Diabetic cystopathy

1. Diabetic cystopathy

2. Definition
Wide variety of voiding complaints from overactive bladder and urge incontinence
to decreased bladder sensation and overflow incontinence

3. Introduction
Middle aged and elderly individuals
Long standing uncontrolled blood glucose

4. Physiology of micrurition
- During bladder filling at low volumes, low frequency impulses activate afferent nerves to
signal the pontine storage and micturition centers, and stimulate sympathetic outflow via
hypogastric and pudendal nerves.
- Released norepinephrine induces detrusor relaxation and enhances bladder compliance,
which is mediated largely through β3-adrenergic receptors, while bladder outlet resistance is
enhanced by activation of α1-adrenergic receptors in the bladder neck, urethra and prostate
- The somatic nerves also participate in the process of increasing bladder outlet resistance by
releasing acetylcholine.
- Increasing urine volume will increase the frequency of afferent impulses, which in turn will
shift efferent signaling from the pontine storage to the micturition center.
- This activates parasympathetic and inhibit sympathetic outflow. The resultant acetylcholine
stimulates detrusor muscle through mainly M3 muscarinic receptor subtypes

5. Stages
Stage of detrusor hyperactivity with urgency, nocturia
Stage of detrusor hyporeflexia , decreased bladder sensation, poor voiding and
overflow incontinence (classical diabetic cystopathy)

6. Pathogenesis
Detrusor muscle impairment
- In the early stage, hyperglycemia and osmotic diuresis lead to bladder distension and increased
detrusor activity with increased density of M3 rexeptors - lead to detrusor hypereflexia
- Later lead to receptor downregulation
Autonomic dysfunction
- Decreased visceral efferent fibre conduction
- Poor symparhetix and parasympathetic activity
Urothelial abnormalities
- Abnormalities due to polyol pathway, O2 free radicals and PKC activation
- Abnormalities in secretion of NO, NGF, Prostacyclins

7. Diagnosis
Early stage : increased frequency, urgency, precipitancy, nocturia
Late stage: decreased bladder sensation, increased residual volume, overflow incontinence
Examine for alternate causes - BPH, CVA, spinal cord diseases, genital prolapse in females
Investigations
- simple cystometrogram
- simultaneous pressure/flow studies
- uroflow
- sphincter electromyography

8. Treatment - general measures
Good glycemic control, BP control and lipid measures
Avoid smoking, alcohol
Pelvic exercises
Thiamine and PUFA supplementation
In atonic bladder
- More frequent voiding (every 3-4 hours)
- Crede’s manouvre : manual compression of lower abdomen to faxilitate
micturition / valsalva manouvre

9. Treatment
Overactive bladder - Tolterodine, Oxybutynin
Atonic bladder - Bethenechol (10-20 mg 3-4 times daily, intermittent self
catheterisation
Imipramine, alpha methyl dopa, phenoxybenzamine
Surgeries
- Selective vesical neck dissection (risk for retrograde ejaculation)
- Sacral neuromodulation
- -Selective pudendal nerve block