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GAIT, WADDLING
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321
footdrop follow a characteristic cycle of periodic
exacerbation and remission. Muscle weakness,
usually affecting the legs, can range from minor
fatigability to paraparesis with urinary urgency
and constipation. Related findings include facial
pain, visual disturbances, paresthesia, incoordination, and sensory loss in the ankle and toes.
◆ Peroneal muscle atrophy. Bilateral step-
page gait and footdrop begin insidiously in this
disorder. Other early signs and symptoms include paresthesia, aching, cramping, coldness,
swelling, and cyanosis in the feet and legs. Foot,
peroneal, and ankle dorsiflexor muscles are affected first. As the disorder progresses, all leg
muscles become weak and atrophic, with hypoactive or absent deep tendon reflexes (DTRs).
Later, atrophy and sensory losses spread to the
hands and arms.
◆ Peroneal nerve trauma. Temporary ipsilat-
eral steppage gait occurs suddenly but resolves
with the release of peroneal nerve pressure.
Steppage gait is associated with footdrop, muscle weakness, and sensory loss over the lateral
surface of the calf and foot.
◆ Poliomyelitis. Steppage gait, usually perma-
nent and unilateral, commonly develops after
the acute stage of poliomyelitis. It’s typically
preceded by fever, asymmetrical muscle weakness, coarse fasciculations, paresthesia, hypoactive or absent DTRs, and permanent muscle paralysis and atrophy. Dysphagia, urine
retention, and respiratory difficulty may also
occur.
◆ Polyneuropathy. Diabetic polyneuropathy is
a rare cause of bilateral steppage gait, which
appears as a late but permanent effect. This
sign is preceded by burning pain in the feet and
is accompanied by leg weakness, sensory loss,
and skin ulcers.
In polyarteritis nodosa with polyneuropathy,
unilateral or bilateral steppage gait is a late finding. Related findings include vague leg pain, abdominal pain, hematuria, fever, and increased
blood pressure.
In alcoholic polyneuropathy, steppage gait
appears 2 to 3 months after the onset of vitamin
B deficiency. The gait may be bilateral, and it resolves with treatment of the deficiency. Early
findings include paresthesia in the feet, leg muscle weakness and, possibly, sensory ataxia.
◆ Spinal cord trauma. In an ambulatory pa-
tient, spinal cord trauma may cause steppage
gait. Its other effects vary with the severity of injury and may include unilateral or bilateral footdrop, neck and back pain, and vertebral tenderness and deformity. Paresthesia, sensory loss,
asymmetrical or absent DTRs, and muscle
weakness or paralysis may occur distal to the
injury. The patient may also develop fecal and
urinary incontinence.
S
PECIAL CONSIDERATIONS
The patient with steppage gait may tire rapidly
when walking because of the extra effort he
must expend to lift his feet off the ground. When
he tires, he may stub his toes, causing a fall. To
prevent this, help the patient recognize his exercise limits, and encourage him to get adequate rest. Refer him to a physical therapist, if
appropriate, for gait retraining and possible application of in-shoe splints or leg braces to
maintain correct foot alignment.
Gait, waddling
Waddling gait, a distinctive ducklike walk, is an
important sign of muscular dystrophy, spinal
muscle atrophy or, rarely, congenital hip displacement. It may be present when the child begins to walk or may appear only later in life.
The gait results from deterioration of the pelvic
girdle muscles—primarily the gluteus medius,
hip flexors, and hip extensors. Weakness in
these muscles hinders stabilization of the
weight-bearing hip during walking, causing the
opposite hip to drop and the trunk to lean toward that side in an attempt to maintain balance.
Typically, the legs assume a wide stance and
the trunk is thrown back to further improve stability, exaggerating lordosis and abdominal protrusion. In severe cases, leg and foot muscle
contractures may cause equinovarus deformity
of the foot combined with circumduction or
bowing of the legs.
H
ISTORY AND PHYSICAL
EXAMINATION
Ask the patient (or a family member if the patient is a young child) when the gait first appeared and if it has recently worsened. To determine the extent of pelvic girdle and leg
muscle weakness, ask if the patient falls frequently or has difficulty climbing stairs, rising
from a chair, or walking. Also, find out if he was
late in learning to walk or holding his head upright. Obtain a family history, focusing on problems of muscle weakness and gait and on congenital motor disorders.
Inspect and palpate leg muscles, especially
in the calves, for size and tone. Check for a
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positive Gowers’ sign (an inability to lift the
trunk without using the hands and arms to brace
and push), which indicates pelvic muscle weakness. Next, assess motor strength and function
in the shoulders, arms, and hands, looking for
weakness or asymmetrical movements.
M
EDICAL CAUSES
◆ Congenital hip dysplasia. Bilateral hip dis-
location produces a waddling gait with lordosis
and pain.
◆ Muscular dystrophy. In Duchenne’s muscu-
lar dystrophy, waddling gait becomes clinically
evident by ages 3 to 5. The gait worsens as the
disease progresses, until the child loses the ability to walk and needs a wheelchair, usually between ages 10 and 12. Early signs are usually
subtle: delay in learning to walk, frequent falls,
gait or posture abnormalities, and intermittent
calf pain. Common later findings include lordosis with abdominal protrusion, a positive Gowers’ sign, and equinovarus foot position. As the
disease progresses, its effects become more
prominent; they commonly include rapid muscle wasting beginning in the legs and spreading
to the arms (although calf and upper arm muscles may become hypertrophied, firm, and rubbery), muscle contractures, limited dorsiflexion
of the feet and extension of the knees and elbows, obesity and, possibly, mild mental retardation. If kyphoscoliosis develops, it may lead
to respiratory dysfunction and, eventually, death
from cardiac or respiratory failure.
In Becker’s muscular dystrophy, waddling gait
typically becomes apparent in late adolescence,
slowly worsens during the third decade, and
culminates in total loss of ambulation. Muscle
weakness first appears in the pelvic and upper
arm muscles. Progressive wasting with selected
muscle hypertrophy produces lordosis with abdominal protrusion, poor balance, a positive
Gowers’ sign and, possibly, mental retardation.
In facioscapulohumeral muscular dystrophy,
which usually occurs late in childhood or during
adolescence, waddling gait appears after muscle wasting has spread downward from the face
and shoulder girdle to the pelvic girdle and legs.
Earlier effects include progressive weakness
and atrophy of facial, shoulder, and arm muscles; slight lordosis; and pelvic instability.
◆ Spinal muscle atrophy. In Kugelberg-We-
lander syndrome, waddling gait occurs early
(usually after age 2) and typically progresses
slowly, culminating in total loss of ambulation
up to 20 years later. Related findings may include muscle atrophy in the legs and pelvis,
progressing to the shoulders; a positive Gowers’
sign; ophthalmoplegia; and tongue fasciculations.
In Werdnig-Hoffmann disease, waddling gait
typically begins when the child learns to walk.
Reflexes may be absent. The gait progressively
worsens, culminating in complete loss of ambulation by adolescence. Associated findings include lordosis with abdominal protrusion and
muscle weakness in the hips and thighs.
S
PECIAL CONSIDERATIONS
Although there’s no cure for waddling gait, daily
passive and active muscle-stretching exercises
should be performed for both arms and legs. If
possible, have the patient walk at least 3 hours
each day (with leg braces if necessary) to maintain muscle strength, reduce contractures, and
delay further gait deterioration. Stay near the
patient during the walk, especially if he’s on unfamiliar or uneven ground. Provide a balanced
diet to maintain energy levels and prevent obesity. Because of the grim prognosis associated
with muscular dystrophy and spinal muscle atrophy, provide emotional support for the patient
and his family.
P
ATIENT COUNSELING
Caution the patient against long, unbroken periods of bed rest, which accelerate muscle deterioration. As indicated, refer him to a local chapter of the Muscular Dystrophy Association.
Suggest genetic testing and counseling for the
parents if they’re considering having another
child.
Gallop, atrial
[S4]
An atrial (or presystolic) gallop is an extra heart
sound (known as S
palpated immediately before the first heart
sound, late in diastole. This low-pitched sound
is heard best with the bell of the stethoscope
pressed lightly against the cardiac apex. Some
clinicians say that an S
“Ten” in Tennessee (Ten ⫽ S
An atrial gallop typically results from hypertension, conduction defects, valvular disorders,
or other problems such as ischemia. Occasionally, it helps differentiate angina from other
causes of chest pain. It results from abnormal
forceful atrial contraction caused by augmented
ventricular filling or by decreased left ventricular
) that’s heard or commonly
4
has the cadence of the
4
; nes ⫽ S1; see ⫽ S2).
4
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EXAMINATION TIP
Locating heart sounds
When auscultating heart sounds, remember that certain sounds are heard best in specific areas.
Use the auscultatory points shown below to locate heart sounds quickly and accurately. Then expand your auscultation to nearby areas.
Sternoclavicular area
Suprasternal notch
Aortic area
Pulmonic area
Erb’s point
Tricuspid area (right
ventricular area)
Mitral area (left
ventricular area)
Midclavicular line
Midsternal line
323
compliance. An atrial gallop usually originates
from left atrial contraction, is heard at the apex,
and doesn’t vary with inspiration. A left-sided S
can occur in hypertensive heart disease, coronary artery disease, aortic stenosis, and cardiomyopathy. It may also originate from right
atrial contraction. A right-sided S
of pulmonary hypertension and pulmonary
stenosis. It’s heard best at the lower left sternal
border and intensifies with inspiration.
An atrial gallop seldom occurs in normal
hearts; however, it may occur in elderly people
and in athletes with physiologic hypertrophy of
the left ventricle.
EMERGENCY INTERVENTIONS Suspect
myocardial ischemia if you auscultate an
atrial gallop in a patient with chest pain. (See
Locating heart sounds. Also see Interpreting
heart sounds, pages 324 and 325.) Take the pa-
tient’s vital signs and quickly assess for signs of
heart failure, such as dyspnea, crackles, and distended jugular veins. If you detect these signs,
connect the patient to a cardiac monitor and obtain an electrocardiogram. Administer an antianginal and oxygen. If the patient has dyspnea,
elevate the head of the bed. Then auscultate for
abnormal breath sounds. If you detect coarse
is indicative
4
crackles, ensure patent I.V. access and give oxygen and diuretics as needed. If the patient has
bradycardia, he may require atropine and a
4
pacemaker.
H
ISTORY AND PHYSICAL
EXAMINATION
When the patient’s condition permits, ask about
a history of hypertension, angina, valvular
stenosis, or cardiomyopathy. If appropriate,
have him describe the frequency and severity of
anginal attacks.
M
EDICAL CAUSES
◆ Anemia. In this disorder, an atrial gallop may
accompany increased cardiac output. Associated findings may include fatigue, pallor, dyspnea,
tachycardia, bounding pulse, crackles, and a
systolic bruit over the carotid arteries.
◆ Angina. An intermittent atrial gallop char-
acteristically occurs during an anginal attack
and disappears when angina subsides. This
gallop may be accompanied by a paradoxical
second heart sound (S
Typically, the patient complains of anginal
chest pain—a feeling of tightness, pressure,
achiness, or burning that usually radiates from
) or a new murmur.
2
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EXAMINATION TIP
Interpreting heart sounds
Detecting subtle variations in heart sounds requires both concentration and practice.
Once you recognize normal heart sounds, the abnormal sounds become more obvious.
Heart sound and cause Timing and cadence
First heart sound (S1)
Vibrations associated with mitral and
tricuspid valve closure
Second heart sound (S2)
Vibrations associated with aortic and
pulmonic valve closure
Ventricular gallop (S3)
Vibrations produced by rapid blood
flow into the ventricles
Atrial gallop (S4)
Vibrations produced by an increased
resistance to sudden, forceful ejection
of atrial blood
systole diastole systole diastole
S
1S2
LUB
dub
S
1
LUB
S
dub
2
systole diastole systole diastole
S
lub
S
1
2
DUB
S
lub
1
S
2
DUB
systole diastole systole diastole
S
lub
ken
1
S
2S3
dubDEE
tucKY
S
lub
ken
1
S
2S3
dubDEE
tucKY
systole diastole systole diastole
S
S
1
2
S
4S1
DEElub
TENnes
S
dub
see
2
DEElub
TENnes
S
1
S
1
S
1
S
4S1
Summation gallop
Vibrations produced in middiastole by
simultaneous ventricular and atrial gallops, usually caused by tachycardia
the retrosternal area to the neck, jaws, left
shoulder, and arm. He may also exhibit dyspnea, tachycardia, palpitations, increased blood
pressure, dizziness, diaphoresis, belching,
nausea, and vomiting.
◆ Aortic insufficiency (acute). This disorder
causes an atrial gallop accompanied by a soft,
short diastolic murmur along the left sternal
systole diastole systole diastole systole
S
1
border. S
S2S3S4S
1
may be soft or absent. Sometimes a
2
S2S
S4S
3
S2S
S
1
3
4
soft, short midsystolic murmur may be heard
over the second right intercostal space. Related
cardiopulmonary findings may include tachycardia, a ventricular gallop (S
), dyspnea, jugular
3
vein distention, crackles and, possibly, angina.
The patient may also be fatigued and have cool
extremities.
Auscultation tips
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Best heard with the diaphragm of the stethoscope at the apex (mitral area).
Best heard with the diaphragm of the stethoscope in the second or third right and left
parasternal intercostal spaces with the patient sitting or in a supine position.
Best heard through the bell of the stethoscope at the apex with the patient in the left
lateral position. May be visible and palpable
during early diastole at the midclavicular line
between the fourth and fifth intercostal
spaces.
Best heard through the bell of the stethoscope at the apex with the patient in the left
semilateral position. May be visible in late diastole at the midclavicular line between the
fourth and fifth intercostal spaces. May also
be palpable in the midclavicular area with the
patient in the left lateral decubitus position.
Best heard through the bell of the stethoscope at the apex with the patient in the left
lateral position. May be louder than S
May be visible and palpable during diastole.
or S2.
1
◆ Aortic stenosis. This disorder usually causes
an atrial gallop, especially if valvular obstruction is severe. Auscultation reveals a harsh,
crescendo-decrescendo, systolic ejection murmur that’s loudest at the right sternal border
near the second intercostal space. Dyspnea,
angina, and syncope are cardinal associated
findings. The patient may also display crackles,
GALLOP, ATRIAL
325
palpitations, fatigue, and diminished carotid
pulses.
◆ Atrioventricular (AV) block. First-degree AV
block may cause an atrial gallop accompanied
by a faint first heart sound (S
). Although the
1
patient may have bradycardia, he’s usually
asymptomatic. In second-degree AV block, an
atrial gallop is easily heard. If bradycardia develops, the patient may also experience hypotension, light-headedness, dizziness, and fatigue. An atrial gallop is also common in
third-degree AV block. It varies in intensity with
S
and is loudest when atrial systole coincides
1
with early, rapid ventricular filling during diastole. The patient with third-degree AV block
may be asymptomatic or have hypotension,
light-headedness, dizziness, or syncope, depending on the ventricular rate. Bradycardia
may also aggravate or provoke angina or symptoms of heart failure such as dyspnea.
◆ Cardiomyopathy. An atrial gallop is a sign
associated with all types of cardiomyopathy—
dilated (most common), hypertrophic, or restrictive (least common). Additional findings may include dyspnea, orthopnea, crackles, fatigue,
syncope, chest pain, palpitations, edema, jugular vein distention, a ventricular gallop, and
transient or sustained bradycardia that’s usually
associated with tachycardia.
◆ Hypertension. One of the earliest findings in
systemic arterial hypertension is an atrial gallop. The patient may be asymptomatic, or he
may experience headache, weakness, epistaxis,
tinnitus, dizziness, and fatigue.
◆ Mitral insufficiency. In acute mitral insuffi-
ciency, auscultation may reveal an atrial gallop
accompanied by an S
, a ventricular gallop
3
that’s heard best at the apex or over the precordium. This murmur radiates to the axilla and
back and along the left sternal border. Other
features may include fatigue, dyspnea, tachypnea, orthopnea, tachycardia, crackles, and jugular vein distention.
◆ Myocardial infarction (MI). An atrial gallop
is a classic sign of life-threatening MI; in fact, it
may persist even after the infarction heals. Typically, the patient reports crushing substernal
chest pain that may radiate to the back, neck,
jaw, shoulder, and left arm. Associated signs
and symptoms include dyspnea, restlessness,
anxiety, a feeling of impending doom, diaphoresis, pallor, clammy skin, nausea, vomiting, and
increased or decreased blood pressure.
◆ Pulmonary embolism. This life-threatening
disorder causes a right-sided atrial gallop that’s
usually heard along the lower left sternal border
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with a loud pulmonic closure sound. Other features include tachycardia, tachypnea, fever,
chest pain, dyspnea, decreased breath sounds,
crackles, a pleural friction rub, apprehension,
diaphoresis, syncope, and cyanosis. The patient
may have a productive cough with blood-tinged
sputum or a nonproductive cough.
◆ Thyrotoxicosis. This disorder may produce
atrial and ventricular gallops. Its cardinal features include an enlarged thyroid gland, tachycardia, bounding pulse, widened pulse pressure,
palpitations, weight loss despite increased appetite, diarrhea, tremors, dyspnea, nervousness,
difficulty concentrating, diaphoresis, heat intolerance, exophthalmos, weakness, fatigue, and
muscle atrophy.
S
PECIAL CONSIDERATIONS
Prepare the patient for diagnostic tests, such as
electrocardiography, echocardiography, cardiac
catheterization, laboratory tests such as creatine kinase-MB and, possibly, a lung scan.
P
EDIATRIC POINTERS
An atrial gallop may occur normally in children,
especially after exercise. However, it may also
result from congenital heart defects, such as
atrial septal defect, ventricular septal defect,
patent ductus arteriosus, and severe pulmonary
valvular stenosis.
G
ERIATRIC POINTERS
Because the absolute intensity of an atrial gallop doesn’t decrease with age, as it does with
an S
, the relative intensity of S4increases com-
1
pared with S
quency of an audible S
why this sound may be considered a normal
finding in older patients.
. This explains the increased fre-
1
in elderly patients and
4
Gallop, ventricular
[S3]
A ventricular gallop is a heart sound (known as
S
) that’s associated with rapid ventricular filling
3
in early diastole. Usually palpable, this lowfrequency sound occurs about 0.15 second after
the second heart sound (S
either the right or left ventricle. A right-sided S
usually sounds louder on inspiration and is
heard best along the lower left sternal border or
over the xiphoid region. A left-sided S
sounds louder on expiration and is heard best at
the apex.
). It may originate in
2
usually
3
Ventricular gallops are easily overlooked because they’re usually faint. Fortunately, certain
techniques make their detection more likely.
These include auscultating in a quiet environment; examining the patient in the supine, left
lateral, and semi-Fowler’s positions; and having
the patient cough or raise his legs to augment
the sound.
A physiologic ventricular gallop normally occurs in children and adults younger than age 40;
however, most people lose this third heart
sound by age 40. This gallop may also occur
during the third trimester of pregnancy. An abnormal S
sign of decreased myocardial contractility, myocardial failure, and volume overload of the ventricle, as in mitral and tricuspid valve regurgitation. Although a physiologic S
timing as a pathologic S
and wanes with respiration. It’s also heard more
faintly if the patient is sitting or standing.
the earliest signs of ventricular failure. It may
result from one of two mechanisms: rapid deceleration of blood entering a stiff, noncompliant ventricle, or rapid acceleration of blood associated with increased flow into the ventricle.
A gallop that persists despite therapy indicates a
poor prognosis.
may develop both a ventricular gallop and an
atrial gallop—a condition known as a summation gallop. (See Summation gallop: Two gallops
in one.)
H
(in adults older than age 40) can be a
3
has the same
3
, its intensity waxes
3
A pathologic ventricular gallop may be one of
Patients with cardiomyopathy or heart failure
ISTORY AND PHYSICAL
EXAMINATION
After auscultating a ventricular gallop, focus
your history and examination on the cardiovascular system. Begin the history by asking the
patient if he has had any chest pain. If so, have
him describe its character, location, frequency,
and duration as well as any alleviating or aggravating factors. Also, ask about palpitations,
dizziness, or syncope. Does the patient have
difficulty breathing after exertion? While lying
down? At rest? Does he have a cough? Ask
about a history of cardiac disorders. Is the patient currently receiving any treatment for heart
failure? If so, which medications is he taking?
3
During the physical examination, carefully
auscultate for murmurs or abnormalities in the
first and second heart sounds. Then listen for
pulmonary crackles. Next, assess peripheral
pulses, noting an alternating strong and weak
pulse. Finally, palpate the liver to detect en-
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largement or tenderness, and assess for jugular
vein distention and peripheral edema.
M
EDICAL CAUSES
◆ Aortic insufficiency. Aortic insufficiency oc-
curs secondary to reduced ejection fraction and
elevated end-systolic volume. Both the acute
and chronic forms may produce a ventricular
gallop. Typically, acute aortic insufficiency also
causes an atrial gallop and a soft, short diastolic
murmur over the left sternal border. S
soft or absent. At times, a soft, short midsystolic
murmur may be heard over the second right intercostal space. Related findings include tachycardia, dyspnea, jugular vein distention, and
crackles.
Chronic aortic insufficiency produces a ventricular gallop and a high-pitched, blowing, decrescendo diastolic murmur that’s best heard
over the second or third right intercostal space
or the left sternal border. An Austin Flint murmur—an apical, rumbling, mid- to late-diastolic
murmur—may also occur. Typical related findings include palpitations, tachycardia, angina,
fatigue, dyspnea, orthopnea, and crackles.
may be
2
◆ Cardiomyopathy. A ventricular gallop is
characteristic in this disorder. When accompanied by an alternating pulse and altered first and
second heart sounds, this gallop usually signals
advanced heart disease. Other effects may include fatigue, dyspnea, orthopnea, chest pain,
palpitations, syncope, crackles, peripheral edema, jugular vein distention, and an atrial gallop.
◆ Heart failure. A ventricular gallop is a cardi-
nal sign of heart failure. When it’s loud and accompanied by sinus tachycardia, this gallop
may indicate severe heart failure. The patient
with left-sided heart failure also exhibits fatigue,
exertional dyspnea, paroxysmal nocturnal dyspnea, orthopnea and, possibly, a dry cough; the
patient with right-sided heart failure also displays jugular vein distention. Other late features
include tachypnea, chest tightness, palpitations,
anorexia, nausea, dependent edema, weight
gain, slowed mental response, diaphoresis,
hypotension, pallor, narrowed pulse pressure
and, possibly, oliguria. In some patients, inspiratory crackles, clubbing, and a tender, palpable
liver may be present. As heart failure progresses, hemoptysis, cyanosis, severe pitting edema,
and marked hepatomegaly may develop.
◆ Mitral insufficiency. Both acute and chronic
mitral insufficiency may produce a ventricular
gallop. In acute mitral insufficiency, auscultation
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Summation gallop:
Two gallops in one
When atrial and ventricular gallops occur simultaneously, they produce a short, lowpitched sound known as a summation
gallop. This relatively uncommon sound occurs during mid-diastole (between S
S
) and is best heard with the bell of the
1
stethoscope pressed lightly against the cardiac apex. It may be louder than either S
S
and may cause visible apical movement
2
during diastole.
Causes
A summation gallop may result from tachycardia or from delayed or blocked atrioventricular (AV) conduction. Tachycardia shortens ventricular filling time during diastole,
causing it to coincide with atrial contraction. When the heart rate slows, the summation gallop is replaced by separate atrial
and ventricular gallops, producing a
quadruple rhythm much like the canter of a
horse. Delayed AV conduction also brings
atrial contraction closer to ventricular filling, creating a summation gallop.
A summation gallop usually results from
heart failure or dilated congestive cardiomyopathy, but it may also accompany other
cardiac disorders. Occasionally, it signals
further cardiac deterioration. For example,
consider the hypertensive patient with a
chronic atrial gallop who develops tachycardia and a superimposed ventricular gallop. If this patient abruptly displays a summation gallop, heart failure is the likely
cause.
may also reveal an early or holosystolic decrescendo murmur at the apex, an atrial gallop,
and a widely split S
plays sinus tachycardia, tachypnea, orthopnea,
dyspnea, crackles, jugular vein distention, and
fatigue.
In chronic mitral insufficiency, a progressively
severe ventricular gallop is typical. Auscultation
also reveals a holosystolic, blowing, highpitched apical murmur. The patient may report
fatigue, exertional dyspnea, and palpitations, or
he may be asymptomatic.
. Typically, the patient dis-
2
◆ Thyrotoxicosis. This disorder may produce
ventricular and atrial gallops, but its cardinal
features are an enlarged thyroid gland, weight
loss despite increased appetite, heat intolerance,
and
2
or
1
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diaphoresis, nervousness, tremors, tachycardia,
palpitations, diarrhea, and dyspnea.
S
PECIAL CONSIDERATIONS
Monitor the patient with a ventricular gallop;
watch for and report tachycardia, dyspnea,
crackles, and jugular vein distention. Give oxygen, diuretics, and other drugs, such as digoxin
and angiotensin-converting enzyme inhibitors,
to prevent pulmonary edema.
Prepare the patient for electrocardiography,
echocardiography, gated blood pool imaging,
and cardiac catheterization.
P
EDIATRIC POINTERS
A ventricular gallop is normally heard in children. However, it may accompany congenital
abnormalities associated with heart failure,
such as a large ventricular septal defect and
patent ductus arteriosus. It may also result from
sickle cell anemia. Clearly, this gallop must be
correlated with the patient’s associated signs
and symptoms to be of diagnostic value.
Genital lesions in the male
Among the diverse lesions that may affect the
male genitalia are warts, papules, ulcers, scales,
and pustules. These common lesions may be
painful or painless, singular or multiple. They
may be limited to the genitalia or may also occur elsewhere on the body. (See Recognizing
common male genital lesions.)
Genital lesions may result from infection,
neoplasms, parasites, allergy, or the effects of
drugs. These lesions can profoundly affect the
patient’s self-image and relationships. In fact,
the patient may hesitate to seek medical attention because he fears cancer or a sexually transmitted disease (STD).
Genital lesions that arise from an STD could
mean that the patient is at risk for human immunodeficiency virus (HIV) infection. Genital ulcers make HIV transmission between sexual
partners more likely. Unfortunately, if the patient is treating himself, he may alter the lesions, making differential diagnosis especially
difficult.
H
ISTORY AND PHYSICAL
EXAMINATION
Begin by asking the patient when he first noticed the lesion. Did it erupt after he began taking a new drug or after a trip out of the country?
Has he had similar lesions before? If so, did he
get medical treatment for them? Find out if he
has been treating the lesion himself. If so, how?
Does the lesion itch? If so, is the itching constant or does it bother him only at night? Note
whether the lesion is painful. Ask for a description of any drainage from the lesion. Next, take
a complete sexual history, noting the frequency
of relations, the number of sexual partners, and
the pattern of condom use.
Before you examine the patient, observe his
clothing. Do his pants fit properly? Tight pants
or underwear, especially those made of nonabsorbent fabrics, can promote the growth of bacteria and fungi. Examine the entire skin surface,
noting the location, size, color, and pattern of
the lesions. Do genital lesions resemble lesions
on other parts of the body? Palpate for nodules,
masses, and tenderness. Also, look for bleeding,
edema, or signs of infection, such as purulent
drainage or erythema. Finally, take the patient’s
vital signs.
M
EDICAL CAUSES
◆ Balanitis and balanoposthitis. Typically,
balanitis (glans infection) and posthitis (prepuce
infection) occur together (balanoposthitis),
causing painful ulceration on the glans, foreskin, or penile shaft. Ulceration is usually preceded by 2 to 3 days of prepuce irritation and
soreness, followed by a foul discharge and edema. The patient may then develop features of
acute infection, such as fever with chills,
malaise, and dysuria. Without treatment, the ulcers may deepen and multiply. Eventually, the
entire penis and scrotum may become gangrenous, resulting in life-threatening sepsis.
◆ Bowen’s disease. This painless, premalig-
nant lesion usually occurs on the penis or scrotum but may appear elsewhere. It appears as a
brownish red, raised, scaly, indurated, welldefined plaque, which may have an ulcerated
center.
◆ Candidiasis. When this infection involves
the anogenital area, it produces erythematous,
weepy, circumscribed lesions, usually under
the prepuce. Vesicles and pustules may also
develop.
◆ Chancroid. This STD is characterized by the
eruption of one or more lesions, usually on the
groin, inner thigh, or penis. Within 24 hours,
the lesion changes from a reddened area to a
small papule. (A similar papule may erupt on
the tongue, lip, breast, or umbilicus.) It then
becomes an inflamed pustule that rapidly
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Recognizing common male genital lesions
A wide variety of lesions may affect the male genitalia. Some of the more common ones and
their causes appear below.
Penile cancer causes a painless ulcerative
lesion on the glans or foreskin, possibly
accompanied by a foul-smelling
discharge.
Genital warts are marked by clusters of
flesh-colored papillary growths that may be
barely visible or several inches in diameter.
Genital herpes begins as a swollen, slightly
pruritic wheal and later becomes a group of
small vesicles or blisters on the foreskin,
glans, or penile shaft.
Syphilis causes a hard, round papule on the
penis. When palpated, this syphilitic chancre
may feel like a button. Eventually, the papule
erodes into an ulcer. You may also note
swollen lymph nodes in the inguinal area.
ulcerates. This painful—and usually deep—ulcer
bleeds easily and commonly has a purulent gray
or yellow exudate covering its base. Rarely
more than 2 cm in diameter, it’s typically irregular in shape. The inguinal lymph nodes also enlarge, become very tender, and may drain pus.
◆ Erythroplasia of Queyrat. This premalig-
nant lesion is a form of Bowen’s disease that
appears exclusively under the foreskin of an uncircumcised penis. It typically appears as a red,
raised, well-defined, velvety, indurated plaque,
which may have an ulcerated center.
◆ Folliculitis and furunculosis. Hair follicle
infection may cause red, sharply pointed, tender
and swollen lesions with central pustules. If folliculitis progresses to furunculosis, these lesions
become hard, painful nodules that may gradually enlarge and rupture, discharging pus and
necrotic material. Rupture relieves the pain, but
erythema and edema may persist for days or
weeks.
◆ Fournier’s gangrene. In this life-threatening
form of cellulitis, the scrotum suddenly becomes tense, swollen, painful, red, warm, and
glossy. As gangrene develops, the scrotum also
becomes moist. Fever and malaise may accompany these scrotal changes.
◆ Genital herpes. Caused by herpesvirus type
I or II, this STD produces fluid-filled vesicles on
the glans penis, foreskin, or penile shaft and,
occasionally, on the mouth or anus. Usually
painless at first, these vesicles may rupture and
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become extensive, shallow, painful ulcers accompanied by redness, marked edema, and tender, inguinal lymph nodes. Other findings may
include fever, malaise, and dysuria. If the vesicles recur in the same area, the patient usually
feels localized numbness and tingling before
they erupt. Associated inflammation is typically
less marked.
◆ Genital warts. Most common in sexually ac-
tive males, genital warts initially develop on the
subpreputial sac, urethral meatus or, less commonly, the penile shaft and then spread to the
perineum and the perianal area. These painless
warts start as tiny red or pink swellings that
may grow to 10 cm and become pedunculated.
Multiple swellings are common, giving the
warts a cauliflower-like appearance. Infected
warts are also malodorous.
◆ Granuloma inguinale. Initially, this rare,
chronic STD causes a single painless macule or
papule on the external genitalia that ulcerates
and becomes a raised, beefy red lesion with a
granulated, friable border. Later, other painless
lesions may erupt and blend together on the
glans penis, foreskin, or penile shaft. Lesions
may also develop on the nose, mouth, or pharynx. Eventually, these lesions become infected,
malodorous, and painful and may be accompanied by fever, weight loss, malaise, and signs of
anemia such as weakness. Later, they’re
marked by fibrosis, keloidal scarring, and depigmentation.
◆ Leukoplakia. This precancerous disorder is
characterized by white, scaly patches on the
glans and prepuce accompanied by skin thickening and occasionally fissures.
◆ Lichen planus. Small, shiny, polygonal, vio-
let papules develop on the glans penis in this
disorder. These papules are less than 3 cm in diameter and have white, lacy, milky striations.
They may be linear or coalesce into plaques.
Occasionally, oral lesions precede genital lesions; lesions may also appear on the lower
back, ankles, and lower legs. Accompanying
findings may include pruritus, distorted nails,
and alopecia.
◆ Lymphogranuloma venereum. One to three
weeks after sexual exposure, this STD may produce a penile erosion or papule that heals
rapidly and spontaneously; in fact, it often goes
unnoticed. A few days or weeks later, the inguinal and subinguinal nodes enlarge, becoming painful, fluctuant masses. If these nodes become infected, they rupture and form sinus
tracts, discharging a thick, yellow, granular
secretion. Eventually, a scar or chronic indurated mass forms in the inguinal area. Systemic
signs and symptoms include a rash, fever with
chills, headache, migratory joint and muscle
pain, malaise, and weight loss.
◆ Pediculosis pubis. This parasitic infestation
is characterized by erythematous, pruritic
papules in the pubic area and around the anus,
abdomen, and thigh. Inspection may detect
grayish white specks (lice eggs) attached to hair
shafts. Skin irritation from scratching in these
areas is common.
◆ Penile cancer. This cancer usually produces
a painless, enlarging wartlike lesion on the
glans or foreskin. The patient may experience
localized pain, however, if the foreskin becomes
unretractable. Examination may reveal a foulsmelling discharge from the prepuce, a firm
lump in the glans, and enlarged lymph nodes.
Late signs and symptoms may include dysuria,
pain, bleeding from the lesion, and urine retention and bladder distention associated with obstruction of the urinary tract.
◆ Psoriasis. Red, raised, scaly plaques typically
affect the scalp, chest, knees, elbows, and lower
back. When they occur on the groin or on the
shaft and glans of the penis, the plaques are
usually redder; on an uncircumcised penis, the
characteristic silver scales are absent. The patient commonly reports itching and, possibly,
pain from dry, cracked, encrusted lesions. Nail
pitting and joint stiffness may also occur.
◆ Scabies. In this disorder, mites that burrow
under the skin may cause crusted lesions or
large papules on the glans and shaft of the penis and on the scrotum. Lesions may also occur
on the wrists, elbows, axillae, and waist.
They’re usually raised, threadlike, and 1 to
10 cm long and have a swollen nodule or red
papule that contains the mite. Nocturnal pruritus is typical and commonly causes excoriation.
◆ Seborrheic dermatitis. Initially, this disorder
causes erythematous, dry or moist, greasy, scaling papules with yellow crusts that enlarge to
form annular plaques. These pruritic plaques
may affect the glans and shaft of the penis,
scrotum, and groin as well as the scalp, chest,
eyebrows, back, axillae, and umbilicus.
◆ Syphilis. Two to four weeks after exposure
to the spirochete Treponema pallidum, one or
more primary lesions, or chancres, may erupt
on the genitalia; occasionally, they also erupt
elsewhere on the body, typically on the mouth
or perianal area. The chancre usually starts as a
small, red, fluid-filled papule and then erodes to
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