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ABDOMINAL PAIN
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21
route and highly contagious, these viruses that
cause gastroenteritis may also produce acuteonset vomiting, nausea, and diarrhea. Less
common symptoms include low-grade fever,
headache, chills, muscle aches, and generalized
fatigue. Individuals who are otherwise healthy
usually recover in 24 to 60 hours without suffering lasting effects.
◆ Ovarian cyst. Torsion or hemorrhage causes
pain and tenderness in the right or left lower
quadrant. Sharp and severe if the patient suddenly stands or stoops, the pain becomes brief
and intermittent if the torsion self-corrects or
dull and diffuse after several hours if it doesn’t.
Pain is accompanied by a slight fever, mild nausea and vomiting, abdominal tenderness, a palpable abdominal mass, and possibly amenorrhea. Abdominal distention may occur if the
cyst is large. Peritoneal irritation, or rupture and
ensuing peritonitis, causes high fever and
severe nausea and vomiting.
◆ Pancreatitis. Life-threatening acute pancre-
atitis produces fulminating, continuous upper
abdominal pain that may radiate to both flanks
and to the back. To relieve this pain, the patient
may bend forward, draw his knees to his chest,
or move about restlessly. Early findings include
abdominal tenderness, nausea, vomiting, fever,
pallor, tachycardia and, in some patients, abdominal rigidity, rebound tenderness, and hypoactive bowel sounds. Turner’s sign (ecchymosis of the abdomen or flank) or Cullen’s sign
(a bluish tinge around the umbilicus) signals hemorrhagic pancreatitis. Jaundice may occur as
inflammation subsides.
Chronic pancreatitis produces severe leftupper-quadrant or epigastric pain that
radiates to the back. Abdominal tenderness, a
midepigastric mass, jaundice, fever, and
splenomegaly may occur. Steatorrhea, weight
loss, maldigestion, and diabetes mellitus are
common.
◆ Pelvic inflammatory disease. Pain in the
right or left lower quadrant ranges from vague
discomfort worsened by movement to deep,
severe, and progressive pain. Sometimes, metrorrhagia precedes or accompanies the onset of
pain. Extreme pain accompanies cervical or
adnexal palpation. Associated findings include
abdominal tenderness, a palpable abdominal or
pelvic mass, fever, occasional chills, nausea,
vomiting, discomfort on urination, and abnormal vaginal bleeding or a purulent vaginal discharge.
◆ Perforated ulcer. In a life-threatening perfo-
rated ulcer, sudden, severe, and prostrating
epigastric pain may radiate through the abdomen to the back or right shoulder. Other
signs and symptoms include boardlike abdominal rigidity, tenderness with guarding, generalized rebound tenderness, absent bowel sounds,
grunting and shallow respirations and, in many
cases, fever, tachycardia, hypotension, and
syncope.
◆ Peritonitis. In this life-threatening disorder,
sudden and severe pain can be diffuse or localized in the area of the underlying disorder;
movement worsens the pain. The degree of abdominal tenderness usually varies according to
the extent of disease. Typical findings include
fever; chills; nausea; vomiting; hypoactive or
absent bowel sounds; abdominal tenderness,
distention, and rigidity; rebound tenderness and
guarding; hyperalgesia; tachycardia; hypotension; tachypnea; and positive psoas and obturator signs.
◆ Pleurisy. Pleurisy may produce upper ab-
dominal or costal margin pain referred from the
chest. Characteristic sharp, stabbing chest pain
increases with inspiration and movement. Many
patients have a pleural friction rub and rapid,
shallow breathing; some have a low-grade
fever.
◆ Pneumonia. Lower-lobe pneumonia can
cause pleuritic chest pain and referred, severe
upper abdominal pain, tenderness, and rigidity
that diminish with inspiration. It can also cause
fever, shaking chills, achiness, headache, bloodtinged or rusty sputum, dyspnea, and a dry,
hacking cough. Accompanying signs include
crackles, egophony, decreased breath sounds,
and dullness on percussion.
◆ Pneumothorax. Pneumothorax is a poten-
tially life-threatening disorder that can cause referred pain from the chest to the upper abdomen and costal margin. Characteristic chest
pain arises suddenly and worsens with deep inspiration or movement. Accompanying signs
and symptoms include anxiety, dyspnea,
cyanosis, decreased or absent breath sounds
over the affected area, tachypnea, and tachycardia. Watch for asymmetrical chest movements
on inspiration.
◆ Prostatitis. Vague abdominal pain or dis-
comfort in the lower abdomen, groin, perineum, or rectum may develop. Other findings
include dysuria, urinary frequency and urgency, fever, chills, low back pain, myalgia,
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arthralgia, and nocturia. Scrotal pain, penile
pain, and pain on ejaculation may occur in
chronic cases.
◆ Pyelonephritis (acute). Progressive lower
quadrant pain in one or both sides, flank pain,
and CVA tenderness characterize pyelonephritis. Pain may radiate to the lower midabdomen
or the groin. Additional signs and symptoms include abdominal and back tenderness, high
fever, shaking chills, nausea, vomiting, and urinary frequency and urgency.
◆ Renal calculi. Depending on their location,
calculi may cause severe abdominal or back
pain. However, the classic symptom is severe,
colicky pain that travels from the CVA to the
flank, suprapubic region, and external genitalia.
The pain may be excruciating or dull and constant and may be accompanied by agitation,
nausea, vomiting, abdominal distention, fever,
chills, hypertension, and urinary urgency with
hematuria and dysuria.
◆ Sickle cell crisis. Sudden, severe abdominal
pain may accompany chest, back, hand, or foot
pain. Associated signs and symptoms include
weakness, aching joints, dyspnea, and scleral
jaundice.
◆ Smallpox (variola major). Worldwide eradi-
cation of smallpox was achieved in 1977; the
United States and Russia have the only known
storage sites for the virus, which is considered a
potential agent for biological warfare. Initial
signs and symptoms include high fever,
malaise, prostration, severe headache, backache, and abdominal pain. A maculopapular
rash develops on the oral mucosa, pharynx,
face, and forearms and then spreads to the
trunk and legs. Within 2 days, the rash becomes
vesicular and later pustular. The lesions develop
at the same time, appear identical, and are
more prominent on the face and extremities.
The pustules are round, firm, and embedded in
the skin. After 8 to 9 days, the pustules form a
crust, which later separates from the skin, leaving a pitted scar. Death may result from encephalitis, extensive bleeding, or secondary
infection.
◆ Splenic infarction. Fulminating pain in the
left upper quadrant occurs with chest pain that
may worsen on inspiration. Pain commonly radiates to the left shoulder with splinting of the
left diaphragm, abdominal guarding and, occasionally, a splenic friction rub.
◆ Systemic lupus erythematosus. General-
ized abdominal pain is unusual in this disease
but may occur after meals. Butterfly rash, pho-
tosensitivity, alopecia, mucous membrane ulcers, and nondeforming arthritis are characteristic signs. Other common signs and symptoms
include anorexia, vomiting, abdominal tenderness with guarding, abdominal distention after
meals, fatigue, fever, and weight loss. Precordial chest pain and a pericardial rub may also
occur.
◆ Ulcerative colitis. Ulcerative colitis may be-
gin with vague abdominal discomfort that leads
to cramping lower abdominal pain. As the disorder progresses, pain may become steady and
diffuse, increasing with movement and coughing. The most common symptom—recurrent
and possibly severe diarrhea with blood, pus,
and mucus—may relieve the pain. The abdomen
may feel soft and extremely tender. Highpitched, infrequent bowel sounds may accompany nausea, vomiting, anorexia, weight loss,
and mild, intermittent fever.
◆ Uremia. Characterized by generalized or
periumbilical pain that shifts and varies in intensity, uremia causes diverse GI signs and
symptoms, such as nausea, vomiting, anorexia,
and diarrhea. Other findings may include bleeding, abdominal tenderness that changes in location and intensity, visual disturbances,
headache, decreased LOC, vertigo, and oliguria
or anuria. Chest pain may occur secondary to
pericardial effusion. Localized or diffuse pruritus is common.
O
THER CAUSES
◆ Drugs. Salicylates and nonsteroidal anti-in-
flammatories commonly cause burning, gnawing pain in the left upper quadrant or epigastric
area as well as nausea and vomiting.
◆ Insect toxins. Generalized, cramping ab-
dominal pain usually occurs with low-grade
fever, nausea, vomiting, abdominal rigidity,
tremors, and burning sensations in the hands or
feet.
S
PECIAL CONSIDERATIONS
Help the patient find a comfortable position to
ease his distress. The patient should lie in a
supine position, with his head flat on the table,
arms at his sides, and knees slightly flexed to relax the abdominal muscles. Monitor him closely
because abdominal pain can signal a lifethreatening disorder. Especially important
indications include tachycardia, hypotension,
clammy skin, abdominal rigidity, rebound
tenderness, a change in the pain’s location or
intensity, or sudden relief from the pain.
ABDOMINAL RIGIDITY 23
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Withhold analgesics from the patient because they may mask symptoms. Also withhold
food and fluids because surgery may be needed. Prepare for I.V. infusion and insertion of a
nasogastric or other intestinal tube. Peritoneal
lavage or abdominal paracentesis may be required.
You may have to prepare the patient for a diagnostic procedure, such as a pelvic and rectal
examination; blood, urine, and stool tests; Xrays; barium studies; ultrasonography; endoscopy; and biopsy.
P
EDIATRIC POINTERS
Because children commonly have difficulty
describing abdominal pain, pay close attention
to nonverbal clues, such as wincing, lethargy,
or unusual positioning (such as a side-lying
position with knees flexed to the abdomen).
Observing the child while he coughs, walks,
or climbs may offer some diagnostic clues.
Also, remember that a parent’s description
of the child’s complaints is a subjective
interpretation of what the parent believes is
wrong.
Abdominal pain in children may signal a
more serious disorder or a disorder that produces different associated signs and symptoms
than in adults. For example, appendicitis is
more likely to result in rupture and death in
children, and vomiting may be its only other
sign. Acute pyelonephritis may cause abdominal pain, vomiting, and diarrhea, but not the
classic urologic signs found in adults. Peptic ulcer, which is becoming increasingly common in
teenagers, causes nocturnal pain and colic that
may not be relieved by food, unlike peptic ulcer
in adults.
Abdominal pain in children can also result
from lactose intolerance, allergic-tensionfatigue syndrome, volvulus, Meckel’s diverticulum, intussusception, mesenteric adenitis,
diabetes mellitus, juvenile rheumatoid arthritis,
and many uncommon disorders, such as heavy
metal poisoning. Remember, too, that a child’s
complaint of abdominal pain may reflect an
emotional need, such as a wish to avoid school
or to gain adult attention.
G
ERIATRIC POINTERS
Advanced age may decrease the manifestations of acute abdominal disease. Pain may be
less severe, fever less pronounced, and signs
of peritoneal inflammation diminished or absent.
EXAMINATION TIP
Recognizing
voluntary rigidity
Distinguishing voluntary from involuntary
abdominal rigidity is a must for accurate assessment. Review the comparison below so
that you can quickly tell the two apart.
Voluntary rigidity
◆ Usually symmetrical
◆ More rigid on inspiration (expiration caus-
es muscle relaxation)
◆ Eased by relaxation techniques, such as
positioning the patient comfortably and
talking to him in a calm, soothing manner
◆ Painless when the patient sits up using his
abdominal muscles alone
Involuntary rigidity
◆ Usually asymmetrical
◆ Equally rigid on inspiration and expiration
◆ Unaffected by relaxation techniques
◆ Painful when the patient sits up using his
abdominal muscles alone
Abdominal rigidity
[Abdominal muscle spasm,
involuntary guarding]
Detected by palpation, abdominal rigidity refers
to abnormal muscle tension or inflexibility of
the abdomen. Rigidity may be voluntary or involuntary. Voluntary rigidity reflects the patient’s
fear or nervousness upon palpation; involuntary
rigidity reflects potentially life-threatening
peritoneal irritation or inflammation. (See Rec-
ognizing voluntary rigidity.)
Involuntary rigidity most commonly results
from GI disorders but may also result from pulmonary and vascular disorders and from the
effects of insect toxins. It’s usually accompanied
by fever, nausea, vomiting, and abdominal tenderness, distention, and pain.
EMERGENCY INTERVENTIONS After pal-
pating abdominal rigidity, quickly take the
patient’s vital signs. Even though the patient may
not appear gravely ill or have markedly abnormal
vital signs, abdominal rigidity calls for emergency
interventions.
Prepare to administer oxygen and to insert an
I.V. catheter for fluid and blood replacement. The
patient may require drugs to support blood
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pressure. Also prepare him for catheterization,
and monitor intake and output.
A nasogastric tube may have to be inserted to
relieve abdominal distention. Because emergency
surgery may be necessary, prepare the patient for
laboratory tests and X-rays.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient’s condition allows further assessment, take a brief history. Find out when the abdominal rigidity began. Is it associated with abdominal pain? If so, did the pain begin at the
same time? Determine whether the rigidity is localized or generalized. Is it always present? Has
its location changed or remained constant?
Next, ask about aggravating or alleviating factors, such as position changes, coughing, vomiting, elimination, and walking.
Then explore other signs and symptoms. Inspect the abdomen for peristaltic waves, which
may be visible in very thin patients. Also check
for a visibly distended bowel loop. Next, auscultate bowel sounds. Perform light palpation to
locate the rigidity and to determine its severity.
Avoid deep palpation, which may exacerbate
abdominal pain. Finally, check for poor skin
turgor and dry mucous membranes, which indicate dehydration.
M
EDICAL CAUSES
◆ Abdominal aortic aneurysm (dissecting).
Mild to moderate abdominal rigidity occurs in abdominal aortic aneurysm, a life-threatening disorder. It’s typically accompanied by constant upper abdominal pain that may radiate to the lower
back. The pain may worsen when the patient lies
down and may be relieved when he leans forward or sits up. Before rupture, the aneurysm
may produce a pulsating mass in the epigastrium, accompanied by a systolic bruit over the aorta. However, the mass stops pulsating after rupture. Associated signs and symptoms include
mottled skin below the waist, absent femoral and
pedal pulses, blood pressure that’s lower in the
legs than in the arms, and mild to moderate abdominal tenderness with guarding. Significant
blood loss causes signs of shock, such as tachycardia, tachypnea, and cool, clammy skin.
◆ Mesenteric artery ischemia. This life-
threatening disorder is characterized by 2 to 3
days of persistent, low-grade abdominal pain
and diarrhea leading to sudden, severe abdominal pain and rigidity. Rigidity occurs in the central or periumbilical region and is accompanied
by severe abdominal tenderness, fever, and
signs of shock, such as tachycardia and hypotension. Other findings may include vomiting,
anorexia, diarrhea, and constipation. Always
suspect mesenteric artery ischemia in patients
older than age 50 who have a history of heart
failure, arrhythmias, cardiovascular infarct, or
hypotension.
◆ Peritonitis. Depending on the cause of peri-
tonitis, abdominal rigidity may be localized or
generalized. For example, if an inflamed appendix causes local peritonitis, rigidity may be localized in the right lower quadrant. If a perforated
ulcer causes widespread peritonitis, rigidity may
be generalized and, in severe cases, boardlike.
Peritonitis also causes sudden and severe abdominal pain that can be localized or generalized. It can also produce abdominal tenderness
and distention, rebound tenderness, guarding,
hyperalgesia, hypoactive or absent bowel
sounds, nausea, and vomiting. Most patients
also experience fever, chills, tachycardia,
tachypnea, and hypotension.
◆ Pneumonia. In lower lobe pneumonia, se-
vere upper abdominal pain and tenderness accompany rigidity that diminishes with inspiration. Associated signs and symptoms include
blood-tinged or rusty sputum, dyspnea, achiness, headache, fever, sudden onset of chills,
crackles, egophony, decreased breath sounds,
dullness on percussion, and a dry, hacking
cough.
O
THER CAUSES
◆ Insect toxins. Insect stings and bites, espe-
cially black widow spider bites, release toxins
that can produce generalized cramping abdominal pain, usually accompanied by rigidity. These
toxins may also cause low-grade fever, nausea,
vomiting, tremors, and burning sensations in
the hands and feet. Some patients develop increased salivation, hypertension, paresis, and
hyperactive reflexes. Children commonly are
restless, have an expiratory grunt, and keep
their legs flexed.
S
PECIAL CONSIDERATIONS
Continue to monitor the patient closely for signs
of shock. Position him as comfortably as possible in a supine position, with his head flat on
the table, arms at his sides, and knees slightly
flexed to relax the abdominal muscles. Because
analgesics may mask symptoms, withhold them
until a tentative diagnosis has been made. Also
withhold food and fluids and administer an I.V.
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25
antibiotic because emergency surgery may be
required. Prepare the patient for diagnostic
tests, which may include blood, urine, and stool
studies; chest and abdominal X-rays; a computed tomography scan; magnetic resonance imaging; peritoneal lavage; and gastroscopy or
colonoscopy. A pelvic or rectal examination
may also be done.
P
EDIATRIC POINTERS
Voluntary rigidity may be difficult to distinguish
from involuntary rigidity if associated pain
makes the child restless, tense, or apprehensive.
However, in any child with suspected involuntary rigidity, your priority is early detection of
dehydration and shock, which can rapidly become life-threatening.
Abdominal rigidity in children can stem from
gastric perforation, hypertrophic pyloric stenosis, duodenal obstruction, meconium ileus, intussusception, cystic fibrosis, celiac disease, and
appendicitis.
G
ERIATRIC POINTERS
Advanced age and impaired cognition decrease
pain perception and intensity. Weakening of abdominal muscles may decrease muscle spasms
and rigidity.
Accessory muscle use
When breathing requires extra effort, the accessory muscles—the sternocleidomastoid, scalene, pectoralis major, trapezius, internal intercostals, and abdominal muscles—stabilize the
thorax during respiration. Some accessory muscle use normally takes place during such activities as singing, talking, coughing, defecating,
and exercising. (See Accessory muscles: Loca-
tions and functions, page 26.) However, more
pronounced use of these muscles may signal
acute respiratory distress, diaphragmatic weakness, or fatigue. It may also result from chronic
respiratory disease. Typically, the extent of accessory muscle use reflects the severity of the
underlying cause.
EMERGENCY INTERVENTIONS If the
patient displays increased accessory muscle use, immediately look for signs of acute respiratory distress. These include decreased level
of consciousness, shortness of breath when
speaking, tachypnea, intercostal and sternal
retractions, cyanosis, external breath sounds
(such as wheezing or stridor), diaphoresis,
nasal flaring, and extreme apprehension or agitation. Quickly auscultate for abnormal, diminished, or absent breath sounds. Check for
airway obstruction and, if detected, attempt to
restore airway patency. Insert an airway or intubate the patient. Then begin suctioning and
manual or mechanical ventilation. Assess oxygen saturation using pulse oximetry, if available. Administer oxygen; if the patient has
chronic obstructive pulmonary disease (COPD),
use only a low flow rate for mild COPD exacerbations. You may need to use a high flow rate
initially, but be attentive to the patient’s respiratory drive. Giving too much oxygen may
decrease the patient’s respiratory drive. An I.V.
catheter may be required.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient’s condition allows, examine him
more closely. Ask him about the onset, duration, and severity of associated signs and symptoms, such as dyspnea, chest pain, cough, and
fever.
Explore his medical history, focusing on respiratory disorders, such as infection or COPD.
Ask about cardiac disorders, such as heart failure, which may lead to pulmonary edema; also
inquire about neuromuscular disorders, such as
amyotrophic lateral sclerosis, which may affect
respiratory muscle function. Note a history of
allergies or asthma. Because collagen vascular
diseases can cause diffuse infiltrative lung disease, ask about such conditions as rheumatoid
arthritis and lupus erythematosus.
Ask about recent trauma, especially to the
spine or chest. Find out if the patient has recently undergone pulmonary function tests or
received respiratory therapy. Ask about smoking
and about occupational exposure to chemical
fumes or mineral dusts such as asbestos. Explore the family history for such disorders as
cystic fibrosis and neurofibromatosis, which can
cause diffuse infiltrative lung disease.
Perform a detailed chest examination, noting
abnormal respiratory rate, pattern, or depth. Assess the color, temperature, and turgor of the
patient’s skin, and check for clubbing. (See Ac-
cessory muscle use: Causes and associated
findings, page 27.)
M
EDICAL CAUSES
◆ Acute respiratory distress syndrome
(ARDS). In ARDS—a life-threatening disorder—accessory muscle use increases in
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Accessory muscles: Locations and functions
Physical exertion and pulmonary disease usually increase the work of breathing, taxing the
diaphragm and external intercostal muscles.
When this happens, accessory muscles provide
the extra effort needed to maintain respirations. The upper accessory muscles assist with
inspiration, whereas the upper chest, sternum,
internal intercostal, and abdominal muscles
assist with expiration.
With inspiration, the scalene muscles elevate, fix, and expand the upper chest. The sternocleidomastoid muscles raise the sternum,
Scalene muscle
External
intercostal
muscles
expanding the chest’s anteroposterior and longitudinal dimensions. The pectoralis major elevates the chest, increasing its anteroposterior
size, and the trapezius raises the thoracic
cage.
With expiration, the internal intercostals depress the ribs, decreasing the chest size. The
abdominal muscles pull the lower chest down,
depress the lower ribs, and compress the abdominal contents, which exerts pressure on
the chest.
Sternocleidomastoid
muscle
Trapezius muscle
Pectoralis major
muscle
response to hypoxia. It’s accompanied by
intercostal, supracostal, and sternal retractions
on inspiration and by grunting on expiration.
Other characteristics include tachypnea, dyspnea, diaphoresis, diffuse crackles, and a cough
with pink, frothy sputum. Worsening hypoxia
produces anxiety, tachycardia, and mental
sluggishness.
◆ Airway obstruction. An acute upper airway
obstruction can be life-threatening; fortunately,
most obstructions are subacute or chronic. Typically, this disorder increases accessory muscle
use. Its most telling sign, however, is inspiratory
stridor. Associated signs and symptoms include
dyspnea, tachypnea, gasping, wheezing, cough-
Abdominal rectus
muscle
ing, drooling, intercostal retractions, cyanosis,
and tachycardia.
◆ Amyotrophic lateral sclerosis (ALS). Be-
cause ALS affects the diaphragm more than
the accessory muscles, increased accessory
muscle use is characteristic of this disorder.
Other signs and symptoms include fasciculations, muscle atrophy and weakness, spasticity, bilateral Babinski’s reflex, and hyperactive
deep tendon reflexes. Incoordination makes
carrying out routine activities difficult for the
patient. Associated signs and symptoms include impaired speech; difficulty chewing or
swallowing and breathing; urinary frequency
and urgency; and, occasionally, choking and
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SIGNS & SYMPTOMS
Accessory muscle use: Causes and associated
findings
Major associated signs and symptoms
27
Common
causes
Acute respiratory
distress syndrome
Airway obstruction
Amyotrophic
lateral sclerosis
Asthma
Chronic bronchitis
Diffuse infiltrative
(or fibrotic) lung
disease
Emphysema
Pneumonia
Pulmonary edema
Pulmonary
embolism
Spinal cord injury
Thoracic injury
Barrel chest
Chest pain
Cough
Crackles
Cyanosis
Diaphoresis
Dyspnea
Fever
Muscle
weakness
Paralysis
Stridor
Tachycardia
Tachypnea
Wheezing
•
•
•••
•
• • • ••••
•
•
• ••••• •••
•••••• ••
••• • •
•••• •
••••••• ••
••• • •••
•••• •• •••
••
•
•
•
•
excessive drooling. (Note: Other neuromuscular disorders may produce similar signs and
symptoms.) Although the patient’s mental status remains intact, his poor prognosis may
cause periodic depression.
◆ Asthma. During acute asthma attacks, the
patient usually displays increased accessory
muscle use accompanied by severe dyspnea,
tachypnea, wheezing, productive cough, nasal
flaring, and cyanosis. Auscultation reveals faint
or possibly absent breath sounds, musical
crackles, and rhonchi. Other signs and symptoms include tachycardia, diaphoresis, and ap-
prehension caused by air hunger. Chronic asthma may also cause barrel chest.
◆ Chronic bronchitis. In this form of COPD,
increased accessory muscle use may be chronic
and is preceded by a productive cough and exertional dyspnea. Chronic bronchitis is accompanied by wheezing, basal crackles, tachypnea,
jugular vein distention, prolonged expiration,
barrel chest, and clubbing. Patients with chronic
bronchitis are sometimes called “blue bloaters”
because of the cyanosis and weight gain from
edema that commonly occur. Low-grade fever
may occur with secondary infection.
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◆ Diffuse infiltrative (or fibrotic) lung dis-
ease. In diffuse infiltrative lung disease, progressive pulmonary degeneration eventually increases accessory muscle use. Typically, though,
the patient reports progressive dyspnea on exertion as his chief complaint. He may also have
a cough, anorexia, weakness, fatigue, vague
chest pain, tachypnea, and crackles at the base
of the lungs.
◆ Emphysema. Increased accessory muscle
use occurs with progressive exertional dyspnea
and a minimally productive cough in this form
of COPD. These patients are sometimes called
“pink puffers” because of their characteristic
pursed-lip breathing, tachypnea, and a pink or
red complexion. Associated signs and symptoms include peripheral cyanosis, anorexia,
weight loss, malaise, barrel chest, and clubbing.
Auscultation reveals distant heart sounds; percussion detects hyperresonance.
◆ Pneumonia. Bacterial pneumonia initially
produces sudden high fever with chills. Associated signs and symptoms include increased accessory muscle use, chest pain, productive
cough, dyspnea, tachypnea, tachycardia, expiratory grunting, cyanosis, diaphoresis, and fine
crackles.
◆ Pulmonary edema. In acute pulmonary ede-
ma, increased accessory muscle use is accompanied by dyspnea, tachypnea, orthopnea,
crepitant crackles, wheezing, and a cough with
pink, frothy sputum. Other findings include restlessness, tachycardia, ventricular gallop, and
cool, clammy, cyanotic skin.
◆ Pulmonary embolism. Although signs and
symptoms vary with the size, number, and location of the emboli, this life-threatening disorder
may cause increased accessory muscle use.
Common findings include dyspnea and tachypnea that may be accompanied by pleuritic or
substernal chest pain. Other signs and symptoms include restlessness, anxiety, tachycardia,
productive cough, low-grade fever and, with a
large embolus, hemoptysis, cyanosis, syncope,
jugular vein distention, scattered crackles, and
focal wheezing.
◆ Spinal cord injury. An injury below Ll typi-
cally doesn’t affect the diaphragm or accessory
muscles, whereas an injury between C3 and C5
affects the upper respiratory muscles and diaphragm, causing increased accessory muscle
use.
Associated signs and symptoms of spinal
cord injury include unilateral or bilateral Babinski’s reflex; hyperactive deep tendon reflexes;
spasticity; and variable or total loss of pain and
temperature sensation, proprioception, and motor function. Horner’s syndrome (unilateral ptosis, pupillary constriction, facial anhidrosis) may
occur in lower cervical cord injury.
◆ Thoracic injury. Increased accessory mus-
cle use may occur, depending on the type and
extent of the injury. Associated signs and
symptoms of this potentially life-threatening
injury include an obvious chest wound or
bruising, chest pain, dyspnea, cyanosis, and
agitation. Signs of shock, such as tachycardia
and hypotension, occur with significant blood
loss.
O
THER CAUSES
◆ Diagnostic tests and treatments. Pul-
monary function tests, incentive spirometry, and
intermittent positive-pressure breathing can increase accessory muscle use.
S
PECIAL CONSIDERATIONS
If the patient is alert, elevate the head of the bed
to make his breathing as easy as possible. Encourage him to get plenty of rest and to drink
plenty of fluids to liquefy secretions. Administer
oxygen. Prepare him for such tests as pulmonary function studies, chest X-rays, lung
scans, arterial blood gas analysis, complete
blood count, and sputum culture.
If appropriate, stress how smoking endangers
the patient’s health, and refer him to an organized program to stop smoking. Also, teach him
how to prevent infection. Explain the purpose of
prescribed drugs, such as bronchodilators and
mucolytics, and make sure he knows their
dosage and schedule.
P
EDIATRIC POINTERS
Because infants and children tire sooner than
adults, they can develop respiratory failure from
respiratory distress more quickly than adults.
Upper airway obstruction—caused by edema,
bronchospasm, or a foreign object—usually produces respiratory distress and increased accessory muscle use. Disorders associated with airway obstruction include acute epiglottitis,
croup, pertussis, cystic fibrosis, and asthma.
Supraventricular, intercostal, or abdominal retractions indicate accessory muscle use.
G
ERIATRIC POINTERS
Because of age-related loss of elasticity in the
rib cage, accessory muscle use may be part of
an elderly person’s normal breathing pattern.
AGITATION
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29
P
ATIENT COUNSELING
Because labored breathing can make the patient
apprehensive, provide a calm environment and
encourage him to perform relaxation techniques
while you provide interventions to reduce the
work of breathing.
Agitation
Agitation refers to a state of hyperarousal, increased tension, and irritability that can lead to
confusion, hyperactivity, and overt hostility. Agitation can result from a toxic (poisons), metabolic, or infectious cause; brain injury; and psychiatric and various other disorders. It can also
result from pain, fever, anxiety, drug use or
withdrawal, and hypersensitivity reactions. It
can arise gradually or suddenly and last for
minutes or months. Whether it’s mild or severe,
agitation worsens with increased fever, pain,
stress, or external stimuli.
Agitation alone merely signals a change in
the patient’s condition, but it can be a useful indicator of a developing disorder. Obtaining a
good history is critical to determining the underlying cause of agitation.
H
ISTORY AND PHYSICAL
EXAMINATION
Determine the severity of the patient’s agitation
by examining the number and quality of agitation-induced behaviors, such as emotional lability, confusion, memory loss, hyperactivity, and
hostility. Obtain a history from the patient or a
family member, including diet, known allergies,
and use of prescribed or over-the-counter
drugs, including supplements and herbal medicines.
Ask if the patient is being treated for any illnesses. Has he had any recent infections, trauma, stress, or changes in sleep patterns? Check
for signs of drug abuse, such as needle tracks
and dilated pupils, and ask about alcohol intake. Obtain baseline vital signs and neurologic
status for future comparison.
M
EDICAL CAUSES
◆ Affective disturbances. Agitation may occur
in either the depressive or manic phase of affective disturbances and in personality disorders,
such as borderline and antisocial personality
disorders. The hallmark of the depressive form
is depressed mood upon awakening, which eases during the day. Chronic anxiety may be mild
or severe. Psychomotor agitation may be characterized by an inability to sit still, hand-wringing, pacing, and irritability. Other findings in the
manic state may include decreased sleep, pressured speech, and grandiosity.
◆ Alcohol withdrawal syndrome. Mild to
severe agitation occurs with hyperactivity,
tremors, and anxiety. In delirium tremens, the
potentially life-threatening stage of alcohol
withdrawal, severe agitation accompanies hallucinations, insomnia, diaphoresis, and depressed mood. Pulse rate and temperature rise
as withdrawal progresses; status epilepticus,
cardiac arrhythmias, and shock can occur.
◆ Anxiety. Anxiety is a common symptom that
produces varying degrees of agitation. The patient may be unaware of his anxiety or may
complain of it without knowing its cause. Other
findings may include nausea, vomiting, diarrhea, cool and clammy skin, frontal headache,
back pain, insomnia, and tremors.
◆ Chronic renal failure. Moderate to severe
agitation occurs in chronic renal failure, which
is marked by confusion and memory loss. The
agitation is accompanied by diverse signs and
symptoms, such as nausea, vomiting, anorexia, mouth ulcers, ammonia breath odor, GI
bleeding, pallor, edema, dry skin, and uremic
frost.
◆ Dementia. Mild to severe agitation can re-
sult from many common dementia syndromes,
such as Alzheimer’s and Huntington’s diseases.
The patient may display a decrease in memory,
attention span, problem-solving ability, and
alertness. Hypoactivity, wandering behavior,
hallucinations, aphasia, and insomnia may also
occur.
◆ Drug withdrawal syndrome. Findings
vary with the drug but include mild to severe
agitation, anxiety, abdominal cramps, diaphoresis, and anorexia. In opioid or barbiturate withdrawal, a decreased level of consciousness (LOC), seizures, and elevated
blood pressure, heart rate, and respiratory rate
can also occur.
◆ Hepatic encephalopathy. Agitation occurs
only in fulminating encephalopathy. Other findings include drowsiness, stupor, fetor hepaticus,
asterixis, and hyperreflexia.
◆ Hypersensitivity reaction. Moderate to se-
vere agitation may be the first sign of a hypersensitivity reaction. Depending on the severity
of the reaction, agitation may be accompanied
by urticaria, pruritus, and facial and dependent
edema.
30 ALOPECIA
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In anaphylactic shock, a potentially lifethreatening reaction, agitation occurs rapidly
along with apprehension, urticaria or diffuse
erythema, warm and moist skin, paresthesia,
pruritus, edema, dyspnea, wheezing, stridor, hypotension, and tachycardia. Abdominal cramps,
vomiting, and diarrhea can also occur.
◆ Hypoxemia. Beginning as restlessness, agi-
tation rapidly worsens in hypoxemia. The patient may be confused and have impaired judgment and motor coordination. He may also
have tachycardia, tachypnea, dyspnea, and
cyanosis.
◆ Increased intracranial pressure (ICP). Agi-
tation usually precedes other early signs and
symptoms, such as headache, nausea, and
vomiting. Increased ICP produces respiratory
changes, such as Cheyne-Stokes, cluster, ataxic,
or apneustic breathing; sluggish, nonreactive, or
unequal pupils; widening pulse pressure; tachycardia; decreased LOC; seizures; and motor
changes, such as decerebrate or decorticate
posture.
◆ Organic brain syndrome. In organic brain
syndrome, agitation is manifested as hyperactivity, emotional lability, confusion, and memory
loss. Slurred or incoherent speech and paranoid
behavior may also occur.
◆ Post–head trauma syndrome. Shortly—or
even years—after injury, mild to severe agitation
develops, characterized by disorientation, loss
of concentration, angry outbursts, and emotional lability. Fatigue, wandering behavior, and
poor judgment are other findings.
◆ Vitamin B
from mild to severe. Other effects include
seizures, peripheral paresthesia, and dermatitis.
Oculogyric crisis may also occur.
deficiency. Agitation can range
6
tient’s vital signs and neurologic status while
the cause is being determined. Eliminate stressors that can increase agitation. Provide adequate lighting, maintain a calm environment,
and allow the patient ample time to sleep. Ensure a balanced diet, and provide vitamin supplements and hydration.
Remain calm, nonjudgmental, and nonargumentative. If appropriate, prepare the patient for
diagnostic tests, such as computed tomography
scanning, skull X-rays, magnetic resonance
imaging, and blood studies.
P
EDIATRIC POINTERS
A common sign in children, agitation accompanies the expected childhood diseases as well as
more severe disorders that can lead to brain damage: hyperbilirubinemia, phenylketonuria, vitamin
A deficiency, hepatitis, frontal lobe syndrome, increased ICP, and lead poisoning. In neonates, agitation can stem from alcohol or drug withdrawal
if the mother abused these substances.
When evaluating an agitated child, remember
to use words that he can understand and to
look for nonverbal clues. For instance, if you
suspect that pain is causing agitation, ask him
to tell you where it hurts, but be sure to watch
for other indicators, such as wincing, crying, or
moving away.
G
ERIATRIC POINTERS
Any deviation from an older person’s usual activities or rituals may provoke anxiety or agitation. Any environmental change, such as a
transfer to a nursing home or a visit from a
stranger in the patient’s home, may trigger a
need for treatment.
O
THER CAUSES
◆ Drugs. Mild to moderate agitation, which is
commonly dose related, is an adverse effect of
central nervous system stimulants—especially
appetite suppressants, such as amphetamines
and amphetamine-like drugs; sympathomimetics such as ephedrine; caffeine; and theophylline.
◆ Radiographic contrast media. Injection of
a contrast medium during various diagnostic
tests may produce moderate to severe agitation
along with other signs of hypersensitivity.
S
PECIAL CONSIDERATIONS
Because agitation can be an early sign of many
different disorders, continue to monitor the pa-
Alopecia
[Hair loss]
Alopecia usually develops gradually and affects
the scalp; it may be diffuse or patchy and can be
classified as scarring or nonscarring. Scarring
alopecia (permanent hair loss) results from hair
follicle destruction, which smoothes the skin
surface, erasing follicular openings. Nonscarring
alopecia (temporary hair loss) results from hair
follicle damage that spares follicular openings,
allowing future hair growth.
One of the most common causes of alopecia
is the use of certain chemotherapeutic drugs.
Alopecia may also result from the use of other
drugs; radiation therapy; a skin, connective
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