lumbar puncture should be
subarachnoid
performed. The non-contrast CT scan
is very sensitive at detecting
hemorrhage

understanding the
hemorrhage occurred less than 24
hours prior to the
limitations of the
but the
sensitivity of the CT scan for this
purpose decreases with time134 and
not performing a CT
scan or not
subarachnoid hemorrhage if the
exam,133
failure to understand
procedure

not performing a lumbar
puncture
lumbar puncture is recommended.123
Some authors feel that if the patient has an acute headache, the CT
scan of the head is negative, and if the onset of the headache was 6
hours or less prior to the performance of the scan a lumbar puncture is
not needed.132 More recent reviews recommend a lumbar puncture
regardless of the CT scan results.123,130
Misdiagnosing a subarachnoid hemorrhage can be potentially
catastrophic. A 2013 review of the literature found a rate of
misdiagnosis that ranged from 2.5% to 21.7%.135 The reasons for
misdiagnosis are: 1) failure to understand the signs and symptoms
associated with subarachnoid hemorrhage; 2) not performing a CT
scan or not understanding the limitations of the procedure, and; 3) not
performing a lumbar puncture.123
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Treatment Of Ischemic Stroke
Patients should be admitted to the ICU and have continuous
hemodynamic and neurologic monitoring. The following
recommendations are from the 2013 guidelines from the American
Heart Association and the American Stroke Association (AHA/ASA).120

Stabilization of ABCs

Patient positioning: If the patient is hypoxic or at risk for airway
obstruction, aspiration, increased intracranial pressure, the head
of the bed should be elevated at a 15-30 degree angle.

Oxygen: Many patients who have had a stroke are hypoxic.
Supplemental oxygen should be used to maintain an oxygen
saturation of greater than 94%.136 Supplemental oxygen should
not be used if the patient is not hypoxic.120

Hyperthermia: Hyperthermia is common after a stroke and it has
been associated with poor outcome.137 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.120

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 recommendations in Table 7 are from the 2013
AHA/ASA 2013 guidelines for managing ischemic stroke.120
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Table 7: 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

IV hydration:
Euvolemia is recommended.120 Hypovolemia decreases perfusion
to the organs and hypervolemia can increase cerebral edema
and is stressful for the myocardium.
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
Serum glucose:
Hyperglycemia is common in patients who have had an ischemic
stroke and several authors have found an incidence of
hyperglycemia to be greater than 40% in this patient
population.138,139 Elevated serum glucose is common in the acute
phase of stroke and may be related to uncontrolled or
undetected diabetes mellitus or stress-induced hyperglycemia
associated with cortisol and norepinephrine release at the time
of insult.
Hyperglycemia has consistently been associated with poor
outcome after stroke,
120,140,141
but it is not clear if
hyperglycemia is a cause of poor outcome or an effect. The 2013
AHA/ASA guidelines recommend: 1) Treating a serum glucose
that is < 60 mg/dL; and, 2) “ . . . treat hyperglycemia during
acute stroke in a manner that avoids excessive resources, labor,
and risk.
It is reasonable to follow the American Diabetes Association
recommendation and maintain the blood glucose in a range of
110-180 mg/dL in all hospitalized patients.”120

Administer recombinant tissue plasminogen activator (rtPA) if
indicated.
Rapid assessment, evaluation, and treatment of ischemic stroke is
essential. The following Table from the 2013 AHA/ASA guidelines
outlines the optimal times for these aspects of stroke care.120,142
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Table 8: Optimal Stroke Care time Limits
Door to physician ≤10 minutes
Door to stroke team ≤15 minutes
Door to CT initiation ≤25 minutes
Door to CT interpretation ≤45 minutes
Door to drug (≥80% compliance) ≤60 minutes
Door to stroke unit admission ≤3 hours
Thrombolytic Therapy
Thrombolytic therapy with rtPA is the only Food and Drug
Administration (FDA) approved therapy for the treatment of ischemic
stroke. The use of rtPA has been shown to improve 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.120,143 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 following guidelines are from the 2013
AHA/ASS guidelines.120 The relative exclusion criteria refer to
circumstances in which the benefit of rtPA may outweigh the risks.
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
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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 dose in
greater than 48 hours and his/her renal function is normal.120 The
recommendations for inclusion and exclusion criteria are outlined in
the Tables on page 54 - 56.
Table 9: rtPA Inclusion Criteria
Ischemic stroke and measurable neurological deficit
Onset of symptoms < 3 hours before beginning treatment
Aged ≥ 18 years
Table 10: 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
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Table 11: rtPA Relative Exclusion Criteria
Acute myocardial infarction (within 3 months)
Gastrointestinal or urinary tract hemorrhage within 21 days
Major surgery or serious trauma within 14 days
Minor or rapidly improving stroke symptoms
Pregnancy
Seizure and postictal residual neurological impairments
Table 12: Inclusion Criteria: Symptom Onset between 3 - 4.5 Hours
Additional
Ischemic stroke causing measurable neurological deficit
Symptoms onset within 3 to 4.5 hours before beginning treatment
Table 13: Relative Exclusion Criteria: Symptom Onset Between 3 - 4.5 hours
Age >80 years
History of diabetes and prior ischemic stroke
NIHSS score >25)
Taking an oral anticoagulant regardless of INR
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Table 14: Administration of rtPA
1. Infuse 0.9 mg/kg (maximum dose 90 mg) over 60 minutes: give
10% of the dose as a bolus over 1 minute.
2. Admit the patient to an intensive care or stroke unit for monitoring.
3. If the patient develops severe headache, hypertension, nausea,
vomiting, or neurologic deterioration, discontinue the rtPA infusion
obtain an emergent CT scan.
4. Measure blood pressure and perform neurological assessments
every 15minutes during and after IV rtPA infusion for 2 hours, then
every 30 minutes for 6 hours, then hourly until 24 hours after rtPA
treatment.
5. 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 7 to maintain blood pressure.
6. Do not place nasogastric tubes, indwelling bladder catheters, or
intra- arterial pressure catheters if the patient can be safely
managed without them.
7. Obtain a follow-up CT or MRI scan at 24 hours after IV rtPA before
starting anticoagulants or antiplatelet agents.
Thrombolysis is an effective treatment for ischemic stroke but it has
significant limitations. It can only be given within 3 - 4.5 hours after
the onset of symptoms and many patients with ischemic stroke
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present to the hospital well outside of that time frame. Thrombolysis
has serious adverse effects; although it has what could be described
as a good success rate, there are certainly people who do not respond.
Additionally, occlusion of certain cerebral vessels cannot be cleared
with rtPA.144
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.144-46 At
this point the evidence for the effectiveness of these techniques has
been described as equivocal,147 and there are no trials that directly
compare them.
120
Other Aspects of Stroke Care
Other aspects of stroke care are outlined below according to the
recommendations in the 2013 AHA/ASS guidelines.120
Anticoagulation
Urgent anticoagulation with heparin or a low molecular weight heparin
does not decrease the risk of early neurological deterioration or
recurrent stroke is not recommended
Platelet Inhibition
Administering aspirin 24-48 hours after the onset of the stroke is
recommended.
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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
predict poor outcome. If the patient has pneumonia or a UTI she/he
should be treated with the appropriate antibiotics.
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DVT Prevention
Subcutaneous heparin is recommended to prevent 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.
Stroke Prevention Measures
Stroke prevention measures should be started as soon as possible.
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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. Patients should be admitted to the ICU and have
continuous hemodynamic and neurologic monitoring. Specific concerns
in the management of these patients includes:

DVT prevention:
Intermittent pneumatic compression should be used to prevent
DVT.148

IV 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.148

Blood pressure control:
Hypertension is common in patients who have had a
hemorrhagic stroke,149 and an elevated blood pressure is
associated with a poor outcome.150 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
effects.151 A 2014 review of the treatment of hemorrhagic stroke
provided these guidelines for blood pressure management.149
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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

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.56,148
Glucocorticoids such as dexamethasone should not be
used to lower ICP.56,148
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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.152 If ICP needs to be
lowered IV infusions of mannitol,
56,148,153
barbiturate
coma,56,148 hyperventilation,56,148 ventriculostomy,
56,148,154
and surgical evacuation of the hematoma154 are
considered reasonable options.

Seizures:
Seizures, both clinical (2.7%-17%) and noted on
electroencephalography monitoring (28%-31%), are
common after intracranial hemorrhage.154,155 There is no
clear evidence about how seizures affect patient
outcome, whether seizures should be treated, or what
medications should use to treat them.154 A 2014 review
noted that “ . . . clinically significant seizures should be
treated with anti-convulsants . . “154 but prophylaxis with
anti-convulsants, especially phenytoin, is not
recommended.155

Patients receiving anti-coagulants:
Warfarin should be discontinued if the INR is elevated, IV
vitamin K should be administered, and specific vitamin Kdependent factors should be given.155 If there is severe
bleeding vitamin K, fresh frozen plasma, and prothrombin
complex concentrates and recombinant factor VIIa can
be given.155-158
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Treatment Of Subarachnoid Hemorrhage
Many of the treatment concern and goals for subarachnoid
hemorrhagic 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.130,159,160 Patients should be
admitted to the ICU and have continuous hemodynamic and neurologic
monitoring. Specific concerns in the management of these patients
includes the following conditions.

Hyponatremia:
Hyponatremia occurs is approximately one-third of all patients
who have had a subarachnoid hemorrhage and it is associated
with poor outcome.160 Hyponatremia is treated by restricting free
water consumptions and 1.5% or 2% sodium chloride
solutions.160 Fludrocortisone or hydrocortisone may help promote
diuresis and correct the hyponatremia.160

Re-bleeding:
Re-bleeding is managed by using anti-fibrinolytic drugs such as
tranexamic acid, aminocaproic acid, or surgical clipping and
endovascular coiling.159,160

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.159,160
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
Seizures:
Prophylactic anticonvulsants should be considered if the patient
has a large hemorrhage that has not yet been surgically
corrected.159

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).160
Delayed cerebral ischemia 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.160 If the patient is symptomatic
the treatments include induced hypertension, inotropic drugs
such as dobutamine and milrinone, transfusions to maintain a
hemoglobin level between 8-10 mg/dL, angioplasty, and intraarterial dilators such as milrinone, nimodipine, nicardipine, and
verapamil.160

Blood pressure management:
The best treatment for hypertension in a patient who has a
subarachnoid hemorrhage is not known. Singer et al., (2013)
recommend keeping the systolic blood pressure below 160 mm
Hg with enalapril, labetalol, or nicardipine.159
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SUMMARY
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 anti-coagulation and anti-platelet 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 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 the NURSECE4LESS.COM course planners evaluate
nursing knowledge needs met following completion of this course by
completing the self-assessment Knowledge Questions after reading the
article. Correct Answers, 69 page.
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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. Treatment priorities for ischemic stroke include
a. the use of rtPA and blood pressure management.
b. ICP monitoring and prophylactic antibiotics.
c. surgical evacuation of the hematoma and therapeutic
hyperglycemia.
d. monitoring for DCI and re-bleeding
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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. Treatment priorities for hemorrhagic stroke include:
a. administration of rtPA and emergent anti-coagulation.
b. therapeutic hypothermia and avoiding hyperglycemia.
c. prophylactic anti-convulsants and prophylactic antibiotics.
d. monitoring ICP and blood pressure control.
8. Subarachnoid hemorrhage is characterized by:
a. temporary neurologic dysfunction.
b. cerebral ischemia that causes an infarct.
c. bleeding into the subarachnoid space.
d. hypercoaguability that causes decreed brain perfusion.
9. Treatment priorities for subarachnoid hemorrhage include:
a. monitoring for rebleeding and DCI.
b. administration of rtPA and antiplatelet therapy.
c. the use of hypertonic glucose solutions and factor Xa inhibitors.
d. anticoagulation with warfarin and carotid endarterectomy.
10. Transient ischemic attacks and strokes are more likely to
occur in patients who:
a. are female, < age 45, and have a normal lipid profile.
b. are elderly and who have atrial fibrillation and/or hypertension.
c. are male, < age 50, and have insulin dependent diabetes.
d. do not smoke, have a normal BNP, and are black.
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Correct Answers
1.
A
2.
B
3.
D
4.
C
5.
A
6.
B
7.
D
8.
C
9.
A
10. B
Footnotes:
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