More about the urethral hanging theory (UHT) and a response to Dr. Peter Petros’ comments

Dear Editor,

I am very pleased that Dr. Peter Petros has taken the time to analyze and criticize the urethral hanging theory (UHT).1 However, with all due respect, I believe Dr. Petros has read the UHT articles hastily and has misunderstood many important points.

Dr. Petros accentuates that challenging of a theory, is subject to the correct interpretation of original scientific proofs and Popper's rule to “better explain” predictions. I am aware of this, and in recent years, I have spent considerable time searching databases for evidence that contradicts the UHT. However, rather than discovering weaknesses and flaws, I have identified reports and studies that support the theory. Therefore, the criticism from Dr. Petros is very welcome.

Dr. Petros lists five allegedly inaccurate statements (1‐5) made by me and identifies two important questions for the UHT to address (6 and 7). Before I deal with these seven issues, I will comment on the three other statements made by Dr. Petros.

Petros: “The UHT relies on abdominal pressure acting on the bladder to physically open out (“funnel”) the urethra.”

This statement indicates a major misreading of the UHT.2 A central principle of the UHT is that a closed miniscule meatus internus (m.i.) is a perfect seal that cannot be pushed open by the intravesical pressure (IVP). There must be a pulling force that shears open/funnels the proximal urethra. The IVP is always perpendicular to the bladder wall and generates no shear forces to allow expansion of the m.i. This is in accordance with the law of elastic collision, meaning that a molecule bouncing against the bladder wall generates a force perpendicular to it. The bladder will rupture before it is opened. This is consistent with the findings of the study by Bush,3 which is referenced by Dr. Petros “where abdominal pressure two orders of magnitude (100 times) greater would be required to forcibly funnel the urethra”.

Petros: “..the posterior urethra opens out concomitantly with depression of the anterior and posterior vaginal walls, and that this can only be explained by muscle action.”

This statement is undeniably incorrect because urethral hanging in the bladder is another possible explanation. The 6th edition of the ICS Book 4 describes the opening of the proximal urethra during stress. The occurrence of shearing/funneling can be observed using dynamic ultrasound. The reported description is said to support the integral theory (IT). However, it is also an excellent description of what happens when the proximal urethra is arrested and funneled by hanging from a filled bladder (UHT). The muscle actions that explain the open out the proximal urethra are the same muscle actions which generate the acutely high intra‐abdominal pressure (Pabd) during stress. During normal micturition, the combined action of the inner longitudinal smooth muscles of the detrusor and urethra opens out the proximal urethra [2].

Petros: “.. nor can UHT explain how supporting the PUL with a hemostat applied to one side of the urethra can prevent funneling and restore geometry and continence with no elevation.”

This statement is incorrect. According to the UHT, the hemostat prevents the urethra from descending and reaching a hanging/funneling position. However, there are women with stress urinary incontinence (SUI), in whom a hemostat with no elevation does not prevent funneling. These women have a hypomobile “fixed” urethra that is hanging/funneling even at rest. To prevent such hanging, the proximal urethra must be elevated above its resting position.5 In 2003, Petros reported about a clinical experiment using two types of virtual‐operation (VO) techniques,6 which are as follows: the hemostat test (HT) described above and a pinch test (PT), which involves a one‐sided fold of the suburethral vagina. Such a folding/tightening maneuver unavoidably results in shortening of the vaginal hammock, thereby causing a small elevation. Therefore, HT provides support with no elevation, whereas PT provides support with elevation. In other words, HT prevents urethral hanging/funneling in hypermobile SUI, whereas PT prevents it in both hypermobile and hypomobile SUI. From the viewpoint of the UHT, I regard HT as a test of the appropriateness of using tension‐free suburethral tape (TVT) and PT as a test of the appropriateness of a lifting support. The two tests differentiate between hypermobile and hypomobile SUI. UHT uses the “therapeutic window” concept to differentiate and to choose the most appropriate procedure.7

Conversely, IT explains the impact of the VO techniques differently and proposes that HT supports the pubourethral ligaments (PUL), which kink, stretch, and narrow the proximal urethra, rather than being funneled when the posterior urethral wall is pulled down like a trapdoor, shearing it from the better supported anterior urethral wall. On the other hand, the PT is proposed to increase the contractile activity of the horseshoe‐shaped rhabdosphincter (RS), because the pinching maneuver improves its insertion points in the vaginal wall.6 Petros reports, “Up to 20% to 30% of patients require tightening of the hammock (‘pinch test’) in addition to a midurethral anchoring to control urine loss on coughing when tested with ‘simulated operations’”.8 The UHT suggests that most of these women have hypomobile SUI. To create a lift without the risk of obstruction, the surgeon can use the “TVT technique” to insert one tuned tape in the paraurethral tissue on each side of the v.p.7

The comments/responses to the seven issues mentioned above are as follow.

Issue 1. “The IT always postulated a tape at mid urethra, never 1 cm from external meatus!”

Comment: Articles by Dr. Ulf Ulmsten, the co‐originator of IT and the inventor of TVT, suggest another view. In 1996, Ulmsten stipulated an incision at the midline of the suburethral vaginal wall, starting approximately 0.5 cm from the outer urethral meatus.9 This was later changed to 1 cm10 and currently Ethicon (Gynecare TVT, US, LLC) stipulates a sagittal incision starting approximately 1.0 cm cephalad from the urethral meatus.

In women with a short urethra (3 cm), an incision starting at 1 cm from the external meatus (m.e.) results in a midurethral tape position. However, in the case of a long urethra, such an incision results in a distal tape position [5]. Dr. Petros uses the term “mid‐urethra”, but what position does that describe? Is it the middle of the anatomical urethra, the functional urethra, or the intra‐abdominal urethra? Dr. DeLancey specified in 1986 that the approximate location of the intramural urethra is 0% to 20% of the anatomical urethral length and that of the mid urethra is 20% to 60%. This means that, in his opinion, the mid urethra ranges from the bladder neck to 60%.11

The UHT avoids the problems associated with different urethral lengths by stipulating that the tape should be inserted starting at 1 cm from the bladder neck. It could be conjectured that, because a short urethra has a foreshortened extra‐abdominal part, the posterior PUL attachment to the vaginal wall is located at approximately the same distance from the bladder neck and at the midpoint of the intra‐abdominal urethra.

According to the UHT, a tape inserted at 1 cm from the meatus externus is, in the case of a short urethra (3 cm), curative for SUI with no postoperative urgency/frequency symptoms (OAB), and, in the case of a long urethra, curative for SUI but with a high risk of OAB. In a woman with a hypomobile urethra, it is infrequently curative for SUI and has a high risk of OAB. If the tape is set tension‐free with no urethral obstruction, the UHT postulates that the OAB is the result of persistent funneling at rest and/or during stress.5

Issue 2. “The cause of urinary stress incontinence (USI) was never “multifactorial.” The IT always postulated USI was caused by a lax pubourethral ligament (PUL) inactivating two separate closure mechanisms, bladder neck, and distal urethra, Figure 1”

Comment: Dr. Ulmsten had a different view: “Considering the multifactorial etiology and pathophysiology of female stress urinary incontinence, as well as the complicated integration of the anatomical structures involved in maintaining continence one must realize that no method can be expected to cure all patients.9

Issue 3. “The IT considers a loose PUL extension into pubococcygeus muscle as key to USI causation!”

Comment: The UHT has the same consideration.12 However, there is a major difference between the two theories. The IT postulates that PUL act as a fulcrum promoting downward kinking of the proximal urethra, whereas the UHT postulates that the PUL act as a backstop2, 5, 7 that prevents the descent of the proximal urethra.

Issue 4. “Dr. Bergström incorrectly states” In cases with hypomobile SUI, the proximal urethra should be lifted above its resting position.” (Quoting Zacharin who never provided radiological proof for this statement). No elevation postoperatively was demonstrated in all 30 prototype TVT patients!”

Comment: I quoted Dr. Zacharin because he stipulates that “urinary continence control … is affected by … upper urethral anatomy on each side … and for a technique to be successful it must exert its influence at this precise point.13 This “precise point” proposed by Zacharin corresponds exactly with the vaginal point (v.p.) stipulated by the UHT. I did not quote Zacharin regarding the presence or absence of lifting.

Issue 5. Dr Bergström incorrectly states “In the IT, the high pressure midurethral zone is flow‐controlling.” The two closure mechanisms work by narrowing the urethra to exponentially increase resistance to flow and to close bladder neck by a kinking mechanism, or as originally described “like a ball valve”

Comment: The flow‐controlling zone is by definition the zone that prevents urine from entering the urethra. This zone can only be the m.i. An open m.i. results in a funneled bladder neck with urine in the proximal urethra, which is not normal and may trigger urgency/frequency symptoms. According to UHT, a closed miniscule m.i. is a perfect seal and is the flow‐controlling zone. The RS and other striated muscles engaging the urethra form a secondary closure mechanism and are important for voluntary interruption of flow, emptying the urethra after micturition, and obstructing retrograde flow during activities such as swimming. Closure of the proximal urethra is affected by its intrinsic muscles and vascular plexus, but not at least, by its rich content of collagen and elastic fibers.

The IT emphasizes urethral resistance to flow. According to IT, three directional muscles kink, stretch, and narrow the proximal urethra with the midurethral PUL as a fulcrum. The resistance to flow in the proximal urethra increases/decreases inversely to its radius, as defined by the Hagen‐Poiseuille law. This control of urethral resistance results in the control of closure and emptying.8 Moreover, the IT underlines the importance of the striated RS.14, 15 A lax anterior vaginal wall is said to result in a suboptimal RS muscle length; therefore, it does not have optimal muscle strength, which will reduce its ability to contract and increase the urethral resistance.8 In 2015, Dr. Petros postulated that “… whether a patient leaks urine or not has nothing to do with pressure, it is to do with musculoelastic closure of the urethral tube and … narrowing the urethral diameter by the external striated muscle closure mechanism…exponentially raising the resistance to flow.16

Nevertheless, why this prevailing major interest in the urethral resistance to flow? In fact, it does not matter whether the resistance is high or low; the IVP is independent of the conditions behind a closed m.i. A pulling/shearing force is required to open the m.i., and this force does not depend on the level of urethral resistance.

Dr. Petros pays attention to a “ball valve” mechanism, wherein the bladder rotates around the insertion point of a pubovesical ligament to close the bladder neck.8 Such mechanism has seldom been suggested.

Issue 6. How does UHT explain continence restoration with a skin graft in Obstetric Fistula patients?

Response: If the women who were successfully treated had SUI, they were cured because their urethra was reconstructed and then supported by a suburethral Singapore flap and a sling. The flap and sling prevent the urethra from descending and reaching a hanging position.17

Issue 7. How does UHT explain an increase in urethral pressure 0.25 seconds before a cough and higher urethral than bladder pressure during, if everything is done by “pressure transmission?”

Response: To cough, the woman has to produce an acutely high Pabd. Such pressure increase is created by simultaneously contracting all the muscles surrounding the abdominal cavity (AC), including the diaphragm and the pelvic floor muscles (PFM). A key element in continence is the attachment of the endopelvic fascia to the levator ani muscles on both sides at the arcus tendineus fascia pelvis.18 Contraction of the PFM elevates the vaginal wall and forces the posterior urethral wall against the anterior urethral wall. The striated RS has the same somatic innervation as the PFM (S2‐S4) and contracts in synchrony with them. These synchronized contractions can also be defined as guarding reflexes (GR).

Predictably, to produce a cough, muscle contractions must start before the cough; hence, the urethral pressure (UP) begins to increase before the cough. The proximal urethra is situated intra‐abdominally, and consequently the Pabd “transmission” is 100%. At the time of a cough, UP = MUP + GR  + Pabd > IVP, where MUP =  maximum urethral pressure at rest. Thus, the increase in UP to levels higher than the bladder pressure begins before the cough. Coughing (short valsalva) indicates the presence of large GR forces because the intention is to expell something out of the mouth. Strain—correctly performed—means little GR forces because the intention is to let something out from the bottom, which is facilitated by relaxation of the pelvic floor.

Finally, Dr Petros argues that the UHT cannot explain the ultrasound events shown in Figure 1 of his article, and states that there is “No indentation of the anterior bladder wall, a prerequisite if intra‐abdominal pressure is to cause funneling; the anterior urethral wall remains in situ.”

Comment: This is a surprising argument. The UHT means exactly what the name suggests. Figure 1.2 shows a hanging urethra.1 The Pabd is the cause of the hanging situation. Perhaps Dr. Petros does not perceive this because the originators of the IT rejected the theory of direct abdominal pressure transmission.^14,15 However, I find Figure 1.5 incomprehensible. In the case of a woman who has loose and lengthened PUL, the urethra is pictured as an upwards bow. This is inconsistent with Figure 1.2, which shows the reverse. I explain below my view of how Pabd affects hanging/forced funneling.

The AC is a closed entity and similar to a water bag. All but 10%‐15% of its content is incompressible water with some gas. The Pabd is the same throughout the cavity, except for a hydrostatic pressure component. Therefore, in a closed entity like the AC, a change in Pabd affects the whole cavity simultaneously. This is in accordance with Pascal's law of fluid pressures, which states that when there is an increase in pressure at any point in a confined fluid, there is an equal increase at every other point in the container. Enhörning's direct abdominal pressure transmission theory (ET),19 is grounded on this pressure law although ET is not correct regarding the lower limit of the AC.2

During straining, the pressure increases concurrently throughout the entire AC. The same pressure increase occurs around/inside the bladder and around/inside the proximal urethra. There is no compression of the abdominal contents and everything stays in approximately the same position. This is a zero‐sum situation even though the pressure is higher. If a woman is continent at rest, she is also continent under stress. An exception to this situation is when the AC is asymmetrically deformed, which is the case in SUI. The urethra and bladder base are both fixed to the endopelvic fascia/anterior vaginal wall but at different points; the urethra is fixed more distally than the bladder base. If the endopelvic fascia (pubocervical fascia) beneath the proximal urethra is defective, and the fascia beneath the bladder base is not, the urethra will descend relative to the bladder and reach a hanging position that generates a pulling/shearing force that funnels the proximal urethra. This, in a nutshell, is the UHT (Figure 1).

Figure 1.

Hypermobile SUI during a valsalva maneuver. The long urethra (4.5 cm) is “wheeling” downward, hanging in between the anterior PUL and bladder. Funneling at Pabd < aLPP. According to Pascal's formula Fd = (Pabd + Pdet) × π × r ². MUP+GR+Pabd resists the Fs/Fd. The intermediate PUL are not attached to the os pubis. Between that part of the PUL and os pubis, there is only fat and the v. clitoridis. The IT stipulates a suburethral tape that starts at 1 cm from the m.e. The UHT stipulates a suburethral tape that starts at 1 cm from the bladder neck, that is, center of tape at v.p. The figure can alternatively be said to demonstrate a urethra with very small mobility (“fixed urethra”), hanging/funneling even at rest. In such severe hypomobile SUI, a suburethral tension‐free tape is of marginal, if any, benefit to the woman. To stop hanging, the proximal urethra at v.p., must accordingly be lifted above its resting position. Abbreviations: aLPP, abdominal leak point pressure; Fd, outflow distending force; Fs, shearing forces; IT, The integral theory; m.e., meatus externus; m.i., meatus internus; MUP, maximum urethral pressure at rest; Pabd, intra‐abdominal pressure; PCF, pubo‐coccygeal fascia; Pdet, detrusor pressure; PUL, pubourethral ligaments; r, radius of m.i.; SUI, stress urinary incontinence; UHT, urethral hanging theory; v.p., vaginal point; GR, guarding reflex.

However, besides better support, relative to the urethra, a full bladder is heavy with a resistance to acceleration (inertia). During cough the “light‐weighted” unsupported urethra rapidly descents in contrast to a full bladder. This increases the risk for urethral hanging. A full bladder is also large and its ability to descend is restrained.

In contrast to the UHT, the IT, rejecting ET, hypothesizes that the increase in UP during stress, is produced by the fast twitch contraction of the RS and by the kinking/stretching/narrowing action (KINK) of the muscles using PUL as a fulcrum. In the UHT, the PUL act as a backstop that sustains the correct spatial relationship between the proximal urethra and the bladder, thereby preventing the urethra from reaching a hanging position.

A closed m.i. has, per definition, a zero or an almost zero radius and accordingly, the outflow distending force (Fd) will be zero or minimal (Fd = IVP × π × r ²). This is analogous to blowing up a rubber balloon, where the initiation of expansion may be nearly impossible without first manually dilating the mouthpiece (“radius”). Thus, there must be a force that pulls open the m.i.—a high IVP cannot push it open. ICS defines genuine stress incontinence as “involuntary urethral loss of urine when the IVP exceeds the maximum UP in the absence of detrusor activity.” Is it time to change this definition?

The so‐called intrinsic sphincter deficiency (ISD) type of SUI, also called type III SUI, in which the fixed “stovepipe” urethra, low maximum urethral closure pressure at rest and funneling at rest, is, according to the UHT, nothing less than a urethra that is hanging/funneling even at rest.

ISD is often described as a form of SUI with a week sphincter and good support. In viewpoint of the UHT the “week sphincter” is the forced funneling of the proximal urethra and the “good support” is the urethra tethered to a less mobile bladder, limiting its descent. Women with “ISD” frequently have severe urgency/frequency symptoms due to the hanging/funneling position even at rest and to situations wherein only a small stressful event causes the Pabd to reach the abdominal leak point pressure (aLPP). Restoration of the defective suburethral support immediately corrects the supposed intrinsic urethral defect, which demonstrates that it has a functional, not a morphological cause. According to the UHT, SUI, and mixed urinary incontinence (MUI) are the same disease.

Approximately 80% to 90% of cases of SUI are hypermobile SUI, which have high success rates almost irrespective of the TVT position, whereas 10% to 20% are hypomobile SUI, which have a high failure rate for surgery. TVT surgery has an overall failure rate of 10% to 20%, and many women cured of SUI have de novo or persistent symptoms of urgency/frequency. About one‐third of all surgical procedures for SUI are performed in women with recurrent SUI and are unfortunately associated with worse outcomes than in case of a primary surgery. As life expectancy is expected to increase, management of recurrent SUI will be an increasing problem until a better understanding of SUI surgery failure is provided.

There has been no change in the rates of failure and adverse events since the introduction of TVT almost 25 years ago. “It appears that we have reached a ceiling in efficacy and complication rates. As a group, we have not been able to eliminate a rather high rate of unwanted and expected complications.”20 Something must be wrong (Figure 2). It should be noted that the rationale for TVT is based on the IT. In June 1992, the originators of IT proclaimed “There has been very little advance in the surgery of female urinary incontinence over the past 20 years. In our opinion this is due to uncritical acceptance of the intraabdominal pressure transmission theory…”.21 Six months later, December 1992, in a review of his 1961 article19, Dr. Enhörning opposed and defended his theory “… it is not possible to accept that kinking could be the mechanism whereby the urethra normally assures closure”.22 I agree with him and infer that the rejection of ET, as well as the uncritical acceptance of IT, have, in almost 30 years, delayed a correct understanding of SUI. The Swedish‐born Dr. Enhörning died 2013 in Florida, USA, at the age of 88 years old.

Figure 2.

Abbreviations: UHT, urethral hangning theory; IT, integral theory; ET, Enhörnings theory; PUL, pubo‐urethral ligaments; IVP, intravesical pressure; Pdet, detrusor pressure; MUP, maximum urethral pressure at rest; UP, urethral pressure; Pabd, intraabdominal pressure; Fs, shearing force; Fd, outflow distending force; KINK, kinking/stretching/narrowing of the proximal urethra against the PUL as a fulcrum; PCM, pubo‐coccygeus muscles (lift the vaginal hammoch and press the posterior urethra wall against its anterior wall); RS, rhabdosphincter – according to IT, both RS and PCM have reduced effect in cases of loose and lengthened PUL; GR, guarding reflexes (RS+PCM); * = Enhörning's pressure transmission theory is incorrect regarding the lower limit of the abdominal cavity but is otherwise correct.2

The UHT suggests that there is a clear continuum between the two types of SUI, hypermobility and ISD. In the chapter on Pathophysiology of Stress Incontinence in the 6th edition ICS Book (2017) the authors stated that “There is a need for a hypothesis which would integrate these various observations regarding hypermobility and ISD” and “Many patients with urodynamic stress incontinence show urethral mobility, though it is not yet known what it is about that mobility which permits urethral opening during stress.” I propose that these two enigmas are resolved by the UHT.

The total number of women who undergo SUI surgery are constantly increasing. A failed operation, consumes the limited resources and is a misery for the woman. It is crucial that SUI surgeries achieve higher success rates. The UHT is a biomechanical model for deeply understanding the pathophysiology of female urinary incontinence.