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Understanding the sense of smell
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ANOSMIA 51
Our noses can distinguish the odors of thousands of chemicals, thanks to a highly developed complex of sensory cells. The olfactory
epithelium contains olfactory receptor cells,
along with olfactory glands and sustentacular cells, both of which secrete mucus to
keep the epithelial surface moist. The mucus
covering the olfactory cells probably traps
airborne odorous molecules, which then fit
into the appropriate receptors on the cell surface. In response to this stimulus, the receptor cell then transmits an impulse along the
olfactory nerve (cranial nerve I) to the olfactory area of the cortex, where it’s interpreted.
Any disruption along this transmission pathway, or any obstruction of the epithelial surface due to dryness or congestion, can cause
anosmia.
Olfactory bulb
Olfactory nerves
Superior nasal
concha
Superior nasal
meatus
Middle nasal
concha
Middle nasal
meatus
Nasal vestibule
Inferior nasal
concha
Inferior nasal
meatus
CLOSE-UP OF SENSORY
CELLS
Olfactory bulb
Olfactory tract
Olfactory nerves
Cribriform plate
Olfactory receptor cell
Sustentacular cell
Olfactory gland
Olfactory epithelium
Cilia
52 ANURIA
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◆ Polyps. Temporary anosmia occurs when
multiple polyps obstruct nasal cavities. Examination reveals the smooth, pale, grapelike polyp
clusters.
◆ Rhinitis. In common acute viral rhinitis,
temporary anosmia occurs with nasal congestion; sneezing; watery or purulent nasal discharge; red, swollen nasal mucosa; dryness or a
tickling sensation in the nasopharynx;
headache; low-grade fever; and chills.
In allergic rhinitis, temporary anosmia accompanies nasal congestion; itching mucosa;
pale, edematous turbinates; thin nasal discharge; sneezing; tearing; and headache.
In atrophic rhinitis, anosmia resolves with
successful treatment of the disorder. Purulent,
yellow-green, foul-smelling crusts on sclerotic
mucous membranes are characteristic, with
paradoxical nasal congestion in an airway that’s
more open than normal. Turbinates are thin and
atrophic. The nasopharynx and pharynx appear
smooth, dry, and shiny rather than pink and
moist.
In vasomotor rhinitis, temporary anosmia is
accompanied by chronic nasal congestion, watery nasal discharge, postnasal drip, sneezing,
and pale nasal mucosa.
◆ Septal fracture. Anosmia is usually tempo-
rary, caused by airflow obstruction, and returns
with septal repositioning. Examination reveals
septal deviation, swelling, epistaxis, hematoma,
nasal congestion, and ecchymoses.
◆ Septal hematoma. Anosmia is temporary,
resolving with repair of the nasal mucosa or
absorption of the hematoma. Associated signs
and symptoms include epistaxis; dusky red, inflamed nasal mucosa; headache; and mouth
breathing.
◆ Sinusitis. Temporary anosmia may be asso-
ciated with nasal congestion; sinus pain, tenderness, and swelling; severe headache; watery
or purulent nasal discharge; postnasal drip; inflamed throat and nasal mucosa; enlarged, purulent turbinates; malaise; low-grade fever; and
chills.
O
THER CAUSES
◆ Drugs. Anosmia can result from prolonged
use of nasal decongestants, which produces rebound nasal congestion. Occasionally, it results
from naphazoline, a local decongestant that
may paralyze nasal cilia. It can also result from
reserpine and, less commonly, amphetamines,
phenothiazines, and estrogen, which cause
nasal congestion.
◆ Radiation therapy. Permanent anosmia
may follow radiation damage to the nasal mucosa or olfactory nerve.
◆ Surgery. Temporary anosmia may result
from damage to the olfactory nerve or nasal
mucosa during nasal or sinus surgery. Permanent anosmia accompanies a permanent tracheostomy, which disrupts nasal breathing.
S
PECIAL CONSIDERATIONS
If anosmia results from nasal congestion, administer a local decongestant or an antihistamine, and provide a vaporizer or humidifier to
prevent mucosal drying and to help thin purulent nasal discharge. Advise the patient to avoid
excessive use of local decongestants, which can
lead to rebound nasal congestion.
If anosmia doesn’t result from simple nasal
congestion, prepare the patient for diagnostic
tests, such as sinus transillumination, skull Xray, or computed tomography scan.
Although permanent anosmia usually doesn’t respond to treatment, vitamin A given orally
or by injection occasionally provides improvement.
P
EDIATRIC POINTERS
Anosmia in children usually results from nasal
obstruction by a foreign body or enlarged adenoids.
Anuria
Clinically defined as urine output of less than
100 ml in 24 hours, anuria indicates either urinary tract obstruction or acute renal failure due
to various mechanisms. (See Major causes of
acute renal failure.)
Fortunately, anuria is rare; even with renal
failure, the kidneys usually produce at least 75
ml of urine daily.
Because urine output is easily measured,
anuria rarely goes undetected. However, without immediate treatment, it can rapidly cause
uremia and other complications of urine retention.
EMERGENCY INTERVENTIONS After de-
tecting anuria, your priorities are to determine if urine formation is occurring and to intervene appropriately. Prepare to catheterize the
patient to relieve any lower urinary tract obstruction and to check for residual urine. You may find
that an obstruction hinders catheter insertion and
that urine return is cloudy and foul smelling. If
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you collect more than 75 ml of urine, suspect lower urinary tract obstruction; if you collect less than
75 ml, suspect renal dysfunction or obstruction
higher in the urinary tract.
H
ISTORY AND PHYSICAL
EXAMINATION
Take the patient’s vital signs and obtain a
complete history. First ask about any changes
in his voiding pattern. Determine the amount
of fluid he normally ingests each day, the
amount of fluid he ingested in the last 24 to 48
hours, and the time and amount of his last urination. Review his medical history, noting especially previous kidney disease, urinary tract
obstruction or infection, prostate enlargement,
renal calculi, neurogenic bladder, or congenital abnormalities. Ask about drug use and
about any abdominal, renal, or urinary tract
surgery.
Inspect and palpate the abdomen for asymmetry, distention, or bulging. Inspect the flank
area for edema or erythema, and percuss and
palpate the bladder. Palpate the kidneys both
anteriorly and posteriorly, and percuss them at
the costovertebral angle. Auscultate over the renal arteries, listening for bruits.
ANURIA
Major causes of acute
renal failure
Prerenal causes
◆Decreased cardiac output
◆Hypovolemia
◆Peripheral vasodilation
◆Renovascular obstruction
◆Severe vasoconstriction
Intrarenal causes
◆Acute tubular necrosis
◆Cortical necrosis
◆Glomerulonephritis
◆Papillary necrosis
◆Renal vascular occlusion
◆Vasculitis
53
M
EDICAL CAUSES
◆ Acute tubular necrosis. Oliguria (occasion-
ally anuria) is a common finding in acute tubular necrosis. It precedes the onset of diuresis,
which is heralded by polyuria. Associated findings reflect the underlying cause and may include signs and symptoms of hyperkalemia
(muscle weakness, cardiac arrhythmias), uremia (anorexia, nausea, vomiting, confusion,
lethargy, twitching, seizures, pruritus, uremic
frost, and Kussmaul’s respirations), and heart
failure (edema, jugular vein distention, crackles,
and dyspnea).
◆ Cortical necrosis (bilateral). Cortical
necrosis is characterized by a sudden change
from oliguria to anuria along with gross hematuria, flank pain, and fever.
◆ Glomerulonephritis (acute). Glomer-
ulonephritis produces anuria or oliguria. Related
effects include mild fever, malaise, flank pain,
gross hematuria, facial and generalized edema,
elevated blood pressure, headache, nausea,
vomiting, abdominal pain, and signs and symptoms of pulmonary congestion (crackles,
dyspnea).
Postrenal causes
◆Bladder obstruction
◆Ureteral obstruction
◆Urethral obstruction
◆ Hemolytic-uremic syndrome. Anuria com-
uremic syndrome and may last from 1 to 10
days. The patient may experience vomiting, diarrhea, abdominal pain, hematemesis, melena,
purpura, fever, elevated blood pressure, hepatomegaly, ecchymoses, edema, hematuria,
and pallor. He may also show signs of upper
respiratory tract infection.
◆ Papillary necrosis (acute). Bilateral papil-
lary necrosis produces anuria or oliguria as well
54 ANXIETY
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as flank pain, costovertebral angle tenderness,
renal colic, abdominal pain and rigidity, fever,
vomiting, decreased bowel sounds, hematuria,
and pyuria.
◆ Renal artery occlusion (bilateral). Renal
artery occlusion produces anuria or severe oliguria, commonly accompanied by severe, continuous upper abdominal and flank pain; nausea and vomiting; decreased bowel sounds;
fever up to 102° F (38.9° C); and diastolic hypertension.
◆ Renal vein occlusion (bilateral). Renal
vein occlusion occasionally causes anuria;
more typical signs and symptoms include acute
low back pain, fever, flank tenderness, and
hematuria. Development of pulmonary
emboli—a common complication—produces
sudden dyspnea, pleuritic pain, tachypnea,
tachycardia, crackles, pleural friction rub, and
possibly hemoptysis.
◆ Urinary tract obstruction. Severe ob-
struction can produce acute and sometimes
total anuria alternating with or preceded by
burning and pain on urination, overflow incontinence or dribbling, increased urinary frequency and nocturia, voiding of small
amounts, or altered urine stream. Associated
findings include bladder distention, pain and a
sensation of fullness in the lower abdomen
and groin, upper abdominal and flank pain,
nausea and vomiting, and signs of secondary
infection, such as fever, chills, malaise, and
cloudy, foul-smelling urine.
◆ Vasculitis. Vasculitis occasionally produces
anuria. More typical findings include malaise,
myalgia, polyarthralgia, fever, elevated blood
pressure, hematuria, proteinuria, arrhythmias,
pallor, and possibly skin lesions, urticaria, and
purpura.
O
THER CAUSES
◆ Diagnostic tests. Contrast media used in ra-
diographic studies can cause nephrotoxicity,
producing oliguria and, rarely, anuria.
◆ Drugs. Many classes of drugs can cause
anuria or, more commonly, oliguria through
their nephrotoxic effects. Antibiotics, especially
the aminoglycosides, are the most commonly
seen nephrotoxins. Anesthetics, heavy metals,
ethyl alcohol, and organic solvents can also be
nephrotoxic. Adrenergics and anticholinergics
can cause anuria by affecting the nerves and
muscles of micturition to produce urine retention.
S
PECIAL CONSIDERATIONS
If catheterization fails to initiate urine flow, prepare the patient for diagnostic studies—such as
ultrasonography, cystoscopy, retrograde pyelography, and renal scan—to detect any obstruction
higher in the urinary tract. If these tests reveal
an obstruction, prepare him for immediate
surgery to remove the obstruction, and insert a
nephrostomy or ureterostomy tube to drain the
urine. If these tests fail to reveal an obstruction,
prepare the patient for further kidney function
studies.
Carefully monitor the patient’s vital signs
and intake and output, saving urine for inspection as appropriate. Restrict the daily fluid allowance to 600 ml more than the previous
day’s total urine output. Restrict foods and
juices high in potassium and sodium, and
make sure the patient maintains a balanced
diet with controlled protein levels. Provide
low-sodium hard candy to help decrease thirst.
Record fluid intake and output, and weigh the
patient daily.
P
EDIATRIC POINTERS
In neonates, anuria is defined as the absence of
urine output for 24 hours. It can be classified as
primary or secondary. Primary anuria results
from bilateral renal agenesis, aplasia, or multicystic dysplasia. Secondary anuria, associated
with edema or dehydration, results from renal
ischemia, renal vein thrombosis, or congenital
anomalies of the genitourinary tract. Anuria in
children commonly results from loss of renal
function.
G
ERIATRIC POINTERS
In elderly patients, anuria is a gradually occurring sign of underlying pathology. Hospitalized
or bedridden elderly patients may be unable to
generate the necessary pressure to void if they
remain in a supine position.
Anxiety
Anxiety is the most common psychiatric symptom and can result in significant impairment. A
subjective reaction to a real or imagined threat,
anxiety is a nonspecific feeling of uneasiness or
dread. It may be mild, moderate, or severe. Mild
anxiety may cause slight physical or psychological discomfort. Severe anxiety may be incapacitating or even life-threatening.
ANXIETY
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55
Everyone experiences anxiety from time to
time—it’s a normal response to actual danger,
prompting the body (through stimulation of the
sympathetic and parasympathetic nervous systems) to purposeful action. It’s also a normal response to physical and emotional stress, which
can be produced by virtually any illness. In addition, anxiety can be precipitated or exacerbated
by many nonpathologic factors, including lack
of sleep, poor diet, and excessive intake of caffeine or other stimulants. However, excessive
unwarranted anxiety may indicate an underlying psychological problem.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient displays acute, severe anxiety,
quickly take his vital signs and determine his
chief complaint; this will serve as a guide for
how to proceed. For example, if the patient’s
anxiety occurs with chest pain and shortness of
breath, you might suspect myocardial infarction
and act accordingly. While examining the patient, try to keep him calm. Suggest relaxation
techniques, and talk to him in a reassuring,
soothing voice. Uncontrolled anxiety can alter
vital signs and exacerbate the causative disorder.
If the patient displays mild or moderate anxiety, ask about its duration. Is the anxiety constant or sporadic? Did he notice any precipitating factors? Find out if the anxiety is
exacerbated by stress, lack of sleep, or excessive caffeine intake and alleviated by rest, tranquilizers, or exercise.
Obtain a complete medical history, especially
noting drug use. Then perform a physical examination, focusing on any complaints that may
trigger or be aggravated by anxiety.
If the patient’s anxiety isn’t accompanied by
significant physical signs, suspect a psychological cause. Determine the patient’s level of consciousness (LOC) and observe his behavior. If
appropriate, refer the patient for psychiatric
evaluation.
M
EDICAL CAUSES
◆ Acute respiratory distress syndrome.
Acute anxiety occurs along with tachycardia,
mental sluggishness and, in severe cases, hypotension. Respiratory signs and symptoms
include dyspnea, tachypnea, intercostal and
suprasternal retractions, crackles, and
rhonchi.
◆ Anaphylactic shock. Acute anxiety is usual-
ly the first sign of anaphylactic shock. It’s accompanied by urticaria, angioedema, pruritus,
and shortness of breath. Soon, other signs and
symptoms develop: light-headedness, hypotension, tachycardia, nasal congestion, sneezing,
wheezing, dyspnea, barking cough, abdominal
cramps, vomiting, diarrhea, and urinary urgency
and incontinence.
◆ Angina pectoris. Acute anxiety may either
precede or follow an attack of angina pectoris.
An attack produces sharp and crushing substernal or anterior chest pain that may radiate to
the back, neck, arms, or jaw. The pain may be
relieved by nitroglycerin or rest, which eases
anxiety.
◆ Asthma. In allergic asthma attacks, acute
anxiety occurs with dyspnea, wheezing, productive cough, accessory muscle use, hyperresonant lung fields, diminished breath sounds,
coarse crackles, cyanosis, tachycardia, and diaphoresis.
◆ Autonomic hyperreflexia. The earliest signs
of autonomic hyperreflexia may be acute anxiety accompanied by a severe headache and dramatic hypertension. Pallor and motor and sensory deficits occur below the level of the lesion;
flushing occurs above it.
◆ Cardiogenic shock. Acute anxiety is ac-
companied by cool, pale, clammy skin; tachycardia; weak, thready pulse; tachypnea; ventricular gallop; crackles; jugular vein
distention; decreased urine output; hypotension; narrowing pulse pressure; and peripheral
edema.
◆ Chronic obstructive pulmonary disease
(COPD). Acute anxiety, exertional dyspnea,
cough, wheezing, crackles, hyperresonant lung
fields, tachypnea, and accessory muscle use
characterize COPD.
◆ Heart failure. In heart failure, acute anxi-
ety is commonly the first symptom of inadequate oxygenation. Associated findings include restlessness, shortness of breath,
tachypnea, decreased LOC, edema, crackles,
ventricular gallop, hypotension, diaphoresis,
and cyanosis.
◆ Hyperthyroidism. Acute anxiety may be an
early sign of hyperthyroidism. Classic signs and
symptoms include heat intolerance, weight loss
despite increased appetite, nervousness,
tremor, palpitations, diaphoresis, an enlarged
thyroid, and diarrhea. Exophthalmos also may
occur.
56 ANXIETY
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◆ Hyperventilation syndrome. Hyperventila-
tion syndrome produces acute anxiety, pallor,
circumoral and peripheral paresthesia and, occasionally, carpopedal spasms.
◆ Hypochondriasis. Mild to moderate chron-
ic anxiety occurs in hypochondriasis. The patient focuses more on the belief that he has a
specific serious disease rather than on the actual symptoms. Difficulty swallowing, back
pain, light-headedness, and upset stomach are
common complaints. The patient tends to
“physician hop” and isn’t reassured by favorable physical examinations and laboratory test
results.
◆ Hypoglycemia. Anxiety resulting from hy-
poglycemia is usually mild to moderate and associated with hunger, mild headache, palpitations, blurred vision, weakness, and
diaphoresis.
◆ Mitral valve prolapse. Panic may occur in
patients with this valvular disorder, also
known as click-murmur syndrome because its
hallmark is a midsystolic click, followed by an
apical systolic murmur. Mitral valve prolapse
also may cause paroxysmal palpitations accompanied by sharp, stabbing, or aching precordial pain.
◆ Mood disorder. Anxiety may be the patient’s
chief complaint in the depressive or manic form
of mood disorder. In the depressive form,
chronic anxiety of varying severity occurs along
with dysphoria; anger; insomnia or hypersomnia; decreased libido, interest, energy, and concentration; appetite disturbance; multiple somatic complaints; and suicidal thoughts. In the
manic form, the patient’s chief complaint may
be a reduced need for sleep, hyperactivity, increased energy, rapid or pressured speech and,
in severe cases, paranoid ideas and other psychotic symptoms.
◆ Myocardial infarction (MI). In this life-
threatening disorder, acute anxiety commonly
occurs with persistent, crushing substernal pain
that may radiate to the left arm, jaw, neck, or
shoulder blades. MI may be accompanied by
shortness of breath, nausea, vomiting, diaphoresis, and cool, pale skin.
◆ Obsessive-compulsive disorder. Chronic
anxiety occurs in obsessive-compulsive disorder, which is marked by recurrent, unshakable
thoughts or impulses to perform ritualistic acts.
The patient recognizes these acts as irrational
but is unable to control them. Anxiety builds if
he can’t perform these acts and diminishes after
he does.
◆ Pheochromocytoma. Acute, severe anxiety
accompanies pheochromocytoma’s cardinal
sign: persistent or paroxysmal hypertension.
Other common findings include tachycardia,
diaphoresis, orthostatic hypotension, tachypnea, flushing, severe headache, palpitations,
nausea, vomiting, epigastric pain, and paresthesia.
◆ Phobias. In phobias, chronic anxiety accom-
panies persistent fear of an object, an activity,
or a situation that results in a compelling desire
to avoid it. The patient recognizes the fear as irrational but can’t suppress it.
◆ Pneumonia. Acute anxiety may occur in
pneumonia because of hypoxemia. Other findings include productive cough, pleuritic chest
pain, fever, chills, crackles, diminished breath
sounds, and hyperresonant lung fields.
◆ Pneumothorax. Acute anxiety occurs in
moderate to severe pneumothorax associated
with profound respiratory distress. It’s accompanied by sharp pleuritic pain, coughing, shortness of breath, cyanosis, asymmetrical chest expansion, pallor, jugular vein distention, and a
weak, rapid pulse.
◆ Postconcussion syndrome. Postconcussion
syndrome may produce chronic anxiety or periodic attacks of acute anxiety. The anxiety is
usually most pronounced in situations demanding attention, judgment, or comprehension.
Associated signs and symptoms include irritability, insomnia, dizziness, and mild
headache.
◆ Posttraumatic stress disorder. Posttrau-
matic stress disorder occurs in patients who
have experienced an extremely traumatic
event. It produces chronic anxiety of varying
severity and is accompanied by intrusive, vivid
memories and thoughts of the traumatic event.
The patient also relives the event in dreams
and nightmares. Insomnia, depression, and
feelings of numbness and detachment are common.
◆ Pulmonary edema. In pulmonary edema,
acute anxiety occurs with dyspnea, orthopnea,
cough with frothy sputum, tachycardia, tachypnea, crackles, ventricular gallop, hypotension,
and thready pulse. The patient’s skin may be
cool, clammy, and cyanotic.
◆ Pulmonary embolism. Acute anxiety is usu-
ally accompanied by dyspnea, tachypnea, chest
pain, tachycardia, blood-tinged sputum, and
low-grade fever.
◆ Rabies. Anxiety signals the beginning of the
acute phase of rabies. This rare disorder is
APHASIA 57
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characterized by painful laryngeal spasms associated with difficulty swallowing and, as a result, hydrophobia.
◆ Somatoform disorder. Somatoform disor-
der, which usually begins in young adulthood, is
characterized by anxiety and multiple somatic
complaints that can’t be explained physiologically. The symptoms aren’t produced intentionally but are severe enough to significantly impair functioning. Pain disorder, conversion
disorder, and hypochondriasis are examples of
somatoform disorder.
O
THER CAUSES
◆ Drugs. Many drugs cause anxiety, especially
sympathomimetics and central nervous system
stimulants. In addition, many antidepressants
may cause paradoxical anxiety.
S
PECIAL CONSIDERATIONS
Supportive care can help relieve anxiety in
many cases. Provide a calm, quiet atmosphere
and make the patient comfortable. Encourage
him to express his feelings and concerns freely.
If it helps, take a short walk with him while
you’re talking. Anxiety-reducing measures, such
as distraction, relaxation techniques, and
biofeedback, may also be helpful.
P
EDIATRIC POINTERS
Anxiety in children usually results from painful
physical illness or inadequate oxygenation. Its
autonomic signs tend to be more common and
dramatic than in adults.
G
ERIATRIC POINTERS
Changes in an elderly patient’s routine may provoke anxiety or agitation.
Aphasia
[Dysphasia]
Aphasia, impaired expression or comprehension of written or spoken language, reflects
disease or injury of the brain’s language centers. (See Where language originates, page 58.)
Depending on its severity, aphasia may slightly impede communication or may make it impossible. It can be classified as Broca’s, Wernicke’s, anomic, or global aphasia. Anomic
aphasia eventually resolves in more than 50%
of patients, but global aphasia is usually irreversible. (See Identifying types of aphasia,
page 59.)
EMERGENCY INTERVENTIONS Quickly
look for signs and symptoms of increased intracranial pressure (ICP), such as pupillary
changes, decreased level of consciousness (LOC),
vomiting, seizures, bradycardia, widening pulse
pressure, and irregular respirations. If you detect
signs of increased ICP, administer mannitol I.V. to
decrease cerebral edema. In addition, make sure
that emergency resuscitation equipment is readily
available to support respiratory and cardiac function, if necessary. You may have to prepare the patient for emergency surgery.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient doesn’t display signs of increased ICP, or if his aphasia has developed
gradually, perform a thorough neurologic examination, starting with the patient history.
You’ll probably need to obtain this history
from the patient’s family or companion because of the patient’s impairment. Ask if the
patient has a history of headaches, hypertension, seizure disorders, or drug use. Also ask
about the patient’s ability to communicate and
perform routine activities before he developed
aphasia.
Check for obvious signs of neurologic
deficit, such as ptosis or fluid leakage from
the nose and ears. Take the patient’s vital
signs and assess his LOC. Be aware, though,
that the patient’s verbal responses may be unreliable, making LOC assessment difficult.
Also, recognize that dysarthria (impaired articulation due to weakness or paralysis of the
muscles necessary for speech) or speech
apraxia (inability to voluntarily control the
muscles of speech) may accompany aphasia,
so speak slowly and distinctly, and allow the
patient ample time to respond. Assess the patient’s pupillary response, eye movements,
and motor function, especially his mouth and
tongue movement, swallowing ability, and
spontaneous movements and gestures. To
best assess motor function, first demonstrate
the motions and then have the patient imitate
them.
M
EDICAL CAUSES
◆ Alzheimer’s disease. In this degenerative
disease, anomic aphasia may begin insidiously
and then progress to severe global aphasia. Associated signs and symptoms include behavioral changes, loss of memory, poor judgment,
58 APHASIA
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Where language originates
Aphasia reflects damage to one or more of the
brain’s primary language centers, which, in
most people, are located in the left hemisphere. Broca’s area lies next to the region of
the motor cortex that controls the muscles
necessary for speech. Wernicke’s area is the
center of auditory, visual, and language com-
prehension. It lies between Heschl’s gyrus, the
primary receiver of auditory stimuli, and the
angular gyrus, a “way station” between the
brain’s auditory and visual regions. Connecting Wernicke’s and Broca’s areas is a large
nerve bundle, the arcuate fasciculus, which
allows repetition of speech.
FRONTAL LOBE
Motor control of voluntary
muscles
Personality
Concentration
Organization
Problem-solving
BROCA’S CENTER
Motor control of speech
HESCHL’S GYRUS
TEMPORAL LOBE
Hearing
Memory of hearing and vision
restlessness, myoclonus, and muscle rigidity. Incontinence is usually a late sign.
◆ Brain abscess. A brain abscess may cause
any type of aphasia. Aphasia usually develops
insidiously and may be accompanied by hemiparesis, ataxia, facial weakness, and signs of increased ICP.
◆ Brain tumor. A brain tumor may cause any
type of aphasia. As the tumor enlarges, other
types of aphasia may occur along with behavioral changes, memory loss, motor weakness,
seizures, auditory hallucinations, visual field
deficits, and increased ICP.
◆ Creutzfeldt-Jakob disease. Creutzfeldt-
Jakob disease is a rapidly progressive dementia
accompanied by neurologic signs and symptoms, such as myoclonic jerking, ataxia, aphasia, visual disturbances, and paralysis. It generally affects adults ages 40 to 65.
◆ Encephalitis. Encephalitis usually produces
transient aphasia. Its early signs and symptoms
PARIETAL LOBE
Sensory areas of touch,
pain, temperature
Understanding speech,
language
Expressing thoughts
ARCUATE FASCICULUS
ANGULAR GYRUS
OCCIPITAL LOBE
Visual recognition
Focusing the eye
WERNICKE’S CENTER
Interpreting speech
include fever, headache, and vomiting. Seizures,
confusion, stupor or coma, hemiparesis, asymmetrical deep tendon reflexes, positive Babinski’s reflex, ataxia, myoclonus, nystagmus, ocular
palsies, and facial weakness may accompany
aphasia.
◆ Head trauma. Severe head trauma may
cause any type of aphasia, which typically occurs suddenly and may be transient or permanent, depending on the extent of brain damage.
Associated signs and symptoms include blurred
or double vision, headache, pallor, diaphoresis,
numbness and paresis, cerebrospinal otorrhea
or rhinorrhea, altered respirations, tachycardia,
disorientation, behavioral changes, and signs of
increased ICP.
◆ Seizures. Seizures and the postictal state
may cause transient aphasia if the seizures involve the language centers.
◆ Stroke. The most common cause of aphasia,
stroke may produce Wernicke’s, Broca’s, or
Identifying types of aphasia
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APHASIA
59
Type
Anomic aphasia
Broca’s aphasia
(expressive aphasia)
Global aphasia
Wernicke’s
aphasia
(receptive
aphasia)
Location of lesion
Temporal-parietal area;
may extend to angular
gyrus, but sometimes
poorly localized
Broca’s area; usually in
third frontal convolution
of the left hemisphere
Broca’s and Wernicke’s
areas
Wernicke’s area; usually
in posterior or superior
temporal lobe
Signs and symptoms
Patient’s understanding of written and spoken language is relatively unimpaired. His
speech, although fluent, lacks meaningful
content. Word-finding difficulty and circumlocution are characteristic. Rarely, the patient also displays paraphasias.
Patient’s understanding of written and spoken language is relatively spared, but
speech is nonfluent, with word-finding difficulty, jargon, paraphasias, limited vocabulary, and simple sentence construction. The
patient can’t repeat words and phrases. If
Wernicke’s area is intact, he recognizes
speech errors and shows frustration. Hemiparesis is common.
Patient’s receptive and expressive ability is
profoundly impaired. He can’t repeat words
or phrases and can’t follow directions. His
occasional speech is marked by paraphasias or jargon.
Patient has difficulty understanding written
and spoken language. He can’t repeat
words or phrases and can’t follow directions. His speech is fluent but may be rapid
and rambling, with paraphasias. He has difficulty naming objects (anomia) and is unaware of speech errors.
global aphasia. Associated findings include decreased LOC, right-sided hemiparesis, homonymous hemianopia, paresthesia, and loss of sensation. (These signs and symptoms may appear
on the left side if the right hemisphere contains
the language centers.)
◆ Transient ischemic attack (TIA). TIA can
produce any type of aphasia, which occurs suddenly and resolves within 24 hours of the attack. Associated signs and symptoms include
transient hemiparesis, hemianopia, and paresthesia (all usually right-sided) as well as dizziness and confusion.
S
PECIAL CONSIDERATIONS
Immediately after aphasia develops, the patient
may become confused or disoriented. Help to
restore a sense of reality by frequently telling
him what has happened, where he is and why,
and what the date is. Carefully explain diagnostic tests, such as skull X-rays, computed tomog-
raphy scan or magnetic resonance imaging, angiography, and EEG. Later, expect periods of depression as the patient recognizes his disability.
Help him to communicate by providing a relaxed, accepting environment with a minimum
of distracting stimuli.
Be alert for sudden outbursts of profanity by
the patient. This common behavior usually reflects intense frustration with his impairment.
Deal with such outbursts as gently as possible
to minimize embarrassment.
When you speak to the patient, don’t assume
that he understands you. He may simply be interpreting subtle clues to meaning, such as social context, facial expressions, and gestures.
To help avoid misunderstanding, use nonverbal
techniques, speak to him in simple phrases, and
use demonstration to clarify your verbal directions.
Remember that aphasia is a language disorder, not an emotional or auditory one, so speak
60 APNEA
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to the patient in a normal tone of voice. Make
sure he has necessary aids, such as eyeglasses
or dentures, to facilitate communication. Refer
the patient to a speech pathologist early to help
him cope with his aphasia.
P
EDIATRIC POINTERS
Recognize that the term childhood aphasia is
sometimes mistakenly applied to children who
fail to develop normal language skills but who
aren’t considered mentally retarded or developmentally delayed. Aphasia refers solely to
loss of previously developed communication
skills.
Brain damage associated with aphasia in
children most commonly follows anoxia—
the result of near drowning or airway obstruction.
Apnea
Apnea, the cessation of spontaneous respiration, is occasionally temporary and self-limiting,
as in Cheyne-Stokes and Biot’s respirations. In
most cases, though, it’s a life-threatening emergency that requires immediate intervention to
prevent death.
Apnea usually results from one or more of six
pathophysiologic mechanisms, each of which
has numerous causes. Its most common causes
include trauma, cardiac arrest, neurologic disease, aspiration of foreign objects, bronchospasm, and drug overdose. (See Causes of
apnea.)
EMERGENCY INTERVENTIONS If you
detect apnea, first establish and maintain a
patent airway. Place the patient in a supine position, and open his airway using the head-tilt,
chin-lift technique. (Caution: If the patient has or
may have a head or neck injury, use the jawthrust technique to prevent hyperextending the
neck.) Next, quickly look, listen, and feel for
spontaneous respiration; if it’s
absent, begin artificial ventilation until it occurs
or until mechanical ventilation can be initiated.
Because apnea may result from (or may
cause) cardiac arrest, assess the patient’s carotid
pulse immediately after you’ve established a
patent airway. Or, if the patient is an infant or
small child, assess the brachial pulse instead. If
you can’t palpate a pulse, begin cardiac compression.
H
ISTORY AND PHYSICAL
EXAMINATION
When the patient’s respiratory and cardiac status is stable, investigate the underlying cause of
apnea. Ask him (or, if he’s unable to answer,
anyone who witnessed the episode) about the
onset of apnea and events immediately preceding it. The cause may become readily apparent,
as in trauma.
Take a patient history, especially noting reports of headache, chest pain, muscle weakness, sore throat, or dyspnea. Ask about a history of respiratory, cardiac, or neurologic disease
and about allergies and drug use.
Inspect the head, face, neck, and trunk for
soft-tissue injury, hemorrhage, or skeletal deformity. Don’t overlook obvious clues, such as oral
and nasal secretions (reflecting fluid-filled airways and alveoli) or facial soot and singed
nasal hair (suggesting thermal injury to the tracheobronchial tree).
Auscultate over all lung lobes for adventitious breath sounds, particularly crackles and
rhonchi, and percuss the lung fields for increased dullness or hyperresonance. Move on
to the heart, auscultating for murmurs, pericardial friction rub, and arrhythmias. Check for
cyanosis, pallor, jugular vein distention, and
edema. If appropriate, perform a neurologic assessment. Evaluate level of consciousness
(LOC), orientation, and mental status; test cranial nerve and motor function, sensation, and
reflexes in all extremities.
M
EDICAL CAUSES
◆ Airway obstruction. Occlusion or compres-
sion of the trachea, central airways, or smaller
airways can cause sudden apnea by blocking
the patient’s airflow and producing acute respiratory failure.
◆ Brain stem dysfunction. Primary or sec-
ondary brain stem dysfunction can cause apnea
by destroying the brain stem’s ability to initiate
respirations. Apnea may arise suddenly (as in
trauma, hemorrhage, or infarction) or gradually
(as in degenerative disease or tumor). Apnea
may be preceded by decreased LOC and various
motor and sensory deficits.
◆ Neuromuscular failure. Trauma or disease
can disrupt the mechanics of respiration, causing sudden or gradual apnea. Associated findings include diaphragmatic or intercostal muscle paralysis from injury, or respiratory
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