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HYPOPIGMENTATION
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391
has noticed other skin changes—such as erythema, scaling, ulceration, or hyperpigmentation—
or if sun exposure causes unusually severe
burning.
Next, examine the patient’s skin, noting erythema, scaling, ulceration, areas of hyperpigmentation, and other findings.
M
EDICAL CAUSES
◆ Albinism. This genetically inherited disease
involves alterations of the melanin pigment system that affects skin, hair, and eyes. There are
various forms of albinism, all of which are present at birth. Skin and hair color vary from
snow white to brown, but the universal finding
of iris translucency confirms the diagnosis. Associated eye findings include nystagmus, decreased visual acuity, decreased pigmentation
of the retina, and strabismus.
Lifelong diligence is needed to protect the
skin from sun exposure, including using sunblock with an SPF greater than 30; wearing
protective clothing, hats, and sunglasses
(even for infants); avoiding the sun during
high solar intensity; and obtaining routine
skin examinations for the development of
skin cancers.
Suggest referral to a support group to assist
patients with problems occurring in daily life.
One such organization is the National Organization for Albinism and Hypomelanosis.
◆ Burns. Thermal and radiation burns can
cause transient or permanent hypopigmentation.
◆ Discoid lupus erythematosus. This form of
lupus erythematosus may produce hypopigmentation after inflammatory skin eruptions. Lesions are sharply defined, separate or fused
macules, papules, or plaques; they vary from
pink to purple, with a yellowish or brown crust
and scaly, enlarged hair follicles. Although they
may occur on other parts of the body, the lesions are typically distributed in a butterfly pattern over the cheeks and bridge of the nose.
Telangiectasia may occur. After the inflammatory eruptive stage, noncontractile scarring and
atrophy commonly affect the face and may also
involve sun-exposed areas of the neck, ears,
scalp (with possible alopecia), lips, and oral mucosa.
◆ Hypomelanosis (idiopathic guttate). Com-
mon in lightly pigmented people older than age
30, this skin disorder produces sharply marginated, angular white spots on sun-exposed
extremities. In blacks, hypopigmentation occurs
mainly on the upper arms.
◆ Inflammatory and infectious disorders.
Skin disorders, such as psoriasis, and infectious
disorders, such as viral exanthemas or syphilis,
can cause transient or permanent hypopigmentation.
◆ Tinea versicolor. This benign fungal skin
infection produces scaly, sharply defined lesions that usually appear on the upper trunk,
neck, and arms. The lesions range from hypopigmented patches in dark-skinned patients
to hyperpigmented patches in fair-skinned
patients.
◆ Tuberculoid leprosy. This chronic disorder
affects the skin and peripheral nervous system.
Erythematous or hypopigmented macules have
decreased or absent sensation for light, touch,
and warmth. Because the lesions don’t sweat,
the skin feels dry and rough; it may be scaly.
Associated effects may include very painful,
palpable peripheral nerves; muscle atrophy
and contractures; and ulcers of the fingers
and toes.
◆ Vitiligo. This common skin disorder produces
sharply defined, flat white macules and patches
ranging in diameter from 1 to over 20 cm. The
hypopigmented areas commonly have hyperpigmented borders. Usually bilaterally symmetrical,
lesions appear on sun-exposed areas; in body
folds; around the eyes, nose, mouth, and rectum;
and over bony prominences. Patches of vitiligo
may coalesce to form universal lack of pigment
and may involve the hair, eyebrows, and eyelashes. Spontaneous repigmentation can occur.
Hypopigmented patches (halo nevi) may surround pigmented moles.
O
THER CAUSES
◆ Chemicals. Most phenolic compounds—for
example, amylphenol (a dye) and paratertiary
butylphenol, which are used in plastics and
glues, and germicides used in many household
and industrial products—can cause hypopigmentation.
◆ Drugs. Topical or intralesional administra-
tion of corticosteroids causes hypopigmentation at the treatment site. Chloroquine, an antimalarial drug, may cause depigmentation of
hair (including eyebrows and lashes) and
poor tanning 2 to 5 months after therapy
begins.
392 HYPOPIGMENTATION
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S
PECIAL CONSIDERATIONS
In fair-skinned patients, a special ultraviolet
(UV) light (Wood’s lamp) can help differentiate
hypopigmented lesions, which appear pale,
from depigmented lesions, which appear white.
Advise patients to use corrective cosmetics to
help hide skin lesions, and to use a sunblock
because hypopigmented areas may sunburn
easily. Encourage regular examinations for early
detection and treatment of lesions that may become premalignant or malignant. Repigmentation therapy may be prescribed, combining a
photosensitizing drug (psoralen) and UV light,
wavelength A. Advise patients with associated
eye problems, such as albinism, to avoid the
midday sun and to wear sunglasses. Refer patients for counseling if lesions cause stress.
P
EDIATRIC POINTERS
In children, hypopigmentation results from genetic or acquired disorders, including albinism,
phenylketonuria, and tuberous sclerosis. In
neonates, hypopigmentation may indicate a
metabolic or nervous system disorder.
G
ERIATRIC POINTERS
In elderly people, hypopigmentation is usually
the result of cumulative exposure to UV light,
which may also cause hyperpigmentation,
telangiectasia, and purpura. These changes are
known as dermatoheliosis.
I
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Impotence
Impotence, or erectile dysfunction, is the inability to achieve and maintain penile erection sufficient to complete satisfactory sexual intercourse; ejaculation may or may not be affected.
Impotence varies from occasional and minimal
to permanent and complete. Occasional impotence occurs in about one-half of adult American men, whereas chronic impotence affects
about 15 million American men.
Impotence can be classified as primary or
secondary. A man with primary impotence has
never been potent with a sexual partner but
may achieve normal erections in other situations. This uncommon condition is difficult to
treat. Secondary impotence carries a more favorable prognosis because, despite his present
erectile dysfunction, the patient has completed
satisfactory intercourse in the past.
Penile erection involves increased arterial
blood flow secondary to psychological, tactile,
and other sensory stimulation. Trapping of blood
within the penis produces increased length, circumference, and rigidity. Impotence results when
any component of this process—psychological,
vascular, neurologic, or hormonal—malfunctions.
Organic causes of impotence include vascular disease, kidney disease, diabetes mellitus,
hypogonadism, a spinal cord lesion, alcohol and
drug abuse, and surgical complications. (The incidence of organic impotence associated with
other medical problems increases after age 50.)
Psychogenic causes range from performance
anxiety and marital discord to moral or religious
conflicts. Fatigue, stress, poor health, age, and
drugs can also disrupt normal sexual function.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient complains of impotence or of a condition that may be causing it, let him describe his
problem without interruption. Then begin your
examination in a systematic way, moving from
less sensitive to more sensitive matters. Begin
with a psychosocial history. Is the patient married, single, or widowed? How long has he been
married or had a sexual relationship? What’s the
age and health status of his sexual partner? Find
out about past marriages, if any, and ask him
why he thinks they ended. If you can do so discreetly, ask about sexual activity outside marriage or his primary sexual relationship. Also ask
about his job history, his typical daily activities,
and his living situation. How well does he get
along with others in his household?
Focus your medical history on the causes of
erectile dysfunction. Does the patient have type
2 diabetes mellitus, hypertension, or heart disease? If so, ask about its onset and treatment.
Also ask about neurologic diseases such as
multiple sclerosis. Obtain a surgical history, emphasizing neurologic, vascular, and urologic
surgery. If trauma may be causing the patient’s
impotence, find out the date of the injury as well
as its severity, associated effects, and treatment.
Ask about intake of alcohol, drug use or abuse,
smoking, diet, and exercise. Obtain a urologic
history, including voiding problems and past
injury.
393
394 IMPOTENCE
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Next, ask the patient when his impotence began. How did it progress? What’s its current status? Make your questions specific, but remember that many patients have difficulty discussing
sexual problems, and many don’t understand
the physiology involved.
The following sample questions may yield
helpful data: When was the first time you remember not being able to initiate or maintain an
erection? How often do you wake in the morning or at night with an erection? Do you have
wet dreams? Has your sexual drive changed?
How often do you try to have intercourse with
your partner? How often would you like to? Can
you ejaculate with or without an erection? Do
you experience orgasm with ejaculation?
Ask the patient to rate the quality of a typical
erection on a scale of 0 to 10, with 0 being completely flaccid and 10 being completely erect.
Using the same scale, also ask him to rate his
ability to ejaculate during sexual activity, with 0
being never and 10 being always.
Next, perform a brief physical examination.
Inspect and palpate the genitalia and prostate
for structural abnormalities. Assess the patient’s
sensory function, concentrating on the perineal
area. Next, test motor strength and deep tendon
reflexes in all extremities, and note other neurologic deficits. Take the patient’s vital signs and
palpate his pulses for quality. Note any signs of
peripheral vascular disease, such as cyanosis
and cool extremities. Auscultate for abdominal
aortic, femoral, carotid, or iliac bruits, and palpate for thyroid gland enlargement.
◆ Penile disorders. With Peyronie’s disease,
the penis is bent, making erection painful and
penetration difficult and eventually impossible.
Phimosis prevents erection until circumcision
releases constricted foreskin. Other inflammatory,
infectious, or destructive diseases of the penis
may also cause impotence.
◆ Peripheral neuropathy. Systemic diseases,
such as chronic renal failure and diabetes mellitus, can cause progressive impotence if the patient develops peripheral neuropathy. This condition affects about 60% of males with diabetes.
Associated signs and symptoms of diabetic neuropathy include bladder distention with overflow
incontinence, orthostatic hypotension, syncope,
paresthesia and other sensory disturbances,
muscle weakness, and leg atrophy.
◆ Psychological distress. Impotence can re-
sult from diverse psychological causes, including depression, performance anxiety, memories
of previous traumatic sexual experiences, moral
or religious conflicts, and troubled emotional or
sexual relationships.
◆ Trauma. Traumatic injury involving the penis,
urethra, prostate, perineum, or pelvis may cause
sudden impotence due to structural alteration,
nerve damage, or interrupted blood supply.
◆ Vascular disorders. Various vascular disorders
can cause impotence. These include advanced arteriosclerosis affecting both major and peripheral
blood vessels, Leriche’s syndrome (slowly developing occlusion of the terminal abdominal aorta),
and arteriosclerosis, thrombosis, or embolization
of smaller vessels supplying the penis.
M
EDICAL CAUSES
◆ Central nervous system disorders. Spinal
cord lesions from trauma produce sudden impotence. A complete lesion above S
motor-neuron lesion) disrupts descending motor
tracts to the genital area, causing loss of voluntary erectile control but not of reflex erection
and reflex ejaculation. However, a complete
lesion in the lumbosacral spinal cord (lowermotor-neuron lesion) causes loss of reflex ejaculation and reflex erection. Spinal cord tumors and
degenerative diseases of the brain and spinal
cord (such as multiple sclerosis and amyotrophic
lateral sclerosis) cause progressive impotence.
◆ Endocrine disorders. Hypogonadism from tes-
ticular or pituitary dysfunction may lead to impotence from deficient secretion of androgens (primarily testosterone). Adrenocortical and thyroid
dysfunction and chronic hepatic disease may also
cause impotence because these organs play a role
(although minor) in sex hormone regulation.
(upper-
2
O
THER CAUSES
◆ Alcohol and drugs. Alcoholism and drug
abuse are associated with impotence, as are
many prescription drugs, especially antihypertensives. (See Drugs that may cause impotence.)
◆ Surgery. Surgical injury to the penis, bladder
neck, prostate, urinary sphincter, rectum,
or perineum can cause impotence, as can injury
to local nerves or blood vessels.
S
PECIAL CONSIDERATIONS
Care begins by ensuring privacy, confirming confidentiality, and establishing a rapport with the patient. No other medical condition affecting males
is as potentially frustrating, humiliating, and devastating to self-esteem and significant relationships as impotence. Help the patient feel comfortable about discussing his sexuality. This begins
with feeling comfortable about your own sexuality and adopting an accepting attitude about the
sexual experiences and preferences of others.
Insomnia
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INSOMNIA
395
Drugs that may cause
impotence
Many commonly used drugs—especially antidepressants and antihypertensives—can
cause impotence, which may be reversible if
the drug is discontinued or the dosage reduced. Here are some examples.
amitriptyline
atenolol
bicalutamide
carbamazepine
cimetidine
clonidine
desipramine
digoxin
diphenhydramine
finasteride
Prepare the patient for screening tests for hormonal irregularities and for Doppler studies of
penile blood pressure to rule out vascular insufficiency. Other tests include voiding studies, nerve
conduction tests, evaluation of nocturnal penile
tumescence, and psychological screening.
Treatment of psychogenic impotence may involve counseling for the patient and his sexual
partner; treatment of organic impotence focuses
on reversing the cause, if possible. Other forms
of treatment include surgical revascularization,
drug-induced erection, surgical repair of a venous leak, and penile prostheses. Encourage the
patient to maintain follow-up appointments and
therapy for underlying medical disorders.
G
ERIATRIC POINTERS
Most people erroneously believe that sexual
performance normally declines with age. Many
also believe (erroneously) that elderly people
are incapable of or aren’t interested in sex or
that they can’t find elderly partners who are interested in sex. Organic disease must be ruled
out in elderly people who suffer from sexual
dysfunction before counseling to improve sexual performance can start.
P
ATIENT COUNSELING
Encourage your patient to talk openly about his
needs and desires, fears and anxieties, or misconceptions. Urge him to discuss these issues
with his partner as well as what role both of
them want sexual activity to play in their lives.
hydralazine
imipramine
methyldopa
nortriptyline
perphenazine
prazosin
propranolol
thiazide diuretics
thioridazine
tranylcypromine
Insomnia is the inability to fall asleep, remain
asleep, or feel refreshed by sleep. Acute and
transient during periods of stress, insomnia may
become chronic, causing constant fatigue, extreme anxiety as bedtime approaches, and psychiatric disorders. This common complaint is
experienced occasionally by about 25% of
Americans and chronically by another 10%.
Physiologic causes of insomnia include jet
lag, arguing, and lack of exercise. Pathophysiologic causes range from medical and psychiatric disorders to pain, adverse effects of a
drug, and idiopathic factors. Complaints of insomnia are subjective and require close investigation; for example, the patient may mistakenly
attribute his fatigue from an organic cause, such
as anemia, to insomnia.
H
ISTORY AND PHYSICAL
EXAMINATION
Take a thorough sleep and health history. Find
out when the patient’s insomnia began and the
circumstances surrounding it. Is the patient trying to stop using a sedative? Does he take a
central nervous system (CNS) stimulant, such as
an amphetamine, pseudoephedrine, a theophylline derivative, phenylpropanolamine, cocaine, or a drug that contains caffeine, or does
he drink caffeinated beverages?
Find out if the patient has a chronic or acute
condition, the effects of which may be disturbing
his sleep, particularly cardiac or respiratory disease or painful or pruritic conditions. Ask if he
has an endocrine or neurologic disorder, or a
history of drug or alcohol abuse. Is he a frequent
traveler who suffers from jet lag? Does he use
his legs a lot during the day and then feel restless at night? Ask about daytime fatigue and regular exercise. Also ask if he often finds himself
gasping for air, experiencing apnea, or frequently repositioning his body. If possible, consult the
patient’s spouse or sleep partner because the patient may be unaware of his own behavior. Ask
how many pillows the patient uses to sleep.
Assess the patient’s emotional status, and try
to estimate his level of self-esteem. Ask about
personal and professional problems and psychological stress. Also ask if he experiences hallucinations, and note behavior that may indicate alcohol withdrawal. After reviewing any
complaints that suggest an undiagnosed disorder, perform a physical examination. (See Differ-
ential diagnosis: Insomnia, pages 396 and 397.)
396 INSOMNIA
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Differential diagnosis: Insomnia
History of present illness
Focused physical examination:
Mental health; respiratory, endocrine, and cardiovascular system
Common signs and symptoms
◆ Diaphoresis
◆ Palpitations
◆ Shortness of breath
◆ Tachycardia
s
Generalized anxiety disorder
Additional signs and symptoms
◆ Fatigue
◆ Restlessness
◆ Dyspepsia
◆ Dry mouth
◆ Light-headedness
◆ Nausea
◆ Diarrhea
◆ Flushes or chills
◆ Excessive worry
◆ Irritability
◆ Difficulty concentrating
Diagnosis: Psychological evaluation
T
eatment: Medication (selective
r
serotonin reuptake inhibitors [SSRIs], antidepressants, beta-adrenergic blockers
[for physical symptoms], short-term
benzodiazepines), cognitive and
behavioral therapies
Follow-up: Reevaluation every 2 to
3 weeks until stabilized on medication
Thyrotoxicosis
Additional signs and symptoms
◆ Difficulty falling asleep, then sleeping for
only a brief period
◆ Dyspnea
◆ Atrial or ventricular gallop
◆ Inability to concentrate
◆ Emotional lability
◆ Weight loss despite increased appetite
◆ Tremors
◆ Nervousness
◆ Diaphoresis
◆ Hypersensitivity to heat
◆ Enlarged thyroid
◆ Polyuria
◆ Polydipsia
Diagnosis: Physical examination,
laboratory tests (thyroid-stimulating
hormone
Treatment: Medication (antithyroid
agents, therapeutic radioiodine, betaadrenergic blockers)
Follow-up: Reevaluation of thyroid function
every 6 months; reevaluation at 6 weeks and
12 weeks, and then every 6 months, if
undergoing radionuclide therapy
, T4, thyroid resin uptake)
, T
3
M
EDICAL CAUSES
◆ Alcohol withdrawal syndrome. Abrupt
cessation of alcohol intake after long-term
use causes insomnia that may persist for up
to 2 years. Other early effects of this acute
syndrome include excessive diaphoresis,
tachycardia, hypertension, tremors, restlessness, irritability, headache, nausea, flushing,
and nightmares. Progression to delirium
tremens produces confusion, disorientation,
INSOMNIA 397
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Depression
Signs and symptoms
◆ Chronic insomnia with difficulty falling
asleep and early waking
◆ Dysphoria
◆ Decreased or increased appetite
◆ Psychomotor agitation or retardation
◆ Loss of interest in usual activities
◆ Feelings of worthlessness or guilt
◆ Fatigue
◆ Difficulty concentrating
◆ Indecisiveness
◆ Recurrent thoughts of death
◆ Tachycardia
◆ Possible suicidal ideation
Diagnosis: Beck Depression In
Zung Self-Rating Depression Scale,
Geriatric Depression Scale, laboratory tests
(complete blood count, erythrocyte
sedimentation rate, Venereal Disease
Research Laboratory, electrolytes, thyroid
profile, drug screening)
Treatment: Medication (SSRIs, tricyclic
antidepressants), cognitive therapy,
support groups, exercise program
Follow-up: Initial reevaluation at 2 weeks,
then every 4 to 8 weeks, then every 3
months; referral to psychologist
ventory
,
Sleep apnea syndrome
Signs and symptoms
◆ Repeated episodes of obstructive apnea
and hypopnea during sleep that end with a
series of gasps and arousal
◆ Morning headache
◆ Daytime sleepiness
◆ Hypertension
◆ Personality changes
Diagnosis: Polysomnography in a sleep
laboratory
T
r
eatment: Treatment of underlying
cause, continuous positive airway pressure
at night, oral appliances, antidepressants,
surgery, weight loss (if indicated), smoking
and alcohol cessation, positional therapy
Follow-up: Referrals to sleep specialist
and pulmonologist
Additional differential diagnoses: alcohol withdrawal syndrome ◆ mood (affective) disorders ◆ nocturnal
myoclonus ◆ pain ◆ pheochromocytoma ◆ pruritus
Other causes: amphetamines ◆ caffeine-containing beverages ◆ cocaine ◆ ginseng ◆ green tea
◆ pseudoephedrine ◆ theophylline derivatives ◆ withdrawal from sedatives or hypnotics
paranoia, delusions, hallucinations, and
seizures.
◆ Generalized anxiety disorder. Anxiety can
cause chronic insomnia as well as symptoms of
tension, such as fatigue and restlessness; signs
of autonomic hyperactivity, such as diaphoresis,
dyspepsia, and high resting pulse and respiratory rates; and signs of apprehension.
◆ Mood (affective) disorders. Depression
commonly causes chronic insomnia with
398 INSOMNIA
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difficulty falling asleep, waking and being unable to fall back to sleep, or waking early in the
morning. Related findings include dysphoria (a
primary symptom), decreased appetite with
weight loss or increased appetite with weight
gain, and psychomotor agitation or retardation.
The patient experiences loss of interest in his
usual activities, feelings of worthlessness and
guilt, fatigue, difficulty concentrating, indecisiveness, and recurrent thoughts of death.
Manic episodes produce a decreased need for
sleep with an elevated mood and irritability. Related findings include increased energy and activity, fast speech, speeding thoughts, inflated
self-esteem, easy distractibility, and involvement in high-risk activities such as reckless
driving.
◆ Nocturnal myoclonus. With this seizure dis-
order, involuntary and fleeting muscle jerks of
the legs occur every 20 to 40 seconds, disturbing sleep.
◆ Pain. Almost any condition that causes pain
can cause insomnia. Related findings reflect the
specific cause.
◆ Pheochromocytoma. This rare disorder
causes paroxysms of acute hypermetabolic activity, which can prevent or interrupt sleep. Its
cardinal sign is severe hypertension, which
may be sustained between attacks. Other
effects include headache, palpitations, and
anxiety.
◆ Pruritus. Localized skin infections and sys-
temic disorders, such as liver failure, can cause
pruritus, resulting in insomnia.
◆ Sleep apnea syndrome. Apneic periods be-
gin with the onset of sleep, continue for 10 to
90 seconds, and end with a series of gasps and
arousal. With central sleep apnea, respiratory
movement ceases for the apneic period; with
obstructive sleep apnea, upper airway obstruction blocks incoming air, although breathing
movements continue. Some patients display
both types of apnea. Repeated possibly hundreds of times during the night, this cycle alternates with bradycardia and tachycardia. Associated findings include morning headache,
daytime fatigue, hypertension, ankle edema,
and personality changes, such as hostility, paranoia, and agitated depression.
◆ Thyrotoxicosis. Difficulty falling asleep
and then sleeping for only a brief period is one
of the characteristic symptoms of this disorder. Cardiopulmonary features include dyspnea, tachycardia, palpitations, and atrial or
ventricular gallop. Other findings include
weight loss despite increased appetite, diarrhea, tremors, nervousness, diaphoresis, hypersensitivity to heat, an enlarged thyroid,
polyuria, and polydipsia.
O
THER CAUSES
◆ Drugs. Use of, abuse of, or withdrawal from
sedatives or hypnotics may produce insomnia.
CNS stimulants—including amphetamines,
theophylline derivatives, pseudoephedrine, cocaine, and caffeinated beverages—may also
produce insomnia.
HERB ALERT Herbal remedies, such as
ginseng and green tea, can also cause
insomnia.
S
PECIAL CONSIDERATIONS
Prepare the patient for tests to evaluate his insomnia, such as blood and urine studies for
17-hydroxycorticosteroids and catecholamines,
polysomnography (including an EEG, electrooculography, and electrocardiography), and
sleep EEG.
P
EDIATRIC POINTERS
Insomnia in early childhood may develop along
with separation anxiety at ages 2 to 3, after a
stressful or tiring day, or during illness or
teething. In children ages 6 to 11, insomnia usually reflects residual excitement from the day’s
activities; a few children continue to have bedtime fears. Sleep problems are common in foster children.
P
ATIENT COUNSELING
Teach the patient comfort and relaxation techniques to promote natural sleep. (See Tips for
relieving insomnia.) Advise him to awaken and
retire at the same time each day and to exercise
regularly. When he can’t sleep, advise him to
get up but remain inactive. Urge him to use his
bed only for sleeping, not for relaxation or
watching television.
Advise the patient to use tranquilizers or
sedatives for acute insomnia only when relaxation techniques fail. If appropriate, refer him
for counseling or to a sleep disorder clinic for
biofeedback training or other interventions.
Tips for relieving insomnia
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INSOMNIA 399
Common
problems
Acroparesthesia
Anxiety
Dyspnea
Pain
Causes
Improper positioning may
compress superficial (ulnar,
radial, and peroneal)
nerves, disrupting circulation to the compressed
nerve. This causes numbness, tingling and stiffness
in an arm or leg.
Physical and emotional
stress produces anxiety,
which causes autonomic
stimulation.
With many cardiac and pulmonary disorders, a recumbent position and inactivity
cause restricted chest expansion, secretion pooling,
and pulmonary vascular
congestion, leading to
coughing and shortness of
breath.
Chronic or acute pain from
any cause can prevent or
disrupt sleep.
Interventions
Teach the patient to assume a comfortable
position in bed, with his limbs unrestricted.
If he tends to awaken with a numb arm or
leg, tell him to massage and move it until
sensation returns completely and then to
assume an unrestricted position.
Encourage the patient to discuss his fears
and concerns, and teach him relaxation
techniques, such as guided imagery and
deep breathing. If ordered, administer a
mild sedative, such as temazepam or another sedative hypnotic, before bedtime.
Emphasize that these medications are to be
used for the short-term only.
Elevate the head of the bed, or provide at
least two pillows or a reclining chair to
help the patient sleep. Suction him when
he awakens, and encourage deep breathing
and incentive spirometry every 2 to
4 hours. Also, provide supplementary oxygen by nasal cannula. If the patient is pregnant, encourage her to sleep on her left
side at a comfortable elevation to ease
dyspnea.
Administer pain medication, as ordered,
20 minutes before bedtime, and teach
deep, even, slow breathing to promote relaxation. If the patient has back pain, help
him lie on his side with his legs flexed. If he
has epigastric pain, encourage him to take
an antacid before bedtime and to sleep
with the head of the bed elevated. If he has
incisions, instruct him to splint during
coughing or movement.
Pruritus
Restless leg
syndrome
A localized skin infection or
a systemic disorder, such as
liver failure, may produce
intensely annoying itching,
even during the night.
Excessive exercise during
the day may cause tired,
aching legs at night, requiring movement for relief.
Wash the patient’s skin with a mild soap
and water, and dry the skin thoroughly. Apply moisturizing lotion on dry, unbroken
skin and an antipruritic such as calamine
lotion on pruritic areas. Administer diphenhydramine or hydroxyzine, as ordered, to
help minimize itching.
Help the patient exercise his legs gently by
slowly walking with him around the room
and down the hall. If ordered, administer a
muscle relaxant such as diazepam.
400 INTERMITTENT CLAUDICATION
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Intermittent claudication
Most common in the legs, intermittent claudication is cramping limb pain brought on by exercise and relieved by 1 to 2 minutes of rest. This
pain may be acute or chronic; when acute, it
may signal acute arterial occlusion. Intermittent
claudication is most common in men ages 50 to
60 with a history of diabetes mellitus, hyperlipidemia, hypertension, or tobacco use. Without
treatment, it may progress to pain at rest. With
chronic arterial occlusion, limb loss is uncommon because collateral circulation usually
develops.
With occlusive artery disease, intermittent
claudication results from an inadequate blood
supply. Pain in the calf (the most common area)
or foot indicates disease of the femoral or
popliteal arteries; pain in the buttocks and upper thigh, disease of the aortoiliac arteries. During exercise, the pain typically results from the
release of lactic acid due to anaerobic metabolism in the ischemic segment, secondary to obstruction. When exercise stops, the lactic acid
clears and the pain subsides.
Intermittent claudication may also have a
neurologic cause: narrowing of the vertebral
column at the level of the cauda equina. This
condition creates pressure on the nerve roots
to the lower extremities. Walking stimulates
circulation to the cauda equina, causing increased pressure on those nerves and resultant
pain.
Physical findings include pallor on elevation,
rubor on dependency (especially the toes and
soles), loss of hair on the toes, and diminished
arterial pulses.
EMERGENCY INTERVENTIONS If the
patient has sudden intermittent claudication with severe or aching leg pain at rest, check
the leg’s temperature and color and palpate
femoral, popliteal, posterior tibial, and dorsalis
pedis pulses. Ask about numbness and tingling.
Suspect acute arterial occlusion if pulses are absent; if the leg feels cold and looks pale, cyanotic,
or mottled; and if paresthesia and pain are present. Mark the area of pallor, cyanosis, or mottling, and reassess it frequently, noting an increase in the area.
Don’t elevate the leg. Protect it, allowing nothing to press on it. Prepare the patient for preoperative blood tests, urinalysis, electrocardiography,
chest X-rays, lower-extremity Doppler studies, and
angiography. Start an I.V. catheter, and administer
an anticoagulant and analgesics.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient has chronic intermittent claudication, gather history data first. Ask how far he
can walk before pain occurs and how long he
must rest before it subsides. Can he walk less
far now than before, or does he need to rest
longer? Does the pain-rest pattern vary? Has
this symptom affected his lifestyle?
Obtain a history of risk factors for atherosclerosis, such as smoking, diabetes, hypertension, and hyperlipidemia. Next, ask about associated signs and symptoms, such as paresthesia
in the affected limb and visible changes in the
color of the fingers (white to blue to pink) when
he’s smoking, exposed to cold, or under stress.
If the patient is male, does he experience impotence?
Focus the physical examination on the cardiovascular system. Palpate for femoral,
popliteal, dorsalis pedis, and posterior tibial
pulses. Note character, amplitude, and bilateral
equality. Diminished or absent popliteal and
pedal pulses with the femoral pulse present may
indicate atherosclerotic disease of the femoral
artery. Diminished femoral and distal pulses
may indicate disease of the terminal aorta or iliac branches. Absent pedal pulses with normal
femoral and popliteal pulses may indicate
Buerger’s disease.
Listen for bruits over the major arteries. Note
color and temperature differences between his
legs or compared with his arms; also note
where on his leg the changes in temperature
and color occur. Elevate the affected leg for
2 minutes; if it becomes pale or white, blood
flow is severely decreased. When the leg hangs
down, how long does it take for color to return?
(Thirty seconds or longer indicates severe disease.) If possible, check the patient’s deep tendon reflexes after exercise; note if they’re diminished in his lower extremities.
Examine his feet, toes, and fingers for ulceration, and inspect his hands and lower legs for
small, tender nodules and erythema along
blood vessels. Note the quality of his nails and
the amount of hair on his fingers and toes.
If the patient has arm pain, inspect his arms
for a change in color (to white) on elevation.
Next, palpate for changes in temperature,
muscle wasting, and a pulsating mass in the
subclavian area. Palpate and compare the radial, ulnar, brachial, axillary, and subclavian pulses to identify obstructed areas.
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