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Chapter 12 • Dizziness 151
https://t.me/med1917
Timing
Vertigo that occurs on rst arising in the morning is
usually the result of a vestibular disorder. Vertigo
that occurs while turning over in bed is characteristic
of benign paroxysmal positional vertigo (BPPV)
(peripheral).
What do characteristics of the episodes
tell me?
Key Questions
n How long do the episodes of dizziness last?
n Is the onset sudden or gradual?
n Do you have any hearing loss?
n Do you have ringing in your ears?
Duration of Episodes
Episodes that last a few seconds are typically caused
by BPPV and are usually elicited by a rapid head
movement. Episodes lasting minutes to hours can be
caused by Meniere disease or recurrent vestibulopathy.
Episodes that last days or weeks are commonly
produced by vestibular neuronitis. Patients can feel
better when they lie completely still. Stroke can also
produce longlasting episodes. The two can be differ
entiated based on medical history and physical exami
nation ndings.
Sudden onset of prolonged dizziness (lasting
$60 minutes) suggests central causes, such as infec
tion, brainstem infarction, inammation, or vestibular
hemorrhage. Trauma can also produce prolonged diz
ziness.
The child with chronic recurrent dizziness (epi
sodes lasting ,30 minutes) can have central causes,
such as seizure problems or migraine headache. The
cause can also be peripheral, such as BPPV. Chronic
persistent episodes can indicate brainstem lesions,
anemia, diabetes, thyrotoxicosis, or a psychosomatic
disorder.
Onset
A gradual onset of dizziness is typical of an acoustic
neuroma or other neoplastic process that is slow
growing. BPPV can also have a gradual onset.
Acute or sudden onset of vertigo is characteristic
of labyrinthitis, Meniere disease, stroke, or vertebro
basilar causes.
Recurrent episodes are typical of BPPV, vertebro
basilar causes, and Meniere disease.
Hearing Loss and Tinnitus
A classic triad of symptoms—vertigo, hearing loss,
and tinnitus—denes Meniere disease. Patients can
also report a sensation of fullness in the ears. The hear
ing loss can be unilateral or bilateral. Patients with
secondary or early tertiary syphilis can have symptoms
identical to those of Meniere disease. Tinnitus, hearing
loss, and pain in the ear point to lesions in the inner ear
or cranial nerve VIII.
Patients with labyrinthitis and perilymphatic stu
las can also experience hearing loss but without tin
nitus. An acoustic neuroma will produce unilateral
hearing loss with tinnitus. Patients with recurrent
vestibulopathy usually do not report hearing loss.
What else should I consider?
Key Questions
n What medications are you taking?
n Are you now or have you recently been ill?
n Have you had any recent injury to your head? Did
you have dizziness before the head injury?
n Have you had any previous ear surgery?
Medications
Mediations that are saltretaining or ototoxic can
produce vertigo, lightheadedness, or unsteadiness.
Saltretaining drugs include steroids and phenylbuta
zone. Ototoxic medications include ethacrynic acid,
streptomycin, gentamicin, aminoglycosides, aspirin,
and furosemide.
Psychotropic drugs can also produce vertigo. Anti
hypertensive drugs can cause hypotension leading to
lightheadedness. Sedatives, alcohol, and anticonvul
sants can cause a sense of disequilibrium.
Current or Recent Illness
Vestibular neuronitis is associated with recent viral
infection, often an upper respiratory tract infection. If
a patient is currently ill, consider labyrinthitis because
it is frequently associated with concomitant bacterial
and viral infection. Current ear or sinus infection can
produce dysfunction of the vestibular apparatus, result
ing in vertigo. Recent abnormalities of middle ear
ventilation and middle ear effusion are the most com
mon cause of balance disturbance in childhood. In
balance disturbance, transmission of pressure gradients
through the labyrinthine windows to the inner ear
uids and the vestibular sensory receptors is altered.
152 Chapter 12 • Dizziness
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History of Head Trauma
Trauma to the head or ear can cause disturbance of
both peripheral and central balance mechanisms. Cer
tain traumas can cause acute destruction of the inner
ear and produce vertigo. Direct trauma can occur to the
labyrinth from a temporal bone fracture. A blow to the
head or a whiplash injury can also produce a concus
sive effect on the labyrinth. Children who have a his
tory of head trauma can present with vertigo caused by
labyrinthine damage.
Vertigo often occurs as a residual symptom and usu
ally gradually improves over the course of a year.
Trauma can also produce a stula between the middle
and inner ear, causing tympanic membrane (TM) dam
age and ossicle disruption.
Previous Otology History and Procedures
Patients with cholesteatoma usually have a history of
chronic middle ear infection, otorrhea, and conductive
hearing loss. Prior surgical procedures of the ear can
produce peripheral vertigo through disruption of the
vestibular apparatus or through formation of a peri
lymph stula.
DIAGNOSTIC REASONING:
FOCUSED PHYSICAL EXAMINATION
Take Vital Signs and Note Blood
Pressure
Assess orthostatic blood pressure to rule out pos
tural hypotension as the cause of vertigo. Assess
ment is made by measuring the blood pressure in
both the supine and standing positions. A drop in
arterial blood pressure of at least 30 systolic and
20 diastolic mm Hg when the patient changes from
the supine to the standing position indicates ortho
static hypotension.
Note General Appearance
In a patient who is currently ill, suspect labyrinthitis.
In a patient who is acutely nauseated and vomiting,
suspect vestibular neuronitis.
Have Patient Hyperventilate and Perform
Valsalva Maneuver
Perform this testing if you suspect psychogenic vertigo
because the maneuver can reproduce the vertigo in
these patients. Ask the patient to perform a Valsalva
maneuver and to breathe in and out or blow vigorously
for 1 to 3 minutes.
Perform Vision Examination
A recent change in visual acuity or new corrective
lenses can cause transient episodes of imbalance.
Perform Ear Examination
Look for the presence of effusion or infection that
signals serous otitis or otitis media. Look for the pres
ence of a cholesteatoma. It will appear as a shiny
white irregular mass; foulsmelling discharge can also
be present. Note the integrity of the TM; trauma can
sometimes cause its disruption. Perform pneumatic
otoscopy (see Chapter 14), which will enable you to
determine whether changes in pressure trigger an epi
sode of vertigo. If the patient has a stula, changes in
pressure transmitted directly to the inner ear will
cause a sudden episode of vertigo.
Perform Screening Hearing Tests
Perform Rinne (AC:BC) and Weber (lateralization)
tests. Expect sensorineural loss with Meniere disease,
labyrinthitis, perilymph stula, and acoustic neuroma.
In sensorineural loss, the sound lateralizes to the unaf
fected ear. With sensorineural hearing loss, bone and
air conductions are both reduced in Rinne tests, but
the ratio remains the same (AC:BC). Patients with
a cholesteatoma, serous otitis, or otitis media can dem
onstrate a conductive hearing loss (see differential
diagnosis table).
Perform Positional Nystagmus
Testing/Provoking Maneuvers
A test for nystagmus assesses the function of the ves
tibular branch of the acoustic nerve (cranial nerve
VIII). The presence and characteristics of nystagmus
are important in determining central versus peripheral
causes of vertigo. Nystagmus is dened by the axis on
which it occurs (horizontal, vertical, rotary, or mixed)
and by the direction in which it occurs. Nystagmus is
composed of quick and slow components that can be
observed. With the eye xated, a slow drift away from
the position of xation is corrected by a quick move
ment back to the original position. The direction of the
nystagmus is determined by the quick component be
cause it is easier to see. The quick component depends
on the interaction between the vestibular system and
the cerebral cortex and represents the compensatory
response to vestibular stimulation. The slow compo
nent moves in the direction of the movement of the
Chapter 12 • Dizziness 153
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endolymph, a clear uid within the membranous laby
rinth of the inner ear.
Fixed nystagmus, which always beats in the same
direction, occurs with peripheral disorders of BPPV,
Meniere disease, vestibular neuronitis, or labyrinthitis.
Vestibular nystagmus typically consists of a horizontal
rotary, jerk motion of both the slow and fast components.
The nystagmus associated with central causes can be
horizontal, vertical, rotary, or inconsistent. Pronounced
rotary, unidirectional upgaze or downgaze nystagmus
always arises from central processes. Nystagmus that is
equally rapid in both directions is characteristic of central
causes. In vertigo of peripheral origin, nystagmus gener
ally resolves on xation within 24 to 48 hours, whereas
nystagmus associated with central vertigo does not. See
Table 121 for a comparison of characteristics.
Positional Maneuvers
(Bárány or Dix-Hallpike Maneuvers)
To determine the origin of vertigo and accompanying
nystagmus, seat the patient on the table with the patient’s
head turned to the left or right. Quickly lower the patient
to a lying position with the head lower than the table
edge so that the ear faces the oor. Repeat, with the head
turned to the other side and then again with the head in
the midline. The maneuver produces intense vertigo in
patients with vestibular problems and can cause mild
vertigo in patients with central causes. Watch for nystag
mus during this maneuver. The patient’s eyes should be
kept open to observe the duration and direction of the
nystagmus. The nystagmus associated with peripheral
causes has a 3 to 10second delay in onset, lessens with
repetition, and is in a xed direction. In contrast, the
nystagmus associated with central causes begins imme
diately, does not fatigue with repetition, and can be in any
and changing directions. With inner ear damage, the
rapid phase of nystagmus is always in the same direction
regardless of the direction of gaze (see EvidenceBased
Practice box).
Provocation Maneuvers
In patients who experience vertigo associated with posi
tion changes or rapid movement of the head, provoke
nystagmus and vertigo by having the patient assume the
positions that cause the vertigo. Provocation assists in the
diagnosis of BPPV. If you suspect a perilymph stula,
perform pneumatic otoscopy. The pressure applied to the
middle ear can provoke nystagmus and vertigo.
Perform Neurological Examination
Look for brainstem or cerebellar dysfunction, which
could cause abnormal neurological ndings. Speci
cally test cranial nerves, looking for sensory and/or
motor decits. With the exception of hearing loss, cra
nial nerve function should be normal in patients with
peripheral vertigo. Patients with brainstem dysfunction
typically have diplopia as well as changes in sensory
and motor function.
Table 12-1
CHARACTERISTICS CENTRAL PERIPHERAL
Severity Can be disproportionate to vertigo Proportionate to vertigo
Axis Horizontal, vertical, rotary; unidirectional
Consistency of direction Can be inconsistent Consistent; always beats in same direction
Type Irregular or rapid in both directions Has both slow and quick components
EVIDENCE-BASED PRACTICE
The Dix-Hallpike maneuver has a positive predictive value of
83% and a negative predictive value of 52% for the diagnosis of BPPV. After the initial test, the induced symptoms are
typically less intense in peripheral vertigo; the intensity stays
Data from Labuguen RH: Initial evaluation of vertigo, Am Fam Physician 73:244, 2006.
Comparison of Nystagmus in Central and Peripheral Vertigo
Horizontal, rotary
upgaze or downgaze
Dix-Hallpike Maneuver
about the same in central vertigo. The combination of a positive
Dix-Hallpike maneuver and a history of vertigo or vomiting suggests a peripheral vestibular disorder. Laboratory tests identify
the etiology of vertigo in less than 1% of patients with vertigo.
154 Chapter 12 • Dizziness
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Test cerebellar function. Testing gait differences while
blindfolded can be helpful. Ataxia from bilateral vestibu
lar loss is worsened by loss of visual input, whereas
ataxia from cerebellar disease remains about the same.
The sensitivity of gait testing is increased by watching
tandem gait (heel to toe). When trying to walk a straight
line, the patient with a cerebellar lesion will tend to fall
toward the side of the lesion. However, gait disturbances
can also be present with peripheral vertigo.
Test the patient’s ability to perform rapid alternating
movements (RAMs) either through pronationsupination
or through touching thumb to ngers sequentially. Move
ments should be smooth and rhythmic, and the patient
should be able to gradually increase speed. Stiff, slowed,
or jerky movements indicate cerebellar dysfunction.
Perform the pastpointing test. Have the patient sit
with arm extended forward and index nger pointed
while you sit in the same position facing the patient.
The tips of your ngers should touch. Then ask the
patient to close the eyes, raise the arm above the head,
and bring the arm and nger back to the same position.
In patients with central lesions or unilateral vestibular
abnormalities, the arm will deviate toward the side of
the lesion.
Test sensory and motor function. Look for focal decits
that can occur with central vertigo. Many patients with
vertigo also report generalized weakness; therefore it is
important to distinguish between generalized weakness
and focal motor impairment caused by brainstem disorder.
Perform Cardiovascular Evaluation
Note the heart rate and rhythm and attempt to detect
dysrhythmias. Auscultate carotid and temporal arteries
for bruits that can alert you to a cardiovascular cause
for the vertigo.
Congenital heart disease can produce episodes of
syncope that might be falsely interpreted as vertiginous
episodes (see Chapter 30).
LABORATORY AND DIAGNOSTIC
STUDIES
Audiometry
Audiometry is used to quantify hearing loss. The patient
is tested at specic frequencies (pure tones) and specic
intensities. Hearing loss is measured in decibels. Audi
ometry is used anytime the patient presents with both
vertigo and hearing loss (i.e., Meniere disease, acoustic
neuroma, labyrinthitis, perilymph stula, or use of oto
toxic medications) (see Chapter 14).
Electronystagmography
Electronystagmography (ENG) electronically detects
nystagmus that cannot be detected visually. Vestibu
lar function is evaluated using gaze testing, posi
tional changes, and caloric stimulation. Eye move
ments are recorded electronically. Caloric stimulation
is produced by ear irrigation with warm and then
cool water.
ENG is most useful in diagnosing chronic periph
eral disorders (i.e., Meniere disease and persistent
BPPV) to determine the degree and progression of the
vestibular decit. It can also be useful in patients with
psychogenic vertigo to provide reassurance that no
organic disease is present.
Magnetic Resonance Imaging
Magnetic resonance imaging (MRI) of the brain is in
dicated when the history and physical examination
point to acoustic neuroma or a central cause of the
vertigo. Consider urgent MRI if vertigo is of sudden
onset; is accompanied by severe headache, direction
changing nystagmus, or neurological signs; or if the
patient has risk factors for stroke.
Computed Tomography
Computed tomography (CT) scanning of the brain is
indicated whenever there is persistent vertigo and in all
cases with additional signs of neurological distur
bance. In patients with medical conditions such as
renal failure, hypertension, or a hematological malig
nancy who have sudden onset of vertigo, CT scan
is used to look for hemorrhage into the cerebellum,
brainstem, or labyrinth.
Electroencephalography
An electroencephalogram (EEG) should be obtained
for patients who have vertigo associated with altera
tions of consciousness.
Cardiac Monitoring
An electrocardiogram (ECG) or Holter monitoring can
provide conrmatory information on cardiovascular
causes of vertigo.
Hematology and Urinalysis
Complete blood count (CBC) can reveal anemia, which
can cause presyncopal lightheadedness. Urine or serum
glucose levels will detect diabetes mellitus, which can
produce vertigo. Urine testing and blood urea nitrogen
https://t.me/med1917
(BUN) level can reveal renal failure, which can also be
associated with vertigo.
Serological Testing for Syphilis
Because secondary syphilis or early tertiary syphilis
can produce the same symptoms that occur in Meniere
disease, screening is advocated by some to rule out
syphilis as a cause.
DIFFERENTIAL DIAGNOSIS
Central Causes
Brainstem Dysfunction and Cerebellar
Dysfunction
Central vertigo produced by disorders of the brain
stem and cerebellum is usually caused by neoplastic
or vascular processes, including recurrent intermittent
vascular insufciency, transient ischemic attack, and
stroke. Neoplasms are usually slow growing; therefore
vestibular dysfunction is of gradual onset and usually
manifests as a problem with equilibrium.
Vascular causes are more common and can produce
acuteonset, longlasting, or recurrent transient epi
sodes of vertigo. Patients usually manifest other neuro
logical decits. With brainstem disorders, patients can
have reports of diplopia, dysarthria, dysphagia, and
paresthesia. They can demonstrate sensory and motor
decits. Cerebellar dysfunction usually results in gait
disturbance and difculties in nemotor coordination,
including rapid alternating movements (RAM) and
ngertonger testing.
Multiple Sclerosis
Multiple sclerosis can produce a range of neurological
symptoms. Vertigo occurs in up to 50% of patients
with multiple sclerosis. Disease onset is usually in the
third or fourth decade of life. MRI shows characteristic
demyelinating plaques.
Migraine Headache
Approximately 30% of persons with migraine head
aches have vertigo. It can be present before the head
ache begins, during the headache, or independent of
the headache. Patients can have other symptoms con
sistent with vertebrobasilar vascular abnormalities
such as visual changes, tinnitus, decreased hearing,
ataxia, or paresthesia. Diagnosis is usually made on the
basis of the history.
Chapter 12 • Dizziness 155
Peripheral Causes
Benign Paroxysmal Positional Vertigo
Episodes of BPPV are characterized by acute onset of
vertigo associated with rapid head movement or position
changes. Many women report dizziness with position
change around the time of their menses. The episodes
are brief, lasting a few seconds. Nystagmus can be elic
ited by positional testing. Testing positional changes can
provoke the vertigo. There is no hearing loss. Diagnosis
is made on the basis of the history and clinical ndings.
This is one of the most common causes of vertigo, espe
cially in older adults.
Benign Paroxysmal Vertigo of Childhood
Benign paroxysmal vertigo (BPV) of childhood occurs
most often in children 23 years old. The disorder tends
to be recurrent with one to four attacks per month. The
episodes occur suddenly, and the child cries out for help.
Vomiting, pallor, sweating, and nystagmus are common
during the episode. The neurological and audiological
examinations are entirely normal. Some children can
have a hypoactive or absent response to caloric testing
(ear irrigation with warm and then cool water).
Meniere Disease
Meniere disease is characterized by a classic triad of
symptoms—vertigo, hearing loss, and tinnitus. A sensa
tion of ear fullness can also be present. The attacks are
abrupt and recurrent and last for minutes to several
hours. The interval between attacks can be weeks or
months. Between episodes, the patient is asymptomatic.
On physical examination, sensorineural hearing loss is
present in the affected ear, or it can be bilateral.
Vestibular Neuronitis
Vestibular neuronitis is frequently preceded by an acute
viral infection. These patients usually present with severe
vertigo, nausea, and vomiting. The vertigo lasts for days
to weeks. Remaining completely motionless can help the
symptoms. Auditory function is not affected. Physical
examination reveals nystagmus that intensies in ampli
tude when the gaze is directed away from the affected
ear. Visual xation minimizes the nystagmus.
Labyrinthitis
Frequently associated with a concurrent viral or bacterial
illness, labyrinthitis produces severe vertigo that lasts for
several days. Labyrinthitis can be a complication of otitis
156 Chapter 12 • Dizziness
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media or meningitis. This condition is distinguished from
vestibular neuronitis by the accompanying hearing loss
that occurs as a result of destruction of the inner ear.
Acoustic Neuroma
Also called a vestibular schwannoma, acoustic neu
roma is a benign tumor that originates most often in the
vestibular portion of cranial nerve VIII (acoustic). It
usually causes unilateral sensorineural hearing loss,
tinnitus, and loss of equilibrium. The neuroma grows
slowly; therefore loss of equilibrium is more often a
symptom than is vertigo. Acoustic neuroma can also
occur in cranial nerve V (trigeminal) with symptoms of
paresthesia consistent with the nerve distribution.
Large tumors of cranial nerve VI (abducens) can com
press the brainstem.
Perilymph Fistula
Fistula formation can occur as a result of ear trauma,
from a direct blow, secondary to otologic surgery, or
indirectly from straining, coughing, or pressure
changes. In this condition there is leakage of perilymph
from either the round or the oval window into the
middle ear. Sensorineural hearing loss is frequently
present as well as vertigo. The stula will often heal
spontaneously but sometimes can require surgery.
Sinusitis and Otitis
Serous otitis, otitis media, and sinusitis can cause disrup
tion of the vestibular apparatus, producing vertigo. His
tory and physical examination ndings will be consistent
with the specic disorder (see Chapters 14 and 22).
Cholesteatoma
Collection of squamous debris often associated with
chronic middle ear infection can form a cholesteatoma,
which enlarges and destroys structures in its way. On
physical examination, the cholesteatoma will appear as
a shiny white irregular mass. Foulsmelling discharge
can be evident, and there can be visible bone destruc
tion. A conductive hearing loss can be present.
Systemic Causes
Psychogenic
Psychogenic causes of vertigo are common. Patients
often describe themselves as anxious or nervous and
can have psychiatric diagnoses (see Chapter 3). Their
symptoms are vague and imprecise. Neurological
examination is normal. No nystagmus is present or
elicited. The vertigo can be reproduced with hyperven
tilation. MRI can be useful to provide reassurance.
Cardiovascular
Orthostatic hypotension and cardiac dysrhythmias can
produce vertigo. The diagnosis of postural hypotension
can be made by taking orthostatic blood pressure read
ings. The diagnosis of cardiac conditions can involve
CBC, blood chemistry, ECG, cardiac stress testing, and
echocardiography.
Neurosyphilis
Secondary or early tertiary syphilis can present
with symptoms similar to those of Meniere disease.
The patient demonstrates various clinical symptoms,
including papilledema, aphasia, monoplegia or hemi
plegia, cranial nerve (CN) palsies, pupillary abnor
malities, or focal neurological decits. The Argyll
Robertson pupil, which occurs almost exclusively in
neurosyphilis, is a small irregular pupil that reacts
normally to accommodation but not to light. Sero
logical testing will be positive for syphilis.
Other Causes
Ototoxic Drugs and Drugs Causing Salt
Retention
Medications that are ototoxic, saltretentive, or psy
chotropic can produce vertigo, lightheadedness, or
unsteadiness. Drugs causing salt retention include
steroids and phenylbutazone. Ototoxic medications
include aspirin, ethacrynic acid, streptomycin, gen
tamicin, aminoglycosides, and furosemide. Psycho
tropic drugs can also produce vertigo. Ototoxic
drugs can produce a sensorineural hearing loss.
Audiometry should be performed with any noted
hearing loss.
Trauma
Injury to the head or ear from labyrinthine concussion,
temporal bone fracture, or perilymph stula can pro
duce disturbance of the vestibular apparatus and result
in vertigo. Head trauma can also produce cerebral
concussion involving the anterior tip of the temporal
lobe. Trauma from otologic procedures can also cause
vertigo.
Chapter 12 • Dizziness 157
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DIFFERENTIAL DIAGNOSIS OF Common Causes of Dizziness
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
Central Causes
Brainstem
dysfunction/
cerebellar
dysfunction
Multiple sclerosis Onset is often in third or
Migraine headache Headache history; other
Peripheral Causes
Benign paroxysmal
positional vertigo
(BPPV)
Benign paroxysmal
vertigo of
childhood
Meniere disease Sudden onset; lasts hours,
Vestibular neuronitis Sudden onset; antecedent
Labyrinthitis Sudden onset, lasts hours
Acoustic neuroma Adults; gradual onset; mild
Perilymph fistula History of trauma;
Otitis/sinusitis Pain in ear or face; history
Cholesteatoma History of chronic middle
Elderly; acute-onset;
recurrent vertigo; tinnitus;
hearing OK
fourth decade of life
migraine symptoms
Adults: associated with
positional changes;
recurrent episodes; lasts
seconds to minutes;
some relief if motionless
Children: usually 2-3 years
of age, sudden onset
with crying by child
recurrent; tinnitus and
fullness in ears
viral infection
to days
vertigo; persistent tinnitus;
facial numbness,
weakness
hearing loss
of ear or sinus infections;
gradual onset of vertigo
ear infections
Symptoms of brainstem/
vertebrobasilar vascular abnormality: ataxia, double vision;
lack of coordination; sensory/
motor deficits; vertical, lateral,
rotary nystagmus; hearing
normal; cerebellar: impaired
RAM, finger-to-finger testing
Can have no other findings or
can have other neurological
symptoms
Can have symptoms of
vertebrobasilar vascular
abnormalities, as above
Lateral or rotary nystagmus; no
tinnitus or hearing loss
Vomiting, pallor, sweating, and
nystagmus common; no loss
of consciousness; neurological
and audiological examination
can be normal
Lateral or rotary nystagmus;
fluctuating hearing loss: low
tones; sensorineural
Nausea and vomiting; nystagmus;
no hearing loss, loss of equilibrium always to the same side
Can currently be ill; lateral
nystagmus; hearing loss; rarely
tinnitus; nausea and vomiting
can be present
Unilateral hearing loss, poor
speech discrimination
Nystagmus and vertigo with
pneumatic otoscopy;
sensorineural hearing loss
Serous otitis, otitis media;
tenderness over sinuses;
purulent nasal discharge; no
nystagmus
Shiny white irregular mass on
otoscopic examination;
foul-smelling discharge can be
present; bone destruction can
be visible; conductive hearing
loss can be present
MRI
MRI
None
Provoke nystagmus and
vertigo by position
that causes response;
Dix-Hallpike maneuver;
ENG
Can have hypoactive
or absent response to
caloric testing
Positional maneuvers,
audiometry, ENG
Positional maneuvers
Positional maneuvers,
audiometry
MRI; audiometry
Audiometry
See Chapters 14 and 22
Audiometry
Continued
158 Chapter 12 • Dizziness
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DIFFERENTIAL DIAGNOSIS OF Common Causes of Dizziness—cont’d
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
Systemic Causes
Psychogenic Vague symptoms; recur-
rent; can describe self as
anxious; can have other
psychiatric diagnoses
Cardiovascular CV history; antihypertensive
medications
Neurosyphilis Vertigo, tinnitus, fullness
in ears
Other Causes
Ototoxic and
salt-retaining
drugs
Trauma History of trauma to head
CT, computed tomography; ENG, electronystagmography; MRI, magnetic resonance imaging; RAM, rapid alternating movements.
Medication history: steroids,
phenylbutazone, ethacrynic
acid, aspirin, streptomycin,
gentamicin, aminoglycosides, furosemide, psychotropic drugs
or ear
Normal neurological and auditory
examinations
Orthostatic blood pressure;
dysrhythmias; carotid or
temporal bruits
Various clinical symptoms; pap-
illedema, aphasia, monoplegia
or hemiplegia, central nervous
palsies, pupillary abnormalities,
Argyll Robertson pupil; focal
neurological deficits
Sensorineural hearing loss Audiometry
Depends on nature and location
of injury; can exhibit peripheral
or central symptoms
Hyperventilation to
reproduce the vertigo
Depends on client
condition and
symptoms
Serology for syphilis
MRI/CT
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DA, ter Riet G: Causes of persistent dizziness in elderly patients
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C H A P T E R
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13
Dyspnea
yspnea, or shortness of breath, is a subjective
sensation of air hunger that results in labored
D
general causes: (1) an increased awareness of normal
breathing, such as with hyperventilation; (2) an increase in the work of breathing, such as in airway
obstruction or restricted volume; and (3) abnormalities in the ventilatory system, such as in neurological
disorders, diseases of the muscles, and chest wall
abnormalities. In disease states it is usually a result
of pulmonary or cardiac pathology. When eliciting
the history, it is helpful to determine if this is newonset acute dyspnea, chronic progressive dyspnea, or
chronic recurrent dyspnea. Carefully directed questioning will provide essential clues for identifying
the differential diagnoses. In children younger than
3 years, who usually cannot express the sensation,
caregivers can observe tachypnea, retractions, stridor,
nasal aring, or feeding difculty.
DIAGNOSTIC REASONING:
FOCUSED HISTORY
breathing. True dyspnea results from three
Is this an emergency?
Severe dyspnea is a medical emergency. If not treated
immediately, respiratory failure and death can occur.
Assess the adequacy of the airway rst. Emergency
measures should be instituted to establish ventilation.
When the patient is stabilized, search for the underlying
cause of the dyspnea.
Key Questions
n Did this occur suddenly, or has it been developing
gradually? Over what period of time (hours, days,
weeks) has it developed?
n What were you (or the child) doing just before having
difculty in breathing?
n Do you (or the child) have other symptoms, such as
itching or swelling?
Onset
New-onset acute dyspnea in a patient in acute distress
can signal a life-threatening problem. In the patient
with no previous history of heart or lung disease,
dyspnea can indicate several conditions that require
immediate treatment, such as aspiration of a foreign
body, anaphylaxis, pulmonary embolism (PE), and
pneumonia. A common cause of acute-onset dyspnea
is left ventricular dysfunction.
Acute upper or lower airway obstruction in children
has the greatest potential to cause serious morbidity
or mortality and therefore must initially be ruled out.
The most serious problem is hypoxemia caused by the
inability to transport oxygen past a blocked upper airway,
such as with epiglottitis, croup, or a foreign body.
Acute dyspnea requires immediate assessment
of the airway and ventilatory status with oxygen
and cardiac monitoring. Often this must occur
before a definitive diagnostic evaluation has been
completed.
Acute epiglottitis in children is caused by Hae-
mophilus inuenzae. Inammation of the epiglottis
causes edema that obstructs the tracheal airway. The
onset is sudden and the course of the disease is rapid.
The patient’s presenting symptoms usually include
drooling, dysphonia, dysphagia, and respiratory distress with inspiratory stridor. The child looks anxious
and sits up and forward with the jaw open to assist in
air intake.
Status asthmaticus is a progressive bronchospasm
from an increase in airow resistance in children who
are having an asthma event that does not respond to
pharmacological intervention. Fever can be present,
and pulse rate and respirations are increased. The use
of accessory respiratory muscles is seen. Sometimes
wheezing is not heard because of lack of air movement. The combination of hypoxia, hypercapnia, and
acidosis can result in cardiovascular depression and
cardiopulmonary arrest.
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160 Chapter 13 • Dyspnea
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Foreign Body Aspiration
The adult patient with foreign body aspiration reports that dyspnea occurred while eating solid foods
or drinking large amounts of alcohol. Children who
put small objects in their mouth are at risk for aspiration of the object into the airway and subsequent
airway obstruction. The patient or the care provider
gives a history of sudden onset of choking, coughing,
or wheezing, without preceding upper respiratory
tract infection. Often the child has been playing
on the oor or outside at the time of the onset of
symptoms.
Anaphylaxis
Anaphylaxis can follow insect bites or the ingestion of
medication or other potential allergens (e.g., shellsh,
peanuts). Primary symptoms include ushing, generalized
pruritus, fear, faintness, and sneezing. An allergic response
can lead to shock, cardiac arrythmia, laryngeal edema, and
death within minutes. The sooner the symptoms occur,
the more severe the reaction.
Is the dyspnea caused by trauma
to the chest?
Key Question
n Have you experienced any trauma to the chest?
Trauma
Limitation of motion of the thoracic cage because
of pain and/or trauma can be associated with
severe alveolar hypoventilation and subsequent
dyspnea.
Pneumothorax occurs most frequently in young
persons during strenuous activity. Spontaneous pneumothorax results in sudden loss of lung volume, hypoxia, hypercapnia, and signicant shortness of breath
(SOB). Blunt chest trauma can be caused by a fall or
motor vehicle accident.
Is the dyspnea caused by a pulmonary
embolus?
Is the dyspnea caused by a secondary
obstruction in the lower respiratory tract?
Key Questions
n Have you had cough or recent cold?
n Do you have a history of asthma?
n Is there a family history of asthma?
Cough
Secondary partial airway obstruction caused by small
airway disease contributes to hypoxemia via intrapulmonary shunting. The pulmonary obstruction can be
intraluminal (distal foreign objects, asthma); intramural (edema, bronchomalacia, bronchiolitis); or extramural (compression from tumor, lymph nodes). The
narrowing increases both airway resistance and turbulence of airow. The imbalance between pulmonary
ventilation and perfusion affects oxygen exchange.
This causes the patient to work harder to maintain
adequate ventilation, resulting in dyspnea.
History of Asthma
Both adults and children can experience airway
obstruction caused by reactive airways disease
or asthma. Personal or family history of asthma
increases the risk of dyspnea from acute bronchospasm.
Key Questions
n Have you recently been conned to bed or been
sitting for a long period of time?
n Have you had recent surgery?
n Have you recently sustained a fracture?
n Are you taking birth control pills or estrogen?
n Do you smoke?
n What medications are you taking?
n Are you feeling anxious or scared?
The person with PE is usually in acute distress
and reports signicant SOB, localized pleuritic chest
pain, apprehension, bloody sputum production, diaphoresis, fever, and history of conditions causing
risk for emboli. These risk factors include age of
greater than 60 years, pulmonary hypertension, congestive heart failure, chronic lung disease, ischemic
heart disease, stroke, and cancer. Predisposing factors that can contri bute to thrombus formation include (1) venous stasis, (2) hypercoagulability, and
(3) endothelial injury with inammation to the vessel
lining. Trauma, muscle spasm, or clot dissolution can
cause the thrombus to dislodge, creating an embolus.
Emboli circulate in the blood to the right side of the
heart and enter the lungs via the pulmonary artery. If
the clot is not dissolved within the lungs, it occludes
the pulmonary artery and obstructs blood ow and
perfusion of the lungs. Patients with suspected PE
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