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PECIAL CONSIDERATIONS
As needed, prepare the patient for cardiopulmonary studies, such as an electrocardiogram
and a lung scan. Perform a venipuncture to collect a serum sample for cardiac enzyme and
other studies. Explain the purpose and procedure of each diagnostic test to the patient to
help alleviate his anxiety. Also explain the purpose of any prescribed drugs, and make sure
that the patient understands the dosage, schedule, and possible adverse effects.
Keep in mind that a patient with chest pain
may deny his discomfort, so stress the importance of reporting symptoms to allow adjustment of his treatment.
P
EDIATRIC POINTERS
Even children old enough to talk may have difficulty describing chest pain, so be alert for
nonverbal clues, such as restlessness, facial
grimaces, or holding of the painful area. Ask
the child to point to the painful area and then
to where the pain goes (to find out if it’s radiating). Determine the pain’s severity by asking
the parents if the pain interferes with the
child’s normal activities and behavior. Remember, a child may complain of chest pain in an
attempt to get attention or to avoid attending
school.
G
ERIATRIC POINTERS
Because older patients have a higher risk of
developing life-threatening conditions (such
as an MI, angina, and aortic dissection), you
must evaluate chest pain carefully in these patients.
P
ATIENT COUNSELING
Teach patients with coronary artery disease
about the typical features of cardiac ischemia as
well as the symptoms that should prompt them
to seek medical attention. If the pain fails to disappear after sublingual nitroglycerin, lasts more
than 20 minutes, or has a different pattern than
the usual angina, the patient must be evaluated
immediately.
Cheyne-Stokes
respirations
CHEYNE-STOKES RESPIRATIONS 151
Recognizing
Cheyne-Stokes
respirations
Cheyne-Stokes respirations are breaths that
gradually become faster and deeper than
normal, then slower, during a 30- to 170second period, alternating with 20- to 60second periods of apnea.
of apnea. This pattern can occur normally in
patients with heart or lung disease. It usually
indicates increased intracranial pressure (ICP)
from a deep cerebral or brain stem lesion, or
a metabolic disturbance in the brain. (See
Recognizing Cheyne-Stokes respirations.)
Cheyne-Stokes respirations may indicate a
major change in the patient’s condition—usually
for the worse. For example, in a patient who
has had head trauma or brain surgery, CheyneStokes respirations may signal increasing ICP.
Cheyne-Stokes respirations can occur normally
in patients who live at high altitudes.
EMERGENCY INTERVENTIONS If you de-
tect Cheyne-Stokes respirations in a patient
with a history of head trauma, recent brain
surgery, or another brain insult, quickly take his
vital signs. Keep his head elevated 30 degrees,
and perform a rapid neurologic examination to
obtain baseline data. Reevaluate the patient’s
neurologic status frequently. If ICP continues to
rise, you’ll detect changes in the patient’s level of
consciousness (LOC), pupillary reactions, and
ability to move his extremities. ICP monitoring is
indicated.
Time the periods of hyperpnea and apnea for 3
to 4 minutes to evaluate respirations and to obtain
baseline data. Be alert for prolonged periods of
apnea. Frequently check blood pressure; also
check skin color to detect signs of hypoxemia.
Maintain airway patency and administer oxygen
as needed. If the patient’s condition worsens, endotracheal intubation is necessary
.
The most common pattern of periodic breathing, Cheyne-Stokes respirations are characterized by a waxing and waning period of hyperpnea that alternates with a shorter period
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient’s condition permits, obtain a brief
history. Ask especially about drug use.
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M
EDICAL CAUSES
◆ Adams-Stokes attacks. Cheyne-Stokes res-
pirations may follow an Adams-Stokes attack—
a syncopal episode associated with atrioventricular block. The patient is hypotensive, with a
heart rate between 20 and 50 beats/minute. He
may also appear pale, shaking, and confused.
◆ Heart failure. In left-sided heart failure,
Cheyne-Stokes respirations may occur with exertional dyspnea and orthopnea. Related findings include fatigue, weakness, tachycardia,
tachypnea, and crackles. The patient may also
have a cough, generally nonproductive but occasionally producing clear or blood-tinged sputum.
◆ Hypertensive encephalopathy. In this life-
threatening disorder, severe hypertension precedes Cheyne-Stokes respirations. The patient’s
LOC is decreased, and he may experience vomiting, seizures, severe headaches, vision disturbances (including transient blindness), and
transient paralysis.
◆ Increased ICP. As ICP rises, Cheyne-Stokes
is the first irregular respiratory pattern to occur.
It’s preceded by a decreased LOC and accompanied by hypertension, headache, vomiting, impaired or unequal motor movement, and vision
disturbances (blurring, diplopia, photophobia,
and pupillary changes). In late stages of increased ICP, bradycardia and widened pulse
pressure occur.
◆ Renal failure. End-stage chronic renal fail-
ure may produce Cheyne-Stokes respirations,
bleeding gums, oral lesions, ammonia breath
odor, and marked changes in every body system.
O
THER CAUSES
◆ Drugs. Large doses of an opioid, a hypnotic,
or a barbiturate can precipitate Cheyne-Stokes
respirations.
S
PECIAL CONSIDERATIONS
When evaluating Cheyne-Stokes respirations,
be careful not to mistake periods of hypoventilation or decreased tidal volume for complete
apnea.
P
EDIATRIC POINTERS
Cheyne-Stokes respirations rarely occur in children, except during late heart failure.
G
ERIATRIC POINTERS
Cheyne-Stokes respirations can occur normally
in elderly patients during sleep.
P
ATIENT COUNSELING
Inform the patient or his family that sleep apnea
and Cheyne-Stokes respirations have different
causes and methods of treatment.
Chills
[Rigors]
Chills are extreme, involuntary muscle contractions with characteristic paroxysms of violent
shivering and teeth chattering. Commonly
caused by an increased body temperature set
by the hypothalamic thermostat, chills are usually accompanied by fever and tend to arise
suddenly, heralding the onset of infection. Certain diseases, such as pneumococcal pneumonia, produce only a single, shaking chill. Other
diseases, such as malaria, produce intermittent
chills with recurring high fever. Still others produce continuous chills for up to 1 hour, precipitating a high fever. (See Why chills accompany
fever.)
Chills can also result from lymphomas, blood
transfusion reactions, and the use of certain
drugs. Chills without fever are a normal response to exposure to cold. (See Rare causes of
chills.)
H
ISTORY AND PHYSICAL
EXAMINATION
Ask the patient when the chills began and
whether they’re continuous or intermittent. Because fever commonly accompanies or follows
chills, take his rectal temperature to obtain a
baseline reading. Then check his temperature
often to monitor fluctuations and to determine
his temperature curve. Typically, a localized infection produces a sudden onset of shaking
chills, sweats, and high fever, whereas a systemic infection produces intermittent chills with
recurring episodes of high fever or continuous
chills that may last up to 1 hour and precipitate
a high fever.
Ask about related signs and symptoms, such
as headache, dysuria, diarrhea, confusion, abdominal pain, cough, sore throat, or nausea.
Does the patient have any known allergies, an
infection, or a recent history of an infectious
disorder? Find out which medications he’s taking and whether any drug has improved or
worsened his symptoms. Has he received any
treatment that may predispose him to an infection (such as chemotherapy)? Ask about
recent exposure to farm animals, guinea pigs,
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153
Why chills
accompany fever
Fever usually occurs when exogenous pyrogens activate endogenous pyrogens to
reset the body’s thermostat to a higher level. At this higher thermostatic setpoint, the
body feels cold and responds through several compensatory mechanisms, including
rhythmic muscle contractions, or chills.
These muscle contractions in turn generate
body heat and help produce fever. This
flowchart outlines the events that link chills
to fever.
Exogenous pyrogens (infectious
organisms, immune complexes,
toxins) enter the body.
Phagocytic leukocytes release
endogenous pyrogens.
Endogenous pyrogens — possibly
with prostaglandins — stimulate
temperature-sensitive receptors
in the hypothalamus and raise the
thermostatic setpoint to a higher
level.
Descending efferent pathways from
the hypothalamus innervate
effectors, such as skeletal muscles,
and stimulate them to rhythmically
contract.
Rhythmic muscle contractions,
or chills, generate body heat,
which helps produce fever.
Rare causes of chills
Chills can result from disorders that are rare
in the United States but may be fairly common worldwide. Remember to ask about recent foreign travel when you obtain a patient’s history. Among the many rare
disorders that produce chills are:
◆ brucellosis (undulant fever)
◆ dengue fever (breakbone fever)
◆ epidemic typhus (louse-borne typhus)
◆ leptospirosis
◆ lymphocytic choriomeningitis
◆ plague
◆ pulmonary tularemia
◆ rat bite fever
◆ relapsing fever.
hamsters, dogs, and such birds as pigeons, parrots, and parakeets. Also ask about recent insect or animal bites, travel to foreign countries,
and contact with persons who have an active
infection.
M
EDICAL CAUSES
◆ Acquired immunodeficiency syndrome.
This commonly fatal disease is caused by infection with human immunodeficiency virus transmitted by blood or semen. The patient usually
develops lymphadenopathy and may also experience fatigue, anorexia and weight loss,
diarrhea, diaphoresis, skin disorders, and signs
of upper respiratory tract infection. Opportunistic infections can cause serious disease in these
patients.
◆ Anthrax (inhalation). This acute infectious
disease is caused by the gram-positive, sporeforming bacterium Bacillus anthracis. Although
the disease most commonly occurs in wild and
domestic grazing animals, such as cattle, sheep,
and goats, the spores can live in the soil for
many years. The disease can occur in humans
exposed to infected animals, tissue from infected animals, or biological agents. Most natural
cases occur in agricultural regions worldwide.
Anthrax may occur in cutaneous, inhalation, or
GI forms.
Inhalation anthrax is caused by inhalation of
aerosolized spores. Initial signs and symptoms
are flulike and include fever, chills, weakness,
cough, and chest pain. The disease generally
occurs in two stages with a period of recovery
after the initial signs and symptoms. The second
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stage develops abruptly, causing rapid deterioration marked by fever, dyspnea, stridor, and
hypotension; death generally results within 24
hours. Radiologic findings include mediastinitis
and symmetrical mediastinal widening.
◆ Cholangitis. Charcot’s triad—chills with
spiking fever, abdominal pain, and jaundice—
characterizes sudden obstruction of the common bile duct. The patient may have associated
pruritus, weakness, and fatigue.
◆ Gram-negative bacteremia. This infection
causes sudden chills and fever, nausea, vomiting, diarrhea, and prostration.
◆ Hemolytic anemia. In acute hemolytic ane-
mia, fulminating chills occur with fever and abdominal pain. The patient rapidly develops
jaundice and hepatomegaly; he may develop
splenomegaly.
◆ Hepatic abscess. This infection usually aris-
es abruptly, with chills, fever, nausea, vomiting,
diarrhea, anorexia, and severe upper abdominal
tenderness and pain that may radiate to the
right shoulder.
◆ Hodgkin’s disease. The patient characteris-
tically experiences several days or weeks of
fever and chills alternating with periods of no
fever and no chills. This disorder commonly
produces regional lymphadenopathy that may
progress to hepatosplenomegaly. Other findings
include diaphoresis, fatigue, and pruritus.
◆ Infective endocarditis. This infection pro-
duces abrupt onset of intermittent shaking chills
with fever. In addition to petechiae, the patient
may have Janeway lesions on his hands and
feet and Osler’s nodes on his palms and soles.
Associated findings include murmur, hematuria,
eye hemorrhage, Roth’s spots, and signs of
heart failure (dyspnea, peripheral edema).
◆ Influenza. Initially, this disorder causes an
abrupt onset of chills, high fever, malaise,
headache, myalgia, and nonproductive cough.
Some patients may also suddenly develop rhinitis, rhinorrhea, laryngitis, conjunctivitis, hoarseness, and sore throat. Chills generally subside
after the first few days, but intermittent fever,
weakness, and cough may persist for up to
1 week.
◆ Influenza type A H1N1 virus (Swine flu).
Influenza type A H1N1, or swine flu, is a respiratory disease of pigs caused by type A influenza
virus. Swine flu viruses cause high levels of illness and low death rates in pigs. Swine flu
viruses normally don’t infect humans. However,
sporadic human infections with swine flu have
occurred. Most commonly, these cases occur in
persons with direct exposure to pigs. The virus
has changed slightly and is known as H1N1 flu.
Outbreaks of H1N1 flu in 2009 showed that the
virus can be transmitted from person to person,
causing transmission across the globe. The
H1N1 flu is similar to influenza, and causes illness and in some cases death. The symptoms
of swine flu include chills, fever, fatigue, myalgia, nonproductive cough, headache, and vomiting. The use of antiviral drugs is recommended
to treat H1N1 flu.
◆ Legionnaires’ disease. Within 12 to 48
hours after the onset of this disease, the patient
suddenly develops chills and a high fever. Prodromal signs and symptoms characteristically
include malaise, headache, and possibly diarrhea, anorexia, diffuse myalgia, and general
weakness. An initially nonproductive cough
progresses to a productive cough with mucoid
or mucopurulent sputum and possibly hemoptysis. Most patients also develop nausea and
vomiting, confusion, mild temporary amnesia,
pleuritic chest pain, dyspnea, tachypnea, crackles, tachycardia, and flushed and mildly diaphoretic skin.
◆ Lung abscess. In addition to chills, a lung
abscess causes sweating, pleuritic chest pain,
dyspnea, clubbing, weakness, headache,
malaise, anorexia, weight loss, and a cough that
produces large amounts of purulent, foulsmelling and, possibly, bloody sputum.
◆ Lyme disease. The bite of a tiny deer tick
can transmit this infection, which causes a red
macule or papule (erythema migrans) to develop at the bite site. It’s accompanied by chills,
fever, malaise, fatigue, lymphadenopathy,
arthralgia, and rash. If untreated, Lyme disease
may cause cranial neuritis with facial palsy,
heart blocks, arthritis, and a characteristic sclerotic rash.
◆ Lymphangitis. Acute lymphangitis produces
chills and other systemic signs and symptoms,
such as fever, malaise, and headache. Its characteristic signs are red streaks radiating from a
wound and cellulitis draining toward tender regional lymph nodes.
◆ Lymphogranuloma venereum. This disor-
der produces chills, fever, lymphadenopathy,
headache, anorexia, myalgia, arthralgia, and
weight loss. The primary genital lesion is a
papule or small erosion that precedes lymphatic
involvement and heals spontaneously within a
few days.
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◆ Malaria. The paroxysmal cycle of malaria
begins with a period of chills lasting 1 to
2 hours. This is followed by a high fever lasting
3 to 4 hours and then 2 to 4 hours of profuse
diaphoresis. Paroxysms occur every 48 to
72 hours when caused by Plasmodium malariae
and every 42 to 40 hours when caused by P. vi-
vax or P. ovale. In benign malaria, the paroxysms
may be interspersed with periods of well-being.
The patient also has a headache, muscle pain,
and possibly hepatosplenomegaly.
◆ Miliary tuberculosis. In the acute form of
this disease, the patient suffers intermittent
chills, high fever, and night sweats. Epididymal
or testicular nodules and splenomegaly may
also occur.
◆ Monkeypox. Many individuals infected with
the monkeypox virus experience chills. Other
common initial symptoms of this rare virus include fever, lymphadenopathy, sore throat, dyspnea, muscle aches, and rash. Although monkeypox occurs primarily in central and western
Africa, it was confirmed in the United States in
2003 when several humans contracted the virus
from infected pet prairie dogs. There is no treatment for this virus; however, given its similarity
to smallpox, the smallpox vaccine is used in
certain circumstances to protect individuals
against monkeypox.
◆ Otitis media. Acute suppurative otitis media
produces chills with fever and severe deep,
throbbing ear pain. The patient usually displays
a mild conductive hearing loss and a bulging,
hyperemic tympanic membrane. He may also
have dizziness, nausea, and vomiting. When the
tympanic membrane ruptures, pus drains externally through the ear canal and the patient feels
relief.
◆ Pelvic inflammatory disease. In this infec-
tion, chills and fever are typically accompanied
by lower abdominal pain and tenderness; profuse, purulent vaginal discharge; or abnormal
menstrual bleeding. The patient may also develop nausea and vomiting, an abdominal mass,
and dysuria.
◆ Plague. Caused by Yersinia pestis, plague is
one of the most virulent and, if untreated, lethal
bacterial infections known. Most cases are sporadic, but the potential for epidemic spread still
exists. Clinical forms include bubonic (the most
common), septicemic, and pneumonic plagues.
The bubonic form is transmitted to man from
the bite of infected fleas. Signs and symptoms
include fever, chills, and swollen, inflamed, and
tender lymph nodes near the site of the fleabite.
Septicemic plague may develop as a complication of untreated bubonic or pneumonic plague
and occurs when the plague bacteria enter the
bloodstream and multiply. The pneumonic form
can be contracted by inhaling respiratory
droplets from an infected person or inhaling the
organism that has been dispersed in the air
through biological warfare. The onset is usually
sudden with chills, fever, headache, and myalgia. Pulmonary signs and symptoms include a
productive cough, chest pain, tachypnea, dyspnea, hemoptysis, increasing respiratory distress,
and cardiopulmonary insufficiency.
◆ Pneumonia. A single shaking chill usually
heralds the sudden onset of pneumococcal
pneumonia; other pneumonias characteristically cause intermittent chills. In any type of pneumonia, related findings may include fever, productive cough with bloody sputum, pleuritic
chest pain, dyspnea, tachypnea, and tachycardia. The patient may be cyanotic and diaphoretic, with bronchial breath sounds and crackles,
rhonchi, increased tactile fremitus, and grunting
respirations. He may also experience achiness,
anorexia, fatigue, and headache.
◆ Psittacosis. This disease typically begins
with the sudden onset of chills, fever, headache,
myalgia, epistaxis, and prostration. A dry, hacking cough occurs initially, progressing to pneumonia with a cough that produces small
amounts of mucoid, blood-streaked sputum.
The patient also experiences tachypnea, fine
crackles, photophobia, abdominal distention
and tenderness, nausea, vomiting, a faint macular rash and, rarely, chest pain.
◆ Pyelonephritis. In acute pyelonephritis, the
patient develops chills, high fever, and possibly
nausea and vomiting over several hours to
days. He generally also has anorexia, fatigue,
myalgia, flank pain, costovertebral angle tenderness, hematuria or cloudy urine, and urinary
frequency, urgency, and burning.
◆ Q fever. Q fever is a rickettsial disease
caused by Coxiella burnetii, an organism found
in cattle, sheep, and goats. Human infection
usually results from exposure to contaminated
milk, urine, feces, or other fluids from infected
animals, but it may also result from inhalation
of contaminated barnyard dust. C. burnetii is
highly infectious and is considered a possible
airborne agent for biological warfare. Signs
and symptoms include fever, chills, severe
headache, malaise, chest pain, nausea,
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vomiting, and diarrhea. The fever may last up to
2 weeks. In severe cases, the patient may develop hepatitis or pneumonia.
◆ Renal abscess. This abscess initially pro-
duces sudden chills and fever. Later effects include flank pain, costovertebral angle tenderness, abdominal muscle spasm, and transient
hematuria.
◆ Rocky Mountain spotted fever. This disor-
der begins suddenly with chills, fever, malaise,
an excruciating headache, and muscle, bone,
and joint pain. Typically, the patient’s tongue is
covered with a thick white coating that gradually turns brown. After 2 to 6 days of fever and
occasional chills, a macular or maculopapular
rash appears on the hands and feet and then
becomes generalized; after a few days, the rash
becomes petechial.
◆ Sepsis, puerperal or postabortal. Chills
and high fever occur as early as 6 hours or as
late as 10 days postpartum or postabortion. The
patient may also have a purulent vaginal discharge, an enlarged and tender uterus, abdominal pain, backache and, possibly, nausea, vomiting, and diarrhea.
◆ Septic arthritis. Chills and fever accompany
the characteristic red, swollen, and painful
joints caused by this disorder.
◆ Septic shock. Initially, septic shock produces
chills, fever and, possibly, nausea, vomiting, and
diarrhea. The patient’s skin is typically flushed,
warm, and dry; his blood pressure is normal or
slightly low; and he has tachycardia and tachypnea. As septic shock progresses, the patient’s
arms and legs become cool and cyanotic, and
he exhibits oliguria, thirst, anxiety, restlessness,
confusion, and hypotension. Later, he develops
cold and clammy skin, a rapid and thready
pulse, severe hypotension, persistent oliguria or
anuria, signs of respiratory failure, and coma.
◆ Sinusitis. In acute sinusitis, chills are accom-
panied by fever, headache, and pain, tenderness, and swelling over the affected sinuses.
Maxillary sinusitis produces pain over the
cheeks and upper teeth; ethmoid sinusitis, pain
over the eyes; frontal sinusitis, pain over the
eyebrows; and sphenoid sinusitis, pain behind
the eyes. The primary indicator of sinusitis is
nasal discharge, which is commonly bloody for
24 to 48 hours before gradually becoming
purulent.
◆ Snake bite. Most pit viper bites that result in
envenomization cause chills, typically with
fever. Other systemic signs and symptoms include sweating, weakness, dizziness, fainting,
hypotension, nausea, vomiting, diarrhea, and
thirst. The area around the snake bite may be
marked by immediate swelling and tenderness,
pain, ecchymoses, petechiae, blebs, bloody discharge, and local necrosis. The patient may
have difficulty speaking, blurred vision, paralysis, bleeding tendencies, and signs of respiratory distress and shock.
◆ Tularemia. Also known as “rabbit fever,”
this infectious disease is caused by the gramnegative, non–spore-forming bacterium Fran-
cisella tularensis. This organism is found in wild
animals, water, and moist soil, typically in rural
areas. It’s transmitted to humans through the
bite of an infected insect or tick, the handling of
infected animal carcasses, the drinking of contaminated water, or the inhalation of the bacterium. It’s considered a possible airborne agent for
biological warfare. Signs and symptoms following inhalation of the organism include the
abrupt onset of fever, chills, headache, generalized myalgia, a nonproductive cough, dyspnea,
pleuritic chest pain, and empyema.
◆ Typhoid fever. This disorder may initially
cause sudden chills and a sharply rising fever.
More commonly, though, the patient’s body
temperature gradually increases for 5 to 7 days
with accompanying chilliness or frank chills.
Headache, abdominal discomfort, constipation,
and demonstrable splenomegaly appear by the
end of the first week. A characteristic rash
called “rose spots” develops on the upper abdomen and anterior thorax during the second
week but lasts only 2 to 3 days. Later, the patient may develop a dry cough, epistaxis, mental
dullness or delirium, marked abdominal distention, significant weight loss, profound fatigue,
and diarrhea. The heart rate may be unusually
slow in relation to the high fever.
◆ Typhus. Typhus is a rickettsial disease trans-
mitted to humans by fleas, mites, or body louse.
Initial signs and symptoms include headache,
myalgia, arthralgia, and malaise followed by an
abrupt onset of chills, fever, nausea, and vomiting. A maculopapular rash may be present in
some cases.
◆ Violin spider bite. This bite produces chills,
fever, malaise, weakness, nausea, vomiting,
and joint pain within 24 to 48 hours. The patient
may also develop a rash and delirium.
O
THER CAUSES
◆ Drugs. Amphotericin B is a drug associated
with chills. Phenytoin is also a common cause
of drug-induced fever that can produce chills.
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157
I.V. bleomycin and intermittent administration
of an oral antipyretic can also cause chills.
◆ I.V. therapy. Infection at the I.V. insertion
site (superficial phlebitis) can cause chills, high
fever, and local redness, warmth, induration,
and tenderness.
◆ Transfusion reaction. A hemolytic reaction
may cause chills during the transfusion or immediately afterward. A nonhemolytic febrile reaction may also cause chills.
S
PECIAL CONSIDERATIONS
Check the patient’s vital signs often, especially if
his chills result from a known or suspected infection. Be alert for signs of progressive septic
shock, such as hypotension, tachycardia, and
tachypnea. If appropriate, obtain samples of
blood, sputum, or wound drainage for culture
tests to determine the causative organism. Give
the appropriate antibiotic. Radiographic studies
and serum and urine samples may be required.
Because chills are an involuntary response to
an increased body temperature, blankets won’t
stop a patient’s chills or shivering. Despite this,
keep his room temperature as even as possible.
Provide adequate hydration and nutrients, and
give an antipyretic to help control fever. Irregular use of an antipyretic can trigger compensatory chills.
P
EDIATRIC POINTERS
Infants don’t get chills because they have poorly
developed shivering mechanisms. In addition,
most classic febrile childhood infections, such
as measles and mumps, don’t typically produce
chills. However, older children and teenagers
may have chills with mycoplasma pneumonia
and acute pyogenic osteomyelitis.
G
ERIATRIC POINTERS
Chills in an elderly patient usually indicate an
underlying infection, such as a urinary tract infection, pneumonia (commonly associated with
aspiration of gastric contents), diverticulitis, or
skin breakdown in pressure areas. Also, consider an ischemic bowel in an elderly patient who
comes into your facility with fever, chills, and
abdominal pain.
P
ATIENT COUNSELING
Advise the patient to measure his temperature
with a thermometer when he experiences chills
and to document the exact readings and times.
This will help reveal patterns that may point to
a specific diagnosis.
Chorea
[Choreiform movements]
Chorea—brief, unpredictable bursts of rapid,
jerky motion that interrupt normal coordinated
movement—indicates dysfunction of the extrapyramidal system.
Unlike tics, choreiform movements are seldom repetitive but tend to appear purposeful
despite their involuntary nature. Although any
muscle can be affected, chorea usually involves
the face, head, lower arms, and hands. It can affect both sides of the body or only one side;
however, when it affects the face, both sides are
usually involved. Chorea may be aggravated by
excitement or fatigue and may disappear during
sleep. In some patients, it may be difficult to distinguish chorea from athetosis (snakelike,
writhing movements), although choreiform
movements are generally more rapid than
athetoid ones. (See Distinguishing athetosis from
chorea, page 73.)
H
ISTORY AND PHYSICAL
EXAMINATION
Ask the patient and his family when they first
noticed the choreiform movements. Do the
movements disappear when the patient is
asleep? Find out if anyone in the patient’s family
exhibits the same type of movements, and ask
about a family history of such diseases as Huntington’s disease. Also ask which medications
the patient is taking. Obtain an occupational
history, noting especially prolonged exposure to
manganese or other metals. As you obtain the
history, observe the patient for excessive restlessness and periodic facial grimaces that may
interrupt his speech.
Perform a physical examination to evaluate
the severity of the patient’s chorea. Ask him to
stick out his tongue and keep it out. Typically,
he’ll be unable to do this; instead, his tongue
will dart in and out of his mouth. Observe the
patient’s arms and legs separately for involuntary jerky movements. Ask him to extend and
flex his hand as if halting traffic; the choreiform
movements will be extremely evident in this position. Also, check for such related signs as
athetosis, rigidity, or tremor.
To assess the patient for choreoathetotic gait,
ask him to walk. He may change the position of
his trunk and upper body parts with each step
and jerk and tilt his head to one side. Because
of superimposed involuntary movements and
postures, the patient’s legs may move slowly
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and awkwardly. (An involuntary movement suspending his leg momentarily with each step
may give a dancing quality to his gait.)
M
EDICAL CAUSES
◆ Cerebral infarction. An infarction that in-
volves the thalamic area produces unilateral or
bilateral chorea. The patient may also experience dysarthria, tremors, rigidity, weakness,
and sensory disturbances such as paresthesia.
◆ Encephalitis. Chorea may occur in the re-
covery phase of encephalitis. Low-grade fever
and athetosis may also be present, in addition
to such focal neurologic signs as hemiparesis,
hemiplegia, and facial droop.
◆ Huntington’s disease. In this inherited dis-
ease, chorea may be the first sign or it may accompany the intellectual decline that leads to
emotional disturbances and dementia. The patient’s movements tend to be choreoathetotic
and may be accompanied by dysarthria, dystonia, prancing gait, dysphagia, and facial grimacing.
◆ Wilson’s disease. Chorea and dystonia af-
fecting the arms and legs are early indicators of
Wilson’s disease. The patient typically experiences dysarthria, tremors, hoarseness, dysphagia, and slowed body movements; he may also
exhibit emotional and behavioral disturbances,
drooling, rigidity, and mental deterioration. The
pathognomonic Kayser-Fleischer ring in the
cornea appears as the disease progresses.
O
THER CAUSES
◆ Carbon monoxide poisoning. A patient
who survives severe carbon monoxide poisoning may have neurologic signs and symptoms,
such as chorea, rigidity, dementia, impaired
sensory function, masklike facies, generalized
seizures, and myoclonus.
◆ Drugs. Phenothiazines (especially the piper-
azine derivatives), haloperidol, thiothixene, and
loxapine commonly produce chorea. Metoclopramide, metyrosine, hormonal contraceptives,
levodopa, and phenytoin may also cause this
sign.
◆ Lead poisoning. In the later stages, lead poi-
soning produces chorea in addition to seizures,
headache, memory lapses, and severe mental
impairment. The patient may also develop
masklike facies, footdrop, wristdrop, dizziness,
ataxia, weakness, lethargy, abdominal pain,
anorexia, nausea, vomiting, constipation, lead
line on the gums, and a metallic taste in his
mouth.
◆ Manganese poisoning. In miners who have
been exposed to manganese dioxide for prolonged periods, chorea characteristically occurs
with a propulsive gait, dystonia, and rigidity. Initially, the patient may have masklike facies, a
resting tremor, and personality changes; later,
extreme muscle weakness and lethargy occur.
S
PECIAL CONSIDERATIONS
Because the patient’s movements are involuntary and increase his risk of severe injury, pad
the side rails of his bed and keep sharp objects
out of his environment. Help him minimize
physical activity and emotional upset to avoid
aggravating the chorea and ensure adequate
periods of rest and sleep.
P
EDIATRIC POINTERS
Sydenham’s chorea occurs in childhood as a delayed manifestation of rheumatic fever. In
Hallervorden-Spatz disease, a rare and inherited
degenerative disorder, choreoathetotic movements occur in late childhood or early adolescence. Chorea can also occur in children with
athetoid cerebral palsy.
Chvostek’s sign
Chvostek’s sign is an abnormal spasm of the
facial muscles that’s elicited by lightly tapping
the patient’s facial nerve near his lower jaw.
(See Eliciting Chvostek’s sign.) This sign usually suggests hypocalcemia but can occur normally in about 25% of people. Typically, it precedes other signs of hypocalcemia and
persists until the onset of tetany. It can’t be
elicited during tetany because of strong muscle contractions.
Normally, eliciting Chvostek’s sign is attempted only in patients with suspected hypocalcemic
disorders. However, because the parathyroid
gland regulates calcium balance, Chvostek’s
sign may also be tested in patients before neck
surgery to obtain a baseline.
EMERGENCY INTERVENTIONS Test for
Trousseau’s sign, a reliable indicator of
hypocalcemia. Closely monitor the patient for
signs of tetany, such as carpopedal spasms or circumoral and extremity paresthesia.
Be prepared to act rapidly if a seizure occurs.
Perform an electrocardiogram to check for
changes associated with hypocalcemia that can
predispose the patient to arrhythmias. Place the
patient on a cardiac monitor.
Eliciting Chvostek’s sign
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Begin by telling the patient to relax his facial muscles. Then stand directly in front of
him, and tap the facial nerve either just anterior to the earlobe and below the zygomatic arch or between the zygomatic arch
and the corner of his mouth. A positive response varies from twitching of the lip at
the corner of the mouth to spasm of all facial muscles, depending on the severity of
hypocalcemia.
H
ISTORY AND PHYSICAL
EXAMINATION
Obtain a brief history. Find out if the patient has
had the parathyroid glands surgically removed
or if he has a history of hypoparathyroidism, hypomagnesemia, or malabsorption disorder. Ask
him or his family if they have noticed any mental
changes, such as depression or slowed responses, which can accompany chronic hypocalcemia.
M
EDICAL CAUSES
◆ Hypocalcemia. The degree of muscle spasm
elicited reflects the patient’s serum calcium level. Initially, hypocalcemia produces paresthesia
in the fingers, toes, and circumoral area that
progresses to muscle tension and carpopedal
spasms. The patient may also complain of muscle weakness, fatigue, and palpitations. Muscle
twitching, hyperactive deep tendon reflexes,
choreiform movements, and muscle cramps
may also occur. The patient with chronic
hypocalcemia may have mental status changes;
diplopia; difficulty swallowing; abdominal
cramps; dry, scaly skin; brittle nails; and thin,
patchy scalp and eyebrow hair.
CLUBBING
O
THER CAUSES
◆ Blood transfusion. A massive transfusion
can lower serum calcium levels and allow
Chvostek’s sign to be elicited.
S
PECIAL CONSIDERATIONS
Collect blood samples for serial calcium studies
to evaluate the severity of hypocalcemia and the
effectiveness of therapy, which consists of oral
or I.V. calcium supplements. Also, look for
Chvostek’s sign when evaluating a patient postoperatively.
P
EDIATRIC POINTERS
Because Chvostek’s sign may be observed in
healthy infants, it isn’t elicited to detect neonatal tetany.
G
ERIATRIC POINTERS
Always consider malabsorption and poor nutritional status in an elderly patient with
Chvostek’s sign and hypocalcemia.
P
ATIENT COUNSELING
Inform patients who will be undergoing thyroidectomy or parathyroidectomy about the early signs and symptoms of hypocalcemia, such
as numbness, tingling, and muscle cramps, and
tell them to seek immediate medical attention if
these occur.
159
Clubbing
A nonspecific sign of pulmonary and cyanotic
cardiovascular disorders, clubbing is the painless, usually bilateral increase in soft tissue
around the terminal phalanges of the fingers or
toes. (See Rare causes of clubbing, page 160.) It
doesn’t involve changes in the underlying bone.
In early clubbing, the normal 160-degree angle
between the nail and the nail base approximates 180 degrees. As clubbing progresses, this
angle widens and the base of the nail becomes
visibly swollen. In late clubbing, the angle
where the nail meets the now-convex nail base
extends more than halfway up the nail.
H
ISTORY AND PHYSICAL
EXAMINATION
You’ll probably detect clubbing while evaluating
other signs of known pulmonary or cardiovascular disease. Therefore, review the patient’s
current plan of treatment because clubbing
may resolve with correction of the underlying
160 CLUBBING
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Rare causes of clubbing
Clubbing is typically a sign of pulmonary or
cardiovascular disease, but it can also result
from certain hepatic and GI disorders, such as
cirrhosis, Crohn’s disease, and ulcerative colitis. Clubbing occurs only rarely in these disorders, however, so first check for more common signs and symptoms. For example, a
patient with cirrhosis usually experiences
right-upper-quadrant pain and hepatomegaly,
a patient with Crohn’s disease typically has
abdominal cramping and tenderness, and a
patient with ulcerative colitis may develop
diffuse abdominal pain and blood-streaked
diarrhea.
disorder. Also, evaluate the extent of clubbing
in both the fingers and toes. (See Checking for
clubbed fingers.)
M
EDICAL CAUSES
◆ Bronchiectasis. Clubbing commonly occurs
in the late stage of this disorder. Another classic
sign is a cough producing copious, foulsmelling, and mucopurulent sputum. Hemoptysis and coarse crackles heard over the affected
area during inspiration are also characteristic.
The patient may complain of weight loss, fatigue, weakness, and exertional dyspnea. He
may also have rhonchi, fever, malaise, and halitosis.
◆ Bronchitis. Clubbing may occur as a late
sign in chronic bronchitis, but it doesn’t reflect
the severity of the disease. The patient has a
chronic productive cough and may display barrel chest, dyspnea, wheezing, increased use of
accessory muscles, cyanosis, tachypnea, crackles, scattered rhonchi, and prolonged expiration.
◆ Emphysema. Clubbing occurs late in this
disease, which may also cause anorexia,
malaise, dyspnea, tachypnea, diminished breath
sounds, peripheral cyanosis, pursed-lip breathing, accessory muscle use, barrel chest, and a
productive cough.
◆ Endocarditis. In subacute infective endo-
carditis, clubbing may be accompanied by fever,
anorexia, pallor, weakness, night sweats, fatigue, tachycardia, and weight loss. The patient
may also develop arthralgia, petechiae, Osler’s
nodes, splinter hemorrhages, Janeway lesions,
splenomegaly, and Roth’s spots. Cardiac murmurs are usually present.
◆ Heart failure. Clubbing is a late sign of heart
failure along with wheezing, dyspnea, and fatigue. Other findings include jugular vein distention, hepatomegaly, tachypnea, palpitations, dependent edema, unexplained weight gain,
nausea, anorexia, chest tightness, slowed mental response, hypotension, diaphoresis, narrow
pulse pressure, pallor, oliguria, a gallop rhythm
(a third heart sound), and crackles on inspiration.
◆ Interstitial fibrosis. Clubbing occurs in al-
most all patients with advanced interstitial fibrosis. Typically, the patient also develops intermittent chest pain, dyspnea, crackles, fatigue,
weight loss and, possibly, cyanosis.
◆ Lung abscess. Initially, this disorder pro-
duces clubbing, which may resolve with resolution of the abscess. It can also cause pleuritic chest pain, dyspnea, crackles, halitosis, and
a productive cough with a large amount of purulent, foul-smelling, and commonly bloody
sputum. The patient may also experience
weakness, fatigue, anorexia, headache,
malaise, weight loss, and fever with chills.
Auscultation may reveal decreased breath
sounds.
◆ Lung and pleural cancer. Clubbing occurs
commonly in these cancers. Associated findings include hemoptysis, dyspnea, wheezing,
chest pain, weight loss, anorexia, fatigue, and
fever.
S
PECIAL CONSIDERATIONS
Don’t mistake curved nails—a normal variation—for clubbing. Remember that the angle between the nail and its base remains normal in
curved nails, but not in clubbed nails.
P
EDIATRIC POINTERS
Clubbing usually occurs in children with cyanotic congenital heart disease or cystic fibrosis.
Surgical correction of heart defects may reverse
clubbing.
G
ERIATRIC POINTERS
Arthritic deformities of the fingers or toes may
disguise clubbing in elderly patients.
P
ATIENT COUNSELING
Inform the patient that clubbing doesn’t always disappear, even if the cause has been
resolved.
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