Disturbances in bladder emptying and/or storage are often asymptomatic to the patient, especially in the beginning of this diabetic complication. In contrast, sexual dysfunctions are readily perceived by the patient. Sexual dysfunctions as erectile or ejaculatory dysfunction and infertility are frequently found in the male diabetic compared with the nondiabetic population. Although these sexual dysfunctions often exert a dramatic negative impact on psychosocial living and self esteem of the patients with diabetes, they remain unacknowledged in many instances. They do not attract medical attention and thereby possible treatment either owing to the shame and embarrassment of the patient or to unawareness or old-fashioned negligence of the problem by the physician. As the impairment of bladder storage and emptying as well as sexual dysfunction may have severe organic and psychosocial consequences, their existence (often in apparent to the patient) should be systematically screened for in the routine diabetes clinic. Given hints of existence, comprehensive evaluation of the impaired organ system is mandatory. For treatment, a wide spectrum of various approaches is available and can be individually offered after appropriate diagnosis (1).

From: Contemporary Diabetes: Diabetic Neuropathy: Clinical Management, Second Edition Edited by: A. Veves and R. Malik © Humana Press Inc., Totowa, NJ

BLADDER DYSFUNCTION Physiology of Micturition

In the adult, storage capacity of the urinary bladder is 300-600 mL. Until the final volume is reached only a minimal intravesical pressure increase is observed and involuntary spinal reflexes avoid uninhibited contractions. During the filling phase, afferent impulses from the bladder are suppressed both by intraspinal and cerebral mechanisms; furthermore, the sphincter apparatus is activated. When the maximal storage capacity is being reached, afferent impulses transmit this information to the conscience level. Then, efferent motor activity from the pontine micturition center through the nuclei intermediolaterales of the spinal micturition centers at the level of Th 10-L 2 and S 2-4 initiate the micturition. These impulses are transmitted to the secondary cholinergic neuron within the pelvic plexus. Peripherally, micturition is initiated by relaxation of the extrinsic striated sphincteric muscle and contraction of the smooth muscles of the bladder wall. In the absence of relevant anatomical subvesical obstruction, complete bladder emptying occurs in the presence of rather low intravesical pressures (1).

Pathophysiology and Clinical Symptomatology of the Diabetic Bladder

In the rat with experimentally induced diabetes, micturition disturbances start with degeneration of the afferent myelinated fibers (2). Neurogenically mediated bladder contraction is altered in the diabetic rats, which show an increased response to electrical field stimulation and a reduced cholinergic response. However, the purinergic response does not appear to be altered, whereas a residual nonadrenergic-noncholiner-gic (NANC) component of contractile response of unknown origin is increased (3). Diabetes-induced decrease in the contractility of bladder wall smooth muscle in rabbits has been linked to an increased expression of thin filament proteins, calponin, tropomyosin, and caldesmon, which might alter the contractile and cytoskeletal structure in bladder myocytes. The overexpression of these thin filament associated proteins, which suppresses actin-myosin interaction and actomyosin adenosine triphosphatase, and the enhancement of this suppression by tropomyosin are likely to have an effect on the relationship between force and myosin light chain phosphorylation. Thus, requiring higher levels of phosphorylation in diabetic detrusor compared with that of control. The downstream effects of high glucose (e.g., oxidative stress) appear to modulate the tran-scriptional regulation of thin filament mediated regulatory proteins in bladder smooth muscle (4).

In man, "diabetic bladder" describes a syndrome of reduced awareness of bladder filling, followed by increased bladder storage capacity and decreased bladder contractility. The reduction of sensation of a filled bladder (caused by the degeneration of the afferent myelinated fibers) is rapidly followed by degeneration of the non-myelinated efferent fibers resulting with detrusor hypocontractility. This hypocon-tractility translates clinically into reduced urinary flow, incomplete bladder emptying, recurrent urinary tract infections (UTI) and, as end stage disease, into bladder desen-sitization and acontractility with overflow incontinence. In contrast to this classical scenario of a diabetic bladder, autonomic neuropathy may cause irritative symptoms as urge, pollakiuria, nocturia, or incontinence in the presence of other urological diseases (5-7).

Bladder Dysfunction in Women With Diabetes

It has been estimated that urinary incontinence may affect nearly 50% of middle aged and older women, leading to significant distress, limitations in daily functioning, and poorer quality of life. Diabetes is associated with an increased risk of incontinence by 30-100%. It has been suggested that interventions that prevent or delay onset of diabetes may also prevent urinary incontinence. In the diabetes prevention program the prevalence of weekly stress incontinence was decreased by the diabetes prevention program intensive lifestyle intervention. Reducing incontinence may be a powerful motivator for women with impaired glucose tolerance to choose lifestyle modification to prevent diabetes (8). Recent large observational studies have identified urge incontinence, an involuntary loss of urine with a feeling of urgency, as increased among women with diabetes, whereas there was no increased risk for stress incontinence, an involuntary loss of urine with physical activity (8). Women with diabetes treated with insulin are at considerably higher risk of urge incontinence than those treated with oral medications or diet (9). However, little is known about how diabetes may contribute to the incidence or severity of urinary incontinence.

Bladder Dysfunction in Men With Diabetes

Lower urinary tract symptoms (LUTS) are common, age-related complaints that are often attributed to benign prostatic hyperplasia (BPH). LUTS and BPH increase rapidly with age starting at about 50 years. Straining, intermittency, postvoid dribbling, and weak stream may signify urethral obstruction from BPH. However, among men with diabetes, similar symptoms may also result from bladder dysfunction because of dener-vation and poor detrusor contractility. Other complex associations of LUTS and BPH among men with diabetes include symptoms of urgency, frequency, and nocturia that may occur from detrusor overactivity resulting from BPH, and/or microvascular complications associated with diabetes, increasing hyperactivity of the detrusor. Because previous studies have failed to differentiate LUTS from BPH in men with diabetes, the effect of diabetes on the development or presence of LUTS and BPH remains controversial (8).

Recent evidence suggests that LUTS may occur more frequently among men with diabetes, with an estimated 25% to nearly twofold increased risk of LUTS in men with diabetes. Furthermore, among men with BPH, diabetes is associated with more LUTS symptoms compared with men without diabetes (8). Experimental evidence suggests that early alterations in sodium and potassium channels occur in both BPH and diabetes similar to neuropathic models. These changes trigger altered excitability, leading to detrusor overactivity and urinary frequency. With time, impaired contractility because of a myopathy can lead to incomplete emptying. Thus, a combination of several factors with differing time courses lead to LUTS and known urodynamic findings, making discerning an etiology and distinguishing classic diabetic cystopathy from neural plasticity accompanying obstruction because of BPH problematic (8).

Diagnostic Approach to Micturition Disturbances

In 40-80% of urologically asymptomatic patients with diabetes, abnormal findings were obtained in a detailed urodynamic work up. Many of these patients were aware of their abnormal micturition patterns only in structured questioning. However, these often asymptomatic micturition disturbances may have deleterious consequences for the upper urinary tract with significant renal impairment or even end stage renal disease. This low incidence of symptoms in the presence of possible severe consequences necessitates the inclusion of specific questions regarding micturition patterns in the yearly routine diabetic check up. Here, frequency, sensation of incomplete bladder emptying, UTI, urge symptoms, dysuria, nocturia, incontinence and necessity to use abdominal strain to empty the bladder should be specifically addressed. In unclear situations, a micturition protocol for three consecutive days and nights may be helpful. A urinary lab completes the routine urinary bladder function check (1).

Given anamnestic hints for micturition disorders or recurrent UTI, a noninvasive uro-logical work up consisting a uroflometry and a postvoid ultrasound of the bladder should be initiated. A full urological work up with formal urodynamics and radiological imaging of the urinary tract is needed in the presence of recurrent UTI or abnormal noninvasive findings. Endoscopic diagnostic procedures will be instituted according to the findings of the aforementioned diagnostics. Depending on the therapeutic option planned, further and mostly highly specialized diagnostic procedures are needed, for example, putting "temporary wires" as time-confined percutaneous testing of the effect of neurostimulation or instruction of self-catheterization before surgical construction of a catheterizable neobladder (see specific procedures) (10).

Therapeutic Options for Micturition Disturbances

The need for treatment of micturition disorders is determined by the subjective and objective severeness of the impairment, by its etiology, its urological (nondiabetic) comorbidities, its secondary negative impact on the upper urinary tract as well as by the intellectual and manual capacities of the patient. Although autonomic neuropathy will most likely be a reason for voiding dysfunctions in a patient with diabetes, other cofac-tors or coetiologies such as hormone deficiency, obstructive prostatic hyperplasia, or ure-thral and meatal stenosis may play an important role and must be taken into account when treatment options are considered and discussed with the patient. To determine these individual variables, the aforementioned rationalized urological approach is mandatory before treatment. The majority of diabetic voiding dysfunctions can be safely managed by conservative approaches. However, close follow-up of the patient might be necessary for early detection of treatment failures and avoidance of secondary complications (1).

Treatment of a large capacity bladder might start with regular voiding intervals (during daytime, three hourly intervals are often appropriate). Furthermore, the patient is advised to take his time to void and to try to relax his pelvic floor during micturition. An hypo- or even acontractile bladder may benefit from pharmacotherapy with parasympathomimetics. In the presence of a mild-to-moderate infravesical prostatic obstruction, an a-blocking drug can be additionally prescribed. If recurrent UTIs are observed inspite of these therapies and residual postvoid urine is significantly more than 100 mL, either clean intermitted self-catheterization (4-5 times daily) should be started or a suprapubic catheter be put. Surgical reduction of the bladder's capacity has not been very successful in the past; the ability of neuromodulation or -neurostimulation to restore bladder emptying in these patients (in the presence of autonomic neuropathy) also seems very limited (10-13).

Anatomical infravesical obstruction is mostly seen in elderly male patients, although urethral strictures are a frequent cause of recurrent UTI in females. In case of a significant bladder outlet obstruction by BPH, ablative procedures (transurethral resection, laser evaporization, thermoablation, open surgery) should be recommended. Urethral or meatal strictures warrant endoscopic or formal repair (14).

Stress incontinence by a descensus of the pelvic floor and insufficiency of the sphinc-teric mechanisms is a frequent finding in elderly women with diabetes. Depending on the severity of symptoms and the individual's preference, various approaches may be chosen. In mild-to-moderate cases, conservative options as functional rehabilitation by regular pelvic floor exercises, local or systemic hormonal replacement, or vaginal electros-timulation result in good therapeutic responses. However, these treatment modalities require regular application and good patient's motivation. The principle of the surgical correction for stress incontinence is elevation of the pelvic floor by various procedures. Here, success rates of minimally invasive sling procedures (Raz, Stamey) are at approximately 50% (or less than that figure) after 5 years, whereas formal surgical repair (fascial sling, Burch) attains rates of 80% dryness after 5 years. Implantation of an artificial sphincter for correction of urinary stress incontinence in an elderly diabetic should be critically discussed and remain a last resort if all other approaches failed as it is accompanied by an increased rate of prosthesis infection compared with the nondiabetic (1).

Pollakiuria, dysuria, urge, or incontinence symptoms may be caused by neurogenic bladder hyperreflexia in the patient with diabetes. Compared with stress incontinence, most of these symptoms respond well to conservative treatment. The mainstay of pharmacotherapy are antimuscarinic or "spasmolytic" (direct smooth muscle relaxant) agents; however, as these pharmacological approaches exert none or only very limited bladder selectivity, their individual effectivity is often limited. Nonpharmacological approaches for the urge symptom complex consist vaginal electrostimulation as well as neuromodulation (electrical stimulation of sacral nerves) (1).

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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