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.