Under Pressure: MUCP Is About More Than SUI

The commercial availability of air charged balloons with their accurate reproducible measurement made tracking of urethral pressure and maximum urethral closing pressure (MUCP) in particular, very easy to achieve. But why would you bother? Oddly, even when SUI improves with bulking agents there may be no change in MUCP, suggesting it is not a great marker of treatment response. MUCP is an index of urethral integrity and loss of integrity related to childbirth and urethral surgery cause it to drop. But is there more to this index of urethral resistance than its utility or not in SUI?

The first element of a voiding contraction starts in the urethra with a drop in MUCP. This is followed by a detrusor contraction into an open outlet. This relaxation function or drop in MUCP usually occurs sub-consciously resulting in good flow through the external sphincter (rhabdosphincter), the site of the MUCP.

The sequence of fall in MUCP heralding a voiding reflex, followed by detrusor contraction may be altered with various types of adversity. Neurogenic dysfunction of the external sphincter does not, however, respond to muscle down training. It may or may not be associated with neurogenic dysfunction in the smooth muscle sphincter which may also be evident on urethral pressure measurement. Tracking of rhabdosphincter behavior by continuous measurement of MUCP during urodynamic testing in patients with neurogenic disorders provides useful information too but it is rarely done. It permits detection of detrusor sphincter dyssynergia (DSD), because MUCP is due to the same entity measured in electromyography (EMG) of the external sphincter. We see activity in the MUCP zone during an involuntary contraction (instead of its relaxation which otherwise occurs during detrusor overactivity) which is most marked in upper spinal pathology such as in multiple sclerosis. Measurement by catheter transducer without the need for EMG i.e., avoiding placement of electrodes while obtaining the functional measurement, may offer an advantage to patients.

When contemplating onabotulinum toxin treatment to the detrusor, the risk of urinary retention necessitates a complex informed consenting conversation. When DSD is demonstrated (EMG or MUCP or both +/- fluoroscopic evidence of urethral sphincter behavior) a conversation about the likely need for self-catheterization is prudent. By comparison, in the presence of detrusor overactivity without such urethral sphincteric behavior, as is seen after a cerebrovascular accident, the risk of self-catheterization is much lower. In practice this translates into a willingness to offer low dose onabotulinum to such patients even when relatively frail and with poor dexterity.

In neurogenic detrusor overactivity due to non-spinal states, such as following a cerebrovascular accident, the symptoms may be the same, but we see involuntary relaxation of the external sphincter as a drop in MUCP prior to the detrusor reflex contraction. Such integration demonstrated on urodynamic studies helps in diagnosis and management because voiding is likely to be intact when detrusor overactivity is ablated successfully by botulinum toxin or medication. In lower spinal cord pathology, there may be loss of the so-called guarding reflex which may be helpful diagnostically.

Excessive activity in the MUCP zone is also seen in Fowlers syndrome. The EMG and urethral pressure profile in the MUCP zone measure the same pathology reflected in a very similar pattern though different mechanism of measurement.

In anxiety states and habitual holding of the pelvic floor and external sphincter, MUCP may fail to relax during voiding resulting in poor flow and other syndromes. Fortunately, this may respond to physical therapy or pelvic floor muscle ‘downtraining’. Whilst the observation of resolution in these syndromes in some women is evident clinically, there is a surprising dearth of collaboration between Urodynamic clinicians and physical therapists who down train the pelvic floor. Combining this with EMG and other techniques may help to unify our concepts in this field if urological endeavor though MUCP may simplify evaluation in this patient cohort prone to pelvic pain.

Finally, but not exhaustively, during an urgency experience, MUCP may drop without the detrusor pressure rising, so called urethral instability. Such a variant of ‘detrusor overactivity’ is still responsive to OAB therapy.

References:

Aw HC, Ranasinghe W, Tan, PHM, O’Connell HE. Overactive pelvic floor muscles (OPFM): improving diagnostic accuracy with clinical examination and functional studies. Transl Androl Urol. 2017 Jul; 6(Suppl 2): S64–S67. doi: 10.21037/tau.2017.05.41

What do you consider as a normal range for MUCP? How much increase do you expect to see in patients with the Fowler's variant of dysfunctional voiding? 

A low MUCP is <30cm H2O though many clinicians use <20 for their definition of “intrinsic sphincter deficiency”. Unfortunately, it can become complicated when neuropathic conditions are considered. For example, a patient with extremely severe intrinsic sphincter deficiency due to spina bifida (myelomeningocoele) may have a high (though fixed) MUCP. This is where Valsalva Leak Point Pressure (VLPP) is useful though there is considerable confusion over how to use VLPP and what it all means. In most non-neuropathic patients, when MUCP is low, VLPP is also low. For the upper limit of normal we have used >95cmH2O.

A great deal more work could be done on this. Fowler’s syndrome is diagnosed when overt urinary retention occurs. But there are plenty of young women particularly who are not in overt urinary retention but have bothersome LUTS, a high MUCP and who may be at risk of urinary retention. Their uroflow is often poor. Their pelvic floor is typically tender, and this appears to respond to expert physical therapy. They would not qualify for SNM though it is possible they would respond to it. What is interesting is botulinum toxin directly into the external sphincter does not work particularly well, suggesting the pathology involves the pelvic floor as a whole rather than the intra-urethral rhabdosphincter component.

Readers may find the following a useful reference:
DasGupta R, Fowler CJ. Urodynamic study of women in urinary retention treated with sacral neuromodulation. J Urol 171: 1161-1164 2004 DOI: 10.1097/01.ju.0000113201.26176.8f

Values for normal range of MUCP are discussed briefly in this paper. In the series reported and our experience, abdominal straining is seen as a saw tooth pattern in the uroflow. Correcting the tendency to strain and restoring relaxation during voiding appears important to rectifying this voiding disorder.

There are papers on the use of dynamic MUCP. Do you perform dynamic MUCP measurement in your practice?

These are useful reports and MUCP has been shown to increase in dynamic maneuvers such as cough or Valsalva. I find VLPP to be a dynamic and useful marker of intrinsic sphincter function. One could debate at length about the literature on this and why only some clinicians find it a useful measurement. Repositioning surgery that causes acute obstruction during a Valsalva or dynamic event is responsive to MUCP as has been demonstrated. When repositioning is not involved e.g., with bulking agents, there may be no change in MUCP though the patient improves clinically with respect to stress continence. The physiology of this is complex and probably not very interesting to most clinicians. ICS offers standards around the process of measuring MUCP.