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ALOPECIA
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31
tissue, endocrine, nutritional, or psychological
disorder; a neoplasm; an infection; a burn; or
exposure to toxins.
Normally, everyone loses about 50 hairs per
day, and these hairs are replaced by new ones.
However, aging, genetic predisposition, and
hormonal changes may contribute to gradual
hair thinning and hairline recession. This type of
alopecia occurs in about 40% of adult men and
may also occur in postmenopausal women.
CULTURAL CUE People who have fine and
relatively scanty hair, such as natives of
tropical areas, may not recognize alopecia right
away.
GENDER CUE In men, hair loss commonly
affects the temporal areas, producing an
M-shaped hairline. In women, diffuse thinning
marks the centrofrontal area.
In both sexes, hair loss may also occur on the
trunk, pubic area, axillae, arms, and legs. Another normal pattern of alopecia occurs 2 to
4 months postpartum. This temporary, diffuse
hair loss on the scalp may be scant or dramatic
and possibly accentuated at the frontal areas.
Anxiety, high fever, and even certain hair styles
or grooming methods may also cause alopecia.
(See Recognizing patterns of alopecia, page 32.)
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient isn’t receiving a chemotherapeutic
drug or radiation therapy, begin by asking when
he first noticed the hair loss or thinning. Does it
affect the scalp alone, or does it occur elsewhere on the body? Is it accompanied by itching
or rashes? Then carefully explore other signs
and symptoms to help distinguish between normal and pathologic hair loss. Ask about recent
weight change, anorexia, nausea, vomiting, excessive stress, and altered bowel habits. Also
ask about urinary tract changes, such as hematuria or oliguria. Has the patient been especially
tired or irritable? Does he have a cough or difficulty breathing? Ask about joint pain or stiffness
and about heat or cold intolerance. Inquire
about exposure to insecticides. If the patient is
female, ask if she has had menstrual irregularities and note her pregnancy history. If the patient is male, ask about sexual dysfunction, such
as decreased libido or impotence.
Next, ask about hair care. Does the patient
frequently use a hot blow dryer or electric
curlers? Does he periodically dye, bleach, or
perm his hair? If the patient is black, ask if he
uses a hot comb to straighten his hair or a long-
toothed comb to achieve an Afro look. Does he
ever braid the hair in cornrows? Check for a
family history of alopecia, and ask what age relatives were when they started experiencing hair
loss. Also ask about nervous habits, such as
pulling the hair or twirling it around a finger.
Begin the physical examination by taking vital signs and then assessing the extent and pattern of scalp hair loss. Is it patchy or symmetrical? Is the hair surrounding a bald area brittle or
lusterless? Is it a different color than other scalp
hair? Does it fall out easily? Inspect the underlying skin for follicular openings, erythema, loss
of pigment, scaling, induration, broken hair
shafts, and hair regrowth.
Then examine the rest of the skin. Note the
size, color, texture, and location of any lesions.
Check for jaundice, edema, hyperpigmentation,
pallor, or duskiness. Examine nails for vertical
or horizontal pitting, thickening, brittleness, or
whitening. As you do so, watch for fine tremors
in the hands. Observe the patient for muscle
weakness and ptosis. Palpate for lymphadenopathy, enlarged thyroid or salivary
glands, and masses in the abdomen or chest.
M
EDICAL CAUSES
◆ Alopecia areata. Alopecia areata is usually
marked by well-circumscribed patches of nonscarring hair loss on the scalp without skin
changes. Occasionally, the patches also appear
on the beard, axillae, pubic area, arms, legs, or
the entire body (alopecia universalis). “Exclamation point” hairs—loose hairs with rough, brushlike tips on narrow, less-pigmented shafts—typically border expanding patches of alopecia.
Although this disorder is recurrent, hair growth
usually returns after several months. In about
20% of patients, alopecia areata also causes
horizontal or vertical nail pitting.
◆ Arsenic poisoning. Most common in
chronic poisoning, alopecia is diffuse and
mainly affects the scalp. Related signs and
symptoms include muscle weakness and wasting, areflexia, partial or total vision loss, and
bronze skin.
◆ Arterial insufficiency. Patchy alopecia oc-
curs in arterial insufficiency, typically on the
lower extremities, and is accompanied by thin,
shiny, atrophic skin and thickened nails. The
skin turns pale when the patient’s legs are elevated and dusky when they’re dependent. Associated findings include weak or absent peripheral pulses, cool extremities, paresthesia, leg
ulcers, and intermittent claudication.
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Recognizing patterns of alopecia
Distinctive patterns of alopecia result from different causes. The illustrations below show four of
the most common patterns.
Tinea capitis, a
fungal infection,
produces irregular bald patches
with scaly, red
lesions.
Alopecia areata causes expanding
patches of nonscarring hair loss
bordered by “exclamation point”
hairs.
Trauma from habitual hair pulling or injudicious grooming habits may cause permanent
peripheral alopecia.
Chemotherapeutic drugs produce diffuse, yet temporary, hair loss.
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33
◆ Burns. Full-thickness or third-degree burns
completely destroy the dermis and epidermis,
leaving translucent, charred, or ulcerated skin.
Scarring or keloid formation associated with
these burns causes permanent alopecia.
◆ Cutaneous T-cell lymphoma. More com-
mon in older patients, cutaneous T-cell lymphoma may be associated with alopecia mucinosa in its first, or premycotic, stage. Scattered
papules or plaques may occur on clothed areas,
such as breasts and buttocks, or a zebralike pattern of scaly erythema may form on the trunk.
Alopecia may persist through the plaque and
tumor stages.
◆ Dissecting cellulitis of the scalp. Resulting
from skin infection, dissecting cellulitis of the
scalp is characterized by small nodules that
eventually rupture and drain. Keloid formation
during healing causes permanent alopecia.
◆ Exfoliative dermatitis. Exfoliative dermatitis
is a transient disorder in which loss of scalp and
body hair is preceded by several weeks of generalized scaling and erythema. Nail loss commonly occurs along with pruritus, malaise,
fever, weight loss, lymphadenopathy, and gynecomastia.
◆ Fungal infections. Tinea capitis (scalp ring-
worm), the most common fungal infection, produces irregular balding areas, scaling, and erythematous lesions. As these lesions enlarge,
their centers heal, causing the classic ringshaped appearance. Surrounding the balding
areas are broken scalp hairs. When they break
off at the scalp surface, hairs resemble black
dots. Other findings include pruritus and thick,
whitish nails.
◆ Hodgkin’s disease. Permanent alopecia may
occur if the lymphoma infiltrates the scalp. It’s
accompanied by edema, pruritus, and hyperpigmentation. Associated signs vary with the degree and location of lymphadenopathy.
◆ Hypopituitarism. In adults, hypopituitarism
varies greatly, depending on its severity and the
number of deficient hormones. Gonadotropin
deficiency in the female causes sparse or absent pubic and axillary hair accompanied by infertility, amenorrhea, and breast atrophy. A
similar deficiency in the male decreases facial
and body hair and causes infertility, decreased
libido, impotence, poor muscle development,
and undersized testes, penis, and prostate
gland. A human growth hormone deficiency at
an early age may cause short stature. Deficiency of thyroid-stimulating hormone produces
signs of hypothyroidism; deficiency of corti-
cotropin produces signs of adrenocortical
insufficiency.
◆ Hypothyroidism. In hypothyroidism, the hair
on the face, scalp, and genitalia thins and becomes dull, coarse, and brittle. Most characteristic, though, is loss of the outer third of the
eyebrows. Typically, alopecia is preceded by fatigue, constipation, cold intolerance, and weight
gain. Other signs and symptoms include dry,
flaky, inelastic skin; puffy face, hands, and feet;
hoarseness; thick, brittle nails; slow mental
function; bradycardia; menorrhagia; and
myalgia.
◆ Lichen planus. Occasionally, lichen planus
disorder produces patchy hair loss on the scalp
with skin inflammation. Angular, flat, purple
papules typically develop on the lower back,
genitalia, arms, and lower legs. Related findings
include pruritus and nail changes, ranging from
grooves to nail loss. Scarring alopecia may develop with scalp skin atrophy.
◆ Lupus erythematosus. Hair loss is a chief
complaint in patients with either discoid or systemic lupus. Hair tends to become brittle and
may fall out in patches; short, broken hairs
(known as lupus hairs) commonly appear above
the forehead. Both types of lupus are characterized by raised, red, scaling plaques with follicular plugging, telangiectasia, and central atrophy.
Facial plaques typically assume a distinctive
butterfly pattern.
In systemic lupus, however, the rash may
vary in severity from malar erythema to discoid
lesions. Unlike discoid lupus, systemic lupus affects multiple body systems. It may produce
photosensitivity, weight loss, fatigue, lymphadenopathy, arthritis, emotional lability, and
other signs and symptoms.
◆ Myotonic dystrophy. Premature baldness
characterizes the adult form of this muscular
dystrophy. However, myotonia—the inability to
normally relax a muscle after its contraction—is
its primary sign. Associated signs include muscle wasting and cataracts.
◆ Protein deficiency. Protein deficiency pro-
duces brittle, fine, dry, and thinning hair and,
occasionally, changes in its pigment. Characteristic muscle wasting may be accompanied by
edema, hepatomegaly, apathy, irritability,
anorexia, diarrhea, and dry, flaky skin.
◆ Sarcoidosis. Sarcoidosis may produce scar-
ring alopecia if it infiltrates the scalp. Accompanied by various lesions on the face and the oral
and nasal mucosa, it may also produce fever,
weight loss, fatigue, lymphadenopathy,
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substernal pain, cough, shortness of breath,
visual muscle weakness, arthralgia, myalgia,
and cranial nerve palsies.
◆ Scleroderma (progressive systemic sclero-
sis). A late sign in scleroderma, permanent
alopecia is accompanied by thickening and
tightening of the skin, especially on the arms
and hands. The skin appears taut and shiny and
loses its pigment. Other findings include dysphagia, dyspepsia, abdominal pain, altered
bowel habits, cough, dyspnea, and signs of renal failure.
◆ Seborrheic dermatitis. Erupting in areas
with many sebaceous glands and in skin folds,
seborrheic dermatitis may produce hair loss on
the scalp. Alopecia begins at the vertex and
frontal areas and may spread to other scalp areas. The patient’s skin is reddened and dry with
branlike scales that flake off easily. Pruritus is
common.
◆ Skin metastasis. Occasionally, cancer from
an internal site, such as the lung, metastasizes
to the skin, causing scarring alopecia that may
develop slowly along with scalp induration and
atrophy. Related findings include weight loss,
fever, altered bowel habits, abdominal pain, and
lymphadenopathy.
◆ Syphilis, secondary. This sexually transmit-
ted disease produces temporary, patchy hair
loss that gives the scalp and beard a “motheaten” appearance. It also produces loss of eyelashes and eyebrows and a pruritic rash. Associated signs and symptoms include slight fever,
weight loss, sore throat, malaise, anorexia, lymphadenopathy, nausea, vomiting, headache, a
maculopapular rash, and condyloma latum.
◆ Thyrotoxicosis. Diffuse hair loss, possibly
accentuated at the temples, occurs in this disorder. Hair becomes fine, soft, and friable. The
skin becomes uniformly flushed and thickened,
marked by red, raised, pruritic patches. Characteristically, this disorder produces fine tremors,
nervousness, an enlarged thyroid, sweating,
heat intolerance, amenorrhea, palpitations,
weight loss despite increased appetite, diarrhea,
and possibly exophthalmos.
O
THER CAUSES
◆ Drugs. Chemotherapeutic agents—such as
bleomycin, cyclophosphamide, dactinomycin,
daunorubicin, doxorubicin, fluorouracil, and
methotrexate—may cause patchy, reversible
alopecia a few weeks after administration. Hair
loss is usually limited to the scalp, but with
long-term chemotherapy, it may also affect the
axillae, arms, legs, face, and pubic area. New
hair—which may differ in thickness, texture,
and color from the patient’s original hair—may
begin to grow after the drug is discontinued or
between successive treatments.
Other common drugs may cause diffuse hair
loss on the scalp a few weeks after administration. These include allopurinol, antithyroid
drugs, beta-adrenergic blockers, carbamazepine, gentamicin, heparin, hormonal contraceptives, indomethacin, lithium, trimethadione, valproic acid, excessive doses of
vitamin A, and warfarin. Hair growth usually
resumes when these drugs are discontinued.
◆ Radiation therapy. Like certain drugs, radia-
tion therapy produces temporary reversible hair
loss a few weeks after exposure. Because Xrays damage hair follicles at the site of therapy,
head or scalp X-rays cause the most obvious
hair loss.
◆ Thallium poisoning. Thallium poisoning
produces diffuse but temporary hair loss on the
scalp. Nausea and vomiting are also common.
In acute poisoning, the patient may experience
arm and leg pain, bilateral ptosis, ataxia, fever,
nasal congestion, conjunctival injection, and
abdominal pain. In chronic poisoning, he may
experience translucent, thin, and shiny skin
and signs of renal damage such as oliguria.
S
PECIAL CONSIDERATIONS
Alopecia can have a devastating impact on the
patient’s self-image, especially if it’s extensive
and occurs suddenly, as with chemotherapeutic
drugs. Make sure you explain to the patient that
this hair loss is reversible. Occasionally, scalp
hypothermia methods—such as a cryogen, an
ice-filled cap, or a scalp tourniquet—may be
used before, during, and after drug administration to cause scalp vasoconstriction, thus decreasing drug delivery to the hair follicles and
minimizing hair loss. However, these methods
are contraindicated in patients with circulating
malignant cancer cells (for example, patients
with lymphoma) or scalp metastases.
A skin biopsy may be performed to determine
the cause of the alopecia, especially if skin
changes are evident. Microscopic examination
of a plucked hair may also aid diagnosis.
For patients with partial baldness or alopecia
areata, topical application of minoxidil (a common antihypertensive that also produces hair
growth) for several months stimulates localized
hair growth. However, hair loss may recur if the
drug is discontinued.
P
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EDIATRIC POINTERS
Alopecia normally occurs during the first
6 months of life, as either a sudden, diffuse hair
loss or a gradual thinning that’s hardly noticeable. Reassure the infant’s parents that this hair
loss is normal and temporary. If bald areas result because the infant is left in one position for
too long, advise the parents to change his position regularly.
Common causes of alopecia in children in-
clude use of chemotherapy or radiation therapy, seborrheic dermatitis (known as cradle
cap), follicular mucinosis, tinea capitis, and
hypopituitarism. Tinea capitis may produce a
kerion lesion—a boggy, raised, tender, and
hairless lesion. Trichotillomania, a psychological disorder more common in children than
adults, may produce patchy baldness with
stubby hair growth due to habitual hair
pulling. Other causes include progeria and
congenital hair shaft defects such as trichorrhexis nodosa.
P
ATIENT COUNSELING
Encourage gentle hair care to avoid further hair
loss. Also, suggest wearing a wig, cap, or scarf,
if appropriate. Remind the patient to cover his
head in cold weather to prevent loss of body
heat. Encourage patients who are frequently exposed to the sun to use sunblock to decrease
the risk of skin cancer.
Amenorrhea
The absence of menstrual flow, amenorrhea can
be classified as primary or secondary. In primary
amenorrhea, menstruation fails to begin before
age 16. In secondary amenorrhea, it begins at
an appropriate age but later ceases for 3 or
more months in the absence of normal physiologic causes, such as pregnancy, lactation, or
menopause.
Pathologic amenorrhea results from anovulation or physical obstruction of menstrual outflow, such as from an imperforate hymen, cervical stenosis, or intrauterine adhesions.
Anovulation itself may result from hormonal
imbalance, debilitating disease, stress or emotional disturbances, strenuous exercise, malnutrition, obesity, or anatomic abnormalities, such
as congenital absence of the ovaries or uterus.
Amenorrhea may also result from drug or hormonal treatments. (See How amenorrhea devel-
ops, pages 36 and 37.)
AMENORRHEA
H
ISTORY AND PHYSICAL
35
EXAMINATION
Begin by determining whether the amenorrhea is
primary or secondary. If it’s primary, ask the patient at what age her mother first menstruated because age of menarche is fairly consistent in families. Form an overall impression of the patient’s
physical, mental, and emotional development because these factors as well as heredity and climate may delay menarche until after age 16.
If menstruation began at an appropriate age
but has since ceased, determine the frequency
and duration of the patient’s previous menstrual
cycles. Ask her about the onset and nature of
any changes in her normal menstrual pattern,
and determine the date of her last menses. Find
out if she has noticed any related signs, such as
breast swelling or weight changes.
Determine when the patient last had a physical examination. Review her health history, noting especially any long-term illnesses, such as
anemia, or use of hormonal contraceptives. Ask
about exercise habits, especially running, and
whether she experiences stress on the job or at
home. Probe the patient’s eating habits, including number and size of daily meals and snacks,
and ask if she has gained weight recently.
Observe her appearance for secondary sex
characteristics or signs of virilization. If you’re
responsible for performing a pelvic examination, check for anatomic aberrations of the outflow tract, such as cervical adhesions, fibroids,
or an imperforate hymen.
M
EDICAL CAUSES
◆ Adrenal tumor. Amenorrhea may be ac-
companied by acne, thinning scalp hair, hirsutism, increased blood pressure, truncal obesity, and psychotic changes. Asymmetrical
ovarian enlargement in conjunction with rapid
onset of virilizing signs is usually indicative.
◆ Adrenocortical hyperplasia. Amenorrhea
precedes characteristic cushingoid signs, such
as truncal obesity, moon face, buffalo hump,
bruises, purple striae, hypertension, renal calculi, psychiatric disturbances, and widened
pulse pressure. Acne, thinning scalp hair, and
hirsutism also typically appear.
◆ Adrenocortical hypofunction. Besides
amenorrhea, adrenocortical hypofunction may
cause fatigue, irritability, weight loss, increased
pigmentation (including bluish black discoloration of the areolas and mucous membranes
of the lips, mouth, rectum, and vagina), nausea,
vomiting, and orthostatic hypotension.
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How amenorrhea develops
A disruption at any point in the menstrual cycle can produce amenorrhea, as illustrated in
the flowchart below.
Hypothalamus secretes gonadotropin-
releasing hormone (GnRH).
GnRH secretion can be
inhibited by:
◆ pseudocyesis
◆ Kallmann syndrome
◆ hypothalamic tumor
◆ stress or exercise.
Low progesterone
and estrogen levels
stimulate the
hypothalamus.
Hormonal regulation
may be disrupted by:
◆ adrenal disorders
◆ excessive production
of corticotropin or
prolactin
◆ thyroid disorders.
Anterior pituitary increases follicle-
stimulating hormone (FSH) and luteinizing
hormone (LH) production.
Ovaries secrete estrogen.
Rising estrogen levels at midcycle stimulate
anterior pituitary to increase LH and FSH production.
Ovulation occurs.
Corpus luteum develops and secretes
estrogen and progesterone.
Corpus luteum recedes, which decreases
estrogen and progesterone secretion.
◆ Amenorrhea-lactation disorders. Amenor-
rhea-lactation disorders, such as ForbesAlbright and Chiari-Frommel syndromes, produce secondary amenorrhea accompanied by
lactation in the absence of breast-feeding. Associated features include hot flashes, dyspareunia,
vaginal atrophy, and large, engorged breasts.
◆ Anorexia nervosa. Anorexia nervosa is a
psychological disorder that can cause either primary or secondary amenorrhea. Related findings include significant weight loss, a thin or
emaciated appearance, compulsive behavior
patterns, blotchy or sallow complexion, constipation, reduced libido, decreased pleasure in
once-enjoyable activities, dry skin, loss of scalp
hair, lanugo on the face and arms, skeletal muscle atrophy, and sleep disturbances.
◆ Congenital absence of the ovaries. Con-
genital absence of the ovaries results in primary
amenorrhea and absence of secondary sex
characteristics.
◆ Congenital absence of the uterus. Primary
amenorrhea occurs with congenital absence of
the uterus. The patient also may fail to develop
breasts.
◆ Corpus luteum cysts. Corpus luteum cysts
may cause sudden amenorrhea as well as acute
abdominal pain and breast swelling. Examina-
Pituitary disease or tumor
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can disrupt production of
FSH and LH.
Anovulation may result
from:
◆ Turner’s syndrome
◆ ovarian insensitivity to
gonadotropins.
Endometrium
proliferates.
AMENORRHEA
Normal uterine changes
may be inhibited by:
◆ absence of uterus
◆ uterine hypoplasia
◆ uterine scarring
◆ radiation therapy.
37
Endometrium
Menstrual flow may be
obstructed by:
◆ endometrial scarring
◆ cervical stenosis
◆ congenital defects.
Menstruation
hypertrophies.
Endometrium sloughs.
tion may reveal a tender adnexal mass and
vaginal and cervical hyperemia.
◆ Hypothalamic tumor. In addition to amen-
orrhea, a hypothalamic tumor can cause endocrine and visual field defects, gonadal underdevelopment or dysfunction, and short stature.
◆ Hypothyroidism. Deficient thyroid hormone
levels can cause primary or secondary amenorrhea. Typically vague, early findings include fatigue, forgetfulness, cold intolerance, unexplained
weight gain, and constipation. Subsequent signs
include bradycardia; decreased mental acuity;
dry, flaky, inelastic skin; puffy face, hands, and
feet; hoarseness; periorbital edema; ptosis; dry,
sparse hair; and thick, brittle nails. Other common findings include anorexia, abdominal distention, decreased libido, ataxia, intention
tremor, nystagmus, and delayed reflex relaxation
time, especially in the Achilles tendon.
◆ Mosaicism. Mosaicism is a genetic disorder
that results in primary amenorrhea and absence
of secondary sex characteristics.
◆ Ovarian insensitivity to gonadotropins.
Ovarian insensitivity to gonadotropins is a hormonal disturbance that leads to amenorrhea
and absence of secondary sex characteristics.
◆ Pituitary infarction. Pituitary infarction usu-
ally causes postpartum failure to lactate and to
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resume menses. Although associated signs and
symptoms depend on the infarction’s severity,
they include headaches, visual field defects,
oculomotor palsies, and an altered level of consciousness. The patient may also lose pubic and
axillary hair.
◆ Pituitary tumor. Amenorrhea may be the
first sign of a pituitary tumor. Associated findings include headache, visual disturbances such
as bitemporal hemianopia, and acromegaly.
Cushingoid signs include moon face, buffalo
hump, hirsutism, hypertension, truncal obesity,
bruises, purple striae, widened pulse pressure,
and psychiatric disturbances.
◆ Polycystic ovary syndrome. Typically,
menarche occurs at a normal age, followed by
irregular menstrual cycles, oligomenorrhea, and
secondary amenorrhea. Alternatively, periods of
profuse bleeding may alternate with periods of
amenorrhea. Obesity, hirsutism, slight deepening of the voice, and enlarged, “oysterlike”
ovaries may also accompany polycystic ovary
syndrome.
◆ Pseudoamenorrhea. An anatomic anomaly,
such as imperforate hymen, obstructs menstrual
flow, causing primary amenorrhea and, possibly,
cyclic episodes of abdominal pain. Examination
may reveal a pink or blue bulging hymen.
◆ Pseudocyesis. In pseudocyesis, amenorrhea
may be accompanied by lordosis, abdominal
distention, nausea, and breast enlargement.
◆ Sertoli-Leydig cell tumor. Sertoli-Leydig
cell tumor is an ovarian tumor that may produce amenorrhea along with acne, hirsutism,
deepening of the voice, balding, muscle mass
development, and clitoral enlargement.
◆ Testicular feminization. Primary amenor-
rhea may signal this form of male pseudohermaphroditism. The patient, outwardly female
but genetically male, exhibits breasts and external genitalia but scant or absent pubic hair.
◆ Thyrotoxicosis. Thyroid hormone overproduc-
tion may result in amenorrhea. Classic signs and
symptoms include an enlarged thyroid (goiter),
nervousness, heat intolerance, diaphoresis,
tremors, palpitations, tachycardia, dyspnea, weakness, and weight loss despite increased appetite.
◆ Turner’s syndrome. Primary amenorrhea
and failure to develop secondary sex characteristics may signal this syndrome of genetic ovarian dysgenesis. Typical features include short
stature, webbing of the neck, low nuchal hairline, a broad chest with widely spaced nipples
and poor breast development, underdeveloped
genitalia, and edema of the legs and feet.
◆ Uterine hypoplasia. Primary amenorrhea
results from underdevelopment of the uterus,
which is detectable on physical examination.
O
THER CAUSES
◆ Drugs. Busulfan, chlorambucil, injectable or
implanted contraceptives, cyclophosphamide,
and phenothiazines may cause amenorrhea.
Hormonal contraceptives may cause anovulation and amenorrhea after they’re discontinued.
◆ Radiation therapy. Irradiation of the ab-
domen may destroy the endometrium
or ovaries, causing amenorrhea.
◆ Surgery. Surgical removal of both ovaries or
the uterus produces amenorrhea.
S
PECIAL CONSIDERATIONS
In patients with secondary amenorrhea, physical and pelvic examinations must rule out pregnancy before diagnostic testing begins. Typical
tests include progestin withdrawal, serum hormone and thyroid function studies, and endometrial biopsy.
P
EDIATRIC POINTERS
Adolescent girls are especially prone to amenorrhea caused by emotional upsets, typically stemming from school, social, or family problems.
G
ERIATRIC POINTERS
In women older than age 50, amenorrhea usually represents the onset of menopause.
P
ATIENT COUNSELING
After diagnosis, answer the patient’s questions
about the type of treatment that will be provided
and its expected outcome. Because amenorrhea
can cause severe emotional distress, provide
emotional support. Be sure to encourage the
patient to discuss her fears and, if necessary, refer her for psychological counseling.
Amnesia
Amnesia—a disturbance in, or loss of,
memory—may be classified as partial or complete and as anterograde or retrograde. Anterograde amnesia denotes memory loss for
events that occurred after the onset of the
causative trauma or disease; retrograde amnesia, for events that occurred before the onset.
Depending on the cause, amnesia may arise
suddenly or slowly and may be temporary or
permanent.
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39
Organic (or true) amnesia results from temporal lobe dysfunction, and it characteristically
spares patches of memory. A common symptom
in patients with seizures or head trauma, organic amnesia can also be an early indicator of
Alzheimer’s disease. Hysterical amnesia has a
psychogenic origin and characteristically causes
complete memory loss. Treatment-induced amnesia is usually transient.
H
ISTORY AND PHYSICAL
EXAMINATION
Because the patient often isn’t aware of his amnesia, you’ll usually need help in gathering information from his family or friends. Throughout your assessment, notice the patient’s
general appearance, behavior, mood, and train
of thought. Ask when the amnesia first appeared and what types of things the patient is
unable to remember. Can he learn new information? How long does he remember it? Does
the amnesia encompass a recent or a remote
period?
Test the patient’s recent memory by asking
him to identify and repeat three items. Retest
him after 3 minutes. Test his intermediate memory by asking, “Who was the president before
this one?” and “What was the last type of car
you bought?” Test remote memory with such
questions as “How old are you?” and “Where
were you born?”
Take the patient’s vital signs and assess his
level of consciousness (LOC). Check his pupils:
They should be equal in size and should
constrict quickly when exposed to direct light.
Also, assess his extraocular movements. Test
motor function by having the patient move his
arms and legs through their range of motion.
Evaluate sensory function with pinpricks on the
patient’s skin. (See Amnesia: Causes and associated findings, page 40.)
M
EDICAL CAUSES
◆ Alzheimer’s disease. Alzheimer’s disease
usually begins with retrograde amnesia, which
progresses slowly over many months or years to
include anterograde amnesia and, eventually,
severe and permanent memory loss. Associated
findings include agitation, inability to concentrate, disregard for personal hygiene, confusion,
irritability, and emotional lability. Later signs include aphasia, incontinence, and muscle rigidity.
◆ Cerebral hypoxia. After recovery from hy-
poxia (brought on by such conditions as carbon
monoxide poisoning or acute respiratory fail-
ure), the patient may experience total amnesia
for the event along with sensory disturbances
such as numbness and tingling.
◆ Head trauma. Depending on the trauma’s
severity, amnesia may last for minutes, hours,
or longer. Usually, the patient experiences brief
retrograde and longer anterograde amnesia as
well as persistent amnesia about the traumatic
event. Severe head trauma can cause permanent amnesia or difficulty retaining recent memories. Related findings may include altered respirations and LOC; headache; dizziness;
confusion; visual disturbances, such as blurred
or double vision; and motor and sensory disturbances, such as hemiparesis and paresthesia,
on the side of the body opposite the injury.
◆ Herpes simplex encephalitis. Recovery
from herpes simplex encephalitis commonly
leaves the patient with severe and possibly permanent amnesia. Associated findings include
signs and symptoms of meningeal irritation,
such as headache, fever, and altered LOC;
seizures; and various motor and sensory disturbances, such as paresis, numbness, and tingling.
◆ Hysteria. Hysterical amnesia, a complete
and long-lasting memory loss, begins and
ends abruptly and is typically accompanied by
confusion.
◆ Seizures. In temporal lobe seizures, amnesia
occurs suddenly and lasts for several seconds to
minutes. The patient may recall an aura or
nothing at all. An irritable focus on the left side
of the brain primarily causes amnesia for verbal
memories, whereas an irritable focus on the
right side of the brain causes graphic and nonverbal amnesia. Associated signs and symptoms may include decreased LOC during the
seizure, confusion, abnormal mouth movements, and visual, olfactory, and auditory hallucinations.
◆ Vertebrobasilar circulatory disorders. Ver-
tebrobasilar ischemia, infarction, embolus, or
hemorrhage may cause complete amnesia that
begins abruptly, lasts for several hours, and
ends abruptly. Associated findings include dizziness, decreased LOC, ataxia, blurred or double
vision, vertigo, nausea, and vomiting.
◆ Wernicke-Korsakoff syndrome. Retrograde
and anterograde amnesia can become permanent without treatment in Wernicke-Korsakoff
syndrome. Accompanying signs and symptoms
include apathy, an inability to concentrate or to
put events into sequence, and confabulation to
fill memory gaps. The syndrome may also cause
40 AMNESIA
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SIGNS & SYMPTOMS
Amnesia: Causes and associated findings
Common
causes
Alzheimer’s
disease
Major associated signs and symptoms
Agitation
Ataxia
Confusion
Decreased level of
consciousness
Diplopia
Dizziness
Emotional lability
Headache
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Nausea
Paresthesia
Vertigo
Visual blurring
Vomiting
Cerebral hypoxia
Head trauma
Herpes simplex
encephalitis
Hysteria
Seizures
Vertebrobasilar
circulatory
disorders
Wernicke-Korsakoff
syndrome
diplopia, decreased LOC, headache, ataxia, and
symptoms of peripheral neuropathy such as
numbness and tingling.
O
THER CAUSES
◆ Drugs. Anterograde amnesia can be precipi-
tated by general anesthetics, especially fentanyl
and isoflurane; barbiturates, most commonly
pentobarbital; and certain benzodiazepines,
especially triazolam.
◆ Electroconvulsive therapy. Sudden onset of
retrograde or anterograde amnesia occurs with
electroconvulsive therapy. Typically, the amnesia
lasts for several minutes to several hours, but
severe, prolonged amnesia occurs with treatments given frequently over a prolonged period.
◆ Temporal lobe surgery. Usually performed
on only one lobe, this surgery causes brief, mild
amnesia. However, removal of both lobes results in permanent amnesia.
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PECIAL CONSIDERATIONS
Prepare the patient for diagnostic tests, such as
computed tomography scan, magnetic resonance
imaging, EEG, or cerebral angiography.
Provide reality orientation for the patient with
retrograde amnesia, and encourage his family
to help by supplying familiar photos, objects,
and music.
Adjust your patient-teaching techniques for
the patient with anterograde amnesia because
he can’t acquire new information. Include his
family in teaching sessions. In addition, write
down all instructions—particularly medication
dosages and schedules—so the patient won’t
have to rely on his memory.
If the patient has severe amnesia, consider
his basic needs, such as safety, elimination, and
nutrition. If necessary, arrange for placement in
an extended-care facility.
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