Either decreased mental status or cranial

nerve dysfunction can compromise airway protection.

Check for spontaneous swallowing. Do not test gag reflex

as this may induce vomiting.

Note the patient's vital signs and breathing pattern. Low

blood pressure can mimic stroke symptoms. High blood pressure may be a cause or compensation. If you choose to lower

blood pressure later, it will be important to know the presenting baseline pressure. Cheyne-Stokes or apneustic breathing

may indicate severe brain injury. Hypoxia can cause strokelike symptoms in the absence of a actual vascular occlusion.

Other important questions to answer on the physical

examination include the following. Is the rhythm irregular

(atrial fibrillation)? Are there murmurs to indicate valvular

disease? Is there peripheral evidence of emboli (splinter

hemorrhages in nails, on the retina)? Are carotid pulses

palpable? Is there a bruit, indicating possible dissection or

plaque as a source of emboli?

Is there a fever? CNS infections can be confused with

stroke. Hypotension from sepsis can cause hypoperfusion and

mimic stroke. Is there evidence of head trauma or other injury?

Neurologic examination need not be comprehensive

initially. Tools such as the National Institute of Health

stroke scale (NIHSS) are available to "quantify" the

extent of the stroke and are widely available ( Table 82-2).

Table 82-2. National I nstitute of Health stroke sca le.

Category Patient Response Score

LOC questions Answers both correctly 0

Answers one correctly 1

Answers none correctly 2

LOC commands Obeys both correctly 0

Obeys one correctly 1

Obeys none correctly 2

Beat gaze Normal 0

Partial gaze palsy 1

Forced deviation 2

Best visual No visual loss 0

Partial hemianopsia 1

Complete hemianopsia 2

Bilateral hemianopsia 3

Facial palsy"' Normal 0

Minor facial weakness

Partial facial weakness 2

No facial movement 3

Best motor arm No drift 0

Right Drift <1 0 seconds

Left Falls <1 0 seconds 2

No effort against gravity 3

No movement 4

Best motor leg No drift 0

Right Drift <5 seconds 1

Left Falls <5 seconds 2

No effort against gravity 3

No movement 4

Limb ataxia* Absent 0

Ataxia in 1 limb

Ataxia in 2 limbs 2

Sensory No sensory loss 0

Mild sensory loss 1

Severe sensory loss 2

Neglect Absent 0

Mild 1

Severe 2

Articulation Normal 0

Mild 1

Severe 2

Language Normal 0

Mild aphasia 1

Severe aphasia 2

Mute or global aphasia 3

LOC, level of consciousness.

''Items deleted from the modified N I HSS.

CHAPTER 82

Do not delay imaging to perform the complete examination.

The details can be obtained after the computed tomography (CT). Focus on key components, including:

Level of consciousness. Is the patient alert, lethargic,

obtunded, or stuporous? Rapid decline may indicate

herniation.

Eye exam. Asymmetric pupils may indicate herniation or

midbrain involvement. Papilledema indicates increased

intracranial pressure or hypertensive encephalopathy.

Retinal hemorrhages or pale spots indicate emboli. Is there

a gaze deviation? Is there evidence of nystagmus?

Cranial nerve exam. The brainstem is a tightly packed

area, and it is extremely rare to have a stroke that involves

only one cranial nerve. Cranial nerve palsies on one side of

the body and contralateral motor/sensory findings are a

hallmark of brainstem strokes.

Motor exam. Assess for asymmetric weakness and classify

as normal, weak, or not moving at all. Check to see if the

deficit is greater in the face/arm distribution (MCA) or the

leg (ACA) or both (carotid bifurcation). Checking for pronator drift is a sensitive test for subtle weakness.

Sensory exam. Compare sensation to pain and light touch

bilaterally. The sensory exam is often limited by neglect,

receptive aphasia, or mental status. Subtle sensory deficits

may be uncovered by checking for extinction to bilateral

simultaneous light touch on the arms, legs, and face.

Reflexes. Initially reflexes are decreased in the involved

regions. Hyperreflexia may indicate old strokes. Assess for

asymmetric release reflexes such as a Babinski sign or myoclonic jerking when feet are pushed dorsally.

Cerebellar exam. If safe, have the patient walk. Look for

wide or narrow gait and perform a Romberg test. Check for

smooth controlled finger-to-nose, knee-heel-shin, and

rapid alternating movements to test cerebellar fine motor

control.

DIAGNOSTIC STUDIES

� Imaging

Noncontrasted head CT is currently the test of choice for

the initial evaluation of stroke patients. Most acute strokes

are not visible on CT. Its role is not to "rule in stroke;' but

rather to rule out other entities that would be a con traindication to fibrinolytic reperfusion therapy. Bleeding is an

obvious contraindication to fibrinolytics. Large strokes

that show early ischemic changes (edema) on the CT scan

are more likely to convert to hemorrhagic strokes and thus

are a relative contraindication to fibrinolytic treatment.

Plain CT is very sensitive for bleeding or mass effects from

other intracranial lesions (Figure 82- 1 and 82-2).

� Laboratory

Important lab studies include rapid blood glucose and coagulation studies (prothrombin time, partial thromboplastin

time). These must be ordered as quickly as possible after

Figure 82-1. CT sca n showing an ischemic

stroke. Note the hypodense area anterior and to

the right of the fourth ventricle (arrow).

Figure 82-2. CT sca ns showing hemorrhagic

stroke (a rrow).

patient arrival. Other common tests include complete blood

count, electrolytes, and renal function. Electrocardiogram

and cardiac enzymes are often ordered to assess for cardiac

causes of the event.

CEREBROVASCULAR ACCIDENT

PROCEDURES

No special procedures are required in stroke patients. It is

important, however, to avoid doing procedures that could

complicate the course of fibrinolytic treatment. Any central

lines should be placed in areas where bleeding can be

monitored and controlled with compression (jugular or

femoral, not subclavian). Peripheral IVs are preferred.

Do not perform a lumbar puncture unless there is a strong

suspicion of subarachnoid hemorrhage or meningitis as

the cause of symptoms.

MEDICAL DECISION MAKING

The first decision that should be considered with an ischernie stroke is eligibility for fibrinolytic reperfusion therapy (Figure 82-3). Critical factors include the following:

1. Is this truly an ischemic stroke (vs hemorrhagic or

other stroke mimic)?

2. Is the time of the onset of symptoms clear?

3. Are there exclusion factors?

4. Is your institution capable of TPA administration, or

do you need to transfer the patient to a stroke center?

History Er physical exam to distinguish typica l

stroke syndromes versus alternative causes

Assess for possibil ity of

thrombolysis

airway

compromise

Admit to general or

telemetry floor

Large infarct with

edema, sh ift and

possibility of ai rway

compromise

Neurosurgical

consultation

Figure 82-3. Cerebrovascu lar accident diagnostic algorithm. BP, blood pressure; CT, computed

tomography; ICU, intensive care unit.

CHAPTER 82

TREATMENT

First, do no harm. Limit further damage by paying attention to the details of supportive care. Intubate if the patient

is unable to protect his or her airway. Provide s upplemental oxygen for hypoxia (generally for 0 2 sats <95%; there is

some evidence that hyperoxia can worsen neuronal damage

by free radical oxidation). In addition, administer IV fluids

if the patient appears hypovolemic or is hypotensive. Aim

for euvolemia; volume overload can worsen cerebral

edema. Severely anemic patients may need blood transfusion to assure good oxygen-carrying capability. Be very

cautious lowering blood pressure, if you lower it at all.

Hypotension is much worse than hypertension. Blood

pressure control for ischemic strokes is not warranted

unless pressures are sustained above 220/120 mmHg.

Blood pressure control for hemorrhagic strokes has less

evidence, but many recommend controlling any blood

pressure over 1 50/90 mmHg.

� Ischemic Strokes

For patients with ischemic strokes or TIA, aspirin (325 mg

orally) helps prevent platelet aggregation. Do not give until

you assure that the patient does not have an intracranial

hemorrhage. If you think the patient might receive fibrinolytics, hold the aspirin for the first 24 hours. Consult a

neurologist and/or stroke team whenever available. If fibrinolytic therapy is administered, the FDA-approved dose is

Reteplase (rTPA) 0.9 mg/kg (max dose 90 mg). Ten percent

should be administered as a bolus, with the remainder of

the infusion over the next hour. Intensive care monitoring

is need for the first 24 hours after treatment. Any worsening of condition should prompt immediate cessation of the

infusion and repeat head CT.

� Hemorrhagic Stroke

Mitigate elevated intracranial pressure by elevating the

head of the bed to 30 degrees. Treat coagulopathy. Patients

on warfarin with high international normalized ratios

should be reversed with fresh-frozen plasma or prothrombin complex concentrate and vitamin K. Do not give

aspmn. Consult neurosurgery. Many intracerebral clots

will benefit from early clot evacuation. Implement seizure

precautions and consider antiepileptic administration in

consultation with the admitting team.

DISPOSITION

� Admission

All stroke patients should be admitted to the hospital.

Patients with large strokes, evidence of edema on CT scan,

or decreases in mental status are at high risk for decompensation and should be admitted to an intensive care unit

(ICU). All patients who receive fibrinolytic therapy should

be monitored in the ICU for the first 24 hours after treatment. Patients with evidence of arrhythmias or other car ­

diac causes for the stroke should be admitted to a

monitored setting. Patients with hemorrhagic strokes

should be admitted to an ICU setting with neurosurgical

consultation. In many hospitals, this will mean transfer to

a facility with higher levels of care. Patients with TIA

symptoms should be admitted to the hospital for an expedited evaluation.

� Discharge

Stable patients with obvious nonstroke etiologies may be

discharged home if other medical conditions do not war ­

rant admission. Ensure that the patient has a safe social

situation and appropriate follow-up.

SUGGESTED READING

G o S , Worman DJ. Stroke, transient ischemic attack and cervical

artery dissection. In: Tintinalli JE, Stapczynski JS, Ma OJ,

Cline DM, Cydulka RK, Meckler GD. Tintinalli's Emergency

Medicine: A Comprehensive Study Guide. 7th ed. New York,

NY: McGraw-Hill, 20 1 1, pp. 1 122-1 135.

Hoffman JR, Schriger DL. A graphic reanalysis of the NINDS

Trial. Ann Emerg Med. 2009;54:329-336.e35.

Tissue plasminogen activator for acute ischemic stroke. The

National Institute of Neurological Disorders and Stroke r t-PA

Stroke Study Group. N Eng! J Med. 1 995;333: 1581-1 588.

Seizu res and Status

Epilepticus

Amer Zia Aldeen, MD

Alison R. Foster, MD

Key Points

• Always check a bedside glucose level in seizure

patients.

• Monitor airway, breathing, and circulation in actively

seizing patients and intervene when needed.

INTRODUCTION

A seizure is an episode of abnormal neurologic function

caused by inappropriate, excessive activation of neurons in

the brain. Seizures account for up to 2% of emergency department (ED) visits and affect approximately 4 million people in

the United States. The incidence of seizures is highest among

those <20 and >60 years of age. Status epilepticus is continuous or intermittent seizure activity for more than 5 minutes

without recovery of consciousness. It has a mortality rate of

up to 20%. Half of all patients presenting to the ED in status

epilepticus have no prior history of seizures. ED management

of seizures should focus on cessation of seizure activity.

Seizures result from abnormal excitation or lack of inhibition of neurons in the brain. The cause may be primary

(idiopathic) or secondary, with an underlying etiology that

may be treatable such as hypoglycemia. In patients with a

known seizure disorder, the most common cause of recurrent seizures includes medication noncompliance, sleep

deprivation, alcohol or substance withdrawal, and infection. Secondary causes of seizures include head trauma,

stroke, intracranial infection or mass, electrolyte abnormalities, alcohol withdrawal, drug overdose, and eclampsia.

Seizures are classified as generalized or partial.

Generalized seizures are characterized by excitation of the

entire cerebral cortex and always cause alteration of mental

status. Generalized seizures can manifest as a staring spell

• Intravenous lorazepam is the drug of choice for actively

seizing patients.

• Search for a secondary cause of seizures in first-time

seizure patients and those with a known seizure

disorder who have new or different features.

(absence or petit mal), diffuse motor activity (tonic-clonic

or grand mal), or drop attacks (myoclonic, tonic, clonic, or

atonic). The postictal period refers to the time (lasting up

to 1 hour) after a generalized seizure when the patient

gradually returns to baseline mental status. The postictal

period often distinguishes generalized seizures from other

causes of sudden altered mental status such as syncope.

Partial seizures are caused by localized neuronal activation

that may remain localized or spread to involve other areas of

the brain (referred to as partial seizure with secondary generalization). Patients with simple partial seizures experience

brief focal motor or sensory symptoms without altered

mental status. Complex partial seizures are characterized by

altered consciousness with autonomic, sensory, motor, and/

or psychological manifestations (Table 83-1).

CLINICAL PRESENTATION

� History

While the history is performed, obtain a blood glucose level

in all patients with altered mental status, including those

suspected of having had a seizure. Hypoglycemic seizures

are easily treated with dextrose and do not respond to standard antiepileptic drugs. To determine whether a seizure

actually occurred, gather a complete and detailed history

from witnesses, emergency medical service, and the patient.

353

 

PROCEDURES

The Dix-Hallpike maneuver can be used to elicit BPPV and

differentiate it from a central cause for vertigo. The procedure involves rapidly moving the patient from a seated to

supine position with the head rotated 45 degrees to the

right with the eyes open. If no symptoms are elicited,

the procedure should be repeated with the head rotated to

the left. The latency, duration, and direction of nystagmus

and presence of vertigo should be noted. With BPPV, the

nystagmus is horizontal or rotatory, has a latency period

(up to 60 seconds), is fatigable, and suppresses with

fixation (Figure 81-2).

MEDICAL DECISION MAKING

The ED evaluation of dizziness requires a broad differen ­

tial diagnosis encompassing benign diagnoses such as labyrinthitis associated with an upper respiratory infection to

DIZZIN ESS

.A. Figure 81-1 . CT sca n showing cerebellopontine

angle tumor (acoustic neuroma).

life-threatening emergencies such as cerebellar infarct or

hemorrhage. The history and physical examination may

lead to a diagnosis or point toward the need for further ED

evaluation and possible admission (Figure 81-3).

TREATMENT

The treatment of patients with dizziness in the ED is

dictated by the working diagnosis after evaluation.

Peripheral vertigo is treated based on the suspected cause.

BPPV can be treated in the ED with canalith repositioning

maneuvers. The Epley maneuver is used to reposition the

particulate debris from the semicircular canal to the utricle

(Figure 81-4). Once the debris is repositioned, the abnormal vestibular input is eliminated. Multiple attempts at

this procedure may be necessary. Vestibular suppressant

medications are also used to decrease abnormal input from

the affected semicircular canal (Table 81-3). For other

Table 81-3. Vestibular suppressant therapy.

Class

Antihistamine

Antiemetic

Benzodiazepines

Medication

Meclizine

Promethazine

Diazepam

Dose

25 mg PO q 8 hr

25 mg PO q 6 hr

2-5 mg PO q 8 hr

CHAPTER 81

A

B

Superior

Posterior canal ampulla

Utriculus

Particles

Superior

canal

Utriculus

.&. Figure 81·2. Dix-Hall pike maneuver to el icit benign positional vertigo (origi nating in the

right ear). The maneuver begins with the patient seated and the head turned to one side at

45 degrees (A), which aligns the right posterior semicircu lar cana l with the sag itta l plane of the

head. The patient is then helped to recline rapidly so that the head hangs over the edge of the

table (B), sti ll turned 45 degrees from the midline. With in several seconds, this el icits vertigo

and nystagmus that is right beati ng with a rota ry (cou nterclockwise) component. If no nystagmus is elicited, the maneuver is repeated after a pause of 30 seconds, with the head turned to

the left. Treatment with the canal ith repositioning maneuver is shown in Figure 81-4. Reprinted

with permission from Ropper AH, Samuels MA. Chapter 1 5. Deafness, Dizziness, and Disorders

of Eq uil ibrium. In: Ropper AH, Samuels MA, eds. Adams and Victor's Principles of Neurology.

9th ed. New York: McG raw-Hill, 2009.

Meniere's

disease,

labyrinthitis,

vestibular

neuritis

Vestibular suppressant therapy

Outpatient ENT referral

DIZZIN ESS

ECG,

card iac

workup.

Dysrhythmia,

valvular hea rt

disease

Admission

abnormal vita l

sig ns, or other

nonspecific

symptoms

Hemoglobin,

el ectrolytes,

renal

function,

medication

list

.A Figure 81-3. Dizzi ness diag nostic algorithm. BPPV, benign paroxysmal positional vertigo; CT, computed

tomography; ECG, el ectroca rdiogram; TIA, transient ischemic attack.

causes of peripheral vertigo such as Meniere disease, labyrinthitis, and vestibular neuronitis, vestibular suppressant

medications are the mainstay of treatment.

Patients with vertigo from central causes ( CNS tumor,

bleed, or infarct) should have appropriate neurology or

neurosurgical consultation in the ED. Patients suspected of

having vertebrobasilar insufficiency should be started on

aspirin, and follow-up (inpatient vs outpatient) decisions

should be made in consultation with their primary

physician.

Patients with cardiovascular risk factors and presyncope

are treated similar to patients with syncope and may

require a telemetry admission to exclude an arrhythmia

(see Chapter 19, Syncope). Patients found to have

noncardiac causes of presyncope, such as dehydration or

anemia, are treated accordingly with fluids and/or blood

transfusion.

Patients with symptoms of disequilibrium or nonspe ­

cific lightheadedness with an unremarkable ED evaluation

may be discharged home after consultation with their

primary physician. As the majority of these patients are

elderly, patients should be assessed for fall risk and home

safety before discharge. Vestibular suppressants should

never be used in these patients because these drugs can

exacerbate their symptoms.

DISPOSITION

� Admission

Patients with central vertigo, focal neurologic findings, a

possible cardiovascular cause (arrhythmia, ischemia), an

electrolyte abnormality, or anemia should be admitted to

the hospital.

A

canal

B

c

D

CHAPTER 81

Utriculus Posterior

Particles

canal

ampulla

Posterior canal

Figure 81-4. Bedside maneuver for the treatment

of a patient with benign paroxysmal positional vertigo

affecting the right ear. The pr

esumed position of the

debris within the labyrinth during the maneuver is

shown on each panel. The maneuver is a 4-step

procedure. First, a Dix-Hallpike test is performed with

the patient's head rotated 45 degrees toward the

(affected) right ear and the neck slightly extended

with the chin poi nted slightly upward . This position

resu lts in the patient's head hanging to the right

(A) Once the vertigo and nystagmus provoked by this

maneuver cease, the patient's head is rotated about

the rostr

a l-caudal body axis until the left ear is down

(B) Then the head and body are further rotated until

the head is almost face down (C) The vertex of the

head is kept ti lted upward throughout the rotation. The

patient should be kept in the final, facedown position

for about 10 to 15 seconds. With the head kept turned

toward the left shoulder, the patient is brought into

the seated position (D) Repri nted with permission

from Rapper AH, Samuels MA. Chapter 1 5. Deafness,

Dizziness, and Disorders of Equil ibrium. In: Rapper AH,

Samuels MA, eds. Adams and Victor's Principles of

Neurology. 9th ed. New York: McGraw-Hilt 2009. � Discharge

Patients with peripheral vertigo may be discharged home.

ENT follow-up may be necessary if the symptoms are

persistent or recurrent. Patients with nonspecific symp

­

toms without serious comorbidities and a normal ED

work-up may be discharged after follow-up with their

. primary physician has been arranged.

Part1cles

Superior canal

SUGGESTED READING

Goldman B. Vertigo and dizziness. In: Tintinalli JE, Stapczynski

JS, Ma OJ, Clince DM, Cydulka, RK, Meckler GD. Tintinalli's

Emergency Medicine: A Comprehensive Study Guide. 7th Ed.

New York, NY: McGraw-Hill, 201 1.

Cerebrovascu lar Accident

Tom Morrissey, MD

Key Points

• Time is brain. Time of symptom onset is key to acute

stroke treatment.

• Hypoglycemia and hypoxia can mimic stroke. Assess

and treat these conditions early in the eval uation of

patients with stroke-like symptoms.

INTRODUCTION

Roughly 750,000 strokes occur annually in the United States,

and this will increase as the population ages. Physical, emotional, and economic damages are multifactorial. The cost of

initial care is only the beginning. Many stroke s urvivors are

not only unable to return to work, they are unable to care for

themselves, placing heavy demands on family and friends.

Stroke is defined as a neurologic deficit resulting from the

interruption of blood supply to neuronal tissue. The brain is

highly metabolically active, consuming roughly 25% of cardiac

output, but has no mechanism for storing energy reserves. This

makes it extremely sensitive to even transient interruption in

its supply of oxygen and glucose. Vascular oomprornise may be

caused by several different mechanisms, but the final oommon

pathway is impaired neuronal perfusion and tissue starvation.

Strokes are often classified in 2 different ways: etiology

and location. Etiologic causes can be classified as either

hemorrhagic or ischemic. Hemorrhagic strokes account for

1 0-20% of all strokes. They sometimes result from the rupture of an aneurysm or arteriovenous malformation (AVM),

usually causing bleeding on the surface of the brain. More

commonly, the bleeding comes from disruption of an intracerebral arteriole, leading to bleeding inside the parenchyma

of the brain. Uncontrolled hypertension is the most

common precipitant of intracerebral bleeding, but other

• Resist the urge to aggressively lower blood pressure. Hypertension is the body's attempt to mainta in perfusion

to ischemic tissue. Hypotension can make things worse.

• Transient ischemic attack (TIA) is a warn ing of a stroke

to come (aborted stroke). Treat TIAs seriously and work

up risk factors expediently.

conditions such as amyloidosis and tumors can increase the

chances of intracerebral bleeding. Vasospasm can occur

from the irritant effects of blood on the surface of the brain,

leading to an even greater decrease in blood flow.

Ischemic strokes are caused primarily by thrombosis of

a blood vessel, very similar to mechanisms involved in myocardial infarction. Conditions such as atherosclerosis,

hypercoagulable states, polycythemia, and vasculitis are

common precipitants. About 20% of ischemic strokes result

from embolic phenomenon. The carotid bifurcation is a

common source of plaque embolism. Cardiac mural thrombus and valve disease are also likely sources of embolism.

Classification by location depends on the blood vessel or

vascular distribution involved (Table 82-1). The blood supply

to the brain comes from paired carotid and vertebral blood

vessels. The carotid distribution (ie, anterior circulation) supplies primarily cerebral and cortical structures, whereas the

vertebrobasilar vascular distribution (ie, posterior circulation)

feeds the cerebellum and brainstem structures. The involved

vessel can often be inferred from the clinical presentation.

Carotid circulation strokes commonly present with motor and

sensory deficits that are fairly obvious. Visual field defects,

neglect, and language difficulties (eg, aphasia) are often apparent on exam. The internal carotid bifurcates into the anterior

carotid artery (ACA), which feeds areas involved in control of

the leg, and the middle carotid artery (MCA), which feeds areas

347

CHAPTER 82

Table 82-1. Vascular supply of common strokes.

cerebral

Circulation Vascular Supply Motor Manifestation Sensory Manifestation Speech

Anterior Anterior cerebral artery Contralateral weakness of leg > Minimal discrimination deficits. Perseveration

circulation arm (face and hand spared)

Middle cerebral artery Contralateral weakness of face Contralateral numbness of face Aphasia, if dominant

and arm > leg and arm > leg hemisphere is involved

(left in 80% of patients)

Posterior Posterior cerebral artery Minimal motor involvement Visual abnormal ities, light touch,

circulation (supplies visual cortex) and pinprick affected (patient

often unaware of deficits)

Vertebral and basilar artery Hallmark is crossed deficits (ipsi lat-

(supplies brainstem and eral cranial nerve deficits with

cerebel lum) contralateral motor weakness)

Vertebrobasilar artery ischemia Cranial nerve palsies, limb weak- Dizziness, vertigo, ataxia Dysarthria

ness, diplopia

Cerebellar artery Drop attack

Lacunar Penetrating arteries (ischemia

infarction of thalamus and internal

(4 types) capsule)

Motor Face, arm, and leg

Sensory

Clumsy hand Clumsiness of one hand

dysarthria

Ataxic Hemiparesis

hemiparesis

more involved in control of the face and arm. Smaller branches

penetrate deeper into areas such as the internal capsule. Strokes

in these vessels can give pure sensory or motor deficits.

Vertebrobasilar strokes cause ischemia in the brainstem or

cerebellum. Large brainstem strokes are usually fatal. Smaller

ones can lead to cranial nerve dysfunction and more subtle

findings, such as vertigo_ Cerebellar strokes can be much harder

to recognize, emphasizing the importance oflooking for ataxia,

balance, and fine motor control on the neurologic exam. These

signs are often not noticed by the patients themselves.

Until the mid 1990s, the treatment for acute ischemic

stroke was almost entirely supportive care. In 1996, the

Food and Drug Administration (FDA) approved the use of

tissue plasminogen activator (TPA). Some facilities are

employing intravascular catheter-guided clot lysis or evacuation. With the availability of these newer treatments, stroke

patients now rank as true medical emergencies that warrant

the focused resources of the emergency department (ED).

With the time dependency of treatment options, much

work has gone into increasing public awareness of stroke

and enhancing prehospital recognition and transport.

Many hospitals have developed dedicated stroke teams and

stroke protocols to expedite care of acute stroke patients.

Transient ischemic attacks ( TIAs) are defined as "a transient episode of neurologic dysfunction caused by focal

Vertigo

Dysarthria

Pure hemisensory deficit

Dysarthria

Ataxia on same side as

weakness

brain, spinal cord or retinal ischemia, without acute infarc ­

tion." Symptoms typically last less than 1-2 hours. These

patients should be assessed and treated as acute strokes, with

the exception of fibrinolytic treatment. TIAs are the equivalent of unstable angina in coronary disease and should be

treated as "warning signs of strokes to come." Some studies

estimate as many as 20% of TIA patients will s uffer a stroke

within 90 days, half of which may occur within 48 hours.

CLINICAL PRESENTATION

� History

Reperfusion strategies are both time-and situation-dependant.

Gathering accurate historical information as quickly as possible is a critical facet of treatment_ Issues such as aphasia and

cognitive dysfunction can make it very difficult to get information directly from the patient. Make efforts to contact

others (family, nursing home staff) who can provide historical

details. Hemineglect and gaze deviation may cause patients

not to be aware of you. Be sure you are in the patient's line of

sight and touch them while you are talking to them.

One of the most important historical considerations is to

determine when the symptoms began. If the patient had

symptoms on awakening, or cannot clearly identify the time

they started, the start time is considered the last time the

CEREBROVASCULAR ACCIDENT

patient was seen as normal. The "time last known well" is

important to obtain early because it will determine whether

fibrinolytics will be considered. The window to administer

fibrinolytics intravenously (IV) is usually an onset of symp ­

toms within the last 3 hours. If fibrinolytics are being considered, ask about contraindications to their administration. Is

there a history of previous intracranial bleeding? Brain tumor?

Head injury? Recent surgery? Is the patient on anticoagulants?

Ask the patient how he or she noticed the symptoms

and what he or she was doing when it started. Is the patient

dizzy, off balance, or falling? Is the patient having pain or

weakness or both? Has the patient had these symptoms

before? Extremity pain is an unusual feature of a stroke and

suggests an alternate diagnosis. Onset of symptoms with

severe headache, seizure, and syncope suggests a hemorrhage stroke. Neck pain or history of neck trauma or

manipulation may indicate carotid or vertebral dissection.

When assessing the past medical history, determine

whether a stroke mimic is possible. Diabetic patients may

be presenting with hypoglycemia. Patients with a history of

seizures may be postictal. Patients with a history of

migraines may also present with stroke-like symptoms.

Lastly, elicit risk factors for stroke. Atrial fibrillation and

valvular disease are common risk factors for emboli. Diabetes

and hypertension are risk factors for thrombotic strokes.

..... Physical Examination

As with history, extensive physical exam should not delay

imaging and treatment. Focus on the airway, breathing,

and circulation (ABCs) and pertinent neurologic findings.

Of greatest importance is the patient's ability to protect his

or her airway.