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EDIATRIC POINTERS
A child who suffers amnesia during seizures
may be mistakenly labeled as “learning disabled.” To prevent this mislabeling, stress the
importance of adhering to the prescribed drug
schedule, and discuss ways that the child, his
parents, and his teachers can cope with
amnesia.
Analgesia
Analgesia, the absence of sensitivity to pain, is
an important sign of central nervous system
disease, often indicating a specific type and
location of spinal cord lesion. It always occurs
with loss of temperature sensation (thermoanesthesia) because these sensory nerve
impulses travel together in the spinal cord. It
can also occur with other sensory deficits—
such as paresthesia, loss of proprioception
and vibratory sense, and tactile anesthesia—in
various disorders involving the peripheral
nerves, spinal cord, and brain. However, when
accompanied only by thermoanesthesia, analgesia points to an incomplete lesion of the
spinal cord.
Analgesia can be classified as partial or total
below the level of the lesion and as unilateral or
bilateral, depending on the cause and level of
the lesion. Its onset may be slow and progressive with a tumor or abrupt with trauma. Transient in many cases, analgesia may resolve
spontaneously.
EMERGENCY INTERVENTIONS Suspect
spinal cord injury if the patient complains
of unilateral or bilateral analgesia over a large
body area, accompanied by paralysis. Immobilize his spine in proper alignment, using a
cervical collar and a long backboard, if possible. If a collar or backboard isn’t available,
place the patient in a supine position on a
flat surface and place sandbags around his
head, neck, and torso. Use correct technique
and extreme caution when moving him to
prevent exacerbating the spinal injury.
Continuously monitor respiratory rate and
rhythm, and observe him for accessory muscle
use because a complete lesion above the T6
level may cause diaphragmatic and intercostal
muscle paralysis. Have an artificial airway
and a handheld resuscitation bag on hand,
and be prepared to initiate emergency
resuscitation measures in case of
respiratory failure.
H
ISTORY AND PHYSICAL
ANALGESIA
41
EXAMINATION
Once you’re satisfied that the patient’s spine
and respiratory status are stabilized—or if the
analgesia isn’t severe and isn’t accompanied by
signs of spinal cord injury—perform a physical
examination and baseline neurologic evaluation. First, take the patient’s vital signs and assess his level of consciousness. Then test pupillary, corneal, cough, and gag reflexes to rule out
brain stem and cranial nerve involvement. If the
patient is conscious, evaluate his speech and
ability to swallow.
If possible, observe the patient’s gait and posture and assess his balance and coordination.
Evaluate muscle tone and strength in all extremities. Test for other sensory deficits over all
dermatomes (individual skin segments innervated by a specific spinal nerve) by applying
light tactile stimulation with a tongue depressor
or cotton swab. Perform a more thorough check
of pain sensitivity, if necessary, using a pin. (See
Testing for analgesia, pages 42 and 43.) Also, test
temperature sensation over all dermatomes,
using two test tubes—one filled with hot water,
the other with cold water. In each arm and leg,
test vibration sense (using a tuning fork),
proprioception, and superficial and deep tendon
reflexes (DTRs). Check for increased muscle
tone by extending and flexing the patient’s elbows and knees as he tries to relax.
Focus your history taking on the onset of
analgesia (sudden or gradual) and on any recent trauma, such as a fall, a sports injury, or an
automobile accident. Obtain a complete medical history, noting especially any incidence of
cancer in the patient or his family.
M
EDICAL CAUSES
◆ Anterior cord syndrome. In anterior cord
syndrome, analgesia and thermoanesthesia occur bilaterally below the level of the lesion
along with flaccid paralysis and hypoactive
DTRs.
◆ Central cord syndrome. In central cord syn-
drome, analgesia and thermoanesthesia typically occur bilaterally in several dermatomes and
may extend in a capelike fashion over the arms,
back, and shoulders. Early weakness in the
hands progresses to weakness and muscle
spasms in the arms and shoulder girdle. Hyperactive DTRs and spastic weakness of the legs
may develop. However, if the lesion affects the
(Text continues on page 44.)
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Testing for analgesia
By carefully and systematically testing your patient’s sensitivity to pain, you can determine
whether his nerve damage has segmental or
peripheral distribution and help locate the
causative lesion.
Tell the patient to relax, and explain that
you’re going to lightly touch areas of his skin
with a small pin. Have him close his eyes.
Apply the pin firmly enough to produce pain
without breaking the skin. (Practice on
ANTERIOR
C2 C2
C2 C2
T1 T1
C6 C6
C8
C7
C2
C3
C4
C5
T1
T2
T3
T4
T5
T6
T7
T8
T9
T10
T11
L1
L2
L3
L4
T12
S2
S3
L1
L2
C8
L3
L4
C7
C5 C5
C8
C7
C2
C3
C4
C7
C8
T1
T2
T3
T4
T5
T5
T6
T8
T9
T10
T11
T12
L1
L2
L3
L4
L5
S1
S2
S3
S4
S5
L1 L1
L2 L2
L3 L3
C6
C8
C7
L5
S1 S1
L4 L4
L5
S1 S2 S2 S1
L4
L5 L5
L4
ANALGESIA 43
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yourself first to learn how to apply the correct
pressure.)
Starting with the patient’s head and face,
move down his body, pricking his skin on alternating sides. Have the patient report when he
feels pain. Use the blunt end of the pin occa-
Peripheral nerves
ANTERIOR LEG
Lateral
cutaneous nerve
of thigh
Lateral
cutaneous nerve
of calf
Superficial
peroneal nerve
sionally, and vary your test pattern to gauge the
accuracy of his response.
Document your findings thoroughly,
clearly marking areas of lost pain sensation
on a dermatome chart (shown on previous
page).
POSTERIOR LEG
Lateral
cutaneous
nerve of thigh
Lateral
cutaneous
nerve of calf
Superficial
peroneal
nerve
ANTERIOR HAND POSTERIOR HAND
Ulnar nerve
Radial nerve
Median
nerve
Radial
nerve
Ulnar nerve
Median nerve
44 ANHIDROSIS
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lumbar spine, hypoactive DTRs and flaccid
weakness may persist in the legs.
With brain stem involvement, additional findings include facial analgesia and thermoanesthesia, vertigo, nystagmus, atrophy of the
tongue, and dysarthria. The patient may also
have anhidrosis, dysphagia, urine retention, decreased intestinal motility, and hyperkeratosis.
◆ Spinal cord hemisection. Contralateral
analgesia and thermoanesthesia occur below
the level of the lesion. In addition, loss of proprioception, spastic paralysis, and hyperactive
deep tendon reflexes develop ipsilaterally. The
patient may also experience urine retention
with overflow incontinence.
O
THER CAUSES
◆ Drugs. Analgesia may occur with use of a
topical or local anesthetic, although numbness
and tingling are more common.
S
PECIAL CONSIDERATIONS
Prepare the patient for spinal X-rays, and maintain spinal alignment and stability during transport to the laboratory.
Focus your care on preventing further injury
to the patient because analgesia can mask injury
or developing complications. Prevent formation
of pressure ulcers through meticulous skin care,
massage, use of lamb’s wool pads, and frequent
repositioning, especially when significant motor
deficits hamper the patient’s movement. Guard
against scalding by testing the patient’s bathwater temperature before he bathes; advise him to
test it at home using a thermometer or a body
part with intact sensation.
P
EDIATRIC POINTERS
Because a child may have difficulty describing
analgesia, observe him carefully during the assessment for nonverbal clues to pain, such as
facial expressions, crying, and retraction from
stimuli. Remember that pain thresholds are high
in infants, so your assessment findings may not
be reliable. Also, remember to test bathwater
carefully for a child who is too young to test it
himself.
Anhidrosis
Anhidrosis, an abnormal deficiency of sweat,
can be classified as generalized (complete) or
localized (partial). Generalized anhidrosis can
lead to life-threatening impairment of ther-
moregulation. Localized anhidrosis rarely interferes with thermoregulation because it affects
only a small percentage of the body’s eccrine
(sweat) glands.
Anhidrosis results from neurologic and skin
disorders; congenital, atrophic, or traumatic
changes to sweat glands; and the use of certain
drugs. Neurologic disorders disturb central or
peripheral nervous pathways that normally activate sweating, causing retention of excess
body heat and perspiration. The absence, obstruction, atrophy, or degeneration of sweat
glands can produce anhidrosis at the skin surface, even if neurologic stimulation is normal.
(See Eccrine dysfunction in anhidrosis, pages 46
and 47.)
Anhidrosis may go unrecognized until significant heat or exertion fails to produce sweat.
However, localized anhidrosis often provokes
compensatory hyperhidrosis in the remaining
functional sweat glands, which, in many cases,
is the patient’s chief complaint.
EMERGENCY INTERVENTIONS If you de-
tect anhidrosis in a patient whose skin feels
hot and flushed, ask if the patient is also experiencing nausea, dizziness, palpitations, and substernal tightness. If he is, quickly take his rectal
temperature and other vital signs, and assess his
level of consciousness (LOC). If a rectal temperature higher than 102.2° F (39° C) is accompanied
by tachycardia, tachypnea, altered blood pressure,
and decreased LOC, suspect life-threatening anhidrotic asthenia (heatstroke). Start rapid cooling
measures, such as placing the patient on a cooling
blanket, and give I.V. fluid replacements. Continue
these measures, and frequently check vital signs
and neurologic status, until the patient’s temperature drops below 102° F (38.9° C). Then place him
in an air-conditioned room.
H
ISTORY AND PHYSICAL
EXAMINATION
If anhidrosis is localized or the patient reports
local hyperhidrosis or unexplained fever, take a
brief history. Ask the patient to characterize his
sweating during heat spells or strenuous activity. Does he usually sweat slightly or profusely?
Ask about recent prolonged or extreme exposure to heat and about the onset of anhidrosis
or hyperhidrosis. Obtain a complete medical
history, focusing on neurologic disorders; skin
disorders, such as psoriasis; autoimmune disorders such as scleroderma; systemic diseases
that can cause peripheral neuropathies such as
diabetes mellitus; and drug use.
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45
Inspect skin color, texture, and turgor. If you
detect any skin lesions, document their location, size, color, texture, and pattern.
M
EDICAL CAUSES
◆ Anhidrotic asthenia (heatstroke). Heat-
stroke is a life-threatening disorder that causes
acute, generalized anhidrosis. In early stages,
the patient may still sweat and be rational, but
his rectal temperature may already exceed
102.2° F (39° C). Associated signs and symptoms
include severe headache and muscle cramps,
which later disappear; fatigue; nausea and vomiting; dizziness; palpitations; substernal tightness; and elevated blood pressure followed by
hypotension. Within minutes, anhidrosis and
hot, flushed skin develop, accompanied by
tachycardia, tachypnea, and confusion progressing to seizures or loss of consciousness.
◆ Burns. Depending on their severity, burns
may cause permanent anhidrosis in affected areas as well as blistering, edema, and increased
pain or loss of sensation.
◆ Cerebral lesions. Cerebral cortex and brain
stem lesions may cause anhidrotic palms and
soles along with various motor and sensory disturbances specific to the site of the lesions.
◆ Horner’s syndrome. A supraclavicular spinal
cord lesion affecting a cervical nerve produces
unilateral facial anhidrosis with compensatory
contralateral hyperhidrosis. Other findings include ipsilateral pupillary constriction and ptosis.
◆ Miliaria crystallina. This usually innocuous
form of miliaria causes anhidrosis and tiny,
clear, fragile blisters, usually under the arms
and breasts.
◆ Miliaria profunda. If severe and extensive,
this form of miliaria can progress to lifethreatening anhidrotic asthenia. Typically, it
produces localized anhidrosis with compensatory facial hyperhidrosis. Whitish papules appear mostly on the trunk but also on the extremities. Associated signs and symptoms include
inguinal and axillary lymphadenopathy, weakness, shortness of breath, palpitations, and fever.
◆ Miliaria rubra (prickly heat). This common
form of miliaria, which typically produces localized anhidrosis, rarely can progress to lifethreatening anhidrotic asthenia if it becomes
severe and extensive. Small, erythematous
papules with centrally placed blisters appear on
the trunk and neck and rarely on the face,
palms, or soles. Pustules may also appear in extensive and chronic miliaria. Related symptoms
include paroxysmal itching and paresthesia.
◆ Peripheral neuropathy. In this disorder, an-
hidrosis commonly appears over the legs with
compensatory hyperhidrosis over the head and
neck. Associated findings mainly involve the extremities and include glossy red skin; paresthesia, hyperesthesia, or anesthesia in the hands
and feet; diminished or absent deep tendon reflexes; flaccid paralysis and muscle wasting;
footdrop; and burning pain.
◆ Shy-Drager syndrome. Shy-Drager syn-
drome is a degenerative neurologic syndrome
that causes ascending anhidrosis in the legs.
Other signs and symptoms include severe orthostatic hypotension, loss of leg hair, impotence, constipation, urine retention or urinary
urgency, decreased salivation and tearing, mydriasis, and impaired visual accommodation.
Eventually, focal neurologic signs—such as leg
tremors, incoordination, and muscle wasting
and fasciculations—may appear.
◆ Spinal cord lesions. Anhidrosis may occur
symmetrically below the level of the lesion, with
compensatory hyperhidrosis in adjacent areas.
Other findings depend on the site and extent of
the lesion but may include partial or total loss of
motor and sensory function below the lesion as
well as impaired cardiovascular and respiratory
function.
O
THER CAUSES
◆ Drugs. Anticholinergics, such as atropine
and scopolamine, can cause generalized anhidrosis.
S
PECIAL CONSIDERATIONS
Because even a careful evaluation can be inconclusive, you may need to administer specific tests to evaluate anhidrosis. These include
wrapping the patient in an electric blanket or
placing him in a heated box to observe the
skin for sweat patterns, applying a topical
agent to detect sweat on the skin, and administering a systemic cholinergic drug to stimulate sweating.
P
EDIATRIC POINTERS
In both infants and children, miliaria rubra and
congenital skin disorders, such as ichthyosis
and anhidrotic ectodermal dysplasia, are the
most common causes of anhidrosis.
Because delayed development of the thermoregulatory center renders an infant—
especially a premature one—anhidrotic for several weeks after birth, caution parents against
overdressing their infant.
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Eccrine dysfunction in anhidrosis
Eccrine glands, located over most of the skin, help regulate body temperature by secreting sweat.
Any change or dysfunction in these glands can result in anhidrosis of varying severity. These illustrations show a normal eccrine gland and some common abnormalities.
NORMAL SKIN
Hair shaft
Opening of
sweat duct
Squamous
epithelial cell
Langerhans’
cell
Melanocyte
Sebaceous
gland
Pacinian
corpuscle
Cutaneous
nerve
Epidermis
Dermis
Subcutaneous
layer
Stratum
corneum
Stratum
granulosum
Stratum
spinosum
Stratum
basale
Papillary dermis
Reticular dermis
Arrector pili
muscle
Eccrine sweat
gland
Hair follicle
P
ATIENT COUNSELING
Advise the patient with anhidrosis to remain in
cool environments, to move slowly during
warm weather, and to avoid strenuous exercise
and hot foods. Warn him about the anhidrotic
effects of any drugs he’s receiving.
Anorexia
Anorexia, a lack of appetite in the presence of a
physiologic need for food, is a common symptom of GI and endocrine disorders and is characteristic of certain severe psychological disturbances such as anorexia nervosa. It can also
result from such factors as anxiety, chronic
pain, poor oral hygiene, increased body temperature due to hot weather or fever, and changes
in taste or smell that normally accompany aging. Anorexia also can result from drug therapy
Arteriole
or abuse. Short-term anorexia rarely jeopardizes health, but chronic anorexia can lead to
life-threatening malnutrition.
H
ISTORY AND PHYSICAL
EXAMINATION
Take the patient’s vital signs and weight. Find
out previous minimum and maximum weights.
Ask about involuntary weight loss greater than
10 lb (4.5 kg) in the last month. Explore dietary
habits, including what the patient eats and
when. Ask what foods he likes and dislikes and
why. The patient may identify tastes and smells
that nauseate him and cause loss of appetite.
Ask about dental problems that interfere with
chewing, including poor-fitting dentures. Ask if
he has difficulty or pain when swallowing or if
he vomits or has diarrhea after meals. Ask the
patient how frequently and intensely he exercises.
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47
OBSTRUCTED
ECCRINE GLAND
(occurs in miliaria)
Sweat duct
obstruction
Retained
sweat
ATROPHY
(occurs with aging)
Atrophic
eccrine
gland
DESTRUCTION
(occurs with burns)
Destroyed
eccrine
gland
CONGENITAL
ABSENCE
(occurs in anhidrotic
ectodermal dysplasia)
Absent eccrine
gland
Check for a history of stomach or bowel disorders, which can interfere with the ability to digest, absorb, or metabolize nutrients. Find out
about changes in bowel habits. Ask about alcohol use and drug use and dosage.
If the medical history doesn’t reveal an organic basis for anorexia, consider psychological
factors. Ask the patient if he knows what’s
causing his decreased appetite. Situational factors—such as a death in the family or problems
at school or at work—can lead to depression
and subsequent loss of appetite. Be alert for
signs of malnutrition, consistent refusal of food,
and a 7% to 10% loss of body weight in the preceding month. (See Is your patient malnour-
ished? page 48.)
M
EDICAL CAUSES
◆ Acquired immunodeficiency syndrome
(AIDS). An infection or Kaposi’s sarcoma
affecting the GI or respiratory tract may lead to
anorexia in a patient with AIDS. Other findings
include fatigue, afternoon fevers, night sweats,
diarrhea, cough, bleeding, lymphadenopathy,
oral thrush, gingivitis, and skin disorders, including persistent herpes zoster and recurrent
herpes simplex, herpes labialis, or herpes genitalis.
◆ Adrenocortical hypofunction. In adreno-
cortical hypofunction, anorexia may begin slowly and subtly, causing gradual weight loss. Other
common signs and symptoms include nausea
and vomiting, abdominal pain, diarrhea, weakness, fatigue, malaise, vitiligo, bronze-colored
skin, and purple striae on the breasts, abdomen,
shoulders, and hips.
◆ Alcoholism. Chronic anorexia commonly ac-
companies alcoholism, eventually leading to
malnutrition. Other findings include signs of liver damage (jaundice, spider angiomas, ascites,
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Is your patient
malnourished?
When assessing a patient with anorexia, be
sure to check for these common signs of
malnutrition.
Hair. Dull, dry, thin, fine, straight, and easily
plucked; areas of lighter or darker spots and
hair loss
Face. Generalized swelling, dark areas on
cheeks and under eyes, lumpy or flaky skin
around the nose and mouth, enlarged
parotid glands
Eyes. Dull appearance; dry and either pale
or red membranes; triangular, shiny gray
spots on conjunctivae; red and fissured eyelid corners; bloodshot ring around cornea
Lips. Red and swollen, especially at corners
Tongue. Swollen, purple, and raw-looking,
with sores or abnormal papillae
Teeth. Missing or emerging abnormally;
visible cavities or dark spots; spongy, bleeding gums
Neck. Swollen thyroid gland
Skin. Dry, flaky, swollen, and dark, with
lighter or darker spots, some resembling
bruises; tight and drawn, with poor skin turgor
Nails. Spoon-shaped, brittle, and ridged
Musculoskeletal system. Muscle wasting,
knock-knee or bowlegs, bumps on ribs,
swollen joints, musculoskeletal hemorrhages
Cardiovascular system. Heart rate above
100 beats/minute, arrhythmias, elevated
blood pressure
Abdomen. Enlarged liver and spleen
Reproductive system. Decreased libido,
amenorrhea
Nervous system. Irritability, confusion,
paresthesia in hands and feet, loss of proprioception, decreased ankle and knee reflexes
edema), paresthesia, tremors, increased blood
pressure, bruising, GI bleeding, and abdominal
pain.
◆ Anorexia nervosa. Chronic anorexia ner-
vosa is an eating disorder that begins insidiously and eventually leads to life-threatening
malnutrition, as evidenced by skeletal muscle
atrophy, loss of fatty tissue, constipation,
amenorrhea, dry and blotchy or sallow skin,
alopecia, sleep disturbances, distorted self-image, anhedonia, and decreased libido. Para-
doxically, many patients exhibit extreme restlessness and vigor and may exercise avidly;
many also have complicated food preparation
and eating rituals.
◆ Appendicitis. Anorexia closely follows the
abrupt onset of generalized or localized epigastric pain, nausea, and vomiting. It can continue
as pain localizes in the right lower quadrant
(McBurney’s point) and other signs and symptoms—abdominal rigidity, rebound tenderness,
constipation or diarrhea, slight fever, and tachycardia—appear.
◆ Cancer. Chronic anorexia may be accompa-
nied by weight loss, weakness, apathy, and
cachexia.
◆ Chronic renal failure. Chronic anorexia is
common and develops insidiously in chronic
renal failure. It’s accompanied by changes in
all body systems, such as nausea, vomiting,
mouth ulcers, ammonia breath odor, metallic
taste, GI bleeding, constipation or diarrhea,
drowsiness, confusion, tremors, pallor, dry and
scaly skin, pruritus, alopecia, purpuric lesions,
and edema.
◆ Cirrhosis. Anorexia occurs early in cirrhosis
and may be accompanied by weakness, nausea,
vomiting, constipation or diarrhea, and dull abdominal pain. It continues after these early
signs and symptoms subside and is accompanied by lethargy, slurred speech, bleeding tendencies, ascites, severe pruritus, dry skin, poor
skin turgor, hepatomegaly, fetor hepaticus,
jaundice, edema of the legs, gynecomastia, and
right-upper-quadrant pain.
◆ Crohn’s disease. Chronic anorexia causes
marked weight loss in Crohn’s disease. Associated signs vary according to the site and extent
of the lesion but may include diarrhea, abdominal pain, fever, abdominal mass, weakness, perianal or vaginal fistulas and, rarely, clubbing of
the fingers. Acute inflammatory signs and symptoms—right-lower-quadrant pain, cramping,
tenderness, flatulence, fever, nausea, diarrhea
(including nocturnal), and bloody stools—mimic
those of appendicitis.
◆ Depressive syndrome. Anorexia reflects an-
hedonia in depressive syndrome. Accompanying signs and symptoms include poor concentration, indecisiveness, delusions, menstrual
irregularities, decreased libido, insomnia or hypersomnia, fatigue, mood swings, poor
self-image, and gradual social withdrawal.
◆ Gastritis. In acute gastritis, anorexia may
have a sudden onset. The patient may experience postprandial epigastric distress accompa-
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49
nied by nausea, vomiting (often with hematemesis), fever, belching, hiccups, and
malaise.
◆ Hepatitis. In viral hepatitis (hepatitis A, B, C,
or D), anorexia begins in the preicteric phase
and is accompanied by fatigue, malaise,
headache, arthralgia, myalgia, photophobia,
nausea and vomiting, mild fever, hepatomegaly,
and lymphadenopathy. It may continue throughout the icteric phase along with mild weight
loss, dark urine, clay-colored stools, jaundice,
right-upper-quadrant pain and, possibly, irritability and severe pruritus.
Signs and symptoms of nonviral hepatitis
usually resemble those of viral hepatitis but may
vary, depending on the cause and the extent of
liver damage.
◆ Hypopituitarism. Anorexia usually develops
slowly in hypopituitarism, which usually begins
with hypergonadism. Accompanying signs and
symptoms vary with the disorder’s severity and
the number and type of deficient hormones.
They may include amenorrhea; decreased libido; lethargy; cold intolerance; pale, thin, and
dry skin; dry, brittle hair; and decreased temperature, blood pressure, and pulse rate.
◆ Hypothyroidism. Anorexia is common and
usually insidious in patients with thyroid hormone deficiency. Vague early findings typically
include fatigue, forgetfulness, cold intolerance,
unexplained weight gain, and constipation.
Subsequent findings include decreased mental
stability; dry, flaky, and inelastic skin; edema of
the face, hands, and feet; ptosis; hoarseness;
thick, brittle nails; coarse, broken hair; and
signs of decreased cardiac output such as
bradycardia. Other common findings include abdominal distention, menstrual irregularities, decreased libido, ataxia, intention tremor, nystagmus, dull facial expression, and slow reflex
relaxation time.
◆ Ketoacidosis. Anorexia usually arises gradu-
ally in ketoacidosis and is accompanied by dry,
flushed skin; fruity breath odor; polydipsia;
polyuria and nocturia; hypotension; weak,
rapid pulse; dry mouth; abdominal pain; and
vomiting.
◆ Pernicious anemia. In pernicious anemia,
insidious anorexia may cause considerable
weight loss. Related findings include the classic
triad of burning tongue, general weakness, and
numbness and tingling in the extremities; alternating constipation and diarrhea; abdominal
pain; nausea and vomiting; bleeding gums;
ataxia; positive Babinski’s and Romberg’s signs;
diplopia and blurred vision; irritability,
headache, malaise, and fatigue.
O
THER CAUSES
◆ Drugs. Anorexia may result from the use of
amphetamines, chemotherapeutic agents,
sympathomimetics such as ephedrine, and
some antibiotics. It also may signal digoxin
toxicity.
◆ Radiation therapy. Radiation treatments
can cause anorexia, possibly as the result of
metabolic disturbances.
◆ Total parenteral nutrition. Maintenance of
blood glucose levels by I.V. therapy may cause
anorexia.
S
PECIAL CONSIDERATIONS
Because the causes of anorexia are diverse,
diagnostic procedures may include thyroid
function studies, endoscopy, upper GI series,
gallbladder series, barium enema, liver and
kidney function tests, hormone assays, computed tomography scans, ultrasonography,
and blood studies to assess nutritional
status.
Promote adequate protein and caloric intake by providing high-calorie snacks or frequent, small meals. Encourage the patient’s
family to supply his favorite foods to help
stimulate his appetite. Take a 24-hour diet history daily. The patient may consistently exaggerate his food intake (common in patients
with anorexia nervosa), so you’ll need to
maintain strict calorie and nutrient counts for
the patient’s meals. In severe malnutrition,
provide supplemental nutritional support,
such as total parenteral nutrition or oral nutritional supplements.
Because anorexia and poor nutrition increase
susceptibility to infection, monitor the patient’s
vital signs and white blood cell count and closely observe any wounds.
P
EDIATRIC POINTERS
In children, anorexia commonly accompanies
many illnesses but usually resolves promptly.
However, be alert for subtle signs of anorexia
nervosa in preadolescent and adolescent girls.
Anosmia
Although usually an insignificant consequence
of nasal congestion or obstruction, anosmia—
absence of the sense of smell—occasionally
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heralds a serious defect. Temporary anosmia
can result from any condition that irritates and
causes swelling of the nasal mucosa and obstructs the olfactory area in the nose, such as
heavy smoking, rhinitis, or sinusitis. Permanent anosmia usually results when the olfactory neuroepithelium or any part of the olfactory
nerve is destroyed. Permanent or temporary
anosmia can also result from inhaling irritants
that paralyze nasal cilia, such as cocaine and
acid fumes. Anosmia may also be reported—
without an identifiable organic cause—by patients suffering from hysteria, depression, or
schizophrenia.
Anosmia is invariably perceived as bilateral;
unilateral anosmia can occur but is seldom recognized by the patient. Because combined stimulation of taste buds and olfactory cells produces the sense of taste, anosmia is usually
accompanied by ageusia, loss of the sense of
taste. (See Understanding the sense of smell.)
H
ISTORY AND PHYSICAL
EXAMINATION
Begin the patient history by asking about the
onset and duration of anosmia and related signs
and symptoms—stuffy nose, nasal discharge or
bleeding, postnasal drip, sneezing, dry or sore
mouth and throat, loss of sense of taste or appetite, excessive tearing, and facial or eye pain.
Pinpoint any history of nasal disease, allergies,
or head trauma. Ask about heavy smoking and
the use of prescribed or over-the-counter nose
drops or nasal sprays. Be sure to rule out cocaine use.
Inspect and palpate nasal structures for obvious injury, inflammation, deformities, and septal
deviation or perforation. Observe the contour
and color of the nasal mucosa and the size and
color of the turbinates. Check for polyps, which
appear as translucent white masses around the
middle meatus. Note the source and character
of any nasal discharge. Palpate the sinus areas
for tenderness and contour.
Assess the patient for nasal obstruction by
occluding one nostril at a time with your
thumb as the patient breathes quietly; listen for
breath sounds and for sounds of moisture or
mucus. Test olfactory nerve (cranial nerve I)
function by having the patient identify common odors.
M
EDICAL CAUSES
◆ Anterior cerebral artery occlusion. Per-
manent anosmia may follow vascular damage
involving the olfactory nerve. Associated signs
and symptoms include contralateral weakness
and numbness (especially in the leg), confusion, and impaired motor and sensory functions.
◆ Degenerative brain disease. Anosmia may
accompany Alzheimer’s disease, Parkinson’s
disease, and other degenerative central nervous system disorders. Associated findings include dementia, tremor, rigidity, and gait disturbance.
◆ Diabetes mellitus. Insidious, permanent
anosmia may occur along with fatigue, polyuria,
polydipsia, weight loss, polyphagia, and weakness.
◆ Head trauma. Permanent anosmia may fol-
low damage to the olfactory nerve. Associated
findings depend on the type and severity of the
trauma but may include epistaxis, headache,
nausea and vomiting, altered level of consciousness, blurred or double vision, raccoon
eyes, Battle’s sign, and otorrhea.
◆ Lead poisoning. Anosmia due to lead poi-
soning may be permanent or temporary, depending on the extent of damage to the nasal
mucosa. Associated findings include abdominal
pain, weakness, headache, nausea, vomiting,
constipation, wristdrop or footdrop, lead line on
the gums, metallic taste, seizures, delirium, and
possibly coma.
◆ Lethal midline granuloma. Permanent
anosmia accompanies lethal midline granuloma—a slowly progressive disease. Examination
reveals ulcerative granulation tissue in the
nose, sinuses, and palate; widespread crust formation and tissue necrosis; septal cartilage destruction; and possibly purulent rhinorrhea,
serous otitis media, and inflammation of the
eyelids and lacrimal apparatus.
◆ Neoplasms (brain, nasal, or sinus). Anos-
mia may be permanent if the neoplasm destroys or displaces the olfactory nerve. Associated signs and symptoms include unilateral or
bilateral epistaxis, swelling and tenderness in
the affected area, visual disturbances, decreased tearing, and elevated intracranial
pressure.
◆ Pernicious anemia. Anosmia from perni-
cious anemia may be temporary or permanent
and is accompanied by the classic triad of
weakness; sore, pale tongue; and numbness
and tingling in the extremities. Related findings
include distortion of taste, pallor, headache, irritability, dizziness, nausea, vomiting, diarrhea,
and shortness of breath.
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