Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2920_Библиотеки_им_академика_М_И_Перельмана
.pdf
218 DIPLOPIA
https://t.me/medicina_free
◆ Brain tumor. Diplopia may be an early
symptom of a brain tumor. Associated signs and
symptoms vary with the tumor’s size and location but may include eye deviation, emotional
lability, decreased LOC, headache, vomiting, absence or generalized tonic-clonic seizures,
hearing loss, visual field deficits, abnormal
pupillary responses, nystagmus, motor weakness, and paralysis.
◆ Cavernous sinus thrombosis. This disorder
may produce diplopia and limited eye movement. Associated signs and symptoms include
exophthalmos, orbital and eyelid edema, diminished or absent pupillary responses, impaired
visual acuity, papilledema, and fever.
◆ Diabetes mellitus. Among the long-term ef-
fects of this disorder may be diplopia due to isolated third cranial nerve palsy. Diplopia typically
begins suddenly and may be accompanied by
pain.
◆ Encephalitis. Initially, this disorder may
cause a brief episode of diplopia and eye deviation. However, it usually begins with sudden
onset of high fever, severe headache, and
vomiting. As the inflammation progresses, the
patient may display signs of meningeal irritation, decreased LOC, seizures, ataxia, and
paralysis.
◆ Head injury. Potentially life-threatening
head injuries may cause diplopia, depending on
the site and extent of the injury. Associated
signs and symptoms include eye deviation,
pupillary changes, headache, decreased LOC,
altered vital signs, nausea, vomiting, and motor
weakness or paralysis.
◆ Intracranial aneurysm. This life-threaten-
ing disorder initially produces diplopia and eye
deviation, perhaps accompanied by ptosis and a
dilated pupil on the affected side. The patient
complains of a recurrent, severe, unilateral,
frontal headache. After the aneurysm ruptures,
the headache becomes violent. Associated signs
and symptoms include neck and spinal pain and
rigidity, decreased LOC, tinnitus, dizziness, nausea, vomiting, and unilateral muscle weakness
or paralysis.
◆ Multiple sclerosis (MS). Diplopia, a com-
mon early symptom of MS, is usually accompanied by blurred vision and paresthesia. As MS
progresses, signs and symptoms may include
nystagmus, constipation, muscle weakness,
paralysis, spasticity, hyperreflexia, intention
tremor, gait ataxia, dysphagia, dysarthria, impotence, emotional lability, and urinary frequency,
urgency, and incontinence.
◆ Myasthenia gravis. This disorder initially
produces diplopia and ptosis, which worsen
throughout the day. It then progressively involves other muscles, resulting in blank facial
expression; nasal voice; difficulty chewing,
swallowing, and making fine hand movements
and, possibly, signs of life-threatening respiratory muscle weakness.
◆ Ophthalmologic migraine. Most common
in young adults, this disorder results in diplopia
that persists for days after the headache resolves. Accompanying signs and symptoms include severe unilateral pain, ptosis, and extraocular muscle palsies. Irritability, depression,
or slight confusion may also occur.
◆ Orbital blowout fracture. This fracture usu-
ally causes monocular diplopia affecting the upward gaze. However, with marked periorbital
edema, diplopia may affect other directions of
gaze. This fracture commonly causes periorbital
ecchymosis but doesn’t affect visual acuity,
although eyelid edema may prevent accurate
testing. Subcutaneous crepitation of the eyelid
and orbit is typical. Occasionally, the patient’s
pupil is dilated and unreactive, and he may have
a hyphema.
◆ Orbital cellulitis. Inflammation of the orbital
tissues and eyelids causes sudden diplopia as
well as eye deviation and pain, purulent
drainage, eyelid edema, chemosis and redness,
exophthalmos, nausea, and fever.
◆ Orbital tumor. An enlarging tumor can
cause diplopia, exophthalmos and, possibly,
blurred vision.
◆ Stroke. Diplopia characterizes this life-
threatening disorder when it affects the vertebrobasilar artery. Other signs and symptoms include unilateral motor weakness or paralysis,
ataxia, decreased LOC, dizziness, aphasia, visual field deficits, circumoral numbness, slurred
speech, dysphagia, and amnesia.
◆ Thyrotoxicosis. Diplopia occurs when ex-
ophthalmos characterizes the disorder. It usually begins in the upper field of gaze because of
infiltrative myopathy involving the inferior rectus muscle. It’s accompanied by impaired eye
movement, excessive tearing, eyelid edema
and, possibly, inability to close the eyelids.
Other cardinal findings include tachycardia,
palpitations, weight loss, diarrhea, tremors, an
enlarged thyroid, dyspnea, nervousness,
diaphoresis, and heat intolerance.
◆ Transient ischemic attack (TIA). A TIA,
which may be a warning sign of a future
stroke, is generally accompanied by diplopia,
DIZZINESS 219
https://t.me/medicina_free
dizziness, tinnitus, hearing loss, and numbness. It can last for a few seconds or up to
24 hours.
O
THER CAUSES
◆ Eye surgery. Fibrosis associated with eye
surgery may restrict eye movement, resulting in
diplopia.
S
PECIAL CONSIDERATIONS
Continue to monitor vital signs and neurologic
status if you suspect an acute neurologic disorder. Prepare the patient for neurologic tests
such as a computed tomography scan. Provide a
safe environment. If the patient has severe
diplopia, remove sharp obstacles and assist him
with ambulation. Also, institute seizure precautions if indicated.
P
EDIATRIC POINTERS
Strabismus, which can be congenital or acquired at an early age, produces diplopia; however, diplopia is a rare complaint in young children because the brain rapidly compensates for
double vision by suppressing one image.
School-age children who complain of double
vision require a careful examination to rule out
serious disorders such as a brain tumor.
Dizziness
A common symptom, dizziness is a sensation of
imbalance or faintness, sometimes associated
with giddiness, weakness, confusion, and
blurred or double vision. Episodes of dizziness
are usually brief; they may be mild or severe
with an abrupt or gradual onset. Dizziness may
be aggravated by standing up quickly and alleviated by lying down and by rest.
Dizziness typically results from inadequate
blood flow and oxygen supply to the cerebrum
and spinal cord. It’s a key symptom in certain
serious disorders, such as hypertension and vertebrobasilar artery insufficiency, and it may also
occur in anxiety, respiratory and cardiovascular
disorders, and postconcussion syndrome.
Dizziness is commonly confused with
vertigo—a sensation of revolving in space or of
surroundings revolving around oneself.
However, unlike dizziness, vertigo is commonly
accompanied by nausea, vomiting, nystagmus,
staggering gait, and tinnitus or hearing loss.
Dizziness and vertigo may occur together, as in
postconcussion syndrome.
EMERGENCY INTERVENTIONS If the pa-
tient complains of dizziness, first ensure his
safety by preventing falls, and then determine the
severity and onset of the dizziness. Ask the patient
to describe it. Is it associated with headache or
blurred vision? Next, take the patient’s blood pressure while he’s lying, sitting, and standing to
check for orthostatic hypotension. Ask about a
history of high blood pressure. Determine if the
patient is at risk for hypoglycemia. Tell the patient
to lie down, and recheck his vital signs every
15 minutes. Insert an I.V. catheter, and prepare to
administer medications as ordered.
H
ISTORY AND PHYSICAL
EXAMINATION
Ask about a history of diabetes and cardiovascular disease. Is the patient taking drugs prescribed for high blood pressure? If so, when did
he take his last dose?
If the patient’s blood pressure is normal, obtain a more complete history. Ask if he’s had a
myocardial infarction, heart failure, kidney disease, or atherosclerosis, which may predispose
him to cardiac arrhythmias, hypertension, and a
transient ischemic attack. Does he have a
history of anemia, chronic obstructive pulmonary disease, anxiety disorders, or head
injury? Obtain a complete drug history.
Next, explore the patient’s dizziness. How often does it occur? How long does each episode
last? Does the dizziness abate spontaneously?
Does it lead to loss of consciousness? Find out if
dizziness is triggered by sitting or standing up
suddenly or by stooping over. Does being in a
crowd make the patient feel dizzy? Ask about
emotional stress. Has the patient been irritable or
anxious lately? Does he have insomnia or difficulty concentrating? Look for fidgeting and eyelid
twitching. Does the patient startle easily? Also,
ask about palpitations, chest pain, diaphoresis,
shortness of breath, and chronic cough.
Next, perform a physical examination. Begin
with a quick neurocheck, assessing the patient’s
level of consciousness (LOC), motor and
sensory function, and reflexes. Then inspect for
poor skin turgor and dry mucous membranes,
signs of dehydration. Auscultate heart rate and
rhythm. Inspect for barrel chest, clubbing,
cyanosis, and use of accessory muscles. Also
auscultate breath sounds. Take the patient’s
blood pressure while he’s lying, sitting, and
standing to check for orthostatic hypotension.
Test capillary refill time in the extremities, and
palpate for edema.
220 DIZZINESS
https://t.me/medicina_free
M
EDICAL CAUSES
◆ Anemia. Anemia typically causes dizziness
that’s aggravated by postural changes or exertion. Other signs and symptoms include pallor,
dyspnea, fatigue, tachycardia, bounding pulse,
and increased capillary refill time.
◆ Cardiac arrhythmias. Dizziness lasts for
several seconds or longer and may precede
fainting in arrhythmias. The patient may experience palpitations; irregular, rapid, or thready
pulse and, possibly, hypotension. He may also
experience weakness, blurred vision, paresthesia, and confusion.
◆ Carotid sinus hypersensitivity. This disor-
der is characterized by brief episodes of dizziness that usually terminate in fainting. These
episodes are precipitated by stimulation of one
or both carotid arteries by seemingly minor
sensations or actions, such as wearing a tight
collar or moving the head. Associated signs
and symptoms include sweating, nausea, and
pallor.
◆ Emphysema. Dizziness may follow exertion
or the chronic productive cough that’s characteristic of this disorder. Associated signs and
symptoms include dyspnea, anorexia, weight
loss, malaise, use of accessory muscles, pursedlip breathing, tachypnea, peripheral cyanosis,
and diminished breath sounds. Barrel chest and
clubbing may occur.
◆ Generalized anxiety disorder. This disorder
produces persistent anxiety (for at least 1
month), insomnia, difficulty concentrating, irritability and, possibly, continuous dizziness that
may intensify as the anxiety worsens. The patient may show signs of motor tension—for example, twitching or fidgeting, muscle aches, a
furrowed brow, and a tendency to be startled.
He may also display signs of autonomic hyperactivity, such as diaphoresis, palpitations, cold
and clammy hands, dry mouth, paresthesia, indigestion, hot or cold flashes, frequent urination, diarrhea, a lump in the throat, pallor, and
increased pulse and respiratory rates.
◆ Hypertension. In patients with hyperten-
sion, dizziness may precede fainting, but it may
also be relieved by rest. Other common signs
and symptoms include headache and blurred
vision. Retinal changes include hemorrhage,
sclerosis of retinal blood vessels, exudate, and
papilledema.
◆ Hyperventilation syndrome. Episodes of
hyperventilation cause dizziness that usually
lasts a few minutes; however, if these episodes
occur frequently, dizziness may persist between
them. Other effects include apprehension, diaphoresis, pallor, dyspnea, chest tightness, palpitations, trembling, fatigue, and peripheral and
circumoral paresthesia.
◆ Hypoglycemia. Dizziness is a central nerv-
ous system (CNS) disturbance that can result
from fasting hypoglycemia. It’s generally accompanied by headache, clouding of vision,
restlessness, and mental status changes.
◆ Hypovolemia. Dizziness may be accompa-
nied by other signs of fluid volume deficit, such
as dry mucous membranes, decreased blood
pressure, and increased heart rate.
◆ Orthostatic hypotension. This condition
produces dizziness that may terminate in fainting or disappear with rest. Related findings include dim vision, spots before the eyes, pallor,
diaphoresis, hypotension, tachycardia and, possibly, signs of dehydration.
◆ Panic disorder. Dizziness may accompany
acute attacks of panic in patients with this disorder. Other findings include anxiety, dyspnea,
palpitations, chest pain, a choking or smothering sensation, vertigo, paresthesia, hot and cold
flashes, diaphoresis, and trembling or shaking.
The patient may feel like he’s dying or losing his
mind.
◆ Postconcussion syndrome. Occurring 1 to
3 weeks after a head injury, this syndrome is
marked by dizziness, headache (throbbing,
aching, bandlike, or stabbing), emotional
lability, alcohol intolerance, fatigue, anxiety and,
possibly, vertigo. Dizziness and other symptoms
are intensified by mental or physical stress. The
syndrome may persist for years, but symptoms
eventually abate.
◆ Rift Valley fever. Typical signs and symp-
toms of this disorder include dizziness, fever,
myalgia, weakness, and back pain. A small percentage of patients may develop encephalitis or
may progress to hemorrhagic fever, which can
lead to shock and hemorrhage. Inflammation of
the retina may result in some permanent vision
loss.
◆ Transient ischemic attack (TIA). Lasting
from a few seconds to 24 hours, a TIA commonly signals an impending stroke and may be
triggered by turning the head to the side. Besides dizziness of varying severity, TIAs are
marked by unilateral or bilateral diplopia,
blindness or visual field deficits, ptosis, tinnitus,
hearing loss, paresis, and numbness. Other
findings may include dysarthria, dysphagia,
vomiting, hiccups, confusion, decreased LOC,
and pallor.
O
https://t.me/medicina_free
THER CAUSES
◆ Drugs. Anxiolytics, CNS depressants, opi-
oids, decongestants, antihistamines, antihypertensives, and vasodilators commonly cause
dizziness.
HERB ALERT Herbal remedies, such as
St. John’s wort, can produce dizziness.
S
PECIAL CONSIDERATIONS
Prepare the patient for diagnostic tests, such as
blood studies, arteriography, computed tomography scan, EEG, magnetic resonance imaging,
and tilt-table studies.
P
EDIATRIC POINTERS
Dizziness is less common in children than in
adults. Many children have difficulty describing
this symptom and instead complain of tiredness, stomachache, or feeling sick. If you suspect dizziness, also assess the patient for vertigo, a more common symptom in children that
may result from a vision disorder, an ear infection, or antibiotic therapy.
P
ATIENT COUNSELING
Teach the patient ways to control dizziness. If
he’s hyperventilating, have him breathe and rebreathe into his cupped hands or a paper bag. If
he experiences dizziness in an upright position,
tell him to lie down and rest and then to rise
slowly. Advise the patient with carotid sinus hypersensitivity to avoid wearing garments that
constrict the neck. Instruct the patient who risks
a TIA from vertebrobasilar insufficiency to turn
his body instead of sharply turning his head to
one side.
DOLL’S EYE SIGN, ABSENT 221
EXAMINATION TIP
Testing for absent
doll’s eye sign
To evaluate the patient’s oculocephalic re-
flex, hold her upper eyelids open and quickly
(but gently) turn her head from side to side,
noting eye movements with each head turn.
In absent doll’s eye sign, the eyes remain
fixed in midposition.
Doll’s eye sign, absent
[Negative oculocephalic reflex]
An indicator of brain stem dysfunction, the absence of the doll’s eye sign is detected by rapid,
gentle turning of the patient’s head from side to
side. The eyes remain fixed in midposition, instead of the normal response of moving laterally
toward side opposite the direction the head is
turned. (See Testing for absent doll’s eye sign.)
The absence of doll’s eye sign indicates injury
to the midbrain or pons, involving cranial
nerves III and VI. It typically accompanies a
coma caused by lesions of the cerebellum and
brain stem. This sign usually can’t be relied
upon in a conscious patient because he can
control eye movements voluntarily. Absent
222 DROOLING
https://t.me/medicina_free
doll’s eye sign is necessary for a diagnosis of
brain death.
A variant of absent doll’s eye sign that devel-
ops gradually is known as abnormal doll’s eye
sign. Because conjugate eye movement is lost,
one eye may move laterally while the other remains fixed or moves in the opposite direction.
An abnormal doll’s eye sign usually accompanies metabolic coma or increased intracranial
pressure (ICP). Associated brain stem dysfunction may be reversible or may progress to deeper coma in patients with this sign.
H
ISTORY AND PHYSICAL
EXAMINATION
After detecting an absent doll’s eye sign, perform a neurologic examination. First, evaluate
the patient’s level of consciousness (LOC), using
the Glasgow Coma Scale. Note decerebrate or
decorticate posture. Examine the pupils for size,
equality, and response to light. Check for signs
of increased ICP—increased systolic blood pressure, widening pulse pressure, and bradycardia.
M
EDICAL CAUSES
◆ Brain stem infarction. This infarction caus-
es absent doll’s eye sign with a coma. It also
causes limb paralysis, cranial nerve palsies (facial weakness, diplopia, blindness or visual field
deficits, and nystagmus), bilateral cerebellar
ataxia, variable sensory loss, a positive Babinski’s reflex, decerebrate posture, and muscle
flaccidity.
◆ Brain stem tumor. Absent doll’s eye sign
accompanies a coma in this type of tumor. This
sign may be preceded by hemiparesis, nystagmus, extraocular nerve palsies, facial pain or
sensory loss, facial paralysis, diminished
corneal reflex, tinnitus, hearing loss, dysphagia,
drooling, vertigo, dizziness, ataxia, and
vomiting.
◆ Central midbrain infarction. Accompany-
ing absent doll’s eye sign are a coma, Weber’s
syndrome (oculomotor palsy with contralateral
hemiplegia), contralateral ataxic tremor, nystagmus, and pupillary abnormalities.
◆ Cerebellar lesion. Whether associated with
abscess, hemorrhage, or tumor, a cerebellar lesion that progresses to a coma may also cause
an absent doll’s eye sign. The coma may be preceded by headache, nystagmus, ocular deviation to the side of the lesion, unequal pupils,
dysarthria, dysphagia, ipsilateral facial paresis,
and cerebellar ataxia. Characteristic signs of increased ICP may also occur, including
decreased LOC, abnormal pupillary responses,
increased systolic blood pressure, widening
pulse pressure, bradycardia, altered respiratory
pattern, papilledema, and vomiting.
◆ Pontine hemorrhage. Absent doll’s eye sign
and a coma develop within minutes in this lifethreatening disorder. Other ominous signs—
such as complete paralysis, decerebrate posture, a positive Babinski’s reflex, and small,
reactive pupils—may rapidly progress to death.
◆ Posterior fossa hematoma. A subdural
hematoma at this location typically causes absent doll’s eye sign and a coma. These signs
may be preceded by characteristic signs and
symptoms, such as headache, vomiting, drowsiness, confusion, unequal pupils, dysphagia, cranial nerve palsies, stiff neck, and cerebellar
ataxia.
O
THER CAUSES
◆ Drugs. Barbiturates may produce severe
central nervous system depression, resulting in
a coma and absent doll’s eye sign.
S
PECIAL CONSIDERATIONS
Don’t attempt to elicit doll’s eye sign in a comatose patient with a suspected cervical spine injury; doing so risks spinal cord damage. Instead,
evaluate the oculovestibular reflex with the cold
caloric test. Normally, instilling cold water in the
ear causes the eyes to move slowly toward the
irrigated ear. Cold caloric testing may also be
done to confirm an absent doll’s eye sign.
Continue to monitor vital signs and neurologic status in the patient with an absent doll’s
eye sign.
P
EDIATRIC POINTERS
Normally, doll’s eye sign isn’t present for the
first 10 days after birth, and it may be irregular
until age 2. After that, this sign reliably indicates
brain stem dysfunction. An absent doll’s eye
sign in children may accompany a coma associated with head injury, near drowning, suffocation, or brain stem astrocytoma.
Drooling
Drooling—the flow of saliva from the mouth—
results from a failure to swallow or retain saliva
or from excess salivation. It may stem from facial muscle paralysis or weakness that prevents
mouth closure, from neuromuscular disorders
or local pain that causes dysphagia or, less
DROOLING 223
https://t.me/medicina_free
commonly, from the effects of drugs or toxins
that induce salivation. Drooling may be scant or
copious (up to 1 L daily) and may cause circumoral irritation. Because it signals an inability to
handle secretions, drooling warns of potential
aspiration.
H
ISTORY AND PHYSICAL
EXAMINATION
If you observe the patient drooling, first determine
the amount. Is it scant or copious? When did it
begin? Ask the patient if his pillow is wet in the
morning. Also, inspect for circumoral irritation.
Then explore associated signs and symptoms. Ask about sore throat and difficulty swallowing, chewing, speaking, or breathing. Have
the patient describe any pain or stiffness in the
face and neck and any muscle weakness in the
face and extremities. Has he noticed any mental
status changes, such as drowsiness or agitation? Ask about changes in vision, hearing, and
sense of taste. Also ask about anorexia, weight
loss, fatigue, nausea, vomiting, and altered
elimination habits. Has the patient recently had
a cold or other infection? Was he recently bitten
by an animal or exposed to pesticides? Finally,
obtain a complete drug history.
Next, perform a physical examination, starting with vital signs. Inspect the face for signs of
paralysis or an abnormal expression. Examine
the mouth and neck for swelling, the throat for
edema and redness, and the tonsils for exudate.
Note halitosis. Examine the tongue for bilateral
furrowing (trident tongue). Look for pallor, skin
lesions, and frontal baldness. Carefully assess
any bite or puncture marks.
Assess cranial nerves II through XII. Then
check pupillary size and response to light. Assess the patient’s speech. Evaluate muscle
strength and palpate for tenderness or atrophy.
Also palpate for lymphadenopathy, especially in
the cervical area. Observe the patient’s ability to
swallow. Test for poor balance, hyperreflexia,
and a positive Babinski’s reflex. Also, assess
sensory function for paresthesia.
M
EDICAL CAUSES
◆ Achalasia. Progressively severe dysphagia
may cause copious drooling late in this disorder. When the patient lies down, food and saliva
in the dilated esophagus flow back to the pharynx and mouth, resulting in drooling. Coughing
or choking and aspiration may follow regurgitation. Other findings include weight loss and,
possibly, spasms or substernal pain after eating.
◆ Acoustic neuroma. When this malignant tu-
mor involves the facial nerve, it produces facial
weakness or paralysis with scant to copious
drooling. The drooling is followed by tinnitus,
unilateral hearing loss, and vertigo. Other
symptoms include dysphagia, poor balance, and
ear or eye pain.
◆ Amyotrophic lateral sclerosis. Brain stem
involvement in this degenerative disorder
weakens muscles of the face and tongue, resulting in constant scant to copious drooling. The
drooling is accompanied by dysarthria and difficulty chewing, swallowing, and breathing. Fasciculations are common along with muscle atrophy and weakness, especially in the forearms
and hands, and hyperreflexia and spasticity in
the legs.
◆ Bell’s palsy. Drooling accompanies the grad-
ual onset of facial hemiplegia in Bell’s palsy.
The affected side of the face sags and is expressionless, the nasolabial fold flattens, and the
palpebral fissure (distance between upper and
lower eyelids) widens. The patient usually complains of pain in or behind the ear. Other cardinal signs and symptoms include a unilateral diminished or absent corneal reflex, decreased
lacrimation, Bell’s phenomenon (upward deviation of the eye with attempt at eyelid closure),
and partial loss of taste or abnormal taste sensation.
◆ Diphtheria. In this infection, moderate
drooling results from dysphagia associated with
sore throat. The hallmark of diphtheria, however,
is a bluish white, gray, or black membrane over
the mucous membranes of the tonsils, pharynx,
larynx, soft palate, and nose. This membrane
causes pooling of saliva, which aggravates
drooling. Other signs and symptoms include
fever, pallor, tachycardia, halitosis, noisy respirations, cervical lymphadenopathy, purpuric
skin lesions, drowsiness, and delirium.
◆ Esophageal tumor. In this type of tumor, co-
pious and persistent drooling is typically preceded by weight loss and progressively severe
dysphagia. Other signs and symptoms include
substernal, back, or neck pain and bloodflecked regurgitation.
◆ Glossopharyngeal neuralgia. Drooling may
accompany the sharp paroxysms of pain that
characterize this rare disorder. The pain may be
precipitated by swallowing, talking, chewing, or
coughing or by external pressure on the ear; it
may affect the posterior pharynx, the ear, or the
base of the tongue or jaw. Associated findings
include hoarseness, soft palate deviation to the
224 DROOLING
https://t.me/medicina_free
unaffected side, absent gag reflex, partial loss of
taste, and trapezius and sternocleidomastoid
muscle weakness.
◆ Guillain-Barré syndrome. The hallmark of
this polyneuritis is ascending muscle weakness
that typically starts in the legs and extends to
the arms and face within 24 to 72 hours. Facial
diplegia and dysphagia set the stage for scant to
copious drooling, which is accompanied by
dysarthria, nasal voice tone, and a diminished
or absent corneal reflex. Other signs and symptoms include paresthesia, signs of respiratory
distress, and signs of sympathetic dysfunction,
such as orthostatic hypotension, loss of bowel
and bladder control, diaphoresis, and
tachycardia.
◆ Hypocalcemia. The chief feature of hypocal-
cemia is tetany, characterized by muscle twitching, cramps, and seizures; carpopedal spasm;
and positive Chvostek’s and Trousseau’s signs.
Moderate to copious drooling may accompany
the resultant dysphagia. In severe hypocalcemia, the patient may have laryngeal spasm
with stridor, cyanosis, and generalized tonicclonic seizures.
◆ Ludwig’s angina. In this disorder, moderate
to copious drooling stems from dysphagia and
local swelling of the floor of the mouth, causing
tongue displacement. Submandibular swelling
of the neck and signs of respiratory distress may
also occur.
◆ Myasthenia gravis. Facial and pharyngeal
muscle weakness causes scant to copious
drooling that’s accompanied by difficulty swallowing, chewing, and speaking. Typically, drooling is preceded by diplopia and ptosis. The patient displays a masklike face and myasthenia
snarl (smile with lips elevated but not retracted). Other features include a weak tongue with
bilateral furrowing (trident tongue) and a sagging jaw if masseter muscles are affected.
Skeletal muscle weakness is characteristic;
muscles typically weaken throughout the day,
especially after exercise.
◆ Myotonic dystrophy. Facial weakness and a
sagging jaw account for constant drooling in
this disorder. Other characteristic findings include myotonia (inability to relax a muscle after
its contraction), muscle wasting, cataracts, testicular atrophy, frontal baldness, ptosis, and a
nasal, monotone voice.
◆ Paralytic poliomyelitis. When this infection
involves the brain stem, it may produce facial
paralysis and dysphagia, resulting in scant to
copious drooling. Typically, the drooling is pre-
ceded by fever, headache, nuchal rigidity, and
intense muscle aches. The patient then develops fasciculations and usually asymmetrical
paralysis in the lower legs and trunk that’s associated with transient urine retention.
◆ Parkinson’s disease. In this degenerative
disorder, the neck is flexed forward, so saliva isn’t directed to the back of the mouth; the result
is drooling. Other cardinal features include a
pill-rolling tremor, rigidity, bradykinesia, a shuffling gait, stooped posture, masklike facies, dysarthria, and a high-pitched, monotone voice.
◆ Peritonsillar abscess. A severe sore throat
causes dysphagia with moderate to copious
drooling in this type of abscess. Accompanying
signs and symptoms are high fever, rancid
breath, and enlarged, reddened, edematous tonsils that may be covered by a soft gray exudate.
Palpation may reveal cervical lymphadenopathy.
◆ Rabies. When this acute central nervous sys-
tem infection advances to the brain stem, it produces drooling (commonly referred to as “foaming at the mouth”) from excessive salivation,
facial palsy, or extremely painful pharyngeal
spasms that prohibit swallowing. It’s accompanied by hydrophobia in about 50% of patients.
Seizures and hyperactive deep tendon reflexes
(DTRs) may also occur before the patient develops generalized flaccid paralysis and a coma.
◆ Retropharyngeal abscess. This disorder
causes painful swallowing, resulting in moderate to copious drooling. The patient complains
of a lump in his throat that he can’t swallow
and of dyspnea in the sitting position that disappears when he lies down. Other cardinal signs
and symptoms include coughing, snoring, choking, noisy breathing, and a “cry of a duck” voice
tone. Cervical lymphadenopathy, pharyngeal
edema and redness, and a high fever may also
occur.
◆ Seizures (generalized). This tonic-clonic
muscular reaction causes excessive salivation
and frothing at the mouth accompanied by loss
of consciousness and cyanosis. In the unresponsive postictal state, the patient may also
drool.
◆ Stroke. Facial paralysis associated with
stroke results in scant to copious drooling. Other
signs and symptoms include diplopia, visual field
deficits, dysarthria, hearing loss, paresthesia,
paralysis, ataxia, headache, dizziness, confusion, nausea, vomiting, unilateral or bilateral hyperactive DTRs, and a positive Babinski’s reflex.
◆ Tetanus. This acute infection may produce
scant to copious drooling associated with
DYSARTHRIA 225
https://t.me/medicina_free
dysphagia. Typically, drooling is preceded by
restlessness and pain and stiffness in the jaw,
abdomen, and back that progress to tonic
spasms. A locked jaw and a grotesque grinning
expression (risus sardonicus) are characteristic
signs. Profuse sweating, low-grade fever, and
tachycardia are also common.
O
THER CAUSES
◆ Drugs. Such drugs as clonazepam, ethion-
amide, and haloperidol can all cause excessive
salivation, which may result in drooling.
◆ Envenomation. Some snakebites trigger ex-
cess salivation, resulting in drooling. The drooling is accompanied by other neurotoxic effects,
such as diaphoresis, chills, weakness, dizziness,
nausea, vomiting, paresthesia, fasciculations,
and tender lymphadenopathy. Local swelling,
pain, and ecchymoses may occur.
◆ Pesticide poisoning. Toxic effects of pesti-
cides may include excess salivation with drooling, diaphoresis, nausea and vomiting, involuntary urination and defecation, blurred vision,
miosis, increased lacrimation, fasciculations,
weakness, flaccid paralysis, signs of respiratory
distress, and coma.
S
PECIAL CONSIDERATIONS
Be alert for aspiration in the drooling patient.
Position him upright or on his side. Provide frequent mouth care, and suction as necessary to
control drooling. Be prepared to perform a tracheostomy and intubation, to administer oxygen, or to execute an abdominal thrust.
Help the patient cope with drooling by providing a covered, opaque collecting jar to decrease odor and prevent transmission of infection. Keep tissues handy and drape a towel
across the patient’s chest at mealtime. Encourage oral hygiene. Also, teach the patient exercises to help strengthen facial muscles, if appropriate. Assist the patient with meticulous skin
care, especially around the mouth and in the
neck area, to prevent skin breakdown. Cornstarch may be placed on the neck to reduce the
risk of maceration.
P
EDIATRIC POINTERS
Normally, an infant can’t control saliva flow until about age 1, when muscular reflexes that initiate swallowing and lip closure mature. Salivation and drooling typically increase with
teething, which begins at about the fifth month
and continues until about age 2. Excessive salivation and drooling may also occur in response
to hunger or anticipation of feeding, and in association with nausea.
Common causes of drooling in children include epiglottiditis, retropharyngeal abscess, severe tonsillitis, stomatitis, herpetic lesions,
esophageal atresia, cerebral palsy, mental deficiency, and drug withdrawal in neonates of addicted mothers. It may also result from a foreign
body in the esophagus, causing dysphagia.
Dysarthria
Dysarthria, poorly articulated speech, is characterized by slurring and a labored, irregular
rhythm. It may be accompanied by a nasal voice
tone caused by palate weakness. Whether it occurs abruptly or gradually, dysarthria is usually
evident in ordinary conversation. It’s confirmed
by asking the patient to produce a few simple
sounds and words, such as “ba,” “sh,” and “cat.”
However, dysarthria is occasionally confused
with aphasia, loss of the ability to produce or
comprehend speech.
Dysarthria results from brain stem damage
that affects cranial nerves IX, X, or XII. Degenerative neurologic disorders and cerebellar disorders commonly cause dysarthria. In fact,
dysarthria is a cardinal sign of olivopontocerebellar degeneration. It may also result from illfitting dentures. (See Dysarthria: Causes and
associated findings, pages 226 and 227.)
EMERGENCY INTERVENTIONS If the pa-
tient displays dysarthria, ask him about associated difficulty swallowing. Then determine
respiratory rate and depth. Measure vital capacity
with a Wright respirometer if available. Assess
blood pressure and heart rate. Tachycardia,
slightly increased blood pressure, and shortness of
breath are usually early signs of respiratory muscle weakness.
Ensure a patent airway. Place the patient in
Fowler’s position and suction him if necessary.
Administer oxygen and keep emergency resuscitation equipment nearby. Anticipate intubation and
mechanical ventilation in progressive respiratory
muscle weakness. Withhold oral fluids in the patient with associated dysphagia.
If dysarthria isn’t accompanied by respiratory
muscle weakness and dysphagia, continue to assess for other neurologic deficits. Compare muscle
strength and tone in the limbs, and evaluate tactile
sensation. Ask the patient about numbness or
tingling. Test deep tendon reflexes (DTRs), and note
gait ataxia. Assess cerebellar function by observing
226 DYSARTHRIA
https://t.me/medicina_free
SIGNS & SYMPTOMS
Dysarthria: Causes and associated findings
Major associated signs and symptoms
Common
causes
Alcoholic cerebellar degeneration
Amyotrophic
lateral sclerosis
Basilar artery
insufficiency
Botulism
Manganese
poisoning
Mercury poisoning
Multiple sclerosis
Myasthenia gravis
Olivopontocerebellar degeneration
Parkinson’s disease
Shy-Drager
syndrome
Aphasia
Ataxia
Bradykinesia
Diplopia
Drooling
Dysphagia
Dyspnea
Fasciculations
Gait, propulsive
Hyperreflexia
Hypotension
Level of conscious-
ness, decreased
Masklike facies
•• •
•
•••• •
••
•••
•••
••
••• •
••••
•
••• • •
••
••
Stroke (brain stem)
Stroke (cerebral)
rapid alternating movement, which should be
smooth and coordinated. Next, test visual fields
and ask about double vision. Check for signs of
facial weakness such as ptosis. Finally, determine
level of consciousness (LOC) and mental status.
H
ISTORY AND PHYSICAL
EXAMINATION
Explore dysarthria completely. When did it begin? Has it gotten better? Speech improves with
••••
••••
resolution of a transient ischemic attack, but
not in a completed stroke. Ask if dysarthria
worsens during the day. Then obtain a drug and
alcohol history. Also, ask about a history of
seizures. Observe dentures for a proper fit.
M
EDICAL CAUSES
◆ Alcoholic cerebellar degeneration. This
disorder commonly causes chronic, progressive
dysarthria along with ataxia, diplopia,
•
Muscle atrophy
https://t.me/medicina_free
Muscle weakness
Ptosis
Spasticity
Tremor
Vertigo
Visual field deficits
•• •
•••
••
•••
••
•••
••
•
••
••
••
ophthalmoplegia, hypotension, and altered
mental status.
◆ Amyotrophic lateral sclerosis. Dysarthria
occurs when this disorder affects the bulbar
nuclei; it may worsen as the disease progresses.
Other signs and symptoms include dysphagia;
difficulty breathing; muscle atrophy and weakness, especially of the hands and feet;
fasciculations; spasticity; hyperactive DTRs in
the legs; and occasionally excessive drooling.
DYSARTHRIA 227
Progressive bulbar palsy may cause crying
spells or inappropriate laughter.
◆ Basilar artery insufficiency. This disorder
causes random, brief episodes of bilateral brain
stem dysfunction, resulting in dysarthria. Accompanying it are diplopia, vertigo, facial
numbness, ataxia, paresis, and visual field loss,
all of which can last from minutes to hours.
◆ Botulism. The hallmark of this disorder is
acute cranial nerve dysfunction that causes
dysarthria, dysphagia, diplopia, and ptosis. Early
findings include dry mouth, sore throat, weakness, vomiting, and diarrhea. Later, descending
weakness or paralysis of muscles in the extremities and trunk causes hyporeflexia and dyspnea.
◆ Multiple sclerosis. When demyelination af-
fects the brain stem and cerebellum, the patient
displays dysarthria accompanied by nystagmus,
blurred or double vision, dysphagia, ataxia, and
intention tremor. Exacerbations and remissions
of these signs and symptoms are common.
Other findings include paresthesia, spasticity,
intention tremor, hyperreflexia, muscle weakness or paralysis, constipation, emotional lability, and urinary frequency, urgency, and incontinence.
◆ Myasthenia gravis. This neuromuscular dis-
order causes dysarthria associated with a nasal
voice tone. Typically, the dysarthria worsens
during the day and may temporarily improve
with short rest periods. Other findings include
dysphagia, drooling, facial weakness, diplopia,
ptosis, dyspnea, and muscle weakness.
◆ Olivopontocerebellar degeneration.
Dysarthria, a cardinal sign of this disorder, accompanies cerebellar ataxia and spasticity.
◆ Parkinson’s disease. This disorder produces
dysarthria and a monotone voice. It also produces muscle rigidity, bradykinesia, an involuntary tremor that usually begins in the fingers, difficulty walking, muscle weakness, and stooped
posture. Other findings include masklike facies,
dysphagia and, occasionally, drooling.
◆ Shy-Drager syndrome. Marked by chronic
orthostatic hypotension, this syndrome eventually causes dysarthria as well as cerebellar
ataxia, bradykinesia, masklike facies, dementia,
impotence and, possibly, stooped posture and
incontinence.
◆ Stroke (brain stem). This type of stroke is
characterized by bulbar palsy, resulting in the
triad of dysarthria, dysphonia, and dysphagia.
The dysarthria is most severe at the onset of the
stroke; it may lessen or disappear with
Соседние файлы в папке Библиотека им академика М.И. Перельмана