6245A.
qxd 8/23/08 7:56 PM Page 25
● Papillary necrosis (acute). Bilateral papil-
lary necrosis produces anuria or oliguria. It
also produces flank pain, costovertebral an-
gle tenderness, renal colic, abdominal pain
and rigidity, fever, vomiting, decreased bow-
el sounds, hematuria, and pyuria.
● Renal artery occlusion (bilateral). Bilateral
renal artery occlusion produces anuria or se-
vere oliguria, commonly accompanied by se-
vere, continuous upper abdominal and flank
pain; nausea and vomiting; decreased bowel
sounds; fever up to 102 F (38.9 C); and di-
astolic hypertension.
● Renal vein occlusion (bilateral). Bilateral
renal vein occlusion occasionally causes
anuria; more typical signs and symptoms in-
clude acute low back pain, fever, flank ten-
derness, and hematuria. Development of
pulmonary emboli — a common complica-
tion — produces sudden dyspnea, pleuritic
pain, tachypnea, tachycardia, crackles, pleu-
ral friction rub, and possibly hemoptysis.
● Urinary tract obstruction. Severe obstruc-
tion can produce acute, and sometimes, total
anuria, alternating with or preceded by burn-
ing and pain on urination, overflow inconti-
nence or dribbling, increased urinary fre-
quency 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 pro-
duces anuria. More typical findings include
malaise, myalgia, polyarthralgia, fever, ele-
vated blood pressure, hematuria, proteinuria,
arrhythmias, pallor, and possibly skin le-
sions, urticaria, and purpura.
OTHER CAUSES
● Diagnostic tests. Contrast media used in
radiographic studies can cause nephrotoxici-
ty, producing oliguria and, rarely, anuria.
● Drugs. Many classes of drugs can cause
anuria or, more commonly, oliguria through
their nephrotoxic effects. Antibiotics, espe-
cially aminoglycosides, are the most typical-
ly seen nephrotoxins. Anesthetics, heavy
metals, ethyl alcohol, and organic solvents
can also be nephrotoxic. Adrenergics and an-
ticholinergics can cause anuria by affecting
the nerves and muscles of micturition to pro-
duce urine retention.
APHASIA
NURSING CONSIDERATIONS
If catheterization fails to initiate urine flow,
prepare the patient for diagnostic studies —
such as ultrasonography, cystoscopy, retro-
grade pyelography, and renal scan — to de-
tect an obstruction higher in the urinary
tract. If these tests fail to reveal an obstruc-
tion, prepare the patient for further kidney
function studies. If these tests reveal an ob-
struction, immediate surgery may be indicat-
ed to remove the obstruction, and a nephros-
tomy or ureterostomy tube may be inserted
to drain urine.
Carefully monitor the patient’s vital signs
and intake and output, initially saving any
urine for inspection. Restrict daily fluid al-
lowance to 600 ml more than the previous
day’s total urine output. Restrict foods and
juices high in potassium and sodium, and
make sure that the patient maintains a bal-
anced diet with controlled protein levels.
Provide low-sodium hard candy to help de-
crease thirst. Record fluid intake and output,
and weigh the patient daily.
PATIENT TEACHING
Explain all tests and procedures to the pa-
tient. Depending on the cause of anuria, re-
view the disorder’s early warning signs and
symptoms. If the patient requires surgery,
withhold food and fluids. Review medica-
tions that may worsen renal function.
Aphasia
◆
Aphasia is an impairment in expressing or
comprehending written or spoken language.
It generally reflects disease or injury to the
brain’s language centers. (See Where language
originates, page 26.) Depending on its severity,
aphasia may slightly impede communication
or may make it impossible. It can be classi-
fied 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 27.)
Act now Quickly look for signs and
symptoms of increased intracranial pressure
(ICP), such as pupillary changes, decreased level of
consciousness (LOC), vomiting, seizures, bradycar-
dia, widening pulse pressure, and irregular respira-
tions. If you detect signs of increased ICP, insert a
25
6245A.qxd 8/23/08 7:56 PM Page 26
W HERE 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 hemi-
sphere. 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-
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
urinary catheter to prevent bladder rupture and
then administer mannitol I.V. to decrease cerebral
edema. In addition, make sure that emergency re-
suscitation equipment is readily available to support
respiratory and cardiac function, if necessary. You
may have to prepare the patient for emergency sur-
gery.
ASSESSMENT
History
A history will probably need to be obtained
from the patient’s family or companion be-
cause of the patient’s impairment. Determine
if the aphasia is new or when it began. De-
termine if the patient has a history of head-
aches, hypertension, seizure disorders, or
drug use.
Physical examination
Perform a complete neurologic examination.
Take the patient’s vital signs and assess his
26 APHASIA
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 enables
speech repetition.
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
LOC. Be aware, though, that assessing LOC
is commonly difficult because the patient’s
verbal responses may be unreliable. Assess
the patient’s pupillary response, eye move-
ments, 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. Don’t give liquids to
drink until ordered due to the risk of aspira-
tion.
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;
therefore, speak slowly and distinctly, and al-
low the patient ample time to respond.
Check for obvious signs of neurologic
6245A.qxd 8/23/08 7:56 PM Page 27

I DENTIFYING TYPES OF APHASIA

TYPE LOCATION OF LESION SIGNS AND SYMPTOMS

Anomic aphasia Temporal-parietal area; may
extend to angular gyrus, but
sometimes poorly localized
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
paraphasia.

Broca’s aphasia Broca’s area; usually in third
(expressive aphasia) frontal convolution of the left
hemisphere
Patient’s understanding of written and spoken
language is relatively spared, but speech is
nonfluent, evidencing word-finding difficulty,
jargon, paraphasia, limited vocabulary, and
simple sentence construction. He can’t repeat
words and phrases. If Wernicke’s area is in-
tact, he recognizes speech errors and shows
frustration. He’s commonly hemiparetic.

Global aphasia Broca’s and Wernicke’s areas Patient has profoundly impaired receptive
and expressive ability. He can’t repeat words
or phrases and can’t follow directions. His oc-
casional speech is marked by paraphasia or
jargon.

Wernicke’s aphasia Wernicke’s area; usually in
(receptive aphasia) posterior or superior tempo-
ral lobe
Patient has difficulty understanding written
and spoken language. He can’t repeat words
or phrases or can’t follow directions. His
speech is fluent but may be rapid and ram-
bling, with paraphasia. He has difficulty naming
objects (anomia) and is unaware of speech
errors.

deficit, such as ptosis or fluid leakage from MEDICAL CAUSES

the nose and ears.
Pediatric 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 the loss of previously developed
communication skills.
Brain damage associated with aphasia in
children most commonly follows anoxia —
the result of near-drowning or airway ob-
struction.
Geriatric pointers
Pre-existing diseases, such as dementia
(Alzheimer’s type, vascular, or others) or pre-
vious stroke may make it more difficult to
assess the patient for aphasia.
● Alzheimer’s disease. With Alzheimer’s dis-
ease, a degenerative disease, anomic aphasia
may begin insidiously and then progress to
severe global aphasia. Associated signs and
symptoms include behavioral changes, mem-
ory loss, poor judgment, restlessness, my-
oclonus, and muscle rigidity. Incontinence is
usually a late sign.
● Brain abscess. Any type of aphasia may
occur with brain abscess. Usually, aphasia
develops insidiously and may be accompa-
nied 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 aphasias may occur along with behav-
ioral changes, memory loss, motor weak-
ness, seizures, auditory hallucinations, visual
field deficits, and increased ICP.

APHASIA 27
6245A.qxd 8/23/08 7:56 PM Page 28
● Creutzfeldt-Jakob disease. Creutzfeldt-Ja-
cob disease is a rapidly progressive dementia
accompanied by neurologic signs and symp-
toms, such as myoclonic jerking, ataxia,
aphasia, vision disturbances, and paralysis. It
generally affects adults ages 40 to 65.
● Encephalitis. Encephalitis usually pro-
duces transient aphasia. Its early signs and
symptoms include fever, headache, and
vomiting. Seizures, confusion, stupor or
coma, hemiparesis, asymmetrical deep ten-
don reflexes, positive Babinski’s reflex, atax-
ia, myoclonus, nystagmus, ocular palsies,
and facial weakness may accompany apha-
sia.
● Head trauma. Any type of aphasia may
accompany severe head trauma, which oc-
curs suddenly and may be transient or per-
manent, depending on the extent of brain
damage. Associated signs and symptoms in-
clude blurred or double vision, headache,
pallor, diaphoresis, numbness and paresis,
cerebrospinal otorrhea or rhinorrhea, altered
respirations, tachycardia, disorientation, be-
havioral 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 apha-
sia, stroke may produce Wernicke’s, Broca’s,
or global aphasia. Associated findings in-
clude decreased LOC, right-sided hemipare-
sis, homonymous hemianopia, paresthesia,
and loss of sensation. (These signs and
symptoms may appear on the left side if the
right hemisphere contains the language cen-
ters.)
● Transient ischemic attack (TIA). A TIA can
produce any type of aphasia, which occurs
suddenly and resolves within 24 hours of the
TIA. Associated signs and symptoms include
transient hemiparesis, hemianopia, and par-
esthesia (all usually right-sided), dizziness,
and confusion.
NURSING CONSIDERATIONS
Maintain reality by frequently explaining
what has happened, where the patient is lo-
cated and why, and what the date is. Later,
expect periods of depression as the patient
recognizes his disability. Facilitate communi-
cation by providing a relaxed, accepting en-
vironment with a minimum of distracting
stimuli. Prepare the patient for a psychiatric
consultation if the depression becomes debil-
28 APNEA
itating or is demonstrated by personality
changes.
When you speak to the patient, don’t as-
sume that he understands you. He may sim-
ply 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 dis-
order, not an emotional or auditory one, so
speak to the patient in a normal tone of
voice. Make sure that 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.
PATIENT TEACHING
Carefully explain diagnostic tests, such as
skull X-rays, computed tomography or mag-
netic resonance imaging, angiography, and
electroencephalography. Explain the related
effects of aphasia to the patient and his fami-
ly, such as possible depression or the use of
profanity.
Apnea
◆
Apnea is the cessation of spontaneous respi-
ration and is usually a life-threatening emer-
gency that requires immediate intervention
to prevent death. It may occur as a tempo-
rary and self-limiting event, such as Cheyne-
Stokes and Biot’s respirations.
Apnea usually results from one or more
of six pathophysiologic mechanisms, each of
which has numerous causes. Its most com-
mon causes include trauma, cardiac arrest,
neurologic disease, aspiration of foreign ob-
jects, bronchospasm, and drug overdose.
(See Causes of apnea.)
Act now Upon discovering a patient with
apnea, immediately begin resuscitative
measures. Place the patient in a supine position.
Open the airway using the head tilt/chin lift tech-
nique, and look, listen, and feel for spontaneous
respirations. (If there’s suspected head, neck, or
spine trauma, use the jaw thrust maneuver to open
the airway). If breaths are absent, begin artificial
ventilation. If apnea was prolonged, full cardiac ar-