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CREPITATION, SUBCUTANEOUS 191
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◆ Rheumatoid arthritis. In advanced rheuma-
toid arthritis, bony crepitation is heard when the
affected joint is rotated. However, this disorder
usually develops insidiously, producing nonspecific signs and symptoms, such as fatigue,
malaise, anorexia, a persistent low-grade fever,
weight loss, lymphadenopathy, and vague
arthralgias and myalgia. Later, more specific
and localized articular signs develop, commonly
at the proximal finger joints. These signs usually
occur bilaterally and symmetrically and may extend to the wrists, knees, elbows, and ankles.
The affected joints stiffen after inactivity. The
patient also has increased warmth, swelling,
and tenderness of affected joints as well as limited range of motion.
S
PECIAL CONSIDERATIONS
If a fracture is suspected, prepare the patient for
X-rays of the affected area, and reexamine his
neurovascular status frequently. Keep the affected part immobilized and elevated until treatment begins. Give an analgesic to relieve pain.
P
EDIATRIC POINTERS
Bony crepitation in a child usually occurs after a
fracture. Obtain an accurate history of the injury, and be alert for the possibility of child
abuse. In a teenager, bony crepitation and pain
in the patellofemoral joint help diagnose chondromalacia of the patella.
G
ERIATRIC POINTERS
Degenerative joint changes, which have usually
begun by age 20 or 30, progress more rapidly
after age 40 and occur primarily in weightbearing joints, such as the lumbar spine, hips,
knees, and ankles.
Crepitation, subcutaneous
[Subcutaneous crepitus,
subcutaneous emphysema]
When bubbles of air or other gases (such as carbon dioxide) are trapped in subcutaneous tissue, palpation or stroking of the skin produces a
crackling sound called subcutaneous crepitation
or subcutaneous emphysema. The bubbles feel
like small, unstable nodules and aren’t painful,
even though subcutaneous crepitation is commonly associated with painful disorders. Usually, the affected tissue is visibly edematous; this
can lead to life-threatening airway occlusion if
the edema affects the neck or upper chest.
The air or gas bubbles enter the tissues
through open wounds from the action of anaerobic microorganisms or from traumatic or spontaneous rupture or perforation of pulmonary or
GI organs.
H
ISTORY AND PHYSICAL
EXAMINATION
Because subcutaneous crepitation can indicate
a life-threatening disorder, you’ll need to perform a rapid initial evaluation and intervene if
necessary. (See Managing subcutaneous crepita-
tion, page 192.)
When the patient’s condition permits, palpate
the affected skin to evaluate the location and
extent of subcutaneous crepitation and to obtain baseline information. Repalpate frequently
to determine if the crepitation is increasing. Ask
the patient if he’s experiencing any pain or having difficulty breathing. If he’s in pain, find out
where the pain is located, how severe it is, and
when it began. Ask about recent thoracic
surgery, diagnostic tests, and respiratory therapy or a history of trauma or chronic pulmonary
disease.
M
EDICAL CAUSES
◆ Gas gangrene. Subcutaneous crepitation is
the hallmark of this rare, but commonly fatal,
infection that’s caused by anaerobic microorganisms. It’s accompanied by local pain,
swelling, and discoloration as well as bullae
and necrosis. The skin over the wound may
rupture, revealing dark red or black necrotic
muscle and a foul-smelling, watery or frothy
discharge. Related findings include tachycardia,
tachypnea, a moderate fever, cyanosis, and
lassitude.
◆ Orbital fracture. This fracture allows air
from the nasal sinuses to escape into subcutaneous tissue, causing subcutaneous crepitation
of the eyelid and orbit. The most common sign
of an orbital fracture is periorbital ecchymosis.
Visual acuity is usually normal, although a
swollen eyelid may prevent accurate testing.
The patient has facial edema, diplopia, a hyphema and, occasionally, a dilated or unreactive
pupil on the affected side. Extraocular movements may also be affected.
◆ Pneumothorax. Severe pneumothorax pro-
duces subcutaneous crepitation in the upper
chest and neck. In many cases, the patient has
chest pain that’s unilateral, rarely localized initially, and increased on inspiration. Dyspnea,
anxiety, restlessness, tachypnea, cyanosis,
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EMERGENCY INTERVENTION
Managing subcutaneous crepitation
Subcutaneous crepitation occurs when air or gas bubbles escape into tissues. It may signal a lifethreatening rupture of an air-filled or gas-producing organ or a fulminating anaerobic infection.
Organ rupture
If the patient shows signs of respiratory distress—such as severe dyspnea, tachypnea, accessory muscle use, nasal flaring, air hunger, or
tachycardia—quickly test for Hamman’s sign to
detect trapped air bubbles in the mediastinum.
To test for Hamman’s sign, help the patient
assume a left-lateral recumbent position. Then
place your stethoscope over the precordium. If
you hear a loud crunching sound that synchronizes with his heartbeat, the patient has a positive Hamman’s sign.
Depending on which organ is ruptured, be
prepared for endotracheal intubation, an
emergency tracheotomy, or chest tube insertion. Start administering supplemental oxygen
immediately. Start an I.V. catheter to adminis-
tachycardia, accessory muscle use, asymmetrical chest expansion, and a nonproductive cough
can also occur. On the affected side, breath
sounds are absent or decreased, hyperresonance or tympany may be heard, and decreased
vocal fremitus may be present.
◆ Rupture of the esophagus. A ruptured
esophagus usually produces subcutaneous
crepitation in the neck, chest wall, or supraclavicular fossa, although this sign doesn’t always
occur. In a rupture of the cervical esophagus,
the patient has excruciating pain in the neck or
supraclavicular area, his neck is resistant to
passive motion, and he has local tenderness,
soft-tissue swelling, dysphagia, odynophagia,
and orthostatic vertigo.
Life-threatening rupture of the intrathoracic
esophagus can produce mediastinal emphysema confirmed by a positive Hamman’s sign. The
patient has severe retrosternal, epigastric, neck,
or scapular pain and edema of the chest wall
and neck. He may also display dyspnea, tachypnea, asymmetrical chest expansion, nasal flaring, cyanosis, diaphoresis, tachycardia, hypotension, dysphagia, and fever.
◆ Rupture of the trachea or major
bronchus. This life-threatening injury produces
abrupt subcutaneous crepitation of the neck
and anterior chest wall. The patient has severe
dyspnea with nasal flaring, tachycardia, accessory muscle use, hypotension, cyanosis, ex-
ter fluids and medication, and connect the patient to a cardiac monitor.
Anaerobic infection
If the patient has an open wound with a foul
odor and local swelling and discoloration, you
must act quickly. Take the patient’s vital signs,
checking especially for fever, tachycardia, hypotension, and tachypnea. Next, start an I.V.
catheter to administer fluids and medication,
and provide supplemental oxygen.
In addition, be prepared for emergency
surgery to drain and debride the wound. If the
patient’s condition is life-threatening, you may
need to prepare him for transfer to a facility
with a hyperbaric chamber.
treme anxiety and, possibly, hemoptysis and
mediastinal emphysema confirmed by a positive
Hamman’s sign.
O
THER CAUSES
◆ Diagnostic tests. Endoscopic tests, such as
bronchoscopy and upper GI tract endoscopy, can
cause rupture or perforation of respiratory or GI
organs, producing subcutaneous crepitation.
◆ Respiratory treatments. Mechanical venti-
lation and intermittent positive-pressure breathing can rupture alveoli, producing subcutaneous
crepitation.
◆ Thoracic surgery. Subcutaneous crepitation
can occur if air escapes into the tissue in the
area of the incision.
S
PECIAL CONSIDERATIONS
Monitor the patient’s vital signs, especially respirations, frequently. Because excessive edema
from subcutaneous crepitation in the neck and
upper chest can cause airway obstruction, be
alert for signs of respiratory distress such as
dyspnea. Tell the patient that the affected tissues will eventually absorb the air or gas bubbles, decreasing the subcutaneous crepitation.
P
EDIATRIC POINTERS
Children may develop subcutaneous crepitation
in the neck from ingestion of corrosive substances that perforate the esophagus.
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P
ATIENT COUNSELING
Warn patients with asthma or chronic bronchitis
to be alert for subcutaneous crepitation, which
can signal pneumothorax, a dangerous complication.
Cry, high-pitched
[Cerebral cry]
A high-pitched cry is a brief, sharp, piercing vocal sound produced by a neonate or an infant.
Whether acute or chronic, this cry is a late sign
of increased intracranial pressure (ICP). The
acute onset of a high-pitched cry demands
emergency treatment to prevent permanent
brain damage or death.
Any change in the volume of one of the
brain’s components—brain tissue, cerebrospinal
fluid, or blood—may cause increased ICP. In
neonates, increased ICP may result from intracranial bleeding associated with birth trauma
or from congenital malformations, such as
craniostenosis and Arnold-Chiari syndrome. In
fact, a high-pitched cry may be an early sign of
a congenital malformation. In infants, increased
ICP may result from meningitis, head trauma, or
child abuse.
H
ISTORY AND PHYSICAL
EXAMINATION
Take the infant’s vital signs, and then obtain a
brief history. Did the infant fall recently or experience even minor head trauma? Be sure to ask
the mother about any changes in the infant’s
behavior during the past 24 hours: Has he been
vomiting? Has he seemed restless or unlike
himself? Has his sucking reflex diminished?
Does he cry when moved? Suspect child abuse
if the infant’s history is inconsistent with physical findings.
Next, perform a neurologic examination. Remember that neurologic responses in neonates
and young infants are primarily reflex responses. Determine the infant’s level of consciousness (LOC). Is he awake, irritable, or lethargic?
Does he reach for an attractive object or turn
toward the sound of a rattle? Observe his posture. Is he in the normal flexed position or in extension or opisthotonos? Examine muscle tone
and observe the infant for signs of a seizure,
such as a tremor and twitching.
Examine the size and shape of the infant’s
head. Is the anterior fontanel bulging? Measure
the infant’s head circumference, and check pupil-
lary size and response to light. Unilateral or bilateral dilation and a sluggish response to light may
accompany increased ICP. Finally, test the infant’s
reflexes; expect Moro’s reflex to be diminished.
After completing your examination, elevate
the infant’s head to promote cerebral venous
drainage and decrease ICP. Start an I.V. catheter,
and give a diuretic and a corticosteroid to decrease ICP. Be sure to keep endotracheal (ET) intubation equipment close by to secure an airway.
M
EDICAL CAUSES
◆ Increased ICP. A high-pitched cry is a late
sign of increased ICP. Typically, the infant also
displays bulging fontanels, increased head circumference, and widened sutures. Earlier signs
and symptoms of increasing ICP include
seizures, bradycardia, dilated pupils, decreased
LOC, increased systolic blood pressure, widened
pulse pressure, altered respiratory pattern and,
possibly, vomiting.
S
PECIAL CONSIDERATIONS
An infant with increased ICP requires specialized care and monitoring in the intensive care
unit. For example, you’ll need to monitor his vital signs and neurologic status to detect subtle
changes in his condition. Also, monitor intake
and output and ICP. Restrict fluids and administer a diuretic. Increase the head of the bed
30 degrees, if the infant’s condition permits, and
keep the head midline. Perform nursing care judiciously because procedures may further increase ICP. For an infant with severely increased
ICP, ET intubation and mechanical hyperventilation may be needed to decrease serum carbon
dioxide levels and constrict cerebral blood vessels. Hyperventilation is used for acute increases in ICP after carefully weighing the risks and
benefits. Alternatively, a barbiturate coma or hypothermia therapy may be needed to decrease
the infant’s metabolic rate.
Remember to avoid jostling the infant, which
may aggravate increased ICP. Comfort him and
maintain a calm, quiet environment because the
infant’s crying or exposure to environmental
stimuli may also worsen increased ICP.
Cyanosis
A bluish or bluish black discoloration of the skin
and mucous membranes, cyanosis results from
excessive concentration of unoxygenated hemoglobin in the blood. This common sign may
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develop abruptly or gradually. It can be classified as central or peripheral, although the two
types may coexist.
Central cyanosis reflects inadequate oxygena-
tion of systemic arterial blood caused by rightto-left cardiac shunting, pulmonary disease, or
hematologic disorders. It may occur anywhere
on the skin and also on the mucous membranes
of the mouth, lips, and conjunctivae.
Peripheral cyanosis reflects sluggish peripher-
al circulation caused by vasoconstriction, reduced cardiac output, or vascular occlusion. It
may be widespread or may affect only one extremity; however, it doesn’t affect mucous
membranes. Typically, peripheral cyanosis appears on exposed areas, such as the fingers, nail
beds, feet, nose, and ears.
Although cyanosis is an important sign of
cardiovascular and pulmonary disorders, it isn’t
always an accurate gauge of oxygenation. Several factors contribute to its development: hemoglobin concentration and oxygen saturation,
cardiac output, and partial pressure of arterial
oxygen (Pa
until the oxygen saturation of hemoglobin falls
below 80%. Severe cyanosis is quite obvious,
whereas mild cyanosis is more difficult to detect, even in natural bright light. In darkskinned patients, cyanosis is most apparent in
the mucous membranes and nail beds.
from environmental factors. For example, peripheral cyanosis may result from cutaneous
vasoconstriction after brief exposure to cold air
or water, and central cyanosis may result from
reduced Pa
other signs of arterial occlusion, protect the affected limb from injury, but don’t massage it. If you
see central cyanosis stemming from a pulmonary
disorder or shock, perform a rapid evaluation.
Take immediate steps to maintain an airway, assist breathing, and monitor circulation.
H
O
). Cyanosis is usually undetectable
2
Transient, nonpathologic cyanosis may result
O
at high altitudes.
2
EMERGENCY INTERVENTIONS If the pa-
tient displays sudden, localized cyanosis and
ISTORY AND PHYSICAL
EXAMINATION
If cyanosis accompanies less acute conditions,
perform a thorough examination. Begin with a
history, focusing on cardiac, pulmonary, and
hematologic disorders. Ask about previous
surgery. Then begin the physical examination by
taking vital signs. Inspect the skin and mucous
membranes to determine the extent of cyanosis.
Ask the patient when he first noticed the
cyanosis. Does it subside and recur? Is it aggravated by cold, smoking, or stress? Is it alleviated
by massage or rewarming? Check the skin for
coolness, pallor, redness, pain, and ulceration.
Also note clubbing.
Next, evaluate the patient’s level of consciousness. Ask about headaches, dizziness, or
blurred vision. Then test his motor strength. Ask
about pain in the arms and legs (especially with
walking) and about abnormal sensations, such
as numbness, tingling, and coldness.
Ask about chest pain and its severity. Can the
patient identify any aggravating or alleviating
factors? Palpate peripheral pulses, and test capillary refill time. Also, check for edema. Auscultate heart rate and rhythm, especially noting
gallops and murmurs. Also auscultate the abdominal aorta and femoral arteries to detect
any bruits.
Does the patient have a cough? Is it productive? If so, have the patient describe the sputum.
Evaluate respiratory rate and rhythm. Check for
nasal flaring and use of accessory muscles. Ask
about sleep apnea. Does the patient sleep with
his head propped up on pillows? Inspect the patient for asymmetrical chest expansion or barrel
chest. Percuss the lungs for dullness or hyperresonance, and auscultate for decreased or adventitious breath sounds.
Inspect the abdomen for ascites, and test for
shifting dullness or a fluid wave. Percuss and
palpate the abdomen for liver enlargement and
tenderness. Also, ask about nausea, anorexia,
and weight loss.
M
EDICAL CAUSES
◆ Arteriosclerotic occlusive disease (chron-
ic). In this disorder, peripheral cyanosis occurs
in the legs whenever they’re in a dependent position. Associated signs and symptoms include
intermittent claudication and burning pain at
rest, paresthesia, pallor, muscle atrophy, weak
leg pulses, and impotence. Leg ulcers and gangrene are late signs.
◆ Blast lung injury. Cyanosis is a serious
sign of blast lung injury. The impact of this
condition on the lungs of affected individuals
varies and may include tearing, contusion,
edema, and hemorrhage. Other signs and
symptoms may include chest pain, wheezing,
hemoptysis, and dyspnea. Treatment for patients with blast lung injury typically involves
high-flow oxygen, careful fluid management,
possible intubation, and close observation in
an intensive care setting.
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195
◆ Bronchiectasis. This disorder produces
chronic central cyanosis. Its classic sign,
though, is a chronic productive cough with copious, foul-smelling, mucopurulent sputum or
hemoptysis. Auscultation reveals rhonchi and
coarse crackles during inspiration. Other signs
and symptoms include dyspnea, recurrent fever
and chills, weight loss, malaise, clubbing, and
signs of anemia.
◆ Buerger’s disease. In this disorder, exposure
to cold initially causes the feet to become cold,
cyanotic, and numb; later, they become red, hot,
and tingly. Intermittent claudication of the instep, a characteristic sign, is aggravated by exercise and smoking and relieved by rest. Associated signs and symptoms include weak
peripheral pulses and, in later stages, ulceration, muscle atrophy, and gangrene.
◆ Chronic obstructive pulmonary disease
(COPD). Chronic central cyanosis occurs in
advanced COPD and may be aggravated by exertion. Associated signs and symptoms include exertional dyspnea, a productive cough
with thick sputum, anorexia, weight loss,
purse-lip breathing, tachypnea, and accessory
muscle use. Examination reveals wheezing
and hyperresonant lung fields. Barrel chest
and clubbing are late signs. Tachycardia,
diaphoresis, and flushing may also accompany
COPD.
◆ Deep vein thrombosis. In this disorder,
acute peripheral cyanosis in the affected extremity is associated with tenderness, painful
movement, edema, warmth, and prominent superficial veins. Homans’ sign can also be elicited.
◆ Heart failure. Acute or chronic cyanosis
may occur in patients with heart failure. It may
be central, peripheral, or both and is typically a
late sign. In left-sided heart failure, central
cyanosis occurs with tachycardia, fatigue, dyspnea, cold intolerance, orthopnea, a cough, ventricular or atrial gallop, bibasilar crackles, and
diffuse apical impulse. In right-sided heart failure, peripheral cyanosis occurs with fatigue, peripheral edema, ascites, jugular vein distention,
and hepatomegaly.
◆ Lung cancer. This disease causes chronic
central cyanosis accompanied by fever, weakness, anorexia, weight loss, dyspnea, chest
pain, hemoptysis, and wheezing. Atelectasis
causes mediastinal shift, decreased diaphragmatic excursion, asymmetrical chest expansion,
a dull percussion note, and diminished breath
sounds.
◆ Peripheral arterial occlusion (acute). This
disorder produces acute cyanosis of one arm or
leg or, occasionally, of both legs. The cyanosis
is accompanied by sharp or aching pain that
worsens when the patient moves. The affected
extremity also exhibits paresthesia, weakness,
and pale, cool skin. Examination reveals decreased or absent pulse and increased capillary
refill time.
◆ Pneumonia. In pneumonia, acute central
cyanosis is usually preceded by fever, shaking
chills, a cough with purulent sputum, crackles,
rhonchi, and pleuritic chest pain that’s exacerbated by deep inspiration. Associated signs and
symptoms include tachycardia, dyspnea,
tachypnea, diminished breath sounds, diaphoresis, myalgia, fatigue, headache, and anorexia.
◆ Pneumothorax. A cardinal sign of pneu-
mothorax, acute central cyanosis is accompanied by dyspnea; sharp chest pain that’s exacerbated by movement, deep breathing, and
coughing; and asymmetrical chest wall expansion. The patient may also exhibit rapid, shallow respirations; a weak, rapid pulse; pallor;
jugular vein distention; anxiety; and absence of
breath sounds over the affected lobe.
◆ Polycythemia vera. A ruddy complexion
that can appear cyanotic is characteristic in this
chronic myeloproliferative disorder. Other findings include hepatosplenomegaly, headache,
dizziness, fatigue, aquagenic pruritus, blurred
vision, chest pain, intermittent claudication, and
coagulation defects.
◆ Pulmonary edema. In this disorder, acute
central cyanosis occurs with dyspnea; orthopnea; frothy, blood-tinged sputum; tachycardia;
tachypnea; dependent crackles; ventricular gallop; cold, clammy skin; weak, thready pulse; hypotension; and confusion.
◆ Pulmonary embolism. Acute central
cyanosis occurs when a large embolus causes
significant obstruction of the pulmonary circulation. Syncope and jugular vein distention may
also occur. Other common signs and symptoms
include dyspnea, chest pain, tachycardia, paradoxical pulse, a dry cough or a productive
cough with blood-tinged sputum, low-grade
fever, restlessness, and diaphoresis.
◆ Raynaud’s disease. In Raynaud’s disease,
exposure to cold or stress initially causes the
fingers or hands to blanch and turn cold, then to
become cyanotic, and finally to redden with return of normal temperature. Numbness and tingling may also occur. Raynaud’s phenomenon describes the same presentation when associated
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with other disorders, such as rheumatoid arthritis, scleroderma, or lupus erythematosus.
◆ Shock. In shock, acute peripheral cyanosis
develops in the hands and feet, which may also
be cold, clammy, and pale. Other characteristic
signs and symptoms include lethargy, confusion, increased capillary refill time, and a rapid,
weak pulse. Tachypnea, hyperpnea, and hypotension may also be present.
◆ Sleep apnea. Chronic and severe sleep ap-
nea causes pulmonary hypertension and cor
pulmonale (right-sided heart failure), which can
produce chronic cyanosis.
S
PECIAL CONSIDERATIONS
Provide supplemental oxygen to relieve dyspnea, improve oxygenation, and decrease
cyanosis. Be sure to deliver small doses (2
L/minute) to patients with COPD, who may retain carbon dioxide. Use a low-flow oxygen rate
for mild COPD exacerbations. However, for
acute situations, a high-flow oxygen rate may
be needed initially. Remember to pay attention
to the patient’s respiratory drive and adjust the
amount of oxygen accordingly. Position the patient comfortably to ease breathing. Administer
a diuretic, a bronchodilator, an antibiotic or a
cardiac drug as needed. Make sure that the patient gets sufficient rest between activities to
prevent dyspnea.
Prepare the patient for such tests as arterial
blood gas analysis and a complete blood count
to determine the cause of cyanosis.
G
ERIATRIC POINTERS
Because elderly patients have reduced tissue
perfusion, peripheral cyanosis can occur even
with a slight decrease in cardiac output or systemic blood pressure.
P
ATIENT COUNSELING
Teach patients with chronic cardiopulmonary
diseases, such as heart failure, asthma, or
COPD, to recognize cyanosis as a sign of severe
disease and to get immediate medical attention
when it occurs.
P
EDIATRIC POINTERS
Many pulmonary disorders responsible for
cyanosis in adults also cause cyanosis in children. In addition, central cyanosis may result
from cystic fibrosis, asthma, airway obstruction
by a foreign body, acute laryngotracheobronchitis, or epiglottiditis. It may also result from a
congenital heart defect, such as transposition of
the great vessels, that causes right-to-left intracardiac shunting.
In children, circumoral cyanosis may precede
generalized cyanosis. Acrocyanosis (also called
“glove and bootee” cyanosis) may occur in infants from excessive crying or exposure to cold.
Exercise and agitation enhance cyanosis, so
provide regular rest periods and make the child
comfortable. Also, administer supplemental
oxygen during cyanotic episodes.
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Earache
[Otalgia]
Earaches usually result from disorders of the external and middle ear associated with infection,
obstruction, or trauma. Their severity ranges
from a feeling of fullness or blockage to deep,
boring pain. At times, it may be difficult to determine the precise location of the earache. Earaches can be intermittent or continuous and
may develop suddenly or gradually.
H
ISTORY AND PHYSICAL
EXAMINATION
Ask the patient to characterize his earache.
How long has he had it? Is it intermittent or
continuous? Is it painful or slightly annoying?
Can he localize the site of the pain? Does he
have pain in any other areas, such as the jaw?
Ask about recent ear injury or other trauma.
Does swimming or showering trigger ear discomfort? Is discomfort associated with itching?
If so, find out where the itching is most intense
and when it began. Ask about ear drainage and,
if present, have the patient characterize it. Does
he hear ringing, “swishing,” or other noises in
his ears? Ask about dizziness or vertigo. Does it
worsen when the patient changes position?
Does he have difficulty swallowing, hoarseness,
neck pain, or pain when he opens his mouth?
Find out if the patient has recently had a head
cold or problems with his eyes, mouth, teeth,
jaws, sinuses, or throat. Disorders in these areas
may refer pain to the ear along the cranial nerves.
Finally, find out if the patient has recently
flown, been to a high-altitude location, or been
scuba diving.
Begin your physical examination by inspecting the external ear for redness, drainage,
swelling, or deformity. Then apply pressure to
the mastoid process and tragus to elicit any tenderness. Using an otoscope, examine the external auditory canal for lesions, bleeding or discharge, impacted cerumen, foreign bodies,
tenderness, or swelling. Examine the tympanic
membrane: Is it intact? Is it pearly gray (normal)? Look for tympanic membrane landmarks:
the cone of light, umbo, pars tensa, and the
handle and short process of the malleus. (See
Using an otoscope correctly.) Perform the watch
tick, whispered voice, Rinne, and Weber’s tests
to assess for hearing loss.
M
EDICAL CAUSES
◆ Abscess (extradural). Severe earache ac-
companied by a persistent ipsilateral headache,
malaise, and recurrent mild fever characterizes
this serious complication of middle ear infection.
◆ Barotrauma (acute). Earache associated
with barotrauma ranges from mild pressure to
severe pain. Tympanic membrane ecchymosis
or bleeding into the tympanic cavity may occur,
producing a blue drumhead; the eardrum
usually isn’t perforated.
◆ Cerumen impaction. Impacted cerumen
(earwax) may cause a sensation of blockage or
fullness in the ear. Additional features include
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EARACHE 255
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EXAMINATION TIP
Using an otoscope correctly
When the patient reports an earache, use an otoscope to inspect ear structures closely. Follow
these techniques to obtain the best view and ensure patient safety.
Child younger than age 3
To inspect an infant’s or a young
child’s ear, grasp the lower part of the
auricle and pull it down and back to
straighten the upward S curve of the
external canal. Then gently insert the
speculum no more than
into the canal.
1
⁄2” (1.2 cm)
Adult
To inspect an adult’s ear, grasp the
upper part of the auricle and pull it up
and back to straighten the external
canal. Then insert the speculum about
1” (2.5 cm) into the canal. Also use
this technique for children ages 3 and
older.
Auricle
External ear canal
Tympanic membrane
External
ear canal
Tympanic
membrane
1.2 cm
partial hearing loss, itching and, possibly, dizziness.
◆ Chondrodermatitis nodularis chronica.
Chondrodermatitis nodularis chronica produces
small, painful, indurated areas along the auricle’s upper rim.
◆ Ear canal obstruction by an insect. An in-
sect lodged in the ear canal may cause severe
pain and distressing noise.
◆ Frostbite. Prolonged exposure to cold may
cause burning or tingling pain in the ear, followed by numbness. The ear appears mottled
and gray or white; it turns purplish blue as it’s
warmed.
2.5 cm
◆ Furunculosis. Infected hair follicles in the
outer ear canal may produce severe, localized
ear pain associated with a pus-filled furuncle
(boil). The pain is aggravated by jaw movement
and relieved by rupture or incision of the furuncle. Pinna tenderness, swelling of the auditory
meatus, partial hearing loss, and a feeling of
fullness in the ear canal may also occur.
◆ Herpes zoster oticus (Ramsay Hunt syn-
drome). Herpes zoster oticus causes burning or
stabbing ear pain that’s commonly associated
with ear vesicles. The patient also complains of
hearing loss and vertigo. Associated signs and
symptoms include transient ipsilateral facial
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paralysis, partial loss of taste, tongue vesicles,
and nausea and vomiting.
◆ Keratosis obturans. Mild ear pain, otorrhea,
and tinnitus are common in keratosis obturans.
Inspection reveals a white glistening plug obstructing the external meatus.
◆ Mastoiditis (acute). Mastoiditis causes a
dull ache behind the ear accompanied by lowgrade fever (99⬚ F to 100⬚ F [37.2⬚ C to 37.8⬚ C]).
The eardrum appears dull and edematous and
may perforate, and soft tissue near the eardrum
may sag. A purulent discharge is seen in the
external canal.
◆ Ménière’s disease. Ménière’s disease is an
inner ear disorder that can produce a sensation
of fullness in the affected ear. Its classic effects,
however, include severe vertigo, tinnitus, and
sensorineural hearing loss. The patient may
also experience nausea and vomiting, diaphoresis, and nystagmus.
◆ Middle ear tumor. Deep, boring ear pain
and facial paralysis are late signs of a malignant
tumor.
◆ Myringitis bullosa. Myringitis bullosa is a
rare bacterial infection that causes sudden, severe ear pain that radiates over the mastoid and
lasts for up to 48 hours. Small serous or bloodfilled vesicles may dot the reddened tympanic
membrane. Transient hearing loss and a
serosanguineous discharge may also occur.
◆ Otitis externa. Earache characterizes both
acute and malignant otitis externa. Acute otitis
externa begins with mild to moderate ear pain
that occurs with tragus manipulation. The pain
may be accompanied by low-grade fever, sticky
yellow or purulent ear discharge, partial hearing loss, and a feeling of blockage. Later, ear
pain intensifies, causing the entire side of the
head to ache and throb. Fever may reach 104⬚ F
(40⬚ C). Examination reveals swelling of the tragus, external meatus, and external canal;
eardrum erythema; and lymphadenopathy. The
patient also complains of dizziness and
malaise.
Malignant otitis externa causes sudden ear
pain that’s aggravated by moving the auricle or
tragus. The pain is accompanied by intense
itching, purulent ear discharge, fever, parotid
gland swelling, and trismus. Examination reveals a swollen external canal with exposed
cartilage and temporal bone. Cranial nerve palsy may occur.
◆ Otitis media (acute). Otitis media is a mid-
dle ear inflammation that can be serous or suppurative. Acute serous otitis media may cause a
feeling of fullness in the ear, hearing loss, and a
vague sensation of top-heaviness. The eardrum
may be slightly retracted, amber colored, and
marked by air bubbles and a meniscus, or it
may be blue-black from hemorrhage.
Acute suppurative otitis media is characterized
by severe deep, throbbing ear pain; hearing
loss; and fever that may reach 102⬚ F (38.9⬚ C).
The pain increases steadily over several hours
or days and may be aggravated by pressure on
the mastoid antrum. Perforation of the eardrum
is possible. Before rupture, the eardrum appears
bulging and fiery red. Rupture causes purulent
drainage and relieves the pain.
Chronic otitis media usually isn’t painful except during exacerbations. Persistent pain and
discharge from the ear suggest cancer or osteomyelitis of the skull base.
◆ Perichondritis. Perichondritis can cause ear
pain accompanied by warmth and tenderness in
the outer ear and a reddened, doughlike auricle.
◆ Petrositis. The result of acute otitis media,
this infection produces deep ear pain with
headache and pain behind the eye. Other findings are diplopia, loss of lateral gaze, vomiting,
sensorineural hearing loss, vertigo and, possibly, nuchal rigidity.
◆ Temporomandibular joint infection. Typi-
cally unilateral, temporomandibular joint infection produces ear pain that’s referred from the
jaw joint. The pain is aggravated by pressure on
the joint with jaw movement; it commonly radiates to the temporal area or the entire side of
the head.
S
PECIAL CONSIDERATIONS
Administer an analgesic, and apply heat to relieve discomfort. Instill eardrops if necessary.
Teach the patient how to instill drops if they’re
prescribed for home use.
P
EDIATRIC POINTERS
Common causes of earache in children are
acute otitis media and insertion of foreign bodies that become lodged or infected. Be alert for
nonverbal clues to earache in a young child,
such as crying or ear tugging.
To examine the child’s ears, place him in a
supine position with his arms extended and
held securely by his parent. Then hold the otoscope with the handle pointing toward the top
of the child’s head, and brace it against him using one or two fingers. Because an ear examination may upset the child with an earache,
save it for the end of your physical examination.
EDEMA, GENERALIZED
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257
Edema, generalized
A common sign in severely ill patients, generalized edema is the excessive accumulation of interstitial fluid throughout the body. Its severity
varies widely; slight edema may be difficult to
detect, especially if the patient is obese, whereas massive edema is immediately apparent.
Generalized edema is typically chronic and
progressive. It may result from cardiac, renal,
endocrine, or hepatic disorders as well as from
severe burns, malnutrition, or the effects of certain drugs and treatments.
Common factors responsible for edema are
hypoalbuminemia and excess sodium ingestion
or retention, both of which influence plasma osmotic pressure. (See Understanding fluid bal-
ance, page 258.) Cyclic edema associated with
increased aldosterone secretion may occur in
premenopausal women.
EMERGENCY INTERVENTIONS Quickly
determine the location and severity of edema, including the degree of pitting. (See Edema:
Pitting or nonpitting? page 259.) If the patient has
severe edema, promptly take his vital signs, and
check for jugular vein distention and cyanotic lips.
Auscultate the lungs and heart. Be alert for signs
of heart failure or pulmonary congestion, such as
crackles, muffled heart sounds, or ventricular gal-
Fowler’s position to promote lung expansion. Prepare to administer oxygen and an I.V. diuretic.
Have emergency resuscitation equipment nearby.
H
ISTORY AND PHYSICAL
EXAMINATION
When the patient’s condition permits, obtain a
complete medical history. First, note when the
edema began. Is the edema worse in the morning or at the end of the day? Is it accompanied
by shortness of breath or pain in the arms or
legs? Find out how much weight the patient has
gained. Has his urine output changed in quantity or quality? Is the edema generalized or localized, dependent or nondependent?
Next, ask about previous burns or cardiac, renal, hepatic, endocrine, or GI disorders. Have
the patient describe his diet so you can determine whether he suffers from protein malnutrition. Explore his drug history, and note recent
I.V. therapy.
Begin the physical examination by comparing
the patient’s arms and legs for symmetrical edema. Also, note ecchymoses and cyanosis. Assess the back, sacrum, and hips of the bedrid-
den patient for dependent edema. Palpate peripheral pulses, noting whether hands and feet
feel cold. Finally, perform a complete cardiac
and respiratory assessment.
M
EDICAL CAUSES
◆ Angioneurotic edema or angioedema. Re-
current attacks of acute, painless, nonpitting
edema involving the skin and mucous membranes—especially those of the respiratory tract,
face, neck, lips, larynx, hands, feet, genitalia, or
viscera—may be the result of a food or drug allergy or emotional stress, or they may be hereditary. Abdominal pain, nausea, vomiting, and diarrhea accompany visceral edema; dyspnea and
stridor accompany life-threatening laryngeal
edema.
◆ Burns. Edema and associated tissue damage
vary with the severity of the burn. Severe generalized edema (4+) may occur within 2 days of a
major burn; localized edema may occur with a
less severe burn.
◆ Cirrhosis. A late sign of chronic cirrhosis,
edema usually starts in the legs and thighs and
may progress to anasarca. Accompanying signs
and symptoms include abdominal pain, anorexia, nausea and vomiting, hepatomegaly, ascites,
jaundice, pruritus, bleeding tendencies, musty
breath, lethargy, mental changes, and asterixis.
◆ Heart failure. Severe, generalized pitting
edema—occasionally anasarca—may follow leg
edema late in heart failure. The edema may improve with exercise or elevation of the limbs
and is typically worse at the end of the day.
Among other classic late findings are hemoptysis, cyanosis, marked hepatomegaly, clubbing,
crackles, and a ventricular gallop. Typically, the
patient has tachypnea, palpitations, hypotension, weight gain despite anorexia, nausea,
slowed mental response, diaphoresis, and pallor. Dyspnea, orthopnea, tachycardia, and fatigue typify left-sided heart failure; jugular vein
distention, hepatomegaly, and peripheral edema
typify right-sided heart failure.
◆ Malnutrition. Anasarca in this disorder may
mask dramatic muscle wasting. Malnutrition
also typically causes muscle weakness; lethargy;
anorexia; diarrhea; apathy; dry, wrinkled skin;
and signs of anemia, such as dizziness and
pallor.
◆ Myxedema. In this severe form of hypothy-
roidism, generalized nonpitting edema is accompanied by dry, flaky, inelastic, waxy, pale
skin; a puffy face; and an upper eyelid droop.
Observation also reveals masklike facies, hair
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