The underactive bladder: detection and diagnosis

Myogenic factors

Any pathological process that changes the normal structure and/or functioning of the extracellular matrix or the myocytes of the detrusor may cause a loss in the generation or transmission of a contraction. Factors that may affect the contractile activity of the myocytes include disruption of important cellular mechanisms (e.g. ion storage/exchange, excitation-contraction coupling, calcium storage, and energy generation). The implication of this is that even if efferent neuronal activity is normal, an impaired contraction will result⁵.

Supporting the idea that myogenic factors may be important, morphological changes have been observed within both the normally aged and the diseased detrusor. Much of this work was conducted by Elbadawi, who suggested that specific ultrastructural features detected by electron microscopy were associated with aging and different bladder dysfunctions including DUA^6–8. The specific pattern associated with DUA was described as the “degeneration” pattern, characterized by widespread disrupted myocytes with axonal degeneration⁶. What is not clear is whether detrusor myocyte disruption is in itself the cause of DUA or the result of an underlying pathological process.

Neurogenic factors

Intact bladder sensation is central to the voiding reflex. The afferent nerves monitor bladder volume during the storage phase and also during the voiding phase. Afferent nerves arising at the level of the urethra may also have a contributory role in perceiving flow through the urethra^9,10. If afferent functioning is reduced, this may lead to a reduction in the strength or premature termination of the voiding reflex¹¹.

Bladder outlet obstruction

It has long been held that DUA occurs as a secondary effect of prolonged bladder outlet obstruction (BOO). This assumption has been largely derived from work in animals, particularly the rodent, where partial BOO is induced by a constricting metal ring or ligature. The process by which DUA occurs has been widely described and includes three phases^12,13:

Relating the insights from this work to humans is problematic, as the animals studied are usually young and female with an acute obstruction induced using a constricting ring. This is unlikely to be a good representation of the common clinical scenario of an elderly man with compressive benign prostatic obstruction. Interestingly, the largest longitudinal study available has shown that in man, prolonged BOO does not usually result in decompensation and DUA. In a group of 170 men with BOO demonstrated on pressure-flow studies, no significant deterioration in urodynamic parameters was observed at a mean follow up of 13.9 years (no change in pdet@Qmax [detrusor pressure at maximum flow] and a reduction in Qmax [maximum flow rate] of only 1 ml/s)¹⁴.

Diabetes mellitus

Diabetic bladder dysfunction (DBD) (or diabetic cystopathy) is a well-recognized cause of DUA. Diabetes mellitus probably affects function through both a myogenic and a neurogenic mechanism leading to a decline in bladder emptying ability throughout the course of the disease^15,16. It is traditionally thought that this predominately occurs through hyperglycemia-induced axonal degeneration and segmental demyelination leading to impaired afferent and efferent bladder function (autonomic neuropathy)¹⁷. Myogenic mechanisms are less clearly elucidated, though it is likely that changes in intercellular connections and excitability, intracellular signaling, and receptor density and distribution are implicated¹⁸.

Detrusor contraction strength

A detrusor contraction generates pressure and flow¹⁹; therefore, many authors have used two measurements to approximate contraction strength and thereby diagnose DUA: the maximal flow (Qmax) and the detrusor pressure at maximal flow (Pdet@Qmax). Most often a reduction in either is considered to be lower than the “normal” range. Historically, for men the normal ranges are derived from a series of men undergoing de-obstructive surgery^20,21. In other groups, such as healthy men and women, in particular, the ranges are less well established^22–24. Although relatively simple to apply, this method has two flaws. Firstly, it is likely to be an inaccurate method of determining the maximal pressure generated by the bladder due to the bladder outlet relation (BOR), the normal inverse correlation between detrusor pressure and urine flow during voiding²⁵. Essentially, the BOR can be summed up as during voiding the pressure is highest when flow is lowest and vice versa, hence the pdet@Qmax represents the point of lowest bladder pressure during voiding. Secondly, the fact that the flow rate is also impacted upon by the degree of bladder outlet resistance is not considered. This is important because when detrusor pressure is low, the cause of low flow may also have its basis in obstruction (e.g. due to BPE) or alternatively a normal Qmax can result from reduced outlet resistance even if detrusor pressure is low (e.g. post-prostatectomy incontinence).

In order to gain a more accurate assessment of contraction strength, different methods of measuring isovolumetric bladder pressure have been introduced:

1. Watts factor

This is an estimate of the power per unit area of the bladder surface that is generated by the detrusor. The formula for calculation is WF = [(pdet + a) (vdet + b) – ab]/2π where vdet is detrusor shortening velocity and a and b are fixed constants (a=25 cmH₂O, b=6 mm/s) derived from experimental and clinical data²⁶. The main pros of the WF are that it is not dependent on bladder volume²⁶ and is not influenced by increased outlet resistance²⁷. There are, however, no validated values for what is considered normal. Currently, the WF is little used in practice due to its complexity as well as the fact that it assesses only strength of contraction, rather than duration.

2. Projected isovolumetric pressure (PIP)

The PIP was proposed by Schäfer, who used a straight line to represent the BOR and then “projected” back to the y-axis (pdet) from the point representing pdet@Qmax to obtain the isovolumetric pressure. This projection is calculated by the formula PIP = Pdet@Qmax + KQmax where K is a fixed constant representing the steepness of the angle of the BOR to x-a axis²⁸. K is dependent on the specific population studied and differs between men and women²⁹; in men it is usually taken as 5. The suggested groupings for PIP are as follows:

There are two other reported variants of the PIP: the detrusor coefficient (DECO), which is the PIP divided by 100, and the bladder contractility index (BCI), which is essentially the same as PIP but with different groupings. The main advantage with these formulae is that they are easy and quick to use; however, they may overestimate PIP and have less test-retest reliability than measuring isovolumetric pressures directly³⁰.

3. Mechanical occlusion of flow

This entails the direct measurement of isovolumetric pressure by the mechanical obstruction of urine flow³¹. There are two methods for this measurement: (1) a stop test, the interruption of flow once it has already started, or (2) continuous occlusion test, where urine flow is impeded before and throughout the duration of the detrusor contraction. Stop tests can be voluntarily induced by the patient by contraction of the rhabdosphincter or alternatively the urodynamicist can impede flow through methods such as manual occlusion of the urethra. The voluntary stop test tends to underestimate pressure by about 20 cmH₂O, which is likely to be attributable to a reflex detrusor inhibition brought on by sphincter contraction^30,32. The voluntary test may not be possible in patients with sphincter weakness and in the elderly, whereas continuous occlusion can be painful and does not provide the opportunity for synchronous flow measurement.