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Checking for clubbed
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fingers
To assess a patient for chronic tissue hypoxia, check his fingers for clubbing. Normally,
the angle between the fingernail and the
point where the nail enters the skin is about
160 degrees. Clubbing occurs when that angle increases to 180 degrees or more, as
shown below.
NORMAL FINGERS
Normal angle
(160 degrees)
CLUBBED FINGERS
Angle greater than
180 degrees
Enlarged and curved nail
Cogwheel rigidity
Cogwheel rigidity, a cardinal sign of Parkinson’s
disease, is marked by muscle rigidity that reacts
with superimposed ratchetlike movements
when the muscle is passively stretched. This
sign can be elicited by stabilizing the patient’s
forearm and then moving his wrist through the
range of motion. (Cogwheel rigidity usually appears in the arms but can sometimes be elicited
in the ankle.) Both the patient and the examiner
can see and feel these characteristic movements, thought to be a combination of rigidity
and tremor.
H
ISTORY AND PHYSICAL
EXAMINATION
After you’ve elicited cogwheel rigidity, take the
patient’s history to determine when he first no-
COGWHEEL RIGIDITY
ticed associated signs of Parkinson’s disease. For
example, has he experienced tremors? Did he
notice tremors of his hands first? Does he have
“pill-rolling” hand movements? When did he first
notice that his movements were becoming slower? How long has he been experiencing stiffness
in his arms and legs? Has his handwriting gotten
smaller? While taking the history, observe the
patient for signs of pronounced parkinsonism,
such as drooling, masklike facies, dysphagia,
monotone speech, and altered gait.
Find out which medications the patient is
taking and ask if they’ve helped relieve some of
his symptoms. If he’s taking levodopa and his
symptoms have worsened, find out if he has exceeded the prescribed dosage. If you suspect an
overdose, withhold the drug. If the patient has
been taking a phenothiazine or another antipsychotic and has no history of Parkinson’s disease, he may be having an adverse reaction.
Withhold the drug as appropriate.
M
EDICAL CAUSES
◆ Parkinson’s disease. In this disorder, cog-
wheel rigidity occurs together with an insidious
tremor, which usually begins in the fingers (unilateral pill-roll tremor), increases during stress
or anxiety, and decreases with purposeful
movement and sleep.
Bradykinesia (slowness of voluntary movements and speech) also occurs. The patient
walks with short, shuffling steps; his gait lacks
normal parallel motion and may be retropulsive
or propulsive. He has a monotonal way of
speaking and a masklike facial expression. He
may also experience drooling, dysphagia,
dysarthria, and loss of posture control, causing
him to walk with his body bent forward. An
oculogyric crisis (eyes fixed upward and involuntary tonic movements) or blepharospasm
(complete eyelid closure) may also occur.
O
THER CAUSES
◆ Drugs. Phenothiazines and other antipsy-
chotics (such as haloperidol, thiothixene, and
loxapine) can cause cogwheel rigidity. Metoclopramide causes it infrequently.
S
PECIAL CONSIDERATIONS
If the patient has associated muscular dysfunction, assist him with ambulation, feeding, and
other activities of daily living, as needed. Provide symptomatic care as appropriate. For example, if the patient develops constipation, administer a stool softener; if he experiences
161
162 COLD INTOLERANCE
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dysphagia, offer a soft diet with frequent small
feedings. Refer the patient to the National
Parkinson Foundation or the American Parkinson Disease Association, both of which provide
educational materials and support.
P
EDIATRIC POINTERS
Cogwheel rigidity doesn’t occur in children.
Cold intolerance
Usually developing gradually, this increased
sensitivity to cold temperatures reflects damage
to the body’s temperature-regulating mechanism, based on interactions between the hypothalamus and the thyroid gland. Typically, the
symptom results from a tumor or a hormonal
deficiency. In elderly patients, cold intolerance
reflects normal age-related physiologic changes.
H
ISTORY AND PHYSICAL
EXAMINATION
Find out when the patient first noticed cold intolerance by asking when he began using more
blankets or wearing heavier clothing. A person
may suffer transitory cold intolerance when
moving from a tropical to a temperate climate;
ask if the patient has recently made such a
move. Ask about associated signs and symptoms, such as changes in vision or in the texture
or amount of body hair. If the patient is female,
ask about changes in her normal menstrual pattern.
Before proceeding with the physical examination, obtain a brief history. Does the patient
have a history of hypothyroidism or hypothalamic disease? Is he taking any medications? If so,
is he complying with the prescribed schedule
and dosage? Has the regimen been changed recently?
Begin the physical examination by taking the
patient’s vital signs and checking for hypothermia, dry skin, and hair loss. Then ask the patient to straighten and extend his arms. Are his
hands shaking? During the examination, note if
the patient shivers or complains of chills. Provide a blanket if necessary.
M
EDICAL CAUSES
◆ Hypopituitarism. Signs and symptoms of
hypopituitarism usually develop slowly and vary
with the disorder’s severity. Cold intolerance
and shivering typically accompany cold, dry,
thin skin with a waxy pallor and fine wrinkles
around the mouth. Other findings include fatigue, lethargy, menstrual disturbances, impotence, decreased libido, nervousness, irritability,
headache, and hunger. If hypopituitarism results
from a pituitary tumor, expect neurologic signs
and symptoms, such as headache, bilateral temporal hemianopsia, loss of visual acuity, and
possibly blindness.
◆ Hypothalamic lesion. A patient with hypo-
thalamic damage may alternate from cold intolerance to heat intolerance. Cold intolerance develops suddenly; the patient typically complains
of feeling chilled, shivering, and wearing extra
clothes to keep warm. Related findings include
amenorrhea, disturbed sleep pattern, increased
thirst and urination, vigorous appetite with
weight gain, impaired vision, headache, and
personality changes, such as attacks of rage,
laughing, and crying.
◆ Hypothyroidism. Cold intolerance develops
early and worsens progressively in patients with
this disorder. Other early findings include fatigue, anorexia with weight gain, constipation,
and menorrhagia. As hypothyroidism progresses, the patient experiences loss of libido and
slowed intellectual and motor activity. His hair
becomes dry and sparse; nails, thick and brittle;
and skin, dry, pale, cool, and doughy. Eventually, the patient displays a dull expression with
periorbital and facial edema and puffy hands
and feet. Relaxation is delayed after deep tendon reflex testing. Bradycardia, abdominal distention, and ataxia may also occur.
S
PECIAL CONSIDERATIONS
Help increase the patient’s comfort by regulating his room temperature and providing extra
clothing and blankets. Prepare him for diagnostic tests to determine the cause of cold intolerance.
P
EDIATRIC POINTERS
Some degree of cold intolerance is normal in infants because fat distribution is decreased and
the temperature-regulating mechanism is immature at birth. Make sure parents understand
that their infant will quickly lose body heat if
he’s exposed to cold temperatures. Instruct
them to dress the infant warmly before sleep
and going outdoors and to avoid chilling him
during his bath.
An infant with cold intolerance due to hypothyroidism may have subtle, nonspecific signs
of the underlying disorder or none at all. Typically, the infant shivers and has a temperature
CONFUSION
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163
below 86° F (30° C), blue lips, and cold, mottled
skin, especially on the extremities.
G
ERIATRIC POINTERS
Cold intolerance is common in older people because of metabolic changes associated with
aging.
P
ATIENT COUNSELING
Allow the patient to openly express his concerns about body image changes related to his
cold intolerance. Instruct him and his family to
adapt the patient’s environment to meet his
needs. After the cause of cold intolerance is
known, explain the disease process to the patient and his family to help alleviate their anxiety. Also explain that, with proper treatment, he
can expect relief from his symptoms.
Confusion
An umbrella term for puzzling or inappropriate
behavior or responses, confusion is the inability
to think quickly and coherently. Depending on
its cause, confusion may arise suddenly or gradually and may be temporary or irreversible. Aggravated by stress and sensory deprivation,
confusion commonly occurs in hospitalized patients—especially the elderly, in whom it may be
mistaken for senility.
Sudden severe confusion combined with hal-
lucinations and psychomotor hyperactivity is
classified as delirium. Long-term, progressive
confusion with deterioration of all cognitive
functions is classified as dementia.
Confusion can result from fluid and electrolyte imbalance or from hypoxemia due to
pulmonary disorders. It can also stem from
metabolic, neurologic, cardiovascular, cerebrovascular, or nutritional disorders; a severe
systemic infection; or the effects of toxins,
drugs, or alcohol. Confusion also may signal
worsening of an underlying and perhaps irreversible disease.
H
ISTORY AND PHYSICAL
EXAMINATION
When you take his history, ask the patient to describe what’s bothering him. He may not report
confusion as his chief complaint but may complain of memory loss, persistent apprehension,
or the inability to concentrate. He may be unable to respond logically to direct questions.
Check with a family member or friend about the
onset and frequency of the patient’s confusion.
Find out, too, if the patient has a history of head
trauma or a cardiopulmonary, metabolic, cerebrovascular, or neurologic disorder. Which
medications is he taking, if any? Ask about any
changes in eating or sleeping habits and in drug
or alcohol use.
Perform an assessment to determine the
presence of systemic disorders. Check vital
signs, and assess the patient for changes in
blood pressure, temperature, and pulse.
Next, perform a neurologic assessment to establish the patient’s level of consciousness.
M
EDICAL CAUSES
◆ Brain tumor. In the early stages of a brain
tumor, confusion is usually mild and difficult to
detect. As the tumor impinges on cerebral structures, however, confusion worsens and the patient may exhibit personality changes, bizarre
behavior, sensory and motor deficits, visual field
deficits, and aphasia.
◆ Cerebrovascular disorders. These disorders
produce confusion due to tissue hypoxia and ischemia. Confusion may be insidious and fleeting, as in a transient ischemic attack, or acute
and permanent, as in a stroke.
◆ Decreased cerebral perfusion. Mild confu-
sion is an early symptom of decreased cerebral
perfusion. Associated findings usually include
hypotension, tachycardia or bradycardia, irregular pulse, ventricular gallop, edema, and
cyanosis.
◆ Fluid and electrolyte imbalance. The ex-
tent of the imbalance determines the severity of
the patient’s confusion. Typically, he’ll show
signs of dehydration, such as lassitude, poor
skin turgor, dry skin and mucous membranes,
and oliguria. He may also develop hypotension
and a low-grade fever.
◆ Head trauma. Concussion, contusion, and
brain hemorrhage may produce confusion at the
time of injury, shortly afterward, or months or
even years afterward. The patient may be delirious, with periodic loss of consciousness. Vomiting, severe headache, pupillary changes, and
sensory and motor deficits are also common.
◆ Heatstroke. This disorder causes pro-
nounced confusion that gradually worsens as
body temperature rises. Initially, the patient may
be irritable and dizzy; later, he may become
delirious, have seizures, and lose consciousness.
◆ Hypothermia. Confusion may be an early
sign of this disorder. Typically, the patient
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displays slurred speech, cold and pale skin, hyperactive deep tendon reflexes, rapid pulse, and
decreased blood pressure and respiratory rate.
As his body temperature continues to drop, his
confusion progresses to stupor and coma, his
muscles become rigid, and his respiratory rate
decreases.
◆ Hypoxemia. Acute pulmonary disorders that
result in hypoxemia produce confusion that can
range from mild disorientation to delirium.
Chronic pulmonary disorders produce persistent
confusion.
◆ Infection. A severe generalized infection,
such as sepsis, commonly produces delirium.
Central nervous system (CNS) infections, such
as meningitis, cause varying degrees of
confusion along with headache and nuchal
rigidity.
◆ Metabolic encephalopathy. Both hyper-
glycemia and hypoglycemia can produce sudden confusion. A patient with hypoglycemia
may also experience transient delirium and
seizures. Uremic and hepatic encephalopathies
produce gradual confusion that may progress to
seizures and coma. Usually, the patient also experiences tremors and restlessness.
◆ Nutritional deficiencies. Inadequate dietary
intake of thiamine, niacin, or vitamin B
duces insidious, progressive confusion and possibly mental deterioration.
pro-
12
◆ Seizure disorders. Mild to moderate confu-
sion may immediately follow any type of
seizure. The confusion usually disappears within several hours.
◆ Thyroid hormone disorders. Hyperthy-
roidism produces mild to moderate confusion
along with nervousness, inability to concentrate, weight loss, flushed skin, and tachycardia.
Hypothyroidism produces mild, insidious confusion and memory loss; weight gain; bradycardia; and fatigue.
O
THER CAUSES
◆ Alcohol. Intoxication causes confusion and
stupor, and alcohol withdrawal may cause delirium and seizures.
◆ Drugs. Large doses of CNS depressants
produce confusion that can persist for several
days after the drug is discontinued. Opioid and
barbiturate withdrawal also causes acute confusion, possibly with delirium. Other drugs
that commonly cause confusion include lidocaine, cardiac glycosides, indomethacin, cycloserine, chloroquine, atropine, and cimetidine.
◆ Heavy metal poisoning. Chronic inges-
tion or inhalation of heavy metals (such as
lead, arsenic, mercury, and manganese) eventually produces confusion and, typically,
weakness and drowsiness. The patient may
also experience headache, vomiting, seizures,
tremors, gait disturbances, and mental deterioration.
HERB ALERT Herbal medicines, such as St.
John’s wort, can cause confusion, especially
when taken in conjunction with an antidepressant
or another serotonergic drug.
S
PECIAL CONSIDERATIONS
Never leave a confused patient unattended to
prevent injury to himself and others. Keep the
patient calm and quiet, and plan uninterrupted
rest periods. To help him stay oriented, keep a
large calendar and a clock visible, and make a
list of his activities with specific dates and
times. Reintroduce yourself to the patient each
time you enter his room.
P
EDIATRIC POINTERS
Confusion can’t be determined in infants and
very young children. However, older children
with acute febrile illnesses commonly experience transient delirium or acute confusion.
Conjunctival injection
A common ocular sign associated with inflammation, conjunctival injection is nonuniform
redness of the conjunctiva from hyperemia. This
redness can be diffuse, localized, or peripheral,
or it may encircle a clear cornea.
Conjunctival injection usually results from
bacterial or viral conjunctivitis, but it can also
signal a severe ocular disorder that, if untreated, may lead to permanent blindness. Conjunctival injection can also result from minor eye irritation due to inadequate sleep, overuse of
contact lenses, environmental irritants, and excessive eye rubbing.
EMERGENCY INTERVENTIONS If the pa-
tient with conjunctival injection reports a
chemical splash to the eye, quickly irrigate the eye
with copious amounts of normal saline solution.
(First, remove contact lenses.) Evert the lids and
wipe the fornices with a cotton-tipped applicator
to remove any foreign body particles and as much
of the chemical as possible.
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165
H
ISTORY AND PHYSICAL
EXAMINATION
When you take the patient’s history, always ask
if he has associated pain. If so, when did the
pain begin, and where is it located? Is it constant or intermittent? Also, ask about itching,
burning, photophobia, blurred vision, halo vision, excessive tearing, or a foreign body sensation in his eye. Does the patient have a history
of eye disease or trauma? If he has suffered ocular trauma, avoid touching the affected eye.
Test his visual acuity and intraocular pressure
(IOP) only if his eyelids can be opened without
applying pressure. Place a metal shield over the
affected eye to protect it, if necessary.
If the patient’s condition permits, examine
the affected eye. First, determine the location
and severity of conjunctival injection. Is it circumcorneal or localized? Peripheral or diffuse?
Note any conjunctival or lid edema, ocular deviation, conjunctival follicles, ptosis, or exophthalmos. Also note the type and amount of any
discharge.
Test the patient’s visual acuity to establish a
baseline. Note if the patient has had vision
changes: Is his vision blurred or his visual acuity
markedly decreased? Next, test pupillary reaction to light.
Perform IOP measurements. To gauge increased IOP without a tonometer, gently place
your index finger over the closed eyelid; if the
globe feels rock-hard, IOP is elevated.
M
EDICAL CAUSES
◆ Blepharitis. This disorder produces diffuse
conjunctival injection. Ulcerations appear on
the eyelids, which burn, itch, and have no
lashes.
◆ Chemical burns. Diffuse conjunctival injec-
tion occurs in this ocular emergency, but severe
pain is the main symptom. The patient also displays photophobia, blepharospasm, and decreased visual acuity in the affected eye; the
cornea may appear gray, and the pupil may be
unilaterally smaller.
◆ Conjunctival foreign bodies and abra-
sions. These conditions feature localized conjunctival injection with sudden, severe eye pain.
The patient may have increased tearing and
photophobia, but his visual acuity usually isn’t
impaired.
◆ Conjunctivitis. Allergic conjunctivitis pro-
duces milky, diffuse peripheral conjunctival injection. Related findings include a watery,
stringy eye discharge; increased tearing; itching;
palpebral conjunctival follicles; and (with hay
fever) conjunctival edema, photophobia, and a
feeling of fullness around the eyes.
Bacterial conjunctivitis causes diffuse peripheral conjunctival injection along with a thick,
purulent eye discharge that contains mucous
threads. The patient’s lids and lashes stick together, and he has excessive tearing, photophobia, burning, and itching. He may have pain and
a foreign body sensation if the cornea is involved.
Besides diffuse peripheral conjunctival injection, the patient with fungal conjunctivitis complains of photophobia and increased tearing,
itching, and burning. The discharge is thick and
purulent, making his eyelids crusted, sticky, and
swollen. Corneal involvement causes pain.
In viral conjunctivitis, the conjunctival injection is bright red, diffuse, and peripheral. The
patient may also have conjunctival edema, follicles on the palpebral conjunctiva, and lid edema; a local viral rash; and signs of upper respiratory tract infection. He complains of itching,
increased tearing and, possibly, a foreign body
sensation.
◆ Corneal abrasion. Diffuse conjunctival in-
jection is extremely painful in this disorder, especially when the eyelids move over the abrasion. The patient may also report photophobia,
excessive tearing, blurred vision, and a foreign
body sensation.
◆ Corneal erosion. Recurrent corneal erosion
produces diffuse conjunctival injection; severe,
continuous pain from rubbing of the eyelid over
the eroded area of the cornea; and photophobia.
◆ Corneal ulcer. Bacterial, viral, and fungal
corneal ulcers produce diffuse conjunctival injection that increases in the circumcorneal area.
Accompanying findings include severe photophobia, severe pain in and around the eye,
markedly decreased visual acuity, and a copious
amount of purulent eye discharge and crusting.
If the patient develops associated iritis, a physical examination will also reveal corneal opacities and an abnormal pupillary response to
light.
◆ Dacryoadenitis. This disorder produces dif-
fuse conjunctival injection, pain over the temporal part of the eye, considerable lid swelling
and, possibly, a purulent eye discharge.
◆ Episcleritis. Conjunctival injection is local-
ized and raised and may be violet or purplish
pink in patients with episcleritis. Associated
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signs and symptoms include an inflamed sclera,
deep pain, photophobia, increased tearing, and
conjunctival edema.
◆ Glaucoma. In acute angle-closure glau-
coma, conjunctival injection is typically circumcorneal. Other signs and symptoms include severe eye pain, nausea and vomiting, severely
elevated IOP, blurred vision, and the perception
of rainbow-colored halos around lights.
Corneas appear steamy because of corneal
edema. The pupil of the affected eye is moderately dilated and completely unresponsive to
light.
◆ Hyphema. Depending on the type and extent
of traumatic injury, a hyphema may produce diffuse conjunctival injection, possibly with lid and
orbital edema. The patient may complain of
pain in and around the eye. The extent of visual
impairment depends on the hyphema’s size and
location.
◆ Iritis. In acute iritis, marked conjunctival in-
jection is found mainly around the cornea. Other findings include moderate to severe pain,
photophobia, blurred vision, constricted pupils,
and poor pupillary response to light.
◆ Kawasaki syndrome. Conjunctival injection
is a characteristic sign of Kawasaki syndrome
and usually occurs bilaterally. This febrile illness, which primarily affects children under age
5, also causes erythema, lymphadenopathy, and
swelling in the peripheral extremities. Treatment with I.V. gamma globulin is extremely effective if given immediately, so early detection
is essential. Delaying treatment may cause
coronary artery dilation and aneurysm, resulting
in ischemic heart disease and, possibly, sudden
death.
◆ Keratoconjunctivitis sicca. This disorder
produces severe diffuse conjunctival injection.
The patient reports generalized eye pain along
with burning, itching, a foreign body sensation,
excessive mucus secretion from the eye, absence of tears, and photophobia.
◆ Lyme disease. Spread by tick bites, Lyme
disease may cause conjunctival injection, diffuse urticaria, malaise, fatigue, headache, fever,
chills, aches, and lymphadenopathy.
◆ Ocular lacerations and intraocular for-
eign bodies. Diffuse conjunctival injection may
be increased in the area of injury. The patient
experiences impaired visual acuity and moderate to severe pain that varies with the type and
extent of injury. He may also develop lid edema,
photophobia, excessive tearing, and an abnormal pupillary response to light.
◆ Ocular tumors. A tumor located in the orbit
behind the globe may produce conjunctival injection together with exophthalmos. Conjunctival edema, ocular deviation, and diplopia usually occur if muscles are involved.
◆ Refractive error. An uncorrected or poorly
corrected refractive error can produce conjunctival injection. The patient may complain of
headache, eye pain, and eye fatigue.
◆ Scleritis. In this relatively rare disorder, con-
junctival injection can be diffuse or localized
over the area of the scleritis nodule. The patient
has severe pain on moving the eye, photophobia, tenderness, and tearing.
◆ Stevens-Johnson syndrome. This disorder
produces diffuse conjunctival injection, a purulent eye discharge, severe eye pain, photophobia, decreased tearing, entropion, and
trichiasis.
◆ Trachoma. Conjunctival injection is an early
sign of trachoma, a leading cause of blindness
in Third World countries and among Native
Americans in the southwestern United States.
Caused by a bacterial infection, trachoma may
also produce eyelid swelling and corneal cloudiness.
◆ Uveitis. Diffuse conjunctival injection, which
may be increased in the circumcorneal area,
characterizes this disorder. Accompanying signs
and symptoms include constricted, irregularly
shaped pupils; blurred vision; tenderness; photophobia; and possibly sudden, severe ocular
pain.
S
PECIAL CONSIDERATIONS
As indicated, prepare the patient for such diagnostic tests as orbital X-rays, ocular ultrasonography, and fluorescein staining. Obtain cultures
of any eye discharge, and record its appearance,
consistency, and amount.
Most forms of conjunctivitis are contagious
and can easily spread to the other eye or to
family members. Stress the importance of frequent hand washing and of not touching the affected eye to prevent contagion.
P
EDIATRIC POINTERS
An infant can develop self-limiting chemical
conjunctivitis at birth from the ocular instillation
of silver nitrate. He may also develop bacterial
conjunctivitis 2 to 5 days after birth from contamination of the birth canal. An infant with congenital syphilis has prominent conjunctival injection and grayish pink corneas.
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167
P
ATIENT COUNSELING
If the patient complains of photophobia, darken
the room or suggest that he wear sunglasses. If
the patient’s visual acuity is markedly decreased, orient him to his environment to ensure his comfort and safety.
Constipation
Constipation is defined as small, infrequent, or
difficult bowel movements. Because normal
bowel movements can vary in frequency and
from individual to individual, constipation must
be determined in relation to the patient’s normal elimination pattern. Constipation may be a
minor annoyance or, occasionally, a sign of a
life-threatening disorder such as acute intestinal
obstruction. Untreated, constipation can lead to
headache, anorexia, and abdominal discomfort
and can adversely affect the patient’s lifestyle
and well-being.
Constipation usually occurs when the urge to
defecate is suppressed and the muscles associated with bowel movements remain contracted.
Because the autonomic nervous system controls bowel movements—by sensing rectal distention from fecal contents and by stimulating
the external sphincter—any factor that influences this system may cause bowel dysfunction.
(See How habits and stress cause constipation,
page 168.)
H
ISTORY AND PHYSICAL
EXAMINATION
Ask the patient to describe the frequency of his
bowel movements and the size and consistency of his stools. How long has he had constipation? Acute constipation usually has an organic cause, such as an anal or rectal disorder. In
a patient over age 45, a recent onset of constipation may be an early sign of colorectal cancer. Conversely, chronic constipation typically
has a functional cause and may be related to
stress.
Does the patient have pain related to constipation? If so, when did he first notice the
pain, and where is it located? Cramping abdominal pain and distention suggest obstipation—extreme, persistent constipation due to
intestinal tract obstruction. Ask the patient if
defecation worsens or helps relieve the pain.
Defecation usually worsens the pain, but in
disorders such as irritable bowel syndrome, it
may relieve it.
Ask the patient to describe a typical day’s
menu; estimate his daily fiber and fluid intake.
Ask him, too, about any changes in eating
habits, medication or alcohol use, or physical
activity. Has he experienced recent emotional
distress? Has constipation affected his family
life or social contacts? Also, ask about his job. A
sedentary or stressful job can contribute to constipation.
Find out whether the patient has a history of
GI, rectoanal, neurologic, or metabolic disorders; abdominal surgery; or radiation therapy.
Then ask about the medications he’s taking, including over-the-counter preparations, such as
laxatives, mineral oil, stool softeners, and enemas.
Inspect the abdomen for distention or scars
from previous surgery. Then auscultate for bowel sounds, and characterize their motility. Percuss all four quadrants, and gently palpate for
abdominal tenderness, a palpable mass, and
hepatomegaly. Next, examine the patient’s rectum. Spread his buttocks to expose the anus,
and inspect for inflammation, lesions, scars, fissures, and external hemorrhoids. Use a disposable glove and lubricant to palpate the anal
sphincter for laxity or stricture. Also palpate for
rectal masses and fecal impaction. Finally, obtain a stool specimen and test it for occult
blood.
As you assess the patient, remember that
constipation can result from several life-threatening disorders, such as acute intestinal obstruction and mesenteric artery ischemia, but it
doesn’t herald these conditions.
M
EDICAL CAUSES
◆ Anal fissure. A crack or laceration in the lin-
ing of the anal wall can cause acute constipation, usually due to the patient’s fear of the severe tearing or burning pain associated with
bowel movements. He may notice a few drops
of blood streaking toilet tissue or his underwear.
◆ Anorectal abscess. In this disorder, consti-
pation occurs together with severe, throbbing,
localized pain and tenderness at the abscess
site. The patient may also have localized inflammation, swelling, and purulent drainage and
may complain of fever and malaise.
◆ Cirrhosis. In the early stages of cirrhosis, the
patient experiences constipation along with
nausea and vomiting, and a dull pain in the
right upper quadrant. Other early findings include indigestion, anorexia, fatigue, malaise,
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How habits and stress cause constipation
Suppression
of urge to
defecate
Inadequate
fluid and fiber
intake
Chronic
anxiety
Acute
emotional
distress
Contraction
of external
sphincter and
associated
muscles
Increased
intestinal
transit time
Generalized
muscle
tension
Sympathetic
response
Absence of
bowel
movement
Increased
reabsorption
of fluid
Decreased
intestinal
motility
Decreased
interstitial
motor activity
Constipation
Infrequent
physical
exercise
flatulence, hepatomegaly and, possibly,
splenomegaly and diarrhea.
◆ Diabetic neuropathy. This type of neuropa-
thy produces episodic constipation or diarrhea.
Other signs and symptoms include dysphagia,
orthostatic hypotension, syncope, and painless
bladder distention with overflow incontinence.
A male patient may also experience impotence
and retrograde ejaculation.
◆ Diverticulitis. In this disorder, constipation
or diarrhea occurs with left-lower-quadrant
Decreased peristalsis
pain and tenderness and possibly a palpable,
tender, firm, fixed abdominal mass. The patient
may develop mild nausea, flatulence, or a lowgrade fever.
◆ Hemorrhoids. Thrombosed hemorrhoids
cause constipation as the patient tries to avoid
the severe pain of defecation. The hemorrhoids
may bleed during defecation.
◆ Hepatic porphyria. Abdominal pain, which
may be severe, colicky, and localized or generalized, precedes constipation in hepatic
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169
porphyria. The patient may also have a fever,
sinus tachycardia, labile hypertension, diaphoresis, severe vomiting, photophobia, urine
retention, nervousness or restlessness, disorientation and, possibly, visual hallucinations.
Deep tendon reflexes may be diminished or absent. Some patients have skin lesions causing
itching, burning, erythema, altered pigmentation, and edema in areas exposed to light. Severe hepatic porphyria can produce delirium,
coma, seizures, paraplegia, or complete flaccid
quadriplegia.
◆ Hypercalcemia. In hypercalcemia, consti-
pation usually is accompanied by anorexia,
nausea, vomiting, polyuria, and polydipsia. The
patient may also display arrhythmias, bone
pain, muscle weakness and atrophy, hypoactive deep tendon reflexes, and personality
changes.
◆ Hypothyroidism. Constipation occurs early
and insidiously in patients with hypothyroidism;
it may be accompanied by fatigue, sensitivity to
cold, anorexia with weight gain, menorrhagia,
decreased memory, hearing impairment, muscle
cramps, and paresthesia.
◆ Intestinal obstruction. Constipation associ-
ated with this disorder varies in severity and onset, depending on the location and extent of the
obstruction. In a partial obstruction, constipation may alternate with leakage of liquid stools.
In a complete obstruction, obstipation may occur. Constipation can be the earliest sign of partial colon obstruction, but it usually occurs later
if the level of the obstruction is more proximal.
Associated findings include episodes of colicky
abdominal pain, abdominal distention, nausea,
and vomiting. The patient may also develop hyperactive bowel sounds, visible peristaltic
waves, a palpable abdominal mass, and abdominal tenderness.
◆ Irritable bowel syndrome. This common
syndrome usually produces intermittent watery diarrhea, although some patients have
chronic constipation and others complain of
alternating constipation and diarrhea. Stress
may trigger nausea and abdominal distention
and tenderness, but defecation usually relieves these signs and symptoms. Many patients have an intense urge to defecate and
feelings of incomplete evacuation. Typically,
the stools are scybalous and contain visible
mucus.
◆ Mesenteric artery ischemia. This life-
threatening disorder produces sudden constipation with failure to expel stool or flatus. Ini-
tially, the abdomen is soft and nontender but
soon severe abdominal pain, tenderness, vomiting, and anorexia occur. Later, the patient
may develop abdominal guarding, rigidity, and
distention; tachycardia; syncope; tachypnea;
fever; and signs of shock, such as cool, clammy skin and hypotension. A bruit may be
heard.
◆ Multiple sclerosis (MS). This disorder can
produce constipation in addition to ocular disturbances, such as nystagmus, blurred vision,
and diplopia; vertigo; and sensory disturbances.
The patient may also have motor weakness,
seizures, paralysis, muscle spasticity, gait ataxia, intention tremor, hyperreflexia, dysarthria, or
dysphagia. MS can also produce urinary urgency, frequency, and incontinence as well as
emotional instability. A male patient may experience impotence.
◆ Spinal cord lesion. Constipation may occur
in this disorder along with urine retention, sexual dysfunction, pain, and possibly motor weakness, paralysis, or sensory impairment below
the level of the lesion.
◆ Tabes dorsalis. In tabes dorsalis, constipa-
tion is accompanied by an ataxic gait; paresthesia; loss of sensation of body position, deep
pain, and temperature; Charcot’s joints; Argyll
Robertson pupils; diminished deep tendon reflexes; and possibly impotence.
◆ Ulcerative colitis. Constipation may occur in
patients with chronic ulcerative colitis, but
bloody diarrhea with pus, mucus, or both is the
hallmark of this disorder. Other signs and symptoms include cramping lower abdominal pain,
tenesmus, anorexia, low-grade fever and, occasionally, nausea and vomiting. Bowel sounds
may be hyperactive. Later, weight loss, weakness, and arthralgias occur.
◆ Ulcerative proctitis. This disorder produces
acute constipation with tenesmus. The patient
feels an intense urge to defecate but is unable
to do so. Instead, he may eliminate mucus, pus,
or blood.
O
THER CAUSES
◆ Diagnostic tests. Constipation can result
from the retention of barium given during certain GI studies.
◆ Drugs. Many patients experience constipa-
tion when taking an opioid analgesic or other
drugs, including vinca alkaloids, calcium channel blockers, antacids containing aluminum
or calcium, anticholinergics, and drugs with
anticholinergic effects (such as tricyclic
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antidepressants). Patients may also experience
constipation from excessive use of laxatives or
enemas.
◆ Surgery and radiation therapy. Constipa-
tion can result from rectoanal surgery, which
may traumatize nerves, and abdominal irradiation, which may cause intestinal stricture.
S
PECIAL CONSIDERATIONS
As indicated, prepare the patient for diagnostic
tests, such as proctosigmoidoscopy, colonoscopy,
barium enema, plain abdominal films, and an
upper GI series. If the patient is on bed rest,
reposition him frequently, and help him perform active or passive exercises as indicated.
Teach him abdominal toning exercises if his
abdominal muscles are weak and relaxation
techniques to help him reduce stress related to
constipation.
P
EDIATRIC POINTERS
The high content of casein and calcium in cow’s
milk can produce hard stools and possibly constipation in bottle-fed infants. Other causes of
constipation in infants include Hirschsprung’s
disease, inadequate fluid intake, and anal fissures. In older children, constipation usually results from inadequate fiber intake and excessive
intake of milk; it can also result from bowel
spasm, mechanical obstruction, hypothyroidism, reluctance to stop playing for bathroom
breaks, and the lack of privacy in some school
bathrooms.
G
ERIATRIC POINTERS
Acute constipation in elderly patients is usually
associated with underlying structural abnormalities. Chronic constipation, however, is chiefly
caused by lifelong bowel elimination and dietary habits and laxative use.
P
ATIENT COUNSELING
Caution the patient not to strain during defecation to prevent injuring rectoanal tissue. Instruct
him to avoid using laxatives or enemas. If he
has been abusing these products, begin to wean
him from them. Use a disposable glove and lubricant to remove impacted fecal contents.
(Check if an oil-retention enema can be given
first to soften the fecal mass.)
Stress the importance of a high-fiber diet, and
encourage the patient to drink plenty of fluids.
(Explain that he may experience temporary
bloating or flatulence after adding fiber to his
diet.) Also, encourage him to exercise at least
1
1
⁄2 hours each week, if possible.
Corneal reflex, absent
The corneal reflex is tested bilaterally by drawing a fine-pointed wisp of sterile cotton from a
corner of each eye to the cornea. Normally,
even though only one eye is tested at a time, the
patient blinks bilaterally each time either cornea
is touched—this is the corneal reflex. When this
reflex is absent, neither eyelid closes when the
cornea of one is touched. (See Eliciting the
corneal reflex.)
The afferent fibers for this reflex are located
in the ophthalmic branch of the trigeminal
nerve (cranial nerve V); the efferent fibers are
located in the facial nerve (cranial nerve VII).
Unilateral or bilateral absence of the corneal
reflex may result from damage to these
nerves.
H
ISTORY AND PHYSICAL
EXAMINATION
If you can’t elicit the corneal reflex, look for other signs of trigeminal nerve dysfunction. To test
the three sensory portions of the nerve, touch
each side of the patient’s face on the brow,
cheek, and jaw with a cotton wisp, and ask him
to compare the sensations.
If you suspect facial nerve involvement, determine whether both the upper face (brow and
eyes) and lower face (cheek, mouth, and chin)
are weak bilaterally. Lower-motor-neuron facial
weakness affects the face on the same side as
the lesion, whereas upper-motor-neuron weakness affects the side opposite the lesion—
predominantly the lower facial muscles.
Because an absent corneal reflex may signify
such progressive neurologic disorders as Guillain-Barré syndrome, ask the patient about associated symptoms, such as facial pain, dysphagia, and limb weakness.
M
EDICAL CAUSES
◆ Acoustic neuroma. This tumor affects the
trigeminal nerve, causing a diminished or absent corneal reflex, tinnitus, and unilateral hearing impairment. Facial palsy and anesthesia,
palate weakness, and signs of cerebellar dysfunction (ataxia, nystagmus) may result if the
tumor impinges on the adjacent cranial nerves,
brain stem, and cerebellum.
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