Fig. 14.1
(a) This is an example of detrusor overactivity (highlighted by the circle) during the filling cystometrogram. The P det tracing is calculated using P ves and P abd values as explained in (b). (b) Using the equation P det = P ves − P abd , the calculated P det (circled) in the figure on the left is zero since the rise in P ves is associated with a rise in P abd (highlighted by the arrow). This can be seen, as in this case, due to a Valsalva maneuver which causes a slow controlled rise in the P abd and P ves tracings for the duration of the maneuver. Conversely, the calculated P det (circled) in the figure on the right represents a true increase in detrusor pressure since the rise in P ves is not associated with a rise in P abd (highlighted by the arrow). In other words, the increase in P det is independent of any intraabdominal pressure activity.
Vesical pressure (P ves) is the measured pressure inside the bladder. It is measured with a pressure transducer catheter placed into the bladder. Abdominal pressure (P abd) is the measured pressure inside the abdomen. It is usually measured with a pressure transducer catheter placed into the rectum. Detrusor pressure (P det) is a calculated value of the difference between P ves and P abd such that P det = P ves − P abd (Fig. 14.1b). P det, though a completely derived number, represents the true value of the pressure generated by the bladder and is distinguished from changes in the pressure tracings due to increased abdominal pressure such as that seen with coughing or straining. From a clinical perspective, evaluating the value of P det is important, as documented by McGuire, due to the potentially deleterious effects on the upper tracts when the detrusor pressure (P det) during filling or voiding is sustained above 40 cm H2O [3].
The normal micturition cycle involves passive low-pressure filling of the bladder and a coordinated detrusor contraction coupled with urinary sphincter relaxation for the evacuation of urine. A normally functioning bladder stores urine at low pressures as a result of the bladder’s viscoelastic properties and compliance. Filling cystometry provides information regarding bladder sensation, bladder capacity, detrusor activity, and bladder compliance. In addition, it is during this phase of the urodynamic study that the bladder outlet can be assessed for weakness (stress urinary incontinence). The two phases of UDS include the filling/storage phase and voiding phase (Fig. 14.2). Detrusor activity is normal during the voiding phase as the bladder contracts to expel urine. Detrusor activity should not be present during the filling and/or the storage phases and when seen is considered involuntary and is referred to as DO. DO can occur spontaneously or as a result of provocation. Provocative maneuvers such as coughing (Fig. 14.3) and Valsalva maneuvers are performed during the storage phase to assess for SUI. These provocative maneuvers can also provoke DO in a phenomenon described as stress-induced DO which will be covered later in the chapter.
Fig. 14.2
The filling phase is indicated by the steady increase in volume in the bladder as it is being filled. The storage phase can be identified by a stable volume in the bladder. The voiding phase begins when the patient is given permission to void. Note that in this instance, the patient is able to void successfully. There is an increase in flow with a concomitant decrease in the post void residual (PVR) volume
Fig. 14.3
Provocative maneuvers such as coughing (indicated by the arrow) result in increases in P ves and P abd. The P det value is the calculated value determined by the difference in the measured P ves and P abd such that P det = P ves − P abd . In the case of a cough, P det is negligible as there is no pressure coming from the detrusor itself. Acute increases in the P det lead during provocative maneuvers such as coughing represent artifact and should not be misinterpreted as detrusor overactivity
The smooth muscle fibers of the bladder can exhibit spontaneous action potentials, a phenomenon thought to be the cause of phasic detrusor activity [4]. According to the 2002 ICS standardization of terminology [5], phasic detrusor overactivity (PDO) is defined as a characteristic waveform, and may or may not lead to urinary incontinence. Although the contour of the characteristic waveform is not specified, as the name suggests one would expect cyclical increases and decreases in the P det tracing (Fig. 14.4).
Fig. 14.4
This UDS demonstrates the “waveforms” in the P det tracing with phasic DO. There is no standardization regarding the characteristics of the “waveform,” but is generally recognized as cyclical increases and decreases in P det. Note that the P abd is silent suggesting that the increases in P det are due to contractions arising in the bladder
Neurogenic detrusor overactivity (NDO) replaces the old terminology “detrusor hyperreflexia” and is defined as DO in a patient with a neurologic condition (Fig. 14.5) [1].
Fig. 14.5
This patient, who is recovering from a cerebral vascular accident, has NDO during the storage phase with associated UUI. It is important to highlight that the NDO occurred during the storage phase and not during the voiding phase. The compensatory EMG recruitment could be erroneously labeled as detrusor sphincter dyssynergia (DSD) which may occur during the voiding phase in patients with neurologic pathology
Idiopathic detrusor overactivity (IDO) (Fig. 14.6) replaces the old term “detrusor instability” and is the term used when there is no identifiable neurological cause for the DO. It is important to note that NDO and IDO may look identical on UDS. These terms are strictly defined by the patient’s neurologic status and not by the presence of IDCs on the UDS tracings.
