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Chapter 32 • Sore Throat
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389
DIFFERENTIAL DIAGNOSIS OF
Common Causes of Sore Throat—cont’d
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
Group A b-hemolytic
streptococcal
pharyngitis
Mononucleosis
(Epstein-Barr
virus)
Gonococcal
pharyngitis
Inflammation
PHARYNGITIS WITH ULCERS
Herpangina
(coxsackievirus)
Fusospirochetal
infection (Vincent
angina)
Aphthous stomatitis Oral trauma, ill-fitting dentures;
Herpes simplex
infection
Candidiasis Immunosuppressed; people taking
CBC, Complete blood count; CT, computed tomography.
Most common in people 5 to
15 years old; known exposure;
fall/winter season; sudden onset
of fever, severe sore throat, and
malaise; absence of cough and
upper respiratory tract symptoms
Young adults; slow onset of
malaise, low-grade fever,
mild sore throat
History of orogenital sexual activity;
may be asymptomatic
Exposure to irritants; postnasal drip;
allergic symptoms
More common in children;
immunosuppressed; painful
throat; fever, malaise
Poor oral hygiene; painful ulcers,
foul breath, bleeding gums
painful ulcers varying in size;
absence of other symptoms
History of trauma to mucosa; pain,
fever, headache
antibiotics or with diabetes; sore
mouth/throat
Temperature .38.5° C (101.5° F);
exudate; anterior cervical
lymphadenopathy
Presence/absence of pharyngeal
exudate, posterior cervical
lymphadenopathy, splenomegaly
Pharyngeal exudate; bilateral
cervical lymphadenopathy
Sinus tenderness, pale or swollen
pharynx, postnasal drainage
visible, no fever or
lymphadenopathy
Lymphadenopathy; small grayish
papulovesicular lesions on soft
palate and pharynx, progressing
to shallow ulcers, usually
,5 mm in diameter
Gray necrotic ulcers without
vesicles on gingival margins
and interdental papillae
Shallow ulcers, no vesicles;
indurated papules that progress
to 1-cm ulcers; ulcer has yellow
membrane and red halo; no
fever or nodes
Perioral lesions; lymphadenitis;
vesicles on palate, pharynx, gingiva
Curdlike white plaques that bleed
when scraped off
Positive rapid strep
antibody screen;
strep culture
Positive Monospot; CBC
with differential;
.50% leukocytes
Gram stain; gonorrhea
culture
Eosinophils in nasal
secretions with
allergies
Serology
Gram stain reveals
spirochetes
None
Viral culture
Potassium hydroxide
smear shows
hyphae; culture
References and Readings
Centor RM: When should patients seek care for sore throat? Ann
Intern Med 159:636, 2013.
Coby BA: Diagnosis and treatment of streptococcal pharyngitis, Am
Fam Physician 79:383, 2009.
Darrow DH, Siemens C: Indications for tonsillectomy and adenoid-
ectomy, Laryngoscope 112:6, 2002.
Ebell MH, Smith MA, Barry HC, et al: The rational clinical exami-
nation: Does this patient have strep throat? JAMA 284:2912, 2000.
Gereige R, Cunill-DeSautu B: Throat infections, Pediatr Rev 32:459,
2011.
Linder JA: Evaluation and management of adult pharyngitis, Compr
Ther 34:196, 2008.
Shulman ST, Bisno AL, Clegg HW, et al: Clinical practice guideline
for the diagnosis and management of group A streptococcal pharyngitis: 2012 update by the Infectious Diseases Society of America,
Clin Infect Dis 55:1279, 2012.
Stevens D: A sore throat or something else? Pract Nurs 19:83, 2008.
Vincent MT, Celstin N, Hussain AN: Pharyngitis, Am Fam Physician
69:1465, 2004.
Wessels MR: Clinical practice: Streptococcal pharyngitis, N Engl J
Med 364:648, 2011.
CHAPTER
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33
Syncope
yncope is the transient loss of consciousness and
S
postural tone that results from a sudden decrease in
cerebral perfusion. It is distinct from coma, seizures,
shock, vertigo, and other states of altered consciousness. It is a symptom that about 10% of adults of any
age will experience at least some time during their
lives, and the incidence increases exponentially in
people over 70 years old. It is less common in children
except when there is a seizure disorder, primary cardiac
arrhythmia, or a breath-holding incident.
The causes of syncope can be difcult to determine
because patients generally are seen after the event
has occurred. Syncope can be quite benign, such as a
vasovagal response, or it can indicate serious disease.
However, even benign syncope can place the patient at
risk for falls or injury. Cardiogenic syncope has high
associated morbidity and mortality, and the emphasis
in diagnosis is to rule out the most serious causes
through a careful history and physical examination,
with a few laboratory and diagnostic tests to establish
a possible diagnosis.
DIAGNOSTIC REASONING: FOCUSED HISTORY
Is this really syncope?
Key Questions
l
Did you lose consciousness?
l
Did you have any warning symptoms?
l
What were you doing when the event occurred?
l
If you lost consciousness, how long did it last?
l
Did your limbs jerk during the event?
l
Did anyone see you faint?
Loss of Consciousness
Distinguish syncope from other symptoms. Dizziness,
vertigo, and presyncope do not cause loss of consciousness or postural tone.
Prodromal Symptoms
Sweating, vertigo, nausea, and/or yawning are prodromal
symptoms that are associated with syncope; seizures may
be associated with an aura or tongue biting. Aura also
suggests migraine etiology.
EVIDENCE-BASED PRACTICE
Syncope is a common symptom with no diagnostic gold standard and a range of prognoses. The authors of this guideline
undertook an extensive review of the literature to help clinicians maximize the diagnostic yield in the workup of syncope
and report the following key points that assist in the evaluation
of syncope:
1. History, physical examination, and electrocardiography
(ECG) are the core of syncope workup (combined diagnostic
yield, 50%).
2. Neurological testing is rarely helpful unless additional
neurological signs or symptoms are present (diagnostic
yield of EEG, CT, and Doppler ultrasound, 2% to 6%).
3. Patients in whom heart disease is known or suspected and
those with exertional syncope who are at higher risk for
Data from Linzer M, Yang EH, Estes NA III, et al: Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography.
Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med 126:989, 1997.
390
Diagnosing Syncope
adverse outcomes should have cardiac testing, including
echocardiography, stress testing, Holter monitoring, or electrophysiology study, alone or in combination (diagnostic
yield, 5% to 35%).
4. Syncope in the elderly often results from polypharmacy
and abnormal physiological responses to daily events.
5. Long-term loop electrocardiography (diagnostic yield,
25% to 35%) and tilt-table testing (diagnostic yield,
#60%) are most useful in patients with recurrent syncope
in whom heart disease is not suspected.
6. Psychiatric evaluation can detect mental disorders associated with syncope in up to 25% of cases.
7. Hospitalization may be indicated for patients at high risk
for cardiac syncope or with acute neurological signs.
Chapter 33 • Syncope
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391
Pre-event Characteristics
Characterize what precipitated the episodes. Loss of
consciousness precipitated by pain, exercise, urination,
defecation, or stressful events is probably not a seizure.
Breath-holding spells commonly cause syncope in
children and are usually precipitated by pain, anger, a
sudden startle, or frustration. Syncope occurs with rest
or when supine during a seizure or arrhythmia. Syncope that occurs without warning symptoms is highly
suspect to have a cardiovascular origin.
Event and Postevent Characteristics
Rhythmic movements of extremities during the event
usually indicate a seizure, although they can occur
with syncope. Disorientation after the event, slowness
in returning to consciousness, and unconsciousness
lasting longer than 5 minutes indicate seizure. Often
children with breath-holding spells have associated
cyanosis, clonic jerks, opisthotonos, and bradycardia.
Witness
The patient is unconscious when the syncopal event
takes place, and therefore is a poor historian. A careful
history is needed from both the patient and a witness to
help in the diagnosis. Adolescents who have psychogenic
syncope episodes generally have an audience when the
event occurs and are able to describe details of the event
that would not be known to an unconscious patient.
l
Are you having chest pain and/or shortness of
breath?
l
Do you have palpitations?
l
Did this occur during or after exercise?
History of Heart Disease/Congenital
Heart Problem
The presence of structural heart disease increases the
risk of sudden death. Patients with a history of coronary artery disease, congestive heart failure, or ventricular arrhythmia should be hospitalized. Cardiac
syncope may be either arrhythmic or mechanical in
origin. Cardiac outow obstruction from aortic or
mitral stenosis or a prosthetic valve may cause syncope. Complete heart block, the result of interruption
of atrioventricular conduction, is a leading cause of
syncope. Children who have had cardiac surgery to
correct severe congenital heart disease are at risk for
arrhythmias.
Palpitations
Supraventricular or ventricular tachycardia are associated with syncope and sudden death. Ventricular tachycardia with a heart rate of 200 beats per minute may be
asymptomatic or cause syncope. Chaotic ventricular
activity of ventricular brillation is always fatal unless
it is reversed with electrical debrillation (see Chapter
26 for Palpitations).
Does this require immediate referral?
Key Questions
l
Do you have a history of heart disease? What is it?
l
Do you have a congenital heart problem?
EVIDENCE-BASED PRACTICE
an Abnormal Heart Rhythm?
Supraventricular tachycardia (SVT) is a common heart
rhythm disturbance that can occur in healthy individuals and
includes symptoms of chest pain, palpitations, dyspnea,
sweating, feeling faint, and loss of consciousness. Treatment
is usually a combination of Valsalva maneuver, medications,
and electro reversion. The Valsalva maneuver stimulates the
vagus nerve (CN X), which in turn leads to slowing of the
heart rate. This maneuver is performed by having a patient
blow into a syringe while lying prone for 15 seconds to
generate increased pressure within the chest cavity and a
slowing of heart rate that may stop the abnormal rhythm.
Data from Smith GD, Fry MM, Taylor D, Morgans A, Cantwell K. Effectiveness of the Valsalva Manoeuvre for reversion of supraventricular tachycardia. Cochrane Database of Systematic Reviews 2015, Issue 2. Art. No.: CD009502. DOI: 10.1002/14651858.CD009502.pub3
Cochrane Reviews are regularly updated as new evidence emerges and in response to feedback, and Cochrane Database of Systematic Reviews
should be consulted for the most recent version of the review.
Chest Pain or Shortness of Breath
Obstructive mechanical blockage may be caused by
pulmonary embolism, cardiac ischemia, or myocardial
infarction with pump failure.
Is the Valsalva Maneuver Effective for Stopping
Three studies involving a total of 316 participants were
included in this review. Results showed that reversion is
between 19.4% and 54.3%. Potential side effects reported
include hypotension and syncope. No side effects were
reported in the three studies reviewed and within the three
studies, reversion was achieved on completion of each Valsalva maneuver. The authors concluded that the Valsalva
maneuver is a simple, noninvasive method of stopping an
abnormal heart rhythm, but its safety and overall effectiveness are difficult to quantify. Further research is required to
improve the evidence surrounding this practice.
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Chapter 33 • Syncope
After Exercise
Syncope that accompanies exercise should be considered of cardiac origin unless it is proven otherwise.
Syncope after exertion in a well-trained athlete who
has no heart disease is likely vasovagal in origin.
What do associated symptoms tell me?
Key Questions
l
What other symptoms did you have?
l
Do you have headaches?
l
Have you experienced vertigo, dizziness, or visual
changes?
Headaches
The pain of migraine headaches and the effect of the
migraine on the brainstem can cause syncope. Generally the patient has associated symptoms, such as vomiting, photophobia, severe headache (often unilateral),
and a strong family history of migraines. The headache
continues after consciousness is regained. Consider
the possibility that the headache may indicate a head
injury secondary to the syncopal episode.
Vertigo, Dizziness, and Visual Symptoms
The presence of vertigo, dizziness, diplopia, or other
visual changes may accompany migraine headache.
Interruption in cerebral perfusion, such as with a transient ischemic attack, also must be considered.
Is this neurocardiogenic in origin?
Key Questions
l
Did this occur in response to a specic situation
(e.g., stressful event, urination, defecation)?
l
Were you sitting, standing, or lying at when you
fainted?
l
Do you have a history of any heart problems?
Situational Fainting
Vasovagal syncope is the most common type seen in
adults and healthy children. It is neurocardiogenic and
tends to occur in families. It is often precipitated by emotional stress, fear, extreme fatigue, or injury. It can occur
without any obvious antecedent cause. Warm temperature, anxiety, blood drawing, and crowded rooms may
cause peripheral vasodilation. Lack of large muscle activity prevents the venous return that is needed for cardiac
lling with consequent bradycardia and fainting. When
supine, venous return to the heart occurs, awakening the
patient. Rapid standing will cause recurrence of the episode. Mental alertness is present.
Situational syncope can occur in response to
urination, defecation, cough, swallowing, or emotional
stress. Posttussive syncope follows paroxysmal coughing caused by increased intrathoracic pressure, which
is then transmitted to the intracranial circulation, increasing intracranial pressure and decreasing cerebral
blood ow. Postmicturition syncope, occurring during
or after urination, is caused by the release of intravascular pressure on urination, which triggers vasodilation
and vagally mediated bradycardia.
Is this orthostasis?
Key Questions
l
What medications are you taking?
l
Have you recently started blood pressure medicine
or has the dose changed?
l
What other health problems/conditions do you have?
Medications
About 10% of syncopal episodes are caused by prescribed medications (e.g., antidepressants, antiarrhythmics, b-blockers, diuretics), over-the-counter medications, and recreational drugs (e.g., alcohol, cocaine)
that produce orthostasis, bradycardia, or prolonged QT
interval. Adolescents may use drugs such as amyl nitrite and butyl nitrite as aphrodisiacs and euphoriants.
These drugs lead to vasodilation, and syncope may
occur.
Children may ingest medications that belong to
family members, and a history of such activity must be
investigated as a cause of the syncope.
Other Health Problems or Conditions
Diabetes may induce hypoglycemia, causing a gradual
syncope. Anemias and chronic gastrointestinal bleeding
from an ulcer or another source may cause syncope.
Patients who are pregnant or dehydrated or who
have been on prolonged bed rest are at risk for orthostatic hypotension and syncope.
Is this explained by other factors?
Key Questions
l
Have you had this before? How often?
l
Did it occur with sudden head turning?
l
If a child: Has the child had Kawasaki disease?
l
Do you have Lyme disease?
Chapter 33 • Syncope
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Frequent Syncope With No Heart Disease
Psychogenic syncope is often associated with repeated
episodes in which unpredictable motor reflexes
appear with a lack of pathological reexes. Blood
pressure and pulse rate measurements show normal
readings, and skin and mucous membranes do not
change color. Panic attacks or hyperventilation are
often interpreted as feeling faint, but the patient
does not usually appear pale, nor are the symptoms
relieved when recumbent.
After Sudden Head Rotation
Carotid sinus hypersensitivity produces a cardioinhibitory response that results in a profound drop in heart
rate or may induce an abrupt vasopressor response
with a drop in blood pressure.
History of Kawasaki Disease
Syncope can occur in children who have had Kawasaki
disease. These children are at risk for coronary heart
disease, which may present as chest pain associated
with exercise.
Lyme Disease
Lyme disease can cause arrhythmia in the form of heart
block, which may result in syncope.
What else do I need to consider?
Key Questions
l
Do you have a family history of sudden death?
l
Do you have a family history of fainting?
l
If a child: Did the mother have systemic lupus
erythematosus (SLE) while pregnant?
Family History of Sudden Death
A family history of idiopathic hypertrophic subaortic
stenosis (IHHS) is a risk factor for sudden death, and
referral is necessary to rule out this condition. A history
of a family member who had a myocardial infarction
before age 30 is a signicant risk factor for sudden
death.
Family History of Fainting
Neurocardiogenic syncope is common in families.
Prenatal Systemic Lupus Erythematosus
Systemic lupus erythematosus (SLE) in a pregnant
woman may cause autoimmune injury, resulting in
congenital complete atrioventricular block.
DIAGNOSTIC REASONING: FOCUSED
PHYSICAL EXAMINATION
Measure Blood Pressure and Pulse Rate
Obtain blood pressure readings in supine, sitting, and
standing positions. Orthostatic hypotension occurs as a
result of a decrease in systolic blood pressure of at least
20 mm Hg or symptoms such as fainting, weakness, or
lightheadedness, which prevent continued standing.
Compare blood pressure readings in the two arms.
Unequal measurements may indicate a cardiac cause of
the syncope.
Bradycardia of 35 to 40 beats per minute usually
does not compromise cerebral blood ow. Rates below
this, however, will impair cerebral circulation and
function. Tachycardia up to 180 beats per minute does
not usually compromise cerebral circulation.
Observe Hydration Status
Poor hydration status secondary to diuretic use, poor
nutrition, or loss of uids from vomiting and diarrhea
may be associated with syncope.
Perform Heart and Lung Examination
Observe for jugular venous distention. Palpate the precordium to assess the point of maximal impulse to estimate the size of the left ventricle. Feel for lifts. Listen
to the heart as the patient moves from a squat to a
standing position. This maneuver may reveal a systolic
ejection murmur related to dynamic left ventricular
outow obstruction. Listen for heart rate and murmurs
and for radiation of murmurs. Listen for an abnormally
loud second heart sound (S
heart sound (S3). Auscultate for carotid bruits and
pericardial rub. Listen to the lungs to assess for rales
associated with congestive heart failure.
Perform a Neurological Examination
Begin with a brief mental status examination. Assess
cranial nerves, deep tendon reexes, and motor function. Perform a Romberg test as well as gait and proprioception evaluation. Assess pupillary asymmetry
and look for nystagmus (see Chapter 13).
Perform an Abdominal Examination
Auscultate and observe for signs of aortic aneurysm.
Examine Extremities
Observe lower extremities for signs of thrombophlebitis,
a source of pulmonary embolism.
) or the presence of a third
2
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Chapter 33 • Syncope
LABORATORY AND DIAGNOSTIC STUDIES
Suspected or Known Cardiac Cause
Electrocardiogram
The usefulness of the electrocardiogram usually lies in
identifying abnormalities that provide clues to underlying cardiac causes of syncope. These ndings include
evidence of conduction disorder or signs of coronary artery disease or left ventricular hypertrophy. A 12-lead
ECG is used for the basic evaluation. This should be
evaluated for rhythm and rate rst. Hand-measured interval measurement should be made. A Q wave found in the
anterolateral lead may indicate abnormal placement of
the left coronary artery. A patient with a prolonged QT
interval or the presence of Q waves must be referred.
Complete heart block requires immediate referral
for pacemaker insertion evaluation.
Carotid Sinus Massage
Carotid sinus massage (CSM) is done to evaluate patients with suspected carotid sinus hypersensitivity. This
can be performed at the bedside with the patient in a
supine or upright position while under continuous ECG
and blood pressure monitoring. Apply rm pressure and
massage for 5 to 10 seconds one side at a time at the site
of the strongest carotid pulsation. Carotid sinus hypersensitivity is diagnosed when CSM causes a 3-second or
longer pause, a 50–mm Hg or larger fall in systolic
blood pressure, or both, and associated syncope.
Event Monitoring or Continuous-Loop Monitoring
These measures are used in patients with suspected
cardiac arrhythmias as the cause of the syncope. Holter
(24 hours) or long-term (weeks, months) event monitoring is used to document electrocardiographic recordings. Holter monitoring is a continuous, 24-hour
electrocardiographic recording to evaluate the type and
amount of irregular heartbeats during regular activities, exercise, and sleep. The patient keeps a 24-hour
diary to record daily activities and any symptoms
experienced.
Cardiac event monitoring is a continuous-loop,
digital memory recorder worn for extended periods of
time (up to 30 days or longer) that saves and records
transient events felt by the patient. These monitors
are patient-activated as symptoms occur or may be
triggered automatically by a predened high or low
heart rate. Loop monitors save information for a predetermined period before the patient trigger and
therefore can help identify the initiation sequence for
arrhythmias. These stored events can be transmitted
through a telephone for review.
Doppler Studies
Transcranial Doppler and carotid ultrasonography are
used to detect hemodynamically signicant stenosis in
the major intracranial or extracranial arteries.
Exercise Stress Test
Cardiac stress testing is performed to evaluate exerciseassociated arrhythmias and syncope. It can conrm the
presence of coronary artery disease.
Echocardiography
Echocardiography is used if underlying structural cardiac disease is suspected. This may include valvular
disease, hypertrophic cardiomyopathy, tumor or thrombus, or left ventricular failure.
Electrophysiological Studies
Electrophysiological studies (EPSs) are invasive tests
that use electrical stimulation and monitoring to
diagnose conduction disorders or the propensity for
the development of tachyarrhythmia. Electrodes are
threaded through arm or leg veins and placed at
strategic positions in the ventricles, atria, or both. The
electrodes record electrical signals and allow mapping
of electrical impulses. The electrodes also can electrically stimulate the heart at programmed rates to trigger
latent ventricular tachycardia.
Suspected Neurological Cause
Baseline Blood Testing
Routine blood tests (electrolyte levels, renal function,
blood glucose level, complete blood count) rarely yield
useful diagnostic information. Most patients with abnormalities in these areas have seizures rather than syncope.
Electroencephalography
Electroencephalography (EEG) may be useful in patients whose history suggests seizure.
Computed Tomography Scanning
Computed tomography (CT) may be useful if the patient has focal neurological ndings.
Unexplained Syncope
Toxicology Screen
Toxicology screening may be indicated on the basis of
the history.
Chapter 33 • Syncope
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Tilt-Table Testing
Tilt-table testing is used to provoke vasovagal syncope
in susceptible patients. Provocative agents such as
isoproterenol or nitroglycerin may be used. Using the
table, the patient is tilted upright while continuous
minute-to-minute blood pressure, heart rate, and
oxygen saturation measurements are recorded. Patient
symptoms are recorded in each position. Patients with
neurocardiogenic syncope develop a sudden drop in
heart rate and/or blood pressure after their body has
been tilted up for several minutes. If symptoms of
lightheadedness or fainting occur during this test, the test
is considered positive for neurocardiogenic syncope.
DIFFERENTIAL DIAGNOSIS
Cardiac Causes
Cardiac causes have a higher rate of mortality than do
other causes of syncope. Cardiac causes include coro-
nary artery disease, congenital and valvular disease,
cardiomyopathy, arrhythmias, and conduction system
disorders. Coronary artery disease, congestive heart
failure, and ventricular hypertrophy can result in
arrhythmias and syncope. Patients with organic heart
disease may have chest pain, dyspnea, and syncope
with exertion. Patients with arrhythmias may have
palpitations or sudden syncope without other physical
symptoms. On physical examination, murmurs or
carotid bruits may be present. Other ndings might
include a loud S2, precordial lift, S3 pericardial rub, or
unequal blood pressure measurements in the arms.
Electrocardiographic testing is indicated; other cardiac
testing may be helpful.
Neurocardiogenic Causes
Vasovagal syncope is the most common type in young
people, but it can occur at any age. It usually occurs in
a standing position and is precipitated by fear, emo-
tional stress, or pain. Autonomic symptoms such as
nausea, sweating, blurred or fading vision, epigastric
discomfort, lightheadedness, and a feeling of warmth
may precede syncope by a few minutes. The syncope
occurs secondary to efferent vasopressor reexes re-
sulting in decreased peripheral vascular resistance.
Physical examination usually has normal ndings. Tilt-
table testing may be useful in establishing a diagnosis.
Situational syncope is vasovagal syncope with a
known precipitant. It is commonly related to conditions that produce a Valsalva maneuver. Micturition,
defecation, and cough are types of situational syncope.
These stimuli result in autonomic reexes with a vasopressor response, ultimately leading to transient
cerebral hypotension. The physical examination has
normal ndings.
Carotid sinus hypersensitivity produces a cardioinhibitory response or vasopressor response that
produces syncope with head turning.
Orthostasis
Orthostatic (postural) syncope indicates variable or
unstable vasomotor reexes. A drop in blood pressure
when one assumes an upright position is caused
by loss of vasoconstriction reexes in the lower
extremities. Sudden standing or rapid movement after
assuming a standing position can trigger syncope; the
prevalence of this type of syncope increases with age.
The syncope is caused by hypotension that occurs as
a blunted baroreceptor response and inability of the
cardiovascular system to respond to hypotensive
stresses. It may also occur from age-related physiological changes, volume depletion, medication, and
autonomic insufciency. Orthostatic hypotension is
produced with testing.
Medication-Related Causes
Use of prescribed medications or recreational drugs
can produce syncope. Medications that can cause syncope include antidepressants, antidysrhythmic medications, b-blockers, and diuretics. Recreational drugs
(e.g., alcohol, cocaine) can produce orthostasis, bradycardia, or prolonged QT interval. Amyl nitrite and
butyl nitrite cause vasodilation and syncope. Physical
ndings depend on the underlying physical condition
of the patient.
Neurological Causes
Neurological causes include transient ischemic attacks,
migraines, and seizures. Prodromal symptoms may
include vertigo, diplopia, and loss of balance. Syncope
results from vertebrobasilar insufciency. In an acute
syncopal attack, circulation is briey obstructed to the
reticular activating system in the brainstem, resulting
in loss of consciousness. Neurological ndings, such
as diplopia, pupillary asymmetry, nystagmus, ataxia,
and gait instability, may be present.
Psychiatric Causes
Syncope of unexplained origin may be psychogenic. Panic and anxiety disorders, somatization,
major depression, and substance abuse are the main
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Chapter 33 • Syncope
psychiatric problems associated with syncope.
Physical examination usually has normal findings.
Psychiatric evaluation may reveal the underlying
disorder.
DIFFERENTIAL DIAGNOSIS OF
Common Causes of Syncope
Unknown Causes
Syncope from unknown causes accounts for about one
third of all episodes of syncope. The workup has normal results.
DISORDER HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
CARDIAC CAUSES
Organic heart disease Shortness of breath, chest pain, palpita-
tions, exercise-associated syncope
Arrhythmias Palpitations; absence of other symptoms Loud S
NEUROCARDIOGENIC CAUSES
Vasovagal Emotional event, standing for long periods,
crowded room, warm environment
Situational Occurs with cough, micturition,
defecation, swallowing
Breath holding Children 6 mo to 5 yr; associated with
anger, pain, brief cry; breath-holding
LOC; may have twitching
Hyperventilation Anxiety- or fear-induced event, shortness
of breath
Cough syncope History of asthma; coughing paroxysm
awakens child from sleep, becomes
flaccid with clonic muscle spasm, LOC
May have bradycardia or
tachycardia, cyanosis
, S3; murmur,
2
lift
None Tilt-table testing,
None None
Cyanosis or pallor None
None None
Wheezes None
Refer
Electrocardiogram,
Holter monitor,
echocardiogram
Doppler studies,
cardiac stress
testing
CSM
ORTHOSTASIS
Orthostatic hypotension Position change from lying/sitting to
MEDICATION-RELATED CAUSES
Prescribed medications History of antidepressants, antiarrhythmic
Drug-induced causes History of use of illicit drugs Arrhythmia may be
NEUROLOGICAL CAUSES
Migraine Headache, vomiting, photophobia,
Seizures Convulsions, incontinence, postictal
PSYCHIATRIC CAUSES
Mental disorder Symptoms consistent with depression,
Hysterical reaction Adolescent, event occurs with audience
Unknown Causes No diagnostic characteristics None Workup normal
CSM, Cardiac sinus massage; LOC, loss of consciousness.
standing, pregnancy, prolonged
bed rest
agents, b-blockers, or diuretics
positive family history
phase
anxiety, panic
present; gentle fall, memory of incident exact
Hypotension on testing
orthostatic blood
pressure
Depends on underlying
condition
present
Usually none; nystagmus,
photophobia
Usually none; nystagmus Electroencephalo-
None Psychiatric
None None
20–mm Hg drop in
systolic pressure
on standing
None
Toxicology screen
None
gram
evaluation
results
Chapter 33 • Syncope
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397
References and Readings
Batra AS, Holn AR: Consultation with the Specialist: Palpitations,
syncope and sudden cardiac death in children: Who’s at risk?
Pediatr Rev 24:269, 2003.
Friedman K, Alexander M: Chest pain and syncope in children: A
practical approach to the diagnosis of cardiac disease, J Pediatr
163:896, 2013.
Gauer, RL: Evaluation of syncope, Am Fam Physician 84:
640, 2011.
Kapoor WN: Syncope, N Engl J Med 343:1856, 2000.
Kenny RA: Syncope in the elderly: Diagnosis, evaluation, and
treatment, J Cardiovasc Electrophysiol 14:S74, 2003.
MacNeill E, Vashist S: Approach to syncope and altered mental status,
Pediatr Clin North Am 60:1083, 2013.
Moodley M: Clinical approach to syncope in children, Semin Pediatr
Neurol 20:12, 2013.
Narchi H: The child who passes out, Pediatr Rev 21:384, 2000.
Schnipper JL, Kapoor WN: Diagnostic evaluation and management
of patients with syncope, Med Clin North Am 85:423, 2002.
Stewart J: Common syndromes of orthostatic intolerance, Pediatrics
131:968, 2013.
Strickberger S, Benson D, Biaggioni I, et al: AHA/ACCF scientic
statement on the evaluation of syncope, J Am Coll Cardiol
47:473, 2006.
Thanavaro JL: Evaluation and management of syncope, Clin Schol
Rev 2:65, 2009.
Ungar A, Mussi C, Del Rosso A, et al: Diagnosis and characteristics
of syncope in older patients referred to geriatric departments,
J Am Geriatr Soc 54:1531, 2006.
CHAPTER
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34
Urinary Incontinence
rinary incontinence is any involuntary loss of urine.
U
It occurs as a result of pathological, anatomical,
psychological, or physiological factors that produce
obstruction, bladder irritability, or interference with
neurological functioning. Environmental factors such as
decreased mobility, or inaccessibility of toilet facilities,
may also produce periodic incontinence.
Urinary incontinence is a common problem, particularly in older adults. It is so common in older women
that some think of it as normal. The prevalence in
women in the United States is 26% during reproductive
years, and 30% to 40% in postmenopausal years. In
noninstitutionalized elderly women, the prevalence is
15% to 30%, and in men it is 8% to 22%. In elderly individuals in nursing homes, the rate rises to almost 50%.
Urinary incontinence in adults is categorized according to the underlying anatomical or physiological
impairment. There are ve main categories of urinary
incontinence: stress incontinence, urge incontinence
(overactive bladder), overow incontinence, mixed
incontinence, and incontinence from reversible causes.
Stress incontinence is leakage of urine during activities
that increase intra-abdominal pressure, such as coughing,
sneezing, laughing, or other physical activities. It occurs
most often in females and is caused by hypermotility
at the base of the bladder and urethra associated with
pelvic oor relaxation or intrinsic urethral weakness.
Urge incontinence is an abrupt and strong desire to
void with the inability to delay urination and is caused
by detrusor muscle hyperactivity or hypersensitive bladders, which are both caused by neurological impairment.
Detrusor muscle overactivity occurs when pathological
brain disorders interfere with central inhibitory centers
and fail to prevent detrusor muscle contractions.
Patients with features of both stress and urge incontinence are considered to have mixed incontinence.
This occurs when incontinence is produced as the result
of several anatomical or physiological factors.
Overow incontinence occurs with overdistention
of the bladder caused by an underactive or acontractile
detrusor muscle; by sphincter-detrusor dyssynergia,
which is loss of the synergistic urinary sphincter relaxation that normally occurs with bladder detrusor
muscle contraction; or from bladder outlet or urethral
obstruction. Sphincter weakness can occur from damage to the urethra or its innervation or from pelvic oor
muscle relaxation.
Incontinence from reversible factors originates outside of the lower urinary tract and is caused by mental
status impairment, immobility, or medication. This is
also called functional or transient incontinence.
Involuntary discharge of urine in children is abnormal beyond the age of 4 years for daytime wetting and
beyond the age of 6 for nighttime wetting. Daytime
wetting refers to diurnal enuresis. Nighttime wetting
is known as nocturnal or sleep enuresis. In children,
enuresis may be organic or nonorganic. Nonorganic
enuresis can be primary or secondary. Primary nonorganic enuresis occurs in 75% to 90% of children with
enuresis. This enuresis is dened as wetting that has
continued since infancy without an established pattern
of dryness. Secondary nonorganic enuresis occurs in
10% to 25% of children with enuresis and is dened
as recurrence of wetting after continence has been
established for at least 6 months. The possibility of
abnormal urinary anatomy is high in young children
who present with urinary tract symptoms.
DIAGNOSTIC REASONING: FOCUSED
HISTORY
ADULTS
Could this be the result of reversible factors?
( Box 34-1)
Key Questions
l
What medications are you taking?
l
Do you have any of the following urinary symptoms:
urgency, frequency, burning, pain, blood in the urine,
or ank pain?
398
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