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BUTTERFLY RASH
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131
abdominal CT scan can determine ectopic involvement. Visual field testing and a skull CT
scan can identify pituitary tumors.
P
EDIATRIC POINTERS
Although rare in children, buffalo hump may occur at any age. In children older than age 7, this
sign usually results from pituitary oversecretion
of corticotropin in bilateral adrenal hyperplasia.
In younger children, it commonly results from
glucocorticoid therapy—for example, overuse of
glucocorticoid eyedrops.
P
ATIENT COUNSELING
Advise the patient about proper diet, drug therapy, and exercise. Provide education and intervention for emotional lability.
Butterfly rash
A butterfly rash is typically a sign of systemic lupus erythematosus (SLE), but it can also signal
dermatologic disorders. Typically, this rash appears in a malar distribution across the nose
and cheeks. (See Recognizing butterfly rash.)
Similar rashes may appear on the neck, scalp,
and other areas. A butterfly rash is sometimes
mistaken for sunburn because it can be provoked or aggravated by ultraviolet rays, but it
has more substance, is more sharply demarcated, and has a thicker feel in relation to surrounding skin.
H
ISTORY AND PHYSICAL
EXAMINATION
Ask the patient when he first noticed the butterfly rash and if he has recently been exposed to
the sun. Has he noticed a rash elsewhere on his
body? Also, ask about recent weight or hair
loss. Does he have a family history of lupus? Is
he taking hydralazine or procainamide (common causes of drug-induced lupus erythematosus)?
Inspect the rash, noting any macules,
papules, pustules, or scaling. Is the rash edematous? Are areas of hypopigmentation or hyperpigmentation present? Look for blisters or
ulcers in the mouth, and note any inflamed lesions. Check for rashes elsewhere on the body.
(See Butterfly rash: Causes and associated
findings.)
Plaques
Pruritus
Scaling
Sore throat
Telangiectasia
•
•
•
•
•• •
•
•
Vomiting
•
•••
Recognizing butterfly
rash
In a classic butterfly rash, lesions appear
on the cheeks and the bridge of the nose,
creating a characteristic butterfly pattern.
The rash may vary in severity from malar
erythema to discoid lesions (plaques).
Weight loss
Characteristic rash
132 BUTTERFLY RASH
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M
EDICAL CAUSES
◆ Discoid lupus erythematosus. Discoid lu-
pus erythematosus is a localized form of lupus
erythematosus characterized by a rash on one
or both sides of the face that consists of erythematous, raised, sharply demarcated plaques
with follicular plugging and central atrophy. The
rash may also involve the scalp, ears, chest, and
any part of the body exposed to the sun. Telangiectasia, scarring alopecia, and hypopigmentation or hyperpigmentation may occur later.
Other accompanying signs include conjunctival
redness, dilated capillaries of the nail fold, bilateral parotid gland enlargement, oral lesions,
and mottled, reddish blue skin on the legs.
◆ Erysipelas. Erysipelas causes rosy or crim-
son swollen lesions, mainly on the neck and
head and commonly along the nasolabial fold. It
may cause hemorrhagic pus-filled blisters. Other
signs and symptoms include fever, chills, cervical lymphadenopathy, and malaise.
◆ Polymorphous light eruption. A butterfly
rash appears as erythema, vesicles, plaques,
and multiple small papules that may later become eczematized, lichenified, and excoriated.
Provoked by ultraviolet rays, the rash appears
on the cheeks and bridge of the nose, the hands
and arms, and other areas, beginning a few
hours to several days after exposure. It may be
accompanied by pruritus.
◆ Rosacea. Initially, the rash may appear as a
prominent, nonscaling, intermittent erythema
limited to the lower half of the nose or including
the chin, cheeks, and central forehead. As
rosacea develops, the duration of the rash increases; instead of disappearing after each
episode, the rash varies in intensity and is commonly accompanied by telangiectasia. In advanced rosacea, the skin is oily, with papules,
pustules, nodules, and telangiectasia restricted
to the central oval of the face. In men with severe rosacea, the butterfly rash may be accompanied by rhinophyma—a thickened, lobulated
overgrowth of sebaceous glands and epithelial
connective tissue on the lower half of the nose
and, possibly, the adjacent cheeks. This is more
common in elderly patients.
◆ Seborrheic dermatitis. In this disorder,
greasy, scaling, slightly yellow macules and
papules of varying size appear on the cheeks
and the bridge of the nose in a butterfly pattern.
The scalp, beard, eyebrows, portions of the forehead above the bridge of the nose, nasolabial
fold, or trunk may also be involved. Associated
signs and symptoms include crusts and fissures
(particularly when the external ear and scalp are
involved), pruritus, redness, blepharitis, styes,
severe acne, and oily skin. Severe seborrheic
dermatitis of the face occurs in acquired immunodeficiency syndrome.
◆ Systemic lupus erythematosus (SLE). Oc-
curring in about 40% of patients with SLE—a
connective tissue disorder—a butterfly rash appears as a red, often scaly, sharply demarcated
macular eruption. The rash may be transient in
patients with acute SLE or may progress slowly
to include the forehead, chin, the area around
the ears, and other exposed areas. Common associated skin findings include scaling, patchy
alopecia, mucous membrane lesions, mottled
erythema of the palms and fingers, periungual
erythema with edema, reddish purple macular
lesions on the volar surfaces of the fingers,
telangiectasia of the base of the nails or eyelids,
purpura, petechiae, and ecchymoses.
The rash may be accompanied by joint pain,
stiffness, and deformities, particularly ulnar deviation of the fingers and subluxation of the
proximal interphalangeal joints. Related findings
include periorbital and facial edema, dyspnea,
low-grade fever, malaise, weakness, fatigue,
weight loss, anorexia, nausea, vomiting, lymphadenopathy, photosensitivity, and hepatosplenomegaly.
O
THER CAUSES
◆ Drugs. Hydralazine and procainamide can
cause a lupuslike syndrome.
S
PECIAL CONSIDERATIONS
Prepare the patient for immunologic studies,
complete blood count, and possibly liver studies. Obtain a urine specimen if needed. Withhold photosensitizing drugs, such as phenothiazines, sulfonamides, sulfonylureas, and
thiazide diuretics. Instruct the patient to avoid
exposure to the sun or to use a sunscreen. Suggest that he use hypoallergenic makeup to help
conceal facial lesions.
P
EDIATRIC POINTERS
Rare in pediatric patients, a butterfly rash may
occur as part of an infectious disease such
as erythema infectiosum (“slapped cheek
syndrome”).
Café-au-lait spots
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An important indicator of neurofibromatosis
and other congenital melanotic disorders,
café-au-lait spots appear as flat, light brown,
uniformly hyperpigmented macules or patches
on the skin surface. They usually appear during the first 3 years of life but may develop at
any age. Café-au-lait spots can be differentiated from freckles and other benign birthmarks
by their larger size (a few millimeters to
[1.6 cm] or larger in diameter) and irregular
shape. They usually have no significance;
however, six or more café-au-lait spots may
be associated with an underlying neurologic
disorder.
H
ISTORY AND PHYSICAL
EXAMINATION
Ask the patient or his parents when the café-aulait spots first appeared. Also ask about a family
history of these spots and of neurofibromatosis.
Review the patient’s history for seizures, frequent fractures, or mental retardation.
Inspect the skin, noting the location and pattern of the spots. Look for distinctive skin lesions, such as axillary freckling, mottling, small
spherical patches, and areas of depigmentation.
Large lesions should be measured along the
longest axis. A wood’s light examination may
help visualize lesions in pale-skinned individuals. Check for subcutaneous neurofibromas
along major nerve branches, especially on the
trunk. Also check for bony abnormalities, such
as scoliosis or kyphosis.
5
⁄8”
C
M
EDICAL CAUSES
◆ Albright’s syndrome. In Albright’s syn-
drome, café-au-lait spots are smaller (about
[1 cm] in diameter) and more irregularly shaped
than those in neurofibromatosis. They may stop
abruptly at the midline and seem to follow a
dermatomal distribution. Usually, fewer than six
spots appear, unilaterally on the forehead, neck,
and lower back. When they occur on the scalp,
the hair overlying them may be more deeply
pigmented. Associated signs include skeletal
deformities, frequent fractures and, in females,
sexual precocity.
◆ Neurofibromatosis. The most common
cause of café-au-lait spots, this disorder (also
called von Recklinghausen’s disease) is characterized by six or more large, smooth-bordered
spots up to
bertal children and more than
diameter in postpubertal children. Associated
signs include axillary and inguinal freckling; irregular, hyperpigmented, and mottled skin; and
multiple skin-colored pedunculated nodules
clustered along nerve sheaths. The nodules develop during childhood, growing larger than
1
⁄4”. They proliferate throughout life, affecting
all body tissues and causing marked deformity.
They grow to
pairment, seizures, hearing loss, exophthalmos,
decreased visual acuity, and GI bleeding can
eventually occur.
◆ Tuberous sclerosis. Mental retardation and
seizures characteristically appear first, followed
several years later by cutaneous facial lesions—
multiple café-au-lait spots, spherical areas of
1
⁄4” (6.4 mm) in diameter in prepu-
5
⁄8” or larger in adults. Mental im-
5
⁄8” (15 mm) in
3
⁄8”
133
134 CAPILLARY REFILL TIME, INCREASED
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rough skin, and areas of yellow-red or depigmented nevi.
S
PECIAL CONSIDERATIONS
Although café-au-lait spots require no treatment, you’ll need to provide emotional support
for the patient and his family. Also, refer them
for genetic counseling. Prepare the patient for
diagnostic tests, such as tissue biopsy and radiographic studies.
Capillary refill
time, increased
Capillary refill time is the duration required for
color to return to the nail bed of a finger or toe
after application of slight pressure, which causes blanching. This duration reflects the quality
of peripheral vasomotor function. Normal capillary refill time is less than 3 seconds.
Increased refill time isn’t diagnostic of any
disorder but must be evaluated along with other
signs and symptoms. However, this sign usually
signals obstructive peripheral arterial disease or
decreased cardiac output.
Capillary refill time is typically tested during a
routine cardiovascular assessment. It isn’t tested with suspected life-threatening disorders because other, more characteristic signs and
symptoms appear earlier.
H
ISTORY AND PHYSICAL
EXAMINATION
If you detect increased capillary refill time, take
the patient’s vital signs and check pulses in the
affected limb. Does the limb feel cold or look
cyanotic? Does the patient report pain or any
unusual sensations in his fingers or toes, especially after exposure to cold?
Take a brief medical history, especially noting
previous peripheral vascular disease. Find out
which medications the patient is taking.
M
EDICAL CAUSES
◆ Aortic aneurysm (dissecting). Capillary re-
fill time is increased in the fingers and toes in a
dissecting aneurysm in the thoracic aorta; it’s
prolonged in just the toes in a dissecting
aneurysm in the abdominal aorta. Common accompanying signs and symptoms include a pulsating abdominal mass, a systolic bruit, and
substernal back or abdominal pain.
◆ Aortic arch syndrome. Increased capillary
refill time in the fingers is an early sign of
aortic arch syndrome. The patient displays
absent carotid pulses and possibly unequal
radial pulses. Other signs and symptoms usually precede loss of pulses and include fever,
night sweats, arthralgia, weight loss, anorexia, nausea, malaise, rash, splenomegaly, and
pallor.
◆ Aortic bifurcation occlusion (acute). In-
creased capillary refill time in the toes is a
late sign in this rare but usually fatal disorder.
All lower-extremity pulses are absent, and the
patient complains of sudden moderate to severe pain in the legs and, less commonly, in
the abdomen, lumbosacral area, or perineum.
Both legs are cold, pale, totally numb, and
flaccid.
◆ Arterial occlusion (acute). Increased capil-
lary refill time occurs early in the affected limb.
Arterial pulses are usually absent distal to the
obstruction; the affected limb appears cool and
pale or cyanotic. Intermittent claudication,
moderate to severe pain, numbness, and paresthesia or paralysis of the affected limb may
occur.
◆ Buerger’s disease. Capillary refill time is in-
creased in the toes in Buerger’s disease. Exposure to low temperatures initially turns the feet
cold, cyanotic, and numb; later they become
red, hot, and tingly. Other findings include intermittent claudication of the instep and weak peripheral pulses; in later stages the patient may
experience ulceration, muscle atrophy, and gangrene. If the disease affects the hands, increased capillary refill time may accompany
painful fingertip ulcerations.
◆ Cardiac tamponade. Increased capillary re-
fill time is a late sign of decreased cardiac output. Associated signs include paradoxical pulse,
tachycardia, cyanosis, dyspnea, jugular vein distention, and hypotension.
◆ Hypothermia. Increased capillary refill time
may appear early as a compensatory response.
Associated signs and symptoms depend on the
degree of hypothermia and may include shivering, fatigue, weakness, decreased level of consciousness (LOC), slurred speech, ataxia, muscle stiffness or rigidity, tachycardia or
bradycardia, hyporeflexia or areflexia, diuresis,
oliguria, bradypnea, decreased blood pressure,
and cold, pale skin.
◆ Peripheral arterial trauma. Any trauma to
a peripheral artery that reduces distal blood flow
also increases capillary refill time in the affected
extremity. Related findings in that extremity include bruising or pulsating bleeding, weakened
CARPOPEDAL SPASM 135
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pulse, cyanosis, paresthesia, sensory loss, and
cool, pale skin.
◆ Peripheral vascular disease. Increased cap-
illary refill time in the affected extremities is a
late sign. Peripheral pulses gradually weaken
and then disappear. Intermittent claudication,
coolness, pallor, and decreased hair growth are
associated signs. Impotence may accompany
arterial occlusion in the descending aorta or
femoral areas.
◆ Raynaud’s disease. Capillary refill time is
prolonged in the fingers, the usual site of this
disease’s characteristic episodic arterial vasospasm. Exposure to cold or stress produces
blanching in the fingers, then cyanosis, and
then erythema before the fingers return to
normal temperature. Warmth relieves the
symptoms, which may include paresthesia.
Chronic disease may produce trophic changes,
such as sclerodactyly, ulcerations, or chronic
paronychia.
◆ Shock. Increased capillary refill time appears
late in almost all types of shock. Accompanying
signs include hypotension, tachycardia, tachypnea, and cool, clammy skin.
◆ Volkmann’s contracture. Increased capil-
lary refill time results from this contracture’s
characteristic vasospasm. The affected
extremity may also exhibit loss of mobility and
strength.
O
THER CAUSES
◆ Diagnostic tests. Cardiac catheterization
can cause arterial hematoma or clot formation
and increased capillary refill time.
◆ Drugs. Drugs that cause vasoconstriction
(particularly alpha-adrenergic blockers)
increase capillary refill time.
◆ Treatments. Increased capillary refill time
can result from an arterial line or umbilical
line (which can cause arterial hematoma and
obstructed distal blood flow) or from an improperly fitting cast (which constricts circulation).
S
PECIAL CONSIDERATIONS
Frequently assess the patient’s vital signs, LOC,
and affected extremity, and report any changes,
such as progressive cyanosis or loss of an existing pulse. Prepare the patient for diagnostic
tests, such as arteriography or Doppler ultrasonography, to help confirm or rule out arterial
occlusion.
P
EDIATRIC POINTERS
Capillary refill time may be increased in
neonates with acrocyanosis; however, this is a
normal finding. Typically, increased capillary
refill time is associated with the same disorders in children as in adults. However, the
most common cause in children is cardiac
surgery, such as the repair of congenital heart
defects.
Carpopedal spasm
Carpopedal spasm is the violent, painful contraction of the muscles in the hands and feet.
(See Recognizing carpopedal spasm, page 136.)
It’s an important sign of tetany, a potentially
life-threatening condition that is commonly associated with hypocalcemia and characterized
by increased neuromuscular excitation and sustained muscle contraction.
Carpopedal spasm requires prompt evaluation and intervention. If not treated promptly,
the patient can also develop laryngospasm,
seizures, cardiac arrhythmias, and cardiac and
respiratory arrest.
EMERGENCY INTERVENTIONS If you de-
tect carpopedal spasm, quickly examine the
patient for signs of respiratory distress (laryngospasm, stridor, loud crowing noises, cyanosis)
or cardiac arrhythmias, which indicate hypocalcemia. Obtain blood samples for electrolyte analysis (especially calcium), and perform an electrocardiogram. Connect the patient to a monitor to
watch for the appearance of arrhythmias. Administer an I.V. calcium preparation, and provide
emergency respiratory and cardiac support. If a
calcium infusion doesn’t control seizures, administer a sedative, such as chloral hydrate or phenobarbital.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient isn’t in distress, obtain a detailed history. Ask about the onset and duration of the spasms and the degree of pain they
produce. Also ask about related signs and
symptoms of hypocalcemia, such as numbness and tingling of the fingertips and feet,
other muscle cramps or spasms, and nausea,
vomiting, and abdominal pain. Check for previous neck surgery, calcium or magnesium
deficiency, tetanus exposure, and hypoparathyroidism.
136 CARPOPEDAL SPASM
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EXAMINATION TIP
Recognizing carpopedal spasm
In the hand, carpopedal spasm involves adduction of the thumb over the
palm, followed by flexion of the
metacarpophalangeal joints, extension
of the interphalangeal joints (fingers
together), adduction of the hyperextended fingers, and flexion of the wrist
and elbow joints. Similar effects occur
in the joints of the feet.
During the history, form a general impression
of the patient’s mental status and behavior. If
possible, ask family members or friends if
they’ve noticed changes in the patient’s behavior because hypocalcemia can cause confusion
and even personality changes.
Inspect the patient’s skin and fingernails, noting any dryness or scaling and ridged, brittle
nails.
M
EDICAL CAUSES
◆ Hypocalcemia. Carpopedal spasm is an
early sign of hypocalcemia. It’s usually accompanied by paresthesia of the fingers, toes, and
perioral area; muscle weakness, twitching, and
cramping; hyperreflexia; chorea; fatigue; and
palpitations. Positive Chvostek’s and
Trousseau’s signs can be elicited. Laryngospasm, stridor, and seizures may appear in
severe hypocalcemia.
Chronic hypocalcemia may be accompanied
by mental status changes; cramps; dry, scaly
skin; brittle nails; and thin, patchy hair and
eyebrows.
◆ Tetanus. Tetanus is an infectious disease
that develops when Clostridium tetani enters a
wound in a nonimmunized individual. The patient develops muscle spasms, painful seizures,
difficulty swallowing, and a low-grade fever.
Without prompt treatment, mortality is very
high.
O
THER CAUSES
◆ Treatments. Multiple blood transfusions and
parathyroidectomy may cause hypocalcemia,
resulting in carpopedal spasm. Surgical proce-
dures that impair calcium absorption, such as
ileostomy formation and gastric resection with
gastrojejunostomy, may also cause hypocalcemia.
S
PECIAL CONSIDERATIONS
Carpopedal spasm can cause severe pain and
anxiety, leading to hyperventilation. If this occurs, help the patient slow his breathing
through your relaxing touch, reassuring attitude, and clear directions about what he should
do. Provide a quiet, dark environment to reduce
his anxiety.
Prepare the patient for laboratory tests,
such as complete blood count and serum calcium, phosphorus, and parathyroid hormone
studies.
P
EDIATRIC POINTERS
Idiopathic hypoparathyroidism is a common
cause of hypocalcemia in children. Carefully
monitor children with this condition because
carpopedal spasm may herald the onset of
epileptiform seizures or generalized tetany
followed by prolonged tonic spasms.
G
ERIATRIC POINTERS
Always ask elderly patients about their immunization record. Suspect tetanus in anyone who
comes into your facility with carpopedal spasm,
difficulty swallowing, and seizures. Such patients may have incomplete immunizations or
may not have had a recent booster shot. Always
ask about any recent wound, no matter how inconsequential it may seem.
P
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ATIENT COUNSELING
Teach the patient the importance of receiving
immunization against tetanus and of keeping a
vaccination record. If you have any doubt about
his vaccination record, you must give him the
vaccine. Tetanus toxoid booster shots must be
given every 10 years after the patient has been
properly immunized in childhood.
Cat’s cry
Occurring during infancy, this mewing, kittenlike sound is the primary indicator of cri du chat
(also known as cat’s cry) syndrome. This syndrome affects about 1 in 50,000 neonates and
causes profound mental retardation and failure
to thrive. Most of those affected can have a normal life span, although a small number have serious organ defects and other life-threatening
medical conditions.
The chromosomal defect responsible for this
disorder (deletion of the short arm of chromosome 5) usually appears spontaneously but may
be inherited from a carrier parent. The characteristic cry is thought to result from abnormal
laryngeal development.
GENDER CUE Cri du chat syndrome is
more common in females than males.
EMERGENCY INTERVENTIONS Suspect
cri du chat syndrome if you detect cat’s cry
in a neonate. Be alert for signs of respiratory distress, such as nasal flaring; irregular, shallow
respirations; cyanosis; and a respiratory rate over
60 breaths/minute. Be prepared to suction the
neonate and to administer warmed oxygen. Keep
emergency resuscitation equipment nearby because bradycardia may develop.
H
ISTORY AND PHYSICAL
EXAMINATION
Perform a physical examination, and note any
abnormalities. If you detect cat’s cry in an older
infant, ask the parents when it developed. Sudden onset of an abnormal cry in an infant with
a previously normal, vigorous cry suggests other disorders. (See “Cry, high-pitched,” page
193.)
M
EDICAL CAUSES
◆ Cri du chat syndrome. A kittenlike cry be-
gins at birth or shortly thereafter in this disorder. It’s accompanied by profound mental retardation, microcephaly, low birth weight,
hypotonia, failure to thrive, and feeding difficul-
CHEST EXPANSION, ASYMMETRICAL
ties. Typically, the infant displays a round face
with wide-set eyes; strabismus; a broad-based
nose with oblique or down-sloping epicanthal
folds; abnormally shaped, low-set ears; and an
unusually small jaw. He may also have a short
neck, webbed fingers, and a simian crease. Other abnormalities may include heart defects and
GI abnormalities.
S
PECIAL CONSIDERATIONS
Connect the infant to an apnea monitor, and
check for signs of respiratory distress. Keep suction equipment and warmed oxygen available.
Obtain a blood sample for chromosomal analysis. Prepare the infant for a computed tomography scan to rule out other causes of microcephaly and for an ear, nose, and throat
examination to evaluate vocal cords.
Because the infant with cri du chat is usually a poor eater, monitor intake, output, and
weight. Instruct the parents to offer the child
frequent small feedings. Prepare the parents
to work long term with a team of specialists
in genetics, neurology, cardiology, and
speech and language. Have a counselor or
support group available for the parents and
family.
Chest expansion,
asymmetrical
Asymmetrical chest expansion is the uneven
extension of portions of the chest wall during
inspiration. During normal respiration, the thorax uniformly expands upward and outward,
then contracts downward and inward. When
this process is disrupted, breathing becomes
uncoordinated, resulting in asymmetrical chest
expansion.
Asymmetrical chest expansion may develop
suddenly or gradually and may affect one or
both sides of the chest wall. It may occur as
delayed expiration (chest lag), as abnormal
movement during inspiration (for example, intercostal retractions, paradoxical movement,
or chest-abdomen asynchrony), or as unilateral absence of movement. This sign usually results from pleural disorders, such as lifethreatening hemothorax or tension
pneumothorax. (See Recognizing life-threaten-
ing causes of asymmetrical chest expansion,
page 138.) However, it can also result from a
musculoskeletal or urologic disorder, airway
obstruction, or trauma. Regardless of its
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138 CHEST EXPANSION, ASYMMETRICAL
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Recognizing life-threatening causes of
asymmetrical chest expansion
Asymmetrical chest expansion can result from several life-threatening disorders. Two common
causes—bronchial obstruction and flail chest—produce distinctive chest wall movements that
provide important clues about the underlying disorder.
In bronchial obstruction, only the unaffected portion of the chest wall expands during inspira-
tion. Intercostal bulging during expiration may indicate that the air is trapped in the chest.
INSPIRATION
Bronchial
obstruction
In flail chest—a disruption of the thorax due to multiple rib fractures—the unstable portion of
the chest wall collapses inward during inspiration and balloons outward during expiration.
INSPIRATION
Fractured
ribs
underlying cause, asymmetrical chest expansion produces rapid and shallow or deep
respirations that increase the work of
breathing.
EMERGENCY INTERVENTIONS If you de-
tect asymmetrical chest expansion, first consider traumatic injury to the patient’s ribs or sternum, which can cause flail chest, a lifethreatening emergency characterized by paradoxical chest movement. Quickly take the patient’s
vital signs and look for signs of acute respiratory
distress—rapid and shallow respirations, tachycardia, and cyanosis. Use tape or sandbags to temporarily splint the unstable flail segment.
Depending on the severity of respiratory distress, administer oxygen by nasal cannula, mask,
or mechanical ventilator. Insert an I.V. catheter to
allow fluid replacement and administration of pain
medication. Draw a blood sample from the patient
EXPIRATION
Bronchial
obstruction
EXPIRATION
Fractured
ribs
for arterial blood gas analysis, and connect the
patient to a cardiac monitor.
Although asymmetrical chest expansion may
result from hemothorax, tension pneumothorax,
bronchial obstruction, and other life-threatening
causes, it isn’t a cardinal sign of these disorders.
Because any form of asymmetrical chest expansion can compromise the patient’s respiratory status, don’t leave the patient unattended, and be
alert for signs of respiratory distress.
H
ISTORY AND PHYSICAL
EXAMINATION
If you don’t suspect flail chest and if the patient
isn’t experiencing acute respiratory distress, obtain a brief history. Asymmetrical chest expansion commonly results from mechanical airflow
obstruction, so find out if the patient is experiencing dyspnea or pain during breathing. If so,
CHEST EXPANSION, ASYMMETRICAL
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139
does he feel short of breath constantly or intermittently? Does the pain worsen his feeling of
breathlessness? Does repositioning, coughing,
or any other activity relieve or worsen the patient’s dyspnea or pain? Is the pain more noticeable during inspiration or expiration? Can he inhale deeply?
Ask if the patient has a history of pulmonary
or systemic illness, such as frequent upper respiratory tract infections, asthma, tuberculosis,
pneumonia, or cancer. Has he had thoracic
surgery? (This typically produces asymmetrical
chest expansion on the affected side.) Also, ask
about blunt or penetrating chest trauma, which
may have caused pulmonary injury. Obtain an
occupational history to find out if the patient
may have inhaled toxic fumes or aspirated a
toxic substance.
Next, perform a physical examination. Begin by gently palpating the trachea for midline positioning. (Deviation of the trachea
usually indicates an acute problem requiring
immediate intervention.) Then examine the
posterior chest wall for areas of tenderness
or deformity. To evaluate the extent of asymmetrical chest expansion, place your hands—
fingers together and thumbs abducted toward
the spine—flat on both sections of the lower
posterior chest wall. Position your thumbs at
the 10th rib, and grasp the lateral rib cage
with your hands. As the patient inhales, note
the uneven separation of your thumbs, and
gauge the distance between them. Then repeat this technique on the upper posterior
chest wall. Next, use the ulnar surface of
your hand to palpate for vocal or tactile
fremitus on both sides of the chest. To check
for vocal fremitus, ask the patient to repeat
“99” as you proceed. Note any asymmetrical
vibrations and areas of enhanced, diminished, or absent fremitus. Then percuss and
auscultate to detect air and fluid in the lungs
and pleural spaces. Finally, auscultate all
lung fields for normal and adventitious
breath sounds. Examine the patient’s anterior
chest wall, using the same assessment
techniques.
M
EDICAL CAUSES
◆ Bronchial obstruction. Life-threatening loss
of airway patency may occur gradually or suddenly in bronchial obstruction. Typically, lack of
chest movement indicates complete obstruction; chest lag signals partial obstruction. If air
is trapped in the chest, you may detect intercostal bulging during expiration and hyperresonance on percussion. You may also note dyspnea, accessory muscle use, decreased or absent
breath sounds, and suprasternal, substernal, or
intercostal retractions.
◆ Flail chest. In this life-threatening injury to
the ribs or sternum, the unstable portion of the
chest wall collapses inward during inspiration
and balloons outward during expiration (paradoxical movement). The patient may have ecchymoses, severe localized pain, or other signs
of traumatic injury to the chest wall. He may
also exhibit rapid, shallow respirations, tachycardia, and cyanosis.
◆ Hemothorax. Hemothorax is life-threatening
bleeding into the pleural space that causes chest
lag during inspiration. Other findings include
signs of traumatic chest injury, stabbing pain at
the injury site, anxiety, dullness on percussion,
tachypnea, tachycardia, and hypoxemia. If hypovolemia occurs, you’ll note signs of shock, such
as hypotension and rapid, weak pulse.
◆ Kyphoscoliosis. Abnormal curvature of the
thoracic spine in the anteroposterior direction
(kyphosis) and the lateral direction (scoliosis)
gradually compresses one lung and distends the
other. This produces decreased chest wall
movement on the compressed-lung side and expands the intercostal muscles during inspiration
on the opposite side. It can also produce ineffective coughing, dyspnea, back pain, and
fatigue.
◆ Myasthenia gravis. Progressive loss of ven-
tilatory muscle function produces asynchrony of
the chest and abdomen during inspiration (“abdominal paradox”), which can lead to acute respiratory distress. Typically, the patient’s shallow
respirations and increased muscle weakness
cause severe dyspnea, tachypnea and, possibly,
apnea.
◆ Phrenic nerve dysfunction. In this disorder,
the paralyzed hemidiaphragm fails to contract
downward, causing asynchrony of the thorax
and upper abdomen on the affected side during
inspiration (“abdominal paradox”). Its onset
may be sudden, as in trauma, or gradual, as in
infection or spinal cord disease. If the patient
has underlying pulmonary dysfunction that contributes to hyperventilation, his inability to
breathe deeply or to cough effectively may
cause atelectasis of the affected lung.
◆ Pleural effusion. Chest lag at end-
inspiration occurs gradually in this life-threatening accumulation of fluid, blood, or pus in the
140 CHEST EXPANSION, ASYMMETRICAL
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pleural space. Usually, some combination of
dyspnea, tachypnea, and tachycardia precedes
chest lag; the patient may also have pleuritic
pain that worsens with coughing or deep
breathing. The area of the effusion is delineated
by dullness on percussion and by egophony,
bronchophony, whispered pectoriloquy, decreased or absent breath sounds, and decreased
tactile fremitus. The patient may have a fever if
infection caused the effusion.
◆ Pneumonia. Depending on whether fluid
consolidation in the lungs develops unilaterally or bilaterally, asymmetrical chest expansion occurs as inspiratory chest lag or as
chest-abdomen asynchrony. The patient typically has fever, chills, tachycardia, tachypnea,
and dyspnea along with crackles, rhonchi,
and chest pain that worsens during deep
breathing. He may also be fatigued and
anorexic and have a productive cough with
rust-colored sputum.
◆ Pneumothorax. Entrapment of air in the
pleural space can cause chest lag at endinspiration. This life-threatening condition also
causes sudden, stabbing chest pain that may
radiate to the arms, face, back, or abdomen
and dyspnea unrelated to the chest pain’s
severity. Other findings include tachypnea, decreased tactile fremitus, tympany on percussion, decreased or absent breath sounds over
the trapped air, tachycardia, restlessness, and
anxiety.
Tension pneumothorax produces the same
signs and symptoms as pneumothorax, but
they’re much more severe. A tension pneumothorax rapidly compresses the heart and
great vessels, causing cyanosis, hypotension,
tachycardia, restlessness, and anxiety. The patient may also develop subcutaneous crepitation of the upper trunk, neck, and face
and mediastinal and tracheal deviation away
from the affected side. Auscultation of a
crunching sound over the precordium with
each heartbeat indicates pneumomediastinum.
◆ Poliomyelitis. In this rare disorder, paralysis
of the chest wall muscles and diaphragm produces chest-abdomen asynchrony (“abdominal
paradox”), fever, muscle pain, and weakness.
Other findings include decreased reflex response
in the affected muscles and impaired swallowing and speaking.
◆ Pulmonary embolism. This acute, life-
threatening disorder causes chest lag; sud-
den, stabbing chest pain; and tachycardia.
The patient usually has severe dyspnea,
blood-tinged sputum, pleural friction rub, and
acute anxiety.
O
THER CAUSES
◆ Treatments. Asymmetrical chest expansion
can result from pneumonectomy and surgical
removal of several ribs. Chest lag or the absence of chest movement may also result from
intubation of a mainstem bronchus, a serious
complication typically due to incorrect insertion
of an endotracheal tube or movement of the
tube while it’s in the trachea.
S
PECIAL CONSIDERATIONS
If you’re caring for an intubated patient, regularly auscultate breath sounds in the lung peripheries to help detect a misplaced tube. If this
occurs, prepare the patient for a chest X-ray to
allow rapid repositioning of the tube. Because
asymmetrical chest expansion increases the
work of breathing, supplemental oxygen is usually given during acute events.
P
EDIATRIC POINTERS
Children are at greater risk than adults for inadvertent intubation of a mainstem bronchus (especially the left bronchus). Their breath sounds
are usually referred from one lung to the other
because of the small size of the thoracic cage,
so use chest wall expansion as an indicator of
correct tube position in children. Children also
develop asymmetrical chest expansion, paradoxical breathing, and retractions with acute
respiratory illnesses, such as bronchiolitis, asthma, and croup.
Congenital abnormalities, such as cerebral
palsy and diaphragmatic hernia, can also cause
asymmetrical chest expansion. In cerebral
palsy, asymmetrical facial muscles usually accompany chest-abdomen asynchrony. In a lifethreatening diaphragmatic hernia, asymmetrical
expansion usually occurs on the left side of the
chest.
G
ERIATRIC POINTERS
Asymmetrical chest expansion may be more
difficult to determine in elderly patients because of the structural deformities associated
with aging.
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