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SA JOURNAL OF DIABETES & VASCULAR DISEASE
REVIEW
VOLUME 8 NUMBER 2 • JUNE 2011
59
vascular accidents or spinal problems. A detailed gynaecological
assessment to rule out pelvic organ prolapse and to assess the
integrity of the pelvic floor muscles should also be carried out.
Diagnostic tests
Laboratory investigations such as urinalysis and culture (assessment
for bacterial cystitis), serum glucose and glycosylated haemoglobin
(diabetes control), and urea and creatinine (end-organ failure)
assays should be carried out.
Urodynamic studies form an integral part of assessment and
can include a simple cystometrogram, pressure flow studies,
uroflowmetry, sphincter electromyography and evaluation of
leak-point pressure, and residual volume tests. Current evidence
suggests that diabetic women have significantly higher nocturia
scores, weaker urinary streams, and higher incidence of overactive
bladder, with a larger percentage of increased bladder sensation
and detrusor muscle over-activity. They also have reduced voided
volumes with lower maximal flow rates, and a larger percentage
has residual volumes greater than 100 ml
27
(Table 3).
Treatment options
The treatment, which may be divided into behavioural,
pharmacological and surgical interventions, is aimed at symptom
relief, prevention of infection and adequate bladder emptying.
Behavioural modifications
Weight reduction of between five and 10% substantially lowers
symptoms of UI in obese women.
28
Other recommendations include
dietary modification, altering the amount and timing of fluid intake
and bladder and pelvic floor muscle training.
Nocturia may be reduced by restricting fluid intake in the late
afternoon and evening, voiding before going to bed, and avoiding
bladder irritants and diuretics such as caffeine, carbonated drinks
and alcohol. Bladder training is recommended for women with
OAB and may be of benefit to older women with stress UI,
29,30
but
the latest
Cochrane Review
suggests that definitive research into
bladder training needs to be conducted.
31
Optimising glycaemic
and blood pressure control and cessation of smoking is also
recommended.
32
Pelvic floor exercises or Kiegel’s exercises with or without
biofeedback have been shown to improve symptoms in urge (OAB),
stress and mixed UI.
33
Frequent voiding and the use of a double-voiding technique
are recommended. This results in more effective bladder emptying
and hence reduces or prevents UI. Valsalva’s manoeuvre or Crede’s
manual compression of the lower abdomen may be useful in
Table 3.
Clinical assessment of the incontinent female (from the Third
International Consultation on Incontinence
48
).
Type of examination Purpose
Tests
Fluid intake/voiding/UI diary, cough test, stress pad
analysis
Abdominal/rectal
Determine ascites, organomegaly, masses, anal
tone, faecal impaction, and postvoid residual
bladder urine
Pelvic/perineal/vaginal
Determine pelvic floor function, advanced pelvic
organ prolapse, urethral diverticulum (rare),
oestrogen status, inflammation, and pelvic floor
sensation
Neurological
To determine sensation and motor innervation
involving especially S2–S4; the somatic and
parasympathetic source for the bladder, urethra,
rectum, and anal canal
Urinalysis
To rule out pyuria and/or nitrate reaction
(infection), haematuria (infection, stones, or
cancer), proteinuria (renal disease), and glycosuria
(diabetes)
Urodynamic studies
Cystometrogram, pressure flow studies,
uroflowmetry, sphincter electromyography and
evaluation of leak point pressure and residual
volume
Table 4.
Surgical options for treatment of urinary incontinence.
49
Retropubic urethropexies (Burch and Marshall-Marchetti-Krantz procedures)
Suburethral sling (‘tension-free vaginal tape’)
Periurethral injection of bovine collagen or carbon-coated beads
Table 2.
Pathogenesis of diabetic bladder dysfunction.
19
Alteration in detrusor muscle function
May be attributed to different mechanisms:
• changes in intracellular connections and excitability
• changes in receptor density and distribution
• alteration in intracellular signalling and genetic change
• increase in smooth muscle sensitivity to calcium
• bladder hypertrophy can also exacerbate oxidative stress.
Neuronal damage
Possible mechanism for hyperglycaemia-induced neuronal damage include:
• Activation of the polyol pathway which results in accumulation of
sorbitol and fructose, increases the production of free radicals, activates
protein kinase C, and enhances the formation of advanced glycated end
products
• These metabolic derangements lead to axonal degeneration and
impairment of nerve conduction, which later manifests as bladder
hyposensation.
• The decreased synthesis of nerve growth factor in the bladder or the
defective transport of nerve growth factor to the lumbar sacral dorsal
root ganglia causes diabetic sensory neuropathy and bladder dysfunction.
• Diabetic neuropathy can also affect the gastrointestinal tract resulting in
constipation, impaired rectal sensation or faecal incontinence. Straining
to defecate can cause weakness of the pelvic floor and subsequent
cystocele, an increased risk of stress incontinence and incomplete bladder
emptying.
Urothelium dysfunction
• M2 and M3 muscarinic receptors increase in the urothelium, resulting in
increased sensory nerve activity to facilitate the detrusor contraction.
• Bradykinin and adenosine triphosphate significantly increase
prostaglandin release from the urothelium, resulting in increased
sensitivity of the detrusor muscle to stimuli.
Urethral dysfunction
• Nitric oxide (NO) is involved in the relaxation of the urethra and urethral
sphincter.
• NO deficiency results in sphincter spasm and outflow obstruction.
The effect of obesity and the metabolic syndrome
• High BMI increases intra-abdominal pressure leading to pelvic floor
dysfunction and urinary incontinence.
• Hyperlipidaemia is also an independent risk factor for overactive bladder.
• The main presentation of metabolic bladder dysfunction is overactive
bladder with impaired contractility.
