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291
blurred vision), and increased secretions (tearing, salivation, pulmonary secretions, or diaphoresis) may also occur.
S
PECIAL CONSIDERATIONS
Prepare the patient for diagnostic studies, such
as spinal X-rays, myelography, computed tomography scan, magnetic resonance imaging,
and electromyography with nerve conduction
velocity tests. Prepare the patient for laboratory
tests such as serum electrolyte levels. Help the
patient with progressive neuromuscular degeneration perform activities of daily living, and
provide appropriate assistive devices.
P
EDIATRIC POINTERS
Fasciculations, particularly of the tongue, are an
important early sign of Werdnig-Hoffmann disease.
P
ATIENT COUNSELING
Teach effective stress management techniques
to the patient with stress-induced fasciculations.
Fatigue
Fatigue is a feeling of excessive tiredness, lack
of energy, or exhaustion accompanied by a
strong desire to rest or sleep. This common
symptom is distinct from weakness, which involves the muscles, but may accompany it.
Fatigue is a normal and important response
to physical overexertion, prolonged emotional
stress, and sleep deprivation. However, it can
also be a nonspecific symptom of a psychological or physiologic disorder, especially viral or
bacterial infection and endocrine, cardiovascular, or neurologic disease.
Fatigue reflects both hypermetabolic and hypometabolic states in which nutrients needed
for cellular energy and growth are lacking because of overly rapid depletion, impaired replacement mechanisms, insufficient hormone
production, or inadequate nutrient intake or
metabolism.
H
ISTORY AND PHYSICAL
EXAMINATION
Obtain a careful history to identify the patient’s
fatigue pattern. Fatigue that worsens with activity and improves with rest generally indicates a
physical disorder; the opposite pattern, a psychological disorder. Fatigue lasting longer than
4 months, constant fatigue that’s unrelieved by
rest, and transient exhaustion that quickly gives
way to bursts of energy are findings associated
with psychological disorders.
Ask about related symptoms and any recent
viral or bacterial illness or stressful changes in
lifestyle. Explore nutritional habits and any appetite or weight changes. Carefully review the
patient’s medical and psychiatric history for any
chronic disorders that commonly produce fatigue, and ask about a family history of such
disorders.
Obtain a thorough drug history, noting use of
any narcotic or drug with fatigue as an adverse
effect. Ask about alcohol and drug use patterns.
Determine the patient’s risk of carbon monoxide
poisoning, and ask whether the patient has a
carbon monoxide detector.
Observe the patient’s general appearance for
overt signs of depression or organic illness. Is
he unkempt or expressionless? Does he appear
tired or sickly, or have a slumped posture? If
warranted, evaluate his mental status, noting
especially mental clouding, attention deficits,
agitation, or psychomotor retardation.
M
EDICAL CAUSES
◆ Acquired immunodeficiency syndrome.
Besides fatigue, this syndrome may cause fever,
night sweats, weight loss, diarrhea, and a
cough, followed by several concurrent opportunistic infections.
◆ Adrenocortical insufficiency. Mild fatigue,
the hallmark of this disorder, initially appears
after exertion and stress but later becomes
more severe and persistent. Weakness and
weight loss typically accompany GI disturbances, such as nausea, vomiting, anorexia, abdominal pain, and chronic diarrhea; hyperpigmentation; orthostatic hypotension; and a
weak, irregular pulse.
◆ Anemia. Fatigue after mild activity is com-
monly the first symptom of anemia. Associated
findings vary but generally include pallor, tachycardia, and dyspnea.
◆ Anxiety. Chronic, unremitting anxiety invari-
ably produces fatigue, often characterized as
nervous exhaustion. Other persistent findings
include apprehension, indecisiveness, restlessness, insomnia, trembling, and increased muscle tension.
◆ Cancer. Unexplained fatigue is commonly
the earliest sign of cancer. Related findings reflect the type, location, and stage of the tumor
and typically include pain, nausea, vomiting,
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anorexia, weight loss, abnormal bleeding, and a
palpable mass.
◆ Chronic fatigue syndrome. This syndrome,
whose cause is unknown, is characterized by
incapacitating fatigue. Other findings are sore
throat, myalgia, and cognitive dysfunction.
◆ Chronic obstructive pulmonary disease.
The earliest and most persistent symptoms of
this disease are progressive fatigue and dyspnea. The patient may also experience a chronic
and usually productive cough, weight loss, barrel chest, cyanosis, slight dependent edema,
and poor exercise tolerance.
◆ Cirrhosis. Severe fatigue typically occurs late
in this disorder, accompanied by weight loss,
bleeding tendencies, jaundice, hepatomegaly,
ascites, dependent edema, severe pruritus, and
decreased level of consciousness.
◆ Cushing’s syndrome (hypercortisolism).
This disorder typically causes fatigue, related in
part to accompanying sleep disturbances. Cardinal signs include truncal obesity with slender
extremities, buffalo hump, moon face, purple
striae, acne, and hirsutism; increased blood
pressure and muscle weakness may also occur.
◆ Depression. Persistent fatigue unrelated to
exertion nearly always accompanies chronic depression. Associated somatic complaints include headache, anorexia (occasionally, increased appetite), constipation, and sexual
dysfunction. The patient may also experience
insomnia, slowed speech, agitation or bradykinesia, irritability, loss of concentration, feelings
of worthlessness, and persistent thoughts of
death.
◆ Diabetes mellitus. Fatigue, the most com-
mon symptom of this disorder, may begin insidiously or abruptly. Related findings include
weight loss, blurred vision, polyuria, polydipsia,
and polyphagia.
◆ Heart failure. Persistent fatigue and lethargy
characterize this disorder. Left-sided heart failure produces exertional and paroxysmal nocturnal dyspnea, orthopnea, and tachycardia. Rightsided heart failure produces jugular vein
distention and possibly a slight but persistent
nonproductive cough. In both types, later signs
and symptoms include mental status changes,
nausea, anorexia, weight gain and, possibly,
oliguria. Cardiopulmonary findings include
tachypnea, inspiratory crackles, palpitations
and chest tightness, hypotension, narrowed
pulse pressure, ventricular gallop, pallor, diaphoresis, clubbing, and dependent edema.
◆ Hypopituitarism. Fatigue, lethargy, and
weakness usually develop slowly. Other insidious effects may include irritability, anorexia,
amenorrhea or impotence, decreased libido, hypotension, dizziness, headache, visual disturbances, and cold intolerance.
◆ Hypothyroidism. Fatigue occurs early in this
disorder along with forgetfulness, cold intolerance, weight gain, metrorrhagia, and constipation.
◆ Infection. Fatigue is commonly the most
prominent symptom—and sometimes the only
one—in a chronic infection. Low-grade fever
and weight loss may accompany signs and
symptoms that reflect the type and location of
the infection, such as burning on urination or
swollen, painful gums. Subacute bacterial endocarditis is an example of a chronic infection that
causes fatigue and acute hemodynamic decompensation.
In an acute infection, brief fatigue typically
accompanies headache, anorexia, arthralgia,
chills, high fever, and such infection-specific
signs as a cough, vomiting, or diarrhea.
◆ 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 fatigue, fever, nonproductive
cough, myalgia, chills, headache, and vomiting.
The use of antiviral drugs is recommended to
treat H1N1 flu.
◆ Lyme disease. Besides fatigue and malaise,
signs and symptoms of this tick-borne disease
include intermittent headache, fever, chills, an
expanding red rash, and muscle and joint aches.
Later, patients may develop arthritis, fluctuating
meningoencephalitis, and cardiac abnormalities, such as a brief, fluctuating atrioventricular
heart block.
◆ Malnutrition. Easy fatigability, lethargy, and
apathy are common findings in patients with
protein-calorie malnutrition. Patients may also
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exhibit weight loss, muscle wasting, sensations
of coldness, pallor, edema, and dry, flaky skin.
◆ Methicillin-resistant Staphylococcus au-
reus (MRSA). MRSA is a strain of staphylococ-
cus that’s resistant to antibiotics commonly
used to treat staphylococcal infections. The incidence of MRSA has greatly increased in recent
years. This increase is thought to be related to
the increase in antibiotic use in hospital and
outpatient settings and the widespread use of
hand sanitizers and disinfectants. Older adults
and patients with compromised immune systems are at greatest risk for MRSA, although it’s
becoming more common in community settings. Patients with MRSA may have a variety of
signs and symptoms (most commonly fatigue
and fever), depending on where the infection is
located.
◆ Myasthenia gravis. The cardinal symptoms
of this disorder are easy fatigability and muscle
weakness, which worsen as the day progresses.
They also worsen with exertion and abate with
rest. Related findings depend on the specific
muscles affected.
◆ Myocardial infarction. Fatigue can be se-
vere but is typically overshadowed by chest
pain. Related findings include dyspnea,
anxiety, pallor, cold sweats, increased or
decreased blood pressure, and abnormal heart
sounds.
◆ Narcolepsy. One or more of the following
characterizes this disorder: hypersomnia, hypnagogic hallucinations, cataplexy, sleep paralysis,
and insomnia. Fatigue is a common symptom
as well.
◆ Popcorn lung disease. Popcorn lung dis-
ease occurs in factory workers who experience
respiratory symptoms after inhaling butter flavoring chemicals such as diacetyl, used in the
manufacture of microwave popcorn. The patient typically complains of gradual onset of a
nonproductive cough that worsens over time,
progressive shortness of breath, and unusual fatigue. Clinical findings include wheezing, chest
pain, fever, night sweats, and weight loss. Bronchiolitis fibrosa obliterans, an irreversible fixed
airway obstructive lung disorder, is the most severe condition reported.
◆ Renal failure. Acute renal failure commonly
causes sudden fatigue, drowsiness, and lethargy. Oliguria, an early sign, is followed by severe
systemic effects: ammonia breath odor, nausea,
vomiting, diarrhea or constipation, and dry skin
and mucous membranes. Neurologic findings
include muscle twitching, personality changes,
and altered level of consciousness, which may
progress to seizures and coma.
Chronic renal failure produces insidious fatigue and lethargy along with marked changes
in all body systems, including GI disturbances,
ammonia breath odor, Kussmaul’s respirations,
bleeding tendencies, poor skin turgor, severe
pruritus, paresthesia, visual disturbances, confusion, seizures, and coma.
◆ Restrictive lung disease. Chronic fatigue
may accompany the characteristic signs and
symptoms: dyspnea, cough, and rapid, shallow
respirations. Cyanosis first appears with exertion; later, even at rest.
◆ Rheumatoid arthritis. Fatigue, weakness,
and anorexia precede localized articular findings: joint pain, tenderness, warmth, and
swelling along with morning stiffness.
◆ Systemic lupus erythematosus. Fatigue
usually occurs along with generalized aching,
malaise, low-grade fever, headache, and irritability. Primary signs and symptoms include
joint pain and stiffness, butterfly rash, and photosensitivity. Also common are Raynaud’s phenomenon, patchy alopecia, and mucous membrane ulcers.
◆ Thyrotoxicosis. In this disorder, fatigue may
accompany characteristic signs and symptoms,
including an enlarged thyroid, tachycardia and
palpitations, tremors, weight loss despite increased appetite, diarrhea, dyspnea, nervousness, diaphoresis, heat intolerance, amenorrhea
and, possibly, exophthalmos.
◆ Valvular heart disease. All types of valvular
heart disease commonly produce progressive
fatigue and a cardiac murmur. Additional signs
and symptoms vary but generally include exertional dyspnea, cough, and hemoptysis.
◆ Vancomycin-resistant enterococci (VRE)
infection. Enterococci are bacteria naturally
present in the intestinal tract of all people; however, some strains of enterococci have become
resistant to vancomycin. Serious VRE infections
may occur in hospitalized patients with such comorbidities as cancer, kidney disease, or immune deficiencies. Elderly patients and those
hospitalized for long periods are also at risk for
developing VRE infections. Symptoms of VRE infection depend on where the infection is; patients with VRE infections may have diarrhea,
fever, and fatigue.
◆ Vancomycin-resistant Staphylococcus
aureus (VRSA). VRSA is a strain of staphylo-
coccus that’s resistant to vancomycin, an antibiotic commonly used to treat staphylococcal
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infections. Patients most susceptible to
VRSA infections include those with diabetes,
kidney disease, or previous infection with
MRSA, and those with I.V. catheters. VRSA
can be difficult to diagnose because of the
patient’s overlying medical problems. Patients
with VRSA commonly complain of fatigue and
fever that don’t respond to treatment with
vancomycin. VRSA is usually diagnosed when
cultures are done to see why the patient isn’t
responding to vancomycin; after the patient is
started on a different antibiotic, the infection
improves.
O
THER CAUSES
◆ Carbon monoxide poisoning. Fatigue oc-
curs along with headache, dyspnea, and confusion; apnea and unconsciousness may occur
eventually.
◆ Drugs. Fatigue may result from various
drugs, notably antihypertensives and sedatives.
In those receiving cardiac glycoside therapy, fatigue may indicate toxicity.
◆ Surgery. Most types of surgery cause tempo-
rary fatigue, probably from the combined effects
of hunger, anesthesia, and sleep deprivation.
S
PECIAL CONSIDERATIONS
If fatigue results from organic illness, help the
patient determine which daily activities he may
need help with and how he should pace himself
to ensure sufficient rest. You can help him reduce chronic fatigue by alleviating pain, which
may interfere with rest, or nausea, which may
lead to malnutrition. He may benefit from referral to a community health nurse or housekeeping service. If fatigue results from a psychogenic
cause, refer him for psychological counseling.
P
EDIATRIC POINTERS
When evaluating a child for fatigue, ask his parents if they’ve noticed any change in his activity
level. Fatigue without an organic cause occurs
normally during accelerated growth phases in
preschool-age and prepubescent children. However, psychological causes of fatigue must be
considered; for example, a depressed child may
try to escape problems at home or school by
taking refuge in sleep. In the pubescent child,
consider the possibility of drug abuse, particularly of hypnotics and tranquilizers.
G
ERIATRIC POINTERS
Always ask older patients about fatigue because
this symptom may be insidious and mask more
serious underlying conditions in this age-group.
Temporal arthritis, which is much more common in people older than age 60, is usually
characterized by fatigue, weight loss, jaw claudication, proximal muscle weakness, headache,
visual disturbances, and associated anemia.
P
ATIENT COUNSELING
Regardless of the cause of fatigue, you may
need to help the patient alter his lifestyle to
achieve a balanced diet, a program of regular
exercise, and adequate rest. Counsel him
about setting priorities, keeping a reasonable
schedule, and developing good sleep habits.
Teach stress management techniques as
appropriate.
Fecal incontinence
Fecal incontinence, the involuntary passage of
feces, follows any loss or impairment of external anal sphincter control. It can result from
various GI, neurologic, and psychological disorders; the effects of drugs; or surgery. In some
patients, it may even be a purposeful manipulative behavior.
Fecal incontinence may be temporary or permanent; its onset may be gradual, as in dementia, or sudden, as in spinal cord trauma. Although usually not a sign of severe illness, it
can greatly affect the patient’s physical and psychological well-being.
H
ISTORY AND PHYSICAL
EXAMINATION
Ask the patient with fecal incontinence about its
onset, duration, and severity and about any discernible pattern—for example, at night or with
diarrhea. Note the frequency, consistency, and
volume of stools passed within the last 24 hours
and obtain a stool specimen. Focus your history
taking on GI, neurologic, and psychological disorders.
Let the history guide your physical examination. If you suspect a brain or spinal cord lesion, perform a complete neurologic examination. (See Neurologic control of defecation.) If a
GI disturbance seems likely, inspect the abdomen for distention, auscultate for bowel
sounds, and percuss and palpate for a mass. Inspect the anal area for signs of excoriation or
infection. If not contraindicated, check for fecal
impaction, which may be associated with incontinence.
Neurologic control of defecation
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FECAL INCONTINENCE 295
Three neurologic mechanisms normally regulate defecation: the intrinsic defecation reflex
in the colon, the parasympathetic defecation
reflex involving sacral segments of the spinal
cord, and voluntary control. Here’s how they
interact.
From conscious cortex
Afferent nerve
Skeletal motor nerve
Parasympathetic nerve
Fecal distention of the rectum activates the
relatively weak intrinsic reflex, causing afferent impulses to spread through the myenteric
plexus, initiating peristalsis in the descending
and sigmoid colon and in the rectum. Subsequent movement of feces toward the anus
causes receptive relaxation of the internal anal
sphincter.
To ensure defecation, the parasympathetic
reflex magnifies the intrinsic reflex. Stimulation
of afferent nerves in the rectal wall propels impulses through the spinal cord and back to the
descending and sigmoid colon, rectum, and
anus to intensify peristalsis (see illustration).
However, fecal movement and internal
sphincter relaxation cause immediate contraction of the external anal sphincter and temporary fecal retention. At this point, conscious
control of the external sphincter either prevents or permits defecation. Except in infants
or neurologically impaired patients, this voluntary mechanism further contracts the sphincter
to prevent defecation at inappropriate times or
relaxes it and allows defecation to occur.
Descending
colon
Sigmoid colon
Rectum
Anal sphincter
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Bowel retraining tips
You can help your patient control fecal incontinence by instituting a bowel retraining
program. Here’s how:
◆ Begin by establishing a specific time for
defecation. A typical schedule is once a day
or once every other day after a meal, usually breakfast. However, be flexible when establishing a schedule, and consider the patient’s normal habits and preferences.
◆ If necessary, help ensure regularity by ad-
ministering a suppository, either glycerin or
bisacodyl, about 30 minutes before the
scheduled defecation time. Avoid the routine use of enemas or laxatives because
they can cause dependence.
◆ Provide privacy and a relaxed environ-
ment to encourage regularity. If “accidents”
occur, assure the patient that they’re normal
and don’t mean that he has failed in the
program.
◆ Adjust the patient’s diet to provide ade-
quate bulk and fiber; encourage him to eat
more raw fruits and vegetables and whole
grains. Ensure a fluid intake of at least 1 qt
(1 L)/day.
◆ If appropriate, encourage the patient to
exercise regularly to help stimulate peristalsis.
◆ Be sure to keep accurate intake and elimi-
nation records.
M
EDICAL CAUSES
◆ Dementia. Any chronic degenerative brain
disease can produce fecal as well as urinary incontinence. Associated signs and symptoms include impaired judgment and abstract thinking,
amnesia, emotional lability, hyperactive deep
tendon reflexes (DTRs), aphasia or dysarthria
and, possibly, diffuse choreoathetoid movements.
◆ Gastroenteritis. Severe gastroenteritis may
result in temporary fecal incontinence manifested by explosive diarrhea. Nausea, vomiting, and
colicky, peristaltic abdominal pain are typical.
Other findings include headache, myalgia, and
hyperactive bowel sounds.
◆ Head trauma. Disruption of the neurologic
pathways that control defecation can cause fecal incontinence. Additional findings depend on
the location and severity of the injury and may
include decreased level of consciousness,
seizures, vomiting, and a wide range of motor
and sensory impairments.
◆ Inflammatory bowel disease. Nocturnal fe-
cal incontinence occurs occasionally with diarrhea. Related findings include abdominal pain,
anorexia, weight loss, blood in the stool, and
hyperactive bowel sounds.
◆ Multiple sclerosis. Fecal incontinence occa-
sionally appears as one of this disorder’s extremely variable signs. Other effects depend on
the area of demyelination and may include
muscle weakness, ataxia, and paralysis; gait
disturbances; sensory impairment, such as
paresthesia and genital anesthesia; visual blurring, diplopia, or nystagmus; urinary disturbances; and emotional lability.
◆ Rectovaginal fistula. Fecal incontinence oc-
curs in tandem with uninhibited passage of
flatus.
◆ Spinal cord lesion. Any lesion that causes
compression or transsection of sensorimotor
spinal tracts can lead to fecal incontinence. Incontinence may be permanent, especially with
severe lesions of the sacral segments. Other
signs and symptoms reflect motor and sensory
disturbances below the level of the lesion,
such as urinary incontinence, weakness or
paralysis, paresthesia, analgesia, and thermanesthesia.
◆ Stroke. Temporary fecal incontinence occa-
sionally occurs in a stroke patient but usually
disappears when muscle tone and DTRs are restored. Persistent fecal incontinence may reflect
extensive neurologic damage. Other findings
depend on the location and extent of damage
and may include urinary incontinence, hemiplegia, dysarthria, aphasia, sensory losses, reflex changes, and visual field deficits. Typical
generalized signs and symptoms include
headache, vomiting, nuchal rigidity, fever, disorientation, mental impairment, seizures, and
coma.
◆ Tabes dorsalis. This late sign of syphilis oc-
casionally results in fecal incontinence. It also
produces urinary incontinence, ataxic gait,
paresthesia, loss of DTRs and temperature sensation, severe flashing pain, Charcot’s joints, Argyll Robertson pupils, and possibly impotence.
O
THER CAUSES
◆ Drugs. Chronic laxative abuse may cause in-
sensitivity to a fecal mass or loss of the colonic
defecation reflex.
◆ Surgery. Pelvic, prostate, or rectal surgery
occasionally produces temporary fecal
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incontinence. A colostomy or an ileostomy causes permanent or temporary fecal incontinence.
S
PECIAL CONSIDERATIONS
Maintain proper hygienic care, including control
of foul odors. Also, provide emotional support
for the patient because he may feel deep embarrassment. For the patient with intermittent or
temporary fecal incontinence, encourage Kegel
exercises to strengthen abdominal and perirectal muscles. (See How to do Kegel exercises, page
232.) For the neurologically capable patient with
chronic incontinence, provide bowel retraining.
(See Bowel retraining tips.)
P
EDIATRIC POINTERS
Fecal incontinence is normal in infants and may
occur temporarily in young children who experience stress-related psychological regression or
a physical illness associated with diarrhea. Pediatric fecal incontinence can also result from
myelomeningocele.
G
ERIATRIC POINTERS
Fecal incontinence is an important factor when
long-term care is considered for an elderly patient. Leakage of liquid fecal material is especially common in males. Age-related changes affecting smooth-muscle cells of the colon may
change GI motility and lead to fecal incontinence. Before age is determined to be the cause,
however, any pathology must be ruled out.
Fetor hepaticus
Fetor hepaticus—a distinctive musty, sweet
breath odor—characterizes hepatic encephalopathy, a life-threatening complication of
severe liver disease. The odor results from the
damaged liver’s inability to metabolize and
detoxify mercaptans produced by bacterial
degradation of methionine, a sulfurous amino
acid. These substances circulate in the blood,
are expelled by the lungs, and flavor the breath.
EMERGENCY INTERVENTIONS If you de-
tect fetor hepaticus, quickly determine the
patient’s level of consciousness. If he’s comatose,
evaluate his respiratory status. Prepare to intubate
him and provide ventilatory support if necessary.
Start a peripheral I.V. catheter for fluid administration, begin cardiac monitoring, and insert an indwelling urinary catheter to monitor output. Obtain arterial and venous samples for analysis of
blood gases, ammonia, and electrolytes.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient is conscious, closely observe him
for signs of impending coma. Evaluate deep
tendon reflexes, and test for asterixis and Babinski’s reflex. Be alert for signs of GI bleeding and
shock, common complications of end-stage liver failure. Also, watch for increased anxiety,
restlessness, tachycardia, tachypnea, hypotension, oliguria, hematemesis, melena, or cool,
moist, pale skin. Place the patient in a supine
position with the head of the bed at 30 degrees.
Administer oxygen if necessary, and determine
the patient’s need for I.V. fluids for albumin replacement. Draw blood samples for liver function tests, serum electrolyte levels, hepatitis
panel, blood alcohol count, a complete blood
count, typing and crossmatching, a clotting profile, and ammonia level. Intubation, ventilation,
or cardiopulmonary resuscitation may be necessary. Evaluate the degree of jaundice and abdominal distention, and palpate the liver to assess the degree of enlargement.
Obtain a complete medical history, relying on
the patient’s family if necessary. Focus on any
factors that may have precipitated liver disease
or coma, such as a recent severe infection;
overuse of sedatives, analgesics, (especially
acetaminophen), alcohol, or diuretics; excessive
protein intake; or recent blood transfusion,
surgery, or GI bleeding.
M
EDICAL CAUSES
◆ Hepatic encephalopathy. Fetor hepaticus
usually occurs in the final, comatose stage of
this disorder but it may occur earlier. Tremors
progress to asterixis in the impending stage,
which is also marked by lethargy, aberrant behavior, and apraxia. Hyperventilation and stupor mark the stuporous stage, during which the
patient acts agitated when aroused. Seizures
and coma herald the final stage, along with decreased pulse and respiratory rates, positive
Babinski’s reflex, hyperactive reflexes, decerebrate posture, and opisthotonos.
S
PECIAL CONSIDERATIONS
Effective treatment of hepatic encephalopathy
reduces blood ammonia levels by eliminating
ammonia from the GI tract. You may have to
administer neomycin or lactulose to suppress
bacterial production of ammonia, give sorbitol
solution to induce osmotic diarrhea, give potassium supplements to correct alkalosis, provide
continuous gastric aspiration of blood, or
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maintain the patient on a low-protein diet. If
these methods prove unsuccessful, hemodialysis or exchange transfusions may be performed.
During treatment, closely monitor the patient’s level of consciousness, intake and output, and fluid and electrolyte balance.
P
EDIATRIC POINTERS
A child who is slipping into a hepatic coma may
cry, be disobedient, or become preoccupied with
an activity.
G
ERIATRIC POINTERS
Along with fetor hepaticus, elderly patients with
hepatic encephalopathy may exhibit disturbances of awareness and mentation, such as
forgetfulness and confusion.
P
ATIENT COUNSELING
Advise the patient to restrict his intake of dietary protein to as little as 40 g/day. Recommend that he eat vegetable protein rather than
animal protein sources. Inform the patient that
medications used to treat and prevent hepatic
encephalopathy do so by causing diarrhea, so
he shouldn’t stop taking the drug when diarrhea
occurs.
Fever
[Pyrexia]
Fever is a common sign that can arise from numerous disorders. Because these disorders can
affect virtually any body system, fever in the absence of other signs usually has little diagnostic
significance. A persistent high fever, though,
represents an emergency.
Fever can be classified as low (oral reading of
99⬚ to 100.4⬚ F [37.2⬚ to 38⬚ C]), moderate (100.5⬚
to 104° F [38.1⬚ to 40⬚ C]), or high (above 104⬚ F).
Fever over 106⬚ F (41.1⬚ C) causes unconsciousness and, if sustained, leads to permanent brain
damage.
Fever may also be classified as remittent, intermittent, sustained, relapsing, or undulant.
Remittent fever, the most common type, is characterized by daily temperature fluctuations
above the normal range. Intermittent fever is
marked by a daily temperature drop into the
normal range and then a rise back to above
normal. An intermittent fever that fluctuates
widely, typically producing chills and sweating,
is called hectic (or septic) fever. Sustained fever
involves persistent temperature elevation with
little fluctuation. Relapsing fever consists of alternating feverish and afebrile periods. Undulant
fever refers to a gradual increase in temperature
that stays high for a few days and then decreases gradually.
Fever can be either brief (less than 3 weeks)
or prolonged. Prolonged fevers include fever of
unknown origin, a classification used when
careful examination fails to detect an underlying cause.
EMERGENCY INTERVENTIONS If you de-
tect a fever higher than 106⬚ F (41.1⬚ C), take
the patient’s other vital signs and determine his
level of consciousness (LOC). Administer an antipyretic and begin rapid cooling measures: Apply
ice packs to the axillae and groin, give tepid
sponge baths, or apply a cooling blanket. These
methods may evoke a cooling response; to prevent
this, constantly monitor the patient’s rectal temperature.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient’s fever is only mild to moderate,
ask him when it began and how high his temperature reached. Did the fever disappear,
only to reappear later? Did he experience any
other symptoms, such as chills, fatigue, or
pain?
Obtain a complete medical history, noting especially immunosuppressive treatments or disorders, infection, trauma, surgery, diagnostic
testing, and use of anesthesia or other medications. Ask about recent travel because certain
diseases are endemic.
Let the history findings direct your physical
examination. (See Differential diagnosis: Fever,
pages 300 and 301.) Because fever can accompany diverse disorders, the examination may
range from a brief evaluation of one body system to a comprehensive review of all systems.
(See How fever develops, page 302.)
M
EDICAL CAUSES
◆ Anthrax, cutaneous. In this disorder, the
patient may experience a fever along with lymphadenopathy, malaise, and headache. After the
bacterium Bacillus anthracis enters a cut or
abrasion on the skin, the infection begins as a
small, painless or pruritic macular or papular
lesion resembling an insect bite. Within 1 to
2 days, the lesion develops into a vesicle and
then into a painless ulcer with a characteristic
black necrotic center.
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299
◆ Anthrax, GI. After ingesting contaminated
meat from an animal infected with the bacterium Bacillus anthracis, the patient experiences
fever, anorexia, nausea, vomiting and, possibly,
abdominal pain, severe bloody diarrhea, and
hematemesis.
◆ Anthrax, inhalation. This acute infectious
disease initially produces flulike signs and
symptoms, including fever, chills, weakness,
cough, and chest pain. The disease generally
occurs in two stages with a period of recovery
after the initial symptoms. The second stage develops abruptly and causes rapid deterioration
marked by fever, dyspnea, stridor, and hypotension; death generally results within 24 hours.
◆ Avian influenza. Avian influenza, also
known as bird flu, is an infection caused by
viruses that originate in the intestines of wild
birds but are highly contagious to domesticated
birds, such as chickens, turkeys, and geese. Infected poultry and surfaces contaminated with
infected bird excretions have recently led to human infections and deaths in several Asian
countries. Fever is commonly an initial symptom of these viruses along with other conventional influenza symptoms, such as muscle
aches, sore throat, and cough. Individuals infected with the most virulent avian virus, influenza A (H5N1), may develop pneumonia,
acute respiratory distress, and other lifethreatening complications.
◆ Escherichia coli O157:H7. Fever, bloody
diarrhea, nausea, vomiting, and abdominal
cramps occur after eating undercooked beef or
other foods contaminated with this strain of
bacteria. Children younger than age 5 and elderly patients may develop hemolytic uremic
syndrome, which can ultimately lead to acute
renal failure.
◆ Immune complex dysfunction. When pre-
sent, fever usually remains low, although moderate elevations may accompany erythema multiforme. Fever may be remittent or intermittent,
as in acquired immunodeficiency syndrome
(AIDS) or systemic lupus erythematosus, or sustained, as in polyarteritis. As one of several
vague, prodromal complaints (such as fatigue,
anorexia, and weight loss), fever produces nocturnal diaphoresis and accompanies such associated signs and symptoms as diarrhea and a
persistent cough (in AIDS) or morning stiffness
(in rheumatoid arthritis). Other disease-specific
findings include headache and vision loss (in
temporal arteritis); pain and stiffness in the
neck, shoulders, back, or pelvis (in ankylosing
spondylitis and polymyalgia rheumatica); skin
and mucous membrane lesions (in erythema
multiforme); and urethritis with urethral discharge and conjunctivitis (in Reiter’s syndrome).
◆ Infectious and inflammatory disorders.
Fever ranges from low (in Crohn’s disease or ulcerative colitis) to extremely high (in those with
bacterial pneumonia, necrotizing fasciitis, Ebola
virus or Hantavirus pulmonary syndrome). It
may be remittent, as in infectious mononucleosis or otitis media; hectic (recurring daily with
sweating, chills, and flushing), as in a lung abscess, influenza, or endocarditis; sustained, as
in meningitis; or relapsing, as in malaria. Fever
may arise abruptly, as in toxic shock syndrome
or Rocky Mountain spotted fever, or insidiously,
as in mycoplasmal pneumonia. In patients with
hepatitis, fever may represent a disease prodrome; in those with appendicitis, it follows the
acute stage. Its sudden late appearance with
tachycardia, tachypnea, and confusion heralds
life-threatening septic shock in patients with
peritonitis or gram-negative bacteremia.
Associated signs and symptoms involve
every system. The cyclic variations of hectic
fever typically produce alternating chills and diaphoresis. General systemic complaints include
weakness, anorexia, and malaise.
◆ 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 fever, nonproductive cough,
fatigue, myalgia, chills, headache, and vomiting.
The use of antiviral drugs is recommended to
treat H1N1 flu.
◆ Kawasaki syndrome. Fever, typically high
and spiking, is the primary characteristic of this
acute illness. The diagnosis of Kawasaki syndrome is confirmed when fever persists for 5
or more days (or until administration of I.V.
gamma globulin if given before the fifth day)
and is accompanied by other clinical signs,
including conjunctival injection, erythema,
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Differential diagnosis: Fever
History of present illness
Focused physical examination: All systems
Common signs and symptoms
◆ Fatigue
◆ Malaise
◆ Anorexia
Thermoregulatory dysfunction
Additional signs and symptoms
◆ Sudden onset of fever that rises rapidly
and remains high
◆ Temperature that may rise to 107° F
(41.7°
C)
◆ Vomiting
◆ Anhidrosis
◆ Decreased level of consciousness (LOC)
◆ Hot, flushed skin
◆ Tachycardia
◆ Tachypnea
◆ Hypotension
Diagnosis: Patient history with additional
signs or symptoms that would indicate
source of thermoregulatory dysfunction
(such as heatstroke
leptic malignant syndrome
hyperthermia, lesions of the central nervous
system)
Treatment: Cooling techniques to decrease
temperature, treatment of cause, antipyretics
Follow-up: As needed (depending on cause
of dysfunction)
, thyroid storm, neuro-
, malignant
Neoplasms
Additional signs and symptoms
◆ Prolonged fever of varying elevations
◆ Nocturnal diaphoresis
◆ Weight loss
◆ Lymphadenopathy
◆ Palpable mass
Diagnosis: V
signs and symptoms but usually includes
imaging studies (computed tomography
scan, magnetic resonance imaging)
reatment: Varies based on type and
T
location of neoplasm but may include
medication (antipyretics, chemotherapy),
radiation therapy and, possibly, surgery
Follow-up: Referral to oncologist
aries depending on additional
lymphadenopathy, and peripheral extremity
swelling. This syndrome occurs worldwide, with
the highest incidence in Japan. It primarily affects children under age 5, is more prevalent in
boys, and can cause serious heart damage and
death without prompt treatment with I.V. gamma globulin.
◆ Listeriosis. Signs and symptoms of this in-
fection include fever, myalgia, abdominal pain,
nausea, vomiting, and diarrhea. If the infection
spreads to the nervous system, it may cause
meningitis, whose symptoms include fever,
headache, nuchal rigidity, and change in LOC.
GENDER CUE Listeriosis during pregnancy
may lead to premature delivery, infection of
the neonate, or stillbirth.
◆ Methicillin-resistant Staphylococcus au-
reus (MRSA). MRSA is a strain of staphylococcus
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