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other signs of shock (such as tachycardia,
tachypnea, and cool, clammy skin) and altered
mental status. Any significant changes can indicate complications, such as massive GI bleeding
or pericarditis with tamponade.
M
EDICAL CAUSES
◆ End-stage chronic renal failure. Ammonia
breath odor is a late finding in end-stage chronic
renal failure. Accompanying signs and symptoms include anuria, skin pigmentation changes
and excoriation, brown arcs under the nail margins, tissue wasting, Kussmaul’s respirations,
neuropathy, lethargy, somnolence, confusion,
disorientation, behavior changes, irritability, and
emotional lability. Later neurologic signs that
signal impending uremic coma include muscle
twitching and fasciculations, asterixis, paresthesia, and footdrop. Cardiovascular findings include hypertension, myocardial infarction, signs
of heart failure, pericarditis, and even sudden
death and stroke. GI findings include anorexia,
weight loss, nausea, heartburn, vomiting, constipation, hiccups, and a metallic taste. Oral signs
and symptoms may include stomatitis, gum ulceration and bleeding, and a coated tongue. The
patient has an increased risk of peptic ulceration
and acute pancreatitis. Uremic frost, pruritus,
and signs of hormonal changes, such as impotence or amenorrhea, may also appear.
S
PECIAL CONSIDERATIONS
Ammonia breath odor is offensive to others, but
the patient may become accustomed to it. As a
result, remind him to perform frequent mouth
care, particularly before meals because reducing
the foul taste and odor may stimulate his appetite. A half-strength hydrogen peroxide mixture or lemon juice gargle helps neutralize the
ammonia; the patient may also want to use
commercial lozenges or breath sprays or to suck
on hard candy. Advise him to use a soft-bristled
toothbrush or sponge to prevent trauma. If he
can’t perform mouth care, do it for him and
teach his family members how to assist him.
Maximize dietary intake by offering the patient frequent small meals of his favorite foods,
within dietary limitations.
P
EDIATRIC POINTERS
Ammonia breath odor also occurs in children
with end-stage chronic renal failure. Provide
hard candy to relieve bad taste and odor. If the
child can gargle, try mixing hydrogen peroxide
with flavored mouthwashes.
P
ATIENT COUNSELING
Involve the patient at an early stage in the various aspects of treatment to help prepare him for
any complicated training that may be needed
later—for example, if he needs dialysis or transplantation. Explain dietary and drug therapies.
Breath with fecal odor
Fecal breath odor typically accompanies fecal
vomiting associated with a long-standing intestinal obstruction or gastrojejunocolic fistula.
It represents an important late diagnostic clue
to a potentially life-threatening GI disorder because complete obstruction of any part of the
bowel, if untreated, can cause death within
hours from vascular collapse and shock.
When the obstructed or adynamic intestine
attempts self-decompression by regurgitating its
contents, vigorous peristaltic waves propel
bowel contents backward into the stomach.
When the stomach fills with intestinal fluid, further reverse peristalsis results in vomiting. The
odor of feculent vomitus lingers in the mouth.
Fecal breath odor may also occur in patients
with a nasogastric (NG) or intestinal tube. The
odor is detected only while the underlying disorder persists and abates soon after its resolution.
EMERGENCY INTERVENTIONS Because
fecal breath odor signals a potentially lifethreatening intestinal obstruction, you’ll need to
quickly evaluate your patient’s condition. Monitor his vital signs, and be alert for signs of
shock, such as hypotension, tachycardia, narrowed pulse pressure, and cool, clammy skin.
Ask the patient if he’s experiencing nausea or
has vomited. Find out the frequency of vomiting
as well as the color, odor, amount, and consistency of the vomitus. Have an emesis basin
nearby to collect and accurately measure the
vomitus.
Anticipate possible surgery to relieve an obstruction or repair a fistula, and withhold all food
and fluids. Be prepared to insert an NG or intestinal tube for GI tract decompression. Insert a peripheral I.V. catheter for vascular access, or assist
with central venous access device insertion for
large-bore access and central venous pressure
monitoring. Obtain a blood sample and send it to
the laboratory for complete blood count and electrolyte analysis because large fluid losses and
shifts can produce electrolyte imbalances. Maintain adequate hydration and support circulatory
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status with additional fluids. Give a physiologic
solution—such as lactated Ringer’s or normal
saline solution or Plasmanate—to prevent metabolic acidosis from gastric losses and metabolic
alkalosis from intestinal fluid losses.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient’s condition permits, ask about previous abdominal surgery because adhesions can
cause an obstruction. Also ask about loss of appetite. Is the patient experiencing abdominal
pain? If so, have him describe its onset, duration, and location. Ask if the pain is intense,
persistent, or spasmodic. Have the patient describe his normal bowel habits, especially noting constipation, diarrhea, or leakage of stool.
Ask when the patient’s last bowel movement
occurred, and have him describe the stool’s color and consistency.
Auscultate for bowel sounds; hyperactive,
high-pitched sounds may indicate an impending
bowel obstruction, whereas hypoactive or absent sounds occur late in obstruction and paralytic ileus. Inspect the abdomen, noting its contour and any surgical scars. Measure abdominal
girth to provide baseline data for subsequent assessment of distention. Palpate the abdomen for
tenderness, distention, and rigidity. Percuss it
for tympany, indicating a gas-filled bowel, and
dullness, indicating fluid.
Rectal and pelvic examinations should be
performed. All patients with a suspected bowel
obstruction should have a flat and upright abdominal X-ray; some will also need a chest
X-ray, sigmoidoscopy, and a barium enema.
M
EDICAL CAUSES
◆ Gastrojejunocolic fistula. Symptoms of
gastrojejunocolic fistula may be variable and intermittent because of temporary plugging of the
fistula. They may include fecal vomiting with resulting fecal breath odor, but the chief complaint is usually diarrhea accompanied by abdominal pain. Related GI findings include
anorexia, weight loss, abdominal distention,
and possibly marked malabsorption.
◆ Large-bowel obstruction. Vomiting is usu-
ally absent at first, but fecal vomiting with resulting fecal breath odor occurs as a late sign.
Typically, symptoms develop more slowly than
in small-bowel obstruction. Colicky abdominal
pain appears suddenly, followed by continuous hypogastric pain. Marked abdominal distention and tenderness occur, and loops of
large bowel may be visible through the
abdominal wall. Although constipation develops,
defecation may continue for up to 3 days after
a complete obstruction because of stool remaining in the bowel below the obstruction.
Leakage of stool is common in a partial obstruction.
◆ Small-bowel obstruction, distal. In late ob-
struction, nausea is present but vomiting may
be delayed. Vomitus initially consists of gastric
contents, then changes to bilious contents, followed by fecal contents with resulting fecal
breath odor. Accompanying symptoms include
achiness, malaise, drowsiness, and polydipsia.
Bowel changes (ranging from diarrhea to constipation) are accompanied by abdominal distention, persistent epigastric or periumbilical
colicky pain, hyperactive bowel sounds, and
borborygmus. As the obstruction becomes complete, bowel sounds become hypoactive or absent. Fever, hypotension, tachycardia, and rebound tenderness may indicate strangulation or
perforation.
S
PECIAL CONSIDERATIONS
After an NG or intestinal tube has been inserted,
keep the head of the bed elevated at least
30 degrees and turn the patient on his right side
to facilitate passage of the intestinal tube
through the GI tract. Don’t tape the intestinal
tube to the patient’s face. Ensure tube patency
by monitoring drainage and checking that suction devices function properly. Irrigate as required. Monitor GI drainage, and send serum
specimens to the laboratory for electrolyte
analysis at least once a day. Prepare the patient
for diagnostic tests, such as abdominal X-rays,
barium enema, and proctoscopy.
P
EDIATRIC POINTERS
Carefully monitor the child’s fluid and electrolyte
status because dehydration can occur rapidly
from persistent vomiting. The absence of tears
and dry or parched mucous membranes are important clinical signs of dehydration.
G
ERIATRIC POINTERS
In older patients, early surgical intervention
may be necessary for a bowel obstruction that
doesn’t respond to decompression because of
the high risk of bowel infarct.
P
ATIENT COUNSELING
Encourage the patient to brush his teeth and
gargle with a flavored mouthwash or a halfstrength hydrogen peroxide mixture to minimize offensive breath odor. Assure him that the
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123
fecal odor is temporary and will abate after
treatment of the underlying cause.
Breath with fruity odor
Fruity breath odor results from respiratory elimination of excess acetone. This sign characteristically occurs in ketoacidosis, a potentially lifethreatening condition that requires immediate
treatment to prevent severe dehydration, irreversible coma, and death.
Ketoacidosis results from the excessive catabolism of fats for cellular energy in the absence of usable carbohydrates. This process begins when insulin levels are insufficient to
transport glucose into the cells, as in diabetes
mellitus, or when glucose is unavailable and
hepatic glycogen stores are depleted, as in lowcarbohydrate diets and malnutrition. Lacking
glucose, the cells burn fat faster than enzymes
can handle the ketones, the acidic end products.
As a result, the ketones (acetone, beta-hydroxybutyric acid, and acetoacetic acid) accumulate
in the blood and urine. To compensate for increased acidity, Kussmaul’s respirations expel
carbon dioxide with enough acetone to flavor
the breath. Eventually, this compensatory mechanism fails, producing ketoacidosis.
EMERGENCY INTERVENTIONS When
you detect fruity breath odor, check for
Kussmaul’s respirations and examine the patient’s level of consciousness (LOC). Take vital
signs and check skin turgor. Be alert for fruity
breath odor that accompanies rapid, deep respirations; stupor; and poor skin turgor. Try to obtain a brief history, noting especially diabetes
mellitus, nutritional problems such as anorexia
nervosa, and fad diets with little or no carbohydrates. Obtain venous and arterial blood samples for complete blood count and glucose, electrolyte, acetone, and arterial blood gas (ABG)
levels. Also obtain a urine specimen to test for
glucose and acetone. Administer I.V. fluids and
electrolytes to maintain hydration and electrolyte
balance, and give regular insulin to patients
with diabetic ketoacidosis to reduce blood glucose levels.
If the patient is obtunded, you’ll need to insert
endotracheal and nasogastric (NG) tubes. Suction
as needed. Insert an indwelling urinary catheter,
and monitor intake and output. Insert central venous pressure and arterial lines to monitor the
patient’s fluid status and blood pressure. Connect
the patient to a cardiac monitor, monitor vital
signs and neurologic status, and draw blood
hourly to check glucose, electrolyte, acetone, and
ABG levels.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient isn’t in severe distress, obtain a
thorough history. Ask about the onset and duration of fruity breath odor. Also ask about any
changes in breathing pattern, increased thirst,
frequent urination, weight loss, fatigue, and abdominal pain. Ask the female patient if she has
had candidal vaginitis or vaginal secretions with
itching. If the patient has a history of diabetes
mellitus, ask about stress, infections, and noncompliance with therapy—the most common
causes of ketoacidosis in known diabetics. If the
patient is suspected of having anorexia nervosa,
obtain a dietary and weight history.
M
EDICAL CAUSES
◆ Anorexia nervosa. Severe weight loss asso-
ciated with anorexia nervosa may produce
fruity breath odor, usually with nausea, constipation, and cold intolerance. Induced vomiting
may cause dental enamel erosion and scars or
calluses in the dorsum of the hand.
◆ Ketoacidosis. Fruity breath odor accompa-
nies alcoholic ketoacidosis, which is usually
seen in poorly nourished alcoholics with a history of vomiting, abdominal pain, and only minimal food intake over several days. Kussmaul’s
respirations begin abruptly and accompany dehydration, abdominal pain and distention, and
absent bowel sounds. Blood glucose levels are
normal or slightly decreased.
In diabetic ketoacidosis, fruity breath odor
commonly acompanies the development of ketoacidosis over 1 to 2 days. Other findings include polydipsia, polyuria, nocturia, weak and
rapid pulse, hunger, weight loss, weakness, fatigue, nausea, vomiting, and abdominal pain.
Eventually, Kussmaul’s respirations, orthostatic
hypotension, dehydration, tachycardia, confusion, and stupor occur. Signs and symptoms
may lead to coma.
Starvation ketoacidosis is a potentially lifethreatening disorder that has a gradual onset.
Besides fruity breath odor, typical findings include signs of cachexia and dehydration, decreased LOC, bradycardia, and a history of
anorexia nervosa.
O
THER CAUSES
◆ Drugs. Any drug known to cause metabolic
acidosis, such as nitroprusside and salicylates,
can result in fruity breath odor.
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◆ Low-carbohydrate diets. Diets that promote
little or no carbohydrate intake may cause ketoacidosis and the resulting fruity breath odor.
S
PECIAL CONSIDERATIONS
Provide emotional support for the patient and
his family. Explain tests and treatments clearly.
When the patient is more alert and his condition
stabilizes, remove the NG tube and start him on
an appropriate diet. Switch his insulin from the
I.V. to the subcutaneous route.
P
EDIATRIC POINTERS
Fruity breath odor in an infant or a child usually
stems from uncontrolled diabetes mellitus. Ketoacidosis develops rapidly in this age-group
because of their low glycogen reserves. As a result, prompt administration of insulin and correction of fluid and electrolyte imbalance are
necessary to prevent shock and death.
P
ATIENT COUNSELING
Patient teaching and referrals should be based
on the underlying cause. For example, teach the
patient with uncontrolled diabetes mellitus to
recognize the signs of hyperglycemia and to
wear a medical identification bracelet. Refer the
patient with starvation ketoacidosis to a psychologist or a support group, and recognize the
need for possible long-term follow-up.
Brudzinski’s sign
A positive Brudzinski’s sign (flexion of the hips
and knees in response to passive flexion of the
neck) signals meningeal irritation. Passive flexion of the neck stretches the nerve roots, causing pain and involuntary flexion of the knees
and hips.
Brudzinski’s sign is a common and important
early indicator of life-threatening meningitis
and subarachnoid hemorrhage. It can be elicited
in children as well as adults, although more reliable indicators of meningeal irritation exist for
infants.
Testing for Brudzinski’s sign isn’t part of a
routine physical examination unless meningeal
irritation is suspected. (See Testing for Brudzins-
ki’s sign.)
EMERGENCY INTERVENTIONS If the pa-
tient is alert, ask him about headache, neck
pain, nausea, and vision disturbances (blurred or
double vision and photophobia)—all indications of
increased intracranial pressure (ICP). Next, observe
the patient for signs and symptoms of increased
ICP, such as an altered level of consciousness
(LOC), pupillary changes, bradycardia, widened
pulse pressure, irregular respiratory patterns
(Cheyne-Stokes or Kussmaul’s respirations), vomiting, and moderate fever.
Keep artificial airways, intubation equipment, a
handheld resuscitation bag, and suction equipment on hand because the patient’s condition may
suddenly deteriorate. Elevate the head of his bed
30 to 60 degrees to promote venous drainage. Administer an osmotic diuretic, such as mannitol, to
reduce cerebral edema.
Be alert for further increases in ICP. You may
have to provide mechanical ventilation and administer a barbiturate and additional doses of a
diuretic. Also, cerebrospinal fluid (CSF) may have
to be drained.
H
ISTORY AND PHYSICAL
EXAMINATION
Continue your neurologic examination by evaluating the patient’s cranial nerve function and
noting any motor or sensory deficits. Be sure to
look for Kernig’s sign (resistance to knee extension after flexion of the hip), a further indication
of meningeal irritation. Also look for signs of
central nervous system infection, such as fever
and nuchal rigidity.
Ask the patient—or his family if necessary—
about a history of hypertension, spinal arthritis,
or recent head trauma. Also ask about dental
work and abscessed teeth (a possible cause of
meningitis), open-head injury, endocarditis, and
I.V. drug abuse. Ask about the sudden onset of
headaches, which may be associated with subarachnoid hemorrhage.
M
EDICAL CAUSES
◆ Arthritis. A positive Brudzinski’s sign can
occasionally be elicited in patients with severe
spinal arthritis. The patient may also report
back pain (especially after weight bearing) and
limited mobility.
◆ Meningitis. A positive Brudzinski’s sign can
usually be elicited 24 hours after the onset of
meningitis, a life-threatening disorder. Accompanying findings may include headache, a positive Kernig’s sign, nuchal rigidity, irritability or
restlessness, deep stupor or coma, vertigo, fever
(high or low, depending on the severity of the infection), chills, malaise, hyperalgesia, muscular
hypotonia, opisthotonos, symmetrical deep tendon reflexes, papilledema, ocular and facial
palsies, nausea and vomiting, photophobia,
diplopia, and unequal, sluggish pupils. As ICP
rises, arterial hypertension, bradycardia,
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Testing for Brudzinski’s sign
Here’s how to test for Brudzinski’s sign when you suspect meningeal irritation:
With the patient in a supine position, place your hands behind her neck and lift her head to-
ward her chest.
sive neck flexion.
widened pulse pressure, Cheyne-Stokes or Kussmaul’s respirations, and coma may develop.
◆ Subarachnoid hemorrhage. A positive
Brudzinski’s sign may be elicited within minutes
after initial bleeding in subarachnoid hemorrhage, a life-threatening disorder. Accompanying signs and symptoms include sudden onset of
a severe headache, nuchal rigidity, altered LOC,
dizziness, photophobia, cranial nerve palsies (as
evidenced by ptosis, pupil dilation, and limited
extraocular muscle movement), nausea and
vomiting, fever, and a positive Kernig’s sign.
Focal signs—such as hemiparesis, vision distur-
bances, and aphasia—may also occur. As ICP
rises, arterial hypertension, bradycardia,
widened pulse pressure, Cheyne-Stokes or Kussmaul’s respirations, and coma may develop.
S
PECIAL CONSIDERATIONS
Many patients with a positive Brudzinski’s sign
are critically ill. They need constant ICP monitoring and frequent neurologic checks in addition to intensive assessment and monitoring of
vital signs, intake and output, and cardiorespiratory status. To promote patient comfort,
maintain low lights and minimal noise and
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elevate the head of the bed. The patient usually
won’t receive an opioid analgesic because it
may mask signs of increased ICP.
Prepare the patient for diagnostic tests. These
may include blood, urine, and sputum cultures
to identify bacteria; lumbar puncture to assess
CSF and relieve pressure; and computed tomography scan, magnetic resonance imaging, cerebral angiography, or spinal X-rays to locate a
hemorrhage.
P
EDIATRIC POINTERS
Brudzinski’s sign may not be a useful indicator
of meningeal irritation in infants because more
reliable signs—such as bulging fontanels, a
weak cry, fretfulness, vomiting, and poor
feeding—appear early.
Bruits
Commonly an indicator of life- or limb-threatening vascular disease, bruits are swishing sounds
caused by turbulent blood flow. They’re characterized by location, duration, intensity, pitch, and
time of onset in the cardiac cycle. Loud bruits
produce intense vibration and a palpable thrill. A
thrill, however, doesn’t provide any further clue
to the causative disorder or its severity.
Bruits are most significant when heard over
the abdominal aorta; the renal, carotid, femoral,
popliteal, or subclavian artery; or the thyroid
gland. (See Preventing false bruits.) They’re also
significant when heard consistently despite
changes in patient position and when heard
during diastole.
H
ISTORY AND PHYSICAL
EXAMINATION
If you detect bruits over the abdominal aorta,
check for a pulsating mass or a bluish discoloration around the umbilicus (Cullen’s sign). Either of these signs—or severe, tearing pain in the
abdomen, flank, or lower back—may signal lifethreatening dissection of an aortic aneurysm.
Also check peripheral pulses, comparing intensity in the upper and lower extremities.
If you suspect dissection, monitor the patient’s vital signs continuously, and withhold
food and fluids until a definitive diagnosis is
made. Watch for signs and symptoms of hypovolemic shock, such as thirst; hypotension;
tachycardia; weak, thready pulse; tachypnea; altered level of consciousness (LOC); mottled
knees and elbows; and cool, clammy skin.
If you detect bruits over the thyroid gland,
ask the patient if he has a history of hyperthyroidism or signs and symptoms of it, such as
nervousness, tremors, weight loss, palpitations,
heat intolerance, and (in females) amenorrhea.
Watch for signs and symptoms of life-threatening thyroid storm, such as tremor, restlessness,
diarrhea, abdominal pain, and hepatomegaly.
If you detect carotid artery bruits, be alert for
signs and symptoms of a transient ischemic attack (TIA), including dizziness, diplopia, slurred
speech, flashing lights, and syncope. These findings may indicate an impending stroke. Be sure
to evaluate the patient frequently for changes in
LOC and muscle function.
If you detect bruits over the femoral,
popliteal, or subclavian artery, watch for signs
and symptoms of decreased or absent peripheral circulation—edema, weakness, and paresthesia. Ask the patient if he has a history of intermittent claudication. Frequently check distal
pulses and skin color and temperature. Pallor,
coolness, or the sudden absence of a pulse may
indicate a threat to the affected limb.
If you detect a bruit, be sure to check for further vascular damage and perform a thorough
cardiac assessment.
M
EDICAL CAUSES
◆ Abdominal aortic aneurysm. A pulsating
periumbilical mass accompanied by a systolic
bruit over the aorta characterizes an abdominal
aortic aneurysm. Associated signs and symptoms include a rigid, tender abdomen; mottled
skin; diminished peripheral pulses; and claudication. Sharp, tearing pain in the abdomen,
flank, or lower back signals imminent dissection.
◆ Abdominal aortic atherosclerosis. Loud
systolic bruits in the epigastric and midabdominal areas are common in this disorder. They
may be accompanied by leg pain, weakness,
numbness, paresthesia, or paralysis or by decreased or absent femoral, popliteal, or pedal
pulses. Abdominal pain is rare.
◆ Anemia. Increased cardiac output in anemia
causes increased blood flow. In patients with severe anemia, short systolic bruits may be heard
over both carotid arteries and may be accompanied by headache, fatigue, dizziness, pallor,
jaundice, palpitations, mild tachycardia, dyspnea, nausea, anorexia, and glossitis.
◆ Carotid artery stenosis. Systolic bruits heard
over one or both carotid arteries may be the only
sign of this disorder. However, dizziness,
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EXAMINATION TIP
Preventing false bruits
Auscultating bruits accurately requires practice and skill. These sounds typically stem from arterial luminal narrowing or arterial dilation, but they can also result from excessive pressure
applied to the stethoscope’s bell during auscultation. This pressure compresses the artery, creating turbulent blood flow and a false bruit.
To prevent false bruits, place the bell lightly on the patient’s skin. Also, if you’re auscultating
for a popliteal bruit, help the patient to a supine position, place your hand behind his ankle, and
lift his leg slightly before placing the bell behind the knee.
NORMAL BLOOD FLOW, NO BRUIT
TURBULENT BLOOD FLOW AND RESULTANT BRUIT CAUSED BY ANEURYSM
TURBULENT BLOOD FLOW AND FALSE BRUIT CAUSED BY COMPRESSION OF ARTERY
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vertigo, headache, syncope, aphasia, dysarthria,
sudden vision loss, hemiparesis, or hemiparalysis signals TIA and may herald a stroke.
◆ Carotid cavernous fistula. Continuous
bruits heard over the eyeballs and temples are
characteristic, as are vision disturbances and
protruding, pulsating eyeballs.
◆ Peripheral arteriovenous fistula. A rough,
continuous bruit with systolic accentuation may
be heard over the fistula; a palpable thrill is also
common.
◆ Peripheral vascular disease. Peripheral
vascular disease characteristically produces
bruits over the femoral artery and other arteries
in the legs. It can also cause diminished or absent femoral, popliteal, or pedal pulses; intermittent claudication; numbness, weakness,
pain, and cramping in the legs, feet, and hips;
and cool, shiny skin and hair loss on the affected
extremity. It also predisposes the patient to lower
extremity ulcers that heal with difficulty.
◆ Renal artery stenosis. Systolic bruits are
commonly heard over the abdominal midline
and flank on the affected side. Hypertension
commonly accompanies stenosis. Headache,
palpitations, tachycardia, anxiety, dizziness,
retinopathy, hematuria, and mental sluggishness may also appear.
◆ Subclavian steal syndrome. In subclavian
steal syndrome, systolic bruits may be heard
over one or both subclavian arteries as a result
of narrowing of the arterial lumen. They may be
accompanied by decreased blood pressure and
claudication in the affected arm, hemiparesis,
vision disturbances, vertigo, and dysarthria.
◆ Thyrotoxicosis. A systolic bruit is commonly
heard over the thyroid gland. Accompanying
signs and symptoms appear in all body systems,
but the most characteristic ones include thyroid
enlargement, fatigue, nervousness, tachycardia,
heat intolerance, sweating, tremor, diarrhea,
and weight loss despite increased appetite. Exophthalmos may also be present.
S
PECIAL CONSIDERATIONS
Because bruits can signal a life-threatening vascular disorder, frequently check the patient’s
vital signs and auscultate over the affected
arteries. Be especially alert for bruits that become louder or develop a diastolic component.
As needed, administer prescribed drugs, such
as a vasodilator, an anticoagulant, an antiplatelet drug, or an antihypertensive. Prepare
the patient for diagnostic tests, such as blood
studies, radiography, an electrocardiogram, cardiac catheterization, and ultrasonography.
P
EDIATRIC POINTERS
Bruits are common in young children but are
usually of little significance—for example, cranial bruits are normal until age 4. However, certain bruits may be significant. Because birthmarks commonly accompany congenital
arteriovenous fistulas, carefully auscultate for
bruits in a child with port-wine spots or cavernous or diffuse hemangiomas.
G
ERIATRIC POINTERS
Elderly people with atherosclerosis may experience bruits over several arteries. Those related
to carotid artery stenosis are particularly important because of the high incidence of associated
stroke. Close follow-up is mandatory as well as
prompt surgical referral when indicated.
P
ATIENT COUNSELING
Instruct the patient to inform the physician if he
develops dizziness, pain, or any symptom that
suggests a stroke because this may indicate a
worsening of his condition.
Buffalo hump
Buffalo hump, characterized by an accumulation of cervicodorsal fat, may indicate hypercortisolism (Cushing’s syndrome). Hypercortisolism
itself may result from long-term glucocorticoid
therapy, adrenal carcinoma, adrenal adenoma,
ectopic corticotropin production, or excessive
pituitary secretion of corticotropin (Cushing’s
disease). Buffalo hump doesn’t help distinguish
between the underlying causes of hypercortisolism, but it may help direct diagnostic testing.
H
ISTORY AND PHYSICAL
EXAMINATION
Ask the patient about recent weight gain and
when he first noticed the buffalo hump. Typically, a history of moderate to extreme obesity,
with accumulation of adipose tissue in the nape
of the neck, face, and trunk and thinning of the
arms and legs, indicates hypercortisolism. (See
Recognizing hypercortisolism.) If the patient has
an old photograph, use it to compare his current
and former weight and distribution of adipose
tissue. Ask if the patient or any family member
has a history of endocrine disorders, cancer, or
obesity. If the patient is a female of childbearing
age, ask the date of her last menses and about
any changes in her normal menstrual pattern.
Next, ask about any changes in diet or drug use.
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Recognizing hypercortisolism
Buffalo hump, moon face, and truncal obesity are the cardinal signs of hypercortisolism. In addition to these and the other signs shown here, hypertension, osteoporosis, and emotional lability
may also occur.
Fluid retention around
eyes and face
Acne, moon face,
hirsutism
Buffalo hump
(cervicodorsal fat)
Ecchymoses
Thinning of extremities
(muscle wasting and
weakness)
Purple striae
Poor wound healing
Protruding abdomen
Girdle obesity
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If the patient is receiving glucocorticoid therapy,
ask about the dosage, schedule, administration
route, and any recent changes in therapy.
Take the patient’s vital signs, height, and
weight. Form an impression of his appearance,
noting obvious signs of hypercortisolism, such as
hirsutism, diaphoresis, and moon (roundish) face.
Inspect the arms, legs, and trunk for striae, and
note skin turgor for thin skin. Assess muscle function by asking the patient to rise from a squatting
position; note any difficulty because this may indicate quadriceps muscle weakness. These patients
will typically have proximal muscle weakness (for
example, limb or girdle weakness).
During your assessment, observe the patient’s behavior. Extreme emotional lability
along with depression, irritability, or confusion
may signal hypercortisolism.
M
EDICAL CAUSES
◆ Hypercortisolism. Buffalo hump varies in
size, depending on the severity of hypercortisolism and the amount of weight gain. It’s commonly accompanied by hirsutism, moon face,
and truncal obesity with slender arms and legs.
The skin may appear transparent, with purple
striae and ecchymoses. Other findings include
acne, muscle weakness and wasting, fatigue,
poor wound healing, elevated blood pressure,
personality changes, and amenorrhea or
oligomenorrhea in women or impotence in
men.
◆ Morbid obesity. The size of the buffalo
hump depends on the amount of weight gain
and the distribution of adipose tissue. Associated signs and symptoms include generalized adiposity, silver striae, elevated blood pressure,
and hypogonadism.
O
THER CAUSES
◆ Drugs. Buffalo hump may result from exces-
sive doses of a glucocorticoid, such as cortisone, hydrocortisone, prednisone, or dexamethasone. Long-term glucocorticoid therapy is
the most common cause in the United States.
S
PECIAL CONSIDERATIONS
Prepare the patient for diagnostic tests. Blood
and urine tests can confirm hypercortisolism;
ultrasonography, computed tomography (CT)
scan, or arteriography can localize adrenal
tumors. Chest X-rays, bronchography, and an
SIGNS & SYMPTOMS
Butterfly rash: Causes and associated findings
Common
causes
Discoid lupus
erythematosus
Erysipelas
Polymorphous
light eruption
Rosacea
Seborrheic
dermatitis
Systemic lupus
erythematosus
Major associated signs and symptoms
Acne
Alopecia
Anorexia
Cervical
adenopathy
Erythema
Fever
Headache
Maculopapular
lesions
•
•
•
•• •
•
•
•
•
•
•
•• •• •
Malaise
Mucous
membrane
lesions
•
Photosensitivity
•
•
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