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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2920_Библиотеки_им_академика_М_И_Перельмана
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Kernig’s sign
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Lymphadenopathy
Malaise
Muscle spasms
Nuchal rigidity
Paralysis
Paresthesia
Swelling
Tenderness
Weakness
NIGHT BLINDNESS
481
Night blindness
[Nyctalopia]
Often difficult to identify, night blindness refers
to impaired vision in the dark, especially after
entering a darkened room or while driving at
night. A symptom of choroidal and retinal degeneration, night blindness occurs in various
ocular disorders and as an early indicator of vitamin A deficiency. In some patients, however,
night blindness occurs without underlying
pathology, simply reflecting poor adaptation to
the dark. In these patients, it’s commonly accompanied by myopia.
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(continued)
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient complains of difficulty seeing at
night, ask when he first noticed the problem. Is
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it intermittent or steadily worsening? Is it worse
at certain times or in certain conditions? Also,
ask about other ocular symptoms, such as eye
pain, blurred or halo vision, floaters or spots,
and photophobia.
Explore any history of glaucoma, cataracts,
and familial degeneration of vision. If no ocular
problems are apparent, briefly evaluate the patient’s nutritional status for vitamin A deficiency.
Examine the eyes for ptosis, abnormal tearing, discharge, and conjunctival injection. Test
visual acuity and visual fields in both eyes and,
if trained and equipped, measure intraocular
pressure. Check pupillary response, and evaluate extraocular muscle function by testing the
six cardinal fields of gaze.
M
EDICAL CAUSES
◆ Cataracts. Night blindness and halo vision
occur early in senile-type cataract formation. As
the cataract matures, it causes gradual, painless
visual blurring and vision loss, sometimes with
visible lens opacity.
◆ Choroidal dystrophies. Night blindness and
decreased peripheral vision may occur early in
choroidal dystrophies. Disease progression
causes loss of central vision.
◆ Fundus albipunctatus. Night blindness is
the chief complaint in this retinal and choroidal
disease. Multiple small, round, yellow-white
dots are present on the retina.
◆ Fundus flavimaculatus. With this disease,
night blindness may be pronounced or may be
an incidental finding. Irregular yellow or white
lesions appear deep in the retina.
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Neck pain: Causes and associated findings (continued)
Major associated signs and symptoms
Common
causes
Rheumatoid
arthritis
Spinous process
fracture
Subarachnoid
hemorrhage
Thyroid trauma
Torticollis
Tracheal trauma
◆ Glaucoma. Night blindness occurs late in
chronic open-angle glaucoma, with halo vision,
gradually impaired bilateral visual acuity, loss of
peripheral vision and, possibly, slight eye pain.
◆ Goldman-Favre dystrophy. With this disor-
der, night blindness is usually the chief complaint. The retina resembles that seen in retinitis
pigmentosa.
◆ Oguchi’s disease. This rare, hereditary reti-
nal and choroidal degeneration produces night
blindness and a retina with a yellowish metallic
sheen.
◆ Optic nerve atrophy. This disorder may
cause night blindness, visual field and color vision defects, and decreased visual acuity. Pupillary reactions are sluggish, and optic disk pallor
is evident.
◆ Retinitis pigmentosa. In this usually heredi-
tary retinal degeneration, night blindness is
characteristically the first symptom, usually arising in adolescence. Scattered black pigmentary
bodies form in a characteristic “bone-spicule”
arrangement on the retina. As the disease progresses, the visual field gradually constricts,
causing tunnel or “gun barrel” vision and eventually total blindness.
Arm pain
Back pain
Brudzinski’s sign
Decreased level of
consciousness
••
Decreased range
of motion
Deformity
Dysphagia
Dyspnea
Ecchymoses
Fatigue
Fever
Headache
Hemoptysis
•• ••
••
•
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•• •
◆ Vitamin A deficiency. Night blindness is typ-
ically the first symptom of vitamin A deficiency.
Associated findings include xerophthalmia (conjunctival dryness) and Bitot’s spots (gray-white
conjunctival plaques). The patient may complain of visual blurring or vision loss. His skin
may be dry and scaly. His mucous membranes
may be shrunken and hardened.
O
THER CAUSES
◆ Drugs. Isotretinoin, used to treat inflamma-
tory acne, rarely causes night blindness.
S
PECIAL CONSIDERATIONS
Because any visual impairment is frightening to
the patient, provide emotional support. Help decrease his anxiety and enhance cooperation by
explaining scheduled diagnostic tests such as
electroretinography in simple terms. Make sure
the patient is safe; explain that he shouldn’t drive and that he should use assistive devices at
night or in darkened or dim lighting as necessary.
P
EDIATRIC POINTERS
Because children generally don’t have adequate
body reserves of vitamin A, they’re especially
Hoarseness
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Kernig’s sign
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Lymphadenopathy
Malaise
Muscle spasms
Nuchal rigidity
Paralysis
Paresthesia
Swelling
Tenderness
Weakness
•••••
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prone to deficiency and resulting night blindness.
G
ERIATRIC POINTERS
Night blindness due to vitamin A deficiency usually occurs in elderly and disadvantaged patients. It’s also a common effect of aging.
Nipple discharge
Nipple discharge can occur spontaneously or
can be elicited by nipple stimulation. It’s characterized as intermittent or constant, unilateral or
bilateral, and by color, consistency, and composition. Its incidence increases with age and parity. This sign rarely occurs (but is more likely to
be pathologic) in men and in nulligravid, regularly menstruating women. It’s relatively common and often normal in parous women. A
thick, grayish discharge—benign epithelial debris from inactive ducts—can often be elicited in
middle-age parous women. Colostrum, a thin,
yellowish or milky discharge, often occurs in the
last weeks of pregnancy.
Nipple discharge can signal serious underly-
ing disease, particularly when accompanied by
NIPPLE DISCHARGE
other breast changes. Significant causes include
endocrine disorders, cancer, certain drugs, and
blocked lactiferous ducts.
H
ISTORY AND PHYSICAL
483
EXAMINATION
Ask the patient when she first noticed the discharge, and determine its duration, extent,
quantity, color, consistency, and smell, if any.
Has she had other nipple and breast changes,
such as pain, tenderness, itching, warmth,
changes in contour, and lumps? If she reports a
lump, question her about its onset, location,
size, and consistency.
Obtain a complete gynecologic and obstetric
history, and determine her normal menstrual
cycle and the date of her last menses. Ask if she
experiences breast swelling and tenderness,
bloating, irritability, headaches, abdominal
cramping, nausea, or diarrhea before or during
menses. Note the number, date, and outcome of
her pregnancies and, if she breast-fed, the approximate time of her last lactation. Also, check
for any risk factors of breast cancer—family history, previous or current malignancies, nulliparity or first pregnancy after age 30, early menarche, or late menopause.
Start your physical examination by characterizing the discharge. If the discharge isn’t frank,
try to elicit it. (See Eliciting nipple discharge,
page 484.) Then examine the nipples and
breasts with the patient in four different positions: sitting with her arms at her sides; with her
arms overhead; and with her hands pressing on
her hips; and leaning forward so her breasts are
suspended. Check for nipple deviation, flattening, retraction, redness, asymmetry, thickening,
excoriation, erosion, or cracking. Inspect her
breasts for asymmetry, irregular contours, dimpling, erythema, and peau d’orange. With the
patient in a supine position, palpate the breasts
and axillae for lumps, giving special attention to
the areolae. Note the size, location, delineation,
consistency, and mobility of any lump you find.
Is the patient taking hormones (hormonal
contraceptives or hormone replacement therapy)? Is the discharge spontaneous, or does it
have to be expressed?
M
EDICAL CAUSES
◆ Breast abscess. This disorder, most com-
mon in breast-feeding women, may produce a
thick, purulent discharge from a cracked nipple
or infected duct. Associated findings include
abrupt onset of high fever with chills; breast
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Eliciting nipple
discharge
If your patient has a history or evidence of
nipple discharge, you can attempt to elicit it
during your examination. Help the patient
into a supine position, and gently squeeze
her nipple between your thumb and index
finger; note any discharge through the nipple. Then place your fingers on the areola,
as shown, and palpate the entire areolar
surface, watching for any discharge through
areolar ducts.
pain, tenderness, and erythema; a palpable soft
nodule or generalized induration; and possibly,
nipple retraction.
◆ Breast cancer. This may cause bloody, wa-
tery, or purulent discharge from a normal-appearing nipple. Characteristic findings include a
hard, irregular, fixed lump; erythema; dimpling;
peau d’orange; changes in contour; nipple deviation, flattening, or retraction; axillary lymphadenopathy; and possibly, breast pain.
◆ Choriocarcinoma. Galactorrhea (a white or
grayish milky discharge) may result from this
highly malignant neoplasm, which can follow
pregnancy. Other characteristics include persistent uterine bleeding and bogginess after delivery or curettage, and vaginal masses.
◆ Herpes zoster. This virus can stimulate the
thoracic nerves, causing bilateral, spontaneous,
intermittent galactorrhea. Other characteristics
include shooting or burning pain, eruption of
small red nodules or vesicles on the thorax and
possibly the arms and legs, pruritus and paresthesia or hyperesthesia in affected areas,
headache, and fever and malaise.
◆ Hypothyroidism. This disorder occasionally
causes galactorrhea. Related findings include
bradycardia; weight gain despite anorexia; decreased mentation; periorbital edema; menorrhagia; constipation; puffy face, hands, and feet;
brittle, sparse hair; and dry, doughy, pale, cool
skin.
◆ Intraductal papilloma. This disorder is the
primary cause of nipple discharge in the nonpregnant, non–breast-feeding woman. Unilateral serous, serosanguineous, or bloody nipple
discharge—usually from only one duct—is its
predominant sign. Discharge may be intermittent or profuse and constant, and can often be
stimulated by gentle pressure around the areola. Subareolar nodules, breast pain, and tenderness may occur.
◆ Mammary duct ectasia. A thick, sticky,
grayish discharge from multiple ducts may be
the first sign of this disorder. The discharge may
be bilateral and is usually spontaneous. Other
findings include a rubbery, poorly delineated
lump beneath the areola, with a blue-green discoloration of the overlying skin; nipple retraction; and redness, swelling, tenderness, and
burning pain in the areola and nipple.
◆ Paget’s disease. With this disorder, serous or
bloody discharge emits from denuded skin on
the nipple, which is red, intensely itchy and,
possibly, eroded or excoriated. The discharge is
usually unilateral.
◆ Prolactin-secreting pituitary tumor. Bilat-
eral galactorrhea may occur with this tumor.
Other findings include amenorrhea, infertility,
decreased libido and vaginal secretions,
headaches, and blindness.
◆ Proliferative (fibrocystic) breast disease.
This benign disorder occasionally causes a bilateral clear, milky, or straw-colored discharge,
which is rarely purulent or bloody. Multiple
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485
round, soft, tender nodules are usually palpable
in both breasts, although they may occur singly.
Usually, nodules are mobile and are located in
the upper outer quadrant. Nodule size, tenderness, and discharge increase during the luteal
phase of the menstrual cycle. Symptoms then
regress after menses.
◆ Trauma. Bilateral galactorrhea can result
from trauma to the breasts.
O
THER CAUSES
◆ Drugs. Galactorrhea can be caused by psy-
chotropic agents, particularly phenothiazines
and tricyclic antidepressants; some antihypertensives (reserpine and methyldopa); hormonal
contraceptives; cimetidine; metoclopramide;
and verapamil.
◆ Surgery. Chest wall surgery may stimulate
the thoracic nerves, causing intermittent bilateral galactorrhea.
S
PECIAL CONSIDERATIONS
Although nipple discharge is usually insignificant, it can be frightening to the patient. Help
relieve the patient’s anxieties by clearly explaining the nature and origin of her discharge. Apply a breast binder, which may reduce discharge
by eliminating nipple stimulation.
Diagnostic tests may include tissue biopsy (if
a breast lump is found), cytologic study of the
discharge, mammography, ultrasonography,
transillumination, and serum prolactin.
P
EDIATRIC POINTERS
Nipple discharge in children and adolescents is
rare. When it does occur, it’s almost always
nonpathologic, as in the bloody discharge that
sometimes accompanies onset of menarche. Infants of both sexes may experience a milky
breast discharge beginning 3 days after birth
and lasting up to 2 weeks due to maternal hormonal influences.
perform breast self-examinations and maintain
appointments for breast examinations by a
physician and mammograms as recommended.
Nipple retraction
Nipple retraction, the inward displacement of
the nipple below the level of surrounding breast
tissue, may indicate an inflammatory breast lesion or cancer. It results from scar tissue formation within a lesion or large mammary duct. As
the scar tissue shortens, it pulls adjacent tissue
inward, causing nipple deviation, flattening, and
finally, retraction.
H
ISTORY AND PHYSICAL
EXAMINATION
Ask the patient when she first noticed retraction
of the nipple. Has she experienced other nipple
changes, such as itching, discoloration, discharge, or excoriation? Has she noticed breast
pain, lumps, redness, swelling, or warmth? Obtain a history, noting risk factors of breast cancer, such as a family history or previous malignancy.
Carefully examine both nipples and breasts
with the patient sitting upright with her arms at
her sides, with her hands pressing on her hips,
and with her arms overhead; and with the patient leaning forward so her breasts hang. Look
for redness, excoriation, and discharge; nipple
flattening and deviation; and breast asymmetry,
dimpling, or contour differences. (See Differenti-
ating nipple retraction from inversion, page 486.)
Try to evert the nipple by gently squeezing
the areola. With the patient in a supine position,
palpate both breasts for lumps, especially beneath the areola. Mold breast skin over the
lump or gently pull it up toward the clavicle,
looking for accentuated nipple retraction. Also,
palpate axillary lymph nodes.
G
ERIATRIC POINTERS
In postmenopausal women, breast changes are
considered malignant until proven otherwise.
P
ATIENT COUNSELING
Counsel your patient to be aware of discharge
characteristics—its consistency (thick or thinning), odor, origin in single or multiple ducts,
and relation to the menstrual cycle. If the discharge becomes bloody, instruct the patient to
seek medical evaluation. Instruct the patient to
M
EDICAL CAUSES
◆ Breast abscess. This disorder, most com-
mon in breast-feeding women, occasionally
produces unilateral nipple retraction. More
common findings include high fever with chills;
breast pain, erythema, and tenderness; breast
induration or soft mass; and cracked, sore nipples, possibly with purulent discharge.
◆ Breast cancer. Unilateral nipple retraction is
commonly accompanied by a hard, fixed, nontender nodule beneath the areola, as well as
486 NOCTURIA
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Differentiating nipple retraction from inversion
Nipple retraction is sometimes confused with nipple inversion, a common abnormality that’s congenital in many patients and doesn’t usually signal underlying disease. A retracted nipple appears
flat and broad, whereas an inverted nipple can be pulled out from the sulcus where it hides.
NIPPLE RETRACTION NIPPLE INVERSION
other breast nodules. Other nipple changes include itching, burning, erosion, and watery or
bloody discharge. Breast changes commonly include dimpling, altered contour, peau d’orange,
ulceration, tenderness (possibly pain), redness,
and warmth. Axillary lymph nodes may be enlarged.
◆ Mammary duct ectasia. Nipple retraction
commonly occurs along with a poorly defined,
rubbery nodule beneath the areola, with a bluegreen skin discoloration; areolar burning, itching, swelling, tenderness, and erythema; and
nipple pain with a thick, sticky, grayish, multiductal discharge.
◆ Mastitis. Nipple retraction, deviation, crack-
ing, or flattening may occur in this disorder with
a firm and indurated or tender, flocculent, discrete breast nodule, warmth, erythema, tenderness, and edema. Fatigue, high fevers, and chills
may also be present.
O
THER CAUSES
◆ Surgery. Previous breast surgery may cause
underlying scarring and retraction.
S
PECIAL CONSIDERATIONS
Prepare the patient for diagnostic tests, including mammography, cytology of nipple discharge, and biopsy.
P
EDIATRIC POINTERS
Nipple retraction doesn’t occur in prepubescent
females.
P
ATIENT COUNSELING
Teach your patient breast self-examination and
advise her to always seek medical evaluation
for breast changes.
Nocturia
Nocturia—excessive urination at night—may
result from disruption of the normal diurnal
pattern of urine concentration or from overstimulation of the nerves and muscles that control urination. Normally, urine is more concentrated during the night than during the day. As
a result, most persons excrete three to four
times more urine during the day, and can sleep
for 6 to 8 hours during the night without being
awakened. The patient with nocturia may
awaken one or more times during the night to
empty his bladder and excrete 700 ml or more
of urine.
Although nocturia usually results from renal
and lower urinary tract disorders, it may result
from certain cardiovascular, endocrine, and
metabolic disorders. This common sign may
also result from drugs that induce diuresis, particularly when they’re taken at night, and from
the ingestion of large quantities of fluids, especially caffeinated beverages or alcohol, at bedtime.
NOCTURIA
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487
H
ISTORY AND PHYSICAL
EXAMINATION
Begin by exploring the history of the patient’s
nocturia. When did it begin? How often does it
occur? Can the patient identify a specific pattern? Precipitating factors? Also, note the volume of urine voided. Ask the patient about any
change in the color, odor, or consistency of his
urine. Has the patient changed his usual pattern
or volume of fluid intake? Next, explore associated symptoms. Ask about pain or burning on
urination, difficulty initiating a urine stream,
costovertebral angle tenderness, and flank, upper abdominal, or suprapubic pain.
Determine if the patient or his family has a
history of renal or urinary tract disorders or endocrine and metabolic diseases, particularly diabetes. Is the patient taking a drug that increases urine output, such as a diuretic, a cardiac
glycoside, or an antihypertensive?
Focus your physical examination on palpating and percussing the kidneys, the costovertebral angle, and the bladder. Carefully inspect the
urinary meatus. Inspect a urine specimen for
color, odor, and the presence of sediment.
M
EDICAL CAUSES
◆ Benign prostatic hyperplasia. Common in
men older than age 50, this disorder produces
nocturia when significant urethral obstruction
develops. Typically, it causes frequency, hesitancy, incontinence, reduced force and caliber of
the urine stream and, possibly, hematuria. Oliguria may also occur. Palpation reveals a distended bladder and an enlarged prostate. The
patient may also complain of lower abdominal
fullness, perineal pain, and constipation. Obstruction may lead to renal failure.
◆ Bladder neoplasm. A late sign of this neo-
plasm, nocturia involves frequent voiding of
small to moderate amounts of urine. Besides
hematuria, the most common sign, associated
characteristics include bladder distention; urinary frequency and urgency; dysuria; pyuria;
bladder, rectal, flank, back, or leg pain; vomiting; diarrhea; and insomnia. Signs and symptoms of urinary tract infection, such as tenesmus, low-grade fever, and perineal pain, may
also occur.
◆ Cystitis. All three forms of cystitis may cause
nocturia marked by frequent, small voidings
and accompanied by dysuria and tenesmus.
Bacterial cystitis may also cause urinary urgency; hematuria; fatigue; suprapubic, perineal,
flank, and lower back pain; and occasionally,
low-grade fever. Most common in women between ages 25 and 60, chronic interstitial cystitis is characterized by Hunner’s ulcers—small,
punctate, bleeding lesions in the bladder; it also
causes gross hematuria. Because symptoms resemble bladder cancer, this must be ruled out.
Viral cystitis also causes urinary urgency,
hematuria, and fever.
◆ Diabetes insipidus. The result of antidiuret-
ic hormone deficiency, this disorder usually produces nocturia early in its course. It’s characterized by periodic voiding of moderate to large
amounts of urine. Diabetes insipidus can also
produce polydipsia and dehydration.
◆ Diabetes mellitus. An early sign of diabetes
mellitus, nocturia involves frequent, large voidings. Associated features include daytime
polyuria, polydipsia, polyphagia, frequent urinary tract infections, recurrent yeast infections,
vaginitis, weakness, fatigue, weight loss and,
possibly, signs of dehydration, such as dry mucous membranes and poor skin turgor.
◆ Heart failure. Nocturia may develop early in
this disorder—the result of increased glomerular
filtration associated with movement of edematous fluid from dependent areas during recumbency. Other early effects include fatigue, jugular vein distention, dyspnea, orthopnea,
tachycardia, and a dry cough with wheezing.
Later, the patient may develop tachypnea,
weight gain, hypotension, oliguria, cyanosis,
and hepatomegaly.
◆ Hypercalcemic nephropathy. With this dis-
order, nocturia involves the periodic voiding of
moderate to large amounts of urine. Related
findings include daytime polyuria, polydipsia,
and occasionally, hematuria and pyuria.
◆ Hypokalemic nephropathy. Again, nocturia
involves the periodic voiding of moderate to
large amounts of urine. Associated findings typically include polydipsia, daytime polyuria, muscle weakness or paralysis, hypoactive bowel
sounds, and increased susceptibility to
pyelonephritis.
◆ Prostate cancer. The second leading cause
of cancer deaths in men, this disorder is usually
asymptomatic in early stages. Later, it produces
nocturia characterized by infrequent voiding of
moderate amounts of urine. Other characteristic
effects include dysuria (most common symptom), difficulty initiating a urine stream, interrupted urine stream, bladder distention, urinary
frequency, weight loss, pallor, weakness,
488 NUCHAL RIGIDITY
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perineal pain, and constipation. Palpation reveals a hard, irregularly shaped, nodular
prostate.
◆ Pyelonephritis (acute). Nocturia is common
with this disorder and is usually characterized
by infrequent voiding of moderate amounts of
urine. The urine may appear cloudy. Associated
signs and symptoms include a high, sustained
fever with chills, fatigue, unilateral or bilateral
flank pain, costovertebral angle tenderness,
weakness, dysuria, hematuria, urinary frequency and urgency, and tenesmus. Occasionally,
anorexia, nausea, vomiting, diarrhea, and hypoactive bowel sounds may also occur.
◆ Renal failure (chronic). Nocturia occurs rel-
atively early in this disorder and is usually characterized by infrequent voiding of moderate
amounts of urine. As the disorder progresses,
oliguria or even anuria develops. Other widespread effects of chronic renal failure include
fatigue, ammonia breath odor, Kussmaul’s respirations, peripheral edema, elevated blood
pressure, decreased level of consciousness,
confusion, emotional lability, muscle twitching,
anorexia, metallic taste in the mouth, constipation or diarrhea, petechiae, ecchymoses, pruritus, yellow- or bronze-tinged skin, nausea, and
vomiting.
O
THER CAUSES
◆ Drugs. Any drug that mobilizes edematous
fluid or produces diuresis (for example, a diuretic or a cardiac glycoside) may cause nocturia;
obviously, this effect depends on when the drug
is administered.
S
PECIAL CONSIDERATIONS
Patient care includes maintaining fluid balance,
ensuring adequate rest, and providing patient
education. Monitor vital signs, intake and output, and daily weight; continue to document the
frequency of nocturia, amount, and specific
gravity. Plan administration of a diuretic for daytime hours, if possible. Also plan rest periods to
compensate for sleep lost because of nocturia.
Prepare the patient for diagnostic tests,
which may include routine urinalysis; urine concentration and dilution studies; serum blood
urea nitrogen, creatinine, and electrolyte levels;
and cystoscopy.
P
EDIATRIC POINTERS
In children, nocturia may be voluntary or involuntary. The latter is commonly known as enure-
sis, or bedwetting. With the exception of
prostate disorders, causes of nocturia are generally the same for children and adults.
However, children with pyelonephritis are
more susceptible to sepsis, which may display
as fever, irritability, and poor skin perfusion. In
addition, girls may experience vaginal discharge
and vulvar soreness or pruritus.
G
ERIATRIC POINTERS
Postmenopausal women have decreased bladder elasticity, but urine output remains constant, resulting in nocturia.
P
ATIENT COUNSELING
Advise patients to reduce fluid intake (especially
of caffeinated and alcoholic beverages) before
bedtime. Also advise them to void 15 to 20 minutes before retiring. Voiding once more just before retiring may be helpful.
Nuchal rigidity
Commonly an early sign of meningeal irritation,
nuchal rigidity refers to stiffness of the neck that
prevents flexion. To elicit this sign, attempt to
passively flex the patient’s neck and touch his
chin to his chest. If nuchal rigidity is present,
this maneuver triggers pain and muscle spasms.
(Be sure that there is no cervical spinal misalignment, such as a fracture or dislocation, before testing for nuchal rigidity. Severe spinal
cord damage could result.) The patient may also
notice nuchal rigidity when he attempts to flex
his neck during daily activities. This sign is not
reliable in children and infants.
Nuchal rigidity may herald life-threatening
subarachnoid hemorrhage or meningitis. It may
also be a late sign of cervical arthritis, in which
joint mobility is gradually lost.
EMERGENCY INTERVENTIONS After elic-
iting nuchal rigidity, attempt to elicit
Kernig’s and Brudzinski’s signs. Quickly evaluate
level of consciousness (LOC). Take vital signs. If
you note signs of increased intracranial pressure
(ICP), such as increased systolic pressure, bradycardia, and widened pulse pressure, start an I.V.
catheter for drug administration and deliver oxygen as necessary, and keep the head of the bed
no lower than 30 degrees. Draw a specimen for
routine blood studies such as a complete blood
count with a white blood cell count and electrolyte levels.
NYSTAGMUS
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489
H
ISTORY AND PHYSICAL
EXAMINATION
Obtain a patient history, relying on family
members if altered LOC prevents the patient
from responding. Ask about the onset and duration of neck stiffness. Were there any precipitating factors? Also ask about associated signs
and symptoms, such as headache, fever, nausea and vomiting, and motor and sensory
changes. Check for a history of hypertension,
head trauma, cerebral aneurysm or arteriovenous malformation, endocarditis, recent infection (such as sinusitis or pneumonia), or recent
dental work. Then, obtain a complete drug
history.
If the patient has no other signs of meningeal
irritation, ask about a history of arthritis or neck
trauma. Can the patient recall pulling a muscle
in his neck? Inspect the patient’s hands for
swollen, tender joints, and palpate the neck for
pain or tenderness.
M
EDICAL CAUSES
◆ Cervical arthritis. With this disorder, nuchal
rigidity develops gradually. Initially, the patient
may complain of neck stiffness in the early
morning or after a period of inactivity. Stiffness
then becomes increasingly severe and frequent.
Pain on movement, especially with lateral motion or head turning, is common. Typically,
arthritis also affects other joints, especially
those in the hands.
◆ Encephalitis. This viral infection may cause
nuchal rigidity accompanied by other signs of
meningeal irritation, such as positive Kernig’s
and Brudzinski’s signs. Usually, nuchal rigidity
appears abruptly and is preceded by headache,
vomiting, and fever. The patient may display a
rapidly decreasing LOC, progressing from
lethargy to coma within 24 to 48 hours of onset.
Associated features include seizures, ataxia,
hemiparesis, nystagmus, and cranial nerve
palsies, such as dysphagia and ptosis.
◆ Listeriosis. If this bacterial infection spreads
to the nervous system, meningitis may develop.
Signs and symptoms include nuchal rigidity,
fever, headache, and change in LOC. Initial
signs and symptoms include fever, myalgias,
abdominal pain, nausea, vomiting, and diarrhea.
◆ Meningitis. Nuchal rigidity is an early sign of
this disorder and is accompanied by other signs
of meningeal irritation—positive Kernig’s and
Brudzinski’s signs, hyperreflexia and, possibly,
opisthotonos. Other early features include fever
with chills, headache, photophobia, and vomiting. Initially, the patient is confused and irritable; later, he may become stuporous and
seizure-prone or may slip into coma. Cranial
nerve involvement may cause ocular palsies, facial weakness, and hearing loss. An erythematous papular rash occurs in some forms of viral
meningitis; a purpuric rash may occur in
meningococcal meningitis.
◆ Subarachnoid hemorrhage. Nuchal rigidity
develops immediately after bleeding into the
subarachnoid space. Examination may detect
positive Kernig’s and Brudzinski’s signs. The patient may experience abrupt onset of severe
headache, photophobia, fever, nausea and vomiting, dizziness, cranial nerve palsies, and focal
neurologic signs, such as hemiparesis or hemiplegia. His LOC deteriorates rapidly, possibly
progressing to coma. Signs of increased ICP,
such as bradycardia and altered respirations,
may also occur.
S
PECIAL CONSIDERATIONS
Prepare the patient for diagnostic tests, such as
computed tomography scans, magnetic resonance imaging, and cervical spinal X-rays.
Monitor vital signs, intake and output, and
neurologic status closely. Avoid routine administration of opioid analgesics because these may
mask signs of increasing ICP. Enforce strict bed
rest; keep the head of the bed elevated at least
30 degrees to help minimize ICP.
Assist the patient in finding a comfortable position to obtain adequate rest.
P
EDIATRIC POINTERS
Tests for nuchal rigidity are generally less reliable in children, especially infants. In younger
children, move the head gently in all directions,
observing for resistance. In older children, ask
the child to sit upright and touch his chin to his
chest. Resistance to this movement may indicate meningeal irritation.
Nystagmus
Nystagmus refers to the involuntary oscillations
of one or, more commonly, both eyeballs. These
oscillations are usually rhythmic and may be
horizontal, vertical, rotary, or mixed. They may
be transient or sustained and may occur spontaneously or on deviation or fixation of the eyes.
490 NYSTAGMUS
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Minor degrees of nystagmus at the extremes of
gaze are normal. Nystagmus when the eyes are
stationary and looking straight ahead is always
abnormal. Although nystagmus is fairly easy to
identify, the patient may be unaware of it unless
it affects his vision.
Nystagmus may be classified as pendular or
jerk. Pendular nystagmus consists of horizontal
(pendular) or vertical (seesaw) oscillations that
are equal in rate in both directions and resemble the movements of a clock’s pendulum. Jerk
nystagmus (convergence-retraction, downbeat,
and vestibular), which is more common than
pendular nystagmus, has a fast component and
then a slow—perhaps unequal—corrective component in the opposite direction. (See Classifying
nystagmus.)
Nystagmus is considered a supranuclear oc-
ular palsy—that is, it’s caused by pathology in
the visual perceptual area, vestibular system,
cerebellum, or brain stem rather than in the
extraocular muscles or cranial nerves III, IV,
and VI. Its causes are varied and include brain
stem or cerebellar lesions, multiple sclerosis,
encephalitis, labyrinthine disease, and drug
toxicity. Occasionally, nystagmus is entirely
normal; it’s also considered a normal response
in the unconscious patient during the doll’s
eye test (oculocephalic stimulation) or the
cold water caloric test (oculovestibular stimulation).
H
ISTORY AND PHYSICAL
EXAMINATION
Begin by asking the patient how long he has
had nystagmus. Does it occur intermittently?
Does it affect his vision? Ask about recent infection, especially of the ear or respiratory tract,
and about head trauma and cancer. Does the
patient or anyone in his family have a history of
stroke? Then explore associated signs and
symptoms. Ask about vertigo, dizziness, tinnitus, nausea or vomiting, numbness, weakness,
bladder dysfunction, and fever.
Begin the physical examination by assessing
the patient’s level of consciousness (LOC) and
vital signs. Be alert for signs of increased intracranial pressure (ICP), such as pupillary
changes, drowsiness, elevated systolic pressure,
and altered respiratory pattern. Next, assess
nystagmus fully by testing extraocular muscle
function: Ask the patient to focus straight ahead
and then to follow your finger up, down, and in
an “X” across his face. Note when nystagmus
occurs, as well as its velocity and direction. Fi-
nally, test reflexes, motor and sensory function,
and the cranial nerves.
M
EDICAL CAUSES
◆ Brain tumor. Insidious onset of jerk nystag-
mus may occur with tumors of the brain stem
and cerebellum. Associated characteristics include deafness, dysphagia, nausea and vomiting, vertigo, and ataxia. Brain stem compression by the tumor may cause signs of increased
ICP, such as altered LOC, bradycardia, widening
pulse pressure, and elevated systolic blood
pressure.
◆ Encephalitis. With this disorder, jerk nystag-
mus is typically accompanied by altered LOC
ranging from lethargy to coma. Usually, it’s preceded by sudden onset of fever, headache, and
vomiting. Among other features are nuchal
rigidity, seizures, aphasia, ataxia, photophobia,
and cranial nerve palsies, such as dysphagia
and ptosis.
◆ Head trauma. Brain stem injury may cause
jerk nystagmus, which is usually horizontal. The
patient may also display pupillary changes, altered respiratory pattern, coma, and decerebrate posture.
◆ Labyrinthitis (acute). This inner ear inflam-
mation causes sudden onset of jerk nystagmus,
accompanied by dizziness, vertigo, tinnitus,
nausea, and vomiting. The fast component of
the nystagmus is toward the unaffected ear.
Gradual sensorineural hearing loss may also occur.
◆ Ménière’s disease. This inner ear disorder is
characterized by acute attacks of jerk nystagmus, severe nausea and vomiting, dizziness,
vertigo, progressive hearing loss, tinnitus, and
diaphoresis. Typically, the direction of jerk nystagmus varies from one attack to the next. Attacks may last from 10 minutes to several
hours.
◆ Multiple sclerosis. With this disorder, jerk or
pendular nystagmus may occur intermittently.
Usually, it’s preceded by diplopia, blurred vision,
and paresthesia. Related signs and symptoms
may include muscle weakness or paralysis,
spasticity, hyperreflexia, intention tremor, gait
ataxia, dysphagia, dysarthria, impotence, and
emotional instability. The patient may also develop constipation, as well as urinary frequency,
urgency, and incontinence.
◆ Stroke. A stroke involving the posterior infe-
rior cerebellar artery may cause sudden horizontal or vertical jerk nystagmus that may be
gaze dependent. Other findings include
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