Year: 2023
Type: article
Abstract: In a recent NAU article Petros claimed that Enhörning's abdominal pressure transmission theory (PTT) is incorrect.1 He compared PTT to the Russian monk Rasputin, who continued to live despite being mortally wounded; the PTT was "mortally wounded" by 11 different invalidations from the 1990 published integral theory (IT) of female stress urinary incontinence (SUI). Petros stated that intra-abdominal pressure (Pabd) does not contribute to urethral pressure at rest or during stress. Instead, Pabd transmission would be an index of the changed intraurethral area caused by a musculoelastic mechanism, in which the posterior pubourethral ligaments (PUL) act as a fulcrum, against which the proximal urethra is kinked, stretched, and narrowed by three-directional muscle forces.2 This is unreasonable. The PTT is based on Pascal's fundamental hydrostatic law and cannot be replaced by an alternative mechanism. Enhörning's theory involves two assumptions, or more precisely, two different theories, one of which is correct.3 The first theory, the correct one, states that in healthy asymptomatic women, the Pabd is equally and simultaneously transmitted to the bladder and proximal urethra; this is Enhörning's theory of abdominal pressure transmission (PTT). The second theory, the false theory, states that in SUI, the suburethral vaginal wall is pressed down by the Pabd without reaching a firm backstop. The counterpressure is partially shifted proximally to the better-supported vaginal wall below the bladder, resulting in a dampening effect in response to pressure transmission to the proximal urethra, with the bladder neck being pushed open when the bladder pressure exceeds the urethral pressure. This is Enhörning's theory of the pathogenesis of SUI. The first theory follows Pascal's hydrostatic law and does not violate any physical laws, whereas the second theory violates Pascal's hydrostatic law, the law of elastic collision, and the Hagen–Poisseuille law.4 Enhörning's first theory, the PTT, is correct, as the bladder and proximal two-thirds of the urethra are contained within the same confined space. This area, known as the abdominal pressure space (APS) or pressure equalization zone, is caudally limited by the pubocervical fascia (PCF), above which the bladder and proximal urethra are located. Human abdominal tissues, including the watery contents of the intestines (with some gas) and the bladder/urethra complex, comprise approximately 85% of water. Therefore, the APS can be considered as a confined space filled with an incompressible fluid to which Pascal's law applies. This law, which also applies to deformable entities such as the APS, states that the pressure is the same at every point of a confined fluid-filled space except for the hydrostatic pressure component caused by the weight of the fluid. Consequently, the Pabd is always completely (100%) transmitted to the bladder and proximal urethra; that is, an increase in the Pabd is equally transmitted to both sides of the bladder neck. This is a zero-sum situation, with neither high nor low Pabd transmission interfering with the urethral closure mechanisms and this is true for both continent and incontinent women, both at rest and during stress. Regarding the urethral closure, the bladder neck—the closed meatus internus—is the primary mechanism, and the pressure in the urethral high-pressure zone (HPZ), that is, the maximum urethral pressure, is the secondary mechanism. The APS is illustrated schematically in Figure 1, in which the red rectangle represents its limits—the PCF, thoracic diaphragm, abdominal wall, os pubis and spine. In healthy asymptomatic women with normal suburethral support, pressure changes in the bladder and proximal urethra, caused by Pabd transmission, are no more or less important than changes in atmospheric pressure, which are transmitted equally and simultaneously to both sides of the bladder neck. Women can urinate normally deep in the water or on top of Mount Everest. In clinical urodynamics, atmospheric pressure is never accounted for, even though it contributes an average of 1033 cm H2O (760 mmHg × 1.36) to urethral pressure at ground level. However, this does not indicate that Pabd transmission to the proximal urethra is unimportant. If atmospheric pressure were not transmitted to the urethra but only to the bladder, it would be disasterous for women's continence mechanisms. Analogously, if Pabd were not transmitted to the proximal urethra, the function of the HPZ as a secondary closure mechanism would be severely affected. This would also mean that in women with defective suburethral support there would be no SUI, as during stress there would be no force to depress the proximal urethra and forced it to be funneled by hanging on a less mobile bladder neck. Furthermore, women would be unable to urinate by straining/pushing.4 The 11 evidence alleged to invalidate Enhörning's PTT are described and commented on below and "challenged for truth or falsity," as suggested by Petros.1 Petros, does not differentiate between the two theories of Enhörning and, consequently, argues against Enhörning's PTT (Pascal's fundamental law) and against Enhörning's theory of the pathogenesis of SUI. It is correct to argue against the latter theory as it violates at least three physical laws and therefore, is false. In the comments, Enhörning's PTT is defined according to Pascal's hydrostatic law, and the bladder and two-thirds of the proximal urethra are considered to be within the same confined space, the APS. The 11 evidence alleged to invalidate the PTT are described in short excerpts from Patros' article; read1 for more details. All 30 patients, even those whose bladder neck was below the symphysis preoperatively were cured without any bladder neck elevation whatsoever. According to Popper's criteria for a valid theory, this finding alone invalidated the PTT as described by Enhörning. Comment: The bladder and proximal urethra are always within the APS; therefore, 100% of the Pabd is always transmitted to the bladder and proximal urethra. A very low bladder neck position indicates that the bladder neck is outside the pelvic bone, but not outside the APS, which is caudally limited by the PCF. Bladder neck elevation does not affect Pabd transmission. Enhörning did not state that a low-lying urethra outside the APS is the cause of SUI or that, for successful surgery, the bladder neck should be elevated to a retropubic position. He stated that the suburethral tissues should be reinforced in order to ensure that the urethra does not yield downwards during stress.3 According to the Urethral Hanging Theory (UHT) of SUI, the 30 women with SUI were cured because the tape prevented the proximal urethra from descending and breaking against/hanging on a less mobile bladder neck and being pulled open/forced funneled, that is, deformed (Figure 2). A video produced by the Sydney Pelvic Floor Health Clinic at the University of Sydney, Australia, provides an excellent demonstration of urethral funneling during the Valsalva maneuver.5 In women with SUI, the Pabd transmitted to the proximal urethra is counterbalanced by the pulling/shearing force (Fs) and the outflow-distending force (Fd); therefore, Pabd does not seem to be 100% transmitted.6 Pressing a hemostat on one side of the urethra immediately behind the symphysis at the origin of PUL, without any elevation of bladder neck, controlled SUI. No PTT hypothesis can explain this. Comment: Pabd transmission is always exactly 100% and elevating the bladder neck does not make any difference; SUI is controlled by the hemostat as it prevents the urethra from descending ("yielding downwards") during stress. See comment 1. First, distal urethral closure, then, bladder neck closure. These findings cannot be explained by any PTT hypothesis. The IT explains both mechanisms by the action of three opposite muscle forces. Comment: The problem in SUI is not to close the urethra; it is to prevent it from being pulled open/funneled. The urethra is tightly closed by the recoiling of its intrinsic smooth (circular) and striated muscles, vascular plexus, and rich content of collagen/elastic fibers. Moreover, the high tonus of the pubococcygeus muscles which are connected to the posterior PUL and the PCF closes the urogenital hiatus and lifts the suburethral vaginal wall, thereby pressing the posterior urethral wall against its anterior wall. Additionally, during stress, signals from the pontine storage center induce reflex contractions of the rhabdosphincter complex, urethral circular smooth muscle and PFM. These reflex contractions are known as the guarding reflex (GR). A closing musculoelastic mechanism is not required. Furthermore, if it were true that a musculoelastic mechanism increases the urethral pressure proportionally to the Pabd increase, the pressure "transmission rate" to the urethra would be more than 200%—that is, 100% according to Pascal's fundamental law, 100% according to the musculoelastic mechanism, and some percentage from the GR. This, however, never happens. Pascal's fundamental law cannot be rejected and replaced by an alternative mechanism. A firm PUL is required for the closure action of the three opposite muscle forces. Comment: (See comment 3). The urethra is closed by the recoiling of its intrinsic structures, pressure transmission, the GR and a tight urogenital hiatus. The cure requires the prevention of bladder neck and proximal urethral funneling. A firm PUL prevents the proximal urethra from descending and being forced funneled by breaking against/hanging on the less mobile bladder neck, and not by restoring a fulcrum/musculoelastic mechanism. Urethra is anatomically shielded. Close examination of the organs at rest, there is no space for pressure transmission. Comment: All tissues within the APS are essentially just water; the APS is deformable, and nothing that shields the proximal urethra is present. A pressure change is equal and simultaneous throughout the entire entity. Bush et al. found that a pressure two orders of magnitude (×100) would be needed for the pressure to distend the urethra to reproduce the funnelling observed during micturition, that is, a column 16 000 cm high (160 × 100 cm) would be needed to compress the same tissues to close the urethra. Comment: This argument, which follows the law of elastic collision, does not invalidate the PTT. However, it invalidates Enhörning's theory of the pathogenesis of SUI. The bladder neck cannot be pushed open by a high bladder pressure either during normal micturition or during stress, it must be pulled open. "Pinch test." taking a fold in urethra restored continence without elevation in women who leaked urine while coughing. A transducer positioned at midurethra recorded raised urethral pressure when the fold was made. Comment: The video Petros refers to has been deleted from YouTube and is unavailable; however, the "Pinch test" is discussed in a recent article.4 Petros refers to the 20-30% of women with SUI who require tightening of the hammock ("pinch") along with midurethral anchoring to control urine loss on coughing when tested with "simulated operations".2 According to the UHT, these women have hypomobile SUI or "fixed type" of SUI with a small therapeutic window, i.e., a short or no distance for the urethra to descend before it breaks against/hangs on the bladder neck. The "Pinch test" involves vaginal folding, which unavoidably results in the shortening of the vaginal hammock, causing a small elevation that prevents the urethra from descending and being forced funneled. The elevation does not make a difference to the Pabd transmission which is always exactly 100%. Petros claimed that these women were cured because the vaginal folding increased the contractile activity of the horseshoe-shaped rhabdosphincer, thereby increasing the urethral pressure.4 This is incorrect because the magnitude of urethral pressure is irrelevant to the opening of the bladder neck. Cure requires preventing the bladder neck and proximal urethra from being pulled open/funneled. It is given that women with SUI, where at rest, the urethra is hanging or is almost hanging on a less mobile bladder neck, i.e. having a small therapeutic window, cannot be treated by an elastic, tension-free tape loosely placed under the posterior urethral wall. To cure, it is necessary to increase the margin to urethral hanging by a lifting support procedure. Vaginal folding is one such procedure. (a) At the level of the bladder, as expected, pressures inside were slightly less than outside. (b) However, urethral pressure on coughing was markedly higher in the urethra than the bladder indicating closure on coughing by a reflex. It would be expected, if the PTT theory were correct, that, during coughing, the pressure inside the urethra would be slightly less than outside. When, as part of the operation, at the time the suburethral vaginal hammock was disconnected, massive urine loss was noted during coughing, even though the intraurethral pressure increase recorded on four patients at midurethra was 78%, 94%, 112%, and 170%. When the suburethral vagina was sutured to the adjacent pubococcygeus muscles, the patients immediately became continent on coughing. This could only be explained by an active closure mechanism, as postulated by the Integral Theory. Comment: (a) The bladder pressure (Pabd + Pdet) is always higher than the pressure just outside the bladder wall, which is the Pabd. In the referenced 1995 clinical study, measurement errors must have occurred.7 (b) This argument does not invalidate the PTT. The proximal urethra is within the APS, and its pressure during stress increases synchronously with the Pabd. In SUI, when the Pabd increase is high enough to press the proximal urethra down and cause it to break against/hang on a less mobile bladder neck, the bladder neck is opened by the two forces Fs/Fd. These forces counteract the high maximum urethral pressure during cough (sMUP; s = stress). This can be described by the following equation: sMUP = MUP + ΔPabd + GR−Fs−Fd < Pabd + Pdet. Pdet is the detrusor pressure, MUP is the maximum urethral pressure at rest including the transmitted Pabd at rest, GR is the guarding reflex and ΔPabd is the increase of Pabd during stress. The magnitude of the increase in sMUP before leakage depends on the extent to which Pabd must increase before the proximal urethra is pressed down to the hanging position. This pressure is called the abdominal leak point pressure (aLPP), which can be low or high, depending on the compliance of the proximal urethral support in relation to the compliance of the bladder neck support, i.e., urethral mobility in relation to bladder neck mobility. Therefore, during stress, the increase in sMUP is the same (exclusive of the GR component) as that in Pabd until the urethra breaks against the less mobile bladder neck and is forced funneled (deformed). At the aLPP, the forces Fs/Fd overwhelmed the sMUP, and the urethra is opened at its full length.8 Accordingly, in SUI cases with high aLPP the intra urethral pressure increase can be very high before leakage occurs. Ultrasound experiment showed the importance of a firm PUL. A hemostat applied immediately behind the symphysis not only controlled urine loss on coughing, it activated closure at the distal urethra and also, bladder neck. Comment: The urethra is closed by recoiling, pressure transmission, the GR and a tight urogenital hiatus (se comment 3). Normal posterior PUL control urine loss by preventing the descent of the urethra into a hanging position and not by restoring a midurethral fulcrum and an alleged musculoelastic mechanism4 (a) The simplest invalidation of the PTT. Three theories/hypotheses, Enhörning, DeLancey, Bergström, rely on increased intraabdominal pressure acting to close the proximal urethra. A single question invalidates all three: "why does pushing down during micturition, which increases intraabdominal pressure, not stop urine flow; rather, it increases flow?" (b) The Integral Theory explains… the forward vector "PCM"… relaxes immediately before micturition; this allows the two posterior vectors LP/LMA, to actively open out the posterior urethral wall ("funneling"). Comment: (a) Healthy continent women can urinate by straining/pushing. The PCM and the connected posterior PUL are then voluntarily/intentionally relaxed, and the proximal urethra is pressed down to a hanging position. This is analogous to what occurs in SUI, which involves defective posterior PUL, when the proximal urethra is "unintentionally" pressed down. Without such a hanging mechanism that further funnels the proximal urethra, straining/pushing would only result in a zero-sum situation without any effect on bladder emptying as the Pabd is equally and simultaneously "transmitted" to both sides of the bladder neck. Thus, SUI occurs when the normal mechanism of urination by straining/pushing is unintentionally triggered. (b) It is unlikely that women, in normal micturition, use an anal muscle – the conjoined longitudinal anal muscle (LMA) - and two pelvic floor muscles (LP and PCM) to control bladder neck closure and opening considering that the bladder-urethra complex constitutes one organ with inherent internal mechanisms for closing, opening, relaxing, and contracting. According to the UHT, in normal micturition, the PCM, urethral circular smooth muscle and rahbdosphincter complex are relaxed and the BN is pulled open and funneled when the curved conjoined inner longitudinal smooth muscles of the bladder and urethra—which are innervated by parasympathetic nerves—contract/shorten and straighten. After cessation of urine flow, the urethra is closed by recoiling its intrinsic structures and resuming the muscle tonus of the PCM.8 It is also unlikely that, during stress, the LMA which consists primarily of smooth muscle fibers situated between the external and internal anal sphincter muscles and surrounds the anal canal, is responsible for the force that executes the partly forward rotational movement seen in SUI; especially as the force vector of the concurrently contracting LP has nearly the opposite direction. According to the UHT, during stress, the anterior vaginal wall/urethra is pressed down by the Pabd, and not pulled down by posterior muscle forces (LMA and LP).9 MUS operation in 1997. There was no elevation of bladder neck on ultrasound, no increase in midurethral pressure. The return of continence after the MUS was explained by tighter closure of the urethra, thus exponentially increasing the internal urethral resistance to flow from the bladder. Comment: Urethra is closed by recoiling, pressure transmission, the GR, and a tight urogenital hiatus. The Pabd is always 100% transmitted to the bladder neck and proximal urethra; this is independent of bladder neck elevation/position. Whether the sMUP is high or low is irrelevant to the opening the meatus internus. A musculoelastic mechanism that further increases urethral pressure/resistance is not required. The cure requires the prevention of bladder neck and proximal urethral funneling. MUS surgery cures SUI by preventing the urethra from hanging on a less mobile bladder neck, and not by restoring a fulcrum/musculoelastic mechanism. The evidence alleged to invalidate Enhörning's PTT violate Pascal's hydrostatic law and are irrelevant.10
Source: Neurourology and Urodynamics
DOI: 10.1002/nau.25312
Author: Bo S. Bergström
Institution: Mora lasarett
Language: English
Subfield: Urology
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Estimated APC paid: $4,530
OpenAlex ID: W4387931048