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Subpart IVD
Chapter
34
Clinical – Neurologic
Transient Ischemic Attack (TIA)
Matthew Tabbut, MD
Jonathan Glauser, MD, FACEP
TIA Definition
Every year in the United States nearly 800,000
people are affected by a new or recurrent stroke.
1
It has historically been the third leading cause of
death and a leading cause of long-term disability.
2
Statistically, 15–30% of all strokes are preceded by
a transient ischemic attack (TIA).
3
In the emergency department (ED), TIA accounts for
approximately 300,000 patient visits annually
though this may be an underestimate of the true
prevalence of TIA as many do not present to a
health care provider.
1,2,4
Traditionally, TIA has been defined as an
“Acute neurologic deficit caused by focal brain
ischemia (attributable to a specific arterial territory) that completely resolves in 24 hours.”
2,5
The
differentiation between TIA and stroke historically was made when advanced brain imaging was
not available and recovery was judged based on
clinical symptoms. With the advent of CT and
MRI, radiographic evidence of infarction can be
seen in many who would have been previously
classified as having a TIA.
5,6
A new definition has been proposed that considers TIA a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia
without evidence of acute infarction. Some
authors include a time window of less than 1
hour, since 75% of TIAs by the old definition
resolve within 60 minutes.
1,3,5,6
Recently there has been an enhanced sense of
urgency regarding the workup of TIA in order to
prevent subsequently de bilitating strokes. The
time window of greatest concern for the emergency physician is the first 48 hours to 7 days.
Approximately half of all strokes that occur
during the first 7 days will occur within the first
24 hours.
7
Risk Stratification
Stroke risk is believed to be 3–5% in 2 days,
5–7% in 7 days, 8.0% in 30 days, and 9.2% in
90 days following a TIA,
8,9,10,11
although higher
risk using a different methodology has also been
reported: 9.9% at 2 days, 13.4% at 30 days, and
17.3% at 90 days.
9
Several scoring rules have
been developed in order to risk stratify patients
who are at increased risk of stroke following
aTIA.
The California rule, ABCD rule, and ABCD2
rule have been used to risk stratify patients into
high and low risk of subsequent stroke. The most
widely used rule is the ABCD score (Table 34.1).
It was derived to determine the risk of stroke
following TIA at 7 days. More recently the
ABCD2 score was developed by adding a history
of diabetes to the ABCD score (Table 34.2).
Though the ABCD and ABCD2 rule was
derived to help determine if patients are safe for
Table 34.1 ABCD Rule
2
Factors Score
Age 60 yrs 1
Elevated BP
Systolic > 140 mmHg
Diastolic > 90 mmHg
1
Unilateral weakness 2
Speech impairment without unilateral
weakness
1
Duration 60 min 2
Duration 10 to 59 min 1
Duration < 10 min 0
Total possible points 6
038
21:05:24
discharge, it has not been used specifically as
entrance or exclusion criteria for ED observation
units (OUs).
Role of Observation
There are no clear guidelines that establish a standard of care for the disposition of TIA patients.
12
The final decision to admit or discharge is often left
to the individual institution and to physician risk
tolerance. Some institutions admit all patients diagnosed with a TIA. Others who have well-established
follow-up in specialized TIA clinics may discharge
patients who are deemed appropriate for outpatient
management to obtain their studies within the next
48 hours.
2, 13
As ED OUs have gained popularity,
it is increasingly clear that patients diagnosed with
TIA can be safely and efficiently managed in the
observation setting as an alternative to inpatient
admission.
14
In particular, OU use results in
reduced risk for subsequent stroke, greater compliance with diagnostic evaluation, shorter length of
stay, lower cost, and decreased hospital overcrowding and ambulance diversion.
14
Because the risk of stroke following a TIA is
highest in the first 48 hours, hospitalization has
been justified in order to identify particular pathologies that may predispose to stroke. Conditions
such as atrial fibrillation, carotid artery stenosis,
extracranial dissections, cardiac thrombus, and
cardiac arrhythmia all hav e been known to be
causes of stroke that are potentially modifiable
in the acute phase. The initial evaluation of TIA
should be aimed at identifying treatable conditions to prevent stroke through a variety of
imaging studies and laboratory assessments.
14
The short-term risk of stroke in the acut e
phase after TIA is typically due to unstable vascular pathology, includi ng critical carotid stenosis, cardiac thrombus, and arrhythmia.
14,15
Accelerated diagnostic protocols in the ED observation setting are aimed at uncovering these
pathologies and consist of neuroimaging, telemetry monitor ing, cardiac echocardiography, and
carotid imaging.
16
The evaluation of TIA in the ED observation
setting provides an efficient and accurate patient
assessment. Additionally it has been found to
reduce unnecessary hospitalization. Rapid evaluation of TIA has been shown to reduce subsequent stroke risk. The EXPRESS trial evaluating
the use of urgent, specialized clinics in the evaluation and initial treatment of TIA found an 80%
reduction in risk of early recurrent stroke.
17
From an economic standpoint, the use of
accelerated diagnostic protocols in the ED OU
compared to inpatient admission showed cost
savings and resulted in shorter length of stay.
In one report, the average cost for inpatient
admission was $1,547 versus $890 for ED observation. The average length of stay for inpatient
admission was 61.2 hours versus 25.6 hours for
ED observation.
16
Some categories of patients are inappropriate
for admission to an OU. Patients with cresc endo
TIA symptoms or repeated TIA symptoms present a high risk for subsequent stroke and should
be admitted to an inpatient unit. Patients with a
stroke or with persistent neurologic deficits
require full inpatient admission.
16
Patients identified in the ED as having a cause
for their TIA should be admitted to an inpatient
unit rather than the ED OU. Thus, any head
CT positive for intracranial hemorrhage, infarct
or mass requires admission to the appropriate
neurology or neurosurgery service. Patients with
known embolic sources should be admitted to the
appropriate cardiology or medical service for
management of their underlying process. Any
patient with known carotid stenosis > 50%
should be evaluated by vascular surgery for urgent
carotid endarterectomy (CEA).
16
A certain percentage of patients will rule in for
stroke even with transient symptoms that clinically appear to be a TIA.
6
Patients in the ED OU
Table 34.2 ABCD2 Rule
2
Factors Score
Age 60 yrs 1
Elevated BP
Systolic > 140 mmHg
Diastolic > 90 mmHg
1
Unilateral weakness 2
Speech impairment without unilateral
weakness
1
Duration 60 min 2
Duration 10 to 50 min 1
Duration < 10 min 1
Diabetes 1
Total possible points 7
Matthew Tabbut and Jonathan Glauser
038
21:05:24
who are found to have evidence of ischemia on
their MRI should be admitted for further management and care of their stroke.
Other neurologic and vascular conditions
can mimic TIA (Table 34.3). Patien ts with these
conditions or patients who have significant
comorbidities requiring > 24-hour stay should
be evaluated in the ED with appropriate
disposition.
16
TIA Workup
The evaluation of TIA is time sensitive. The goal of
the ED observation evaluation of TIA is to identify
reversible causes of subsequent stroke. The initial
ED evaluation should evaluate TIA mimics
(Table 34.3), differentiate TIA from stroke and
detect high-risk pathologies that require immediate
intervention and admission (Table 34.4).
Purposes of an accelerated diagnostic protocol
for TIA in the ED OU include confirmation of the
diagnosis of TIA, evaluation for reversible causes
of TIA, and determination of the need for additional therapeutic intervention to prevent subsequent stroke. Standardized protocols may consist
of continuous monitoring (neurologic assessment
and telemetry monitoring), brain imaging,
carotid imaging, cardiac imaging, and neurology
consultation (Table 34.5).
Brain Imaging
Non-Contrast CT Brain
The primary utility of CT brain imaging is to differentiate ischemic lesions versus non-ischemic lesions
(i.e., tumor, aneurysm, intracranial hemorrhage) as
Table 34.3 Differential Diagnosis for TIA
2,16
Stroke
Complex migraine
Focal seizure
Todd’s paralysis
Hypertensive encephalopathy
Intracranial hemorrhage
Syncope
Labyrinthine disorders
Vasospasm
Hypoglycemia
Hypernatremia
Hydrocephalus
Intracranial mass
Arteritis
Focal neuropathy
Table 34.4 ED Evaluation
2
Glucose check Evaluate for
hypoglycemia
EKG Evaluate for
precipitating
arrhythmias (i.e., atrial
fibrillation)
Brain imaging
(CT scan)
Differentiate between
hemorrhagic lesion,
mass lesion or
ischemic lesion
Laboratory assessment
– Complete blood count
– Basic metabolic panel
– Coagulation studies
– Lipid profile
Evaluate for metabolic
causes of symptoms
and guide for medical
management
Table 34.5 Observation Unit Protocol
16
Diffusion
weighted MRI
Differentiates TIA from ischemic
stroke
Carotid imaging Evaluates for stenosis that would
require carotid revascularization
(MRA vs CTA vs Doppler
Ultrasound)
Cardiac imaging
(e.g.,
echocardiogram)
Evaluates for cardioembolic
source of TIA and for patent
foramen ovale (PFO) allowing for
embolism from venous
circulation
Continuous
telemetry
monitoring
Evaluates for paroxysmal
arrhythmia contributing to
ischemic symptoms or
differential diagnosis
Frequent
neurologic
assessments
Monitors for changing or
evolving symptoms
Patient
education
Education on stroke risk
following transient ischemic
attack, risk factor modification
(blood pressure control, lipid
control, antiplatelet agents) and
smoking cessation counseling
Transient Ischemic Attack (TIA)
038
21:05:24
the source of a patient’s neurologic deficits.5CT
should be performed in the ED prior to admission
to the ED OU as the results have a direct impact
on the need for admission and consultation.
MRI
Diffusion weighted magnetic resonance imaging
(DW-MRI) serves two purposes in the ED OU. It
primarily aids in the diagnostic differentiation
between TIA and st roke. This technique has identified approximately 30% to 67% of patients who
were clinical ly classified as TIA as having evidence of acute ischemia suggestive of stroke.
3, 18
Additionally DW-MRI can assist in the risk
stratification of patients with TIA. While the
exact results have been somewhat variable it has
been consistently sho wn that patients with a
negative DW-MRI are at less than 1% risk for
stroke at 48 hours and 7 days.
18
As DW-MRI is
often not readily available initially in the ED,
patients can be evaluated by MRI as part of the
ED observation protocol.
Vascular Imaging
Intracranial and extracranial arterial stenosis are
risk factors for TIA and stroke. For those with
intracranial artery stenosis the 90-day risk of
stroke is 32.6% for those who also have evidence
of ischemia on DW-MRI and 10.8% for those
without evidence of ischemia on DW-MRI.
3
All
patients evaluated in the ED OU should undergo
imaging to determine the presence or absence of
carotid artery stenosis with a goal of detecting
carotid artery stenosis of > 50%. For patients with
carotid artery stenosis < 50% there is no benefit
to surgical management over medical management in reduction of stroke risk.
1
Carotid artery
ultrasonography, CT angiography or MR angiography can be used to evaluate vascular caliber.
Carotid Artery Duplex Ultrasound
Carotid artery duplex ultrasonography has been
considered the standard imaging modality for
evaluation of carotid artery stenosis. Its major
benefits include lack of radiation and its ability
to evaluate the stiffness of the carotid vasculature.
It is believed that increased stiffness predisposes
to plaque rupture secondary to pulsatile stress
from increased pulse pressure.
2
Carotid artery
duplex ultrasonography has been shown to perform well in the evaluation of 70–99% stenosis
with sensitivities and specificities ranging from
86–89% and 84–87% respectively.
19, 20
Computed Tomography Angiography
CT angiography (CTA) has become a fast, accurate, and noninvasive method of evaluating the
intracranial and extracranial vasculature. It can
be paired with the CT scan that patients receive
in the routine workup of TIA and stroke, and is
widely available .
3
Unlike duplex ultrasonography,
it can provide an evaluation of the anterior and
posterior carotid and cerebral vasculature. The
use of CTA involves additional radiation exposure
and risk for contrast induced nephropathy.
3
However, when compared to ultrasonography, CTA
compared favorably with a reported sensitivity
of 76% and specificity of 94% for 70–99% carotid
artery stenosis.
19
Magnetic Resonance Angiography
Magnetic resonance angiography (MRA) and
contrast enhanced MRA (CE-MRA) are becoming
increasingly available in the evaluation of TIA.
Like CTA, it is able to provide visualization of
the carotid, posterior, and intracranial vasculature. The added benefit to MRA over CTA is
the avoidance of ionizing radiation.
2
The use of
MRA is limited by patient tolerance, previously
implanted metal devices, length of evaluation, and
cost.
3
Various studies have evaluated the performance of MRA compared with gold standard arteriography and other carotid imaging modalities in
the evaluation of 70–99% stenosis. Of all the noninvasive modalities evaluated, contrast enhanced
MRA had the highest sensitivity and specificity of
94–95% and 90–93%.
19,20
One study reported a
sensitivity of 98% and specificity of 100% for
complete arterial occlusion.
20
This data suggests
that MRA (particularly CE-MRA) is the most
effective noninvasive imaging modality in
detecting high-grade carotid artery stenosis.
Cardiac Imaging
It is believed that 20–40% of ischemic strokes are
from a cardiogenic embolism.
2
Various conditions that predispose to thrombus formati on or
embolization include atrial fibrillation, ventricular aneurysm, heart failure with reduced ejection
fraction, valvular heart disease including endocarditis, regurgitation and stenosis, and persistent
foramen ovale (PFO).
3
Matthew Tabbut and Jonathan Glauser
038
21:05:24
Echocardiography is the primary means of
evaluation for potential cardiogenic processes. It
is able to provide not only a structural evaluation
of the heart but a functional evaluation as well.
Transthoracic echocardiography (TTE) is generally considered adequate in the initial evaluation
of TIA in the ED OU for the detection of intracardiac thrombus.
3, 5
ED OU protocol should at
minimum include TTE. If concern exists for cardiac thrombus in patients with a normal TTE, a
trans-esophageal echo can be obtained. This
modality has been shown to be more sensitive
for detection of thrombus particularly in the left
atrial appendage, aortic arch plaque, PFO or atrial
septal aneurysm.
2,3,5
Prevention of Stroke
Medical Management
Antiplatelet agents are considered the mainstay
preventative treatment for atherosc lerotic, ischemic cardiovascular disease. They reduce the risk
for subsequent myocardial infarction, ischemic
stroke, and vascular death.
21
For patients who
have experienced a TIA or stroke there are currently four antiplatelet medications that are
approved by the FDA. These include aspirin,
aspirin/dipyridamole, clopidogrel, or ticlopidine.
1
Aspirin
Aspirin has long been used in the secondary prevention of stroke after TIA or stroke. This cyclooxygenase (COX1) inhibitor of platelet aggregation
has been shown to provide a 15% relative risk
reduction for any type of subsequent stroke.
1, 21
As
with any anticoagulant or antiplatelet agent, there
is a risk of major and minor bleeding events while
taking aspirin; however this risk is smaller than
that of recurrent ischemic stroke.
1
Current guide-
lines recommend 50–325 mg daily.
1
There is no
additional benefit for doses exceeding 325 mg.
Higher doses are associated with a greater risk of
bleeding complications.
22
Even for patients who
experience cerebral ischemic events, increasing
the dosage of aspirin is not recommended.
21
Other
agents have been found to be as effective or more
effective than aspirin. However, aspirin is by far
the least expensive of the antiplatelet agents.
1
Aspirin/Dipyridamole
Dipyridamole is a phosphodiesterase type 5
inhibitor that decreases platelet aggregation and
adhesiveness.
1,22
There have been several studies
performed looking at the effectiveness of dipyridamole alone and in combination with aspirin
or clopidogrel in t he secondary prevention of
stroke. They found the risk of stroke was reduced
more with a combination of aspirin and dipyridamole than with either agent alone.
23, 24
Studies i ndicate that there is no benefit to using
dipyridamole alone; however, when used in combination with aspirin there is a significant benefit
in preventing subsequent stroke.
2, 5, 23, 24
There
was no statistically different rate in major and
minor bleeding complications when both medications were used.
23, 24
Thebenefitoftheaspirin
plus dipyridamole is limited by s ide effects, particularly headache, with the combination.
23,24
Current guidelines indicate that the combinati on
of aspirin plu s extended release dipyridamole
is at least as effective in preventing subsequent
stroke and is an acceptable alternative to aspirin.
1
Given the side effect profile, it is not necessarily
considered the first-line agent.
5
Clopidogrel
Clopidogrel irreversibly inhibits a major adenosine diphosphate receptor on the platelet surface.
It has been used both individually and in combination with aspirin in the prevention of cardiovascular disease.
There have been several major studies comparing the combination of clopidogrel and aspirin
with either aspirin alone or clopidogrel alon e.
Taken in aggregate, studies demonstrate that the
combination of aspirin and clopidogrel has not
been shown to be superior to either agent alone.
21
Clopidogrel has been shown to be equally as
effective as aspirin and aspirin plus extended
release dipyridamole, but has not been shown to
be more effective than either option. Current
guidelines recommend the use of clopidogrel
75 mg daily as monotherapy as an alternative to
aspirin or aspirin plus dipyrimadole, but recommends against the use of clopidogrel plus aspirin.
1
Ticlopidine
Ticlopidine is thienopyridine similar to clopidogrel.
The use of ticlopidine has been limited by the
increased rate of side effects, especially skin
reactions, neutropenia, and thrombotic thrombocytopenia.
1
Ticlopidine is recommended as a
second-line agent for secondary prevention of stroke
and has largely been replaced by clopidogrel.
22
Transient Ischemic Attack (TIA)
038
21:05:24
Observation Recommendations
Patients who are being evaluated in the ED OU
for non-cardioembolic ischemic stroke and not
already taking daily antiplatelet agents should be
started on an antiplatelet agent. Options listed in
the AHA guidelines incl ude aspirin 50–325 mg
daily, clopidogrel 75 mg daily or aspirin/extended
release dipyridamole 25/200 mg twice daily.
Aspirin is typically the first-line agent given its
affordable cost and safety profile. For those who
fail aspirin therapy, there is no need to increase
the dosage beyond 325 mg daily. Changing to a
different a gent can be done in consultation with
a neurologist.
2
Anticoagulation
Cardioembolism accounts for approximately 20%
of ischemic strokes.
1
Anticoagulation has been
shown to be effective in reducing risk of subsequent stroke in patients at risk for cardioembolic
disease. Warfarin has been found to provide a
68% relative risk reduction for subsequent stroke
in patients with atrial fibrillation. This exceeds the
risk of major hemorrhage.
1,2
For patients with previously diagnosed atrial
fibrillation and already on anticoagulation, there
is no evidence that changing levels of anticoagulation, if therapeutic (INR 2–3), will provide any
additional protection against future TIA or stroke.
1
For patients with non-cardioembolic ischemic
disease there is no benefit to anticoagulation compared to antiplatelet agents. Since there is
increased risk of major bleeding for patients being
treated with anticoagulation, AHA guidelines recommend antiplatelet agents rather than anticoagulation for patients with non-cardioembolic
ischemic stroke or TIA.
1
Surgical Management
Carotid artery stenosis is a risk factor for cerebral
ischemic symptoms. Traditionally, stenosis has
been divided into < 30%, 30–49%, 50–69%,
70–99% and total occlusion where 50–69% is considered moderate stenosis and 70–99% is considered high-grade stenosis.
2,25
Symptomatic
carotid artery stenosis has been shown to benefit
from revascularization procedures. Traditionally
CEA has been that procedure of choice. Recently
carotid angioplasty and stenting have become
alternatives to CEA with similar success rates.
1
The exact procedure to be performed is best
determined in consultation with vascular surgery.
A 2011 Cochrane review found that there was no
benefit for surgical intervention over medical
management for patients with carotid artery
stenosis < 50%.
1,25
One study found that patients with high-grade
stenosis had a 30% reduction in their 5-year
stroke risk if they had surgery within 2 weeks of
their TIA.
2
The AHA guidelines recommend CEA
within 2 weeks for patients who have no contraindications to carotid revascularization.
1
Patients
found to have moderate or high-grade carotid
artery stenosis during workup in the ED observation setting benefit from urgent carotid revascularization procedures.
Risk Factor Modification
Hypertension
Hypertension is a risk factor for TIA and stroke.
A decrease in blood pressure is associated with a
lower incidence of recurrent stroke. AHA guidelines recommend an average 10/5 mmHg decrease
in blood pressure.
1
In addition to lifestyle modification (low salt
diet, weight loss, exercise), diuretics with or
without angiotensin converting enzyme (ACE)
inhibition provide benefit.
1
There is little evidence for the utility of blood pressure management in the acute phase. Unless a patient is
experiencing a hypertensive emergency, the
optimization of blood pressure may be accomplished as an outpatient.
1
However if patients
are in need of blood pressure control, a diuretic
and ACE inhibitor can be started prior to discharge from the OU.
Diabetes
Diabetes mellitus is a risk factor for TIA and
stroke. Several studies have been done comparing
standard glycemic control (A1C ≤ 7–7.9%) to
intensive glycemic control (A1C ≤ 6–6.5%) and
have not shown benefit in reducing recurrent
stroke. The AHA guidelines recommend standard
glycemic control.
1
Hyperlipidemia
Cholesterol lowering has been shown to provide
benefit in long-term risk mitigation for patients
who experience a TIA.
2
The AHA guidelines recommend statin therapy with a goal LDL reduction
of at least 50% or absolute level < 70 mg/dL for
Matthew Tabbut and Jonathan Glauser
038
21:05:24
patients who experience ischemic stroke or
TIA and have evidence of atherosclerosis,
LDL 100 mg/dL, and no coronary heart disease
(CHD).
1
LDL goals should be based on the
National Cholesterol Education Program (NCEP)
goal of LDL < 100 mg/dL. Statin therapy may be
initiated upon discharge from the ED OU.
2
Additional Risk Factors
Other risk factors for stroke include tobacco
smoking, significant alcohol consumption,
obesity, and physical inactivity. The AHA guidelines recommend counseling for smoking cessation, reducing consumption of alcohol, weight
loss, and 30 minutes of moderate intensity physical activity as ways of preventing stroke.
1
Patient
education either verbally or video during the
observation stay or written on discharge instructions may help encourage compliance.
2
Disposition
Admission to the OU is predicated on the basis
that patients will be discharged within 24 hours.
14
Consultation
During admission to the ED OU, all patients
should be evaluated by the neurology consult
service. Additionally, patients found to have
reversible causes of TIA and stroke (i.e., carotid
artery stenosis) should be seen by the appropriate
service to expedite further care.
Admission
Approximately 15% of patients will be found to
have high-risk factors discovered that will require
inpatient admission.
16
Factors that require inpatient admission include recurrent neurologic symptoms, evidence of acute ischemia on imaging,
evidence of thromboembolism requiring anticoagulation, evidence of carotid stenosis requiring
urgent revascularization or recommendation of
the neurologist.
16
Discharge
Upon presentation to the ED, patients have a 5%
risk (9.9% using a different methodology) of
stroke in 48 hours and 7% risk in 7 days.
8
Physicians will undoubtedly have varying levels of risk
tolerance, but it is fairly universally held that
patients who can be classified as having < 1% risk
of adverse events are safe for discharge and
follow-up for further outpatient management.
8
For patients who are found to have an unremarkable evaluation in the ED OU the risk of stroke was
found to be 0.96% at 2 days and 1.2% at 7 days.
14
Table 34.6 Risk Factor Modification
1
Antiplatelet
Agent
If patients are not already on an
agent, one should be started
prior to discharge
line)
– Additional options
• Aspirin/dipyridamole
• Clopidogrel
• Ticlopidine (reserved for
intolerance of other
agents)
– Changing agents based on
failure of one agent can be
done at the
recommendation of
neurology
Hypertension Consider starting blood pressure
control if BP > 140/90 mmHg
– Encourage lifestyle
modification
– First-line therapy: Diuretic
– Additional Coverage:
Diuretic + ACEI
(angiotensin-converting
enzyme inhibitor)
– Goal: reduction of 10/5
mmHg
Glycemic
Control
Manage diabetes according to
existing guidelines
– Lifestyle modification
– Oral agents
– Insulin
Hyperlipidemia Consider starting statins if
LDL100 mg/dL
– Target 50% decrease
LDL-C or
– LDL-C < 70 mg/dL
Smoking Patients should be counseled
in smoking cessation
Lifestyle
Modifications
Patients should be counseled
about lifestyle modification
– 30 minutes of moderate-
intensity physical
activity daily
– weight loss
Transient Ischemic Attack (TIA)
038
21:05:24
For those who have undergone DW-MRI and
foundtohavenoevidenceofischemia,stroke
risk is < 1%.
18
Patients who complete the observation protocol for T IA who have no recurrent
deficits, a negative workup and normal serial
exams can be discharged after neurology c onsultation. If patients are not already on
an antiplatelet agent prior to admission, they
should be started on an appropriate agent.
1
For
a summary of the discharge management see
Table 34.6.
Follow-Up
Patients discharged from the ED OU are still in
need of urgent follow-up for long-term risk
factor modification as the ongoing risk of stroke
beyond the acute phase is related to vascular
risk factors.
15
Patients with carotid artery
stenosis not requiring immediate admission
should be given urgent follow-up with vascular
surgery. When discharged, patients should
be given appropriate return instructions that
include warning symptoms for recurrent ischemic symptoms.
Summary
The evaluation and management of TIA in the ED
observation setting is primarily concerned with
mitigation of future stroke risk as disability from
stroke places a major burden on patients, families,
and the health care system. In the ED, patients
should be evaluated for TIA mimics and factors
that require immediate inpatient admission. The
workup prior to ED OU admission should at
minimum consist of glucose check, electrocardiogram (EKG), head CT, and a basic laboratory
assessment. Patients on discharge should be
started on an appropriate antiplatelet or anticoagulation therapy and be educated about risk factor
mitigation.
Cerebral ischemia is a time-sensitive disease.
Emergency physicians will play an increasing role
in TIA care and prevention of disability from
subsequent stroke.
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RJ, et al. Guidelines for the
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Transient Ischemic Attack (TIA)
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Subpart IVD
Chapter
35
Clinical – Neurologic
Headaches
Sharon E. Mace, MD, FACEP, FAAP
Introduction
Headaches are extremely common. During a
given year, nine out of ten people (90%) suffer
from headaches.
1
Headache is the chief complaint
in 1–4% of emergency department (ED)
patients,
2–4
which accounts for approximately
5 million ED visits each year.
4,5
More than
45 million Americans suffer from chronic, recurring headaches.
6
Of the two most common head-
aches,
7
tension headaches have an annual
prevalence of 11% with 78% of adults suffering
from a tension headache at some point in time,
2
while migraine headaches affect 18% of American
women and 7% of American men with an estimated 28 million individuals with migraines in
the United States.
8
One-third of the US population will suffer from a migraine headache in their
lifetime.
8
Approximately 70% of all headache suf-
ferers are women.
6
Headaches are the most common neurologic
disorder, followed by stroke, Alzheimer’s disease
and seizures.
9,10
Headache is the ninth most
common cause of physician visits.
8
Headache is
the most frequent complaint in children and adolescents.
11
About 20% of the pediatric population
has a significant headache.
6
Headaches are the
number one reason for absenteeism from work
and school. Migraine sufferers alone miss more
than 157 million work and school days every year
because of headaches.
6
Headache, or cephalgia, is defined as a pain
anywhere in the region of the head or neck. There
are a multitude of conditions that can lead to a
headache. Most of the causes of headache are
benign and self-limited; although the pathology
responsible for some headaches, such as meningitis, subarachnoid hemorrhage (SAH) or increased
intracranial pressure from a tumor or other
causes, can lead to major complications and even
death if undiagnosed and untreated. It is estimated that 3.8% of ED patients with a headache
have a serious or life-threatening etiology for their
headache,
4
although an older study noted 17% of
patients had significant lesions.
3
The key is to differentiate the benign headache
from the headache due to a significant or serious
pathology, which can be quite difficult,
2,3
as
evidenced by studies of SAH as an example.
12,13
Of patients with SAH, 23% were not diagnosed on
their initial presentation to the ED.
12
In another
study of SAH, one-third of patients died before
reaching the ED and another 25% of patients died
after having seen a physician for their headache.
13
The purpose of an observation stay is to identify those with a life-threatening etiology for their
headache, while concurrently managing the
patient’s headache pain and, if possible, begin
specific treatment for the underlying etiology of
the headache.
3,14
Primary and Secondary Headaches
Headaches are categorized into primary and secondary headaches.
4
Primary headaches account
for more than 90% of all headaches. Tension
headaches and migraines are the most common
primary headaches, while the other primary headaches, cluster headaches and trigeminal autonomic neuralgias, are much less common.
Secondary headaches are caused by an underlying condition or disease, which range from headaches due to any injury or painful condition of the
head, neck or facial structures including the temporomandibular joints (TMJ), jaws, teeth, ears/
nose/throat (ENT) structures (e.g., sinuses. ears,
nasopharynx), head or neck musculature, to major
intracranial disease or injury such as an intracranial bleed, malignancy, increased intracranial pressure, inflammatory disease (central nervous system
[CNS] sarcoid, Behcet’s disease, as examples) or
infection (e.g., meningitis, encephalitis).
Secondary headaches also include headaches
due to medications (from use, ingestion, or
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