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significant microscopic hematuria as three or more red blood cells/high power field from two
of three properly collected urine specimens (1).
II. PATHOPHYSIOLOGY
A. Etiology.
The list of the potential causes of hematuria is lengthy and includes diseases
of the urinary tract, as well as nonurologic causes. Some of these are life threatening (e.g.,
renal and bladder cancer), whereas others are insignificant (e.g., exercise-induced hematu-
ria, bladder polyps, and renal cysts). It is important to note that hematuria in an adult is
more often urologic than renal in origin. The extent of the workup should be determined
by considering factors such as the likelihood of coexisting illnesses, potential complications
from procedures, and the cost to the patient. Benign causes such as menstruation, infection,
and trauma should always be excluded before further evaluation and referral to urology or
nephrology is initiated.
B. Epidemiology. Overall prevalence varies greatly (0.1–13%) and depends on many vari-
ables (e.g., the number of screening tests performed and the type of population studied).
However, screening of the general population for microscopic hematuria is not recom-
mended. The decision to check for hematuria should depend on various risk factors for
significant underlying disease and remains a physician’s judgment call. Risk factors of signifi-
cant urological disease include age > 40 years, cigarette smoking (past or present, including
second-hand smoke), history of urinary tract infections, history of hematuria, exposure to
various drugs (analgesics, anti-inflammatory drugs, cyclophosphamide, and human immu-
nodeficiency virus therapy), exposure to occupational hazards (benzenes, 2-naphthylamine,
aromatic amines, and aniline dyes), and pelvic radiation. In many cases of microhematuria,
no cause can be found despite a complete evaluation.
III. EVALUATION
A. History.
A thorough history is of utmost importance.
1. General questions should cover the type of hematuria (macro/gross/microscopic) and
the relationship between urination and the timing of hematuria. The three-container
method assists in separating the micturition into three portions—initial, middle, and
final portions. Anatomically, initial hematuria usually originates from anterior urethral
disease, and final hematuria results from disease of the bladder neck, posterior urethra,
or prostate. Hematuria throughout the micturition suggests pathology more proximal.
Worm-like clots suggest a location above the bladder neck. Urine color should be ques-
tioned, which can be affected by the following: phenazopyridine (orange), nitrofurantoin
(brown), rifampin (yellow-orange), l-dopa, methyldopa, and metronidazole (reddish-
brown), phenolphthalein in laxatives, red beet and rhubarb consumption, food coloring,
and vegetable dyes (red).
2. Associated symptoms can hint at various particular problems; for example, a recent sore
throat, fever, chills, and flu-like symptoms may be the first signs of immunoglobulin A
nephropathy or postinfectious glomerulonephritis. Urinary frequency, urgency, dysuria,
fever, and chills point to an infectious process. Diminished urine flow and abdominal or
flank pain radiating into the groin can indicate the presence of urinary tract obstruction.
Vaginal discharge or bowel movement changes may hint at a nonurinary tract cause such
as a foreign body (especially in children). A rash, joint pain, photosensitivity, flu-like
symptoms, and Raynaud’s phenomenon point to a collagen vascular disease.
3. Past medical history should also include travel history. If the patient has traveled to
areas where bilharzia (Schistosoma haematobium) is endemic, parasitic infestation is
highly probable. Furthermore, if the history includes the use of analgesics, especially
anti-inflammatory drugs, renal papillary necrosis should be considered. Past exposure to
cyclophosphamide may cause chemical cystitis, because past exposure to antibiotics (e.g.,
penicillin and cephalosporins) may cause interstitial nephritis. Of special note is that the
mere use of oral anticoagulants does not cause hematuria. To the contrary, these patients
may in fact present earlier in their disease process and should be evaluated promptly (2).
4. Family history may lead to suspicion of polycystic kidney disease, sickle cell trait and
disease, nephrolithiasis, various glomerular diseases, tuberculosis, and benign familial
218
hematuria. The combination of renal failure, deafness, and hematuria suggests Alport’s
hereditary nephritis.
B. Physical Examination. Examination should focus on signs of systemic disease (e.g.,
fever, rash, lymphadenopathy, joint swelling, and abdominal or pelvic mass) and underlying
medical or renal disease (e.g., hypertension, peripheral and generalized edema). Multiple
telangiectasias and mucous membrane lesions indicate hereditary hemorrhagic telangiecta-
sia (Rendu-Osler-Weber disease). The finding of an abdominal mass may indicate Wilms’
tumor in children and abdominal cancer and aneurysm in adults. On rectal and genitouri-
nary examination, one can find signs of prostatitis, prostate hypertrophy, prostate cancer,
vaginal and urethral changes, and pelvic masses.
C. Testing
1. Laboratory testing initially begins with examining a freshly voided, clean catch urine
sample by a dipstick. It is important to confirm hematuria by a microscopic examination
of the urine sediment. This sediment is obtained by centrifugation of a fixed volume of
urine (5 mL) for 5 minutes at 3,000 rotations/min. Afterward, the supernatant is poured
off, and the remaining sediment is resuspended in the centrifuge tube by gently tapping
the bottom of the tube. A pipette is used to sample the residual fluid and transfer it to
a glass slide, and a cover slip is applied to the slide for microscopic evaluation (3). The
specimen is examined under high magnification (400×) to determine cell type and
distinct morphologic features. Results are recorded as the number of red blood cells per
high-power field. If a patient is asymptomatic and has no particular risk factors, two
additional urine analyses should be obtained. If one of them is abnormal, it is necessary
to proceed with further workup. For those asymptomatic patients with one to two red
blood cells/high-power field and risk factors for significant underlying disease, consider
full urologic evaluation (1). When the dipstick testing is positive for blood, but urine
microscopy reveals no red blood cells, hemoglobinuria or myoglobinuria should be
considered. The use of a benzidine dipstick allows the differentiation of these discolor-
ations from those of hematuria and myoglobinuria. As a next step, a urine culture can be
obtained to rule out an infection. The urine could also be sent for cytology to assess for
abnormal cells.
2. Blood tests include a renal panel and a complete blood count with differential, sedimen-
tation rate, prothrombin time, and partial thromboplastin time. Any further evaluation
is highly dependent on the suspected cause. Further blood tests may include serum
complement titer (significant if low), antistreptolysin-O titer (significant if high), anti-
nuclear antibody and extended panels with anti-deoxyribonuclease B titer (significant if
high), and hemoglobin electrophoresis.
3. A tuberculin skin test or chest x-ray can be done to detect tuberculosis. Upper urinary
tract workup such as intravenous pyelogram (limited sensitivity for small renal lesions),
abdominal and pelvic ultrasound (limited ability to detect solid tumors that are less
than 3 cm), computed tomography (high sensitivity for renal calculi and small lesions),
or magnetic resonance imaging (high cost and not widely supported in the literature)
(3) may detect benign conditions such as urolithiasis, obstructive uropathy, renal cysts,
parenchymal abnormalities, and nonurinary tract lesions, as well as malignancies of vari-
ous anatomic areas. Abnormalities of the urethra and bladder maybe found using cystos-
copy. Biopsies of various areas, as well as invasive vascular studies, may be necessary. At
any time during an evaluation, it remains within the physician’s judgment to refer the
patient to a subspecialist.
IV. DIAGNOSIS. The keys to the diagnosis of hematuria are the clinical history and the physical
examination. Laboratory and imaging studies only aid to confirm or rule out initial suspicions.
The goal is to diagnose a variety of serious illnesses, including malignancies and renal parenchy-
mal diseases. In general, the degree of hematuria is of little diagnostic or prognostic value (4).
As little as 1 mL of blood can cause a visible color change. In addition, a variety of drugs,
foods, and food coloring can discolor the urine. Also, it is necessary to remember that transient
hematuria, especially in a young individual, is quite common and rarely indicative of significant
219
pathology (5). When present in patients older than 40 years, however, transient hematuria war-
rants a comprehensive evaluation to rule out malignancy. Similarly, a diagnostic workup should
be performed when persistent hematuria is found in patients of any age. A summary of the best
practice policy recommendations by the American Urologic Association can be obtained from
the article “Asymptomatic Microscopic Hematuria in Adults (1).” It contains an excellent flow-
chart of the workup of asymptomatic microscopic hematuria plus a strategy to identify patients
with significant disease, while minimizing cost and morbidity associated with unnecessary tests.
Repeat evaluations are indicated for those patients with a negative evaluation and in whom
a malignancy is suspected (mainly older adults). A reasonable time frame appears to be 3–6
months for less invasive tests and 1–5 years for more invasive tests (6, 7).
Other clinical manifestations should also be considered. Until otherwise proven, painless
gross hematuria in the absence of infection in elderly men is caused by malignancy, just as
hematuria associated with “sterile” pyuria is caused by genitourinary tuberculosis or interstitial
nephritis. Finally, other medical problems such as prostate hypertrophy, diabetes mellitus (neph-
rosclerosis), nephrolithiasis, trauma (including vigorous masturbation), previous urinary tract
malignancies with recurrence, and sickle cell disease (papillary necrosis) may cause hematuria.
REFERENCES
1. Grossfeld GD, Wolf JS Jr, Litwan MS, et al. Asymptomatic microscopic hematuria in adults: summary
of the AUA best practice policy recommendations. Am Fam Physician 2001;63(6):1145–1154.
2. Yun EJ, Meng MV, Carroll PR. Evaluation of the patient with hematuria. Med Clin North Am
2004;88(2):329–343.
3. McDonald MM, Swagerty D, Wetzel L. Assessment of microscopic hematuria in adults. Am Fam
Physician 2006;73(10):1748–1754.
4. Thaller TR, Wang LP. Evaluation of asymptomatic microscopic hematuria in adults. Am Fam Physician
1999;60(4):1143–1152, 1154.
5. Murakami S, Igarashi T, Hara S, Shimazaki J. Strategies for asymptomatic microscopic hematuria: a
prospective study of 1,034 patients. J Urol 1990;144(1):99–101.
6. Messing EM, Young TB, Hunt VB, et al. Hematuria home screening: repeat testing results. J Urol
1995;154(1):57–61.
7. Loo R, Whittaker J, Rabrenivich V. National practice recommendations for hematuria: how to evaluate
in the absence of strong evidence? Perm J 2009;13(1):37–46, PMCID: 3034463.
10.3
I. BACKGROUND. Erectile dysfunction (ED), previously commonly labeled “impotence,”
defined as the consistent inability to get or maintain an erection sufficient for intercourse, is in
essence a patient-defined diagnosis (1,2). The role of the clinician is to confirm ED, rule out
correctable secondary causes, and expeditiously restore sexual function. To encourage hopeful-
ness, clinicians would do well to explain at the outset that essentially 100% of men can have
restoration of sexual function using currently available treatments.
II. PATHOPHYSIOLOGY. The most recent large epidemiologic survey of American men found
some degree of impotence in 52% of men older than 40 years of age. Most organic ED is on
a vascular basis. Because integrity of the endothelium is necessary to provide adequate penile
engorgement, disorders that cause endothelial dysfunction are predictably associated with ED.
Diabetes, smoking, hypertension, dyslipidemia, and peripheral vascular disease are all associated
with impaired endothelial function and may hence induce or contribute to ED. Whether the
E
rectile Dysfunction
Louis Kuritzky and Michel B. Diab
220
correction of these pathogenic vasculopathic factors improves erectile function in men with ED
remains to be determined. Studies that have looked at global implementation of cardiovascular
risk factor reduction (i.e., weight loss, blood pressure control, lipid control, diet modulation,
smoking cessation, and exercise in combination) have shown improvements in erectile function,
although it is difficult to ascertain—due to the combination of interventions—which specific
intervention(s) can be confirmed to be efficacious.
III. EVALUATION
A. History
1. Although written questionnaires may elicit sexual dysfunction, most patients prefer to
communicate such issues in the privacy of verbal communication with their primary
care provider. Initial inquiry can simply be “Are you sexually active?” For sexual dys-
function evaluation, gender orientation is not relevant to diagnosis or therapy, so that
whether the patient is homosexual, heterosexual, or bisexual has no distinct bearing
on the diagnostic or therapeutic direction. For individuals who are not sexually active,
the next inquiry should be to determine whether this is a matter of choice or due to
an obstacle that prevents sexual activity (e.g., lack of partner, impotence, and physical
disorder).
2. For individuals who are sexually active, a series of follow-up questions uncovers most
relevant psychosexual pathology. You could begin with “How would you rate your sex
life on a scale of 1 to 10?” If the response is 10, sexual dysfunction is decidedly unlikely.
However, most individuals respond “Oh, about a 7.” You can follow with, “What would
have to be different to change your sex life from a 7 to a 10?” This forced-choice inquiry
often produces responses that directly indicate problematic underlying issues such as
“Well, if I could just get a good erection” or “If my erection could last >30 seconds.”
Inquiry about libido is a crucial diagnostic point for testosterone deficiency. Men who
present with good libido only have a remote possibility of having testosterone deficiency.
Although testosterone enhances response of nitric oxide synthase, and hence can aug-
ment the response to erectogenic stimuli, testosterone is not necessary to have erections.
Most experts suggest routine measurement of testosterone, nonetheless.
3. A medication history should be taken. Most medication-induced ED is evident by the
temporal relationship between the onset of ED and medication initiation. On the other
hand, agents such as thiazides may produce ED after months of use. Similarly, some anti-
depressants may produce sexual dysfunction early or after weeks of therapy. Relationship
of medications to ED can often be clarified by a drug holiday.
B. Physical Examination. Although physical examination is usually not enlightening, there
is general agreement that the genitals should be examined for evidence of overt testicular
atrophy and the penis for Peyronie’s disease. Peyronie’s disease produces palpable plaques in
the corpora cavernosa that can lead to angulation upon erection, pain, or both. Treatment is
surgical. A rectal examination to document rectal sensation as well as tone can be comple-
mented by the bulbocavernosus reflex. This reflex is elicited by briskly squeezing the glans
penis in one hand while a single digit from the other is in the rectum. A normal examina-
tion, indicating an intact reflex arc, is manifest as a rectal contraction in response to the glans
squeeze. Prostate examination is pertinent at this point, in the event testosterone therapy is
required.
C. Testing. Reasonable screening tests for ED include plasma glucose, lipid profile (seeking
vasculopathic risk factors), total morning testosterone, and a urinalysis. If total morning
testosterone is low, luteinizing hormone (LH) and follicle-stimulating hormone (FSH)
levels should be measured, because an increase in these indicates gonadal failure, for which
testosterone replacement is indicated; a normal or decreased LH/FSH indicates potential
hypothalamic or pituitary insufficiency, necessitating central nervous system (CNS) imaging
to rule out a mass lesion. Recently, expert consensus guidance has suggested that because
some midlife males do not respond with a vigorous LH or FSH elevation to testicular fail-
ure, only men with distinctively low testosterone levels (<150 ng/dL) and nonelevated LH/
FSH require CNS imaging.
221
Similarly, testosterone may be suppressed by an elevated prolactin, whether induced by a
CNS lesion, hypothyroidism, medications, or other factors. A low (or low-normal) total tes-
tosterone should be repeated and confirmed; equivocal total morning testosterone levels should
be further clarified by means of measuring the free testosterone, sex hormone binding globulin
or both.
IV. DIAGNOSIS
A. Differential Diagnosis.
ED is broadly divided into psychogenic and organic categories,
although there is often a substantial degree of overlap. Men who report sudden, complete
loss of sexual function, or “circumstantial” ED: (i) good function with one partner, but not
another; (ii) good erections with masturbation but not with a partner; (iii) good morning
erections, but not with a partner, are much more likely to have psychogenic ED. Because
organic ED generally leads to psychological consequences, many patients suffer a combina-
tion of psychogenic and organic ED.
B. Clinical Manifestations
1. Psychogenic ED may reflect depression, relationship conflict, performance anxiety, or
partner-directed hostility. The history is definitive in most cases. Sudden complete loss of
function, situation or partner variability, along with maintenance of morning or mastur-
batory erections, is typical. Occasionally, patients with dysfunctions other than ED seek
advice; for instance, mistaking premature ejaculation for ED. In such cases, corrective
education combined with appropriate attention to the alternate diagnosis is the logical
next step.
2. Organic sexual dysfunction is characterized by incremental loss of erectile function. In
middle age, men with organic ED note reduced erectile turgidity, increasing require-
ment for tactile stimulation to produce an erection, and a lengthening refractory
period (i.e., the amount of time required after ejaculation before the male is receptive
to restimulation and erection). Such stepwise loss of sexual function corroborates
organicity.
3. In primary care, as many as 98% of patients have no correctable cause of impotence
discerned after appropriate history and physical examination. This is not to say that
hypertension, diabetes, and dyslipidemia are not remediable, but rather that correc-
tion of such risk factors has not been confirmed to ameliorate ED. Additionally, the
presence of such additional risk factors need not delay the immediate provision of
highly effective oral agents (PDES inhibitor [phosphodiesterase type 5 inhibitors]),
Tadalafil 5 mg daily (3), vacuum constriction devices, or intra-corporeal injection,
any of which may be provided in the primary care setting. However, before provid-
ing any tool which can restore sexual function, clinicians should be confident that
the patient’s cardiovascular status is sufficient that vigorous physical activity—sexual
activity, exercise, or work exertion—is safe. In general, an adult who can tolerate 4
mets of activity (brisk walking) can safely engage in other vigorous activities such as
sexual activity. Patients who fail to respond to the standard treatment tools should be
referred (4).
REFERENCES
1. Kuritzky L. Primary care issues in the management of erectile dysfunction. In: Seftel AD, ed. Male and
female sexual dysfunction. Edinburgh: Mosby, 2004:1–15.
2. Kuritzky L, Ahmed O, Kosch S. Management of impotence in primary care. Comp Ther
1998;24(3):137–146.
3. Egerdie RB, Auerbach S, Roehrborn CG, et al. Tadalafil 2.5 mgor 5 mg administration once a daily for
12 weeks in men with both erectile dysfunction and symptoms of benign prostatic hyperplasia: results
of a randomized, placebo-controlled, double blind study. J Sex Med 2012:9:271–281.
4 Gupta BP, Murad HM, Clifton MM, Prokop L, Nehra A, Kopecky SL. The effect of lifestyle modifi-
cation and cardiovascular risk factor reduction on erectile dysfunction a systematic review and meta-
analysis. Arch Intern Med 2011;171(20):1797–1803. doi:10.1001/archintemmed.2011.440
222
10.4
I. BACKGROUND. Urinary incontinence (UI) is defined by the International Continence Society
as the “complaint of involuntary loss of urine.” Rates of UI increase with age and are as high
as 34% in women and 11% in men (1). It is a major cause of social withdrawal and loss of
independent living. Patients are often too embarrassed to discuss this problem, even with their
physician. Some even view it as a natural part of aging, but this is not the case. UI is a symptom,
not a disease. Understanding the types of disorders that cause incontinence is the key to correct
diagnosis and effective treatment (2–5).
A. Definition. UI is the involuntary loss of urine.
B. Classification. The classification of UI is presented in Table 10.4.1.
C. UI can be acute or chronic.
1. Acute causes include
a. infection
b. medications
c. delirium
d. exacerbation of systemic diseases (e.g., diabetes mellitus, diabetes insipidus, congestive
heart failure, or stroke)
Urinary Incontinence
Richard Rathe and David M. Quillen
TABLE 10.4.1 Types of Incontinence
Type Definition Mechanism Disorders
Urge Inability to delay voiding
once the urge occurs
Detrusor hyperactivity Idiopathic (common in the
elderly)
Genitourinary conditions
(cystitis, stones)
Stress Loss of urine with
increased abdominal
pressure
Sphincter failure Weak or injured pelvic
muscles
Sphincter weakness
Overflow Partial retention of urine
behind an obstruction
Outlet obstruction
Loss of innervation
Obstruction (prostate,
cystocele)
Neuropathic (diabetes,
nerve injury)
Functionality Inability to get to the
toilet
Physical or cognitive
impairment
Dementia or delirium
Physical limitations (lack of
mobility)
Psychological or behavioral
causes
Mixed Any combination of the
above
223
2. Chronic conditions that are associated with UI fall into two categories:
a. local
i. pelvic floor weakness following childbirth
ii. bladder tumor or deformity
iii. tumors
iv. obstruction by an enlarged prostate or cystocele
v. postsurgic
b. systemic
i. menopause
ii. neuropathy (diabetes, alcoholism)
iii. dementia
iv. depression
v. stroke
vi. tumor
vii. Parkinson’s disease
D. The DRIP mnemonic is often cited as a way to remember the reversible (and curable)
causes of UI:
1. D: Delirium and drugs
2. R: Restricted mobility and retention
3. I: Infection, inflammation, and (fecal) impaction
4. P: Polyuria from uncontrolled diabetes and other conditions
II. EVALUATION
A. History
1. Voiding History. It is important to fully characterize the patient’s problem by taking a
detailed history, including the duration of the symptoms, timing of voluntary or invol-
untary voiding, amounts voided involuntarily, and the relationship to voluntary voiding.
Focus on the following areas:
a. Need for pads or diapers (measure of severity)
b. Loss of urine with coughing or laughing (suggests stress type)
c. Inability to hold urine after having the urge to urinate (suggests urge type)
d. Pain or discomfort (suggests infection or inflammation)
e. Inability to fully empty bladder (suggests obstruction)
f. Decreased urinary stream (suggests obstruction)
g. What impact does UI have on the patient’s life?
h. What does the patient think is going on?
2. Major Medical Problems.
a. Does the patient have any known condition that is associated with UI?
i. Diabetes
ii. Heart failure
iii. Menopause
iv. Neurologic problems
b. Does the patient have other genitourinary symptoms? In female patients, be sure to
take a detailed obstetric history.
3. Medication History. Since medications are a major cause of incontinence, a thorough
medication history is essential. Offending agents include
a. Diuretics
b. Older antidepressants
c. Antihypertensives
d. Narcotics
e. Alcohol
4. Special Concern. Central and nephrogenic diabetes insipidus can present with UI
because of increased urine output (many liters per day). These patients frequently have
224
a concomitant polydipsia that closely matches their water loss. Consider this diagnosis
when the patient gives a history of voiding large volumes of urine.
B. Physical Examination. The physical examination is often normal in cases of UI. Focus
efforts in an attempt to uncover the underlying cause(s):
1. General. Is the patient physically capable of getting to the toilet?
2. Mental Status. Can the patient understand and act on the urge to void?
3. Neurologic, including the anal reflex; focal signs suggest a neurologic cause.
4. Abdominal Examination. Is the bladder distended?
5. Rectal or Prostate. Does the patient have a fecal impaction or an enlarged prostate?
6. Pelvic Examination. Look for atrophic vaginitis, uterine prolapse, or a pelvic mass.
C. Testing
1. Voiding Journal. A voiding journal is a good way to get additional information about
the patient’s problem. Have the patient record the time and approximate amount of each
voiding, and whether they were wet or dry.
2. Urinalysis. Be cautious when interpreting the urine analysis; in the absence of other
symptoms, bacteriuria is seldom the primary cause of UI. Treat cystitis or urethritis when
the rest of the clinical picture confirms them. Unexplained, persistent microhematuria
requires investigation.
3. Postvoiding Urine Volume. The patient should be catheterized immediately after
voiding. In general, the postvoid urine volume should be less than 50 mL. Volumes in
the range of 100–200 mL may suggest impaired bladder contractility or obstruction.
Volumes greater than 200 mL strongly suggest obstruction.
4. Blood Urea Nitrogen, Creatinine, and Glucose are simple blood tests that help rule
out underlying renal disease and diabetes.
5. Special tests are available via urologic consultation to further delineate the cause of UI.
These include cystoscopy, cystometry, and other voiding studies. Up to two-thirds of
patients can be successfully treated without urologic referral.
III. DIAGNOSIS. The clinical history is the most important factor leading to the correct diagnosis
and successful treatment of UI. However, it is an imperfect tool at best. In one review, clinical
history had a sensitivity and specificity for stress incontinence of 0.90 and 0.50, respectively.
For detrusor instability, the figures were 0.74 and 0.55, respectively (2).
The task becomes even more problematic when considering the reluctance of patients
to talk about their symptoms and the tendency for UI to be of a mixed type. Response
to therapy (or lack thereof) often drives the practical management of this condition. Lack
of response to multiple trials of therapy is a good indication for consulting a urologist.
Remember that your initial assessment will often be incorrect, so keep an open mind and
consider all possible diagnoses. Finally, recall that UI frequently involves more than one
causal factor. For example, many elderly people have a functional component (can’t get to
the toilet quickly) in addition to one of the other types.
REFERENCES
1. Fong E, Nitti VW. Urinary incontinence. Prim Care 2010;37(3):599–612, ix.
2.
Jensen JR, Nielsen FR, Ostergard DR. The role of patient history in the diagnosis of urinary inconti-
nence. Obstet Gynecol 1994;83(5):904–910.
3. Finding Out about Incontinence. AAFP patient information handout. Am Fam Physician
1998;57(11):2688–2690.
4. Goode PS, Burgio KL. Pharmacologic treatment of lower urinary tract dysfunction in geriatric patients.
Am J Med Sci 1997;314(4):262–267.
5. Weiss BD. Diagnostic evaluation of urinary incontinence in geriatric patients. Am Fam Physician
1998;57(11):2665–2687.
225
10.5
I. BACKGROUND. Nocturia is defined as the need for an individual to wake up one or more
times from sleep during the night to void. The prevalence of nocturia increases with age, rang-
ing from 4% in children aged 7–15 years to approximately 70% in patients >60 years of age.
Although the prevalence of nocturia does increase with age, it would be difficult to conclude
that nocturia is a normal part of aging, because it is not universally present in all older adults.
The clinical significance of nocturia has been increasingly recognized because of its association
with reduced quality of life and increased morbidity and mortality (1–3).
II. PATHOPHYSIOLOGY. The pathophysiology of nocturia is complex and multifactorial.
A number of conditions can result in alteration of more than one regulatory pathway control-
ling normal voiding. The underlying pathophysiology may depend on some conditions being
purely mechanical and for others may involve complex neurohormonal mechanisms. Atrial
natriuretic peptide (ANP) and vasopressin appear to be two of the known hormones associated
with pathophysiology of some conditions resulting in nocturia.
A. The etiology of nocturia can be divided into four main categories:
1. Diurnal Polyuria. A continuous overproduction of urine, not limited only to sleep
hours, with a 24-hour urine output of more than 40 mL/kg. Diurnal polyuria may be
related to either free water diuresis or to osmotic diuresis.
a. Free water diuresis.
i. Diabetes insipidus (DI): Defect in production of arginine vasopressin (AVP; cen-
tral DI) or impaired response to AVP, medications, hereditary (nephrogenic DI)
ii. Gestational DI
iii. Primary polydipsia
b. Osmotic dieresis
i. Diabetes mellitus
ii. Medications
Sorbitol and mannitol
Diuretics (multiple mechanisms)
Lithium
Calcium channel blockers (variable affect)
Selective serotonin re-uptake inhibitor (SSRI)
iii. AVP suppression caused by low calcium and potassium
2. Nocturnal Polyuria. This is defined as an increase in nighttime urine production with a
corresponding decrease in daytime urine production, resulting in a normal 24-hour urine
production
a. Nocturnal Polyuria Syndrome. This is thought to be caused by a lack of normal
diurnal variation in the production of urine and lack of nocturnal AVP level increase,
which occurs normally.
b. Edema-Forming States. CHF, chronic kidney disease (CKD), hypoalbulinemia,
chronic liver disease, venous insufficiency, enhanced ANP release resulting from a
redistribution and mobilization of fluid and solute at night.
c. Obstructive Sleep Apnea (OSA). AVP production through hypoxic-induced vaso-
constriction.
d. Alzheimer Disease. Loss of circadian AVP release.
e. Medications. Tetracycline AVP inhibition.
f. Behavioral. Excessive late night fluid intake, late evening diuretic usage.
3. Reduced Bladder Capacity. This includes
a. Overactive bladder, e.g., detrusor over- or underactivity
Nocturia
Umar Ghaffar
226
b. Reduced bladder capacity due to benign prostatic hypertrophy, bladder cancer,
neurogenic bladder, tuberculosis, interstitial cystitis
c. Others, e.g., infection, stones, pelvic floor laxity
d. Medications, e.g., SSRIs
e. Fecal impaction
f. Obstetric or gynecologic disease
4. Mixed Nocturia. A significant number of nocturia patients may have more than one
etiology for their symptoms, and therefore a thorough history taking is crucial.
a. History. A comprehensive history should be elicited to obtain information regarding
any of the above-mentioned conditions that would contribute toward nocturia.
i. History of: Lower urinary tract symptoms (e.g., urgency, hesitancy, straining,
and feeling of incomplete bladder evacuation) that may suggest bladder storage/
capacity-related issues.
ii. History of: Symptoms related to conditions resulting in diurnal polyuria, e.g.,
diabetes mellitus, DI, CKD.
iii. Conditions causing edema-forming state (CHF, chronic liver disease (CLD),
hypoalbulinemia)
iv. Underlying neurologic disorders (prior cerebrovascular accident (CVA), Alzheimer’s
spinal cord injuries)
v. Attention should be paid to daily fluid intake schedule, baseline voiding pattern
and changes therein, severity of nocturia, sleep pattern, and quality
vi. Use of frequently used medications such as diuretics, SSRIs, tetracycline, and
calcium channel blockers as well as their time of dosing should be sought.
III. EVALUATION
A. Physical Exam. A thorough system-wise approach is warranted:
1. General vitals: include body weight (obesity contributing to OSA) and orthostatic blood
pressure (possibly indicating autonomic dysfunction).
2. Cardiopulmonary exam: Should focus on clues to CHF, OSA, and edema-forming states.
3. Abdominal exam: bladder distention, prostate enlargement, ascites, rectal exam for sphincter lax-
ity, tumors, impaction, and signs of spinal cord damage, each pointing toward a specific etiology.
4. Neurologic exam: general appearance and visual field testing to evaluate for pituitary or
endocrine dysfunction.
B. Testing
1. Labs including
a. Urinalysis by dipstick
b. Urine culture
c. Selected cases: microscopy may identify a urologic cause
d. Elevated PSA may point toward a prostatic etiology
e. Blood urea nitrogen (BUN), creatinine, and electrolytes can help in evaluating for
renal disease as well as hypercalcemia
f. Serum glucose and osmolality and urine electrolytes and water deprivation tests can
identify diabetes mellitus or DI
g. Liver function tests (LFTs) and albumin can be obtained for liver function
2. Postvoid residual volume measurement can help distinguish bladder outlet obstruction
or neurogenic bladder.
3. Urodynamic studies although very helpful require interpretation by specialists.
IV. DIAGNOSIS. The key to diagnosis of the etiology of nocturia in a given patients is:
A. Obtaining a thorough history and physical exam.
B. Identifying other medical conditions and an accurate medication history will often give
a strong clue toward the underlying pathology.
C. Identifying the pattern of normal baseline voiding.
D. Identifying the pattern of fluid intake, frequency and severity of nocturia.
E. Appropriate diagnostic testing.
F. Referral to a urological specialist may, however, be required in some cases for further
evaluation with urodynamic studies and cystoscopy.
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