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REVIEW
SA JOURNAL OF DIABETES & VASCULAR DISEASE
58
VOLUME 8 NUMBER 2 • JUNE 2011
An approach to urinary incontinence in the diabetic female
T D NAIDOO
Abstract
D
iabetes mellitus has reached epidemic proportions
worldwide. It is also evident that urinary incontinence
among adult women is increasing in prevalence,
especially with advanced age. Bladder dysfunction, occurring
as a complication of diabetes mellitus, usually presents with
a variety of symptoms ranging from overactive bladder, urge
incontinence to overflow incontinence, reduced bladder
sensation, and even stress urinary incontinence. This article
focuses on the association between urinary incontinence
in women and diabetes mellitus. We highlight the possible
pathophysiological processes involved and examine the
evidence regarding management of these patients.
Introduction
The increasing prevalence of diabetes mellitus (DM) worldwide can
be attributed to changing lifestyles, increasing rates of obesity and
the longevity of the population.
1
This in turn results in an increasing
prevalence of diabetes-associated complications.
2
The International Continence Society defines urinary incon-
tinence (UI) as ‘the complaint of any involuntary leakage of urine’.
3
Incontinence may be divided into stress UI, urge UI (overactive blad-
der), mixed UI, overflow UI and continuous UI (Table 1).
Prevalence rates of UI among women vary between 23 and
40%,
4
with recent studies highlighting an increased incidence.
3,5-7
Women with UI may experience social isolation, psychosocial stress
and decreased quality of life.
6,8,9
Pathophysiology of UI in DM
DM-induced microvascular damage, with the resultant alterations
in innervation and function of the detrusor muscle and function of
the neuronal component, leads to urge UI, with glycosuria, detrusor
muscle over-activity, recurrent urinary tract infections and diabetic
cystopathy being implicated in the pathopysiological process.
10-13
In the past it was felt that stress UI was due to dysfunction
of the striated muscle of the urethral sphincter and pelvic floor
supports and their innervation,
14
and that DM did not play a role in
its development. However, more recent studies suggest that obesity
as a result of DM leads to higher levels of stress UI due to increased
intra-abdominal and pelvic pressure.
15-17
Overflow UI results from
urinary retention and elevated residual volume as a result of an
acontractile detrusor muscle. The resultant increased bladder
distension and rise in intravesical pressure due to glucosuria and
osmotic diuresis leads to bladder hypertrophy, and subsequent high
residual volumes.
18
Diabetic cystopathy
Historically, diabetes-associated lower urinary tract dysfunction
has been known as diabetic cystopathy.
19
Patients’ symptoms
vary from overactive bladder (OAB) and urge UI to decreased
bladder sensation and overflow incontinence.
20
Prevalence rates
of urodynamically diagnosed bladder cystopathy range from 25
to 90%.
21
The pathogenesis is believed to be multifactorial with
alteration in detrusor muscle physiology, neuronal impairment,
and urethelium and urethral dysfunction being considered as
contributory mechanisms
22
(Table 2).
Patient evaluation
Twenty-five to 50% of patients do not volunteer information about
voiding problems unless specifically asked.
23
Ueda
et al.
24
in their
study of asymptomatic diabetic patients showed that upon direct
questioning, 40% admitted to having some degree of voiding
abnormality. Symptoms of reduced bladder contractility include
hesitancy, weak stream, dribbling, and a sense of incomplete
emptying, leaking with increased abdominal pressure and
infrequent voiding.
25
Patients’ complaints vary, with one study
showing that 17% of patients present with urinary retention,
and 76% with involuntary bladder contractions presenting as
urgency and/or nocturia.
26
Hence a thorough history of symptoms
is important in determining management, with details about their
DM and glycaemic control indicating the severity of the disease.
The patient should be assessed for other causes of vesico-urethral
dysfunction, including neurological disorders such as cerebral
Correspondence to: TD Naidoo
Department of Obstetrics and Gynaecology, Grey’s Hospital,
Pietermaritzburg
e-mail: Thinagrin.Naidoo@kznhealth.gov.za
S Afr J Diabetes Vasc Dis
2011;
8
: 58–61.
Table 1.
Types of urinary incontinence.
Type of UI
Underlying cause
Symptoms/signs
Stress
Sphincter dysfunction due to
pelvic floor weakness
Involuntary leakage of urine
upon effort or exertion, or
upon sneezing or coughing
Urge
(overactive
bladder)
Involuntary and uninhibited
detrusor contractions, due to
detrusor muscle instability
Involuntary leakage of
urine accompanied by or
immediately preceded by
urgency
Mixed
A combination of bladder
and urethral dysfunction
causing stress and urge
incontinence
Involuntary leakage of urine
associated with urgency and
also with exertion, effort,
sneezing or coughing
Overflow An acontractile detrusor
(diabetic neuropathy)
Palpable/percussable
bladder large postvoid
residual capacity, diminished
functional capacity with
frequency
Continuous
incontinence
Vesico-vaginal fistula
Constant leakage of urine.
No desire to void
