The Challenge of Identifying and Managing Detrusor Underactivity

Detrusor underactivity (DU) is a common cause of lower urinary tract symptoms that is important to identify, but once identified may be difficult to treat. DU implies that a patient has a bladder contraction that is insufficient to effectively empty the bladder and is essentially a urodynamic diagnosis. The primary thing to distinguish DU from bladder outlet obstruction (BOO) as both may cause a slow stream, prolonged voiding time and difficulty emptying. With BOO there are very clear anatomic and functional causes which when identified may be treated and lead to much improved voiding and symptom reduction. In contrast, even if the cause of DU is identified, there may not be many effective treatment options.

The primary etiologies of DU include myogenic, neurogenic, and idiopathic causes. Myogenic may include chronic overdistention and aging, while neurogenic causes include metabolic, both central and peripheral neurologic and infectious conditions. While the treatment or natural course of an infectious cause may allow resolution and return of normal function, many of the other neurologic and metabolic causes may not have good treatment options. Much pharmacologic investigation is ongoing to identify compounds that may be able to safely treat DU due to these causes. Currently though, self-catheterization or other treatments to manage the symptoms are all that is possible in many cases.

On the other hand, many patients with idiopathic DU may respond to sacral neuromodulation (SNM). Given that in many cases the exact etiology of DU is unclear and since SNM generally involves a minimally invasive trial stage, SNM may be a very useful treatment option in the right patient population. In fact, idiopathic, non-obstructive, urinary retention (not exactly the same as DU but many DU patients may fall into this category) is one of the FDA approved indications for SNM. In particular, younger otherwise healthy patients with idiopathic DU seem to do well with SNM.

In summary, DU is a relatively common cause of LUTS often seen in older adults and those with neurologic or metabolic comorbidities. It is important to distinguish it from BOO as BOO has many treatment options. Current treatment options for DU are rather limited except in those with idiopathic DU where SNM appears to play an important management role. Hopefully, new treatments which are effective for those with other etiologies of DU will be available in the future and allow for more robust treatment options.

Does the Bladder Contractility Index (BCI) have any role in women with detrusor underactivity? Do you use it in your practice?

No, we don’t really use the BCI in our practice. I guess we have looked at urodynamics reports for so long that we get a good sense for what is going on by just looking at the graph and not doing calculations.

This is a bit provocative, but does the fact that SNM may have a role to play in DU mean that the DU is secondary to pelvic floor-external sphincter dyssynergia? Is there some merit to the work of Kuo et. al.? Does pelvic floor/external sphincter spasm lead to negative reflexes being sent to the detrusor muscle?

I think there is a subgroup of patients who do have bladder inhibition due to external sphincter activity or perhaps some abnormal firing of the sphincter (Fowlers’ patients).

The diagnosis of DU is so dependent on ruling out BOO. However, what does one do in the patients in whom the voiding reflex is not initiated either in the UDS lab or while doing micturating cystourethrography? The patients just sit there not being able to void. There are so many patients like that. In them, it is difficult to diagnose if BOO is responsible and hence exclude DU.

Yes, that is a big challenge and then you often have to rely on the rest of the clinical picture. They may have BOO and DU or perhaps just have trouble voiding in a test setting.