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Causes of apnea
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Various disorders may cause apnea.
Airway obstruction
◆ Asthma
◆ Bronchospasm
◆ Chronic bronchitis
◆ Chronic obstructive pul-
monary disease
◆ Foreign body aspiration
◆ Hemothorax or pneumotho-
rax
◆ Mucus plug
◆ Obstruction by tongue or
tumor
◆ Obstructive sleep apnea
◆ Secretion retention
◆ Tracheal or bronchial
rupture
Brain stem dysfunction
◆ Brain abscess
◆ Brain stem injury
◆ Brain tumor
◆ Central nervous system de-
pressants
◆ Central sleep apnea
◆ Cerebral hemorrhage
◆ Cerebral infarction
◆ Encephalitis
◆ Head trauma
◆ Increased intracranial pres-
sure
◆ Medullary or pontine
hemorrhage or infarction
◆ Meningitis
◆ Transtentorial herniation
Neuromuscular failure
◆ Amyotrophic lateral
sclerosis
◆ Botulism
◆ Diphtheria
◆ Guillain-Barré syndrome
◆ Myasthenia gravis
◆ Phrenic nerve paralysis
◆ Rupture of the diaphragm
◆ Spinal cord injury
APNEA
Parenchymatous
disease
◆ Acute respiratory distress
syndrome
◆ Diffuse pneumonia
◆ Emphysema
◆ Near drowning
◆ Pulmonary edema
◆ Pulmonary fibrosis
◆ Secretion retention
Pleural pressure
gradient disruption
◆ Flail chest
◆ Open chest wounds
Pulmonary capillary
perfusion decrease
◆ Arrhythmias
◆ Cardiac arrest
◆ Myocardial infarction
◆ Pulmonary embolism
◆ Pulmonary hypertension
◆ Shock
61
weakness or paralysis from acute or degenerative disease.
◆ Parenchymatous lung disease. An accu-
mulation of fluid within the alveoli produces apnea by interfering with pulmonary gas exchange
and producing acute respiratory failure. Apnea
may arise suddenly, as in near drowning and
acute pulmonary edema, or gradually, as in emphysema. Apnea also may be preceded by
crackles and labored respirations with accessory muscle use.
◆ Pleural pressure gradient disruption. Con-
version of normal negative pleural air pressure
to positive pressure by chest wall injuries (such
as flail chest) causes lung collapse, producing
respiratory distress and, if untreated, apnea. Associated signs include an asymmetrical chest
wall and asymmetrical or paradoxical respirations.
◆ Pulmonary capillary perfusion decrease.
Apnea can stem from obstructed pulmonary circulation, most commonly due to heart failure or
lack of circulatory patency. It occurs suddenly in
cardiac arrest, massive pulmonary embolism,
and most cases of severe shock; it occurs progressively in septic shock and pulmonary hypertension. Related findings include hypotension,
tachycardia, and edema.
O
THER CAUSES
◆ Drugs. Central nervous system (CNS) depres-
sants may cause hypoventilation and apnea.
Benzodiazepines may cause respiratory depression and apnea when given I.V. along with other CNS depressants to elderly or acutely ill patients.
Neuromuscular blockers—such as curariform
drugs and anticholinesterases— may produce
sudden apnea due to respiratory muscle paralysis.
◆ Sleep-related apneas. These repetitive ap-
neas occur during sleep from airflow obstruction or brain stem dysfunction.
S
PECIAL CONSIDERATIONS
Closely monitor the apneic patient’s cardiac and
respiratory status to prevent further apneic
episodes.
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P
EDIATRIC POINTERS
Premature neonates are especially susceptible
to periodic apneic episodes because of CNS immaturity. Other common causes of apnea in infants include sepsis, intraventricular and subarachnoid hemorrhage, seizures, bronchiolitis,
and sudden infant death syndrome.
In toddlers and older children, the primary
cause of apnea is acute airway obstruction from
aspiration of foreign objects. Other causes include acute epiglottitis, croup, asthma, and systemic disorders, such as muscular dystrophy
and cystic fibrosis.
G
ERIATRIC POINTERS
In elderly patients, increased sensitivity to analgesics, sedative-hypnotics, or any combination
of these drugs may produce apnea, even with
normal dosage ranges.
P
ATIENT COUNSELING
Educate the patient about safety measures related to aspiration of medications. Encourage
cardiopulmonary resuscitation training for all
adolescents and adults.
Apneustic respirations
Apneustic respirations are characterized by prolonged, gasping inspiration with a pause at full
inspiration. This irregular breathing pattern is
an important localizing sign of severe brain
stem damage.
Involuntary breathing is primarily regulated
by groups of neurons located in respiratory
centers in the medulla oblongata and the pons.
In the medulla, neurons react to impulses from
the pons and other areas to regulate respiratory rate and depth. In the pons, two respiratory
centers regulate respiratory rhythm by interacting with the medullary respiratory center to
smooth the transition from inspiration to expiration and back. The apneustic center in the
pons stimulates inspiratory neurons in the
medulla to precipitate inspiration. These inspiratory neurons, in turn, stimulate the pneumotaxic center in the pons to precipitate expiration. Destruction of neural pathways by
pontine lesions disrupts normal regulation of
respiratory rhythm, causing apneustic respirations.
Apneustic respirations must be differentiated
from bradypnea and hyperpnea (disturbances in
rate and depth, but not in rhythm), CheyneStokes respirations (rhythmic alterations in rate
and depth, followed by periods of apnea), and
Biot’s respirations (irregularly alternating periods of hyperpnea and apnea).
EMERGENCY INTERVENTIONS Your first
priority for a patient with apneustic respirations is to ensure adequate ventilation. You’ll
need to insert an artificial airway and administer
oxygen until mechanical ventilation can begin.
Next, thoroughly evaluate the patient’s neurologic status, using a standardized tool such as
the Glasgow Coma Scale. Finally, obtain a brief
patient history from a family member, if
possible.
M
EDICAL CAUSES
◆ Pontine lesions. Apneustic respirations usu-
ally result from extensive damage to the upper
or lower pons due to infarction, hemorrhage,
herniation, severe infection, tumor, or trauma.
Typically, these respirations are accompanied by
profound stupor or coma; pinpoint midline
pupils; ocular bobbing (a spontaneous downward jerk, followed by a slow drift up to midline); quadriplegia or, less commonly, hemiplegia with the eyes pointing toward the weak
side; a positive Babinski’s reflex; negative oculocephalic and oculovestibular reflexes; and, possibly, decorticate posture.
S
PECIAL CONSIDERATIONS
Constantly monitor the patient’s neurologic and
respiratory status. Watch for prolonged apneic
periods or signs of neurologic deterioration.
Monitor the patient’s arterial blood gas levels,
or use a pulse oximetry device. If appropriate,
prepare him for neurologic tests, such as EEG
and computed tomography scan or magnetic
resonance imaging.
P
EDIATRIC POINTERS
In young children, avoid using the Glasgow
Coma Scale because it requires verbal responses and assumes a certain level of language development.
Apraxia
Apraxia is the inability to perform purposeful
movements in the absence of significant weakness, sensory loss, poor coordination, or lack of
comprehension or motivation. This neurologic
APRAXIA
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How apraxia interferes with purposeful movement
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Type of apraxia
Ideational apraxia
Ideomotor apraxia
Kinetic apraxia
sign usually indicates a lesion in the cerebral
hemisphere. Its onset, severity, and duration
vary.
Apraxia is classified as ideational, ideomotor, or kinetic, depending on the stage at
which voluntary movement is impaired. It can
also be classified by type of motor or skill impairment. For example, facial apraxia and gait
apraxia involve specific motor groups and are
easily perceived. Constructional apraxia refers
to the inability to copy simple drawings or
patterns. Dressing apraxia refers to the inability to correctly dress oneself. Callosal apraxia
refers to normal motor function on one side
of the body accompanied by the inability to
reproduce movements on the other side. (See
How apraxia interferes with purposeful movement.)
H
ISTORY AND PHYSICAL
Description
The patient can physically
perform the steps required to
complete a task but fails to
remember the sequence in
which they’re performed.
The patient understands and
can physically perform the
steps required to complete a
task but can’t formulate a
plan to carry them out.
The patient understands the
task and formulates a plan to
complete it but fails to set the
proper muscles in motion.
EXAMINATION
If you detect apraxia, ask about previous neurologic disease. If the patient fails to report such
disease, begin a neurologic assessment. First,
take the patient’s vital signs and assess his level
of consciousness. Be alert for any evidence of
aphasia or dysarthria. Ask the patient if he has
recently experienced headaches or dizziness.
Then test the patient’s motor function, observing for weakness and tremors. Next, use a small
pin or another pointed object to test sensory
Examination technique
Ask the patient to tie his shoelace.
Typically, he’ll be able to grasp the
shoelace, loop it, and pull on it. However, he’ll fail to remember the sequence of steps needed to tie a knot.
Ask the patient to wave or cross his
arms. Typically, he won’t respond, but
he may be able to spontaneously perform the gesture.
Ask the patient to comb his hair. Typically, he’ll fail to move his arm and
hand correctly to do so. However, he’ll
be able to state that he needs to pick
up the comb and draw it through his
hair.
function. Check deep tendon reflexes for quality
and symmetry. Finally, test the patient for visual
field deficits.
Be alert for signs and symptoms of increased intracranial pressure (ICP), such as
headache and vomiting. If you detect these, elevate the head of the bed 30 degrees and monitor the patient closely for altered pupil size
and reactivity, bradycardia, widened pulse
pressure, and irregular respirations. Have
emergency resuscitation equipment nearby,
and be prepared to give mannitol I.V. to decrease cerebral edema.
If the patient is experiencing seizures, stay
with him and have another nurse notify the
physician immediately. Avoid restraining the patient. Help him to a supine position, loosen tight
clothing, and place a pillow or other soft object
beneath his head. If the patient’s teeth are
clenched, don’t force anything into his mouth. If
his mouth is open, protect the tongue by placing
a soft object, such as a washcloth, between his
teeth. Turn the patient’s head to provide an
open airway.
After completing the examination and ensuring the patient’s safety, take a history. Ask about
previous cerebrovascular disease, atherosclerosis, neoplastic disease, infection, or hepatic disease. Then assess the apraxia further to help
determine its type. (See Apraxia: Causes and
associated findings, page 64.)
64 APRAXIA
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SIGNS & SYMPTOMS
Apraxia: Causes and associated findings
Common
causes
Alzheimer’s disease
Brain abscess
Brain tumor
Hepatic
encephalopathy
Major associated signs and symptoms
Amnesia
Aphasia
Decreased level of
consciousness
Decreased mental
acuity
Dysarthria
Headache
Hyperreflexia
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Incontinence
Seizures
Tremors
Visual field deficits
•
•
•
•
•
•
•
•
••
Stroke
M
EDICAL CAUSES
◆ Alzheimer’s disease. Alzheimer’s disease
sometimes causes gradual and irreversible
ideomotor apraxia. It can also cause amnesia,
anomia, decreased attention span, apathy,
aphasia, restlessness, agitation, paranoid delusions, incontinence, social withdrawal, ataxia,
and tremors.
◆ Brain abscess. Apraxia occasionally re-
sults from a large brain abscess but usually resolves spontaneously after the infection subsides. Depending on the location of the
abscess, apraxia may be accompanied by
headache, fever, drowsiness, decreased mental acuity, aphasia, dysarthria, hemiparesis,
hyperreflexia, incontinence, focal or generalized seizures, and ocular disturbances, such
as nystagmus, visual field deficits, and unequal pupils.
◆ Brain tumor. In a brain tumor, progressive
apraxia may be preceded by decreased mental
acuity, headache, dizziness, and seizures. It
may occur with or directly after early signs of
increased ICP, such as pupil changes. It may
also occur with other localizing signs and symptoms of the tumor, such as aphasia, dysarthria,
visual field deficits, weakness, stiffness, and hyperreflexia in the extremities.
••
•
•
◆ Hepatic encephalopathy. Hepatic en-
cephalopathy may cause gradual onset of constructional apraxia, which may be reversible
with treatment. Early associated signs and
symptoms include disorientation, amnesia,
slurred speech, dysarthria, asterixis, and lethargy. Later signs include hyperreflexia, positive
Babinski’s reflex, agitation, seizures, fetor hepaticus, stupor, and coma.
◆ Stroke. Stroke commonly causes sudden on-
set of apraxia, which typically resolves spontaneously but may persist. Associated signs and
symptoms vary according to the affected artery
but can include headache, confusion, stupor or
coma, hemiplegia, unilateral or bilateral visual
field deficits, aphasia, agnosia, dysarthria, and
urinary incontinence.
S
PECIAL CONSIDERATIONS
Prepare the patient for diagnostic studies, such
as computed tomography and radionuclide
brain scans. Because weakness, sensory
deficits, confusion, and seizures may accompany apraxia, take measures to ensure safety. For
example, assist the patient with gait apraxia in
walking.
Explain the patient’s apraxia to him, and encourage his participation in normal activities.
Help him to overcome his frustration at being
••
ARM PAIN
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Causes of localized arm pain
Various disorders cause hand, wrist, elbow, or shoulder pain. In some disorders, pain may radiate
from the injury site to other areas.
65
Hand pain
◆ Arthritis
◆ Buerger’s disease
◆ Carpal tunnel syndrome
◆ Dupuytren’s contracture
◆ Elbow tunnel syndrome
◆ Fracture
◆ Ganglion
◆ Infection
◆ Occlusive vascular
disease
◆ Radiculopathy
◆ Raynaud’s disease
◆ Shoulder-hand syndrome
(reflex sympathetic dystrophy)
◆ Sprain or strain
◆ Thoracic outlet
syndrome
◆ Trigger finger
Wrist pain
◆ Arthritis
◆ Carpal tunnel syndrome
◆ Fracture
◆ Ganglion
◆ Sprain or strain
◆ Tenosynovitis (de Quer-
vain’s disease)
Elbow pain
◆ Arthritis
◆ Bursitis
◆ Dislocation
◆ Fracture
◆ Lateral epicondylitis (tennis
elbow)
◆ Tendinitis
◆ Ulnar neuritis
Shoulder pain
◆ Acromioclavicular separa-
tion
◆ Acute pancreatitis
unable to perform routine tasks by demonstrating each step in these tasks and giving
him sufficient time to imitate each step. Avoid
giving complex directions, and enlist the help
of family members in rehabilitation. Also, refer
the patient to a physical or occupational
therapist.
◆ Adhesive capsulitis (frozen
shoulder)
◆ Angina pectoris
◆ Arthritis
◆ Bursitis
◆ Cholecystitis or cholelithia-
sis
◆ Clavicle fracture
◆ Diaphragmatic pleurisy
◆ Dislocation
◆ Dissecting aortic aneurysm
◆ Gastritis
◆ Humeral neck fracture
◆ Infection
◆ Pancoast’s syndrome
◆ Perforated ulcer
◆ Pneumothorax
◆ Ruptured spleen (left shoul-
der)
◆ Shoulder-hand syndrome
◆ Subphrenic abscess
◆ Tendinitis
ing aware of his limitations. Also provide emotional support because playmates may tease a
child who can’t perform normal physical activities.
Arm pain
P
EDIATRIC POINTERS
Detecting apraxia in children can be difficult.
However, any sudden inability to perform a previously accomplished movement warrants
prompt neurologic evaluation because a brain
tumor—the most common cause of apraxia in
children—may be treated effectively if detected
early.
Brain damage in a young child may cause developmental apraxia, which interferes with the
ability to learn activities that require sequential
movement, such as hopping, jumping, dancing,
or hitting or kicking a ball. When caring for a
child with apraxia, provide an environment
that’s conducive to rehabilitation while remain-
Arm pain usually results from musculoskeletal
disorders, but it can also stem from neurovascular or cardiovascular disorders. (See Causes of
localized arm pain.) In some cases, arm pain
may be referred from another area, such as the
chest, neck, or abdomen. Its location, onset,
and character provide clues to its cause. The
pain may affect the entire arm or only the upper
arm or forearm. It may arise suddenly or gradually and be constant or intermittent. Arm pain
can be described as sharp or dull, burning or
numbing, and shooting or penetrating. Diffuse
arm pain, though, may be difficult to describe,
especially if it isn’t associated with injury.
66 ARM PAIN
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SIGNS & SYMPTOMS
Arm pain: Causes and associated findings
Major associated signs and symptoms
Common
causes
Angina
Biceps rupture
Cellulitis
Cervical nerve
root compression
Compartment
syndrome
Fractures
Muscle contusion
Muscle strain
Myocardial
infarction
Neoplasm of the
arm
Osteomyelitis
Chest pain
Crepitus
Decreased motion
Decreased reflex
response
Deformity
Ecchymosis
Edema
Impaired
circulation
Muscle weakness
•
•• •
•
•••
•••••
•• •••• •
••
••
•
•• •
•
•
Nausea
•
Paresthesia
Vomiting
•
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient reports arm pain after an injury,
take a brief history of the injury from the patient. Then quickly assess him for severe injuries requiring immediate treatment. If you’ve
ruled out severe injuries, check pulses, capillary
refill time, sensation, and movement distal to
the affected area because circulatory impairment or nerve injury may require immediate
surgery. Inspect the arm for deformities, assess
the level of pain, and immobilize the arm to
prevent further injury.
If the patient reports continuous or intermit-
tent arm pain, ask him to describe it and to re-
late when it began. Is the pain associated with
repetitive or specific movements or positions?
Ask him to point out other painful areas because arm pain may be referred. For example,
arm pain commonly accompanies the characteristic chest pain of myocardial infarction, and
right shoulder pain may be referred from the
right-upper-quadrant abdominal pain of cholecystitis. Ask the patient if the pain worsens in
the morning or in the evening, if it prevents him
from performing his job, and if it restricts any
movements. Also ask if heat, rest, or drugs relieve it. Finally, ask about any preexisting illnesses, a family history of gout or arthritis, and
current drug therapy.
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67
Next, perform a focused examination. Observe the way the patient walks, sits, and holds
his arm. Inspect the entire arm, comparing it
with the opposite arm for symmetry, movement,
and muscle atrophy. (It’s important to know if
the patient is right- or left-handed.) Palpate the
entire arm for swelling, nodules, and tender areas. In both arms, compare active range of motion, muscle strength, and reflexes.
If the patient reports numbness or tingling,
check his sensation to vibration, temperature,
and pinprick. Compare bilateral hand grasps
and shoulder strength to detect weakness.
If the patient has a cast, splint, or restrictive
dressing, check for circulation, sensation, and
mobility distal to the dressing. Ask the patient
about edema and if the pain has worsened
within the last 24 hours.
Examine the neck for pain on motion, point
tenderness, muscle spasms, or arm pain when
the neck is extended with the head toward the
involved side. (See Arm pain: Causes and associ-
ated findings.)
M
EDICAL CAUSES
◆ Angina. Angina may cause inner arm pain as
well as chest and jaw pain. Typically, the pain
follows exertion and persists for a few minutes.
Accompanied by dyspnea, diaphoresis, and apprehension, the pain is relieved by rest or vasodilators such as nitroglycerin.
◆ Biceps rupture. Rupture of the biceps after
excessive weight lifting or osteoarthritic degeneration of bicipital tendon insertion at the
shoulder can cause pain in the upper arm. Forearm flexion and supination aggravate the pain.
Other signs and symptoms include muscle
weakness, deformity, and edema.
◆ Cellulitis. Cellulitis typically affects the legs,
but it can also affect the arms. It produces pain
as well as redness, tenderness, edema and, at
times, fever, chills, tachycardia, headache, and
hypotension. Cellulitis usually follows an injury
or insect bite.
◆ Cervical nerve root compression. Com-
pression of the cervical nerves supplying the
upper arm produces chronic arm and neck pain,
which may worsen with movement or prolonged sitting. The patient may also experience
muscle weakness, paresthesia, and decreased
reflex response.
◆ Compartment syndrome. Severe pain with
passive muscle stretching is the cardinal symptom of compartment syndrome, which may also
impair distal circulation and cause muscle
weakness, decreased reflex response, paresthesia, and edema. Ominous signs include paralysis and absent pulse.
◆ Fractures. In fractures of the cervical ver-
tebrae, humerus, scapula, clavicle, radius, or
ulna, pain can occur at the injury site and radiate throughout the entire arm. Pain at a
fresh fracture site is intense and worsens with
movement. Associated signs and symptoms
include crepitus, which is felt and heard from
bone ends rubbing together (don’t attempt to
elicit this sign); deformity if bones are misaligned; local ecchymosis and edema; impaired distal circulation; paresthesia; and decreased sensation distal to the injury site.
Fractures of the small wrist bones can manifest with pain and swelling several days after
the trauma.
◆ Muscle contusion. Muscle contusion may
cause generalized pain in the injured area as
well as local swelling and ecchymosis.
◆ Muscle strain. Acute or chronic muscle
strain causes mild to severe pain with movement. The resultant reduction in arm movement
may cause muscle weakness and atrophy.
◆ Myocardial infarction. In this life-
threatening disorder, the patient may complain
of left arm pain in addition to the characteristic
deep and crushing chest pain. He may display
weakness, pallor, nausea, vomiting, diaphoresis, altered blood pressure, tachycardia, dyspnea, and feelings of apprehension or impending doom.
◆ Neoplasm of the arm. A neoplasm of the
arm produces continuous, deep, and penetrating arm pain that worsens at night. Occasionally, redness and swelling accompany arm pain;
later, skin breakdown, impaired circulation, and
paresthesia may occur.
◆ Osteomyelitis. Osteomyelitis typically begins
with vague and evanescent localized arm pain
and fever and is accompanied by local tenderness, painful and restricted movement and, later,
swelling. Associated findings include malaise
and tachycardia.
S
PECIAL CONSIDERATIONS
If you suspect a fracture, apply a sling or a splint
to immobilize the arm, and monitor the patient
for worsening pain, numbness, or decreased
circulation distal to the injury site. Also, monitor
vital signs and be alert for tachycardia, hypotension, and diaphoresis. Withhold food, fluids, and
68 ASTERIXIS
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Recognizing asterixis
In asterixis, the patient’s wrists and fingers
are observed to “flap” because of a brief,
rapid relaxation of wrist dorsiflexion.
analgesics until potential fractures are evaluated. Promote the patient’s comfort by elevating
his arm and applying ice. Clean abrasions and
lacerations and apply dry, sterile dressings if
necessary. Also, prepare the patient for X-rays
or other diagnostic tests.
P
EDIATRIC POINTERS
In children, arm pain commonly results from
fractures, muscle sprain, muscular dystrophy, or
rheumatoid arthritis. In young children especially, the exact location of the pain may be difficult
to establish. Watch for nonverbal clues, such as
wincing or guarding.
If the child has a fracture or sprain, obtain a
complete account of the injury. Closely observe
interactions between the child and his family,
and don’t rule out the possibility of child
abuse.
G
ERIATRIC POINTERS
Elderly patients with osteoporosis may experience fractures from simple trauma or even from
heavy lifting or unexpected movements. They’re
also prone to degenerative joint disease that
can involve several joints in the arm or neck.
P
ATIENT COUNSELING
Advise a patient with a cast to notify his physician if he detects worsening swelling, purple
discoloration of fingers, or numbness or tingling
because these signs may represent vascular
compliance due to a tight cast. Also, inform a
patient with angina that arm pain, usually leftsided, may represent an ischemic event, espe-
cially if accompanied by diaphoresis, nausea,
vomiting, and anxiety.
Asterixis
[Liver flap, flapping tremor]
A bilateral, coarse movement, asterixis is characterized by sudden relaxation of muscle
groups holding a sustained posture. This elicited
sign is most commonly observed in the wrists
and fingers but may also appear during any sustained voluntary action. Typically, it signals hepatic, renal, or pulmonary disease.
To elicit asterixis, have the patient extend his
arms, dorsiflex his wrists, and spread his fingers
(or do this for him, if necessary). Briefly observe
him for asterixis. Alternatively, if the patient has
a decreased level of consciousness (LOC) but
can follow verbal commands, ask him to
squeeze two of your fingers. Consider rapid
clutching and unclutching indications of asterixis. Or, elevate the patient’s leg off the bed and
dorsiflex the foot. Briefly check for asterixis in
the ankle. If the patient can tightly close his
eyes and mouth, watch for irregular tremulous
movements of the eyelids and corners of the
mouth. If he can stick out his tongue, observe
it for continuous quivering. (See Recognizing
asterixis.)
EMERGENCY INTERVENTIONS Because
asterixis may signal serious metabolic deterioration, quickly evaluate the patient’s neurologic
status and vital signs. Compare these data with
his baseline, and watch carefully for acute
changes. Continue to closely monitor neurologic
status, vital signs, and urine output.
Watch for signs of respiratory insufficiency, and
be prepared to provide endotracheal intubation
and ventilatory support. Also, be alert for complications of end-stage hepatic, renal, or pulmonary
disease.
If the patient has hepatic disease, assess him
for early indications of hemorrhage, including
restlessness, tachypnea, and cool, moist, pale
skin. (If the patient is jaundiced, check for pallor
in the conjunctivae and mucous membranes of
the mouth.) Be aware that hypotension, oliguria,
hematemesis, and melena are late signs of hemorrhage. Prepare to insert a large-bore I.V.
catheter for fluid and blood replacement. Position
the patient flat in bed with his legs elevated 20
degrees. Begin or continue to administer oxygen.
If the patient has renal disease, briefly review
the therapy he has received. If he’s on dialysis, ask
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69
about the frequency of treatments to help gauge
the disease’s severity. Question a family member if
the patient’s LOC is significantly decreased.
Then assess the patient for hyperkalemia and
metabolic acidosis. Look for tachycardia, nausea,
diarrhea, abdominal cramps, muscle weakness,
hyperreflexia, and Kussmaul’s respirations. Prepare to administer sodium bicarbonate, calcium
gluconate, dextrose, insulin, or sodium polystyrene sulfonate (Kayexalate).
If the patient has pulmonary disease, check for
labored respirations, tachypnea, accessory muscle
use, and cyanosis, which are critical signs.
Prepare to provide ventilatory support by nasal
cannula, mask, or intubation and mechanical
ventilation.
M
EDICAL CAUSES
◆ Hepatic encephalopathy. A life-threatening
disorder, hepatic encephalopathy initially
causes mild personality changes and a slight
tremor. The tremor progresses to asterixis—a
hallmark of hepatic encephalopathy—and is accompanied by lethargy, aberrant behavior, and
apraxia. Eventually, the patient becomes stuporous and displays hyperventilation. After slipping into a coma, the patient exhibits characteristic hyperactive reflexes, positive Babinski’s
reflex, and fetor hepaticus. He also may experience bradycardia, decreased respirations, and
seizures.
◆ Respiratory insufficiency, severe. Charac-
terized by life-threatening respiratory acidosis,
severe respiratory insufficiency initially produces headache, restlessness, confusion, apprehension, and decreased reflexes. Eventually,
the patient becomes somnolent and may
demonstrate asterixis before slipping into a
coma. Associated signs and symptoms of respiratory insufficiency include difficulty breathing
and rapid, shallow respirations. The patient
may be hypertensive in early disease but hypotensive later.
◆ Uremic syndrome. Uremic syndrome is a
life-threatening disorder that initially causes
lethargy, somnolence, confusion, disorientation,
behavior changes, and irritability. Eventually,
signs and symptoms appear in diverse body systems. Asterixis is accompanied by stupor, paresthesia, muscle twitching, fasciculations, and
footdrop. Other signs and symptoms include
polyuria and nocturia followed by oliguria and
then anuria, elevated blood pressure, signs of
heart failure and pericarditis, Kussmaul’s respirations, anorexia, nausea, vomiting diarrhea, GI
bleeding, weight loss, ammonia breath odor,
and metallic taste (dysgeusia).
O
THER CAUSES
◆ Drugs. Certain drugs, such as the anticonvul-
sant phenytoin, may cause asterixis.
S
PECIAL CONSIDERATIONS
Provide simple comfort measures, such as allowing frequent rest periods to minimize fatigue
and elevating the head of the bed to relieve dyspnea and orthopnea. Administer oil baths and
avoid soap to relieve itching caused by jaundice
and uremia. Provide emotional support to the
patient and his family.
If the patient is intubated or has a decreased
LOC, provide enteral or parenteral nutrition.
Closely monitor serum and urine glucose levels
to evaluate hyperalimentation. Because the patient will probably be on bed rest, reposition him
at least once every 2 hours to prevent skin breakdown. Also observe strict hand-washing and
aseptic techniques when changing dressings and
caring for invasive lines because the patient’s debilitated state makes him prone to infection.
P
EDIATRIC POINTERS
End-stage hepatic, renal, and pulmonary disease may also cause asterixis in children.
Ataxia
Classified as cerebellar or sensory, ataxia refers
to incoordination and irregularity of voluntary,
purposeful movements. Cerebellar ataxia results
from disease of the cerebellum and its pathways
to and from the cerebral cortex, brain stem, and
spinal cord. It causes gait, trunk, limb, and possibly speech disorders. Sensory ataxia results
from impaired position sense (proprioception)
due to interruption of afferent nerve fibers in the
peripheral nerves, posterior roots, posterior
columns of the spinal cord, or medial lemnisci
or, occasionally, from a lesion in both parietal
lobes. It causes gait disorders. (See Identifying
ataxia, page 70.)
Ataxia occurs in acute and chronic forms.
Acute ataxia may result from stroke, hemorrhage, or a large tumor in the posterior fossa. In
this life-threatening condition, the cerebellum
may herniate downward through the foramen
magnum behind the cervical spinal cord, or upward through the tentorium on the cerebral
hemispheres. Herniation may also compress the
70 ATAXIA
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Identifying ataxia
Ataxia may be observed in the patient’s
speech, in the movements of his trunk and
limbs, or in his gait.
In speech ataxia, a form of dysarthria, the
patient typically speaks slowly and stresses
usually unstressed words and syllables.
Speech content is unaffected.
In truncal ataxia, a disturbance in equilibrium,
the patient can’t sit or stand without falling, and
his head and trunk may bob and sway (titubation). If he can walk, his gait is reeling.
In limb ataxia, the patient loses the ability to
gauge distance, speed, and power of movement, resulting in poorly controlled, variable,
and inaccurate voluntary movements. He may
move too quickly or too slowly, or his movements may break down into component parts,
giving him the appearance of a puppet or a ro-
brain stem. Acute ataxia may also result from
drug toxicity or poisoning. Chronic ataxia can
be progressive and may result from acute disease. It can also occur in metabolic and chronic
degenerative neurologic disease.
EMERGENCY INTERVENTIONS If ataxic
movements develop suddenly, examine the
patient for signs of increased intracranial pressure
and impending herniation. Determine his level of
consciousness (LOC), and be alert for pupillary
changes, motor weakness or paralysis, neck stiffness or pain, and vomiting. Check vital signs, especially respirations; abnormal respiratory patterns may quickly lead to respiratory arrest.
Elevate the head of the bed. Have emergency resuscitation equipment readily available. Prepare
the patient for a computed tomography scan or
surgery.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient isn’t in distress, review his history.
Ask about multiple sclerosis, diabetes, central
nervous system infection, neoplastic disease,
previous stroke, and a family history of ataxia.
Also ask about chronic alcohol abuse or prolonged exposure to industrial toxins such as
mercury. Find out if the ataxia developed suddenly or gradually.
If necessary, perform Romberg’s test to help
distinguish between cerebellar and sensory
ataxia. Instruct the patient to stand with his feet
bot. Other effects include a coarse, irregular
tremor in purposeful movement (but not at
rest) and reduced muscle tone.
In gait ataxia, the patient’s gait is wide
based, unsteady, and irregular.
In cerebellar ataxia, the patient may stagger
or lurch in zigzag fashion, turn with extreme
difficulty, and lose his balance when his feet
are together.
In sensory ataxia, the patient moves
abruptly and stomps or taps his feet. This occurs because he throws his feet forward and
outward, and then brings them down first on
the heels and then on the toes. The patient
also fixes his eyes on the ground, watching
his steps; if he can’t watch his steps, staggering worsens. When he stands with his
feet together, he sways or loses balance.
together and his arms at his side. Note his posture and balance, first with his eyes open and
then with them closed. Test results may indicate
normal posture and balance (minimal swaying),
cerebellar ataxia (swaying and inability to maintain balance with eyes open or closed), or sensory ataxia (increased swaying and inability to
maintain balance with eyes closed). Stand close
to the patient during this test to prevent his
falling.
If you test for gait and limb ataxia, be aware
that motor weakness may mimic ataxic movements, so check motor strength, too. Gait ataxia
may be severe, even when limb ataxia is minimal. Ask the patient with gait ataxia if he tends
to fall to one side and if he falls more at night.
With truncal ataxia, remember that the patient’s
inability to walk or stand, combined with the
absence of other signs while he’s lying down,
may give the impression of hysteria or drug or
alcohol intoxication.
M
EDICAL CAUSES
◆ Cerebellar abscess. Cerebellar abscess
commonly causes limb ataxia on the same side
as the lesion as well as gait and truncal ataxia.
Typically, the initial symptom is headache localized behind the ear or in the occipital region,
followed by oculomotor palsy, fever, vomiting,
altered LOC, and coma.
◆ Cerebellar hemorrhage. Cerebellar hemor-
rhage is a life-threatening disorder in which
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