DEVELOPING GERIATRIC SERVICES FOR INCONTINENCE IN

THE ELDERLY
Almira J. Amin-Ong, M.D., FPOGS

Urinary incontinence (UI) is a condition where there is involuntary urine

loss in sufficient amount that causes a social and/or health problem. It is difficult
to know the exact prevalence or the incidence rate for urinary incontinence
because it is part of a symptom complex of pelvic floor dysfunction which
includes namely, pelvic organ prolapse, bowel, and, sexual dysfunction. There is
a heterogeneity of studies about the condition (terminology, demographics,
methodology, outcome measure, etc) such that the incidence ranges from 5 –
30% of a population like the United States. Furthermore, there may be an
underestimation of the incidence because patients themselves do not voluntarily
consult nor talk about the UI with their physicians for a lot of reasons like
embarrassment, belief that is a part of the aging process, a part of menopause,
or a natural consequence of vaginal delivery.

When one talks about urine leakages, one has to classify among the
different types of incontinence – stress, urge, mixed, functional or overflow. One
of the commonest causes of UI in the elderly is overactivity of the bladder (OAB).
OAB remains to be a global problem affecting 50% of women aged 60-80 years,
or roughly 17 million of the US population. In a study among 24,222 Asian
women by Lapitan et. al. in 2000, the incidence is between 4-17%.

Overactive bladder is a clinical diagnosis based on a triad of symptoms –

frequency, urgency and nocturia, which may or may not be accompanied by urge
incontinence. In the 2009 International Consultation on Incontinence
standardization of terminology, increased daytime frequency is defined as the
complaint of the patient who considers that she voids too often by the day,
generally more than 7 times a day. Nocturia is its equivalent in the night, defined
as the complaint that the individual has to wake up at night one or more times to
void. Urgency is a sudden compelling desire to urinate which is difficult to defer.
For many elderly patients on whom these symptoms predominate, the notion that
OAB symptoms are “normal, just a part of aging, or related to fluid intake” is
untrue. Only when these same symptoms pose a significant problem will they
consult a physician. Likewise, a number of physicians also assume the same,
“normal, just a part of aging, or related to fluid intake”.
 Frequency, urgency, nocturia and incontinence are storage disorder
symptoms. Understanding the normal physiology of micturition will explain, at
least in theory, how the above symptoms occur.

During filling, the normal bladder passively accommodates to the

increasing volume of urine. As the bladder distends, the stretch receptors in the
bladder wall are activated and generate low level afferent sensory signals that
are transmitted to the brain. Once the brain perceives that micturition is still
inappropriate, it sends inhibitory signals to the pontine micturition center (PMC)
that induces the following actions to maintain continence: (1) activates the
efferent fibers of the sympathetic hypogastric nerves to release norepinephrine
(NE) that inhibits detrusor muscle action through activation of the B
adrenoreceptors in the bladder wall. Norepinephrine, however, has a stimulatory
action on the alpha adrenoceptors in the bladder neck and proximal urethra that
results to contraction of the above to ensure a closed outlet while filling; (2)
inhibits parasympathetic outflow to the detrusor via the pelvic nerve, and; (3)
stimulates the somatic pudendal nerve to contract the striated urethral sphincter
muscle. The above actions are maintained until such time that the normal
capacity of the bladder between 400-600cc is reached, which now shifts the
bladder into an emptying or a voiding mode. The higher centers in the brain,
particularly the prefrontal cortex and the hypothalamus send stimulatory signals
to the PMC which activates the efferent nerve fibers of the parasympathetic
pelvic nerve to release acetylcholine. Acetylcholine acts on the muscarinic
receptors in the bladder wall to facilitate detrusor contraction. At the same time,
sympathetic and somatic stimulation in the bladder neck and urethral sphincters
are inhibited during voiding.

Any alteration in either the storage or the voiding phase of micturition

naturally will result to lower urinary tract symptoms. Frequency, urgency and
nocturia happen when the bladder afferents generate low level signals which are
acted upon by the spinal reflex pathways through the sacral micturition center, in
effect by-passing inhibitory signals from the brain. These triggers result to
involuntary detrusor contractions that can be objectively demonstrated in a
urodynamic tracing and subjectively felt by the patient as “urge” hence the
frequent trips to the toilet. These same involuntary contractions that are
independent of higher brainstem control do not enter a period of quiescence at
nighttime, hence, nocturia occurs. Hence, patients with the syndrome generally
have poor quality of life (loss of self-esteem, depression, social isolation,
anxiety).
 Other factors to consider in maintaining continence are the following:
efficient urethral sphincters, efficient support of the urethra through its fascial and
muscular attachments, and, a hermetic mucosal seal of the urothelium. Once
any of the above is anatomically, vascularly or neurologically impaired, urine
leakage occurs. This is what happens in stress urinary incontinence (SUI)
where there is urine loss on effort or exertion, or on sneezing and coughing that
is a result of a deficient sphincter and/or urethral hypermobility. A combination of
OAB symptoms and SUI is a mixed type of incontinence.

Work-up of patients with urinary dysfunction should include a thorough

history, physical examination, evaluation for postvoid residual volume, urinalysis
and a bladder diary. This is where a center manned by people who are trained to
cater to urinary, or at most, pelvic floor dysfunction ideally should be set up in all
hospitals. During history taking, for example, specialists may ask about the
voiding habit of the patient including pertinent symptoms using a standardized
and validated questionnaire. Investigation of bladder and urethral function can be
carried out simultaneously in the center by virtue of urodynamic studies. These
studies (simple office tests and multichannel ones) help in elucidating the cause
of lower urinary tract dysfunction, prognosticating the disorder and employing
treatment strategy. In the local setting, urodynamic studies are reserved for
patients with symptoms of stress incontinence who are candidates for surgery
and patients with neurologic impairment (multiple sclerosis, diabetic neuropathy,
Parkinson’s disease, dementia, cerebrovascular accident, etc).

Treatment is directed towards the cause. Patients with OAB respond well
to anticholinergics and bladder training. Lifestyle interventions like reducing
caffeine and carbonated drinks, weight loss, cessation of smoking, limiting
strenuous exercises or gym activity are also advised. Rarely is OAB surgically
managed. Patients with urinary stress incontinence demonstrated through
history, physical examination and urodynamic studies can be managed
conservatively and/or surgically through continence procedures. Role of topical
hormones is unclear. It can be given to reduce atrophic changes in the lower
genitourinary tract. It does not have a role in urinary stress incontinence. For
patients with mixed type of incontinence, therapy is directed towards the
predominant symptom.
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