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Detecting congenital murmurs
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Heart defect
Type of murmur
MURMURS 451
Aortopulmonary
septal defect
Atrial septal defect
Bicuspid aortic
valve
Coarctation of the
aorta
Common
atrioventricular
canal defects
(endocardial
cushion defect)
Ebstein’s anomaly
Small defect: a continuous rough or crackling murmur best heard at the
upper left sternal border and below the left clavicle, possibly accompanied by a systolic ejection click.
Large defect: a harsh systolic murmur heard at the left sternal border.
A midsystolic, spindle-shaped murmur of grade II or III intensity heard at
the upper left sternal border, with a fixed splitting of S
may also produce a low- to medium-pitched early diastolic murmur over
the lower left sternal border.
An early systolic, loud, high-pitched ejection sound or click that’s best
heard at the apex and is commonly accompanied by a soft, early or
midsystolic murmur at the upper right sternal border. The aortic component of S
recognized until early childhood.
Usually a systolic ejection click at the base of the heart, at the apex, and
occasionally over the carotid arteries, often accompanied by a systolic
ejection murmur at the base. This disorder may also produce a blowing
diastolic murmur of aortic insufficiency or an apical pansystolic murmur
of unknown origin.
With a competent mitral valve: a midsystolic, spindle-shaped murmur of
grade II or III intensity heard at the upper left sternal border, with a fixed
splitting of S
diastolic murmur over the lower left sternal border.
decrescendo murmur at the apex, along with a widely split S
an S
A soft, high-pitched holosystolic blowing murmur that increases with inspiration (Carvallo’s sign); best heard over the lower left sternal border
and the xiphoid area; possibly accompanied by a low-pitched diastolic
rumbling murmur at the apex. Fixed splitting of S
also occur.
is usually accentuated at the apex. This murmur may not be
2
; may be accompanied by a low- to medium-pitched early
2
With an incompetent mitral valve: an early systolic or holosystolic
.
4
. Large shunts
2
and often
2
and a loud split S
2
4
Left ventricular–
right atrial
communication
Mitral atresia
Partial anomalous
pulmonary venous
connection
Patent ductus
arteriosus
Pulmonic
insufficiency
A holosystolic, decrescendo murmur of grades II to IV intensity heard
along the lower left sternal border, accompanied by a normal S
shunts also produce a diastolic rumbling murmur over the apex.
A nonspecific systolic murmur and a diastolic flow rumble at the lower
left sternal border, with one loud S
A midsystolic, spindle-shaped grade II to III murmur at the upper left
sternal border, possibly accompanied by a low- to medium-pitched early
diastolic murmur over the lower left sternal border.
A continuous rough or crackling murmur best heard at the upper left
sternal border and below the left clavicle. The murmur is accentuated
late in systole.
An early to middiastolic, soft, medium-pitched crescendo-decrescendo
murmur best heard at the second or third right intercostal space.
.
2
; large
2
(continued)
452 MURMURS
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Detecting congenital murmurs (continued)
Heart defect
Type of murmur
Pulmonic stenosis
Single atrium
Supravalvular
aortic stenosis
Tetralogy of Fallot
Tricuspid atresia
Trilogy of Fallot
Ventricular septal
defect
An early systolic, harsh, crescendo-decrescendo murmur of grades IV to
VI intensity heard at the second left intercostal space, possibly radiating
along the left sternal border.
A holosystolic regurgitant murmur at the apex, accompanied by a fixed
splitting of S
A systolic ejection murmur best heard over the second right intercostal
space or higher in the episternal notch or over the lower right side of the
neck. The aortic closure sound is usually preserved, and no ejection
clicks are heard.
A midsystolic murmur with a systolic thrill palpable at the left midsternal
border; softer murmurs occurring earlier in systole generally indicate a
more severe obstruction.
Variable, depending on associated defects.
A systolic, harsh, crescendo-decrescendo murmur, best heard at the upper left sternal border with radiation toward the left clavicle. The pulmonic component of S
grees of obstruction.
Small defect: usually a holosystolic (but may be limited to early or midsystole), grades II to IV decrescendo murmur heard along the lower left sternal border, accompanied by a normal S
Large defect: a holosystolic murmur at the lower left sternal border and a
midsystolic rumbling murmur at the apex, accompanied by an increased S
at the lower left sternal border and an increased pulmonic component of S2.
.
2
pain, dyspnea, and fatigue. (See Differential
diagnosis: Murmurs, pages 454 and 455.) Explore the patient’s medical history, noting especially any incidence of rheumatic fever, recent
dental work, heart disease, or heart surgery,
particularly prosthetic valve replacement.
Perform a systematic physical examination.
Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient’s liver tender or
palpable? Does he have peripheral edema?
M
EDICAL CAUSES
◆ Aortic insufficiency. Acute aortic insuffi-
ciency typically produces a soft, short diastolic
murmur over the left sternal border that’s best
heard when the patient sits and leans forward
and at the end of a forced held expiration. S
2
may be soft or absent. Sometimes, a soft, short
midsystolic murmur may also be heard over the
second right intercostal space. Associated findings include tachycardia, dyspnea, jugular vein
becomes progressively softer with increasing de-
2
.
2
distention, crackles, increased fatigue, and pale,
cool extremities.
Chronic aortic insufficiency causes a highpitched, blowing, decrescendo diastolic murmur
that’s best heard over the second or third right
intercostal space or the left sternal border with
the patient sitting, leaning forward, and holding
his breath after deep expiration. An Austin Flint
murmur—a rumbling, mid-to-late diastolic murmur best heard at the apex—may also occur.
Complications may not develop until ages 40 to
50; then, typical findings include palpitations,
tachycardia, angina, increased fatigue, dyspnea,
orthopnea, and crackles.
◆ Aortic stenosis. With this valvular disorder,
the murmur is systolic, beginning after S
1
ending at or before aortic valve closure. It’s
harsh and grating, medium-pitched, and
crescendo-decrescendo. Loudest over the second right intercostal space when the patient is
sitting and leaning forward, this murmur may
also be heard at the apex, at the suprasternal
notch (Erb’s point), and over the carotid arteries.
1
and
Identifying common murmurs
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MURMURS 453
The timing and configuration of a murmur
can help you identify its underlying cause.
Learn to recognize the characteristics of
these common murmurs.
Aortic insufficiency (chronic)
Thickened valve leaflets fail to close correctly, permitting backflow of blood into the left
ventricle.
Systole Diastole
S
1
S
2
S
1
Aortic stenosis
Thickened, scarred, or calcified valve leaflets
impede ventricular systolic ejection.
Systole
S
1
Diastole
S
2
S
1
If the patient has advanced disease, S2 may
be heard as a single sound, with inaudible aortic closure. An early systolic ejection click at the
apex is typical but is absent when the valve is
severely calcified. Associated signs and symptoms usually don’t appear until age 30 in congenital aortic stenosis, ages 30 to 65 in stenosis
due to rheumatic disease, and after age 65 in
calcific aortic stenosis. They may include dizziness, syncope, dyspnea on exertion, paroxysmal
nocturnal dyspnea, fatigue, and angina.
◆ Cardiomyopathy (hypertrophic). This dis-
order generates a harsh late systolic murmur,
ending at S
. Best heard over the left sternal
2
border and at the apex, the murmur is commonly accompanied by an audible S
or S4. The
3
murmur decreases with squatting and increases
with sitting down. Major associated symptoms
are dyspnea and chest pain; palpitations, dizziness, and syncope may also occur.
◆ Mitral insufficiency. Acute mitral insuffi-
ciency is characterized by a medium-pitched
blowing, early systolic or holosystolic decrescendo murmur at the apex, along with a
Mitral prolapse
Incompetent mitral valve bulges into the left
atrium because of an enlarged posterior
leaflet and elongated chordae tendineae.
Systole
S
1
Diastole
S
2
S
1
Mitral insufficiency (chronic)
Incomplete mitral valve closure permits
backflow of blood into the left atrium.
Systole
S
1
Diastole
S
2
S
1
Mitral stenosis
Thickened or scarred valve leaflets cause
valve stenosis and restrict blood flow.
Systole
S
1
widely split S
and commonly an S4. This mur-
2
Diastole
S
2
S
1
mur doesn’t get louder on inspiration as with
tricuspid insufficiency. Associated findings typically include tachycardia and signs of acute pulmonary edema.
Chronic mitral insufficiency produces a highpitched, blowing, holosystolic plateau murmur
that’s loudest at the apex and usually radiates to
the axilla or back. Fatigue, dyspnea, and palpitations may also occur.
◆ Mitral prolapse. This disorder generates a
midsystolic to late-systolic click with a highpitched late-systolic crescendo murmur, best
heard at the apex. Occasionally, multiple clicks
may be heard, with or without a systolic murmur. Associated findings include cardiac awareness, migraine headaches, dizziness, weakness,
syncope, palpitations, chest pain, dyspnea, severe episodic fatigue, mood swings, and anxiety.
◆ Mitral stenosis. With this valvular disorder,
the murmur is soft, low-pitched, rumbling,
crescendo-decrescendo, and diastolic, accompanied by a loud S
or an opening snap—a car-
1
dinal sign. It’s best heard at the apex with the
454 MURMURS
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Differential diagnosis: Murmurs
History of present illness
Focused physical examination:
Cardiovascular and pulmonary systems
Common signs and symptoms
◆ Arrhythmias
◆ Crackles
◆ Fatigue
◆ Jugular vein distention
◆ Palpitations
◆ Shortness of breath
◆ Tachycardia
Mitral insufficiency
Additional signs and symptoms
Acute
◆ Early systolic or holosystolic decrescendo
murmur at the apex
◆ Widely split S
◆ S
4
Chronic
◆ High-pitched, blowing, holosystolic mur-
mur at the apex that radiates to the axilla or
back
◆ Weight loss
◆ Nocturia
Diagnosis: Physical examination,
angiography
reatment: Medication (antibiotics [if
T
infection is present], anticoagulants [if atrial
fibrillation is present], diuretics)
Follow-up: Referral to cardiologist
2
, echocardiogram
patient in the left lateral position. Mild exercise
will help make this murmur audible.
With severe stenosis, the murmur of mitral
insufficiency may also be heard. Other findings
include hemoptysis, exertional dyspnea and fatigue, and signs of acute pulmonary edema.
◆ Myxomas. A left atrial myxoma (most com-
mon) usually produces a middiastolic murmur
and a holosystolic murmur that’s loudest at the
apex, with an S
, an early diastolic thudding
4
sound (tumor plop), and a loud, widely split S
Related features include dyspnea, orthopnea,
chest pain, fatigue, weight loss, and syncope.
Aortic insufficiency
Additional signs and symptoms
Acute
◆ Short diastolic murmur over the left
sternal border
◆ Soft or absent S
◆ Soft, midsystolic murmur over the sec-
ond right intercostal space (possibly)
Chr
onic
◆ High-pitched, blowing, decrescendo di-
astolic murmur that’s best heard over the
second or third right intercostal space
Diagnosis: Physical examination,
imaging studies (ultrasound, angiography,
echocardiogram), cardiac catheterization
Treatment: As needed (based on the
severity of symptoms), medications
(diuretics, digoxin)
Follow-up: Referral to cardiologist
A right atrial myxoma causes a late diastolic
rumbling murmur, a holosystolic crescendo
murmur, and tumor plop, best heard at the lower left sternal border. Other findings include fatigue, peripheral edema, ascites, and hepatomegaly.
A left ventricular myxoma (rare) produces a
systolic murmur, best heard at the lower left sternal border, arrhythmias, dyspnea, and syncope.
A right ventricular myxoma commonly generates a systolic ejection murmur with delayed
.
1
S
and a tumor plop, best heard at the left ster-
2
nal border. It’s accompanied by peripheral
2
Common signs and symptoms
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◆ Angina
◆ Arrhythmias
◆ Dizziness
◆ Dyspnea
◆ Fatigue
◆ Hypotension
MURMURS 455
Aortic stenosis
Additional signs and symptoms
◆ Harsh, grating systolic murmur over the
second right intercostal space, the apex, Erb’
point, or the carotid arteries
Diagnosis: Physical examination, imaging
studies (angiography, Doppler ultrasound,
chest X-ray)
Treatment: Avoidance of strenuous activity,
medication (diuretics, digoxin)
Follow-up: Reevaluation every 6 to 12
months
Additional differential diagnoses: mitral prolapse ◆ mitral stenosis ◆ myxomas ◆ papillary
muscle rupture ◆ tricuspid insufficiency ◆ tricuspid stenosis
Other causes: prosthetic valve replacement
s
edema, hepatomegaly, ascites, dyspnea, and
syncope.
◆ Papillary muscle rupture. With this life-
threatening complication of an acute MI, a loud
holosystolic murmur can be auscultated at the
apex. Related findings include severe dyspnea,
chest pain, syncope, hemoptysis, tachycardia,
and hypotension.
◆ Rheumatic fever with pericarditis. A peri-
cardial friction rub along with murmurs and gallops are heard best with the patient leaning forward on his hands and knees during forced
expiration. The most common murmurs heard
Additional signs and symptoms
◆ Harsh, late systolic murmur that ends at S
◆ Murmur located over the left sternal border
and apex
◆ S
◆ Palpitations
◆ Sudden cardiac death
Diagnosis: Physical examination, imaging
studies (chest X-ray
scan, magnetic resonance imaging,
angiography), echocardiogram
T
therapy
Follow-up: Referral to cardiologist
are the systolic murmur of mitral insufficiency, a
midsystolic murmur due to swelling of the
leaflet of the mitral valve, and the diastolic murmur of aortic insufficiency. Other signs and
symptoms include fever, joint and sternal pain,
edema, and tachypnea.
◆ Tricuspid insufficiency. This valvular ab-
normality is characterized by a soft, highpitched, holosystolic blowing murmur that increases with inspiration (Carvallo’s sign),
decreases with exhalation and Valsalva’s maneuver, and is best heard over the lower left
sternal border and the xiphoid area. Following a
Cardiomyopathy
or S4(possibly)
3
, computed tomography
reatment: Symptomatic treatment, oxygen
2
456 MUSCLE ATROPHY
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lengthy asymptomatic period, exertional dyspnea and orthopnea may develop, along with
jugular vein distention, ascites, peripheral
cyanosis and edema, muscle wasting, fatigue,
weakness, and syncope.
◆ Tricuspid stenosis. This valvular disorder
produces a diastolic murmur similar to that of
mitral stenosis, but louder with inspiration and
decreased with exhalation and Valsalva’s maneuver. S
and symptoms include fatigue, syncope, peripheral edema, jugular vein distention, ascites,
hepatomegaly, and dyspnea.
O
◆ Treatments. Prosthetic valve replacement
may cause variable murmurs, depending on the
location, valve composition, and method of operation.
S
PECIAL CONSIDERATIONS
Prepare the patient for diagnostic tests, such as
electrocardiography, echocardiography, and angiography. Administer an antibiotic and an anticoagulant as appropriate. Because any cardiac
abnormality is frightening to the patient, provide emotional support.
P
Innocent murmurs, such as Still’s murmur, are
commonly heard in young children and typically
disappear in puberty. Pathognomonic heart
murmurs in infants and young children usually
result from congenital heart disease, such as
atrial and ventricular septal defects. Other murmurs can be acquired, as with rheumatic heart
disease.
P
ATIENT COUNSELING
Instruct the patient to contact his physician before undergoing invasive procedures or dental
work because prophylactic antibiotics may be
necessary.
may also be louder. Associated signs
1
THER CAUSES
EDIATRIC POINTERS
Muscle atrophy
[Muscle wasting]
Muscle atrophy results from denervation or prolonged muscle disuse. When deprived of regular
exercise, muscle fibers lose both bulk and
length, producing a visible loss of muscle size
and contour and apparent emaciation or deformity in the affected area. Even slight atrophy
usually causes some loss of motion or power.
Atrophy usually results from neuromuscular
disease or injury. However, it may also stem
from certain metabolic and endocrine disorders
and prolonged immobility. Some muscle atrophy also occurs with aging.
H
ISTORY AND PHYSICAL
EXAMINATION
Ask the patient when and where he first noticed
the muscle wasting and how it has progressed.
Also ask about associated signs and symptoms,
such as weakness, pain, loss of sensation, and
recent weight loss. Review the patient’s medical history for chronic illnesses; musculoskeletal or neurologic disorders, including trauma;
and endocrine and metabolic disorders. Ask
about his use of alcohol and drugs, particularly
steroids.
Begin the physical examination by determining the location and extent of atrophy. Visually
evaluate small and large muscles. Check all major muscle groups for size, tonicity, and
strength. (See Testing muscle strength, pages 464
and 465.) Measure the circumference of all
limbs, comparing sides. (See Measuring limb cir-
cumference.) Check for muscle contractures in
all limbs by fully extending joints and noting
any pain or resistance. Complete the examination by palpating peripheral pulses for quality
and rate, assessing sensory function in and
around the atrophied area, and testing deep
tendon reflexes.
M
EDICAL CAUSES
◆ Amyotrophic lateral sclerosis. Initial symp-
toms of this progressive disease include muscle
weakness and atrophy that typically begin in
one hand, spread to the arm, and then develop
in the other hand and arm. Eventually, weakness and atrophy spread to the trunk, neck,
tongue, larynx, pharynx, and legs; progressive
respiratory muscle weakness leads to respiratory insufficiency. Other findings include muscle
flaccidity, fasciculations, hyperactive deep tendon reflexes, slight leg muscle spasticity, dysphagia, impaired speech, excessive drooling,
and depression.
◆ Burns. Fibrous scar tissue formation, pain,
and loss of serum proteins from severe burns
can limit muscle movement, resulting in atrophy.
◆ Compartment syndrome and Volkmann’s
ischemic contracture. With this acute disorder,
muscle atrophy is a late sign of irreversible ischemia, along with contractures, paralysis, and
loss of pulses. Earlier signs and symptoms
include severe pain that increases with passive
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muscle movement, along with weakness and
paresthesia.
◆ Herniated disk. Here, pressure on nerve
roots leads to muscle weakness, disuse, and ultimately, atrophy. The primary symptom is severe lower back pain, possibly radiating to the
buttocks, legs, and feet and commonly accompanied by muscle spasms. Diminished reflexes
and sensory changes may also occur.
◆ Hypercortisolism. This disorder may cause
limb weakness and eventually atrophy. Related
cushingoid features include buffalo hump,
moon face, truncal obesity, purple striae, thin
skin, acne, easy bruising, poor wound healing,
elevated blood pressure, fatigue, hyperpigmentation, and diaphoresis. The male patient may
be impotent; the female patient may develop
hirsutism and menstrual irregularities.
◆ Hypothyroidism. Reversible weakness and
atrophy of proximal limb muscles may occur
in hypothyroidism. Associated findings commonly include muscle cramps and stiffness;
cold intolerance; weight gain despite anorexia; mental dullness; dry, pale, cool, doughy
skin; puffy face, hands, and feet; and bradycardia.
◆ Meniscal tear. Quadriceps muscle atrophy,
resulting from prolonged knee immobility and
muscle weakness, is a classic sign of this traumatic disorder.
◆ Multiple sclerosis. This degenerative dis-
ease may produce arm and leg atrophy as a result of chronic progressive weakness; spasticity
and contractures may also develop. Associated
signs and symptoms typically wax and wane
and include diplopia and blurred vision, nystagmus, hyperactive deep tendon reflexes, sensory
loss or paresthesia, dysarthria, dysphagia, incoordination, ataxic gait, intention tremors, emotional lability, impotence, and urinary dysfunction.
◆ Osteoarthritis. This chronic disorder even-
tually causes atrophy proximal to involved
joints as a result of progressive weakness and
disuse. Other late signs and symptoms include
bony joint deformities, such as Heberden’s
nodes on the distal interphalangeal joints,
Bouchard’s nodes on the proximal interphalangeal joints, crepitus and fluid accumulation,
and contractures.
◆ Parkinson’s disease. With this disorder,
muscle rigidity, weakness, and disuse may
produce muscle atrophy. The patient may exhibit insidious resting tremors that usually begin in
MUSCLE ATROPHY 457
Measuring limb
circumference
To ensure accurate and consistent limb circumference measurements, mark and use a
consistent reference point each time and
measure with the limb in full extension.
The illustration below shows the correct
reference points for arm and leg measurements.
ARM
Biceps
circumference
Olecranon
process
Forearm
circumference
LEG
Quadriceps
circumference
Patella
Calf
circumference
458 MUSCLE ATROPHY
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the fingers (pill-rolling tremor), worsen with
stress, and ease with purposeful movement and
sleep. He may also develop bradykinesia; a
characteristic propulsive gait; a high-pitched,
monotone voice; masklike facies; drooling; dysphagia; dysarthria; and occasionally, oculogyric
crisis or blepharospasm.
◆ Peripheral nerve trauma. Injury to or pro-
longed pressure on a peripheral nerve leads to
muscle weakness and atrophy. Associated findings include paresthesia or sensory loss, pain,
and loss of reflexes supplied by the damaged
nerve. Paralysis may also occur.
◆ Peripheral neuropathy. With this disorder,
muscle weakness progresses slowly to flaccid
paralysis and eventually atrophy. Distal extremity muscles are generally affected first. Associated findings include loss of vibration sense;
paresthesia, hyperesthesia, or anesthesia in the
hands and feet; mild to sharp, burning pain; anhidrosis; glossy red skin; and diminished or absent deep tendon reflexes.
◆ Protein deficiency. If chronic, this may lead
to muscle weakness and atrophy. Other findings
include chronic fatigue, apathy, anorexia, dry
skin, peripheral edema, and dull, sparse, dry hair.
◆ Radiculopathy. Damaged spinal nerve roots
can cause muscle atrophy as well as weakness,
paralysis, severe pain and, at times, loss of feeling in the areas supplied by the affected nerves.
◆ Rheumatoid arthritis. Muscle atrophy oc-
curs in the late stages of this disorder, as joint
pain and stiffness decrease range of motion and
discourage muscle use.
◆ Shy-Drager syndrome. This rare, progressive
neurologic syndrome is characterized by muscle
atrophy, orthostatic hypotension, incontinence,
tremor, rigidity, incoordination, and ataxia. It’s
most common in young and middle-aged adults.
◆ Spinal cord injury. Trauma to the spinal
cord can produce severe muscle weakness and
flaccid, then spastic, paralysis, eventually leading to atrophy. Other signs and symptoms depend on the level of injury but may include respiratory insufficiency or paralysis, sensory
losses, bowel and bladder dysfunction, hyperactive deep tendon reflexes, positive Babinski’s reflex, sexual dysfunction, priapism, hypotension,
and anhidrosis (usually unilateral).
◆ Stroke. Stroke may produce contralateral
or bilateral weakness and eventually atrophy
of the arms, legs, face, and tongue. Associated
signs and symptoms depend on the site and
extent of vascular damage and may include
dysarthria, aphasia, ataxia, apraxia, agnosia,
and ipsilateral paresthesia or sensory loss.
The patient may develop visual disturbance,
altered level of consciousness, amnesia and
poor judgment, personality changes, and emotional lability. He may also report bowel and
bladder dysfunction, vomiting, headache, and
seizures.
◆ Thyrotoxicosis. This disorder may produce
insidious, generalized muscle weakness and atrophy. Related findings include extreme anxiety,
fatigue, heat intolerance, diaphoresis, tremors,
tachycardia, palpitations, ventricular or atrial
gallop, dyspnea, weight loss, and an enlarged
thyroid. Exophthalmos may be present.
O
THER CAUSES
◆ Drugs. Prolonged steroid therapy interferes
with muscle metabolism and leads to atrophy,
most prominently in the limbs.
◆ Immobility. Prolonged immobilization from
bed rest, casts, splints, or traction may cause
muscle weakness and atrophy.
S
PECIAL CONSIDERATIONS
Because contractures can occur as atrophied
muscle fibers shorten, help the patient maintain
muscle length by encouraging him to perform
frequent, active range-of-motion exercises. If he
can’t actively move a joint, provide activeassistive or passive exercises, and apply splints
or braces to maintain muscle length. If you find
resistance to full extension during exercise, use
heat, pain medication, or relaxation techniques
to relax the muscle. Then slowly stretch it to full
extension. (Caution: Don’t pull or strain the
muscle; you may tear muscle fibers and cause
further contracture.) If these techniques fail to
correct the contracture, use moist heat, a
whirlpool bath, resistive exercises, or ultrasound therapy. If these techniques aren’t effective, surgical release of contractures may be
necessary.
Teach the patient to use necessary assistive
devices properly to ensure his safety and prevent falls. Have the patient consult a physical
therapist for a specialized therapy regimen.
Prepare the patient for electromyography,
nerve conduction studies, muscle biopsy, and Xrays or computed tomography scans.
P
EDIATRIC POINTERS
In young children, profound muscle weakness
and atrophy can result from muscular dystrophy. Muscle atrophy may also result from
cerebral palsy and poliomyelitis, and from
paralysis associated with meningocele and
myelomeningocele.
MUSCLE FLACCIDITY
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459
Muscle flaccidity
[Muscle hypotonicity]
Flaccid muscles are profoundly weak and soft,
with decreased resistance to movement, increased mobility, and greater than normal range
of motion. The result of disrupted muscle innervation, flaccidity can be localized to a limb or
muscle group or generalized over the entire
body. Its onset may be acute, as in trauma, or
chronic, as in neurologic disease.
EMERGENCY INTERVENTIONS If the
patient’s muscle flaccidity results from trauma,
make sure his cervical spine has been stabilized.
Quickly determine his respiratory status. If you note
signs and symptoms of respiratory insufficiency—
dyspnea, shallow respirations, nasal flaring,
cyanosis, and decreased oxygen saturation—
administer oxygen by nasal cannula or mask.
Intubation and mechanical ventilation may be
necessary.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient isn’t in distress, ask about the onset and duration of muscle flaccidity and any
precipitating factors. Ask about associated
symptoms, notably weakness, other muscle
changes, and sensory loss or paresthesia.
Examine the affected muscles for atrophy,
which indicates a chronic problem. Test muscle
strength, and check deep tendon reflexes in all
limbs.
M
EDICAL CAUSES
◆ Amyotrophic lateral sclerosis. Progressive
muscle weakness and paralysis are accompanied by generalized flaccidity. Typically, these effects begin in one hand, spread to the arm, and
then develop in the other hand and arm. Eventually, they spread to the trunk, neck, tongue,
larynx, pharynx, and legs; progressive respiratory muscle weakness leads to respiratory insufficiency. Other findings include muscle cramps
and coarse fasciculations, hyperactive deep tendon reflexes, slight leg muscle spasticity, dysphagia, dysarthria, excessive drooling, and depression.
◆ Brain lesions. Frontal and parietal lobe le-
sions may cause contralateral flaccidity, weakness or paralysis, and eventually, spasticity and
possibly contractures. Other findings include
hyperactive deep tendon reflexes, positive
Babinski’s sign, loss of proprioception, stereognosis, graphesthesia, anesthesia, and thermanesthesia.
◆ Cerebellar disease. With this disease, gener-
alized muscle flaccidity or hypotonia is accompanied by ataxia, dysmetria, intention tremor,
slight muscle weakness, fatigue, and dysarthria.
◆ Guillain-Barré syndrome. This disorder
causes muscle flaccidity. Progression is typically
symmetrical and ascending, moving from the
feet to the arms and facial nerves within 24 to
72 hours of onset. Associated findings include
sensory loss or paresthesia, absent deep tendon
reflexes, tachycardia (or, less often, bradycardia), fluctuating hypertension and orthostatic
hypotension, diaphoresis, incontinence, dysphagia, dysarthria, hypernasality, and facial diplegia. Weakness may progress to total motor
paralysis and respiratory failure.
◆ Huntington’s disease. Besides flaccidity,
progressive mental status changes up to and including dementia and choreiform movements
are major symptoms. Others include poor balance, hesitant or explosive speech, dysphagia,
impaired respirations, and incontinence.
◆ Muscle disease. Muscle weakness and flac-
cidity are features of myopathies and muscular
dystrophies.
◆ Peripheral nerve trauma. Flaccidity, paraly-
sis, and loss of sensation and reflexes in the innervated area can occur.
◆ Peripheral neuropathy. Flaccidity usually
occurs in the legs as a result of chronic progressive muscle weakness and paralysis. It may also
cause mild-to-sharp burning pain, glossy red
skin, anhidrosis, and loss of vibration sensation.
Paresthesia, hyperesthesia, or anesthesia may
affect the hands and feet. Deep tendon reflexes
may be hypoactive or absent.
◆ Poliomyelitis. Damage to the anterior horn
cells in the spinal cord and brain stem causes
flaccid weakness and loss of reflexes. The large,
proximal muscles of the limbs are most commonly affected.
◆ Seizure disorder. Brief periods of syncope
and generalized flaccidity commonly follow a
generalized tonic-clonic seizure.
◆ Spinal cord injury. Spinal shock can result
in acute muscle flaccidity or spasticity below the
level of injury. Associated signs and symptoms
also occur below the level of injury and may include paralysis; absent deep tendon reflexes;
analgesia; thermanesthesia; loss of proprioception and vibration, touch, and pressure sensation; and anhidrosis (usually unilateral).
Hypotension, bowel and bladder dysfunction,
and impotence or priapism may also occur. Injury in the C1 to C5 region can produce respiratory paralysis and bradycardia.
460 MUSCLE SPASMS
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S
PECIAL CONSIDERATIONS
Provide regular, systematic, passive range-ofmotion exercises to preserve joint mobility and
to increase circulation. Reposition a patient
with generalized flaccidity every 2 hours to protect him from skin breakdown. Pad bony
prominences and other pressure points, and
prevent thermal injury by testing bath water
yourself before the patient bathes. Treat isolated flaccidity by supporting the affected limb in a
sling or with a splint. Ensure patient safety and
reduce the risk of falls by introducing assistive
devices and their proper use. Consult a physician and occupational therapist to formulate a
personalized therapy regimen and foster independence.
Prepare the patient for diagnostic tests, such
as cranial and spinal X-rays, computed tomography scans, and electromyography.
P
EDIATRIC POINTERS
Pediatric causes of muscle flaccidity include
myelomeningocele, Lowe’s disease, WerdnigHoffmann disease, and muscular dystrophy. An
infant or young child with generalized flaccidity
may lie in a froglike position, with his hips and
knees abducted.
Muscle spasms
[Muscle cramps]
Muscle spasms are strong, painful contractions.
They can occur in virtually any muscle but are
most common in the calf and foot. Muscle
spasms typically occur from simple muscle fatigue, after exercise, and during pregnancy.
However, they may also develop in electrolyte
imbalances and neuromuscular disorders, or as
the result of certain drugs. They’re typically precipitated by movement, especially a quick or
jerking movement, and can usually be relieved
by slow stretching.
EMERGENCY INTERVENTIONS If the pa-
tient complains of frequent or unrelieved
spasms in many muscles, accompanied by paresthesia in his hands and feet, quickly attempt to
elicit Chvostek’s and Trousseau’s signs. If these
signs are present, suspect hypocalcemia. Evaluate
respiratory function, watching for the development
of laryngospasm; provide supplemental oxygen as
necessary, and prepare to intubate the patient and
provide mechanical ventilation. Draw blood for
calcium and electrolyte levels and arterial blood
gas analysis, and insert an I.V. catheter for
administration of a calcium supplement. Monitor
cardiac status, and prepare to begin resuscitation
if necessary.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient isn’t in distress, ask when the
spasms began. Is there any particular activity
that precipitates them? How long did they last?
How painful were they? Did anything worsen or
lessen the pain? Ask about other symptoms,
such as weakness, sensory loss, or paresthesia.
Evaluate muscle strength and tone. Then,
check all major muscle groups and note
whether any movements precipitate spasms.
Test the presence and quality of all peripheral
pulses, and examine the limbs for color and
temperature changes. Test capillary refill time
(normal is less than 3 seconds), and inspect for
edema, especially in the involved area. Observe
for signs and symptoms of dehydration such as
dry mucous membranes. Obtain a thorough
drug and diet history. Ask the patient if he has
had recent vomiting or diarrhea. Finally, test reflexes and sensory function in all extremities.
M
EDICAL CAUSES
◆ Amyotrophic lateral sclerosis. With this
disorder, muscle spasms may accompany progressive muscle weakness and atrophy that typically begin in one hand, spread to the arm, and
then spread to the other hand and arm. Eventually, muscle weakness and atrophy affect the
trunk, neck, tongue, larynx, pharynx, and legs;
progressive respiratory muscle weakness leads
to respiratory insufficiency. Other findings include muscle flaccidity progressing to spasticity,
coarse fasciculations, hyperactive deep tendon
reflexes, dysphagia, impaired speech, excessive
drooling, and depression.
◆ Arterial occlusive disease. Arterial occlu-
sion typically produces spasms and intermittent
claudication in the leg, with residual pain. Associated findings are usually localized to the legs
and feet and include loss of peripheral pulses,
pallor or cyanosis, decreased sensation, hair
loss, dry or scaling skin, edema, and ulcerations.
◆ Cholera. Muscle spasms, severe water and
electrolyte loss, thirst, weakness, decreased
skin turgor, oliguria, tachycardia, and hypotension occur along with abrupt watery diarrhea
and vomiting.
◆ Dehydration. Sodium loss may produce limb
and abdominal cramps. Other findings include a
slight fever, decreased skin turgor, dry mucous
membranes, tachycardia, orthostatic hypoten-
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