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Chapter 30 • Syncope 371
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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, emotional 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 resulting in decreased peripheral vascular resistance. Physical examination is usually
negative. 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 is
negative.
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 agerelated 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, antidysrhythmics,
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 psychiatric
problems associated with syncope. Physical examination is usually negative. Psychiatric evaluation may
reveal the underlying disorder.
Unknown Causes
Syncope from unknown causes accounts for about one
third of all episodes of syncope. The workup is negative.
372 Chapter 30 • Syncope
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DIFFERENTIAL DIAGNOSIS OF Common Causes of Syncope
DISORDER HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
Cardiac Causes
Organic heart
disease
Arrhythmias Palpitations; absence of other
Neurocardiogenic Causes
Vasovagal Emotional event, standing for long
Situational Occurs with cough, micturition,
Breath holding Children 6 mo to 5 yr; associated with
Hyperventilation Anxiety- or fear-induced event, short-
Cough syncope History of asthma; coughing paroxysm
Orthostasis
Orthostatic
hypotension
Medication-Related Causes
Prescribed
medications
Drug-induced
causes
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 negative
CSM, cardiac sinus massage; LOC, loss of consciousness.
Shortness of breath, chest pain,
palpitations, exercise-associated
syncope
symptoms
periods, crowded room, warm
environment
defecation, swallowing
anger, pain, brief cry; breath-holding
LOC; may have twitching
ness of breath
awakens child from sleep, becomes
flaccid with clonic muscle spasm, LOC
Position change from lying/sitting to
standing, pregnancy, prolonged bed
rest
History of antidepressants, antidysrhyth-
mic agents, b-blockers, or diuretics
History of use of illicit drugs Arrhythmia may be
positive family history
phase
anxiety, panic
present; gentle fall, memory of incident
exact
May have bradycar-
dia or tachycardia,
cyanosis
Loud S2, S3; murmur,
lift
None Tilt-table testing, CSM
None None
Cyanosis or pallor None
None None
Wheezes None
Hypotension on
testing orthostatic
blood pressure
Depends on underly-
ing condition
present
Usually none; nystag-
mus, photophobia
Usually none;
nystagmus
None Psychiatric evaluation
None None
Refer
Electrocardiogram,
Holter, echocardiogram
Doppler studies, cardiac stress testing
20 mm Hg drop in
systolic pressure on
standing
None
Toxicology screen
None
Electroencephalogram
Chapter 30 • Syncope 373
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REFERENCES AND READINGS
Batra AS, Holn AR: Palpitations, syncope and sudden cardiac death
in children: who’s at risk? Pediatr Rev 24:269, 2003.
Brignole M, Alboni P, Benditt DG, Bergfeldt L, Blanc JJ, Thomsen
PE et al: Guidelines on management (diagnosis and treatment) of
syncope: update 2004. Executive summary, Eur Heart J 25:22,
2004.
Kapoor WN: Syncope, N Engl J Med 343:1856, 2000.
Kenny RA: Syncope in the elderly: diagnosis, evaluation, and treat-
ment, J Cardiovasc Electrophysiol 14:9, 2003.
Lewis D, Dhala A: Syncope in the pediatric patient, Pediatr Clin
North Am 46:205, 1999.
Limmer DD, Mistovich JJ, Krost WS: Beyond the basics: syncope,
EMS Magazine March:76, 2009.
Miller TH: Evaluation of syncope, Am Fam Physician 72:1492,
2005.
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 2:423, 2002.
Strickberger S, Benson D, Biaggioni, I, Callans D, Cohen M, El-
lenbogen K et al: AHA/ACCF scientic statement on the evaluation of syncope, J Amer Coll Cardiol 47:474, 2006.
Taylor B, Green MS: Evaluating and managing syncope, Clin Rev
10:55, 2000.
Thanavaro JL: Evaluation and management of syncope, Clin Schol
Rev 2:65, 2009.
Ungar A, Mussi C, Del Rosso A, Noro G, Abete P, Ghirelli L et al:
Diagnosis and characteristics of syncope in older patients referred
to geriatric departments, J Am Geriatr Soc 54:1531, 2006.
Willis J: Syncope, Pediatr Rev 21:201, 2001.
C H A P T E R
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31
Urinary Incontinence
rinary incontinence is any involuntary loss
of urine. It occurs as a result of pathological,
U
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.
ularly in older adults. It is so common in older women
that some think of it as “normal.” The prevalence in
U.S. women 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 persons in
nursing homes, the rate rises to almost 50%.
cording to the underlying anatomical or physiological
impairment—specically, stress incontinence, urge
incontinence (overactive bladder), overow incontinence, and incontinence from reversible causes.
that increase 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.
to void with the inability to delay urination and is
caused by bladder hyperactivity or hypersensitive
bladder. Detrusor muscle overactivity occurs when
pathological brain disorders interfere with central
inhibitory centers and fail to prevent detrusor muscle
contractions.
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
374
anatomical, psychological, or physiological
Urinary incontinence is a common problem, partic-
Urinary incontinence in adults is categorized ac-
Stress incontinence is leakage of urine during activities
Urge incontinence is an abrupt and strong desire
Overow incontinence occurs with overdistention
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. Some
sources term this functional or transient incontinence.
A nal category of incontinence is called mixed
incontinence. This occurs when the incontinence is
produced as the result of several anatomical, physiological, or functional factors. 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 constitutes
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. 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
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
(see Box 31-1)?
Key Questions
n What medications are you taking?
n Do you have any of the following urinary symp-
toms: urgency, frequency, burning, pain, blood in
the urine, ank pain?
Chapter 31 • Urinary Incontinence 375
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Box 31-1
Reversible Factors that Can
Cause Urinary Incontinence
in Adults
D Delirium, dementia, depression
I Infection
A Atrophic vaginitis/urethritis
P Pharmaceuticals
E Endocrine/excess urine production
R Restricted mobility, retention
S Stool impaction
Modified from Resnick NM: Initial evaluation of the incontinent patient,
J Am Geriatr Soc 38:311, 1990.
n Do you have vaginal dryness or itching?
n Do you have pain/discomfort with sexual activity?
n Have you had changes in bowel function?
n When was your last bowel movement?
n Are you feeling depressed or “blue”?
n Are you aware of incontinence?
n How active are you?
n Are you able to get to the toilet easily?
n Do you have any chronic health problems?
Medications
Hypnotic-sedatives, diuretics, anticholinergic agents,
adrenergic agents, and calcium channel blockers
can cause incontinence. a-Adrenergic agonists and
b-adrenergic agonists increase sphincter tone and
may cause retention. Anticholinergics, prostaglandin
inhibitors, calcium channel blockers, and narcotic
analgesics decrease detrusor tone. Diuretics can
cause incontinence because of increased production
of urine. Central nervous system (CNS) depressants,
such as hypnotic-sedatives, can interfere with func-
tional ability.
Table 31-1 lists categories of medications and their
mechanism of action in urinary incontinence.
Urinary Tract Infection, Vaginal Dryness,
and Dyspareunia
Urinary tract infection (UTI) and atrophic vaginitis can
cause incontinence through local irritation and loss of
muscle tone.
Bowel Function
Fecal impaction can cause incontinence through me-
chanical obstruction of the urethra.
Mental Status, Mobility, and Chronic Health
Problems
Excessive urine production may be a problem if mo-
bility is restricted, health is poor, or orientation is
variable. Chronic health problems, psychological
factors, and restricted mobility can result in inconti-
nence because of loss of functional ability and/or
mentation.
Table 31-1
MEDICATION CATEGORY TYPE OF INCONTINENCE MECHANISM OF ACTION
Anticholinergics Overflow Decreased bladder contractions with retention
Antidepressants Overflow Decreased bladder contractions with retention
Antipsychotics Overflow Decreased bladder contractions with retention
Sedative-hypnotics Overflow Decreased bladder contractions with retention
Antihistamines Overflow Decreased bladder contractions with retention
Narcotics Overflow Decreased bladder contractions with retention
Alcohol Overflow Decreased bladder contractions with retention
Calcium channel blockers Overflow Decreased bladder contractions with retention
b-Adrenergic agonists Overflow Decreased bladder contractions with retention
a-Adrenergic agonists Overflow Sphincter contraction with outflow obstruction
a-Adrenergic antagonists Stress Sphincter relaxation with urinary leakage
Diuretics Urge Contractions stimulated by high urine flow
Caffeine Urge Diuretic effect
Sedative-hypnotics Urge Depressed CNS inhibition of micturition
Alcohol Urge Diuretic effect and depressed CNS inhibition
Adapted from Weiss BD: Diagnostic evaluation of urinary incontinence in geriatric patients, Am Fam Physician 57:2675, 2688, 1998.
Medications that Can Cause or Contribute to Urinary Incontinence
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What do the presenting symptoms tell me?
Key Questions
n What is the primary symptom (e.g., urgency; drib-
bling; lack of sensation; nocturia; abdominal discomfort; leakage with laughing, coughing, or sneezing)?
n How frequently do you urinate?
n How much urine is voided each time?
n Do you have difculty starting to urinate?
n Does your urine stream start and stop while you are
urinating?
Primary Symptom
Urgency is the primary symptom of detrusor instability.
Dribbling indicates overow incontinence, and sphincter weakness usually increases with postural changes.
Men often report nocturia and dribbling with overow
incontinence. Abdominal discomfort often occurs with
overow incontinence because of bladder distention.
Incontinence with an increase in intraabdominal pressure is usually stress incontinence but can also be the
result of detrusor overactivity and bladder irritability.
Frequency of Voiding
Increase in frequency of voiding occurs with detrusor
instability or hyperactivity and may occur with some
transient causes such as use of diuretics or large-volume
uid intake. Decreased frequency is common in overow incontinence.
Amount of Urine Lost with Each Episode
Involuntary loss of small amounts of urine occurs with
stress incontinence and overow incontinence.
Character of Stream
Voiding a small-caliber or intermittent stream or difculty
in starting the stream indicates obstructive uropathy. In
males, this may be secondary to an enlarged prostate.
Are there any other symptoms that will point
me in the right direction?
Key Questions
n How much uid do you drink in a day?
n How much caffeine and alcohol do you drink?
n What time of day do you drink uids?
n How thirsty are you?
n Have you lost or gained weight recently?
Fluid Intake
A signicant increase in the amount of uid intake or
an unusually large volume may indicate diabetes mellitus (DM). Caffeine and alcohol can act as diuretics
and may be a cause of reversible incontinence. Caffeine can also be a bladder irritant and either produce
or exacerbate urge incontinence. A large volume of
uid intake may produce enuresis secondary to a large
urine volume, particularly if uids are consumed in the
evening before bedtime.
Thirst
Unusual thirst accompanied by an unusually large intake of uid may indicate DM.
Weight Loss or Gain
Weight loss may indicate a chronic health problem,
tumor, or dementia. Weight gain may indicate congestive heart failure, DM, or loss of mobility.
Children
Is this primary or secondary enuresis?
Key Question
n Has the child ever had consistent dryness for at least
6 months?
Primary enuresis occurs when a child has never
achieved consistent dryness. Secondary enuresis is involuntary voiding of urine in a child who has had a
period of dryness of more than 6 months. Secondary
enuresis is often indicative of some other form of voiding dysfunction or signicant underlying pathology. In
children, daytime urinary incontinence beyond the age
of 4 years may indicate congenital abnormalities in the
urinary tract or nervous system.
Is this organic enuresis?
Key Questions
n Does the child have pain on urination?
n Does the child have intermittent daytime wetness?
n Does the child seem thirsty and urinate a lot?
n Has the child had nervous system trauma?
n Does the child have constipation or encopresis?
n Does the child have constant wetness or dribbling
throughout the day?
n Does the child have an abnormal stream, such as
dribbling or hesitancy?
Chapter 31 • Urinary Incontinence 377
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n Has the child had a change in gait?
n Has the child had a recent lumbar puncture?
n Does the child snore or have apnea at night?
n Does the child report rectal itching at night?
Organic explanations of enuresis focus primarily on
the genitourinary and nervous systems.
Genitourinary System
Fifteen percent of children with a UTI present with
enuresis. It is unclear whether UTI causes the enuresis or
vice versa. A wet perineum predisposes to ascending infection, and prompt treatment of the infection cures the
enuresis in about one third of the cases. Asymptomatic
bacteremia in school children is associated with enuresis.
Fecal retention that is chronic or intermittent is
responsible for production of “functional” bladder
neck obstruction. Displacement of the bladder and
posterior urethra by the full rectum in the xed and
limited space of the bony pelvis causes detrusor perineal dysynergism, which is thought to be the mechanism responsible for urinary stasis and interference
with micturition produced by constipation.
Abnormal daytime voiding suggests urological
abnormality. Dribbling suggests the presence of an
ectopic ureter, labial fusion, a deep positioned meatus
or a hymen covering the meatus. Chronic leakage of
urine in females may indicate an ectopic ureter
that terminates in the vagina. Partial distal urethral
obstruction can cause straining to urinate. Polyuria
from glucose-induced osmotic diuresis can be seen in
patients with DM. Renal tubules lose their ability to
concentrate urine, resulting in the production of large
volumes of very dilute urine.
Sleep apnea interferes with the child’s ability to
wake appropriately in response to stimuli to void.
Other
Pinworms (Enterobius vermicularis) primarily inhabit
the cecum and lower bowel and are the most common
cause of rectal itching in children. Pinworms have been
implicated in incontinence in children, although the
reason is not clear.
What risk factors does this child have for
nonorganic enuresis?
Key Questions
n Is the child a boy or a girl?
n Is there a history of bedwetting in the family?
n Is the child a twin?
n What is the child’s birth order?
n Has the child been institutionalized?
n Does the child have sickle cell disease?
n What is the child’s daily uid intake?
Gender
Boys are more likely to have nocturnal enuresis. Girls
are more likely to have diurnal enuresis related to UTI.
Family History
Children with nonorganic enuresis often have a very
strong family history of fathers who had nocturnal
enuresis as a child.
Twin/Birth Order
Nocturnal enuresis is most common in the rstborn
and in twins.
Nervous System
Lumbosacral disorders affect bladder innervation and
may cause enuresis. Head injury or brain tumor can
cause polyuria and polydipsia. If the kidneys are unable
to concentrate urine because of deciency in the hypothalamic production of antidiuretic hormone (ADH),
central diabetes insipidus (DI) develops, while renal
unresponsiveness to ADH causes nephrogenic DI.
Interference with the nerve supply to the bladder
causes a neurogenic bladder and obstruction. This can
be functional, resulting from an imbalance between
detrusor muscle contraction and urethral sphincter
relaxation. It can also be congenital or acquired, such
as with meningomyelocele or spinal cord injury.
Institutionalization
Institutionalized children have a greater tendency for
enuresis because of developmental delay.
Sickle Cell Disease
Children with sickle cell anemia may have a concentrating defect and excrete low specific gravity
urine in large volumes, which may make the child
wet the bed.
Fluid Intake
A large volume of uid intake may produce enuresis
secondary to a large urine volume, particularly if the
uids are consumed in the evening before bedtime.
378 Chapter 31 • Urinary Incontinence
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DIAGNOSTIC REASONING:
FOCUSED PHYSICAL EXAMINATION
Perform Mental Status Examination
Assess orientation and cognitive function. In adults,
incontinence can occur as the result of disorientation,
delirium, or dementia.
In children, secondary enuresis can be caused by
the presence of stress factors during the developmental period from 2 to 4 years of age. Separation
from family, death of a parent, birth of a sibling, a
move, marital conict, and other stress-related
causes may produce transient and intermittent
enuresis.
Observe Gait
The urinary bladder receives extensive autonomic as
well as somatic innervation. Lesions at all levels of the
neuraxis from the cortex to peripheral nerves produce
abnormalities of micturition.
Take Vital Signs
Blood pressure readings in children are important to
rule out nephrotic causes of enuresis. When chronic
renal failure is the result of an inadequate amount of
normally functioning renal tissue, the clinical presentation may be enuresis. Fever in infants without any
other signs is likely caused by UTI.
Examine the Abdomen
Palpate for masses, suprapubic tenderness, or fullness.
Palpate the bladder. Abdominal distention or palpable
bladder is suggestive of urinary retention and overow
incontinence.
Examine Genitalia in Males
Look for abnormalities of the foreskin, glans, meatus,
penis, and perineal skin that might contribute to or
produce incontinence.
Perform Pelvic Examination in Females
Note signs of pelvic prolapse (cystocele, rectocele).
Palpate for pelvic mass and perivaginal muscle tone.
Note condition of the vaginal mucosa and look for atrophic vaginitis. Vaginitis can cause urinary incontinence
in children and adults, whereas atrophic vaginitis will
produce incontinence only in adults.
Observe for evidence of sexual abuse such as abra-
sions, tears, or bruising. Urethral irritation, especially
if discharge is present, may suggest sexual abuse in
children.
Perform Provocative Stress Testing
During the pelvic examination, ask the patient to relax and then cough vigorously (or perform a Valsalva
maneuver); watch for urine loss from the urethra. A
positive test indicates stress incontinence.
Perform Digital Rectal Examination
Assess for perineal sensation, resting and active sphincter tone, rectal mass, fecal impaction, and ssures. A lax
sphincter suggests spinal cord involvement.
In men, assess consistency and contour of the
prostate. Prostate enlargement or masses suggest
the possibility of overow incontinence from
obstruction.
Conduct a Neurological Examination
Assess the intactness of the neurological system. Note
focal decits, test deep tendon reexes, and test for
sensation in the perineal and perirectal areas. Assess
nerve roots S2 to S4. Test for muscle tone and strength.
Decits may point to a neurological cause for the incontinence.
Examine and Palpate the Spine in
Children
Look for an undetected birth defect that may be causing a neurological disturbance. A spinal dimple or hair
tuft may alert you to a potential problem.
Perform Musculoskeletal Examination
Assess mobility, strength, and functional ability. In
many older adults, the inability to get to a toilet causes
incontinence.
An easy assessment of mobility is the timed get-upand-go test. Time the patient getting up from a chair,
walking 10 feet, and sitting back down. Although the
time required to perform this test will vary, a mobile,
independent, older adult can perform this activity in
about 10 seconds.
Additional Procedures
Postvoid Residual
Have the patient void without straining and then catheterize. A residual volume greater than 100 mL suggests either bladder weakness (stress incontinence) or
outlet obstruction (overow incontinence).
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Observe Voiding
Note hesitancy, dribbling, interrupted stream, and decreased force or caliber of stream. These symptoms
suggest outlet obstruction and overow incontinence.
LABORATORY AND DIAGNOSTIC
STUDIES
Urinalysis
Dipstick urinalysis (U/A) can rule out or point to infection or systemic disease as a cause of the incontinence.
Note hematuria, pyuria, bacteriuria, or the presence of
leukocyte esterase or nitrites as indicators of UTI. Glycosuria or proteinuria suggests DM or renal disease.
Specific Gravity
A specic gravity greater than 1.015 rules out diabetes
insipidus as the cause of incontinence.
Urine Culture
A culture can be used to determine the organism(s)
producing a UTI and can conrm the diagnosis.
Urine Cytology
Urine for cytology is indicated if microscopic or gross
painless hematuria is present in the absence of infection.
Bladder Diary
A 24-hour bladder diary (3-day voiding diary for children) can provide an accurate record of urine output;
average voided volume; frequency of voiding; frequency and nature of incontinent episodes; and type of
volume of uid intake. Patients or parents can catch
and measure urine output in a measuring cup.
Blood Urea Nitrogen and Creatinine
Use these indicators of renal function if you suspect
obstruction or urinary retention.
Vaginal Specimen Microscopy,
DNA Testing, or Culture
These tests can conrm vaginal infection. See Chapter 34
for the procedures for these tests.
Office Cystometrography
Have the patient void and empty the bladder. Have
men lie supine and place women in the dorsal lithot-
omy position. Insert a sterile 12 to 14 French (nonbal-
looned) catheter and empty the bladder. (Measure the
postvoid residual and collect urine for U/A at that
time.) Insert a 50-mL syringe with plunger removed
into the end of the catheter and position it about 15 cm
above the urethra. Fill the syringe by pouring sterile
water into it in 25- to 50-mL increments. Record cumu-
lative total uid instillation in the bladder and note the
volume at which the patient rst reports the urge to
void. Continue adding uid slowly until the uid level
in the syringe rises, indicating an increase in intrablad-
der pressure and contraction of the detrusor muscle.
The rise may be gradual or sudden. Detrusor contrac-
tion at less than 300 to 350 mL of bladder volume in-
dicates detrusor instability (urge incontinence). Have
the patient void at the end of the procedure. The
amount instilled minus the amount voided will also
provide a measure of postvoid residual.
Urodynamic Testing
Complete urodynamic testing includes uroowmetry,
cystometrography, perineal electromyelography, and
voiding cystourethrography (VCUG). It is indicated
when patient symptoms do not correlate with objec-
tive physical ndings, when results may change man-
agement, after treatment failure, or if more informa-
tion is needed in order to plan further therapy (see the
Evidence-Based Practice box, Urodynamic Testing).
EVIDENCE-BASED PRACTICE
A Cochrane systematic review compared outcomes in
women with urinary incontinence based on urodynamic
testing. The authors concluded that women assessed using
urodynamic testing in addition to clinical methods were
more likely to receive medication or surgical treatment.
However, there was insufficient evidence to show whether
Data from Glazener CMA, Lapitan MCM: Urodynamic investigations for management of urinary incontinence in children and adults, Cochrane
Database of Systematic Reviews 2002. Available online at www.cochrane.org. Accessed May 28, 2010.
Urodynamic Testing
they were less likely to be incontinent after treatment than
women who did not have urodynamic tests. The additional
cost of testing may not be justifiable given the lack of
evidence for improvement in clinical outcomes. No data
were available to evaluate the use of urodynamics in other
patient groups.
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Cystoscopy and Contrast Radiography
These procedures are indicated for detection of neoplasms or stones.
Ultrasound
Ultrasonography may be useful in determining the
presence of an obstruction.
DIFFERENTIAL DIAGNOSIS
Incontinence from Anatomical Causes
Stress Incontinence
Stress incontinence is associated with activities that
increase intraabdominal pressure, such as coughing,
sneezing, running, or laughing. The underlying abnormality is typically urethral hypermotility as a result of
inadequate pelvic support of the bladder neck (urethrovesical junction). Normally increased intraabdominal
pressure is transmitted evenly across the bladder neck
and body. When adequate support is lacking, an increase in intraabdominal pressure displaces the bladder
neck outside the abdominal cavity. The subsequent
disproportionate increase in bladder pressure as compared to urethral pressure results in urine loss. Poor
urethral sphincter function also contributes to stress
incontinence. The amount of urine lost with each episode is small. The patient usually has a history of
childbirth. On examination, pelvic oor relaxation
may be evident with the presence of a cystocele and/or
rectocele. The urethral sphincter may appear lax, and
there is loss of urine with provocative testing. Atrophic
vaginitis is a common nding in postmenopausal
women. U/A and culture may be performed to rule out
infections or urinary tract problems. Postvoid residual
is normal.
Urge Incontinence
Urge incontinence is characterized by an uncontrolled
urge to void, secondary to detrusor muscle irritability or
hyperactivity or to a hypersensitive bladder. Most cases
result from an idiopathic inability to suppress detrusor
contraction. The urine volume lost is large. Physical
examination results are usually normal. Postvoid residual is normal. Diagnostic testing includes U/A and culture to rule out infection, and determination of blood
urea nitrogen and creatinine levels to rule out nephropathy. On ofce cystometrography, the urine volume is
less than 300 to 350 mL before the urge to void occurs.
Complete urodynamic testing can conrm the diagnosis.
For more information, see the Evidence-Based Practice box, Determining the Type of Urinary Incontinence.
Overflow Incontinence
Overow incontinence occurs in the presence of obstruction or interruption in the nervous system. It is a
result of overdistention of the bladder from an underactive or acontractile detrusor muscle, from sphincterdetrusor dyssynergia (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.
Overow incontinence is small-volume incontinence, with symptoms of dribbling and hesitancy. In
men, symptoms of an enlarged prostate may be present
(i.e., nocturia, dribbling, hesitancy, and decreased force
and caliber of stream). On examination, look for distended bladder, prostate hypertrophy, evidence of spinal cord disease, or diabetic neuropathy. Postvoid residual is more than 100 mL. Diagnostic testing includes
EVIDENCE-BASED PRACTICE
The authors of a recent systematic review of evidence of the
most accurate way to determine the type of urinary incontinence
during office assessment concluded that when evaluating a
woman with urinary incontinence, a systematic approach that
includes a history, physical examination, and stress test increases the likelihood of correctly classifying the type of incontinence (for stress: positive LR*, 3.7; negative LR, 0.20; and
for urge: positive LR, 2.2; negative LR, 0.63). The most helpful
* LR 5 Likelihood Ratio
Data from Holroyd-Leduc JM, Tannenbaum C, Thorpe KE, Straus SE: What type of urinary incontinence does this woman have? JAMA 299:1446,
2008.
Determining the Type of Urinary Incontinence
component of the assessment for determining the presence of
urge incontinence is a history of urine loss associated with urinary urgency (positive LR, 4.2). A stress test (preferably a filled
bladder stress test) may be helpful for diagnosing stress incontinence (filled bladder stress test: positive LR, 9.4; negative LR,
0.07). Measurement of the postvoid residual urine volume detects incomplete bladder emptying, but there are no data to
support using this in women to determine incontinence type.
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